When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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EMERGENTEM

Toxicology & Overdose

Toxidromes guide initial management; specific antidotes save lives. ABCs first, identify the toxidrome, then antidote + supportive care. NEVER intubate a salicylate-toxic patient unless absolutely necessary.

Overview

Acetaminophen

Rumack-Matthew nomogram, APAP level vs time to determine NAC need
NAC: N-acetylcysteine 150mg/kg/1h → 50mg/kg/4h → 100mg/kg/16h Prescott 1979
AST/ALT may be normal initially (peaks 72–96h). King’s College for transplant referral

Salicylate

Tinnitus, tachypnea (resp alkalosis + AG met acidosis). Alkalinize urine: bicarb drip, target urine pH 7.5–8
Dialysis if level >90 or severe symptoms

NEVER intubate a salicylate-toxic patient unless absolutely necessary. They hyperventilate to compensate for metabolic acidosis. Losing that compensation during intubation → sudden severe acidosis → cardiac arrest.

TCA

Wide QRS (>100ms), sodium channel blockade, seizures
Sodium bicarbonate 1–2 mEq/kg IV bolus (narrows QRS)
NEVER flumazenil in TCA/benzo co-ingestion (lowers seizure threshold)

🔄 Updated Practice: Old teaching: flumazenil (Romazicon) for all benzodiazepine overdoses. Current practice: AVOID flumazenil in chronic benzo users (precipitates withdrawal seizures) and in mixed overdose with TCAs (removes seizure protection). Flumazenil is only safe for iatrogenic oversedation in benzo-naive patients (e.g., post-procedure). When in doubt, don't give it.

Opioid

Naloxone 0.04–0.4mg IV titrate (start low). Drip for long-acting opioids

BB / CCB

BB: Glucagon 3–5mg IV
CCB: High-dose insulin 1u/kg/hr + D10W

Digoxin

Presentation: nausea/vomiting, visual disturbance (yellow-green halos, "Van Gogh"), confusion, bradyarrhythmia + ectopy (classic: PAT with block, bidirectional VT). Hyperkalemia in acute toxicity (Na/K-ATPase block).
DigiFab (digoxin-specific Fab fragments). Empiric 10–20 vials for acute OD; calculated # vials = (level × weight) / 100.
Indications: hemodynamic instability, K⁺ > 5, symptomatic bradycardia/heart block, dig level > 10 (acute) or > 6 (chronic), ingestion > 10 mg adult / 4 mg child.
Avoid IV calcium in dig toxicity (theoretical "stone heart" from intracellular Ca overload, though contested). Use DigiFab instead.

Warfarin / Long-Acting Anticoagulant Rodenticide

Vitamin K 10 mg IV slow (peaks at 12–24h, restores factor synthesis).
4-factor PCC (Kcentra) 25–50 units/kg IV for life-threatening bleed (reverses INR within minutes). FFP if PCC unavailable.
Long-acting rodenticides ("superwarfarins" e.g. brodifacoum) require weeks to months of oral vitamin K.

Organophosphate / Carbamate

Cholinergic toxidrome (SLUDGE / DUMBBBELS): miosis, salivation, lacrimation, urination, diarrhea, bradycardia, bronchospasm, bronchorrhea, fasciculations, seizures.
Atropine 2 mg IV, double q3–5 min until secretions dry (titrate to lung exam, NOT pupils or HR). No upper-limit dose; severe poisonings need 10–100+ mg.
Pralidoxime (2-PAM) 1–2 g IV over 15–30 min, then 500 mg/hr infusion. Reactivates AChE if given before "aging" (12–48h). Best within 6h.
Decontaminate skin/clothing (provider PPE: nitrile gloves, gown, eye protection, nerve agent exposure can affect responders).

Benzodiazepine

Supportive care first. Pure benzo overdoses rarely cause death; respiratory depression worse with co-ingestion.
Flumazenil (Romazicon) 0.2 mg IV q1 min (max 3 mg). Rarely used.
Avoid flumazenil in: chronic benzo users (precipitates withdrawal seizures), TCA / proconvulsant co-ingestion (removes seizure protection), unknown overdose. Safe only for iatrogenic oversedation in benzo-naive patients.

Local Anesthetic Systemic Toxicity (LAST)

Trigger: inadvertent IV bupivacaine / ropivacaine / lidocaine. Presents with seizures → cardiac arrest (refractory to ACLS).
Intralipid 20% 1.5 mL/kg IV bolus, then 0.25 mL/kg/min infusion. Lipid sink pulls drug out of cardiac tissue. Continue until hemodynamic stability + 10 min.
Avoid vasopressin (worsens outcomes); use low-dose epinephrine (≤ 1 mcg/kg).

