Emergency Medicine

Every critical presentation, resuscitation protocol, acute diagnosis, procedure, disposition decision, and management strategy in one place.

01 The Emergency Medicine Approach

Emergency medicine is the only specialty defined not by an organ system or patient demographic but by acuity and undifferentiated presentation. The ED physician sees every chief complaint, from cardiac arrest to laceration repair, and must risk-stratify within minutes. The central question is never "what is the complete diagnosis?" but rather "does this patient have a life-threatening condition that I must identify and treat right now?"

Classification of the four types of shock: hypovolemic, cardiogenic, distributive, and obstructive, with their primary organ system associations
Figure 1 — Classification of Shock Types. Synoptic view of the four major categories of shock (hypovolemic, cardiogenic, distributive, obstructive) and the organ systems primarily associated with each type. Understanding shock classification is fundamental to emergency medicine resuscitation.

Triage — Emergency Severity Index (ESI)

ESI is the standard 5-level triage system used in US emergency departments. It combines acuity with expected resource utilization to prioritize patient flow.

ESI LevelDescriptionClinical ExampleExpected Resources
1Immediate life-saving intervention requiredCardiac arrest, respiratory failure, active massive hemorrhageResuscitation bay
2High-risk situation, confused/lethargic, severe pain/distressChest pain with ECG changes, stroke symptoms, unstable vital signsImmediate bedside evaluation
3Stable but likely needs multiple resources (labs, imaging, IV meds)Abdominal pain needing CT, renal colic, pneumonia2+ resources
4Stable, needs 1 resourceSimple laceration, UTI needing UA, ankle sprain needing X-ray1 resource
5Stable, needs 0 resources (exam only)Prescription refill, suture removal, medication question0 resources

Primary Survey — ABCDE

The primary survey is performed on every critically ill or injured patient. It is a systematic, sequential assessment that identifies and treats life threats in the order they will kill the patient fastest.

StepAssessmentImmediate Interventions
A — AirwayIs the airway patent? Look for stridor, gurgling, obstruction, facial trauma, angioedemaJaw thrust, suction, OPA/NPA, intubation, surgical airway
B — BreathingRR, SpO2, breath sounds bilateral? Chest wall excursion symmetric? Trachea midline?O2, BVM, needle decompression for tension PTX, chest tube, intubation
C — CirculationHR, BP, skin (cool/clammy = shock), active bleeding? Pulse quality?2 large-bore IVs, fluid bolus, blood products, pressors, tourniquet, direct pressure
D — DisabilityGCS, pupils (size, reactivity, symmetry), gross motor exam, glucoseDextrose for hypoglycemia, naloxone for opioid overdose, mannitol/hypertonic saline for herniation
E — Exposure/EnvironmentFully undress patient, log-roll, temperatureWarm blankets (prevent hypothermia), identify posterior wounds, rectal exam in trauma if indicated
In trauma, C-A-B-C is increasingly used: control catastrophic hemorrhage first (tourniquet), then airway, breathing, circulation. This reflects lessons from military medicine — exsanguination from extremity hemorrhage is the most preventable cause of trauma death.
Pathophysiology of shock showing hemodynamic parameters and compensatory mechanisms across shock types
Figure 2 — Shock Pathophysiology and Hemodynamic Parameters. Detailed pathophysiological mechanisms underlying each type of shock, including key hemodynamic parameters (cardiac output, SVR, preload) that differentiate them clinically.

Secondary Survey

Performed only after the primary survey is complete and life threats are addressed. This is the comprehensive head-to-toe physical exam: HEENT (pupil response, TMs, oropharynx), neck (JVD, tracheal deviation, c-spine tenderness), chest (heart sounds, lung fields), abdomen (tenderness, guarding, rigidity, peritoneal signs), pelvis (stability), extremities (pulses, deformity, compartments), neuro (cranial nerves, strength, sensation, reflexes, cerebellar), skin (rashes, wounds, track marks), and a detailed history (SAMPLE: Signs/symptoms, Allergies, Medications, Past medical history, Last meal, Events preceding).

02 Resuscitation Fundamentals

ACLS — Cardiac Arrest Algorithms

The 2020 AHA Guidelines define two pathways based on initial rhythm:

Shockable (VF/pVT)Non-Shockable (Asystole/PEA)
Defibrillate immediately (biphasic 120–200 J, mono 360 J)CPR × 2 min, then rhythm check
Resume CPR × 2 min, rhythm checkEpinephrine 1 mg IV/IO q3–5 min (give ASAP)
Epinephrine 1 mg IV/IO q3–5 min (after 2nd shock)Identify and treat reversible causes (H's and T's)
Amiodarone 300 mg IV (first dose), then 150 mg (second dose)Continue CPR with rhythm checks q2min

The H's and T's — reversible causes of cardiac arrest: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo/hyperkalemia, Hypothermia, Tension pneumothorax, Tamponade (cardiac), Toxins, Thrombosis (coronary/pulmonary). High-quality CPR is the single most important intervention: rate 100–120/min, depth 2–2.4 inches (5–6 cm), full chest recoil, minimize interruptions (< 10 sec for rhythm checks).

Intubation checklist for critically ill adults showing preparation, equipment, and steps for rapid sequence intubation
Figure 3 — Intubation Checklist for Critically Ill Adults. Standardized RSI checklist covering patient preparation, equipment verification, team briefing, and failed airway contingency planning. Checklists reduce adverse events during emergency intubation.

Airway Management Hierarchy

Airway interventions escalate in invasiveness: positioning (head tilt–chin lift, jaw thrust in trauma) → basic adjuncts (OPA in unconscious without gag, NPA if gag intact) → bag-valve-mask (BVM)supraglottic airway (LMA, King tube — rescue device or prehospital) → endotracheal intubation (RSI is the ED standard) → surgical airway (cricothyrotomy — "can't intubate, can't oxygenate" scenario).

Shock Recognition & Classification

TypeMechanismClassic FindingsExamplesInitial Treatment
HypovolemicDecreased preload (volume loss)Tachycardia, hypotension, flat neck veins, cool extremitiesHemorrhage, dehydration, burnsIV fluids, blood products, control hemorrhage
CardiogenicPump failureHypotension, JVD, pulmonary edema, cool extremitiesMI, cardiomyopathy, myocarditis, valvular catastropheVasopressors (norepinephrine), inotropes (dobutamine), mechanical support
DistributiveVasodilation (decreased SVR)Hypotension, warm extremities (early), tachycardia, wide pulse pressureSepsis, anaphylaxis, neurogenic, adrenal crisisFluids + vasopressors (norepinephrine), treat cause
ObstructiveMechanical obstruction to flowHypotension, JVD, muffled heart sounds (tamponade) or absent breath sounds (tension PTX)Tension PTX, cardiac tamponade, massive PENeedle decompression, pericardiocentesis, thrombolytics

Hemorrhagic Shock Staging (ATLS)

ClassBlood LossHRBPRRMental StatusFluid Replacement
I< 750 mL (< 15%)< 100Normal14–20Slightly anxiousCrystalloid
II750–1500 mL (15–30%)100–120Normal20–30AnxiousCrystalloid
III1500–2000 mL (30–40%)120–140Decreased30–40ConfusedCrystalloid + blood
IV> 2000 mL (> 40%)> 140Very low> 35Lethargic/obtundedMassive transfusion protocol
Massive Transfusion Protocol (MTP)

Activated for anticipated need of ≥10 units pRBCs in 24 hours or ≥4 units in 1 hour. Target ratio: 1:1:1 (pRBC : FFP : platelets). Tranexamic acid (TXA) 1 g IV over 10 min within 3 hours of injury (CRASH-2 trial). Monitor: calcium (citrate in blood products chelates Ca → hypocalcemia → give calcium chloride 1 g IV or calcium gluconate 3 g IV), temperature (hypothermia worsens coagulopathy), potassium, ionized calcium, fibrinogen (target > 150 mg/dL — give cryoprecipitate if low). The lethal triad of trauma: hypothermia + acidosis + coagulopathy.

03 Key Terminology & Abbreviations

Emergency medicine uses a dense layer of abbreviations across triage, resuscitation, trauma, and disposition. A comprehensive list is provided in Section 50. Below are the foundational terms every EM reference requires:

ABCDEAirway, Breathing, Circulation, Disability, Exposure ACLSAdvanced Cardiovascular Life Support ATLSAdvanced Trauma Life Support BVMBag-valve-mask CPRCardiopulmonary resuscitation EDEmergency department ESIEmergency severity index FASTFocused Assessment with Sonography for Trauma GCSGlasgow Coma Scale IOIntraosseous MTPMassive transfusion protocol NIHSSNIH Stroke Scale ROSCReturn of spontaneous circulation RSIRapid sequence intubation STEMIST-elevation myocardial infarction

04 Acute Coronary Syndromes CV

ACS is a spectrum of acute myocardial ischemia ranging from unstable angina (UA) to non-ST-elevation MI (NSTEMI) to ST-elevation MI (STEMI). ACS is the leading cause of death worldwide and the most common high-acuity cardiac presentation in the ED. The critical ED task is rapid ECG interpretation (< 10 minutes from arrival) to identify STEMI, which requires emergent reperfusion.

ECG diagnosis and classification of acute coronary syndromes showing STEMI, NSTEMI, and unstable angina patterns
Figure 4 — ECG Classification of Acute Coronary Syndromes. Electrocardiographic patterns differentiating STEMI from NSTEMI and unstable angina. ST-segment elevation in contiguous leads is the hallmark of transmural ischemia requiring emergent reperfusion.

ACS Spectrum

EntityECGTroponinPathologyUrgency
Unstable AnginaNormal or ST depression/T-wave changesNegativePartial coronary occlusion, no necrosisAdmit, serial troponins, risk stratify
NSTEMIST depression, T-wave inversion, or non-specific changesElevatedPartial occlusion with myocardial necrosisAdmit, anticoagulate, cardiology consult, cath within 24–72 hrs
STEMI≥1 mm ST elevation in ≥2 contiguous leads (or new LBBB)Elevated (may be initially negative)Complete coronary occlusionEmergent PCI (door-to-balloon < 90 min) or thrombolytics (door-to-needle < 30 min)
12-lead ECG showing anterior STEMI with ST elevation in leads V1-V4
Figure 5 — Anterior STEMI on 12-Lead ECG. ST-segment elevation in the precordial leads (V1-V4) indicating LAD territory infarction. Anterior STEMI carries the highest risk of cardiogenic shock and ventricular arrhythmias.

STEMI Localization by ECG

Leads with ST ElevationTerritoryCulprit ArteryWatch For
V1–V4Anterior/LADLADLarge territory → cardiogenic shock, VT/VF
II, III, aVFInferiorRCA (85%) or LCxRight ventricular involvement (get V4R), bradycardia, avoid nitrates if RV infarct
I, aVL, V5–V6LateralLCxOften with inferior or anterior MI
V7–V9 (posterior leads)PosteriorRCA or LCxSuspect if prominent R wave + ST depression V1–V3 (mirror image)
12-lead ECG showing inferior STEMI with ST elevation in leads II, III, aVF
Figure 6 — Inferior STEMI on 12-Lead ECG. ST elevation in the inferior leads (II, III, aVF) indicating RCA or LCx occlusion. Always obtain right-sided leads (V4R) to assess for right ventricular involvement, which contraindicates nitroglycerin.

Initial ED Management of ACS

MONA (Morphine, Oxygen, Nitroglycerin, Aspirin) is the classic mnemonic but has evolved: Aspirin 325 mg chewed (non-enteric coated, immediate), Nitroglycerin 0.4 mg SL q5min × 3 (hold if SBP < 90, RV infarct, or PDE5 inhibitor within 24–48 hrs), heparin (UFH 60 U/kg bolus max 4000 U, then 12 U/kg/hr infusion; or enoxaparin 1 mg/kg SQ), P2Y12 inhibitor (clopidogrel 600 mg load or ticagrelor 180 mg load — check with interventional cardiologist before cath as some prefer to load in the lab). Oxygen only if SpO2 < 94%. Morphine with caution — may increase mortality in NSTEMI.

The HEART score (History, ECG, Age, Risk factors, Troponin) stratifies chest pain patients for 30-day MACE risk. Score 0–3: low risk (safe for early discharge); 4–6: moderate (observation, serial troponins); 7–10: high risk (admit, early invasive strategy). The HEART pathway has been validated in >10,000 patients (Than et al., Lancet 2019).

05 Acute Heart Failure & Pulmonary Edema CV

Acute decompensated heart failure (ADHF) presents as sudden or worsening dyspnea, orthopnea, and hypoxia from pulmonary venous congestion. The ED must rapidly distinguish cardiogenic pulmonary edema from pneumonia, COPD, and PE. BNP > 400 pg/mL (or NT-proBNP > 900 pg/mL) strongly supports HF; < 100 (< 300) makes it unlikely. CXR shows cephalization of vessels, Kerley B lines, bilateral pleural effusions, and perihilar edema ("butterfly" or "bat wing" pattern).

Doppler echocardiography showing respiratory variation in mitral and tricuspid valve flows indicating tamponade physiology
Figure 7 — Doppler Assessment in Pericardial Effusion. Doppler echocardiography demonstrating exaggerated respiratory variation in atrioventricular valve flow velocities, a hallmark of hemodynamically significant pericardial effusion and impending tamponade.

Acute Management

The mainstay is preload and afterload reduction, NOT fluid boluses. Nitroglycerin 400 mcg SL, then IV infusion 10–200 mcg/min (titrate to symptom relief and SBP > 100). Furosemide (Lasix) 40–80 mg IV (if on chronic diuretics, give ≥ home dose IV). BiPAP (CPAP 10–12 cmH2O or BiPAP 10/5) dramatically reduces work of breathing and intubation rates — start immediately in moderate-to-severe respiratory distress. For flash pulmonary edema with hypertension: aggressive nitroglycerin (high-dose bolus 2 mg IV followed by infusion) is highly effective.

Cardiogenic Shock

When ADHF progresses to cardiogenic shock (SBP < 90, signs of end-organ hypoperfusion, CI < 2.2 L/min/m²): start norepinephrine (first-line vasopressor per SOAP II trial) and dobutamine (5–20 mcg/kg/min for inotropy). Avoid fluids unless clear hypovolemia. Emergent cardiology consult for mechanical circulatory support (Impella, IABP, ECMO). Mortality exceeds 40%.

