CoreEM: Recent Episodes

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     Group A strep in the pediatric ED: from strep throat to invasive disease and toxic shock.

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

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Group\_A\_Strep.mp3   Download Leave a Comment Tags: Infectious Diseases, Pediatrics    Show Notes Background* **Group A strep = *Streptococcus pyogenes*** — gram-positive organism that colonizes the pharynx, but also the **perianal and genital mucosa** (worth remembering when the source isn’t the throat).

• Extremely common. The episode cites an estimated ~289 million cases/yr of strep pharyngitis in children 5–14 (NIH). For a U.S.-specific, verifiable anchor: the CDC estimates strep throat drives ~5.2 million outpatient visits/yr in people <65.
• No true beta-lactam resistance. GAS remains uniformly susceptible to penicillin and amoxicillin. Note this is not true for macrolides/clindamycin — roughly 1 in 3 invasive isolates are now erythromycin/clindamycin resistant.

Pathophysiology — the throughline Exotoxins (superantigens) tie the whole spectrum together — they drive scarlet fever, streptococcal toxic shock syndrome (STSS), and are implicated in the Kawasaki overlap discussed below. * The organism is the same from a sore throat to a life-threat; what changes is host response and toxin burden.*

Clinical Presentation Core findings: tonsillar inflammation/exudate, tender anterior cervical lymphadenopathy, fever. * Classic strep tells to hunt for: + Palatal petechiae + Strawberry tongue + Perioral pallor * Scarlet fever — fine, sandpapery rash, typically starts on the trunk and spreads outward; later desquamation of the fingers and toes. * Extrapharyngeal clues: kids commonly present with abdominal pain or headache even when the throat looks unimpressive. Low threshold to test with fever + abd pain or fever + headache*.

Diagnosis / WorkupCentor / Modified (McIsaac) Score Centor Score (Modified/McIsaac) — MDCalc * One point each: fever, tonsillar exudates, tender anterior cervical lymphadenopathy, absence of cough. The Modified (McIsaac) version adds age. * Developed and validated in adults (≥16). It is not reliable in young children* — don’t lean on it in peds the way you would in an adult. * For reference, McIsaac culture-positive probabilities: ~2.5% (0 criteria), 6.5% (1), 15% (2), 32% (3), 56% (4).

Testing Rapid PCR — high sensitivity and specificity; increasingly the front-line test. * Rapid antigen detection test (RADT) — highly specific but less sensitive. Per IDSA, a negative RADT in a child/adolescent should be backed up with a throat culture (culture is the more sensitive gold standard). Backup culture is not* required in adults.

Who not to test Generally don’t test/treat children <3 — acute rheumatic fever is rare in this group. * Exception: the symptomatic young child with a close contact recently diagnosed* with strep.

Management First-line: amoxicillin 50 mg/kg once daily, max 1 g/dose. GAS stays beta-lactam susceptible (penicillin and amoxicillin remain treatments of choice per IDSA 2012). * IM penicillin G / benzathine (bicillin) for kids who can’t tolerate oral meds — one shot, done. * Return to school: after one full day of treatment (~12–24 h), provided afebrile and feeling well. * Contact prophylaxis: + Pharyngitis — routine prophylaxis of asymptomatic contacts is not standard; consider it for households with recurrent infection or a history of rheumatic fever. + Invasive GAS — more aggressive. Prophylaxis is recommended for household contacts who are immunosuppressed, pregnant, post-recent-surgery, or have an open wound* (CDC).

The Bounce-Back / Treatment FailureThe kid who finishes amox and is back a week later. Sort into three buckets:

1. Chronic carrier — GAS carriage in children runs 2–20%. Carriers test positive but are asymptomatic, with low risk of transmission or complications. Don’t chase them.
2. New infection.
3. True treatment failure → ask why:
   • The shield effect — the throat is co-colonized with beta-lactamase producers (Staph aureus, H. influenzae, Moraxella) that degrade amoxicillin before it can act, effectively shielding the GAS.
   • This is NOT true resistance — the strep is still beta-lactam susceptible; the neighbors are the problem.
   • Fix: switch to a beta-lactamase–stable agent — amoxicillin-clavulanate or a first-generation cephalosporin.

Complications Suppurative: peritonsillar abscess, sinusitis, meningitis, bacteremia. * Non-suppurative: + Acute rheumatic fever — typically 1–5 wks post-infection; Jones criteria (AHA 2015 revision · ACC summary · CDC). + Post-infectious...*

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Authors: Jonathan Kobles, MD and Matthew Generoso, MD

Case: A 25-year-old female with no significant past medical history presents to the Emergency Department with right jaw pain and inability to close her mouth. She reports an episode of nausea and stomach cramping and a sensation that she was about to vomit. After running to the bathroom and attempting to vomit, she felt a clicking sensation in her jaw (worse on the right side) and afterward was unable to close her mouth. She states this has never happened to her before, and she denied any direct trauma to her face, jaw, or mouth. * On exam, her mouth is held open and she is unable to fully close her mouth. She has no significant facial swelling, and no evidence of intraoral trauma. She has mild tenderness to her right temporomandibular joint (TMJ), where she is suspected to have an anterior TMJ dislocation. * She is given 30 mg of intramuscular ketorolac and 5 mg of intramuscular diazepam. * Reduction of her anterior TMJ dislocation is attempted with both extra-oral and intra-oral manipulation, without success and with significant discomfort from the patient. Background: Temporomandibular joint (TMJ) dislocation occurs when the mandibular condyle becomes trapped anterior to the articular eminence, preventing spontaneous reduction and leaving the patient unable to close their mouth. * Most ED presentations involve acute anterior dislocations following routine activities that require excessive mouth opening, including yawning, laughing, vomiting, singing, dental procedures, or endoscopy. * Traditional reduction methods rely on provider-applied force and may require procedural sedation. The syringe technique offers a patient-driven alternative that can often be performed without sedation and may be particularly useful in patients with recurrent atraumatic dislocations. Epidemiology*** Anterior dislocations account for the overwhelming majority of TMJ dislocations encountered in clinical practice. Bilateral dislocations occur more commonly than unilateral dislocations and are frequently associated with atraumatic mechanisms. * Patients at highest risk for recurrence include those with prior dislocations, generalized ligamentous laxity, connective tissue disorders, abnormal joint anatomy, and neuromuscular conditions that alter normal jaw mechanics. * Recurrent dislocators represent the population most likely to benefit from learning the syringe technique as a future self-reduction maneuver.

Clinical Presentation: Patients typically present with an inability to close their mouth accompanied by preauricular pain, difficulty speaking, excessive salivation, and inability to chew normally. * On examination, the jaw is fixed in an open position. Bilateral dislocations generally produce a symmetric appearance, whereas unilateral dislocations often cause deviation of the mandible toward the unaffected side. * The diagnosis is usually clinical. Imaging should be reserved for patients with significant trauma, concern for fracture, atypical findings, or failed reduction attempts. Differential Diagnosis: Mandibular fractures, particularly condylar fractures, should be considered in patients with traumatic mechanisms, persistent malocclusion, facial deformity, or focal bony tenderness. * Deep neck space infections, peritonsillar abscesses, and epiglottitis may mimic TMJ dislocation by causing drooling, muffled speech, and difficulty handling secretions, though associated infectious symptoms are typically present. * TMJ internal derangement, acute dystonic reactions, and tetanus can all produce abnormal jaw positioning or restricted jaw movement and should be considered when the clinical presentation is atypical. The Syringe Technique:*Patient Selection Ideal candidates are awake, cooperative patients with an acute atraumatic anterior dislocation and no evidence of associated fracture. * The technique should generally be avoided in patients with significant facial trauma, altered mental status, inability to cooperate, or concern for mandibular fracture.

Procedure1. Place a 5- or 10-mL syringe between the upper and lower posterior molars on the affected side. 2. Instruct the patient to bite gently and slowly roll the syringe back and forth. 3. Continue until reduction occurs. 4. If the initial attempt is unsuccessful, repeat the maneuver on the contralateral side.

Mechanism* Rolling the syringe creates gradual rotational movement of the mandible while promoting relaxation of the muscles of mastication. As muscular tension decreases, the condyle...

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     A guide to diagnosing, imaging, and managing acute renal colic and nephrolithiasis in the ED.

Hosts:
Brian Gilberti, MD
Avir Mitra, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Nephrolithiasis.mp3   Download Leave a Comment Tags: Kidney Stones, Urology    Show Notes 1. CLINICAL CORE & PHYSIOLOGIC FRAMEWORK* **Epidemiologic Risk Profiles**
+ Lifetime incidence parameters hover around **1 in 11**, presenting with a prominent male sex skew.
+ Peak demographic manifestation concentrated within the **30–60 age band**.
+ **High-yield temporal parameter:** 50% recurrence vector within a 5-year post-initial-insult window.

• Mineralogical Composition Vectors
  • Calcium oxalate crystals represent the predominant structural matrix.
  • Struvite configurations (magnesium ammonium phosphate matrix) account for 1–2% of cohorts.
  • Struvite stones function explicitly as infection-driven configurations secondary to upper tract proliferation; higher distribution index noted in female cohorts.
• Etiological & Modifiable Relational Dynamics
  • Profound systemic dehydration or low baseline fluid throughput states.
  • High-sodium diet structures and heavy animal-protein consumption loads.
  • Positive genetic/familial history variables.
  • Relative risk modulation: Each variable independently operates to expand baseline risk by a factor of 2x to 3x.
• Pathophysiologic Symptom Complexes
  • Acute, sudden-onset, maximum-intensity (10/10) unilateral flank pain.
  • Classic structural radiation vector tracking downward toward the ipsilateral groin/genitourinary dermatomes.
  • Distinctive behavioral marker: Renal colic pacing/writhing behavior with zero antalgic position availability.
  • Concomitant autonomic triggers: Nausea and emesis manifest in 50% of acute presentations.
• Physical Exam Discordance Metrics
  • Severe subjective distress contrasted with a characteristically soft, completely non-tender abdominal palpation exam.
  • CVA tenderness is completely variable and lacks reliable negative predictive value.
  • Atypical Presentation Classifications
  • Vague, poorly localized abdominal pain presentations occurring in up to 20% of active cases.
  • Isolated lower urinary tract irritative signs including acute frequency or severe urgency.

• Incidental & Asymptomatic Dynamics

  • Silent intrarenal or ureteral stones found incidentally.
  • Longitudinal tracking demonstrates up to 33.3% of initially asymptomatic cohorts convert to fully symptomatic renal colic within a multi-year tracking window.

• EXCLUSION DIAGNOSES & CRITICAL PATHWAY RED FLAGS Vascular Mimics:* AAA rupture/expansion. This is a mandatory exclusion pathway in elderly cohorts presenting with acute flank or back pain. Physical tracking requires active exploration for an expansile, pulsatile abdominal mass.

• Gynecologic Emergencies: Ruptured ectopic pregnancy. Demands universal screening protocols via rapid beta-hCG testing in all female patients of childbearing potential presenting with lower abdominal/pelvic localization.
• Infectious Upper Tract Decompensation: Acute uncomplicated pyelonephritis. Differentiated via persistent high spikes, high fevers, systemic shaking chills, and profound pyuria.
• Genitourinary Structural Crises: Acute testicular torsion. Mandates a thorough, explicit scrotal/testicular structural exam if the flank pain radiates into the scrotum.

• Gastrointestinal and Adnexal Torsional Confounds: Acute appendicitis variants, acute mesenteric/bowel ischemia, and ovarian torsion syndromes.

