CoreEM: Recent Episodes

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Author: Natalie Bertrand, MD

Editor: Naillid Felipe, MD

Background:

• Definition: adverse reaction to blood product administration
• Incidence: more common in children than adults, except for delayed hemolytic transfusion reactions
  • Allergic (non-anaphylaxis) – Platelets 1-3%; RBCs 0.1-0.3%
  • Febrile Non-hemolytic (FNHTR) – 1%
  • Transfusion-associated circulatory overload (TACO) – 1%
  • Transfusion-related acute lung injury (TRALI) – <0.01%
  • Anaphylaxis/ABO incompatibility – 1:20,000 – 1:50,000
  • Acute Hemolytic – 1:76,000
  • Sepsis – Platelets 1:50,000; RBCs 1:5,000,000
  • Hypotensive Reaction – <0.01%

• Mortality – 0.6-2.3 per 1,000,000 Pathophysiology and General Management

• Monitor for any adverse reaction from the onset of transfusion for 24 hours-10 days

  • Most common clinical presentation – fever/chills, pruritus, and urticaria
  • Severe reaction – respiratory distress/hypoxia, hypotension, altered mental status, syncope, hemoglobinuria, flank/back pain, jaundice, abnormal bleeding, oliguria
  • Management immediate actions:
  • • Always stop the transfusion
  • Assess the patient
  • Keep an open IV line
  • Re-confirm the correct product/patient
  • Inform the transfusion service/blood bank
  • Main signs and symptoms:
  • • Fever and chills
    • Febrile Non-Hemolytic Transfusion Reaction, Acute Hemolytic Transfusion Reaction, Delayed Hemolytic Transfusion Reaction, Sepsis, Transfusion Related Acute Lung Injury
  • Respiratory distress
    • Transfusion Associated Circulatory Overload, Transfusion Related Acute Lung Injury, Anaphylaxis
  • Hypotension
    • Hypotensive Transfusion Reaction, Anaphylaxis, Acute Hemolytic Transfusion Reaction, Sepsis, Transfusion Related Acute Lung Injury Transfusion Reactions: Allergic

Allergic Reaction (Mild)

• Clinical Presentation
  • Symptom Onset: 0-4 Hours
  • Pruritus, Urticaria
• Pathophysiology
  • Antigen-antibody interaction
  • Type I immediate hypersensitivity (IgE mediated)
  • Usually against donor serum proteins
• Management
  • Antihistamines:
    • Diphenhydramine 25-50 mg
    • Famotidine (20-40 mg)
  • Observe for 30 minutes
  • May continue transfusion once symptoms stabilize or resolve
  • Work-up: No labs needed for isolated pruritus/urticaria

Anaphylaxis

• Clinical Presentation:
  • Symptom Onset: 0-10 minutes
  • Pruritus/Urticaria, Respiratory Distress, Wheezing, Angioedema, Hypotension, Nausea/Vomiting
• Pathophysiology:
  • IgA-deficient recipient with anti-IgA antibodies to the IgA in the transfused product

• Management:

  • Epinephrine IM 0.01mg/kg every 5-15min OR Epipen IM 0.3 mg
  • IF requiring IM Epi >3x, switch to IV Epi, 0.05-0.1 mg
  • IVF bolus
  • Diphenhydramine 25-50 mg
  • Famotidine 20-40 mg
  • Inhaled bronchodilators or supplemental O2 > BIPAP > Intubation
  • Work-up: CXR, IgA titers Transfusion Reactions: Febrile

• Differential Diagnosis: Febrile Non-Hemolytic Transfusion Reaction, Acute Hemolytic Transfusion Reaction, Delayed Hemolytic Transfusion Reaction, Sepsis, Transfusion Related Acute Lung Injury

Febrile Non-Hemolytic Transfusion Reaction

• Clinical Presentation:
  • Symptom Onset: 0-4 hours
  • Fevers/chills
  • Diagnosis of exclusion
• Pathophysiology:
  • Cytokine release from non-leukoreduced blood product
• Management:
  • Symptom management with antipyretics: Acetaminophen 325-1000mg
  • Work-up: Recommend ruling out hemolysis and sepsis

Acute Hemolytic Transfusion Reaction

• Clinical Presentation:
  • Symptom Onset: 0-4 hours
  • Fever/chills, flank and back pain, bleeding, oliguria, pink urine/hemoglobinuria, pink serum (rare), negative direct antiglobulin test (DAT)
• Pathophysiology:
  • Recipient immune cells attack transfusion product leading to intravascular hemolysis
  • Often due to ABO incompatibility due to lab or administration error
• Management:
  • Dilution – IV hydration – 500ml NS/hr until resolution of hemoglobinuria
  • Diuresis – Furosemide IV to main renal output of 1 mL/kg/hr
  • IF DIC, consider need for additional platelets, plasma, or cryoprecipitate transfusion
  • Work-up: CBC (smear), CMP, reticulocyte count, coags, LDH, haptoglobin, fibrinogen, dimer, DAT, consider nephrology, heme, and ICU consult

Delayed Hemolytic Transfusion Reaction

• Clinical Presentation:
  • Symptom Onset: > 24 hours
  • Fever/chills, chest pain, dyspnea, light-headedness, jaundice, anemia with low reticulocyte count, hemolysis (elevated d-dimer, bilirubin, LDH), positive direct antiglobulin test (DAT), kidney injury
• Pathophysiology:
  • More common in sickle cell disease
  • Re-exposure to antigens from prior transfusions leading to intravascular hemolysis
• Management:
  • Similar to acute hemolytic transfusion reaction

Sepsis

• Clinical Presentation:
  • Symptom Onset: 0-1 hours
  • Fever/chills, hypotension, SIRS
  • Must exclude AHTR and TRALI
• Pathophysiology:
  • IV administration of microorganism, typically higher volume of organism delivery than peripheral infection or other typical infection sources
  • More common in platelet transfusion due to storage at room temperature

• Management:

  • IVF resuscitation per sepsis guidelines
  • Broad spectrum antibiotics
  • Hemodynamic support
  • Work-up: Blood cultures on patient and transfusion product, UA, CXR, EKG Transfusion Reactions: Respiratory Distress

• Differential Diagnosis: Transfusion Associated Circulatory Overload, Transfusion Related Acute Lung Injury, Anaphylaxis

Transfusion Associated Circulatory Overload (TACO)

• Clinical Presentation:
  • Symptom Onset: 4-6 hours
  • Respiratory distress, hypoxia, hypertension, elevated central venous pressure, elevated BNP, evidence of pulmonary edema (CXR or POCUS)
• Pathophysiology:
  • Pulmonary edema caused by volume overload
  • Most common in elderly, children, patients with underlying heart failure or who receive large volume of blood products
  • Transudative pulmonary edema fluid due to cardiogenic source
• Management:
  • Diuresis – Furosemide IV, dosing dependent on diuretic naivety
  • Respiratory support – Oxygen > BIPAP > Intubation
  • Work-up: CXR, EKG, BNP, Troponin, ABG, consider cardiology consult

Transfusion Related Acute Lung Injury

• Clinical Presentation:
  • Symptom Onset: 4-6 hours
  • Fever/chills, respiratory distress, hypoxia, hypotension, pink/frothy sputum, bilateral chest x-ray infiltrates
• Pathophysiology:
  • Transfusion product with anti-HLA/anti-HNA causing recipient immune system to activate in lungs causing local cytotoxic effects
  • Exudative pulmonary edema fluid due to inflammatory source
• Management:
  • Respiratory support
  • ARDS management: https://coreem.net/podcast/episode-195-ards/ Transfusion Reaction: Hypotension

Differential Diagnosis: Hypotensive Transfusion Reaction, Anaphylaxis, Acute Hemolytic Transfusion Reaction, Sepsis, Transfusion Related Acute Lung Injury

Hypotensive Transfusion Reaction

• Clinical Presentation:
  • Symptom Onset: 0-1 hours
  • Hypotension SBP drop by > 30 mm Hg or SBP < 80 mm Hg
  • Rapid improvement after halting transfusion
  • Must exclude other etiologies of hypotension
• Pathophysiology:
  • Unclear mechanism, likely bradykinin induced
  • Risk factors: ACE inhibitor use and leukocyte reduced product
  • Most common with platelet transfusion

• Management:

  • IV Fluids as needed
  • Hold ACE inhibitors prior to transfusion
  • Work-up for alternative etiologies as indicated Transfusion Reaction: Transfusion Associated Graft vs Host

• Clinical Presentation:

  • Symptom onset: 3-30 days
  • Fever/chills, rash/pruritus, nausea and vomiting, diarrhea, dyspnea
• Pathophysiology:
  • Donor T-cells attack recipient cells and tissue
  • More common in patients with hematologic malignancies or stem cell transplants
  • Labs demonstrate pancytopenia
  • Mortality 90%
• Management:
  • Emergent Hematology/Oncology consult (might need immunosuppression or urgent stem cell transplant) Diagnosis

Assessment

• Always:
  • Vitals
  • Blood glucose
  • Detailed history of event and PMHx
  • Repeat physical exam
  • Re-confirm the correct product/patient
• Often:
  • Complete Blood Counts
  • Complete Metabolic Panel (including LFTs)
  • Repeat ABO compatibility
  • Additional antibody screen
  • Repeat crossmatch with pre-and post-transfusion specimens
• Symptom Specific
  • VBG/ABG
  • Direct antiglobulin testing (Coombs)
  • Hemolysis labs – haptoglobin, LDH, unconjugated bilirubin, and reticulocyte count
  • Cardiac labs – Trop, BNP
  • DIC labs – PT, PTT, fibrinogen, and D-dimer
  • UA – pink color and analysis for free hemoglobin
  • Serial H/H
  • CXR
  • IgA levels

Information to send with the sample to blood bank for transfusion reaction:

• • Patient label with MRN
  • Reason for the transfusion
  • Vital signs before, during, and current
  • PMHx of transfusion reaction
  • Pretransfusion medications
  • Time of transfusion initiation, symptom onset, and transfusion stop
  • Detailed patient symptoms Disposition and Next Steps

• Restart the transfusion?

  • YES, restart
    • Stable vital signs, symptoms resolved, correct product confirmed
    • AND Minor allergic reaction, TACO, FNHR
    • AND <4 hours from onset of transfusion (regulations may be facility dependent)
  • NO, do NOT restart
    • AHTR, TRALI, anaphylaxis, sepsis
    • OR Unstable vitals signs, persistent symptoms, incorrect product/patient
• Admit for:
  • Persistently unstable VS
  • Sepsis
  • Hemolysis
  • Respiratory distress
  • Need for further transfusions
• When to discharge:
  • Stable VS
  • Symptoms resolved
  • Underlying need for transfusion has been addressed

• Prevention of Transfusion Reactions

  • Correct labeling of T&S in ED level and cross matching at blood bank level
  • Allergic Reactions – use WASHED products for patients with IgA deficiency or prior allergic reactions
  • Delayed HTR – use LEUKOREDUCED products for patients with SCD or prior hemolytic reactions
  • Transfusion Associated GVHD – use IRRADIATED products for patient with hematologic malignancies & stem cell transplants
  • TACO – transfuse slower or with HD for high risk patients (HF, ESRD etc)
  • No evidence for use of APAP or benadryl prophylactically References:

• Benson AB, Moss M, Silliman CC. Transfusion-related acute lung injury (TRALI): a clinical review with emphasis on the critically ill. Br J Haematol. 2009 Nov;147(4):431-43. https://doi.org/10.1111/j.1365-2141.2009.07840

• Emery, M. Blood and blood components. In: Marx J, ed. Rosen’s emergency medicine. 8th ed. Philadelphia, PA: Elsevier; 2014:75-80.
• Hendey G. Transfusion Reactions and Complications. In: Wolfson A, ed. Harwood-Nuss’ Clinical Practice of Emergency Medicine. 6th ed. Philadelphia, PA: Wolters Kluwer; 2015:979-984.
• Hirayama F. Current understanding of allergic transfusion reactions: incidence, pathogenesis, laboratory tests, prevention and treatment. Br J Haematol. 2013 Feb;160(4):434-44. https://doi.org/10.1111/bjh.12150
• Kwon, S. S., Kim, S., & Kim, H. O. (2022). Incidence and characteristics of hypotensive transfusion reaction: 10-Year experience in a single center. Transfusion, 62(11), 2245–2253. https://doi.org/10.1111/trf.17099
• Metcalf, R. A., Bakhtary, S., Goodnough, L. T., & Andrews, J. (2016). Clinical pattern in hypotensive transfusion reactions. Anesthesia & Analgesia, 123(2), 268–273. https://doi.org/10.1213/ane.0000000000001387
• Osterman, J. L., & Arora, S. (2017). Blood product transfusions and reactions. Hematology/Oncology Clinics of North America, 31(6), 1159–1170. https://doi.org/10.1016/j.hoc.2017.08.014
• Pollard R, Boraski M, Block JG. Hypotensive Transfusion Reaction Treated With Vasopressin in a Patient Taking an Angiotensin-Converting Enzyme Inhibitor: A Case Report. A A Case Rep. 2017 Jul 1;9(1):4-8. https://doi.org/10.1213/XAA.0000000000000507
• Savage, W. J., Tobian, A. A. R., Savage, J. H., Wood, R. A., Schroeder, J. T., & Ness, P. M. (2012). Scratching the surface of allergic transfusion reactions. Transfusion, 53(6), 1361–1371. https://doi.org/10.1111/j.1537-2995.2012.03892.x
• Skeate, R. C., & Eastlund, T. (2007). Distinguishing between transfusion related acute lung injury and transfusion associated circulatory overload. Current Opinion in Hematology, 14(6), 682–687. https://doi.org/10.1097/moh.0b013e3282ef195a
• Vamvakas, E. C., & Blajchman, M. A. (2009). Transfusion-related mortality: The ongoing risks of allogeneic blood transfusion and the available strategies for their prevention. Blood, 113(15), 3406–3417. https://doi.org/10.1182/blood-2008-10-167643
• Vlaar, A. P. J., Toy, P., Fung, M., Looney, M. R., Juffermans, N. P., Bux, J., Bolton‐Maggs, P., Peters, A. L., Silliman, C. C., Kor, D. J., & Kleinman, S. (2019). A consensus redefinition of transfusion‐related acute lung injury. Transfusion, 59(7), 2465–2476. https://doi.org/10.1111/trf.15311

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     We discuss migraines with one of the authorities in the field.

Hosts:
Benjamin Friedman, MD of Montefiore
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Migraines.mp3   Download Leave a Comment Tags: Neurology    Show Notes **Initial Approach to Diagnosing Migraines:**

• Differentiating between primary headaches (migraine, tension-type, cluster) and secondary causes (e.g., subarachnoid hemorrhage).
• The importance of patient history and reevaluation after initial treatment.
• Recognizing the unique presentation of cluster headaches and their management implications.

Effective Acute Migraine Treatments:

• First-line treatments including anti-dopaminergic medications like metoclopramide (Reglan) and prochlorperazine (Compazine), and parenteral NSAIDs like ketorolac (Toradol).
• The limited role of triptans in the ED due to side effects and less efficacy compared to anti-dopaminergics.
• The use of nerve blocks (greater occipital nerve block and sphenopalatine ganglion block) as effective treatments without systemic side effects.

Treatments to Avoid or Use with Caution:

• Diphenhydramine (Benadryl): Studies show it does not prevent akathisia from anti-dopaminergics nor improve migraine outcomes.
• IV Fluids: Routine use is not supported unless the patient shows signs of dehydration.
• Magnesium: Conflicting evidence with some studies showing no benefit or even harm.

Managing Refractory Migraines:

• Second-line treatments including additional doses of metoclopramide combined with NSAIDs or dihydroergotamine (DHE).
• Considering opioids as a last resort when other treatments fail.
• The potential use of newer medications like lasmiditan and CGRP antagonists.

Preventing Recurrence of Migraines:

• Administering a single dose of dexamethasone (4 mg IV) to reduce the risk of headache recurrence after discharge.
• Prescribing NSAIDs or triptans upon discharge for outpatient management.
• Recognizing and addressing chronic migraine, and initiating preventive therapies like propranolol when appropriate.

Key Takeaways

• Differentiate Primary from Secondary Headaches and Reassess After Treatment:
  • Use patient history and reevaluation post-treatment to distinguish migraines from more serious conditions, reducing unnecessary imaging and procedures.
• First-Line Treatments Are Effective:
  • Anti-dopaminergic medications and NSAIDs are the mainstay of acute migraine treatment in the ED.
  • Reserve opioids for cases unresponsive to multiple lines of treatment.
• Avoid Unnecessary Interventions:
  • Diphenhydramine and routine IV fluids do not have proven benefits and can be excluded to streamline care.
• Utilize Nerve Blocks for Refractory Cases:
  • Greater occipital nerve blocks and sphenopalatine ganglion blocks are effective alternatives for patients not responding to medication.
• Prevent Recurrence with Dexamethasone and Outpatient Planning:
  • A single IV dose of dexamethasone can help prevent recurrence.
  • Provide prescriptions and consider preventive therapies to reduce future ED visits.

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Author: Allison Tu

About me: I’m a second-year medical student at NYU planning to pursue a career in emergency medicine. I graduated from Harvard in 2023 with a degree in psychology and global health, and during medical school, I’ve co-directed NYU’s asylum clinic and volunteered for the suicide prevention lifeline. I am also interested in teaching, and I hope to pursue a medical education fellowship in the future. Outside of medical school, I love social dance, baking, and long-distance running.

To get a sense of how medical students feel about emergency medicine, we interviewed three students who are interested in EM: Nick, a graduating M4 pre-matched into EM residency, Charlotte, an M2 currently planning to pursue EM, and Annie, an M1 considering EM.

What sparked your interest in emergency medicine?

Nick: My interest in EM began when I was working in EMS as an undergrad, and I was always pretty committed to the field. I enjoyed the approach to the undifferentiated patient and the challenge of ruling out worst-case scenarios. The role of the emergency room as part of the social safety net and the importance of patient-provider interactions in this context also drew me to EM. During medical school, I did consider other specialties, but realized what I liked most about EM: being a generalist, always learning from the specialists you consult, and making the final call on patient care.

Charlotte: My interest in EM stems from the variety it offers – you see patients who have little other contact with the healthcare system alongside many high acuity patients. I also appreciate the culture in EM, which I’ve found to generally be down-to-earth and less hierarchical. There’s more focus on maintaining balance and interests outside of medicine, which I think is important for a sustainable career in medicine.

Annie: I developed an interest in EM while working as a scribe in the ED during college. In addition to what Charlotte and Nick said, I can envision myself staying calm in the stressful situations that come up in the ED. I’m also passionate about advocacy, so I appreciate the focus on the social safety net. The culture is also great – I’ve heard crazy stories about surgeons with tempers, but have never seen that in the ED.

How does your medical school support interest in emergency medicine careers?

Nick: Throughout medical school, I noticed that most of the teaching, across the entire curriculum, is done by specialists rather than generalists. This setup encourages students to think about the cutting edge of each subspecialty, which is great, but I believe it’s more important for us at this stage to master the basics needed to be a good clinician. I usually had to seek out role models in generalist-type fields on my own.

Charlotte: The EM department does an exceptional job of supporting interest in the field. I had an early exposure to EM through shadowing shifts during my first year, and then participated in an EM summer fellowship program. These experiences helped me better understand the specialty and start envisioning myself in the field.

Annie: The EM department does most of the heavy lifting in supporting student interest. There’s minimal EM exposure in the curriculum, but as an EM Interest Group co-leader, I’ve seen how much effort the department puts in. They’ve set up amazing workshops and shadowing experiences, which were so valuable, especially given the condensed preclinical curriculum.

What have people said to you to discourage you from going into EM?

Nick: Over my years in medical school, doctors have expressed concerns about the high burnout rate, mid-level creep, unsafe working conditions, and insufficient compensation in EM. On the medicine floors, I’ve heard that EM doctors don’t engage in slow, methodical thinking. However, I think there’s room in the ER for both fast and slow thinking.

Charlotte: Most of the discouraging comments I’ve encountered concerning EM have originated from sub-specialty services on my clerkships. EM interacts with a variety of other divisions, oftentimes seeking consults or admissions, so I believe some of the frustration comes from the differing goals of each service. Similarly, I’ve encountered a bias towards physicians becoming increasingly specialized, while EM is one of the few areas in which broad medical skillsets are particularly important.

Annie: I think the general public’s perceptions about EM often focus on intensity of the work and the crazy traumas, so they’re concerned about burnout. I’ve run into the sense that EM really grinds on you, which I believe is a misconception, though I realize that might change as I spend more time in the ER.

If you end up not pursuing EM, what would be the reason(s) why?

Nick: EM is sometimes viewed as less academic, which is a concern for me. I enjoy reading studies, discussing their implications, and teaching, which is why I’m considering a critical care fellowship. It does seem like many MICUs and SICUs prefer to hire people who are IM or anesthesia trained, so that’s one drawback, but it was balanced out by a lot of benefits of EM. I strongly considered general surgery and internal medicine, specifically pulmonary critical care or cardiac critical care. Both fit the generalist aspect I enjoy, but I did not end up loving the OR. Internal medicine felt too slow for me, and I missed seeing cases like musculoskeletal injuries or pediatrics.

Charlotte: I’ve enjoyed different aspects of many clerkships, which sometimes made me consider other specialties. In particular, I enjoyed the detailed diagnostic exams in neurology, the interpretation of echocardiograms in cardiology, and the patient and family contact in OBGYN and pediatrics. The appeal of EM is that it incorporates aspects with each of these, in addition to providing critical interventions. I see the appeal of focusing on a single area of medicine in depth, but I always come back to EM.

Annie: As an MD-PhD, I’m passionate about research, particularly in basic science and neuroscience. EM definitely has less of that sort of research, so I’m grappling with the decision between pursuing a more academically research-oriented career or staying in EM. Of course, there are also plenty of EM physicians who do a lot of research, and I have plenty of time to figure it all out in the interim.

What do you view as the biggest challenges in emergency medicine?

Nick: Triaging your time and priorities as an ED doc on shift is so challenging. There’s always an endless list of tasks for you at any given time, plus more patients in the waiting room that need to be seen, and having the executive function skills to figure out which tasks take priority takes a lot of practice. It’s something I definitely haven’t mastered just yet, and might not master for a really long time.

Charlotte: I suspect that the biggest challenge I will face will be the combination of a high-volume and fast-paced work environment. In particular, I think the cognitive and mental burden of caring for critically ill and complex patients, and patients with significant social stressors, can stretch even very empathetic clinicians.

Annie: Insurance issues, such as the cost of medications and procedures, and disparities in healthcare access, especially in rural areas, are significant challenges. Despite EM being more diverse than other specialties, there’s still work to be done in making the field more inclusive and addressing overrepresentation of certain groups. Emergency medicine is uniquely positioned to tackle these issues, but it remains an elite profession with many systemic challenges to overcome.

What is your perspective on the 2021 job report?

Nick: The 2021 job report, which predicts an excess of emergency physicians by 2030, has encouraged me to think critically about my career. I’ve asked folks about their job search experiences and reconsidered other specialties, but I can’t see myself doing anything other than EM. However, I am considering pursuing some kind of fellowship to have a fallback option or to make myself a more competitive candidate. I’m thinking about a fellowship in addiction medicine or critical care.

Charlotte: I think the practice of medicine is always changing, and the responsibilities of each specialty will evolve, especially with advancements in AI. Despite the report, I think there will still be EM jobs available and that other fields may experience greater changes due to AI. EM is still the field that most closely aligns with my interests.

Annie: I wasn’t aware of this report until recently, and it hasn’t trickled down much to first-year medical students. The narrative has always been about a physician shortage, so I was pretty surprised. This might be the PhD student in me coming out, but I’m curious about the prediction models and factors they used, because emergencies happen all the time and there are plenty of rural places without enough healthcare. I’m taking it pretty neutrally and am interested to see how it plays out, especially since I’ll graduate in 2030.

What are your thoughts on the role of private equity companies in EM?

Nick: It is scary to hear the horror stories of what happens to hospitals and EDs taken over by private equity companies. In some ways I feel like the situation is a consequence of having a system that’s constantly being pushed to its limits. It seems like there is legislation coming to limit the amount of control that non-physician PE groups can have over ED care and staffing – I’m thinking of a particular ongoing lawsuit in Florida that seems to be a step in the right direction.

Charlotte: There’s been a shift in healthcare overall towards working for hospital or medical groups owned by private entities, which changes the incentives away from providing the best care. I’m glad that EM is recognizing this and discussing solutions, but the overall trend is concerning.

Annie: As someone who realizes the value of single-payer systems, it’s frustrating to see the US moving in the opposite direction. It’s very concerning, but I’m still hopeful that there will be improvements and perhaps regulations in the future.

Lots of Gen Z and millennials are getting most of their healthcare in the ED. What do we think about the increased burden of healthcare in the ED?

Nick: It’s definitely posing a new challenge to EDs, and possibly even expanding the skillset of ED providers to know more about how to treat more low acuity complaints. It also speaks to the low availability of primary care docs in certain areas and poses the need for better systems of linking folks from the ED to longitudinal outpatient care.