06 Aortic Dissection & Aortic Emergencies CV

Aortic dissection is a tear in the aortic intima allowing blood to enter the media, creating a false lumen. Mortality increases 1–2% per hour if untreated. Classic presentation: sudden-onset "tearing" or "ripping" chest/back pain that is maximal at onset, radiating to the back (descending) or anterior chest (ascending). Risk factors: uncontrolled hypertension, Marfan syndrome, bicuspid aortic valve, prior cardiac surgery, cocaine use.

Cross-sectional diagram of the aortic wall showing intima, media, and adventitia layers relevant to dissection pathology
Figure 8 — Structure of the Aortic Wall. The aortic wall consists of three layers: intima, media, and adventitia. Dissection occurs when blood enters through an intimal tear and tracks within the media, creating a false lumen that can propagate proximally or distally.

Stanford Classification

TypeInvolvementManagementMortality (untreated)
AAscending aorta involved (regardless of distal extent)Emergent open surgical repair~1–2% per hour for 48 hrs
BDescending aorta only (distal to left subclavian)Medical management (anti-impulse therapy); TEVAR if complicated~10% at 30 days with medical management
Stanford and DeBakey classification of aortic dissection showing Type A (ascending) and Type B (descending) dissections
Figure 9 — Stanford Classification of Aortic Dissection. Type A involves the ascending aorta (regardless of distal extent) and requires emergent surgical repair. Type B involves the descending aorta only and is typically managed medically unless complicated by malperfusion or rupture.

ED Management

Anti-impulse therapy: target HR < 60 bpm and SBP 100–120 mmHg. Start IV esmolol (500 mcg/kg bolus, then 50–200 mcg/kg/min) or labetalol (20 mg IV bolus, then 1–2 mg/min infusion). Beta-blocker FIRST — do not give vasodilators (nitroprusside, nicardipine) without beta-blockade, as reflex tachycardia increases aortic shear stress. Add nitroprusside (0.25–10 mcg/kg/min) only after HR is controlled. CTA chest/abdomen/pelvis is the gold-standard diagnostic study (sensitivity > 95%).

Physical exam clues: blood pressure differential > 20 mmHg between arms (subclavian involvement), new aortic regurgitation murmur (ascending dissection disrupting the valve), pulse deficits, malperfusion syndromes (stroke, limb ischemia, mesenteric ischemia, renal failure). D-dimer < 500 ng/mL has >95% negative predictive value and can help rule out dissection in lower-risk patients.

07 Cardiac Arrest & Post-Arrest Care CV

Cardiac arrest survival depends on the chain of survival: early recognition, early CPR, early defibrillation, and advanced resuscitation. Out-of-hospital cardiac arrest (OHCA) survival to discharge averages 10–12% nationally; in-hospital cardiac arrest (IHCA) survival is approximately 25%. Shockable rhythms (VF/pVT) carry significantly better prognosis than non-shockable (asystole/PEA).

Post-Arrest Care

Echocardiographic evaluation showing pericardial effusion with fluid surrounding the heart
Figure 10 — Echocardiographic Evaluation of Pericardial Effusion. Bedside echocardiography demonstrating pericardial fluid collection. The anechoic stripe surrounding the heart is the key diagnostic finding. Right ventricular diastolic collapse indicates tamponade physiology.

After ROSC, immediate priorities: 12-lead ECG (emergent cath if STEMI or high suspicion of coronary occlusion), targeted temperature management (TTM) — the TTM2 trial (2021) found no benefit of 33°C vs. 36°C, and current guidelines recommend maintaining temperature ≤ 37.5°C and actively preventing fever. Hemodynamic optimization: MAP > 65 mmHg (vasopressors as needed), avoid hypotension and hypoxia (target SpO2 94–98%, avoid hyperoxia). Neuroprognostication should be delayed ≥ 72 hours after rewarming — never withdraw care based on exam alone within the first 72 hours.

08 Arrhythmia Management CV

Tachyarrhythmias

RhythmECG FeaturesStable ManagementUnstable Management
SVT (AVNRT/AVRT)Narrow complex, regular, rate 150–250, no visible P wavesVagal maneuvers (modified Valsalva) → Adenosine 6 mg rapid IV push (may repeat 12 mg × 2)Synchronized cardioversion 50–100 J
AFib with RVRIrregularly irregular, narrow complex, no distinct P waves, rate > 100Rate control: diltiazem 0.25 mg/kg IV (15–20 mg) over 2 min, then 5–15 mg/hr infusion; or metoprolol 5 mg IV q5min × 3Synchronized cardioversion 120–200 J (biphasic)
AFlutterSawtooth pattern (leads II, III, aVF), rate usually 150 (2:1 block) or 75 (4:1)Rate control same as AFib; cardioversion very effective at low energySynchronized cardioversion 50–100 J
Monomorphic VTWide complex, regular, rate > 100, AV dissociationAmiodarone 150 mg IV over 10 min, then 1 mg/min × 6 hrs; or procainamide 20–50 mg/min until arrhythmia resolves (max 17 mg/kg)Synchronized cardioversion 100 J
Polymorphic VT (Torsades)Wide complex, undulating axis, often preceded by long QTMagnesium sulfate 2 g IV over 10 min; isoproterenol or overdrive pacingDefibrillation (unsynchronized) 120–200 J
Unstable = hypotension, altered mental status, ischemic chest pain, or acute heart failure. If the patient is unstable from any tachycardia, the answer is synchronized cardioversion (except pulseless VT/VF, which gets unsynchronized defibrillation).

Bradyarrhythmias

Symptomatic bradycardia (HR < 50 with hypotension, AMS, chest pain, or acute HF): Atropine 1 mg IV q3–5 min (max 3 mg) — will not work in Mobitz II or third-degree block (infranodal). If atropine fails: transcutaneous pacing (start at 60 mA, increase until capture, then add 10 mA safety margin; sedate the patient with fentanyl/midazolam). Dopamine infusion (5–20 mcg/kg/min) or epinephrine infusion (2–10 mcg/min) as bridge to transvenous pacing.

09 Hypertensive Emergencies CV

A hypertensive emergency is severely elevated BP (often > 180/120) with acute end-organ damage: encephalopathy, acute stroke, aortic dissection, acute MI, pulmonary edema, eclampsia, acute renal failure, or retinal hemorrhage. Hypertensive urgency is severely elevated BP without end-organ damage — manage with oral agents and outpatient follow-up; aggressive IV reduction is not indicated and may cause harm.

Treatment by End-Organ

ScenarioAgent of ChoiceBP Target
Aortic dissectionEsmolol or labetalol (beta-blocker first)SBP 100–120, HR < 60 within 20 min
Acute pulmonary edemaNitroglycerin infusion + furosemide25% reduction in MAP over 1 hr
Acute ischemic strokeNicardipine or labetalol< 185/110 if thrombolytic candidate; otherwise < 220/120
Hemorrhagic stroke (ICH)Nicardipine or clevidipineSBP < 140 (per INTERACT2)
EclampsiaMagnesium sulfate (seizure prevention) + labetalol or hydralazineSBP < 160, DBP < 110
Sympathomimetic crisis (cocaine)Benzodiazepines first, then nitroglycerin/phentolamine — avoid beta-blockersSymptom-guided

10 Pulmonary Embolism CV

PE is the third leading cause of cardiovascular death. The ED challenge is identifying PE among the high volume of patients with chest pain and dyspnea while avoiding unnecessary CT angiography. Risk stratification begins with clinical probability assessment.

CT pulmonary angiography showing pulmonary embolism with filling defects in the pulmonary arteries
Figure 11 — CT Pulmonary Angiography in Pulmonary Embolism. CTA demonstrating intraluminal filling defects within the pulmonary arteries, the gold-standard imaging finding for PE diagnosis. CTA has sensitivity exceeding 95% for clinically significant PE.

Wells Score for PE

CriterionPoints
Clinical signs/symptoms of DVT3.0
PE is #1 or equally likely diagnosis3.0
Heart rate > 1001.5
Immobilization (≥3 days) or surgery in prior 4 weeks1.5
Previous DVT/PE1.5
Hemoptysis1.0
Active cancer (treatment within 6 months or palliative)1.0

Score ≤4: PE unlikely → check D-dimer (if < 500 ng/mL, PE excluded). Score >4: PE likely → proceed to CTA. PERC rule: if clinical gestalt is "PE unlikely" AND all 8 PERC criteria are negative (age < 50, HR < 100, SpO2 ≥ 95%, no hemoptysis, no estrogen use, no prior DVT/PE, no unilateral leg swelling, no surgery/trauma requiring hospitalization in past 4 weeks), D-dimer is unnecessary — PE is effectively excluded.

CT showing right ventricular enlargement and strain in massive pulmonary embolism
Figure 12 — RV Strain Signs on CT in Pulmonary Embolism. CT angiography demonstrating right ventricular enlargement (RV/LV ratio > 1.0) and interventricular septal bowing, indicating hemodynamically significant PE with right heart strain.

Management by Severity

CategoryHemodynamicsRV StrainTreatment
Low-riskStableNoAnticoagulation (heparin → DOAC). Some qualify for outpatient treatment (Hestia criteria)
Submassive (intermediate-risk)StableYes (RV dilation on CT/echo, elevated troponin/BNP)Anticoagulation + close monitoring in ICU; consider catheter-directed therapy if decompensating
MassiveHemodynamically unstable (SBP < 90)YesSystemic thrombolytics (alteplase 100 mg IV over 2 hrs), surgical embolectomy, or catheter-directed therapy. Bolus fluids cautiously (250–500 mL — excessive fluids worsen RV)

11 Cardiac Tamponade CV

Pericardial fluid accumulation compressing the heart, impairing diastolic filling. The physiologic consequence is obstructive shock — reduced cardiac output despite adequate volume. Causes: malignancy (most common cause of large effusions), uremia, post-MI (Dressler syndrome), trauma (hemopericardium), aortic dissection (rupture into pericardium), infection (TB, viral). Beck's triad: hypotension, muffled heart sounds, JVD. Pulsus paradoxus > 10 mmHg (SBP drop with inspiration) is a key sign. Electrical alternans on ECG (beat-to-beat alternation in QRS amplitude) is specific but not sensitive.

Echocardiogram showing right ventricular diastolic collapse in cardiac tamponade
Figure 13 — Cardiac Tamponade: RV Diastolic Collapse. M-mode and 2D echocardiography demonstrating right ventricular diastolic collapse, the earliest echocardiographic sign of hemodynamically significant tamponade physiology requiring emergent pericardiocentesis.

Bedside echo is the diagnostic study of choice — pericardial effusion with RV diastolic collapse (earliest sign of tamponade physiology) and RA systolic collapse. Treatment: emergent pericardiocentesis (subxiphoid approach, ultrasound-guided, advance 18-gauge needle at 30–45° toward the left shoulder). Even removing 20–50 mL can dramatically improve hemodynamics. IV fluid bolus (500–1000 mL) as temporizing measure to increase preload. Traumatic tamponade often requires emergent thoracotomy rather than pericardiocentesis.

12 Acute Asthma & Status Asthmaticus Resp

Asthma exacerbation severity drives treatment intensity. Mild-moderate: speaks in sentences, RR < 30, SpO2 ≥ 90%, PEF > 50% predicted. Severe: speaks in words, RR > 30, accessory muscle use, SpO2 < 90%, PEF < 50%. Status asthmaticus: severe exacerbation refractory to initial bronchodilator therapy, representing a life-threatening emergency.

Stepwise ED Management

First-line: continuous nebulized albuterol (10–15 mg/hr) + ipratropium 0.5 mg nebulized q20min × 3. Corticosteroids early: prednisone 60 mg PO or methylprednisolone 125 mg IV (onset 4–6 hrs, but give early). Magnesium sulfate 2 g IV over 20 min for severe exacerbation (NNT = 4 for preventing admission). Epinephrine 0.3–0.5 mg IM for impending respiratory failure. For patients failing NIV: intubation is dangerous in status asthmaticus (post-intubation hypotension from air trapping — use ketamine for induction, permissive hypercapnia strategy, low RR 8–10, long expiratory time, I:E 1:4–1:5).

The "silent chest" is an ominous sign — absence of wheezing in a dyspneic asthmatic indicates such severe bronchospasm that there is insufficient airflow to generate wheezing. This patient is about to crash. Also monitor for paradoxical: a normal or rising pCO2 in acute asthma indicates respiratory muscle fatigue and impending arrest (a healthy asthmatic should be hyperventilating with a LOW pCO2).

13 COPD Exacerbation Resp

Acute worsening of respiratory symptoms (dyspnea, cough, sputum volume/purulence) beyond normal day-to-day variation requiring a change in medication. Most common triggers: viral/bacterial infection (60–80%), air pollution, PE, and pneumothorax. COPD patients live with chronic CO2 retention; their respiratory drive may be hypoxic rather than hypercarbic. Target SpO2 88–92% — excessive oxygen can worsen hypercapnia through the Haldane effect and V/Q mismatch redistribution.

Treatment

Bronchodilators: albuterol + ipratropium nebulized. Systemic corticosteroids: prednisone 40 mg PO × 5 days (or methylprednisolone IV). Antibiotics if purulent sputum or requiring mechanical ventilation: azithromycin 500 mg × 1 day then 250 mg × 4 days, or doxycycline 100 mg BID, or amoxicillin-clavulanate. BiPAP (IPAP 10–15 cmH2O, EPAP 5 cmH2O) is first-line for COPD exacerbation with respiratory acidosis (pH < 7.35, pCO2 > 45) — reduces intubation rate by 60% and mortality by 50% (Cochrane review).

14 Pneumonia (CAP, HAP, Aspiration) Resp

Community-acquired pneumonia (CAP) is the most common infectious cause of death in the US. Typical pathogens: S. pneumoniae (most common), H. influenzae, M. catarrhalis. Atypical: Mycoplasma, Chlamydophila, Legionella. Viral: influenza, RSV, SARS-CoV-2.

