PICU Doc On Call - SoundSage

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In this episode, Drs. Pradip Kamat, Monica Gray, and Rahul Damania talk through a heartbreaking case involving a 14-year-old girl with a history of psychiatric illness who intentionally took 45 tablets of metformin and empagliflozin. Things went downhill quickly—she developed severe lactic acidosis, hypoglycemia, acute kidney injury, and eventually suffered a cardiac arrest that required ECMO and continuous dialysis. Sadly, even with the most aggressive care, she didn’t make it. The doctors walk listeners through the pharmacology and toxicity of metformin and empagliflozin, discuss how these drugs can cause harm, and share key management strategies. They really stress the importance of early recognition, using extracorporeal therapies, and working as a multidisciplinary team when dealing with severe pediatric overdoses of antidiabetic medications.

Show Highlights:

Case study of a 14-year-old girl with intentional ingestion of an oral antidiabetic agent
Presentation of severe lactic acidosis, hypoglycemia, acute kidney injury, and cardiac arrest
Discussion of the pharmacology and toxicology of metformin and empagliflozin
Mechanisms of metformin toxicity and its effects on metabolic processes
Differentiation between types of lactic acidosis related to metformin
Importance of early recognition and management of metformin toxicity
Supportive care strategies for managing severe metformin overdose
Role of extracorporeal therapies, including ECMO and dialysis, in treatment
Multidisciplinary approach involving intensivists, nephrologists, and toxicologists
Clinical implications and outcomes of severe metformin toxicity in pediatric patients

Resources:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter: Nothing found
Reference 1: Noites I, Figueiredo M, Shchomak Z, Boto L, Camilo C. Fatal Pediatric Metformin-Associated Lactic Acidosis: When Severity Goes Unnoticed. Cureus. 2026 Feb 16;18(2):e103719.
Reference 2: Bebarta VS, Pead J, Varney SM. Lacticemia After Acute Overdose of Metformin in an Adolescent Managed Without Intravenous Sodium Bicarbonate or Extracorporeal Therapy. Pediatr Emerg Care. 2015 Aug;31(8):589-90.

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In this episode of Pediatric Critical Care Insights, Dr. Monica Gray and Dr. Pradip Kamat chat about how capnography, specifically end-tidal CO2 monitoring, is used in the pediatric ICU. They walk through a real-life case of a 9-year-old with respiratory failure from influenza A, showing how ETCO2 monitoring helps confirm endotracheal tube placement, guides ventilation, spots cardiac arrest, and even helps assess the quality of CPR. Along the way, they break down how to interpret capnography waveforms, discuss different types of devices, and explain the key physiological concepts. The episode is packed with practical, bedside tips for intensivists caring for critically ill kids.

Show Highlights:

Importance of capnography (end-tidal CO2 monitoring) in the pediatric intensive care unit (PICU)
Clinical case study of a 9-year-old boy with respiratory failure due to influenza A
Use of capnography for confirming endotracheal tube placement and assessing ventilation status
Detection of cardiac arrest and guidance for CPR quality through ETCO2 monitoring
Overview of capnography physics and physiology, including terminology distinctions
Types of capnography: mainstream vs. sidestream, and their applications in pediatric patients
Assumptions for accurate ETCO2 approximation of arterial CO2 and conditions affecting this relationship
Analysis of capnography waveform phases and their clinical significance
Prognostic value of ETCO2 during cardiac arrest and its correlation with patient outcomes
Practical applications of ETCO2 monitoring in critical care, focusing on airway, breathing, and circulation management

References:

Noninvasive respiratory monitoring and assessment of gas exchange. David F. Butler; Kenneth A. Schenkman. Fuhrman and Zimmerman's Pediatric Critical Care, 43, 483-491.e3
Humphreys S, Schibler A, von Ungern-Sternberg BS. Carbon dioxide monitoring in children—A narrative review of physiology, value, and pitfalls in clinical practice. Pediatr Anaesth. 2021;31:839–845. https://doi.org/10.1111/pan.14208
Lasa JJ, Dhillon GS, Duff JP, et al. Part 8: Pediatric Advanced Life Support: 2025 American Heart Association and American Academy of Pediatrics Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Pediatrics. 2026;157(1):e2025074351
O'Flaherty. Capnography: principles and practice. London: BMJ Publishing Group; 1994.
Aminiahidashti H, Shafiee S, Zamani Kiasari A, Sazgar M. Applications of End-Tidal Carbon Dioxide (ETCO2) Monitoring in Emergency Department; a Narrative Review. Emerg (Tehran). 2018;6(1):e5. Epub 2018 Jan 15. PMID: 29503830; PMCID: PMC5827051.

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In this special episode of PICU Doc on Call, hosts Dr. Monica Gray and Dr. Rahul Damania welcome new pediatric critical care fellows across the U.S. with practical advice for day one of fellowship. Joined by third-year PICU fellow Dr. Alexandra Bryant, the episode covers three key areas: navigating PICU logistics, protecting mental health, and managing the overwhelming volume of critical care knowledge. Dr. Bryant shares candid insights from her own training journey, offering actionable strategies for success. The hosts remind listeners that fellowship is a learning process and that new fellows can make a meaningful impact.

Show Highlights

Introduction to pediatric critical care fellowship for new fellows and learners
Key insights and advice for first-year fellows in pediatric intensive care
Importance of understanding logistics in the PICU environment
Strategies for effective communication and collaboration within the PICU team
Managing mental health and self-care during fellowship
Techniques for absorbing and retaining vast knowledge in pediatric critical care
Recommendations for organizing study materials and resources
Emphasis on lifelong learning and accessing information effectively
Practical tips for time management and responsibility organization
Suggested resources for mindfulness and emotional support in medical training

Resource:

PICU Doc on Call Episode 31

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In this episode of PICU Doc on Call Shorts, pediatric ICU physicians Dr. Pradip Kamat and Dr. Rahul Damania discuss respiratory time constants and their clinical relevance in pediatric critical care. Using a case of a six-year-old with near-fatal status asthmaticus on mechanical ventilation, they explain how prolonged time constants from high airway resistance cause air trapping, dynamic hyperinflation, and intrinsic PEEP. They emphasize recognizing these issues through ventilator waveforms and highlight that increasing respiratory rate can worsen hypercapnia in obstructive disease. Key management strategies include reducing respiratory rate, extending expiratory time, and accepting permissive hypercapnia to ensure hemodynamic stability.

Show Highlights

Respiratory time constants and their clinical significance in pediatric patients
Case study of a six-year-old boy with near-fatal status asthmaticus
Management of severe obstructive respiratory failure in pediatric patients
Understanding airway resistance and lung compliance in relation to time constants
Impact of ventilator settings on patient outcomes, including air trapping and intrinsic PEEP
Importance of adequate expiratory time to prevent dynamic hyperinflation
Recognizing signs of inadequate expiratory time in mechanically ventilated patients
Strategies for managing hypercapnia and optimizing ventilator settings
Differences in time constants related to various pediatric respiratory conditions
Key takeaways for pediatric critical care practice and ventilator management

References1. Depta F, Kallet RH, Gentile MA, Kassis EN. Expiratory time constants in mechanically ventilated patients: rethinking the old concept — a narrative review. Intensive Care Medicine Experimental. 2025;13:40. The review summarizes the definition of expiratory time constant, the relationship to resistance and compliance, the 63/86/95/98/99% rule, and clinical applications in obstructive and acute lung injury states. 2. Depta F, et al. Six methods to determine expiratory time constants in mechanically ventilated patients: a prospective observational physiology study. Intensive Care Medicine Experimental. 2024. This study describes expiratory time constant as a parameter that can guide respiratory rate and I:E adjustment to support complete exhalation. 3. Alibrahim O, Rehder KJ, Miller AG, Rotta AT. Mechanical Ventilation and Respiratory Support in the Pediatric Intensive Care Unit. Pediatric Clinics of North America. 2022;69(3):587–605. This pediatric review specifically discusses passive exhalation, the expiratory time constant, and why asthma and bronchiolitis require longer expiratory times to avoid gas trapping. 4. Arnal JM. Monitoring respiratory mechanics in mechanically ventilated patients. Hamilton Medical Knowledge Base. This source provides a practical bedside description of time constants, waveform-based respiratory mechanics, and typical RCexp ranges, while emphasizing dependence on resistance and compliance. 5. Emeriaud G, López-Fernández YM, Iyer NP, et al.; PALICC-2 Group; PALISI Network. Executive summary of the second international guidelines for the diagnosis and management of pediatric ARDS. Pediatric Critical Care Medicine. 2023;24(2):143–168. The PALICC-2 guideline framework supports lung-protective ventilation in PARDS, including attention to tidal volume, PEEP, plateau pressure, and driving pressure.

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In this episode of PICU Doc on Call, hosts Dr. Monica Gray and Dr. Pradip Kamat explore procedural sedation in the pediatric ICU. They cover sedation levels, pre-screening, risk stratification using ASA classifications, and medication selection tailored to each patient's hemodynamic and respiratory status. Through real-world case discussions involving respiratory failure, septic shock, and acute neurological decline, they highlight the importance of end-tidal CO2 monitoring and early adverse event recognition. Key takeaways include avoiding the term "conscious sedation," preparing rescue plans, and prioritizing patient safety through careful assessment and monitoring.

Show Highlights:

Definitions and levels of sedation (minimal, moderate, deep sedation, and general anesthesia)
Importance of terminology in procedural sedation
Monitoring sedation levels using scales like the Richmond Agitation-Sedation Scale (RASS)
Pre-screening and risk stratification considerations for pediatric patients
ASA physical status classification system for assessing patient risk
Unique challenges of procedural sedation in critically ill children
Adverse events associated with pediatric procedural sedation, particularly respiratory complications
Management strategies for specific cases requiring sedation (e.g., respiratory failure, septic shock)
Importance of end-tidal CO2 monitoring during sedation
Key takeaways for safe sedation practices in the pediatric ICU setting

References:

Nir Atlas; Rahul C. Damania; Pradip P. Kamat In Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 135, 1624-1628
Statement on Continuum of Depth of Sedation: Definition of General Anesthesia and Levels of Sedation/Analgesia by Committee on Quality Management and Departmental Administration. Last Amended: October 23, 2024.
Coté CJ, Wilson S; AMERICAN ACADEMY OF PEDIATRICS; AMERICAN ACADEMY OF PEDIATRIC DENTISTRY. Guidelines for Monitoring and Management of Pediatric Patients Before, During, and After Sedation for Diagnostic and Therapeutic Procedures. Pediatrics. 2019 Jun;143(6):e20191000. doi: 10.1542/peds.2019-1000. PMID: 31138666.x
Krauss B, Green SM. Procedural sedation and analgesia in children. Lancet. 2006 Mar 4;367(9512):766-80. doi: 10.1016/S0140-6736(06)68230-5. PMID: 16517277.
Sharif S, Kang J, Sadeghirad B, Rizvi F, Forestell B, Greer A, Hewitt M, Fernando SM, Mehta S, Eltorki M, Siemieniuk R, Duffett M, Bhatt M, Burry L, Perry JJ, Petrosoniak A, Pandharipande P, Welsford M, Rochwerg B. Pharmacological agents for procedural sedation and analgesia in the emergency department and intensive care unit: a systematic review and network meta-analysis of randomised trials. Br J Anaesth. 2024 Mar;132(3):491-506. doi: 10.1016/j.bja.2023.11.050. Epub 2024 Jan 6. PMID: 38185564.
Smith, Heidi A. B. MD, MSCI (Chair)1,2; Besunder, James B. DO, FCCM3,4; Betters, Kristina A. MD1; Johnson, Peter N. PharmD, BCPS, BCPPS, FCCM, FPPA, FASHP5,6; Srinivasan, Vijay MBBS, MD, FCCM7,8; Stormorken, Anne MD9,10; Farrington, Elizabeth PharmD, FCCM11; Golianu, Brenda MD12,13; Godshall, Aaron J. MD14; Acinelli, Larkin CPNP-AC, ACHPN15; Almgren, Christina CPNP16; Bailey, Christine H. MD17; Boyd, Jenny M. MD18,19; Cisco, Michael J. MD20; Damian, Mihaela MD, MPH21,22; deAlmeida, Mary L. MD23,24; Fehr, James MD13,25; Fenton, Kimberly E. MD, FCCM14; Gilliland, Frances DNP, CPNP-AC/PC26,27; Grant, Mary Jo C. CPNP-AC, PhD, FAAN28; Howell, Joy MD29; Ruggles, Cassandra A. PharmD, BCCCP, BCPPS30; Simone, Shari DNP31,32; Su, Felice MD21,22; Sullivan, Janice E. MD33,34; Tegtmeyer, Ken MD, FAAP, FCCM35,36; Traube, Chani MD, FCCM29; Williams, Stacey CPNP-AC37; Berkenbosch, John W. MD, FAAP, FCCM (Chair)33,34. 2022 Society of Critical Care Medicine Clinical Practice Guidelines on Prevention and Management of Pain, Agitation, Neuromuscular Blockade, and Delirium in Critically Ill Pediatric Patients With Consideration of the ICU Environment and Early Mobility. Pediatric Critical Care Medicine 23(2):p e74-e110, February 2022. | DOI: 10.1097/PCC.0000000000002873
Benzoni T, Agarwal A, Cascella M. Procedural Sedation. [Updated 2025 Mar 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2026 Jan-. Available from:https://www.ncbi.nlm.nih.gov/books/NBK551685/
Kerson AG, DeMaria R, Mauer E, Joyce C, Gerber LM, Greenwald BM, Silver G, Traube C. Validity of the Richmond Agitation-Sedation Scale (RASS) in critically ill children. J Intensive Care. 2016 Oct 26;4:65. doi: 10.1186/s40560-016-0189-5. PMID: 27800163; PMCID: PMC5080705.
Tel-Dan SF, Shavit D, Nates R, Samuel N, Shavit I. Emergency Physician-Administered Sedation for Thoracostomy in Children With Pleuropneumonia. Pediatr Emerg Care. 2021 Dec 1;37(12):e1209-e1212. doi: 10.1097/PEC.0000000000001975. PMID: 31929389.
Cosgrove P, Krauss BS, Cravero JP, Fleegler EW. Predictors of Laryngospasm During 276,832 Episodes of Pediatric Procedural Sedation. Ann Emerg Med. 2022 Dec;80(6):485-496. doi: 10.1016/j.annemergmed.2022.05.002. Epub 2022 Jun 23. PMID: 35752522.
Cravero JP, Blike GT, Beach M, Gallagher SM, Hertzog JH, Havidich JE, Gelman B; Pediatric Sedation Research Consortium. Incidence and nature of adverse events during pediatric sedation/anesthesia for procedures outside the operating room: report from the Pediatric Sedation Research Consortium. Pediatrics. 2006 Sep;118(3):1087-96. doi: 10.1542/peds.2006-0313. PMID: 16951002.

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In this episode of PICU Doc on Call, Dr. Monica Gray and Dr. Pradip Kamat are joined by fellow Dr. Hope Vancleve to discuss a complex case of a 12-year-old with MRSA septic shock requiring VA ECMO. The conversation covers sepsis-induced myocardial dysfunction, including its pathophysiology, diagnosis, and management. The hosts also explore differential hypoxia, or Harlequin syndrome, a serious VA ECMO complication causing upper body deoxygenation, and discuss monitoring strategies and circuit reconfiguration to prevent cerebral and myocardial ischemia.

Show Highlights:

Clinical case discussion of a 12-year-old male patient with MRSA septic shock.
Complications of sepsis, including sepsis-induced myocardial dysfunction and refractory shock.
Management strategies for septic shock, including antibiotic therapy and fluid resuscitation.
Use of venoarterial ECMO support in pediatric patients with severe cardiac dysfunction.
Pathophysiology of sepsis-induced myocardial dysfunction and its impact on cardiac function.
Differential hypoxia (North-South syndrome) in patients on femoral VA ECMO.
Diagnostic approaches for sepsis-induced myocardial dysfunction, including echocardiography and biomarkers.
Importance of monitoring and managing end-organ function in septic patients.
Strategies for addressing differential hypoxia in ECMO patients, including circuit reconfiguration.
Discussion of the risks and benefits of various ECMO configurations and management techniques.

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter
Reference 1: Torre DE, Pirri C. Harlequin Syndrome in Venoarterial ECMO and ECPELLA: When ECMO and Native or Impella Circulations Collide - A Comprehensive Review. Rev Cardiovasc Med. 2025 Aug 26;26(8):39992. doi: 10.31083/RCM39992. PMID: 40927093; PMCID: PMC12415751.
Reference 2 : Cove ME. Disrupting differential hypoxia in peripheral veno-arterial extracorporeal membrane oxygenation. Crit Care. 2015 Jul 22;19(1):280. doi: 10.1186/s13054-015-0997-3. PMID: 27391473; PMCID: PMC4511033.

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In this episode of PICU Doc on Call, hosts Dr. Monica Gray and Dr. Pradip Kamat discuss a 15-year-old girl who attempted suicide by ingesting rat poison, acetaminophen, ibuprofen, and amlodipine. The episode focuses on long-acting anticoagulant rodenticides (LAARs), such as brodifacoum, which inhibit vitamin K epoxide reductase, causing delayed coagulopathy. Key topics include clinical presentation, diagnostic evaluation, and management, emphasizing vitamin K1 as the primary antidote and prothrombin complex concentrate or fresh-frozen plasma for major bleeding. The patient stabilized with aggressive supportive care, including vasoactive agents and NAC therapy, alongside psychiatric intervention. Listen to learn more!

Show Highlights

Clinical case of a 15-year-old girl who attempted suicide through polypharmacy ingestion
Ingestion of multiple substances, including chewable rat poison, acetaminophen, ibuprofen, and amlodipine
Discussion of toxicology related to long-acting anticoagulant rodenticides (LAARs) like brodifacoum
Symptoms and clinical presentation following acute ingestion, including metabolic acidosis and elevated lactate
Diagnostic evaluation and laboratory findings, including coagulation studies and liver function tests
Management strategies for LAAR poisoning, including the use of vitamin K and supportive care
Importance of monitoring for delayed coagulopathy and serial INR testing
Consideration of calcium channel blocker toxicity in the context of the patient's clinical instability
Overview of the mechanisms of action of LAARs and their impact on vitamin K-dependent clotting factors
Key take-home points regarding the recognition and management of rodenticide ingestion in pediatric patients

References

Reference: King N, Tran MH. Long-Acting Anticoagulant Rodenticide (Superwarfarin) Poisoning: A Review of Its Historical Development, Epidemiology, and Clinical Management. Transfus Med Rev. 2015 Oct;29(4):250-8.

Reference 2: Feinstein DL, Akpa BS, Ayee MA, et al. The emerging threat of superwarfarins: history, detection, mechanisms, and countermeasures. Ann N Y Acad Sci. 2016 Jun;1374(1):111-22.

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In this episode of PICU Doc on Call, Dr. Monica Gray and Dr. Pradip Kamat chat about flexible fiberoptic bronchoscopy (FFB) in the pediatric ICU. They walk through a case involving an eight-year-old who’s dealing with respiratory failure after a stem cell transplant. Along the way, they talk about when and why you might use bronchoscopy both for diagnosis and treatment—plus how to approach sedation and what effects the procedure can have on the heart and lungs. They also dive into important topics like managing hypoxia, handling increased airway and pulmonary vascular resistance, and what to keep in mind if your patient has a traumatic brain injury. The episode wraps up with tips for managing fever after the procedure and a quick look at how rigid bronchoscopy compares.

Show Highlights:

Use of flexible fiberoptic bronchoscopy (FFB) in the pediatric ICU (PICU)
Indications for performing bronchoscopy (diagnostic and therapeutic)
Management of sedation and analgesia during bronchoscopy
Cardiovascular effects associated with bronchoscopy procedures
Respiratory effects and complications during bronchoscopy
Special considerations for bronchoscopy in patients with traumatic brain injury (TBI)
Post-procedure complications, including fever and its management
Overview of rigid bronchoscopy and its indications
Importance of understanding physiological changes during bronchoscopy
Educational focus on acute pediatric care for current and aspiring PICU interns

References:

Reference 1: Sachdev A, Chhawchharia R. Flexible Fiberoptic Bronchoscopy in Pediatric Practice. Indian Pediatr. 2019 Jul 15;56(7):587-593. PMID: 31333214.

Reference 2: Li SX, Tao XF, Wu HJ, Jin F, Zhu GH, Wang YS, Tang LF, Chen ZM, Wu L. Advances in pediatric flexible bronchoscopy. World J Pediatr. 2025 Oct;21(10):945-956. doi: 10.1007/s12519-025-00967-7. Epub 2025 Oct 4. PMID: 41045338; PMCID: PMC12578761.

Reference 3: Truitt BA, Kasi AS, Kamat PP, Fundora MP, Simon DM, Guglani L. Cryoextraction via flexible bronchoscopy in children with tracheobronchial obstruction. Pediatr Pulmonol. 2023 Sep;58(9):2527-2534. doi: 10.1002/ppul.26540. Epub 2023 Jun 23. PMID: 37350368.

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In this episode of "PICU Doc on Call," Drs. Monica Gray and Pradip Kamat from Children's Healthcare of Atlanta dive into the use of inhaled anesthetics, especially isoflurane, in the pediatric ICU. We’re focusing on those tough cases: refractory status asthmaticus and status epilepticus.

We’ll chat about why isoflurane is our go-to over other agents like sevoflurane, desflurane, or nitrous oxide, and break down its bronchodilatory and anticonvulsant properties. We’ll also touch on important pharmacology concepts, such as MAC and the blood-gas partition coefficient, and discuss how we approach dosing and ventilator management when using isoflurane.

Of course, we’ll also discuss the potential adverse effects that can come with prolonged use, and why it’s important to stop other sedatives and beta-agonists once you start isoflurane. Join us as we walk through the practical aspects and pearls for using inhaled anesthetics in the PICU!

Show Highlights:

Use of inhaled anesthetics in pediatric intensive care units (PICU)
Focus on isoflurane for managing refractory status asthmaticus and status epilepticus
Comparison of inhaled anesthetic agents: isoflurane, sevoflurane, nitrous oxide, and desflurane
Importance of minimum alveolar concentration (MAC) and blood-gas partition coefficient in anesthetic pharmacodynamics
Mechanism of action of isoflurane in airway management and bronchodilation
Clinical administration techniques for isoflurane in critically ill children
Ventilator management principles for intubated children with status asthmaticus
Role of isoflurane in refractory and super-refractory status epilepticus
Potential adverse effects and considerations for prolonged isoflurane use
Summary of pharmacologic concepts essential for safe isoflurane therapy in pediatric patients

References:

Rogers Text Book of Pediatric Intensive Care: Chapter 47: Acute Severe Asthma. Stewart C, Brilli RJ. pages 763-775
Reference 1: Stetefeld HR, Schaal A, Scheibe F, Nichtweiß J, Lehmann F, Müller M, Gerner ST, Huttner HB, Luger S, Fuhrer H, Bösel J, Schönenberger S, Dimitriadis K, Neumann B, Fuchs K, Fink GR, Malter MP; IGNITE Study Group, with support from the German Neurocritical Care Society (DGNI). Isoflurane in (Super-) Refractory Status Epilepticus: A Multicenter Evaluation. Neurocrit Care. 2021 Dec;35(3):631-639. doi: 10.1007/s12028-021-01250-z. Epub 2021 Jul 20. PMID: 34286464; PMCID: PMC8692280.
Reference 2: Zeiler FA, Zeiler KJ, Teitelbaum J, Gillman LM, West M. Modern inhalational anesthetics for refractory status epilepticus. Can J Neurol Sci. 2015 Mar;42(2):106-15. doi: 10.1017/cjn. 2014.121. Epub 2015 Jan 9. PMID: 25572922.
Reference 3: Werner HA. Status asthmaticus in children: a review. Chest. 2001 Jun;119(6):1913-29. doi: 10.1378/chest. 119.6.1913. PMID: 11399724.
Reference 4: Gill B, Bartock JL, Damuth E, Puri N, Green A. Case report: Isoflurane therapy in a case of status asthmaticus requiring extracorporeal membrane oxygenation. Front Med (Lausanne). 2022 Nov 8;9:1051468. doi: 10.3389fmed. .2022.1051468. PMID: 36425104; PMCID: PMC9679515.

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In this episode of PICU Doc on Call, Drs. Monica Gray, Pradip Kamat, and Rahul Damania chat about a 17-year-old girl who ended up with acute liver failure after she intentionally took 22.5 grams of acetaminophen. She came in 48 hours later with really high transaminases and an INR of 5.5, so she was admitted to the PICU. The hosts break down how acetaminophen affects the body, walk through its four clinical stages, and discuss how to manage it—focusing on N-acetylcysteine as the primary antidote. They also touch on other treatments, like fomepizole. Thankfully, this patient recovered without needing a liver transplant, which really shows how important it is to have a team approach with intensivists, hepatologists, toxicologists, and psychiatry all working together.

Show Highlights:

Clinical case presentation of a 17-year-old girl with acetaminophen ingestion leading to acute liver failure
Mechanism of acetaminophen toxicity and its metabolic pathways
Epidemiology of acetaminophen toxicity in pediatric populations
Pathophysiology of acetaminophen overdose and its effects on liver function
Clinical manifestations and progression of acetaminophen toxicity through various stages
Evaluation and diagnostic criteria for assessing acetaminophen toxicity
Management strategies for acetaminophen overdose, including the use of N-acetylcysteine (NAC).
Discussion of adjunctive therapies such as fomepizole in severe cases.
Importance of supportive care in managing complications of acute liver failure
An interdisciplinary approach to treatment involving various medical specialties

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter ***.

Reference 1: 2019 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 37th Annual Report. Gummin DD, Mowry JB, Beuhler MC, Spyker DA, Brooks DE, Dibert KW, Rivers LJ, Pham NPT, Ryan ML. Clin Toxicol (Phila). 2020;58(12):1360.

Reference 2: Pepin L, Matsler N, Fontes A, Heard K, Flaherty BF, Monte AA. Fomepizole Therapy for Acetaminophen-Induced Liver Failure in an Infant. Pediatrics. 2023 Oct 1;152(4):e2022061033. doi:10.1542/peds. 2022-061033. PMID: 37681263.

Reference 3. Chiew AL, Buckley NA. Acetaminophen Poisoning. Crit Care Clin. 2021 Jul;37(3):543-561.

Reference 4. Squires JE, Alonso EM, Ibrahim SH, Kasper V, Kehar M, Martinez M, Squires RH. North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition Position Paper on the Diagnosis and Management of Pediatric Acute Liver Failure. J Pediatr Gastroenterol Nutr. 2022 Jan 1;74(1):138-158. doi: 10.1097/MPG.0000000000003268. PMID: 34347674.

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In this episode of "PICU Doc on Call," Drs. Monica Gray, Pradip Kamat, and Rahul Damania discuss the use of intranasal medications in pediatric intensive care. Using the case of a four-month-old infant needing an MRI, they explore when and why intranasal drugs are preferred over IV access, the science behind nasal drug delivery, safe administration techniques, and common medications used. The episode highlights the benefits of intranasal sedation—such as rapid onset and needle-free delivery—while emphasizing teamwork and careful monitoring for safe, effective pediatric care.

Show Highlights:

Use of intranasal medications in pediatric intensive care settings
Case study of a four-month-old infant requiring sedation for an MRI.
Advantages of intranasal delivery over IV access
Pharmacokinetics and neuroanatomy related to intranasal drug absorption
Techniques for safe and effective administration of intranasal medications
Comparison of intranasal dosing to oral and IV routes
Common intranasal medications used in the pediatric ICU
Importance of timing and monitoring during sedation procedures
Teamwork and communication in administering intranasal medications
Clinical applications and implications for patient comfort and care delivery

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter ***.
Reference 1: Tsze DS, Woodward HA, McLaren SH, Leu CS, Venn AMR, Hu NY, Flores-Sanchez PL, Stefan BR, Shen ST, Ekladios MJ, Cravero JP, Dayan PS. Optimal Dose of Intranasal Midazolam for Procedural Sedation in Children: A Randomized Clinical Trial. JAMA Pediatr. 2025 Sep 1;179(9):979-986. doi: 10.1001/jamapediatrics. 2025.2181.
Reference 2: Prescott MG, Iakovleva E, Simpson MR, Pedersen SA, Munblit D, Vallersnes OM, Austad B. Intranasal analgesia for acute moderate to severe pain in children - a systematic review and meta-analysis. BMC Pediatr. 2023 Aug 18;23(1):405. doi: 10.1186/s12887-023-04203-x.
Reference 3: Chabowski L, Mahboobi Z, Navolokina A. Intranasal ketamine for procedural sedation in children. Am J Emerg Med. 2023 Jun;68:195. doi: 10.1016/j.ajem.2023.04.013.
Reference 4: Sulton C, Kamat P, Mallory M, Reynolds J. The Use of Intranasal Dexmedetomidine and Midazolam for Sedated Magnetic Resonance Imaging in Children: A Report From the Pediatric Sedation Research Consortium. Pediatr Emerg Care. 2020 Mar;36(3):138-142. doi: 10.1097/PEC.0000000000001199.

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In this special “PICU Doc On Call Shorts” episode, pediatric ICU physicians Dr. Monica Gray, Dr. Pradip Kamat, and Dr. Rahul Damania break down the concept of Mean Arterial Pressure (MAP). Using a case of a six-year-old in septic shock, they discuss how to calculate MAP, normal pediatric values, and the physiological determinants and clinical significance of MAP. The hosts highlight MAP’s role in guiding management of critically ill children, review autonomic and endothelial regulation, and reinforce learning with a board-style question. This episode emphasizes practical bedside application for pediatric interns and ICU providers.

Show Highlights:

Overview of Mean Arterial Pressure (MAP) and its clinical significance in pediatric critical care.
Introduction of a clinical case involving a 6-year-old child in septic shock.
Explanation of the formula for calculating MAP and its application to the clinical case.
Discussion of normal reference values for MAP in children and their clinical implications.
Physiological determinants of MAP, including cardiac output and systemic vascular resistance.
Role of the autonomic nervous system in regulating MAP through baroreceptor reflexes.
Importance of maintaining adequate MAP for organ perfusion, particularly in critically ill patients.
Clinical applications of MAP monitoring and management strategies in the PICU.
Summary of key takeaways regarding MAP calculation, physiological determinants, and clinical relevance.
Mention of related topics, such as invasive versus non-invasive blood pressure monitoring.

References:

DeMers D, Wachs D. Physiology, Mean Arterial Pressure. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing.
Pediatric Blood Pressure Metrics and Hypotension Thresholds (details the task force data used to derive the 5th and 50th percentile MAP estimation formulas for children)
Berlin DA, Bakker J. Starling curves and central venous pressure. Crit Care. 2015 Feb 16;19(1):55.
Magder S. Volume and its relationship to cardiac output and venous return. Crit Care. 2016 Sep 10;20(1):271

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In this episode of "PICU Doc on Call," Drs. Pradip Kamat and Rahul Damania dive into a pediatric ICU case involving a 4-year-old girl who presents with severe anemia and bleeding, ultimately diagnosed with von Willebrand disease (VWD). They chat about the causes and different types of VWD, walk through the key clinical features, and break down how to diagnose and manage this condition. Drs. Kamat and Damania highlight the important roles of desmopressin and factor concentrates in treatment. Throughout the episode, they stress the need to recognize VWD in kids who have mucosal bleeding and offer practical tips for intensivists on lab evaluation and treatment strategies for this common inherited bleeding disorder.

Show Nighlights:

Clinical case discussion of a 4-year-old girl with severe anemia and bleeding symptoms
Diagnosis of von Willebrand disease (VWD) and its significance in pediatric critical care
Etiology and pathogenesis of von Willebrand disease
Classification of von Willebrand disease into types (Type 1, Type 2 with subtypes, Type 3)
Clinical manifestations and symptoms associated with VWD
Diagnostic approach for identifying von Willebrand disease, including laboratory tests
Management strategies for VWD, including desmopressin and von Willebrand factor concentrates
Role of adjunctive therapies such as antifibrinolytics and hormonal treatments
Importance of multidisciplinary collaboration in managing complex bleeding disorders
Overview of the pathophysiology of von Willebrand factor and its role in hemostasis

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter ***.
Reference 1: Leebeek FW, Eikenboom JC. Von Willebrand's Disease. N Engl J Med. 2016 Nov 24;375(21):2067-2080.
Reference 2: Ng C, Motto DG, Di Paola J. Diagnostic approach to von Willebrand disease. Blood. 2015 Mar 26;125(13):2029-37.
Platton S, Baker P, Bowyer A, et al. Guideline for laboratory diagnosis and monitoring of von Willebrand disease: A joint guideline from the United Kingdom Haemophilia Centre Doctors' Organisation and the British Society for Hematology. Br J Haematol 2024 May;204(5):1714-1731.
Mohinani A, Patel S, Tan V, Kartika T, Olson S, DeLoughery TG, Shatzel J. Desmopressin as a hemostatic and blood-sparing agent in bleeding disorders. Eur J Haematol. 2023 May;110(5):470-479. doi: 10.1111/ejh.13930. Epub 2023 Feb 12. PMID: 36656570; PMCID: PMC10073345.

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In this episode of "PICU Doc On Call," Drs. Pradip Kamat and Rahul Damania discuss the acute management of a 14-year-old boy with severe rectal bleeding and hypertension, ultimately diagnosed with inflammatory bowel disease (IBD). They review the approach to pediatric lower GI bleeding, diagnostic workup, and imaging, emphasizing early recognition and resuscitation. They outline IBD management, including steroids, biologics such as infliximab, and nutritional support, while highlighting the importance of screening for infections before immunosuppression. The episode provides practical insights for PICU physicians on handling acute GI emergencies in children.

Show Nighlights:

Clinical case of a 14-year-old male with hypertension and rectal bleeding.
Diagnosis of inflammatory bowel disease (IBD) following significant blood loss.
Approach to pediatric rectal bleeding and its implications.
Diagnostic workup including laboratory tests and imaging modalities.
Management strategies for IBD in acute pediatric care.
Importance of early recognition and resuscitation in cases of shock.
Physiological principles related to blood loss and shock in children.
Differential diagnoses for lower gastrointestinal bleeding in pediatrics.
Initial evaluation and stabilization protocols for pediatric patients.
Nutritional support and multidisciplinary care in managing IBD.

References:

Romano C, Oliva S, Martellossi S, et al. Pediatric gastrointestinal bleeding: Perspectives from the Italian Society of Pediatric Gastroenterology. World J Gastroenterol. 2017;23(8):1326-1337.
Pai AK, Fox VL. Gastrointestinal bleeding and management. Pediatr Clin North Am. 2017;64(3):543-561.
Padilla BE, Moses W. Lower gastrointestinal bleeding and intussusception. Surg Clin North Am. 2017;97(1):63-80.
Kaur M, Dalal RL, Shaffer S, Schwartz DA, Rubin DT. Inpatient management of inflammatory bowel disease-related complications. Clin Gastroenterol Hepatol. 2020;18(11):2417-2428.
Ashton JJ, Ennis S, Beattie RM. Early-onset paediatric inflammatory bowel disease. Lancet Child Adolesc Health. 2017;1(2):147-158.
Bouhuys M, Lexmond WS, van Rheenen PF. Pediatric inflammatory bowel disease. Pediatrics. 2022;150(6):e2022059341.
Rosen MJ, Dhawan A, Saeed SA. Inflammatory bowel disease in children and adolescents. JAMA Pediatr. 2015;169(11):1053-1060.
Conrad MA, Rosh JR. Pediatric Inflammatory Bowel Disease. Pediatr Clin North Am. 2017 Jun;64(3):577-591.
Turner D, Ruemmele FM, Orlanski-Meyer E, et al. Management of Paediatric Ulcerative Colitis, Part 1: Ambulatory Care-An Evidence-based Guideline From European Crohn's and Colitis Organization and European Society of Paediatric Gastroenterology, Hepatology and Nutrition. J Pediatr Gastroenterol Nutr. 2018 Aug;67(2):257-291, correction can be found in J Pediatr Gastroenterol Nutr 2020 Dec;71(6):794.

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In this episode of "PICU Doc on Call," Dr. Pradip Kamat and Dr. Rahul Damania dive into a fascinating case of a 9-month-old infant who comes in with hypoglycemia and seizures. Together, they break down the basics of glucose metabolism, walk through the causes of hypoglycemia, and discuss the best diagnostic strategies and acute management steps. They put a special spotlight on using diazoxide for hyperinsulinemic hypoglycemia, discussing not only how it works but also its potential side effects. The conversation also discusses dietary interventions for metabolic disorders and highlights the importance of rapid diagnosis and personalized treatment.

Show Highlights:

Pediatric hypoglycemia and its implications in infants
Case study of a 9-month-old infant with hypoglycemia and seizures
Physiology of glucose metabolism and its regulation
Causes of hypoglycemia, categorized into primary and secondary etiologies
Diagnostic approaches for identifying the cause of hypoglycemia
Initial management strategies for acute hypoglycemia
Long-term treatment options based on underlying causes
Importance of timely diagnosis and intervention in the PICU setting
Pharmacologic management of hyperinsulinemic hypoglycemia, including the use of diazoxide
Multidisciplinary care and follow-up for pediatric patients with hypoglycemia

References:1. Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 84 Alder M et al. Pediatric Sepsis. Pages 1293-1309 2. Honarmand K, Sirimaturos M, Hirshberg EL, Bircher NG, Agus MSD, Carpenter DL, Downs CR, Farrington EA, Freire AX, Grow A, Irving SY, Krinsley JS, Lanspa MJ, Long MT, Nagpal D, Preiser JC, Srinivasan V, Umpierrez GE, Jacobi J. Society of Critical Care Medicine Guidelines on Glycemic Control for Critically Ill Children and Adults 2024. Crit Care Med. 2024 Apr 1;52(4):e161-e181. doi: 10.1097/CCM.0000000000006174. Epub 2024 Jan 19. PMID: 38240484. 3. Rosenfeld E, Thornton PS. Hypoglycemia in Neonates, Infants, and Children. 2023 Aug 22. In: Feingold KR, Ahmed SF, Anawalt B, Blackman MR, Boyce A, Chrousos G, Corpas E, de Herder WW, Dhatariya K, Dungan K, Hofland J, Kalra S, Kaltsas G, Kapoor N, Koch C, Kopp P, Korbonits M, Kovacs CS, Kuohung W, Laferrère B, Levy M, McGee EA, McLachlan R, Muzumdar R, Purnell J, Rey R, Sahay R, Shah AS, Singer F, Sperling MA, Stratakis CA, Trence DL, Wilson DP, editors. Endotext [Internet]. South Dartmouth (MA):MDText.com, Inc.; 2000–. PMID: 37665756. 4. Rayas MS, Salehi M. Non-Diabetic Hypoglycemia. 2024 Jan 27. In: Feingold KR, Ahmed SF, Anawalt B, Blackman MR, Boyce A, Chrousos G, Corpas E, de Herder WW, Dhatariya K, Dungan K, Hofland J, Kalra S, Kaltsas G, Kapoor N, Koch C, Kopp P, Korbonits M, Kovacs CS, Kuohung W, Laferrère B, Levy M, McGee EA, McLachlan R, Muzumdar R, Purnell J, Rey R, Sahay R, Shah AS, Singer F, Sperling MA, Stratakis CA, Trence DL, Wilson DP, editors. Endotext [Internet]. South Dartmouth (MA):MDText.com, Inc.; 2000–. PMID: 27099902. 5. Nakrani MN, Wineland RH, Anjum F. Physiology, Glucose Metabolism. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from:https://www.ncbi.nlm.nih.gov/books/NBK560599/ 6. Chen X, Feng L, Yao H, Yang L, Qin Y. Efficacy and safety of diazoxide for treating hyperinsulinemic hypoglycemia: A systematic review and meta-analysis. PLoS One. 2021 Feb 11;16(2):e0246463. doi: 10.1371/journal.pone.0246463. PMID: 33571197; PMCID: PMC7877589. 7. Kucharczyk P, Albano G, Deisl C, Ho TM, Bargagli M, Anderegg M, Wuest S, Konrad D, Fuster DG. Thiazides Attenuate Insulin Secretion Through Inhibition of Mitochondrial Carbonic Anhydrase 5b in β -Islet Cells in Mice. J Am Soc Nephrol. 2023 Jul 1;34(7):1179-1190. Doi: 10.1681/ASN.0000000000000122. Epub 2023 Apr 17. PMID: 36927842; PMCID: PMC10356162.

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Today, Dr. Monica Gray, Dr. Pradip Kamat, and Rahul Damania discuss a critical case involving a 10-year-old boy who developed post-intubation desaturation. Using the DOPE mnemonic (Displacement, Obstruction, Pneumothorax, Equipment failure), they systematically troubleshoot the emergency, highlighting the importance of teamwork, capnography, and manual ventilation. The team emphasizes structured approaches, simulation training, and essential bedside tools to ensure rapid, effective management of acute deterioration in intubated children, turning a life-threatening crisis into a controlled, solvable situation.

Show Highlights:

Clinical case discussion of a ten-year-old boy with post-intubation desaturation in the pediatric ICU
Use of the "DOPE" mnemonic (Displacement, Obstruction, Pneumothorax, Equipment failure) for troubleshooting
Systematic approaches in emergency situations in pediatric critical care
Assessment and management of sudden desaturation in intubated patients
Evaluation of potential causes of desaturation, including tube displacement and obstruction
Role of equipment failure in acute deterioration and strategies to address it
Significance of continuous capnography and manual ventilation techniques
Prevention strategies for unplanned extubation in pediatric ICU settings
Emphasis on teamwork, communication, and simulation training in crisis management
Review of literature insights related to hypoxemia and equipment issues in pediatric intubation

References:

Topjian AA, et al. Part 4: Pediatric Basic and Advanced Life Support—2020 AHA PALS Guidelines. Circulation. 2020.Foundational pediatric resuscitation guidance endorsing early switch to manual ventilation and structured troubleshooting for the deteriorating intubated child.
Cook TM, et al. Major complications of airway management in the UK: NAP4. British Journal of Anaesthesia. 2011.Seminal audit highlighting ICU/ED airway failures and the critical role of waveform capnography in preventing unrecognized esophageal intubation.
Volpicelli G, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Medicine. 2012. High-impact consensus placing lung ultrasound at the bedside to rapidly diagnose pneumothorax during post-intubation deterioration.
Prekker ME, et al. Video vs direct laryngoscopy for ED intubation—randomized trial. New England Journal of Medicine. 2023.NEJM RCT showing higher first-pass success with video laryngoscopy—relevant to preventing displacement/misplacement drivers of desaturation.
Chrimes N, et al. Preventing unrecognised oesophageal intubation: consensus guideline. Anaesthesia. 2022.Modern, practice-changing guidance: sustained waveform capnography is the mainstay to exclude esophageal placement and avert catastrophic hypoxemia.

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Welcome to "PICU Doc on Call," the podcast where the world of pediatric critical care comes alive! Today, Dr. Monica Gray, Dr. Pradip Kamat, and Rahul Damania delve into a fascinating case involving a 16-year-old male presenting with headache, photophobia, anemia, and cerebral venous thrombosis. After some detective work, the diagnosis? Paroxysmal nocturnal hemoglobinuria, or PNH.

Join us as we break down the pathogenesis and clinical features of PNH, walk through the diagnostic workup, and discuss management strategies, especially the game-changing role of complement inhibitors like Eculizumab. We’ll also review this patient’s clinical journey, highlighting the key pearls for recognizing and treating PNH in the pediatric intensive care unit.

So, tune in to hear more!

Show Highlights:

Clinical case presentation of a 16-year-old male with symptoms including headache, photophobia, and anemia
Diagnosis of paroxysmal nocturnal hemoglobinuria (PNH) and its clinical significance
Pathogenesis of PNH, including the role of the PIGA gene mutation and GPI-anchored proteins
Clinical features and complications associated with PNH, such as thrombosis and hemolysis
Diagnostic workup for PNH, including laboratory tests and flow cytometry
Management strategies for PNH, focusing on complement inhibitors like Eculizumab
Importance of supportive care in the PICU for patients with PNH
Discussion of emerging therapies and advancements in PNH treatment
Patient outcome and clinical course following treatment for PNH
Key takeaways regarding the diagnosis and management of PNH in pediatric intensive care

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care.
Reference 1: Brodsky RA. Paroxysmal nocturnal hemoglobinuria. Blood. 2014 Oct 30;124(18):2804-11.
Reference 2 Waheed A, Shammo J, Dingli D. Paroxysmal nocturnal hemoglobinuria: Review of the patient experience and treatment landscape. Blood Rev. 2024 Mar;64:101158.
Reference 3: Kokoris S, Polyviou A, Evangelidis P, Grouzi E, Valsami S, Tragiannidis K, Gialeraki A, Tsakiris DA, Gavriilaki E. Thrombosis in Paroxysmal Nocturnal Hemoglobinuria (PNH): From Pathogenesis to Treatment. Int. J. Mol. Sci. 2024 Nov 11;25(22):12104.

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In today’s episode, Dr. Monica Gray and Dr. Pradip Kamat sit down with neurosurgeon Dr. Neal Laxpati, MD, PhD, to chat about intracranial pressure (ICP) monitoring in pediatric critical care. Using real case studies, they dive into how and when to use external ventricular drains (EVDs) and ICP bolts, walking listeners through setup, potential risks, and everyday challenges. The group discusses device complications, ways to prevent infections, how to interpret waveforms, and shares practical bedside tips. It’s a must-listen for intensivists looking for hands-on advice and key insights to help optimize care for kids with brain injuries or hydrocephalus.

Show Highlights:

Pediatric critical care unit (PCU) case discussions
Intracranial pressure (ICP) monitoring in pediatric patients
Case studies involving a 10-year-old girl with diffuse midline glioma and a 16-year-old male with a ruptured arteriovenous malformation (AVM)
Cerebrospinal fluid (CSF) physiology and its role in ICP management
Types of ICP monitoring devices: external ventricular drains (EVDs) and intraparenchymal monitors
Indications and complications associated with ICP monitoring
Interpretation of ICP waveforms and their clinical significance
Management strategies for elevated ICP and CSF drainage
Risks and challenges of ICP monitoring, including infection and device malfunction
Importance of interdisciplinary communication and meticulous bedside care in pediatric critical care settings

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 118. Traumatic brain injury. Kochaneck et al. Page 1375 -1400
Rogers textbook:
Reference 1: Forsyth RJ, Parslow RC, Tasker RC, Hawley CA, Morris KP; UK Paediatric Traumatic Brain Injury Study Group; Paediatric Intensive Care Society Study Group (PICSSG). Prediction of raised intracranial pressure complicating severe traumatic brain injury in children: implications for trial design. Pediatr Crit Care Med. 2008 Jan;9(1):8-14. doi: 10.1097/01.PCC.0000298759.78616.3A. PMID: 18477907.
Reference 2: Appavu B, Burrows BT, Foldes S, Adelson PD. Approaches to Multimodality Monitoring in Pediatric Traumatic Brain Injury. Front Neurol. 2019 Nov 26;10:1261. doi: 10.3389/fneur.2019.01261. PMID: 32038449; PMCID: PMC6988791.

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Ever wondered how PICU teams make those critical calls about blood pressure and vasoactive meds? On this episode, Dr. Monica Gray and Dr. Pradip Kamat dive into the real-world questions that come up during pediatric intensive care rounds. They break down the pros and cons of arterial line versus non-invasive cuff measurements, talk through blood pressure targets for tough cases like sepsis and brain injury, and share practical tips for weaning kids off vasoactive drugs. With a focus on the latest guidelines and research, Monica and Pradip offer actionable advice to help you fine-tune hemodynamic management for your sickest patients. Tune in!

Show Highlights:

Relationship between blood pressure and cardiac output in pediatric patients
Comparison of arterial line (invasive) versus non-invasive cuff measurements for blood pressure monitoring in the PICU
Blood pressure targets for critical illnesses such as sepsis, traumatic brain injury, and respiratory failure in children
Strategies for weaning vasoactive medications in critically ill pediatric patients
Importance of accurate blood pressure measurement and monitoring in the PICU
Discussion of organ autoregulation and its impact on blood pressure management
Clinical assessment and individualized care in setting blood pressure goals
Recommendations for initial vasoactive agents in pediatric septic shock
Challenges and considerations in vasoactive medication selection and weaning
Need for further research on pediatric vasoactive medication management strategies

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 110. Alder M et al. Pediatric Sepsis. Pages 1293-1309.
Rogers Textbook of Pediatric Critical Care Medicine. Chapter 88. Fitzgerald J et al. Bacterial Sepsis.Pages 1469-1485.
Reference 1 Weiss S. Vasoactive Selection for Pediatric Septic Shock-Where to begin. JAMA Network Open, 2025;8(4):e254726.
Reference 2 Schlapbach LJ, Watson RS, Sorce LR, Argent AC, Menon K, Hall MW, Akech S, Albers DJ, Alpern ER, Balamuth F, Bembea M, Biban P, Carrol ED, Chiotos K, Chisti MJ, DeWitt PE, Evans I, Flauzino de Oliveira C, Horvat CM, Inwald D, Ishimine P, Jaramillo-Bustamante JC, Levin M, Lodha R, Martin B, Nadel S, Nakagawa S, Peters MJ, Randolph AG, Ranjit S, Rebull MN, Russell S, Scott HF, de Souza DC, Tissieres P, Weiss SL, Wiens MO, Wynn JL, Kissoon N, Zimmerman JJ, Sanchez-Pinto LN, Bennett TD; Society of Critical Care Medicine Pediatric Sepsis Definition Task Force. International Consensus Criteria for Pediatric Sepsis and Septic Shock. JAMA. 2024 Feb 27;331(8):665-674.

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Welcome to PICU Doc on Call, the podcast where we break down real-life cases from the pediatric intensive care unit and share practical insights for clinicians everywhere! I’m Dr. Monica Gray, and I’m joined by my co-host, Dr. Pradip Kamat.

Today, we’re diving into a fascinating case: a 13-year-old boy who suddenly developed muscle weakness and was found to have severe hypokalemia. After some detective work, he was diagnosed with familial hypokalemic periodic paralysis, a rare but important condition to recognize in the PICU.

We’ll discuss the genetic underpinnings, classic clinical features, and common triggers associated with this disorder. Additionally, we’ll guide you through the differential diagnosis, key management strategies, such as potassium supplementation, and explain why genetic testing is so crucial. We’ll also cover essential considerations for anesthesia and cardiac monitoring in these patients.

Whether you’re a pediatric intensivist or just interested in acute neuromuscular care, stick around for some practical pearls you can use on your next shift!

Show Highlights:

Clinical case discussion of a 13-year-old male patient with muscle weakness and hypokalemia
Diagnosis and management of familial hypokalemic periodic paralysis
Genetic basis and mutations associated with hypokalemic periodic paralysis (CACNA1S and SCN4A)
Physiological mechanisms underlying hypokalemic periodic paralysis
Common clinical presentations and triggers for episodes of muscle weakness
Differential diagnoses for muscle weakness and hypokalemia in pediatric patients
Laboratory investigations to confirm hypokalemic periodic paralysis
Treatment options for hypokalemic periodic paralysis, including potassium supplementation and prophylactic medications
Importance of avoiding triggers and coordinating care with anesthesia

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 68: Weimer M et al. Acute neuromuscular disease and disorders page 840
Rogers Textbook of Pediatric Intensive Care Medicine: Management of Sodium and Potassium Disorders. Pages 1876- 1883
Reference 1: Weber F, Lehmann-Horn F. Hypokalemic Periodic Paralysis. 2002 Apr 30 [Updated 2018 Jul 26]. In: Adam MP, Feldman J, Mirzaa GM, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2025. Available from: https://www.ncbi.nlm.nih.gov/books/NBK1338/
Reference 2: Channelopathies. Clin Exp Pediatr. 2014;57(1):1-18. Published online January 31, 2014DOI: https://doi.org/10.3345/kjp.2014.57.1.1
Reference 3: Statland JM, Fontaine B, Hanna MG, Johnson NE, Kissel JT, Sansone VA, Shieh PB, Tawil RN, Trivedi J, Cannon SC, Griggs RC. Review of the Diagnosis and Treatment of Periodic Paralysis. Muscle Nerve. 2018 Apr;57(4):522-530.