Charlotte: It’s tough because, while great PCPs are valuable for continuity, many young people struggle to find a PCP – I tried to find one myself and many physicians don’t have appointments for a year or more. Younger generations are also used to services being more on-demand, so more of them end up in urgent cares or the ED. Since I’m not working yet, I don’t know how it actually affects clinical practice, but I can see how the model fits better with Gen Z and millennials.

Annie: The narrative that more people are using the ED for healthcare highlights broader issues in the healthcare system, like the difficulty in accessing PCPs. While it can be frustrating, it’s important to understand that people come to the ED because they need help, even if it’s not strictly an emergency.

EM offers lots of flexibility to engage in other facets of medicine, from medical education to toxicology. What EM-adjacent fields might you be interested in pursuing throughout your career?

Nick: I’ve thought a lot about improving my future job security, which definitely includes potentially pursuing a fellowship. I’m interested in addiction medicine, which aligns with the ED’s role in the social safety net, and critical care, which is full of slower, detailed thinking.

Charlotte: Before med school, I worked in public health, and I see a lot of potential for implementing programs and conducting research related to public health in the ED. Additionally, I really enjoy ultrasound. While I might not pursue a formal ultrasound fellowship, it’s a valuable diagnostic skill that I’m aiming to develop during residency.

Annie: I only recently realized how many fellowships EM offers. I’m currently most interested in education, policy, and toxicology. The variety is exciting, and it’s truly wild how many opportunities there are. I think I might even pursue multiple fellowships, as there’s so much to explore and that happens to be an option.

What qualities do you view as being most important in an EM physician?

Nick: I think it’s important to be introspective of how you are thinking, switching between fast, intuitive system one and slow, deliberate system two. You have to be aware of what you’re doing and able to switch depending on what the situation calls for.

Charlotte: Above all else, I think adaptability is key. In EM we are often balancing clinical triage, resource limitations, social barriers, and the challenges of making first-impression diagnoses. It is essential to transition from task to task, monitor the board, proactively help peers, and prioritize actions efficiently. It’s also important to be able to bring your full self to each interaction, whether it is delivering safe discharge instructions or discussing a life-altering diagnosis.

Annie: Hard work, empathy, and resilience are crucial. You need to be quick on your feet and stay level-headed when chaos is around you, and have a huge breadth of information that you’re comfortable drawing from. It’s also so important to be able to work effectively on a team, given the collaborative nature of EM.

What qualities are most helpful to you in EM mentors, residents, and attendings?

Nick: In EM, people are generally very open and quick to share their genuine selves with mentees, which has helped me imagine my future career. Although we often work with an attending for just a single ED shift, people are great about understanding my goals for each shift and providing specific, actionable feedback. It’s clear that they want to help me become a better doctor.

Charlotte: I’ve had mentors in the EM department who are very thoughtful and understanding. This has been particularly important during my clerkship year, as I’ve been juggling many different commitments including applying for the three-year program (which admits med students directly to residency) during my surgery clerkship. The willingness of these mentors to be available, even giving me their phone numbers for any questions, has been so helpful.

Annie: EM physicians love students and are eager to help. I’ve attended several women in EM events, which are so wholesome, because you can really see the genuine care EM physicians and the department itself have for the students.

How do you anticipate adapting to and incorporating new innovations into your career?

Nick: In the future, I envision an emergency department with minimal physician-computer interaction, where documentation is fully automated, allowing us to focus more on medical decision-making. However, I think the element of clinician gestalt will remain irreplaceable, especially in making diagnoses where clinical decision-making tools are not fully reliable. I also think patient-provider interactions will still require a human touch – people come to the ED to be seen by a doctor.

There are also big implementation barriers to new technology in healthcare. Even with a perfectly functioning AI system, widespread adoption could take decades, just as EHRs have still not been universally implemented.

Charlotte: Documentation is the lowest hanging fruit for AI integration, but the more complex aspects of healthcare – decision-making and patient communication – are much harder to automate. Prior to medical school, students sometimes work as scribes because much of the documentation doesn’t require the same understanding of medicine or carry the same liability as making management decisions, which will be more challenging for AI to replace.

Annie: I don’t think AI will be fully integrated into healthcare anytime soon. AI has developed rapidly, but the necessary regulations and considerations haven’t kept pace. There are significant biases in AI data, like algorithms that spit out gender-biased results, which can lead to harmful outcomes. There’s a lot of buzz about using AI to lead patient care, but I don’t think it’ll happen to any significant extent for a while, beyond what’s already been implemented.

Imagine yourself at the end of your career in EM. What impact do you hope to have made?

Nick: I think at the end of the day, I just want to be a good doctor that’s thoughtfully treated a lot of patients and had an influence on a lot of trainees. I think a lot of people have aspirations to make enormous system-wide changes in their field, which is fantastic, but my motivations in medicine have always been on a more individual level.

Charlotte: Being realistic, I hope that I will have been an excellent EM doctor and positively impacted my patients. If I want to be ambitious, I hope to incorporate healthcare policy into my career, helping to shape laws and regulations that ensure that all patients receive the care they need.

Annie: Realistically, I want to be the best doctor I can be, always reminding myself that I’m doing this for the patients. Beyond that, I hope to explore what I can do with my PhD, possibly incorporating translational or basic science research into my career. I’m also interested in education and policy, as they all tie back to improving patient care. Alas, it’s early in my career, and I think I’ll figure it out more as time goes on.

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The Case A 96-year-old female with a history of coronary artery disease, hypertension, and complete heart block status post dual-chamber pacemaker (remote) presents to the ED by EMS with generalized weakness and lethargy.

EKG Show Details EKG Characteristics * Rate 130 * Rhythm Wide Complex Tachycardia, Paced * Intervals QRS 180, QT/QTc 406/596 * Axis Left axis deviation * ST Segments Non-specific * Additional Features Paced Rhythm with LBBB morphology

Diagnosis Pacemaker-Mediated Tachycardia

Questions 1. What is the differential diagnosis for these ECG findings? Pacemaker Associated Tachycardia, Rapidly-Sensed Atrial Rate (with underlying atrial tachycardia), Ventricular Arrhythmia 2. What is the next best step in evaluating this patient? Applying a magnet to the pacemaker inhibits its ability to sense atrial rhythms and reverts it to an asynchronous pacing mode. Terminating the tachycardia by applying a magnet suggests a pacemaker-mediated tachycardia and further pacemaker interrogation and evaluation should occur. If there is no change with the magnet application, an underlying arrhythmia is likely present, and standard ACLS algorithms should be applied.

 Discussion **Discussion:**

Pacemaker-mediated tachycardia is typically caused by atrial sensing of a ventricular impulse through a retrograde AV node or a re-entrant pathway. Other forms of pacemaker-mediated tachycardia include sensor-induced tachycardia caused by malfunctioning physiologic sensors, which normally increase the pacemaker rate based on underlying physiologic parameters. Consider a pacemaker-mediated tachycardia when a patient presents with a regular, paced tachycardia at or around 130 bpm, a standard upper limit of pacemaker rate. P-waves are typically absent. This rhythm will be terminated with magnet application.

A pacemaker-mediated tachycardia’s primary differential diagnosis includes a rapidly-sense atrial rate, which occurs when any (native) atrial tachycardia (sinus tachycardia, atrial fibrillation, etc.) results in rapid ventricular pacing. The ECG will demonstrate a native atrial rhythm with a paced ventricular rhythm. In this situation, non-paced P-waves are likely to be present.

Consider secondary/physiologic etiologies of tachycardia (infection, dehydration, bleeding, embolism, substance use/withdrawal) in addition to underlying atrial arrhythmias. This rhythm will not result in cessation with magnet application.

ED Course:

The patient presented mild hypotension but was alert without signs of respiratory distress and a reassuring perfusion exam.

EKG initially showed a ventricular paced rhythm at 130 with expected left-bundle branch block morphology and no evidence of ischemia per Modified Sgarbossa’s criteria.

The chest X-ray demonstrated normal pacemaker lead placement with mild pulmonary edema. The patient was connected to Zoll Pads, a magnet was obtained, and Electrophysiology was consulted.

During EP evaluation, the patient’s rhythm reverted to her baseline, paced rhythm without intervention.

EP interrogated the device, which determined that an inappropriate rate response parameter, likely related to the battery replacement three days prior, confirming a sensor-induced pacemaker-mediated tachycardia.

The patient was ultimately admitted, treated with gentle diuretics, and underwent re-programming of her pacemaker.

Pearls * Consider pacemaker-mediated tachycardia in patients presenting with paced, wide-complex tachycardia, especially when the rate remains constant at 130, the typical upper limit of pacemaker settings. * Magnet application can differentiate pacemaker-mediated tachycardia from a rapidly sensed atrial rate by reverting the pacemaker to an asynchronous pacing mode.

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     We discuss a new class of medications, Immune Checkpoint Inhibitors, and their side effects.

Hosts:
Avir Mitra, MD
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Immune\_Checkpoint\_Inhibitors.mp3   Download Leave a Comment Tags: Oncology    Show Notes **Overview of Immune Checkpoint Inhibitors (ICIs)*** ICIs are a relatively new class of oncologic drugs that have revolutionized cancer treatment.

• Unlike chemotherapy, ICIs help the immune system develop memory against cancer cells and adapt as the cancer mutates.
• Since their release in 2011, ICIs have expanded to 83 indications for 17 different cancers, with approximately 230,000 patients using them.

Mechanism of Action* Cancer cells can evade the immune system by binding to T cell receptors that downregulate the immune response. * ICIs work by blocking these receptors or ligands, preventing the downregulation and allowing T cells to proliferate and attack cancer cells. * Common ICIs

Risks and Toxicities of ICIs* ICIs can lead to autoimmune attacks on healthy cells due to immune system upregulation. * Immune-related adverse effects (irAEs) include colitis, pneumonitis, dermatitis, hepatitis, and endocrine issues (e.g., hypothyroid, hypocortisolemia, hypophysitis). * These toxicities can present as infections, making diagnosis challenging in the emergency room.

Management of ICI Toxicities in the ER* Diagnosis: Look for signs that mimic infections (e.g., cough and fever in pneumonitis). * Diagnostic Imaging in pneumonitis: If CXR is normal but suspicion is high, consider CT scans to differentiate conditions like pneumonitis from other issues such as malignancy-associated pleural effusion or acute pulmonary embolism. * Treatment: The primary treatment for irAEs is steroids (e.g., prednisone 1 mg/kg). Start steroids early and hold the ICI to manage symptoms effectively and increase the likelihood of resuming ICI therapy later. * Consider using antibiotics in combination with steroids if there is uncertainty about whether symptoms are due to infection or ICI toxicity. * Coordinate care with the patient’s oncologist if possible

Disposition Decisions* Patient disposition (admit vs. discharge) should depend on clinical presentation and severity. * Coordination with oncology is crucial; they are often comfortable with starting steroids even if there is a potential infection. * Patients can be discharged if symptoms are mild, but sicker patients with more complex presentations may require admission.

Take-Home Points* ICIs are a new class of cancer drugs that effectively target cancer cells but come with unique immune-related toxicities. * Diagnosing irAEs can be challenging due to symptom overlap with infections. * The cornerstone of treatment is early administration of steroids and temporarily holding the ICI. * Close collaboration with oncology teams is essential for optimal patient management.

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Medical Education FellowshipNYU Langone’s Ronald O. Perelman Department of Emergency Medicine is excited to introduce our new fellowship, starting July 2025. The Medical Education Fellowship is designed for emergency physicians aspiring to advance their careers in medical education. This two-year fellowship provides an extensive curriculum aimed at developing skills necessary for roles such as program directors, clerkship directors, and academic leaders in the field of emergency medicine.

Fellowship HighlightsFellows practice at multiple NYU Langone locations, including the Ronald O. Perelman Center for Emergency Services in Manhattan, NYU Langone Hospital—Brooklyn, and NYU Langone Health—Cobble Hill Emergency Department at the Joseph S. and Diane H. Steinberg Ambulatory Care Center, as well as NYC Health + Hospitals/Bellevue. These sites feature high-acuity emergency departments, a Level 1 Trauma Center, a freestanding emergency department, and comprehensive urgent care and telehealth services.

In partnership with Maastricht University’s Master of Health Professions Education (MHPE) Program, fellows engage in educational administrative and leadership training during the first year, assuming roles such as associate program director in their chosen domain: undergraduate medical education, graduate medical education (residency or pediatric emergency medicine fellowship programs), or continuing medical education and faculty development.

The second year focuses on educational scholarship, including content generation and completing a master’s thesis, leveraging collaborations with institutional programs such as NYU Langone’s globally recognized FOAM platform, CORE Emergency Medicine, the Institute for Innovations in Medical Education, the Program for Medical Education Innovations and Research Projects, and the Research on Medical Educations Outcomes group. Throughout the fellowship, participants engage in a variety of teaching methods, including didactic sessions, bedside instruction, and simulation-based learning, all within the Bellevue Emergency Medicine Residency Program and NYU Grossman School of Medicine.

Fellowship Leadership and FacultyJonathan Kobles, MD. Program Director

Selin T. Sagalowsky, MD, MPH.Vice Chair for Education

Lily Liang Senior Fellowship Program Coordinator

Fellowship Curriculum OverviewBased on holistic learning, the curriculum focuses on following criteria:

• clinical: 16 hours per week as a junior attending at our NYU Langone and Bellevue clinical sites
• MHPE: two-year part-time MHPE program focused on self-directed learning and delivered predominantly through flexible distance-learning technologies and requires completion of a master’s thesis
• experiential learning: a diversity of proscribed and mentored teaching activities to build an educational portfolio, paired with a longitudinal fellowship curriculum and leadership role as an acting associate program director

Fellowship Eligibility CriteriaWe are looking for candidates who are dedicated to patient care, passionate about education and leadership, and meet the following criteria:

• MD or DO graduate of an Accreditation Council for Graduate Medical Education (ACGME)–accredited emergency medicine residency program or American Osteopathic Association (AOA)–accredited pediatric emergency medicine fellowship program
• American Board of Emergency Medicine (ABEM) or American Board of Pediatrics (ABP, pediatric emergency medicine) board-certified or -eligible
• three- or four-year residency programs accepted

How to ApplyApplications are being accepted from July 1, 2024, to October 15, 2024, for a start date of July 1, 2025. You can submit your CV, statement of interest, and three letters of recommendation.

Contact UsTo submit an inquiry or to begin the application process, please email Lily Liang, program coordinator, at Lily.Liang@NYULangone.org.

This fellowship offers a competitive salary and benefits package, providing a unique opportunity for professional growth and leadership in medical education within emergency medicine.

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Author: Erica Cohen, MD

Editor: Brian Gilberti, MD

Definition:

• Naturally occurring electric arc between a cloud and the ground
• Most common during thunderstorms
• Direct strikes can be > 10 million volts [1]
• Usually last between 1/10-1/1000 of a second [1]

Epidemiology:

• ~300-500 injuries/year, ~50-100 deaths/year [2,3]
• Most commonly occurs in young males and those who perform outdoor work or pursue outdoor recreational activities.
  • Most common during the spring and summer months (i.e., fishing, golfing, camping).
• Lightning strikes may injure a group of people simultaneously.

• Lightning strikes occur most frequently in areas with higher incidence of thunderstorms such as unexposed areas at higher elevations (i.e. mountain terrain will have more lightning strikes than surrounding lower elevations) Pathophysiology:

• Flashover: lightning travels across the body’s surface

  • Wet skin allows current to travel along the outside of the body
  • Less likely to result in internal injuries
  • Higher survival incidence
• Mechanisms of Injury:
  • Electric current travels through the body (not common)
  • The conversion of electrical energy to thermal energy results in burn injury
  • Mechanical trauma (i.e. being thrown from a transmitted shock wave or direct strike from a bolt)
  • Rapid expansion and contraction of air (ex., TM perforations)
• Keraunoparalysis (Stunning): flashover effect on the peripheral nervous and vascular systems [4,5]
  • Benign and reversible (transient) paralysis from peripheral vascular spasm
  • Signs: sensory abnormalities, pallor, coolness, diminished or absent pulses
    • Usually in the lower extremities > upper extremities
  • Avoid performing a fasciotomy on these patients as these findings are likely to resolve spontaneously within hours to days, though rarely they can be permanent
    • More permanent symptoms: muscular weakness, pain, photophobia, neurotic behavior
• Types of lightning strikes [3]:
  • Direct (5%), contact (15%), side flash (30%), ground strike (50%)
    • Direct strike: struck directly by lightning discharge
    • Contact strike: lightning strikes an object held by a person and travels through the person to the ground
    • Side flash: current jumps to the victim from a nearby object via air (no physical contact)
    • Ground current (Step Voltage): current travels through the ground from the strike point
      • Stride Potential: The foot closer to the strike point will receive higher electrical potential compared to the foot farther away

Causes of Death:

• Most deaths that occur within 1 hour of injury are from cardiac arrest due to fatal arrhythmia or respiratory arrest
  • Depolarization of the myocardium can result in asystole
  • Depolarization and paralysis of the medullary respiratory center leads to respiratory arrest
    • Spontaneous cardiac activity usually resumes before respiratory activity, resulting in secondary hypoxic cardiac arrest
  • Ventricular dysrhythmias such as ventricular fibrillation are less common. Evaluation:

Pre-Hospital: Reverse triage system – in mass casualty events, treat those with respiratory arrest and cardiac arrest first

• After a lightning strike, prehospital providers should be advised to leave the scene as soon as possible and continue resuscitation and stabilizing efforts en route to the hospital, as the environmental conditions that led to a lightning strike in that location may persist (ie, lightning can strike twice!).

ED: Follow ATLS guidelines

• Full trauma exam, including primary and secondary exam
  • Cutaneous burns demonstrate the current pathway
• Labs: CBC, CMP (electrolytes, creatinine and BUN for kidney function), glucose
  • CK (though rhabdomyolysis is rare), troponin, EKG
  • UA to evaluate for myoglobinuria

Unique workup considerations:

• Spinal fractures can occur from muscle contractions, therefore maintain spinal immobilization during initial resuscitation
• Parkland Formula for extensive burns (& transfer to burn center if appropriate)
• Aggressive IV fluid replacement is not always needed [6]
• Consider hemorrhagic blood loss as the etiology of hypotension
• Monitor for compartment syndrome and rhabdomyolysis (rare)
  • If concerned for compartment syndrome, fasciotomy should be performed within 6 hours of injury
• Myotonic contractions can lead to shoulder dislocations Organ Injury:

Cutaneous Injury:

• Look for singed clothing, holes as below
• Patients should be completely exposed to evaluate for cutaneous injuries
• Treatment: tetanus prophylaxis, irrigation, debridement, wound dressings
• Lichtenberg Figures
  • Pathognomonic, red superficial feathering or ferning pattern
  • Not true thermal burns, disappear within 24 hours
• Flash Burns
  • Mild erythema
  • May involve cornea
• Punctate Burns
  • Circular burns (cigarette shaped)
  • < 1cm, full thickness
• Contact Burns
  • Metal close to the skin is heated resulting burn pattern unique to shape
• Superficial Erythema and Blistering Burns
• Linear Burns:
  • < 5 cm, skinfolds (axilla, groin)

Cardiac Injury:

• Sympathetic activation may result in hypertension and tachycardia
  • Should resolve spontaneously
• Effects: global depression of myocardial contractility, coronary artery spasm, pericardial effusion, and arrhythmias
• EKG: ST elevation, QT prolongation, non-specific T wave inversions [5,7]
• True MIs are rare… but initial EKG can mimic STEMI (ECG changes usually resolve, trend troponins)
• Cardiac arrest secondary to a lightning strike has a better prognosis compared to other etiologies (ex., Occlusive MI); therefore, consider prolonged code

Neurologic Injury:

• Peripheral nerve damage can present with abnormal sensory and/or motor findings
• Other findings include:
  • AMS and depressed consciousness
  • Lower extremity paralysis
  • Seizures
• Autonomic damage, such as fixed, dilated, and asymmetric or non-reactive pupils are an unreliable indicator of death and do not correlate with the degree of brain injury [6]
• Most lethal injuries include heat-induced coagulation of the cerebral cortex, epidural or subdural hematomas, and intracranial hemorrhage
• Pursue CT in cases of coma, persistent altered mental status, focal neurologic deficit, or persistent headache

Metabolic

• Cerebral Salt Wasting
  • Symptoms: hyponatremia + extracellular volume depletion (i.e. hypotension, decreased skin turgor, increased hematocrit) [8]
  • Treatment: Sodium correction

Ophthalmic Injury:

• Lightning-induced cataracts, usually bilateral, can form weeks to years after lightning injury
• Other occular findings: hyphema, vitreous hemorrhage, corneal abrasion, uveitis, retinal detachment or hemorrhage, and optic nerve damage [5,6]
• Perform an ocular exam on all patients and consider ophthalmology consultation for persistent pain or vision changes (dilated exam, etc)

Auditory Injury:

• Blast effect results in tympanic membrane (TM) rupture (seen in 50-80% of patients) [9,10,11]
• Other findings: sensorineural hearing loss, tinnitus, ataxia, vertigo, and injury to the facial nerve [12]

Special Populations: [3]

• Pregnant patients: Fetus is especially prone to injury
  • ~50% of lightning strikes result in fetal demise in utero
  • May also cause placental abruption
  • Pregnant patients should undergo fetal monitoring for at least 4 hours

• Electronic Control Devices (ECDs): taser, stun gun, during arrest

  • Most are treat and release injuries
  • Rare to have electrical injuries
  • Barbs or hooks can cause superficial punctures, minor lacerations, cutaneous burns
  • Consider injury from falls and other trauma Hospital Course:

• Cardiac symptoms lasting more than 6 hours, including persistent ECG changes, dysrhythmia, cardiac arrest, elevated troponin, new cardiac dysfunction (e.g., new cardiomyopathy), or suspicion of direct lightning strike warrant inpatient admission for at least 24 hours for telemetry monitoring and cardiology consultation.

• Consider ICU admission with signs of instability (i.e. hypotension), significant trauma, large burns, or deep tissue injury.
• Once stabilized, patients with significant burns or deep tissue injury should be transferred to a burn center.

• Patients with a reassuring physical exam with no additional risk factors can be watched on telemetry in the ED for 4-6 hours and discharged if no dysrhythmia is apparent [5] Ways to Avoid Lightning Strikes:

• “When thunder roars, go indoors” — ideally inside a large building

• Stay in a metal-roofed vehicle with doors and windows closed (Faraday cage)
• Remove metal objects to avoid contact burns
• Avoid open, exposed areas, summits, and ridgelines, as well as doors and windows
• Avoid tall structures
• If in a group space, stay >20 feet (6 m) apart
• If outdoors, use the ‘lightning position’ as a last resort: crouch with feet together to make one contact point
  • Alternatively, if sitting – lift feet off the ground; insulate from the ground if possible (e.g. sit on a pack)
• Stay indoors until 30 minutes after the last thunderclap is heard (to ensure a 10-mile buffer)
• Exit any water and stay away from the water edge

• Be aware that lightning can strike despite clear skies (typically after a storm – ‘bolt from the blue’) References:

• Browne BJ, Gaasch WR. Electrical injuries and lightning. Emerg Med Clin North Am. 1992;10(2):211-229.

• Zafren K, Durrer B, Herry JP, Brugger H; ICAR and UIAA MEDCOM. Lightning injuries: prevention and on-site treatment in mountains and remote areas. Official guidelines of the International Commission for Mountain Emergency Medicine and the Medical Commission of the International Mountaineering and Climbing Federation (ICAR and UIAA MEDCOM). Resuscitation. 2005;65(3):369-372. doi:10.1016/j.resuscitation.2004.12.014
• Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9. McGraw-Hill Education; 2016.
• ten Duis HJ, Klasen HJ, Reenalda PE. Keraunoparalysis, a ‘specific’ lightning injury. Burns Incl Therm Inj. 1985;12(1):54-57. doi:10.1016/0305-4179(85)90183-4
• Davis C, Engeln A, Johnson E, et al. Wilderness medical society practice guidelines for the prevention and treatment of lightning injuries. Wilderness Environ Med. 2012;23(3):260-269. doi:10.1016/j.wem.2012.05.016
• Jain S, Bandi V. Electrical and lightning injuries. Crit Care Clin. 1999;15(2):319-331. doi:10.1016/s0749-0704(05)70057-9
• Lichtenberg R, Dries D, Ward K, Marshall W, Scanlon P. Cardiovascular effects of lightning strikes. J Am Coll Cardiol. 1993;21(2):531-536. doi:10.1016/0735-1097(93)90699-2
• Emet M, Caner I, Cakir M, Aslan S, Cakir Z. Lightning injury may cause abrupt cerebral salt wasting syndrome. Am J Emerg Med. 2010;28(5):640.e1-640.e6403. doi:10.1016/j.ajem.2009.07.010
• Patten BM. Lightning and electrical injuries. Neurol Clin. 1992;10(4):1047-1058.
• 10.Gluncić I, Roje Z, Gluncić V, Poljak K. Ear injuries caused by lightning: report of 18 cases. J Laryngol Otol. 2001;115(1):4-8. doi:10.1258/0022215011906858
• 11.Wetli CV. Keraunopathology. An analysis of 45 fatalities. Am J Forensic Med Pathol. 1996;17(2):89-98. doi:10.1097/00000433-199606000-00001
• 12.Liew L, Morrison GA. Bilateral hearing loss following electrocution. J Laryngol Otol. 2006;120(1):65-66. doi:10.1017/S0022215105000514
• 13.O’Keefe KP. Electrical injuries and lightning strikes: Evaluation and management. UpToDate. November 3, 2023. Accessed July 4, 2024. https://www.uptodate.com/contents/electrical-injuries-and-lightning-strikes-evaluation-and-management/print.
• 14.Nickson, C. Lightning injury. Life In The Fast Lane. November 3, 2020. Accessed July 4, 2024. https://litfl.com/lightning-injury/

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- Importance of Catheter Selection:

• The catheter’s diameter and length are critical factors affecting the flow rate.
• Shorter, wider catheters provide a higher flow rate, making them preferable for rapid resuscitation.
• Diameter and Flow Rate:
• A larger diameter increases flow rate, and this relationship is proportional to the fourth power. For instance, doubling the diameter results in a 16-fold increase in maximum flow rate.
• Peripheral 16-gauge IVs can sometimes outtransfuse larger central lines like a Cordis, due to their shorter length and adequate diameter.
• Length and Flow Rate:
• Longer catheters, such as triple-lumen catheters, can restrict flow due to increased resistance.
• Practical Implications:
• In emergency situations requiring rapid volume infusion, such as trauma or severe GI bleeding, bilateral 16-gauge IVs are often more effective and quicker to place than a central line.
• Always refer to the packaging for flow rate information, which highlights the differences between catheter types.