• LABORATORY TESTING & PHYSIOLOGIC EVALUATION Urinalysis Interpretation Nuances*

  • Microscopic or gross hematuria presents in approximately 66% to 90% of acute cases.
  • Critical Pathological Caveat: Complete absence of hematuria documented in 20% to 33.3% of confirmed, acute obstructing ureteral stones.
  • Diagnostic rule: A pristine urinalysis with zero red blood cells is entirely insufficient to exclude acute ureterolithiasis.
• Urinary pH as a Composition Clue
  • Consistently low urinary pH parameters (pH < 5.5) point strongly toward a uric acid crystalline composition.
  • Elevated urinary pH parameters (pH > 7.5) indicate the presence of urease-producing microbial pathogens, pointing toward a struvite infection stone.
• Infectious Screening Metrics
  • Active tracking for marked pyuria, positive leukocyte esterase, and bacterial nitrites to rule out an obstructed, infected upper urinary tract system.
• BMP
  • Immediate quantification of baseline serum creatinine to establish accurate eGFR values.
  • Targeting detection of post-renal AKI from bilateral obstruction, unilateral obstruction in a single functioning kidney, or severe volume depletion.
• CBC
  • Evaluation for marked leukocytosis.
  • Physiologic Nuance: Mild-to-moderate white blood cell count elevations frequently represent non-specific stress demargination driven by severe pain and repetitive vomiting.
  • High-grade white blood cell shifts demand immediate exclusion of systemic bacteremia or an infected, obstructed urinary system.

• Adjunctive Lab Pathways

  • Rapid qualitative urine hCG testing.
  • Reflex urine culture execution whenever urinalysis metrics display significant inflammatory profiles or clinical suspicion of UTI is high.

• IMAGING MODALITIES & ALGORITHMIC CLINICAL SELECTION Non-Contrast CT Diagnostics*

  • Gold standard; diagnostic sensitivity and specificity parameters exceed 95% for stones >2 mm.
  • Provides precise quantification of stone diameter (mm), exact localization (proximal, mid, or distal ureter), and degree of secondary hydronephrosis.
  • Excellent structural visualization for detecting or ruling out alternate retroperitoneal, vascular, or intra-abdominal pathologies.
• Contrast-Enhanced CT Protocols
  • Indicated when alternative intra-abdominal surgical pathology is highly suspected over isolated renal colic.
  • Retains diagnostic capability to identify urinary tract stones >3 mm even within contrast-enhanced phases.
• NCCT Structural Architecture Limitations
  • Standard stone protocol CT scans are executed in a prone position without IV contrast enhancement. It does not opacify the ureteral lumen.
  • Presents a cumulative radiation exposure penalty when utilized serially across recurrent ED presentations.
• POCUS / Radiology Ultrasound
  • Direct stone visualization capabilities are modest, operating at approximately 50% to 60% sensitivity, and is highly dependent on anatomical positioning at the extreme pr...

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     Diagnosis, workup, and the four-step treatment protocol for thyroid storm.

Hosts:
Annaliese Elam, MD
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Thyroid\_Storm.mp3   Download Leave a Comment Tags: Critica Care, Endocrine, Thyroid Storm    Show Notes I. Pathophysiology & Diagnosis**Definition:** Life-threatening hypermetabolic state resulting from decompensated thyrotoxicosis.

Hormonal Profile: Absolute levels of total T₄/T₃ often mirror uncomplicated thyrotoxicosis; storm is driven by rapid rate of rise, increased catecholamine sensitivity, or increased free T₄/T₃ concentrations.

Clinical Presentation:

• Hyperpyrexia (e.g., 104.2°F)
• Tachycardia/Arrhythmias (e.g., 155 bpm)
• Altered Mentation: Agitation, delirium, or psychosis; often the primary differentiator between “storm” and “compensated” hyperthyroidism
• Warm, moist skin

Precipitating Events:

• Infection, trauma, or surgery
• Parturition
• Abrupt cessation of antithyroid medications

Burch-Wartofsky Point Scale (BWPS):

• ≥ 45: Highly suggestive of Thyroid Storm
• 25–44: Suggestive of impending storm
• < 25: Storm unlikely
• Note: High sensitivity but low specificity; can be skewed by unrelated febrile illness.

II. Laboratory & Ancillary FindingsThyroid Panel: Characteristically low TSH with elevated free T₄ and T₃.

Metabolic Abnormalities:

• Mild hyperglycemia (catecholamine-induced insulin inhibition)
• Mild hypercalcemia
• Elevated LFTs and leukocytosis

Cardiovascular: EKG may show sinus tachycardia or atrial fibrillation with rapid ventricular response.

III. Management: The Four-Step Blocking Strategy Step 1: Sympathetic Blockade (Beta Blockers) + Agent of Choice: Propranolol + Mechanism: Non-selective blockade; in high doses, inhibits peripheral conversion of T₄ to T₃. + Dosing: - PO: 60–80 mg every 4–6 hours - IV: 0.5–1 mg over 10 minutes + Critical Pitfall: Avoid in patients with acute decompensated heart failure with systolic dysfunction; risk of cardiovascular collapse. * Step 2: Inhibition of Hormone Synthesis (Thionamides) + Agent of Choice: Propylthiouracil (PTU) preferred over Methimazole in life-threatening storm. + Mechanism: Blocks synthesis of new hormone and inhibits peripheral T₄-to-T₃ conversion (decreases T₃ by ~45% in 24 hours). + Dosing: 200–250 mg PO every 4 hours * Step 3: Inhibition of Hormone Release (Iodine) + Agents: Potassium iodide (SSKI) or Lugol’s solution + Critical Timing: Must wait at least 60 minutes AFTER thionamide administration. + Rationale: Immediate iodine administration provides substrate for new hormone synthesis (Wolff-Chaikoff effect bypass), potentially worsening thyrotoxicosis. * Step 4: Inhibition of Peripheral Conversion & Adrenal Support + Agent: Glucocorticoids (Hydrocortisone) + Mechanism: Inhibits peripheral T₄ to T₃ conversion and treats potential relative adrenal insufficiency. + Dosing:* 300 mg IV loading dose, followed by 100 mg IV every 8 hours

IV. Supportive Care & Avoidance MeasuresHyperpyrexia Management:

• Acetaminophen is the standard of care
• Avoid Aspirin: Salicylates displace thyroid hormone from thyroid-binding globulin (TBG), increasing free T₄/T₃ levels

Volume Resuscitation:

• Aggressive IV fluids; patients are often profoundly dehydrated
• May require 3–5 liters of isotonic crystalloid per 24 hours

Take Home PointsI. Diagnostic Essentials Clinical Diagnosis: Based on hyperpyrexia, cardiovascular dysfunction, and altered mentation. * Key Differentiator: Altered mentation (agitation, delirium, psychosis) is often the sole finding distinguishing “storm” from “compensated” thyrotoxicosis. * Burch-Wartofsky Point Scale (BWPS): + ≥ 45: Highly suggestive of storm. + 25–44: Suggests impending storm. + < 25: Storm unlikely. + Note: High sensitivity, low specificity (e.g., hyperthyroid + flu can score > 45). * Triggers:* Infection, trauma, parturition, or abrupt cessation of antithyroid drugs.

II. The Four-Step Blocking Strategy1. Beta Blockade (Propranolol): * Dose: 60–80 mg PO q4–6h or 0.5–1 mg IV over 10 min. * Action: Blocks symptoms and inhibits peripheral T4 to T3 conversion. * Caution: Avoid in acute decompensated heart failure with systolic dysfunction. 2. Thionamides (PTU): * Dose: 200 to 250 mg every four hours. (note: some resources suggest a loading dose beforehand) * Action: Preferred over methimazole; blocks new hormone synthesis and peripheral T4 to T3 conversion. 3. Iodine (SSKI/Lugol’s): * Timing: Must wait ≥ 60 minutes AFTER thionamide dose. * Action: Blocks hormone release. * Pitfall: Early iodine provides substrate for new hormone synthesis, worsening the condition. 4. Glucocorticoids (Hydrocortisone): * Dose: 300 mg IV load, then 100 mg IV q8h. * Action: Blocks conversion and provides adrenal support.

III. Critical Supportive Care Hyperpyrexia: Use Acetaminophen. + NEVER Use Aspirin: Displaces thyroid hormone from binding proteins, acutely increasing free T4/T3 levels. * Volume:* Aggressive fluid resuscitation; patients may require 3–5 L/day due to profound dehydration.

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The Case A 40 year old male with a history of obstructive coronary artery disease (remote percutaneous intervention), heart failure with severely reduced ejection fraction (10%), left ventricular assist device (LVAD) placed 2022, presents to the emergency department with acute onset of chest pressure and light-headedness. The patient denies any LVAD alarms prior to arrival. The following ECG is obtained:

EKG Show Details EKG Characteristics * Rate 231 * Rhythm Wide QRS Tachycardia * Intervals QRS 142 ms, QTc 419 ms

Diagnosis Ventricular Tachycardia

Wide complex tachycardia should be presumed ventricular tachycardia until proven otherwise, especially if no prior history of widened QRS. Comparison to prior ECG’s may reveal a prior intra-ventricular conduction delay (bundle branch block) to support a supra-ventricular tachycardia with aberrancy.

Other features that support ventricular tachycardia include:

• AV dissociation (P waves marching through QRS complexes)
• Capture and/or fusion beats
• Extreme axis deviation
• Concordance in pre-cordial leads

Questions 1. What is the differential diagnosis for this patient? Ventricular tachycardia, supraventricular tachycardia with aberrancy.

 Discussion Ventricular tachycardia (VT) is common in the LVAD population (> 50% of patients). Underlying risk factors for VT include:

• Underlying cardiomyopathy
• Right-ventricular (RV) failure
• Mechanical compression of the ventricle by the inflow cannula
• Less commonly, VT can be due to myocardial ischemia/infarction from native coronary artery disease

Due to the degree of physiologic support afforded by the LVAD (continuous flow physiology), otherwise fatal arrhythmias are often well-tolerated, and may present with vague symptoms such as fatigue, nausea, light-headedness, or chest pressure.

As VT or VF may be tolerated for a short period in LVAD patients, clinicians often have time to try medical interventions prior to resorting to electrical cardioversion. In the hemodynamically stable LVAD patient:

1. Evaluate for mechanical etiology of VT.
   1. Point-of-care ultrasound may demonstrate an overly decompressed LV with collapse and septal shift
   2. Decreasing LVAD speed or a fluid bolus may allow for increased ventricular filling and resolve the arrhythmia
2. Anti-arrhythmic agents such as amiodarone and lidocaine should be considered in the absence of a mechanical cause of arrhythmia.
3. Cardioversion and defibrillation are not contraindicated and can be performed without disconnection of the LVAD device.
   1. Use an anterior-posterior pad placement
   2. Avoid placing pads over the LVAD pump
   3. Consider sedation if the patient is concious
4. Patients with recurrent VT from increased sympathetic tone may benefit from high-dose beta-blockers.

The patient was treated with an amiodarone bolus which terminated the rhythm. He was subsequently admitted to advanced cardiology for further diagnostics and cardiac monitoring.

Pearls * Assume ventricular tachycardia until proven otherwise in patients presenting with wide QRS tachycardia. * ECG's obtained on LVAD patients may contain considerable artifact, compare to prior ECG's when possible. * Typically unstable arrhythmias may be well-tolerated in patients with LVADs due to the continuous flow physiology of the mechanical pump. In hemodynamically stable patients, evaluate for mechanical etiology of arrhythmias and consider appropriate anti-arrhythmic medications. * Electrical cardioversion is safe in LVAD patients. Avoid placing pads directly over the LVAD pump. Pursue an anterior-posterior approach and use sedation on the concious patient.