Severity & Disposition — CURB-65

CriterionDefinitionPoints
ConfusionNew mental confusion1
UreaBUN > 20 mg/dL1
Respiratory rate≥ 30 breaths/min1
Blood pressureSBP < 90 or DBP ≤ 601
Age≥ 65 years1

Score 0–1: outpatient. 2: consider short hospitalization. 3–5: admit, 4–5 consider ICU.

Empiric Antibiotic Regimens

SettingEmpiric Regimen
Outpatient (healthy, no comorbidities)Amoxicillin 1 g TID × 5 days; OR doxycycline 100 mg BID; OR azithromycin 500 mg day 1, then 250 mg × 4 days
Outpatient (comorbidities: DM, CKD, COPD, CHF)Amoxicillin-clavulanate 875/125 BID + azithromycin; OR respiratory fluoroquinolone (levofloxacin 750 mg daily)
Inpatient (non-ICU)Ceftriaxone 1–2 g IV daily + azithromycin 500 mg IV daily; OR levofloxacin 750 mg IV daily
Inpatient (ICU)Ceftriaxone 2 g IV + azithromycin 500 mg IV; add vancomycin + piperacillin-tazobactam if MRSA/Pseudomonas risk factors
Aspiration pneumoniaAmpicillin-sulbactam 3 g IV q6h; OR clindamycin 600 mg IV q8h + ceftriaxone (if community-acquired)

15 Pneumothorax Resp

Chest X-ray showing spontaneous pneumothorax with visible visceral pleural line and absent lung markings
Figure 14 — Pneumothorax on Chest Radiograph. Erect chest X-ray demonstrating a visible visceral pleural line with absent lung markings beyond the line, the classic radiographic finding of pneumothorax.

Types

TypeMechanismPresentationManagement
Simple spontaneous (primary)Rupture of apical bleb; tall, thin young malesAcute pleuritic chest pain, dyspnea, decreased breath sounds unilaterallySmall (< 2 cm apex-to-cupola): observe, supplemental O2. Large or symptomatic: aspiration or chest tube (pigtail 14 Fr or standard 20–24 Fr)
Secondary spontaneousUnderlying lung disease (COPD, CF, Marfan)More symptomatic due to reduced reserveLower threshold for chest tube; higher risk of recurrence
TensionOne-way valve mechanism; air accumulates under pressureHypotension, tracheal deviation (away), JVD, absent breath sounds, cardiac arrest (PEA)Immediate needle decompression (14-gauge needle, 2nd ICS midclavicular line or 5th ICS anterior axillary line) followed by chest tube
Open ("sucking chest wound")Penetrating trauma with persistent chest wall defectAir sucked in/out of wound with respirationThree-sided occlusive dressing (allows air out but not in) → chest tube remote from wound
Chest X-ray demonstrating tension pneumothorax with mediastinal shift, tracheal deviation, and flattened hemidiaphragm
Figure 15 — Tension Pneumothorax on Chest Radiograph. CXR showing complete lung collapse with contralateral mediastinal shift and tracheal deviation. Tension pneumothorax is a clinical diagnosis requiring immediate needle decompression; do not delay treatment for imaging.

16 Acute Respiratory Failure & Mechanical Ventilation Resp

Type I (hypoxemic): PaO2 < 60 mmHg on room air. Caused by V/Q mismatch, shunt, diffusion impairment (pneumonia, ARDS, PE, pulmonary edema). Type II (hypercapnic): PaCO2 > 50 mmHg with respiratory acidosis. Caused by alveolar hypoventilation (COPD, neuromuscular disease, drug overdose, obesity hypoventilation).

Initial Ventilator Settings (Post-Intubation)

ParameterARDS / Lung-ProtectiveObstructive (COPD/Asthma)
ModeVolume control (AC/VC)Volume control
Tidal Volume6–8 mL/kg ideal body weight6–8 mL/kg IBW
Rate14–208–12 (lower to allow exhalation)
FiO2Start 100%, wean to SpO2 92–96%Titrate to SpO2 88–92%
PEEPStart 5–10 cmH2O, titrate per ARDSNet PEEP/FiO2 tableLow (3–5 cmH2O, match auto-PEEP)
Plateau Pressure Goal< 30 cmH2O< 30 cmH2O; watch for auto-PEEP
Oxygen delivery and consumption relationship diagram showing the pathophysiology of septic shock and supply dependence
Figure 16 — DO2/VO2 Relationship in Septic Shock. The relationship between oxygen delivery (DO2) and oxygen consumption (VO2) in septic shock. Below a critical delivery threshold, consumption becomes supply-dependent, leading to tissue hypoxia and lactate production.

ARDSNet protocol (ARMA trial, NEJM 2000): low tidal volume ventilation (6 mL/kg IBW) reduces mortality by 22% in ARDS. Target plateau pressure < 30 cmH2O. Permissive hypercapnia acceptable (pH ≥ 7.20). Prone positioning for 16+ hrs/day in moderate-severe ARDS (P/F < 150) reduces mortality (PROSEVA trial).

17 Acute Ischemic Stroke Neuro

Stroke is a time-critical emergency — "time is brain." Approximately 1.9 million neurons are lost per minute during a large-vessel occlusion. The ED role is rapid recognition (NIHSS assessment), immediate CT to exclude hemorrhage, and initiation of reperfusion therapy within the time window.

CT imaging of acute ischemic stroke showing early ischemic changes and CT perfusion maps
Figure 17 — CT Imaging in Acute Ischemic Stroke. Non-contrast CT and CT perfusion imaging in acute ischemic stroke. CT perfusion maps (CBF, CBV, MTT, Tmax) delineate the ischemic core and salvageable penumbra, guiding reperfusion therapy decisions.

Reperfusion Windows

TherapyTime WindowEligibilityKey Details
IV alteplase (tPA)≤ 4.5 hours from last known wellAge ≥18, disabling deficit, no hemorrhage on CTDose: 0.9 mg/kg (max 90 mg), 10% bolus over 1 min, remainder over 60 min. BP must be < 185/110 before and < 180/105 for 24 hrs after. Exclusion: recent surgery, active bleeding, platelets < 100K, INR > 1.7
IV tenecteplase≤ 4.5 hoursEmerging as alternative to alteplase0.25 mg/kg single bolus (max 25 mg); easier administration, gaining guideline support
Mechanical thrombectomy≤ 24 hours (with imaging selection)Large-vessel occlusion (ICA, M1, M2 MCA), NIHSS ≥ 6, salvageable penumbra on CT perfusion/MRIExtended to 24 hrs by DAWN and DEFUSE-3 trials. NNT = 2.8 for functional independence
Stroke Mimics vs. Stroke

Common mimics: hypoglycemia (always check glucose before CT), Todd's paralysis (post-ictal), complex migraine, conversion disorder, brain tumor. CT head without contrast is the initial study — its primary role is to exclude hemorrhage, not to "see the stroke." Early ischemic changes are subtle (loss of gray-white differentiation, sulcal effacement, hyperdense vessel sign). CTA head and neck should be obtained simultaneously to identify large-vessel occlusion for thrombectomy candidacy.

18 Hemorrhagic Stroke (ICH & SAH) Neuro

CT head showing intracerebral hemorrhage with hyperdense blood in the basal ganglia region
Figure 18 — Hemorrhagic Stroke on CT Head. Non-contrast CT demonstrating hyperdense (bright white) intraparenchymal blood. CT is the first-line study in stroke to differentiate ischemic from hemorrhagic stroke, as the management differs fundamentally.

Intracerebral Hemorrhage (ICH)

Spontaneous ICH accounts for 10–15% of all strokes but carries 40–50% 30-day mortality. Most common cause: hypertensive arteriopathy (deep structures: basal ganglia, thalamus, pons, cerebellum). Other causes: cerebral amyloid angiopathy (lobar hemorrhages in elderly), anticoagulant use, vascular malformations, hemorrhagic conversion of ischemic stroke. CT head shows hyperdense (bright white) intraparenchymal blood.

Management: aggressive BP control (SBP target < 140 mmHg within 1 hr — INTERACT2; use nicardipine infusion). Reverse anticoagulation immediately if applicable (warfarin → 4-factor PCC + vitamin K 10 mg IV; DOAC → idarucizumab for dabigatran, andexanet alfa for Xa inhibitors, or 4-factor PCC if specific reversal unavailable). Neurosurgery consult for cerebellar hemorrhage > 3 cm (may need emergent evacuation) or hydrocephalus (EVD placement).

CT head scan showing subarachnoid hemorrhage with hyperdense blood in the basal cisterns and Sylvian fissures
Figure 19 — Subarachnoid Hemorrhage on CT Head. Non-contrast CT showing hyperdense blood in the basal cisterns, Sylvian fissures, and interhemispheric fissure, the classic distribution of aneurysmal SAH. CT sensitivity is highest within 6 hours of onset.

Subarachnoid Hemorrhage (SAH)

85% from ruptured cerebral aneurysm. Classic presentation: "worst headache of my life," sudden onset, maximal intensity at onset ("thunderclap headache"), with or without neck stiffness, photophobia, vomiting, syncope, or coma. CT head sensitivity: 95–100% within 6 hours, drops to ~85% at 24 hours and further with time. If CT is negative and clinical suspicion remains: lumbar puncture looking for xanthochromia (yellow discoloration of CSF from bilirubin, most reliable at 12+ hours after onset) or elevated RBCs that do not clear with sequential tubes.

After SAH diagnosis: CTA to locate the aneurysm, neurosurgery/neurointerventional consult for definitive treatment (endovascular coiling preferred over surgical clipping for most aneurysms per ISAT trial). Nimodipine 60 mg PO q4h × 21 days (prevents vasospasm-related delayed cerebral ischemia — the only medication proven to improve outcomes in SAH). Keep SBP < 160 until aneurysm secured.

Diagnostic algorithm for subarachnoid hemorrhage evaluation in patients presenting with thunderclap headache
Figure 20 — SAH Diagnostic Algorithm. Algorithmic approach to evaluating suspected subarachnoid hemorrhage, from initial CT through lumbar puncture and CTA. A systematic approach prevents missed diagnosis of this potentially fatal condition.

19 Status Epilepticus Neuro

Defined as continuous seizure activity lasting ≥ 5 minutes or ≥ 2 seizures without return to baseline. A true time-critical neurological emergency — prolonged seizure activity causes excitotoxic neuronal injury, rhabdomyolysis, hyperthermia, and systemic acidosis. Mortality approaches 20% and increases with duration of seizure.

Stepwise Treatment Protocol

StageTimingIntervention
1st line0–5 minBenzodiazepines: lorazepam 0.1 mg/kg IV (max 4 mg, may repeat ×1) OR midazolam 10 mg IM (if no IV). Prehospital: diazepam 20 mg rectal or midazolam 10 mg IM/intranasal
2nd line5–20 minIf seizures persist after 2 doses of benzodiazepine: fosphenytoin 20 mg PE/kg IV (rate ≤ 150 mg PE/min); OR levetiracetam (Keppra) 60 mg/kg IV (max 4500 mg) over 15 min; OR valproic acid 40 mg/kg IV (max 3000 mg) over 10 min
Refractory> 20 minIntubation + continuous IV infusion: propofol (1–2 mg/kg bolus, 20–80 mcg/kg/min), midazolam (0.2 mg/kg bolus, 0.1–2 mg/kg/hr), or pentobarbital (5 mg/kg load, 1–5 mg/kg/hr). Continuous EEG monitoring required
Always check glucose, electrolytes (Na, Ca, Mg), and toxic screen in all seizing patients. Hypoglycemia and hyponatremia are rapidly reversible causes. For eclamptic seizures: magnesium sulfate 4–6 g IV is the agent of choice, not standard antiepileptics.

20 Meningitis & Encephalitis Neuro

Bacterial meningitis carries 20–25% mortality even with treatment and requires emergent antibiotics — do not delay for LP or imaging. Classic triad: fever, nuchal rigidity, altered mental status (present in only ~44% of bacterial meningitis). Kernig's sign (pain with knee extension when hip flexed) and Brudzinski's sign (involuntary hip flexion with passive neck flexion) have low sensitivity but moderate specificity.

Empiric Antibiotics by Age

Age GroupCommon PathogensEmpiric Regimen
< 1 monthGBS, E. coli, ListeriaAmpicillin + cefotaxime (or gentamicin)
1–23 monthsS. pneumoniae, N. meningitidis, GBSVancomycin + ceftriaxone (or cefotaxime)
2–50 yearsS. pneumoniae, N. meningitidisVancomycin + ceftriaxone
> 50 years or immunocompromisedS. pneumoniae, N. meningitidis, ListeriaVancomycin + ceftriaxone + ampicillin (Listeria coverage)

Dexamethasone 0.15 mg/kg IV q6h × 4 days — give with or just before the first antibiotic dose. Reduces mortality and neurological sequelae in pneumococcal meningitis (de Gans et al., NEJM 2002).

LP Interpretation

ParameterBacterialViralTB/Fungal
Opening pressureElevated (> 25 cmH2O)Normal to mildly elevatedElevated
WBC1000–10,000+ (PMN predominant)10–500 (lymphocyte predominant)100–500 (lymphocyte predominant)
GlucoseLow (< 40 or CSF:serum < 0.4)NormalLow
ProteinHigh (> 250 mg/dL)Normal to mildly elevatedHigh
Gram stainPositive in 60–90%NegativeAFB smear (low sensitivity)

21 Spinal Cord Compression Neuro

Acute spinal cord compression is a neurosurgical/oncologic emergency. Most common cause: metastatic disease (breast, lung, prostate account for >50%). Other causes: epidural abscess, disk herniation, epidural hematoma. Presentation: progressive back pain (often the first symptom, present for weeks before neurological deficits), bilateral leg weakness, sensory level, urinary retention or incontinence. A sensory level (loss of sensation below a dermatomal line) is highly specific for cord compression.

CT and CT angiography showing middle cerebral artery occlusion with hyperdense vessel sign and loss of gray-white differentiation
Figure 21 — Large Vessel Occlusion Imaging. CT and CTA demonstrating middle cerebral artery territory ischemia. The hyperdense vessel sign on non-contrast CT and vessel cutoff on CTA identify large vessel occlusions amenable to mechanical thrombectomy.