Conclusion:

When faced with a patient who requires rapid volume resuscitation, prioritize the use of bilateral peripheral IVs with larger diameters over central lines when possible. This strategic choice can maximize flow rates, enhance resuscitation efforts, and improve patient outcomes.

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     We discuss a case of ataxia in children and how to approach the evaluation of these pts.

Hosts:
Ellen Duncan, MD, PhD
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Ataxia\_in\_Children.mp3   Download Leave a Comment Tags: Neurology, Pediatrics    Show Notes **Introduction**

• The episode focuses on ataxia in children, which can range from self-limiting to life-threatening conditions.
• Pediatric emergency medicine specialist shares insights on the topic.

The Case

• An 18-month-old boy presented with ataxia, unable to keep his head up, sit, or stand, and began vomiting.
• Previously healthy except for recurrent otitis media and viral-induced wheezing.
• The decision to take the child to the emergency department (ED) was based on acute symptoms.

Differential Diagnosis

• Common causes include acute cerebellar ataxia, drug ingestion, Guillain-Barre syndrome, and basilar migraine.
• Less common causes include cerebellitis, encephalitis, brain tumors, and labyrinthitis.

Importance of History and Physical Examination

• A detailed history and physical exam are essential in diagnosing ataxia.
• Key factors include time course, recent infections, signs of increased intracranial pressure, and toxic exposures.
• Look for signs such as bradycardia, hypertension, vomiting, and overall appearance.

Diagnostic Workup

• Initial tests include point-of-care glucose and neuroimaging for concerns about trauma or increased intracranial pressure.
• MRI is preferred for posterior fossa abnormalities, but non-contrast head CT is commonly used due to accessibility.
• Lumbar puncture may be needed if meningismus is present.

Treatment Approach

• Treatment depends on the underlying cause:
  • Acute cerebellar ataxia is self-limiting and typically resolves with time.
  • Antibiotics are required for meningitis or encephalitis.
  • Steroids may be useful for cerebellitis and acute disseminated encephalomyelitis (ADEM).
  • Specialist consultations are necessary for severe diagnoses like intracranial masses.

Outcome of the Case Study

• The child had a normal fast T2 MRI and improved during the ED stay.
• Diagnosed with a combination of cerebellar ataxia and labyrinthitis.
• Received myringotomy tubes and experienced no further neurologic changes or otitis media episodes.

Take-Home Points

1. Diverse Etiologies: Ataxia in children can have various causes that range from self-limiting to life-threatening
2. Comprehensive Assessment: History and physical exams guide diagnosis and workup direction, focusing on symptom time course, infections, and toxic exposures.
3. Physical Examination Clues: Vital signs and appearance offer clues; increased ICP may present with bradycardia, hypertension, and vomiting.
4. Diagnostic Imaging: Point-of-care glucose testing and neuroimaging are key; MRI is preferred for posterior fossa abnormalities.
5. Tailored Treatment: Treatment varies by cause; acute cerebellar ataxia typically resolves over time without specific intervention.

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Author:

• Sarah Beth Spiegel MD

Editor:

• Sarah Battistich, MD
• Jonathan Kobles, MD

Facial nerve blocks offer an applicable option for achieving analgesia in the emergency department.

Potential Indications:

• Burn care
• Fractures and dislocations
• Large lacerations that would require a harmful dose of anesthetic
• Facial lacerations where distortion of the wound would affect the quality of repair
• Wound exploration
• Pain control (headaches, toothaches)

Contraindications:

• Infection around the injection site
• Bleeding disorders
• Preexisting nerve damage is a relative contraindication and should be well-documented before the procedure

Risks

• Nerve Injury
  • Avoid intraneural injection and permanent nerve damage by advancing the needle slowly and monitoring for paresthesia. Parasthesia indicates that the needle tip is within the nerve sheath. Withdraw the needle 1-2mm, wait for the paresthesia to resolve, and then inject anesthetic.1
  • Ultrasound guidance may also decrease the risk of intraneural injection.

Equipment:

• Chlorhexidine
• 18g draw up needle
• 20-27g injection needle
• Syringe

Commonly Used Anesthetics:

Lidocaine (1%) :

• Max dose: 3 mg/kg
• Duration: 30-120 mins

Lidocaine (1%) with epi :

• Max dose: 5 mg/kg
• Duration: 60-400 mins

Bupivacaine (0.25%) :

• Max dose: 1.75 mg/kg
• Duration: 120-240 mins

Bupivacaine (0.25%) with epi:

• Max dose: 2.25 mg/kg
• Duration: 240-480 mins

Tips and tricks for Pain Reduction:

• Consider the use of topical anesthetic (especially for pediatric patients )
• Use buffered anesthesia (3:1 ratio of 1% lidocaine to sodium bicarbonate)
• Warming anesthetic (allow to warm up by holding in pocket or hand) Supraorbital Nerve Block:

Anatomy:

• The supraorbital nerve is a branch of the ophthalmic division of the trigeminal nerve.
• It emerges through the supraorbital foramen at the midline of the superior orbital ridge in line with the pupil.
• It is generally blocked together with the supratrochlear nerve.

Technique:

1. Palpate the supraorbital notch.
2. Insert the needle in the subcutaneous space superior to the eyebrow in line with the pupil.
3. Direct the needle tip medially to create a horizontal wheel extending from the medial border of the brow using 2-5cc of anesthetic. Infraorbital Nerve Block

Anatomy:

• The infraorbital nerve is a branch of the maxillary division of the trigeminal nerve. It runs out of the infraorbital foramen ~1cm inferior to the mid-infraorbital ridge and in line with the pupil.
• It provides sensory innervation to the medial cheek and upper lip.
• The infraorbital nerve branches into the anterior and middle superior alveolar nerves, providing sensation to maxillary incisors, canine, and premolar teeth.

Extraoral Technique:

1. Palpate the infraorbital foramen.
2. Insert needle just inferior to foramen until needle touches maxilla.
3. Inject 1-2cc anesthetic.

Intraoral Technique:

1. Provide topical anesthetic to the mucosa superior to the maxillary canine.
2. Dry the mucosa.
3. Using your non-dominant hand, place your index finger on the infraorbital foramen and use your thumb to retract the lip.
4. Insert your needle into the gingival reflection superior to the maxillary canine. Direct the needle superiorly until you reach the foramen (about halfway between the orbital rim and gingival reflection). Inject 3-5cc of anesthetic. Mental Nerve Block

Anatomy:

• The mental nerve is a branch of the mandibular division of the trigeminal nerve.
• It exits the skull at the mental foramen. The mental foramen is vertically in line with the supraorbital foramen, infraorbital foramen, and pupil. It is horizontally in line with the middle of the body of the mandible.
• It provides sensation to the skin of the lower lip and chin.

Extraoral approach:

1. Palpate the mental foramen using the above approach.
2. Place a wheel superior to the foramen.
3. Insert the needle through the wheel until it contacts the mandible.
4. Inject 1-2cc of anesthetic.

Intraoral approach

1. Provide topical anesthetic to the mucosa at the junction of the lower canine and first premolar (mouth can be open or closed).
2. Dry the mucosa.
3. Insert the needle inferiorly and posteriorly through the gingival mucosa.
4. Advance ⅓ of the depth of the mandible body and make contact with the mandible.

5. Inject 1-2 cc of anesthetic. Occipital Nerves:

6. Anatomy: The occipital nerves are a group of nerves that arise from C2-C3 and provide innervation to the posterior scalp and ear. They include the greater occipital nerve, the lesser occipital nerve, and the third occipital nerve.

7. Indications: occipital neuralgia, cluster headache, occipital migraine

Greater occipital Nerve block:

Anatomy:

• The greater occipital nerve branches off C2 and provides sensory to the posterior neck up to the scalp vertex.
• The greater occipital nerve runs just medial to the posterior occipital artery.

Technique:

1. Palpate the occipital protuberance and mastoid process. Draw an imaginary line between the two.
2. The occipital artery can be palpable about ⅓ of the occipital protuberance.
3. Inject a small amount of anesthetic to make a wheel over the occipital artery.
4. Inject 1 ml of anesthetic 1-2mm to the left and right of the artery—aspirate before injection to avoid intravascular injection.

If the occipital artery cannot be palpated, divide the imaginary line between the mastoid process and external occipital protuberance into thirds. Infiltrate the middle third with 5-8cc of anesthetic (will also anesthetize the lesser occipital nerve)

Lesser occipital nerve block:

Anatomy:

• The lesser occipital nerve is a branch of the cervical plexus.
• It provides innervation to the skin between the skin and scalp, between the ear and the mastoid process.
• The lesser occipital nerve emerges from the middle third of the posterior border of the sternocleidomastoid muscle and travels superiorly towards the mastoid process.

Technique:

1. Make a wheel just posterior to the mastoid process.
2. Insert the needle through the wheel towards the posterior ear.
3. Once the posterior ear is contacted, aspirate and inject anesthetic while pulling back towards the wheel to anesthetize the area between the mastoid process and the posterior ear. Aurical Block:

Anatomy:

• The ear is innervated by two nerves.
  • The auriculotemporal nerve innervates the anterior ear.
  • The greater auricular nerve innervates the posterior ear.

Technique: This technique is a ring block and will anesthetize the entire ear.

1. 1. Insert the needle into the skin just inferior to the attachment of the ear lobe to the scalp.
   2. Advance the needle towards the tragus while aspirating. Inject 2-3cc of anesthetic while withdrawing.
   3. Redirect the needle posteriorly and superiorly aspirating while advancing. Inject 2-3 cc of anesthetic while withdrawing.
   4. Interior the needle into the skin just superior to where the ear’s helix attaches to the scalp.
   5. Advance the needle towards tragus aspirating while advancing. Inject 2-3cc of anesthetic while withdrawing.
   6. Redirect the needle posterior and inferiorly aspirating while advancing. Inject 2-3cc of anesthetic while withdrawing. Ultrasound Guidance:

US guidance may lead to fewer complications (intravascular injection, vascular puncture, intraneural injection), higher success rate, shorter procedure time, and less total anesthetic used.5 Ultrasound guidance can be applied to all the techniques discussed above.

Technique:

1. Identify the foramen using the landmark technique.
2. Use a linear probe to confirm the location of the foramen.
3. Use your non-dominant hand to hold the US probe and your dominant hand to insert the needle in the longitudinal axis and inject around the foramen (avoid injecting directly into the foramen, as increased pressure can result in nerve necrosis).

References:

1. Tintinalies chapter 156.
2. https://www.nuemblog.com/blog/occipital-nerve-block
3. Chapter 156: Regional Nerve Blocks (Regional Anesthesia), Eric F. Reichman; Jehangir Meer
4. Atlas of Pain Medicine Procedures. Sudhir Diwan, Peter S. Staats. Chapter 20: Periorbital Nerve Blocks (Supraorbital, Supratrochlear, and Infraorbital Nerves), Sanford Silverman. ©2021 McGraw Hill. All Rights Reserved
5. Kasia Rubin, Denise Sullivan, Senthilkumar Sadhasivam. Are peripheral and neuraxial blocks with ultrasound guidance more effective and safe in children? Paediatr Anaesth. 2009 Feb;19(2):92-6.

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     We discuss the approach to diagnosing and managing hypernatremia in the emergency department.

Hosts:
Abigail Olinde, MD
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hypernatremia.mp3   Download Leave a Comment Tags: Electorlye    Show Notes **Episode Overview:**

• Introduction to Hypernatremia
• Definition and basic concepts
• Clinical presentation and risk factors
• Diagnosis and management strategies
• Special considerations and potential complications

Definition and Pathophysiology:

• Hypernatremia is defined as a serum sodium level over 145 mEq/L.
• It can be acute or chronic, with chronic cases being more common.
• Symptoms range from nausea and vomiting to altered mental status and coma.

Causes of Hypernatremia based on urine studies:

• Urine Osmolality > 700 mosmol/kg
  • Causes:
    • Extrarenal Water Losses: Dehydration due to sweating, fever, or respiratory losses
    • Unreplaced GI Losses: Vomiting, diarrhea
    • Unreplaced Insensible Losses: Burns, extensive skin diseases
    • Renal Water Losses with Intact AVP Response:
    • Diuretic phase of acute kidney injury
    • Recovery phase of acute tubular necrosis
    • Postobstructive diuresis
• Urine Osmolality 300-600 mosmol/kg
  • Causes:
    • Osmotic Diuresis: High glucose (diabetes mellitus), mannitol, high urea
    • Partial AVP Deficiency: Incomplete central diabetes insipidus
    • Partial AVP Resistance: Nephrogenic diabetes insipidus
• Urine Osmolality < 300 mosmol/kg
  • Causes:
    • Complete AVP Deficiency: Central diabetes insipidus
    • Complete AVP Resistance: Nephrogenic diabetes insipidus
• Urine Sodium < 25 mEq/L
  • Causes:
    • Extrarenal Water Losses with Volume Depletion: Vomiting, diarrhea, burns
    • Unreplaced Insensible Losses: Sweating, fever, respiratory losses
• Urine Sodium > 100 mEq/L
  • Causes:
    • Sodium Overload: Ingestion of salt tablets, hypertonic saline administration
    • Salt Poisoning: Deliberate or accidental ingestion of large amounts of salt
• Mixed or Variable Urine Sodium
  • Causes:
    • Diuretic Use: Loop diuretics, thiazides
    • Adrenal Insufficiency: Mineralocorticoid deficiency
    • Osmotic Diuresis with Renal Water Losses: High glucose, mannitol

Risk Factors:

• Patients with impaired thirst response or those unable to access water (e.g., altered or ventilated patients) are at higher risk.
• Important to consider underlying conditions affecting thirst mechanisms.

Diagnosis:

• Initial assessment includes history, physical examination, and laboratory tests.
• Key tests: urine osmolality and urine sodium levels.
• Lab errors should be considered if the clinical picture does not match the lab results.

Management Strategies:

• Calculate the Free Water Deficit (FWD) to guide treatment.

• Administration routes include oral, NGT, G-tube, or IV with D5W for larger deficits.

• Safe correction rate is 10-12 mEq/L per day or 0.5 mEq/L per hour to avoid cerebral edema.
• Address hypovolemia with isotonic fluids before correcting sodium.

Monitoring and Follow-Up:

• Monitor sodium levels every 4-6 hours.
• Assess urine output and adjust free water administration as needed.
• Admission to ICU for symptomatic patients or those with severe hypernatremia (sodium >160 mEq/L).
• Decision to discharge vs admit is a complicated one that factors in symptoms, etiology, degree of hypernatremia, patient preference, access to follow up, etc.

Take Home Points:

• Hypernatremia is a serum sodium level over 145 mEq/L, with symptoms ranging from nausea to coma.
• It is primarily caused by water loss exceeding intake due to various factors like sweating, vomiting, diarrhea, and renal issues.
• Correcting hypernatremia too quickly can lead to cerebral edema, so a safe correction rate is essential.
• Initial treatment involves calculating the Free Water Deficit and selecting the appropriate administration route.
• Monitor sodium levels frequently and decide on admission or discharge based on symptoms, sodium levels, and patient’s ability to follow up.

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     We discuss an approach to the acutely agitated patient and review medications commonly used.

Hosts:
Jonathan Kobles, MD
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Acute\_Agitation.mp3   Download Leave a Comment Tags: Agitation, psychiatry, Toxicology    Show Notes **Background/Epidemiology**

•Definition and Scope: Agitation encompasses behaviors from restlessness to severe altered mental states. It’s a common emergency department presentation, often linked with acute medical or psychiatric emergencies.

•Significance: Patients with agitation are at high risk for morbidity and mortality, necessitating prompt and effective management to prevent harm to themselves and healthcare providers.

A Changing Paradigm in Describing Agitation

•Terminology Shift: Move away from terms like ‘excited delirium’ due to their politicization and stigmatization. Focus on describing agitation by severity and underlying causes.

Agitation as a Multifactorial Process

•Complex Nature: Recognize agitation as a result of various factors, including medical, psychiatric, and environmental influences.

Recognizing Agitation

•Signs and Symptoms: Identify agitation early by monitoring for behaviors such as hostility, pacing, non-compliance, and verbal aggression.

Initial Evaluation

•Severity Assessment: Determine the severity of agitation and prioritize reversible causes and life-threatening conditions.

•Diagnostic Steps: Perform vital signs check, blood glucose levels, ECG, and a targeted medical screening exam.

Life Threats

•Immediate Concerns: Identify and address immediate life threats such as hypoxia, hypoglycemia, trauma, and acute neurological emergencies.

Forming a Differential Prior to Treatment

•Prioritization: Severe agitation requires immediate treatment to facilitate further evaluation and reduce risk of harm.

Physician/Staff Safety

•Safety Measures: Ensure personal and team safety by maintaining a calm environment and preparing for potential violence.

Multimodal Approach

•Self-check In: Physicians should mentally prepare and approach the situation calmly to ensure effective management.

•Verbal De-escalation: Use techniques focused on safety, therapeutic alliance, and patient autonomy to manage agitation non-pharmacologically.

Medication Administration

•Oral/Sublingual Medications: Consider oral medications for less severe cases to maintain patient autonomy and avoid invasive procedures.

•IM or IV Medications: Use intramuscular or intravenous medications for rapid control in severe cases.

Specific Medication Regimens

•PO Regimens:

•Medications: Antipsychotics like Zyprexa (olanzapine) 5-10 mg, benzodiazepines like Ativan (lorazepam) 1-2 mg.

•Benefits: Empower patients with a sense of autonomy, avoid injection-related trauma.

•Pharmacokinetics:

•Olanzapine: Onset in 15-45 minutes, peak effect in 1-2 hours, duration 12-24 hours.

•Lorazepam: Onset in 30-60 minutes, peak effect in 2 hours, duration 6-8 hours.

•IV/IM Regimens:

•Medications: Droperidol, haloperidol, midazolam, ketamine.

•ACEP 2023 Guidelines: Recommend droperidol with midazolam or an atypical antipsychotic for severe agitation.

•Pharmacokinetics (IM):

•Haloperidol: IM onset in 15, time to sedation ~25 minutes, can last for 2 hours

•Droperidol: IM onset in 5-10 minutes, duration 2-4 hours but can last as long as 12 hours

•Midazolam: IM onset ~15 minutes, , duration 20 minutes – 2 hours.

•Lorazepam: IM onset ~15-30 minutes, , duration up to 3 hours

•Ketamine: IM onset in ~5 minutes, duration 5-30 minutes.

Special Situations

•Elderly/Dementia: Optimize environment, use non-pharmacologic measures, avoid benzodiazepines to reduce delirium risk.

•Parkinson’s Disease: Avoid antipsychotics that can precipitate a Parkinsonian crisis.

•Autism/Pediatrics: Engage caregivers, create a calming environment, avoid aggressive measures.

•Alcohol Withdrawal: Utilize benzodiazepines and phenobarbital.

Re-dosing and Physical Restraints

•Re-dosing: Use the lowest effective dose, consider continuous monitoring, and reassess frequently.

•Physical Restraints: Employ as a last resort, ensuring close monitoring for any adverse effects.

Final Points

•Clinical Leadership: Physicians should lead with clear communication, planning, and support for the team.

•Continuous Learning: Regular debriefing and assessment after each incident to improve future responses.

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Optimizing Trauma Resuscitation Education: A Year-Long In-Situ Simulation Curriculum

Ashika Jain, MD, Nelly Parisot, MD, Michael J. Klein, MD, Janice Shin-Kim, MD, Brian Lin, MD, Julia Paris, MD, Shannon McNamara, MD, Jessica Strauss, MD, Soma Pathak, MD

Delivering optimal care in a trauma resuscitation requires a highly coordinated and skilled team. Traditional learning methods, while valuable, may not fully prepare healthcare professionals for the high-pressure environment of a real-life trauma situation. In-situ simulation (ISS) training offers a powerful alternative by enabling teams to practice within their actual working environment with realistic scenarios. This curriculum was written by our Emergency Medicine and Trauma Surgery faculty and outlines a year-long in-situ program designed for our Level I trauma centers. The program aims to enhance the knowledge, skills, and teamwork of healthcare professionals involved in trauma care. It fosters a collaborative learning environment for interdisciplinary and interprofessional teams.

Multiple studies have demonstrated the effectiveness of in-situ simulation training in trauma care. A review by Steinemann et al. showed that ISS training led to improvements in team communication, leadership, and resource management [1]. Similarly, Miller et al. found that ISS training significantly improved non-technical skills, including situational awareness and prioritization, during real trauma resuscitations [2]. These findings suggest that ISS training can translate theoretical knowledge into improved clinical practice.

This curriculum features monthly ISS scenarios focusing on a variety of common and challenging trauma presentations. Each scenario is designed to be completed within a one-hour timeframe, minimizing disruption to patient care. Each scenario is followed by a facilitated debriefing session led by experienced faculty. Debriefing focuses on performance strengths and weaknesses, promoting reflection and improvement. By practicing in a realistic environment and receiving targeted feedback, healthcare professionals can develop the skills and teamwork necessary to optimize patient outcomes in time-critical trauma situations.

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Curriculum:

MVA: Pneumothorax

• https://docs.google.com/document/d/11Jbbcu4T0VfIKx1XLzg902BmBplu7o6J/edit

MVA: Liver Laceration

• https://docs.google.com/document/d/10CQ6fZ6y340ykp-z5m5nNNP16P8DUFly/edit?dls=true

Fall: Open Pelvic Fracture

• https://docs.google.com/document/d/1LZJyPxMYh2M_onjrciXUqciRRk06jLpT/edit

MVA: Femur Fracture with Hemorrhagic Shock

• https://docs.google.com/document/d/1M5oEfMTJ64HUEDHEUld-SxDSYmA8Wh3N/edit

MVA: Pregnant Patient

• https://docs.google.com/document/d/1sJg53IM2dszKaxMZozhy0o33MJ2fDSQ6/edit

Neurogenic Shock

• https://docs.google.com/document/d/1lzIq9SffTTXmooHVWzOaTtj3MW2Dxw3W/edit

Stab Wound: Pericardial Effusion

• https://docs.google.com/document/d/1A4dHV_I7WotRIn0-Xa3JGXBjUAs1RQUn/edit

GSW: Tension Pneumothorax

• https://docs.google.com/document/d/19k7igX52C85PeVVG9XvV6qtSMa-cdeQY/edit

Fall: Epidural Hematoma

• https://docs.google.com/document/d/1wKt76lyiYo9ba7la7fuQtEd3NAgVVIID/edit

Surgical Airway in Trauma

• https://docs.google.com/document/d/15de9Dmom_T8bRAr82ANFHGRClWDXxGac/edit?dls=true

AKA

• https://docs.google.com/document/d/1KCCIbGqsqZDKDaVHSYw82kWbuFAsol91/edit

MVA: Liver Laceration and AMS

• https://docs.google.com/document/d/1o1E0Ozn2-HUFYndR1uE5tGpslxr5jKdl/edit

References

• Steinemann, S., et al. (2011). In situ simulation-based trauma team training: A pilot study. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, 19(1), 1-7.
• Miller, R. D., et al. (2012). The impact of in situ simulation on trauma team performance. The American Journal of Surgery, 204(2), 225-232

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• Author: Melissa A. Socarras, MD MS
• Editor: Jonathan Kobles, MD

Definition and Background:

• Pneumocystis is an atypical fungal microorganism that can cause potentially life-threatening pulmonary infection in immunocompromised individuals.
• Highest risk patients: HIV positive with CD4 < 200
  • PJP is the most common initial opportunistic infection that establishes the diagnosis of AIDS
  • PJP infection is the most common identifiable cause of death in patients with AIDS
• Other at-risk patients:
  • Hematologic or solid organ transplant recipients
  • Malignancies (especially hematologic)
  • Chronic glucocorticoids, chemotherapeutics agents, and other immunosuppressive medications.

