Core EM - Emergency Medicine Podcast

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 Findings

Thyroid 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 Measures

Hyperpyrexia 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 Points

I. 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 Strategy

1. 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.

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 & Prevention

Patient-Specific Risk Factors

• 
  

  Extremes of Age: Neonates (low $\alpha$-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 $4.5\text{ mg/kg}$.

    
    
  
  
  • 
    

    Lidocaine (with Epi): Max $7\text{ mg/kg}$.

    
    
  
  
  • 
    

    Bupivacaine: Max $2.5\text{–}3\text{ mg/kg}$.

    
    
  
  
  
  


• 
  

  Incremental Injection: $3\text{–}5\text{ mL}$ aliquots with frequent aspiration.

  
  


• 
  

  Intravascular Marker: Use Epinephrine ($1:200,000$) to detect accidental IV placement (HR increase $>10\text{ bpm}$or SBP increase $>15\text{ mmHg}$).

  
  

III. Clinical Presentation

Neurologic Phase (Early to Late)

• 
  

  Subjective: Metallic taste, tinnitus, circumoral numbness/tingling.

  
  


• 
  

  Objective: Visual disturbances, agitation, confusion, tremors.

  
  


• 
  

  Critical: Generalized tonic-clonic seizures, rapid progression to CNS depression, coma, and apnea.

  
  


• 
  

  Note: Early phases are often masked in patients receiving midazolam or propofol.

  
  

Cardiovascular Phase

• 
  

  Initial: Hypertension and tachycardia (if epi used) or transient stimulatory phase.

  
  


• 
  

  Conduction Defects: PR prolongation, QRS widening (classic sign), bundle branch blocks.

  
  


• 
  

  Dysrhythmias: Bradycardia (most common), VT/VF, PEA, asystole.

  
  


• 
  

  Contractility: Profound, refractory hypotension and cardiogenic shock.

  
  

IV. Immediate Management Algorithm

Goal: Prevent hypoxia/acidosis and sequester the toxin.

1. Initial Actions

• 
  

  Stop Injection: Immediately halt all LA administration.

  
  


• 
  

  Call for Help: Specify “LAST Protocol” and “Intralipid Kit.”

  
  


• 
  

  Airway Management:

  
  
  
  
  • 
    

    100% O2​.

    
    
  
  
  • 
    

    Hyperventilate slightly if needed to counter respiratory acidosis.

    
    
  
  
  • 
    

    Low threshold for intubation (hypoxia/acidosis rapidly worsen LAST).

    
    
  
  
  
  

2. Seizure Control

• 
  

  First-line: Benzodiazepines (e.g., Midazolam).

  
  


• 
  

  Avoid: Propofol if hemodynamically unstable (exacerbates cardiac depression).

  
  


• 
  

  Neuromuscular Blockers: May be needed for ventilation, but remember they do not stop CNS seizure activity.

  
  

3. Lipid Emulsion Therapy 20%

• 
  

  Indications: Start at first sign of serious toxicity (airway compromise, seizures, or CV instability).

  
  


• 
  

  Bolus: $1.5\text{ mL/kg}$ IV over $1\text{ minute}$.

  
  


• 
  

  Infusion: $0.25\text{ mL/kg/min}$ immediately following bolus.

  
  


• 
  

  If Instability Persists:

  
  
  
  
  • 
    

    Repeat bolus (up to 2 times).

    
    
  
  
  • 
    

    Increase infusion to $0.5\text{ mL/kg/min}$.

    
    
  
  
  
  


• 
  

  Upper Limit: $\approx 12\text{ mL/kg}$ total dose.

  
  

4. Modified ACLS

• 
  

  Epinephrine: Use low doses ($<1\text{ mcg/kg}$) to avoid worsening arrhythmias and interfering with lipid rescue.

  
  


• 
  

  Antiarrhythmics: Amiodarone is preferred.

  
  


• 
  

  CONTRAINDICATED:

  
  
  
  
  • 
    

    Lidocaine: (Class Ib antiarrhythmic—will worsen toxicity).