Diagnosis: MRI of the entire spine (urgent, within hours). Treatment: dexamethasone 10 mg IV bolus followed by 4 mg IV q6h (reduces cord edema). Urgent neurosurgery or radiation oncology consult for surgical decompression vs. radiation therapy. Functional outcomes correlate directly with neurological status at the time of treatment — ambulatory patients have >80% chance of remaining ambulatory; paraplegic patients have <10% chance of walking again.

22 Traumatic Brain Injury Trauma

Glasgow Coma Scale (GCS)

ComponentResponseScore
Eye Opening (E)Spontaneous4
To voice3
To pain2
None1
Verbal (V)Oriented5
Confused4
Inappropriate words3
Incomprehensible sounds2
None1
Motor (M)Obeys commands6
Localizes pain5
Withdrawal (flexion)4
Abnormal flexion (decorticate)3
Extension (decerebrate)2
None1

GCS 13–15: mild TBI; 9–12: moderate; 3–8: severe (intubate for airway protection). The motor score is the single most predictive component.

CT head showing multiple cerebral contusions with hemorrhagic foci in the temporal and frontal lobes
Figure 22 — Cerebral Contusions on CT Head. CT demonstrating hemorrhagic contusions, typically located in the inferior frontal and anterior temporal lobes where the brain impacts bony ridges. Contusions can expand significantly in the first 24-48 hours, requiring serial imaging.
CT head showing epidural hematoma with characteristic biconvex lens-shaped hyperdense collection
Figure 23 — Epidural Hematoma on CT Head. CT demonstrating the classic biconvex (lens-shaped) hyperdense collection between the skull and dura mater, typically from rupture of the middle meningeal artery. Epidural hematomas classically present with a lucid interval followed by rapid deterioration.

Herniation Syndromes

Signs of herniation: unilateral fixed, dilated pupil (CN III compression from uncal herniation), Cushing's triad (hypertension, bradycardia, irregular respirations — a late and ominous sign), decerebrate posturing. Emergency management of herniation: elevate HOB 30°, mannitol 1–1.5 g/kg IV (osmotic diuresis) or hypertonic saline 3% 250 mL or 23.4% 30 mL IV over 15 min, hyperventilation to pCO2 30–35 mmHg (temporizing only — causes vasoconstriction reducing ICP but also reducing cerebral perfusion), emergent neurosurgery consult for decompressive craniectomy.

CT head showing acute subdural hematoma with crescent-shaped hyperdense collection and midline shift
Figure 24 — Acute Subdural Hematoma on CT Head. CT demonstrating a crescent-shaped hyperdense collection conforming to the cerebral convexity, with associated midline shift and effacement of sulci indicating mass effect. Subdural hematomas requiring surgery have mortality exceeding 50%.
CT head showing transtentorial herniation with uncal herniation, midline shift, and effacement of basal cisterns
Figure 25 — Transtentorial Herniation on CT. CT findings of uncal herniation including midline shift, effacement of the basal cisterns, and compression of the brainstem. These findings demand emergent osmotherapy and neurosurgical consultation for decompressive craniectomy.

Canadian CT Head Rule

For minor head injury (GCS 13–15) — CT is required if ANY of the following are present:

High Risk (for neurosurgical intervention)Medium Risk (for brain injury on CT)
GCS < 15 at 2 hours post-injuryRetrograde amnesia > 30 min before impact
Suspected open or depressed skull fractureDangerous mechanism (pedestrian struck, ejected from vehicle, fall > 3 feet / 5 stairs)
Any sign of basal skull fracture (hemotympanum, raccoon eyes, Battle's sign, CSF otorrhea/rhinorrhea)
≥ 2 episodes of vomiting
Age ≥ 65

23 Cervical Spine Injury Trauma

The ED must identify or confidently exclude c-spine injury in every trauma patient. Clinical decision rules allow safe clearance without imaging in low-risk patients.

CT cervical spine showing various types of cervical fractures in sagittal and axial views
Figure 26 — Cervical Spine Fractures on CT. Multiplanar CT images demonstrating cervical spine fractures. CT with sagittal and coronal reformats is the imaging modality of choice for cervical spine evaluation in trauma, offering superior sensitivity over plain radiographs.

NEXUS Criteria & Canadian C-Spine Rule

NEXUS: C-spine imaging NOT needed if ALL 5 criteria met: no posterior midline tenderness, no focal neurological deficit, normal alertness, no intoxication, no distracting injury. Canadian C-Spine Rule (more sensitive than NEXUS): Step 1 — any high-risk factor mandating imaging? (age ≥ 65, dangerous mechanism, paresthesias in extremities). If yes → image. Step 2 — any low-risk factor allowing safe ROM assessment? (simple rear-end MVC, sitting in ED, ambulatory at any time, delayed onset neck pain, no midline tenderness). If yes → Step 3: can patient actively rotate neck 45° left and right? If yes → no imaging needed.

CT showing odontoid (dens) fracture of C2 vertebra in sagittal and coronal views
Figure 27 — Odontoid Fracture on CT. CT imaging of the C2 odontoid process (dens) fracture. Type II fractures at the base of the dens are the most common and most unstable, particularly prevalent in elderly patients following falls.

High-Yield C-Spine Injuries

InjuryMechanismLevelKey Point
Atlas (C1) fracture (Jefferson)Axial loading (diving)C1Lateral mass spread on open-mouth view; usually stable
Odontoid (dens) fractureFlexion/extensionC2Type II (base of dens) most common and most unstable; common in elderly falls
Hangman's fractureHyperextension + axial loadC2 pediclesBilateral pars fracture; often paradoxically stable (spinal canal widened)
Facet dislocationFlexion-rotationSubaxial (C3–C7)Unilateral: 25% subluxation; Bilateral: 50% subluxation with high SCI risk
SCIWORAFlexion/extension in childrenAnySpinal cord injury without radiographic abnormality; MRI required. More common in pediatric patients due to ligamentous laxity

24 Chest Trauma Trauma

CT pulmonary angiography demonstrating various PE presentations including central, segmental, and subsegmental emboli
Figure 28 — Pulmonary Embolism: Spectrum of CT Findings. CTA images showing different presentations of PE from central (saddle) emboli to segmental and subsegmental filling defects. The clot burden and presence of right heart strain determine clinical severity and treatment approach.

Chest trauma is responsible for 25% of trauma deaths. Most life-threatening injuries can be identified on primary survey and CXR. The "deadly dozen" includes tension PTX, open PTX, massive hemothorax, flail chest, cardiac tamponade, and tracheobronchial disruption (identified during primary survey), plus aortic injury, diaphragmatic rupture, esophageal perforation, pulmonary contusion, myocardial contusion, and simple PTX/hemothorax (identified during secondary survey).

Key Chest Trauma Entities

InjuryDiagnosisManagement
Massive hemothorax (>1500 mL initial or >200 mL/hr × 2–4 hrs)CXR: opacification of hemithorax; absent breath sounds, dullness to percussion, hypotensionChest tube (36–40 Fr) + autotransfusion; if criteria met → emergent thoracotomy
Flail chest (≥3 consecutive ribs fractured in ≥2 places)Paradoxical chest wall movement, crepitus, severe painPain control (epidural or intercostal nerve block), positive-pressure ventilation if respiratory failure; underlying pulmonary contusion is the real threat
Blunt cardiac injury (BCI)Sternal fracture, ECG changes (new RBBB, ST changes), elevated troponinMonitoring, treat arrhythmias; echocardiography if hemodynamically significant; rarely causes tamponade
Traumatic aortic injuryWidened mediastinum on CXR; confirmed by CTA (intimal flap at aortic isthmus distal to left subclavian)HR/BP control (same as dissection), emergent TEVAR or open repair. 85% die at scene; of survivors, 50% die within 24 hrs without repair

25 Abdominal Trauma & FAST Exam Trauma

FAST exam probe positions and ultrasound windows including RUQ, LUQ, suprapubic, and subxiphoid views
Figure 29 — FAST Exam Probe Positions and Views. The four standard FAST exam windows: right upper quadrant (Morison's pouch), left upper quadrant (splenorenal recess), suprapubic (pelvis), and subxiphoid (pericardium). The FAST exam rapidly detects free intraperitoneal fluid in the trauma bay.

Blunt abdominal trauma: spleen is the most commonly injured solid organ (left-sided mechanism), followed by liver (right-sided). In penetrating trauma, liver is most commonly injured (stab wounds), followed by small bowel (gunshot wounds). The FAST exam (Focused Assessment with Sonography for Trauma) is performed in the resuscitation bay to detect free fluid (blood) in four windows: RUQ (Morison's pouch — most sensitive for free fluid), LUQ (splenorenal recess), suprapubic (pelvis), and subxiphoid (pericardial). FAST is 85–95% sensitive for significant hemoperitoneum.

Positive FAST exam showing free fluid in Morison's pouch between liver and right kidney
Figure 30 — Positive FAST Exam: RUQ View (Morison's Pouch). Ultrasound demonstrating anechoic free fluid (blood) in the hepatorenal recess (Morison's pouch), the most sensitive location for detecting hemoperitoneum on the FAST exam.

Management Algorithm

Hemodynamically unstable + positive FAST: emergent exploratory laparotomy. Hemodynamically stable + positive FAST or high-energy mechanism: CT abdomen/pelvis with IV contrast for injury grading. FAST negative + stable: serial exams; CT if clinical concern persists (FAST misses retroperitoneal, hollow viscus, and diaphragm injuries).

Splenic Injury Grading (AAST)

GradeInjuryManagement
ISubcapsular hematoma < 10% surface; capsular laceration < 1 cmNon-operative (observation, serial exams, Hgb q6h)
IISubcapsular 10–50%; intraparenchymal < 5 cm; laceration 1–3 cmNon-operative in most stable patients
IIISubcapsular > 50% or expanding; intraparenchymal > 5 cm; laceration > 3 cmNon-operative with angioembolization vs. operative (patient-dependent)
IVLaceration involving segmental or hilar vessels; >25% devascularizedAngioembolization or splenectomy
VShattered spleen or hilar vascular injury with complete devascularizationSplenectomy

26 Pelvic Fracture & Hemorrhage Trauma

CT cervical spine showing facet dislocation with subluxation and spinal canal compromise
Figure 31 — Cervical Facet Dislocation on CT. CT demonstrating facet joint dislocation with vertebral subluxation. Bilateral facet dislocations cause approximately 50% subluxation with high risk of spinal cord injury requiring emergent reduction.

Unstable pelvic fractures (open-book, vertical shear) can cause massive hemorrhage from the presacral venous plexus and pelvic arterial branches, with blood loss exceeding 3–5 liters. Mechanism: high-energy (MVC, motorcycle, pedestrian struck, fall from height). Exam: pelvic instability on gentle AP compression (perform ONCE — repeated rocking worsens hemorrhage). Do NOT perform a rocking exam if instability is obvious or if a pelvic binder is already in place.

Management: pelvic binder (commercially available or bedsheet wrapped tightly at the level of the greater trochanters) to reduce pelvic volume and tamponade hemorrhage. Activate MTP. If hemodynamically unstable despite binder + MTP: angioembolization (if CTA shows arterial blush) or preperitoneal pelvic packing (direct surgical packing of the pelvic space). REBOA (Resuscitative Endovascular Balloon Occlusion of the Aorta) in Zone III (infrarenal) is an emerging temporizing measure.

27 Orthopedic Emergencies Trauma

Open Fractures — Gustilo-Anderson Classification

TypeWound SizeSoft Tissue InjuryContaminationAntibiotic
I< 1 cmMinimalCleanCefazolin 2 g IV
II1–10 cmModerateModerateCefazolin 2 g IV
IIIA> 10 cmExtensive, adequate coverageHighCefazolin + gentamicin
IIIB> 10 cmExtensive, requires flap coverageHighCefazolin + gentamicin
IIICAnyVascular injury requiring repairAnyCefazolin + gentamicin + PCN if soil contamination

All open fractures need: tetanus prophylaxis, IV antibiotics within 1 hour, irrigation and debridement in the OR (ideally within 6–24 hours), and orthopedic consult.

Cross-sectional anatomy of the lower leg showing the four fascial compartments involved in compartment syndrome
Figure 32 — Lower Leg Compartments and Compartment Syndrome. Cross-sectional anatomy of the lower leg showing the four fascial compartments (anterior, lateral, superficial posterior, deep posterior). Elevated pressure within any compartment compromises perfusion, requiring emergent fasciotomy.

Compartment Syndrome

Elevated pressure within a closed fascial compartment compromising perfusion. Most common after tibial fractures, crush injuries, and reperfusion after vascular repair. The 6 P's (Pain out of proportion, Pain with passive stretch — the earliest and most reliable sign, Paresthesias, Pressure/tense compartment, Pallor, Pulselessness — a LATE finding). Normal compartment pressure: 0–8 mmHg. Delta pressure (diastolic BP minus compartment pressure) < 30 mmHg = fasciotomy indicated. Treatment: emergent fasciotomy. Delay beyond 6–8 hours causes irreversible muscle necrosis and Volkmann's contracture.

High-Risk Dislocations

JointDirectionNeurovascular RiskUrgency
Shoulder (anterior, 95%)Anterior-inferiorAxillary nerve (deltoid weakness, lateral shoulder numbness)Reduce promptly; pre/post reduction neurovascular exam mandatory
Hip (posterior, 90%)PosteriorSciatic nerve; AVN risk increases after 6 hrsReduce within 6 hours to prevent femoral head AVN
KneeAnterior or posteriorPopliteal artery injury in 30–40%; peroneal nerveVascular emergency: reduce immediately, ABI, CTA if any concern for vascular injury
Lunate/perilunate (wrist)Volar (lunate) or dorsal (perilunate)Median nerve (carpal tunnel)Often missed on initial X-ray; look for "spilled teacup" sign on lateral

28 Acute Abdomen & Imaging Approach GI

The "acute abdomen" is not a diagnosis but a clinical presentation: acute abdominal pain requiring urgent evaluation and often intervention. The ED approach centers on identifying surgical emergencies (appendicitis, perforated viscus, bowel obstruction, mesenteric ischemia, ruptured AAA, ectopic pregnancy) and time-critical medical conditions (DKA, ACS with epigastric pain, adrenal crisis).