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Learn how to sharpen your pediatric intubation skills and make evidence-based decisions at the bedside. Today, Dr. Pradip Kamat, Dr. Monica Gray, and Dr. Rahul Damania expertly dissect the nuances of selecting optimal induction agents for critically ill children in the PICU. Through engaging, real-world case scenarios, our hosts guide you through drug choices in complex situations such as cardiogenic shock, septic shock, and elevated intracranial pressure—always prioritizing hemodynamic stability and patient safety. Gain valuable insights into the advantages, limitations, and clinical pearls of agents like propofol, fentanyl, ketamine, and midazolam, along with practical strategies for rapid sequence intubation, neuromuscular blockade, and individualized patient care. Don’t miss this high-yield discussion, packed with actionable knowledge!

Show Highlights:

Induction agents for endotracheal intubation in critically ill children
Clinical scenarios highlighting optimal choices of induction agents and neuromuscular blockers
Importance of maintaining hemodynamic stability during intubation
Pharmacology and clinical considerations of various induction agents (e.g., propofol, ketamine, fentanyl, etomidate)
Use of neuromuscular blocking agents (NMBAs) in pediatric intubation
Differences between depolarizing and non-depolarizing neuromuscular blockers
Risks associated with specific induction agents in patients with cardiac dysfunction or septic shock
Modified rapid sequence intubation (RSI) techniques for unstable patients
Key takeaways for managing critically ill pediatric patients requiring intubation
Practical tips for optimizing intubation conditions and minimizing complications

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care 6th Edition. Chapters 127 - 135, Pages 1510 - 1610
Hendrix JM, Regunath H. Intubation Endotracheal Tube Medications. [Updated 2025 Jan 19]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459276/
Agrawal, Dewesh. Rapid sequence intubation (RSI) in children for emergency medicine: Medications for sedation and paralysis. UpToDate. Last updated Dec 4, 2024.
Vanlinthout LE, Geniets B, Driessen JJ, Saldien V, Lapré R, Berghmans J, Uwimpuhwe G, Hens N. Neuromuscular-blocking agents for tracheal intubation in pediatric patients (0-12 years): A systematic review and meta-analysis. Paediatr Anaesth. 2020 Apr;30(4):401-414. doi: 10.1111/pan.13806. Epub 2020 Mar 9. PMID: 31887248.
Tarquinio KM, Howell JD, Montgomery V, Turner DA, Hsing DD, Parker MM, Brown CA 3rd, Walls RM, Nadkarni VM, Nishisaki A; National Emergency Airway Registry for Children; Pediatric Acute Lung Injury and Sepsis Investigators Network. Current medication practice and tracheal intubation safety outcomes from a prospective multicenter observational cohort study. Pediatr Crit Care Med. 2015 Mar;16(3):210-8. doi: 10.1097/PCC.0000000000000319. PMID: 25581629.
Conway JA, Kharayat P, Sanders RC Jr, Nett S, Weiss SL, Edwards LR, Breuer R, Kirby A, Krawiec C, Page-Goertz C, Polikoff L, Turner DA, Shults J, Giuliano JS Jr, Orioles A, Balkandier S, Emeriaud G, Rehder KJ, Kian Boon JL, Shenoi A, Vanderford P, Nuthall G, Lee A, Zeqo J, Parsons SJ, Furlong-Dillard J, Meyer K, Harwayne-Gidansky I, Jung P, Adu-Darko M, Bysani GK, McCarthy MA, Shlomovich M, Toedt-Pingel I, Branca A, Esperanza MC, Al-Subu AM, Pinto M, Tallent S, Shetty R, Thyagarajan S, Ikeyama T, Tarquinio KM, Skippen P, Kasagi M, Howell JD, Nadkarni VM, Nishisaki A; National Emergency Airway Registry for Children (NEAR4KIDS) and for the Pediatric Acute Lung Injury and Sepsis Investigators (PALISI). Ketamine Use for Tracheal Intubation in Critically Ill Children Is Associated With a Lower Occurrence of Adverse Hemodynamic Events. Crit Care Med. 2020 Jun;48(6):e489-e497. doi: 10.1097/CCM.0000000000004314. PMID: 32317603.
Zanza C, Piccolella F, Racca F, Romenskaya T, Longhitano Y, Franceschi F, Savioli G, Bertozzi G, De Simone S, Cipolloni L, La Russa R. Ketamine in Acute Brain Injury: Current Opinion Following Cerebral Circulation and Electrical Activity. Healthcare (Basel). 2022 Mar 17;10(3):566. doi: 10.3390/healthcare10030566. PMID: 35327044; PMCID: PMC8949520.
Zeiler FA, Teitelbaum J, West M, Gillman LM. The ketamine effect on ICP in traumatic brain injury. Neurocrit Care. 2014 Aug;21(1):163-73. doi: 10.1007/s12028-013-9950-y. PMID: 24515638.

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Ready for a deep dive into a real-life pediatric ICU situation? Today, Dr. Pradip Kamat, Dr. Monica Gray, and Dr. Rahul Damania will walk you through the case of a seven-year-old girl with Hemoglobin SC (HbSC) disease, who presents with abdominal swelling, pneumonia, low oxygen, and pain.

In this episode, our team unpacks the spleen’s anatomy and its crucial role in immunity, then zooms in on how sickle cell disease can throw a wrench in splenic function. You’ll hear how they approach the diagnosis and management of acute splenic sequestration crisis, sharing clinical pearls along the way. Plus, they’ll break down why quick recognition is so important and discuss strategies for both immediate and long-term care in pediatric sickle cell patients. Don’t miss these practical insights from the frontlines of pediatric critical care!

Show Highlights:

Case study of a seven-year-old girl with hemoglobin SC disease
Presentation of symptoms: abdominal distension, pneumonia, hypoxia, and body pain
Discussion of acute splenic sequestration crisis as a complication of sickle cell disease
Anatomy and physiology of the spleen
The role of the spleen in sickle cell disease and how sickled cells affect splenic function
Acute splenic sequestration crisis, including clinical features and laboratory evaluations
Management strategies for acute splenic sequestration crisis in the ICU
Importance of blood transfusions and supportive care in treatment
Prophylactic measures to prevent recurrence of splenic sequestration
Educational emphasis on recognizing clinical signs and the need for timely intervention

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 88. Hemoglobinopathies. Baender, MA, Marsh Anne. Pages: 1457-1470
Rogers' textbook of pediatric intensive care: Hematologic Emergencies. McCory MC, Bhar S, and Blaine E. Pages 2003-2005
Brousse V, Buffet P, Rees D. The spleen and sickle cell disease: the sick(led) spleen. Br J Haematol. 2014 Jul;166(2):165-76. doi: 10.1111/bjh 12950. Epub 2014 May 26. PMID: 24862308.
Waleed S, Aldabsa M, Gouher S. Splenic Sequestration Induced by Parvovirus B19: A Case Report. Cureus. 2024 May 23;16(5):e60937. doi: 10.7759/cureus. 60937. PMID: 38915956; PMCID: PMC11195323.
Solanki DL, Kletter GG, Castro O. Acute splenic sequestration crises in adults with sickle cell disease. Am J Med. 1986 May;80(5):985-90. doi: 10.1016/0002-9343(86)90649-2. PMID: 3706382.
Karna B, Jha SK, Al Zaabi E. Hemoglobin C Disease. [Updated 2023 May 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559043/

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Welcome to "PICU Doc on Call," the podcast where real cases meet real expertise at the bedside! Join Dr. Monica Gray, Dr. Pradip Kamat, and Dr. Rahul Damania as they unravel the mysteries of pediatric critical care. In today’s episode, our team dives into the compelling case of a previously healthy seven-year-old girl who arrives with seizures, right arm weakness, and sudden respiratory failure. Together, they’ll break down the diagnosis and management of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease, also known as MOGAD. This autoimmune demyelinating disorder can challenge even the most seasoned clinicians.

Tune in as our experts walk you through the clinical features, essential diagnostic workup, and the critical importance of early immunosuppressive therapy. Whether you’re at the bedside or on the go, this episode is packed with practical pearls and a multidisciplinary approach to recognizing and treating acute pediatric neuroimmunological emergencies in the PICU. Let’s get started!

Show Highlights:

Presentation of a complex pediatric case involving a seven-year-old girl with new-onset seizures and acute respiratory failure
Discussion of Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD) as an autoimmune demyelinating disorder
Overview of the clinical presentation and diagnostic criteria for autoimmune encephalitis
Importance of a broad differential diagnosis, including infectious and autoimmune causes, in pediatric patients with seizures and neurological deficits
Diagnostic approach involving MRI, lumbar puncture, and antibody testing for MOGAD
Management strategies for MOGAD, including stabilization, seizure control, and immunosuppressive therapy
Neurocritical care considerations for monitoring and treating elevated intracranial pressure
Long-term management challenges and the need for multidisciplinary care in pediatric patients with MOGAD
Discussion of potential outcomes and the risk of relapse in children with MOGAD.
Emphasis on the importance of early and comprehensive diagnostic testing to avoid misdiagnosis

References:

Fuhrman & Zimmerman - Pediatric Critical Care 6th Edition, Chapter 64
Gole S, Anand A. Autoimmune Encephalitis. [Updated 2023 Jan 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK578203/
Salama S, Khan M, Pardo S, Izbudak I, Levy M. MOG antibody-associated encephalomyelitis/encephalitis. Mult Scler. 2019 Oct;25(11):1427-1433. doi: 10.1177/1352458519837705. Epub 2019 Mar 25. PMID: 30907249; PMCID: PMC6751007
Lancaster E. The Diagnosis and Treatment of Autoimmune Encephalitis. J Clin Neurol. 2016 Jan;12(1):1-13. doi: 10.3988/jcn.2016.12.1.1. PMID: 26754777; PMCID: PMC4712273.
Fisher KS, Illner A, Kannan V. Pediatric neuroinflammatory diseases in the intensive care unit. Semin Pediatr Neurol. 2024 Apr;49:101118. Doi: 10.1016/j.spen.2024.101118. Epub 2024 Feb 1. PMID: 38677797.
Hébert J, Muccilli A, Wennberg RA, Tang-Wai DF. Autoimmune Encephalitis and Autoantibodies: A Review of Clinical Implications. J Appl Lab Med. 2022 Jan 5;7(1):81-98. Doi: 10.1093/jalm/jfab102. PMID: 34996085.
Lopez JA, Denkova M, Ramanathan S, Dale RC, Brilot F. Pathogenesis of autoimmune demyelination: from multiple sclerosis to neuromyelitis optica spectrum disorders and myelin oligodendrocyte glycoprotein antibody-associated disease. Clin Transl Immunology. 2021 Jul 26;10(7):e1316. doi: 10.1002/cti2.1316. PMID: 34336206; PMCID: PMC8312887.

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Have you ever wondered what happens when a toddler gets into something they definitely shouldn’t? Today, Dr. Monica Gray, Dr. Pradip Kamat, and Dr. Rahul Damania discuss the case of an 18-month-old boy who accidentally ingested concentrated bleach, presenting with stridor, drooling, and vomiting. They review the clinical approach to caustic ingestions in children, including airway management, diagnostic workup, and the roles of endoscopy, steroids, and multidisciplinary care. The episode also highlights potential complications such as esophageal strictures and cancer, emphasizes prevention strategies, and provides key takeaways for intensivists managing similar pediatric emergencies. If you’re an intensivist or just want to know what to do in a pediatric emergency, don’t miss these essential takeaways for managing one of the scariest situations in the ER.

Show Highlights:

Case study of an 18-month-old boy who ingested concentrated bleach
Clinical presentation including symptoms like stridor, drooling, and vomiting
Management strategies for caustic ingestions in children
Importance of airway management and monitoring in cases of caustic ingestion
Diagnostic workup including imaging and endoscopy
Differential diagnosis considerations for similar presentations (e.g., button batteries, laundry detergent pods)
Mechanism of injury caused by alkaline substances like bleach
Long-term complications associated with caustic ingestions, such as esophageal strictures and cancer
Multidisciplinary approach to treatment involving various medical specialties
Prevention strategies to reduce the incidence of accidental caustic ingestions in children

References:

American Academy of Pediatrics – Pediatric Care Online: Esophageal Caustic Injury (AAP clinical guidance on caustic ingestions).
Fuhrman & Zimmerman’s Pediatric Critical Care textbook – Chapters on toxicology and gastrointestinal emergencies (covering caustic injury management and critical care approach).
Hoffman RS, et al. “Ingestion of Caustic Substances.” New England Journal of Medicine. 2020; 382(18):1739-1748. A comprehensive review of caustic ingestion injuries and management.
Arnold M, Numanoglu A. “Caustic ingestion in children – a review.” Semin Pediatr Surg. 2017;26(2):95-104. Review of epidemiology, pathophysiology, and treatment of caustic injuries in kids.
Johnson CM, Brigger MT. “The public health impact of pediatric caustic ingestion injuries.” Arch Otolaryngol Head Neck Surg. 2012;138(12):1111-1115. (Epidemiology study showing declining incidence).
Pediatric Critical Care Medicine (PCCM) Journal – various case reports and series on caustic ingestion (for case-based insights), and annual National Poison Data System reports (for statistics on pediatric poisonings).
Tringali A, et al. ESGE/ESPGHAN Pediatric GI Endoscopy Guidelines (Endoscopy, 2017) – Includes recommendations for endoscopy timing and steroid use in caustic ingestions.
Usta M, et al. “High doses of methylprednisolone in the management of caustic esophageal burns.” Pediatrics. 2014;133(6):E1518-24. (Key study demonstrating steroids benefit in grade 2b injuries).
Royal Children’s Hospital Melbourne – Clinical Practice Guidelines: Caustic Ingestions (2019) – Practical hospital guidelines emphasizing early intubation for airway threat, endoscopy within 24h, IV PPI, and supportive care.

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Today, Dr. Monica Gray, Dr. Pradip Kamat, and Dr. Rahul Damania discuss two real-life pediatric cases of hyponatremia in the PICU. They talk through a case of a six-month-old baby with severe sodium depletion and a teenager dealing with cancer-related hyponatremia. The team breaks down the pathophysiology, walks us through the diagnostic workups, and discusses the careful management needed for these cases. They emphasize the importance of correcting sodium levels gradually and addressing the root cause of the problem. They share practical tips for intensivists and highlight why staying vigilant and following evidence-based care is so crucial when managing critically ill kids with electrolyte disturbances. Tune in to hear more!

Show Highlights:

Discussion of hyponatremia in pediatric patients, particularly in the PICU
Presentation of two case studies illustrating different presentations of hyponatremia
Examination of the pathophysiology of hyponatremia, including its classification into hypovolemic, euvolemic, and hypervolemic types
Overview of diagnostic investigations for hyponatremia, including volume status assessment and serum/urine electrolyte measurements
Management strategies for hyponatremia, emphasizing the importance of gradual correction of sodium levels
Risks associated with rapid correction of hyponatremia
Importance of fluid management in different types of hyponatremia
Role of pharmacological interventions in specific cases, such as SIADH
Clinical presentation and symptoms associated with hyponatremia in pediatric patients
Emphasis on continuous monitoring of sodium levels and clinical status during treatment

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 71. Fluid and electrolyte issues in pediatric critical illness. Evans I, Joyce E. Page 866-872
Rogers' textbook of Pediatric Intensive Care Chapter 108: Disorders of Water, Sodium and Potassium homeostasis: Schneider J & Glater-Welt L. Pages 1868-1880
Harrison’s Principles of Internal Medicine Volume 1. Chapter 53: Fluid and Electrolyte Disturbances. Mount D. Pages 338-347

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Today, Dr. Rahul Damania, Dr. Pradip Kamat, and Dr. Monica Gray, pediatric intensivists, sit down to chat about the diagnosis and management of acute myocarditis in children. They focus on a real-life case involving a one-month-old infant who presented with poor feeding, respiratory distress, and fever. Together, they break down the possible causes, key clinical signs, diagnostic approaches, and treatment options for pediatric myocarditis. Throughout the discussion, they highlight the importance of early recognition, a multidisciplinary team approach, and supportive care in improving outcomes for these critically ill infants. This episode is packed with practical insights and is designed to help pediatric intensivists tackle this challenging and potentially life-threatening condition. Tune in to hear more!

Show Highlights:

Definition and etiology of acute myocarditis in pediatric patients
Clinical case presentation of a one-month-old infant with acute myocarditis
Symptoms and clinical manifestations of acute myocarditis in children
Diagnostic approaches for identifying acute myocarditis, including echocardiography and laboratory tests
Management strategies for acute myocarditis, including intensive care and medication
Importance of recognizing atypical presentations in infants
Prognosis and risk factors associated with acute myocarditis
Role of multidisciplinary collaboration in managing acute myocarditis
Impact of viral infections on the development and severity of myocarditis
Outcomes and potential complications related to acute myocarditis in pediatric patients

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 108. Life-threatening viral diseases and their treatment. Vora S et al. Pages 1273-1278
Rogers’ textbook of Pediatric Intensive Care. Chapter 74: cardiomyopathy, myocarditis, and mechanical circulatory support. Harmon WG et al. Pages 1247-1255
Robinson J, Hartling L, Vandermeer B, Sebastianski M, Klassen TP. Intravenous immunoglobulin for presumed viral myocarditis in children and adults. Cochrane Database Syst Rev. 2020 Aug 19;8(8): CD004370. Doi: 10.1002/14651858.CD004370.pub4. PMID: 32835416

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In this episode of "PICU Doc on Call," pediatric intensivists Dr. Rahul Damania, Dr. Pradip Kamat, and Dr. Monica Gray discuss a critical case involving a 16-year-old male who experienced severe carbon monoxide poisoning after being found unresponsive in a garage. They chat about the pathophysiology, clinical manifestations, diagnostic workup, and management of carbon monoxide toxicity. Furthermore, they cover the importance of early oxygen administration, recognizing potential delayed neurological sequelae, and keeping an eye out for cardiac complications. Tune in and hear more about a comprehensive approach to treatment and the significance of multidisciplinary support for achieving the best patient outcomes.

Show Highlights:

Case presentation of a 16-year-old male with severe carbon monoxide poisoning
Pathophysiology of carbon monoxide toxicity and its effects on hemoglobin
Clinical manifestations and symptoms associated with carbon monoxide poisoning
Diagnostic workup for suspected carbon monoxide exposure
Management principles for treating carbon monoxide poisoning in pediatric patients
Sources and scenarios leading to carbon monoxide poisoning
Complications arising from carbon monoxide exposure including neurological injuries
Importance of early oxygen administration and monitoring in treatment
Discussion of hyperbaric oxygen therapy and its indications
Key takeaways for clinicians regarding the management and follow-up of carbon monoxide poisoning cases

We welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our websitepicudoconcall.org.

References:

Tapking, C., et al. (2021). Burn and inhalation injury. In J. J. Zimmerman & A. T. Rotta (Eds.), Fuhrman and Zimmerman’s Pediatric Critical Care (6th ed., pp. 1347–1362). Elsevier.
Nañagas KA, Penfound SJ, Kao LW. Carbon Monoxide Toxicity. Emerg Med Clin North Am. 2022 May;40(2):283-312. doi: 10.1016/j.emc.2022.01.005. Epub 2022 Apr 5. PMID: 35461624.
Smollin C, Olson K. Carbon monoxide poisoning (acute). BMJ Clin Evid. 2010 Oct 12;2010:2103. PMID: 21418677; PMCID: PMC3217756.
Palmeri R, Gupta V. Carboxyhemoglobin Toxicity. [Updated 2023 Apr 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan.

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Welcome to another exciting episode of PICU Doc on Call! Today, we're diving deep into the world of pediatric critical care with our expert hosts, Dr. Rahul Damania, Dr. Pradip Kamat, and Dr. Monica Gray. Get ready to unravel the mysteries of the oxygen extraction ratio (O2ER) and its pivotal role in managing pediatric acute respiratory distress syndrome (ARDS) and multi-organ dysfunction.

Picture this: a seven-year-old girl battling severe pneumonia that spirals into ARDS and septic shock. Our hosts walk you through this gripping case, shedding light on calculating O2ER and why central venous oxygen saturation (ScvO2) is a game-changer. They'll share their top strategies for optimizing oxygen delivery and cutting down on oxygen demand.

But that's not all! This episode is all about the holistic approach to managing critically ill pediatric patients. Tune in to discover how these insights can lead to better outcomes for our youngest and most vulnerable patients. Don't miss out on this vital conversation!

Show Highlights:

Clinical significance of the oxygen extraction ratio (O2ER) in pediatric critical care
Importance of understanding oxygen delivery and consumption in critically ill patients
Calculation and interpretation of O2ER and its relationship to central venous oxygen saturation (ScvO2)
Physiological concepts related to oxygenation, including intrapulmonary shunting and ventilation-perfusion mismatch
Management strategies for increasing oxygen delivery and reducing oxygen demand in ARDS and septic shock
Interventions such as blood transfusions, sedation, and optimization of cardiac output
Implications of lactic acidosis and anaerobic metabolism in the context of inadequate oxygen delivery
Holistic approach to patient management, focusing on both numerical values and overall metabolic needs

We welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our websitepicudoconcall.org.

References:

Fuhrman B.P. & Zimmerman J.J. (Eds.). Pediatric Critical Care, 6th ed. Elsevier; 2021. (Key concepts of oxygen delivery, consumption, and extraction in shock states are discussed in Chapter 13) .
Nichols D.G. (Ed.). Roger’s Textbook of Pediatric Intensive Care, 5th ed. Wolters Kluwer; 2016. (Comprehensive review of oxygen transport and utilization in critically ill children, including ARDS and shock).
Lucking S.E., Williams T.M., Chaten F.C., et al. Dependence of oxygen consumption on oxygen delivery in children with hyperdynamic septic shock and low oxygen extraction. Crit Care Med. 1990;18(12):1316–1319. doi:10.1097/00003246-199012000-00002.
Ronco J.J., Fenwick J.C., Tweeddale M.G., et al. Pathologic dependence of oxygen consumption on oxygen delivery in acute respiratory failure. Chest. 1990;98(6):1463–1466. doi:10.1378/chest.98.6.1463 .
Carcillo J.A., Davis A.L., Zaritsky A. Clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock. Crit Care Med. 2002;30(6):1365–1378. (ACCM guidelines emphasizing ScvO₂ targets in shock) .
Emeriaud G, López-Fernández YM, Iyer NP, et al; PALICC-2 Group; PALISI Network. Executive summary of the second international guidelines for the diagnosis and management of pediatric ARDS (PALICC-2). Pediatr Crit Care Med. 2023;24(2):143–168. doi:10.1097/PCC.0000000000003147.

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In this episode, Dr. Rahul Damania, Dr. Pradip Kamat, and Dr. Monica Gray dive into a critical case involving a five-week-old baby facing acute respiratory failure due to pertussis. They chat about how this condition shows up, how it's diagnosed, and the best ways to manage it, especially considering the serious complications it can cause in infants, like pulmonary hypertension and the potential need for ECMO. The conversation underscores the importance of catching it early and providing supportive care, while also highlighting how crucial vaccination is in preventing pertussis. Tune in to learn how severe this disease can be and why staying alert in pediatric care is so important.

Show Highlights:

Clinical case of a five-week-old infant with acute respiratory failure and pertussis diagnosis
Epidemiology and public health impact of pertussis, including vaccination rates and outbreak patterns
Pathophysiology of pertussis and its effects on respiratory health, particularly in infants
Clinical presentation of pertussis, including stages of the disease and atypical symptoms in infants
Diagnostic approaches for pertussis, including laboratory findings and PCR testing
Management strategies for severe pertussis, including supportive care and antibiotic therapy
Potential complications associated with pertussis, especially in young infants
Differential diagnosis considerations for pertussis and distinguishing features from other infections
Importance of vaccination in preventing pertussis and reducing morbidity and mortality
ECMO as a treatment option for severe cases and its associated challenges, and outcomes

We welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org.

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter and Rogers texbook of Pediatric intensive care -both do not have any Pertussis mentioned in their index.
Rowlands HE, Goldman AP, Harrington K, Karimova A, Brierley J, Cross N, Skellett S, Peters MJ. Impact of rapid leukodepletion on the outcome of severe clinical pertussis in young infants. Pediatrics. 2010 Oct;126(4):e816-27. doi: 10.1542/peds.2009-2860. Epub 2010 Sep 6. PMID: 20819895.
Lauria AM, Zabbo CP. Pertussis. [Updated 2022 Oct 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK519008/
Berger JT, Carcillo JA, Shanley TP, Wessel DL, Clark A, Holubkov R, Meert KL, Newth CJ, Berg RA, Heidemann S, Harrison R, Pollack M, Dalton H, Harvill E, Karanikas A, Liu T, Burr JS, Doctor A, Dean JM, Jenkins TL, Nicholson CE; Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Collaborative Pediatric Critical Care Research Network (CPCCRN). Critical pertussis illness in children: a multicenter prospective cohort study. Pediatr Crit Care Med. 2013 May;14(4):356-65. doi: 10.1097/PCC.0b013e31828a70fe. PMID: 23548960; PMCID: PMC3885763.
Cousin, V.L., Caula, C., Vignot, J. et al. Pertussis infection in critically ill infants: meta-analysis and validation of a mortality score. Crit Care 29, 71 (2025). https://doi.org/10.1186/s13054-025-05300-2
Domico M, Ridout D, MacLaren G, Barbaro R, Annich G, Schlapbach LJ, Brown KL. Extracorporeal Membrane Oxygenation for Pertussis: Predictors of Outcome Including Pulmonary Hypertension and Leukodepletion. Pediatr Crit Care Med. 2018 Mar;19(3):254-261. doi: 10.1097/PCC.0000000000001454. PMID: 29319632.
Centers for Disease Control: https://www.cdc.gov/schoolvaxview/data/index.html; https://www.cdc.gov/pertussis/php/surveillance/pertussis-incidence-by-age-group-and-year.html; https://www.cdc.gov/pertussis/media/pdfs/2025/01/pertuss-surv-report-2024_PROVISIONAL-508.pdf (various links)
Tuan, Ta Anh MD, PhD1; Xoay, Tran Dang MD1; Nakajima, Noriko MD, PhD2; Nakagawa, Satoshi MD3; Phuc, Phan Huu MD, PhD1; Hung, Dau Viet MD, PhD1; Dung, Nguyen Trong MD1; Dong, Ngo Tien MD1; Dung, Tran Ba MD1; Thuy, Phung Thi Bich PhD4; Hai, Le Thanh MD, PhD5; Dien, Tran Minh MD, PhD6. Pertussis Infants Needing Mechanical Ventilation and Extracorporeal Membrane Oxygenation: Single-Center Retrospective Series in Vietnam. Pediatric Critical Care Medicine 22(9):p e471-e479, September 2021. | DOI: 10.1097/PCC.0000000000002723

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In today’s episode, Dr. Rahul Damania and Dr. Pradip Kamat welcome their new co-host, Dr. Monica Gray. They’ll dive into the topic of upper airway obstruction in children and explore a case involving a 12-month-old girl who presents with stridor and fever. Throughout the discussion, they delve into the underlying causes, possible diagnoses, and management strategies. Key takeaways include the significance of keeping the child calm, ensuring proper positioning, and utilizing treatments such as dexamethasone and Racemic epinephrine. They’ll also touch on advanced therapies and serious infections like epiglottitis. The episode highlights the importance of recognizing stridor, knowing when to consider PICU admission, and the effectiveness of low-dose dexamethasone. Tune in to learn more!

Show Highlights:

Overview of upper airway obstruction in pediatric patients
Case presentation of a 12-month-old girl with stridor and fever
Discussion on the pathophysiology of stridor and its clinical significance
Differential diagnoses for stridor, including croup, epiglottitis, and foreign body aspiration
Management strategies for upper airway obstruction, including stabilization and medication
Importance of calming the child and optimal positioning during treatment
Use of dexamethasone and racemic epinephrine in managing croup
Advanced therapies, such as Helios, for specific cases
Indicators for pediatric intensive care unit (PICU) admission
Key clinical points and takeaways for healthcare professionals managing airway emergencies

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 47 Otteson T, Richardson C, Shah J: Diseases of the upper Airway. Pages 524-535
Rogers Textbook of Pediatric Intensive Care: Chapter 25; Ong May Soo Jacqueline, Tijssen J, Bruins BB and Nishisaki A: Airway management. Pages 341-365
Reference: Asmundsson AS, Arms J, Kaila R, Roback MG, Theiler C, Davey CS, Louie JP. Hospital Course of Croup After Emergency Department Management. Hosp Pediatr. 2019 May;9(5):326-332. doi: 10.1542/hpeds.2018-0066. PMID: 30988017; PMCID: PMC6478427.
Reference: Aregbesola A, Tam CM, Kothari A, Le ML, Ragheb M, Klassen TP. Glucocorticoids for croup in children. Cochrane Database Syst Rev. 2023 Jan 10;1(1):CD001955. doi: 10.1002/14651858.CD001955.pub5. PMID: 36626194; PMCID: PMC9831289.

Previous Episode Mentioned:

PICU Doc On Call Episode 80

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In this episode of PICU DOC on Call, Dr. Rahul Damania and Dr. Pradip Kamat discuss the resurgence of measles in the United States. They explore the virus's pathophysiology, clinical features, diagnostic methods, treatment options, and complications. They emphasize the critical role of vaccination in preventing measles outbreaks and address the historical context and public health challenges related to vaccine hesitancy. The speakers highlight the severe complications of measles, especially in immunocompromised patients, and advocate for robust vaccination efforts to protect vulnerable populations and prevent the spread of this preventable disease. Tune in to hear more!

Show Highlights:

Resurgence of measles in the United States
Historical context of measles outbreaks and vaccination impact
Current statistics and recent cases of measles
Pathophysiology of the measles virus
Clinical features and progression of measles infection
Diagnostic approaches for confirming measles
Differential diagnosis considerations for fever and rash
Treatment options and the role of vaccination
Complications associated with measles, including severe outcomes
Public health challenges related to vaccine hesitancy and advocacy for immunization

Resources:

CDC Measles Info Page

WHO Measles Global Surveillance

References:

Fuhrman & Zimmerman. Textbook of Pediatric Critical Care, Ch. 52

Long S et al. Principles and Practice of Pediatric Infectious Diseases, Ch. 227

Moss WJ. Measles. Lancet. 2017;390(10111):2490-2502

Paules CI, Marston HD, Fauci AS. NEJM. 2019;380(23):2185-2187

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In this episode of PICU DOC on Call, Dr. Rahul Damania and Dr. Pradip Kamat chat about a challenging case involving a 15-year-old girl dealing with acute myocarditis and worsening respiratory failure. They explore the intricate dance between the heart and lungs, especially how positive pressure ventilation can affect heart function. They cover important topics like cardiac output, preload, and afterload, and discuss the delicate balance needed to manage myocarditis effectively. The episode offers practical tips for optimizing care for critically ill children, underscoring the importance of personalized treatment plans and teamwork in pediatric critical care. Tune in!

Show Highlights:

Clinical case of a 15-year-old girl with acute myocarditis and respiratory failure
Importance of understanding cardiopulmonary interactions in pediatric critical care
Effects of positive pressure ventilation on cardiac function
Key concepts of cardiac output, preload, and afterload in the context of myocarditis
Challenges of managing hemodynamic instability in critically ill pediatric patients
Differences between spontaneous breathing and positive pressure ventilation
Strategies for optimizing preload and fluid management in myocarditis patients
Tailoring ventilatory support and transitioning to invasive mechanical ventilation
Monitoring for arrhythmias and managing myocardial function with inotropic support
Importance of frequent assessments and collaboration with cardiac ICU teams for patient care

Management StrategiesOptimizing Preload:

Volume depletion is common in patients with hypotension and tachycardia. A careful fluid challenge is important to restore circulatory volume, but fluid overload should be avoided, especially with impaired left ventricular function.

Tailoring Ventilatory Support:

Adjust BiPAP settings to improve oxygenation without overloading the heart with excessive positive pressures.
Use the optimal level of PEEP to recruit alveoli while maintaining adequate venous return to the heart.

Supporting Myocardial Function:

Inotropic support (e.g., milrinone) may be necessary to improve myocardial contractility. Milrinone also provides vasodilation, which can reduce afterload but must be used cautiously due to its potential to lower blood pressure.

Frequent Reassessments:

Bedside echocardiography and regular monitoring of biomarkers (lactate, BNP) and clinical status are essential for ongoing evaluation.
In severe cases, advanced therapies like ECMO may be required if the patient’s hemodynamic status continues to deteriorate.

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Today, pediatric intensivists Dr. Pradip Kamat and Dr. Rahul Damania discuss a complex case of a 12-year-old girl who suffered a seizure and unresponsiveness due to a subarachnoid hemorrhage from a ruptured aneurysm. They explore the multi-system effects of traumatic brain injury (TBI) and intracranial hemorrhage, focusing on non-neurologic organ dysfunction.

They’ll also highlight the impact on cardiovascular, respiratory, renal, and hepatic systems, emphasizing the importance of understanding these interactions for better patient management.

Tune in to hear relevant studies and management strategies to improve outcomes in pediatric TBI cases.

In This Episode:

Clinical case of a 12-year-old girl with seizure and unresponsiveness due to subarachnoid hemorrhage from a ruptured aneurysm
Management of non-neurologic organ dysfunction in traumatic brain injury (TBI) and intracranial hemorrhage
Multi-system effects of brain injuries, including cardiovascular, respiratory, renal, and hepatic complications
Importance of recognizing non-neurologic organ dysfunction in pediatric patients
Epidemiology and prevalence of non-neurologic organ dysfunction in patients with aneurysms or subarachnoid hemorrhage
Mechanisms of organ dysfunction following brain injury, including inflammatory responses and cytokine release
Management strategies for cardiovascular complications in TBI patients.
Discussion of respiratory complications, such as acute lung injury and ARDS, in the context of TBI
Renal and hepatic dysfunction associated with traumatic brain injury and their management
Emphasis on the need for a comprehensive understanding of organ interactions to improve patient outcomes in pediatric critical care

Conclusion

In summary, the episode underscores the complex interplay between brain injury and multi-system organ dysfunction. The hosts emphasize the need for a comprehensive understanding of these interactions to improve patient outcomes in pediatric TBI cases. They advocate for a team-based approach to management, focusing on individual patient physiology and the delicate balance required to address the challenges posed by non-neurologic organ dysfunction.

Connect With Us!

We hope you found value in this case-based discussion. Please share your feedback, subscribe, and leave a review on our podcast. For more resources, visit our website at PICUoncall.org.

Thank you for joining us, and stay tuned for our next episode!

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Welcome to another insightful episode of PICU on Call, a podcast dedicated to current and aspiring intensivists. In this episode, our hosts, Dr. Pradip Kamat, Dr. Rahul Damania, and their colleague, Dr. Jordan Dent, delve into the complexities of managing pneumonia in pediatric patients. The discussion is anchored around a clinical case involving a 10-year-old girl presenting with difficulty breathing and a fever, suggestive of pneumonia. We will break down the key themes and insights from the case, providing a comprehensive guide to understanding and managing pediatric pneumonia.

Case Presentation

The episode begins with a detailed case presentation:

Patient: 10-year-old girl, 28-week preemie with chronic lung disease.
Symptoms: Progressive respiratory distress over eight days, worsening cough, increased work of breathing, hypoxemia (oxygen saturation in the low 80s despite supplemental oxygen).
Findings: Chest X-ray reveals bilateral lower lobe infiltrates and a left-sided pleural effusion. Lab results show elevated CRP and a positive respiratory PCR for a bacterial pathogen.

This case sets the stage for an in-depth discussion on the various aspects of pediatric pneumoRisk Factors for Pneumonia

Understanding the risk factors for pneumonia is crucial for early identification and prevention.

These risk factors can be categorized into three main groups:

Host Factors

Incomplete Immunization Status: Children who are not fully vaccinated are at higher risk
Young Age: Infants and young children have immature immune systems, making them more susceptible
Lower Socioeconomic Status: Limited access to healthcare and poor living conditions can increase risk

Environmental Factors

Exposure to Tobacco Smoke: Secondhand smoke can damage the respiratory tract and impair immune function
Seasonal Variations: Pneumonia cases peak during fall and winter due to increased circulation of respiratory viruses
Contact with Other Children: Daycare settings and schools can facilitate the spread of infections

Healthcare-Associated Factors

Prolonged Mechanical Ventilation: Increases the risk of ventilator-associated pneumonia (VAP)
Nasogastric Tube Placement: Can introduce pathogens into the respiratory tract.
Neuromuscular Blockade: Impairs the ability to clear secretions
Inadequate Humidification: Dry air can damage the respiratory mucosa

Pathogenesis of Pneumonia

Pneumonia occurs when pathogens invade the lower respiratory tract, triggering an inflammatory response. This leads to fluid accumulation and white blood cell infiltration in the alveoli, resulting in:

Decreased Lung Compliance: The lungs become stiffer and harder to expand.
Increased Airway Resistance: Narrowing of the airways makes breathing more difficult.
Ventilation-Perfusion (V/Q) Mismatch: Impaired gas exchange leads to hypoxia and tachypnea.

Etiology by Age Group

The causative pathogens of pneumonia vary by age group:

Neonates: Group B Streptococcus, E. coli, Listeria, Klebsiella
Children Under 5: Viral causes (50% of cases) such as RSV, human metapneumovirus, and influenza, with bacterial causes like Streptococcus pneumoniae and Haemophilus influenzae
Older Children and Teens: Mycoplasma pneumonia, Chlamydia pneumonia, and Streptococcus pneumoniae

Classification of Pneumonia

Pneumonia can be classified based on the acquisition setting:

Community-Acquired Pneumonia (CAP): Occurs in patients not hospitalized in the past month
Hospital-Acquired Pneumonia (HAP): Develops after 48 hours of hospitalization
Ventilator-Associated Pneumonia (VAP): Occurs within 48 hours of intubation
Aspiration Pneumonia: Results from inhaling gastric or oral contents
Necrotizing Pneumonia: Caused by aggressive bacteria, often requiring CT imaging for diagnosis

Clinical Presentation

When a child presents with suspected pneumonia, clinicians should look for:

Systemic Symptoms: Fever, lethargy, poor appetite
Respiratory Symptoms: Tachypnea, hypoxia, and classic findings like crackles
Key Indicators: Moderate hypoxemia (SpO2 < 96%) and increased respiratory effort (nasal flaring, intercostal retractions)

Diagnostic Approach

The diagnostic workup for bacterial pneumonia typically includes:

Basic Labs: CBC, inflammatory markers (CRP, procalcitonin), and a comprehensive metabolic panel
Cultures: Blood cultures have low yield; pleural fluid cultures are more definitive
Imaging: Chest X-rays can overestimate pneumonia; point-of-care ultrasound may help identify effusions

Management Framework

Management begins with assessing whether the child can be treated at home or requires hospitalization. Key considerations for admission include:

Hypoxemia: SpO2 < 92%
Rapid Respiratory Rates: Indicative of severe respiratory distress
Toxic Appearance or Poor Oral Intake: Suggests a need for closer monitoring and supportive care

In the PICU, management involves:

Respiratory Support

Nasal Cannula: For mild cases
High-Flow Nasal Cannula (HFNC): For moderate cases
Mechanical Ventilation: For severe cases of respiratory failure

Antibiotic Therapy

Empiric Therapy: Based on age, severity, and local resistance patterns
Targeted Therapy: Adjusted based on culture results and clinical response

Supportive Care

Fluid Management: To maintain hydration and electrolyte balance
Nutrition: Ensuring adequate caloric intake
Fever Control: Using antipyretics to manage fever

Complications of Pneumonia

Complications occur in about 3% of pneumonia cases and include:

Pleural Effusion: Managed with chest tube placement and fibrinolytic therapy
Necrotizing Pneumonia: May require drainage if abscesses develop
Systemic Complications: Such as ARDS, sepsis, and multi-organ dysfunction

Conclusion

Early diagnosis and management of bacterial pneumonia are crucial to prevent complications and mortality. Key indicators include moderate hypoxemia and increased work of breathing. Diagnostic imaging findings such as large pleural effusions and cavitation strongly suggest bacterial infection.

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In today’s episode, we explore a tragic but educational case involving a 15-year-old girl who suffered severe inhalation injury following a house fire. While heroically rescuing her brother and his friend, she endured prolonged cardiac arrest and severe multi-organ dysfunction. We’ll focus on the pathophysiology, investigation, and management of inhalation injuries, including the critical role of recognizing carbon monoxide and cyanide poisoning in these complex cases.

Key Learning Points:

Exposure to house fire and prolonged cardiac arrest
Signs of inhalation injury and airway compromise
Pathophysiology of inhalation injuries and their impact on multiple organ systems
Management strategies for inhalation injury, including airway protection and ventilation
Differentiating carbon monoxide and cyanide poisoning in pediatric fire victims

Case Presentation

A 15-year-old previously healthy girl is brought to the Pediatric Intensive Care Unit (PICU) after experiencing cardiac arrest during a house fire. She was found unconscious by firefighters after a heroic rescue attempt where she saved her brother and his friend. Upon arrival at the hospital, she was unresponsive, intubated, and in severe cardiovascular distress with signs of multi-organ dysfunction.

Key findings include:

Soot deposits and superficial burns on extremities
Prolonged resuscitation (45 minutes of field CPR and 47 minutes of in-hospital CPR)
Cardiovascular compromise with PVCs, cool extremities, and delayed capillary refill
Metabolic acidosis, AKI, coagulopathy, transaminitis
Severe hypoxic-ischemic encephalopathy on EEG

These findings raise immediate concern for inhalation injury, which is the primary focus of today's discussion.

Pathophysiology of Inhalation Injury

When a patient is exposed to smoke and hot gases during a fire, inhalation injury results in significant damage to the respiratory system. Inhalation injury has three main components:

Upper airway involvement – Thermal injury can cause swelling and obstruction.
Chemical pneumonitis – Noxious chemicals like carbon monoxide and cyanide trigger inflammation in the lungs.
Systemic toxicity – Toxins such as carbon monoxide and cyanide can affect cellular oxygen utilization.

The primary damage occurs in the lower respiratory tract, leading to airway edema, mucosal damage, and bronchial cast formation. This process can result in bacterial pneumonia, respiratory failure, and the need for aggressive intervention.

Investigating Inhalation Injury

A thorough diagnostic approach is essential when assessing patients with suspected inhalation injury:

Basic Imaging: A chest X-ray (CXR) should be obtained, although a normal film doesn't rule out injury.
Gold Standard – Bronchoscopy: Direct visualization allows for assessment and removal of bronchial casts.
Laboratory Tests: Key labs include CBC, CMP, blood gas, lactate, co-oximetry (to assess CO levels), and toxicology screens.
CO and Cyanide Testing: Critical for identifying toxic exposure, especially when a patient presents with altered mental status or unexplained metabolic acidosis.

Managing Inhalation Injury: A Structured Approach

Management revolves around three key pillars:

Airway Protection: Intubation is essential for airway security. Signs such as progressive hoarseness, soot around the nose, or face burns should prompt early intervention.
Ventilation Strategies: Use low tidal volumes and optimized PEEP for lung protection. In severe cases, consider advanced modalities like APRV, HFOV, or ECMO.
Secretion Management: Aggressive pulmonary toilet and medications such as nebulized heparin, tPA, and N-acetylcysteine may help manage airway inflammation and obstructions.

Recognizing and Treating Carbon Monoxide (CO) Poisoning

In cases of suspected CO poisoning, the key is early recognition and treatment:

CO Blood Levels: Measure carboxyhemoglobin levels immediately.
Classic Symptoms: Look for the “cherry red” skin color and neurologic symptoms such as confusion or dizziness.
First-Line Therapy: Administer 100% oxygen via a non-rebreather mask or endotracheal tube.
Hyperbaric Oxygen: While 100% O2 works well, HBO therapy is crucial for preventing delayed neuropsychiatric complications.

Fun Fact: CO has a much higher affinity for hemoglobin than oxygen, which leads to a "tissue oxygen famine," even with normal PaO2 levels.

Identifying Cyanide Poisoning in Fire Victims

Cyanide poisoning can be particularly challenging to diagnose but is crucial in fire victims. Look for:

Classic Triad: Metabolic acidosis, elevated venous oxygen saturation, and CNS symptoms (confusion, mydriasis).
Late Signs: Cardiovascular collapse, hypotension, and bradycardia.
Treatment: Hydroxocobalamin is the first-line antidote (70 mg/kg IV), with the caveat that purple-red urine is a normal side effect.
Avoid Nitrites: In burn victims, nitrite-based cyanide kits can worsen CO poisoning by forming methemoglobin.

Clinical Tip: Unlike CO poisoning, cyanide poisoning presents with seizures and dilated pupils.

Clinical Course of Our Patient

The patient’s clinical course was marked by rapid deterioration despite aggressive treatment:

Initially managed with high-frequency oscillatory ventilation (HFOV) due to pulmonary hemorrhage
Developed severe PARDS, cardiac dysfunction, and multi-organ failure within 12 hours
Ultimately, neuroimaging revealed anoxic brain injury with cerebral edema and herniation, leading to brain death

This heartbreaking case highlights the importance of early intervention and recognition of inhalation injury in burn victims.

Key Takeaways:

Act quickly to protect the airway in pediatric fire victims—early intubation can be life-saving.
Protect the lungs with proper ventilation strategies and aggressive secretion management.
Time is critical when dealing with CO and cyanide poisoning. Immediate recognition and treatment are key to survival.
Inhalation injuries can result in rapid multi-organ failure, and management requires a multi-disciplinary approach.

Join Us for More Insights

We hope this case-based discussion provides valuable insights into the complex management of inhalation injuries in pediatric burn victims. Stay tuned for our next episode and be sure to share your feedback and subscribe to the podcast!

For more episodes, visit our website at picudoconcall.org.

References:

Tapking C., et al. "Burn and Inhalation Injury." Fuhrman & Zimmerman - Textbook of Pediatric Critical Care, Chapter 116, Pages 1347-1362.
Bergman, et al. "Burns and Smoke Inhalation." Rogers Textbook of Pediatric Intensive Care, 6th edition, Chapter 33, Pages 484-497.
Goh CT, Jacobe S. "Ventilation strategies in pediatric inhalation injury." Paediatr Respir Rev. 2016 Sep;20:3-9.
Rodeberg DA, Housinger TA, et al. "Improved ventilatory function in burn patients using volumetric diffusive respiration." J Am Coll Surg. 1994 Nov;179(5):518-522.

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Welcome and Episode Introduction* Hosts: Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital) * Mission: A podcast dedicated to current and aspiring pediatric intensivists, exploring intriguing PICU cases and acute care pediatric management * Focus of the Episode: Managing toxic alcohol ingestion in the PICU with emphasis on ethanol, methanol, ethylene glycol, propylene glycol, and isopropyl alcohol

Case Presentation* Patient Details: A 7-month-old male presented with accidental ethanol ingestion after his formula was mixed with vodka * Key Symptoms: Lethargy, uncoordinated movements, decreased activity, and ethanol odor * Initial Labs & Findings: * EtOH level: 420 mg/dL. * Glucose: 50 mg/dL. * Normal CXR and EKG. * PICU Presentation: Tachycardic, normotensive, lethargic, with signs of CNS depression * Initial Management: Dextrose infusion, glucose monitoring, neurological observation, and ruling out complications

Key Learning Points from the Case* Toxic alcohol ingestion in pediatrics requires rapid stabilization and targeted interventions * Hypoglycemia and CNS depression are common features of ethanol toxicity in infants * Management prioritizes glucose correction, airway support, and close neurological monitoring

Deep Dive: Toxic Alcohols in the PICU1. Ethanol

Typical Presentation in Infants/Toddlers: Hypotonia, ataxia, coma, hypoglycemia, hypotension, and hypothermia
Diagnostic Workup:
Focus on CNS and metabolic effects
Labs: Glucose, electrolytes, bicarbonate, anion gap, ketones, toxicology screen
Imaging (head CT) if indicated
Management: Stabilization, IV dextrose for hypoglycemia, NPO status until alert, and consultation with poison control and social work

2. Methanol

Sources: Windshield fluids, cleaning agents, moonshine

Clinical Stages:

Early: Dizziness, nausea, vomiting (0–6 hours)
Latent: Asymptomatic (6–30 hours)
Late: Vision disturbances, seizures, respiratory failure (6–72 hours)
Key Symptoms: “Snowstorm blindness” from retinal toxicity
Management: Fomepizole, correction of metabolic acidosis, and hemodialysis in severe cases

3. Ethylene Glycol

Sources: Antifreeze, brake fluids, household cleaners
Pathophysiology: Metabolism to glycolic acid (acidosis) and oxalic acid (renal failure due to calcium oxalate crystals)
Red Flags: Hypocalcemia, renal failure, QT prolongation
Management: Fomepizole, supportive care, and hemodialysis for severe toxicity

4. Propylene Glycol

Sources: Medications like lorazepam and pentobarbital
Presentation: High anion gap metabolic acidosis at high doses, with renal and liver dysfunction
Management: Discontinue offending agent, supportive care, and hemodialysis if severe

5. Isopropyl Alcohol

Sources: Disinfectants, hand sanitizers
Presentation: CNS depression, GI irritation, fruity acetone breath, but no metabolic acidosis
Management: Supportive care; fomepizole and ethanol are ineffective

Key Laboratory Insights* Osmolar Gap Formula: * Measured Osmolality - Calculated Osmolality * A high osmolar gap indicates unmeasured osmoles like toxic alcohols. * Lactate Gap in Ethylene Glycol: Discrepancy between bedside and lab lactate levels due to glycolate interference

Management Pearls* Ethanol and Ethylene Glycol: Fomepizole as first-line treatment; hemodialysis for severe cases * Methanol: Similar approach with additional focus on preventing blindness * Propylene Glycol: Monitor lactate and renal function, discontinue offending medications * Isopropyl Alcohol: Supportive care, no acidosis present

Mnemonics for Toxic AlcoholsMEGA GAP:

Methanol and Ethylene Glycol: Anion Gap Acidosis with elevated Osmolar Gap
Isopropyl Alcohol: Isolated Osmolar Gap (no acidosis)
Propylene Glycol: Mimics ethylene glycol with HAGMA at high doses

Takeaway Messages* Early recognition of toxic alcohol ingestion is critical for successful management * Differentiate between toxic alcohols using anion gap, osmolar gap, and clinical presentation * Engage poison control and social work early in the process

Conclusion* Pediatric toxic alcohol ingestions are rare but potentially life-threatening * Fomepizole is a cornerstone therapy for methanol and ethylene glycol toxicity * Supportive care remains essential across all toxic alcohol ingestions

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Did you know that Multi-Organ Dysfunction Syndrome (MODS) can result from both infectious and non-infectious causes? In our latest episode, we delve deep into the pathophysiology of MODS, exploring how different organs interact and fail in sequence. We discuss key concepts like organ functional reserve and the kinetics of organ injury, which aren’t as straightforward as they seem. Tune in to learn about the non-linear progression of organ damage and how it impacts management strategies in pediatric critical care.

We break down the case into key elements:

Patient Background: A 15-year-old girl with chronic TPN dependence and a PICC line presented with septic shock and respiratory failure.
Initial Presentation: Blood cultures confirmed Gram-negative rod bacteremia. She developed multi-system complications, including acute kidney injury (AKI), thrombocytopenia, and cardiac dysfunction.
Management: Broad-spectrum antibiotics, mechanical ventilation, vasoactive agents, and supportive care for MODS.

Key Case Highlights:* Clinical case of a 15-year-old girl with sepsis from a gram-negative rod * Dependence on total parenteral nutrition (TPN) and prolonged PICC line use * Discussion of septic shock, acute respiratory failure, and acute kidney injury * Overview of multiple organ dysfunction syndrome (MODS) and its definitions * Pathophysiology of MODS, including organ functional reserve and kinetics of organ injury * Molecular mechanisms involved in MODS, such as mitochondrial dysfunction and immune responses * Specific phenotypes of sepsis-induced MODS, including TAMOF and IPMOF * Management strategies for MODS, emphasizing multidisciplinary approaches * Role and complications of therapeutic plasma exchange (TPE) in treating MODS * Importance of recognizing signs of MODS and timely intervention in pediatric patients

Segment 1: MODS Definitions and Phenotypes* Key Definition: MODS is the progressive failure of two or more organ systems due to systemic insults (infectious or non-infectious). * Phenotypes: * TAMOF (Thrombocytopenia-Associated Multi-Organ Failure): Characterized by thrombocytopenia, hemolysis, and decreased ADAMTS13 activity. * Immunoparalysis: Persistent immunosuppression and risk of secondary infections. * Sequential Liver Failure: Often associated with viral triggers.