;

Epidemiology:

• During WWI, PJP was first observed in humans through malnourished and premature infants.
• In the 1980s, there was a steep rise in PJP infections correlating to the AIDS epidemic as pneumocystis became an AIDS-defining illness.

;

Pathophysiology:

• Transmission is via airborne route, and acquisition of new infections is likely person-to-person.
• Pneumocystis attaches to Type 1 alveolar epithelial cells in the host, prompting the fungus to transition from the trophic state to the cystic state. This attachment initiates a cascade of cellular responses in both the pneumocystis organism and the host lung tissue, resulting in lung injury.
• CD4+ T cells are essential for the control of pneumocystis infection.

;

Clinical Presentation:

• Symptoms and physical examination are typically non-specific.
  • Symptoms:
    • Nonproductive and dry cough (95% of patients)
    • Low-grade fever (80% of patients)
    • Progressive dyspnea (95% of patients)
  • Exam:
    • 50% of cases will have clear lung sounds; abnormal findings often include crackles and rhonchi.
    • Hypoxemia, tachypnea, and tachycardia will be present in more severe cases. However, some of these can be elicited with exertion in mild cases.
    • Ambulatory saturation can be a valuable tool in the ED to identify subtle hypoxia with exertion.
• HIV-positive patients: More likely to present with indolent and subtle onset of symptoms over weeks
  • • Mortality: 17-30%
• Non-HIV immunocompromised patients: More likely to present with more abrupt onset of symptoms; will present with fulminant infection, especially if onset is shortly after receiving corticosteroids.
  • • Mortality: 28 – 53%
• Consider PJP and undiagnosed HIV in patients who present with:
  • Hypoxemia without any other explanation
  • History of high-risk sexual behavior or injection drug use
  • History of constitutional symptoms, including unexpected weight loss, night sweats, fatigue, and lymphadenopathy
  • Signs and symptoms of pneumonia with bilateral chest x-ray infiltrates (see below)

;

Evaluation and Differential Diagnosis:

Most laboratory findings are non-specific.

• Lymphocyte count: A value < 10% of normal has been associated with a poor prognosis.
• Beta-d-glucan: Elevated value should raise suspicion if one is already concerned about possible PJP infection, but a positive test in isolation cannot be considered diagnostic.
• LDH:
  • Extracellular LDH indicates lung tissue cellular damage and death.
  • An elevated level is not specific to PJP infection; however, infection has been associated with levels > 500.
  • LDH values can help exclude PJP in HIV-positive patients.
    • HIV positive: sensitivity 100% / specificity 47%
      • A negative result can exclude Disease, but a positive result does not confirm the diagnosis.
    • HIV negative: sensitivity 63% / specificity 43%
• ABG: Routine testing in hypoxic patients is important to calculate the alveolar-arterial (A-a) oxygen gradient. PJP increases the A-a gradient.

;

Radiographic findings are non-specific and cannot provide a definitive diagnosis.

• CXR:
  • Classic findings are bilateral, diffuse interstitial infiltrates (bat-wing pattern); however, they may also present with focal consolidation, nodular lesions, cavitary lesions, and adenopathy.
  • 15 to 25% of CXR may appear negative, especially in the early stages of the Disease.
• Chest CT:
  • Ground glass opacities with a patchy distribution, predominantly in the perihilar region of the lungs.
  • CT chest is more sensitive than CXR and can show infection in early stages.
  • Early Stage PJP: 20% of CTs demonstrate GCOs.
  • Mid Stage PJP: 47% of CTs demonstrate GCOs and patchy consolidations.
  • Late Stage PJP: 80% of CTs demonstrate predominant consolidations.

;

Microbiological Testing:

• Confirmation of PJP infection involves inpatient diagnostics, including bronchoscopy with specimen analyses.
• Pneumocystis cannot be cultured.
• PCR of BAL: sensitivity 100% / specificity 87%
• PCR of induced sputum: sensitivity 97% / specificity 93%

;

Consider a broad differential diagnosis in HIV patients presenting with symptoms and findings suggestive of respiratory infection, including:

• Bacterial Pneumonia
  • Streptococcus pneumoniae is the most common cause of HIV-associated pneumonia in the US and Western Europe.
• Tuberculosis
  • 10% of new cases in the US occur in HIV-infect4ed patients
  • TB should be considered in any HIV-infected patient presenting with pulmonary symptoms, and appropriate precautions should be taken to avoid transmission.
• Mycobacterium avium-intracellulare complex (MAC)
• Viral Pneumonia
  • CMV, common respiratory viruses including influenza and COVID
• Fungal infection
  • Histoplasmosis, Coccidioidomycosis, Cryptococcus (abnormal pulmonary adenopathy)
• Kaposi’s Sarcoma (nodular lesions)

;

Management:

• Treatment for PJP should begin immediately when clinical suspicion is high. Treatment should not be delayed to obtain diagnostic confirmation.
• Treatment of PJP is determined by disease severity.
  • Mild Disease: A-a O2 gradient < 35 mmHg or PaO ≥70 mmHg.
  • Moderate disease: A-a O2 gradient of 35-45 mmHg or PaO ≥60 and <70 mmHg
  • Severe Disease: A-a O2 gradient of ≥45 mmHg or PaO <60 mmHg or signs of respiratory failure.
• Treat fulminant respiratory failure with ARDS principles:
  • Review an up-to-date approach to the management of ARDS: https://coreem.net/podcast/episode-195-ards/

;

Antibiotics:

• Trimethoprim-sulfamethoxazole: mainstay of treatment
  • Mild to Moderate Disease: TMP 15 to 20 mg/kg/day and SMX 75 to 100 mg/kg/day PO in 3-4 divided doses OR TMP-SMX DS two tablets three times a day.
  • Severe Disease: TMP 15 to 20 mg and SMX 75 to 100 mg/kg/day IV every 6 – 8 hours; switch to PO when the patient demonstrates clinical improvement.
• In cases of allergy or adverse reaction to TMP-SMX:
  • Adverse reactions to TMP-SMX are common in patients with AIDS and may present with rash, fever, or neutropenia.
    • • Mild allergy: patients should undergo desensitization treatment.
      • Severe allergy: desensitization is not recommended.
  • Alternative regimens for mild to moderate Disease:
    • • Atovaquone 750 mg, PO BID
      • Trimethoprim 15 mg/kg/day PO BID + dapsone 100 mg PO QD
      • Primaquine 30 mg QD + clindamycin 450 mg PO Q6 or 600 mg Q8
  • Alternative regimens for severe Disease:
    • • Pentamidine 4 mg/kg IV QD over 60 minutes
      • Primaquine 30 mg PO QD + clindamycin IV 600 mg Q6 or 900 mg Q8
• Duration of Treatment:
  • • HIV Positive Patients: at least 21 days
    • Non-HIV Patients: at least 14 days
• PJP Prophylaxis
  • • Recommended for all patients with CD4+ T-cell counts of < 200 to mitigate PJP
    • The preferred regimen is TMP-SMX, one double-strength tablet daily.

;

Steroids:

• Studies evaluating the benefits of steroids have almost exclusively been done in HIV-positive patients. Evidence in non-HIV-positive patients is sparse.
• HIV-positive patients with moderate to severe Disease (A-a > 35 or PaO2 < 70):
  • 21-day prednisone taper:
    • • 40 mg PO BID x 5 days
      • 40 mg PO QD x 5 days
      • 20 mg PO QD x 11 days
  • If IV dosing is necessary:
    • • Methylprednisolone at 75% of prednisone dose

;

Take Home Points:

• Clinical presentation of PJP Pneumonia may vary, with notable differences in disease progression between HIV-positive and non-HIV-positive patients.
• Symptoms are typically non-specific and include cough, fever, and dyspnea. Hypoxia presents in fulminant or late states of PJP infection; however, subtle hypoxia may be identified with ambulatory saturations in the ED.
• Maintain a broad differential diagnosis in immunocompromised patients presenting with respiratory symptoms.
• Treatment is dependent on the severity of the illness.
  • Mild Disease: oral Bactrim
  • Moderate Disease (A-a O2 gradient of 35-45 mmHg or PaO ≥60 and <70 mmHg): oral Bactrim with a 21-day steroid taper.
  • Severe Disease (A-a O2 gradient of ≥45 mmHg or PaO <60 mmHg or signs of respiratory failure): IV Bactrim with a 21-day steroid taper.

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References:

1. Avino LJ, Naylor SM, Roecker AM. Pneumocystis jirovecii Pneumonia in the Non–HIV-Infected Population. Annals of Pharmacotherapy. 2016;50(8):673-679. doi:https://doi.org/10.1177/1060028016650107
2. Catherinot E, Lanternier F, Bougnoux ME, Lecuit M, Couderc LJ, Lortholary O. Pneumocystis jirovecii Pneumonia. Infectious Disease Clinics of North America. 2010;24(1):107-138. doi:https://doi.org/10.1016/j.idc.2009.10.010
3. Cushion MT, Stringer JR. Has the Name Really Been Changed? It Has for Most Researchers. Clinical Infectious Diseases. 2005;41(12):1756-1758. doi:https://doi.org/10.1086/498158
4. Sax P. Epidemiology, clinical presentation, and diagnosis of Pneumocystis pulmonary infection in patients with HIV. UpToDate. Published April 13, 2023. Accessed April 18, 2024.
5. Sax P. Treatment and prevention of Pneumocystis infection in patients with HIV. UpToDate. Published September 12, 2022. Accessed April 18, 2024.
6. Stringer JR, Beard CB, Miller RF, Wakefield AE. A New Name forPneumocystisfrom Humans and New Perspectives on the Host-Pathogen Relationship. Emerging Infectious Diseases. 2002;8(9):891-896. doi:https://doi.org/10.3201/eid0809.020096
7. Thomas C, Limper A. Epidemiology, clinical manifestations, and diagnosis of Pneumocystis pneumonia in patients without HIV. UpToDate. Published November 16, 2023. Accessed April 18, 2024.
8. Thomas C, Limper A. Treatment and prevention of Pneumocystis pneumonia in patients without HIV. UpToDate. Published January 9, 2024. Accessed April 18, 2024.
9. Tintinalli J, J. Stapczynski, O. John Ma, Cline D, Cydulka R, Meckler G. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, Seventh Edition. McGraw Hill Professional; 2010.
10. Truong J, Ashurst JV. Pneumocystis jirovecii Pneumonia. [Updated 2023 Jan 21]. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482370/
11. Weyant RB, Kabbani D, Doucette K, Lau C, Cervera C. Pneumocystis jirovecii: a review with a focus on prevention and treatment. Expert Opinion on Pharmacotherapy. 2021;22(12):1579-1592. doi:https://doi.org/10.1080/14656566.2021.1915989
12. White PL, Backx M, Barnes RA. Diagnosis and management of Pneumocystis jirovecii infection. Expert Review of Anti-infective Therapy. 2017;15(5):435-447. doi:https://doi.org/10.1080/14787210.2017.1305887

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    We discuss an approach to the critically ill infant.

Hosts:
Ellen Duncan, MD, PhD
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/The\_Critically\_Ill\_Infant.mp3   Download Leave a Comment Tags: Pediatrics    Show Notes **The Critically Ill Infant: THE MISFITS****Trauma*** ‘T’ in the mnemonic stands for trauma, which includes both accidental and intentional causes.

• Considerations for Non-accidental Trauma:
  • Stresses the importance of considering non-accidental trauma, especially given that it may not always present with obvious external signs.
• Anatomical Vulnerabilities:
  • Highlights specific anatomical considerations for infants who suffer from trauma:
    • Infants have proportionally larger heads, increasing their susceptibility to high cervical spine (c-spine) injuries.
    • Their liver and spleen are less protected, making abdominal injuries potentially more severe.

Heart 5 T’s of Cyanotic Congenital Heart Disease: Introduces a mnemonic to help remember key right-sided ductal-dependent lesions: + Truncus Arteriosus: Single vessel serving as both pulmonary and systemic outflow tract. + Transposition of the Great Arteries: The pulmonary artery and aorta are switched, leading to improper circulation. + Tricuspid Atresia: Absence of the tricuspid valve, leading to inadequate development of the right ventricle and pulmonary circulation issues. + Tetralogy of Fallot: Comprises four defects—ventricular septal defect, pulmonary stenosis, right ventricular hypertrophy, and an overriding aorta. + Total Anomalous Pulmonary Venous Connection (TAPVC): Pulmonary veins do not connect to the left atrium but rather to the right heart or veins, causing oxygen-rich blood to mix with oxygen-poor blood. * Other Significant Conditions: + Ebstein’s Anomaly: Malformation of the tricuspid valve affecting right-sided heart function. + Pulmonary Atresia/Stenosis: Incomplete formation or narrowing of the pulmonary valve obstructs blood flow to the lungs. * Left-sided Ductal-Dependent Lesions: + Conditions such as aortic arch abnormalities (coarctation or interrupted arch), critical aortic stenosis, and hypoplastic left heart syndrome are highlighted. These generally present with less obvious cyanosis and more pallor. * Diagnostic and Management Considerations: + Routine prenatal ultrasounds detect most cases, but conditions like coarctation of the aorta and TAPVC might not be apparent until after birth when the ductus arteriosus closes. + Emphasizes the importance of a thorough physical exam: checking for murmurs, assessing hepatosplenomegaly, feeling for femoral pulses, measuring pre- and post-ductal saturations, and taking blood pressures in all four limbs. * Treatment Recommendations*: + Early initiation of alprostadil (a prostaglandin) for patients with suspected ductal-dependent lesions to maintain ductal patency. + Preparedness for potential complications from alprostadil treatment, such as apnea and hypotension, which may necessitate intubation and hemodynamic support.

Endocrine* Focuses on acute salt-wasting crisis in undiagnosed Congenital Adrenal Hyperplasia (CAH). * Electrolyte imbalances: ↓Na, ↑K, ↓HCO3, ↓Glu. * Treatment: hydrocortisone (25mg for babies, 50mg for kids, 100mg for adults).

Metabolic* Electrolyte abnormalities such as hypoglycemia (values: <60 in infants, <40 in neonates). * Broad differential. * Rule of 50s for correction: D% x #ml/kg fluid = 50.

Inborn Errors of Metabolism* Major classes include organic acidurias (profound anion gap metabolic acidosis) and urea cycle defects (hyperammonemia) * Recommendation: Draw gas and ammonia level.

Sepsis Emphasized as a critical condition in the differential diagnosis for ill infants, though placed later in the mnemonic for easier recall. * Presentation and Diagnosis: + Sepsis in infants often presents nonspecifically, making early detection challenging. + Immediate drawing of blood cultures upon suspicion of sepsis. * Initial Treatment: + Prompt initiation of antimicrobials and fluids. + Use of vancomycin for gram-positive and MRSA coverage, a third-generation cephalosporin or pip-tazo for broad bacterial coverage, and acyclovir for HSV. (tailor based on age and institutional guidelines) * Supportive Care*: + Highlights the necessity of fluid resuscitation to stabilize the patient.

Formula Formula-Related Electrolyte Imbalances: + Incorrect mixing of infant formula can cause hypo- or hypernatremia. * Consequences of Electrolyte Imbalances: + Both conditions can lead to severe outcomes including altered mental status, seizures, coma, and potentially death. * Management Strategies*: + Treatment varies based on the sodium levels: - Symptomatic hyponatremia is treated with hypertonic saline. - Hypernatremia requires fluid resuscitation.

Intestinal Catastrophe Specific Conditions: + Malrotation with Midgut Volvulus: Twisting of the intestines that can obstruct blood flow. + Necrotizing Enterocolitis (NEC): Can occur in both full-term and preterm infants, involves inflammation and bacterial infection that can destroy bowel tissue. + Hirschsprung-associated Enterocolitis: Complication of Hirschsprung’s disease involving blockage and infection. + Intussusception: Older infants might only show altered mental status instead of the typical intermittent pain and lethargy. * Symptoms: + Common symptoms include bilious emesis (green vomit) or hematemesis (vomiting blood). * Emergency Response*: + Urges early mobilization of pediatric surgery and radiology teams upon suspicion of these conditions.

Toxins* Includes intentional or unintentional ingestion. * One pill killers include: calcium channel blockers (CCB), tricyclic antidepressants (TCA), opiates, sulfonylureas, Class 1 antiarrhythmics, antimalarials, camphor, oil of wintergreen.

Seizures The second ‘S’ in the mnemonic refers to seizures, which can be triggered by various conditions such as hypoglycemia, sepsis, inborn errors of metabolism, and trauma. * First-Line Treatment: + Actively seizing patients should initially be treated with benzodiazepines. * Second-Line Medications: + Includes fosphenytoin, phenobarbital, levetiracetam (Keppra), and valproic acid. * Management of Reversible Causes: + Urges prompt treatment of any identifiable causes like hypoglycemia or electrolyte imbalances. * Special Consideration*: + Notes the possibility of pyridoxine-dependent epilepsy in neonates, recommending pyridoxine (vitamin B6) for intractable seizures unresponsive to multiple antiepileptic drugs (AEDs).

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     We revisit the topic of Hyperkelamia to update our prior episode from 2015 (pre-Lokelma)

Hosts:
Brian Gilberti, MD
Jonathan Kobles, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hyperkalemia.mp3   Download Leave a Comment Tags: Renal Colic    Show Notes **Introduction**

1. Background
2. • Physiology: - Normal range and the significance of deviations (>5.5 mEq/L)
   • Epidemiology:
     • Prevalence of hyperkalemia in the ER
     • ESRD missed HD → ECG, monitor

Causes / Risk Factors

• • Causes - Kidney Dysfunction, Medications, Cellular Destruction, Endocrine Causes, Pseudohyperkalemia
• • High-Risk Medications:
• • • Antibiotics: Bactrim, antifungals
• • • Calcineurin inhibitors
• • • Beta-blockers
• • • ACE/ARB
• • • K+ Sparing diuretics
• • • NSAIDs
• • • Digoxin
• • • SUX – high risks in neuromuscular disease
• • Lab errors, hemolysis in samples - VBG vs Chem accuracy - When to repeat a hemolyzed sample - 2023 study: Of the 145 children with hemolyzed hyperkalemia, 142 (97.9%) had a normal repeat potassium level. Three children (2.1%) had true hyperkalemia: one had known chronic renal failure and was referred to the ED due to concern for electrolyte abnormalities; the other 2 patients had diabetic ketoacidosis (DKA).

Clinical Presentation / eval

• Symptomatic vs. Asymptomatic:
  • “First symptom of hyperkalemia is death”
  • If severe, ascending muscle weakness → paralysis
    • Point at which patients experience symptoms depends on chronicity

      • 7 mEq/L if chronic and can be lower if acute

  • Hyperkalemia can be a cause of non-specific GI symptoms
• EKG Changes:
  • ECG findings may be the first marker the ER doc gets that something is wrong
  • Typical changes:
    • Peaked T-waves, shortened QT
    • Lengthening of PR interval and QRS duration
    • Bradycardia / Junctional rhythm
      • Hyperkalemia can produce bradycardia without other ECG findings
    • Ones associated with VT/VF/code, death in one study: QRS widening (RR = 4.74), Junctional Rhythm (RR = 7.46), HR <50 (RR = 12.29) while no adverse outcomes with just peaked T waves or PR prolongation (Durfey, 2017)
  • Don’t be fooled by a normal ECG, may be normal, but it’s also on case report level to have K > 9 and a normal ECG
    • Series of 127 patient (K 6-9.3), no serious arrhythmia noted, only 46% had ECG changes, (Acker, 1998)
  • ECG changes are not linear, there is no exact association between K+ levels and ECG changes
  • ECG changes may be hidden and subtle in patients with underlying inter-ventricular conduction delay (BBBs)
    • Be suspicious of the patient with LBBB > 160 ms or RBBB > 140 ms
  • BRASH Syndrome
    • Synergism between hyperkalemia, renal failure/injury and AV nodal blocking agents -> may produce ECG changes out of proportion to serum potassium levels.
• Labs
  • Chem, VBG, +/- CK if you think muscle breakdown is at play (Tintinalli talks about looking at urine K, but this is not most people’s practice)
  • Consider evaluation for adrenal insufficiency
  • Waiting for labs may not be an option
    • Renal dysfunction + consistent ECG findings → prompt treatment before chem results
    • Realistically 2 hours to get back chemistry in most settings ≈ eternity

Management in the ER

• Discontinue/hold any nephrotoxins or medications in suspected medication-induced hyperkalemia
• A. Acute Management Strategies:
  • Cardiac protection with calcium
    • 1g over 5-10 mins
      • Lasts 30-60 mins, may have to redose
      • Dose considerations if on digoxin
      • AEs: Calciphylaxis and hypercalcemia
        • Fast pushes can result in hypotension, arrhythmia
    • Calcium chloride vs calcium gluconate
    • Caution in patients taking Digoxin
  • IVF choice – NS vs LR
    • Caution/Avoid fluid in patients with ESRD/CHF or signs of VOL
  • Shifting potassium:
    • insulin/glucose
      • 5 units vs 10 units
        • 5 similar effect, less hypoglycemic episodes (LaRue 2017)
        • If doing 10 units, start D10W at 50-75 cc/h after amp of d50 but be mindful that anuric patient who missed HD may not have much room for volume
      • Decrease but about 0.5-1.2 mEq/L
      • Effect starts 10-20 mins after administration and can last 4-6 hours
    • Albuterol
      • 10-20 mg over 10 mins (NB: higher dose than for asthma)
      • Peak effect at 90 mins
      • Decreases by 0.5 – 1.0 mEq/L alone
        • With insulin, ~1.2 mEq/L, additive effect
    • Bicarbonate
      • Controversy. Useless in hyperkalemic, nonacidotic patient. Useful as drip but takes hours to work, again, volume in anuric patient an issue
        • May be most useful in patients with renal failure and hyperkalemia 2/2 volume loss
      • Hypertonic Bicarb is ineffective – More potassium is pulled out of cells due to osmotic shift.
  • Removal:
    • Lokelma (Sodium Zirconium cyclosilicate)
      • Luckily residents have never had to use Kayexalate
      • Can start working in 1-2 hours of administration
      • 0.37 mEq/L reduction at 4 hours after 10 g
      • Not a magic bullet in patients who need dialysis
    • Diuretics
      • No studies that demonstrate effectiveness in this ED setting
        • May be effective in patients with normal renal function
      • If patient not anuric, may be worth using, can give 40 mg, but again, should not be the only attempted method of removing K
      • Nephron BOMB
        • Loop Diuretic (160-250 mg IV Lasix or 4-5 mg IV Bymex)
        • Thiazide (500-1000 mg IV chlorothiazide or 5-10 mg metolazone)
        • +/- Acetazolamide
        • +/- Fludrocortisone
          • May help stimulate the kidneys to secrete potassium
          • Primarily helpful in patients with mineralocorticoid deficiencies
    • Dialysis
      • Involve renal early because it takes a while to call in an HD nurse sometimes
      • If no access and emergent HD is required → HD catheter placement
  • Strategies for suspected Brash syndrome
    • Epinephrine/Levo (if hypotensive/bradycardic)
    • Calcium gtt
• Disposition/wrap up
  • Many factors at play here – patient preference, access, degree of hyperkalmia, identifiable / corrected cause

Take Home points

• • Hyperkelamia causes can be put into three categories, pseudohyperkalemia, due to redistribution, and due to total body increase in potassium. Check out the show notes for a more complete list
  • Hyperkalemia can be difficult to pick up on before the labs come back because it can lurk without symptoms or even ECG changes
  • If a patient does have ECG changes, they may not follow that linear pattern that is traditionally taught and ECGs can be poorly sensitive. Now, if you do see changes, the ones that are more commonly associated with adverse events are QRS widening, junctional rhythm, and bradycardia
  • Treatment is a numbers game, calcium for cardiac stabilization can last just 30-60 minutes, insulin will be the fastest way to shift potassium back into cells, but be mindful that 10 units is associated with increased episodes of hypoglycemia whereas 5 units may have the same effect in reducing potassium. And albuterol is at a much higher dose than what is given for asthma
  • Lokelma is now a pillar of treatment for removal of potassium.
  • Diuretics with the goal of kiuresis may have a role in the oliguric patient, and increased doses along with other agents may buy time in patients with severe hyperK when HD is not readily available
  • Involve renal early if you think that the patient will require HD

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Diagnostic accuracy of the physical examination in emergency department patients with acute vertigo or dizziness: A systematic review and meta-analysis for GRACE-3 Academic Emergency Medicine, 2023 Background GRACE Background

• The GRACE guidelines – “Guidelines for Reasonable and Appropriate Care in the Emergency Department” – are a Society for Academic Emergency Medicine (SAEM) program designed to “reduce wasteful testing, provide explicit criteria to reduce foreseeable risk, and define sensible and prudent medical care”. The GRACE-1 guidelines were about chest pain, and the GRACE-2 guidelines were about abdominal pain.
• GRACE guidelines are written by a diverse group of clinicians with content expertise. GRACE-3 guidelines included emergency physicians, oto-neurologists, neuro-otologists, and patient advocates.