Abdominal Pain Differential by Location

LocationKey Diagnoses
RUQCholecystitis, hepatitis, Fitz-Hugh-Curtis, hepatic abscess, RLL pneumonia, nephrolithiasis
LUQSplenic pathology (infarct, rupture), gastric ulcer, pancreatitis (tail), LLL pneumonia
RLQAppendicitis, ovarian torsion/cyst, ectopic pregnancy, Meckel's, inguinal hernia, mesenteric adenitis
LLQDiverticulitis, ovarian torsion/cyst, ectopic pregnancy, sigmoid volvulus, inguinal hernia
EpigastricPeptic ulcer, pancreatitis, ACS (inferior MI), AAA, gastritis, biliary disease
PeriumbilicalEarly appendicitis (visceral pain), SBO, mesenteric ischemia, AAA
SuprapubicUTI, urinary retention, ovarian torsion, ectopic pregnancy, PID
DiffusePeritonitis (any cause), DKA, mesenteric ischemia, SBO, IBD flare
In every woman of reproductive age with abdominal pain: obtain a pregnancy test before imaging. Ectopic pregnancy is the most dangerous missed diagnosis in this population. Ruptured ectopic is a surgical emergency with potentially fatal hemorrhage.

29 Appendicitis & Cholecystitis GI

Appendicitis

Lifetime incidence 7–8%. Classic presentation: periumbilical pain migrating to RLQ (visceral → somatic pain as inflammation reaches the parietal peritoneum), anorexia, nausea/vomiting, low-grade fever. McBurney's point tenderness (1/3 of the distance from ASIS to umbilicus). Special signs: Rovsing's (RLQ pain with LLQ palpation), psoas sign (pain with right hip extension — retrocecal appendix), obturator sign (pain with internal rotation of flexed right hip — pelvic appendix).

Diagnosis: CT abdomen/pelvis with IV contrast is the gold standard (sensitivity 98%). Ultrasound is first-line in pregnant patients and children. Alvarado (MANTRELS) score: Migration, Anorexia, Nausea, Tenderness (RLQ), Rebound, Elevation of temperature, Leukocytosis, Shift to left; score ≥7 strongly suggests appendicitis. Treatment: appendectomy (laparoscopic preferred). Antibiotics alone are an option for uncomplicated appendicitis in selected patients (CODA trial), though recurrence rate is ~30% at 2 years.

Acute Cholecystitis

Gallstone impacted in the cystic duct causing gallbladder inflammation. Presentation: persistent RUQ pain (>4–6 hrs, distinguishing it from biliary colic which resolves), fever, Murphy's sign (inspiratory arrest during RUQ palpation). Diagnosis: RUQ ultrasound showing gallstones + gallbladder wall thickening > 3 mm + pericholecystic fluid + sonographic Murphy's sign. HIDA scan if ultrasound equivocal (non-filling of gallbladder = cystic duct obstruction). Treatment: NPO, IV fluids, antibiotics (piperacillin-tazobactam or ceftriaxone + metronidazole), surgical consult for cholecystectomy (ideally within 72 hours of admission).

30 Bowel Obstruction & Mesenteric Ischemia GI

Small Bowel Obstruction (SBO)

Causes: adhesions from prior surgery (75%), hernias (15%), malignancy, Crohn's disease, volvulus. Presentation: crampy abdominal pain, nausea/vomiting (earlier and more profuse in proximal obstruction), obstipation/constipation, distension. X-ray: dilated small bowel loops (> 3 cm), air-fluid levels, decompressed colon. CT with IV and oral contrast is the definitive study — identifies transition point, closed-loop obstruction, and signs of strangulation (mesenteric haziness, wall thickening, reduced enhancement, pneumatosis).

Treatment: NGT decompression (Salem sump), IV fluids, NPO, electrolyte correction. Surgery if: signs of strangulation/ischemia, closed-loop obstruction, peritonitis, complete obstruction without improvement in 48–72 hours, or incarcerated hernia.

Mesenteric Ischemia

Acute mesenteric ischemia is a surgical emergency with 60–80% mortality. The hallmark: "pain out of proportion to exam" — severe abdominal pain with a benign abdominal examination (early). As bowel infarction develops: peritoneal signs, bloody stool, lactic acidosis. Causes: SMA embolism (~50%), SMA thrombosis (~25%), NOMI (~15%), mesenteric venous thrombosis (~10%). CTA is diagnostic (filling defects, bowel wall changes). Treatment: heparin, emergent surgical embolectomy or revascularization, bowel resection if necrotic; second-look laparotomy at 24–48 hours.

31 GI Hemorrhage GI

Upper GI Bleeding (UGIB)

Source proximal to the ligament of Treitz. Presentation: hematemesis (bright red or coffee-ground emesis), melena (black tarry stool), or hematochezia (if massive). Most common causes: peptic ulcer disease (35–50%), esophageal/gastric varices (10–20%), Mallory-Weiss tear, erosive gastritis/esophagitis. Glasgow-Blatchford Score (GBS): BUN, hemoglobin, SBP, HR, melena, syncope, hepatic disease, heart failure. Score 0–1: safe for outpatient management. Score ≥6: high risk, needs intervention.

Management: 2 large-bore IVs, fluid resuscitation, type and cross. Restrictive transfusion (Hgb target ≥ 7 g/dL, ≥ 8 if active CAD per Villanueva et al., NEJM 2013). PPI: pantoprazole 80 mg IV bolus, then 8 mg/hr infusion for suspected ulcer bleeding. EGD within 24 hours (12 hours if high-risk features). Variceal bleed: octreotide 50 mcg IV bolus then 50 mcg/hr, antibiotics (ceftriaxone 1 g IV), urgent EGD for band ligation. If uncontrolled variceal bleeding: Blakemore/Minnesota tube or TIPS.

Lower GI Bleeding (LGIB)

Source distal to ligament of Treitz. Presentation: hematochezia (bright red blood per rectum). Common causes: diverticular bleeding (most common cause of massive LGIB), hemorrhoids, AV malformations, colitis (IBD, ischemic, infectious), colorectal cancer. Most LGIB stops spontaneously (80–85%). Hemodynamically significant LGIB: resuscitate, CTA if unstable (identifies active extravasation/source), colonoscopy within 24 hours if stabilized.

32 Pancreatitis GI

Diagnosis requires 2 of 3: (1) characteristic abdominal pain (epigastric, radiating to back, worse after eating), (2) serum lipase ≥ 3× upper limit of normal, (3) imaging findings (CT showing pancreatic edema/necrosis/peripancreatic stranding). Lipase is preferred over amylase (more sensitive and specific, stays elevated longer). Most common causes: gallstones (40%) and alcohol (30%). Other: hypertriglyceridemia (> 1000 mg/dL), post-ERCP, medications (valproic acid, azathioprine), autoimmune.

Management: aggressive IV fluid resuscitation (LR preferred, 1.5 mL/kg/hr for 24 hrs per WATERFALL trial — though subsequent evidence favors moderate resuscitation), pain control (IV opioids, NSAIDs), early enteral nutrition (within 24 hrs if tolerated — no need to wait for pain resolution). CT is NOT needed at presentation unless the diagnosis is uncertain or complications are suspected. CT should be obtained at 48–72 hours if not improving to assess for necrosis. Ranson's criteria and BISAP score predict severity. Gallstone pancreatitis requires cholecystectomy during the same admission (to prevent recurrence).

33 Sepsis & Septic Shock Infxn

Clinical criteria for sepsis and septic shock definitions showing SOFA score, qSOFA, and diagnostic criteria
Figure 33 — Sepsis-3 Clinical Criteria and Definitions. Diagnostic framework for sepsis and septic shock per the 2016 Sepsis-3 definitions. Sepsis requires suspected infection plus acute organ dysfunction (SOFA increase of 2 or more points). Septic shock adds vasopressor requirement and lactate > 2 mmol/L.

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection. The Sepsis-3 (2016) definition requires suspected infection + acute change in SOFA score ≥ 2 points. qSOFA (quick bedside screen): RR ≥ 22, altered mentation, SBP ≤ 100. Two or more qSOFA criteria should prompt further evaluation. Septic shock: sepsis + vasopressor requirement to maintain MAP ≥ 65 + lactate > 2 mmol/L despite adequate fluid resuscitation. Septic shock mortality: 30–40%.

Hour-1 Bundle (Surviving Sepsis Campaign 2021)

InterventionDetails
Measure lactateIf lactate > 2 mmol/L, remeasure within 2–4 hours to guide resuscitation
Blood cultures before antibioticsAt least 2 sets (aerobic + anaerobic) from different sites; do NOT delay antibiotics for cultures
Broad-spectrum antibioticsWithin 1 hour of sepsis recognition. Common regimens: vancomycin + piperacillin-tazobactam; or vancomycin + cefepime; or meropenem for critically ill
IV fluids30 mL/kg crystalloid (LR preferred over NS) for hypotension or lactate ≥ 4 mmol/L. Reassess after each bolus; do NOT give all 30 mL/kg blindly if patient develops volume overload
VasopressorsIf hypotension persists after initial fluid resuscitation: norepinephrine is first-line (start 5–10 mcg/min, titrate to MAP ≥ 65). Add vasopressin 0.04 units/min as second-line. Consider hydrocortisone 200 mg/day IV if shock refractory to vasopressors
Every hour of delay in appropriate antibiotic administration increases mortality by approximately 4–8% in septic shock. Source control (drainage of abscess, removal of infected device, debridement of necrotic tissue) is equally important and should be achieved within 6–12 hours when feasible.

34 Skin & Soft Tissue Infections Infxn

CT imaging of necrotizing fasciitis showing soft tissue gas tracking along fascial planes
Figure 34 — Necrotizing Fasciitis: CT Imaging. CT demonstrating gas within the soft tissues tracking along fascial planes, a specific but not sensitive finding in necrotizing fasciitis. CT sensitivity is approximately 93% for necrotizing soft tissue infections.

Spectrum of SSTIs

EntityDescriptionTreatment
Cellulitis (non-purulent)Spreading erythema, warmth, tenderness without drainable collection; typically beta-hemolytic strepMild: cephalexin 500 mg QID or amoxicillin-clavulanate. Moderate/severe: cefazolin 1–2 g IV q8h or ceftriaxone 1 g IV daily. Mark borders with pen to track progression
Abscess (purulent)Fluctuant, tender collection; often CA-MRSAI&D is the primary treatment. Antibiotics for surrounding cellulitis, systemic symptoms, or high-risk patients: TMP-SMX DS BID or doxycycline 100 mg BID × 7–10 days
Necrotizing fasciitisRapidly progressive deep infection destroying fascia and subcutaneous tissue. Pain out of proportion, crepitus, skin necrosis, bullae, "dishwater" gray drainage, systemic toxicityEmergent surgical debridement + broad-spectrum antibiotics (vancomycin + piperacillin-tazobactam + clindamycin for toxin suppression). CT showing gas in soft tissue is specific but not sensitive. LRINEC score ≥6 suggests necrotizing infection
Red Flags for Necrotizing Fasciitis

Pain out of proportion to visible findings, rapid progression despite antibiotics, bullae/skin necrosis, crepitus on palpation, systemic toxicity (fever, tachycardia, hypotension), WBC > 15,000 or < 4,000, elevated CK. If suspected, do NOT delay surgical consult for imaging. Mortality exceeds 30% even with treatment; approaches 100% without surgery.

35 Toxidrome Recognition & General Approach Tox

A toxidrome is a constellation of signs and symptoms that suggests a particular class of poisoning. Recognizing the toxidrome narrows the differential immediately and guides empiric treatment before confirmatory labs return.

ToxidromeVital SignsPupilsKey FindingsAgentsAntidote
SympathomimeticHypertension, tachycardia, hyperthermiaMydriasisAgitation, diaphoresis, tremor, seizuresCocaine, amphetamines, MDMA, synthetic cathinonesBenzodiazepines (primary treatment); avoid beta-blockers with cocaine
AnticholinergicTachycardia, hyperthermia, hypertensionMydriasis"Hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter." Dry skin, urinary retention, ileus, deliriumDiphenhydramine, TCAs, atropine, jimsonweed, scopolaminePhysostigmine 1–2 mg IV slow push (for pure anticholinergic; avoid in TCA overdose)
CholinergicBradycardia, hypotensionMiosisDUMBBBELS: Diarrhea, Urination, Miosis, Bronchospasm/Bradycardia, Emesis, Lacrimation, SalivationOrganophosphates, nerve agents, carbamatesAtropine (high doses, 2–4 mg IV, double q5min until secretions dry) + pralidoxime (2-PAM)
OpioidBradypnea, hypotension, bradycardiaMiosis (pinpoint)CNS depression, respiratory depression, decreased bowel soundsHeroin, fentanyl, morphine, oxycodone, methadoneNaloxone 0.04–2 mg IV/IM/IN (start low, titrate to respiratory effort, not alertness)
Sedative-HypnoticBradypnea, hypotensionNormal or miosisCNS depression, normal pupils (distinguishes from opioid)Benzodiazepines, barbiturates, GHB, zolpidemFlumazenil 0.2 mg IV (rarely used — seizure risk in chronic benzodiazepine users or co-ingestion with seizure-threshold-lowering drugs)
Serotonin SyndromeTachycardia, hypertension, hyperthermiaMydriasisClonus (spontaneous, inducible, ocular), hyperreflexia, agitation, diaphoresis, diarrheaSSRIs + MAOIs, tramadol, linezolid, dextromethorphan, MDMACyproheptadine 12 mg PO load, then 4 mg q6h; benzodiazepines for agitation; avoid paralysis (masks clonus)

36 Acetaminophen & Salicylate Toxicity Tox

Acetaminophen (APAP) Overdose

The most common cause of acute liver failure in the US. Toxic dose: > 150 mg/kg or > 7.5 g in adults. Metabolism: at therapeutic doses, APAP is metabolized via glucuronidation/sulfation. In overdose, these pathways saturate, and CYP2E1 converts APAP to NAPQI, a toxic metabolite that depletes glutathione and causes hepatocellular necrosis. Stages: (1) 0–24 hrs: nausea, vomiting, normal labs; (2) 24–72 hrs: RUQ pain, rising AST/ALT; (3) 72–96 hrs: peak hepatotoxicity (AST/ALT > 10,000, coagulopathy, renal failure, encephalopathy); (4) Recovery or death.