Segment 2: Pathophysiology of MODSMolecular Insights:

Mitochondrial dysfunction and damage-associated molecular patterns (DAMPs)
Innate and adaptive immune dysregulation
Microcirculatory dysfunction and ischemia-reperfusion injury
Organ Interactions: MODS evolves through complex multi-organ interdependencies

Segment 3: Diagnosis and Evidence-Based Management* Key Diagnostic Pearls: * MODS is not solely infection-driven; it requires a shared mechanism and predictable outcomes. * Use biomarkers like ADAMTS13 and TNF-α response for phenotypic classification. * Management Highlights: * Supportive Care: Multisystem approach including lung-protective ventilation, renal replacement therapy, and hemodynamic support. * Therapeutic Plasma Exchange (TPE): Especially effective in TAMOF by restoring ADAMTS13 and removing inflammatory mediators.

Segment 4: Practical Tips for Intensivists* Early recognition of MODS phenotypes for targeted therapy * Importance of multidisciplinary teamwork in critical care settings * Monitoring for complications like TMA and immunoparalysis during prolonged ICU stays

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In this episode, we discuss the case of a 15-year-old girl who presents with progressive headache, nausea, vomiting, and difficulty ambulating. Her condition rapidly evolves into altered mental status and severe hydrocephalus, leading to a compelling discussion about the evaluation, diagnosis, and management of hydrocephalus in pediatric patients.

We break down the case into key elements:

A comprehensive look at acute hydrocephalus, including its pathophysiology and causes
Epidemiological insights, clinical presentation, and diagnostic approaches
Management strategies, including temporary and permanent CSF diversion techniques
A review of complications related to shunts and endoscopic third ventriculostomy

Key Case Highlights:* Patient Presentation: * A 15-year-old girl with a 3-day history of worsening headaches, nausea, vomiting, and difficulty walking * Altered mental status and bradycardia upon PICU admission * CT scan revealed severe hydrocephalus without a clear mass lesion * Management Steps in the PICU: * Hypertonic saline bolus improved her mental status and pupillary reactions * Neurosurgery consultation recommended MRI and close neuro checks * Initial management included dexamethasone, keeping the patient NPO, and hourly neuro assessments * Differential Diagnosis: * Obstructive (non-communicating) vs. non-obstructive (communicating) hydrocephalus * Consideration of alternative diagnoses like intracranial hemorrhage and idiopathic intracranial hypertension

Episode Learning Points:* Hydrocephalus Overview: * Abnormal CSF buildup in the ventricles leading to increased intracranial pressure (ICP) * Key distinctions between obstructive and non-obstructive types

Epidemiology and Risk Factors:

Congenital causes include genetic syndromes, neural tube defects, and Chiari malformations
Acquired causes: post-hemorrhagic hydrocephalus (e.g., from IVH in preemies), infections like TB meningitis, and brain tumors

Clinical Presentation:

Infants: Bulging fontanelles, sunsetting eyes, irritability
Older children: Headaches, vomiting, papilledema, and gait disturbances

Management Framework:

Temporary CSF diversion via external ventricular drains (EVD) or lumbar catheters
Permanent interventions include VP shunts and endoscopic third ventriculostomy (ETV)

Complications of Shunts and ETV:

Shunt infections, malfunctions, over-drainage, and migration
ETV-specific risks, including delayed failure years post-procedure

Clinical Pearl:

Communicating hydrocephalus involves symmetric ventricular enlargement and is often linked to inflammatory or post-treatment changes affecting CSF reabsorption.

Hosts’ Takeaway Points:

Dr. Pradip Kamat emphasizes the importance of timely recognition and intervention in hydrocephalus to prevent complications like brain herniation.
Dr. Rahul Damania highlights the need for meticulous neurological checks in PICU patients and an individualized approach to treatment.

Resources Mentioned:* Hydrocephalus Clinical Research Network guidelines. * Recent studies on ETV outcomes in pediatric populations.

Call to Action:If you enjoyed this discussion, please subscribe to PICU Doc On Call and leave a review. Have a topic you’d like us to cover? Reach out to us via email or on social media!

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Twitter: @PICUDocOnCall
Email: contact@picudoconcall.com

Stay tuned for more cases that challenge and inspire us as PICU clinicians!

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Introduction* Hosts: Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital) * Mission: A podcast dedicated to current and aspiring pediatric intensivists, exploring intriguing PICU cases and acute care pediatric management * Focus of the Episode: Managing toxic alcohol ingestion in the PICU with emphasis on ethanol, methanol, ethylene glycol, propylene glycol, and isopropyl alcohol

Deep Dive: Toxic Alcohols in the PICU1. Ethanol

Typical Presentation in Infants/Toddlers: Hypotonia, ataxia, coma, hypoglycemia, hypotension, and hypothermia
Diagnostic Workup:
Focus on CNS and metabolic effects
Labs: Glucose, electrolytes, bicarbonate, anion gap, ketones, toxicology screen
Imaging (head CT) if indicated
Management: Stabilization, IV dextrose for hypoglycemia, NPO status until alert, and consultation with poison control and social work

2. Methanol

Sources: Windshield fluids, cleaning agents, moonshine
Clinical Stages:
Early: Dizziness, nausea, vomiting (0–6 hours)
Latent: Asymptomatic (6–30 hours)
Late: Vision disturbances, seizures, respiratory failure (6–72 hours)
Key Symptoms: “Snowstorm blindness” from retinal toxicity
Management: Fomepizole, correction of metabolic acidosis, and hemodialysis in severe cases

3. Ethylene Glycol

Sources: Antifreeze, brake fluids, household cleaners
Pathophysiology: Metabolism to glycolic acid (acidosis) and oxalic acid (renal failure due to calcium oxalate crystals)
Red Flags: Hypocalcemia, renal failure, QT prolongation
Management: Fomepizole, supportive care, and hemodialysis for severe toxicity

4. Propylene Glycol

Sources: Medications like lorazepam and pentobarbital
Presentation: High anion gap metabolic acidosis at high doses, with renal and liver dysfunction
Management: Discontinue offending agent, supportive care, and hemodialysis if severe

5. Isopropyl Alcohol

Sources: Disinfectants, hand sanitizers
Presentation: CNS depression, GI irritation, fruity acetone breath, but no metabolic acidosis
Management: Supportive care; fomepizole and ethanol are ineffective

Mnemonics for Toxic AlcoholsMEGA GAP:

Methanol and Ethylene Glycol: Anion Gap Acidosis with elevated Osmolar Gap
Isopropyl Alcohol: Isolated Osmolar Gap (no acidosis)
Propylene Glycol: Mimics ethylene glycol with HAGMA at high doses

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Email: contact@picudoconcall.com

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Introduction:Today, Dr. Rahul Damania, Dr. Pradip Kamat, and their guest, Dr. Jordan Dent, discuss a critical case involving a 15-year-old male who collapsed during football practice due to exertional heat stroke. The discussion emphasizes the clinical presentation, risk factors, pathophysiology, and evidence-based management of heat stroke and other heat-related illnesses in pediatric patients. The episode also delves into the role of rapid cooling interventions and long-term care to minimize mortality and morbidity.

Case Summary: A 15-year-old male with ADHD collapsed during football practice on a hot, humid day. He presented with:

Normotension (BP: 101/67 mmHg)
Tachycardia (HR: 157 bpm)
Tachypnea (RR: 40 breaths/min)
Febrile (Rectal temp: 41.8°C/107.2°F)
Dry, hot skin, GCS of 9
Lab abnormalities: hyponatremia, hypokalemia, hypoglycemia, elevated creatinine, liver enzymes, lactate, CK, and troponin

After suffering cardiac arrest and undergoing resuscitation, the patient developed multiorgan dysfunction, including seizures, encephalopathy, and cerebral edema. Despite severe initial complications, the patient demonstrated neurological improvement with left-side hemiparesis before discharge.

Key Discussion Points:

Etiology and Pathophysiology of Heat Stroke:
Heat stroke occurs when the body’s thermoregulatory mechanisms fail, leading to dangerous elevations in core body temperature. Exertional heat stroke is common during strenuous physical activity in hot, humid environments.
Key physiological breakdowns include inadequate sweating, vasodilation dysfunction, and subsequent cellular damage due to hyperthermia.
Risk Factors for Exertional Heat Stroke:
Environmental factors: High temperature, humidity, lack of hydration, and breaks.
Athlete-related factors: Hypohidrosis, dehydration, medical conditions, and medications (e.g., Adderall).
Heat illness is the third leading cause of death in high school athletics, with American football players particularly at risk.
Spectrum of Heat-Related Illness:
Heat Cramps: Involuntary muscle contractions due to dehydration and electrolyte imbalance.
Heat Syncope: Transient loss of consciousness due to heat exposure.
Heat Exhaustion: Milder heat illness with core temperature < 104°F, potentially progressing to heat stroke if untreated.
Heat Stroke: Life-threatening with core temperature ≥ 104°F, CNS dysfunction, and risk of multiorgan failure.
Management of Heat Stroke:
Rapid Cooling: Immediate cooling to bring core temperature down to 39°C within 30 minutes is critical. Methods include ice packs, cold water immersion, and core cooling techniques (cold IV fluids, gastric lavage).
Supportive Care: Management of shock, electrolyte imbalances, rhabdomyolysis, DIC, and ARDS.
Monitoring and Long-Term Care: Continuous EEG, fluid management, and rehabilitation are key in managing neurological and systemic complications.
Differentiating Heat Stroke from Fever:
Fever results from a reset of the hypothalamic setpoint due to pyrogens, while heat stroke involves the failure of thermoregulation without a change in the hypothalamic setpoint.
Case Outcome:
The patient initially suffered significant neurological damage but improved with intensive care and rehabilitation. By discharge, the patient showed notable recovery, though with some lasting deficits.

Key Takeaways:

Heat stroke is a medical emergency with a high risk of mortality and long-term complications if not treated promptly.
Early recognition, rapid cooling, and a multidisciplinary approach are critical to improving outcomes.
Athletes and children engaging in strenuous activities in hot environments should be closely monitored for signs of heat-related illness.

References:

Fuhrman, B., & Zimmerman, J. J. (2020). Hyperthermic Injury. In Textbook of Pediatric Critical Care (pp. 1327-1331).
Rogers, M. C., et al. (2016). Thermoregulation. In Rogers' Textbook of Pediatric Intensive Care (pp. 546-552).
Ishimine, P. (2022). Heat Stroke in Children. UpToDate. Retrieved from www.uptodate.com/contents/heat-stroke-in-children.
Jardine, D. S. (2007). Heat Illness and Heat Stroke. Pediatrics in Review, 28(7), 249–258. https://doi.org/10.1542/pir.28-7-249.
Patel, J., et al. (2023). Critical illness aspects of heatstroke: A hot topic. Journal of Intensive Care Society, 24(2), 206-214. https://doi.org/10.1177/17511437221148922.
Ramirez, O., Malyshev, Y., & Sahni, S. (2018). It’s Getting Hot in Here: A Rare Case of Heat Stroke in a Young Male. Cureus, 10(12), e3724. https://doi.org/10.7759/cureus.3724.

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IntroductionWelcome to PICU Doc On Call, a podcast dedicated to current and aspiring pediatric intensivists. I'm Dr. Pradip Kamat from Children’s Healthcare of Atlanta/Emory University School of Medicine, and I’m Dr. Rahul Damania from Cleveland Clinic Children’s Hospital. We are two Pediatric ICU physicians passionate about medical education in the PICU. This podcast focuses on interesting PICU cases and their management in the acute care pediatric setting.

Episode OverviewIn today’s episode, we are excited to welcome Dr. Karen Zimowski, Assistant Professor of Pediatrics at Emory University School of Medicine and a practicing pediatric hematologist at Children’s Healthcare of Atlanta at the Aflac Blood & Cancer Center. Dr. Zimowski specializes in pediatric bleeding and clotting disorders.

Case PresentationA 16-year-old female with a complex medical history, including autoimmune thyroiditis and prior cerebral infarcts, was admitted to the PICU with acute chest pain and difficulty breathing. Despite being on low-dose aspirin, her oxygen saturation was 86% on room air. A CT angiography revealed a pulmonary embolism (PE) in the left lower lobe and signs of right heart strain. The patient was hemodynamically stable, and thrombolytic therapy was deferred in favor of anticoagulation. She was placed on BiPAP to improve her respiratory status. Her social history was negative for smoking, illicit drug use, or oral contraceptive use.

Key Case Points* Diagnosis: Pulmonary embolism (PE) * Hemodynamics: Stable with no right ventricular (RV) strain on echocardiogram * Management Focus: Anticoagulation and consultation with the hematology/thrombosis team

Expert Discussion with Dr. Karen ZimowskiRisk Factors and Epidemiology of VTE in Pediatrics* Pathophysiology: Venous thromboembolism (VTE) in children involves components of Virchow’s triad: stasis of blood flow, endothelial injury, and hypercoagulability. * Incidence: VTE is rare in the general pediatric population but increases significantly in hospitalized children. * Age Distribution: Bimodal peaks in infants and adolescents aged 15-17 years. * Risk Factors: Central venous lines, infections, congenital heart disease, cancer, and autoimmune disorders.

Clinical Manifestations of DVT* Symptoms: Swelling, pain, warmth, and skin discoloration in the affected extremity. * Specific Presentations: * SVC syndrome from superior vena cava thrombosis * Abdominal pain from portal vein thrombosis * Hematuria from renal vein thrombosis * Neurological symptoms from cerebral sinus venous thrombosis

Diagnostic Approach for DVT Imaging: * Compression Doppler Ultrasonography: Primary method for diagnosing DVT in pediatric patients. * MR Venography (MRV) and CT Venography (CTV): Used for abdominal and cerebral sinus thrombosis. * Laboratory Studies:* * D-dimer: Useful in adults; limited specificity in children. * Other Labs: Renal and liver function tests, CBC with differential, DIC panel.

Management of DVTAnticoagulation Strategies* Unfractionated Heparin (UFH): * Targets factors IIa and Xa; requires frequent monitoring. * Adverse events: Bleeding and thrombocytopenia. * Low Molecular Weight Heparin (LMWH): * More predictable pharmacokinetics than UFH. * Advantages include ease of administration and lower risk of HIT. * Vitamin K Antagonists (VKAs): * Used for long-term anticoagulation. * Requires regular INR monitoring. * Direct Oral Anticoagulants (DOACs): * Dabigatran, Rivaroxaban, and Apixaban used in pediatric VTE. * Advantages: No routine monitoring required, predictable effects.

ConclusionIn this episode, we discussed the intricacies of VTE diagnosis and management in pediatric patients. We thank Dr. Karen Zimowski for sharing her expertise on anticoagulation and hemostasis in the PICU. For more episodes and our Doc on Call management cards, visit picudoconcall.org.

Stay tuned for our next episode, and thank you for listening!

References1. Fuhrman & Zimmerman - Textbook of Pediatric Critical Care: Thrombosis in Pediatric Critical Care. 2. American Society of Hematology 2018 Guidelines for Management of Venous Thromboembolism: Treatment of Pediatric Venous Thromboembolism. 3. Antithrombotic Therapy in Neonates and Children: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. 4. O’Brien, SH, Stanek JR, Witmer CM, Raffini L. The Continued Rise of Venous Thromboembolism Across US Children’s Hospitals. Pediatrics (2022).

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Welcome to PICU Doc On Call, where Dr. Pradip Kamat from Children’s Healthcare of Atlanta/Emory University School of Medicine and Dr. Rahul Damania from Cleveland Clinic Children’s Hospital delve into the intricacies of Pediatric Intensive Care Medicine. In this special episode of PICU Doc on Call shorts, we dissect the Alveolar Gas Equation—a fundamental concept in respiratory physiology with significant clinical relevance.

Key Concepts Covered:

Alveolar Gas Equation Demystified: Dr. Rahul explains the Alveolar Gas Equation, which calculates the partial pressure of oxygen in the alveoli (PAO2). This equation, PAO2 = FiO2 (Patm - PH2O) - (PaCO2/R), is essential in understanding hypoxemia and the dynamics of gas exchange in the lungs.
Calculating PAO2: Using the Alveolar Gas Equation, the hosts demonstrate how to calculate PAO2 at sea level, emphasizing the influence of atmospheric pressure, fraction of inspired oxygen (FiO2), water vapor pressure, arterial carbon dioxide pressure (PaCO2), and respiratory quotient (R) on oxygenation.
A-a Gradient and Hypoxemia: The A-a gradient, derived from the Alveolar Gas Equation, is discussed in the context of hypoxemia evaluation. Understanding the causes of hypoxemia, including ventilation/perfusion (V/Q) mismatch, anatomical shunt, diffusion defects, and hypoventilation, is crucial for clinical diagnosis and management.
Clinical Scenarios and A-a Gradient Interpretation: Through a clinical scenario, the hosts elucidate how different conditions affect the A-a gradient and oxygenation, providing insights into respiratory pathophysiology and differential diagnosis.
Clinical Implications and Management Strategies: The hosts highlight the clinical significance of the Alveolar Gas Equation in assessing oxygenation status, diagnosing gas exchange abnormalities, and tailoring respiratory management strategies in the pediatric intensive care setting.

Key Takeaways:

Utility of the Alveolar Gas Equation: Understanding and applying the Alveolar Gas Equation is essential for evaluating oxygenation and diagnosing respiratory abnormalities.
Interpreting A-a Gradient: A normal A-a gradient suggests alveolar hypoventilation as the likely cause of hypoxemia, whereas elevated gradients indicate other underlying pathologies.
Clinical Relevance: Recognizing the clinical implications of the Alveolar Gas Equation aids in accurate diagnosis and optimal management of respiratory conditions in pediatric intensive care patients.

Conclusion:

Join Dr. Kamat and Dr. Damania as they unravel the complexities of the Alveolar Gas Equation, providing valuable insights into respiratory physiology and its clinical applications. Don’t forget to subscribe, share your feedback, and visit picudoconcall.org for more educational content and resources.

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter: Physiology of the respiratory system. Chapter 42. Khemani et al. Pages 470-481
Rogers textbook of Pediatric intensive care: Chapter 44. Respiratory physiology. Akong K et al. Pages 691-721
Respiratory Physiology for the Anesthesiologist. Bigatello L and Pesenti A, Anesthesiology 2019; 130: 1064-77

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

Hosts:
Dr. Pradip Kamat: Children’s Healthcare of Atlanta/Emory University School of Medicine
Dr. Rahul Damania: Cleveland Clinic Children’s Hospital

Introduction:

Pediatric Intensive Care Unit (PICU) physicians passionate about medical education in the acute care pediatric setting
Episode focus: A case of a 23-month-old ex-28 week premie presenting with sudden high fever and rapidly rising ETCO2 during surgery

Case Presentation:

Presented by Dr. Rahul Damania
23-month-old ex-28 week premie intubated during hernia repair surgery
Noticed rapidly rising ETCO2, unprovoked tachycardia, and elevated temperature
Transferred to PICU, exhibiting rigidity, clenched jaw, metabolic acidosis, and elevated lactate.
Consideration of Malignant Hyperthermia (MH) crisis

Key Points:

Elevated temperature, hypercapnia, metabolic acidosis, and unprovoked tachycardia raise concern for MH
Organized discussion on pathophysiology, clinical signs, symptoms, and management

Multiple Choice Question:

Diagnosis of MH crisis during scoliosis repair
Correct Answer: D) Sarcoplasmic reticulum
Dantrolene acts on the sarcoplasmic reticulum to inhibit calcium release, crucial in MH management

Clinical Presentation of MH Crisis:

Tachycardia, acidosis, muscle stiffness, and hyperthermia are hallmark features
Potential life-threatening complications underscore the urgency of recognition and treatment

Triggers and Pathophysiology of MH Crisis:

Triggered by inhalational agents and depolarizing neuromuscular blocking agents
Pathophysiology involves defective Ryanodine receptor leading to uncontrolled calcium release

Differential Diagnosis:

Includes sepsis, thyroid storm, pheochromocytoma, and neuroleptic malignant syndrome
Differentiation from similar conditions crucial for accurate management

Diagnostic Approach:

High clinical suspicion
Genetic testing (ryanodine receptor gene sequencing) and Caffeine Halothane Contracture Test (CHCT) for diagnosis
Immediate workup during crisis includes blood gas, lactate, CPK, CMP, and urine analysis

General Management Framework:

MH crisis is a medical emergency requiring rapid intervention
Dantrolene Na administration, supportive measures, and continuous monitoring in PICU
Utilization of Malignant Hyperthermia carts and involvement of specialized hotlines

Clinical Pearls and Pitfalls:

Early recognition is crucial.
Proper administration of Dantrolene Na without delay
Extended monitoring period in PICU to ensure stability

Conclusion:

Importance of recognizing and managing MH crisis
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Website picudoconcall.org for additional resources

References:

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter
Malignant Hyperthermia Association of the United States
What is MH?
Managing a crisis
Rosenbaum HK, Rosenberg H. UpToDate: Malignant hyperthermia: diagnosis and management of acute crisis.

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Show Introduction

Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists.
Hosted by Dr. Pradip Kamat and Dr. Rahul Damania

Case Presentation

A 14-year-old female with a history of depression and oppositional defiant disorder presents with dizziness, slurring speech, and is pale appearance.
The mother noticed symptoms of dizziness, stumbling, and sleepiness.
The patient had a prior suicide attempt.
Vital signs: HR 50 bpm, BP 75/40, GCS 10.
The initial workup reveals hyperglycemia, and she is stabilized and admitted to the PICU.

Key Aspects of Ingestion Work-up

History and physical exam are crucial.
Stratify acute or chronic ingestions.
Consider baseline medications and coingestants.
Perform initial screening examination to identify immediate measures for stabilization.

Diagnostic Studies

Pulse oximetry, continuous cardiac monitoring, ECG, capillary glucose measurement.
Serum acetaminophen, ASA levels
Consider extended toxicology screen.

Differentiating CCB vs. Beta-Blocker Overdose

ECG findings: PR interval prolongation and Bradydysrhythmia suggest CCB poisoning.
Hyperglycemia in non-diabetic patients may indicate CCB overdose

Approach to CCB Overdose

Initial resuscitation and stabilization
ABC approach
Consult Poison Control Center
Empiric use of glucagon, IV fluids, and vasopressors
Consideration of orogastric lavage and activated charcoal

Specific Medical Therapies

Vasopressors: norepinephrine/epinephrine infusion
Atropine for bradycardia
IV calcium salts to overcome cardiovascular effects
High-dose insulin and dextrose for myocardial function
Investigational therapies: methylene blue, lipid emulsion

Procedures

Transvenous pacemaker placement if needed
ECMO in refractory hypotension

Key Takeaways

Hypotension and bradycardia indicate life-threatening toxidromes.
Differential includes CCB, BB, digoxin, clonidine, and CNS depressants.
Stepwise approach includes close monitoring of ABCs and specific medical therapies.

Thank you for listening to PICU Doc On Call. We would love for you to share your feedback, subscribe, and review our podcast.

Visit picudoconcall.org for more information and resources.

Stay tuned for our next episode!

References

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 125 and 126.
St-Onge M et al. Treatment for calcium channel blocker poisoning: a systematic review.
DeRoos F. Calcium channel blockers. In: Goldfrank's Toxicologic Emergencies, 8th edition.

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Hosts:

Pradip Kamat, Children’s Healthcare of Atlanta/Emory University School of Medicine
Rahul Damania, Cleveland Clinic Children’s Hospital

Introduction

Today, we discuss the case of an 8-month-old infant with severe bronchospasm and abnormal blood gas. We'll delve into the epidemiology, pathophysiology, and evidence-based management of acute bronchiolitis.

Case Summary

An 8-month-old infant presented to the ER with decreased alertness following worsening work of breathing, preceded by URI symptoms. The infant was intubated and transferred to the PICU, testing positive for RSV. Initial blood gas showed 6.8/125/-4, and CXR revealed massive hyperinflation. Vitals: HR 180, BP 75/45, SPO2 92% on 100% FIO2, RR 12 (prior to intubation), now around 16 on the ventilator, afebrile.

Discussion Points

Etiology & Pathogenesis: Bronchiolitis is primarily caused by RSV, with other viruses and bacteria playing a role. RSV bronchiolitis is the most common cause of hospitalization in infants, particularly in winter months. Immuno-pathology involves an unbalanced immune response and can lead to various extra-pulmonary manifestations.
Diagnosis: Diagnosis is clinical, based on history and examination. Key signs include upper respiratory symptoms followed by lower respiratory distress. Blood gas, chest radiography, and viral testing are generally not recommended unless warranted by severe symptoms or clinical deterioration.
Management Framework: For patients requiring PICU admission, focus on oxygenation and hydration. High-flow therapy and nasal continuous positive airway pressure (CPAP) can be used. Hydration and feeding support are crucial. Antibiotics, steroids, and bronchodilators are generally not recommended. Mechanical ventilation and ECMO may be necessary in severe cases.
Immunoprophylaxis & Nosocomial Infection Prevention: Palivizumab and nirsevimab are used for RSV prevention in high-risk infants. Strict infection control measures, including hand hygiene and isolation, are essential to prevent nosocomial infections.

Conclusion

RSV bronchiolitis is a common and potentially severe respiratory illness in infants. Management focuses on supportive care, with a careful balance between oxygenation and hydration. Immunoprophylaxis and infection control are crucial in preventing the spread of the virus.

Thank you for listening to our episode on acute bronchiolitis. Please subscribe, share your feedback, and visit our website at picudoconcall.org for more resources. Stay tuned for our next episode!

References

Rogers - Textbook of Pediatric Critical Care Chapter 49: Pneumonia and Bronchiolitis. De Carvalho et al. page 797-823

Reference 1: Dalziel, Stuart R; Haskell, Libby; O'Brien, Sharon; Borland, Meredith L; Plint, Amy C; Babl, Franz E; Oakley, Ed. Bronchiolitis. The Lancet. , 2022, Vol.400(10349), p.392-406. DOI: 10.1016/S0140-6736(22)01016-9; PMID: 35785792

Reference 2: Schroeder AR, Destino LA, Ip W, Vukin E, Brooks R, Stoddard G, Coon ER. Day of Illness and Outcomes in Bronchiolitis Hospitalizations. Pediatrics. 2020 Nov;146(5):e20201537. doi: 10.1542/peds.2020-1537. PMID: 33093138.

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Hosts:

Pradip Kamat, Children’s Healthcare of Atlanta/Emory University School of Medicine
Rahul Damania, Cleveland Clinic Children’s Hospital

Case Introduction:

6-year-old patient admitted to PICU with severe pneumonia complicated by pediatric Acute Respiratory Distress Syndrome (pARDS).
Presented with respiratory distress, hypoxemia, and significant respiratory acidosis.
Required intubation and mechanical ventilation.
Despite initial interventions, condition remained precarious with persistent hypercapnia.

Physiology Concept: Dead Space

Defined as the volume of air that does not participate in gas exchange.
Consists of anatomic dead space (large airways) and physiologic dead space (alveoli).
Physiologic dead space reflects ventilation-perfusion mismatch.

Pathological Dead Space:

Occurs due to conditions disrupting pulmonary blood flow or ventilation.
Common in conditions like pulmonary embolism, severe pneumonia, or ARDS.

Clinical Implications:

Increased dead space fraction (DSF) in PARDS is a prognostic factor linked to severity and mortality.
Elevated DSF indicates worse lung injury and inefficient gas exchange.
DSF can be calculated using the formula: DSF = (PaCO2 – PetCO2) / PaCO2.

Practical Management:

Optimize Mechanical Ventilation
Enhance Perfusion
Consider Positioning (e.g., prone positioning)

Summary of Physiology Concepts:

Bohr equation for physiologic dead space.
Importance of lung-protective ventilation strategies.
Monitoring and trending dead space fraction.
Strategies to improve airway patency and mucociliary clearance.

Connect with us!

PICU Doc on Call provides concise explanations of critical concepts in pediatric intensive care.
Feedback, subscriptions, and reviews are encouraged.
Visit picudoconcall.org for episodes and Doc on Call infographics.
Hosted by Dr. Pradip Kamat and Dr. Rahul Damania.

Reference:

Yehya N, Bhalla AK, Thomas NJ, Khemani RG. Alveolar Dead Space Fraction Discriminates Mortality in Pediatric Acute Respiratory Distress Syndrome. Pediatr Crit Care Med. 2016 Feb;17(2):101-9. doi: 10.1097/PCC.0000000000000613. PMID: 26669646; PMCID: PMC4740261.

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Today's episode promises an insightful exploration into a unique case centered on retropharyngeal abscess in the PICU, offering a comprehensive analysis of its clinical manifestations, pathophysiology, diagnostic strategies, and evidence-based management approaches.

Today, we unravel the layers of a compelling case involving a 9-month-old with a retropharyngeal abscess, delving into the intricacies of its diagnosis, management, and the critical role played by PICU specialists. Join us as we navigate through the clinical landscape of RPA, providing not only a detailed analysis of the presented case but also valuable takeaways for professionals in the field and those aspiring to enter the world of pediatric intensive care. Welcome to PICU Doc On Call – where MED-ED meets the real challenges of the PICU.

Case Presentation* Patient: 9-month-old male with rapid symptom onset, left neck swelling, fever, noisy breathing, and decreased oral intake. * Initial presentation: Left neck swelling, limited neck mobility, and deteriorating condition. * Imaging: Neck X-ray and CT scan with IV contrast confirmed Retropharyngeal Abscess (RPA). * Management: High-flow nasal cannula, intravenous antibiotics, and consultation with ENT. PICU admission for comprehensive care.

Key Elements* Rapid Symptom Onset * Neck Swelling & Drooling * Limited Neck Mobility

Problem Representation* A previously healthy 9-month-old male with a recent upper respiratory infection, presenting with rapid-onset left neck swelling, fever, and respiratory distress. Imaging suggestive of a Retropharyngeal Abscess, requiring urgent PICU management for airway protection and antibiotic therapy.

Pathophysiology of RPA* Anatomy of retropharyngeal space * Rapid communication of infections via lymph nodes * Infection sources: dental issues, trauma, localized infections (e.g., otitis, URI)

Dangers of RPA* Airway compromise and posterior mediastinitis * Progression from cellulitis to abscess * Microbial suspects: Group A Streptococcus, anaerobes, Staphylococcus aureus, Haemophilus influenza, Klebsiella, Mycobacterium avium-intracellulare

Clinical Manifestations* Seen predominantly in children aged 3-4 years * Non-specific symptoms in the acute setting * Pronounced symptoms in PICU: neck pain, stiffness, torticollis, muffled voice, stridor, respiratory distress

Diagnostic Workup* Thorough history and physical examination * CT scan with contrast as the gold standard * Blood culture, CRP, and procalcitonin for infection severity

Clinical Pearls* Limited neck mobility is the most specific physical exam finding * Younger age and signs of airway obstruction indicate a complicated course

Management of RPA* Antibiotic therapy: Up to 50% cases can be treated with IV antibiotics * Surgical drainage may be needed if no improvement or persistent respiratory distress * Duration of therapy: 10 to 14 days * Controversial use of steroids for reducing airway swelling

Complications of RPA* Upper airway obstruction, aspiration pneumonia, internal jugular thrombosis, carotid artery sheath rupture * Mediastinitis: severe inflammation, infection of mediastinal tissues

Patient's Clinical Course* Respiratory viral panel: RSV, adenovirus, rhino/enterovirus * Intubation due to worsening respiratory distress * Incision and drainage (I&D) by ENT * Cultures grew MRSA * Extubation after air leak detection; discharged on oral Clindamycin

Clinical Takeaways* Maintain a low threshold for suspecting RPA * Initiate broad-spectrum antibiotics early * Prioritize airway assessment and intervene early in cases of worsening upper airway obstruction or hypoxia * Consider surgical drainage for non-responders, escalating respiratory distress, or immunocompromised patients

Conclusion* Emphasize the critical nature of RPA in children and the importance of early intervention. * Complications include upper airway obstruction, aspiration pneumonia, and potential vascular complications.

References* Villanueva-Fernández E, et al. (2022) Role of steroids in conservative treatment of parapharyngeal and retropharyngeal abscess in children. Eur Arch Otorhinolaryngol. * Akhavan M. (2021) Ear, Nose, Throat: Beyond Pharyngitis: Retropharyngeal Abscess, Peritonsillar Abscess, Epiglottitis, Bacterial Tracheitis, and Postoperative Tonsillectomy. Emerg Med Clin North Am. * Reilly BK, Reilly JS. (2012) Retropharyngeal abscess: diagnosis and treatment update. Infect Disord Drug Targets.

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Today, Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University School of Medicine) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital), are excited to speak with Matthew Kirschen, MD, PhD, FAAN, FNCS, regarding a very sensitive topic involving pediatric brain death guidelines published in 'Neurology' in October 2023. Dr. Matthew Kirschen, a leader in pediatric neurocritical care and one of the authors of the new guidelines.

Guest Introduction:

Dr. Matthew Kirschen is an Assistant Professor of Anesthesiology and Critical Care Medicine, Pediatrics, and Neurology at the Children's Hospital of Philadelphia. A proud alumnus of Brandeis University and Stanford, where he secured both his MD and PhD in neuroscience. Dr. Kirschen’s journey includes a residency at Stanford followed by a unique dual fellowship in neurology and pediatric critical care at CHOP. Notably, he's among the rare professionals dual-boarded in both PCCM and Neurology.

Dr. Kirschen’s tireless endeavors in pediatric neuro-critical care, especially his work on multimodal neuro-monitoring to detect and prevent brain injuries in critically ill children, have garnered significant attention. His expertise also extends to predicting recovery post-severe brain injuries. Pertinent to today's discussion, Dr. Kirschen has displayed a keen interest in the precise diagnosis of brain death and proudly stands as one of the authors of the new guidelines on the topic of Pediatric and Adult Brain death/death by neurologic criteria.

Discussion:

1. Understanding Brain Death Criteria:

Brain Death/Death by Neurologic Criteria (BD/DNC) declared with permanent cessation of all brain functions, including brainstem
Important considerations before BD/DNC determination:
No evaluation in infants < 37 weeks corrected gestational age
Absence of coma, intact brainstem reflexes, and spontaneous breathing inconsistent with BD/DNC

2. Who Can Perform BD/DNC Evaluations:

Attending clinicians must be credentialed and trained in BD/DNC evaluation.
Two attending clinicians are needed for evaluation, with exceptions for advanced practice providers.

3. Prerequisites for BD/DNC Determination:

Importance of identifying the etiology of BD/DNC to avoid reversible processes
Observation periods based on age and type of brain injury
Maintaining core body temperature before evaluation

4. Blood Pressure Management:

Hypotension can lead to impermanent coma; clinicians should manage with fluids or vasopressors.
Specific blood pressure targets for different ECMO support types

5. Medication Considerations:

Excluding medications affecting CNS function before BD/DNC evaluation
Recommendations for drug level monitoring and metabolic derangement exclusion

6. Performing the BD/DNC Neurologic Examination:

Two independent examinations by different clinicians with a minimum 12-hour interval
Central components including assessing irreversible coma and brainstem reflexes

7. Apnea Testing:

Two apnea tests after each neurologic examination
Procedures, complications, and baseline PCO2 and pH considerations

8. Ancillary Tests:

BD/DNC remains a clinical evaluation; ancillary tests are used in specific circumstances.
Conditions and circumstances for using or not using ancillary tests

9. Case Presentation and Family Communication:

Real-life case presented and discussed following the new AAN guidelines.
No need for consent before evaluation; communication with the family emphasized.
Maintaining transparency and involvement in the BD/DNC process

10. Public Trust in BD/DNC:

Building trust through education, transparency, public involvement, and ethical considerations
Continuous improvement, professional collaboration, and legal frameworks

We welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org which showcases our episodes as well as our Doc on Call management cards. PICU Doc on Call is co-hosted by Dr. Pradip Kamat and Dr. Rahul Damania. Stay tuned for our next episode! Thank you!

References:

Greer D, Kirschen MP et al. Pediatric and Adult Brain Death/Death by Neurologic Criteria Consensus Guideline Report of the AAN Guidelines Subcommittee, AAP, CNS, and SCCM. Neurology 2023; 101:1-21. doi:10.1212/WNL.0000000000207740
Pediatric Neurocritical Care Educational Series - Lecture_ Brain Death 2023 Guidelines

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Today’s case presentation involves a 2-year-old girl who was previously healthy and was admitted to the Pediatric Intensive Care Unit (PICU) for acute respiratory distress characterized by increased work of breathing and wheezing.

Case PresentationA 2-year-old girl with acute respiratory distress due to RSV infection

Presented with increased work of breathing, wheezing, and no fever
Started on High Flow Nasal Cannula (HFNC) therapy in the PICU

Key Elements:

Prodrome of URI symptoms
Increased respiratory effort (nasal flaring, intercostal retractions, decreased lung base air entry)
HFNC improved the work of breathing and oxygen saturation

Physiology of HFNCMechanisms of ActionWashout of Nasopharyngeal Dead Space:

HFNC clears nasopharyngeal dead space, improving oxygen efficiency.
Reduces re-breathing of CO2 from the anatomical dead space.
Enhances ventilation efficiency and oxygenation.

Reduction in Upper Airway Resistance:

HFNC reduces resistance in the upper airway.
Delivers rapid gas flow matching or exceeding natural inhalation rate.
Eases breathing, especially in neonates and infants with narrow airways.

Optimal Conditioning of Gas:

HFNC delivers heated and humidified oxygen, matching the body's conditions.
Reduces energy expenditure and risk of airway irritation
More comfortable and effective compared to cold, dry air delivery

Debunking the PEEP Theory (Positive End-Expiratory Pressure) * HFNC generates minimal and variable PEEP. * Amount of PEEP depends on factors like flow rate and cannula size * Not as high or consistent as other respiratory support devices

Research Findings* A 2022 CHEST study by Khemani et al. on children with bronchiolitis challenged the conventional understanding of HFNC's mechanisms. * HFNC primarily reduces breathing effort but does not consistently increase lung volume (EELV) or tidal volume (VT). * Reduction in the pressure rate product (PRP) indicates decreased breathing effort, but not significant alterations in EELV or VT.

Physiological Effects* HR, RR, and SpO2 are key indicators of HFNC efficacy. * HR and RR should approach normal ranges for the child's age. * Improvement in SpO2 levels while maintaining or reducing FiO2 indicates a positive response.

Conclusion* HFNC is a valuable tool in pediatric care for alleviating respiratory distress. * Not a one-size-fits-all solution; vigilant monitoring and reassessment are crucial * Recognizing HFNC's mechanisms allows for optimized bedside application.

Closing Remarks:

Subscribe, share feedback, and leave a review on the podcast.
Visit picudoconcall.org for more episodes and management cards.
Hosted by Dr. Pradip Kamat and Dr. Rahul Damania

ReferencesMiller AG, Gentle MA, Tyler LM, Napolitano N. High-Flow Nasal Cannula in Pediatric Patients: A Survey of Clinical Practice. Respir Care 2018; 63:894.

Wraight TI, Ganu SS. High-flow nasal cannula use in a pediatric intensive care unit over 3 years. Crit Care Resusc 2015; 17:197.

Hutchings FA, Hilliard TN, Davis PJ. Heated humidified high-flow nasal cannula therapy in children. Arch Dis Child 2015; 100:571.

Lee JH, Rehder KJ, Williford L, et al. Use of high flow nasal cannula in critically ill infants, children, and adults: a critical review of the literature. Intensive Care Med 2013; 39:247.

Wing R, James C, Maranda LS, Armsby CC. Use of high-flow nasal cannula support in the emergency department reduces the need for intubation in pediatric acute respiratory insufficiency. Pediatr Emerg Care 2012; 28:1117.

Bressan S, Balzani M, Krauss B, et al. High-flow nasal cannula oxygen for bronchiolitis in a pediatric ward: a pilot study. Eur J Pediatr 2013; 172:1649.

Mayfield S, Bogossian F, O'Malley L, Schibler A. High-flow nasal cannula oxygen therapy for infants with bronchiolitis: pilot study. J Paediatr Child Health 2014; 50:373.

Kelly GS, Simon HK, Sturm JJ. High-flow nasal cannula use in children with respiratory distress in the emergency department: predicting the need for subsequent intubation. Pediatr Emerg Care 2013; 29:888.

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Welcome to PICU Doc on Call, a podcast dedicated to current and aspiring intensivists. I'm Pradeep Kumar coming to you from Children's Healthcare of Atlanta, Emory University School of Medicine, and I'm Rahul Damania from Cleveland Clinic Children's Hospital. We are two pediatric ICU physicians passionate about all things medical education in the PICU.

Episode Overview:

PICU.com call focuses on interesting PICU cases and management in the acute care Pediatric setting. In this episode, we discuss the case of an eight-year-old boy with chest pain, fatigue, and shortness of breath. This case presentation by Rahul highlights the complexity of pediatric care in the PICU.

Case Presentation:

An eight-year-old boy with up-to-date immunizations and no recent travel or pet exposure presented to the PICU with chief complaints of chest pain, fatigue, and decreased oral intake. His history over the preceding two weeks included a diminishing appetite, episodes of vomiting, and shortness of breath.

On examination, he exhibited various cardiac findings, including a hyperdynamic left ventricle, murmurs, and a noted gallop. Abdominal and neurological findings were also concerning. Diagnostic studies revealed an enlarged heart, and sinus tachycardia with left ventricular hypertrophy, and echocardiography confirmed severe valvular and ventricular abnormalities.

Laboratory Findings:

Laboratory findings included elevated BNP, slightly elevated troponin, and elevated inflammatory markers (ESR and CRP). Strep throat culture was negative, but ASO and anti-DNAse B titers were markedly elevated. MRI confirmed multiple punctate infarctions, likely due to valvular heart disease.

Diagnosis:

Given the complex multisystem presentation, the child was admitted to the PICU for intensive monitoring and comprehensive management of this multisystem pathology. The working diagnosis is rheumatic fever.

The episode is organized into three parts:

Pathophysiology of Acute Rheumatic Fever
Approach to Diagnosis and Investigations
Management and Prevention

Pathophysiology of Acute Rheumatic Fever:

Acute rheumatic fever is an autoimmune disease initiated by a response to group A strep infection, primarily due to molecular mimicry. The streptococcal M protein has structural similarities with host proteins, leading to organ damage, especially in the heart.

Epidemiology:

Acute rheumatic fever is most prevalent in low to middle-income areas, affecting over 80% of cases. It mainly affects children between 5 to 14 years of age, and overcrowded households and limited healthcare access increase the risk. Globally, rheumatic heart disease affects millions of people annually and claims many lives.

Jones Criteria for Diagnosis:

The Jones criteria help diagnose acute rheumatic fever. For a definitive diagnosis, evidence of a preceding group A strep infection is required. Major manifestations include carditis, arthritis, erythema marginatum, subcutaneous nodules, and Sydenham's chorea. Minor criteria include fever, elevated inflammatory markers, prolonged PR interval on EKG, and mild joint issues.

Differentiating Low and High-Risk Populations:

The criteria differentiate between low and high-risk populations based on the epidemiology of acute rheumatic fever. The presentation of arthritis varies, and the thresholds for fever or inflammatory marker elevation are lower in high-risk populations.

Diagnostic Approach:

Diagnosis includes throat swab, anti-streptolysin O antibody titers, anti-DNAse B titers, CBC with differential, blood cultures, inflammatory markers, EKG, chest X-ray, and echocardiography. Joint analysis may be performed if needed.

Sydenham's Chorea:

Sydenham's chorea is marked by involuntary movements, primarily in the trunk and limbs, and it often resolves within 12 to 15 weeks with treatment.

Management of Acute Rheumatic Fever:

Management includes eradicating the remaining strep infection, controlling inflammation, and preventing recurrence. Penicillin or amoxicillin is used to treat the infection, while aspirin or NSAIDs are used to manage inflammation. In severe cases, systemic steroids may be considered. Cardiac surgery should be delayed until acute inflammation resolves. Prophylactic antibiotics are used for prevention.

Conclusion:

Rheumatic fever management requires a holistic approach, encompassing infection control, inflammation management, and long-term prevention. Early recognition, thorough diagnostics, and prophylactic antibiotics play essential roles in managing this condition.

Future Directions:

Research is needed for early detection using biomarkers and the development of a group A strep vaccine.

Closing Remarks:

As pediatric intensivists, we play a pivotal role in primary prevention by advocating for awareness and prompt treatment of group A strep infections.

Thank you for listening to PICU Doc on Call. Please subscribe, share your feedback, and visit our website at picudoconcall.org for more information. Stay tuned for our next episode.

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Introduction:

Welcome to "PQ Doc On Call," a podcast dedicated to current and aspiring intensivists. Hosted by Dr. Pradeep Kamar from Children's Healthcare of Atlanta, Emory University School of Medicine, and Dr. Rahul Damia from Cleveland Clinic Children's Hospital, both passionate PICU physicians.

You will hear:

This episode dives into the management of pediatric drowning cases in the PICU, providing valuable insights into assessment, pathophysiology, and practical management strategies.

Case Presentation:

An 18-month-old girl was admitted to the PICU following a submersion incident in a residential pool. The child's initial unresponsiveness and subsequent clinical deterioration presented challenges for the PICU team, including respiratory distress, electrolyte imbalances, and potential neurological complications.

Key Elements from the Case:

Severe acute respiratory failure following submersion
Abnormal electrolytes (hyponatremia)
Neurological insult requiring ongoing monitoring

Definitions and Terminology:

Clarification of drowning terminology, emphasizing uniform definitions and avoiding outdated terms like "near drowning." Key terms include primary vs. secondary drowning, saltwater vs. freshwater, intentional vs. non-intentional, and fatal vs. non-fatal drowning incidents.

Pathophysiology:

Airway Reflexes: Initial reflex laryngospasm triggered by liquid penetration, followed by relaxation due to hypoxia, hypercarbia, and acidosis.
Gas Exchange Compromise: Decreased functional residual capacity leading to impaired oxygen uptake and CO2 elimination.
Pulmonary Complications: Pulmonary edema, surfactant washout, increased pulmonary vascular resistance, and shunting, impacting oxygen delivery.

Management Strategies:

Out-of-Hospital: Aggressive on-site CPR and advanced life support are crucial for favorable outcomes. Swift control of hypoxia and acidosis is vital.
In-PICU: Ventilation strategies resembling ARDS management (low tidal volume, low plateau pressures, high PEEP). Consider neurological exam, continuous EEG, and neuromuscular blockade if needed.
Prognostic Factors: Duration of submersion, time to effective CPR, initial GCS, apnea persistence, pH levels, and neurologic status.

Prevention:

Empowering prevention through measures like fencing around pools, teaching children to swim, and vigilant adult supervision can significantly reduce the risk of pediatric drowning incidents.

Conclusion:

"PQ Doc On Call" underscores the importance of timely, effective CPR, swift management...

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In this episode of PICU Doc On Call, your hosts Pradip Kamat and Rahul Damania, experienced Pediatric ICU physicians, take you on an enlightening journey through the intricate landscape of lactic acidosis. Join us as we unravel the complexities, share clinical insights, and provide practical guidance on diagnosing and managing this critical condition in the acute care pediatric setting.

You will hear:

Case Presentation:

4-year-old boy with hypotension, fatigue, rash, and respiratory distress

Recent COVID-19 exposure, concerning respiratory symptoms

Hypotensive, tachycardic, tachypneic, low pulse oximetry reading

Swollen red lips, erythematous rash, hepatomegaly

High-flow nasal cannula, resuscitation, epinephrine infusion

Initial arterial blood gas: pH 7.22, lactate 4.5 mMol/L

Definition of Lactic Acidosis:

Hyperlactatemia and lactic acidosis criteria
Causes: impaired tissue oxygenation or mitochondrial dysfunction

Types of Lactic Acidosis:

Type A: Impaired O2 delivery, shock-related
Type B: Impaired O2 utilization, toxins, infections

Lactate Measurement:

Comparability between POCT and central lab analysis
Role of lactate measurement in pediatric sepsis

Lactic Washout:

Rising lactate with re-established oxygen delivery
Impaired clearance in microcirculation, liver, kidney
Monitoring trends with clinical exams and lab surrogates

Bicarbonate Therapy:

Role in Type A lactic acidosis
Controversy, indications, and potential complications

Conclusion:

PICU Doc On Call podcast explores the intriguing case of a 4-year-old boy with lactic acidosis, highlighting the clinical intricacies of diagnosing and managing this condition. The hosts, Pradip Kamat and Rahul Damania provide insightful discussions on the different types of lactic acidosis, the physiological mechanisms behind it, and the role of bicarbonate therapy. The episode emphasizes the importance of addressing underlying causes and offers valuable clinical pearls for managing pediatric patients with lactic acidosis.

Stay tuned for more engaging episodes from PICU Doc On Call! Don't forget to subscribe, share your feedback, and review the podcast on your preferred platform. For more information and resources, visit picudoconcall.org.

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In this episode of PICU Doc On Call, Dr. Pradip Kamat and Dr. Rahul Damania discuss a case of a 4-year-old girl with bite marks and swelling of her foot, presenting with concerning vital signs and abnormal labs. They explore snake envenomation and its management in the pediatric critical care setting.

Classifying Snake EnvenomationSnakes with venom-delivering fangs, primarily Elapidae and Viperidae, are responsible for most human envenomations and fatalities. We're focusing on Pit Vipers today, including rattlesnakes, cottonmouths, and the copperhead. Elapids, such as the coral snake, differ by having round pupils, short fangs, and no facial pit.

Risk Factors for Pediatric SnakebitesSnakebite incidents can happen when toddlers unintentionally disturb snakes, particularly in low-light conditions or grassy areas. Teenagers trying to capture snakes are another frequent group presenting with upper extremity bites.

Pathophysiology of Snake Envenomation

Snake venoms contain toxic proteins that affect various physiological systems, leading to neurotoxic, hemotoxic, myotoxic, or cytotoxic effects. Envenomation can happen immediately or be delayed, presenting with various clinical and laboratory anomalies.

Syndromes Observed After Snake EnvenomationThe impact of a snakebite depends on the snake type, fang size, and venom injection site. Effects may include cytotoxicity, lymphatic system damage, platelet dysfunction, neurotoxicity, cardiotoxicity, hypotension, and nephrotoxicity.

General Management FrameworkIn snakebite cases, prehospital care involves immediate EMS call and ensuring airway, breathing, and hemodynamic stability. In the hospital, general supportive care is crucial, and antivenin administration depends on clinical presentation and snake type.

Antivenin ConsiderationsAntivenin dosage is challenging due to unknown venom load, and its choice depends on safety, kinetics, cost, and the specific snake involved. Smaller fragments of antivenin have larger distribution volumes and shorter half-lives. Recurrence, anaphylaxis, and serum sickness are potential side effects of antivenin.

Clinical Pearls* A high index of suspicion is required to diagnose snake envenomation. * Antivenin is the mainstay of therapy, and rapid transport to a facility with antivenin is crucial. * Patients should be educated about recurrence, serum sickness, and lifestyle adjustments after a pit viper bite.

Thank you for listening to this episode on snake envenomation in the PICU. For more episodes, visit our website picudoconcall.org. Stay tuned for our next episode! Don't forget to share your feedback and subscribe to our podcast.

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In this episode PICUDoc On Call, we discuss the case of a six-month-old ex-preemie with bacterial meningitis who presents with symptoms of cerebral sinus venous thrombosis. We explore the anatomy of the venous distribution in the brain and the clinical syndromes associated with sinus venous thrombosis. Our focus is on the imaging techniques, laboratory tests, and management strategies involved in diagnosing and treating this challenging condition.

You will learn:

A six-month-old ex-preemie presents with persistent fever, recurrent emesis, and increased somnolence.
The patient experiences eye rolling and decreased oxygen saturation, prompting a visit to the emergency department.
Physical examination reveals rigidity in all four limbs, and a head CT shows dilated ventricles and encephalomalacia.
Lumbar puncture confirms an infection, and the patient is admitted to the hospital.
After a 14-day course of antibiotics, the patient's clinical status worsens, leading to intubation and neurosurgery consultation.
An MRI confirms cerebral venous sinus thrombosis.

Anatomy of Venous Distribution in the Brain:

Dural venous sinuses serve as conduits for venous blood return from the brain to the internal jugular veins.
The superior sagittal sinus, cortical veins, transverse sinus, sigmoid sinus, and internal jugular vein are key components of the venous drainage system.

Clinical Syndromes of Sinus Venous Thrombosis:

Symptoms can be related to elevated intracranial pressure or focal brain damage from venous ischemia, infarction, or hemorrhage.
Headache, seizures, focal neurologic deficits, and cranial nerve paralysis are common presentations.
Cavernous sinus thrombosis can cause periorbital pain, ocular chemos, and paralysis of cranial nerves passing through the sinus.

