USMLE Vault · Divine Intervention Emergency Medicine
Step 2 / 3 · Study Guide
Emergency Medicine System

Emergency Medicine

7 episodes · 3 Rapid Review inline · Divine Intervention Podcast

High-yield emergency medicine for USMLE Step 2/3 — airway management, hemorrhagic shock, toxicology, neurologic emergencies, and trauma resuscitation, extracted from Divine Intervention and organized by clinical cluster for exam performance.

2 episodes
Cardiovascular Emergencies
ACS, acute decompensated heart failure, arrhythmias, and pericardial emergencies are the cardiovascular crises tested most heavily on Step 2/3 EM questions. The key distinction is hemodynamic stability — it determines whether you cardiovert, medicate, or intubate. Kussmaul sign and Beck's triad are the clinical shortcuts for pericardial emergencies.
RR 121EP595
Acute Decompensated HF, ACS & Pulmonary Edema
  • Polycythemia vera → increased viscosity → thrombosis: High hematocrit raises total peripheral resistance (Poiseuille's Law: viscosity directly proportional to TPR) → hypertension → concentric LVH → diastolic dysfunction → S4 heart sound
  • Epstein's anomaly: Lithium use in pregnancy → downward displacement of tricuspid valve leaflets + right ventricle underdevelopment → tricuspid regurgitation + ASD or PFO in ~50% of cases. Classic exam: newborn with HF whose mom has bipolar disorder on lithium
  • Marfan's cardiac associations: Mitral valve prolapse + aortic aneurysm/dissection. Sudden severe chest pain in tall young person → rule out pneumothorax AND aortic dissection. Needs regular echocardiographic surveillance
  • ADPKD cardiac: Mitral valve prolapse + intracranial aneurysms (Circle of Willis) → risk of SAH. Clusters: liver cysts, renal cysts (→ RCC risk), MVP, berry aneurysms
  • SVT management algorithm: Stable → vagal maneuvers → adenosine → beta-blocker or non-DHP CCB (verapamil/diltiazem). Unstable → synchronized cardioversion immediately. Defibrillation (unsynchronized) = VFib or pulseless VTach only
Epstein's AnomalyLithiumSVTAdenosineSynchronized CardioversionMarfan'sADPKD

SVT — Full Management Algorithm

StepStable PatientUnstable Patient
FirstVagal maneuvers (carotid massage, Valsalva, cold water immersion)Synchronized cardioversion immediately
SecondIV adenosine (terminates AV-nodal reentry)
MaintenanceBeta-blocker or verapamil/diltiazem
Critical — Synchronized vs Unsynchronized

Synchronized cardioversion: Any unstable tachyarrhythmia with a pulse (SVT, atrial flutter, AFib, stable VTach). Defibrillation (unsynchronized): VFib only OR pulseless VTach. Never shock asystole or PEA — that worsens outcome.

Congenital Cardiac Defect Associations (High-Yield Table)

Syndrome / ExposureCardiac Defect
Down syndromeEndocardial cushion (AV canal) defect
DiGeorge syndromeTruncus arteriosus, Tetralogy of Fallot
Lithium exposure (fetal)Epstein's anomaly (+ ASD/PFO in 50%)
Fetal alcohol syndromeVSD
Marfan syndromeMitral valve prolapse + aortic aneurysm
ADPKDMitral valve prolapse + berry aneurysms
Turner syndromeBicuspid aortic valve + coarctation of aorta
Polycythemia Vera Integration Chain

JAK2 mutation → EPO-independent RBC proliferation → ↑ hematocrit → ↑ blood viscosity → ↑ TPR → hypertension → LV afterload → concentric LVH → diastolic dysfunction → S4. Simultaneously: viscosity → stasis (Virchow's triad) → thrombosis → consumed vWF → bleeding. Treatment: phlebotomy + aspirin.