Rumack-Matthew nomogram plotting serum acetaminophen concentration against time after ingestion to determine NAC treatment threshold
Figure 35 — Rumack-Matthew Nomogram for Acetaminophen Toxicity. The nomogram plots serum acetaminophen levels against time since ingestion. Levels at or above the treatment line (starting at 150 mcg/mL at 4 hours) indicate need for N-acetylcysteine (NAC) therapy.

Rumack-Matthew Nomogram: Plot the 4-hour post-ingestion APAP level on the nomogram. Treatment line starts at 150 mcg/mL at 4 hours. If level is above the line: N-acetylcysteine (NAC) — IV protocol: 150 mg/kg over 1 hour, then 50 mg/kg over 4 hours, then 100 mg/kg over 16 hours (total 21 hours). Oral: 140 mg/kg load, then 70 mg/kg q4h × 17 additional doses. NAC is most effective within 8 hours but should be given at ANY time if clinical concern for toxicity. Always check an APAP level on every overdose patient regardless of reported ingestion.

Salicylate Toxicity

Acute ingestion > 150 mg/kg is toxic; > 500 mg/kg is potentially lethal. Chronic salicylism occurs at lower levels in elderly patients on aspirin. Pathophysiology: uncouples oxidative phosphorylation, stimulates respiratory center, causes metabolic acidosis. Classic ABG: mixed respiratory alkalosis + metabolic acidosis (early: respiratory alkalosis from central stimulation; late: AG metabolic acidosis predominates). Symptoms: tinnitus, nausea, vomiting, hyperpnea, diaphoresis, altered mental status, seizures.

Treatment: sodium bicarbonate infusion (150 mEq in 1 L D5W at 1.5–2× maintenance) targeting urine pH 7.5–8.0 (alkalinize the urine to trap salicylate in its ionized form for renal excretion). Monitor K+ closely (hypokalemia prevents urine alkalinization). Hemodialysis indications: salicylate level > 90 mg/dL (acute) or > 60 mg/dL (chronic), altered mental status, renal failure, pulmonary edema, refractory acidosis. Do NOT intubate salicylate patients unless absolutely necessary — their compensatory hyperventilation is maintaining acid-base balance; matching their minute ventilation post-intubation is extremely difficult, and loss of respiratory compensation leads to rapid acidemia, cardiovascular collapse, and death.

37 Alcohol Withdrawal & Sedative-Hypnotic Toxicity Tox

Alcohol withdrawal is a spectrum from mild (tremor, anxiety, insomnia, 6–24 hrs after last drink) to moderate (hallucinations, 12–48 hrs) to seizures (12–48 hrs) to delirium tremens (48–96 hrs: confusion, agitation, autonomic instability, hyperthermia, seizures — mortality 5–15% without treatment, up to 35% untreated). Use the CIWA-Ar score (Clinical Institute Withdrawal Assessment for Alcohol, Revised) to guide benzodiazepine dosing: 10 parameters scored 0–7 each (max 67). CIWA < 10: mild, monitoring. 10–18: moderate, treat. > 18: severe, aggressive treatment.

Treatment: benzodiazepines are the mainstay. Symptom-triggered dosing (CIWA-guided) is preferred over fixed-schedule. Diazepam 10–20 mg IV q10–15 min (active metabolites provide smooth taper) or lorazepam 2–4 mg IV q15–30 min (preferred in liver failure — no active metabolites). For refractory DTs: phenobarbital 130–260 mg IV, propofol infusion, or dexmedetomidine adjunct. IV thiamine 500 mg before glucose (prevent Wernicke's encephalopathy), IV magnesium, folate, multivitamins.

38 Anaphylaxis Tox

Clinical features and severity grading of anaphylaxis showing cutaneous, respiratory, cardiovascular, and gastrointestinal manifestations
Figure 36 — Anaphylaxis: Clinical Features and Severity Grading. Clinical manifestations of anaphylaxis across organ systems. Skin findings (urticaria, angioedema) occur in 90% of cases but may be absent in rapidly progressive anaphylaxis. Cardiovascular collapse can occur without skin findings.

Anaphylaxis is a severe, life-threatening systemic allergic reaction involving ≥2 organ systems (skin/mucosal, respiratory, cardiovascular, GI). Triggers: foods (peanuts, tree nuts, shellfish), medications (antibiotics, NSAIDs), insect stings, latex. Can occur within seconds to minutes of exposure. Presentation: urticaria/angioedema (90%), bronchospasm/stridor, hypotension/tachycardia, nausea/vomiting/cramping.

Emergency treatment algorithm for anaphylaxis showing step-by-step management including epinephrine administration, positioning, and adjunctive therapies
Figure 37 — Anaphylaxis Emergency Treatment Algorithm. Stepwise management algorithm for anaphylaxis. Intramuscular epinephrine is the first-line treatment. The algorithm emphasizes airway management, positioning (supine with legs elevated unless respiratory distress), and monitoring for biphasic reactions.

Epinephrine is the ONLY first-line treatment: 0.3–0.5 mg IM (1:1000 concentration) in the anterolateral thigh. May repeat q5–15 min. IV epinephrine (1:10,000, 0.1 mg boluses or infusion 1–10 mcg/min) for refractory shock. Adjuncts: IV fluids (1–2 L bolus for hypotension), albuterol nebulized (bronchospasm), diphenhydramine 50 mg IV (H1 blocker), famotidine 20 mg IV (H2 blocker), methylprednisolone 125 mg IV (prevents biphasic reaction — occurs in 5–20% at 1–72 hours). Observe 4–6 hours post-treatment; prescribe EpiPen and refer to allergist on discharge.

Delayed or withheld epinephrine is the leading cause of death from anaphylaxis. There are NO absolute contraindications to epinephrine in anaphylaxis. Elderly patients, those on beta-blockers, and cardiac patients may need escalating doses or IV glucagon (1–5 mg IV for beta-blocker-resistant anaphylaxis).

39 Environmental Emergencies Tox

Heat Emergencies

EntityCore TempKey FeaturesTreatment
Heat exhaustion< 40°C (104°F)Heavy sweating, weakness, headache, nausea, normal mentationRest, cool environment, oral/IV rehydration
Heat stroke≥ 40°C (104°F)Altered mental status (confusion, seizures, coma) + hot skin (may be dry or sweaty)Aggressive cooling: cold water immersion (most effective, target < 39°C within 30 min), evaporative cooling (mist + fans), ice packs to axillae/groin/neck. Stop cooling at 38.5°C. Intubate if needed, IV fluids, treat rhabdomyolysis
Accidental hypothermia management algorithm showing staging, rewarming methods, and cardiac arrest management based on core temperature
Figure 38 — Hypothermia Management Algorithm. Staging and treatment algorithm for accidental hypothermia. Management escalates from passive external rewarming (mild) to active internal rewarming including ECMO (severe). Resuscitation should continue until the patient is warm.

Hypothermia

SeverityCore TempSignsTreatment
Mild32–35°C (90–95°F)Shivering, confusion, tachycardiaPassive external rewarming (warm blankets, warm environment)
Moderate28–32°C (82–90°F)Shivering stops, paradoxical undressing, atrial fibrillation, decreased LOCActive external rewarming (forced warm air, warm blankets) + warm IV fluids (40–42°C)
Severe< 28°C (82°F)Unresponsive, VF risk, fixed dilated pupils (do not pronounce dead until warm and dead)Active internal rewarming: warm IV fluids, warm humidified O2, peritoneal/pleural lavage with warm saline, ECMO for cardiac arrest
Hypothermia staging system showing clinical signs, ECG findings, and treatment approach at each temperature range
Figure 39 — Hypothermia Staging and Clinical Features. Clinical staging of accidental hypothermia with corresponding signs, ECG changes (including Osborn J-waves), and treatment strategies. Shivering ceases below 32 degrees C, and the risk of VF increases significantly below 28 degrees C.
"Nobody is dead until they're warm and dead." In profound hypothermia, patients can appear clinically dead (fixed dilated pupils, absent pulses, asystole) but may be fully resuscitatable after rewarming. Continue CPR and rewarming to core temp ≥ 32°C before considering termination. Defibrillation is often ineffective below 30°C; limit to 3 attempts and rewarm before retrying.

Drowning

Leading cause of unintentional death in children 1–4 years. Primary insult is hypoxia from water aspiration and laryngospasm. All drowning patients who are symptomatic or have any submersion > 1 minute require ED evaluation. Treatment is supportive: supplemental O2, positive-pressure ventilation if needed, intubation for respiratory failure. Monitor for ARDS (may develop 6–24 hours post-submersion). Hypothermia from cold-water submersion may be neuroprotective and is not a reason to terminate resuscitation early. Cervical spine precautions if diving mechanism.

40 Pediatric Emergencies Peds

Febrile Seizures

Most common seizure type in children (2–5% of children aged 6 months to 5 years). Simple febrile seizure: generalized, < 15 minutes, does not recur within 24 hours. Complex: focal, > 15 minutes, or recurrent within 24 hours. Simple febrile seizures are benign — no increased epilepsy risk, no need for LP or EEG in well-appearing children ≥ 12 months with first simple febrile seizure. Treat the fever and reassure parents.

Croup (Laryngotracheobronchitis)

Viral (parainfluenza most common), ages 6 months to 3 years. Presentation: barking "seal-like" cough, inspiratory stridor, hoarseness, worse at night. "Steeple sign" on AP neck X-ray (subglottic narrowing). Treatment: mild (stridor at rest) → dexamethasone 0.6 mg/kg PO/IM (single dose); moderate-severe → nebulized racemic epinephrine (0.5 mL of 2.25% in 3 mL NS) + dexamethasone. Observe ≥ 3–4 hours after racemic epi for rebound.

Abdominal radiograph and ultrasound showing the target sign of intussusception in a pediatric patient
Figure 40 — Intussusception: Target Sign on Imaging. The characteristic target sign (also known as the bull's-eye sign) on imaging, formed by concentric rings of intussuscipiens wall surrounding the echogenic intussusceptum. Ultrasound sensitivity exceeds 98% for pediatric intussusception.

Intussusception

Telescoping of proximal bowel into distal segment. Peak incidence: 6–36 months. Most common cause of bowel obstruction in infants. Classic triad: colicky abdominal pain (intermittent, severe, with drawing up of legs), vomiting, and "currant jelly" stool (bloody mucus — a LATE sign). Palpable "sausage-shaped" mass in RUQ. Diagnosis: ultrasound showing "target sign" or "pseudokidney sign." Treatment: air-contrast or hydrostatic enema (both diagnostic and therapeutic, 80–95% success for reduction). Surgery if enema fails, peritonitis, or perforation.

Non-Accidental Trauma (NAT)

Suspect when: injury inconsistent with developmental stage, changing history, delay in seeking care, multiple injuries at different stages of healing, specific injury patterns (posterior rib fractures, metaphyseal "corner" or "bucket handle" fractures, retinal hemorrhages, patterned bruising/burns). Mandatory reporting is required in all US states when NAT is suspected. Workup: skeletal survey (children < 2 years), head CT, ophthalmologic exam, labs (CBC, CMP, coags, lipase, UA for hematuria).

41 Obstetric Emergencies OB

Ectopic Pregnancy

Implantation outside the uterine cavity (95% in fallopian tube). Risk factors: prior ectopic, PID, tubal surgery, IUD. Presentation: abdominal/pelvic pain + vaginal bleeding + positive pregnancy test. Ruptured ectopic causes acute abdomen with hemoperitoneal shock. Diagnosis: transvaginal ultrasound (absence of IUP with beta-hCG above discriminatory zone, typically ≥1500–2000 mIU/mL) + adnexal mass or free fluid. Treatment: hemodynamically stable + unruptured → methotrexate (50 mg/m² IM single dose) if criteria met (no fetal cardiac activity, mass < 4 cm, beta-hCG < 5000). Ruptured or hemodynamically unstable → emergent salpingectomy.

Eclampsia & Severe Preeclampsia

Preeclampsia: new-onset hypertension (≥140/90 after 20 weeks) + proteinuria or end-organ dysfunction. Severe features: SBP ≥ 160 or DBP ≥ 110, platelets < 100K, elevated liver enzymes (2× normal), renal insufficiency (Cr > 1.1), pulmonary edema, headache/visual disturbances. Eclampsia: seizures in preeclamptic patient. Treatment: magnesium sulfate 4–6 g IV over 20 min (seizure prophylaxis and treatment), then 1–2 g/hr maintenance; antihypertensives (IV labetalol or hydralazine); definitive treatment is delivery.

Perimortem Cesarean Delivery

If a pregnant patient (fundus at or above the umbilicus, roughly ≥ 20 weeks) suffers cardiac arrest and does not have ROSC within 4 minutes of CPR, perimortem C-section should be performed at the bedside. The goal is delivery within 5 minutes of arrest (the "4-minute rule" — decision at 4 min, delivery by 5 min). This is performed to improve maternal resuscitation (relieving aortocaval compression) as much as for fetal survival. The procedure is performed at the patient's current location — do not move to the OR.

42 Psychiatric Emergencies Psych

Suicidal Patient

Risk assessment: SAD PERSONS (Sex, Age, Depression, Previous attempt, Ethanol abuse, Rational thinking loss, Social supports lacking, Organized plan, No spouse, Sickness). High-risk features: specific plan, access to means (especially firearms), active psychosis, recent discharge from psychiatric facility, male > 45, history of prior attempts. Columbia Suicide Severity Rating Scale (C-SSRS) is the standard structured assessment. All patients with active suicidal ideation with plan or intent require psychiatric evaluation and safety precautions (1:1 observation, search for sharps, remove cords/ligatures from room).