Risk Factors for Cerebral Sinus Venous Thrombosis:

Dehydration, CNS or sinus infections, intracranial surgery, autoimmune disorders, genetic syndromes, metabolic syndromes, medications, and genetic thrombophilic states can predispose children to thrombosis.
Thorough evaluation for risk factors, including thrombophilia, is recommended in children with cerebral venous thrombosis.

Imaging and Laboratory Tests:

CT and MRI with contrast-enhanced venography are preferred imaging tools to detect cerebral sinus venous thrombosis.
Non-enhanced CT scans and T1/T2-weighted MRI scans show characteristic signs of thrombosis.
Lab tests include CBC with differential, DIC panel, comprehensive metabolic panel, ESR, and specific thrombophilia tests.

Management...

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Welcome to PICU Doc on Call, a podcast dedicated to intense wisdom in the field of pediatric critical care. In this episode, hosts Pradeep Kama and Rahul Damania, both pediatric ICU physicians, discuss the case of a five-year-old male who presents to the emergency department with unexplained fatigue and fever. The patient's symptoms include fatigue, intermittent fevers, tachycardia, and significantly low hemoglobin levels.

The hosts delve into the possible causes of the patient's condition, considering a blood cell disorder and the potential for severe anemia due to aplastic crisis. They explain the physiological adaptations that occur in severe acute anemia, including the shifting of the oxyhemoglobin curve to the right and the increase in cardiac output through tachycardia and increased stroke volume.

The podcast episode also covers different forms of hemolytic anemia, including extravascular and intravascular hemolysis, autoimmune hemolytic anemia, and paroxysmal nocturnal hemoglobinuria. The hosts discuss the workup for hemolytic anemias, such as complete blood count, peripheral smear, LDH levels, haptoglobin levels, and Coombs tests. They emphasize the importance of involving hematology and infectious disease specialists for accurate diagnosis and management.

The case of the five-year-old with hereditary spherocytosis is explored, highlighting the characteristic spherocytic shape of red blood cells and potential complications like hemolytic crisis, splenic sequestration, and aplastic crisis. The hosts provide insights into the pathophysiology and presentations of these complications, emphasizing the need for prompt recognition and appropriate interventions.

In summary, this episode of PICU Doc on Call provides valuable information on the evaluation and management of a pediatric patient with fatigue, fever, and anemia, shedding light on different forms of hemolytic anemias and their associated complications.

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine

And I'm Rahul Damania from Cleveland Clinic Children’s Hospital and we are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode:

Welcome to our Episode featuring a 16-year-old male with high-grade fever & abdominal pain.

Here's the case:

A 16-year-old male patient presents with high-grade fever, abdominal pain, and rash. The patient began experiencing a high-grade fever (102°F/38.9°C) and fatigue for the past 5 days. Over the past 2 days, he has developed diffuse abdominal pain, accompanied by vomiting and diarrhea. The patient also noticed a non-pruritic, maculopapular rash on his trunk and extremities yesterday. The patient has a history of mild asthma, controlled with a rescue inhaler. No history of hospitalizations, surgeries, or other significant medical issues. He uses an albuterol inhaler as needed for asthma symptoms. Up-to-date on all immunizations, including a COVID-19 vaccine booster 4 months ago. The persistence of the high-grade fever, worsening abdominal pain, the appearance of the rash, and the patient becoming increasingly lethargic led the family to seek medical attention urgently.
Vital Signs on arrival: Temperature: 103.2°F (39.6°C) Heart rate: 135 bpm Respiratory rate: 24 bpm Blood pressure: 88/50 mmHg Oxygen saturation: 95% on room air
The patient appears acutely ill, uncomfortable, and lethargic. There is a diffuse, non-pruritic, maculopapular rash on the trunk and extremities, with areas of petechiae. A cardiovascular exam reveals tachycardia and muffled heart sounds. Perfusion is 4-5 seconds peripherally. Respiratory exam demonstrates labored breathing with decreased breath sounds at the bases bilaterally. The abdomen is markedly distended, diffusely tender with rebound and guarding. Neurologically, the patient is somnolent but arousable to verbal stimuli, without focal deficits.
Laboratory findings show elevated WBC, moderate anemia, thrombocytopenia, markedly elevated liver enzymes, and elevated creatinine. Inflammatory markers, including CRP and ESR, are significantly elevated. Imaging reveals bilateral pleural effusions on chest X-ray and a moderately enlarged liver with mild ascites on abdominal ultrasound. Blood cultures are pending, and COVID-19 PCR is negative.
Patient received aggressive IV fluid resuscitation, antipyretics, and was started on broad-spectrum empiric antibiotics. Supplemental oxygen was administered via a high-flow nasal cannula to maintain adequate oxygen saturation.

To summarize key elements from this case:

A 16-year-old male presents with a 5-day high-grade fever, abdominal pain, rash, and recent onset of lethargy.
Exhibits tachycardia, hypotension, and respiratory distress.
Labs indicate elevated WBC, anemia, thrombocytopenia, liver enzymes, creatinine, and inflammatory markers.
Imaging reveals pleural effusions and liver enlargement with ascites.

Pradip, do you mind at this point giving me an idea of your thought process at this point and what you feel is the working diagnosis?

The patient was admitted to the PICU because of a high fever, fast heart rate, low blood pressure, and difficulty breathing, which all suggest a quickly worsening, potentially life-threatening situation. Based on the details from this case, there are a few possible diagnoses we should consider:
Severe bacterial infection such as septic shock secondary to complicated pneumonia- characterized by the sudden onset of fever, elevated WBC count, and hypotension on exam.
Atypical presentation of appendicitis or cholecystitis - considering the patient's abdominal pain, distention, and elevated liver enzymes, albeit with nonspecific imaging findings.
Toxic shock syndrome - suggested by the presence of fever, rash, and multiorgan involvement, including cardiovascular, respiratory, and hepatic manifestations.
And finally, a systemic inflammatory process:
This includes Multisystem Inflammatory Syndrome in Children (MIS-C) which is plausible given the patient's age, recent COVID-19 vaccination, and symptoms involving multiple organ systems, along with the elevated inflammatory markers. I would also add an atypical presentation of Kawasaki disease - while less likely due to the patient's age, it cannot be ruled out, given the fever, rash, and cardiovascular involvement.

This is a great differential, and as we narrow down what this patient might have, I think it is important for us to consider that if we have a branchpoint decision to make, what would be an appropriate pressor to use in this patient?

Sure! Let's talk about using cardiovascular agents in the context of this case. As a quick background, vasopressors are often necessary when a patient's heart or circulatory function isn't improving even after making sure even after fluid resuscitation is adequate. These medications work by influencing the biochemical and neurochemical pathways that help control blood vessel tone, contractility, and heart rate.

It's crucial to understand how these vasoactive agents work and their specific pharmacological properties, as well as how the patient's own response to their critical illness might impact how they react to the drug. Also, it’s important to note that a patient's critical condition can also influence drug clearance, so the effects we read about in textbooks might not be exactly what we see at the bedside.

Let’s organize the decision of which pressor to choose by going thru each of the potential vasopressor options we have in our armamentarium, how they work, and the pros & cons of each one.

That sounds like a great idea, but before we get into that when it comes to shock one of the classical teachings which we think about is to categorize the shock as cold shock where the patient has cool extremities, delayed capillary refill, and poor perfusion versus warm shock where the patient is flushed, has flash capillary refill, and hyperdynamic perfusion. Can you shed some light on this cold vs. warm shock characterization?

That's an interesting question! Classically, we've been taught to think about shock in terms of cold and warm categories. As you alluded to, cold shock is typically associated with cool extremities, delayed capillary refill, and poor perfusion, while warm shock is characterized by flushed skin, rapid capillary refill, and hyperdynamic perfusion. However, recent guidelines have moved away from relying solely on these bedside clinical signs to categorize septic shock in children. The 2020 Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-associated Organ Dysfunction in Children suggest not using these clinical signs in isolation to label septic shock as "warm" or "cold." This recommendation stems from the weak recommendation and very low quality of evidence supporting this classification. Instead, it's crucial to take a more comprehensive approach when evaluating and managing shock in pediatric patients, considering a variety of factors beyond these traditional bedside signs.

Interestingly, an article published in PCCM in 2021 entitled, ‘Clinical Classification of Cold and Warm Shock: Is there a signal in the noise?’ played a bit of a devil’s advocate on the Surviving Sepsis guidelines — in fact, it brought up, the fact that this may be a bit of an uncomfortable recommendation as we frequently rely on our bedside assessments to drive care. It also noted that we are subject to bias, and at times, it’s hard for us to understand what portion of the assessment is true ‘signal’ vs. ‘noise.’

You've brought up a great point! It's important to remember that skin blood flow, as determined by factors like capillary refill time and extremity temperature, may not accurately represent the true state of a patient's circulation. This is because various organs, such as the muscles, gut, coronary, renal, and brain, all have their own unique autoregulation processes.

Interestingly, research has shown that there's no clear benefit to choosing a vasoactive agent based on the traditional classification of "shock type." In a study comparing vasoactive choices and clinical outcomes, investigators found that factors like extremity temperature, capillary refill, and pulse strength were the primary drivers for clinicians to categorize a patient as having warm or cold shock. Pulse pressure and diastolic blood pressure, however, didn't play a significant role in this decision-making process.

Even more fascinating, when the study simulated random allocations of shock type, the vasoactive agent choices were just as likely to match these random classifications as the ones made by clinicians. This finding further emphasizes the need to move beyond the traditional "warm" or "cold" shock categorization and focus on a more comprehensive approach when evaluating and managing pediatric shock patients.

In summary, selecting the right pressor for pediatric patients involves several challenges, including a lack of standardization in clinical examination, discordance between shock elements, and individual variability in response to medications. Additionally, skin perfusion might not accurately reflect vital organ perfusion and optimal therapeutic hemodynamic goals for children are unknown. Recognizing trends in surrogates of CO and constantly reevaluating are at least some mitigation strategies that we can consider to address these challenges.

Let’s go thru a quick multiple-choice question to really kick off our rapid review of pressors:

A 14-year-old with toxic shock syndrome due to osteomyelitis and Staphylococcus aureus bacteremia presents with tachycardia (heart rate of 133 bpm), hypotension (blood pressure of 82/25 mmHg), and tachypnea (respiratory rate of 30 breaths/min). Clinical exam reveals diffuse erythema, bounding pulses, and flash capillary refill. After aggressive fluid resuscitation and central venous catheter placement, his blood pressure slightly improves to 90/21.

Which vasoactive infusion should be initiated? A. Dobutamine B. Dopamine C. Norepinephrine D. Epinephrine E. Milrinone

Rahul, in this particular case, the most appropriate choice of vasoactive infusion would be option C, Norepinephrine. The patient is presenting with toxic shock syndrome, which often involves a distributive shock characterized by vasodilation and low systemic vascular resistance. Norepinephrine, a potent α-adrenergic agonist, helps increase vascular tone and subsequently improves blood pressure. It also has some β-adrenergic effects, which can aid in supporting cardiac function. Given the patient's hypotension and the clinical context, Norepinephrine seems to be the most suitable option to address the patient's hemodynamic instability.

What would be the pros and cons of using NE in a distributive shock picture?

The pros of using Norepinephrine (NE) in distributive shock include its potent vasoconstrictive effects, which are beneficial in shock states characterized by excessive vasodilation. NE also possesses inotropic activity at the myocardial β1-adrenoceptor, supporting cardiac function without significant chronotropic effects, as its low binding affinity for β2-adrenoceptors limits its impact on heart rate. Additionally, NE increases venous tone, facilitating increased venous return, and generally has little effect on pulmonary vascular resistance in patients with normal pulmonary vasculature.

This is very helpful, what about the cons of NE use?

There are cons to using NE in distributive shock as well. Its use should be limited to situations with adequate intravascular volume, as improper use can decrease end-organ perfusion and lead to ischemia, particularly in the kidney and gut. In patients with pulmonary hypertension or increased muscularization of the pulmonary vasculature, NE may increase pulmonary vascular resistance and right ventricular afterload. Furthermore, extravasation of NE can cause severe tissue necrosis, so it should be infused only through central venous sites. If extravasation occurs, treatment with the α-adrenergic antagonist phentolamine can help manage the affected area.

In summary, NE, commonly viewed as a vasoconstrictor, remember also has a high affinity for cardiac β1-adrenoceptors due to its role as a neurotransmitter in sympathetic nerves. This enables it to produce inotropic actions alongside increased vascular resistance. With minimal effect on β2-adrenoceptors, it also has little impact on the atrial pacemaker. In adult studies of cardiogenic shock, NE has been shown to be superior to Epi.

Alright, the next pressor we want to highlight is epinephrine, and to effectively talk about this, let’s contrast it to NE.

Epinephrine and NE differ in their actions on adrenergic receptors and their effects on various circulations. Epinephrine acts on all adrenergic receptors, with low infusion doses primarily impacting β1 & 2-adrenoceptors. It is initially used in postarrest settings but it can typically be transitioned to another vasoactive depending on the clinical state. In contrast to NE, epinephrine has hemodynamic and metabolic effects to keep in mind. At low to moderate doses, epinephrine redirects increased cardiac output towards skeletal muscles and away from splanchnic and renal circulations.

Adding to our discussion, it's worth noting that epinephrine has different effects on coronary perfusion depending on the infusion dose. At lower doses, it can reduce diastolic blood pressure due to its β2-adrenergic effect, while still increasing systolic blood pressure with its positive inotropic effect. This leads to increased pulse pressure. However, the rise in contractility and heart rate also increases myocardial oxygen demand, which in turn boosts coronary blood flow.

At higher infusion doses, epinephrine increases systemic vascular resistance, leading to increased afterload. This, combined with an increased heart rate, significantly elevates myocardial oxygen demand, which is not favorable for patients with cardiogenic shock.

Alright, so here’s a quick active-recall question.

Which vasopressor acts on the alpha-1 receptor that is structurally similar to epinephrine and elevates the SVR and PVR?

If you said Phenylephrine, you’re absolutely correct!
Phenylephrine, similar to NE, causes significant arterial vasoconstriction and thus elevates SVR and PVR. It has no inotropic properties; therefore, if cardiac function is impaired, cardiac output may be reduced by the increase in afterload even though the blood pressure increases.

At this juncture, it's essential to underscore a fundamental principle: whenever vasopressors come into the conversation, concurrently, we should be discussing access. Given that these vasopressors have the potential to inflict considerable peripheral and systemic harm if they inadvertently leak into the soft tissue, securing a central line access becomes a vital priority. It's not just important—it's an absolute necessity for effective team coordination and patient safety! These children likely will need an arterial line to see beat-to-beat changes in BP.

Alright, to wrap up this episode, let’s do a quick rapid review of common vasopressors in the PICU.

Ready Pradip?

Yes! Let’s do it!

Let’s talk about Dopamine
What is Dopamine's mechanism of action?
It's a dose-dependent effect:
Low dose (1–5 mcg/kg/min) → Renal/splanchnic vasodilation, natriuresis via a D1 receptor effect.
As you increase the dose, it has more B and alpha effects → typically at 5–8 mcg/kg/ min, you will see an Increased inotropy, whereas at a high dose (> 10 mcg/kg/min) you will see increased SVR, PVR.

Please note, that there is little to no evidence to support the use of renal low-dose dopamine in children with shock and typically we go for the direct-acting vasoactive agents.

Let’s talk about Dobutamine next:

What's the mechanism of...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania from Cleveland Clinic Children’s Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode.

In today's episode, we're bringing together some of the best content from our previous podcasts to present a comprehensive clinical case. We're also excited to share with you some of the most highly cited articles from the past year, presented in a practical, case-based format. This episode will offer you valuable insights into the latest research findings while also highlighting the real-world application of this knowledge in a clinical setting.

We'll start by presenting an interesting case of a toddler who was transferred to the PICU due to increasing respiratory distress:

A 2-year-old male was brought to the emergency department with a chief complaint of increased work of breathing and URI symptoms, including a cough and runny nose. The child had no significant past medical history, was not taking any medications, and had no known allergies. The child was up-to-date on immunizations, and there were no significant sick contacts.

The family brought the child to the emergency department after noticing a significant increase in work of breathing, including the use of accessory muscles, nasal flaring, and chest retractions. The initial physical exam revealed tachypnea and decreased breath sounds on the right side. The child's vital signs were concerning for respiratory distress, with a heart rate of 170 beats per minute, respiratory rate of 50 breaths per minute, and oxygen saturation of 85% on room air. Chest X-ray revealed right lower lobe pneumonia.

The child was started on supplemental oxygen, and broad-spectrum antibiotics, and trialed with albuterol. Despite initial treatment, the child's respiratory distress worsened, and the decision was made to transfer the child to the PICU and place the patient on HFNC 1.5 L/kg. Upon admission to the PICU, the child's vital signs were still concerning, he was afebrile, with a heart rate of 180 beats per minute, respiratory rate of 60 breaths per minute, and oxygen saturation of 85% on 1.5L/kg HFNC at 75% FiO2. Given the persistent respiratory distress, the decision was made to intubate the child in the PICU for acute hypoxemic respiratory failure. Shortly after intubation, a central line is placed in the R internal jugular vein.

To summarize key elements from this case:

2-year-old with a prodrome of URI symptoms
Is otherwise previously healthy with no significant medical history or allergies
Developed respiratory distress and diagnosed with pneumonia
Transferred to PICU, intubated for respiratory failure

Let's fast forward in the case and talk about a scenario that frequently arises in the PICU.

It's hospital day 2, and the patient's RSV swab is positive, and we're seeing some improvement on the X-ray. Blood culture from the outside hospital has continued to be negative. The patient on hospital day 2 has developed a fever of 38.5 degrees C, and the nurse needs to check with the peds resident about whether to take a blood culture and whether it needs to come from the central venous line or peripheral IV. Let’s dive into the literature on this specific topic: fever and a central line.

This is a very common clinical scenario seen in the PICU. The question is often raised, at what point do we obtain a blood culture from a patient in the PICU who is febrile? I would stratify the thought process by assessing whether or not the patient is immunocompetent vs. compromised. I also think that as pediatric intensivists, it's important to reduce unnecessary cultures.
In fact, there was a fascinating study by Woods-Hill et al. in JAMA Pediatrics (May 2022), which explored blood culture practices in the PICU before and after implementing a local quality improvement (QI) program. The program led to a 33% reduction in blood culture rates, a 13% decrease in broad-spectrum antibiotic use, and an 8% drop in initiating new antibiotics. It was also found that CLABSI rates showed a 33% relative reduction. What's noteworthy is that there was no change in mortality, length of stay, readmission, or sepsis rates. So, it's essential to keep in mind the benefits of reducing unnecessary cultures.

What is the relevance of this study to our general PICU practice?

This study shows us that there are ways to reduce blood culture and antibiotic use in the PICU. And it's crucial to do so because blood culture contamination can lead to all sorts of problems like increased costs, longer hospital stays, and a higher likelihood of antibiotic resistance. But there are solutions. For instance, a study published in Pediatrics by El Feghaly and colleagues found that standardizing blood culture collection methods, optimizing blood volume, creating checklists, and reinforcing nurse education could significantly reduce blood culture contamination rates.

So, in our index case, the patient is an immunocompetent host on antibiotics for pneumonia and has an RSV infection with low-grade fever. Given the circumstances, we can reasonably monitor the patient without additional blood cultures or workups at this time. However, we need to be vigilant and keep an eye out for any changes in the fever curve, hemodynamic instability, or laboratory data indicating rising WBC count, CRP, or procalcitonin. If any of these indicators start to worsen, then it's reasonable to obtain cultures both centrally and peripherally. We also need to check the site of the CVL and look out for any signs of skin or soft tissue infection. At present, there were no signs of local infection at the CVL insertion site or symptoms suggestive of sepsis or septic shock, which makes it reasonable to forego blood cultures in this case.

Okay, let's switch gears for a moment and talk about septic shock.

The most recent Surviving Sepsis guidelines define it as a severe infection that causes cardiovascular dysfunction, including hypotension, the need for treatment with a vasoactive medication, or impaired perfusion. In children, sepsis-associated organ dysfunction is also considered a form of septic shock, which involves severe infection leading to cardiovascular dysfunction as well as other organ dysfunction.

It's crucial to note that diagnosing sepsis requires clinical judgment and decision-making. There's no single test, biomarker, or decision rule that can perfectly differentiate serious bacterial infections. And while blood cultures remain the gold standard for diagnosing sepsis resulting from bloodstream infections in children, they are often overused in practice, especially in the context of central lines.

We need to be mindful of the risks and benefits of taking blood cultures from our patients, particularly in the PICU. As we've seen in previous studies, implementing multidisciplinary diagnostic stewardship interventions and standardizing blood culture collection methods can help reduce blood culture contamination rates and unnecessary antibiotic use. Ultimately, it's up to us as pediatric intensivists to use our clinical judgment and balance the need for diagnostic testing with the potential risks and benefits for our patients.

Okay, Pradip, let's imagine our patient had not quite this dramatic of a presentation of hypoxemic respiratory failure and presented with respiratory distress due to RSV+ bronchiolitis and placed initially on HFNC 1 L/kg 40%, but now we're wondering if we should switch to CPAP or RAM. Can you discuss the current literature on this decision?

Absolutely. So, there was a randomized controlled trial published in JAMA (June 2022) by Ram-Narayan and colleagues that looked at whether the first-line use of HFNC was non-inferior to CPAP for time to liberation from all forms of respiratory support. They had 600 children receive either HFNC or CPAP at a pressure of 7-8cmm H2O and measured the primary outcome, which was the time from randomization to liberation from respiratory support. The study found that there was no difference in mortality, rate of intubation, or use of sedation between the two groups. The authors reported that the median time to liberation from respiratory support was slightly longer in the HFNC group compared to CPAP, but the difference was not statistically significant.

So, based on this study, we can say with confidence that HFNC can be safely continued in our patient, unless there are other red flag signs, and there's no need to switch to CPAP or RAM.

These decisions are highly case-specific for our patients, but it's always helpful to have these studies to guide our decisions and provide us with more information to help us manage our patients effectively.

So Pradip, at our institution, we have a step-down ICU model. Let’s say this patient on 1L/kg was kept in the step-down unit, are there data-driven tools, which can help us identify early deterioration and the need for transfer to our main PICU?

That's a great question. When it comes to detecting which patients are at risk for deterioration and need for transfer to the main PICU, we have a few tools at our disposal. One of the most commonly used tools is the Pediatric Early Warning Score (PEWS) system, which relies on vital signs and patient assessment to identify early signs of patient deterioration. This score can predict patient deterioration 6-8 hours prior to a code event. Each vital sign or patient assessment is assigned points, resulting in a score from 0-6, with a higher score or trend of increasing score indicating a higher risk of deterioration. PEWS 3-4: intermediate risk — recommended to alert charge nurse and staff MD. Several studies have validated the PEWS, including one by Duncan et al which found an area under the receiver operating characteristic curve of 0.90, with 78% sensitivity and 95% specificity at a score of 5.

Yes, I remember classically using this score to trigger a Rapid Response - are there other models out there?

Yes, very recently, researchers have started using automated clinical prediction models in electronic health records. Mayampurath and colleagues published an article in Pediatric Critical Care Medicine that used an automated vital sign-based model to predict clinical deterioration in hospitalized children. They found that the vital sign model outperformed the modified Bedside PEWS in predicting ICU transfers at 12 and 24 hours before transfer, and outperformed the modified Bedside PEWS in predicting critical deterioration events at multiple time points from 6 to 24 hours before transfer. In busy healthcare settings, healthcare providers may become desensitized to the constant beeping and ringing of alarms from multiple monitors. This can result in decreased capture of vital signs, as clinicians may turn off alarms or avoid continuous monitoring to reduce the noise level. However, decreased vital sign capture can impact the accuracy of these models, potentially leading to delayed recognition and intervention of early warning signs of patient deterioration.

In summary, to determine which patients on the floor require transfer to the PICU, we need to use a combination of bedside clinical assessment skills, vital sign-based Early Warning Scores, and newer clinical prediction models. Ultimately, we also need to rely on our "gut feeling" as experienced clinicians to determine when something isn't right with a patient.

As we wrap up this episode, I want to shift gears a bit and discuss a crucial aspect of patient care that often goes overlooked - social determinants and needs. How can we effectively screen our patients and their families for these factors, and what resources can we provide to address them?

Absolutely, this is such a crucial topic so we can take care of our patients holistically! One study by Maholtz and colleagues published in Pediatric Critical Care Medicine in 2022 looked at how we can screen for social needs in critically ill patients. They surveyed parents using the 2020 Social Determinants of Health (SDOH) domains and found that 60% of participants had at least one unmet social need, with 36% of those participants requesting assistance. The most commonly identified needs were difficulties with utilities and living costs, housing instability, adjusting to hospitalization, and food insecurity.

Interestingly, 73% of parents screened appreciated the screening during their child's PICU admission. This suggests that children, especially those in areas with high child poverty rates like the county studied in this research, are at significant risk of exposure to negative social influences on health. The most common interventions needed were providing meal tickets or gas-fuel cards for urgent needs, or connecting families with community resources for non-urgent needs. Overall, screening for social determinants of health is an important aspect of caring for critically ill children and their families.

It's important for pediatric intensivists to not only focus on a patient's medical needs but also on their social determinants of health. As research has shown, poverty is linked to increased utilization of critical care resources and morbidity. We must develop an effective process to screen the social needs of patients admitted to the PICU. This is where early consultation with social workers comes in. By collaborating with social workers early on, we can identify and address social needs, such as housing instability, food insecurity, and difficulties with utilities and living costs. I think it is so key that we work with our patients and their families to move towards a more comprehensive healthcare model.

Rahul, can you summarize some of the key takeaways from the articles we spoke about:

Having an algorithmic approach to fever and central lines in the PICU. It is crucial to consider host status, the underlying reason why the patient is intubated, the time period between illness and fever, and hemodynamic instability, and take into account labs alluding to new infection. Having an institutional approach can reduce unnecessary cultures and also prevent central line-associated bloodstream infections.
We also spoke today about HFNC being non-inferior to CPAP in the setting of bronchiolitis. It is essential that we continue to reevaluate physiologic parameters once patients are started on non-invasive support and have a shared mental model on when to escalate.
Finally, we spoke about the PEWs scoring system, and, in the age of AI, new predictive models are going to be integrated into the critical care setting. It's clear that we need to take a more personalized approach in light of the new data and tools we discussed today, and this means considering both objective data and our own clinical judgment. We have to remember that every patient is unique, with their own set of circumstances and needs, and we need to be able to adapt our care to meet those individual requirements. You taught me in fellowship, Pradip, to identify, intervene, and reevaluate!

This concludes our integrated journal club episode. We hope you found value in our short, case-based podcast. We welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our websitepicudoconcall.org which showcases our episodes as well as our Doc on Call management cards. PICU Doc on Call is co-hosted by myself Dr. Pradip Kamat and Dr. Rahul Damania. Stay tuned for our next episode! Thank you!

References
Marquez L, Palazzi DL. An Integrated Approach to Blood Culture Stewardship. JAMA Pediatr. 2022 Jul 1;176(7):642-643. doi: 10.1001/jamapediatrics.2022.1034. PMID: 35499842.
Mayampurath A, Jani P, Dai Y, et al. A Vital Sign-Based Model to Predict Clinical Deterioration in Hospitalized Children. Pediatr Crit Care Med2020; 21:820–826

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine. I'm Rahul Damania from Cleveland Clinic Children’s Hospital and we are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode.

Today, we are going to discuss the management of the postoperative patient admitted to the PICU. Our discussion will focus on the non-cardiac and non-transplant admission. Our objective in this episode is to create a framework on what areas of care to focus on when you have a patient admitted to the PICU post-operatively. Each surgery and patient is unique; however, we hope that you will garner a few pearls in this discussion so you can be proactive.

in your management. Without any further delay, let’s get started with today’s case:

We begin with a 13-year-old child, Alexa, with h/o of a genetic syndrome, who presents today with a history of thoracolumbar kyphoscoliosis. Over the years, Alexa's curvature has progressively worsened, resulting in difficulty breathing and chronic back pain. The decision was made to proceed with a complex spinal surgery, including posterior spinal fusion and instrumentation.

In the weeks leading up to the surgery, Alexa underwent a thorough preoperative evaluation, including consultations with specialists and relevant imaging studies. Pulmonary function tests revealed a restrictive lung pattern, while the echocardiogram showed no significant cardiac abnormalities. Preoperative labs, including CBC, electrolytes, and coagulation profile, were within normal limits.

During the surgery, Alexa was closely monitored by the anesthesia team, who administered general anesthesia with endotracheal intubation. The surgery was performed by the pediatric neurosurgery and orthopedics, with intra-operative neuromonitoring to assess spinal cord function. The surgical team encountered an unexpected dural tear, which was repaired using sutures and a dural graft. Due to the prolonged surgical time, a temporary intra-operative loss of somatosensory evoked potentials was noted. However, signals were restored after adjusting the patient's position and optimizing blood pressure. The posterior spinal fusion and instrumentation were completed successfully, but the surgery lasted 8 hours. Total intra-operative blood loss was 800 mL, and Alex received 2 units of packed red blood cells and was on NE for a little over half the case before weaning off.

Alexa was admitted to the PICU intubated and sedated for postoperative care. The initial assessment showed stable vital signs, with a systolic blood pressure of 100 mmHg, heart rate of 90 bpm, and oxygen saturation of 99% on mechanical ventilation. Postoperative pain was managed with a continuous morphine infusion. The surgical team placed a closed suction drain near the surgical site and a Foley catheter for urinary output monitoring. You are now at the bedside for OR to PICU handoff…

To summarize key components from this case:

This is a patient with thoracolumbar kyphoscoliosis, underwent complex spinal surgery (posterior spinal fusion and instrumentation) due to progressive curvature, breathing difficulties, and chronic pain.

She had a course intra-operatively, where an unexpected dural tear occurred, requiring repair with sutures and a dural graft. Temporary loss of somatosensory evoked potentials was resolved through patient repositioning and blood pressure optimization with NE.

She had a moderate amount of blood loss in the case and is back intubated, sedated, with surgical drains in place.

So Pradip, we see patients such as Alex in our PICU commonly, if we take a step back what is your general approach with children who are admitted to the PICU post operatively?

I think it's crucial to approach the care of postoperative children in the PICU systematically and proactively. This involves closely monitoring their changing physiology, anticipating potential complications, and collaborating with the surgical team to address any concerns. By maintaining open communication and following evidence-based guidelines, we can optimize patient outcomes and facilitate a smooth recovery process.

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Just as a quick tid-bit, while some of these PICU admissions are scheduled, there is literature to suggest that up to 24% of non-cardiac surgeries may result in unanticipated admissions to the PICU. An single center study published in 2017 in PCCM looked at their rates of unanticipated PICU admissions from the OR, and they found that these children spend twice as much time on mechanical ventilation and that airway abnormalities, anesthetic factors, and intra-operative hypoxia contribute to such admissions.

Alright, Pradip, we are now at the post operative handoff and the first person who is going to be giving report is the anesthesia team. Can you please highlight what are some key things to listen out for during their sign out and what are some questions to ask?

Great question! The anesthesiologist plays a crucial role in ensuring the patient's airway and hemodynamics are properly managed during surgery, which is essential for a safe and successful procedure. It's important for the anesthesiologist to communicate with the PICU team regarding: induction, intraoperative course, line & tubes, as well as pain management.

Let’s break these down:

So for induction, you want to know were the anesthetics administered through IV or general anesthesia, was it a smooth process or were there difficulties, and what was used for anesthesia maintenance.

Next you want to know about the airway.

You want to gather essential information about the patient's airway management. Find out if an LMA or ETT was used during the procedure. If the patient was intubated, inquire about the ease of bag-mask ventilation and laryngoscopy, as well as the grade of the glottic view (e.g., Grade 1) and the type of laryngoscope used, including if video laryngoscopy was employed. It's also important to know the number of intubation attempts. Additionally, gather details about the type of ETT (regular or neo-cuff), its size, and the length at which it is taped to the gum or teeth. Finally, ask if any airway adjuncts were utilized during bag-mask ventilation or intubation.

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Remember that a key management point as soon as handout is completed is to obtain a CXR to confirm tube placement, and work closely with your RT to secure the tube in the correct position.

That’s so true!

As you wrap up anesthesia sign out, here are some other things to think about:

Oxygenation/Ventilation: Determine if the patient was easily oxygenated and ventilated, or if any bronchospasm or laryngospasm occurred during the case.

Lines & Tubes: Inquire about IV or central access, arterial line usage, and the presence of any drains or tubes (e.g., NG, Foley).

I/Os: Understand the management of fluid, electrolyte, and glucose homeostasis during anesthetic care, including the types and rates of fluids administered, blood product usage, and estimated blood loss.

Pain Management: Gather information on the analgesics, sedatives, and neuromuscular blockers used.

Other Medications: Be aware of antibiotics, antiemetics, anticholinergics, and other medications administered during the procedure.

Duration of the Case & Patient Position: Obtain information on the duration of the surgery and the patient's position (e.g., supine or prone, as in spinal cases).

Latest Set of Vital Signs: Ensure you have the most recent vital signs recorded.

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A nice mnemonic that I use is:

A - Airway: LMA/ETT, ease of ventilation, glottic view, laryngoscope type

P - Pain Management: Analgesics, sedatives, neuromuscular blockers

I - I/Os: Fluids, blood products, estimated blood loss

L - Lines & Tubes: IV/central access, arterial line, drains, NG, Foley

O - Oxygenation/Ventilation: Oxygenation ease, bronchospasm, laryngospasm

T - Time & Position: Duration of case, patient position (supine or prone)

Especially when it comes to access, coordinating with your PICC team, surgery colleagues, or anesthesia teams of long term access or additional PIVs which can be placed while the patient is under anesthesia is key!

Absolutely, Rahul! It’s important for us to also recognize that general anesthesia can cause vasodilation, and when combined with surgical blood loss and insensible losses, it increases the need for fluids postoperatively. Factors like prone positioning and mechanical ventilation can also affect urine output, making it a less reliable indicator of intravascular volume. In the postoperative period, it's important to administer isotonic fluids to avoid hyponatremia and watch for SIADH. Additionally, since operating rooms can be cold, it's crucial to monitor the patient's temperature, especially in infants, to prevent complications like arrhythmias and coagulation disturbances due to hypothermia.

Let’s transition, Pradip. When admitting a postoperative patient to the PICU, what essential questions should we ask the surgeons?

As we have our patient post-op in the PICU, we need to have a clear understanding of the type of surgery performed. Additionally, we should ask these key questions to ensure comprehensive patient management. Communication is essential!

We have arranged this into organ systems, and while not all of these questions would be applicable to every case, this list is relatively comprehensive!

Let’s start with our first organ system:

CNS:

What are the acceptable pain management medications for the immediate post-op period? Can we consider PCA, non-opioids like ketorolac or other NSAIDs, or IV acetaminophen?

Are there any activity restrictions for the patient, or can they be mobilized early? When can we involve PT/OT and speech therapy in the patient's care?

Respiratory:

2) If the patient is admitted to the PICU intubated, when can they be extubated?

If extubation is unsuccessful, can non-invasive positive pressure ventilation, such as HFNC or BiPAP, be used? This is especially true for intra-abdominal procedures.

Is perioperative dexamethasone appropriate?

Are there any procedures like MRI or a revisit to the operating room needed prior to extubation?

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Just to loop back to a prior concept which we discussed, you want to know if the patient at minimum can be bag masked, was the airway difficult, if there is an acute airway event should the PICU team be the primary team to intubate or should this be an intubation by Anesthesia or ENT.

Cardiovascular:

3) What are the target blood pressure goals (systolic or MAP) for the patient postoperatively?

This will be especially true for neurosurgical procedures and even transplant patients.

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If you have yet to check them out, please consider listening to our prior episodes on the post operative approach to Renal transplant and Liver tranplant in the PICU!

Fluid, Electrolytes, and Nutrition/GI:

4) When can the patient begin clear fluids and advance their diet?

Renal:

5) Can the Foley catheter be discontinued, and if so, when?

Talk about urine output goals when applicable.

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Also note that another output which you may have to keep in mind will be how much drainage will be coming out of your peritoneal, penrose, CSF drain — clarifying thresholds of quality and quantity of drainage with your surgical teams can really help with effective recognition of post operative complications. Coordinating a plan to replace the excessive out fluid and with type of fluid is key?

Hematology:

6) Which labs (such as CBC, electrolytes, or coagulation profile) need to be obtained, and how frequently?

Are there any specific transfusion goals?

Infectious Diseases:

7) What antibiotics are prescribed, and for what duration? If the patient becomes febrile, should cultures be obtained?

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Alright summary, analgesia, airway, BP goals, diet/activity, transfusion thresholds, antibiotics & repeat imaging.

Rahul, there seem to be several logistical questions to consider as well. Could you please highlight the key aspects for us?

Certainly, it's crucial to address logistical factors in postoperative care. Firstly, we need to determine when a patient, who is extubated and on room air and hemodynamically stable, can be transferred out, especially if bed capacity is limited. Secondly, it's essential to verify whether the child's family or guardians have been updated on their condition. Lastly, we should inquire about any additional consults that need to be placed for the PICU team to ensure comprehensive patient care.

We want to conclude this episode by delving deep into a few of the patients which are commonly admitted to the PICU post operatively. Our goal here is to apply the principles of management we just learned.

The first case we want to return to is our post-operative spinal fusion.

How does their pre-op status influence the post-op course?

The post-op course depends on pre-op status, pulmonary function, degree of curvature, and extent of repair. Key concerns include paralysis, pain management, airway maintenance, and pulmonary hygiene.

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The key here is to work closely with your pulmonary colleagues and RT to coordinate an effective bronchopulmonary hygiene regimen while admitted in the hospital as effective airway clearance can optimize cardiorespiratory status.

What complications should we watch for due to spinal cord manipulation?

Watch for SIADH and check sodium levels if urine output decreases. A high heart rate might be due to pain, so check intra-operative records for more information.

Alright our next Rapid Fire Case: ENT or OMFS procedures like tracheostomy, TNA, SGP, and airway reconstruction!

What should we know about post-op management for typical ENT procedures like tracheostomy or airway reconstruction?

Get information on bag-mask ventilation and intubation options in case of unplanned extubation. Check if NIPPV is contraindicated. Be prepared for blood loss, post-op swelling, and airway emergencies with wire cutters and spare tracheostomy.

How should we handle a dislodged tracheostomy in a fresh case?

Consult the ENT surgeon for a fresh tracheostomy dislodgment. Forcing a trach can create a false track. Some trachs have stay sutures for guidance. Difficult airway patients may need deep sedation or paralysis until the first tracheostomy change.

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In airway emergencies it is vital to remember that what...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

Here's the case of a 12-week-old girl old who is limp and seizing presented by Rahul.

Chief Complaint: A 12-week-old previously healthy female infant was found limp in her crib and developed generalized tonic-clonic seizures on the way to the hospital.
History of Present Illness: The mother returned from work on a Saturday to find her daughter unresponsive in her crib. The infant had been left in the care of her mother's boyfriend, who stated that the daughter had been sleeping all day and had a small spit up. As the patient continued to have low appetite throughout the day and continued to be unresponsive in her crib, mother called EMS to bring her to the emergency department. En route, the patient had tonic movement that did not resolve with intranasal benzodiazepines.
ED Course: The infant presents to the ED being masked. Upon arrival at the ED, the infant was in respiratory distress, with a heart rate of 190 beats per minute, respiratory rate of 50 breaths per minute, and oxygen saturation of 85% with bagging. She was intubated for seizure control upon arrival at the ED. Physical examination in the ED revealed bruising on the right neck region but was otherwise unremarkable. A non-contrast head CT showed no acute intracranial abnormalities. The initial diagnostic workup revealed normal CBC, mildly elevated hepatic enzymes, and pancreatic enzymes which were within normal limits. The blood gas showed metabolic acidemia with PCO2 in the 60s.
Admission to PICU: Upon admission to the PICU, neurosurgery and trauma teams were consulted. A skeletal survey and ophthalmology consult for a fundoscopic examination were ordered, as there were concerns of non-accidental trauma. Further investigation is underway to determine the cause of the infant's condition.

To summarize key elements from this case, this patient has:

Patient left with mother's boyfriend
Infant found limp and had seizures requiring intubation
Neck bruise
All of these bring up a concern for Non-Accidental Trauma (NAT) the topic of our discussion.

Let's start with a short multiple-choice question:

Which imaging modality is the most appropriate for establishing a diagnosis of abusive head trauma (AHT) in a 12-week-old infant with an open fontanelle on the exam?

A. CT scan of the brain without contrast B. MRI of the brain without contrast C. Skull X-ray D. Doppler ultrasound of the head

Rahul, the correct answer is A.

Though ultrasound may be less invasive, the penumbra effect in cranial ultrasound makes it hard to visualize the parts of the brain located just under the convexity of the skull such as a subdural hematoma. Regardless of the small radiation risk, noncontrast head CT is the method of first choice in imaging traumatic brain injury for both fractures and intracranial pathology. CT scan has a short scan time and is widely available. Non-contrast-enhanced CT has a high sensitivity for detecting acute hemorrhage and midline shift.

Thanks for that detailed explanation, I agree CT scan is a valuable diagnostic tool that provides detailed recon images for understanding the mechanism of fractures.

What about the role of MRI in diagnosing abusive head trauma?

MRI has lower sensitivity for acute hemorrhage compared to a CT scan and takes longer to acquire images, which may require anesthesia to provide immobility. However, a systematic review by Kemp and colleagues published in 2009 (Clin Radiol. 2009;64:473–483) reported that MRI performed following an abnormal CT scan in children with abusive head trauma revealed new information in at least 25% of cases, such as cranial shearing, ischemia, infarction, parenchymal hemorrhages, and cerebral contusions. It's important to note that the role of MRI in cases where the initial CT scan is normal is unclear. Additionally, MRI is more accurate in evaluating time points in certain lesions, making it a valuable tool in the diagnosis and management of abusive head trauma in pediatric patients.

💡 In summary, a CT scan is the preferred imaging modality for assessing traumatic brain injury in cases of suspected abusive head trauma, while cranial ultrasonography may be useful in some cases. It's important to remember that interpretation of imaging in cases of suspected AHT requires complete clinical information.

Alright, Pradip, very interesting that our initial CT scan did not show any signs of bleeding, once the patient became more stable in the PICU, what did the skeletal survey show?

The skeletal survey showed multiple fractures of varying ages, including multiple rib fractures, and an unhealed clavicle fracture. The team closely monitored the infant's condition and initiated treatment as necessary.

Rahul, can you give us a brief introduction to non-accidental trauma in the pediatric ICU?

Child abuse, also known as battered child syndrome, can take multiple forms such as physical abuse, sexual abuse, neglect, psychological maltreatment, general neglect, and medical neglect. Today, we'll focus on physical abuse that intensivists may encounter in their practice.
In the Pediatric Intensive Care Unit (PICU), the team is more likely to see cases of abusive head trauma, abdominal trauma, burns, complex fractures, and rib fractures, which may be identified when a chest radiograph is obtained after intubation. These are serious and often life-threatening conditions that require a multidisciplinary team approach and specialized care.

💡 To summarize, physical abuse in children, particularly infants, can present with nonspecific symptoms and signs, such as vomiting or apnea. This highlights the importance of considering the possibility of abusive head trauma in such cases.

Please also remember that the term, abusive head trauma replaced "shaken baby syndrome," and it's a serious and often life-threatening condition that requires prompt recognition and intervention. Therefore, it's essential for us as intensivists to be familiar with the various forms of physical abuse, including abusive head trauma, and work closely with other specialists to ensure that the patient receives the best possible care.

Pradip, let’s dive deep into abusive head trauma, do you mind talking about the spectrum of symptoms we can see?

Abusive head trauma is the most common presentation of child abuse in the PICU: As seen in our case presentation infants may present with apnea, altered mental status, loss of consciousness, limpness, vomiting, seizure, poor feeding, or have subtle signs like swelling of the scalp.

In a third of abusive head trauma cases, the infant was seen by another physician in the preceding 2-3 weeks. The diagnosis requires a high level of suspicion especially in an infant with fractures, ecchymosis, and failure to gain weight. AHT is the leading cause of fatal injuries in children.

📖 AHT is responsible for 53% of all severe TBI cases in infants.

What is the pathophysiology of injury in abusive head trauma?

The pathophysiology of abusive head trauma in infants is complex and multifactorial. The skull of a neonate is soft and malleable, which allows forces applied to the skull to propagate directly to the brain tissue. Additionally, the higher water content and lack of myelination make the brain more susceptible to shearing forces, which occur with shaking. Infants have a larger head in proportion to their body, constituting about 15-20% of total body weight as opposed to 2-3% in adults.

So, we've discussed how the pathophysiology of abusive head trauma in infants is complex and multifactorial. Can you tell me more about how the soft and malleable skull of a neonate plays a role in this type of injury?

A heavier head with a lack of nuchal muscular strength predisposes the head to sustain severe injury as opposed to an older child. Furthermore, due to a lack of coordination of the head and body motion, the infant is unable to protect themselves. Injuries in abusive head trauma can be due to blunt impact, shaking with blunt impact, or shaking alone. Whiplash shaking and jerking subjects the brain to rotational acceleration and deceleration forces, which explains brain injuries and retinal hemorrhages in the absence of external trauma. The resulting traumatic brain injuries can have devastating and long-lasting effects on the child's cognitive and physical development.

Rahul, how would an intensivist assess a child with physical abuse?

As the pediatric intensive care unit is a team sport, it's important to consult with multiple teams early on in cases of suspected abusive head trauma. This includes the trauma and neurosurgery teams, radiologists, child advocacy services, and social workers. In some states, early referral to Child Protective Services or law enforcement is mandatory to protect other siblings from harm. By involving these specialized teams and agencies, we can ensure a comprehensive approach to the diagnosis and management of abusive head trauma in pediatric patients.
Absolutely, Rahul. The first step in diagnosing abusive head trauma is to obtain a detailed history from parents or caregivers. It's important to determine if the child was brought for medical attention or neglected after the traumatic event. Additionally, we need to assess whether the child's development level is consistent with the proposed mechanism of injury and whether the alleged events account for all injuries.

What are some key historical features that can help diagnose child abuse in cases of suspected abusive head trauma?

In a retrospective study of 163 children, 30% of whom met the criteria for physical abuse, certain historical features had high specificity and positive predictive value for diagnosing child abuse. Having no history of trauma had a specificity of 0.97 and a positive predictive value of 0.92 for abuse. Among the subgroup of patients with persistent neurological abnormality at hospital discharge, having a history of no or low-impact trauma had a specificity and positive predictive value of 1.0 for definite abuse.

A detailed history is crucial in diagnosing abusive head trauma, as certain negative historical features such as no history of trauma and low-impact trauma have high specificity and positive predictive value for diagnosing child abuse when the clinical suspicion is high

Certainly. In our case, the mother's boyfriend claimed that the baby fell from the crib onto the hardwood floor. However, falls from less than five feet are unlikely to cause moderate or large subdural hematomas in children and are rarely fatal. It's important to note that scalp contusions or lacerations are common in such falls, while a skull fracture is typically linear and located in the parietal region without associated intracranial hemorrhage.
Rahul, in our case the patient had mild transaminitis, can you comment on abusive abdominal trauma?
Certainly, abdominal trauma in the PICU is an important topic to discuss. In our case, the patient had mild transaminitis which leads us to question the possibility of abusive abdominal trauma. It's important to note that AAT is actually the most common cause of abdominal injuries in children under two years of age.
The outcome for patients with AAT is also worse than those with accidental trauma, with a mortality rate ranging from 9-30%, as opposed to 4.7% for those with accidental injuries. Symptoms such as vomiting may be initially attributed to medical conditions like gastroenteritis, which can lead to a delay in diagnosis. The most common injuries in AAT involve the liver, kidney, spleen (with the liver being more common than the spleen), and the stomach/intestines. If a child presents with pancreatitis after a "reported fall," it should raise suspicion for abusive abdominal trauma.

Let’s keep building on this diagnostic framework, besides history what else would you emphasize?

Certainly, in addition to obtaining a thorough history, the next step in evaluating a child for non-accidental trauma in the PICU is to conduct a comprehensive physical exam. It's essential to document any skin findings, oral lesions, or eye findings, as well as to take photographs and place them in the patient's electronic medical records with the appropriate date/time. The next step is to obtain imaging, with CT being most helpful in the acute phase to determine the need for neurosurgical intervention, while MRI may be needed to evaluate for diffuse axonal injury, ischemia, cranial shearing, or infarction.
A skeletal survey should also be obtained to assess for fractures, and if abdominal injuries are suspected, a CT or MRI of the abdomen should be obtained. Additionally, CBC, CMP, coagulation studies, and pancreatic enzymes should be ordered. An ophthalmology consult for retinal hemorrhages is crucial, as they cannot be specifically dated and may clear quickly, so early examination is important. Lastly, postmortem examination is recommended for children who died from unexplained causes or abusive injuries.

To summarize, retinal hemorrhages are a common finding in fatal cases of AHT seen in 85% of cases with a spectrum of disease such as extensive hemorrhages leading to retinal tears, detachment, and vitreal hemorrhage. While retinal hemorrhages are not specific to AHT, they can be easily distinguished based on history, imaging, and clinical evaluation. Conditions such as birth trauma can cause retinal hemorrhages; the presence of these retinal hemorrhages can be correlated with the mode of delivery, with vacuum extractions having a higher correlation compared to NSVD and C-sections. It is important to note that retinal hemorrhages should not be attributed to birth trauma after 6 weeks of age. Other differentials for retinal hemorrhages in infants to keep in mind include leukemia, meningitis, vasculitis, and severe hypertension. However, by and large, please keep NAT on top of your differential.

How would you outline your general management framework if the history, physical examination, and diagnostic investigation suggest a diagnosis of abusive head trauma?

In managing a child with NAT, the first step is to prioritize acute medical and surgical management of the child's clinical condition, which includes following the same principles used for traumatic brain injury and polytrauma. This involves early consultation with neurosurgery and trauma teams, implementing cerebroprotective measures for intracranial pressure management and prevention of secondary brain injury, using lung protective ventilation strategies, providing adequate analgosedation, maintaining judicious fluid balance, and correcting any necessary laboratory abnormalities. The TAXI guidelines can be followed for blood and platelet transfusion. These topics have been discussed in detail in previous podcast episodes.

Rahul, let's close this episode with some key summary take-homes.

Our case highlighted the importance of maintaining a high index of suspicion for non-accidental trauma in infants and young children. The infant in our case had clinical findings inconsistent with the history provided by the caregiver, leading to a diagnosis of abusive head trauma. Abusive abdominal trauma should also be considered in cases of non-accidental trauma, with a high mortality rate and common injuries to the liver, kidney, spleen, and intestines. A team approach is crucial in the management of NAT in the PICU, involving specialists from trauma, neurosurgery, child advocacy, radiology, and social services. Early recognition and intervention are essential in improving outcomes for these vulnerable patients.

This concludes our episode on child abuse We hope you found value in our short, case-based podcast. We welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org which showcases our episodes as well as our Doc on Call management cards. PICU Doc on Call is co-hosted by...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania, from Cleveland Clinic Children’s Hospital. We are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode:

Welcome to our Episode about a 14-year-old male who collapsed on the baseball field.

Here’s the case presented by Rahul:

A 14-year-old male athlete was playing in a high school baseball tournament when he was hit in the chest with a pitched ball. The impact caused him to collapse on the field. Bystander CPR was begun given his unresponsiveness and emergency medical services were immediately called. The patient was transported to the hospital. Upon arrival, he was unresponsive and had no pulse. An electrocardiogram (ECG) showed ventricular fibrillation, and advanced cardiac life support was initiated. After several shocks and cardiac compressions, the patient regained a pulse and was transferred to the pediatric intensive care unit for further evaluation and management.

To summarize key elements from this case, this patient has:

Been struck by a high-velocity object in the chest
Suffered a cardiac arrest, likely due to an arrhythmia from the blunt chest trauma

The presentation brings up a concern for Commotio Cordis, our topic of discussion today!

We wanted to create this educational episode in light of the recent medical event experienced by the Buffalo Bill’s safety Damar Hamlin. His blunt chest trauma, which led to cardiac arrest, has been postulated to be due to commotio cordis. At the date of this record, we are glad that Damar Hamlin is on the road to recovery.

Absolutely, let’s dive in more into this topic, Let's start with a short multiple-choice question:

The 14-year-old described in our case suffered cardiac arrest after blunt chest trauma. Based on the working diagnosis of comottio cordis, what is the most likely EKG finding which may be seen in this patient?