Quick Antidote Reference

Poison	Antidote	Dose	Pearl
Acetaminophen	NAC	150 mg/kg/1h → 50 mg/kg/4h → 100 mg/kg/16h	Plot 4h level on Rumack-Matthew. Effective > 24h still.
Salicylate	Sodium bicarbonate + dialysis	Bicarb drip, target urine pH 7.5–8	Dialysis if level > 90 or severe symptoms. Avoid intubation.
Opioid	Naloxone	0.04–0.4 mg IV titrate to RR	Goal is breathing, not consciousness. Drip 2/3 effective bolus/hr for long-acting.
Benzodiazepine	Flumazenil	0.2 mg IV q1 min (max 3 mg)	Rarely used. Avoid in chronic users, TCA co-ingestion.
TCA	Sodium bicarbonate	1–2 mEq/kg IV bolus → drip pH 7.45–7.55	QRS > 100 ms or R in aVR > 3 mm. NO flumazenil.
Beta-blocker	Glucagon + HIE	3–10 mg IV bolus → 3–5 mg/hr; insulin 1 u/kg/hr	Glucagon causes vomiting (aspiration risk).
Calcium channel blocker	Calcium + HIE + lipid	CaCl 1–2 g IV; insulin 1 u/kg/hr + D10	HIE is the primary therapy for severe CCB OD.
Methanol / ethylene glycol	Fomepizole + dialysis	15 mg/kg IV load → 10 mg/kg q12h	Dialysis if pH < 7.25, AKI, visual symptoms, level > 50.
Organophosphate	Atropine + 2-PAM	Atropine 2 mg double q3–5 min; 2-PAM 1–2 g IV	Titrate atropine to dry secretions. No upper-limit dose.
Warfarin / superwarfarin	Vitamin K + 4F-PCC	Vit K 10 mg IV; PCC 25–50 u/kg if bleeding	Superwarfarins need weeks of oral vit K.
Digoxin	DigiFab	10–20 vials acute; calc = (level × kg)/100	K⁺ > 5 = strong indication. Avoid IV calcium.
Valproate	L-carnitine ± dialysis	100 mg/kg IV load → 15 mg/kg q4h	Check ammonia even with normal LFTs and therapeutic level.
Local anesthetic (LAST)	Intralipid 20%	1.5 mL/kg bolus → 0.25 mL/kg/min	Bupivacaine arrest is refractory to ACLS without lipid.
Iron	Deferoxamine	15 mg/kg/hr IV (max 6 g/24h)	"Vin rose" urine = chelation working. Level > 500 mcg/dL.
Methemoglobinemia	Methylene blue	1–2 mg/kg IV over 5 min	SpO2 stuck at ~85% despite O2; chocolate-brown blood. Avoid in G6PD deficiency.
Cyanide	Hydroxocobalamin	5 g IV over 15 min, repeat if needed	Smoke inhalation + altered mental status + lactate > 8.

Valproate (Depakote)

VPA (valproate / valproic acid). Toxic level > 150 mcg/mL; severe toxicity > 450.

Presentation: CNS depression / coma (dose-related), hyperammonemic encephalopathy often disproportionate to LFTs, anion gap metabolic acidosis (lactate from mitochondrial dysfunction), hypotension, cerebral edema in severe cases. Delayed: pancreatitis, thrombocytopenia.
Workup: VPA level (repeat q4–6h until falling, sustained-release peaks late), ammonia, lactate, lipase, LFTs, CBC, BMP, ABG/VBG, APAP + salicylate co-ingestion screen.
L-carnitine 100 mg/kg IV load (max 6 g) over 30 min, then 15 mg/kg q4h. Treats and prevents hyperammonemia and hepatotoxicity (VPA depletes carnitine, shunting metabolism to toxic omega-oxidation pathway).
Hemodialysis if: level > 850 mcg/mL, level > 450 with severe symptoms, refractory shock, cerebral edema, or severe acidosis. VPA is dialyzable once protein binding saturates.
Activated charcoal if < 1–2h post-ingestion and airway protected. Multi-dose charcoal (MDAC) for sustained-release Depakote ER.
Lactulose / rifaximin if hyperammonemic encephalopathy persists despite L-carnitine.
Naloxone is NOT effective. Supportive care for CNS depression: airway, fluids, pressors as needed.

Hyperammonemia pearl: VPA can cause encephalopathy with normal LFTs and a normal VPA level. Always check ammonia in any patient on chronic VPA with altered mental status, even if drug level is therapeutic.