Sources Givertz MM, DeFilippis EM, Colvin M, et al. HFSA/SAEM/ISHLT clinical expert consensus document on the emergency management of patients with ventricular assist devices. J Heart Lung Transplant. 2019;38(7):677–698. doi:10.1016/j.healun.2019.05.004

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     We discuss this ominous complication of providing local anesthesia.

Hosts:
Elaine Jonas, MD
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/LAST.mp3   Download Leave a Comment Tags: Critical Care, Toxicology    Show Notes I. Pathophysiology & Mechanisms* **Definition:** Systemic toxicity secondary to local anesthetic (LA) via accidental intravascular injection or excessive systemic absorption.

• Threshold: Occurs when plasma concentration exceeds the safety threshold for cardiac and neural tissue.

• Agent Profile: Bupivacaine (High Risk)

  • Highly lipophilic with high protein binding.
  • “Fast-on, Slow-off” Kinetics: Strong Na+ channel binding with extremely slow dissociation during diastole.
  • Myocardial Depression: Direct inhibition of Ca2+ release from the sarcoplasmic reticulum, impairing contractility.
  • Low CC:CNS Ratio: The dose required for cardiac collapse is very close to the dose that triggers seizures (narrow safety margin).

  • Contributing Factors:

  • Acidosis/Hypercapnia: Increases the fraction of free drug and promotes ion trapping in the brain/heart; shifts the LA-binding curve toward higher toxicity.

  • Hypoxemia: Exacerbates myocardial depression and lowers seizure threshold.

II. Risk Assessment & PreventionPatient-Specific Risk Factors Extremes of Age: Neonates (low α-1-acid glycoprotein) and elderly (reduced clearance). * Body Composition: Low muscle mass/frailty (decreased volume of distribution). * Organ Dysfunction:*

+ **Hepatic:** Reduced metabolism of amide LAs.
+ **Renal:** Accumulation of metabolites; risk of metabolic acidosis lowering seizure threshold.
+ **Cardiac:** Reduced cardiac output slows hepatic delivery/clearance; heart failure patients are more sensitive to Na+ channel blockade.

• Pregnancy: Increased sensitivity to cardiotoxicity.

Procedural Risk Factors Vascularity of Site (Highest to Lowest Risk):*

1. Intercostal blocks (highest absorption rate).
2. Caudal/Epidural.
3. Interfascial plane blocks (e.g., TAP block).
4. Psoas compartment/Sciatic.
5. Brachial plexus.

• Technique: Large volume infiltration, lack of ultrasound, lack of incremental injection.

Prevention Mandates Weight-Based Dosing:*

+ **Lidocaine (Plain):** Max 4.5 mg/kg.
+ **Lidocaine (with Epi):** Max 7 mg/kg.
+ **Bupivacaine:** Max 2.5–3

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Author: Leia Kessler, MD

Editors: David Guernsey, MD, Ellen Duncan, MD/PHD

Introduction:

• Asthma is a chronic inflammatory airway disease characterized by reversible lower airway obstruction due to bronchoconstriction, mucosal edema, and mucus plugging
• Common triggers include viral respiratory infections, exercise, and allergen exposure.
• Asthma is one of the most common chronic pediatric conditions and a leading cause of emergency department (ED) visits and hospitalizations.

• Early recognition and management of exacerbations is essential to prevent life-threatening complications such as respiratory failure, cardiopulmonary arrest, and death. Clinical Manifestations:

• Patients typically present with a combination of:

  • Shortness of breath
  • Wheezing
  • Chest tightness
  • Cough (especially nocturnal or triggered by exercise)
• Risk factors for severe disease and asthma-related mortality include:
  • Prior ICU admission or need for respiratory support (i.e., HFNC, BiPAP, or intubation)
  • Frequent ED visits or hospitalizations for asthma
  • Poor symptom perception, incorrect inhaler technique, or nonadherence to controller medications
• Vital sign abnormalities may include tachypnea, tachycardia, and/or hypoxemia; because asthma is an obstructive disease of the lower airways, significant hypoxemia (SaO2<92%) suggests marked airflow limitation and impaired gas exchange
• Patients may have inspiratory, expiratory, or biphasic wheeze; while expiratory wheeze typically indicates mild-moderate obstruction, inspiratory and/or biphasic wheeze suggest more significant airflow limitation.
• Absence of wheeze (“silent chest”) reflects critically reduced airflow, worsening of obstruction, and impending respiratory failure.

| Physical Exam Findings | | Mild/Moderate | Severe | | Wheezing | Tripod position |

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     We discuss the diagnosis and treatment of one of EM's paradoxes: High-Output Heart Failure.

Hosts:
Nicolas Gonzalez, MD
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/HOHF.mp3   Download Leave a Comment Tags: Cardiology    Show Notes **Core EM Modular CME Course**Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.

Course Highlights:

• Credit: 12.5 AMA PRA Category 1 Credits™
• Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics.
• Cost:
  • Free for NYU Learners
  • $250 for Non-NYU Learners

Click Here to Register and Begin Module 1

1. Core Definition & Hemodynamic Profile Clinical Paradox:* Congestive symptoms (pulmonary edema, JVD, peripheral edema) in the setting of a hyperdynamic, supranormal cardiac function.

2. Hemodynamic Criteria:

   • Cardiac Index (CI): >4.0 L/min/m2.
   • Cardiac Output (CO): >8 L/min.
   • Systemic Vascular Resistance (SVR): Pathologically low (vasodilated or shunted state).
   • The “Warm” Phenotype: Unlike standard HFrEF/HFpEF (often “Cold and Wet”), HOHF presents as “Warm and Wet” due to low SVR and bounding pulses.

3. Pathophysiology: The Hemodynamic Paradox Primary Insult:* Decreased SVR (either via peripheral vasodilation or arteriovenous shunting).

4. Effective Arterial Blood Volume: Paradoxically low despite high total CO.

5. Neurohormonal Cascade:

   • Activation of Renin-Angiotensin-Aldosterone System (RAAS).
   • Increased Sympathetic Nervous System tone.
   • Increased Antidiuretic Hormone (ADH) secretion.
   • Resultant State: Avid renal salt and water retention leading to massive plasma volume expansion.
   • Cardiac Response: Chronic volume overload → eccentric remodeling → chamber dilation → eventual secondary myocardial failure/dilated cardiomyopathy.

1. Differential Diagnosis: Etiological “Buckets”Category A: Increased Metabolic Demand (Systemic) Hyperthyroidism/Thyrotoxicosis:*

   • Direct T3 effects: increased chronotropy/inotropy.
   • Indirect effects: metabolic byproduct accumulation causing peripheral vasodilation.

   • Myeloproliferative Disorders:

   • High cell turnover and increased oxygen consumption drive compensatory CO increase.

   • Sepsis (Hyperdynamic Phase):

   • Cytokine-mediated global vasodilation.

   • Note: Often transient; may transition to sepsis-induced myocardial depression.

Category B: Peripheral Vascular Effects (Shunting/Vasodilation) Arteriovenous Fistulas (AVF) / Malformations (AVM):*

+ **Most Common Cause:** Iatrogenic AVF for Hemodialysis (ESRD population).
+ Bypasses high-resistance capillary beds, dumping arterial blood directly into venous circulation.

• Chronic Liver Disease (Cirrhosis):

  • Formation of “spider angiomataR...

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     We explore how to refine and optimize care in the vital minutes following ROSC.

Hosts:
Jonathan Elmer, MD, MS
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Post-ROSC\_care.mp3   Download Leave a Comment    Show Notes **Core EM Modular CME Course**Maximize your commute with the new Core EM Modular CME Course, featuring the most essential content distilled from our top-rated podcast episodes. This course offers 12 audio-based modules packed with pearls! Information and link below.

Course Highlights:

• Credit: 12.5 AMA PRA Category 1 Credits™
• Curriculum: Comprehensive coverage of Core Emergency Medicine, with 12 modules spanning from Critical Care to Pediatrics.
• Cost:
  • Free for NYU Learners
  • $250 for Non-NYU Learners

Click Here to Register and Begin Module 1

I. Phase 1: Stabilization (Minutes 0–10)The “Rearrest” Window & Pathophysiology High-Risk Period: Rearrest rates reach 30% within the first minutes post-ROSC. * Shock Incidence: Two-thirds of patients develop profound hypotension/shock as initial resuscitative efforts subside. * Catecholamine Washout: Super-physiologic “code-dose” epinephrine (1mg IV) typically wears off within ~3 minutes post-ROSC, leading to predictable hemodynamic collapse. * Secondary Injuries*: Evaluate for “CPR-induced trauma” (blunt thoracic trauma, rib fractures, pneumothorax, liver/splenic lacerations).

Immediate Resuscitative Actions Vascular Access: + Transition rapidly from IO to reliable IV access within 1–2 minutes. + Prioritize Intraosseous (IO) placement within 5 minutes if IV attempts fail; intra-arrest data suggests no significant difference in early outcomes. * Vasoactive “Bridge”: + Maintain a “bolus-dose” pressor at the bedside for immediate push-dose titration. + Options: Phenylephrine, dilute Epinephrine, or dilute Norepinephrine (titrated to effect rather than rigid dosing). * Physician-Specific Task: Arterial Line: + Goal: Placement within 5 minutes of ROSC. + Preferred Site: Femoral (by landmarks/blind if necessary) for speed; should be a <2-minute procedure. + Utility*: Immediate detection of rearrest and beat-to-beat titration of vasopressors.

II. Phase 2: Diagnostic Workup (Minutes 10–40)Etiology Epidemiology ACS Shift: Acute Coronary Syndrome (ACS) is the cause in only 6–10% of resuscitated survivors (lower than historical estimates). * Common Etiologies: * Respiratory*: COPD, pneumonia, mucus plugging.

+ **Cardiac**: Arrhythmia (cardiomyopathy/scar), RV failure (PE), or LV failure.
+ **Neurological**: Intracranial hemorrhage (SAH/ICH), status epilepticus (**4–5%**).
+ **Metabolic**: Dialysis-related disarray/hyperkalemia.
+ **Toxicology**: Overdose accounts for **~10%** of cases in urban centers.

The “Broad Net” Strategy “Rainbow Labs”: Comprehensive panel including toxicology and serial biomarkers. * Pan-Scan Protocol: + Components: CT/CTA Head/Neck, Contrast CT Chest/Abdomen/Pelvis. + Diagnostic Yield: 50% for clinically significant findings (causes or consequences of arrest). + Contrast Risk: Negligible (1–2% increase in AKI risk) compared to the high diagnostic utility. * Avoid Anchoring: Do not assume ischemic EKG changes are the cause; they are frequently a consequence* of the global arrest-induced ischemia.

III. Hemodynamic & Respiratory TargetsMean Arterial Pressure (MAP) Autoregulation Shift: In acute brain injury/post-arrest, the lower limit of cerebral autoregulation shifts right, often requiring MAPs of 110–120 mmHg for adequate perfusion. * Clinical Target: Aim for MAP >80 mmHg. * The BOX Trial Nuance*: While the BOX trial showed no difference between MAP 63 vs. 77, its cohort (Denmark) had exceptionally high survival rates (70% back to work) and short response times, which may not generalize to North American populations...