EP571
Chest Trauma, Pericardial Emergencies & Flail Chest
  • Chest trauma = leading cause of trauma mortality on USMLE exams — high-value organs (heart, lungs, aorta). Aortic transection = near-uniform fatality. Always pick chest-related answer when asked most common cause of trauma death
  • Tension pneumothorax: Sudden SOB + unilateral absent breath sounds + hypotension → needle thoracostomy FIRST (2nd intercostal space, mid-clavicular line, above rib 3). Converts tension to open pneumo. Then tube thoracostomy (chest tube) for definitive management
  • Flail chest: ≥2 ribs fractured in ≥2 places → paradoxical chest wall movement (inward on inspiration, outward on expiration). Most common complication = pulmonary contusion. Tx: O2, judicious fluids, pain control; intubate if deteriorating
  • Kussmaul sign: JVD that increases (rather than decreases) on inspiration. Normal physiology: inspiration → ↑ intrathoracic volume → ↓ intrathoracic pressure → blood rushes into heart → JVD collapses. Kussmaul = heart can't relax → JVD expands. Causes: cardiac tamponade, constrictive pericarditis
  • Cardiac tamponade management: Pericardiocentesis + aggressive IV fluids to maintain preload. Beck's triad: hypotension + muffled heart sounds + JVD
Tension PneumothoraxNeedle DecompressionFlail ChestKussmaul SignCardiac TamponadeBeck's Triad

Needle Thoracostomy — Anatomy Specifics

Insert needle in the 2nd intercostal space, mid-clavicular line, ABOVE rib 3 (not directly below rib 2, which risks damage to the intercostal neurovascular bundle that runs in the groove below each rib). This converts tension → open pneumothorax and buys time. Follow with tube thoracostomy for definitive management.

Chest Wall Movement — Normal vs Flail

PhaseNormal ChestFlail Chest (Paradoxical)
InspirationChest wall moves outwardFlail segment moves inward
ExpirationChest wall moves inwardFlail segment moves outward
Kussmaul Sign — Mechanism

On inspiration, the normal response is JVD collapse (blood rushes from neck veins into the low-pressure thoracic heart). When pericardial pathology prevents cardiac relaxation (tamponade or constrictive pericarditis), the heart cannot accept the rush of blood → JVD paradoxically expands → Kussmaul sign.

Pericardial Disease — Differentiation

Cardiac TamponadeConstrictive Pericarditis
CauseFluid in pericardial spaceCalcified/fibrotic pericardium
Kussmaul signPresent (classic)Present (classic)
Pulsus paradoxusPresent (>10 mmHg drop with inspiration)Can be present
TreatmentPericardiocentesis + IV fluidsSurgical pericardiectomy
USMLE clueTrauma, malignancy, uremia, TBTB, radiation, post-viral
2 episodes
Toxicology & Overdose
Toxicology on Step 2/3 is about recognizing toxidrome patterns, not memorizing antidotes in isolation. The key differentiators: pupil size (pinpoint = opioid, mydriatic = cocaine/meth/anticholinergic), respiratory status (depression = opioid/benzo), and the presence or absence of an identifiable trigger. Alcohol and benzo withdrawal are the two withdrawals that kill — treat aggressively.
RR 92EP442
Alcohol Intoxication, Drug Toxidromes & Withdrawal
  • Alcohol intoxication: Disinhibition, slurred speech, ataxia, NO respiratory depression. Labs: ↑ GGT, AST>ALT (ratio ≥2:1), hypoglycemia (NAD⁺ consumed by alcohol dehydrogenase → impaired glycolysis and gluconeogenesis). Give thiamine BEFORE glucose
  • Alcohol vs other toxidromes: No conjunctival redness or hunger (≠ marijuana), no respiratory depression (≠ opioids), no identifiable trigger (≠ specific phobia). Benzo similar but can have respiratory depression — reverse with flumazenil
  • Opioid intoxication: Respiratory depression + bilateral pinpoint pupils (↓ norepinephrine release). Reverse with naloxone (not naltrexone). Naltrexone = maintenance therapy for opioid use disorder
  • Cocaine intoxication: ↑↑ BP + bilateral mydriasis (α1 stimulation) + chest pain (MI risk) + pressured speech + tachycardia. Treatment: benzodiazepines (NO beta-blockers — risk of unopposed alpha)
  • Meth vs cocaine: Meth has more prominent hallucinations in addition to sympathomimetic signs. Cocaine tends more toward MI/ACS presentation
  • Fatal withdrawals: Alcohol and benzodiazepines — both must be treated aggressively. Alcohol withdrawal → delirium tremens → long-acting benzo (chlordiazepoxide). Benzo withdrawal also managed with benzos (taper)
Alcohol IntoxicationWernicke'sOpioid OverdoseNaloxoneCocaineBenzo WithdrawalFlumazenil