A. Ventricular fibrillation

B. Ventricular tachycardia

C. Complete heart block

D. Asystole

The correct answer is A. In a study published in JAMA (2002; 287(9):1142-1146) which used data from the US Commotio Cordis registry maintained by the Minneapolis Heart Institute Foundation, reported that the most common arrhythmia out of the 128 confirmed cases, 82 of which had EKGs which could be analyzed was ventricular fibrillation. Three patients had Vtach, 3 had Bradyarrhythmia and 1 had complete heart block. Although 40 patients had asystole, this was unlikely to be the initial rhythm after impact. Interestingly, the majority of these rhythms were recorded at the scene.

Rahul, What is the definition of Commotio Cordis?

Commotio cordis is Latin for "commotion of the heart." It refers to a type of sudden cardiac arrest that occurs when a blunt impact to the chest disrupts the normal electrical activity of the heart and causes ventricular fibrillation. It is a primary arrhythmic event that occurs when the mechanical energy generated by a blow is confined to a small area of the precordium and profoundly alters the electrical stability of the myocardium, resulting in ventricular fibrillation. (NEJM Marron BJ et al. N Engl J Med 2010; 362:917-927)

So Pradip, the case we have involves an athlete, do you mind talking a bit about the demographics and epidemiology of this condition?

Absolutely! As you mentioned, Commotio cordis is Latin for agitation of the heart. Interestingly, it is the 3rd most common cause of sudden death in athletes after hypertrophic cardiomyopathy and congenital coronary-artery anomalies. Commotio cordis shows a predilection for children and adolescents with 26% of victims being younger than 10 years of age, & a minority of patients 25 years of age or older. It has a predilection for males, up to 95% in some reports. Commotio cordis can result from blows to the chest from projectiles (predominantly baseballs, softballs, lacrosse balls, or hockey pucks) or blunt bodily contact with other athletes, especially in children < 15 years of age group.

In summary, here are some patients at risk:

Male gender
Young age (typically between 5 and 25 years old)
Participation in high-impact sports such as baseball, ice hockey, and lacrosse.
Chest wall size and anatomy

Heart rate and rhythm at the time of impact.

It is important to note that commotio cordis can occur in anyone who sustains a sudden blow to the chest, regardless of age or level of physical fitness.

Rahul, what is the pathophysiology of Commotio Cordis?

The ventricular fibrillation seen after the mechanical energy of the blow is delivered to the chest has been shown to have certain determinants and triggers from animal studies.

Important determinants include:

Location of the blow must be directly over the heart (near the center of the cardiac silhouette);
Timing of the blow, which must occur within a narrow window of 10 to 20 msec on the upstroke of the T wave, just before its peak. That is an electrically vulnerable period, when inhomogeneous dispersion of repolarization is greatest, creating a susceptible myocardial substrate for provoked ventricular fibrillation.

Contributing variables include greater hardness of the projectile, small sphere, direct orientation, and thinner more compliant chest wall (with immature intercostal musculature).

At a molecular level: It is possible that ventricular depolarization induced by a blow to the chest in commotio cordis, has something in common with the pathophysiological mechanisms that give rise to primary arrhythmogenic conditions, such as ion channelopathies. The increased pressure in the ventricle after the impact, causes the cell membranes to stretch and activates ion channels. The candidate ion channels include the ATP-sensitive potassium channel, which contributes to the initiation of ventricular fibrillation in commotio cordis.

The incidence of Commotio Cordis in adults is low even in sports like kickboxing and boxing. A probable explanation for this may be that their mature and fully developed chest cage may be protective.

Pradip, if a child collapses during sports, what should be the approach of the bystanders prior to the arrival of the paramedics?

Early recognition of cardiac arrest is important. Sudden collapse with unresponsiveness, or no breathing or agonal breathing and no pulse, is cardiac arrest unless proven otherwise.

Immediate high-quality chest compressions should be initiated without interruptions while 911 call is initiated. If an AED is available, then the pads need to be applied to the chest without delay.

Another common scenario is that the child starts to seize after the collapse. This should not be erroneously blamed on a seizure disorder but could be most likely due to brain hypoxia from cardiac arrest.

Rahul, after the initial resuscitation, what are some of the investigations which should be considered?

Early consultation with the cardiologist and electro-physiologist is necessary. Electrocardiography, echocardiography, stress testing, ambulatory ECG monitoring, and cardiac MRI must be considered provided the patient is stable for transport. Electrocardiographic features suggestive of long QT and Brugada syndrome should be pursued if appropriate. Other tests include- CBC, CMP, cardiac enzymes, urine analysis, and even a toxicology screen. Cardiac genetic testing should be considered on a case-by-case basis.

Rahul, what is the management of such a patient in the PICU?

Usual good supportive care with attention to airway, breathing, and circulation should be provided. CVL and arterial lines should be placed and continuous cardiac monitoring initiated. The child may initially require a pressor, like epinephrine, immediately after the arrest for cardiogenic shock. Early extubation when a child is clinically stable should be attempted. Maintenance of judicious fluid balance and correction of electrolytes must be done. Physical and occupational therapy should be initiated early as should the early mobility program to prevent de-conditioning. In the absence of any underlying cardiac disease, there is no indication for any medical or device therapy for survivors of commotio cordis. Such individuals, generally, should have no restrictions for returning to athletic activity.

Check out our episode on post-cardiac arrest care. This two-part episode provides a systems-based breakdown of how to manage the multi-system dysfunction after cardiac arrest.

Pradip, what are some of the community approaches we can use in commotio cordis?

Improved design of sports equipment (using air-filled balls over the dense hardcore balls-although may not be practical as this may change the nature of the game).

Coaching young players to avoid getting hit in the chest by an errant pitch or avoid defending the goal in hockey or lacrosse using the player's chest

Chest protection devices, commercially available protectors, which were originally designed to reduce the likelihood of trauma from blunt bodily injury, do not offer absolute protection from arrhythmia after a blow to the chest. Wearing chest protectors is ineffective in consistently preventing ventricular fibrillation and reducing the risk of sudden death.

AEDs have substantial life-saving capability, and it is appropriate to disseminate them widely at youth sporting events and recreational settings where commotio cordis may occur. Prevention of sudden cardiac death from commotio cordis should be focused on the wider availability of automated external defibrillators and prompt recognition and resuscitation of victims.

Commotio cordis is usually, although not invariably, fatal. The availability of AEDs, public awareness, and early activation of the survival chain has improved survival.

As we close our episode, Rahul, can you summarize some key take-home points?

Commotio cordis is a primary arrhythmic event that occurs when the mechanical energy generated by a blow is confined to a small area of the precordium and profoundly alters the electrical stability of the myocardium, resulting in ventricular fibrillation.

Early recognition of cardiac arrest with prompt initiation of CPR and defibrillation can improve outcomes in patients who suffer severe blunt trauma & commotio cordis.

AEDs should be made available as a public health measure in youth sports or recreational settings! We are pediatricians at heart; thus prevention is key!

This concludes our episode on Commotio Cordis. We hope you found value in our short, case-based podcast. We welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org which showcases our episodes as well as our Doc on Call management cards. PICU Doc on Call is co-hosted by myself Dr. Pradip Kamat and Dr. Rahul Damania. Stay tuned for our next episode! Thank you!

References

Fuhrman & Zimmerman - Textbook of Pediatric Critical Care. Fitzgerald T and Reed C. Pediatric Thoracic trauma. Chapter 119: page 1405

Marron BJ, Estes N. A.M. Commotio Cordis. N Engl J Med 2010; 362:917-927

Estes, N A M; Weinstock, J. My APPROACH to Commotio Cordis. Trends in cardiovascular medicine, 2019, Vol.29(4), p.248

Clinical Profile and Spectrum of Commotio Cordis. Marron BJ et al. JAMA. 2002;287(9):1142-1146. doi:10.1001/jama.287.9.1142

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Approach to Pediatric Trauma Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

Welcome to our Episode today of a 7 yo M who presents to the PICU after a severe Motor Vehicle Accident.

Here is the case presented by Rahul

A 7-year-old male child is admitted to the PICU after sustaining severe trauma. The patient was brought to the emergency department after a motor vehicle accident that involved an 18-wheeler truck & the family’s car; in this severe accident the 7 yo was noted to be restrained however upon impact was ejected from the vehicle. He was unconscious and had multiple injuries, including a laceration on the head and bruising on the chest. The EMS was activated and the patient presented to the ED for acute stabilization. Upon examination, the patient was found to have a Glasgow Coma Scale score of 8, indicating a serious head injury. He had multiple bruises and abrasions on the chest and arms, and his pulse was rapid and weak. The patient was resuscitated with colloid and blood products, intubated, and transferred to the pediatric intensive care unit for further management.

Notably, a CT scan of the head showed a skull fracture and a subdural hematoma. A chest X-ray showed multiple rib fractures and bilateral pulmonary opacities with no evidence of pneumothorax. The patient was also found to have a grade 2 liver laceration and a splenic injury. Pelvic x-ray and cardiac FAST exam were unrevealing.

To summarize key elements from this case, this patient has:

A traumatic brain injury
Pulmonary contusions and is at risk for PARDS
Liver and spleen injury
Anemia
Pertinent negative includes: No pelvic injuries or injuries to great vessels in the chest

Rahul, let's approach the PICU medical management of this case based on a culmination of various guidelines published in the Pediatric Critical Care literature. Namely, let's use this case to dive deep into guidelines for:

Traumatic brain injury (TBI)

*Transfusion and Anemia Expertise Initiative (*TAXI)

pediatric blunt liver and spleen injury management, are also known as the ATOMAC protocol, as well as general PICU management of acute trauma.

As we take the management of this pediatric trauma patient in a systems-based fashion let's first go into the Management of Pediatric Traumatic Brain Injuries, can you start us off with some key management considerations?

Based on the March 2019 TBI guidelines published in Pediatric Critical Care Medicine in 2019 (PCCM20(3S):p S1-S82, March 2019)
This patient should have an ICP monitor or even an EVD placed for CSF diversion in consultation with the NS and trauma team. A CPP of at least >50 in our 7 yo patient and ICP < 20 mm Hg has been shown to improve outcomes and reduce mortality.

Just as a quick review, CPP stands for cerebral perfusion pressure, which is the pressure that maintains blood flow to the brain. The formula for CPP is:

CPP = MAP (mean arterial pressure) - ICP (intracranial pressure)

Monitoring does not affect outcomes directly; rather the information from monitoring can be used to direct treatment decisions. Treatment informed by data from monitoring may result in better outcomes than treatment informed solely by data from clinical assessment. In short, it is important to have qualitative and quantitative data to optimize your decision-making.

As we talked about ICP control is so crucial for this patient, Pradip, can you talk to us about some practical points in controlling ICP?

Appropriate patient position (head midline and elevated 15-30, make certain that cervical collar is not too tight but allows for venous drainage from the skull) is recommended. Control fever, treat hypoxia, and hypercarbia, and avoid hypotension.
Sedation and analgesia are at the discretion of the treating physician but routine boluses must be avoided to prevent cerebral hypoperfusion. Also, continuous use of propofol for sedation or ICP management is not recommended.

That's a great initial set of practical management tips, head position, temperature control to avoid hyperthermia, and avoidance of hypotension to ensure optimal CPPs. Propofol may have a deleterious effect in some patients as it can reduce the SVR and predispose patients to hypotension, especially when employed in a bolus fashion.

Rahul, what about NMB?

Neuromuscular blockade may be required if ICP remains elevated despite adequate sedation. Muscle relaxation can also prevent shivering, fighting against the ventilator, and permit hyperventilation if it is required. Intermittent dosing of short-acting agents (eg, vecuronium or rocuronium) is preferred.
Seizure prophylaxis with levetiracetam or phenytoin to prevent post-traumatic seizures is recommended for the first 7 days. Uncontrolled seizures can increase ICP.
For ICP management: Any ICP > 20 mmHg for > 5 minutes requires intervention:
First-tier therapies include: CSF drainage, bolus/infusion of hypertonic saline, sedation-analgesia/NMB
Second-tier therapies used for refractory intracranial hypertension (20-40% of severe TBI cases) include Hyperventilation, surgery for decompressive craniectomy or to remove mass lesion (a repeat CT scan may be required), hyperventilation, moderate hypothermia (32-34), barbiturate coma, higher levels of osmolar therapy.

I think this is a great time to incorporate an essential physiologic concept, of cerebral metabolic rate of oxygen consumption.

CMRO2 refers to the cerebral metabolic rate of oxygen consumption, which is a measure of the amount of oxygen used by the brain. CMRO2 can be increased during periods of Increased neural activity, Hypercapnia, Hypoxia, increased temperature and increased ICP

It is important to note that these factors can impact the brain's oxygen consumption, and in some cases, an increase in CMRO2 can lead to a decline in brain function if the brain is not able to adequately meet its increased oxygen demand.

Let's pivot to the next organ system in this patient — our patient had bilateral pulmonary contusions, about this patient meet at-risk PARDS criteria? and what would be your mechanical ventilation strategy?
The patient has bilateral contusions. One study (Intensive Care Med Nov 2019, 36(7):) reported that Pediatric ARDS in children with pulmonary contusion is independently associated with lower GCS scores. This patient is at risk for PARDS based on the presence of bilateral contusions and initial GCS < 8. The incidence of PARDS in TBI is ~ 9%, and its presence is associated with significantly increased morbidity and mortality. (Nair AB, Cohen MJ, Flori HR. Pediatr Crit Care Med 2020; 21:122–128). There are no clear oxygenation/Ventilation guidelines in TBI-associated PARDS. We should avoid high positive pressures (PIP) and high positive end-expiratory pressures (PEEP) as long as oxygenation remains adequate; otherwise high PIP and PEEP may increase intrathoracic pressure and impede venous drainage. We target a PCO2 35-45 mmHg and avoid hyperventilation to prevent cerebral ischemia due to decreased cerebral blood flow.

To summarize, PARDS in trauma is a heterogenous disease — it is important to pay attention to the cardiopulmonary interactions of increased positive intrathoracic pressure as this can have effects on preload to the heart as well as venous drainage of the cerebral vasculature.

Pradip, What about fluid status?

Additionally, we should pay close attention to fluid status: Treat hypovolemia with isotonic fluids (eg, normal saline) to achieve normal, rather than excess, volume status. We should avoid the administration of hypotonic fluids (eg, D5W). Although recent evidence from basic science research, observational research, and clinical trials suggests that using balanced crystalloids rather than saline may have beneficial effects on acid–base balance, renal physiology, and patient outcomes, we need to be careful about using balanced fluids in TBI so as to not cause iatrogenic hyponatremia. Although adult studies have reported poor outcomes with fluid overload in pediatric patients, the role of FO in pediatric TBI outcomes is not clear. Drawing from adult studies it is best to be vigilant about fluid balance and avoid fluid overload.

Intensivists should pay close attention to serum electrolytes and glucose while managing Trauma patients: Serum Na should be monitored at least twice daily in TBI patients. If hyponatremia develops despite the use of NS, we should think of SIADH or CSW.

Our patient in our case was noted in the PICU to become progressively hypothermic, Rahul can you highlight the effect of hypothermia in the setting of pediatric trauma?

Yes, I think it is important for us to review the terrible triad of trauma. The "triad of death" in trauma refers to a combination of three physiological conditions that often occur together and significantly increase the risk of death in trauma patients. The triad of death is a dangerous state, as each component can contribute to the others, exacerbating the risk of death. The triad includes acidosis, hypothermia, and coagulopathy. Early recognition and aggressive management of these conditions are crucial in improving outcomes in trauma patients.

Rahul, let’s wrap this section up by talking about hyperglycemia, our patient was noted to have a few blood sugars around 200 mg/dl during the first four hours of his PICU admission, can you shed some light on this?

Hyperglycemia is also commonly seen in TBI patients. The optimal strategy for glucose administration or control remains controversial although it's reasonable to withhold glucose in the IVF in the first 48hrs with close monitoring to prevent hypoglycemia.

The last part of this episode will cover a bit on transfusion in the critical care setting as well as the management of blunt abdominal trauma.

Our patient was noted to have a Hgb of 6.8 mg/dL and an INR of 1.8. How should we tackle anemia and also balance the elevated INR?
Per the Pediatric Transfusion and Anemia Expertise Initiative–Control/Avoidance of Bleeding (TAXI-CAB)guidelines published as a supplement in the January 2022 Vol 23, supplement 15 of PCCM journal, the guideline concluded that there is insufficient pediatric evidence to support specific thresholds for coagulation tests, including INR, and platelet count, and the transfusion of plasma and platelets in critically ill pediatric patients with severe trauma, moderate-to-severe TBI, or nontraumatic ICH.
It is unclear if an INR of 1.8 would change much with an FFP transfusion. Some studies have reported a significant change in INR with FFP only when INR > 2.5 (Arch Surg 2010; 145:899–906). If a procedure such as an ICP monitor or EVD was being placed, the NS team would suggest FFP administration for an INR > 1.5. Similarly it's reasonable to target a platelet count > 100K during the neurosurgical procedure. Although it is not necessary to continue to maintain a platelet count of > 100K once hemostasis is achieved.

What about blood transfusion?

Even though there is a lack of evidence in pediatric patients, the TAXI-CAB experts concluded that a balanced resuscitation strategy/ratio for RBC/plasma/ platelet of 1:1:1 or 2:1:1 in injured children with hemorrhagic shock or with life-threatening hemorrhage might be considered. This transfusion strategy can be stopped once the hemorrhage is controlled. In our case, the patient currently has no ongoing bleeding or shock. The Hgb is 6.8. Per the September 2018 TAXI_CAB guidelines published in the PCCM supplement (Vol 19, supplement 3): In Critically ill children with acute brain injury (e.g., severe traumatic brain injury, or cerebrovascular stroke), an RBC transfusion could be considered if the Hb falls between 7 – 10 g/dL. They also recommended against the use of invasive brain oxygenation monitoring to guide RBC transfusion. Based on these guidelines, I would transfuse blood to this patient.

Once hemostasis is achieved it is reasonable to watch the trend in CBC, coagulation profile every 12 hours. It is not necessary to maintain a platelet count of > 100K once hemostasis is achieved. Similarly, the routine correction of an INR below 2 with FFP is not recommended as studies show a significant change in INR with FFP only when INR > 2.5. In patients with acute brain injury, RBC transfusion must be considered if hgb falls between 7-10g/dL

Finally, in our case, the patient sustained a liver and splenic injury, can you use this case to tell us more about the ATOMAC guidelines?

Absolutely, so the Arizona-Texas-Oklahoma-Memphis-Arkansas Consortium (ATOMAC) consists of a group of Level I pediatric trauma centers from across the United States dedicated to performing clinical and preclinical studies aimed at optimizing management and functional outcomes for injured children. The strongly recommended guidelines include:

Management of pediatric BLSI may be based on hemodynamic status, rather than injury grade.
A shortened period of bed rest of 1 day or less for stable children with unchanged hemoglobin levels.
A transfusion threshold of 7.0 g/dl is reasonable for children undergoing non-operative management.
Unstable patients should be considered for surgery, urgent embolization, or continued non-operative management, depending on other injuries and the center's resources

A recent study (Stewart et al Trauma Acute Care Surg. 2023 Jan 16.) reported that the ATOMAC guideline fostered high rates of non-operative management with low ICU utilization and LOS, while demonstrating safety in implementation, irrespective of injury grade.

In this patient, I would recommend serial CBC monitoring every 4 to 6 hours!

To summarize, the most commonly injured abdominal organ in blunt trauma is the spleen followed by the liver. Intra-abdominal solid organ injuries are graded by the appearance on the computed tomography scans. Higher the grade, the more injury. Most intra-abdominal blunt trauma injuries are managed non-operatively provided the patient is hemodynamically stable. Pay close attention to, localized tenderness, ecchymosis, abrasion, flank tenderness, and flank or abdominal mass along with elevation of liver enzymes or drops in hgb.

For any trainees out there, we would highly recommend familiarizing yourself with TBI guidelines TAXI guidelines and the ATOMAC protocols as these will provide a framework for the management of Pediatric Trauma.

Pediatric trauma like many diagnoses in the PICU involves a multidisciplinary approach with close communication. The approach sense outside of the pediatric ICU as many of these patients undergo long-term rehab in inpatient and outpatient facilities.

This concludes our episode on the PICU management of the patient with trauma. We hope you found value in our short, case-based podcast. We welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org which showcases our episodes as well as our Doc on Call management cards. PICU Doc on Call is co-hosted by myself Dr. Pradip Kamat and Dr. Rahul Damania. Stay tuned for our next episode! Thank you!

References
Fuhrman & Zimmerman - Textbook of Pediatric Critical Care Chapter 117 Evaluation, Stabilization, and initial management after trauma (Naiditch JA et al) pages 1363-1374. Also Chapter 118 Traumatic Brain Injury(Kochanek PM et al.) page 1375-1399. Also Chapter 119 Pediatric Thoracic Trauma (Fitzgerald et al) pages 1401-1407. Also Chapter 120. Pediatric Abdominal trauma (Vogel AM et al) pages 1408-1416
Kochanek, Patrick M.; Tasker, Robert C.; Carney, Nancy; Totten, Annette M.; Adelson, P. David; Selden, Nathan R.; Davis-O’Reilly, Cynthia; Hart, Erica L.; Bell, Michael J.; Bratton, Susan L.; Grant, Gerald A.; Kissoon, Niranjan; Reuter-Rice, Karin E.; Vavilala, Monica S.; Wainwright, Mark S. Guidelines for the Management of Pediatric Severe Traumatic Brain Injury, Third Edition: Update of the Brain Trauma Foundation Guidelines. Pediatric Critical Care Medicine. 20(3S):S1-S82, March 2019
Emeriaud, Guillaume, Khemani R et al. on behalf of the Second Pediatric Acute Lung Injury Consensus Conference (PALICC-2) Group on behalf of the Pediatric Acute Lung Injury and Sepsis Investigators (PALISI) Network Executive Summary of the Second International Guidelines for the Diagnosis and Management of Pediatric Acute Respiratory Distress Syndrome (PALICC-2). Pediatric Critical Care Medicine. 24(2):143-168, February 2023
Nellis ME, Karam O, Valentine SL, Bateman ST, Remy KE, Lacroix J, Cholette JM, Bembea MM, Russell RT, Steiner ME, Goobie SM, Tucci M, Stricker PA, Stanworth SJ, Delaney M, Lieberman L, Muszynski JA, Bauer DF, Steffen K, Nishijima D, Ibla J, Emani S, Vogel AM, Haas T, Goel R, Crighton G, Delgado D, Demetres M, Parker RI; Pediatric Critical Care Transfusion and Anemia EXpertise Initiative—Control/Avoidance of Bleeding (TAXI-CAB), in collaboration with the Pediatric Critical Care Blood Research Network (BloodNet), and the Pediatric Acute Lung Injury and Sepsis Investigators (PALISI) Network. Executive Summary of Recommendations and Expert Consensus for Plasma and Platelet Transfusion Practice in Critically Ill Children: From the Transfusion and Anemia EXpertise Initiative-Control/Avoidance of Bleeding (TAXI-CAB). Pediatr Crit Care Med. 2022 Jan 1;23(1):34-51. doi: 10.1097/PCC.0000000000002851. PMID: 34989711; PMCID: PMC8820267.
Tasker, Robert C. MA, MBBS, MD, FRCP1,2, Turgeon, Alexis F. MD, MSc, FRCPC3; Spinella, Philip C. MD, FCCM4; for the Pediatric Critical Care Transfusion and Anemia Expertise Initiative (TAXI), in collaboration with Pediatric Critical Care Blood Research Network (BloodNet), and the Pediatric Acute Lung Injury and Sepsis Investigators (PALISI) Network. Recommendations on RBC Transfusion in Critically Ill Children With Acute Brain Injury From the Pediatric Critical Care Transfusion and Anemia Expertise Initiative. Pediatric Critical Care Medicine 19(9S):p S133-S136, September 2018. | DOI: 10.1097/PCC.0000000000001589
Stewart S, Fraser JA, Shah N, Rentea RM, Aguayo P, Juang D, Fraser JD, Snyder CL, Hendrickson RJ, St Peter SD, Oyetunji TA. INSTITUTIONAL OUTCOMES OF BLUNT LIVER & SPLENIC INJURY IN THE ATOMAC ERA. J Trauma Acute Care Surg. 2023 Jan 16. doi: 10.1097/TA.0000000000003870. Epub ahead of print. PMID: 36649594.

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Dear Listeners & Peds ICU community, WE are back on air!

Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists.

I'm Pradip Kamat coming BACK to you from Children’s Healthcare of Atlanta/Emory University School of Medicine

and I'm Rahul Damania from Cleveland Clinic Children’s Hospital and we are two Pediatric ICU physicians passionate about all things MED-ED in the PICU.

PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting.

As we turn into a new year, we would like to introduce Season 2 of PICU Doc on Call.

Yes Pradip, I am super excited for this year & I want to take this moment to thank YOU all, our listener community for making PICU Doc on Call such a success as we share our passion for medical education thru this forum!

This episode will give you a quick layout of how we will be organizing each episode of PICU doc on call this year. We will also highlight some tips and tricks on how to best learn from a medical podcast. Our goal in this episode is to provide you a framework on some best practices in medical podcasting and how to retain information from a podcast. Especially for our past & future episodes, we hope you can use this audio learning platform to assist you in applying the knowledge at the bedside when you are working in the acute care setting.

Let’s get into our first learning objective,

Rahul, did you know that learning via podcasts can actually benefit your brain & change the neural chemistry.

In fact, a 2016 med ed study published out of UC Berkeley concluded that listening to narrative stories from podcasts can stimulate multiple parts of your brain such as the limbic system and can enhance mood as it modulates dopamine and serotonin driven neural pathways. Think about listening to your favorite true-crime podcast — the suspense actually allows for you to stimulate centers in your medulla that increase the amount of endorphines, dopamine and serotonin that keep you on the edge of your seat.

That is so unique, so based on this, I do want to highlight some of the key elements which will make our podcast or any medical podcast you listen to beneficial. These pearls will also help you if you are developing a medical podcast of your own!

The first concept here is that many podcasts provide narratives.

When it comes to medical podcasts, narratives are in the form of medical cases which allow for you to retain content knowledge as a patient case invokes emotion and this can help you remember information more robustly.

When listening to a podcast, you have to use your imagination to picture what’s going on. For example, if I painted a 2 yo M with a history of rhinorrhea at home for about a week who now presents to the ED with subcostal & intercostal retractions that then progresses to intubation in the PICU, you not only are envisioning a patient in front of you, but also are shifting your mind across settings. Our brain has to work at the pace of the audio, so hopefully your mind doesn’t wander off like it does when reading a textbook page. And because you have to actively think, you can retain much more.

The second advantage of audio learning is that it provides flexibility and accessibility

When it comes to incorporating a podcast into your daily learning, it is easy, at any time of the day, you can open up your smart phone and access your Apple podcast or Spotify app and listen to a short episode on a certain topic. I would really encourage you to have a portion of the day, whether it is your commute, during chores, or even during a workout to incorporate listening to a podcast in your daily learning. Especially for PICU DOC ON CALL, our episodes are on average around 20 minutes to really capture your attention span.

In fact, a very interesting study published in 2022 by Wolpaw et al. looking at knowledge retention from a podcast showed that

trainees preferred podcast learning over reading for many topics.

When compared to textbook reading, podcast learning (seated or on a treadmill) produced significantly better learning gain, and equivalent retention for two of the three topics which they piloted in the study. This study even hooked the resident & med student participants to an EEG to highlight increased attention when using an audiobased tool.

Finally, a good medical podcast follows a consistent outline or organization & is rooted in principles of multi-media learning.

Multi-media learning theory specifically comes from Dr. Richard Mayer from UC Santa Barbara. His lab focuses on learning science and use of ed technologies.

Some of the key multi-media principles which make podcasts such a unique form of learning involve:

Dual channel processing — the fact that we can utilize both visual and audio representations.

WE are really passionate about this theory on PICU Doc on Call, so make sure you check out our chalk talk infographic & show notes which are paried with each episode; they will help you garner a visual representation of the content we cover!

That’s great, I think another unique multi-media principle is to have a minimization of extraneous load, i.e. the fact is that effective podcasts cut out redudancy, have optimal length of segments, & have user controls like double speed, etc.

The key summary which we would like to impart on you:

Utilize medical podcasts to actively learn — try to identify relevant material which is new to you and create a schema so that you are able to connect the information to your prior knolwedge. This idea of knowledge construction where you can integrate new information with prior experience is crucial in creating long-term memory with podcasts. Podcasts are unique to Adult Learning theory because they are a great self directed way to enhance your learning. Imagine this, you see a patient with ARDS in the PICU or on transport, you can easily direct your learning to a podcast to help solidify what you see & optimize your management decisions.

This is great, Pradip, do you have other tips on how we can effectively learn from a medical podcast?

Yes, I like to hit the pause button often during an in-depth podcast. It helps me stop for a moment and digest the information so I can link it to my clinical experience or knowledge which I have read in the past.

I also try to keep a small notebook in my pocket which I can write out anything that resonates with me — writing it down helps me remember & I can have an area which acts as my second brain as I develop lectures or even teach on rounds.

Such great advice, I also think listening to a podcast and discussing the contents with a colleague or your learner group is so essential. This principle comes from a highly recommended book on learning science called Make it Stick by Peter Brown and colleagues out of their research lab in St Louis and one of the quotes which really resonate with me is:

“Learning is deeper and more durable when it’s effortful. Learning that’s easy is like writing in sand, here today and gone tomorrow.”

Taking that extra effort to construct a mini-chalk talk for your learner group after you listen to the podcast or incorporate it into your next fellow didactics may be helpful for you to retain the new information!

To wrap up this episode, Rahul do you mind sharing with our listeners on how each of our upcoming podcasts in Season 2 will be organized?

Start with a case to highlight the PICU topic at hand

We will provide you a case summary highlighting the pertinent positives and negatives

Go into a board style multiple choice question to help assess your knowledge

Provide diagnostic and management frameworks highlighting relevant literature which surround the topic.

We aim to make this season’s podcasts very dynamic, engaging, & practical. We hope to have you listen to our podcast and actually garner some content that you can incorporate in your practice as well as even utilize to teach your learners/colleagues

Just a quick anecdote, I recently gave a lecture to the EM residency at Cleveland Clinic & before the didactic session, I did assign a podcast to listen to! I see this flipping the class room idea in the undergraduate medical school realm & I really think leveraging this model in the graduate med ed realm is on the horizon.

This concludes our first Season 2 episode on How to Learn & Retain Knowledge from a Medical Podcast. We hope you found value in our short podcast. We really would like to welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org which showcases our episodes as well as our Doc on Call infographics. PICU Doc on Call is co-hosted by myself Dr. Pradip Kamat and Dr. Rahul Damania. Stay tuned for our next episode! Thank you!

References:

Wolpaw J, Ozsoy S, Berenholtz S, Wright S, Bowen K, Gogula S, Lee S, Toy S. A Multimodal Evaluation of Podcast Learning, Retention, and Electroencephalographically Measured Attention in Medical Trainees. Cureus. 2022 Nov 9;14(11):e31289. doi: 10.7759/cureus.31289. PMID: 36514626; PMCID: PMC9733582.

Brown, Peter C. Make It Stick : the Science of Successful Learning. Cambridge, Massachusetts :The Belknap Press of Harvard University Press, 2014.

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The Cannabis sativa plant contains over 500 chemical components called cannabinoids, which exert their psychoactive effect on specific receptors in the central nervous system and immune system. The 2 best-described cannabinoids are THC and cannabidiol (CBD)—and are the most commonly used for medical purposes. Patients with intractable epilepsy or chronic cancer pain may be using these drugs. THC is the active ingredient of the cannabis plant that is responsible for most symptoms of central nervous system intoxication. The term cannabis and the common name, marijuana, are often used interchangeably).

Rahul, can you shed some light on the pharmacokinetics/pharmacodynamics of cannabis? Cannabis exists in various forms: marijuana (dried, crushed flower heads, and leaves), hashish (resin), and hash oil (concentrated resin extract), which can be smoked, inhaled, or ingested. THC is the active ingredient of the cannabis plant that is responsible for most symptoms of central nervous system intoxication, in contrast to CBD, the main non-psychoactive component of cannabis. The potency of cannabis is usually based on the THC content of the preparation. The THC is lipid soluble and highly protein bound and has a volume of distribution of 2.5 to 3.5...

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The presence of a grandparent is a risk factor for unintentional pediatric exposure to pharmaceuticals commonly referred to as the Granny Syndrome. Grandparents’ medications account for 10% to 20% of unintentional pediatric intoxications in the United States. To kids, all pills look like candy. Let’s start with a multiple choice. An overdose of which of the following medications may mimic the presentation of Metoprolol overdose? A. Verapamil toxicity B. Ketamine toxicity C. Valium toxicity D. Lithium toxicity

The correct answer is A, verapamil toxicity. Verapamil is a non DHP CCB. It acts at the level of the SA and AV node similar to Metoprolol, a beta-1-specific antagonist. Both cause bradycardia and AV node block. Valium though a CNS depressant, can cause CV depression as well, however, would have fewer changes on the conduction system compared to a non-DHP CCB.

What is the mechanism of toxicity with beta-blockers?

Beta-blockers are competitive inhibitors at beta-adrenergic binding sites, which results in decreased production of intracellular cyclic adenosine monophosphate (cAMP) with a resultant blunting of multiple metabolic and cardiovascular effects of circulating catecholamines.

They attenuate the effect of adrenergic catecholamines on the heart Decrease inotropic and chronotropic response. Some drugs like Propranolol can act as Na channel blockers (myocyte membrane stabilizing activity) at high doses resulting in arrhythmias and seizures. Toxic doses of drugs like Sotalol can result in K channel blockade giving rise to prolonged QT and risk for...

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Rahul, let's start with a short multiple choice question: Of the following biochemical enzymes, which of the following is deficient in classic galactosemia? A. UDP Glucoronyl Transferase B. Aldolase B C. Galactose 1 Uridyl Transferase D. Galactokinase

The correct answer is C. Galactose 1 Uridyl Transferase aka GALT. Classic galactosemia is caused by a complete deficiency of galactose-1-phosphate uridyl transferase (GALT). We should contrast this with galactokinase deficiency. These two present quite differently — GALT deficiency presents like our patient with jaundice, vomiting, hepatomegaly, renal dysfunction, and sepsis. Galactokinase deficiency has less of systemic symptoms and these patients similar to GALT deficiency have cataracts that are usually bilateral and resolved with dietary therapy. To go through our other answer choices, remember that Aldolase B is the rate-limiting enzyme in fructose metabolism, thus a deficiency in this enzyme would cause hereditary fructose intolerance. With this lead in question, let’s pivot into the biochemistry of galactose and review key lab findings in our patient with galactosemia. Rahul, can you give us a quick summary of how galactose is metabolized in our body? Galactose is a sugar found primarily in human milk and milk products as part of the disaccharide lactose. Lactose is hydrolyzed to glucose and galactose by the intestinal enzyme lactase. The galactose then is converted to glucose for use as an energy source, however it needs a series of reactions: Galactokinase → which catalyzes the rxn galactose to galactose 1 PO4 Our rate limiting enzyme Galactose-1-phosphate uridyl transferase (GALT). GALT helps place a sugar moiety on galactose 1 PO4 to turn it into glucose 1 Phos which can then be utilized in glycolysis or glycogenesis.

A complete deficiency in GALT is known as classic...

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The correct answer is methadone. Methadone prolongs QT interval due to its interactions with the cardiac potassium channel (KCNH2) and increases the risk for Torsades in a dose-dependent manner. Besides the effect on cardiac repolarization, methadone is also associated with the development of bradycardia mediated via its anticholinesterase properties and through its action as a calcium channel antagonist. Hypokalemia, hypocalcemia, hypomagnesemia, and concomitant use of other drugs belonging to the family of CYP3A4 system inhibitors such as erythromycin can prolong Qtc. Even in absence of these risk factors, methadone alone can prolong QTc. Thanks for that, I think it is very important to involve your Pediatric Pharmacy team to also help with management as children may be concurrent qt prolonging meds.

Rahul, what are some of the pharmacological and clinical features of methadone poisoning?

Methadone is a synthetic opioid analgesic made of a racemic mixture of two enantiomers d-methadone and l-methadone. besides its action on mu and kappa receptors, it is also an NMDA receptor antagonist. Due to its long action, methadone is useful as an analgesic and to suppress opioid withdrawal symptoms (hence used for opioid...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine. Today we are joined by two wonderful clinical pharmacists — Whitney Moore & Stephanie Yasechko. Whitney is a Clinical Pharmacy Specialist at Children’s Healthcare of Atlanta. She is on Twitter at @MoorephinRx. Stephanie is a Pediatric Lung Transplant Clinical Pharmacy Specialist at Cincinnati Children’s Hospital Medical Center. We are so excited to have you both on today. My name is Rahul Damania and I am a Pediatric Intensivist at Cleveland Clinic Children’s Hospital; Welcome to PICU Doc On Call where we focus on all things MED-ED in the PICU. Our podcast focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode: Welcome to our Episode an 18 yo immunocompromised patient with headache & sore throat Here's the case presented by Rahul: An 18-year-old female (40 kg) with PMH significant for fibrolamellar carcinoma of the liver, presents to the ED with headache and sore throat. She is febrile to 38.3, tachycardic, tachypneic, and has a WBC of 27K on her CBC. She is markedly hypotensive with BP on the arrival of 99/65. Cultures were drawn, the patient was given x1 doses of vancomycin and meropenem, and she was transported to the PICU for further workup and management. Due to her progressive hemodynamic instability, increased inflammatory markers, and marked immunocompromised state, the team is considering broadening her anti-microbial coverage. To summarize key elements from this case, this patient has: Fibrolamellar carcinoma of the liver A presentation of headache, sore throat, and hemodynamic instability with concern for sepsis A current regimen of just antibacterials, which brings up the consideration of adding anti-fungal coverage in her clinically ill state.

Our episode today will be covering anti-fungal agents in the PICU. We will review general mycology, understand different classes of antifungals, and highlight practical clinical pearls in the acute care setting. As mentioned, this patient has risk factors for an immunocompromised state due to her underlying liver condition. As we dive deeper into antifungals, Whitney, can you please give us an overview of common fungal pathogens in the PICU? Before we discuss the major drugs, it’s important that we take some time to briefly review the most common fungi we encounter clinically since it’s hard to choose the right agent when you don’t know exactly what you are treating. Clinically, Candida is probably the most common fungal pathogen encountered, especially in warm, moist environments. It is important to determine what type of species is growing. The three major species known to cause infection are C. albicans, C. glabrata, and C. krusei, but it is important to differentiate these species when identified since they have different resistance patterns. Cryptococcus is another type of fungus that is known to cause meningitis or fungemia, especially in immunocompromised or cirrhotic patients. Both Candida and Cryptococcus are classified as yeast on Gram stain. Treating cryptococcus will require the use of an agent that has good penetration to the CNS. Endemic fungi known as Coccidia, Histoplasma, and Blastomyces are known to cause disseminated infections in immunocompromised hosts; however, each fungus is associated with a different geographic region in the United States. With any type of infection, it is always very important to consider your patients’ exposures and recent travel history. And finally, there are two major molds that have the potential to be pathogenic. The first is Aspergillus which is identified via hyphae (tall filaments) on Gram stain well known to cause invasive pulmonary infections in the immunocompromised, specifically those who are neutropenic and/or received a lung transplant.

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Rahul, can you inform our listeners about the epidemiology of brain abscesses? Only about 25% of brain abscesses occur in children. Incidence in developed countries is about 1-2% while in developing countries it's about 8%. Peak incidence in children is seen between the ages of 4-7 years and is more common in males. Brain abscess in the neonatal age group is rare but are associated with a higher risk of complications and mortality. Risk factors for brain abscess include Otologic infections (ear, sinus, and dental infections), Congenital heart disease (30% of patients with BA have an underlying heart defect) with intra-cardiac or intrapulmonary shunting (pulmonary AV malformations in hemorrhagic telangiectasis), immunodeficiencies (solid organ transplantation, HIV, etc), prolonged steroid use, diabetes, alcoholism neurosurgical procedures, trauma. Other rare causes can be airway foreign bodies, congenital dermal sinuses, and esophageal procedures (such as dilatations). Brain abscess typically begins with a localized area of cerebritis which evolves through various stages (typically 10-14 days) to develop into an encapsulated collection of purulent material with peripheral gliosis or fibrosis. 40-50% of the spread of infection is via a contiguous site of infection such as otitis, sinusitis or mastoiditis or from head trauma or neurosurgical procedure. 30-40% is spread through the hematogenous route from endocarditis, pulmonary infections, or dental abscess. 90% of brain...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat coming to you from Children’s Healthcare of Atlanta/Emory University School of Medicine and I'm Rahul Damania from Cleveland Clinic Children’s Hospital and we are two Pediatric ICU physicians passionate about all things MED-ED in the PICU. PICU Doc on Call focuses on interesting PICU cases & management in the acute care pediatric setting so let’s get into our episode: Welcome to our Episode an 18 -year old with sore throat, and unilateral L-sided neck pain for ~2 weeks. Here's the case presented by Rahul: An 18-year-old female presents to the ED with cough, fever, fatigue, sore throat, and unilateral L-sided neck pain for ~2 weeks. The patient also has been having non-specific chest pain, weight loss, and decreased appetite for ~ 1 month. Patient has no recent travel h/o, no h/o of vaping or illicit drug use, and there were no sick contacts at home. Vitals revealed an HR 105, BP 116/66, Temp 38.3, and respiratory rate 35, She was 65 Kg and SPO2 on 2L NC was 100%. Physical exam was negative except (L) neck tender to palpation. There was no goiter, lymphadenopathy or hepatosplenomegaly. An initial chest x-ray was significant for possible multi-lobar pneumonia versus metastases. A Chest CT revealed multifocal septic emboli in the lungs. Echo did not show any gross vegetation. She has no rash or any trauma to the neck or difficulty swallowing, no oral ulcers, joint pain, or diarrhea. She had no recent dental work or drinking of unpasteurized milk or eating raw fish or meat. She was admitted to the PICU as she had hypotension requiring fluid boluses, and lab works significant for hyponatremia, rhabdomyolysis, worsening AKI, elevated ferritin, and elevated D-dimer. Her serum uric acid was 9.9, LDH = 230 (normal) ,ESR 78 (normal = 20 or less). Her serum lactate and serum troponin and BNP were all normal. Pertinently, US neck revealed an occlusive thrombus in the (L) IJ vein (done so as to avoid contrast in face of AKI), and blood cultures sent. To summarize key elements from this case, this 18-year-old female presents with fever +cough+sore throat Fatigue + Weight loss (L) neck pain Hypotension with abnormal labs including a concerning WBC with (L) shift, anemia, AKI, elevated uric acid, and ESR Chest CT with possible pulmonary emboli US showing occlusion. All of which brings up a concern for possible malignancy or pulmonary emboli from a septic focus in the neck and a possible diagnosis of Lemierre syndrome This episode will be organized… Definition Diagnosis (physical, laboratory) Management Rahul: What is the definition of Lemierre’s syndrome? Lemierre’s syndrome, also known as post-anginal septicemia or necrobacillosis, is characterized by bacteremia, internal jugular vein thrombophlebitis, and metastatic septic emboli secondary to acute pharyngeal infections. All of which are seen in our above case presentation. Previously called as the forgotten disease as its incidence was decreasing due to the increasing use of antibiotics especially penicillin for URI. However, recently there is an increase in Lemierre’s disease cases with decreased use of antibiotics due to antibiotic stewardship. The recent increase in Lemierre disease due to decreased antibiotic use has not been proven and remain controversial. Rahul what are some of the causative organisms of Lemierre syndrome? The most common causative agent of Lemierre’s syndrome is Fusobacterium necrophorum, followed by Fusobacterium nucleatum and anaerobic bacteria such as streptococci, staphylococci, and Klebsiella pneumoniae. Rahul: Can you tell our listeners about the pathophysiology of Lemierre’s syndrome? Lemierre syndrome can occur in health adults (more common in males in the age group of 14-24 years). Risk factors include immunocompromised patients, organisms, and environmental conditions. Lipopolysaccharides in F. necrophorum have endotoxic...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. Welcome to our Episode a 16-year-old who is coughing up blood. Here's the case: A 16-year-old female with h/o SLE was transferred to the PICU due to hypoxia requiring increasing FIO2. A few hours prior to admission to the PICU patient also started coughing up blood and had difficulty breathing. The patient was admitted to the general pediatric floor 2 days earlier for pneumonia requiring an IV antibiotic and O2 via NC. Once transferred to the PICU, she had a rapid deterioration with progressive hematemesis, worsening respiratory distress, and saturations in the low 70s requiring escalating FIO2. The patient was emergently intubated using ketamine + fentanyl and rocuronium. Chest radiograph showed: Worsening bibasilar alveolar and interstitial airspace disease concerning pulmonary hemorrhage. The patient was initially placed on HFOV Paw 26, FIO2 70%, Hz 8, Dp 70, and later transitioned to airway pressure release ventilation or APRV. The patient was also started on inhaled tranexamic acid or TXA and high-dose pulse steroids. The patient initially continued to have some blood coming out from the ETT with suctioning but secretions became clear in ~24 hours. The mother reported that the patient has never had hematemesis/hemoptysis before, or bleeding from any site in the past. Denied history of frequent respiratory infections or recent URI symptoms. The patient has been vaccinated/boosted x3 vs covid. Her COVID PCR is negative. The mother states that she does not engage in tobacco products or alcohol. A physical exam revealed a well-developed teenage girl laying supine in bed deeply sedated and mechanically ventilated. There was decreased AE at lung bases and coarse breath sounds throughout. There was no hepatosplenomegaly and exams of the heart, abdomen and other systems were normal. There was no skin rash and extremities were well perfused with no clubbing in the fingers. The pulmonary team was consulted and a workup was started for pulmonary hemorrhage. To summarize key elements from this case, this patient has: Autoimmune disease: Systemic lupus erythematosus Respiratory Failure warranting MV 2/2 Pulmonary hemorrhage Her presentation and deterioration bring up a concern for diffuse alveolar hemorrhage our topic of discussion for today. This episode will be organized… Definition Etiology Pathophysiology Diagnosis Management Rahul: How do we define pulmonary hemorrhage (PH): PH is defined as the extravasation of blood into airways and/or lung parenchyma. Blood in the airways produces a diffusion barrier resulting in hypoxemia. Due to the reduction of airway diameter from accumulated blood, there is increased airway resistance and even airway obstruction. Subsequently, ventilation can be impaired leading to increased WOB as well as myocardial work required for O2 delivery. Repeated episodes of PH can result in interstitial fibrosis thus changing lung compliance. Hemoptysis by definition is any bleeding from below the vocal cords. PH can be classified as focal or diffuse. Diffuse is further classified as diffuse immune or diffuse nonimmune.

Loss of 10% of a patient’s circulating blood volume into the lungs, regardless of age, causes a significant alteration in cardiorespiratory function and should be considered massive. In adults, massive pulmonary hemorrhage is defined as blood loss of 600mL or more in 24 hours. In infants, the involvement of at least two pulmonary lobes by confluent foci of extravasated RBCs constitutes as massive PH. “Enough bleeding to make one nervous is probably massive.” Let's pivot and talk about etiologies. Pradip, What are some of the causes of pulmonary hemorrhage in the PICU? Non-immune diffuse PH is usually seen in patients with congenital heart disease (TAPVR, pulmonary atresia, mitral stenosis, hypoplastic left heart syndrome to name a few) neonates (secondary to sepsis, HIE, BW < 1500...

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We will use a physiologic approach to cover this topic! Pradip, can you give us a quick overview of some general principles when it comes to tackling this high-yield critical care topic? Absolutely, internal acid base homeostasis is paramount for maintaining life. Moreover, we know that accurate and timely interpretation of an acid–base disorder can be lifesaving. When we conceptualize acid base today, we will focus on pH, HCO3, and CO2. As we go into each disorder keep in mind to always correlate your interpretation of blood gasses to the clinical status of the patient. Going back to basic chemistry, can you comment on the relationship between CO2 and HCO3? Yes, now this is a throwback. However, we have to review the Henderson–Hasselbalch equation. The equation has constants & logs involved, however in general this equation shows that the pH is determined by the ratio of the serum bicarbonate (HCO3) concentration and the PCO2, not by the value of either one alone. In general, an acid–base disorder is called “respiratory” when it is caused by a primary abnormality in respiratory function (i.e., a change in the PaCO2) and “metabolic” when the primary change is attributed to a variation in the bicarbonate concentration. Now that we have some fundamentals down, let’s move into definitions. Can you define acidemia and alkalemia and comment on how...

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Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat My name is Rahul Damania, a current 3rd-year pediatric critical care fellow and we are coming to you from Children’s Healthcare of Atlanta Emory University School of Medicine Today's episode is dedicated to the transition between NICU & PICU. We will focus on the ventilation of the ex-premature infant who graduated from NICU care and transitioned to the PICU. I will turn it over to Rahul to start with our patient case. Case: A 4-month-old ex-27 week baby boy is transferred to our PICU after an echo at an outside hospital showed elevated pulmonary pressures. The infant was born via a stat C-section due to maternal complications during pregnancy. His birth weight was 560 g. The patient was intubated shortly after delivery and had a protracted course in the NICU which included a sepsis rule out, increased ventilator settings, and a few weeks on inhaled nitric oxide (iNO).

The intubation course was complicated pulmonary hemorrhage on day 1 after intubation. After such an extensive NICU course, thankfully, the infant survived & was sent home on 1/2 LPM NC, diuretics, albuterol, inhaled corticosteroids, Synthroid, multivitamin with iron as well as Vitamin D. The patient was able to tolerate breast milk via NG tube and had a home apnea monitor with pulse oximetry.

After about a week’s stay at home, the mother noted that the patient’s SPO2 was in the low 80s. The mother took the patient to the local hospital, where the patient was started on HFNC which improved his saturations. An echo done at the OSH showed elevated RV pressures (higher than the prior echo). The patient was subsequently transferred to our hospital for further management. At our hospital, the patient presented hypoxemic, tachycardic, and tachypneic. On physical exam: Baby appeared well developed, had a systolic murmur heard throughout the precordium, and there was increased WOB with significant intercostal retraction. There was no hepatosplenomegaly. Due to worsening respiratory distress, and increasing FIO2 requirement despite maximum RAM cannula, the patient was intubated and placed on conventional MV. A blood gas prior to intubation revealed a pH of 7.1/PCO2 of 100. An arterial line and a central venous line were also placed for better access and monitoring. Initial vent settings post intubation PRVC ventilation: TV 32cc, (25/10), 0.7 time, rate 0 (patient sedated/paralyzed).

To summarize, What are some of the features in H&P that are concerning for you in this case: Ex-27 week prematurity with a birth weight of 560 gms Prolonged MV in the NICU Home O2 requirement Abnormal echo showing high pulmonary pressures hypercarbia despite the use of RAM cannula

As mentioned, our patient was intubated, can you tell us pertinent diagnostics which were obtained? CXR revealed: Hazy airspace opacification in the right upper lung concerning developing pneumonia. Streaky airspace opacity in the left lung base medially may represent atelectasis.

I do want to highlight that the intubation of an ex-premie especially with elevated RV pressures is a high-risk scenario, it is best managed by a provider with experience, in a very controlled setting with optimal team dynamics. Adequate preparation to optimize the patient prior to the intubation as well as the knowledge to manage the post intubation cardiopulmonary interactions are essential. I would highly advise you to re-visit our previous podcast on intubation of the high-risk PICU patient by Dr. Heather Viamonte. Like many Peds ICU conditions, the management of the EX-NICU graduate in the PICU is a multidisciplinary team sport. Our patient likely has the diagnosis of Bronchopulmonary Dysplasia or BPD, Pradip, can you comment on the evolving definition of this diagnosis? Let me first define BPD — Clinically, BPD is defined by a requirement of oxygen supplementation either at 28 days...