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The Case 61yo M PMH HTN, AUD, HFpEF, CAD, hypothyroidism, anemia is brought in by EMS after being found down at his shelter in the middle of winter. He was discovered surrounded by empty alcohol bottles and covered in feces. Per shelter staff, the patient was last seen 7 days ago and appeared well at that time. On arrival to the ED, the patient is not responding to questions or commands and is intermittently combative. Vital signs are notable for hypotension with systolic blood pressures in the 70s. He is cold to the touch.

EKG Screenshot

  Show Details     EKG Characteristics * Rate 118 bpm

• Rhythm Irregularly irregular rhythm without discernible p-waves
• Intervals Normal PR and QRS, prolonged QTc at 549ms
• Axis Normal Axis
• ST Segments No significant ST elevations or depressions
• Additional Features Positive J-point deflection in leads II, III, aVF, V3, V4

Diagnosis What Is the Diagnosis?

Hypothermia with Osborne (J) waves

Questions 1. What is the differential diagnosis for this patient? Sepsis, unstable Afib with RVR, myxedema coma, environmental hypothermia, ACS,adrenal insufficiency, alcohol withdrawal

 Discussion **Case Discussion:**

• In this case, a temperature-sensing foley was placed on arrival and the patient’s core temperature was noted to be 79 degrees Farenhiet. Active rewarming was initiated with warm IV fluids and patient was placed on the bairhugger warming device. A central line and A-line were placed for central rewarming access and accurate BP management and the patient was admitted to the MICU for refractory shock and continued rewarming.

Osborne (J) Waves

• Osborne waves are positive deflections at the junction of the QRS complex and ST segment
  • Generally sharp, dome-like appearance as opposed to the slurred or notched
• J-point (“fish-hook” appearance) of benign early repolarization
• Most commonly seen in moderate to severe hypothermia (typically <32°C)
• Often best visualized in inferior and lateral precordial leads
• Amplitude generally increases as core temperature decreases
• Presence does not correlate with prognosis, but signals significant hypothermia

Pathophysiology

• Hypothermia alters myocardial repolarization and creates a transmural voltage gradient between epicardial and endocardial layers which results in the characteristic J-point deflection.

Differential Diagnosis of J Waves

• Osborne waves are not specific to hypothermia. Other causes include:
• Hypercalcemia
• Brugada syndrome
• Early repolarization
• Acute neurologic injury (e.g., SAH)
• Post–cardiac arrest states

Clinical context and core temperature are critical

Management Pearls

• Treat the patient, not the EKG
• Hypothermic patients are extremely arrhythmia-prone, especially with rapid electrolyte shifts during rewarming
  • Atrial fibrillation common
  • Ventricular dysrhythmias possible with minimal stimulation
    • Rough handling, intubation, or invasive procedures can precipitate arrest
• Primary treatment is rewarming
  • Passive external (blankets, warm environment)
  • Active external (forced-air warming)
  • Active internal if severe (warm IV fluids, lavage, ECMO in select cases)
• Avoid unnecessary movement and invasive procedures
• Osborne waves may be misread as ST elevation, especially in patients with CAD
• Bradycardia and atrial fibrillation often resolve with rewarming
  • Aggressive pharmacologic rate control or electrical cardioversion in hypothermic patients can precipitate malignant ventricular arrhythmias. The primary treatment remains correction of the underlying hypothermia.
• Remember, many medications (such as pressors) may be ineffective until temperature improves

Pearls * Osborne (J) waves are a classic ECG finding in moderate to severe hypothermia * They appear as dome-like (camel’s hump) elevations at the J-point, not true ST-elevation MI * Always interpret ECG findings in clinical and temperature context * The definitive treatment is rewarming, not antiarrhythmics or cath lab activation

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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.

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. References:

• 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

• 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
• 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
• Sax P. Epidemiology, clinical presentation, and diagnosis of Pneumocystis pulmonary infection in patients with HIV. UpToDate. Published April 13, 2023. Accessed April 18, 2024.
• Sax P. Treatment and prevention of Pneumocystis infection in patients with HIV. UpToDate. Published September 12, 2022. Accessed April 18, 2024.
• 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
• 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.
• Thomas C, Limper A. Treatment and prevention of Pneumocystis pneumonia in patients without HIV. UpToDate. Published January 9, 2024. Accessed April 18, 2024.
• 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.
• 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/
• 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
• 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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Background:

The lumbar puncture (LP or spinal tap) is a procedure that has been in the medical arsenal since first described in 1891 by German physician Heinrich Quincke. It can be both diagnostic and therapeutic, utilized in the diagnosis (meningitis, Guillain-Barre syndrome, subarachnoid hemorrhage) and symptomatic treatment (idiopathic intracranial hypertension, normal pressure hydrocephalus) of diseases of the central nervous system, respectively.

LP is an invasive procedure in which a spinal needle is inserted into an intervertebral space to obtain samples for cerebrospinal fluid testing. Prior to needle insertion, landmarks must be identified to ensure procedural success. LPs are one of the most challenging procedures for clinicians. A study by Duniec et al. reported that landmark-based assessment of intervertebral space can be inaccurate up to 30% of the time, in part due to patients’ varying body habitus and positional limitations. This, of course, is less than ideal, as the inability to correctly identify landmarks can lead to repeated attempts, patient discomfort, and increased rate of post-procedural complications.

Ultrasound can be a useful tool to ensure procedural success of a LP on the first attempt. It can optimize visualization of the intervertebral spaces and spinous processes to provide a better static approach for performance of the procedure.

Technique:

Probe selection:

The linear probe is more ideal for pediatric patients and adults with a leaner body habitus. For all other patients, a curvilinear probe would be more preferable.

Positioning:

A LP can be performed in either the lateral recumbent/prone position or upright position. To accurately measure the patient’s intracranial pressure, the procedure should be performed in the lateral recumbent/prone position. However, you can outline the intervertebral spaces using the ultrasound in either position.

• Find Tuffier’s Line: Tuffier’s line is the transverse line connecting the superior aspects of the posterior iliac crests, passing through the L3-L4 intervertebral space.

• Find the anatomic midline: with the probe in the transverse orientation (indicator to the patient’s right) and identify the spinous process. It will appear as a hyperechoic rim with posterior shadowing. Position the spinous process in the middle of your screen and use a marker on the skin to indicate the anatomic midline.

• Identify the intervertebral space: with the probe in the sagittal orientation (indicator cephalad) and maintaining midline using your previous mark (see above), identify the spinous processes and slide your probe slightly up or down until you are between two spinous processes. Position the intervertebral space in the middle of your screen and make a horizontal mark.

• Estimate depth of needle insertion: after identifying the spinous processes and intervertebral space in the sagittal view, you can increase the depth and the gain to view the mixed echogenicity soft tissue and ligaments, and then see the hypoechoic subarachnoid space underneath the dura mater.

• Identify your space for needle insertion: connect the marks/lines you made for the anatomic midline and the intervertebral space. The intersection will be the optimal needle insertion site. Proceed with the LP.

Supporting Literature:

The use of ultrasound guidance for LPs has been studied extensively. Here are a handful of these studies and their conclusions:

Nomura et al., 2007 (randomized controlled trial)

• 46 patients – 22 in palpation landmark (PL) group and 24 in ultrasound landmark (UL) group
• Reported LP failure in 6/22 patients in PL group, 1/24 in UL group
• There were 12 obese patients in study: LP failure in 4/7 PL patients, 0/5 UL patients
• No statistical differences in the number of attempts, traumatic LPs, patient comfort, or procedure length

Ferre and Sweeney, 2007 (prospective cohort study)

• 2 operators, 76 patients – investigated visualization time for 5 anatomical structures (spinous processes or laminae, ligamentum flavum, dura mater, epidural space, subarachnoid space).
• High-quality images obtained in <1 minute in 87.9% of scans conducted and in <5 minutes in 100% of scans

Ferre et al., 2009 (pilot study)

• Used ultrasound as means of identifying site of skin puncture and needle depth needed to access the subarachnoid space
• CSF obtained in 36/39 patients in the first interspinous space attempted

Peterson et al., 2014 (randomized controlled trial)

• 50 patients in the landmark group and 50 patients in the ultrasound group
• Primary outcome: number of needle insertion attempts and LP success
• Secondary outcomes: pain associated with procedure, time to perform procedure, # traumatic taps, patient satisfaction
• Reported no significant differences in primary and secondary outcomes

Evans et al., 2018 (randomized controlled trial)

• Operators were residents in an emergency medicine residency program; underwent training on both landmark and ultrasound-guided techniques
• 35 patients total: 18 in landmark group and 17 in the ultrasound group
• Primary outcome: LP success in obtaining CSF
  • No significant difference between groups
• Secondary outcomes: number of attempts, time to CSF flow, pain
  • No significant differences in time to obtain CSF or mean pain scores
  • Significant decrease in number of attempts—1.54 times more attempts in the landmark group and up to 1.7 times more attempts when adjusted for BMI

Gottlieb et al., 2019 (meta-analysis)

• Included 12 pediatric and adult studies (n=957 patients; 505 adults and 452 children)
• Primary outcome: LP success in obtaining CSF
  • Ultrasound guided LP was successful in 90% of patients versus 81.4% for landmark LP
  • Odds ratio 2.22 in favor of the ultrasound guided group
• Secondary outcomes: rate of traumatic LPs, time to procedural success, number of needle passes, patient pain score
  • Fewer traumatic LPs in US group (10.7% vs. 26.5%; OR 0.28)
  • Ultrasound guided LP associated with shorter time to successful LP by approximately one minute. However, this did not account for time taken to perform ultrasound, which may be substantial.
  • Also reported fewer mean needle passes, lower patient pain scores for ultrasound guided LP

Take Home Points:

If you are anticipating a more challenging LP, due to a patient’s body habitus or positioning limitation, operator comfort or experience, or other factors, consider using the ultrasound. Take the time to pick up the probe and map out your procedure. This can make an otherwise challenging and uncomfortable procedure less painful and more successful on your first attempt.

References:

Evans, David P., et al. “Comparison of Ultrasound-Guided and Landmark-Based Lumbar Punctures in Inexperienced Resident Physicians.” Journal of Ultrasound in Medicine, vol. 38, no. 3, 2018, pp. 613–620., https://doi.org/10.1002/jum.14728.

Duniec, L, et al. Anatomical landmarks based assessment of intravertebral space level for lumbar puncture is misleading in more than 30%. Anaesthesiol Intensive Ther 2013; 45:1–6.

Ferre, R M, et al. “Ultrasound Identification of Landmarks Preceding Lumbar Puncture: A Pilot Study.” Emergency Medicine Journal, vol. 26, no. 4, 2009, pp. 276–277., https://doi.org/10.1136/emj.2007.057455.

Ferre, Robinson M., and Timothy W. Sweeney. “Emergency Physicians Can Easily Obtain Ultrasound Images of Anatomical Landmarks Relevant to Lumbar Puncture.” The American Journal of Emergency Medicine, vol. 25, no. 3, 2007, pp. 291–296., https://doi.org/10.1016/j.ajem.2006.08.013.

Gottlieb, Michael, et al. “Ultrasound-Assisted Lumbar Punctures: A Systematic Review and Meta-Analysis.” Academic Emergency Medicine, 2018, https://doi.org/10.1111/acem.13558.

Margarido, Clarita B., et al. “The Intercristal Line Determined by Palpation Is Not a Reliable Anatomical Landmark for Neuraxial Anesthesia.” Canadian Journal of Anesthesia/Journal Canadien D’anesthésie, vol. 58, no. 3, 2010, pp. 262–266., https://doi.org/10.1007/s12630-010-9432-z.

Millington, Scott J., et al. “Better with Ultrasound.” Chest, vol. 154, no. 5, 2018, pp. 1223–1229., https://doi.org/10.1016/j.chest.2018.07.010.