Toxidrome Comparison Table

DrugPupilsRespiratoryKey FeatureReversal
AlcoholNormalNormal (rare depression)Ataxia, disinhibition, hypoglycemiaThiamine + glucose + fluids
OpioidsPinpoint (bilateral)Respiratory depressionDecreased LOC, no responseNaloxone
BenzodiazepinesNormalRespiratory depressionNo identifiable trigger, sedationFlumazenil
CocaineMydriasis (bilateral)Normal/↑ rate↑↑ BP, chest pain, pressured speechBenzodiazepines
MethamphetamineMydriasis (bilateral)Normal/↑ rateProminent hallucinations + sympathomimeticBenzodiazepines
MarijuanaConjunctival injectionNormalHunger, slow reaction time, red eyesSupportive
Alcohol Metabolism — Why Hypoglycemia Occurs

Alcohol is metabolized by alcohol dehydrogenase and acetaldehyde dehydrogenase — both consume NAD⁺ to produce NADH. When NAD⁺ is depleted: (1) glycolysis cannot run (requires NAD⁺), (2) gluconeogenesis is impaired → hypoglycemia. Also drives lactic acidosis (pyruvate → lactate requires NADH) and increased VLDL/triglycerides.

Wernicke's Encephalopathy — Protocol

Classic triad: confusion + ophthalmoplegia + ataxia. In ANY alcoholic admitted to hospital → give IV thiamine FIRST, then glucose (giving glucose without thiamine can precipitate acute Wernicke's by consuming the remaining B1 for glucose metabolism).

Alcohol Withdrawal — Timeline & Treatment

6–24h: Tremors, anxiety, tachycardia. 12–48h: Alcoholic hallucinations (intact orientation). 24–72h: Seizures. 48–96h: Delirium tremens (confusion, fever, autonomic instability — potentially fatal). Treatment: long-acting benzos (chlordiazepoxide or diazepam). Maintenance: naltrexone or acamprosate. AA referral.

EP429
Crystalloid Resuscitation: Normal Saline vs Lactated Ringer's
  • Normal saline problems: Supraphysiologic chloride (154 mEq/L vs normal 96–107) → afferent arteriolar constriction (↓ prostaglandins from macula densa) → AKI risk. Heavy chloride load displaces bicarb → hyperchloremic metabolic acidosis. Redistribution of K⁺ from cells → hyperkalemia despite no K⁺ in bag
  • Lactated Ringer's: More physiologic, lower chloride, slightly better outcomes in ICU studies (SALT-ED, SMART-MED trials). Contains potassium — but ↑K rise is slower and less than with NS-induced metabolic acidosis redistribution
  • Fluid distribution rule: Only ~25–33% of crystalloid stays in vascular space (rest redistributes intracellularly/interstitially). To replace 1L blood loss: give 3–4L crystalloid
  • Transfusion threshold: Hgb <7 in stable patient. Give blood if: still unstable after fluids, OR ongoing active bleed, OR significant cardiac disease (threshold higher). Always give O-negative blood empirically in emergencies
  • Response to resuscitation: Best marker = urine output (Foley catheter). Kidneys retain fluid when volume depleted → diuresis indicates adequate resuscitation. Do NOT place Foley if blood at urethral meatus, scrotal hematoma, or high-riding prostate (→ retrograde urethrogram instead)
Normal SalineLactated Ringer'sHyperchloremic AcidosisTransfusion ThresholdO-Negative BloodUrine Output

Crystalloid Comparison

PropertyNormal Saline (0.9%)Lactated Ringer'sPlasma-Lyte
Na⁺ (mEq/L)154130140
Cl⁻ (mEq/L)154 (supraphysiologic)10998
K⁺ (mEq/L)045
pH5.0 (acidic)6.57.4 (physiologic)
CostCheapestModerateExpensive
Best useHyponatremia, TBI/↑ICP, wound irrigationMost resuscitation scenariosICU patients (if cost acceptable)
NS Causes Hyperkalemia — Mechanism (Counterintuitive)

Normal saline contains zero potassium. Yet massive NS infusion can cause hyperkalemia. Why: heavy chloride load → hyperchloremic metabolic acidosis → body compensates by shifting H⁺ into cells in exchange for K⁺ → serum K⁺ rises. This K⁺ redistribution, not the NS itself, causes hyperkalemia.