Acute Agitation Management

ApproachDetails
Verbal de-escalationFirst-line always. Calm tone, validate feelings, offer choices, maintain safe distance
PO medications (cooperative patient)Olanzapine 5–10 mg ODT or risperidone 2 mg + lorazepam 2 mg PO
IM medications (uncooperative)"B52": haloperidol 5 mg + lorazepam 2 mg + diphenhydramine 50 mg IM. Alternative: olanzapine 10 mg IM (do NOT combine IM olanzapine with IM benzodiazepine — respiratory depression risk). Ketamine 4 mg/kg IM for severe agitation/excited delirium
Physical restraintsLast resort. 4-point leather restraints. Requires physician order, Q15 min checks, neurovascular assessment, offer food/water/toileting q2h. Document ongoing need
Always rule out medical causes of agitation before attributing to psychiatric illness: hypoglycemia, hypoxia, head injury, sepsis, meningitis, thyroid storm, drug intoxication/withdrawal, urinary retention (elderly). A medical workup (vitals, glucose, consider BMP, UA, UDS, CT head) should be performed before psychiatric clearance.

43 Geriatric Emergencies Geri

Elderly patients (≥ 65 years) present atypically: MI without chest pain (dyspnea, confusion), sepsis without fever (hypothermia is a worse prognostic sign), UTI presenting as altered mental status, appendicitis without peritoneal signs. Falls are the leading cause of injury-related death in the elderly. Always consider: medication effects (polypharmacy, anticoagulants), baseline cognitive function (delirium vs. dementia), occult fractures, and disposition challenges (can the patient safely return home?).

Occult Fractures in the Elderly

FracturePresentationImaging PitfallNext Step
Hip fracture (femoral neck)Pain with weight bearing, shortened/externally rotated legX-ray negative in 2–10% of occult hip fracturesMRI (gold standard) or CT if MRI unavailable
C2 (odontoid) fractureNeck pain after fall, especially if on anticoagulantsOften missed on lateral c-spine X-rayCT c-spine (not plain films) for elderly trauma patients
Vertebral compression fractureBack pain after fall or spontaneous (osteoporosis)May be subtle on X-rayMRI to assess acuity if treatment decisions hinge on it
Pelvic rami fracturesGroin/hip pain, difficulty ambulatingCan be subtle on AP pelvis X-rayCT pelvis for definitive evaluation
Anticoagulation & Head Trauma in the Elderly

Any elderly patient on anticoagulation (warfarin, DOACs) who falls and strikes their head requires a CT head even if asymptomatic and GCS 15. Delayed intracranial hemorrhage can occur hours later. Consider observation for 6–24 hours or reliable return precautions. Check INR for warfarin patients; reverse anticoagulation if intracranial hemorrhage is identified.

44 Airway Management & RSI Procedures

Rapid Sequence Intubation (RSI)

RSI is the standard of care for emergency intubation in the ED. It involves simultaneous administration of a sedative and neuromuscular blocking agent to facilitate endotracheal intubation while minimizing aspiration risk.

PhaseActionDetails
PreparationEquipment, positioning, preoxygenationSOAP-ME: Suction, Oxygen, Airway equipment, Pharmacy, Monitoring/End-tidal CO2. Preoxygenate with 100% O2 × 3 min or 8 vital capacity breaths. Position: sniffing/ramped. Apneic oxygenation: 15 L/min NC during attempt
InductionPush sedativeEtomidate 0.3 mg/kg IV (hemodynamically neutral; avoid in sepsis/adrenal insufficiency). Ketamine 1.5–2 mg/kg IV (preferred in hypotension/asthma; does NOT raise ICP in ventilated patients). Propofol 1.5 mg/kg IV (hypotension risk). Midazolam 0.1–0.3 mg/kg (avoid in hypotension)
ParalysisPush neuromuscular blockerSuccinylcholine 1.5 mg/kg IV (onset 45 sec, duration 6–10 min; contraindicated in hyperkalemia, burns >24 hrs, crush >72 hrs, denervation injuries, malignant hyperthermia history). Rocuronium 1.2 mg/kg IV (onset 60 sec, duration 45–60 min; reversible with sugammadex 16 mg/kg)
PlacementIntubateVideo laryngoscopy (preferred in most EDs) or direct laryngoscopy. Confirm with continuous waveform capnography (ETCO2) — the gold standard for tube confirmation. Also: bilateral breath sounds, condensation in tube, chest rise, SpO2
Post-intubationSecure, ventilate, sedateSecure ETT (tape or commercial holder), CXR for depth (2–4 cm above carina), start sedation (propofol or ketamine infusion + fentanyl) and long-acting paralytic if needed
Surgical technique for four-compartment fasciotomy of the lower leg showing incision locations and compartment decompression
Figure 41 — Four-Compartment Fasciotomy Technique. Dual-incision fasciotomy technique for lower leg compartment syndrome. The anterolateral incision releases the anterior and lateral compartments; the posteromedial incision releases the superficial and deep posterior compartments.

Surgical Airway (Cricothyrotomy)

Indicated when intubation and ventilation both fail ("can't intubate, can't oxygenate"). Technique: identify cricothyroid membrane (between thyroid and cricoid cartilages), vertical skin incision, horizontal stab through membrane, insert bougie, railroad a 6.0 cuffed ETT or tracheostomy tube over bougie. Contraindicated in children < 8–10 years (needle cricothyrotomy with jet ventilation instead due to small anatomy).

Non-Invasive Ventilation & High-Flow Nasal Cannula

ModalitySettingsBest IndicationsContraindications
HFNC (High-Flow Nasal Cannula)40–60 L/min, FiO2 titrated, heated/humidifiedHypoxemic respiratory failure, bridge during RSI preoxygenation, post-extubationSevere facial trauma, complete upper airway obstruction
CPAP5–15 cmH2O continuousPulmonary edema (cardiogenic), obstructive sleep apneaVomiting, AMS (aspiration risk), pneumothorax
BiPAPIPAP 10–20 / EPAP 5–10 cmH2OCOPD exacerbation, CHF, obesity hypoventilation, bridge to intubationSame as CPAP; facial trauma making mask seal impossible

45 Vascular Access & Chest Procedures Procedures

Vascular Access Hierarchy

Access TypeGauge/SizeFlow RateWhen to Use
Peripheral IV (PIV)18G (green) or 16G (gray)~200–350 mL/min (16G with pressure bag)First-line; 2 large-bore IVs for trauma/resuscitation
Intraosseous (IO)15G (EZ-IO drill)~80–125 mL/min (pressure infusion)If IV not obtained within 60–90 sec in critical patient. Sites: proximal tibia (preferred in adults), proximal humerus, distal tibia (pediatric). Can give any medication or fluid including blood products
Central venous catheter (CVC)Triple-lumen 7 Fr~70–100 mL/min (distal port)Vasopressor administration, no peripheral access, CVP monitoring. Sites: IJ (preferred, US-guided), subclavian, femoral. IJ and subclavian carry pneumothorax risk; femoral has highest infection rate
Introducer sheath (Cordis)8.5 Fr~300–500 mL/minRapid volume resuscitation (massive hemorrhage); PA catheter introduction

Chest Tube Insertion

Indications: pneumothorax (traumatic, large spontaneous), hemothorax, empyema, large symptomatic pleural effusion. Technique: safe triangle (bordered by anterior border of latissimus dorsi, lateral border of pectoralis major, line of the 5th intercostal space, apex of the axilla). Position: 4th–5th ICS, anterior to mid-axillary line. Incise skin, blunt dissect through intercostal muscles ABOVE the rib (neurovascular bundle runs below each rib), enter pleural space, finger sweep, insert tube directed posteriorly-superiorly for air or posteriorly-inferiorly for fluid. Tube size: 28–36 Fr for hemothorax, 20–24 Fr for pneumothorax. Connect to closed drainage system (Pleur-Evac) with 20 cmH2O suction. Confirm with CXR.

Imaging findings in necrotizing fasciitis showing fascial thickening, fluid collections, and tissue gas on CT and MRI
Figure 42 — Necrotizing Fasciitis: Advanced Imaging Findings. Cross-sectional imaging showing fascial thickening, subfascial fluid collections, and soft tissue inflammatory changes characteristic of necrotizing fasciitis. If clinical suspicion is high, do not delay surgical consultation for imaging.

Needle Decompression

For tension pneumothorax when clinical diagnosis is made (do NOT wait for imaging). Site: 5th ICS, anterior axillary line (preferred over the traditional 2nd ICS midclavicular line due to greater chest wall thickness at the 2nd ICS). Use a 14-gauge angiocatheter, at least 8 cm long. Insert perpendicular to chest wall, above the rib. Rush of air confirms decompression. This is a temporizing measure — follow immediately with chest tube.

46 Wound Management & Procedural Sedation Procedures

Laceration Repair

Assessment: mechanism, contamination, depth (tendon/nerve/vessel/joint involvement?), foreign body, neurovascular status distal to wound, time since injury. Anesthesia: local infiltration with lidocaine 1% (max 4.5 mg/kg without epi, 7 mg/kg with epi) or bupivacaine 0.25% (longer duration). LET gel (lidocaine-epinephrine-tetracaine) for pediatric face/scalp lacerations. Closure: simple interrupted sutures (nylon for skin, absorbable for deep layers), running sutures (rapid closure of clean linear wounds), deep dermal sutures (Vicryl for dead space closure), wound adhesive (2-octyl cyanoacrylate / Dermabond) for clean superficial lacerations, staples for scalp. Suture removal timing: face 3–5 days, scalp 7–10 days, trunk 7–10 days, extremities 10–14 days, joints 14 days.

Procedural Sedation

AgentDoseOnset/DurationProsCons
Propofol0.5–1 mg/kg IV, titrate with 0.25–0.5 mg/kg boluses q30–60 sec30 sec / 5–10 minUltra-short acting, reliable, rapid recoveryApnea, hypotension, no analgesia (combine with fentanyl)
Ketamine1–2 mg/kg IV or 4 mg/kg IMIV: 1 min / 15–30 min; IM: 5 min / 30–60 minMaintains airway reflexes, bronchodilation, analgesia, hemodynamically stableEmergence reactions (adults > children; pretreat with midazolam 0.05 mg/kg), laryngospasm (rare), vomiting
Etomidate0.1–0.15 mg/kg IV30 sec / 5–10 minHemodynamically neutralMyoclonus, no analgesia, adrenal suppression
Midazolam + FentanylMidazolam 0.05 mg/kg + Fentanyl 1 mcg/kg IV2–5 min / 30–60 minTitratable, reversible (flumazenil/naloxone)Slower onset/recovery, respiratory depression with combination

47 Reduction Techniques & Bedside Ultrasound Procedures

Shoulder Dislocation Reduction

Multiple techniques exist; selection depends on patient body habitus, cooperation, and provider experience. External rotation method: patient supine, elbow at 90°, slowly externally rotate the arm (adducted) until relocates. Cunningham technique: patient seated, provider massages biceps, deltoid, and trapezius muscles (no traction). Stimson technique: patient prone, arm hanging off stretcher with 5–10 lb weight; gravity reduces. Traction-countertraction: sheet around patient's chest for countertraction, steady traction on the arm. Pre-reduction X-ray to confirm dislocation and rule out fracture. Post-reduction: neurovascular exam (check axillary nerve), X-ray to confirm reduction, sling × 2–3 weeks, orthopedic follow-up.

Positive FAST exam LUQ view showing free fluid in the splenorenal recess between spleen and left kidney
Figure 43 — Positive FAST Exam: LUQ View (Splenorenal Recess). Ultrasound demonstrating free fluid in the splenorenal recess. The LUQ view is more challenging than the RUQ view due to the spleen's smaller acoustic window and the splenorenal ligament, which can compartmentalize fluid.

Emergency Bedside Ultrasound Applications

ApplicationProbeWhat You're Looking For
FAST examCurvilinearFree fluid in RUQ (Morison's), LUQ (splenorenal), pelvis, pericardium
Cardiac (focused echo)Phased arrayPericardial effusion, RV dilation (PE), global LV function, tamponade physiology
Lung ultrasoundLinear or curvilinearLung sliding (rules out PTX if present), B-lines (pulmonary edema), consolidation (pneumonia), pleural effusion
AortaCurvilinearAAA (≥ 3 cm diameter), dissection flap
IVC assessmentCurvilinear/phased arrayIVC diameter and collapsibility (estimates volume status; IVC < 1 cm with complete collapse = low CVP)
Vascular access guidanceLinearVessel identification, real-time needle guidance for IJ CVC, peripheral IV, arterial line
Soft tissueLinearAbscess vs. cellulitis, foreign body, tendon injury
Renal/biliaryCurvilinearHydronephrosis (renal colic), gallstones, gallbladder wall thickening
DVTLinear2-point compression: CFV and popliteal vein. Non-compressible vein = DVT
First-trimester pregnancyCurvilinear (transabdominal) or endocavitaryIUP vs. ectopic; fetal heart rate; free fluid (ruptured ectopic)

48 Clinical Decision Rules & Scoring Systems

Rule/ScoreApplicationKey Thresholds
HEART ScoreChest pain risk stratification0–3: low risk (safe for discharge); 4–6: moderate; 7–10: high (early invasive)
Wells PEPE probability≤4: unlikely (D-dimer to rule out); >4: likely (CTA)
Wells DVTDVT probability≤1: unlikely (D-dimer); ≥2: likely (compression US)
PERC RulePE exclusion without D-dimerAll 8 criteria negative in low-risk = PE excluded
Ottawa Ankle RulesAnkle X-ray necessityX-ray if: unable to bear weight (4 steps) OR bone tenderness at posterior edge/tip of lateral or medial malleolus
Ottawa Knee RulesKnee X-ray necessityX-ray if: age ≥55, isolated patellar tenderness, fibular head tenderness, inability to flex 90°, inability to bear weight (4 steps)
Canadian C-Spine RuleC-spine imaging3-step algorithm as described in Section 23
Canadian CT Head RuleCT head for minor head injuryHigh-risk and medium-risk criteria as described in Section 22
GCSConsciousness level13–15: mild; 9–12: moderate; 3–8: severe TBI (intubate)
NIHSSStroke severity0: no deficit; 1–4: minor; 5–15: moderate; 16–20: moderate-severe; 21–42: severe
CURB-65Pneumonia severity/disposition0–1: outpatient; 2: consider admission; 3–5: admit/ICU
qSOFASepsis bedside screen≥2 of: RR ≥22, AMS, SBP ≤100
Glasgow-BlatchfordUGIB risk0–1: outpatient management; ≥6: high risk, likely intervention needed
CIWA-ArAlcohol withdrawal severity<10: mild; 10–18: moderate; >18: severe (aggressive treatment)
Alvarado (MANTRELS)Appendicitis probability≤4: unlikely; 5–6: equivocal; ≥7: probable
Centor/McIsaacStrep pharyngitis0–1: no testing; 2–3: rapid antigen test; 4–5: empiric antibiotics or test
PECARNPediatric head CT decisionIdentifies very low-risk children (<2% bleed risk) who can safely avoid CT
Ranson's CriteriaPancreatitis severity≥3 criteria: severe (predicted mortality 15–40%)
BISAPPancreatitis mortality prediction≥3: >20% mortality
CHA₂DS₂-VAScAFib stroke risk (for anticoagulation decision)≥2 (men), ≥3 (women): anticoagulate
HAS-BLEDBleeding risk on anticoagulation≥3: high risk (does not contraindicate, but requires monitoring)