Nomura, Jason T., et al. “A Randomized Controlled Trial of Ultrasound-Assisted Lumbar Puncture.” Journal of Ultrasound in Medicine, vol. 26, no. 10, 2007, pp. 1341–1348., https://doi.org/10.7863/jum.2007.26.10.1341.

Peterson, Michael A., and Jennifer Abele. “Bedside Ultrasound for Difficult Lumbar Puncture.” The Journal of Emergency Medicine, vol. 28, no. 2, 2005, pp. 197–200., https://doi.org/10.1016/j.jemermed.2004.09.008.

Peterson, Michael A., et al. “Ultrasound for Routine Lumbar Puncture.” Academic Emergency Medicine, vol. 21, no. 2, 2014, pp. 130–136., https://doi.org/10.1111/acem.12305.

Strony, Robert. “Ultrasound-Assisted Lumbar Puncture in Obese Patients.” Critical Care Clinics, vol. 26, no. 4, 2010, pp. 661–664., https://doi.org/10.1016/j.ccc.2010.07.002.

“How To: Ultrasound Guided Lumbar Puncture Procedure 3D Video.” https://www.youtube.com/watch?v=ndnZxAcNjdg&ab_channel=Sonosite

“Lumbar Puncture.” https://oxfordmedicaleducation.com/clinical-skills/procedures/lumbar-puncture/

“Lumbar Puncture with Ultrasound.” https://www.youtube.com/watch?v=rbbpwE_ijm0&ab_channel=BCEmergencyMedicineNetwork

sinaiem.org/foam/try-ultrasound-for-your-next-lumbar-puncture

www.emdocs.net/ultrasound-lumbar-puncture-maximize-first-pass-success-patients-large-body-habitus

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Background:

• An update to our 2015 post on HIET for beta-adrenergic receptor and calcium channel antagonists overdose.
• Beta-adrenergic receptor antagonists (Beta blockers, BB) and calcium channel antagonists (calcium channel blockers) are common drugs that can produce profound cardiac depression and shock when taken in overdose.
• 2020 National Poison Data System report:
  • 10,994 beta blocker overdoses
    • 18 deaths
  • 6,132 calcium channel blocker overdoses
    • 45 deaths
  • High case fatality rate, behind only acetaminophen, opiates, and stimulants

Mechanism of toxicity – Calcium Channel Blockers (CCB)

• In a normal state, depolarization of the myocyte opens the L-type calcium channel; resulting influx of calcium causes the concentration dependent release of more calcium from the sarcoplasmic reticulum, ultimately leading to myocyte contraction.
• Calcium channel receptors are also present on smooth muscle in vasculature and in pancreatic beta cells.
• Blockade at the trans-membrane receptor inhibits downstream calcium release. As a result, myocytes cannot contract, vasculature cannot contract, and beta cells cannot release insulin.
  • Consequently results in hypotension, bradycardia, and hyperglycemia

Mechanism of toxicity – Beta Blockers

• Beta blockers block the beta-adrenergic G-protein coupled receptors on the heart, with different members of the class exerting variable effects on the other adrenergic receptors.
• Beta-adrenergic G-protein stimulation activates adenyl cyclase, increases cAMP, leading to activation of protein-kinase-A and other cAMP dependent protein-kinases. They result in the stimulation of pace-maker cells via effects of the calcium clock and increased myocyte contractility via effects on calcium channel influx and calcium storage in the sarcoplasmic reticulum.
• Beta blocker overdose produces profound bradycardia and hypotension due to blockade of these receptors.
  • Can see hypoglycemia, useful for distinguishing between CCB/BB overdose
• At toxic doses, there also appears to be a catecholamine-independent effect on myocyte contractility through dysregulation of intracellular calcium release.

Overdose – general management:

• Consider GI decontamination if overdose is recent
  • Activated charcoal 1g/kg up to 50g by mouth if patient is alert or by NG tube if airway has been secured
    • Avoid in altered mental status as aspiration can lead to severe pneumonitis
  • Gastric lavage/ whole bowel irrigation (WBI) can be indicated for recent massive overdose or extended-release formulations; however decision to proceed should be made in consultation with toxicology
• Trial of calcium gluconate IV and glucagon IV
• If non-responsive to first line therapies and signs of cardiac depression present (hypotension, bradycardia, acidosis, elevated lactate, reduced EF on echo) escalate to high dose insulin euglycemic therapy.
• However, given the logistics of implementing HIET and the delayed onset of action, vasopressors should be initiated early to maintain adequate blood pressure until HIET becomes effective.
• Backup plans for mechanical supports such as venous-arterial ECMO should be included for patients refractory to HIET.

High Dose Insulin Euglycemic Therapy – why we do it:

• Mechanism not fully understood and is certainly multifactorial
  • Insulin increases myocardial contractility via stimulation of phosphatidylinositol-3-kinase (PI3-K), resulting in reverse-mode sodium-calcium exchange and increased calcium concentration in the sacroplasmic reticulum (von Lewinski 2005).
  • Stimulation of PI3K also increase myocardial contractility via calcium-independent mechanism (von Lewinski 2005).
  • Stressed myocardium prefers glucose metabolism. Calcium channel blockers inhibits insulin release and decreases the number of cellular glucose transporters (GLUT); HIET improves glucose utilization.
• Other factors:
  • Restores lactate metabolism in the heart (Kline 1997).
  • Overcomes calcium channel blockade (Bechtel 2008).
• Largest evidence base is animal models:
  • Multiple studies comparing HIET at doses 1-10 units/kg/hr to traditional vasopressors, glucagon, and placebo.
  • Strong trend across different study designs for superiority of HIET.
• HIET improves contractility without increasing SVR, while vasopressin and epinephrine transiently increase SVR/MAP but worsen cardiac output in anesthetized dogs given propranolol (Holger 2007).

HIET Implementation:

• Combination therapy of highly concentrated insulin and dextrose to maintain euglycemia.
  • Potassium supplementation as needed
• Resource intensive requiring coordination across disciplines – emergency medicine, intensive care, toxicology, nursing, and pharmacy.
• Special attention should be directed at the insulin concentrations and programming of the infusion pump.
• Concentrated formulations of both dextrose and insulin to avoid iatrogenic fluid overload
  • Insulin concentration for infusion should be at 10 units/mL.
  • 70 kg patient, insulin at 3 units/kg/hr and dextrose at 0.5g/kg/hr
    • Normal concentration of insulin 1 unit/mL and D10, would receive 560 mL of fluid/hr.
    • HIET with insulin concentration of 10 units/mL and D50, would receive 90 mL of fluid/hr.
  • Central line access required
  • Takes about 30 minutes to take effect, can temporize with traditional vasopressors with the goal of turning them off when insulin is working.
  • Insulin
    • 1 unit/kg bolus
    • 1 unit/kg/hr drip, titrated every 30-60 minutes to end organ perfusion to relative max of 10 units/kg/hr
      • May not see change in MAP due to vasodilation from insulin; assess for improved cardiac output, urine output, acidosis, and lactate
      • Some studies included max of 15 units/kg/hr without increased adverse effects (Page, 2018)
    • Dextrose
      • 0.5-1 g/kg/hr
      • D50 or D20
      • Central line access is required due to the high osmolarity of the glucose infusion.
      • Supplement additional dextrose prn, if hypoglycemia occurs do not stop the insulin, increase the rate of the dextrose drip.
      • Monitoring:
        • Fingerstick glucose every 15 minutes for the first hour and after any up-titration; every 30 minutes if stable x 1 hour; then every hour for the duration of therapy.
        • Will have prolonged need (18-24 hours) for dextrose supplementation after insulin is stopped.
      • Potassium
        • Shifted intracellularly by insulin, total body potassium is normal
        • Replete to goal 3-3.5 mEq/L
          • Goal is to prevent arrhythmia, not normalize potassium
        • Monitoring:
          • Every 1 hour while up or down-titrating insulin
          • Every 4 hours while insulin requirement stable

Safety:

• Multiple retrospective reviews of HIET demonstrate high incidence of hypoglycemia and hypokalemia
  • Page et al, 2018, 22 patients mixed CCB/BB overdose
  • 16/22 hypoglycemia, 9/22 with severe (<45 mg/dL), none symptomatic
  • 18/22 hypokalemia, none with arrhythmia
• Minimal clinical significance to these events, all responded promptly to additional supplementation.
• Reinforces importance of close monitoring and intervention.

Summary:

• High dose insulin with dextrose supplementation is indicated for patients with calcium channel blocker and beta blocker overdose and signs of cardiac toxicity.
• Mechanisms are not completely elucidated, but mostly related to the stimulation of PI3K.
• Evidence comes from animal models and 20 years of successful use in humans.
• Highly concentrated forms of insulin and dextrose via central line.
• Coordinate with toxicology, pharmacy, and nursing to avoid dosing errors.
• Takes 30 minutes to see effect, temporize with traditional vasopressors (norepinephrine, vasopressin).
• Titrate to end organ perfusion as MAP may not change significantly.
• Disposition to ICU.
• Back up plans for mechanical support such as venous-arterial ECMO such be considered early for refractory patients.

References:

Yuan TH, Kerns WP, Tomaszewski CA, et al. Insulin-glucose as adjunctive therapy for severe calcium channel antagonist poisoning. Journal of Toxicology: Clinical Toxicology. 1999;37(4):463-474.

Bechtel LK, Haverstick DM, Holstege CP. Verapamil toxicity dysregulates the phosphatidylinositol 3-kinase pathway. Academic Emergency Medicine. 2008;15(4):368-374.

von Lewinski D, Bruns S, Walther S, et al. Insulin Causes [Ca 2+ ] i -Dependent and [Ca 2+ ] i -Independent Positive Inotropic Effects in Failing Human Myocardium. Circulation. 2005;111(20):2588-2595.

Cole JB, Corcoran JN, Engebretsen KM, et al. Use of a porcine model to evaluate the risks and benefits of vasopressors in propranolol poisoning. J Med Toxicol. 2020;16(2):212-221.

Holger JS, Engebretsen KM, Fritzlar SJ, et al. Insulin versus vasopressin and epinephrine to treat β-blocker toxicity. Clinical Toxicology. 2007;45(4):396-401.

Kerns W, Schroeder D, Williams C, et al. Insulin improves survival in a canine model of acute β-blocker toxicity. Annals of Emergency Medicine. 1997;29(6):748-757.

Kline JA, Tomaszewski CA, Schroeder JD, et al. Insulin is a superior antidote for cardiovascular toxicity induced by verapamil in the anesthetized canine. J Pharmacol Exp Ther. 1993,267(2), 744-50.

Greene SL, Gawarammana I, Wood DM, et al. Relative safety of hyperinsulinaemia/euglycaemia therapy in the management of calcium channel blocker overdose: a prospective observational study. Intensive Care Med. 2007;33(11):2019-2024.

Page CB, Ryan NM, Isbister GK. The safety of high-dose insulin euglycaemia therapy in toxin-induced cardiac toxicity. Clinical Toxicology. 2018;56(6):389-396.

St-Onge M, Anseeuw K, Cantrell FL, et al. Experts consensus recommendations for the management of calcium channel blocker poisoning in adults: Critical Care Medicine. 2017;45(3):e306-e315.

Goldfrank’s Toxicologic Emergencies. Edited by Nelson LS, Howland MA, Lewin NA, Goldfrank LR, Hoffman RS. McGraw-Hill Education, New York, 11th edition, 2019.