Foley Catheter Contraindications in Trauma

  • Blood at urethral meatus → urethral injury → retrograde urethrogram first
  • Scrotal hematoma (pulsatile/bloody) → urethral disruption likely
  • High-riding prostate on rectal exam (prostate farther from anus than normal) → urethral tear
  • In all above: image first, do not blindly insert catheter
O-Negative Blood — Rationale

O = no A or B antigens on RBC surface → cannot be attacked by recipient's anti-A or anti-B antibodies. Negative = no Rhesus antigen → avoids sensitization (critical in women of childbearing age to prevent future hemolytic disease of the newborn). Give O-negative empirically whenever crossmatch is not possible in trauma.

3 episodes
Trauma & Resuscitation
Trauma management on Step 2/3 follows a strict sequence: primary survey → identify life threats → stabilize airway/breathing/circulation before definitively treating injuries. The USMLE favors applied anatomy (where to place the needle, why to avoid the Foley) and management sequencing over pure factual recall. Cervical spine injury and neurogenic shock are particularly high-yield.
EP572
Hemorrhagic Shock, Volume Resuscitation & Transfusion
  • Volume resuscitation sequence: Fluids first (normal saline), then blood if still unstable or Hgb <7. Give 3–4× the estimated blood loss in crystalloid (only 25–33% stays intravascular)
  • Empiric blood type: O-negative in emergencies. O = no ABO antigens. Negative = no RhD antigen (prevents sensitization in women of childbearing age, preventing future hemolytic disease of newborn)
  • RH sensitization — beyond the classic rule: Hemolytic disease of newborn CAN occur in first pregnancy if mom was previously sensitized by trauma, ectopic pregnancy, molar pregnancy, or prior transfusion. Do not assume first pregnancy is always safe
  • Urine output = best resuscitation marker: Kidneys retain fluid when volume-depleted (RAAS active, ADH active). Onset of diuresis signals adequate preload restoration. Place Foley for continuous monitoring
  • Gunshot wounds and law enforcement: When you suspect homicide or criminal activity → notify law enforcement. Mandatory reporting regardless of whether patient is stabilized
Hemorrhagic ShockFluid ResuscitationHemolytic Disease NewbornUrine Output MonitoringLaw Enforcement Reporting

Hemorrhagic Shock — Classification

ClassBlood LossHRBPUrine Output
Class I<15% (<750 mL)NormalNormal>30 mL/hr
Class II15–30%↑ (100–120)Normal (↑ diastolic)20–30 mL/hr
Class III30–40%↑↑ (120–140)↓ systolic5–15 mL/hr
Class IV>40%>140↓↓Negligible
Hematocrit → Hemoglobin Conversion

On USMLE, they may give hematocrit instead of hemoglobin. Conversion: Hemoglobin = Hematocrit ÷ 3. Example: Hct 18% → Hgb ~6 g/dL → below transfusion threshold of 7 → transfuse.

Ethics in Trauma — Consent Rules

  • Unconscious/altered patient: implied consent → treat without consent, do not delay for advanced directive unless one clearly exists
  • Conscious suicidal patient refusing care: ignore refusal and treat — suicidal patients' refusal of life-saving care is not legally binding
  • Advanced directive clearly documented: follow it even if patient cannot currently consent
  • Gunshot wounds / suspected homicide: notify law enforcement — mandatory regardless of stabilization status
EP574
C-Spine Trauma, Neurogenic Shock & Spinal Cord Syndromes
  • C-spine assessment: Cervical X-ray first (>90% sensitive) — preferred over CT on exams unless XR not available. At-risk populations for atlantoaxial subluxation: rheumatoid arthritis, Down syndrome, ankylosing spondylitis → always get cervical XR
  • C-spine fracture pearl: If cervical fracture found → image thoracic and lumbar spine BEFORE going to OR. ~20% of cervical fractures have concurrent thoracic/lumbar fractures. Know all fractures before operating
  • Spinal cord lesion at C5 or above: Destroys phrenic nerve supply (C3-C4-C5 = diaphragm). Next step = immediate intubation. "C345 keeps the diaphragm alive"
  • Neurogenic shock (spinal shock): Damage to thoracic spinal cord → loss of sympathetic (thoracolumbar outflow) → parasympathetic unopposed → hypotension + bradycardia. Mechanism: ↓ venous constriction → ↓ preload + ↓ SVR + ↓ HR. Treatment: fluids + atropine (bradycardia) + norepinephrine (vasopressor for vascular tone)
  • Cauda equina syndrome: Decreased rectal tone + urinary incontinence + saddle anesthesia → emergent MRI + neurosurgical consultation. Do not miss this
Cervical Spine TraumaAtlantoaxial SubluxationPhrenic Nerve C345Neurogenic ShockCauda EquinaSpinal Cord Syndromes