    
    
  
  
  • 
    

    Vasopressin: Associated with poor outcomes in animal LAST models.

    
    
  
  
  • 
    

    Calcium Channel Blockers / Beta Blockers: Exacerbate myocardial depression.

    
    
  
  
  
  


• 
  

  Refractory Arrest: Early consultation for ECMO or Cardiopulmonary Bypass (CPB).

  
  

V. Differential Diagnosis for the Peri-Procedural Patient

• 
  

  High Spinal: Ascending sensory/motor block, profound sympathectomy (hypotension/bradycardia).

  
  


• 
  

  Anaphylaxis: Urticaria, wheezing (rare with amides, more common with esters).

  
  


• 
  

  Air/Gas Embolism: Sudden dyspnea, “mill-wheel” murmur, acute right heart strain.

  
  


• 
  

  Vasovagal Syncope: Bradycardia/hypotension, usually lacks the QRS widening or seizure activity.

  
  

VI. Post-Resuscitation & Complications

• 
  

  Observation:

  
  
  
  
  • 
    

    At least 2 hours after a CNS-only event.

    
    
  
  
  • 
    

    At least 4–6 hours after a CV event.

    
    
  
  
  
  


• 
  

  Lipid Complications:

  
  
  
  
  • 
    

    Lab Interference: Lipemia interferes with hemoglobin, creatinine, and electrolyte measurements (draw labs before ILE if possible).

    
    
  
  
  • 
    

    Pancreatitis: Rare, delayed complication of high-dose ILE.

    
    
  
  
  • 
    

    Fat Embolism/Overload: Rare pulmonary complications.

    
    
  
  
  
  

VII. Clinical “Red Flags” for Toxicity

• 
  

  Unexpected Agitation: In a patient who just received a block, don’t assume “anxiety.”

  
  


• 
  

  Wide QRS: Any widening of the QRS complex post-injection is LAST until proven otherwise.

  
  


• 
  

  Refractory Arrest: Standard ACLS failing in a patient who received LA. Lipid must be given.

  
  

Critical Note: LAST is a clinical diagnosis. Do not wait for serum lidocaine levels or laboratory confirmation to initiate Lipid Emulsion Therapy. Immediate correction of pH and PaCO2​ is as vital as the lipid itself.

Show Notes

Core EM Modular CME Course

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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
  
  
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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.

  
  


• 
  

  Hemodynamic Criteria:

  
  
  
  
  • 
    

    Cardiac Index (CI): >4.0 L/min/m2.

    
    
  
  
  • 
    

    Cardiac Output (CO): $>8\text{ L/min}$.

    
    
  
  
  • 
    

    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.

  
  

2. Pathophysiology: The Hemodynamic Paradox

• 
  

  Primary Insult: Decreased SVR (either via peripheral vasodilation or arteriovenous shunting).

  
  


• 
  

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

  
  


• 
  

  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 $\to$ eccentric remodeling $\to$ chamber dilation $\to$ eventual secondary myocardial failure/dilated cardiomyopathy.

  
  

3. 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 angiomata” and internal AV shunts.

    
    
  
  
  • 
    

    Impaired clearance of endogenous vasodilators (e.g., Nitric Oxide).

    
    
  
  
  
  


• 
  

  Thiamine Deficiency (Wet Beriberi):

  
  
  
  
  • 
    

    Accumulation of pyruvate/lactate $\to$ systemic vasodilation.

    
    
  
  
  • 
    

    Histopathology: Vacuolation, myofiber hypertrophy, and interstitial edema.

    
    
  
  
  
  


• 
  

  Chronic Lung Disease:

  
  
  
  
  • 
    

    Hypoxia/Hypercapnia-driven systemic vasodilation.

    
    
  
  
  • 
    

    Concomitant pulmonary HTN (RV remodeling) but preserved/high LV output.

    
    
  
  
  
  


• 
  

  Others: Paget’s disease of bone (extensive micro-shunting), Carcinoid syndrome, Mitochondrial diseases, Acromegaly, Erythroderma.

  
  

4. Special Focus: Hemodialysis Access-Induced HOHF

Physiologic Phases of AVF Creation:

1. 
   