Hsu C, Wei J, Chen Y, Yang S, et al. Cellular mechanisms responsible for the inotropic action of insulin on failing human myocardium. The Journal of Heart and Lung Transplantation. 2006;25(9):1126-1134.

St-Onge M, Dubé PA, Gosselin S, et al. Treatment for calcium channel blocker poisoning: A systematic review. Clinical Toxicology. 2014;52(9):926-944.

Gummin DD, Mowry JB, Beuhler MC, et al. 2020 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 38th Annual Report. Clinical Toxicology. 2021; 59(12), 1282–1501.

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Relevance:

In 07/2021, the CDC released the first updates to their guidelines in 5 years on the treatment of sexually transmitted infections (STIs). These are consensus guidelines meant to provide an approach for those providers treating suspected and documented sexually transmitted infections, especially in the setting of increasing antibiotic resistance and globalization resulting in increasing prevalence of STIs previously seen mostly abroad. Although some of these guidelines have been previously stated by the CDC, this is the first comprehensive set of guidelines in the last 5 years. This core post will provide a summary of the most relevant aspects of the CDC recommendations.

Primary and Secondary Prevention:

Although as Emergency Medicine providers we are often used to treating patients for active infections, we must also be prepared to encourage primary and secondary prevention among our patients, given many patients do not see providers outside of the ED. When relevant, it is important to encourage and, when possible, offer vaccination for HPV, HAV, and HBV. This is especially relevant to populations at higher risk of contracting these diseases, such as the HAV vaccine for men who have sex with men (MSM). In addition, current recommendations are to offer pre-exposure prophylaxis (PrEP) for HIV to any sexually active adult and adolescent with an STI infection or an HIV-negative person at risk for contracting HIV. In particular, one in 15 MSM will contract HIV within one year of infection with rectal gonorrhea or chlamydia, demonstrating the importance of encouraging prevention among this population. For patients with newly diagnosed HIV, it is important to reinforce that those with HIV with an undetectable viral load cannot transmit HIV to potential partners, so treating themselves provides protection to potential partners.

Partner Co-Treatment:

All patients experiencing symptoms of STIs or with confirmed STI testing should be encouraged to notify their sex partners and urge them to seek evaluation and treatment when relevant. In many states, expedited partner therapy (EPT) is legal and is encouraged where available. Almost every state has some form of EPT for various STIs so it is important to be aware of treatment options. Three US clinical trials involving heterosexual men and women with chlamydia and gonorrhea have shown that offering EPT results in a statistically significant decrease in rates of reinfection. Co-testing for other infections, especially HIV, should also be encouraged.

Gonorrhea and Chlamydia:

Gonorrhea and chlamydia remain the two most commonly reported bacterial communicable diseases in the US. Although they are often asymptomatic, they can cause urethritis, cervicitis, and widespread symptoms in extreme cases (conjunctivitis, arthritis, skin lesions, meningitis, endocarditis). For a simple chlamydial infection, the recommended treatment is 100 mg of doxycycline PO BID for 7 days. For patients with concern for treatment compliance, you can consider a single dose of azithromycin. For a simple gonorrheal infection, the recommended treatment is 500 mg of IM ceftriaxone (note: this is double the previously recommended dose). Co-treatment with azithromycin or doxycycline for gonorrheal infections where chlamydia co-infection has been excluded is no longer recommended. Given rising resistance among strains of both gonorrhea and chlamydia, if patients do not have symptom resolution within 3-5 days, it is recommended that they get re-tested and possibly re-treated with alternative regimens. It is also important to test all relevant exposed mucous membranes in our patients, including rectal and pharyngeal testing in those patients who practice receptive anal or oral sex.

Pelvic Inflammatory Disease:

Pelvic inflammatory disease (PID) constitutes a series of infections of various pelvic organs involving any combination of endometritis, salpingitis, tubo-ovarian abscess, and pelvic peritonitis. The clinical criteria include cervical motion tenderness, uterine tenderness, or adnexal tenderness. Although initially thought to be caused predominantly by gonorrhea or chlamydia, recent studies have shown that the number of cases attributable to those organisms are falling, with some studies showing that only about 50% of women with PID had positive tests for gonorrhea or chlamydia with organisms compromising the vaginal flora such as Gardnerella vaginalis and H. influenzae acting as other causative organisms. As a result, treatment for PID is with ceftriaxone or cefoxitin PLUS doxycycline PLUS metronidazole. Importantly, due to an increasing number of women presenting with more advanced PID after initially presenting with vague, non-specific symptoms, the CDC recommends presumptive PID treatment for women at risk for STIs if they are experiencing pelvic or lower abdominal pain and no other cause for this pain can be identified.

Epididymo-orchitis:

Epididymo-orchitis is defined by pain, swelling, and inflammation of the epididymis or testicle. It is typically unilateral although may be bilateral. Importantly, this is a clinical diagnosis and, although often seen on ultrasound, a negative ultrasound does not rule out epididymitis. It is caused by either STIs or enteric organisms and treatment should be based on a given patient’s risk factors. For patients at higher risk for STIs, treatment should with ceftriaxone and doxycycline targeted at gonorrhea and chlamydia. For men who practice insertive anal sex, treatment should target both enteric and STIs so recommended treatment is with ceftriaxone and levofloxacin. For men who are at low risk for an STI, treatment for enteric organisms with levofloxacin alone is appropriate.

Mycoplasma genitalium:

Mycoplasma genitalium can cause urethritis in men and has associations with infertility, spontaneous abortion, cervicitis, PID, and preterm delivery in women. It is often asymptomatic, although can be symptomatic in men. Current evidence indicates that M. genitalium is responsible for 15-20% of non-gonococcal urethritis, 20%-25% of non-chlamydial non-gonococcal urethritis, and 40% of persistent or recurrent urethritis. Rectal and pharyngeal infections have also been identified and are typically asymptomatic. There is NAAT testing available for urine and urethral, penile, vaginal, and endocervical samples. Testing is recommended for men with recurrent non-gonococcal urethritis and women with recurrent cervicitis, as well as considered for women with PID. Resistance testing should be ordered if available as both macrolide and quinolone resistance is increasing. Resistance-guided therapy should be used whenever possible and should begin with empiric doxycycline as initial therapy, followed by treat with either high-dose azithromycin or moxifloxacin pending resistance testing. Screening for asymptomatic infections is not recommended.

Lymphogranuloma Venereum:

Lymphogranuloma venereum (LGV) is a common STI globally with the causative organism chlamydia trachomatis serovars L1, L2, or L3. The most common presentation is proctocolitis which can mimic inflammatory bowel disease with mucoid or hemorrhagic discharge, anal pain, constipation, fever, and tenesmus. In heterosexual patients, they may solely have unilateral tender inguinal or femoral lymphadenopathy (buboes). Occasionally patients may have a self-limited ulcer or papule. It is recommended that all patients with proctocolitis be tested for LGV (if available) and suspicion should be high among MSM, especially those with a recent positive rectal chlamydia test as our common assays for chlamydia do not distinguish LGV from typical chlamydial infections. For persons with acute proctitis, if a rectal chlamydia NAAT test is positive and severe symptoms such as rectal ulcers, bleeding, or anal discharge are present, then they should be treated empirically for LGV. Treatment is with doxycycline for three weeks.

Chancroid:

Chancroid is characterized by one or more deep and painful genital ulcers along with tender suppurative inguinal lymphadenopathy, although this is seen in less than 50% of cases. It is caused by Haemophilus ducreyi. Per CDC recommendations, it is reasonable to treat any patient with one or more painful ulcers (factoring in their appearance) if syphilis testing is negative and HSV is either unlikely or testing is negative. Treatment is with either azithromycin or ceftriaxone.

HSV-1 and HSV-2:

HSV-1 and HSV-2 are very common causes of both oral and genital lesions. The lesions are self-limited, recurrent, painful, and vesicular or ulcerative lesions. It is estimated that 11.9% of people between ages 14-49 are infected and most of these individuals have not had their condition diagnosed due to mild or unrecognized infection. Despite this, those patients intermittently shed the virus. Treatment is recommended based on a suspected first episode of genital herpes as both of length of infection and rates of recurrence can depend on prompt initiation of initial treatment. Infection can be confirmed with testing by NAAT or culture of the lesions if they are present, but treatment should not wait pending test results. Type-specific serologic tests can be helpful in diagnosing HSV infection if no lesions are present and can be valuable for prognostic reasons. Presence of HSV-2 type-specific antibodies implies anogenital infection since HSV-2 is almost entirely sexually acquired, while HSV-1 type specific antibodies may indicate previous oral or anogenital infection. Possible treatment options include acyclovir, valacyclovir, and famciclovir depending on the patient’s insurance status.

References:

1. Barrow, RY, Ahmed F, Bolan GA, Workowski KA. Recommendations for Providing Quality Sexually Transmitted Diseases Clinical Services, 2020. MMWR REcomm Rep 2020;68(No. RR-5):1-20. http://dx.doi.org/10.15585/mmwr.rr6805a1.
2. Davidson KW, Barry MI, et al. Screening for Chlamydia and Gonorrhea: US Preventive Services Task Force Recommendation Statement. JAMA 2021; 326:949.
3. Hazra A, Collison MW, Davis AM. CDC Sexually Transmitted Infections Treatment Guidelines, 2021. 2022;327(9):870–871. doi:10.1001/jama.2022.1246
4. Summary of CDC STI Treatment Guidelines, 2021. Centers for Disease Control and Prevention. July 22, 2021. Accessed December 20, 2021. https://www.cdc.gov/std/treatment-guidelines/provider-resources.htm.
5. Workowski KA, Bachmann LH, Chan PA, et al. Sexually transmitted infections treatment guidelines, 2021. Centers for Disease Control and Prevention. July 26, 2021. Accessed December 20, 2021. https://www.cdc.gov/std/treatment-guidelines/toc.htm

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Background and Pathophysiology:

• Comorbidities, physiologic changes, and medication-associated effects leave elderly patients more susceptible to injury from “minor” mechanisms. Diminished functional reserves decrease compensatory ability for any injury, regardless of severity.1
• Despite adjustments for injury severity, significantly increased mortality occurs ≥70 years regardless of mechanism, compared to younger counterparts. ATLS and many prehospital guidelines recommend >55 years criteria for referral to a dedicated trauma center due to lack of clear age cutoff in existing data/studies.2
• In patients ≥65 years, falls are the most common cause (>75% of all trauma), followed by motor vehicle crashes. Despite a “benign” mechanism, falls lead to dire medical economic and quality of life consequences for older patients, who sustain more injuries of all types, compared to younger patients.3
• 5% of adults aged ≥65 years report at least one fall in the past year, and 10.2% of those report a fall-related injury. More than 1/3 of geriatric trauma patients presenting to the ED after a fall return to the ED or die within one year of initial evaluation.4
• Elderly patients, who comprise only 8-12% of total ED major trauma cases, represent a disproportionate 15-30% of trauma mortalities and costs.5
• Compared with hospitalization due to other conditions, hospitalizations from falls resulting in a hip fracture or other injuries lead to worse outcomes and greater chance of nursing home admissions.6

Assessment and Initial Evaluation: What’s different?