49 Medications Master Table Meds

RSI & Airway Medications

Drug (Brand)MechanismDoseIndicationCritical Pearl
Etomidate (Amidate)GABA-A agonist0.3 mg/kg IVRSI inductionHemodynamically neutral; single-dose adrenal suppression clinically insignificant
Ketamine (Ketalar)NMDA antagonist1.5–2 mg/kg IVRSI inductionPreferred in hypotension and asthma; sympathomimetic effect supports BP
Propofol (Diprivan)GABA-A agonist1.5 mg/kg IVRSI induction, sedationCauses hypotension; use lower doses in elderly/hypovolemic
Succinylcholine (Anectine)Depolarizing NMB1.5 mg/kg IVRSI paralysisCI: hyperkalemia, burns >24h, denervation, MH history. Fastest onset (45 sec)
Rocuronium (Zemuron)Non-depolarizing NMB1.2 mg/kg IVRSI paralysisOnset 60 sec at intubating dose. Reversible with sugammadex 16 mg/kg

Vasopressors & Inotropes

DrugMechanismDose RangePrimary UseCritical Pearl
Norepinephrine (Levophed)α1 >> β15–50 mcg/minFirst-line for septic shock, cardiogenic shockCentral line preferred but can run peripherally short-term via large PIV; titrate to MAP ≥ 65
Epinephrine (Adrenalin)α1 + β1 + β21–20 mcg/minAnaphylaxis, cardiac arrest, refractory septic shockIncreases HR, contractility, and SVR; may cause lactic acidosis at high doses
Vasopressin (Pitressin)V1 receptor agonist0.04 units/min (fixed)Second-line in septic shockNot titrated; add to norepinephrine, not as replacement
Dobutamine (Dobutrex)β1 > β25–20 mcg/kg/minCardiogenic shock (inotropy)Can cause hypotension (vasodilation); usually combined with vasopressor
Phenylephrine (Neo-Synephrine)Pure α140–360 mcg/minNeurogenic shock, SVT-related hypotensionPure vasoconstrictor; avoid in cardiogenic shock (increases afterload)
DopamineDose-dependent: D1 → β1 → α15–20 mcg/kg/minBradycardia-related hypotension (alternative to transcutaneous pacing)Higher arrhythmia risk than norepinephrine in septic shock; largely replaced

Antidotes

PoisonAntidoteDoseKey Note
AcetaminophenN-acetylcysteine (NAC / Acetadote)150 mg/kg over 1 hr → 50 mg/kg over 4 hr → 100 mg/kg over 16 hr (IV)Most effective within 8 hrs; give at any time if indicated
OpioidsNaloxone (Narcan)0.04–2 mg IV/IM/INStart low, titrate to respiratory effort; duration shorter than most opioids → resedation risk
BenzodiazepinesFlumazenil (Romazicon)0.2 mg IV q1min (max 3 mg)Rarely used; risk of seizures in chronic benzo users; contraindicated with TCA co-ingestion
OrganophosphatesAtropine + pralidoximeAtropine 2–4 mg IV q5min; pralidoxime 1–2 g IV over 30 minTitrate atropine to drying of secretions; no maximum dose
Warfarin (life-threatening bleed)4-factor PCC (Kcentra) + Vitamin KPCC: 25–50 units/kg IV; Vit K 10 mg IV over 10 minPCC reverses INR within minutes; Vitamin K sustains reversal
DabigatranIdarucizumab (Praxbind)5 g IV (two 2.5 g boluses)Complete reversal within minutes
Xa inhibitors (rivaroxaban, apixaban)Andexanet alfa (Andexxa)400–800 mg IV bolus, then infusionExpensive; 4-factor PCC 50 units/kg is the practical alternative
Beta-blockers / CCBsGlucagon, high-dose insulin euglycemia (HIE)Glucagon 3–10 mg IV; Insulin 1 unit/kg bolus + 1 unit/kg/hr + D10WHIE is first-line for CCB overdose; give with dextrose, monitor glucose and K+
DigoxinDigoxin-specific Fab (DigiFab)Based on ingested dose or serum level; empiric 10–20 vials for acute toxicityFor life-threatening arrhythmia or K+ > 5.0 in digoxin toxicity
Methanol / Ethylene glycolFomepizole (Antizol)15 mg/kg IV load, then 10 mg/kg q12hBlocks alcohol dehydrogenase; also hemodialysis if severe acidosis or level > 50 mg/dL
CyanideHydroxocobalamin (Cyanokit)5 g IV over 15 minSuspect in fire/smoke inhalation victims with lactic acidosis + normal SpO2
Carbon monoxide100% O2 (hyperbaric if severe)High-flow 100% O2 via NRB maskPulse ox is unreliable (reads falsely normal). Use co-oximetry for COHb level

Analgesics & Sedatives

Drug (Brand)DoseRouteDurationPearl
Fentanyl0.5–1 mcg/kgIV30–60 minPreferred in hemodynamic instability; no histamine release
Morphine0.1 mg/kg (4–8 mg)IV3–4 hrsHistamine release → hypotension; use with caution in ACS
Ketorolac (Toradol)15–30 mgIV/IM4–6 hrsNSAID; avoid in renal impairment, GI bleed risk, anticoagulation
Acetaminophen (Ofirmev)1 gIV4–6 hrsExcellent adjunct; reduces opioid requirement by 30%
Ketamine (subdissociative)0.1–0.3 mg/kg IV or 0.5 mg/kg INIV/IN15–30 minEffective for pain; opioid-sparing; minimal respiratory depression

Common EM Antibiotics

Drug (Brand)DoseCommon EM IndicationKey Note
Ceftriaxone (Rocephin)1–2 g IV dailyPneumonia, UTI, meningitis, gonorrheaBroad gram-negative coverage; do not mix with calcium-containing solutions in neonates
Piperacillin-tazobactam (Zosyn)3.375–4.5 g IV q6–8hSepsis, necrotizing fasciitis, intra-abdominal infectionBroad-spectrum including Pseudomonas and anaerobes
Vancomycin15–20 mg/kg IV (based on actual body weight)Sepsis (MRSA), meningitis, severe SSTILoad with 25–30 mg/kg for critically ill; monitor troughs or AUC/MIC
Metronidazole (Flagyl)500 mg IV/PO q8hIntra-abdominal infection (anaerobic), C. diffAvoid alcohol (disulfiram reaction)
Azithromycin (Zithromax)500 mg IV/PO × 1 day, then 250 mg × 4CAP atypical coverage, STIQT prolongation risk
TMP-SMX (Bactrim DS)1–2 DS tabs PO BIDUncomplicated UTI, MRSA SSTIHyperkalemia risk; avoid in pregnancy (folate antagonist)

50 Abbreviations Master List

General & Resuscitation

ABCDEAirway, Breathing, Circulation, Disability, Exposure ACLSAdvanced Cardiovascular Life Support ACSAcute coronary syndrome AEDAutomated external defibrillator AMSAltered mental status ATLSAdvanced Trauma Life Support BLSBasic life support BVMBag-valve-mask CPRCardiopulmonary resuscitation EDEmergency department EMSEmergency medical services ESIEmergency severity index ETCO2End-tidal carbon dioxide ETTEndotracheal tube GCSGlasgow Coma Scale IOIntraosseous MAPMean arterial pressure MTPMassive transfusion protocol NRBNon-rebreather mask OPAOropharyngeal airway NPANasopharyngeal airway PALSPediatric Advanced Life Support ROSCReturn of spontaneous circulation RSIRapid sequence intubation TTMTargeted temperature management

Diagnoses

AAAAbdominal aortic aneurysm ADHFAcute decompensated heart failure AFibAtrial fibrillation AKIAcute kidney injury ALIAcute limb ischemia ARDSAcute respiratory distress syndrome CAPCommunity-acquired pneumonia CVACerebrovascular accident (stroke) DKADiabetic ketoacidosis DVTDeep vein thrombosis ICHIntracerebral hemorrhage MIMyocardial infarction NSTEMINon-ST-elevation myocardial infarction PEPulmonary embolism PEAPulseless electrical activity PTXPneumothorax SAHSubarachnoid hemorrhage SBOSmall bowel obstruction STEMIST-elevation myocardial infarction TBITraumatic brain injury TIATransient ischemic attack UAUnstable angina UTIUrinary tract infection VFVentricular fibrillation VTVentricular tachycardia

Procedures & Imaging

BiPAPBilevel positive airway pressure CPAPContinuous positive airway pressure CTACT angiography CVCCentral venous catheter CXRChest X-ray EGDEsophagogastroduodenoscopy FASTFocused Assessment with Sonography for Trauma HFNCHigh-flow nasal cannula I&DIncision and drainage IJInternal jugular LPLumbar puncture NGTNasogastric tube NIVNon-invasive ventilation PEEPPositive end-expiratory pressure PCIPercutaneous coronary intervention REBOAResuscitative Endovascular Balloon Occlusion of the Aorta TEVARThoracic endovascular aortic repair TIPSTransjugular intrahepatic portosystemic shunt

Medications & Labs

APAPAcetaminophen ASAAspirin BNPB-type natriuretic peptide CBCComplete blood count CMPComprehensive metabolic panel DAPTDual antiplatelet therapy DOACDirect oral anticoagulant FFPFresh frozen plasma INRInternational normalized ratio LRLactated Ringer's NACN-acetylcysteine NMBNeuromuscular blocker NSNormal saline (0.9%) PCCProthrombin complex concentrate pRBCPacked red blood cells TXATranexamic acid UFHUnfractionated heparin

Scoring & Decision Rules

CIWA-ArClinical Institute Withdrawal Assessment for Alcohol, Revised CURB-65Confusion, Urea, RR, BP, age ≥65 (pneumonia severity) HEARTHistory, ECG, Age, Risk factors, Troponin (chest pain risk) NIHSSNIH Stroke Scale PECARNPediatric Emergency Care Applied Research Network (head CT rule) PERCPulmonary Embolism Rule-out Criteria qSOFAQuick Sequential Organ Failure Assessment SOFASequential Organ Failure Assessment

51 Disposition Decision Framework & References

Disposition Decision Framework

Every ED patient requires a disposition decision: discharge home, observe (observation unit), admit to the floor, or admit to the ICU. This decision integrates acuity, diagnosis, clinical trajectory, and patient factors.

DispositionCriteriaExamples
DischargeDiagnosis benign or treatable as outpatient; vital signs stable; pain controlled; able to tolerate PO; reliable follow-up; safe home environmentSimple laceration, sprained ankle, uncomplicated UTI, low-risk chest pain (HEART 0–3)
Observation (23-hr)Diagnosis uncertain; need serial assessments or short-interval testing; not clearly requiring inpatient admissionChest pain rule-out (serial troponins), TIA workup, syncope with moderate-risk features, mild CHF responding to diuretics
Floor admissionDiagnosis requiring inpatient treatment; IV medications, serial monitoring, or procedures neededPneumonia requiring IV antibiotics, SBO with NGT, pyelonephritis, new AFib requiring rate control
ICU admissionHemodynamic instability, respiratory failure, continuous infusions (vasopressors, antiarrhythmics), need for invasive monitoring, high risk for rapid deteriorationSeptic shock, intubated patients, STEMI post-cath, massive PE, status epilepticus, DKA with pH < 7.1
Bounce-back risk: Conditions with highest 72-hour return rates include abdominal pain (especially in elderly and women of reproductive age), chest pain, and headache. These patients need clear discharge instructions, specific return precautions, and designated follow-up. The phrase "return if worsening symptoms or new concerns" is insufficient — list specific red flags (e.g., "return immediately for fever > 101, inability to keep fluids down, blood in stool, or worsening pain").

Consolidated References

TopicSource
ACLS/BLS GuidelinesPanchal AR et al. 2020 AHA Guidelines for CPR and ECC. Circulation 2020
CRASH-2 (TXA in trauma)CRASH-2 Collaborators. Lancet 2010;376:23–32
ARDSNet (Low TV ventilation)ARDS Network. NEJM 2000;342:1301–8
PROSEVA (Prone positioning)Guérin C et al. NEJM 2013;368:2159–68
TTM2 TrialDankiewicz J et al. NEJM 2021;384:2283–94
Stroke thrombectomy (DAWN)Nogueira RG et al. NEJM 2018;378:11–21
Stroke thrombectomy (DEFUSE-3)Albers GW et al. NEJM 2018;378:708–18
SAH aneurysm treatment (ISAT)Molyneux AJ et al. Lancet 2005;366:809–17
ICH BP management (INTERACT2)Anderson CS et al. NEJM 2013;368:2355–65
Sepsis-3 DefinitionsSinger M et al. JAMA 2016;315:801–10
Meningitis dexamethasonede Gans J, van de Beek D. NEJM 2002;347:1549–56
GI Bleed transfusion thresholdVillanueva C et al. NEJM 2013;368:11–21
Septic shock vasopressors (SOAP II)De Backer D et al. NEJM 2010;362:779–89
NIV in COPDLightowler JV et al. Cochrane Review 2003
Pancreatitis fluid resuscitationde-Madaria E et al. NEJM 2022;387:989–98 (WATERFALL)