   Acute Phase:

   
   
   
   
   1. 
      

      Immediate $\downarrow$ SVR.

      
      
   
   
   2. 
      

      $\uparrow$ Stroke volume and Heart Rate (SNS-mediated).

      
      
   
   
   3. 
      

      Endothelial shear stress $\to$ Nitric Oxide release $\to$ further arterial dilation.

      
      
   
   
   
   


2. 
   

   Subacute Phase (Days to 2 Weeks):

   
   
   
   
   1. 
      

      RAAS-driven volume expansion.

      
      
   
   
   2. 
      

      $\uparrow$ Right Atrial, Pulmonary Artery, and LV End-Diastolic Pressures (LVEDP).

      
      
   
   
   3. 
      

      Natriuretic peptide surge (BNP/ANP) peaks around Day 10.

      
      
   
   
   
   


3. 
   

   Chronic Phase (Weeks to Months):

   
   
   
   
   1. 
      

      Adaptive hypertrophy.

      
      
   
   
   2. 
      

      Decompensation occurs when dilation exceeds contractility limits.

      
      
   
   
   
   

5. Point-of-Care Physical Exam & Maneuvers

• 
  

  Nicoladoni-Branham Sign (Pathognomonic for Shunt-driven HOHF):

  
  
  
  
  • 
    

    Maneuver: Manually compress the AVF (or inflate cuff to $>50\text{ mmHg}$ above SBP) for 30 seconds.

    
    
  
  
  • 
    

    Positive Result: Reflexive bradycardia or a transient rise in systemic BP.

    
    
  
  
  • 
    

    Significance: Confirms the shunt is a major contributor to the cardiac workload.

    
    
  
  
  
  


• 
  

  Peripheral Pulse Assessment:

  
  
  
  
  • 
    

    Water Hammer Pulses: Rapid upstroke and collapse.

    
    
  
  
  • 
    

    Quincke’s Pulse: Visible capillary pulsations in the nail beds.

    
    
  
  
  • 
    

    Traube’s Sign: “Pistol-shot” sounds auscultated over the femoral arteries.

    
    
  
  
  
  


• 
  

  Volume Status: Rales, S3 gallop, peripheral edema (standard HF signs).

  
  

6. Diagnostic Workup (Technical Targets)

POCUS / Echocardiography:

• 
  

  Left Ventricle: Hyperdynamic function; EF typically $>60\%$.

  
  


• 
  

  Left Atrium: Significant dilation (Left Atrial Volume Index >34 mL/m2; Case study noted 72 mL/m2).

  
  


• 
  

  IVC: Plethoric with minimal respiratory variation.

  
  


• 
  

  Doppler: High flow velocities across the AV access if applicable.

  
  

Laboratory Evaluation:

• 
  

  BNP/NT-proBNP: Often markedly elevated (e.g., $>70,000$ in severe cases), though mean values in literature hover around $700\text{–}800\text{ pg/mL}$.

  
  


• 
  

  Hematology: CBC to evaluate for severe anemia (trigger for HOHF if $\text{Hgb}<7\text{–}8\text{ g/dL}$) or myeloproliferative markers.

  
  


• 
  

  Endocrine/Metabolic: TSH (Thyrotoxicosis), Serum Thiamine (Beriberi), LFTs (Cirrhosis).

  
  

7. Management Strategy: A Stepwise Approach

Phase 1: Immediate Stabilization (Volume Offloading)

• 
  

  Diuresis: Aggressive IV loop diuretics (Bumetanide/Furosemide).

  
  


• 
  

  Ultrafiltration: Preferred in ESRD patients failing to respond to dialysis or with refractory congestion.

  
  


• 
  

  Vasodilator Caution: Avoid aggressive Nitroglycerin or ACE-inhibitors initially.

  
  
  
  
  • 
    

    Rationale: Baseline SVR is already pathologically low; further reduction may precipitate profound hypotension/circulatory collapse.

    
    
  
  
  
  

Phase 2: Targeted Therapy (Etiology Specific)

• 
  

  Anemia: Transfuse to goal $\text{Hgb}>7\text{–}8\text{ g/dL}$ to reduce demand.