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Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. I am Pradip Kamat. I am Rahul Damania, a current 3rd year pediatric critical care fellow. I am Kate Phelps- a second year pediatric critical care medicine. We come to you from Children's Healthcare of Atlanta Emory University School of Medicine. We are delighted to be joined by guest expert Dr Stephanie Jernigan Assistant Professor of Pediatric-Pediatric nephrology, Medical Director of the Pediatric Dialysis Program at Children’s Healthcare of Atlanta. She is the Chief of Medicine and Campus Medical Director at Children’s Healthcare of Atlanta, Egleston Campus. Her research interests include chronic kidney disease, and dialysis. She is on twitter @stephaniejern13 I will turn it over to Rahul to start with our patient case... A 3 year old previously healthy male presents with periorbital edema. Patient was initially seen by a pediatrician who prescribed anti-histamines for allergy. After no improvement in the eye swelling after a two week anti-histamine course, the patient was given a short course of steroids, which also did not improve his periorbital edema. The patient progressed to having abdominal distention and was prescribed miralax for constipation. Grandparents subsequently noticed worsening edema in his face, eyes, and feet. The patient subsequently had low urine output, low appetite and lack of energy patient was subsequently brought to an ED and labs were obtained. Grandparents denied any illness prior to presentation, fever, congestion, sore throat, cough, nausea, vomiting, gross hematuria, or diarrhea. In ED patient was noted to be hypertensive (Average systolic 135-highest 159mm HG), tachycardic (HR 130s-140s), breathing ~20-30 times per minute on RA with SpO2 92%. Admission weight was recorded at 16.5Kg. Physical exam showed periorbital edema, edema of ankles, there was mild abdominal distention (no tenderness and no hepatosplenomegaly), heart and lung exams were normal. There were no rashes on extremities.

Labs at the time of transfer to the PICU: WBC 10 (62% neutrophils, 26% lymphocytes) Hgb 7.2, Hct 21, Platelets 276. BMP: Na 142/K 8.4/Cl 102/HCO3 19/BUN 173/creatinine 5.8. Serum phosphorus was 10.5, Total Ca 6.4 (ionized Ca= 3.4), Mag 2.0, albumin 2.6, AST/ALT were normal. An urine analysis showed: 1015, ph 7.5, urine protein 300 and rest negative. Chest radiograph revealed small bilateral pleural effusions. After initial stabilization of his hyperkalemia-patient was admitted to the PICU. PTH intact 295 (range 8.5-22pg/mL). Respiratory viral panel including for SARS-COV-2 was negative. C3 and C4 were normal. A nephrotic syndrome/FSGS genetic panel was sent. A renal US showed: bilateral echogenic kidneys and ascites (small volume). Pradip: Dr Phelps what are the salient features of the above case presented? Kate Phelps: This patient has a subacute illness characterized by edema, anemia, and proteinuria. His labs show that he has severe acute kidney injury with significantly elevated BUN and Creatinine, hyperkalemia, hyperphosphatemia, and hypocalemia. Rahul: Dr Jernigan welcome to PICU Doc on Call Podcast. Thanks Kate, Rahul and Pradip for inviting me to your podcast. This is a such a great way to provide education and it is my pleasure to come today to speak about one of my favorite topics, pediatric dialysis. I have no financial disclosures or conflicts of interest and am ready to get started. Rahul: Dr Jernigan as you get that call from the ED and then subsequently from the PCCM docs, as a nephrologists whats going on in your mind ? When I get the call from the outside hospital my first job is to make sure the patient is safe and stable for transfer to a tertiary care center. This includes concern about airway, breathing and level of alertness. From a renal standpoint, I am worried about elevated blood pressure, electrolyte abnormalities, in this case primarily the hyperkalemia, and fluid...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat I'm Rahul Damania, a third-year PICU fellow. I’m Kate Phelps, a second-year PICU fellow and we are all coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine, joining Pradip and Rahul today. Welcome to our episode, where will be discussing gastrointestinal bleeding. Kate: Let’s start with a case: A 4-year-old, previously healthy male presents to the emergency room after a large, bloody stool at home. He notably had an episode of dark emesis and an episode of blood-tinged emesis on the day prior. In triage, he is altered and unable to answer questions coherently. Initial vital signs are temperature 36.1 C, RR 24, HR 146, BP 110/54. Point-of-care labs show hemoglobin to be 5.1 with hematocrit 15. His venous blood gas is reassuring against respiratory disease, and he is in no respiratory distress. Further labs are sent and a massive transfusion protocol is initiated before transfer to the PICU. Before arrival in the PICU, he receives two aliquots of RBCs, 1 aliquot of FFP, and 1 aliquot of platelets. Additional labs are sent from the PICU, post-transfusion. His post-transfusion hemoglobin is 8.8. Other labs are notable for normal MCV, elevated total bilirubin to 4.1 (with direct component 3.4), and elevated AST and ALT to 309 and 495 respectively. Rahul: To summarize key elements from this case, this patient has: An undifferentiated gastrointestinal bleed with both hematemesis and hematochezia. He has symptomatic anemia, as evidenced by tachycardia Altered mental status. He is initially stabilized via transfusion of several blood products and liver function labs are shown to be very abnormal — which we will get more into later!

PK: Let’s get into important parts of the history and physical. Kate, can you tell me what some key history items in this patient are — and what are some areas to make sure to touch on when a patient has a GI bleed? Kate: Yeah! I’d love to. First - in our patient, some important elements are his rather acute onset. His parents mention he has had one day of bleeding symptoms - first with emesis yesterday, with components of old, partially digested blood, as well as some fresh blood. Second, he has a frankly bloody stool at home. Given his clinical instability, history taking was probably limited at first, so it’s important to ask follow-up questions and really dig into the case after stabilization! I like to put my questions about gastrointestinal bleeding into buckets based on the questions I need to answer. I need to answer: is this active bleeding or old blood? Is this slow, insidious bleeding or fast, life-threatening bleeding? Is this an upper GI bleed or a lower GI bleed? Bright red blood in emesis tells us that bleeding is active, whereas coffee-ground or dark emesis tells us that, while recent, the blood has been partially digested in the stomach and may not be ongoing. Similarly, melena (dark, tarry stool), tells us blood has come through the colon. While coffee-ground emesis and melena don’t rule out an active bleed, they do tell us the bleeding may be slower, as large volume, active bleedy is irritating to the stomach and gastrointestinal tracks and moves through the system quickly. The next question I want to answer is: what is the cause of this bleed? Easy bruising, petechiae and mucosal bleeding may point to a coagulation disorder. Abdominal cramping, frequent stooling, and weight loss may point to inflammatory bowel disease. Past medical history, family history, and a thorough review of systems are key here. Rahul: Yeah, that’s great! Let’s talk about your question of upper GI vs lower GI bleed. First, a definition: an upper GI bleed is bleeding that occurs above the ligament of Treitz — which is ligamentous tissue that supports the end of the duodenum and beginning of the jejunum at their junction. While not 100% specific, some...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kama and I'm Rahul Damania, a third-year PICU fellow. I’m Kate Phelps, a second-year PICU fellow and we are all coming to you from Children's Healthcare of Atlanta, Emory University School of Medicine, joining Pradip and Rahul today. Welcome to our episode, where will be discussing rhabdomyolysis and associated acute kidney injury in the ICU. Rahul: Here's the case, a 7-year-old female presents to the ED with three days of fever, poor PO, and diffuse myalgia. In the ED, her vital signs are T 39.1C, HR 139, BP 82/44, RR 32. She is pale and diaphoretic, complaining weakly about how much her legs hurt. Her parents note that she has not been peeing very well since yesterday, and when she does pee it is “very concentrated, almost brown.” She’s also been spending all her time on the couch and has asked to be carried to the bathroom when she does need to go. An IV is placed by the emergency room team, and she is given a fluid bolus, acetaminophen, and initial labs are drawn (CMP, CBC, RSV/Flu swab) before she is admitted to the PICU. In the PICU, her fever is better and her vitals have improved to T 37.7, HR 119, BP 115/70, and RR 25. Her respiratory swab has just resulted positive for Influenza A. Further labs are sent, including creatine kinase (CK), coagulation studies, and a urinalysis. Labs are notable for K 3.9, Bicarb 22, BUN 15, Cr 0.8, and CK 5768 IU/L. Her urinalysis is notable for 1 WBC, 2 RBC, +3 blood, negative nitrites, and leukocyte esterase. Kate: To summarize key elements from this case, this patient has: Influenza A, as evidenced by her respiratory swab, as well as her clinical prodrome. She has diffuse myalgias, as well as fevers, diaphoresis, and hypotension. Labs are most notable for elevated creatinine and elevated creatine kinase, as well as an abnormal urinalysis. All of which brings up a concern for rhabdomyolysis and myoglobin-induced acute kidney injury.

Before we get into this episode — let's create a mental framework for this episode — we will dissect our case by highlighting key H&P components, visit a differential diagnosis, pivot to speaking about pathophysiology, and finally, speak about management! Rahul: Let's transition into some history and physical exam components of this case. The classic presentation of rhabdomyolysis is myalgias, muscle weakness, and tea-colored urine, all of which our patient has. Decreased urinary output can also accompany, a variety of reasons, but most notably if the patient has myoglobin-induced acute kidney injury. In our patient, poor PO is also probably contributing to her decrease in urine output. Red flag signs or symptoms will include anuria, hypotension, and altered mental status (which is rare but may indicate severe acidemia and deterioration) Pradip: As we think about our case, what other disease processes might be in our differential? As we dive in a bit more, we’ll come up with ways to distinguish between rhabdo and other things! Viral myositis - inflammation in the muscles in the setting of a viral illness, which can definitely happen with influenza and other common viruses Some other things which may cause reddish-brown urine, including hematuria, hemoglobinuria, porphyria, some specific foods or drugs (like rifampin, beets, food coloring — even ibuprofen) We also have to investigate a bit more to convince ourselves that our patient’s AKI is due to rhabdomyolysis, as it could be from dehydration, sepsis, NSAIDS, etc.

Kate: Let’s dive further into rhabdomyolysis! Rhabdomyolysis affects over 25,000 adults and children every year. While toxins (including prescription drugs, alcohol, and illicit drugs) and trauma are two common causes of rhabdo in adults (and teens), infections, especially viruses, are the most common cause in young children. Influenza, EBV, and CMV are three most commonly reported. What’s the pathophysiology of...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode about a 14- year- old female who presented with hypotension after a suicide attempt. Here's the case: A 14 yo F with PMH of depression and oppositional defiant disorder presents with dizziness. Her mother states she was in her normal state of health when on the day of admission she noticed the patient to be dizzy, slurring speech, and pale. The mother became very concerned about the dizziness as the patient was stumbling and a few hours prior to presentation, became increasingly sleepy. The patient does have a history of depression and is controlled on sertraline. Other medications in the home include Metformin, Amlodipine, and Clonidine. The patient denies ingesting any substance. She does have a prior attempt two years prior, after an argument with her mother; however, her mother was able to “stop” her prior to the attempt. She presents to the ER via EMS. Her vital signs are notable for HR 50 bpm with occasional PACs and non-conducted QRS complexes on telemetry; BP of 75/40. A physical exam is notable for AMS and GCS of 10. She is noted to have clear breath sounds, with a cardiac exam notable for slowed and delayed pulses. Initial laboratory work is notable for serum glucose 180 mg/dL and B HCG negative. Initial resuscitation is begun with IV fluids and atropine. Serum acetaminophen and ASA levels are sent and upon stabilization, the patient presents to the PICU for admission.

To summarize key elements from this case, this patient has: A history of depression with prior attempt An acute bout of altered mental status Bradycardia, hypotension, and hyperglycemia. All of which brings up a concern for an acute ingestion Let’s take a step back and talk about the approach to ingestions in the PICU.

What are key aspects to consider in the work-up of these patients?

History and physical are key: Stratifying acute or chronic ingestions Baseline prescription medications a patient may be taking or have access to in the household Whether the ingestion involves a single drug or co-ingestants are all first steps in evaluating your patient. In an undifferentiated patient, management is paramount. Initial management is focused on pattern recognition and acute stabilization. A brief initial screening examination should be performed on all patients to identify immediate measures required to stabilize and prevent deterioration of the patient. Assess the airway, vital signs, mental status, pupil size, and skin temperature and moisture.

These components of your physical exam should help allude to a toxidrome, and these syndromes are frequently tested on board examinations. Any time a patient has hypotension and bradycardia other drugs that should be considered include beta blockers, digoxin, clonidine, as well as ingestion of barbiturates, opioids, and even benzodiazepines.

What are some diagnostic studies you will want to send immediately in a patient with suspected ingestion? Immediate diagnostic studies to be performed include pulse oximetry, continuous cardiac monitoring, an electrocardiogram (ECG), and a capillary glucose measurement (in altered patients). Intravenous (IV) access should be obtained in all cases of serious ingestion. You also want to send beta-hcg and acetaminophen and salicylate levels. an extended toxicology screen may be required on a case-by-case basis.

One study found detectable serum acetaminophen concentrations in 9.6 percent of all overdose patients; almost one-third of this subset denied ingestion of acetaminophen.

Now that you’ve focused on ABCs are there more detailed laboratory studies to send in patients with toxidromes? Symptomatic patients and those with an unreliable or unknown history should, at a minimum, undergo...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Here's the case: A 6-year-old child with a known h/o craniopharyngioma who has been endocrinologically intact with exception of needing thyroid replacement was admitted to the PICU prior to craniotomy to proceed with further tumor resection as well as the removal of a secondary cyst impacting his brainstem. The patient is receiving Keppra for seizures and per mother, he has recently been significantly more sleepy at school. On POD Op day 5: the PICU the bedside nurse notices increased urine output (6cc/kg/hr to as high as 10cc/kg/hr). Initially, there was an increase in Na to 157mEq/L within 48-72 hours the serum Na dropped to 128mEq/L To summarize key elements from this case, this patient has: Increase UOP Rapidly increasing Na initially followed by a drop All of which brings up a concern for Na abnormality post craniotomy

In today’s episode, we will be breaking down all things Sodium & the Brain. We will discuss diagnostic & management frameworks related to three pathologies: Central Diabetes Insipidus Syndrome of inappropriate Anti-Diuretic Hormone or SIADH Cerebral Salt Wasting

These diagnoses can certainly be seen individually inpatients or as a spectrum of diseases — as we go through each of these diagnoses, pay particular attention to patient characteristics and lab abnormalities. Namely, serum sodium, serum osm, and urine osm. To build the fundamentals, lets first start with classic nephrology saying: Serum Na represents Hydration This takes us into a brief review of normal physiology — talking about three important hormones: ADH Aldosterone Atrial Natriuretic Peptide (ANP)

Let’s go through a quick multiple-choice question. A patient is recently started on DDAVP for pan-hypopituitarism. The medication acts similarly to a hormone that is physiologically synthesized in which of the following from which are in the body? A. Paraventricular Nucleus of the Hypothalamus B. Supraoptic Nucleus of the Hypothalamus C. Anterior Pituitary D. Vascular Endothelium The correct answer here is B the Supraoptic Nucleus of the Hypothalamus. Remember that ADH is synthesized in the hypothalamus and released from the posterior pituitary. What are the physiologic actions of ADH? ADH Increases H2O permeability by directing the insertion of aquaporin 2 (AQP2) H2O channels in the luminal membrane of the principal cells. Thus, as we will see with Central Diabetes insipidus, in the absence of ADH, the principal cells are virtually impermeable to water. Let's talk about our next hormone, aldosterone. What are the important physiologic considerations? Aldosterone is secreted from the adrenal cortex as a byproduct of the RAAS. Aldosterone increases Na+ reabsorption by the renal distal tubule, thereby increasing extracellular fluid (ECF) volume, blood volume, and arterial pressure. It also helps in secreting K and H. This physiology is applied directly at the bedside when we have patients in the ICU who have a contraction alkalosis secondary to diuretics. The increase in aldosterone as these patients lose free water from their Lasix administration results in hypokalemia and metabolic alkalosis.

Alright, what about the third hormone, ANP? Atrial natriuretic peptide (ANP) is released from the atria in response to an increase in blood volume and atrial pressure. ANP causes relaxation of vascular smooth muscle, dilation of arterioles, and decreased TPR. causes increased excretion of Na+ and water by the kidney, which reduces blood volume and attempts to bring arterial pressure down to normal.

As ANP causes natriuresis, diuresis, and inhibition of renin, you can consider this hormone as having a complementary & opposite effect to ADH and aldosterone. Alright, now that we...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat. I’m Dr. Ali Towne, a rising 3rd-year pediatrics resident interested in a neonatology fellowship, and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode a 5-month-old, ex-28 week female with abdominal distention. Here's the case: A 5-month-old, ex 28 week, female with a past medical history of severe BPD, pulmonary hypertension, home oxygen requirement, and G-tube dependence presents with hypoxemia and increased work of breathing. The patient has a history of prolonged NICU stay with 8 weeks of intubation. The patient developed worsening respiratory distress requiring increased support and eventual intubation for hypoxemic respiratory failure. Echo showed worsened pulmonary hypertension with severe systolic flattening of the ventricular septum and a markedly elevated TR jet. The patient had poor peripheral perfusion, and upon intubation was started on milrinone and epinephrine. The patient improved, but the patient then developed abdominal distention and increasing FiO2 requirements prompting an abdominal x-ray. X-ray showed diffuse pneumatosis with portal venous gas. The patient was made NPO and antibiotic therapy was initiated. To summarize key elements from this case, this patient has NEC. NEC is not a homogenous disease, but rather a collection of diseases with similar phenotypes. Some people split NEC into two categories: Cardiac NEC and Inflammatory NEC. Babies who develop cardiac NEC tend to be significantly older than babies who develop inflammatory NEC (about 1 month vs 2 weeks). There are three main contributory factors to the development of NEC: gut prematurity, abnormal bacterial colonization, and ischemia-reperfusion injury. Many cases result from an ischemic insult to the bowel, resulting in translocation of intra-luminal bacteria into the wall of the bowel, but the etiology and course of NEC can be very variable. This translocation can cause sepsis and death; the ischemia of the bowel can result in intestinal perforation and/or necrosis.

Necrotizing enterocolitis (NEC) is one of the most common gastrointestinal emergencies in the newborn infant. It is estimated to occur in 1 to 3 per 1000 live births. More than 90 percent of cases occur in very low birth weight (VLBW) infants (BW <1500 g) born at <32 weeks gestation, and the incidence of NEC decreases with increasing gestational age (GA) and BW. What are key risk factors for the development of NEC? Prematurity and Birth Weight NEC incidence is inversely proportional to gestational age. Congenital Heart Disease Puts children at risk for NEC due to (1) decreased stroke volume, and (2) improperly oxygenated blood which reduced oxygen supply to the SMA and decreases intestinal wall perfusion. On the repair of the cardiac lesion, patients develop reperfusion injury due to their now improved perfusion to their gut. This reperfusion causes hyper inflammation via neutrophil activation resulting in NEC. NEC primarily occurs in healthy, growing, and feeding VLBW preterm infants. It presents with sudden changes in feeding tolerance (increase in gastric residuals) with both nonspecific systemic signs (eg, apnea, respiratory failure, poor feeding, lethargy, or temperature instability) and abdominal signs (eg, abdominal distension, bilious gastric retention and/or vomiting, tenderness, rectal bleeding, and diarrhea). Physical findings may include abdominal wall erythema, crepitus, and induration.

Other than the immediate risk of death, what are some consequences of NEC long-term? Higher risk of malnutrition and short gut. BPD Developmental delay.

What are some areas of current research and development on the topic of NEC? Improved biomarkers for early recognition of NEC prior to the development of radiographic findings. Preventative...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I’m Kate Phelps, a second-year pediatric critical care fellow joining Pradip and Rahul today! I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Today we are honored to have Dr. John Berkenbosch- senior author of the Prevention and Management of Pain, Agitation, Neuromuscular Blockade, and Delirium in Critically Ill Pediatric Patients with consideration of the ICU Environment and Early Mobility (PANDEM) guidelines recently published in February 2022 issue of the Pediatric Critical Care journal. Dr. Berkenbosch is a Professor of Pediatrics and Pediatric Critical Care at the University of Louisville School of Medicine, and continues to be nationally recognized as an expert in pediatric procedural sedation with multiple publications relating to sedation practices, particularly novel uses of procedural sedation medications and regimens. He currently also serves as co-chair for the American College of Critical Care Medicine’s Task Force guidelines for sedation and analgesia in critically ill children which we will be discussing in today’s episode. Dr. Berkenbosch’s research interests have primarily focused on pediatric procedural sedation and implementation of technology advances in Pediatric Critical Care and have resulted in 57 publications as well as several book chapters Rahul: Dr. Berkenbosch welcome to the PICU Doc ON call podcast. I would also like to point out that the free full access to the PANDEM guidelines is available online athttp://pccmjournal.org ( pccmjournal.org) Dr. Berkenbosch: Thanks Rahul and Pradip. I am excited to be on the PICU Doc on Call Podcast to discuss the PANDEM guidelines. I want to first start by giving a huge shout-out to all the team members who contributed to these guidelines’ development. This is a topic about which I am quite passionate but also one that provides much-needed guidance regarding pain/agitation/delirium to our entire pediatric critical care community! KATE: Dr. Berkenbosch, the rationale for the development of the PANDEM guidelines was the high variability in pediatric sedation and analgesia. Can you speak to this variability and why it was important to address that variability? That is a great question, the variability has been one of the key motivators in the creation of these guidelines. We also wanted to develop a guideline that was broader in scope than what was currently available. The ICU Liberation bundle provided a paradigm for liberating critically ill patients from mechanical ventilation and the ICU environment and as we delved into developing these guidelines, we realized that many elements of the ICU liberation bundle aligned very closely with PICU sedation and analgesia so it made imminent sense to incorporate all of these topics into the guidelines, an acknowledgment if you will, that PICU liberation & sedation go hand in hand! Absolutely, as we have stated in our prior episodes, the paradigm is: intubate → ventilate → liberate, and sedation/analgesia is intertwined in each of these processes. Dr. Berkenbosch, as we get into the guidelines, can you please highlight how the search strategy for these guidelines were derived? Of course, this was a remarkable group effort solicited by the Society of Critical Care Medicine. We were initially modeled after the adult PAD (pain, agitation, and delirium) guidelines task force but, as described already, extended beyond that to include Pediatric Pain, Agitation, Neuromuscular Blockade, and Delirium in addition to the PICU Environment and Early Mobility. It was comprised of 29 national experts who collaborated over a ten-year period. The full task force gathered annually in person during the Society of Critical Care Medicine Congress for progress reports and further strategizing with the final face-to-face meeting occurring in...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. I will turn it over to Rahul to start with our patient case... A 2 yo Asian M presents with difficulty feeding. He has a history of epilepsy and recently was switched to Valproic Acid for seizure control as well as OTC deficiency diagnosed at birth. He has had a 3-day history of URI, cough, which now progressed to this difficulty feeding. His parents state he was initially very fussy however in the past few hours he has been more sleepy. He has not had any fevers. They have noticed that while he is sleeping he has been breathing "fast." Prior to arrival at the emergency room, he was noted to have a large non-bloody, non-bilious emesis. Upon transfer to the trauma bay, the patient suddenly has a seizure. A quick POC glucose is normal. His care is escalated & diagnostic workup is initiated. Pradip, our case had two key elements in his history, namely the h/o OTC deficiency & VPA use, which place him, particularly at high risk to have hyperammonemia. As this is our topic of discussion today, would you mind starting with a general background & definition of hyperammonemia? Sure, this is a classic case of not only hyperammonemia but also a metabolic crisis in this case related to a urea cycle defect. As background, the urea cycle is the metabolic pathway that transforms nitrogen to urea for excretion from the body. We get nitrogen sources from a few areas in the body: from peripheral (muscle) enteral sources (protein ingestion)

The urea cycle occurs in the liver and once the ammonia is converted to urea in the hepatocyte, it is excreted into the kidney as urea. We will dive into this deeper soon, however, pathologies that impair adequate hepatocyte function, can impair the urea cycle and thus lead to hyperammonemia. This is a great basic science summary, would you mind commenting about this patient's enzyme defect — the OTC deficiency? Yes, Ornithine transcarbamylase, or OTC for short, is one of the first few enzymes in the urea cycle. As a background, the inheritance pattern of majority, all of the urea-cycle-defects (UCD) is autosomal recessive, however, OTC deficiency is different — it is X linked. In a 21-year, multi-center retrospective study, it was noted that only 34 % of patients with UCD presented during the neonatal period (<30 days of age) — and around 25% of cases present in the 2-12-year-old range. This is why I would like to drive home this clinical point to have a urea cycle defect or any inborn error of metabolism in your differential, especially in a child who presents in a critically ill, undifferentiated state.

Why do you think there are subsets of populations who present later? This is a great question and the cause may be multi-factorial — it is worth noting that patients may have partial enzyme deficiencies and this may be a major reason why patients may have atypical presentations after the newborn period. This delayed presentation is most commonly seen in patients with partial ornithine transcarbamylase (OTC) deficiency.

As we have highlighted key pathophysiologic components, do you mind highlighting the typical clinical presentation of a child with a UCD & hyperammonemia? The presentation may be variable, however, let’s break down some key features which were in our case: Patients typically have a preceding illness such as a URI or gastroenteritis, which triggers a more catabolic state. As a result, patients end up having increased ammonia levels — this ends up creating a picture of somnolence, inability to maintain normal body temperature, poor feeding, vomiting, and in severe cases lethargy, and This is a similar presentation to sepsis and thus keeping your differential broad, having fine attention to trends in vitals or clinical exam,...

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Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat. My name is Rahul Damania and we come to you from Children’s Healthcare of Atlanta-Emory University School of Medicine. Today's episode Is part two of our pediatric post-cardiac arrest care syndrome If you have not yet listened to part one, I would highly encourage you to visit that episode prior to delving into this one. Part 1 addressed the epidemiology, causes, and pathophysiology of POST CARDIAC ARREST SYNDROME. Part 2 Today will discuss management and complications related to post-cardiac arrest syndrome in the ICU. To revisit our index case we had a: 11 yo previously healthy M who was admitted to the PICU after cardiac arrest. After stabilization: The patient was taken to head CT which showed diffuse cerebral edema and diffusely diminished grey-white differentiation most pronounced in the basal ganglia. He is now 18-24 hours post-cardiac arrest and the team is dealing with hemodynamic changes, arrhythmias, and difficulty with ventilation. The patient’s neurological exam still remains poor with fixed 5 mm pupils and upper motor neuron signs in the lower extremities.

Let’s get right into it: What are some of the principles in management of patients with post cardiac arrest syndrome (PCAS)? Where do we keep the patients blood pressure? Hypotension after ROSC is commonly encountered in children with PCAS. Early hypotension occurred in 27% of children after cardiac arrest is associated with lower survival to hospital discharge and unfavorable neurological outcome. When post-cardiac arrest hypotension is present, it is not clear whether increasing the blood pressure through administration of fluids and inotropes/vasopressors can mitigate harm, despite this 41% of patients under 18 receive vasopressor therapy within the first 6 hours after ROSC. Currently, there is no high-quality evidence to support any single specific strategy for post-cardiac arrest hemodynamic optimization in children. Treatment of post-cardiac arrest hypotension and myocardial dysfunction may be assisted by monitoring and evaluating arterial lactate and central venous oxygen saturation. Parenteral fluids, inotropes, and vasoactive drugs are to be used as needed to maintain a systolic blood pressure greater than the fifth percentile for age. Appropriate vasoactive drug therapies should be tailored to each patient and adjusted as needed. What about cardiac arrhythmia's such as Vtach seen in our patient? The rhythm disturbances observed during the post-cardiac arrest period include premature atrial and ventricular contractions, supraventricular tachycardias, and ventricular tachycardias. Heart block is unusual but can be observed as a manifestation of myocarditis. There is inadequate evidence in adults and no published studies in children to support the routine administration of prophylactic antiarrhythmics after ROSC, but rhythm disturbances during this period may warrant therapy. Treatment depends on the cause and hemodynamic consequences of the arrhythmias. Premature depolarizations, both atrial and ventricular, usually do not require therapy other than maintenance of adequate perfusion and normal fluid and electrolyte balance. Ventricular arrhythmias may signify more serious myocardial dysfunction. QT prolonging agents must be avoided. Many of the vasoactive agents used to support myocardial function can increase myocardial irritability and risk of arrhythmias. Premature atrial or ventricular depolarizations are frequently observed and can be controlled by optimizing the dose of the vasoactive drugs. Bradycardia is frequently seen in TTM and typically requires no therapy. During PCAC, mechanical circulatory support (ECMO) may be considered if significant cardiorespiratory instability persists despite appropriate volume expansion and administration of inotropes, vasopressors, and, if indicated,http://antiarrhythmics.in (...

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Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat. My name is Rahul Damania, a current 2nd-year pediatric critical care fellow. We come to you from Children’s Healthcare of Atlanta-Emory University School of Medicine. Today's episode is dedicated to pediatric post-cardiac arrest care. We are going to split this topic into two episodes, part one of pediatric post-cardiac arrest syndrome will address the epidemiology, causes, and pathophysiology. I will turn it over to Rahul to start with our patient case... 11 yo previously healthy M who is admitted to the PICU after cardiac arrest. The patient was noted to be found unresponsive and submerged in a neighborhood pool. He was pulled out by bystanders and CPR was started for 5 minutes with two rounds of epinephrine prior to achieving ROSC. During transport to the OSH, the patient developed hypotension requiring a continuous epinephrine infusion. His initial blood gas was notable for a mixed respiratory and metabolic acidosis: 7.0/60/-20 His initial serum lactate was 6.8 mmol/L. He presents to the PICU with a temperature of 36.6, HR 130s, MAPs 50s on Epinephrine infusion at 0.03mcg/kg/min He is mechanically ventilated with notable settings PEEP of 10, FiO2 65%. The patient is taken to head CT which shows diffuse cerebral edema and diffusely diminished grey-white differentiation most pronounced in the basal ganglia.

Great Rahul, can you please comment on his physical exam & PMH? Important physical exam findings include an unresponsive intubated patient with a cervical collar and bilateral non-reactive pupils at 4mm. The patient received mechanical ventilation with coarse breath sounds. A heart exam revealed tachycardia with no murmur or gallop. The patient does not respond to stimuli, intermittent jerking movements of arms and legs were observed. There was no evidence of rash or trauma. No past medical history of seizures or any heart disease. No home medications or toxic ingestions are suspected.

So now he is transferred to the ICU, what did we do? An arterial line, central venous line, urinary catheter, esophageal temperature probe was placed. The patient was ventilated using a TV of 6cc/kg and a PEEP of 10 (FIO2 ~65%) to keep SPO2 >94%. The patient initially had runs of ventricular tachycardia for which lidocaine was used. Although the initial EKG showed mild QTc prolongation, it subsequently normalized and was considered to be due to his cardiac arrest and resuscitation. An echocardiogram revealed normal biventricular systolic function (on epinephrine) and also showed normal origins of the coronary arteries. Comprehensive Arrhythmia Panel did not identify a specific genetic cause for the patient's sudden cardiac arrest. The patient was placed on continuous EEG, which demonstrated severe diffuse encephalopathy with myoclonic status likely from anoxic brain injury Patient was also started on Levetiracetam and valproic acid. Initial portable CT scan done on day # of admission showed diffuse cerebral edema and diffusely diminished gray-white differentiation (most pronounced in the basal ganglia). MRI was deferred due to patient instability.

The case we talked about highlights a patient who had a trigger that then resulted in cardiac arrest is common is one of the common reasons for admission to the PICU at Children's hospitals whether from submersion injury, trauma, ingestion, cardiac arrhythmia, sepsis, etc. Can we start by defining post-cardiac arrest syndrome? Successful resuscitation from cardiac arrest results in a post-cardiac arrest syndrome, which can evolve in the days to weeks after the return of spontaneous circulation. The components of post-cardiac arrest syndrome are brain injury, myocardial dysfunction, systemic ischemia/reperfusion response, and persistent precipitating pathophysiology. Prior to 2008, the AHA pediatric advanced life support (PALS) guidelines focused...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode a 2-year-old with severe pallor and O2 desaturation. Here's the case presented by Rahul: A two-year-old presents to the PICU with severe pallor + O2 requirement. The patient went for a routine check with her primary care who noted the patient appeared severely pale. He sent the patient to the ED. An initial Hgb check revealed a Hgb of 1.5gm/dL. Per mother, she is otherwise healthy but a very picky eater. She also reports the patient drinks milk as a soothing adjunct at night, consuming between 12 - 36oz a day. No family h/o of anemia or any other blood disorders. No h/o recent illness. Mother had a normal spontaneous full-term delivery. The patient is up to date on her immunizations. Per mother, developmental milestones are normal. The mother also denies any history of decreased activity in the child. Given the low Hgb, the patient was admitted to the PICU. Let's transition into some history and physical exam components of this case? What are key history features in this child? Severe pallor in a 2-year-old H/o being a picky eater H/o excessive milk consumption Pertinent negatives include: No obvious blood loss, No petechia, bruising, or jaundice

What did the physical exam show? The patient was hypertensive, tachycardic to the 140s, and 10th% weight for growth percentiles On physical exam, the patient was in no acute distress. Her lips, gums, and conjunctiva were pale. She had a systolic ejection murmur. As a pertinent negative, she had no hepatosplenomegaly. She also has no rash, bruising, or petechiae.

The lack of hepatosplenomegaly may indicate that the patient has no signs of extramedullary hematopoiesis. Patients with hemolytic processes resulting in anemia may present with signs of scleral icterus, jaundice, and hepatosplenomegaly resulting from increased red cell destruction. In fact, in an emergency department setting, the clinical detection of jaundice was found to have sensitivity and specificity of only approximately 70 percent. To continue with our case, then what were the patient's labs consistent with: Initial CBC showed: WBC 8.5K, RBC 1.14 (L), Hgb 1.5gm/dL; Hct 6.1, MCV 53.5, and an elevated RDW 37.7. Initial platelet count was 50K, reticulocyte count 1.1% Peripheral smear revealed no blasts, thrombocytopenia - with occasional medium-sized platelets - ghost cells and anisocytosis/poikilocytosis- which appears most consistent with iron deficiency. It was interesting that the patient had thrombocytopenia

Absolutely, typically with Iron deficiency, there is thrombocytosis (erythropoietin is increased which closely mimics thrombopoietin stimulates platelets). In fact, both act via the non-TK, JAK-STAT pathway. OK, to summarize, we have: Two year old with severe anemia most likely secondary to iron deficiency. As you think about our case, what would be your differential? For any patient with acute severe anemia presenting to the PICU- One has to think in terms of blood loss, decreased or impaired production (i.e bone marrow failure), or peripheral blood destruction (i.e hemolysis). Here would be the organizations: Blood loss Decreased or impaired production Increased destruction

Let’s go into detail for each: Blood loss can be internal or external (due to trauma, excessive blood draws, due to surgery)-typically gives rise to normochromic normocytic anemia. Decreased or impaired production: Deficiency of substances needed for Hgb & RBC production such as iron Vit B12 etc. Depression of BM due to infection (parvo B), chemicals, pharmacologic agents or immune mechanisms. Bone marrow aplasia can be idiopathic with or without congenital anomalies. Infiltration of BM due to malignancies such as leukemia, Hodgkin disease,...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our episode, which is Part 2 of our acute severe asthma management. Today we discuss invasive mechanical ventilation of the acute asthmatic. A patient with a history of asthma presents to the PICU with decreased air entry. Somnolence. Hypercarbia and drooling. The patient is hypoxemic and has see-saw breathing. Rahul: Let’s dive right into this. What are the indications for intubating a child with acute severe asthma? Absolute indications include: Altered mental status which may be preceded by obtundation, agitation Cardiac and respiratory arrest

Relative indications decided on a case by case basis: Progressive exhaustion-despite, despite maximal therapy. Profound hypoxemia refractory to supplemental oxygen administration, and respiratory failure. The decision to intubate should not be solely determined based on blood gas results. Pradip, can you shed light on how we prepare for the intubation of the patient with acute severe asthma? Rahul, first and foremost- we take the intubation of an asthmatic very seriously. In fact we try the whole “kitchen sink” to avoid intubation. But there will be times when we have to intubate especially for the indications you mentioned above. The intubation will worsen the patient’s bronchospasm, put the patient at risk for barotrauma as well as cardiovascular collapse. Preparation is the key- A team huddle and mapping prior to proceeding to intubate is the key. Every person in the room should have clear roles and responsibilities. Scenarios of what to do if “X” happens should be clearly laid out to the team by the team leader (preferably the attending or a senior fellow). The senior-most experienced person should manage the airway. At least two dedicated RTs to provide bag-mask ventilation as well as manage the ventilator are required. Nursing roles to push meds, chart the vitals and other activities as well a role for the resource nurses to help in case of cardiac arrest should be clearly laid out. Additionally, facilities that have access to isoflurane should have that ready to go. We typically give a heads up to our ECMO team to be on stand-by. Prior to Intubation: Have central access or multiple large-bore PIVs if possible. Keep crystalloids boluses ready for hypotension. We also have peri-arrest epinephrine as well as an epinephrine infusion ready for any hypotension, bradycardia, or cardiac arrest. For intubation, we typically use Ketamine, fentanyl, and rocuronium (some centers may use succinylcholine). We use cuffed endotracheal tube. We don't bag-mask at fast rates but rather wait for a full expiration prior to the next breath being delivered. These patients require slow respiratory rates with very prolonged expiratory times to allow for adequate gas exchange and lung volumes. A helpful technique is to use a stethoscope to auscultate at the lower neck for the disappearance of expiratory wheezes prior to starting the next inspiration. We sometimes place a nasogastric tube to prevent gastric distension. If there is hypoxemia, hypotension, not improving with fluids, ventilator manipulation, - A consideration for tension pneumothorax should be given especially if there is asymmetric chest rise. Bedside POCUS can be used to make a diagnosis. Intubation of an asthmatic is a high-risk procedure and requires a team approach, proactiveness, and anticipation. Intubation should be approached cautiously in patients with severe acute asthma exacerbations because manipulation of the airway can cause laryngospasm and worsening bronchoconstriction. Rahul, what are some of the principles we should all follow prior to initiation of mechanical ventilation in an asthmatic after intubation? It is important to note that most complications of intubating...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode a 15 mo F with respiratory distress and runny nose. Here's the case: A 15 mo F presents to the ED with cough, runny nose, and increased work of breathing. Her mother states that the patient has had these symptoms for the past three days, however, the work of breathing progressed. The patient has had 2 fevers during this course, with the highest 101F. She says that her 3 yo cousin who she visited for the holidays had similar symptoms. Mother notes decreased PO and wet diapers. The patient presented to the ED with the following vital signs: T 38.5C, HR 155, BP 70/48 (MAP 50), RR 48, 92% on RA. The patient on the exam was noted to be tachypneic with abdominal retractions, grunting, and nasal flaring. The patient was nasally suctioned and initiated on 12 L 40% of HFNC. The patient was then transferred to the PICU for further management. To summarize key elements from this case, this patient has: Increased work of breathing indicates respiratory distress. She has a prodrome of symptoms that worsened prior to presentation And a sick contact. All of which brings up a concern for acute respiratory failure requiring non-invasive positive pressure ventilation in the form of HFNC. Let's transition into some history and physical exam components of this case?

What are key history features in this child who presents with respiratory distress & URI sx?

Usually, children under the age of two with bronchiolitis will present with cough, respiratory distress, and crackles on lung exam. The crackles indicate atelectatic alveoli that are filled with fluid which occurs due to inflammatory processes in the lung triggered by respiratory viruses. Respiratory distress, increased work of breathing, respiratory rate, and oxygenation all can change rapidly with crying, coughing, and agitation.

Are there some red-flag symptoms or physical exam components in a child with acute respiratory distress which you could highlight?

That is a great question. We really want to highlight the distinction between respiratory distress and respiratory failure. Children with respiratory failure in our case may have issues with oxygenation or ventilation as well as increased work of breathing that necessitates higher levels of respiratory support like HFNC. In a 2003 Journal of Pediatrics study, infants who were most severely affected with bronchiolitis were born prematurely, <12 weeks of age, or who have underlying cardiopulmonary disease or immunodeficiency. These children are at risk for apnea and respiratory failure which may require escalation to mechanical ventilation. Finally, Infants with bronchiolitis may have difficulty maintaining adequate hydration because of increased fluid needs and metabolic demand. Remember these children will have increased insensible losses due to fever and tachypnea, as well as decreased oral intake related to their systemic illness.

To continue with our case, the patient's labs were consistent with: Mild hyper NA 149 All other electrolytes were within normal limits. The patient had a respiratory viral panel which was positive for Rhino/Entero and RSV. Her COVID PCR was negative. A CXR was performed and showed alveolar airspace disease consistent with I would like to highlight an important point, with the exception of otitis media, a secondary bacterial infection is uncommon among infants and young children with bronchiolitis. In a nine-year prospective study of 565 children (<3 yo) hospitalized with documented RSV infection published in the Journal of Pediatrics, subsequent bacterial pneumonia was present in only 0.9 percent of these.

Yes, Rahul, that is a great point. The risk of secondary bacterial pneumonia is increased among children...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our discussion today on airway clearance in the critically-ill patient in the PICU. We will focus on the use of pharmacological as well as non-pharmacological techniques in critically ill children admitted to the ICU. This episode will be a general overview as specific clinical scenarios such as NM disease may warrant specific therapeutics. Let’s get started with the case: We have an 8-month old ex-34 week premie intubated for acute respiratory failure secondary to RSV bronchiolitis. The patient is on a conventional mechanical ventilator receiving a TV of 6ml/kg, rate of 20, PEEP 6, 40% FiO2 inspiratory time of 0.7 CXR shows a pattern suggestive of viral pneumonia with minimal hyperinflation and atelectasis of the right middle lobe. The patient has excessive secretions when the suction catheter is assessed. The patient is hemodynamically stable and is on feeds via a NG tube. Rahul, Can you comment on how a child clears his/her pulmonary secretions normally when not ill? That's an excellent question. Normally some baseline secretions are produced by all humans. Normal bronchial secretions are made up of contributions from mucus-secreting (goblet)cells as well as cells secreting serous fluid. The ciliary epithelium made of columnar cells line the entire tracheobronchial tree up to the alveolar ducts. This ciliary epithelium provides the coordinated rhythmic force that propels the overlying “mucus blanket” towards the central airways and upper respiratory tract. Primary mechanisms of tracheobronchial clearance of these secretions consist of (1) The mucociliary (MC) escalator in the smaller airways and (2) Cough in central and larger airways. The co-ordinating activity of the beating cilia and their interaction with the overlying viscoelastic layer of mucus makes up the mucociliary escalator. The MC escalator helps remove both healthy and pathologic secretions from the airways as well as the removal of inhaled particles. This MC transport can be affected by mycoplasma, influenza and other viruses as well as exposure to toxins (cigarette smoke, vaping) as well as in CF, asthma, COPD, and ciliary dyskinesia just to name a few. Once the secretions are in large or central airways they are coughed out or swallowed. Let’s transition and talk a little on how one generates an effective cough: For an effective cough one needs firstly to take a sufficiently deep breath in. The glottis needs to close briefly to allow an increase in intrathoracic pressure This is followed by expulsive glottic opening together with abdominal contraction, which results in air being forcibly expelled.

Individuals with neuromuscular disease, bulbar insufficiency, obtunded patients, those on MV with chemical neuromuscular blockade, severe skeletal deformity may have decreased cough expiratory airflow. Reduced ability to cough results in secretion retention, mucus plugging, atelectasis and pre-disposition to infection even if the MC escalator function is normal. Q2. Pradip can you tell us about atelectasis This is a great question. The term atelectasis means “imperfect expansion” and indicates reversible loss of aerated lung with otherwise normal lung parenchyma. Thats a nice concise definition, so if atelectasis reperesents imperfect expansion, what are mechanisms which keep our lungs open? There are three major mechanisms: 1. Pulmonary Surfactant 2. Collateral Ventilation 3. Lung & Chest Wall Balance Let’s go into each of these in more detail: A pulmonary surfactant that covers the large alveolar surface is composed of phospholipids (mostly phosphatidylcholine), neutral lipids, and surfactant-specific apoproteins (termed surfactant proteins A , B , C , and D ). By reducing...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our episode of a three-year-old girl presenting with a cough and difficulty breathing Here's the case presented by Rahul: A previously healthy 3-year-old girl presented to the OSH for difficulty breathing. She had a two-day h/o of cough (worse at night) and congestion but no fever. She has no h/o of emesis, h/o recent travel, or exposure to some/toxins. Initially, she received steroids, albuterol, and O2 but due to continued worsening of breathing and hypoxia-She was transferred to our PICU for initiation of High Flow Nasal Cannula. She has no allergies and her immunizations are up to date. There is a strong family history of asthma and atopic dermatitis. The mother also noted that the patient has h/o of coughing episodes while playing outside with her siblings. Initial Vitals: Temp 37.9, HR 100, BP 97/73, respiratory rate 49, SPO2 98% on 15LPM HFNC at 60% FIO2 , weight 17.5kg On PE: The child is awake, playful. she is tachycardic with no murmur. She has subcostal, intercostal, supra-sternal retractions. There is bilateral symmetric chest expansion. The air entry is decreased with diffuse (B) wheeze. There is atopic dermatitis in the flexor areas of the elbows/knees. The rest of the physical examination was normal. No hepatosplenomegaly. Viral panel: positive for HMP, SARS COV-2 negative CXR: Atelectasis superimposed upon viral pneumonitis versus multifocal bronchopneumonia. No evidence of parapneumonic effusion or air leak. CBC and BMP are normal. To summarize key elements from this case, this 3-year-old girl has: Cough and congestion Increased WOB and difficulty breathing Hypoxia No fever or rash No recent ingestions or exposure to tobacco smoke All of which brings up a concern for a lower airway obstructive process most likely acute asthma

Let's transition into some history and physical exam components of this case? Rahul, what are key history features in this child who presents with increased work of breathing? Cough and congestion Difficulty breathing No h/o suggestive of atopic dermatitis Increased WOB: retractions (subcostal, intercostal, suprasternal). Important to note there is no nasal flaring, head bobbing or grunting. Decreased AE Diffuse (B) wheezing. No subcutaneous emphysema on palpation of the chest or cervical region. Hypoxia needing oxygen Atopic dermatitis No crackles No hepatomegaly No altered mental status

Not all respiratory distress arises within the respiratory tract. Important physical examination to note in any infant or toddler with increased work of breathing is to palpate for hepatomegaly as well as carefully listen for bilateral inspiratory crackles. The presence of hepatomegaly or (B) crackles should raise concern for myocarditis or congestive heart failure. In Newborns with respiratory distress-always make a habit to feel femoral pulses. Acidosis, intracranial hemorrhage, foreign body, panic attacks can also present as respiratory distress. To continue with our case, Pradip, the patient’s labs/diagnostic were consistent with: CBC, BMP were normal Respiratory viral panel positive for HMP virus, Negative for SARS-COV-2 Chest radiograph: Atelectasis superimposed upon viral pneumonitis versus multifocal bronchopneumonia

OK, to summarize, we have: A 3-year-old with acute respiratory distress, wheezing, hypoxia after 2 days h/o of cough/congestion. Rahul, let's start with a short multiple-choice question: A 15-year-old teenager with know h/o asthma presents to the ED in severe respiratory distress, increased work of breathing, hypoxia, and diffuse wheezing. Of the following the presentation that would most likely require intubation in this teenager include- A) Inability to talk in complete sentences B) A blood gas that...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode an 8-year-old admitted for PRESS syndrome with altered mental status secondary to seizures. Here's the case presented by Rahul: Our patient today is an eight-year-old who was admitted to the floor with a diagnosis of MIS-C. On his initial echo, his EF had mildly depressed systolic function, dilatation of coronaries, and worsening of inflammatory markers. As a result, the care team increased the dosing of the methylprednisolone administered to this patient. Since the initiation of methylprednisone, The patient's SBP had been steadily increasing with the latest systolic values approaching 140s-150s. On hospital day 3 patient had a generalized tonic-clonic seizure and became unresponsive for which a rapid response on the floor was called. The patient was emergently bagged and brought to the PICU for airway protection and intubation Initial vitals on PICU admission: He was afebrile, mildly tachycardic, and hypertensive to 160s even after sedation. In the PICU an initial head CT scan done after intubation and stabilization of the patient showed no bleeding or mass. cEEG monitoring was initiated, neurology consulted and an MRI was ordered for the following day. As his AMS was thought to be related to his BP, the team pursued BP control with Nicardipine. To summarize key elements from this case, this patient has: Seizure Altered mental status Hypertension Acute respiratory failure All of which brings up a concern for an acute CNS pathology.

Absolutely, the differential is broad, however, right now I am thinking of an acute stroke categorized as hemorrhagic, ischemic, or venous thrombotic; a meningoencephalitis, CNS vasculitis, acute demyelinating encephalomyelitis, metabolic encephalopathy, tumor, or AMS related to hypertension. Pradip, let's transition into some history and physical exam components of this case? What are key history features in this child? MIS-C with cardiac dysfunction and coronary anomalies Increase in steroid dosage Progressive increase in BP as a result of this increase

Rahul, are there some red-flag symptoms or physical exam components which you could highlight? The patient's physical exam was relatively normal. Of note, the fundoscopic exam did not reveal papilledema and no renal bruit was auscultated. His Pupils were equal, round, and reactive to light. The face was symmetric. Normal bulk and tone. The patient was sedated and did not withdraw extremities to noxious stimuli. Tendon reflexes were equal throughout. and no clonus is noted. Fundoscopic exam revealed no papilledema which may rule out increased ICP as a cause for our AMS.

To continue with our case, Rahul ,what were the patient’s labs were consistent with: Down trending CRP, ESR, BNP, and troponin ECHO is consistent with improved cardiac function as well as improvement of coronary dilatation. CT scan with no bleed MRI suggestive of changes in the posterior brain with distinct edema pattern

OK to summarize, we have: An eight-year-old, with acute severe hypertension, seizure altered mental status, and MRI changes suggestive of vasogenic edema in the posterior part of the brain -all this brings up the concern for posterior reversible encephalopathy syndrome (PRES) the topic of our discussion today. Rahul ,Let's start with a short multiple-choice question: A 19-year-old with h/o of renal transplant on tacrolimus and recent initiation of steroids for rejection presents with acute severe hypertension and a GTC seizure. The patient is afebrile with no rash. CT scan at OSH reveals no mass or hemorrhage. After stabilization and initiation of antihypertensive therapy, the next study of choice for diagnosis is A) Continuous EEG B) MRI C) Lumbar puncture D) Positron...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania, and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode a 24-month-old girl with increased seizure frequency. Here's the case: A 24-month old girl presents to the ED with h/o shaking/jerking episodes in her sleep. The patient was in the care of her aunt when this acute episode occurred. When the father arrived from work, he saw his daughter having episodes of her body shaking alternating with heavy breathing. The patient would not wake up in between episodes. There was pertinently no history of trauma. 911 was called and when EMS arrived, she was starting to arouse and respond to stimuli. The patient was transported to the ED. In the ambulance, the patient continued to have similar shaking and jerking episodes and was given rectal diazepam. On arrival to ED, the patient had a fever of 38.5 Centigrade. Due to ongoing seizures, the patient was loaded with Fosphenytoin, after having been given a total of two doses of IV Lorazepam. The patient was subsequently intubated for airway protection and respiratory failure. A respiratory viral panel was negative for SARS-COV-2 but positive for Rhino-enterovirus. The patient was admitted to the PICU with cEEG monitoring and placed on mechanical ventilation with fentanyl + dexmedetomidine infusions with as needed Midazolam administrations Her physical examination on arrival to the PICU was unremarkable. She wasn't interactive as she had just received sedation after intubation. On her neuro-examination, Pupils are equal and punctiform. The face is symmetric. The tongue is midline. Normal bulk and tone. No spontaneous movements were noted. No withdrawal to painful stimuli. Tendon reflexes were equal throughout. No clonus is noted. Rahul, to summarize key elements from this case, this patient has: Fever Viral infection with Rhinoentero virus Generalized Tonic clonic seizure lasting > 5minutes Acute respiratory failure All of which brings up a concern for status epilepticus

Absolutely, we will get to this later on in the episode; however, remember that Status epilepticus is historically defined as single epileptic seizure of >30 minutes duration or a series of epileptic seizures during which function is not regained between ictal events in a 30-minute period Let's transition into some history and physical exam components of this case?

What are key history features in this child who presents with status epilepticus?

Prolonged Seizures Fever with viral symptomatology which may act as a trigger A pertinent negative is that this patient had no history of trauma or co-morbid conditions such as a genetic syndrome. The patient also had no presumed ingestions as well.

Are there some red-flag symptoms or physical exam components which you could highlight?