Spinal Cord Injury — Classic Findings Pattern

  • Sensory level: Below a certain dermatome, all pain/temperature/vibration/fine touch is lost → think spinal cord, not peripheral nerve
  • Spinothalamic tract (pain/temperature): Crosses in anterior white commissure of spinal cord → crossed findings (deficit contralateral to lesion side)
  • Dorsal columns (vibration/fine touch): Cross in medulla → ipsilateral findings in spinal cord lesions
  • Upper motor neuron signs: Below level of lesion (ipsilateral) — spasticity, hyperreflexia, Babinski
  • Lower motor neuron signs: At level of lesion — flaccidity, fasciculations, areflexia
  • Brown-Séquard syndrome: Hemisection → ipsilateral loss of vibration/UMN + contralateral loss of pain/temperature below lesion
Neurogenic Shock vs Hemorrhagic Shock — Key Difference

Both cause hypotension. But: hemorrhagic shock → tachycardia (sympathetic response). Neurogenic shock → bradycardia (sympathetic system destroyed). If you see trauma + hypotension + bradycardia → neurogenic shock until proven otherwise.

Neurogenic Shock — Treatment Rationale

ProblemMechanismTreatment
↓ PreloadNo venous constriction → blood pools in veinsIV fluids
BradycardiaParasympathetic unopposed (no sympathetic counter)Atropine
↓ Vascular toneNo arteriolar constriction → ↓ SVRNorepinephrine (pressors)
EP571
Airway Management, Epiglottitis & Foreign Body Aspiration
  • Epiglottitis presentation: High fever + audible stridor + drooling + tripod position → airway closure = kill risk. Do NOT give antibiotics first. INTUBATE first (controlled environment ideally OR). If intubation fails → cricothyroidotomy (surgical airway)
  • Epiglottitis cause: H. influenzae type B (unvaccinated children and adults). Staphylococcus aureus in adults. After securing airway → IV antibiotics (3rd-gen cephalosporin)
  • Foreign body aspiration: Child found suddenly unresponsive after playing with toys → foreign body aspiration. Next step = flexible laryngoscopy. Most common site: right mainstem bronchus (wider, more vertical than left)
  • Basal skull fracture signs: Raccoon eyes (periorbital ecchymosis) + hemotympanum + CSF otorrhea/rhinorrhea + Battle's sign (retroauricular ecchymosis). Indicates severe head injury → non-contrast head CT immediately
  • Cushing's reflex: Hypertension + bradycardia + irregular respirations = ↑ ICP. Fastest treatment: intubation + hyperventilation (↓ CO2 → cerebral vasoconstriction → ↓ ICP). Also: mannitol, head-of-bed elevation
EpiglottitisCricothyroidotomyForeign Body AspirationBasal Skull FractureCushing's ReflexRaised ICP

Airway Management Decision Tree

  • Any concern for C-spine → immobilize in collar until cleared
  • Difficult airway anticipated → secure in OR with ENT/anesthesia backup
  • Epiglottitis: intubate first, antibiotics second
  • Intubation fails → surgical airway (cricothyroidotomy)
  • C5 or above spinal cord lesion → emergent intubation (phrenic nerve disrupted)
  • ↑ ICP with altered consciousness → intubation + hyperventilate (set ventilator to high RR)
ICP Reduction — Fastest Method

Hyperventilation → ↓ PaCO2 → cerebral arteriolar vasoconstriction → ↓ cerebral blood volume → ↓ ICP. On exams: if "hyperventilation" not listed as answer, pick "endotracheal intubation" — because you cannot hyperventilate an obtunded trauma patient without a tube. Mannitol and hypertonic saline are alternatives but slower acting.