• Geriatric Trauma is highly under-triaged due to traditional triage tools that are insensitive for signs of injury in older patients (vital signs, mechanisms of injury, ACTLS criteria). Multiple studies suggest activating Trauma Teams for all trauma patients ≥70 years old regardless of mechanism/vital signs, due to the physiologically blunted responses to hypoxia, hypercarbia, and acidosis.7
• History and physical examinations of geriatric trauma patients are less sensitive for injury compared to younger counterparts
• Traumatic brain injury is common in older adults, can occur with minimal head trauma, and may be asymptomatic.
• In the thorax, there is a higher risk for sternal and rib fractures, pulmonary contusions, and pneumothorax, and an increased risk for pneumonia.
• In the abdomen, the goal is early diagnosis, close monitoring, as examination can be unreliable. FAST should be part of the initial evaluation, with a low threshold to obtain advanced imaging.
• Extremity fractures are more common due to osteopenia.
• Vertebral Fractures/Spinal cord injury (SCI): cervical spine fractures can occur from seemingly minor mechanisms (including fall from standing). Age-related changes to vertebrae, intervertebral disks, and the spinal canal place older adults at greater risk of fractures, resulting in a greater likelihood of SCI. Liberal CT use is advocated.8

Primary and Secondary Surveys:

Trauma examination for all Geriatric Trauma should include:

Primary Survey

• Airway / Breathing: should intubation be required, the dose of induction drugs, even etomidate, may require reduction by ~30-50% to minimize risk of cardiovascular depression in this age group.9
• Circulation: Recognizing shock can be more difficult, as older patients can present with a “normal” blood pressure that actually represents relative hypotension. Mortality increases in Geriatric Trauma when the heart rate rises above 90/min, while the same increase is not evident in younger counterparts until heart rate reaches 130/min.10 Evaluate other signs: mental status, capillary refill, tachypnea, and urine output. Adjuncts should evaluate occult shock (e.g., VBG, lactate, base deficit).
• Disability: GCS is a less sensitive indicator in geriatric patients.

Secondary Survey:

• Ensure all Geriatric trauma patients are gowned on arrival and examined carefully from head-to-toe regardless of mechanism/vitals.
• Assess medications that can compromise initial evaluation and further care (anticoagulants, antiplatelets, antihypertensives, antiglycemics, etc.).

Management and Disposition Considerations:

• All patients who present after a fall need a complete trauma assessment, in addition to evaluating potential triggers/cause of the fall (e.g., syncope)
• The window to intervene is narrow in Geriatric trauma patients. Do not delay recognition of shock through false reassurance of “normal” vitals: VBG, lactate, and base deficit should be used as adjunct to VS early, and ECG may be necessary for subtle signs of ischemia
• Increased incidence of intracranial bleeding and cervical injuries, even in minor cases, should prompt liberal CT scanning use.11
• Geriatric trauma patients require increased immediate and delayed ICU resources compared to younger counterparts with the same injuries.12
• Anticipate ambulatory needs, assist devices, PT/OT, pain control strategies, and care coordination early as part of disposition planning12

References:

1.Perdue &al. Differences in mortality between elderly and younger adult trauma patients: geriatric status increases risk of delayed death. J Trauma. 1998;45:805.

1. Caterino &al. Identification of an age cutoff for increased mortality in patients with elderly trauma. Am J Emerg Med. 2010;28:151.

2. Sterling &al. Geriatric falls: injury severity is high and disproportionate to mechanism. J Trauma. 2001;50:116.

3. Liu &al. Frequency of ED revisits and death among older adults after a fall. Am J Emerg Med. 2015;33:1012-1018.

4. CDC Data and Statistics (WISQARSTM): Cost of Injury Reports Data Source: NCHS Vital Statistics System for Numbers of Deaths. https://www.cdc.gov/injury/wisqars/index.html.

5. Gill &al. Association of injurious falls with disability outcomes and nursing home admissions in community-living older persons. Am J Epidemiol. 2013;178:418-25.

6. Demetriades D &al. Old age as a criterion for trauma team activation. J Trauma. 2001;51:754.

7. Goode &al. Evaluation of cervical spine fracture in the elderly: can we trust our physical examination? Am Surg. 2014;80:182.

8. Hasegawa &al. Increased incidence of hypotension in elderly patients who underwent emergency airway management: an analysis of a multi-centre prospective observational study. Int J Emerg Med 2013; 6:12.

9. Heffernan &al. Normal presenting vital signs are unreliable in geriatric blunt trauma victims. J Trauma. 2010;69:813.

10. Li &al. Mild head injury, anticoagulants, and risk of intracranial injury. Lancet. 2001; 357:771-2.

11. Konda &al. Who Is the Geriatric Trauma Patient? An Analysis of Patient Characteristics, Hospital Quality Measures, and Inpatient Cost. Geriatr Orthop Surg Rehabil. 2020 Sep 15;11:2151459320955087.

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Background & Pathophysiology:

• An inflammatory colitis caused by fecal impaction
• Marked distension and increased intraluminal pressure leads to ischemic pressure necrosis of the colonic wall and compromise of vascular supply and mucosal perfusion
• Risk of progression to colonic perforation and peritonitis
• Multiple areas of ulceration occur adjacent to the fecaloma; most commonly in the rectosigmoid colon

Diagnosis:

• Lab findings are non-specific – may reveal increased WBC and/or acute phase reactants
• Increased lactate and anion gap metabolic acidosis should raise concern for ischemia and/or perforation
• Supine and erect chest & abdominal radiographs are needed to eval for intraperitoneal free air under the diaphragm, dilated loops of bowel, and air-fluid levels
• CTAP with IV contrast will reveal dilation of the sigmoid colon, colonic wall thickening, thickened rectum, presence of fecal impaction/fecaloma, and/or pericolonic fat stranding
• If extraluminal bubbles of gas or abscess are visualized, this suggests perforation has already occurred.

Clinical Presentation:

• Typically elderly patients with chronic constipation; especially those with dementia, nursing home, or bedbound
• Younger patients with psychiatric conditions, patients with chronic opioid use, pediatric patients with severe constipation are also be at risk
• Can present sub-acutely with complaints of constipation (acute on chronic), generalized or localized (LLQ) abdominal pain, urinary retention
• Patients who have perforation may present in extremis with signs of peritonitis and sepsis

Management:

• Joint management with gastroenterology and surgical services
• Stable patients may undergo aggressive bowel regimen with laxatives, enemas, and disimpaction
• GI Endoscopically guided disimpaction may be necessary
• Operative indications: perforation, large segments of bowel involvement, or failure of conservative management
• If fecal impaction is not relieved, colonic perforation with peritonitis and decompensation can occur.
  • Treat aggressively with IVF, antibiotics (covering gram negative and anaerobic organisms), and rapid transfer to the OR to resect the affected colon
• A 32-60% mortality rate has been reported when stercoral colitis is associated with perforation!
• Patients with stercoral colitis should be admitted for decompression of the bowel and close monitoring

Pearls:

• Stercoral colitis is an uncommon but potentially fatal complication of chronic constipation
• A high index of suspicion is necessary and should be considered in all patients who present with abdominal pain and constipation, particularly in the elderly
• Active co-management and care coordination with medicine, gastroenterology, and general surgery
• While conservative treatment with bowel regimens and disimpaction may prevent progression, there is a significant potential for perforation
• Imaging: CTAP is the modality of choice for diagnosis
• If starting with plain radiographs, supine & erect films or decubitus are needed to evaluate for free air (multi-view supine x-rays are inadequate) – ensure appropriate views are ordered

References:

1. Morano C, Sharman T. Stercoral Colitis. In: StatPearls. StatPearls Publishing; 2021. Accessed August 17, 2021. http://www.ncbi.nlm.nih.gov/books/NBK560608/
2. Hudson J, Malik A. A fatal faecaloma stercoral colitis: a rare complication of chronic constipation. BMJ Case Reports. Published online September 3, 2015:bcr2015211732. doi:10.1136/bcr-2015-211732
3. Heffernan C, Pachter HL, Megibow AJ, Macari M. Stercoral Colitis Leading to Fatal Peritonitis: CT Findings. American Journal of Roentgenology. 2005;184(4):1189-1193. doi:10.2214/ajr.184.4.01841189
4. Naseer M, Gandhi J, Chams N, Kulairi Z. Stercoral colitis complicated with ischemic colitis: a double-edge sword. BMC Gastroenterol. 2017;17(1):129. doi:10.1186/s12876-017-0686-6
5. Proulx E, Glass C. Constipation-Associated Stercoral Colitis: Pediatric Emergency Care. 2018;34(9):e159-e160. doi:10.1097/PEC.0000000000001600
6. Tajmalzai A, Najah DM. Stercoral colitis due to massive fecal impaction: a case report and literature review. Radiol Case Rep. 2021;16(8):1946-1950. doi:10.1016/j.radcr.2021.04.067
7. Weerakkody, Y. Stercoral colitis. 1/22/22. https://radiopaedia.org/articles/stercoral-colitis

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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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Prehospital Narrow Pulse Pressure Predicts Need for Resuscitative Thoracotomy and Emergent Intervention After Trauma J Surg Res., 2021

Background Prehospital trauma team activation criteria allow for prompt mobilization of personnel and resources. Prehospital hypotension is one of those criteria. Pulse pressure is the difference between systolic and diastolic blood pressure. This is variously defined as a difference of 30-40 mmHg. A narrow pulse pressure occurs due to compensatory increased systemic vascular resistance in the setting of decreased cardiac output. A narrow pulse pressure has been shown to predict the need for hemorrhage control in the ED setting but has not been assessed as a predictor in the prehospital setting.

Clinical Question In trauma patients, 16-60 years of age, presenting to a level one trauma center, is a prehospital narrow pulse pressure (< 30 mmHg) with a systolic blood pressure of > 90 mmHg, associated with in-hospital mortality, need for a resuscitative thoracotomy, need for an emergent intervention (NFEI), need for a trauma intervention (NFTI) and mortality?

Design Observational: Retrospective Cohort

POPULATION:

Inclusion:

• Age 16-60 years

Exclusion:

• Age < 16 (lower BP range) or < 60 years (higher BP range)
• Unrecorded prehospital vital signs
• Transferred from an outside hospital
• On-scene cardiac arrest
• Missing discharge disposition

Setting:

Single Level I Trauma Center (Trauma registry data), (1/2008-5/2020)

EXPOSURE:

• Narrow pulse pressure (PP): Systolic BP 90 mmHg AND PP < 30 mmHg
• (PP = Systolic BP – Diastolic BP)
• Hypotensive: Systolic BP < 90 mmHg (regardless of pulse pressure)

NO EXPOSURE:

• Normotensive: Systolic BP 90 mmHg AND Pulse Pressure 30 mmHg

OUTCOMES:

• Resuscitative thoracotomy
• Mortality
• Need For Emergent Intervention (NFEI): Transfer directly from the ED to the:
  • Operating room
  • Interventional radiology
• Need For Trauma Intervention (NFTI): 1 of the following:
  • Packed red cell transfusion < 4 hours after arrival
  • Need for operative intervention or angioembolization < 90 minutes of arrival
  • Admission to the ICU from the ED with LOS ≥ 3 days
  • Mechanical ventilation initiated within 72 hours of arrival

Primary Results

Univariable Analysis: patients with a narrow pulse pressure were intermediate in risk of:

• resuscitative thoracotomy, need for trauma intervention, need for any operative intervention, central line insertion, chest tube insertion, and mortality compared to normotensive patients and hypotensive groups

Multivariable Analysis:

• A narrow pulse was an independent predictor of the need for a trauma intervention (aOR 45, 95% CI (1.20, 1.75)), the need for resuscitative thoracotomy (aOR 2.04 95% CI (1.46, 2.84)) and the need for an emergent intervention (aOR 1.38, 95% CI (1.15, 1.66)).
• A narrow pulse was not an independent predictor of mortality (p value 0.15, aOR 1.31 with 95% CI not presented).
• A penetrating mechanism, trauma team activation and injury severity score were also independent predictors of all three outcomes.