Dizziness Background

• Acute dizziness represents ~1-3% of ED visits and has a disproportionately high cost, resource use, and length of stay, largely due to imaging (much of which is unnecessary).
• Only about 3.2-6% of patients presenting with dizziness had central causes whereas the rest had cardiac, orthostatic, peripheral vestibular, otological processes.
• Roughly 9-10 times as many patients with dizziness get a CT as those who get an MRI, even though CT is likely only about 10% sensitive in diagnosing a stroke, while MR is up to 95% sensitive.
• The subjective-description paradigm taught in medical school, e.g., “world-spinning” vs. “lightheadedness” vs. “imbalance,” developed in the early 1970s, while commonly used today, is a poor predictor of central vs. peripheral cause. Studies have shown that patients’ descriptions of their symptoms can frequently switch between these categories every few minutes.

GRACE-3 Population of Interest

• Adult ED patients with dizziness present less than 2 weeks and without an apparent medical or neurological cause of dizziness.

GRACE-3 Methodology: GRACE-3 team consisted of 18 members, including emergency physicians, otoneurologist, neuro-otologist, and patient advocates.

• All team members were trained on the Grading of Recommendations Assessment Development and Evaluation (GRADE) framework.
  • This framework assesses literature and provides a systematic review and recommendations on a clinical subject.
• Based on the GRADE framework, recommendations are assigned direction “for, against, or either” and strength “strong or weak”.
• Medicare data was reviewed to assess direct costs for tests and procedures.
• The authors came up with 15 recommendations based on timing and triggers of dizziness.

GRACE-3 recommended paradigm for dizziness

The GRACE committee recommends a ‘’timing and triggers’’ categorization

1. Acute vestibular syndrome (AVS) = acute onset of persistent and continuous dizziness lasting >24 hours
2. Spontaneous episodic vestibular syndrome (s-EVS) = episodes of dizziness without a clear trigger
3. Triggered episodic vestibular syndrome (t-EVS) = episodes of dizziness triggered by something, such as moving head

Figure 1 from cited article.

These clinical syndromes have been endorsed by experts over the last 15 years or so and lend itself to a convenient breakdown of differential diagnoses:

Table 1 from cited article.

 Strengths * Assembles cohesive expert recommendations on a familiar yet confusing and contentious chief complaint.

• Gives strong recommendations, based on the evidence, that can be implemented at the systems level, i.e., additional training.

  Author's Conclusions Overarching GRACE-3 recommendation:

1. EM physicians should receive training in the HINTS exam, Epley, and Dix-Hallpike maneuvers.

Key official GRACE-3 recommendations regarding patients with AVS:

2. In patients with AVS with nystagmus, use HINTS to evaluate for peripheral vs. central causes.

• If HINTS exam suggests a central cause, obtain a Neurologic consult and initiate stroke evaluation.
• If HINTS exam suggests a peripheral cause, there is no need for further imaging.
• Recommend MRI if no clinician is available who is trained for HINTS
• Do not pursue CT/CTA; they have inferior sensitivity for posterior fossa abnormalities.

3. In patients with AVS, add on the “finger-rub” test for unilateral hearing loss.

4. In patients with AVS without nystagmus, do NOT do HINTS. Assess the degree of gait instability to help differentiate between peripheral(mild) and central(severe) etiologies

5. In patients with AVS with or without nystagmus, do NOT pursue CTs or CTAs to distinguish between central and peripheral etiologies.

6. In patients with AVS with nystagmus, HINTS (by a trained person) should be used before MRI for distinguishing central and peripheral etiologies

7. If the HINTS exam is equivocal in these patients or indicates a central etiology, use a stroke protocol MRI.

Comments: These recommendations are based on extensive data showing that the HINTs and Dix-Hallpike exams are better than any imaging available, and the Epley maneuver is better than medication. Furthermore, several studies show that EM physicians can perform these maneuvers with high sensitivity/specificity and efficacy if trained. HOWEVER, untrained EM physicians perform them incorrectly and use them in the incorrect clinical scenarios. They also recommend videos on acep.org/dizzy, and an iphone app from Hopkins developed specifically for GRACE-3 to assist with these exam maneuvers and in interpreting nystagmus.

Key official GRACE-3 recommendations regarding patients with s-EVS:

8. In patients with s-EVS, perform a thorough history and physical, focusing on the cranial nerves, (especially visual fields and eye movements), limb coordination, and gait to distinguish between central and peripheral etiologies.

9/10. In patients with s-EVS we should NOT use CT to distinguish between central and peripheral causes, but instead should use CTA or MRA to rule out posterior circulation vascular pathology if there is concern for TIA.

Comments: Even though symptoms of many TIAs may have already resolved on arrival, diagnosis is important since, if untreated, ~5% of patients will have a stroke in the coming days. Of the peripheral etiologies on the differential, vestibular migraine sufferers are about 5 times more common than patients with Meniere’s disease (Neuhauser 2009).

Key official GRACE-3 recommendations regarding patients with t-EVS:

11. EM physicians should receive training in the Dix-Hallpike and Epley maneuver since they work very well.

12. Do NOT use CT or CTA on these patients

13. In patients with t-EVS, use the Dix-Hallpike to diagnose BPPV. If the Dix-Hallpike is positive, do NOT obtain MRI or MRA.

15. In patients diagnosed with BPPV, use the Epley maneuver to treat them.

Comments: Central causes of positional / triggered vertigo AKA “CPPV” are very rare compared to BPPV. There are (at least) two types of BPPV, with posterior-canal being the most common. If the Dix-Hallpike maneuver is negative or evokes the wrong type of nystagmus in a patient with a strong suspicion for BPPV, they may have horizontal canal BPPV and require the Lempert “barbeque” roll instead of the Epley.

Key official GRACE-3 recommendations regarding patients with vestibular neuritis:

14. Use shared decision-making on whether or not to use steroids if patients present within 3 days of symptom onset.

Comments: All comparative studies have been underpowered and of limited quality. If given at all, the prescription should be for a short duration.

Bottom Line * Forget about “What do you mean, ‘dizzy’?”. Instead, focus on timing and triggers of symptoms. * Brush up your physical exam and maneuvers. * Educational videos about dizziness and vertigo on Dr. Peter Johns channel (https://www.youtube.com/ c/peterjohns). * Smartphone app on diagnosis and treatment of patients with acute dizziness created by GRACE-3 committee (https:// www.hopkinsmedicine.org/armstrong_institute/centers/center_for_ diagnostic_excellence/resources.html). * HINTS exam is instrumental as an aid for dizziness diagnosis but is currently still not standard of care. Additional training is needed for EM physicians in how to accurately perform the HINTS exam. * Stop obtaining non-contrast CT brain imaging for dizziness – if you’re concerned about a central cause of vertigo, obtain an MRI.

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     We go over the essential and complex topic of vasopressors in the ED.

Hosts:
Brian Gilberti, MD
Catherine Jamin, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Vasopressors.mp3   Download Leave a Comment Tags: Critical Care    Show Notes **Introduction**

• Host: Brian Gilberti, MD
• Guest: Catherine Jamin, MD
  • Associate professor of Emergency Medicine at NYU Langone Health
  • Vice Chair of Operations
  • Triple-boarded in Emergency Medicine, Internal Medicine, and Critical Care Medicine
• Topic: Vasopressors: Essential agents for supporting critically ill patients in the ED

What Are Vasopressors and When to Use Them

• Two primary mechanisms to increase blood pressure:
  1. Increasing systemic vascular resistance via vasoconstriction
  2. Increasing cardiac output via augmenting inotropy and chronotropy
• Indicators for vasopressor use:
• • MAP <65, systolic BP <90, or significant drop from baseline BP
  • Signs of organ dysfunction like altered mental status, decreased urine output, elevated lactate
  • Fluid resuscitation either ineffective or contraindicated (e.g., in CHF patients)

Commonly Used Vasopressors in the ED

• Norepinephrine
• Epinephrine
• Vasopressin
• Phenylephrine

Norepinephrine

• Mechanism: Stimulates alpha-1 (vasoconstriction) and beta-1 receptors (increases inotropy & chronotropy)
• Starting Dose: 10 mcg/min, titrate to MAP >65
• Max Dose: No strict limit but usually add a 2nd pressor at 15-20 mcg/min
• Situational Preference: First-line for most cases of shock (septic, undifferentiated, hypovolemic, cardiogenic)
• Pros: Can be infused peripherally via large bore IV

Vasopressin

• Mechanism: Activates V1a receptors causing vasoconstriction
• Dose: Fixed, non-titratable dose of 0.04 units/min
• Situational Preference: Second-line in septic shock
• Concerns: Potential for peripheral ischemia

Phenylephrine

• Mechanism: Stimulates alpha-1 receptors causing vasoconstriction
• Starting Dose: 100 mcg/min, titrate to MAP >65
• Situational Preference: High cardiac output states, tachyarrhythmias, peri-intubation
• Concerns: Increases afterload, can worsen low cardiac output states

Epinephrine

• Mechanism: Stimulates alpha-1, beta-1 and beta-2 receptors
• Starting Dose: 5-10 mcg/min, titrate to MAP >65
• Situational Preference: Anaphylactic shock, septic cardiomyopathy
• Limitations: Can induce tachycardia, may elevate lactate levels

Escalation Strategy in Refractory Shock

• Norepinephrine -> Vasopressin (with stress dose steroids) -> Epinephrine
• Consider POCUS, lactate, central venous saturation, and acid-base status

Peripheral Pressors

• Can safely be administered peripherally via large bore IVs in proximal upper extremity
• Sites: Cephalic or basilic veins
• Adverse Events: Low at 1.8% based on meta-analysis
• Actions in case of extravasation: Phentolamine injection, nitroglycerin paste

Push-Dose Pressors

• Primarily Phenylephrine (peri-intubation, during procedures)
• Also Epinephrine for peri-code situations
• Doses: Epi – 5-20 mcg every 2-5 min

Take-Home Points

• Most used medications are going to be norepinephrine, vasopressin, phenylephrine, and epinephrine.
• Consider these medications if there are signs of end-organ dysfunction, there is a considerable delta in baseline BP, systolic is less than 90 and/or MAP is less than 65
• Norepinephrine is a good pressor for a lot of the situations that we encounter in the emergency department, such as septic shock, undifferentiated shock and hypovolemic shock.
• Vasopressin is commonly the second we reach for in most of these scenarios
• Epinephrine will be first for anaphylactic shock and may be the third agent in septic shock
• Think about phenylephrine in high-output states (patients with tachydysrhythmias), or with AS, though be cautious in patient with low cardiac output
• The benefits outweigh risks for peripheral pressors in situations where you promptly have to increase blood pressure while you work on central access
• Push-dose pressures can help you in a peritinbatuion or pericode situation because it is going to be one of the fastest ways we can boost BP while we work on other measures to stabilize the patient

Additional References

• Importance of RUSH (Rapid Ultrasound in SHock) exam for diagnosis and treatment planning: https://emcrit.org/rush-exam/

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The Case A 41-year-old male presents to the ED with constant palpitations for one day. The patient's medical history is notable for a congenital bicuspid aortic valve, four months post aortic valve replacement with a post-surgical ejection fraction of 30%. The following ECG is obtained:

EKG Show Details EKG Characteristics * Rate Fast * Rhythm Wide complex tachycardia * Intervals Wide complex QRS (146 ms) * Axis Left axis deviation * ST Segments Non-specific * Additional Features Right bundle branch block morphology

Diagnosis Idiopathic Fascicular Ventricular Tachycardia

Questions 1. What is the differential diagnosis for this ECG? The differential diagnosis for this patient includes Ventricular Tachycardia (VT) and Supraventricular Tachycardia (SVT) with aberrancy. Differentiating between the two is difficult as multiple proposed diagnostic criteria have yet to demonstrate sufficient sensitivity or specificity for a definitive diagnosis.

 Discussion Fascicular VT is a distinct subgroup of idiopathic VT. Fascicular VT is reentrant tachycardia due to an ectopic focus within the left ventricle, most commonly in the fascicles. Unlike other forms of VT, Fascicular VT may be more likely to be misidentified as SVT with aberrancy, given RBBB morphology and lack of precordial concordance.

The location of the re-entry circuit determines the morphology of Fascicular VT:

Posterior fascicular VT (most common):

• RBBB + left axis deviation; arises close to the left posterior fascicle

Anterior fascicular VT:

• RBBB + right axis deviation; arises close to the left anterior fascicle

Upper septal fascicular VT (rare):

• Usually RBBB but can be LBBB, narrow QRS with normal axis; arises from the upper septum

Treatment of fascicular VT:

Unstable: Synchronized Cardioversion

Stable:

• IV Verapamil
• Sotalol and Amiodarone
• Radio-frequency ablation

Vagal maneuvers, adenosine, lidocaine, and beta-blockers are unlikely to affect this rhythm. Adenosine may reveal capture or fusion beats to assist in diagnosis; however, this should be performed in conjunction with specialty recommendation.

Ventricular Tachycardia vs. Suprabentricular Tachycardia with Aberrancy:

Factors that may suggest Ventricular Tachycardia or Supraventricular Tachycardia include:

Up to 80% of all patients who present with a wide complex tachycardia will be diagnosed with ventricular tachycardia. Risk factors that increase the likelihood of VT include history of previous myocardial infarction, known coronary artery disease, and structural heart disease. Increased age is also an independent risk factor for increased likelihood of VT in wide complex tachycardia. When in doubt, treat as ventricular tachycardia.

Case Outcome:

The patients EKG performed in the ED showed a Wide Complex Tachycardia at a rate of 142 bpm. He was mentating appropriately with a blood pressure of 105/77.

This patient was given a bolus of Amiodarone and subsequently started on a drip. With the guidance of cardiology, the patient was given adenosine to assist in determining the underlying rhythm. A capture beat was noted on the rhythm strip, suggesting ventricular tachycardia as the underlying rhythm. The patient did not respond to medical therapies trialed in the emergency department and ultimately underwent radio-frequency ablation with the return of normal sinus rhythm. His condition remained stable, and he was discharged home the following day.

Pearls * Consider ventricular tachycardia in any unexplained tachycardia with a widened QRS (especially in patients history of narrow QRS on prior ECG or no previous ECG for comparison). * Fascicular VT is a distinct subgroup of ventricular tachycardia; it may commonly be mistaken for SVT with aberrancy due to “innocuous” RBBB appearance. * Fascicular VT can occur in young, healthy patients with and without structural heart disease. * Fascicular VT often does not respond to typical VT (or SVT) therapies; however, it is likely to be responsive to Verapamil or radio-frequency ablation.

Sources 1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1501077/ 2. https://emj.bmj.com/content/19/5/477 3. https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-9/Idiopathic-fascicular-left-ventricular-tachycardia 4. https://accessemergencymedicine.mhmedical.com/content.aspx?bookid=2969§ionid=250463206#:~:text=When%20a%20person%20with%20a,a%20ventricular%20tachycardia%20(VT). 5. Brady WJ, Skiles J. Wide QRS complex tachycardia: ECG Differential diagnosis. AM J Emerg Med. 1999;17(4):376-381

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Written by: Sadakat Chowdhury MD

Edited by: Mak Sarich MD, Jay Lin MD, Jonathan Kobles MD

Background:

Ultrasound (US) guided nerve blocks offer an applicable option for achieving analgesia in the emergency department. As an alternative to parenteral or oral analgesia, nerve blocks have the potential for improved pain control, decreased risk of harm (hypoventilation, compromised airway or perfusion, potential for addiction), and decreased length of hospital stay.1 2 3 4 This article will focus on three lower extremity (LE) nerve blocks commonly used for acute lower extremity pain in the ED.

Anatomy:

• The lumbar plexus (T12-L4) breaks off into the femoral, lateral femoral cutaneous, obturator, genitofemoral, ilioinguinal, and iliohypogastric nerves which are the main sources of sensory and motor innervation in the anterior LE.
• The femoral nerve branches into its terminal sensory portion, the saphenous nerve.
• The sciatic nerve (L4-S3) courses posteriorly along the thigh and divides into the tibial (which subdivides into the sural nerve) and common peroneal (which subdivides into the superficial and deep peroneal) nerves. These nerves serve most of the sensory and motor innervation for the posterior LE. The sensory distributions of each nerve are depicted in the figure below.

Preparation:

Probe Selection: The linear transducer is ideal for most patients; the curvilinear transducer can be used for patients with larger body habitus where greater depth is needed to visualize the anatomy.

Materials Needed:

• 10 cc sterile saline
• IV tubing
• US-guided nerve block needle or 18-22 gauge Quincke spinal needle
• 60 mL syringe
• US probe cover
• Antiseptic wipes
• Local anesthetic (LA) of choice
• Ensure that your ED has easily assessable intralipid in the case of systemic toxicity

Procedures should be carried out by two operators:

1. Primary operator utilizing sterile technique to operate ultrasound and needle-guidance to nerve
2. Second operator to flush and aspirate syringe

Commonly Used Local Anesthesia:

| Local Anesthesia | Maximum Dose (mg/kg) with and without Epinephrine | Onset (min) | Duration of analgesia (hours) | | Lidocaine 1% | 4/7 | 10-20 | 3-8 | | Bupivacaine 0.5% | 2/3 | 15-20 | 6-30 | | Ropivacaine 0.5% | 3/3.5 | 15-30 | 5-24 |

Adverse effects:

• Infection
• Vascular injury including hematoma or pseudoaneurysm formation
• Nerve damage
• Local anesthesia systemic toxicity (LAST) – confusion, anxiety, headache, drowsiness, hypotension, arrhythmias including ventricular tachycardia or fibrillation.
• • • Blocks with larger volumes of anesthetic carry higher risk of LAST. - Treatment of LAST is supportive care and administration of intralipid * + Intralipid 20% 1.5 mL/kg over 1 min, then 0.25 mL/kg/min for 20 mins is suggested is case of LAST
• Bupivacaine carries a higher risk of cardiotoxicity.

Contraindications:

• Inability to safely cooperate with procedure
• Allergy to local anesthetic
• Overlying infection
• Anticoagulation and coagulopathies are relative contraindications

General Setup and Technique:

• Obtain appropriate consent from the patient.
• Perform a neurovascular assessment of the patient before and after the procedure.

• Ensure all your supplies are at the bedside with your IV tubing connected to the nerve block needle. Fascia Iliaca Nerve Block:

• Blocks the lateral femoral cutaneous nerve, femoral nerve, and obturator nerve by spreading anesthetic across a fascial plane. This will affect sensory innervation to most of the anterior thigh and medial lower leg.

• Indications include hip fracture, proximal femoral shaft fractures, proximal tibial fractures, patellar fractures, burns, anterior thigh lacerations, or abscesses.

Set up:

• Have the patient on monitors and in a supine position.
• Prepare a 60 cc syringe filled with 15-20 mL of LA mixed with 15 mL of sterile saline. Calculate the maximum safe local anesthetic dosage for the patient.
• Don a set of sterile gloves, and using sterile technique, drape and prep the patient’s infra-inguinal area with antiseptic wipes. Use an assistant to apply a sterile probe cover over the US transducer.

Identification of landmarks:

Identify the femoral vein and artery in a transverse orientation. The femoral nerve should be a hyperechoic triangle-shaped structure coursing laterally and housed under the fascia iliaca,the fascial plane above the iliacus muscle.

• Using the in-plane technique, identify the location where you will insert your needle lateral to the femoral nerve and coursing towards the fascia iliaca. Insert the needle through the skin with visualization of the needle tip at all times.
• Advance the needle until entering the fascia iliaca space. You should feel two distinct popping sensations, one when breaking the fascia lata and another when breaking the fascia iliaca.
• Have your assistant aspirate, and then hydrodissect the fascial place with sterile saline. After confirming appropriate location in the fascia iliaca, have your assistant inject your preparation of LA and sterile saline in 5 mL aliquots with gentle aspiration between injections. You should visualize the femoral nerve being pushed medially and an anechoic spread of the fascia iliaca.

• Repeat a neurovascular assessment of the patient after the procedure. Popliteal Sciatic Nerve Block:

• Blocks the sciatic nerve, tibial nerve, and common peroneal nerve. This will affect sensory innervation to the posterior and lateral distribution of lower leg and ankle.

• Indications include: Distal tibia/fibula injuries, ankle injuries, achilles tendon injuries, lower leg burns, lacerations, abscesses.

Set up:

• Place the patient in a prone position. If the patient cannot lie prone, you may elevate their ankle using sheets while they lie supine.
• Prepare a 60cc syringe with 10-15m LA and 10 mL sterile saline. Calculate the maximum safe local anesthetic dosage before performing this procedure.
• Don a set of sterile gloves, and using sterile technique, drape and prep the patient’s popliteal area with antiseptic wipes. Use an assistant to apply a sterile probe cover over the US transducer.

Identification of landmarks:

Identify the popliteal vein and artery in the popliteal fossa using a transverse orientation. The sciatic nerve will be a hyperechoic structure coursing superficially and medially. The sciatic nerve splits into the tibial and common peroneal nerve as you move the transducer distally. The target will be the perineurium between the tibial and common peroneal nerve.

• Using the in-plane technique, identify where you will insert your needle lateral to the nerve bundle. Insert the needle through the skin. Maintain visualization of needle tip through the entirety of the procedure.
• Once you have entered the perineurium, have your assistant aspirate, and then hydrodissect with sterile saline. After confirming that the tibial and common peroneal nerves are moving peripherally, have your assistant inject your local anesthetics and sterile saline preparations in 5 mL aliquots with gentle aspiration between injections.

• Repeat a neurovascular assessment of the patient after the procedure. PENG Nerve Block:

• This block will target the pericapsular nerve group (PENG), which innervates the pelvis. These are branches of the femoral and obturator nerve. This is a motor sparing block – so it will allow your patients to ambulate.8

• This nerve block is typically performed with a curvilinear probe, though a linear probe can be used for patients with a smaller body habitus.
• Indications includeacetabular, pubic rami, femoral neck, and intertrochanteric hip fractures.

Set up:

• Place the patient in a supine position.
• Prepare a 60cc syringe with 10mL LA and 10 mL sterile saline. Calculate the maximum safe local anesthetic dosage before performing this procedure.
• Don a set of sterile gloves, and using sterile technique, drape and prep the patient’s popliteal area with antiseptic wipes. Use an assistant to apply a sterile probe cover over the US transducer.

Identification of landmarks:

Place your transducer in a transverse orientation (rotated 45 degrees) on the proximal thigh directly adjacent to the inguinal ligament. Identify the femoral head and the femoral artery coursing superficially to it. Move the transducer superiorly and medially, and you will be able to identify the anterior inferior iliac spine (AIIS), the ilium, the ileopubic eminence (IPE), and the psoas tendon (PT).

• Using the in-plane technique, identify where you will insert your needle in a lateral to medial direction course. Insert the needle through the skin, with visualization of the needle tip at all times. Advance the needle past the AIIS and directly lateral to the bony surface of the ilium under the PT.
• Once under the PT, have your assistant aspirate and then hydrodissect with sterile saline. After confirming that the tendon is moving superficially above the ileum, have your assistant inject your preparation of LA and sterile saline in 5 mL aliquots with gentle aspiration between injections.
• Repeat a neurovascular assessment of the patient after the procedure. References:

[1] Bhoi S, Sinha TP, Rodha M, Bhasin A, Ramchandani R, Galwankar S. Feasibility and safety of ultrasound-guided nerve block for management of limb injuries by emergency care physicians. J Emerg Trauma Shock. 2012;5(1):28-32. doi:10.4103/0974-2700.93107

[2] Nagdev A. Ultrasound-Guided Nerve Blocks. EMRA. Published June 2020. https://www.emra.org/books/pain-management/ultrasound-guided-nerve-blocks/

[3] Morrison RS, Magaziner J, Gilbert M, et al. Relationship between pain and opioid analgesics on the development of delirium following hip fracture. J Gerontol A Biol Sci Med Sci. 2003;58(1):76-81. doi:10.1093/gerona/58.1.m76

[4] Johnson B, Herring A, Shah S, Krosin M, Mantuani D, Nagdev A. Door-to-block time: prioritizing acute pain management for femoral fractures in the ED. Am J Emerg Med. 2014;32(7):801-803. doi:10.1016/j.ajem.2014.03.027

[5] Jeng C. Lower extremity nerve blocks: Techniques. UpToDate. Published February 4, 2022. Accessed September 29, 2022, https://www-uptodate-com/contents/lower-extremity-nerve-blocks-techniques

[6] Pepe J, Ausman C, Madhani NB. Ultrasound-guided Fascia Iliaca Compartment Block. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 31, 2021.

[7] Gulec, Nazey. Popliteal Sciatic Nerve Block. American Academy of Emergency Physicians, Published 31 Jan. 2022, Accessed September 29, 2022, https://www.acep.org/emultrasound/newsroom/january-2022/popliteal-sciatic-nerve-block/.

[8] Luftig J, Dreyfuss A, Mantuani D, Howell K, White A, Nagdev A. A new frontier in pelvic fracture pain control in the ED: Successful use of the pericapsular nerve group (PENG) block. Am J Emerg Med. 2020;38(12):2761.e5-2761.e9. doi:10.1016/j.ajem.2020.05.085

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     We discuss the diagnosis and management of septic arthritis in the pediatric population.