Important to look for rash (darkening of the skin = adrenoleukodystrophy), genetic facies, evidence of trauma —-all of which are absent in this girl To continue with our case, the patients labs were consistent with: Initial Labs: WBC 27K, with neutrophilic predominance, Hgb and platelets were normal. Initial CMP was normal except for a glucose of 233. Gas prior to intubation in the ED was 6.9/102/85/-9. (repeat after intubation 7.19/49/40/-9). Ionized ca 4.9mg/dl. A urine analysis was unremarkable. Head CT negative

OK to summarize, we have: 24-month-old girl who presented with prolonged seizures and acute respiratory failure All of which brings up the concern for status epilepticus the topic of our discussion today. Let's start with a short multiple-choice question:

A 14-year-old girl is brought to the PICU from the floor with new-onset status epilepticus. She was admitted to the floor on her second day after a posterior spinal fusion surgery and is still receiving intravenous fluids. Her seizure is...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our episode, A Three-Year-Old with recent cough and leg weakness. Here's the case presented by Rahul. A 3-year-old previously healthy female presented to the hospital with a 2-week history of productive cough and congestion and the new 1-day onset of bilateral weakness. Today, the mother noticed weakness and inability to stand/walk following after shower as well as her voice becoming hoarse. She also noticed her lying more limp sitting on her lap, unable to sit up fully without her mother supporting her. She had no trouble holding up her head. The mother endorses increased fussiness but is able to be consoled. Decreased p/o intake, last meal was yesterday. About 1-2 weeks prior to this patient also had non-bloody diarrhea that resolved spontaneously after a few days. UOP normal with 2-3 wet diapers. No difficulty breathing. No history of head trauma or trauma to lower extremities, no erythema/swelling to joints. No pain associated with leg movement. No previous difficulty with walking - developing normally otherwise. No fever, recent travel, H/O sick contact at home (sibling with URI). No allergies, immunization UTD. CMP largely unremarkable. CBC with leukocytosis to 19.72 with L shift and platelets of 647. CRP 0.3, ESR 12. Afebrile, RR 24/min, HR 130, BP 140/86. On PE: Patient was coughing, had a hoarse voice heart and lung exam was normal. Normal abdominal exam. No rash Neurological exam: PERRL, (A+O) X3, 3-4/5 strength at ankles and knees and 5/5 in arms, +UE DTR's but none at patella or ankles. Has a wide-based ataxic gait and needs to hold on to the wall/furniture to ambulate. Rahul, to summarize key elements from this case, this patient has: A cough with a hoarse voice No fever Inability to stand/walk (i.e. lower extremity weakness) with no DTRs in patellae or ankle Normal mental status Diarrhea (non-bloody) preceding neurological weakness All of these bring up a concern for Guillain-Barré syndrome-An immune-mediated disease possibly triggered by a recent infection and targeting the peripheral nervous system.

Let's transition into some history and physical exam components of this case? What are key history features in this 3-year-old child

Acute (B) leg weakness Cough with hoarse Diarrheal illness No fever, no /o rash or trauma

Pradip, Are there some red-flag symptoms or physical exam components which you could highlight?

Bilateral lower leg weakness with absent patellar and AJ DTRs Normal mental status No rash, trauma Rahul continues with our case, the patient's initial labs and imaging were consistent with: The CMP, CBC with differential, and blood gas were unremarkable ESR = 12, CRP 0.29, pro-cal 0.09(all normal) Normal CPK Normal Urine analysis A lumbar puncture revealed colorless CSF with 4 white cells, 0 reds, Glucose 73 (serum Glucose 90) and protein 94, Gram stain and culture-negative MRI of the brain and lumbar spine with and without contrast was completely normal Chest radiograph with no infiltrate or atelectasis Nerve conduction studies were not performed

Any patient with acute ascending lower extremity flaccid paralysis with CSF showing acellular protein predominance should be considered to have Guillain-Barré syndrome unless proven otherwise. MRI brain spine is necessary to rule out any other etiologies such as brain tumor or spinal pathologies. Features strongly supporting the diagnosis of Guillain-Barré syndrome include a progression of onset over several days to less than 4 weeks, symmetrical involvement, painful onset, mild/absent sensory symptoms, cranial nerve involvement, autonomic dysfunction, absence of fever, and recovery 2 to 4 weeks after the onset of peak or plateauing of symptoms. Rahul Let's start with a...

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Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat. And my name is Rahul Damania, we come to you from Children's Healthcare of Atlanta/Emory University School of Medicine. Today's episode is dedicated to Noninvasive and Invasive ventilation in children post-hematopoietic cell transplantation. We are delighted to be joined by Dr. Courtney Rowan, MD, MSCR, Associate Professor of Pediatrics, and the Director of the Pediatric Critical care Fellowship at Indiana University School of Medicine/Riley Children’s Health. Dr. Rowan's research interest is in improving the outcomes of immunocompromised children with respiratory failure. She is active in this field of research and has led and participated in multi-centered studies. She is the co-chair of the committee of the hematopoietic cell transplantation subgroup of the Pediatric acute lung injury and sepsis investigators network. In our podcast today we will be asking Dr. Rowan about the findings of her recent study published in the journal-Frontiers in Oncology reporting on the risk factors for noninvasive ventilation failure in children post hematopoietic cell transplant. She is on twitter @CmRowan. Patient CaseI will turn it over to Rahul to start with our patient case... A 15-year-old female with a history of AML s/p Allogeneic hematopoietic stem cell transplantation T+15 days presents with tachypnea and a new O2 requirement. She has been on the BMT floor for 48 hrs after being admitted for respiratory distress and fevers. Her blood cultures are negative but she is febrile intermittently. Her CXR shows nonspecific haziness, no focal opacity, and underinflation. Her weight is up 2KG in the last 48 hours. She is found to have increased work of breathing and mild desaturations to 88%. She is placed on HFNC and continued on broad-spectrum antibiotics. A respiratory viral panel and Sars-CoV-2 PCR is sent. Transfer to the Pediatric ICU is initiated.

Episode DialogueDr. Rowan, welcome to our PICU Doc on-call podcast. Dr. Rowan: Thanks Rahul & Pradip for having me. I am delighted to be here to discuss one of my favorite topics. I have no conflicts of interest but I have funding from the NHLBI. Today we will be discussing the up-to-date evidence for NIV (HFNC and NIPPV) use in children who have had BMT. Additionally, we will also be discussing the use of invasive MV strategies including HFOV in the pediatric BMT population. To start us off, Dr. Rowan, why is the BMT cohort different from other patients admitted to the PICU? There is an increase in the # of patients undergoing BMT as indications for BMT are being expanded to different disease processes. The Etiologies for lung disease in BMT patients can be infectious (common organisms as well as opportunistic organisms). They can have lung disease from non-infectious causes and even fluid overload from renal dysfunction/medications given and there is a constant threat of alloreactivity which can manifest as GVHD or engraftment syndrome. 75% of PICU admits of immunocompromised children come from the heme-onc inpatient services. BMT patients have a higher risk to progress to ARDS. Recent reports show the incidence of ARDS in the intubated BMT population reaching upwards of 92%. These patients are also at high risk for MODS and can have a mortality rate close to 60%. 💡 To summarize, the BMT population is a unique ever-growing population that represents a relatively large cohort of immunocompromised children in the PICU with a risk of high mortality. As we have set this basis, we will be focusing the rest of our episode on the need for early recognition and intervention in this special population. Dr. Rowan: A common conundrum faced by the PICU team given limited resources and bed availability is when to transfer a patient with BMT to the PICU especially when they start requiring respiratory support on the floor. Are there any risk factors we as PICU physicians...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our episode of a 14-year-old girl with sudden acute outbursts of aggression and severe agitation. Here's the case presented by Dr. Damania: A 14-year-old previously healthy teenager with no significant past h/o presents to the PICU with a three-day h/o of aggressive behavior, agitation, and screaming. Her mother reports that her daughter has recently developed insomnia, abnormal movements and is more irritable with temper tantrums and episodic unintelligible verbal output. Parents report no recent stressors at home or at school. She has been also complaining of headaches for the past week along with things "being too loud". She denies any vertigo symptoms or tinnitus. The patient is brought to the ER due to persistent auditory/visual hallucinations followed by agitation, aggressive behavior, and catatonia. There is no h/o of recent illnesses, head trauma, fevers, rash, abdominal pain, diarrhea, or vomiting. Social history is negative for drugs of abuse in the home. Family h/o negative for seizures, and psychiatric disorders. The patient is sent to the ED and upon arrival has an unprovoked convulsive episode concerning a GTC seizure. The patient was initially admitted to the floor but transferred to the PICU for management of severe agitation, aggressive behavior, and fluctuations of blood pressure and heart rate. Initial vitals in the PICU were notable for tachycardia. The patient was found to be afebrile, normotensive for age, and SpO2 96% on RA. Her physical exam though limited by her aggressive behaviors was normal. The heart, lung, and abdominal exams are normal with no rash or bruising on her body. Initials lab work includes a negative: U preg Serum and Urine tox screen CBC, CMP, and UA are all within normal limits Inflammatory markers — including ESR CRP are unremarkable. A head CT which was normal and an A lumbar puncture revealed colorless CSF with 8 white and 0 red cells. Serum and CSF glucose were within normal limits and protein count in CSF was negligible. An extended multi-disciplinary work-up is initiated.

To summarize key elements from this case, Rahul this teenage girl has: Sudden outbursts of agitation, and aggression Recent difficulty in sleeping Irritability, and decreased verbal output Auditory and visual hallucinations Potential autonomic dysfunction as she has fluctuating BP and HR All of which brings up a concern for neuropsychiatric symptoms that could be organic in nature. Let's transition into some history and physical exam components of this case? Rahul, what are key history features in the patient presented this case. Seizures, Agitation, and aggressive behavior which could reflect CNS dysfunction are seen in this case. The patient additionally has concern for hallucinations which point to a primary psychiatric disturbance as well. Remember the incidence of new-onset psychosis or schizophrenia in a child <13 is increasingly rare — 1 in 40K and thus identification and thorough workup for an organic cause is increasingly important. Rahul, are there some red-flag symptoms or physical exam components which you could highlight? The physical examination (although limited by her behavior) in this patient is negative I would particularly stress the need for a detailed neurological and skin exam. For many of the differentials we will discuss, we must evaluate for rashes, changes in nails or hair, bruising or cutting marks in her arms, and even evidence of trauma to the (head and spine), and considering both an abdominal exam to r/o organomegaly as well as bi-manual pelvic exam is important to perform. Pradip, to continue with our case, the patient’s labs were consistent with? Rahul, actually her labs were normal. Besides the CBC, CMP...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamatand I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode of a 19 month old female with bloody stool, petechiae and no urine output Here's the case presented by Rahul: A 19 month old previously healthy female was brought to the pediatric emergency department for blood in her stool. Patient was at daycare the previous day where she developed a low grade fever, congestion and URI symptoms along with non-bloody-non-bilious vomiting and diarrhea. Patient had a rapid COVID test which was negative and was sent home with instructions for oral hydration. That evening, patient began having vomiting/diarrhea which worsened. She was unable to retain anything by mouth and her parents also noted blood in her stool. Due to this, she was rushed to the Emergency Department. In the ED here, she was hypertensive for age BP of 124/103 mm Hg, febrile, and ill. Specks of blood were noted on the diarrheal stool in the diaper. On her physical exam she was noted to be pale with petechiae on neck and chest. Her abdomen was soft, ND, with some hyperactive bowel sounds, and no hepatosplenomegaly. The rest of her physical examination was normal. In the ED, initial labs were significant for WBC 19, Hgb 8.8, and Platelets 34. CMP was significant for BUN of 74mg/dL and Cr of 3.5mg/dL, Na 131 mmol/L, and K of 5.5mmol/L, Ca 8.3mg/dL (corrected for albumin of 2.2g/dL), Phosphorous 8.5 AST 413, and ALT of 227, LDH > 4000. BNP was 142 and troponin negative. She was given 1 dose of CTX 50mg/kg and a 20cc/kg NS bolus. Stool PCR was sent. She was given labetalol for her hypertension, started on maintenance IV fluids and transferred to the PICU for further management. Rahul to summarize key elements from this case, this patient has: We have a 19-month old child with Diarrhea and emesis X 2 days No urine output for over 24 hours Bloody stool Petechiae on the neck and chest Anemia and thrombocytopenia

All of which bring up a concern for hemolytic uremic syndrome the topic of our discussion today Let's transition into some history and physical exam components of this case. What are the key historical features in this child who presents with above? Bloody stool which alludes to an invasive diarrhea No urine output and an ill appearing state which points to a systemic inflammatory condition and end organ dysfunction.

Are there some red-flag symptoms or physical exam components which you could highlight? Presence of petechiae which are physical exam features of thrombocytopenia Her pallor which is a physical exam sign of anemia Hypertension which is related to her renal dysfunction

To continue with our case, the patient's labs were consistent with: Anemia Thrombocytopenia Elevated BUN and creatinine Elevated serum LDH The patient did not have hyperkalemia, or acidosis on initial presentation

OK to summarize, we have a 19 month old girl with: Anemia, thrombocytopenia, and renal failure. This brings up the concern for Hemolytic uremic syndrome →

Rahul Let's start with a short multiple choice question: A 2-year old boy is admitted to the PICU with acute respiratory failure secondary to pneumococcal pneumonia. On day # 3 of admission, the nurse reports the patient appears pale and has petechiae on his chest. The patient also has not had urine output for > 12 hours and appears to be fluid overloaded. Of the following the lab findings would be most consistent with the above clinical findings in the patient? A) Elevation of serum haptoglobin B) Low serum lactate dehydrogenase (LDH) C) Negative Direct Coombs test D) Peripheral smear showing schistocytes The correct answer is D-Peripheral smear showing schistocytes.

Patient in the above case most likely has streptococcus pneumoniae associated hemolytic uremic syndrome commonly...

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Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat My name is Rahul Damania, a current 2nd year pediatric critical care fellow. We come to you from Emory University,School of Medicine, Children’s Healthcare of Atlanta, Atlanta, GA. Today's episode is dedicated to O2 delivery in the PICU. We would like to highlight in this episode Stanford University School of Medicine Pediatric Critical Care's LearnPICU website. Thehttp://learnpicu.com ( LearnPICU.com) website Is dedicated to reviewing clinical topics related to pediatric critical care, and is an open access resources which Is widely accessed worldwide. The website has over 10,000 visits each month, and is managed by Dr. Kevin Kuo - Clinical associate professor of pediatrics pediatric critical care at Stanford University. Dr. Kuo has Been featured on our prior episode entitled seven habits of highly effective Picu fellows, and we are very excited to collaborate with his educational resources to provide you the listener a comprehensive educational experience. Rahul, let's go ahead and get into today's case. A 17-year old boy is admitted after he was struck by a car at slow speed while crossing the street. He is has SPO2 of 98%, HR 98 bpm with a normal capillary refill and perfusion. His blood gas at admission to the PICU reveals a ph of 7.3/PCO2 35/PaO2 196 mm Hg on 50% NRB with 100% O2 flowing at 12LPM. His admission hgb is 10.5 gm%. 4 hours post admission, the nurses noticed that the patient is tachycardic to 150s, with a drop in his BP, delayed capillary refill, with cool extremities and increased output from the chest tube. His SpO2 has decreased to 86% and PaO2 on his blood gas is now 65mm HG. He is found to have a POC Hgb of 6.8 mg/dL. Let’s take this case and highlight key components of O2 delivery and O2 consumption. Lets focus on O2 delivery first. Rahul What are the components of O2 delivery ? Pradip, O2 delivery is made of O2 content X Cardiac output Simply put, O2 content is the amount of blood present in 100ml of arterial or venous blood. Its is denoted by CaO2 or CvO2 and its unit is mL O2 / dL blood or mL O2 per 100 mL of blood. Before we introduce the complicated formula, let's just appreciate the variables within the equation. Oxygen content is going to be a function of three variables: This is going to be Hgb, Saturations on the hemoglobin also known as SaO2, and the amount of oxygen that is dissolved within the blood also known as your PaO2. Pradip, Can you elucidate further about O2 content? O2 content is given by the formula: CaO2 = (1.34X Hgb gm/dl X SaO2) + (0.003X PaO2) Important points to remember about above formula is that the constant 1.34 (or 1.36 as given by some textbooks) is the amount of O2 in mL bound by one gm of Hgb and is called as the O2 carrying capacity of Hgb. In a healthy person say with 15gm% of Hgb, the O2 carrying capacity is about 15X1.34 = 20gm%. Now many times amount of O2 bound to Hgb may not always reflect 100% saturation So we need to factor the % oxygen saturation into the oxygen carrying capacity of the Hgb. The final element is to understand that some oxygen is dissolved in the plasma and is calculated using a constant 0.003 X PaO2. Typically 100ml of arterial blood with a saturation of 100 will contain 100 X 0.003 = 0.30ml of dissolved oxygen. Rahul can you calculate the pre-decompensation oxygen content in the above case? The above patients hgb pre-decompensation = 10.5gm%. His room air saturation 98% and his PaO2 is 196. CaO2 = (1.34X10.5X0.98) + 0.003 X 196 = 13.7 + 0.58 = 14.2ml O2/dL blood. Great - what is the post decompensation CaO2.? The post decompensation CaO2 can be estimated using same formula as above: CaO2 = (1.34 X 6.8 X0.86) + (0.003 X 65) = 7.8 + 0.195 = 7.9 O2/dL blood. Exactly So if you see the pre and post bleed O2 content just with a drop in Hgb from 10.5 to 7.5gm/dL: There is almost a 38% decrease in...

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Acute pulmonary Hypertensive Crises. Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode a 7 month old boy ex-26 week premature infant with acute hypoxemia, bradycardia episodes, poor perfusion Here's the case: A 7 month old ex-26 week male was transferred from the outside hospital to our PICU for tracheostomy evaluation. Patient was intubated on second day of life. He had a prolonged course, on inhaled Nitric Oxide for first 2-3 months of life in the setting of severe pulmonary hypertension, requiring HFOV for a prolonged period of time. Failed extubation attempts multiple times. Received steroid burst x2. BPD settings trialed (lower rate, longer iTime, high PEEP, larger TV) without improvement. At time of transfer he was in PRVC mode on the ventilator — TV ~10ml/kg, 50%, PEEP 8, rate 28 (Peak pressures 27-32). Patient received albuterol Q4 for bronchospasm/wheezing and pulmicort BID. Patient was deeply sedated with morphine and midazolam. Interstitial lung disease panel was negative. ECHO showed: systolic septal flattening, moderate RV hypertrophy with normal systolic functioning. Patient was not on any PH medications at transfer. Patient is also on furosemide, hydrochlorothiazide and spironolactone. Patient has completed a course of antibiotics for klebsiella tracheitis from a ETT CX a week prior to admission to our picu. Patient tolerated feeds via an NJ tube. The team continues to evaluate his case as the Patient continues to have episodes of acute desaturation, tachycardia, cool extremities and poor perfusion. To summarize key elements from this case, we have a 7month old who is ex-26 week premie Patient has BPD and is on high vent settings and failing extubation Abnormal echocardiogram with flat septum and hypertrophied Right ventricle Episodes of cold shock-tachycardia, poor perfusion, and cool extremities Hypoxia

All of which bring up a concern for acute pulmonary hypertensive crisis Rahul Let's transition into some history and physical exam components of this case? What are key history features in this infants who presents with an acute pulmonary hypertensive crisis Prematurity BPD

Remember BPD is defined by a requirement of oxygen supplementation either at 28 days postnatal age or 36 weeks postmenstrual age. Are there some red-flag symptoms or physical exam components which you could highlight? Presence of cold shock: tachycardia, cool extremities and poor perfusion Hypoxia Cardiac exam will reveal a bounding right ventricle, prominent loud single S2 Although not obvious in this patient: some patients can have a palpable liver, cardiac gallop, peripheral edema and jugular venous distention

S2 heart sound represents the closure of the PV very close to AV — In pulmonary hypertension this PE sign is seen with equal right and left ventricular pressures. To continue with our case, the patient's labs were consistent with: Respiratory acidosis (PCO2 > 100) CMP, CBC are normal BNP < 100, serum lactate normal

Echocardiography findings in these patients can show tricuspid regurgitation. We can estimate right ventricular systolic pressure on echo and, by extension, systolic PAP (sPAP), by using tricuspid regurgitant (TR) jet velocity in combination with other echocardiographic findings. Using the modified bernoulli principle 4 x TR jet velocity squared, we can estimate the sPAP. If sPAP >2/3 systemic sBP with severe flattening or posterior bowing of the interventricular septum the patient can be diagnosed with severe pHTN. Pradip, what if the patient had a PDA on echo — what would you see? Rahul, when you see Predominantly right-to-left shunting across the PDA suggests suprasystemic sPAP. And as a result these patients can be hypoxemic Ok, to summarize, we have: A 7-month ex-26 week

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Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat. My name is Rahul Damania, a current 3rd year pediatric critical care fellow. We come to you from Emory University School of Medicine-Children's Healthcare of Atlanta. Today's episode is very special as we are going to be discussing 7 Habits of Highly Effective PICU fellows. As many trainees, both residents and fellows are settling into the year, We wanted to make a special podcast which highlights some key, high value habits Which can make the pediatric critical care experience very fruitful longitudinally! We are delighted to be joined by Dr. Kevin Kuo and Dr. Paige Stevens. Dr. Kuo is a Clinical Associate Professor, Pediatrics - Critical Care as well as the Program Director, Pediatric Critical Care Fellowship at Stanford University. Notably, Dr. Kuo is also the site creator and editor of the informational & well-known PICU websitehttp://learnpicu.org ( learnpicu.)com- which accumulates over 10K views a month. Dr. Paige Stevens is a PCCM fellow at Stanford University and is here to provide the trainee perspective. Dr. Kuo and Dr Stevens - we are delighted to have you. Welcome to PICU doc on call podcast. Dr Kuo or Stevens: Thank You Pradip and Rahul for having us on PICU Doc on Call. We have no relevant financial disclosures or conflicts of interest.

Our episode will be a series of actionable steps which can optimize your passion and performance in the PICU. This episode was inspired by the very famous book: The 7 Habits of Highly Effective People by Steven Covey which is an international bestseller. To start with our episode, Dr. Kuo, do you mind highlighting the 7 Habits which we will cover: KK: Sure, here they are: From Dr. Covey's book we wanted to start with Begin with the End in Mind as the first habit Second, Embrace a Growth Mindset Third, Eat a Piece of Humble Pie Daily Fourth, Remember the ABCs Fifth, Put on Your Own Oxygen Mask First Sixth, Be Aware of the Meta Seventh, Sing in the Rain

Awesome, I can't wait to get into each of these. Dr. Kuo can you start us off with the first habit — Begin with the End in Mind? Dr. Kuo: sure 3 years goes by very quickly - what do you want your career to look like, what skills do you want to have gained, what things do you want to accomplish by the end of your three years, where do you want to work when you finish (academic vs community)? Be honest with what your interests and career goals are - i.e. not everyone needs to be an R01 funded basic scientist (although that is certainly needed and a wonderful career path). This is also great advice for people interviewing for fellowship. If you have a clear idea of who you want to be at the end of training, it will be easier to find a program that is going to help you get there. If you don’t know, you might want to choose a program where fellows go on to successfully do a broad range of things well.

Excellent approach and mindset especially for residents applying for PICU and matching in a few short months. Dr. Stevens: What about the Growth Mindset? PS: Starting with the Growth Mindset is to Be active in the continual process of self-reflection and evaluating your strengths and areas for growth- use those ILP’s and conversations with your mentors. Be active in the continual process of seeking out feedback from others. You may not always be able to see the full perspective so seek it out from everyone you interact with. When you find areas for improvement after self-reflection or receive feedback from others, embrace a growth mindset and a desire to incorporate that feedback and enact change.

This habit reminds me of a great book known as Mindset: The New Psychology of Success by Carol Dwek, a PhD psychologist who has transformed the way we think about personal development, resilience, and optimism — definitely a trainee read. Dr. Kuo, as you grow your experience as an attending...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode with a 15 year old Male having hypotension and bradycardia. Here's the case presented by Rahul: A 15 year old M presents to the PICU after sustaining an acute trauma. The patient was brought to the ER by his family after being on a boat and lifting a heavy object. He did not fall, sustain any head or extremity trauma, but did feel an achy non-radiating back pain shortly after the event. His grandmother states that the patient kept complaining about the back-pain and over the next few hours the patient became increasingly fatigued and flushed in the face. The patient was able to move his arms and legs and still walk, however family became concerned when the patient had abdominal fullness and was unable to urinate properly. He presents to the emergency department for further evaluation. In the emergency department he is noted to be awake however intermittently sleepy. His vital signs are notable for a HR of 58 bpm and a blood pressure of 85/60. He has 3/5 motor strength in his lower extremities with decreased sensation in his feet. Patellar reflexes are 1+ bilaterally. Rectal tone is normal. Acute resuscitation is begun for this patient. To summarize key elements from this case, this patient has: Acute trigger Back pain Vital sign instability and lower motor neuron signs. All of which bring up a concern for a spinal cord injury. Let's transition and discuss some history and physical exam components of this presentation:

What are key history features in a child who presents with hypotension and bradycardia?

As our worry is primarily spinal cord in etiology you would want to ask about trauma — this could be blunt or penetrating trauma You also would like to ask about the nature of the injury and scene. It is especially important to inquire with the pre-hospital providers about the nature of the injury and the patient course in transport. Besides our normal ABCs, it is important to ask the care taken regarding spinal cord restriction (such as use of a cervical collar or backboard) Another high yield history component when you think about hypotension and bradycardia is to assess for Numbness, weakness, or changes in bowel or bladder habits. In this case the patient had abdominal fullness which maybe due to bladder dysfunction.

This is a great summary of key history findings for patients who present with hypotension and bradycardia as it relates to spinal cord issues. Remember that patients who have Down's syndrome may have a predilection to have lax ligaments especially in the upper verterbrae. As a result, you should have an increased index of suspicion if a Down's Syndrome patient presents with hypotension and bradycardia in the presence or absence of trauma. In a study published in 2017 in Neurocrit Care it was estimated that about 20% of patients with Trisomy 21 may have atlantoaxial instability. A great point which you just highlighted. Remember that when you approach hypotension and bradycardia, it is also important to focus on cardiac etiologies: Bradycardia directly pulls down the cardiac output, potentially causing shock, and especially if you have a blunted vasoconstrictor response you can couple this bradycardia with hypotension.I do not want to delve too much out of the scope of today's episode but there is a wide differential for bradycardia but specifically related to history you should consider intoxication as a cause of bradycardia and hypotension. This includes: Beta-blocker or calcium-channel blocker. Central alpha-2 agonist (e.g., clonidine, dexmedetomidine, guanfacine).

Going back to our case, are there some red-flag symptoms or physical exam components which you could highlight when you approach? Yes, in this patient who we suspect...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode of 17-year old with h/o of SLE and now acute liver failure. Here's the case presented by Rahul: A 17-year old teenage female year old presents to the PICU with acute liver failure. Important past h/o includes a diagnosis of SLE on therapy with prednisone, mycophenolate (cellcept), and plaquenil. 4 days prior to this admission, patient presented to an OSH with RUQ pain, vomiting (non bloody & no bilious), fever & malaise. Initially due to concern for "lupus Flare" patient was given steroids at the OSH. At the OSH notable initial labs included a mild transaminitis and an INR of 1.5. She suddenly at the OSH developed fluid refractory hypotension and was started on a pressor. Due to continued worsening of her transaminitis well as a rising INR on her repeat labs she was referred to our tertiary PICU for further management. Pertinent history also includes a negative urine pregnancy test. No recreational drug use, and only as needed use of Tylenol. She now is in the PICU. She generally appears tired and ill. She is tachypneic on 4 LPM of nasal canulla and her oxygen saturation is 98%. She has a non-focal lung exam. Her cardiac exam is notable for tachycardia, and pertinently no gallop, rub or murmur. Her abdominal exam is non-focal except for mild discomfort on palpation of the RUQ with a palpable liver edge. Her extremities are cool with 3-4 capillary refill time. She is able to answer questions but intermittently doses off. No rash is noted. To summarize key elements from this case, this patient has: H/o of lupus and is on immunosuppressive medications New onset fever/malaise This sounds like a LUPUS flare as she has a clinical picture of generalized inflammation.

Rahul: Lets pause right here and take a look at key history and physical exam components in a patient who has a chronic auto-immune condition: Fever, malaise and feeling tired all signs of constitutional symptoms. She has abdominal pain and vomiting that could again be related to systemic inflammation but also an intra-hepatic lesion.

Are there some red-flag symptoms or physical exam components which you could highlight? This patient has signs of shock! Tachycardia with delayed cap refill and cool extremities Tachypnea & hepatomegaly which could indicate increased central venous pressures. Initially her outside presentation of fluid refractory shock is of utmost concern! Fluid refractory shock with multi organ presentation involving liver, kidney and the blood/coagulation systems All of these elements bring up a concern for some acute life threatening process such as sepsis, or even immune dys-regulation due to her h/o of Lupus To continue with our case, the patients labs were consistent with:Acute liver dysfunction (Elevated AST and ALT in the thousands, Total bilirubin 1.6, GGT 56) although the total bilirubin is not elevated to a degree I would expect. AKI (creatinine 2.18) An uptrending Coagulopathy with elevated PT and INR: PT 120 and a peak INR of 16 Thrombocytopenia: Platelets < 50K She had a peak lactate 9.2 and concurrent Metabolic acidemia: serum HCO3 7, and pH 7.18. A Pertinent negative: Normal serum ammonia <38 micromol/L (nl < 50) Finally, she had an elevated WBC 20.5K/ Hgb 9.7, Platelet 42. CRP 4.2/ESR 5

OK to summarize, we have: a 17 yr old female with SLE on mycophenolate (cellcept) who presents with fever, hypotension, AKI and liver dysfunction with severe coagulopathy, although we do not have other labs- This brings up the concern for acute macrophage activation syndrome (MAS) the topic of our discussion today. Let's start with a short multiple choice question: 12 year old male with h/o systemic onset juvenile idiopathic arthritis (JIA) presents

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania. We are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode of 17-year old with h/o of SLE and now acute liver failure. Here's the case presented by Rahul: A 17-year old teenage female year old presents to the PICU with acute liver failure. Important past h/o includes a diagnosis of SLE on therapy with prednisone, mycophenolate (cellcept), and plaquenil. 4 days prior to this admission, patient presented to an OSH with RUQ pain, vomiting (non bloody & no bilious), fever & malaise. Initially due to concern for "lupus Flare" patient was given steroids at the OSH. At the OSH notable initial labs included a mild transaminitis and an INR of 1.5. She suddenly at the OSH developed fluid refractory hypotension and was started on a pressor. Due to continued worsening of her transaminitis well as a rising INR on her repeat labs she was referred to our tertiary PICU for further management. Pertinent history also includes a negative urine pregnancy test. No recreational drug use, and only as needed use of Tylenol. She now is in the PICU. She generally appears tired and ill. She is tachypneic on 4 LPM of nasal canulla and her oxygen saturation is 98%. She has a non-focal lung exam. Her cardiac exam is notable for tachycardia, and pertinently no gallop, rub or murmur. Her abdominal exam is non-focal except for mild discomfort on palpation of the RUQ with a palpable liver edge. Her extremities are cool with 3-4 capillary refill time. She is able to answer questions but intermittently doses off. No rash is noted. To summarize key elements from this case, this patient has: H/o of lupus and is on immunosuppressive medications New onset fever/malaise This sounds like a LUPUS flare as she has a clinical picture of generalized inflammation.

To continue with our case, the patients labs were consistent with: Acute liver dysfunction (Elevated AST and ALT in the thousands, Total bilirubin 1.6, GGT 56) although the total bilirubin is not elevated to a degree I would expect. AKI (creatinine 2.18) An uptrending Coagulopathy with elevated PT and INR: PT 120 and a peak INR of 16 Thrombocytopenia: Platelets < 50K She had a peak lactate 9.2 and concurrent Metabolic acidemia: serum HCO3 7, and pH 7.18. A Pertinent negative: Normal serum ammonia <38 micromol/L (nl < 50) Finally, she had an elevated WBC 20.5K/ Hgb 9.7, Platelet 42. CRP 4.2/ESR 5

OK to summarize, we have: a 17 yr old female with SLE on mycophenolate (cellcept) Who presents with fever, hypotension, AKI and liver dysfunction with severe coagulopathy. Although we do not have other labs- This brings up the concern for acute macrophage activation syndrome (MAS) the topic of our discussion today. Let's start with a short multiple choice question: 12 year old male with h/o systemic onset juvenile idiopathic arthritis (JIA)...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine in Atlanta, GA.Today we are going to present a case of a 3 year old presenting with bilateral hyper-flexed wrists. Here is Rahul with our case: A 3 yo previously healthy M presents to the emergency department after his mother noted his wrists becoming completely stiff and flexed. Despite several attempts to stretch out his wrist, his mother was unable to place them back into position. She brought him to the ED for further evaluation. Importantly, mother denies any trauma or injury. Mom notes that this happened once before one month ago. The episode lasted 10 min and self-resolved. She did not seek medical attention at that time. Patient has no history of bleeding, bruising or chronic medical conditions. His immunizations are UTD. Family hx was relatively unremarkable however the mother states that she gets admitted to the hospital for Kidney Stones 4-5 times per year. She usually follows with a urologist. Though she is on diuretic therapy for recurrent renal stones, she denies that her son has any access to these medications & also denies any ingestion. She does state that patient is a picky eater and does not drink milk but will eat cheese often with 4-5 cups of juice. Mother denies any recent upper respiratory tract symptoms, vomiting, constipation, urinary abnormalities or changes in gait. Upon presentation to the ED, his vital signs were stable. His physical exam is normal except for Bilateral hands in flexion with digits on flexion as well. After some resistance the examiner was able to extend hands. There were no abrasions or signs of cutaneous injury in his bilateral hands. Full range of motion of elbow and shoulder as well as full range of motion of ankle and knee as well as hip. Prior to drawing blood for a diagnostic work-up the patient undergoes an EKG which shows some artifact but is notable for a prolonged QTc interval of 560. To summarize key elements from this case so far, we have a toddler with Bilateral hyper-flexion of the wrists which seem to be in a tonic state and is recurrent A family history of renal metabolic disease. and finally, an EKG abnormality. Rahul one key pertinent negative at this stage is that there is no trauma & patient has full range of motion at other large joints Rahul, let's transition to key history and physical elements when you think about bilateral wrist flexion.

This is an interesting chief complaint, however I would tailor my history to assess for trauma as this seems to be a primary MSK issue.

The key feature here is that the patient has bilateral wrist involvement which brings up the concern for an underlying systemic cause such as an electrolyte abnormality, connective tissue disorder, or muscular abnormality. The family history of recurrent kidney stones points more towards a familial renal or electrolyte problem. I would ask about any trauma related to skin wounds. As this patient is in a tonic state, I would worry about tetanus. I would also get a good dietary history as excessive juice consumption may have limited nutritional value.

On physical exam, I would look for any other MSK abnormalities with this bilateral wrist flexion. Especially if we are heading down the route of nutritional abnormality, electrolyte disturbance or renal anomaly, I would like to assess for any bowing of the legs, joint flaring, any metacarpal shortening, or rib abnormality.

Pradip, I would love to hear more about the emergency room diagnostic work-up in this patient... To continue with our case, the patients labs were consistent with: A very low ionized calcium of 2.2 (normal 4.4-5.4mg/dl). Also, his total serum Ca was low — < 5mg/dL (Nl range 8.9-10.4mg/dl) with a relatively normal albumin. His CMP was notable for an elevated...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode of a 16 year old with fever and a rash. Here's the case: A 16 year old F presents to the PICU with generalized weakness, fever and a diffuse rash. Three days prior to admission she stated that she was feeling lightheaded and the day after she started having frequent non-bloody diarrhea. She states that she has otherwise been healthy, no sick contacts or travel, and the only change in her life was her menstrual cycle which ended a few days before her symptoms started. She says that about two weeks ago, she went to her primary care physician to get an in-grown toe nail drained, but was able to recover after some analgesia and antibiotics for a week. On day of admission her mother brings her into the ED as she says her rash continues to progress. Her mother states that the rash looks like a sunburn. Mother noticed on day of admission that her daughter now had red injected eyes bilaterally without discharge, and was becoming increasingly confused with her fevers. Of note, the patient has also has had decreased oral intake as she says her mouth quote hurts when she swallows. She has had no sore throat, congestion, dysuria, or headache. She presents to the ED febrile to 39 C and tachycardic to 130 bpm. She is ill appearing and has orthostatic vital signs. Her exam is notable for palpable diffuse myalgia, oropharyngeal hyperemia, diffuse erythroderma, and conjunctival injection. She is noted to have a hyperdynamic precordium and faint crackles bilaterally. Her L toe is mildly erythematous with no discharge, necrosis or pain to palpation. Acute resuscitation and diagnostics are begun and patient is transferred to the pediatric intensive care unit. To summarize key elements from this case, this patient has: Hx of a fever and multisystem involvement including GI manifestations, myalgias, confusion, mucositis, and rash This is in the setting of a local drainage procedure and course of antibiotics. In addition, she presents now with fever, hypotension, and tachycardia. These elements so far bring up a broad differential but for now we can agree that it seems that she has signs of acute inflammation or infection throughout her body.

nsition into some history and physical exam components of this case. If we take a step back, what are key history features in a child who presents with fever & rash?

Understanding the characteristics of the rash, the evolution, and progression of the rash is important. In the setting of myalgias, fever, headache, and rash you should think of assessing for any recent travel as tick-borne illnesses commonly present with this symptomatology. You also want to assess for recent antibiotic exposures, sexual history, and surgical history - in our case, our patient had a recent procedure on her toe

Are there some red-flag symptoms or physical exam components which you could highlight?

Absolutely, when a child presents with fever and a rash, it is important to stratify two major elements:

You want to assess the degree of toxicity in relation to the symptomatology: Lethargy, irritatbility, altered sensorium, poor perfusion, pallor or cyanosis may indicate serious illness. Understanding the duration of fever in the setting of suspected total body inflammation is important, however the importance of the heigh of fever in predicting the risk of serious illness is unclear. We will visit a differential a bit later in this podcast, however I do want to highlight that the presence of tachycardia and tachypnea in any patient with fever and rash suggests the possibility of sepsis. When you notice these red-flag symptoms it is important to focus on resuscitation and treatment rather than pursuing diagnostics.

To continue with our case, our

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our PICU Doc On Call Mini-Case series. In this episode, we present a 15 year old girl who is admitted for shock after returning from her recent travel to NIgeria. Here's the case: 13y F with no significant past medical history presents with 4 days of fever, headache, watery, non-bloody diarrhea, non-bloody, non-bilious emesis, decreased PO intake with worsening myalgias, fatigue, and weakness. She had traveled with her mother to Nigeria earlier this month and returned a week ago. Over the weekend mom consulted her pediatrician who prescribed an antiemetic without significant improvement of her symptoms. Once patient progressed to becoming light headed and weak, the mom decided to bring her to ED where she was found to be have tachycardia and hypotension. She required 3 L of crystalloid resuscitation was started an epinephrine continuous infusion and transferred to the PICU. Patient was found to have acute kidney injury with an elevated Cr, as well as a primarily direct hyperbilirubinemia and associated anemia and thrombocytopenia. Her other history elements were notable for fever and difficulty breathing. Prior to traveling to Nigeria she did receive travel vaccinations and took mefloquine prophylaxis. She also had a negative COVID screen. While in Nigeria she denies exposure to animals, raw food intake, and only recalls that she may have had a few mosquito bites but this was well after returning from Nigeria until 7 days prior to presentation to the ED. She presents to the PICU with hypotension, tachycardia at 160 bpm, tachypnea, and normal saturations. Her physical exam is notable for cool peripheral extremities, RUQ tenderness, and bilateral crackles. She had no murmurs or gallops on her initial exam. Pertinently, she had no rash, lymphadenopathy or scleral icterus. This is a teenage girl who has fever and constitutional symptoms after returning from travel abroad She now presents with fluid refractory shock, tachycardia that is out of proportion to dehydration and signs of end-organ failure. Notable negatives include: No LNadenopathy, hepatosplenomegaly, or a rash Synthesizing these symptoms together → we are thinking that this picture may be related to a contracted infection or inflammatory condition related to her travel. Let's transition into some history and physical exam components of this case.

What are key history features in this child who presents with fever and shock after a recent travel outside the US (Nigeria-West Africa)

Diarrhea and emesis days before presentation High Fever with no rash Mental status is maintained although she did have an headache Light headed and weakness are symptoms suggestive of dehydration and even shock Physical exam findings of importance here include- patient presenting with tachycardia, signs of poor perfusion such as delayed cap refill, cool extremities, hypotension. It is unique that even though she has RUQ pain there is no jaundice.

Are there some red-flag symptoms or physical exam components which you could highlight in a patient with the above history and recent travel. Weakness, light-headedness, shock, tachycardia, poor perfusion, fever and evidence of multi-organ dysfunction are suggestive of an acute and possibly life threatening infection acquired during travel. Given her travel to West Africa: I would be worried about falciparum malaria, dengue fever, typhoid fever, and cholera. Other diseases to be concerned about especially given her travel h/o include leptospirosis, chickungunya, Crimean-Congo hemorrhagic fever, African tick bite fever etc. I would be also concerned about bacterial sepsis with a source such as the kidney, bowel, or intrapelvic organs. To continue with our case, the patients labs were

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our Episode of a 9 year old girl with worsening seizures in the setting of an electrolyte abnormality. Here's the case: A 9 year old girl presents to the ED with increased frequency of seizures, dehydration and listlessness. She has h/o of global developmental delay, congenital hydrocephalous (with VP shunt in place with her last revision 3 years prior, and seizure d/o treated with Leviteracetam. She usually has one or two focal seizures per day but on day of admission she had multiple prolonged seizures which were also generalized tonic clonic in semiology. Per her caregiver, the patient usually eats by mouth and mother typically gives her 3 cups of water daily. There is no history of diarrhea but patient has had 2-3 bouts of non-bloody non-bilous emesis on day of presentation. Looking at her growth chart, the patient has also lost ~ 2KG of her weight in the last 3 months and has had poor follow up with her PCP. In the ED she has a hypovolemic shock picture as she is hypothermic, tachycardic, tachpneic, and hypotensive with appropriate saturations. Blood gas is notable for a mild metabolic acidosis. Patient receives abortive seizure rescue. A head CT showed no increased in hydrocephalus, no mass or hemorrhage and a shunt series confirms patency of her VP shunt. Most pertinently to this case, her serum sodium on her RFP was undetectable at a value of = >200mEQ/dL; this was confirmed by a repeat lab draw and POC value. Other notable findings included an elevated Cr for age, an elevated BUN and a microcytic anemia. Patient was given a NS bolus, had cultures drawn, was started on broad spectrum abx therapy, stabilized and sent to the PICU. To summarize key elements from this case, this patient has: A history of GDD with epilepsy and shunted hydrocephalus. A stigmata of cachexia. And a presentation of hypovolemic shock secondary to decreased intake, increased loss, and potential underlying concern for sepsis. The most important element of this case is her extreme hypernatremia All of these factors in this case point to our topic of discussion today → the approach to hypovloemic hypernatremia 2/2 to dehydration. Let's transition into some history and physical exam components of hypovolemic hypernatremia?

Key history features in patients who present with Hypovolemic HyperNa include:

Increased losses such as emesis Decreased intake, and in this setting potentially lack of access to free water Listlessness which could be related to cerebral hypoperfusion Increase in seizure frequency due to increased rapid depolarization of Na channels in the brain and fluid shifts And weight loss → all of these factors were seen in our case. Of note if this patient was a neonate considering a high-pitched cry in the setting of hyperNa & dehydration could be a subtle history finding.

Are there some red-flag symptoms or physical exam components which you could highlight?

Our patient is Non verbal and has global delay secondary to a remote neurological insult She may not have intact ability to communicate or vocalize thirst. Apart from her mucous membranes, dry cracked lips, decreased skin turgor that can be described as doughy, and prolonged capillary refill, I think it is important to highlight her hypotension - as BP is one of the last vital signs in pediatrics to be abnormal in intravascular volume depletion. To me, this really stratifies this patient into severe dehydration and potentially septic shock.

This is a great point — understanding % volume loss and its correlation to vital sign and PE anomalies is key. Remember a sensitive marker for dehydration in pediatrics is tachycardia and a late finding if you are primarily dealing with dehydration is hypotension. This...

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An 8-year-old female (24 kg, 130 cm) with PMH significant for severe persistent asthma and history of multiple PICU admissions presents to the ED with swelling, redness and inability to bear weight in her (L) lower leg. Patient had just finished soccer practice the evening prior to her ED visit when she first noticed swelling and redness of her left lower leg. She also had a fever as well as some non-bloody, non-bilious emesis. Her past h/o is significant for poorly controlled asthma with multiple admissions to the PICU. Upon arrival to the ED, patient's BP was hypotensive, tachycardic, and tachypneic. She was given two 20 mL/kg NS boluses, and blood cultures were drawn in addition to a CBC, BMP, and UA. Labs were notable for an elevated white count, lactate, and serum Cr. Patient was given a dose of antibiotic, and transported to the PICU for further workup and management. Whitney and Stephanie welcome to PICU Doc on call. Thanks Rahul and Pradip for having us. Neither one of us have any financial disclosures or conflicts of interest. We want to divide today's discussion into 3 segments- antibiotic selection, transition into dosing and end with therapeutic monitoring Whitney, what are some of the factors to consider prior to choosing an antibiotic regimen in our patient case with a preliminary diagnosis of cellulitis of the left lower extremity with possible sepsis? Whitney: First and foremost you want to consider your host so really diving deep into the patient’s past medical history and secondly we should consider the likely pathogens that are causing the patient’s infection. In this case given the invasive nature of her infection and recent hospital admissions I would start Vancomycin and Cefepime. Once blood cultures results are back, we can then tailor or narrow her antibiotics based on susceptibilities.

Stephanie what are some of the other factors to consider prior to starting antibiotics in this patient? Other things to consider include her multiple previous hospitalizations, significant exposure to broad-spectrum antibiotics, whether or not she is immunocompromised, the presence of chronic conditions like lung disease, ventilator/trach dependency, and if patient was a resident of a long term care facility. Additionally any history of organ or bone marrow transplant or malignancy with use of chemotherapy/radiation, and/or a history of growth of multiple drug resistant organisms.

This is an important point - infectious disease is not just about the relevant pathogen or "bug" but it is also about understanding the host status! Stephanie -why vancomycin and cefepime in this case? In this patient the major pathogens to consider include: P. aeruginosa (give her multiple previous PICU admissions). Also she has extensive cellulitis which necessitates antibiotic coverage against Methicillin resistant staph aureus (MRSA) and Streptococcus pyogenes . So our options in this case include vancomycin for broad-spectrum gram positive coverage, and generally either piperacillin/tazobactam or cefepime for broad-spectrum gram negative and pseudomonal coverage. As you can see by patient’s Scr, it appears that she is presenting in AKI since we have no history of her having any type of renal impairment at baseline; therefore, to minimize additional AKI risk, cefepime would be our most appropriate choice for the time being. There is literature that shows us that the combination of...

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Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat My name is Rahul Damania, a current 2nd year pediatric critical care fellow. We come to you from Children's Healthcare of Atlanta and the Emory University School of Medicine Atlanta, GA Today's episode is dedicated to How to Read And Critically Review a Paper not only for the Journal club presentation at the fellows conferences but also for use in your clinical practice as a pediatric intensivist. We are delighted to be joined by Jocelyn Grunwell, MD, PhD. Dr. Grunwell is an Assistant Professor of Pediatrics-Pediatric Critical Critical Care at Emory University School of Medicine in Atlanta, GA. She is a K-scholar with research interests in mitochondrial dysfunction in critical illness, the airway immune response in pediatric acute respiratory distress syndrome, and near-fatal asthma. She is on twitter @GrunwellJocelyn. Rahul: Dr Grunwell welcome to picu doc on call. We are delighted to have you on our podcast today to discuss how to read & critically review a manuscript. Grunwell: Thank you Rahul and Pradip for having me on PICU DOC on Call. I have no conflicts of interest or financial disclosures. Q1. Rahul: Dr Grunwell: Why should a pediatric intensivist (whether in training or as a faculty) read journal articles? Grunwell: There are several reasons you might want to read journal articles, and your reading should be tailored to your goals. For example, first, you may want to learn more about a clinical topic to understand how to diagnose, treat or manage a disease. 2nd you may want to find the best evidence for how to treat a patient. 3rd, you may want to learn about the basic biology or mechanisms of a disease. Finally, you may want to identify gaps in a particular field of research to develop a research plan and write a proposal to explore a new research area. Q2: Dr Grunwell: Where do you find manuscripts relevant to intensivists? First, I would like to suggest that the learners and faculty in pediatric critical care make a habit of reading at the very least the abstracts in various pediatric journals even if they don't have the time to read an entire article. I generally go to Pediatric Critical Care Medicine, Critical Care Medicine, Critical Care Explorations, Pediatrics, Journal of Pediatrics, NEJM, JAMA Pediatrics, and the family of American Thoracic Society journals on a weekly basis. You can set-up your account so that the table of contents of these journals will be emailed to you. There are apps available, such as ReadQxMD, where you can be alerted to new content of interest to you. You can sign up and follow the accounts of several journals of interest to you on Twitter. There is also a useful, free website sponsored by Dr. Hari Krishnan called http://picujournalwatch.com/ (picujournalwatch.com) in which Dr Krishnan has journal articles well-organized. The website is constantly updated to show the latest manuscripts relevant to our field. You can keep your articles organized by topic in software such as EndNote. Also doing a search on PubMed, OVID etc. can also be helpful to find latest information on a topic. Talking to a medical library scientists is very useful to structure a systematic search for articles or to get a article from a journal that is not available at your institution. Q3: Dr Grunwell can you define the term level of evidence? Grunwell: the term level of evidence - or traditional hierarchy of evidence - refers to what degree that information can be trusted based on the study design. The most common question is related to therapy or an intervention. Levels of therapy are typically represented as a pyramid with systematic reviews or meta-analyses positioned at the top of the pyramid followed by well-designed randomized control trials, and then observational studies. Observational studies include cohort studies or case-control studies. Case studies,...

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Welcome to PICU Doc On Call, A Podcast Dedicated to Current and Aspiring Intensivists. I'm Pradip Kamat and I'm Rahul Damania and we are coming to you from Children's Healthcare of Atlanta - Emory University School of Medicine. Welcome to our PICU Mini-Series Episode a 10 month old who is intubated for acute respiratory failure secondary to RSV bronchiolitis. Here's the case: A 10-month-old full-term infant girl old is intubated for acute respiratory failure secondary to RSV bronchiolitis. Patient was brought to the ED by parents on day 3 of her illness with h/o cough, congestion and worsening respiratory distress. She has had increasing WOB and grunting. After assessment in the ED where the patient had a brief trial of HFNC, she was intubated with a 4.0 ETT due to persistent hypoxemia. Pertinently, her viral panel was positive for RSV, and the patient was transferred to the PICU. In the PICU, patient was ventilated using PRVC: Set TV of 90cc (patient is 11KG), PEEP 6, PS 10, and FIO2 40%. Throughout her course, she was mechanically ventilated and sedated for about a week. She required a continuous infusion of rocuronium due to decreased lung compliance and high peak pressures. Patient weaned on her ventilator settings by ICU day 7 and the decision to move towards extubation was made. To summarize key elements from this case, this patient has: 10 month old with acute respiratory failure secondary to RSV infection and with a secondary bacterial infection due to H.Influenza. Had about a six day course on the ventilator requiring sedation and NMB and now we are at the discussion of extubation readiness.Rahul, do you mind summarizing the patient's peri-extubation course?

Sure Pradip, so on day 6 of hospitalization our patient was weaned to low mechanical ventilator settings. The chest radiograph, which initially showed evidence of interstitial pneumonitis and atelectasis now improved and the patient had improved secretion burden. The patient was on ceftriaxone throughout the hospital course as her ETT cx with which grew Hemophilus Influenzae. What about the patient's neurological status? The patient was initially on fentanyl, dexmedetomidine and a rocuronium infusion — a day prior to considering extubation, the patient was off of the continuous rocuronium infusion oxygenating and ventilating well. The patient prior to extubation was wide awake and appropriate during the morning sedation holiday. Any other important clinical markers? Yes, the patient's clinical exam including lung exam was reassuring. The patient underwent a pressure support trial PEEP 5, CPAP 10 and had a normal respiratory effort with exhaled of about 5 mL/kg. The RT, however mentioned that the patient did not have a "leak" when performing the leak test. The finally the patient was given a few doses of furosemide for diuresis prior to extubation. Awesome, today's episode we really want to focus on extubation readiness however prior to this discussion, can we take a step back and talk about some red-flag symptoms which led to intubation for this patient? This patient had severe respiratory distress which progressed to failure. The tachypnea, decreased mentation, and grunting were key signs that the patient was progressing to endotracheal intubation. Grunting is important to highlight as this refers to the child generating auto-PEEP to combat the atelectasis present in bronchiolitis. Remember that a child's chest wall has a high compliance and a decreased propensity for outward elastic recoil — this in essence reduces FRC and thus there is a more balance towards the inward recoil of the long (closing capacity). The highly compliant chest wall and the natural inward recoil of the infant lung creates a propensity towards atelectasis and subsequent impairments in breathing. Low FRC can also create increase PVR which can thus imbalance optimal cardiopulmonary interactions.