Strengths * Large sample size though * + High percentage excluded due to missing data (? Selection bias) + Only 5% with narrow pulse pressure * Mean blood pressure on ED arrival was normal with a normal pulse pressure in the narrow pulse pressure group, strengthening its predictive ability (not just a marker for ED narrow pulse pressure) * Regression analysis to account for baseline difference in blood pressure groups * Trauma registry data prospectively collected though retrospective analysis * BP groups mutually exclusive and collectively exhaustive

Limitations * Single center with high proportion of penetrating trauma * + Subgroup analysis penetrating vs blunt would have been helpful * Generalizability to centers with less penetrating trauma, non-level one trauma centers, pediatric and geriatric patients is unclear * NTEI and NFTI are composite outcomes. Results for individual outcomes that make up the composite are not provided * There was no table for the multivariable analysis primary outcome of in-hospital mortality.

Author's Conclusions “As we continuously seek methods to improve our care of the injured patient, prompt control of hemorrhage to reduce morbidity and mortality remains one of the central tenets of trauma surgery. For this reason, appreciation of early indicators of blood loss are invaluable. In the current study, narrow pulse pressure in the field was independently associated with the need for resuscitative thoracotomy, emergent intervention for hemorrhage control, and the presence of major traumatic injuries. We propose that narrow pulse pressure be further studied in the future as a possible addition to existing American College of Surgeons Committee on Trauma prehospital trauma team activation criteria.”

Our Conclusions Prehospital narrow pulse pressure with a systolic blood pressure > 90 mmHg was an independent predictor of resuscitation thoracotomy, need for emergent intervention and need for trauma intervention but not in-hospital mortality. A subgroup analysis by trauma mechanism (blunt vs penetrating) would have been helpful as penetrating trauma patients were more likely to have a prehospital narrow pulse pressure.

Potential Impact To Current Practice A pre-hospital narrow pulse pressure could serve as a marker of intermediate risk when compared to normotensive and hypotensive patients and prompt mobilization of personnel (e.g. trauma team activation) and resources (e.g. initiation of a massive transfusion protocol). A prospective, multicenter study to examine the impact of a narrow pre-hospital pulse pressure on trauma interventions and outcomes would validate its importance and improve the study’s generalizability.

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Patient Case:

History:

• A 60-year-old male with history of schizophrenia and depression on multiple unknown antipsychotic medications presents with unresponsiveness x 1 day. One week prior to ED arrival, the patient was becoming progressively despondent, less interactive with peers, exhibiting slow speech and movements, and was not eating.

Physical exam:

• Vital signs – febrile, tachycardic, hypertensive
• General – posturing with arms stretched out in front, eyes open without blinking, akinetic, no signs of trauma
• HEENT – dry mucous membranes, trismus with repetitive dystonic movements of the jaw, pupils mildly dilated bilaterally
• Neuro: no verbal or motor response to noxious stimuli, diffuse hyperreflexia, bilateral ankle myoclonus, tremulous, hypertonia
• GU: low urine output without retention despite 3 liters of IV fluids

Pertinent lab findings:

• Mildly elevated CPK
• Leukocytosis
• Urinalysis concentrated with large ketones

Summary:

• 60-year-old male with history of psychotic and mood disorders on antipsychotic medications presenting with 1 day of stupor, mutism, akinesia with posturing associated with autonomic excitation, upper motor neuron signs, and dehydration preceded by 1 week of retarded catatonia, consistent with malignant catatonia.

Course:

• The patient’s vital signs and catatonic features began improving with IV fluids and benzodiazepines in the emergency room. The patient was admitted to the medicine step down unit, managed by the psychiatry inpatient team, and transitioned to standing IV lorazepam during preparation for electroconvulsive therapy (ECT).

Definition:

Catatonia:

• A behavioral motor dysregulation syndrome marked by an inability to move normally despite full physical capacity, which can occur in the context of many underlying psychiatric and general medical disorders [4].
• According to the DSM-5, catatonia is diagnosed (classified as associated with another mental disorder, due to another medical condition, or unspecified catatonia) when 3 or more of the following symptoms are present: mutism, stupor, catalepsy, waxy flexibility, negativism, posturing, mannerism, stereotypy, unresponsive agitation, grimacing, echolalia, and echopraxia [1].

Malignant Catatonia (AKA “lethal catatonia”):

• An acute onset life-threatening subtype of catatonia that is characterized by fever, autonomic instability, delirium, and rigidity [4].

Epidemiology:

Who typically suffers from catatonia?

• Severely ill patients with an underlying psychiatric or medical disorder.
• An estimated 7% to 15% of acutely hospitalized psychiatric patients and psychiatric emergency department patients exhibit catatonia [4].

Who typically suffers from malignant catatonia?

• This has not been widely studied and remains unknown.

What are risk factors for catatonia?

• Underlying mood disorders such as unipolar depression and bipolar disorder, psychotic disorders such as schizophrenia, and autism spectrum disorder [8,2].
• Antipsychotic drugs with high D2-blockade (i.e. first-generation antipsychotics) [5]. However, neuroleptic drug use is not required for diagnosis.
• Sociodemographic risk factors are unknown.

How serious is malignant catatonia?

• High morbidity and mortality, sometimes with permanent cognitive and behavioral deficits.
• Death rates may be as high as 20% [3].

Pathophysiology:

• Largely unknown, but data have revealed some possibilities.

Neuropathologic and neuroimaging studies:

• suggest catatonia may involve alterations in the basal ganglia, thalamus, and prefrontal, orbitofrontal, and parietal cortices [7, 6]

Neurotransmitter studies:

• have linked catatonia with decreased activity at GABA-A and dopamine D2 receptors, and increased activity at NMDA receptors [6]

Presentation:

Features of catatonia:

• Immobility (hypokinesis or akinesis)
• Mutism
• Stupor
• Negativism (resistance to instructions or attempts to be moved)
• Waxy flexibility (as opposed to lead pipe rigidity seen in NMS)
• Posturing
• Excessive purposeless motor activity
• Staring
• Echophenomena (repeating another’s words or movements)

Malignant catatonia = catatonia PLUS:

• Fever (less likely in older patients)
• Autonomic instability (labile or elevated blood pressure, tachycardia, tachypnea)
• Autonomic excitation (pupil dilation, hyperreflexia, diaphoresis, tremors, clonus)
• Rigidity
• Delirium

Course:

• May be preceded by a catatonic prodrome (retarded or excited)
• Fulminant and progresses rapidly within a few days

Differential:

• CNS or systemic infections
• Brain mass lesions
• Stroke
• Seizures/status epilepticus
• Alcohol withdrawal/delirium tremens
• Metabolic abnormalities
• Toxidromes (i.e. neuroleptic malignant syndrome (NMS), malignant hyperthermia, serotonin syndrome, lithium toxicity, etc.)

Diagnosis:

• Largely clinical and a diagnosis of exclusion.

Key history:

• Psychiatric comorbidity
• Neuroleptic or psychotropic medications (especially first-generation antipsychotics including Haloperidol, Prochlorperazine, and Droperidol)
• Prior history of catatonia
• Retarded or excited catatonic features preceding onset of autonomic changes
  • this is especially helpful to differentiate malignant catatonia from NMS, serotonin syndrome, and other potential diagnoses

Workup (to assess for alternative life-threatening diagnoses):

• ED: EKG, CXR, urine studies, full set of labs (including CK, electrolytes, CBC, LFTs, serum iron), VBG, head CT, LP, cultures, consider Utox, Tylenol level, salicylate level, psychiatry consult
• Floor: EEG, advanced neuroimaging (i.e. MRI)

Lab findings (common but nonspecific):

• Elevated CK
• Elevated lactate
• Leukocytosis
• Low serum iron

Lorazepam (Ativan) challenge:

• 1 to 2 mg IV bolus of lorazepam
• Can repeat dose after 5 to 10 minutes if no change in patient’s catatonic symptoms
• Partial temporary relief of catatonic signs 5 to 10 minutes after IV administration of lorazepam is consistent with a diagnosis of catatonia
• A negative response occurs commonly and does not rule out any subtype of catatonia

Management:

Supportive care:

• Volume resuscitation with IV fluids
• Benzodiazepines (lorazepam 1 to 2 mg q8 hours) are used to bridge patients to ECT
• Cardiac monitor while hemodynamically unstable
• 1:1 observation

Psychiatry consult:

• Obtain collateral, assess for suicidality, prepare for ECT

Definitive management:

• Treatment of underlying condition

Disposition:

• Psychiatry floor: resolution of vital sign abnormalities in the emergency department
• Step down unit: persistent but improved autonomic excitation (tachycardia and hypertension)
• MICU: Autonomic instability (severe tachycardia, severe hypertension or hypotension, persistent fever)

Key Points:

• Malignant catatonia is a life-threatening subtype of catatonia, marked by autonomic excitation and instability, rigidity, and delirium.
• It is critical to quickly diagnose and treat malignant catatonia, as its course is fulminant and progresses rapidly, and morbidity and mortality is high.
• The most common underlying psychopathology of malignant catatonia are psychotic disorders, mood disorders, and autism spectrum disorder, and first-generation anti-psychotic medications especially may precipitate or worsen disease.
• Malignant catatonia is a clinical diagnosis guided largely by history, mental status exam, and physical exam.
• Malignant catatonia closely resembles both NMS and serotonin syndrome; past medical history, medication history, and clinical history of a catatonic prodrome prior to the onset of delirium and autonomic excitation is helpful in differentiating malignant catatonia from related presentations.
• An IV lorazepam challenge can help diagnose malignant catatonia and management should include standing IV lorazepam boluses and IV fluid resuscitation until the patient can undergo ECT.
• Disposition to the psychiatry floor, medicine step down unit, or MICU should be guided by the degree of the patient’s vital sign abnormalities, the presence or absence of autonomic instability, and the patient’s response to therapy in the emergency room.

Further Reading:

• Recognize malignant catatonia early: it is well treatable! A case report and review of literature.
• Malignant catatonia mimics tetanus: a case report.
• Catatonia: a case report by Brown Emergency Medicine.
• Catatonia: an approach to diagnosis and treatment.

References:

1. American Psychiatric Association. (2013). In Diagnostic and statistical manual of mental disorders (5th ed.).
2. Burrow JP, Spurling BC, Marwaha R. Catatonia. Treasure Island (FL): StatPearls Publishing; 2021 Jan. Available from: https://www.ncbi.nlm.nih.giv/books/NBK430842
3. Fink M and Taylor MA. Catatonia: a clinician’s guide to diagnosis and treatment, Cambridge University Press, Cambridge, UK 2003.
4. Fink M and Taylor MA. The catatonia syndrome: forgotten but not gone. JAMA Psychiatry. 2009;66(11):1173-1177. doi:10.1001/archgenpsychiatry.2009.141
5. Lee JW. Neuroleptic-induced catatonia: clinical presentation, response to benzodiazepines, and relationship to neuroleptic malignant syndrome. J Clin Psychopharmacol 2010;30(1):3. doi:10.10.1097/JCP.0b013e3181c9bfe6
6. Northoff G. Brain imaging in catatonia: current findings and a pathophysiologic model. CNS Spectr 2000; 5:34.
7. Northoff G. What catatonia can tell us about “top-down modulation”: a neuropsychiatric hypothesis. Behav Brain Sci 2002; 25:555.
8. Taylor MA and Fink M. Catatonia in psychiatric classification: a home of its own. AM J Psychiatry. 2003;160(7):1223.

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