Hosts:
Brian Gilberti, MD
Ellen Duncan, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Septic\_Joint\_in\_Children.mp3   Download Leave a Comment Tags: Infectious Diseases, Pediatrics    Show Notes * General


+ Pain in joint for pediatric patient has a broad differential, including transient synovitis and septic arthritis
+ Transient synovitis, also known as toxic synovitis, is a common condition affecting kids aged 3-10 and often occurs after a viral infection. It is typically self-limiting and not considered a serious condition.
+ Septic arthritis is an infection in the joint space, typically affecting only one joint. It is often difficult to diagnose due to the fact that many patients, particularly under the age of 3, may not be able to localize their pain to a specific joint.

• Workup

  • Diagnostic work-up for septic arthritis begins with blood work, which includes a complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and blood cultures. Lyme disease studies may also be necessary since Lyme disease can cause joint pain.
  • Patients with transient synovitis typically have mild elevation in inflammatory markers, while those with septic arthritis usually show a significant elevation.
  • Imaging studies, including X-rays, ultrasound to evaluate for a joint effusion, and MRI to assess for associated osteomyelitis, are also part of the diagnostic approach.
  • The Kocher criteria, developed specifically for septic arthritis of the hip, are a useful tool for clinical decision-making. The criteria include fever above 38.5 C, inability to bear weight, ESR above 40, and a white blood cell count above 12,000.

1 criterion met = 3% probability of septic arthritis

2 criteria met = 40% probability of septic arthritis

3 criteria met = 93% probability of septic arthritis

4 criteria met = 99+% probability of septic arthritis

• If septic arthritis is suspected, orthopedics should be consulted immediately. Joint fluid aspiration is necessary for diagnosis and should not be delayed. The fluid should be sent for cell count, gram stain, glucose, culture, and PCR if available.
• Septic arthritis is most commonly caused by bacterial infections, with Staph aureus being the most common organism. In school-age children, other bacteria such as Strep pyogenes, Strep pneumoniae, and Haemophilus influenzae should also be considered. In preschool-aged children, K. kingae is also considered. In older children and neonates, the range of potential bacteria varies.

• Management

  • Empiric antibiotic therapy should target the most likely organisms and should not be delayed. Antibiotics may be narrowed once culture results are obtained.
  • The choice of antibiotics is dependent on the age group, with specific combinations suggested for neonates, children between 1 month and 4 years, and children aged 5 and older.
  • Cultures are only positive in 50-60% of cases. Synovial fluid PCR studies can help narrow antibiotic treatment.

  • Take Home Points

  • Limp in the pediatric population can commonly be transient synovitis but we should always consider septic arthritis

  • Some clues in the history and physical that would point you towards septic arthritis include fever, refusal to bear weight, and limited range of motion on exam
  • We are going to have to get labs, including CBC, inflammatory markers, and preoperative labs, along with an XR and possibly an ultrasound
  • Kocher criteria is one tool that can help us determine if this is a patient that requires a joint tap.
  • Arthrocentesis is the gold standard for diagnosis, but antibiotics should be started promptly if the diagnosis is suspected.

  • The choice of antibiotics is dependent upon age group.

    • Neonates get vanc/cefepime, kids 1-4 yo get vanc / ceftriaxone

    • Older than 5 yo get vancomycin

      • Add ceftriaxone to them if patient has sickle cell disease, are immunocompromised, or Lyme or STI are suspected
        • Always cross check with institutional preferences / guidelines when choosing antibiotics

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The SQuID Protocol (Subcutaneous Insulin in Diabetic Ketoacidosis): Impacts on ED Operational Metrics. Academic Emergency Medicine, 2023 Background Diabetic ketoacidosis (DKA) is an endocrine emergency. The standard of care of treating DKA is fluid resuscitation, electrolyte management, and intravenous insulin infusion in the intensive care unit (ICU) setting for close glucose and electrolyte monitoring. Recent research aims at investigating the treatment of DKA with subcutaneous insulin in non-ICU settings.

  Clinical Question Are subcutaneous insulin analogs in mild-to-moderate DKA efficacious, safe, and cost-effective, thus allowing treatment in non-ICU settings?

Population This study occurred in an urban academic hospital with over 90,000 annual visits. Of these, 177 were mild-to-moderate DKA patients, defined as evidence of DKA (hyperglycemia, ketosis, and an anion gap) without severe features (HCO3 < 10 or arterial pH < 7.0). Of this group, 78 patients were placed in the SQuID protocol (subcutaneous insulin in DKA), and 99 were in the traditional cohort.

Intervention SQuID protocol: IV fluids, electrolyte replacement, POC glucose every two hours, and insulin lispro (subcutaneous short-acting insulin). Patients were admitted to an inpatient observation unit managed by a hospital medicine service.

Control A total of 99 mild-to-moderate DKA patients were placed in a traditional cohort during the study period.

Prior cases used as a control included 163 pre-intervention and 161 pre-COVID historical control patients.

Outcomes Primary: operational impacts (EDLOS, ICU admission)

Secondary: fidelity, safety

Design A prospective experimental study with retrospective data to evaluate outcome measures. Data was collected from August 1, 2021 – February 20, 2022. Providers screening a patient for DKA were given a Best Practice Advisory to consider placing the patient on SQuID protocol. Fidelity was examined by the frequency of required q2h glucose checks, safety by seeing how many patients required rescue dextrose for hypoglycemia, and operational impacts including ED LOS and ICU admission.

Image from cited article.

Excluded * Patients with severe DKA (HCO3 < 10 mmol/L or arterial pH < 7.0) * Patients <18 years of age * Exclusion criteria for the SQuID protocol: + Pregnancy + Serious infections + Concerns for myocardial infarction + Altered mental status + Active comorbidities (ESRD, CHF, on immunosuppressants) + Need for a surgical intervention + ED or inpatient team determined the patient was too ill for the designated floor (an inpatient observation unit run by hospitalist physicians) Primary Results 177 patients with mild to moderate severity DKA (78 SQuID, 99 traditional)

• • 76 were admitted to an ICU
  • Among those admitted to a medical floor:
    • 73 patients were managed on the SQuID protocol
    • 28 were managed on an insulin infusion

Fidelity

• High fidelity for patients in the SQuID pathway

Safety

• No differences in safety issues in patients in the SQuID pathway compared to the traditional cohort

EDLOS

• Significantly shorter for patients in the SQuID pathway

ICU admission

• Reductions in ICU admissions were observed though not statistically significant

Strengths Variety of controls, including pre-COVID, pre-protocol, and current controls.

Limitations Generalizability (single center, level 1 urban hospital with limited ICU beds available).

Implementation requires a new hospital specific protocol involving provider education and inpatient unit for SQuID protocol.

 Author's Conclusions “In this single academic medical center study, subcutaneous fast-acting insulin analogs for the treatment of mild to moderate–severity diabetic ketoacidosis in the ED was effective, demonstrated equivalent safety, and reduced ED length of stay.”

Potential Impact To Current Practice ED boarding continues to be a major nationwide issue, and ICU bed availability is often limited. Implementing a DKA protocol where patients’ safety and fidelity are not compromised and patients can be treated promptly is ideal for both patients and throughput for EDLOS.

Bottom Line Using subcutaneous fast-acting insulin for diabetic ketoacidosis can be safe for patients with mild to moderate DKA. However, significant medical education and protocol implementations still need to be implemented to practice a protocol like SQuID safely.

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Written by:
Samantha Kerester, MD
Naillid Felipe, MD

Edited by:
Gregg Chesney, MD
Jonathan Kobles, MD

Background:

Thrombotic thrombocytopenic purpura (TTP) is a hematologic disorder caused by platelet aggregation and thrombus formation in the microvasculature, resulting in severe thrombocytopenia, hemolytic anemia, and multi-organ ischemia.

Annual incidence of approximately 2-4 cases/million/year (Kappler, 2017), with 90% of cases occurring in adulthood. (Joly, 2017)

Risk factors include:

• Female, 2:1 female to male predominance (Terrell, 2010)
• Black race
• Obesity

TTP is a life-threatening condition with mortality of 10-20% despite targeted therapies. (Kappler, 2017)

Pathophysiology:

TTP is caused by a severe deficiency in ADAMTS-13, a protease that cleaves the glycoprotein von Willebrand factor (vWF) necessary for platelet adhesion in the coagulation cascade.

• In the paucity of ADAMTS-13, large vWF multimers accumulate and activate platelets, leading to platelet consumption and unregulated microthrombi formation.
• Microvascular plugging results in tissue ischemia in any organ, though it is most common in high-pressure vasculature, including the brain, heart, kidneys, and pancreas.
• Lung and liver involvement are uncommon due to low pressure and low shearing forces. (Sadler, 2017)

Acquired TTP:

• IgG autoantibodies against ADAMTS-13 inhibit its proteolytic activity towards vWF.
• Deficient ADAMTS-13 activity alone typically does not result in TTP; therefore, it is essential to consider contributing precipitants, including pregnancy, HIV, acute infection, inflammation (SLE, malignancy, pancreatitis) and medication use (ex., fluoroquinolones, quinine, clopidogrel, and ticlopidine)

Congenital/Familial TTP: 2% of cases occur in childhood via autosomal recessive mutations in the ADAMTS-13 gene.

Clinical Presentation:

Classic pentad (mnemonic FAT RN) is rare and seen in less than 7% of cases. (Long, 2021)

• Fever
• Anemia (microangiopathic hemolytic anemia)
• Thrombocytopenia with purpura
• Renal dysfunction (acute kidney injury)
• Neurologic abnormalities

Suspect TTP in all patients with:

• Severe thrombocytopenia (<30×10^9/L)
• Microangiopathic hemolytic anemia with schistocytes on the blood smear

Clinical symptoms may be transient and relate to microvascular ischemia in specific organs (Fodil, 2022):

• CNS injury (60%): headache, confusion, seizure, stroke, focal neurological deficits
• Cardiac injury (25%): chest pain, isolated EKG changes, elevated troponin, congestive heart failure, myocardial infarction
• GI injury (35%): abdominal pain, vomiting, elevated lipase >3x normal limit, bloody diarrhea
  • In TTP, bloody stools occur during the initial presentation, whereas bloody stools often precede the development of symptoms in HUS.
• Renal injury: isolated proteinuria or hematuria, moderate acute kidney injury with serum creatinine levels <2 mg/dL
• Skin: petechiae and purpura
• Despite severe thrombocytopenia, clinically significant bleeding is rare Figure 1. An example of petechiae and purpura frequently seen with thrombocytopenic disorders.

(source: “Thrombotic Thrombocytopenic Purpura (TTP)”, 2022, National Heart, Lung, and Blood Institute. https://www.nhlbi.nih.gov/health/thrombotic-thrombocytopenic-purpura)

Laboratory Evaluation:

Clinical presentation and laboratory findings can help suggest TTP in the emergency department. Patients should undergo comprehensive work-up to rule out alternative causes of thrombocytopenia, evaluate for end-organ damage, and identify underlying infectious or autoimmune etiologies.

• • CBC with differential and peripheral smear
  • Severe thrombocytopenia (<30×10^9/L)
  • Mild anemia
  • Presence of schistocytes
  • Comprehensive metabolic panel to assess for renal involvement
    • • While TTP and hemolytic uremic syndrome have considerable overlap in presentation, renal involvement is more commonly seen in hemolytic uremic syndrome
  • Hemolysis labs and coagulation testing (PT/INR/PTT, Fibrinogen, and D-dimer)
    • • An elevated fibrinogen level or abnormal coagulation (elevated PT/PTT/INR) suggests an alternative diagnosis, such as DIC
  • Evidence of hemolytic anemia:
    • • Increased LDH
      • Increased indirect bilirubin
      • Decreased haptoglobin
      • Increased reticulocyte count
  • β-hCG (for female patients of reproductive age)
    • • Pregnancy-related TTP often occurs during 2nd and 3rd trimester (Joly, 2017)
      • May have features similar to pre-eclampsia-eclampsia, HELLP syndrome, and fatty liver disease of pregnancy
  • Type and screen
  • Troponin, serum lactate, lipase, viral serologies (HIV, HCV, HBV), anti-nuclear antibody, urine analysis for proteinuria and hematuria, urine/blood/stool cultures, EKG, imaging studies including a chest x-ray or head CT as clinically indicated

Confirmatory testing is often not available in the emergency department. Do not delay treatment for confirmatory testing.

• ADAMTS13 activity (sensitivity 97%, specificity 100%) (Chiasakul, 2018)
• Anti-ADAMTS13 antibodies confirm the majority of cases of immune-mediated TTP
• ADAMTS-13 antigen levels and ADAMTS-13 gene analysis confirm congenital TTP The Plasmic Score:

The PLASMIC score can help stratify the likelihood of TTP, as patients ought to have therapy initiation prior to confirmatory testing results.

Patients with a score < 5 are unlikely to have TTP, with a negative predictive value of 99%. (Paydary, 2020) Patients with a score of 5 or greater require ADAMTS-13 levels to be sent along with expert consultation and likely initiation of empiric therapy.

• The factors considered include:
  • Platelets <30×10^9/L
  • One or more indicators of hemolysis (reticulocyte count >2.5%, undetectable haptoglobin, or indirect bilirubin >2 mg/dL)
  • MCV <90 fL
  • INR <1.5
  • creatinine <2 mg/dL
  • No active cancer in the preceding year
  • No history of solid organ or hematopoietic stem cell transplant Management:

TTP requires prompt initiation of treatment in the emergency department in conjunction with a hematology consultation to select the best combination of therapies for each patient

• Therapeutic plasma exchange (TPE) is the cornerstone of treatment for all patients with TTP. It repletes functioning ADAMTS-13 and removes circulating autoantibodies when present.
  • TPE requires the placement of a hemodialysis catheter.
  • Platelet transfusion (correction of thrombocytopenia) before the placement of a hemodialysis catheter is not indicated and may worsen disease course.
  • The first TPE session should be completed prior to administration of any biologic therapies.
  • Prompt initiation of TPE has significantly decreased mortality for an initial episode of TTP from 90% to 10-20%. (Joly, 2017; Sawler, 2020)
• Fresh frozen plasma (FFP) (contains ADMTS-13) may be used to supplement ADAMTS-13 if there is a delay in initiating TPE in the emergency department (i.e. if the patient is being transferred to another hospital).
• Steroids reduce the production of auto-antibodies in acquired TTP.
  • Oral prednisone 1 mg/kg/day.
  • IV methylprednisolone 1000 mg/day may be used in the presence of severe neurological deficits or cardiac injury. (Balduini, 2010)
• Rituximab, the humanized anti-CD20 monoclonal antibody.
  • Decreases production of anti-ADAMTS13 antibodies by removing the B cells that mature into autoantibody-secreting plasma cells. In conjunction with TPE, its use has been associated with reduced hospital length-of-stay and fewer relapses. Initiation and dosing should be discussed with hematology.
• Caplacizumab, a humanized monoclonal antibody, binds to vWF to block its interaction with platelet glycoproteins and ultimately reduce the formation of microthrombi.
  • Its use has been associated with decreased time to normalization of platelet count and decreased mortality; however, the therapy does not address the underlying autoimmune pathology and has been associated with a high risk of 30-day relapse. Initiation and dosing should be discussed with hematology.

Special considerations

• TTP with severe features may require critical care interventions, including PRBC transfusion, anticonvulsants, antihypertensives, and hemodialysis.
• Discontinue inciting medications in all cases of suspected drug-associated TTP.
• Platelet transfusion should only be considered for clinically significant bleeding or intracranial hemorrhage, as it has been associated with acutely worsening thrombosis, renal failure, and death.

• Immune TTP during pregnancy should be managed with TPE, despite the risk of removing pregnancy-maintaining hormones, given the high risk of maternal and fetal mortality without treatment. Rituximab can be given during the first trimester when immunoglobulins do not cross the placenta. Of note, there is no clinical indication for premature delivery. Next Steps:

• TTP is a life-threatening hematologic disorder that requires rapid clinical diagnosis and prompt initiation of therapeutic plasma exchange in the emergency setting.

• TTP relapse (new case onset that occurs 30 days after discontinuation of remission achieving interventions) occurs in approximately 1/3 of patients. Those with low residual ADAMTS-13 activity are at the highest risk of recurrence. (Scully, 2012) Citations:

Balduini CL, et al. High versus standard dose methylprednisolone in the acute phase of idiopathic thrombotic thrombocytopenic purpura: a randomized study. Ann Hematol. 2010 Jun;89(6):591-6. doi: 10.1007/s00277-009-0877-5.

Chiasakul T, Cuker A. Clinical and laboratory diagnosis of TTP: an integrated approach. Hematology Am Soc Hematol Educ Program. 2018 Nov 30;2018(1):530-538. doi: 10.1182/asheducation-2018.1.530.

Fodil S, Zafrani L. Severe Thrombotic Thrombocytopenic Purpura (TTP) with Organ Failure in Critically Ill Patients. J Clin Med. 2022 Feb 19;11(4):1103. doi: 10.3390/jcm11041103.

Joly BS, Coppo P, Veyradier A. Thrombotic thrombocytopenic purpura. Blood. 2017;129(21):2836-2846. doi:10.1182/blood-2016-10-709857.

Kappler S, Ronan-Bentle S, Graham A. Thrombotic Microangiopathies (TTP, HUS, HELLP). Hematol Oncol Clin North Am. 2017;31(6):1081-1103. doi:10.1016/j.hoc.2017.08.010.

Long B, Bridwell RE, Manchanda S, Gottlieb M. Evaluation and Management of Thrombotic Thrombocytopenic Purpura in the Emergency Department. J Emerg Med. 2021;61(6):674-682. doi:10.1016/j.jemermed.2021.07.045.

Paydary, Koosha, et al. “Diagnostic Accuracy of the PLASMIC Score in Patients with Suspected Thrombotic Thrombocytopenic Purpura: A Systematic Review and Meta‐Analysis.” Transfusion, 2020;60(9):2047-2057. doi:10.1111/trf.15954.

Sadler JE. Pathophysiology of thrombotic thrombocytopenic purpura. Blood. 2017 Sep 7;130(10):1181-1188. doi: 10.1182/blood-2017-04-636431.

Sawler D, Parker A, Britto J, et al. Time from suspected thrombotic thrombocytopenic purpura to initiation of plasma exchange and impact on survival: A 10-year provincial retrospective cohort study. Thrombosis Research. 2020;193:53-59. doi: 10.1016/j.thromres.2020.05.045.

Scully M, Hunt BJ, Benjamin S, et al. Guidelines on the diagnosis and management of thrombotic thrombocytopenic purpura and other thrombotic microangiopathies. Br J Haematol. 2012;158(3):323-335. doi:10.1111/j.1365-2141.2012.09167.x.

Terrell DR, Vesely SK, Kremer Hovinga JA, Lämmle B, George JN. Different disparities of gender and race among the thrombotic thrombocytopenic purpura and hemolytic-uremic syndromes. Am J Hematol. 2010 Nov;85(11):844-7. doi: 10.1002/ajh.21833.

Figure 1: From “Thrombotic Thrombocytopenic Purpura (TTP)”, 2022, National Heart, Lung, and Blood Institute. https://www.nhlbi.nih.gov/health/thrombotic-thrombocytopenic-purpura

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Written By: Kaitlynn Tracy, MD

Edited By: Sean Schnarr, MD and Gregg Chesney, MD

Definition/Background:

• Burns are classified as being major, moderate, or minor in severity. The American Burn Association classifies a burn as “minor” if it meets the following criteria:2
  • Partial thickness < 15% BSA in a patient between the ages of 10-50
  • Partial thickness < 10% BSA in a patient younger than 10 or older than 50
  • Full thickness < 2% BSA

• In general, a “minor” burn should also be without any following characteristics:2

  • No signs of associated inhalation injury
  • Not from a chemical or electric burn injury
  • Not involving the face, hands, perineum, or feet
  • Not crossing any major joints
  • Not circumferential Epidemiology:

• Every year there are over 500,000 ED visits are due to burn injuries, with 45,000 of those visits requiring hospital admission.7

• 86% of burn injuries are thermal burns (as opposed to chemical or electric), with 43% resulting from a direct exposure to fire, 34% from scalding liquid, and 9% from a hot object.4
• Risk factors for sustaining a burn injury include young age (children more frequently come into contact with hot objects), male gender (higher occupational risks and higher rates of alcohol consumption), and a lack of smoke detectors in the home.4

• Survival rate for all burn injuries is around 97%, which is a notable increase from 75% in the 1960’s.4 Pathophysiology:

• Thermal burns occur when tissue is exposed to excessive heat, most commonly by direct fire, hot liquid, steam, or a hot surface.4

• The physiologic response to thermal injury results in three separate zones of injury:7

  • The center of the injury is the “zone of coagulative necrosis” where irreversible tissue necrosis results from the direct thermal exposure.
  • Surrounding that is the “zone of ischemia,” where a large inflammatory response and fluid shift results in reduced blood flow and decreased circulation at the site of injury.
  • The outermost area on the periphery of the injury is the “zone of hyperemia,” where the inflammatory response causes vasodilation and increased capillary permeability, resulting in tissue edema. Clinical Presentation:

• Burn size is the percentage of body surface area (BSA%) involved in the injury. Methods for calculating the BSA% of a thermal injury are listed below:1

  • The most commonly used: Rule of 9’s
  • The most accurate (especially in pediatric patients): Lund and Browder Chart
  • The most accurate for small burns: Rule of Palm
• Burn depth is determined by the extent of tissue layers involved in the injury. The categorizations and their associated clinical presentations are as follows:4,5
  • Superficial: Epidermis involvement only
    • Dry, red, blanches with pressure
    • Does not blister
    • Painful to touch
    • Heals within 3-4 days without scarring
  • Superficial Partial Thickness: Epidermis + the upper layer of dermis
    • Moist, pink, blanching
    • May blister
    • Hypersensitive to touch
    • Heals in 7-21 days without scarring
  • Deep Partial Thickness: Epidermis + the deeper layer of dermis
    • Dry, red/mottled
    • Do often blister
    • Painful only to pressure
    • Heals in 2-9 weeks with scarring expected
  • Full Thickness: All epidermal layers + subcutaneous tissue or fat
    • Dry, leathery, white
    • Does not blister
    • Painless
    • Will not heal without skin grafting
  • Fourth Degree: All epidermal layers + underlying bone, fat, or muscle
    • Painless
    • Will not heal without skin grafting (and occasional amputation)
• Wounds can continue to increase in depth for up to 72 hours after the injury, so the true depth of the wound may be increased from initial presentation.5

• Consider the possibility of physical abuse if the burn is in an immersion scald pattern (a burn with well-demarcated lines), there is delayed presentation for evaluation, or the wound is in a specific shape (such as a cigarette butt or the shape or an iron).5 Diagnosis:

• Physical exam remains the most common technique for diagnosing burn depth and size.8

• Additional techniques to aid in the categorization and diagnosis of thermal injuries are actively being studied and include:8

  • Vital dyes, ultrasound, or tissue biopsy for detecting dead cells or denatured collagen
  • Fluorescein, laser doppler, or thermography to monitor the amount of blood flow in injured tissue
  • MRI to evaluate the extent of hyperemia in injured tissue Complications:

• Patients with joint involvement of a burn may need to start early range of motion exercises, stretching, or occupational therapy to avoid the formation of contractures and permanent disability of the joint.2

• Hypertrophic scars may form in some patients, which may benefit from pressure garments or topical silicone treatment.6

• The major systemic processes and metabolic derangements commonly managed in patients with severe thermal injuries rarely occur in patients with minor burns alone.2 Management:

• Cool the injured area by running cold tap water over it for up to 5 minutes.2

  • After 5 minutes there is a risk of vasoconstriction and further tissue damage.
  • Avoid direct contact with ice, which can cause vasoconstriction and increased burn depth.
• Decontaminate/Cleanse with warm saline irrigation or soapy water.2
  • Do not use skin disinfectants (eg. betadine, iodine), which have been shown to increase inflammation and inhibit the healing process.
• Debride any loose or dead skin.2
• Large blisters should be aspirated, while small blisters can be left intact.2
  • This is an area of considerable debate, with varying guidelines between sources.
  • One of the original studies on this topic from 1976 showed evidence that wounds with an intact overlying blister heal faster than those exposed from a ruptured blister, leading to the conclusion that a blister provides a moist environment that benefits healing. There have since been many subsequent studies showing evidence to the contrary.9
• Apply a topical antimicrobial (eg. Bacitracin, Polymyxin B, or Neomycin) to areas with partial or full thickness burns.2
  • There is no evidence showing a benefit of application to superficial burns.
  • Silver sulfadiazine and silver nitrate have long been a common agent of choice, however recent studies have shown evidence of increased cellular irritation and longer healing times with their use. In accordance, most burn centers have stopped recommending their use. 10
  • There is no indication for prescribing prophylactic systemic antibiotics.
• Dress the burn with a nonadherent gauze (eg. Xeroform, Telfa, Adaptic), which will cause less pain with removal during dressing changes.2
  • Cover with an outer layer of elastic gauze roll (eg. Kerlix) for additional coverage.
• Pain can usually be controlled with Acetaminophen, NSAIDS. Also offer second-generation antihistamines (eg. cetirizine) to help alleviate any associated pruritis.2

• Tetanus immunization should be verified, or a booster vaccine offered.2 Disposition/Next Steps:

• Patients with minor burns very rarely require hospitalization, and are considered safe for discharge.