  
  


• 
  

  Beriberi: High-dose IV Thiamine ($100\text{–}500\text{ mg}$).

  
  


• 
  

  Thyrotoxicosis: Beta-blockers (Propranolol) + Antithyroid meds (PTU/Methimazole).

  
  

Phase 3: Surgical/Interventional Salvage (Refractory AVF Cases)

1. 
   

   Closure of Accessory Sites: If multiple fistulas exist, close the non-dominant/unused sites.

   
   


2. 
   

   Flow Reduction (Banding): Surgical narrowing of the fistula to target flow $<600\text{ mL/min}$.

   
   


3. 
   

   RUDI Procedure: Revision Using Distal Inflow (moving inflow to a smaller, more distal artery).

   
   


4. 
   

   Ligation: Complete closure of the AVF.

   
   
   
   
   • 
     

     Note: Requires bridge to Tunneled Dialysis Catheter or AV graft (higher resistance than fistulas).

     
     
   
   
   
   

8. Key Clinical Takeaways

• 
  

  The “Normal EF” Trap: Do not be reassured by an EF of $55\text{–}65\%$; in the context of pulmonary edema and high CO, this is potentially HOHF.

  
  


• 
  

  Pulse Pressure: Look for a wide pulse pressure (e.g., $180/60$) as a marker of low SVR.

  
  


• 
  

  ESRD Logic: If an ESRD patient is “wet” immediately after HD, the problem is likely flow (AVF), not just fluid.

  
  

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 Targets

Mean 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 with lower shockable rhythm incidence.
  
  


• Permissive Hypertension: If the patient is “self-driving” to higher pressures, do not aggressively lower them, as this may be a physiologic demand for cerebral blood flow.
  
  

Ventilation and Oxygenation

• PaCO2 Management:
  
  
  
  • Target: High-normal to slightly hypercarbic (45–55 mmHg).
    
    
  
  
  • Rationale: Avoid accidental hyperventilation (PaCO2 <30), which can cut cerebral blood flow by 50%.
    
    
  
  
  
  


• PaO2 Management: Maintain normoxia; avoid extreme hyperoxia, though trial data (BOX trial) suggests small variances (70 vs 90 mmHg) are likely neutral.
  
  

IV. Neurological Prognostication & Communication

The “Stunned” Brain

• Anoxic Depolarization: Occurs within ~2 minutes of pulselessness as ATP-dependent ion pumps fail.
  
  


• Clinical Pitfall: Early neurological exams (absent pupils, no motor response) are unreliable in the first hours as they reflect global neuronal “stunning” rather than definitive permanent injury.
  
  


• Time Horizon: Meaningful recovery is measured in days/weeks, not minutes/hours.
  
  

Family Engagement

• Presence: Bring family to the bedside immediately, including during procedures or continued resuscitation.
  
  


• Psychological Impact: Significantly reduces PTSD, anxiety, and depression in survivors’ families.
  
  


• Prognostic Honesty: Explicitly state “I don’t know” regarding etiology and outcome.
  
  


• Framing: Define “No News” as the best possible early outcome (preventing rearrest and stabilization).

Show Notes

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Patient Presentation & Workup

• Patient: 36-year-old male, currently shelter-domiciled, presenting with 3 weeks of generalized weakness, fevers, weight loss, and headaches.


• Vitals (Initial): BP 147/98, HR 150s, Temp 100.2°F, RR 18, O2 99% RA.


• Clinical Evolution: Initial assessment noted cachexia and a large ventral hernia. Following initial workup, the patient became acutely altered (A&O x0) and febrile to 102.9°F.


• Physical Exam Findings:
  
  
  
  • Brudzinski Sign: Positive (knees flexed upward upon passive neck flexion).
  
  
  • Kernig Sign: Discussed as highly specific (resistance/pain during knee extension with hip flexed at 90°).
  
  
  • Meningeal Triad: Fever, nuchal rigidity, and AMS (present in 40% of cases; 95% of patients have at least two of the four cardinal symptoms including headache).
  