Basal Skull Fracture — Signs Summary

SignMechanism / Location
Raccoon eyesBlood tracks into periorbital space (anterior fossa fracture)
Battle's signBlood tracks to mastoid process (posterior fossa / temporal bone fracture)
HemotympanumBlood in middle ear (temporal bone fracture)
CSF otorrhea / rhinorrheaDural tear allows CSF to drain through ear or nose
3 episodes
Neurologic & Miscellaneous Emergencies
Stroke, seizure, and altered mental status dominate the neurologic emergency category. The EM physician must distinguish stroke mimics (hypoglycemia, Todd's paralysis, conversion disorder) from true cerebrovascular events, and recognize when IV tPA is indicated versus contraindicated. Rapid Review Series 72 integrates neurology and pharmacology in the context of emergency presentations.
RR 72EP380
Stroke, Drug Toxicities & Neurological Emergencies
  • Herpetic whitlow: Vesicular lesions at nail fold → oral acyclovir (NOT IV — IV acyclovir only for severe/systemic herpes). Acyclovir = DNA-dependent DNA polymerase inhibitor. IV reserved for altered patients or those who cannot tolerate PO
  • Aminoglycosides — dual toxicity: Nephrotoxic + ototoxic (shared transporters between kidney and inner ear). Same cluster: vancomycin, loop diuretics (especially ethacrynic acid), cisplatin. Use in gram-negative infections (UTI → aminoglycosides, NOT vancomycin)
  • TMP-SMX hyperkalemia mechanism: Trimethoprim acts like a potassium-sparing diuretic — blocks ENaC channels in principal cell, reducing luminal negative charge, preventing K⁺ efflux from cell. Net result: K⁺ retention → hyperkalemia. Also can cause G6PD hemolysis in susceptible patients
  • G6PD deficiency: X-linked recessive → males. Heinz bodies + bite cells on smear. Cannot handle oxidant stress → drugs (dapsone, primaquine, TMP-SMX, nitrofurantoin), fava beans trigger hemolysis. NADPH deficiency also impairs respiratory burst (similar to CGD but less severe)
  • Derivative answers on USMLE: DNA polymerase inhibitor = acyclovir. RNA-dependent DNA polymerase inhibitor = NRTI (HIV). DNA-dependent RNA polymerase inhibitor = rifampin. Recognize the mechanism → pick the right derivative answer
Herpetic WhitlowAcyclovirAminoglycosidesTMP-SMX HyperkalemiaG6PD DeficiencyDerivative Answers

Oral vs IV Therapy — USMLE Rule

IV therapy is appropriate ONLY in two situations on NBMEs: (1) Patient is hemodynamically unstable, severely ill, or has organ damage. (2) Patient cannot tolerate oral intake. For everything else → oral is preferred. Trap: NBMEs often list both oral and IV formulations as answers for the same drug — use these rules to choose.

Polymerase Inhibitor Derivatives — Quick Reference

DrugUSMLE Derivative AnswerMechanism
Acyclovir, GanciclovirInhibitor of DNA-dependent DNA polymerasePrevents viral DNA replication
NRTIs (zidovudine, tenofovir)Inhibitor of RNA-dependent DNA polymeraseBlocks HIV reverse transcriptase (RNA→DNA)
RifampinInhibitor of DNA-dependent RNA polymeraseBlocks bacterial transcription
Aminoglycoside Contraindications

Never give aminoglycosides in: myasthenia gravis, ALS, Lambert-Eaton syndrome, polymyositis. Mechanism: aminoglycosides block nicotinic receptors at the NMJ → neuromuscular blockade → worsens pre-existing NMJ disease. High-yield trap on Step 2/3.