• Patients should be instructed to change their first dressing after 48 hours, and continue dressing changes every 3-5 days until epithelialization of the wound.6
• Follow up with a primary physician is recommended within 2-3 days of discharge.2
• Indications for an outpatient referral to a burn center include:2
  • A burn with delayed healing past one week
  • A wound developing signs of infection or tissue necrosis
• Indications for emergent consult with or transfer to a burn center include:
  • “Bad Burn:” these burns may require skin grafting or surgical intervention to heal
    • A deep partial or full thickness burn
    • Burns involving > 10-15% TBSA
  • “Bad Patient:” these burns are at higher rate of superinfection and significant burns lead to a significant cardiovascular demand during the wound healing process
    • A patient less than 5 years of age or greater than 60
    • A patient with significant comorbidities that increase the healing time or rate of infection (eg. peripheral vascular disease, immunosuppression)
  • “Bad Location:” these burns have a higher risk of significant cosmetic defect or disability if strictures develop
    • A burn located on the face, perineum, feet, or hands

– A partial thickness burn (characterized by the blisters, and background erythema of the epidermis) on the volar aspect of a patient’s forearm.

https://phil.cdc.gov/Details.aspx?pid=22127

Take Home Points:

1. Thermal injuries are classified by severity as major, moderate, or minor with specific guidelines for categorization.
2. Diagnosis of a thermal injury is based on physical exam findings. Thermal injuries are broadly categorized based on the percentage of body surface area that they cover, as well as the depth of tissue injury they cause.
3. Thermal injuries continue to increase in depth for up to 72 hours after injury, so the final categorization of depth may be different from initial presentation.
4. Wounds should be cooled with tap water for up to 5 minutes, before being cleaned with soapy warm water.
5. Though there is no official recommendation, in general large blisters can be removed, while small blisters can be left intact.
6. Antimicrobial ointment should be applied to areas with partial or full thickness burned, but is unnecessary in areas with superficial burns.
7. Burns should be dressed with a nonadherent gauze, and changed by the patient at home after 48 hours. Subsequent dressing changes can occur every 3-5 days.
8. Acetaminophen, NSAIDS, and antihistamines can provide patients with symptomatic relief.

9. Most minor thermal injuries are safe for discharge home with outpatient follow up after 2-3 days, while some patients will require follow up with specialized care at a burn center. References:

10. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. Tintinalli J.E., & Ma O, & Yealy D.M., & Meckler G.D., & Stapczynski J, & Cline D.M., & Thomas S.H.(Eds.),Eds. Judith E. Tintinalli, et al.

11. Wiktor, Arek, and David Richards. “Treatment of Minor Thermal Burns.” UpToDate, https://www.uptodate.com/contents/treatment-of-minor-thermal-burns?topicRef=350&source=see_link.#H20.
12. ​​Swain AH, Azadian BS, Wakeley CJ, Shakespeare PG. “Management of blisters in minor burns.” Br Med J (Clin Res Ed). 1987 Jul 18;295(6591):181. doi: 10.1136/bmj.295.6591.181. PMID: 3115367; PMCID: PMC1247035.
13. Schaefer TJ, Tannan SC. Thermal Burns. [Updated 2022 May 30]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430773/
14. Helman, Anton. “EM Cases – Burn and Inhalation Injuries: Ed Wound Care, Resuscitation and Airway Management.” EmDOCs.net – Emergency Medicine Education, 10 Jan. 2020, http://www.emdocs.net/em-cases-burn-and-inhalation-injuries-ed-wound-care-resuscitation-and-airway-management/.
15. Hudspith J, Rayatt S. “First aid and treatment of minor burns.” BMJ. 2004 Jun 19;328(7454):1487-9. doi: 10.1136/bmj.328.7454.1487. PMID: 15205294; PMCID: PMC428524.
16. Singer, Adam J., et al. “Management of Local Burn Wounds in the Ed.” The American Journal of Emergency Medicine, W.B. Saunders, 30 June 2007, https://www.sciencedirect.com/science/article/abs/pii/S0735675706004499#preview-section-cited-by.
17. D. Heimbach, L. Engrav, B. Grube, J. Marvin. “Burn depth: a review.” World J Surg, 16 (1992), pp. 10-15
18. E.S. Wheeler, T.A. Miller. “The blister and the second degree burn in guinea pigs: the effect of exposure.” Plast Reconstr Surg, 57 (1976), p. 83
19. (10)J.F. Frazer, J. Bodman, R. Sturgess, J. Faoagali, R.M. Kimble. “An in vivo study of the anti-microbial efficacy of a 1% silver sulfadiazine and 0.2% chlorhexidine digluconate cream, 1% silver sulfadiazine cream and a silver coated dressing.” Burns, 30 (2004), pp. 35-41

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Background: The immediate post intubation period in the ED is a critical time for continued patient stabilization. While physical adjuncts like securing the tube, in line suctioning, and head positioning are part of general post intubation management, a better understanding of analgesics and sedatives have offered newer approaches and improved outcomes down the line during the patient’s hospital stay. The reality of ever increasing ED volumes and longer boarding times to the ICU makes it imperative for emergency physicians to learn how to manage these critical patients.

Early Interventions in the ED Can Have an Effect:

• The SPICE trial was a multi-center cohort study examining the hospital courses of 251 mechanically ventilated patients. Assessments of the administration of sedative agents, ventilation time and sedation depth via RASS were made. Outcomes measured included delirium and hospital plus 180 day mortality. The authors found that deep early sedation within the first four hours was an independent predictor for delayed extubation and increased mortality. (Shehabi 2012)
• The multi-center cohort ED-SED study examined 324 mechanically ventilated patients. It was found that patients exposed to deep sedation in the ED had an independent higher incidence of continued deep sedation on ICU day one (Fuller, 2019). Analgesia:

Rapid Sequence Intubation (RSI) provides paralysis and amnesia to the patient during the process of endotracheal intubation however analgesia is typically not administered peri-intubation. Immediately following intubation, it is important to address analgesia as part of the post-intubation management.

• Endotracheal tubes are painful
  • A study measuring hemodynamic and respiratory variables during endotracheal suctioning showed a significant increase in RASS scores, systolic, and diastolic blood pressure in mechanically ventilated patients in patients receiving sedation only when compared to patients also receiving analgesia (Jeitziner 2012)
• Not all mechanically ventilated patients require sedatives.
  • A randomized controlled trial of 140 patients compared a protocol of analgesia alone (Morphine IV bolus) versus sedation + analgesia (Propofol/Midazolam IV infusion + Morphine IV bolus). Patients in the analgesia only group had statistically significantly more days without mechanical ventilation and on average shorter ICU length of stays. (Strom 2010)
  • Non-opiate adjuncts such as acetaminophen, intravenous lidocaine, ketamine infusion, and neuropathic medications may all improve pain relief and decrease opiate requirements and should be considered in addition to opiates for appropriate patients.

| Analgesic | Onset | Elimination Half Life | IV Infusion Rates | Side Effects and Other Information | | Fentanyl | 1 – 2 min | 2 – 4 hr | 0.7 – 10 μg/kg/hr | Rapid onset. Lipophilic with adipose deposition, withdrawal symptoms after prolonged infusion | | Hydromorphone | 5 – 15 min | 2 – 3 hr | 0.5 – 3 mg/hr | No active metabolites however parent drug can accumulate in renal failure | | Morphine | 5 – 10 min | 3 – 4 hr | 2 – 30 mg/hr | Active metabolites can accumulate in renal failure | | Remifentanil | 1 – 3 min | 3 – 10 min | Loading dose: 1.5 μg/kg IVMaintenance dose: 0.5 – 15 μg/kg/hr | Rapid onset. Short acting. Not affected by hepatic or renal failure. Associated with development of hyperalgesia | | Ketamine*(subdissociative pain dose is lower than infusion dose used for sedation) | 30-40 sec | 2 – 3 hr | Loading dose 0.1 – 0.5 mg/kg IV followed by 0.05 – 0.4 mg/kg/hr | Attenuates the development of acute tolerance to opioids. Can cause hallucinations and other psychological disturbances. |

Adapted from Clinical Practice Guidelines for the Management of Pain, Agitation, and Delirium in Adult Patients in the Intensive Care Unit. Critical Care Medicine 2018

Sedation:

After absence of pain is ensured, pharmacologic sedation may be indicated to help relieve discomfort, improve synchrony with mechanical ventilation and decrease oxygen requirements and overall work of breathing. (Patel 2012)

• Peri and Immediate Post Intubation Sedation
  • When using a long-acting paralytic (rocuronium and vecuronium), it is essential to provide a sedative and amnestic through the duration of the paralysis.
• Assessing the Sedated Patient
  • Goal in the emergency department should be to titrate to light sedation as objectively measured by a validated scale like the Richmond Agitation-Sedation Scale (RASS)
  • Patients in the immediate post-intubation period may require escalating doses to control initial agitation and assist in ventilator tolerance and synchrony and may require deeper levels of sedation initially

Richmond Agitation Sedation Scale (RASS) – resus.com.au

• Light Sedation vs Deep Sedation
  • Various studies have shown detrimental effects of prolonged deep sedation including longer mechanical ventilation times, 6 month mortality and increased incidence of delirium (Shehabi 2013).
  • Depth of sedation should be regularly assessed in the emergency department
  • When clinically appropriate, sedation should be titrated to achieve light sedation (RASS 0 to -2) as early as possible in the emergency department

Pharmacology of Sedative Medications

| Agent | Onset | Elimination Half Life | Loading Dose (IV) | Usual Maintenance Dose (IV) | Side Effects and Other Information | | Midazolam | 2 – 5 min | 3 – 11 hr | 0.01 mg – 0.05 mg/kg over several minutes | 0.02 – 0.1 mg/kg/hr | Respiratory depression, hypotension | | Lorazepam | 15 – 20 min | 8 – 15 hr | 0.02 – 0.04 mg/kg | 0.01 – 0.1 mg/kg/hr | Respiratory depression, hypotension; nephrotoxicity, propylene glycol toxicity | | Diazepam | 2 – 5 min | 20 – 120 hr | 5-10 mg | 0.03 – 0.1 mg/kg | Respiratory depression, hypotension, phlebitis | | Propofol | 1 – 2 min | Short term ~ 3- 12 hrLong term ~ 50 + 18.6 hr | 5 μg/kg/min over 5 min | 5 – 50 μg/kg/min | Pain on injection, hypotension, respiratory depression, hypertriglyceridemia, pancreatitis, propofol related infusion syndrome | | Dexmedetomidine | 5 – 10 min | 1.8 – 3.1 hr | No bolus | 0.2 – 0.7 (up to 1.5) μg/kg/hr | Bradycardia hypotension, loss of airway reflexes | | Ketamine | 1 – 2 min | ~80 mins | 0.5 – 1 mg/kg | 0.5 – 4 mg/kg/hr | Hypertension, hypersalivation, agitation, emergence reactions, transient respiratory depression |

Adapted from Clinical Practice Guidelines for the Management of Pain, Agitation, and Delirium in Adult Patients in the Intensive Care Unit. Critical Care Medicine 2013

• Nonbenzodiazepines vs benzodiazepines for sedation
  • SCCM PADIS guidelines recommended a preference for infusions of nonbenzodiazepine sedatives (propofol, dexmedetomidine) over benzodiazepine infusions (midazolam or lorazepam) as some trials have demonstrated that benzodiazepines may be associated with longer mechanical ventilation, longer time to light sedation, and higher rates of delirium.
  • With studies suggesting that early onset analgosedation affects downstream ICU outcomes, we suggest that this concept should also be applied in the ED.
  • Benzodiazepines may still be considered in the appropriate patient such as resistant alcohol withdrawal or refractory seizures.
• Propofol vs dexmedetomidine
  • Propofol is a highly lipophilic GABA-agonist that rapidly crosses the blood brain barrier to provide sedation.
  • Dexmedetomidine is a centrally acting α-2 agonist sedative that provides light sedation without respiratory depression.
  • Two recent high profile RCTs comparing propofol to dexmedetomidine demonstrated no difference in outcomes between the two medications.
  • The SPICE III trial was multicenter RCT of nearly 4000 patients comparing dexmedetomidine as the primary sole sedation agent versus usual care (propofol or midazolam or both) and demonstrated no difference in 90-day (primary outcome) or 180-day mortality. 74% of patients in the dexmedetomidine arm required additional sedation (with propofol or midazolam or both) because sedation goals were not met with dexmedetomidine alone and dexmedetomidine was associated with high rates of bradycardia and hypotension (Shehabi 2019).
  • The MENDS2 trial was a multicenter double blind RCT with 422 patients comparing sedation with dexmedetomidine versus propofol for mechanically ventilated patients with sepsis and demonstrated no differences in any outcomes such as number of days alive without delirium or coma, ventilator-free days, and death at 90 days, with no difference in safety outcomes. Patients in this trial were on relatively low doses of both dexmedetomidine and propofol and higher doses of fentanyl which may limit the ability to adequately compare the two agents well (Hughes 2021).
  • Given the lack of outcome difference, the longer time to onset of peak effect, frequently inadequate level of sedation, and the risk of hypotension and bradycardia, propofol may be a more practical choice of sedative in the emergency department when clinically appropriate.

• Ketamine

  • NDMA antagonist that provides analgesia as well as dissociative sedation, tends to afford hemodynamic stability
  • May be used as a primary or adjunctive sedation agent for continuous infusion
  • Well demonstrated to be safe and effective in retrospective studies but a lack of prospective RCTs evaluating its use
  • When used as an adjunctive sedative has been shown in a multicenter retrospective review, when used as an adjunct, patients receiving ketamine achieved pain and sedation goals more often and had decreased requirements for opiates and for other sedative medications (Groth 2022). Take Home Points

• Employ an analgesic-first approach to post intubation pharmacologic management to ensure that pain is adequately addressed.

• Once pain is addressed, additional sedation may be needed. If sedation is needed, after initial sedation goals are met (e.g. ventilator synchrony), sedation dosing should be titrated early to target light sedation (RASS 0 to -2) and degree of sedation should be routinely assessed.
• When using a long-acting paralytic for induction for intubation, ensure sedation and amnesia for the duration of paralysis.
• We recommend considering fentanyl plus propofol or dexmedetomidine as the routine first options for the choice of analgosedation agents in the emergency department. Propofol may often be preferable in the emergency department due to its rapid onset, ease of titration, and reliable capacity for sedation. Read More

emDocs: Post-intubation analgesia/sedation regimens in ED: Pearls & Pitfalls

PulmCrit: Internet Book of Critical Care: Sedation

References

Barr J, Gilles L, Puntillo K, et al: Clinical Practice Guidelines for the Management of Pain, Agitation, and Delirium in Adult Patients in the Intensive Care Unit. Critical Care Medicine 2013; 41: 263-295 PMID: 23269131

Jeitziner MM, Schwendimann R, Hamers JP, et al: Assessment of pain in sedated and mechanically ventilated patients: An observational study. Acta Anaesthesiol Scand 2012; 56: 645-654 PMID: 22404146

Patel S, Kress J: Sedation and Analgesia in the Mechanically Ventilated Patient: Am J Respir Crit Care Med 2012; 185: 486-497 PMID: 22016443

Shehabi Y, Bellomo R, Reade M, et al: Early Intensive Care Sedation Predicts Long-Term Mortality in Ventilated Critically Ill Patients. Am J Respir Crit Care Med 2012; 186: 724-731 PMID: 22859526

Shehabi Y, Chan L, Kadiman S, et al: Sedation Practice in Intensive Care Evaluation (SPICE) Study Group investigators: Sedation depth and long-term mortality in mechanically ventilated critically ill adults: A prospective longitudinal multicenter cohort study. Intensive Care Med 2013; 39: 910-918 PMID: 23344834

Strom T, Martinussen T, Toft P: A protocol of no sedation for critically ill patients receiving mechanical ventilation: a randomized trial. The Lancet 2010; 375: 475-480 PMID: 20116842

Fuller BM, Roberts BW, Mohr NM, et al: The ED-SED Study: A Multicenter, Prospective Cohort Study of Practice Patterns and Clinical Outcomes Associated With Emergency Department SEDation for Mechanically Ventilated Patients. Crit Care Med. 2019 Nov;47(11):1539-1548. PMID: 31393323; PMCID: PMC7323907.

Shehabi Y, Howe BD, Bellomo R, Arabi YM, et al: Early Sedation with Dexmedetomidine in Critically Ill Patients. N Engl J Med. 2019 Jun 27;380(26):2506-2517. PMID: 31112380.

Hughes CG, Mailloux PT, Devlin JW, et al: Dexmedetomidine or Propofol for Sedation in Mechanically Ventilated Adults with Sepsis. N Engl J Med. 2021 Apr 15;384(15):1424-1436. PMID: 33528922.

Groth CM, Droege CA, Connor KA, et al: Multicenter Retrospective Review of Ketamine Use in the ICU. Crit Care Explor. 2022 Feb 10;4(2):e0633. PMID: 35187497

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BACKGROUND:

Necrotizing soft tissue infections are a rare but potentially lethal condition that can quickly lead to severe morbidity and mortality if not identified by clinical history and physical exam. It is a rapidly progressing infection that moves along fascial planes, often evading the immune system. This is a tricky diagnosis that can often be inconspicuous, so clinical gestalt is key. The definitive treatment of a necrotizing soft tissue infection is surgical debridement and removal of the necrotic tissue. Studies have shown that early surgical intervention is associated with reduced mortality, making early identification of this process very important.

While CT and MRI are commonly used imaging modalities for the evaluation of necrotizing soft tissue infections, they can be time consuming and potentially unsafe for an unstable patient. Point of care ultrasound (POCUS) can be a highly valuable tool for safe and rapid identification of necrotizing soft tissue infections.

EVALUATION:

Scan the affected and contralateral body part for comparison with a sterile cover (or Tegaderm) overlying a high frequency linear probe.

Ultrasound findings include STAFF:

• S/T for subcutaneous thickening
• A for air or emphysema in the subcutaneous tissue, which will appear as dirty shadowing – reverberation artifact from the interface where the air meets the tissue
• FF for a fascial fluid layer greater than or equal to 2 mm

Necrotizing soft tissue infections are diagnosed definitively via surgical exploration. However, the presence of these POCUS findings can prompt early surgical consultation and initiation of broad-spectrum antibiotics.

SUMMARY:

Upon initial evaluation of patients in the emergency department with clinical signs of soft tissue infections, consider using POCUS as a valuable tool to gather more information in patients with a high suspicion for the diagnosis and/or are too unstable to undergo CT imaging.

REFERENCES:

Castleberg E, Jenson N, Dinh VA. Diagnosis of necrotizing faciitis with bedside ultrasound: The staff exam. Western Journal of Emergency Medicine. 2014;15(1):111-113.

Clark ML, Fisher KL. Sonographic Detection of Necrotizing Fasciitis. Journal of Diagnostic Medical Sonography. 2017;33(4):311-316.

Joaquín Valle Alonso, Ganapathiram Lakshmanan, Yasser Saleem, Use of POCUS Ultrasound in sepsis, bedside diagnosis of necrotizing fasciitis, QJM: An International Journal of Medicine, Volume 110, Issue 10, October 2017, Pages 687–688.

Magalhães L, Martins SR, Nogué R. The role of point-of-care ultrasound in the diagnosis and management of necrotizing soft tissue infections. The Ultrasound Journal. 2020;12(1). doi:10.1186/s13089-020-0153-4

McHenry CR, Piotrowski JJ, Petrinic D, Malangoni MA. Determinants of mortality for necrotizing soft-tissue infections. Ann Surg 1995; 221:558–563.

Sarani B. Necrotizing fasciitis. Necrotizing Fasciitis. https://rarediseases.org/rare-diseases/necrotizing-fasciitis/. Published October 28, 2019. Accessed March 9, 2022.

VA; CEJND. Diagnosis of necrotizing fasciitis with bedside ultrasound: The staff exam. The western journal of emergency medicine. https://pubmed.ncbi.nlm.nih.gov/24578776/. Accessed February 28, 2022.

Voros D, Pissiotis C, Georgantas D, Katsaragakis S, Antoniou S, Papadimitriou J. Role of early and extensive surgery in the treatment of severe necrotizing soft tissue infection. Br J Surg 1993; 80:1190–1191.

Wallace HA, Perera TB. Necrotizing Fasciitis. [Updated 2021 Jul 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan.

Wronski M; Slodkowski M; Cebulski W; Karkocha D; Krasnodebski IW; Necrotizing fasciitis: Early sonographic diagnosis. Journal of clinical ultrasound: JCU.

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A quick primer on hypocalcemia in the ED.

Hosts:

Joseph Offenbacher, MD

Audrey Bree Tse, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/hypocalcemia.mp3

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Tags: calcium, Critical Care, Endocrine

Show Notes

Swami’s CoreEM Post

Hypocalcemia Repletion:

• IV calcium supplementation with 100-300 mg Ca2+ raises serum Ca2+ by 0.5 – 1.5 mEq
• For acute but mild symptomatic hypocalcemia: 200-1000mg calcium chloride IV or 1-2g IV calcium gluconate over 2 hours
• For severe hypocalcemia: 1g calcium chloride IV or 1-2g IV calcium gluconate IV over 10 minutes repeated q 60 min until symptoms resolve

References:

• Cooper MS, Gittoes NJ. Diagnosis and management of hypocalcaemia. BMJ 2008; 336:1298.
• ​​Desai TK, Carlson RW, Geheb MA. Prevalence and clinical implications of hypocalcemia in acutely ill patients in a medical intensive care setting. Am J Med 1988; 84:209.
• Goltzman, D. Diagnostic approach to hypocalcemia. UpToDate. UpToDate; Jul 17, 2020. Accessed April 29, 2022. https://www.uptodate.com/contents/plantar-fasciitis
• Kelly A, Levine MA. Hypocalcemia in the critically ill patient. J Intensive Care Med 2013; 28:166.
• Pfenning CL, Slovis CM: Electrolyte Disorders; in Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 125: p 1636-53.
• Swaminathan, A. (2016, January 27). Hypocalcemia. CoreEM. Retrieved April 29, 2022, from https://coreem.net/core/hypocalcemia/
• Vantour L, Goltzman D. Regulation of calcium homeostasis. In: rimer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 9th ed, Bilezikian JP (Ed), Wiley-Blackwell, Hoboken, NJ 2018. p.163.

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How and when to reverse anticoagulation in the bleeding EM patient.

Hosts:

Joe Offenbacher, MD

Audrey Bree Tse, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/AC_reversal.mp3

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Tags: Anticoagulation, Critical Care, Resuscitation

Show Notes Coagulation Cascade:

Algorithm for Anticoagulated Bleeding Patient in the ED:

Indications for Anticoagulation Reversal:

References:

1. Baugh CW, Levine M, Cornutt D, et al. Anticoagulant Reversal Strategies in the Emergency Department Setting: Recommendations of a Multidisciplinary Expert Panel. Ann Emerg Med. 2020;76(4):470-485. doi:10.1016/j.annemergmed.2019.09.001
2. Eikelboom JW, Quinlan DJ, van Ryn J, Weitz JI. Idarucizumab: The Antidote for Reversal of Dabigatran. Circulation. 2015 Dec 22;132(25):2412-22. doi: 10.1161/CIRCULATIONAHA.115.019628. PMID: 26700008.
3. Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885.
4. Fariborz Farsad B, Golpira R, Najafi H, et al. Comparison between Prothrombin Complex Concentrate (PCC) and Fresh Frozen Plasma (FFP) for the Urgent Reversal of Warfarin in Patients with Mechanical Heart Valves in a Tertiary Care Cardiac Center. Iran J Pharm Res. 2015;14(3):877-885.
5. Palta S, Saroa R, Palta A. Overview of the coagulation system. Indian J Anaesth. 2014;58(5):515-523. doi:10.4103/0019-5049.144643
6. Siegal DM, Curnutte JT, Connolly SJ, Lu G, Conley PB, Wiens BL, Mathur VS, Castillo J, Bronson MD, Leeds JM, Mar FA, Gold A, Crowther MA. Andexanet Alfa for the Reversal of Factor Xa Inhibitor Activity. N Engl J Med. 2015 Dec 17;373(25):2413-24. doi: 10.1056/NEJMoa1510991. Epub 2015 Nov 11. PMID: 26559317.

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A primer on this airway/ ID/ ENT emergency.