  
  
  


• Imaging:
  
  
  
  • Chest X-ray: Scattered opacities (pneumonia) and a small pneumothorax.
  
  
  • CT Abdomen/Pelvis: Confirmed asplenia (secondary to 2011 GSW/exploratory laparotomy).
  
  
  • Head CT: Ventricle enlargement concerning for obstructive hydrocephalus and diffuse sulcal effacement.
  
  
  
  

CSF Analysis & Microbiology

• Bacterial Meningitis
  
  
  
  • Opening Pressure: Elevated (Normal is $<170$ mm H2​O).
  
  
  • Color: Cloudy or turbid.
  
  
  • Gram Stain: Positive in 60%–80% of cases before antibiotics; drops to 7%–41% after antibiotics.
  
  
  • Cell Count: Very high ($>1000$–2000/mm3 WBC); dominated by neutrophils ($>80\%$ PMN).
  
  
  • Glucose: Low ($<40$ mg/dL); CSF/blood glucose ratio is $<0.3$–$0.4$.
  
  
  • Protein: High ($>200$ mg/dL).
  
  
  • Cytology: Negative.
  
  
  
  


• Viral Meningitis
  
  
  
  • Opening Pressure: Normal.
  
  
  • Color: Clear or bloody.
  
  
  • Gram Stain: Negative.
  
  
  • Cell Count: Slightly elevated (<300/mm3 WBC); dominated by lymphocytes ($<20\%$ PMN).
  
  
  • Glucose: Normal.
  
  
  • Protein: Moderately elevated ($<200$ mg/dL).
  
  
  • Cytology: Negative.
  
  
  
  


• Fungal Meningitis
  
  
  
  • Opening Pressure: Normal to elevated.
  
  
  • Color: Clear or cloudy.
  
  
  • Gram Stain: Negative.
  
  
  • Cell Count: Elevated (<500/mm3 WBC).
  
  
  • Glucose: Normal to slightly low.
  
  
  • Protein: High ($>200$ mg/dL).
  
  
  • Cytology: Negative.
  
  
  
  


• Neoplastic (Cancer-related) Meningitis
  
  
  
  • Opening Pressure: Normal.
  
  
  • Color: Clear or cloudy.
  
  
  • Gram Stain: Negative.
  
  
  • Cell Count: Elevated (<300/mm3 WBC).
  
  
  • Glucose: Normal to slightly low.
  
  
  • Protein: High ($>200$ mg/dL).
  
  
  • Cytology: Positive (this is the key differentiator).
  
  
  
  

Management Protocol

• Immediate Treatment: Early administration of antibiotics/antivirals is critical to reduce mortality.
  
  
  
  • Antibiotics: Ceftriaxone 2g IV q12h + Vancomycin (or Rifampin in cephalosporin-resistant areas).
  
  
  • Listeria Coverage: Add Ampicillin for patients > 50 years old.
  
  
  • Antivirals: Acyclovir 10 mg/kg q8h.
  
  
  • Steroids: Dexamethasone 10 mg IV q6h for 4 days (proven to reduce mortality and improve outcomes).
  
  
  
  


• Surgical Intervention: Neurosurgery performed an emergent EVD in the ED to relieve pressure from obstructive hydrocephalus.


• Post-Exposure Prophylaxis: Indicated only for N. meningitidis (not S. pneumoniae) for contacts < 24 hours from diagnosis.
  
  
  
  • Regimens: Rifampin for 2 days, single-dose Ciprofloxacin, or IM Ceftriaxone (if pregnant).
  
  
  
  

Stats & Clinical Pearls: Austrian Syndrome

• The Triad: Concurrent pneumonia, endocarditis, and meningitis caused by Streptococcus pneumoniae.


• Risk Factors: Asplenia (due to the spleen’s role in filtering encapsulated bacteria), alcohol use disorder, and immunosuppression.


• Mortality Rate: Extremely high at 28%; mortality is highest when there is CNS involvement.


• Incidence: Worldwide, S. pneumoniae is the leading cause of bacterial meningitis, accounting for 3,000–6,000 cases annually.