TMP-SMX — Full Side Effect Profile

  • Hyperkalemia (potassium-sparing diuretic mechanism on ENaC)
  • Megaloblastic anemia (folate synthesis inhibition)
  • Bone marrow suppression (at high doses)
  • G6PD hemolysis (sulfamethoxazole = oxidizing agent)
  • Nephrotoxicity (crystalluria in dehydrated patients)
EP571
Elevated ICP, Head Trauma & Cushing's Reflex
  • Cushing's reflex (triad): Hypertension + bradycardia + irregular/shallow respirations → ↑ ICP. Do NOT treat hypertension — it is a compensatory response to maintain cerebral perfusion pressure
  • ICP reduction hierarchy: (1) Intubation + hyperventilation (fastest — cerebral vasoconstriction). (2) Mannitol (osmotic agent draws water from brain cells). (3) Hypertonic saline (same mechanism). (4) Head-of-bed elevation. (5) Treat underlying cause
  • Hypertonic saline indications: Severe hyponatremia with seizing (Na <120 + seizures). Also: ↑ ICP as adjunct. Correct hyponatremia slowly — too fast → central pontine myelinolysis (quadriplegia, dysphagia, dysarthria, only extraocular muscles spared)
  • Mannitol mechanism: Non-reabsorbable sugar stays in vascular lumen → osmotic pull → draws water from brain cells → reduces cerebral edema → ↓ ICP
  • Emergent imaging in head trauma: Non-contrast head CT first — sensitive for hemorrhage, fractures, edema. MRI preferred for posterior fossa, early ischemia, MS plaques — but too slow in emergencies
Cushing's ReflexRaised ICPHyperventilationMannitolHypertonic SalineCentral Pontine Myelinolysis

ICP Management — Decision Table

InterventionMechanismSpeedUSMLE Priority
ETT + Hyperventilation↓ CO2 → cerebral vasoconstriction → ↓ CBF → ↓ ICPMinutesFirst-line (fastest)
Mannitol IVOsmotic diuresis, draws water from brain cells30–60 minSecond-line
Hypertonic salineOsmotic — shrinks brain cells30–60 minAlternative to mannitol
HOB elevation 30°↑ venous drainage from headMinutesAdjunct
AcetazolamideCarbonic anhydrase inhibitor → ↓ CSF productionHoursPseudotumor cerebri only
Hyponatremia Correction Rate

Maximum correction rate: 8–10 mEq/L per 24 hours. Overcorrection → central pontine myelinolysis (osmotic demyelination syndrome). Mechanism: brain cells adapt to chronic hyponatremia by generating idiogenic osmoles (inositol, glutamine, betaine). Rapid correction creates acute extracellular hyperosmolarity → water drawn out of brain cells → myelin damage → locked-in–like syndrome.

EP572
Ethics, Consent & Legal Obligations in Emergency Medicine
  • Emergency implied consent: Unconscious, altered, or unable to consent in an emergency → treat under doctrine of implied consent. Do NOT delay care to seek consent
  • Suicidal patient refusing care: A lucid suicidal patient who refuses life-saving treatment → IGNORE the refusal and treat. Suicidal intent means the patient lacks the capacity for autonomous decision-making regarding self-harm. This is one of the few absolute exceptions to respecting patient autonomy
  • Advanced directives override emergency consent: If a clearly documented advanced directive exists, follow it — even in an emergency when the patient cannot currently communicate their wishes
  • Mandatory reporting: Suspected homicide (gunshot wound), child abuse, certain communicable diseases → notify law enforcement or public health authorities regardless of patient stability or preference
  • USMLE trap: In any trauma question, if you've fixed the immediate emergency but see an answer about "inform law enforcement" → that is frequently also correct and may be the answer being tested on a follow-up question
Implied ConsentSuicidal PatientsAdvanced DirectivesMandatory ReportingPatient Autonomy Exceptions

Emergency Consent — Decision Framework

ScenarioCorrect Action
Unconscious trauma patient, no advanced directiveImplied consent → treat immediately
Conscious suicidal patient refuses treatmentIgnore refusal → treat (exception to autonomy)
Advanced directive clearly states no resuscitationFollow advanced directive even in arrest
Unconscious patient, family present, no advanced directiveTreat immediately; family provides surrogate consent while care proceeds
Gunshot wound, patient conscious but police not notifiedNotify law enforcement — mandatory reporting
Why Suicidal Patients Cannot Refuse Care

Decision-making capacity requires the ability to understand information, appreciate consequences, reason through options, and communicate a choice. Suicidal intent reflects a desire to end life — by definition, the patient is not exercising autonomous decision-making but acting from a psychiatric emergency. The physician's duty to prevent imminent death supersedes the expressed refusal.