Hosts: Joe Offenbacher MD, A Bree Tse, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/ludwigs_2.mp3

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Tags: Airway, ENT, Infectious Diseases

Show Notes

References:

1. Botha A, Jacobs F, Postma C. Retrospective analysis of etiology and comorbid diseases associated with Ludwig’s Angina. Ann Maxillofac Surg 2015; 5:168.
2. Boscolo-Rizzo P, Da Mosto MC. Submandibular space infection: a potentially lethal infection. Int J Infect Dis 2009; 13:327.
3. Brook I. Microbiology and principles of antimicrobial therapy for head and neck infections. Infect Dis Clin North Am. 2007 Jun;21(2):355-91, vi. doi: 10.1016/j.idc.2007.03.014. PMID: 17561074.
4. Chong W, Hijazi M, Abdalrazig M, Patil N. Respect the Floor of the Mouth. J Emerg Med. 2020 Jul;59(1):e27-e29. doi: 10.1016/j.jemermed.2020.04.015. Epub 2020 May 19. PMID: 32439254.
5. http://www.emdocs.net/ludwigs-angina-2/
6. Mohamad I, Narayanan MS. “Double Tongue” Appearance in Ludwig’s Angina. N Engl J Med 2019; 381:163.
7. Saifeldeen K, Evans R. Ludwig’s angina. Emerg Med J. 2004 Mar;21(2):242-3. doi: 10.1136/emj.2003.012336. PMID: 14988363; PMCID: PMC1726306.
8. Wolfe MM, Davis JW, Parks SN. Is surgical airway necessary for airway management in deep neck infections and Ludwig angina? J Crit Care. 2011 Feb;26(1):11-4. doi: 10.1016/j.jcrc.2010.02.016. PMID: 20537506.

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A quick overview of pneumothorax for the EM physician: the what, why, diagnosis, and treatment.

Hosts:

Joe Offenbacher, MD

Audrey Tse, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Pneumothorax_CoreEM_podcast.mp3

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Tags: #pneumothorax #FOAMed

Show Notes Shownotes:

CoreEM Pulmonary Ultrasound Post

References:

Bense L, Lewander R, Eklund G, et al. Nonsmoking, non-alpha 1-antitrypsin deficiency-induced emphysema in nonsmokers with healed spontaneous pneumothorax, identified by computed tomography of the lungs. Chest 1993; 103:433.

Bense L, Wiman LG, Hedenstierna G. Onset of symptoms in spontaneous pneumothorax: correlations to physical activity. Eur J Respir Dis 1987; 71:181.

Brown SGA, Ball EL, Perrin K, Asha SE, Braithwaite I, Egerton-Warburton D, Jones PG, Keijzers G, Kinnear FB, Kwan BCH, Lam KV, Lee YCG, Nowitz M, Read CA, Simpson G, Smith JA, Summers QA, Weatherall M, Beasley R; PSP Investigators. Conservative versus Interventional Treatment for Spontaneous Pneumothorax. N Engl J Med. 2020 Jan 30;382(5):405-415. doi: 10.1056/NEJMoa1910775. PMID: 31995686.

Chardoli M, Hasan-Ghaliaee T, Akbari H, Rahimi-Movaghar V. Accuracy of chest radiography versus chest computed tomography in hemodynamically stable patients with blunt chest trauma. Chin J Traumatol 2013; 16:351.

Chan KK, Joo DA, McRae AD, et al. Chest ultrasonography versus supine chest radiography for diagnosis of pneumothorax in trauma patients in the emergency department. Cochrane Database Syst Rev 2020; 7:CD013031.

Ebrahimi A, Yousefifard M, Mohammad Kazemi H, et al. Diagnostic Accuracy of Chest Ultrasonography versus Chest Radiography for Identification of Pneumothorax: A Systematic Review and Meta-Analysis. Tanaffos 2014; 13:29.

Gobbel Jr WG, Rhea Jr WG, Nelson IA, Daniel RA. Spontaneous pneumothorax. J Thorac Cardiovasc Surg 1963; 46:331.

Lesur O, Delorme N, Fromaget JM, et al. Computed tomography in the etiologic assessment of idiopathic spontaneous pneumothorax. Chest 1990; 98:341.

Lichtenstein DA, Mezière G, Lascols N, et al. Ultrasound diagnosis of occult pneumothorax. Crit Care Med 2005; 33:1231.

Melton LJ 3rd, Hepper NG, Offord KP. Influence of height on the risk of spontaneous pneumothorax. Mayo Clin Proc 1981; 56:678.

Ohata M, Suzuki H. Pathogenesis of spontaneous pneumothorax. With special reference to the ultrastructure of emphysematous bullae. Chest 1980; 77:771.

Sahn SA, Heffner JE. Spontaneous pneumothorax. N Engl J Med 2000; 342:868.

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An interesting back story on this must-not-miss EKG finding in the ED!

Hosts:

Joseph Offenbacher, MD

Audrey Bree Tse, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/CoreEM_Wellens.mp3

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Tags: #FOAMed, #wellens, Cardiology, EKG, STEMI

Show Notes Hosts: Joe Offenbacher MD, Audrey Bree Tse MD

EKG Findings in de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481.

Table 1 in de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481.

REFERENCES:

de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982 Apr;103(4 Pt 2):730-6. doi: 10.1016/0002-8703(82)90480-x. PMID: 6121481.

Lee, M., & Chen, C. (2015). Myocardial Bridging: An Up-to-Date Review. Journal of Invasive Cardiology, 27(11), 521–528.

https://lifeinthefastlane.com/ecg-library/wellens-syndrome/

Lin AN, Lin S, Gokhroo R, Misra D. Cocaine-induced pseudo-Wellens’ syndrome: a Wellens’ phenocopy. BMJ Case Rep. 2017 Dec 14;2017:bcr2017222835. doi: 10.1136/bcr-2017-222835. PMID: 29246935; PMCID: PMC5753703.

Rhinehardt, J., Brady, W. J., Perron, A. D., & Mattu, A. (2002). Electrocardiographic manifestations of Wellens’ syndrome. The American Journal of Emergency Medicine, 20(7), 638–643. https://doi.org/10.1053/ajem.2002.34800

Tandy, TK; Bottomy DP; Lewis JG (March 1999). “Wellens’ syndrome”. Annals of Emergency Medicine. 33 (3): 347–351. PMID 10036351. doi:10.1016/S0196-0644(99)70373-2. (via Wikipedia)

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We discuss EM presentation, diagnosis, and management of subarachnoid hemorrhage.

Hosts:

Mark Iscoe, MD

Brian Gilberti, MD

Bree Tse, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/SAH.mp3

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Tags: Critical Care, Neurology, Subarachnoid Hemorrhage

Show Notes Non-contrast head CT showing SAH (Case courtesy of Dr. David Cuete, Radiopaedia.org, rID: 22770)

Hunt-Hess grade and mortality (from Lantigua et al. 2015.)

| Hunt-Hess grade | Mortality (%) | | 1. Mild Headache | 3.5 | | 2. Severe headache or cranial nerve deficit | 3.2 | | 3. Confusion, lethargy, or lateralized weakness | 9.4 | | 4. Stupor | 23.6 | | 5. Coma | 70.5 |

Ottawa Subarachnoid Hemorrhage Rule, and appropriate population for rule application (from Perry et al. 2017)

Apply to patients who are:

• Alert
• ≥ 15 years old
• Have new, severe, atraumatic headache that reached maximum intensity within 1 hour of osnet

Do not apply to patients who have:

• New neurologic deficits
• Previous diagnosis of intracranial aneurysm, SAH, or brain tumor
• History of similar headaches (≥ 3 episodes over ≥ 6 months)

SAH cannot be ruled out if the patient meets any of the following criteria:

• Age ≥ 40
• Symptom of neck pain or stiffness
• Witnessed loss of consciousness
• Onset during exertion
• “Thunderclap headache” (defined as instantly peaking pain)
• Limited neck flexion on examination (defined as inability to touch chin to chest or raise head 3 cm off the bed if supine)

___________________________

Special Thanks To:

• Dr. Mark Iscoe, MD (Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue)

___________________________

References:

Bellolio MF, Hess EP, Gilani WI, et al. External validation of the Ottawa subarachnoid hemorrhage clinical decision rule in patients with acute headache. Am J Emerg Med. 2015;33(2):244-9.

Carstairs SD, Tanen DA, Duncan TD, et al. Computed tomographic angiography for the evaluation of aneurysmal subarachnoid hemorrhage. Acad Emerg Med. 2006;13(5):486-492.

Connolly ES, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012;43(6):1711-1737.

Czuczman AD, Thomas LE, Boulanger AB, et al. Interpreting red blood cells in lumbar puncture: distinguishing true subarachnoid hemorrhage from traumatic tap. Acad Emerg Med. 2013;20(3):247-256.

Dugas C, Jamal Z, Bollu PC. Xanthochromia. [Updated 2020 Aug 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526048/

Goldstein JN, Camargo CA, Pelletier AJ, Edlow JA. Headache in United States emergency departments: demographics, work-up and frequency of pathological diagnoses. Cephalalgia. 2006;26(6):684-90.

Kumar A, Niknam K, Lumba-brown A, et al. Practice Variation in the Diagnosis of Aneurysmal Subarachnoid Hemorrhage: A Survey of US and Canadian Emergency Medicine Physicians. Neurocrit Care. 2019.

Lantigua H, Ortega-Gutierrez S, Schmidt JM, et al. Subarachnoid hemorrhage: who dies, and why? Crit Care. 2015;19:309.

Macdonald RL, Schweizer TA. Spontaneous subarachnoid haemorrhage. Lancet. 2017;389(10069):655-666.

Mayer PL, Awad IA, Todor R, et al. Misdiagnosis of symptomatic cerebral aneurysm. Prevalence and correlation with outcome at four institutions. Stroke. 1996;27(9):1558-63.

Meurer WJ, Walsh B, Vilke GM, Coyne CJ. Clinical guidelines for the emergency department evaluation of subarachnoid hemorrhage. J Emerg Med. 2016;50(4):696-701.

Perry JJ, Spacek A, Forbes M, et al. Is the combination of negative computed tomography result and negative lumbar puncture result sufficient to rule out subarachnoid hemorrhage? Ann Emerg Med. 2008;51(6):707-713

Perry JJ, Stiell IG, Sivilotti MLA, et al. High risk clinical characteristics for subarachnoid haemorrhage in patients with acute headache: prospective cohort study. BMJ. 2010;341:c5204.

Perry JJ, Stiell IG, Sivilotti MLA, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. BMJ. 2011;343(jul18 1):d4277-d4277.

Perry JJ, Stiell IG, Sivilotti ML, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. JAMA. 2013;310(12):1248-55.

Perry JJ, Sivilotti MLA, Sutherland J, et al. Validation of the Ottawa Subarachnoid Hemorrhage Rule in patients with acute headache. CMAJ. 2017;189(45):E1379-E1385.

Vermeulen MJ, Schull MJ. Missed diagnosis of subarachnoid hemorrhage in the emergency department. Stroke. 2007;38(4):1216-21.

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We discuss the (F)utility(?) of ED Utox screens with our very own Dr. Phil DiSalvo.

Hosts:

Bree Tse, MD

Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Urine_Drug_Screen_final.mp3

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Tags: Toxicology

Show Notes

Special Thanks To:

Dr. Philip DiSalvo, MD

Ronald O. Perelman Department of Emergency Medicine at NYU Langone Health, NYC Health + Hospitals/ Bellevue

New York City Poison Control Center

References:

Christian MR, et al. Do rapid comprehensive urine drug screens change clinical management in children? Clin Toxicol (Phila). 2017;57:977-980.

Grunbaum AM, Rainey PM (2019). Chapter 7: Laboratory Principles. In Goldfrank’s toxicologic emergencies. New York, NY: McGraw-Hill Education.

Moeller K, Kissack J, Atayee R, Lee K. Clinical Interpretation of Urine Drug Tests: What Clinicians Need to Know About Urine Drug Screens. Mayo Clinic Proceedings Review. Volume 92, Issue 5, p774-796, May 1, 2017. https://www.mayoclinicproceedings.org/article/S0025-6196(16)30825-4/fulltext

Table 2: Approximate Drug Detection Time in the Urine

Table 4: Summary of Agents Contributing to Results by Immunoassay

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EM management of the rare but potentially complicated precipitous vaginal breech delivery.

Hosts:

Audrey Bree Tse, MD

Masashi Rotte, MD MPH

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Breesashi_Breech_CoreEM.mp3

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Tags: Obstetrics, Precipitous Deliveries, Pregnancy

Show Notes Frank Breech Presentation:

Complete Breech Presentation:

Incomplete Breech (“Footling”) Presentation:

Pinard Maneuver:

Mauriceau Maneuver:

References:

• Cunningham FG et al. Breech Presentation and Delivery. Williams Obstetrics, 22nd ed. 2005.
• Desai S, Henderson SO. Labor and Delivery and Their Complications. Rosen’s Emergency Medicine, 8e. 2014. Chapter 181.
• Gabbe SG et al. Obstetrics: Normal and Problem Pregnancies, 2nd e. 1991. p.479.
• Stitely ML, Gherman RB. Labor with abnormal presentation and position. Obstet Gynecol Clin North Am. 2005; 32: 165.
• VanRooyen MJ, Scott J. Emergency Delivery. Tintanelli’s Emergency Medicine, 7th e. 2011. Chapter 105.
• http://www.emdocs.net/the-complicated-delivery-what-do-you-do/#:~:text=Deliveries%20that%20occur%20in%20the,in%20denial%20of%20their%20pregnancies.
• https://ranzcog.edu.au/womens-health/patient-information-resources/breech-presentation-at-the-end-of-your-pregnancy
• https://wikem.org/wiki/Breech_delivery

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The speech given by Dr. Goldfrank at the 2020 NYU / Bellevue Emergency Medicine Graduation Ceremony

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Goldfrank_Graduation_Speech_2020.mp3

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Tags: Graduation. Goldfrank

Show Notes Graduation 2020

Lewis R. Goldfrank, MD

June 17, 2020

WELCOME TO THE GRADUATES

Congratulations to a wonderful group of physicians. It is a pleasure to recognize your great accomplishments in the presence of your friends, families, loved ones and the residents and faculty who have learned so much from and with you. I would first like to recognize those of you who are members of the Gold Humanism Honor Society.

There are a remarkable number of awardees in our graduating class of 2020.

CLASS OF 2020

Joe Bennett (R)

Max Berger (R)

Ashley Miller (R)

Leigh Nesheiwat (S)

Kristen Ng (R)

Emily Unks (S)

AND

Arie Francis (R)

Nisha Narayanan (S)

FUTURE PGY-4

Elena Dimiceli (S)

Kamini Doobay (S)

Mark Iscoe (R)

FUTURE PGY-3

Stasha O’Callaghan (S)

Nicholus Warstadt (S)

FUTURE PGY-1

Aaron Bola (S)

Alison (Ali) Graebner (S)

Aron Siegelson (S)

Melissa Socarras (S)

Sarah Spiegel (S)

Thomas Sullivan (S)

Christy Williams (S)

GOLD HUMANISM CORE VALUES

Integrity, Excellence, Compassion, Altruism, Respect, Empathy, Service

These are the values you want as a doctor for yourself or a loved one,

• to have outstanding listening skills with patients
• to be at your side during a medical emergency,
• to have exceptional interest in service to the community,
• to have the highest standards of professionalism
• to integrate a humanistic approach in patient care.

These values are what brought all of you to NYU-Bellevue and that you have honed throughout your training. The remainder of this talk shows how all of you have been successful and demonstrated these values some of you were elected to the Gold Humanism—all of you have achieved humanistic success.

Your personal efforts in the face of uncertainty of the evolution of the pandemic, the inadequate supplies, the hospital and governmental problematic decisions are remarkable. In our country, the President did not mourn the loss of more than a 100,000 human beings and the needs of society. Nor did he provide the leadership and moral support that the country desperately needed to optimally handle this unprecedented crisis. You, in contrast, demonstrate unflappable commitment to address and overcome obstacles to care for your patients, assist your peers, educate and care for your families and friends, while also caring for yourselves. This is a tribute to your humanism. You created essential ways to help patients who were isolated from families and friends during the critical phases of COVID-19. You utilized new tools to communicate your sorrow, your compassion and love, to maintain essential humanistic traditions of medicine while you could not talk, touch or utilize other essential skills to the fullest extent of a physician.

When you recognized that all your knowledge of the social determinants of medicine was playing out as COVID-19 assaulted the poorest in our country, the people of color, the people with essential jobs without personal protective equipment, the people crowded in apartments and subways and buses, you spoke up and acted with appreciation and understanding of these disparities. You recognized that our system of using medicine to correct the societal social institutionally entrenched disparities was inadequate. George Floyd’s death, and that of Breonna Taylor and innumerable others document the racism in America that destroys a part of us each and every day and by extension reinforces and normalizes white privilege. The ever increasing body of video evidence of the horrors of systemic racism is indisputable. You recognized that the American system of criminalization of social determinants is unacceptable. You spoke up and demonstrated that you saw our blind spots on policing and race. You protested to demand change in America.

Change for equity and justice must occur throughout our society. “Black Lives Matter” will only be realized when the social determinants are truly addressed through changes that impact every vulnerable person. We must recognize that person, institutional and societal failures will not be corrected by medicalizing or criminalizing of socially determined inequities. Racism is systemic. Today you are seeking to create essential changes in medicine that will only occur when all the workplaces and governmental sites across the country, are enriched to allow a full representation of all the voices of all the people.

You are leaders in the response to COVID-19 and the fight against racism. You will not only be remembered for having been present, but particularly for how you have responded. Thank you for your courage, creativity, resiliency and ability to transition and advance under duress. It was a privilege to watch you demonstrate the importance of your core values and the impact that your training here at NYU/Bellevue has had on your ability to integrate them into your practice.

You are truly individuals of immense potential, ideal for advancing our world. How you keep these values and grow them in the next developmental stage of your careers will be critical. Each of you will contribute according to your talent, resources and priorities whether in clinical practice, academics, advocacy or public health. Always in every encounter with patients and their families “Be the change that you wish to see in the world” Mahatma Ghandi.

THANK YOU AND CONGRATULATIONS!

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An overview and management tips of hemoptysis in the ED.

Hosts:

Brian Gilberti, MD

Audrey Bree Tse, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hemoptysis.mp3

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Tags: Critical Care, Pulmonary

Show Notes OVERVIEW:

• Definition:
  • expectoration/ coughing of blood originating from tracheobronchial tree
• Sources:
  • Bronchial arteries (90%): under systemic circulatory pressure to supply supporting structures of the lung → heavier bleeding
  • Pulmonary arteries (5%): under low pressure to supply alveoli → milder bleeding
  • Nonbronchial arteries (5%): intercostal arteries, coronary arteries, thoracic/ upper/ inferior phrenic arteries

• Quantification:

  • Mild: <20mL/ 24h
  • Massive defined anywhere from >300mL-1L/ 24hr
  • Mortality: 38% for massive (>500mL/ 24hr) vs 4.5% for nonmassive

• Etiology (in adults):

  • Infectious (most common):
    • Bronchitis
    • PNA (necrotizing, lung abscess)
    • TB
    • Viral
    • Fungal
    • Parasitic
  • Malignancy:
    • Primary lung cancer vs metastatic disease
  • Pulmonary:
    • Bronchiectasis
    • COPD
    • PE/ infarction
    • Bronchopleural fistula
    • Sarcoidosis
  • Cardiac:
    • Mitral stenosis
    • Tricuspid endocarditis
    • CHF
  • Rheumatological:
    • Goodpasture Syndrome
    • SLE
    • Vasculitis (Wegener’s, HSP, Behcet)
    • Amyloidosis
  • Hematological:
    • Coagulopathy/ thrombocytopenia/ platelet dysfunction
    • DIC
  • Vascular:
    • Pulmonary HTN
    • AA
    • Pulmonary artery aneurysm
    • Aortobronchial fistula
    • Pulmonary angiodysplasia
  • Toxins:
    • Anticoagulation/ aspirin/ antiplatelets
    • Penicillamine, amiodarone
    • Crack lung
    • Organic solvents
  • Trauma:
    • Tracheobronchial rupture
    • Pulmonary contusion
  • Other:
    • bronchoscopy/ lung biopsy
    • Pulmonary artery or central venous catheterization
    • Foreign body aspiration
    • Pulmonary endometriosis (catamenial hemoptysis)
    • Idiopathic (up to 25% of cases)
  • Pseudohemoptysis:
    • Sinusitis
    • Epistaxis
    • Rhinorrhea
    • Pharyngitis
    • URI
    • Aspiration
    • GIB

WORKUP:

• HPI:
  • CP, SOB
  • B symptoms: fever, weight loss, chills, night sweats
  • Lymphadenopathy
  • Timeframe: acute vs chronic
  • Prior lung/ renal/ cardiac disease
  • Recreational drug/ cigarette/ chemical exposures
  • travel/ infectious exposure
  • Medications
  • Any other sites of bleeding
  • Precipitating factors
  • Description of blood clots
  • Patients are unable to accurately estimate degree of bleeding
• PE:
  • Petechiae, edema, ecchymosis, ulcers, clubbing (chronic lung disease)
  • Cardiopulmonary
  • Sputum samples
• Labs:
  • CBC w/ diff, BMP, LFTs, coags, T&S
  • ABG
  • UA
  • Infectious workup if suspected: cultures, grain stains
• Imaging:
  • CXR: 20% will be normal. May see tumour, cavity, effusion, infiltrate, PTX. Early pulmonary hemorrhage may present as infiltrate
  • CT: only for stable patients! May see bronchiectasis, cavitary lesions, acinar nodules, tumours
  • CTA: bronchial arteries, aneurysms, PE
  • ECHO: identify valvular abnormalities, signs of PE, aortic aneurysm
• Bronchoscopy:
  • Not often performed in ED, but therapeutic & diagnostic
  • Allows direct visualization of tumours, foreign bodies, granulomas, infiltration, as well as local therapy (vasoconstrictive agents, stent/ balloon tamponade, electrocautery, procoagulants)

MANAGEMENT:

• Goals:
  • Control airway
  • Protect healthy lung
  • Identify and treat underlying cause
  • Stabilize hemodynamics with volume resuscitation
• Provider precautions (respiratory & contact)
• ABCs, close monitoring
  • Early airway management: massive hemoptysis, respiratory compromise, hypoxia, risk factors (elderly, AMS, coagulopathic)
  • 2 x suction, preoxygenation, patient positioned upright, >8Fr ETT to facilitate suctioning/ bronch
  • If bleeding side can be identified, consider “selective intubation” into nonbleeding lung to minimize further aspiration of blood and to provide ventilation
  • Life threat = asphyxiation, not exsanguination. ~Only 150cc anatomic dead space in major airways
• 2 x large bore IVs
• MTP prn vs volume resuscitation
• “Bad lung down” in lateral position: theoretical belief to minimize reflux of blood into normal lung
• Correct coagulopathy
• Consider nebulized TXA for nonmassive hemoptysis (500mg w/ NS per neb)
  • Double-blind, randomized controlled trial in 2018
  • Nebulized TXA (500mg TID) vs placebo (normal saline) in hemodynamically stable adult patients admitted with mild hemoptysis (<200 mL/ 24hr) and no respiratory instability
    • Additional exclusion criteria included those with renal failure, hepatic failure, or coagulopathy
  • Assessed mortality and hemoptysis recurrence rate at 30 days and 1 year
  • 25 patients randomized to receive TXA nebs, 22 randomized to receive normal saline nebs
  • Results:
    • Resolution of hemoptysis within 5 days of admission was significantly higher in TXA-treated patients than placebo patients (96% vs 50%; P < 0.0005)
    • Mean hospital length of stay was shorter for TXA group (5.7 +- 2.5 days vs 7.8 +- 4.6 days; P = 0.046)
    • Fewer patients in TXA group required invasive procedures to control bleeding vs placebo group (0% vs 18.2%; P = 0.041)
    • No side effects were noticed in either group
• Antibiotics if infectious
• Bronchoscopy: local therapy (vasoconstrictive agents, stent/ balloon tamponade, electrocautery, procoagulants)
  • Rigid bronch for unstable patients to evacuate clots vs fiberoptic bronch for stable patients
• Bronchial artery embolization (call IR early!)
• May require lobectomy or pneumonectomy (consult thoracic surgery)

DISPOSITION:

• Low threshold for higher level of care: only mild, hemodynamically stable hemoptysis on floor
• Discharge: only if certain regarding etiology in healthy, hemodynamically stable patients with scant, resolved hemoptysis, no coagulopathy, and reassuring workup
  • Ensure patients have reliable follow up and avoid smoking. Strict return precautions!

REFERENCES:

• Kiraly A, Pang P, Cheema N. Hemoptysis. In: Schaider J, Barkin R, Hayden S, Wolfe R, Barkin A, Shayne P, Rosen P. Rosen and Barkin’s 5-Minute Emergency Medicine Consult. 5th Edition. Philadelphia, PA: Wolters Kluwer; 2015; 504-505.
• Nickson, C. Haemoptysis. Life in the Fastlane. [litfl.com/haemoptysis/]. Updated April 9, 2019. Retrieved February 10, 2020.
• Wand O, Guber E, Guber A, Schochet GE, Israeli-Shani L, Shitrit D. Inhaled Tranexamic Acid for Hemoptysis Treatment: A Randomized Controlled Trial. Chest. December 2018; 154(6): 1379-1384.
• Young WF. Hemoptysis. In: Cline, David,eds. Tintinalli’s Emergency Medicine Manual. 7th Edition. New York : McGraw-Hill Medical; 2011; 473-476.

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