OK let's transition to our topic of discussion by a quick summary: A...

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Welcome to PICU Doc On Call, a podcast dedicated to current and aspiring intensivists. My name is Pradip Kamat and my name is Rahul Damania and we come to you from Children's Healthcare of Atlanta Emory University School of Medicine. Today's episode is dedicated to optimizing your Pediatric Critical Care Knowledge and study skills by utilizing your medical librarian. We are delighted to be joined by Ms. Carrie Price a health Professions librarian. Carrie was formerly at the Welch Medical Library, serving the faculty, students and staff of Johns Hopkins Medical Institutions. Ms Price is currently at the Albert S. Cook Library of Towson University in Towson, Maryland. Ms Price is an expert searcher with a strong interest in user-centered and instructional design, evidence-based medicine, and inter-professional education. Ms Price also maintains and updates a YouTube Channel with videos about citation management, searching, and evidence-based medicine. Carrie is on twitter @carrieprice78 Q1. Carrie welcome to PICU DOC on Call Podcast. Our topic today— Value of the librarian in PedsICU education and it is one of the first in our series of how learners can organize their study habits while rotating in the PEDS ICU. Carrie: Thanks Rahul and Pradip for having me on PICU DOC on Call podcast. I have no conflicts of interest or financial disclosures. Q2. Carrie tell us your story and how you came to be an expert medical librarian ? Carrie: I came into librarianship as a second career, after a first career in nonprofit development. I was fortunate to start my work in libraries at Johns Hopkins University, where I worked as a library assistant in access services while getting my masters degree in library science. During this time my mom was diagnosed with appendix cancer, a rare cancer, (she's okay now), and through the time we spent together in the hospital, I noticed there was a medical library in the building. I had this epiphany that librarians weren't limited by traditional career paths. From then I started focusing on health and consumer health classes. Later, at a work all-staff meeting, I literally bumped into the former director of the Welch Medical Library, and the rest is history! I applied for an open position, was hired, and started working at the Welch Medical Library in 2012. It has been an incredible experience. I am fortunate to work extensively with a number of departments and divisions at Johns Hopkins and now at Towson University, so my experiences have been really multidisciplinary. In the past I worked as a physical therapy technician, which was awesome and helped inform the knowledge I brought to the profession. I've taken a lot of professional development in the field. I just never stop learning, and I love sharing information on Twitter, YouTube, and on my website, which is http://carrieprice78.github.io/ (carrieprice78.github.io). This is such an amazing story! Q3: Carrie the practice of critical care medicine requires that learners in the Peds ICU remain current in their knowledge of the literature. Given an overwhelming amount of information out there how should these learners drink from that fire hydrant without being blown away? Carrie: I think that's an excellent question. Prior to the arrival of internet, most additional knowledge was acquired from physically going to a library and perusing through peer reviewed journals and textbooks. Now, things are digital and even "born-digital" — and there is so much information available online and on your phone.... I understand that given how much information is out there, a learner can feel overwhelmed and have difficulty trusting the information they see. That's why critical appraisal is a key part of evidence-based practice. Studies have shown the value of readily-available information in patient care and have highlighted the role of the library and librarian in support of clinical practice. In 1996 Sackett et al (BMJ 1996). defined...

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Today’s episode focuses on salicylate toxicity, specifically in the case of a teenager with abdominal pain and emesis. Join us in this discussion of symptoms, patient history, diagnosis, management, and treatment. Show Highlights: Our case: A 15-year-old female is admitted to the PICU for intentionally ingesting a large amount of aspirin tablets. She had epigastric abdominal pain with some non-biliary, non-bloody emesis when she presented to the outside emergency department twelve hours post-ingestion. She denies any neurological symptoms, including tinnitus but appears anxious and tachypneic. In the emergency department, her salicylate level was 45 mg/dL after her ingestion of about 250 aspirin tablets of 325 mg each. The patient is previously healthy, denies the use of illicit drugs and alcohol, is not sexually active, and has no allergies. To summarize the key elements of this case and patient history, she has ingested potentially toxic amounts of aspirin and has suicidal ideation but has no tinnitus or other neurological symptoms. Physical examination results show stable vital signs except for a temp of 38.8C; she has persistent tachypnea and mild epigastric tenderness but no rashes or previous cutting scars. Patient labs were consistent with a 12-hour salicylate level of 45 mg/dL, liver function, Bun/Creatinine, and coagulation profile are all normal. Her anion gap is slightly elevated, urine pH is 6, specific gravity is normal, and urine pregnancy test is negative. Based on patient history, physical exam, and labs, it appears that the patient has GI symptoms of early salicylate toxicity. Ingesting potentially toxic amounts of aspirin brings concern for life-threatening injuries to organs and possible loss of life. Let’s quiz ourselves with a short multiple-choice question: A teenager with a previous history of suicidal attempt now presents with confusion, increased respiratory rate, fever, and diaphoresis. Her physical exam including the pupillary exam is normal. Her labs are remarkable for a pH of 7.45, CO2 of 19, HCO3 of 11, serum anion gap of 20meQ/L, serum K of 2.9, and serum glucose of 180 mg/dL. There are weakly positive ketones in the urine. The next step in management of this patient is: A) NaHCO3 infusion B) Insulin infusion C) Oral activated charcoal D) Hemodialysis dialysis The correct answer to this question is A) Sodium bicarbonate infusion. Insulin therapy is not the answer because serum glucose is low, and a patient with a pH>7.25 is unlikely to have DKA. While activated charcoal can be used, especially followed by sorbitol given with the first dose, we need to be cautious about its use with an altered mental status as in the patient above. Since we do not have a salicylate level at this stage, offering hemodialysis should not be the first step, although it can be considered later given the neurological symptoms. Remember: Any patient with a previous history of suicidal ideation who presents with confusion, fever, and diaphoresis with the above labs is suggestive of mixed respiratory alkalosis with high anion gap metabolic acidosis is highly suggestive of aspirin poisoning. Always examine the pupils in any case of poisoning, as that may point one towards a possible toxidrome. Let’s highlight how basic science correlates with ASA poisoning: Remember the mechanism of action. Aspirin is a cyclo-oxygenase inhibitor which blocks prostaglandin production and has an antithrombotic effect by inhibiting platelet generation of thromboxane A2. Salicylates are weak acids which interfere with the Krebs cycle and specifically uncouple oxidative phosphorylation. This leads to acidosis, heat production, and hypoglycemia. Although not common, neuromuscular irritability manifested as paratonia (inability to relax muscles) and extreme muscle rigidity can develop, further contributing to hyperthermia and increasing the risk of rhabdomyolysis. Salicylates induce...

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Today’s episode is dedicated to the approach to thyroid storm. It’s the first in our Mini-Case series. Show Highlights: Our case, symptoms, and diagnosis: A 12-year-old female presents to the PICU with chest discomfort. She was noted to be anxious by her parents over the past few days. They felt she was a bit "off," as she would constantly drop items and have a tremor. A few weeks prior to these symptoms, she was noted to have rhinorrhea, congestion, and progressive neck swelling. Her parents became increasingly concerned this morning as her temperature was 104F. Per her parents, she was agitated throughout the night and became increasingly somnolent in the early morning. To summarize key elements from this case, this patient has: Chest pain likely due to a cardiac etiology or musculoskeletal cause. Tremor likely due to a primary neurologic cause or increased metabolic drive. Neck swelling with fever after a prodrome of URI symptoms which could be concerning for lymphadenitis or thyroid goiter. Synthesizing these symptoms together, this patient likely has a systemic etiology such as hyperthyroidism, with the most severe manifestation being thyroid storm, a toxidrome, or a pheochromocytoma. Given the fever and altered mental status, considering sepsis is key.

Key history features in this child with tachycardia and signs of hyperthyroidism: High fevers up to 104F Altered mental status Neck swelling

Red flag symptoms and physical exam components in a patient with severe hyperthyroidism include: Airway Check for dyspnea or stridor when the patient is supine. Do a Mallampati assessment. Auscultate for a bruit in the neck. Cardiovascular system Concerns include congestive heart failure and cardiac dysrhythmias. Widened pulse pressure is common

The American Thyroid Association has advocated for the Burch-Wartofsky Point Scale (BWPS) for severe thyrotoxicosis. A score of 45 or higher indicates thyroid storm. A case-control study published in 2015 in the Journal of Endocrinology noted that the BWPS may overdiagnose up to 20% of patients. Clinical criteria on the BWPS include the following: Thermoregulatory dysfunction Central nervous system effects Gastrointestinal-hepatic dysfunction Cardiovascular dysfunction Congestive heart failure Presence or absence of a precipitant history of URI or underlying thyroid condition

Back to our specific case, the patient's labs are consistent with low TSH and elevated free T4, indicating primary hyperthyroidism, positive for TSH-receptor antibodies, and the diagnosis of thyroid storm was confirmed. Other lab findings included elevated WBC, high ALT and AST, elevated glucose, and elevated cortisol. Her cardiac evaluation was notable for sinus tachycardia with occasional PACs. Other important labs include a coagulation panel, BNP and lactate, CRP, procalcitonin, blood cultures, and basic blood chemistries.

Let’s quiz ourselves with a multiple choice question: A patient with thyroid storm is admitted to the PICU. He is started on thyroid modulating therapy. Which of the following mechanisms of action does this medication likely work by? A. Activate Thyroid Peroxidase B. Inhibit Thyroid Peroxidase C. Inhibit Iodine Uptake within the Thyroid D. Increase conversion from T4 to T3

The correct answer is B. The most likely medication which is used in thyroid storm is methimazole or propylthiouracil. Both of these medications block thyroid peroxidase. In terms of differential in our case, you want to think about other causes of fever, tachycardia, and CNS dysfunction, including, but not limited to sepsis, serotonin syndrome, neuroleptic malignant syndrome, heatstroke, and drug intoxication. The diagnostic approach for our patient should focus on her history and physical examination. Be sure to include thyroid function tests, cardiac evaluation via EKG or Echo, chest x-ray, blood...

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We've got an exciting new series for the show and we can't wait to share with you our PICU Doc On Call Mini Case Series. Coming this weekend!

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Today's episode is dedicated to Critical Illness In Children With Hematopoietic Stem Cell Transplants. We are delighted to be joined by Dr. Muna Qayed, Associate Professor of Pediatrics Emory University School of Medicine , Atlanta, GA. She is also the Director of the Blood and Marrow Transplant Program at the Aflac Cancer and Blood Disorders Center at Children's Healthcare of Atlanta. Our Case: A 10 year old female with refractory high-risk ALL s/p mismatched unrelated donor transplantation T+13 days presents as a transfer to the PICU with abdominal distention, worsening jaundice, and escalating nasal cannula requirements. The patient's post-transplant course was complicated by gram-negative bacteremia requiring fluid resuscitation. A CXR upon transfer to the PICU is notable for bilateral airspace disease, a right sided pleural effusion, and hypoexpanded lung fields. The patient is promptly intubated, sedated and started on renal replacement therapy. Echo labs, and further imaging are pending. What are the classic pediatric indications for BMT? Autologous BMT (where donor cells are from the patient/recipient) is used as consolidation in some solid tumors such as High risk neuroblastoma, brain tumors like medulloblastoma, and germ cell tumors, and are a standard treatment approach in relapsed Hodgkin lymphoma Allogeneic BMT-where in the donor cells are derived from another individual are typically used for hematologic malignancies. ALL and AML are most common pediatric indications. Also allogeneic BMT are used for wide spectrum of nonmalignant hematology conditions such as hemoglobinopathies ( Sickle cell disease, Thalassemia), and severe aplastic anemia, and inherited bone marrow failure syndromes, as well as some metabolic disorders and immune-deficiency disorders such as SCID, HLH and other primary immune regulatory disorders.

The sources of graft in BMT? Stem cells (which give rise to different types of blood cells - red cells, white cells and platelets are derived from the bone marrow. Thus the overall process is known as Bone Marrow Transplantation. Stem cells can be also derived from peripheral blood - when the donor is treated with granulocyte colony stimulating factor or G-CSF. There are some key advantages here, which include the ability to collect a much higher stem cell dose, with faster hematopoietic recovery. However the downside is a higher T cell content of the graft with subsequent increased risk of graft versus host disease. Umbilical cord blood is also used as a source of stem cells. Mega doses of stem cells are used to overcome histocompatibility barriers of mismatched transplantation. Majority of T cells have to be removed from donor pool to prevent severe GVHD., Increase risk of infection and relapse of patients original disease.

Explain the human leucocyte antigen (HLA) and its role in BMT? The Major Histocompatibility complex (MHC) system known as the human leukocyte antigen (HLA) in humans is located on the short arm of chromosome 6 and contains the most polymorphic gene cluster of the entire human genome. The HLA consists of regions designated as "classes". Class I and class II are relevant to stem cell transplant. The main function of HLA class I gene products (HLA-A, -B, and -C) is to present endogenous peptides to responding CD8+ T Cells, HLA class I antigens are expressed on all nucleated cells and platelets. While the class II coded molecules HLA-DR, -DP, and –DQ have restricted expression and process exogenous peptides for presentation to CD4+ helper T Cells, and are expressed on antigen presenting cells. HLA-A, HLA-B, HLA-C and HLA-DR are traditionally the loci critical for matching for stem cell donor. In addition to deciding on the source of the graft, we have to make decisions on who the donor will be. If a matched sibling donor is not available (or in some inherited conditions that may not be an option as a donor), then matched unrelated donors or matched cord...

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Today's episode is dedicated to the approach to the unstable neonate. Join us as we discuss the anatomic and physiological considerations for the neonate, initial investigations, and management framework on stabilizing a child. We are delighted to be joined by Dr. Michael Wolf, Associate Professor of Pediatrics at Emory University School of Medicine, and Associate Medical Director of the Cardiac Intensive Care Unit at Children's Healthcare of Atlanta. The CICU at Children’s is one of the highest volume pediatric heart centers in the nation. Dr. Wolf is also Chair of the "You Matter Program" at Children's Healthcare of Atlanta, which addresses physician resilience and second victim syndrome in providers. Show Highlights: Our case, symptoms, and diagnosis: A 4-day-old former full-term neonate delivered via C-section for non-reassuring fetal heart tones is to be discharged from the well-child nursery. On the day of discharge, the child is noted to have progressive tachypnea, tachycardia, and progressive acrocyanosis. The extremities are cool, and the child has delayed capillary refill. Pulse-oximetry is notable for a discordance between upper and lower extremity saturations. Femoral pulses are poorly palpable. Blood gas is significant for metabolic acidosis. The patient is rushed to the NICU, and the process to transfer the baby to a pediatric cardiac intensive care facility is initiated. Important considerations to keep in mind for the neonatal or infant population are according to the traditional Airway-Breathing-Circulation model: Airway--The infant airway is prone to dynamic obstruction due to a larger tongue and epiglottis, compliant soft tissues, and their obligatory nose breathing. Breathing--Differences in chest wall dynamics, oxygen metabolism, and respiratory musculature place the small infant at greater risk for respiratory failure than the older child. Cardiac--Considerations focus on key events in the transition from fetal to neonatal circulation, and include the initiation of prostaglandins and calcium administration to drive contractility.. Shock categories to consider for the neonate include hypovolemic shock from hemorrhage, obstructive entities like severe pulmonary hypertension, and septic shock. Initial stabilization of the neonate includes the following lab testing and imaging: blood gas and glucose determination, basic electrolytes, vital signs and clinical exam data, and prostaglandin infusions to reestablish blood flow. The loop of intervention and reassessment is imperative as you acutely stabilize a child with neonatal shock! Other key diagnostics include four extremity blood pressure and low extremity pulses, pre- and post-ductal saturations, bedside echocardiography, and delving into the history with prenatal screening. The management framework focuses on prostaglandins and dosage protocols, the availability of intubation equipment, and the risk of necrotizing enterocolitis (NEC). Besides congenital heart defects, other considerations for the unstable neonate are sepsis, infusions of ionotropes, cardiac catheterizations, and possible balloon valvuloplasty. Takeaway clinical pearls regarding the unstable neonate: Always think about prostaglandins when approaching the neonate with shock. Use a physical exam to check pulses and blood pressure. Remember that a focused, rapid, bedside echocardiogram can help diagnose shock. We hope you learned something from today’s discussion of the importance of a broad differential, key presentation features of congenital heart disease, and the importance of early PG initiation in the management of an unstable neonate.

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Today’s episode is dedicated to venous/arterial thrombi, also known as catheter directed thrombolysis. We are delighted to be joined by Dr. Anne E. Gill, Assistant Professor of Radiology and Imaging Sciences at Emory University School of Medicine. She is a pediatric interventional radiologist at Children’s Healthcare of Atlanta. Her areas of expertise include pediatric thromboembolic disease, vascular malformations, enteric feeding tube access, and interventional oncology. Dr. Gill is on Twitter @AnneGillMD. Show Highlights: Our case, symptoms, and diagnosis: A 17-year old girl with antithrombin III deficiency presented with bilateral leg pain to an outside ED. Duplex ultrasound of the bilateral lower extremities revealed extensive acute bilateral deep vein thrombosis. A CT scan of the abdomen and pelvis showed an extensive occlusive clot in the inferior vena cava involving the infrarenal and suprarenal IVC. She was transferred to our hospital and admitted to the ICU for thrombolysis and initiation of catheter-directed TPA infusion. In interventional radiology, an IVC filter was placed in the suprarenal IVC; additionally, the venogram in IR showed complete thrombosis of the right upper femoral, external iliac, common iliac, and IVC, with collateral veins in the right lower extremity draining into the thrombosed upper femoral vein. Interventional radiology performed pharmacomechanical thrombolysis and balloon angioplasty of right external iliac, common iliac, and IVC and placed infusion catheter to drip tPA from right femoral vein to the IVC filter. The patient was also placed on continuous heparin drip for systemic anticoagulation management. Morphine and Dexmedetomidine were used for pain management. The overall prevalence of systemic venous occlusion in children is difficult to ascertain due to their asymptomatic quality. Congenital SVOs in children can be due to developmental hypoplasia or agenesis of major conducting veins; they can happen in utero or manifest as neonatal thrombosis. Acquired causes of SVOs can include catheter acquired obstruction, hypercoagulability/thrombophilia, mechanical obstruction, and trauma. A careful history is necessary to determine whether the occlusion was a congenital or acquired SVO. This is challenging because symptoms of venous obstruction in children may not present until later in life. This distinction is important as it affects the procedures that can be done. Better outcomes are possible if a native pathway is present, even if it’s diminished from chronic obstruction and scarring. Clinical presentations of systemic venous occlusions in children include head and neck swelling coupled with shortness of breath. In patients with acute DVT, venous congestion can manifest as prolonged capillary refill, coolness of extremities, and bluish discoloration to frank venous ischemia with loss of pulses. Chronic DVT in extremities can present with a sense of heaviness, aching pain, and fatigue with activity; these symptoms are collectively described as post-thrombotic syndrome. Remember that obstruction to flow can compromise oxygen delivery! Common causes of venous occlusions are mal-positioned or wrongly sized central venous catheters, May-Turner syndrome, and long-standing central venous access lines in dialysis patients. CDT is not recommended for DVTs below the inguinal ligament, based on the ATTRACT trial in 2017 that showed that CDT is most beneficial in veins above the inguinal ligament. Contraindications for CDT in children include allergy to tPA, active bleeding, surgery within the last 14 days, any invasive procedures in the last three days, recent seizures, recent trauma, or coagulopathy which can’t be easily corrected. Caution is needed with premature infants and those with HTN or other risk factors for bleeding. Diagnostics needed prior to consulting on a patient with venous occlusion include Doppler US, CT or MRI to visualize...

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Today’s episode is dedicated to the differentiation and management of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) We are delighted to be joined by Dr. Eric Felner. Dr. Felner is a Professor of Pediatrics/Pediatric Endocrinology at the Emory University School of Medicine and is an Adjunct Professor of Chemical and Biomedical Engineering at Georgia Tech. Show Highlights: Our case, symptoms, and diagnosis: A 15-year-old male presents with a one-week history of increased urination. He is otherwise healthy except for a viral URI last week. He is found to be disoriented and tachycardic, with an exam notable for delayed peripheral capillary refill and cool extremities. The patient has deep, labored respirations upon examination, and labs confirm hyperglycemia with a serum glucose of 850, mild acidosis, and 2+ ketones. His CPK level is elevated, and a crystalloid fluid bolus is started. Hyperosmolar hyperglycemic state is defined as a serum glucose greater than 600 mg/dL, serum osmolality of 330 mOsm/kg, and the absence of ketosis and acidosis. The key difference between HHS and DKA is that DKA is characterized by the presence of ketones in the blood and acidosis, but HHS means these are completely absent. Even though DKA and HHS are similar, their management strategies have their own nuances. In DKA, the lack of insulin leads to management strategies, while HHS is marked by complete dehydration and excessive urination. Factors that point to HHS will be a very overweight child, family history, and ethnicity; Type-2 diabetes is much more common in African-American, Latin-American, and Native-American children, while Type-1 is more common in Caucasians. Specific labs for patients with suspected DKA or HHS include a comprehensive metabolic panel (CMP), blood gas, and CPK for HHS. For both conditions, management strategies focus on insulin and fluid administration, but there are key differentiations: DKA is managed using the triple bag therapy that was pioneered by Dr. Felner. There is a risk for cerebral edema with administering fluid. The most important data relating to fluid administration with regard to neurological outcomes is what we have learned in calculating fluids with the “2x maintenance formula” to guard against mistakes that could result in cerebral edema. Key considerations regarding low-dose vs. standard-dose insulin therapy revolve around the weight and age of the pediatric patient. For HHS, the key is to manage fluids and give insulin; for Type-1 diabetics, the key is to eliminate acidosis. Key PICU management pearls in minimizing cerebral edema risks are to determine the level of sickness by the PCO2 level, high BUN, and by not giving bicarbonate. Remember that children under age 5 have a higher risk for cerebral edema. In the management of both DKA and HHS, remember that it comes down to how sick a patient is and not necessarily following the numbers. In general pediatrics, managing a sick DKA patient means giving an IV, administer fluids, and call a specialist management team right away. Dr. Felner discusses the association between COVID-19 and Type 1 diabetes based on his experience. As intensivists and endocrinology teams work together to transition patients to an intermittent insulin regimen, it’s important to remember how to convert from IV insulin to subQ insulin. Takeaway clinical pearls include the key diagnostic elements between DKA and HHS. In HHS, patients will have higher glucose levels, milder acidosis, mild ketosis, and increased dehydration. Both conditions will have insulin and fluid management, and HHS patients may require increased fluid resuscitation.

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Today, we welcome Dr. Stella Shin, Assistant Professor of Pediatrics-Pediatric Nephrology at The Emory University School of Medicine. Dr Shin is also the Director of General Pediatric Nephrology and the Director of Acute Kidney Replacement Therapy at The Children's Healthcare of Atlanta in Atlanta, GA. Her interests include nephrotoxic medication stewardship, health informatics and healthcare quality improvement. She is on twitter @BabyBeanDoc A 17 year old previously healthy thinly built male teenager is brought to the emergency department for sudden development of blurred vision. Patient has a h/o headaches for the last few months accompanied by abdominal pain and relieved by vomiting. He has also felt his heart racing during such episodes and accompanied by profuse sweating. Patient had tried various over the counter pain medications without much improvement in his headaches or abdominal pain. An initial CT scan of the head reveled no intracranial pathology. ED physician noted a a blood pressure of 200/120 mm HG and a pulse of 132beats/minute. He is started on nicardipine in the ICU. Definitions for normal and high blood pressure come from the AAP clinical practice guidelines for screening and management of high blood pressure. According to these guidelines: Normal BP is a blood pressure reading that is < 90%ile for children 1-12 yrs of age: A normal BP for teenagers 13 years and older = <120/<80. High blood pressure is divided into three categories: Elevated BP, Stage 1 HTN, and Stage 2 HTN. This is further delineated into categories for children 1-12 yo and 13 or older. For children 1-12 yo: Elevated BP is a BP that is >/= 90%ile but <95%ile, or a BP of 120/80 up to <95%ile, whichever is lower. Stage 1 HTN is a BP that is ≥95%ile to <95%ile+12 mmHg, or a BP of 130/80 to 139/89, whichever is lower. Stage 2 HTN is a BP that is ≥95%ile+12 mmHg, or a BP that is ≥140/90, whichever is lower. It's much more simple for children 13 and older: Elevated BP is 120/<80 to 129/<80 Stage 1 HTN is 130/80 to 139/89 Stage 2 HTN is >/= 140/90 That's a lot of numbers and cut offs to remember. To make it easy, in general, hypertension in children and adolescents is defined as a sustained systolic and/or diastolic blood pressure elevation ≥ 95%ile for age, gender, and height. And adult BP cut offs are used for teenagers 13 years or older.

Acute severe hypertension is defined as significant blood pressure elevation with or without of acute target-organ damage from the hypertension. This is further classified based on target organ involvement into hypertensive urgency and hypertensive emergency. The key difference between the two is whether target organ injury is present. Hypertensive Urgency is acute severe hypertension WITHOUT acute target-organ damage. Hypertensive urgency is not associated with adverse short-term outcomes and can be managed in the ambulatory setting. Hypertensive Emergency is acute severe hypertension that is accompanied by acute target-organ injury. It is a medical emergency with substantial morbidity and mortality requiring immediate treatment in an ICU. It is important to note for our listeners that acute sever hypertension is on a spectrum with hypertensive urgency and emergency, and these diagnoses exist on a spectrum! Our discussion focused on acute severe hypertension, which is a medical emergency especially when there is target organ injury. A titratable infusion of an antihypertensive such as nicardipine should be the first line to lower the BP by 25% in first 8 hours as precipitous drop may cause cerebral ischemia. While there are multiple IV antihypertensives, the pediatric critical care team should be should be aware of the pharmacology and relevant side effects of these agents in efforts to choose the best drug for the patients condition. Early consultation with nephrology is warranted in these patients along with monitoring of end organ function.

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Today’s episode is dedicated to acute management of hyperkalemia in the PICU. Join us as we discuss the patient case, symptoms, and treatment. We are delighted to be joined by Dr. Roshan George, Associate Professor of Pediatrics, a practicing Pediatric Nephrologist at Children’s Healthcare of Atlanta, and the Program Director of Pediatric Nephrology Fellowship at Emory University School of Medicine. Show Highlights: Our case, symptoms, and diagnosis: A two-year-old male with a history of focal segmental glomerulosclerosis controlled on chronic prednisone therapy presents to the PICU for respiratory failure. The patient is noted to be hypotensive and tachycardic. Potassium is elevated at 6.4 with no hemolysis noted. The EKG is notable for peak T waves, and the patient is also noted to be anuric. Definition of hyperkalemia: a potassium serum level higher than 5.5 (Be sure to correlate your lab sample with clinical and telemetry changes to rule out pseudohyperkalemia) Common causes of hyperkalemia: Increased intake of potassium Transcellular shift Decreased renal excretion Inborn error of metabolism, especially adrenal problems Why it’s important to be vigilant about hyperkalemia in patients with chronic kidney disease, end-stage renal disease, acute kidney injury, and those with a transplanted kidney Clinical manifestations of hyperkalemia: The risk is for cardiac conduction abnormalities and muscle weakness/paralysis. Adverse events can occur with levels > 5.5mEq/L, and the risk increases as levels rise. Any serum K level > 6mEq/L is significant, regardless of EKG changes. Two hallmarks that can drive effective management of hyperkalemia are EKG findings and laboratory confirmation of elevated serum potassium. Other important labs for patients with hyperkalemia include a basic electrolyte panel to assess kidney function, CBC, and serum blood gas to assess acid/base balance. (A medication check for K supplements or ACE inhibitors should also be done.) Steps in the management of hyperkalemia: First, caution should be exercised that any K level > 5.5 is a medical emergency and should be addressed immediately without finding the etiology. Stabilize the cardiac membrane. Shift potassium with insulin and glucose, bicarbonate, and B2 adrenergic agents. The long-term goal should be to improve excretion with Kayexalate or Furosemide (Remember the mnemonic: “Loops lose K.”) General considerations about dialysis are: CVVH vs. HD Severe hyperkalemia is a key indication for RRT in acutely ill patients. Hemodialysis can be used in an emergency. Takeaway clinical pearls regarding hyperkalemia: Make sure the potassium level is accurate. Consider the next steps in potassium removal. Remember that etiology is the last step.

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Today’s episode is dedicated to the intubation of the critically ill pediatric patient. Join us as we discuss the patient case, symptoms, and treatment. We are delighted to be joined by Dr. Heather Viamonte. Dr. Viamonte is an Assistant Professor of Pediatrics at Emory University School of Medicine. She is a Pediatric Cardiac Intensivist at the Children’s Heart Center and the Director of Cardiac ECMO. The Children’s Heart Center is a 30-bed, dedicated cardiac intensive care unit at the Children’s Healthcare of Atlanta at Egleston. She is a newly published author whose book, Wilde Type, has already been released, and a second novel is on its way to publication. Dr. Viamonte is on Twitter as @hk_jacobs. Show Highlights: Our case, symptoms, and diagnosis: A four-month-old patient is admitted to the PICU from the emergency department for acute respiratory failure on high-flow nasal cannula. The child’s condition has slowly deteriorated over the last few hours and now requires intubation. An echo is performed pre-intubation due to enlarged cardiac silhouette on chest radiograph demonstrating left ventricular dysfunction with ejection fraction in the low 40s. The patient’s saturations are dipping to the mid-80s despite being on maximal HFNC support. Common indications for intubation in the PICU or CICU include acute respiratory failure, upper airway obstruction, hemodynamic instability, management of increased ICP, mediastinal masses, protection of the airway, as well as for procedures and safe transport. Patient conditions with a high risk prior to endotracheal intubation include congenital or acquired heart disease, an infant or child with hemodynamic instability, pulmonary hypertension, upper airway obstruction, increased ICP, and mediastinal masses. Factors in infants and children with congenital heart disease that make them high risk for intubation include anatomical or physiologic issues that could lead to cardiac arrests, such as systemic ventricular dysfunction, single ventricle physiology, arrhythmias, pulmonary hypertension, and coronary artery anomalies. Why an understanding of the patient’s past medical history and overall physiology are important for risk stratification Anatomical concerns that should be assessed in infants and children prior to intubation include genetic syndrome heart defects that could interfere with bag-mask ventilation, airway visualization, or laryngoscopy. These could include morbid obesity and abnormalities of the face, mouth, and teeth. In conceptualizing congenital heart defects prior to intubation, the overriding concern is blood flow to the heart and lungs. Three factors to consider are volume overload, pressure overload, and systemic hypoxemia. Patients can have anatomical and physiological difficulties with regards to airway management, especially in those who are critically ill and those with cardiac disease. Four important clinical scenarios for physiologic derangements are hypoxemia, hypotension, metabolic acidosis, and congenital heart lesion pathophysiology. Remember that infants and children have a higher fragility factor and are at a higher risk for rapid desaturation, hypoxic brain injury, and cardiac arrest. Key factors for the intensivist are fine attention to detail, optimizing your monitoring equipment, and anticipating risk factors for peri-intubation cardiac arrest. Special considerations with intubation for the patient with severe metabolic acidosis are necessary to prevent cardiovascular collapse and pulmonary hypertension. How systolic dysfunction from either ventricle plays into the process of intubation Factors to consider to mitigate risk in intubation include preparation, a multidisciplinary approach, intubation equipment nearby, and management of the post-intubation period. Dr. Viamonte shares her perspectives on sedation and other medications to consider with intubation. Takeaway clinical pearls regarding intubation...

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Today’s episode is dedicated to the acute management of anterior mediastinal mass in the PICU. Join us as we discuss the patient case, symptoms, and treatment. We are delighted to be joined by Dr. Lisa Lima and Dr. Tom Austin. Dr. Tom Austin is the Director of General Pediatric Anesthesiology at Children’s Healthcare of Atlanta-Egleston. He is also an Associate Professor of Anesthesiology and Pediatrics at Emory University School of Medicine. Dr. Lisa Lima is a Fourth Year Advanced Technology Fellow in the Division of Critical Care at Children’s Healthcare of Atlanta. She’s also the Senior Associate in the Department of Pediatrics at Emory University School of Medicine. She’s one of the only pediatric-trained ECMO Fellows in the country. Show Highlights: Our case, symptoms, and diagnosis: A 17-year-old female has facial swelling and shortness of breath. She recently went to her primary care physician and received a steroid burst and Benadryl for the facial swelling. On the day of admission, her mother noticed that the patient had a deep voice and a “funny” inspiratory sound. The patient presented to the ER and was noted to have a widened mediastinum on a chest x-ray, bringing up concern for an anterior mediastinal mass. Key presentation features for mediastinal masses What defines a widened mediastinum? Important differentials to consider with mediastinal masses: Take the patient’s history and presentation into context, like if there was a high-impact motor vehicle collision, history of congestive heart failure, lupus, transplant, leukemia, or lymphoma Pay attention to the Four T’s: thymoma, teratoma, ATLL(lymphoma), and thyroid masses Key principles that might put pediatric patients with mediastinal masses at risk for anesthetic agents Important pathophysiologic issues for patients with mediastinal mass include compressed trachea, blocked access to lungs, and right ventricular failure; these effects can be magnified under general anesthesia Why we need to have great appreciation of the risk of cardiovascular collapse in patients in a tenuous physiological state General management strategies for those patients who are unable to lie flat or may not tolerate a diagnostic scan: patient history, personal physical exam, determining a rescue position Key considerations for the patient in the PICU: Keep the patient spontaneously breathing Have adequate access with large-bore IVs in sites with no anatomic compression Have a rescue position Have a backup plan for rapid deterioration Communicate with others on the patient care team Why the Chamberlain procedure is used to obtain a tissue biopsy when there isn’t another primary biopsy site Key anesthesia principles for patients needing intrathoracic biopsies: Have clear role assignments in the multidisciplinary team approach Keep the patient spontaneously breathing Manage the patient’s pain Employ liberal use of local anesthetics Avoid intubation if possible If necessary, use fiber optic intubation Keep large-bore IVs in extremities Why it’s important to stress interdisciplinary involvement early in management Key factors to consider in patients headed to the OR about airway compression and vascular compression Takeaway clinical pearls regarding anterior mediastinal masses: Remember the Four T’s The pathophysiology of local compression Emphasize a streamlined multidisciplinary approach with important considerations for contingency planning

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Today’s episode is dedicated to Tumor Lysis Syndrome management in the PICU. Join us as we discuss the patient case, symptoms, and treatment. We are delighted to be joined by Dr. Himalee Sabnis, Assistant Professor of Pediatrics at Emory University School of Medicine. She is also a pediatric hematologist/oncologist and the Co-Director of the High-Risk Leukemia Team at the AFLAC Cancer & Blood Disorders Center at Children’s Healthcare of Atlanta. Show Highlights: Our case, symptoms, and diagnosis: A three-year-old female with pre-B ALL presents on Day 2 of chemotherapy to the PICU. She is admitted with telemetry findings of arrhythmia, decreased urine output, and an EKG notable for peaked T waves. Her labs are notable for elevated WBC, hyperkalemia, hyperphosphatemia, and low ionized calcium. Tumor Lysis Syndrome is a life-threatening medical emergency stemming from rapid tumor cell destruction that overwhelms the usual metabolic and excretory pathways. Why TLS is the most common pediatric oncologic emergency for pediatric cancer patients When the tumor cells die or lyse, what’s inside those cells comes out into the blood Key metabolic abnormalities that affect organ function are too much potassium and phosphorus, low calcium, and uric acid buildup. Those metabolic abnormalities can result in cardiac arrhythmia and kidney failure. Certain patient populations have an increased risk for TLS: Hematological cancers have a higher risk than solid tumors Patients with fast-growing tumors, like lymphoma and leukemia, are at high risk Key pathophysiologic principles that drive TLS: The imbalance of electrolytes can impact heart function TLS is characterized by hyperkalemia, hyperphosphatemia, hypocalcemia, and uric acid, which is a by-product of DNA breakdown If untreated, the uric acid can lead to acute kidney injury and renal failure Electrolyte and metabolic disturbances can progress to renal insufficiency, cardiac arrhythmias, seizures, and death TLS releases cytokines that can cause a systemic inflammatory response and multi-organ failure Other lab markers in patients with TLS include uric acid, LDH, CBC, DIC panel, and daily blood gas (these are typically trended every 4-6 hours). Key factors in TLS management are to understand the risk and know your resources. Steps taken would be continuous cardiac monitoring, uric acid control, administering Allopurinol to combat uric acid formation, and managing electrolyte disturbances in conjunction with an intensivist. Chemotherapy would not be delayed due to TLS because the patient’s condition won’t improve until the cancer is treated. How the complications of TLS are treated: Hyperphosphatemia should be treated by using oral phosphate binders such as aluminum hydroxide. Hypocalcemia does not require therapy unless cardiac function is affected. How renal replacement therapy might be required and indications are similar to other forms of acute kidney injury. Besides Allopurinol being given at the initiation of chemotherapy, patients at high risk for TLS may receive low-intensity initial therapy to prevent rapid cell lysis. Takeaway clinical pearls regarding TLS: Know what you’re dealing with because every cancer is different. Fluid management is important and will vary from patient to patient. Be proactive in monitoring. Intervene early and quickly.

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Today’s episode is dedicated to post-operative management in the PICU of the pediatric renal transplant patient. Join us as we discuss the patient case, symptoms, and treatment. Joining the conversation is Dr. Rouba Garro, Associate Professor of Pediatrics at Emory University School of Medicine and the Medical Director of the Kidney Transplant Program at Children’s Healthcare of Atlanta. Children’s Healthcare of Atlanta has one of the largest kidney transplant programs in the country and is the largest in the Southeast US with excellent patient and graft survival. Show Highlights: Our case, symptoms, and diagnosis: a five-year-old is transferred to the PICU after a related living kidney transplant for end-stage renal disease due to obstructive uropathy. The patient has a history of post-urethral valves and is on room air, IV fluids, an arterial line, and a Foley catheter is in place. The top indicators for renal transplant in pediatrics vary according to age, but congenital anomalies are the most common in children younger than six. The criteria for being considered for kidney transplantation include several factors, including when kidney function drops below 20%. The keys for successful transplantation: An experienced pre-transplant team A robust and experienced team for perioperative care and graft outcome A comprehensive and multidisciplinary post-transplant team The process of organ procurement for cadaveric and living donor renal transplants includes the following: Multiple factors determine the points a patient receives toward transplant priority Deceased donor kidneys are classified using the KDPI (kidney donor profile index) A thorough evaluation is performed for living donors Advantages to living donation include a shorter time on dialysis and waitlists, improved graft survival, and shorter ischemia time than from a deceased donor Information from the operating team that is vital for the PICU team to know for post-op success includes patient history, transplant details, ischemia time, and transplant complications. Red flags for the critical care post-op team are in the three categories of blood pressure, urine output, and kidney function/electrolytes. The need to watch for signs of infection in the post-op phase How immunosuppressive medications might be used for the pediatric renal transplant patient Why the post-op transplant patient might need dialysis Clinical pearls for post-op care of the pediatric renal transplant patient in the PICU: Teamwork and collaboration are key elements for success. The most important task is to monitor blood pressure, urine output, and electrolytes.

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Today’s episode is dedicated to post-operative management of liver transplant patients in PICU. Join us as we discuss the patient case, symptoms, and treatment. Joining us is Dr. Joe Magliocca, Associate Professor of Surgery in the Department of Surgery at Emory University School of Medicine. He is also the Surgical Director of Adult and Pediatric Liver Transplantation at Children’s Healthcare of Atlanta. Also joining the conversation is Dr. Rene Romero, Professor of Pediatrics at Emory University School of Medicine and Medical Director of the Liver Transplant Program at Children’s Healthcare of Atlanta, which is one of the largest liver transplant programs in the country with over 600 pediatric liver transplants to date. https://www.dropbox.com/s/bktel3qza7y50j4/Post%20Op%20Liver%20Transplant.jpg?dl=1 (>>Click here to download the PICU card for this episode<<) Show Highlights: Our patient, symptoms, and treatment: An 18-month-old with a history of biliary atresia is admitted to PICU after an orthotopic whole liver transplant. The patient is intubated, and Doppler ultrasound shows vascular patency post-operatively. AST and ALT are pending. Common indications for pediatric liver transplantation: 500-700 pediatric liver transplants are performed annually in the US 40% of the transplants are done on children born with biliary atresia 10-15% of the transplants are due to acute liver failure 5% of the transplants are due to malignancies The rest of the transplants are due to different childhood diseases and metabolic diseases How the PELD (Pediatric End-Stage Liver Disease in children under 12) score relates to prioritization for liver transplant Criteria for the PELD score are bilirubin, albumin, age, growth parameters, and INR The major differences between whole organ vs. split liver transplantation (long-term outcomes are similar and good for both situations) Why liver transplantation requires less immunosuppression than other organ transplants Three phases of the liver transplant process are the hepatectomy phase, anhepatic phase, and reperfusion phase Specifics of the time intervals during the transplant process, where the major risk is for primary non-function during cold ischemia and warm ischemia times Major red flags to look for during the immediate post-operative period Acute post-op management includes extubation in the OR, CV monitoring, pain management, checking urine and electrolyte levels, and communication with the transplant surgeon and liver team How treatment and management have evolved over time with standardized post-op management, protocols, and parameters Two important aspects of post-op management are nutrition and immunosuppression Clinical pearls of wisdom: The need for organ donors is great. Teamwork and collaboration are essential for good patient outcomes. The transformation in the field of liver transplantation has saved many children’s lives.

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Today’s episode is dedicated to pediatric acute liver failure. Join us as we discuss the patient case, symptoms, and treatment. Joining the conversation is Dr. Rene Romero, Professor of Pediatrics at Emory University School of Medicine and the Medical Director of the Liver Transplant Program at Children’s Healthcare of Atlanta. https://www.dropbox.com/s/qz4v8pctqc0k6ri/Acute%20Liver%20Failure.jpg?dl=1 (>>Click here to download the PICU card for this episode<<) Show Highlights: Our case, symptoms, and diagnosis: a three-year-old child presents in the PICU with decreased arousal; the patient is hypoglycemic. The coagulation panel is significant for increased PTT and INR, and AST and ALT are significantly elevated. The patient is hyperammonemic, and the acetaminophen level is normal. The diagnosis is acute liver failure. Basic functions of the liver, the “workhorse of the body” that plays major roles in interactions with other organs Why pediatric acute liver failure is more difficult to diagnose than in adults; key indicators are coagulopathy along with biochemical disruptions The most important contributing factors to pediatric acute liver failure, and why most pediatric cases are children under four years of age Causes of pediatric acute liver failure in the US include HSV, adenovirus, enterovirus, metabolic causes, and acetaminophen, especially in older children The diagnostic approach considers infectious etiologies, toxins, vascular issues, and immune dysregulation In treatment, care should be given to the correction of abnormal lab values and possible renal replacement therapy Why the use of prophylactic antifungal antibiotics is controversial and varies from institution to institution How to discern hyperammonemia and neurologic status The role of intracranial pressure monitoring for cerebral edema, which is the mode of death for these patients Key Clinical Pearls: acute liver failure is a systemic disease that requires a broad diagnostic approach, and the need for standardized approaches still exists.

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Today’s episode is dedicated to acute metabolic emergencies. Join us as we discuss the patient case, symptoms, and treatment. Joining us is Dr. Lori-Anne Schillaci, trained in clinical pediatric genetics with additional training in metabolism. She had a dual appointment in the Department of Pediatric Emergency Medicine at Rainbow Babies and Children’s Hospital, as well as an appointment in the Department of Genetics and Metabolism. Dr. Schillaci is currently embarking on a fellowship in Pediatric Emergency Medicine at Wake Forest Brenner Children’s Hospital. https://www.dropbox.com/s/4439vvu5794g5n2/Acute%20Metabolic%20Emergencies.png?dl=1 (>>Click here to download the PICU card for this episode<<) Show Highlights: Our case: A three-month-old infant presents with seizures and decreased oral intake History, symptoms, and treatment: The child is hypothermic and tachypneic. Blood gas is notable for anion-gap metabolic acidosis. Blood cultures are drawn, and antibiotics are started. Urine organic acids and serum ammonia are both pending. A metabolic emergency is defined as a defect in the breakdown or storage of the body’s energy sources (sugar, fat, and protein) at the cellular level Why metabolic conditions can be inherited or result from a spontaneous mutation How the toxic products form in the body and can affect children in three categories (protein, fat, and sugar metabolism) Common lab tests would be for ammonia, gas, and blood sugar Why the physician should save a purple top tube before any transfusion General management should include treatment of the underlying acute issues, early dextrose fluids, normal saline fluid boluses, IV lipid emulsion (except in patients with known fatty acid oxidation defects) Advice to colleagues in managing a patient with inborn error: Keep in mind that the presentation can occur in older kids Get early labs when they are sick Start high dextrose fluids Keep the patient NPO Treat fever, hypoglycemia, seizures, infection, etc. The goal is to prevent catabolism and be aggressive early in treatment Dr. Schillaci’s final thoughts: “Be vigilant. Assume an inborn error of metabolism unless proven otherwise. Be aware of late presentations of inborn errors of metabolism.”

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Today’s episode is dedicated to PICU applications of lipid emulsion therapy. Join us as we discuss the patient case, symptoms, and treatment. Joining us is Dr. Ziad N. Kazzi, Associate Professor of Emergency Medicine at Emory University School of Medicine, Director of the International Toxicology Fellowship Program at Emory, and Assistant Medical Director of the Georgia Poison Center. Dr. Kazzi is also a board member of the American College of Medical Toxicology and current president of the Middle East North Africa Toxicology Association. https://www.dropbox.com/s/htbyhre5zictxke/Lipid%20Emulsion%20Therapy.jpg?dl=1 (>>Click here to download the PICU card for this episode<<) Show Highlights: Our case: a 14-year-old girl has been admitted to PICU after acute ingestion of the calcium channel blocker Amlodipine in a suicide attempt Symptoms: profound hypotension Acute management: After fluid resuscitation, norepinephrine infusion, and high-dose insulin therapy, lipid emulsion therapy is considered How lipid emulsion therapy began How lipids work in the toxicology realm Applications in PICU for indicators and efficient doses of lipid emulsion therapy Examples of cases that call for lipid emulsion therapy Considerations of propofol as a substitute for lipid emulsion therapy To minimize complications from lipid emulsion therapy, pay attention to dosing guidelines, limit the duration of the infusion, and focus on systemic toxicities Final thoughts: Know when to use (and when not to use) antidotes and be aware of publication bias with any studies

Resources: Download the PICU Card for this episode https://www.dropbox.com/s/htbyhre5zictxke/Lipid%20Emulsion%20Therapy.jpg?dl=1 (here) http://www.lipidrescue.org (www.lipidrescue.org)

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Today’s episode is dedicated to the acute management of pediatric stroke. Join us as we discuss the patient case, symptoms, and treatment. Joining us is Dr. Elissa Ortolani, Assistant Professor of Pediatrics in the Division of Child Neurology and Assistant Professor of Neurology at Emory University School of Medicine. Dr. Ortolani has a strong clinical interest in pediatric vascular disease and is one of the few pediatric neurologists who has completed a formal adult stroke fellowship. She is actively helping to develop a pediatric stroke program at Children’s Healthcare of Atlanta. https://www.dropbox.com/s/2c31vmoubh7w5a6/Pediatric%20Stroke.jpg?dl=1 (>>Click here to download the PICU card for this episode<<) Show Highlights: Our case: a five-year-old male, previously healthy, has had cold symptoms for two days; he presents to the ER with possible stroke symptoms Symptoms: the patient has had left arm and left leg weakness during the past day, and his mother noticed a subtle left side lip droop with drooling Acute management: In the ER, a CT revealed a subtle hypodensity in the right basal ganglia region; the patient was admitted to PICU for further monitoring and workup Causes of an acute pediatric vascular event can include stroke, seizure, migraine, and toxidrome Definition of stroke: an acute neurologic change identified by advanced imaging Practical tools in evaluating stroke include F-facial droop, A-arm weakness, S-speech difficulty, T-time. (Now, amended to FASTER to include stability and eyes/vision) Risk factors for pediatric stroke include vascular issues like sickle cell disease, congenital heart problems, thrombophilia, and mitochondrial, inflammatory, or connective tissue disease In pinpointing pediatric stroke or stroke mimic, which is very common, MRI is the preferred imaging method Important considerations in the diagnosis of pediatric stroke are that mild sedation is sufficient for the 10-12 minutes needed for MRI In the management of pediatric stroke, TPA should be administered within 4.5 hours, and endovascular therapy (if needed) should be administered within 24 hours Why the diagnosis and management of pediatric stroke is delayed, and how ER and ICU physicians can change that Developing a pediatric stroke program is a collaborative effort among emergency care providers, radiologists, pharmacists, adult neuro interventionalists, ICU team, neurosurgeons, hematologists, and rehab physicians A key in the diagnosis of pediatric stroke is recognizing altered mental status

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Today’s episode is dedicated to acute management of laryngospasm. Join us as we discuss the patient case, symptoms, and treatment. Joining us is Dr. Tom Austin, director of General Pediatric Anesthesiology at Children’s Healthcare of Atlanta-Egleston. He’s also an associate professor of anesthesia and pediatrics at Emory University School of Medicine. https://www.dropbox.com/s/sw67ofshib2p2gi/Laryngospasm.jpg?dl=1 (>>Click here to download the PICU card for this episode<<) Show Highlights: Our case: a two-year-old male with a history of Wilms’ tumor presents in a sedation suite for post-surveillance MRI History, symptoms, and treatment: One-week history of nasal congestion with no active nasal discharge and clear lung sounds. Patient was placed on continuous pulse ox symmetry and CO2 monitoring. With sedation for the MRI, the patient had a sudden cough, which progressed to perioral cyanosis and loss of end-tidal CO2. How this case illustrates laryngospasm Definition of laryngospasm: complete or partial closure of the larynx due to some manner of external stimulation Why laryngospasm leads to acute respiratory failure in children How laryngospasm differs from airway obstruction Characteristic breathing pattern with laryngospasm Acute management of laryngospasm includes a bag-mask and positive pressure ventilation, followed by deepened sedation, and a breathing tube Why early recognition of laryngospasm is the key

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Welcome to the first episode of our podcast for current and aspiring intensivists. Our panel of medical professionals and students will examine specific patient cases, symptoms, and treatments. Today’s episode focuses on anaphylaxis. Join us! https://www.dropbox.com/s/3mtdeas0hqu6j9j/Anaphylaxis%20Card.jpg?dl=1 (>>Click here to download the PICU card for this episode<< ) Show Highlights: Our case: a four-year-old is admitted to PICU, and TPN has been administered. Symptoms: dyspnea, wheezing, strider, and urticaria Vitals: hypotensive, tachycardic, with stats dropping rapidly What is anaphylaxis? An acute, life-threatening, systemic allergic reaction that can lead to death by airway obstruction or cardiovascular collapse. Anaphylaxis symptoms include skin, mucosal, respiratory, cardiovascular, and gastrointestinal symptoms that develop within one hour of exposure to the allergen. Anaphylaxis triggers can include allergens, biologics, immunotherapy, and radio-contrast media. The anaphylaxis reaction ends with distributive shock, manifested by low cardiovascular output, low systemic vascular resistance, and high pulmonary vascular resistance. Acute management of an anaphylaxis reaction includes airway, circulation, and breathing management, and epinephrine (the dosing is different from code dose). Watch out for hypotension and lower airway obstruction as possible complications, which can be managed with fluids and nebulized albuterol. Adjunctive therapies include histamine blockers and steroids. Post-anaphylaxis care: Focus on observation of the patient for 10-24 hours. Watch for a biphasic reaction. At discharge, provide two prescriptions for epinephrine, education for the patient and family, and a medical alert bracelet for the patient to wear.

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