Activated charcoal: Only within 1–2h, alert patient, protected airway. NOT for caustics, hydrocarbons, metals, alcohols.

🔄 Updated Practice: Old teaching: gastric lavage ('stomach pumping') for overdose. Current practice: gastric lavage is rarely performed, risk of aspiration, esophageal perforation, and no proven mortality benefit. Activated charcoal within 1-2 hours of ingestion (alert patient, protected airway) is the only recommended GI decontamination in most cases.

Toxidrome Recognition

Toxidrome	Pupils	HR	Temp	Skin	Mental Status	Examples
Sympathomimetic	Mydriasis	↑↑	↑	Diaphoretic	Agitation, psychosis	Cocaine, amphetamines, MDMA
Anticholinergic	Mydriasis	↑	↑	Dry, flushed	Delirium, hallucinations	Diphenhydramine, TCAs, atropine
Cholinergic	Miosis	↓ or ↑	Normal	Diaphoretic, secretions	Confusion, coma	Organophosphates, nerve agents
Opioid	Miosis (pinpoint)	↓	↓	Normal	CNS depression, coma	Heroin, fentanyl, morphine
Sedative-hypnotic	Normal or miosis	↓	↓	Normal	CNS depression, coma	Benzodiazepines, barbiturates, GHB
Serotonin syndrome	Mydriasis	↑	↑↑	Diaphoretic	Agitation, clonus, hyperreflexia	SSRI + tramadol / MAOI / linezolid; MDMA

Sympathomimetic vs Anticholinergic: Both have mydriasis and tachycardia. The KEY differentiator is skin: sympathomimetics are diaphoretic (wet), anticholinergics are dry (“dry as a bone, red as a beet, hot as a hare, blind as a bat, mad as a hatter”).

Cholinergic Mnemonics: DUMBBBELS, Diarrhea, Urination, Miosis, Bradycardia, Bronchospasm, Bronchorrhea, Emesis, Lacrimation, Salivation. Or SLUDGE, Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis.

GI Decontamination Indications

Method	Indication	Timing	Contraindications
Activated Charcoal	Most oral ingestions of adsorbable substances	Within 1–2 hours (may extend for sustained-release)	Caustics, hydrocarbons, metals (iron, lithium, lead), alcohols, unprotected airway
Whole Bowel Irrigation	Sustained-release preps, iron, lithium, body packers	Any time if substance still in GI tract	Bowel obstruction, perforation, ileus, hemodynamic instability
Gastric Lavage	Rarely indicated, life-threatening ingestion within 1h	Within 1 hour	Caustics, hydrocarbons, impaired airway without intubation

Activated Charcoal Dose: 1 g/kg (max 50g) single dose. Multi-dose activated charcoal (MDAC) q4h for: theophylline, carbamazepine, dapsone, quinine, phenobarbital.

Toxic Alcohol Workup

Step 1, Osmolar Gap: Calculated Osm = 2(Na) + Glucose/18 + BUN/2.8 + EtOH/4.6. Gap = Measured − Calculated. Gap > 10 suggests toxic alcohol
Step 2, Anion Gap: As toxic alcohols are metabolized, osmolar gap falls and anion gap rises (formic acid from methanol, glycolic/oxalic acid from ethylene glycol)
Key point: A normal osmolar gap does NOT rule out toxic alcohol if presentation is delayed (parent compound already metabolized)
Methanol: Visual disturbance (“snowfield vision”), optic disc hyperemia, formic acid → retinal toxicity
Ethylene glycol: Flank pain, calcium oxalate crystals in urine (envelope-shaped), AKI
Isopropanol: Elevated osmolar gap but NO anion gap (metabolized to acetone, not an acid). Ketonemia without acidosis

Treatment: Fomepizole 15 mg/kg IV load (inhibits alcohol dehydrogenase). Dialysis if: pH < 7.25, renal failure, visual changes (methanol), level > 50 mg/dL.

Acetaminophen Nomogram (Rumack-Matthew)

Draw APAP level at 4 hours post-ingestion (or ASAP if > 4h)
Treatment line: 150 mcg/mL at 4h declining to 4.7 mcg/mL at 24h
Level above the treatment line → start NAC immediately
Unknown ingestion time or staggered: start NAC empirically if APAP > 10 mcg/mL or AST elevated
NAC IV protocol (21h): 150 mg/kg/1h → 50 mg/kg/4h → 100 mg/kg/16h Prescott 1979
NAC stop criteria: APAP undetectable, AST/ALT trending down, INR < 2, clinically improving

Anaphylactoid Reactions to NAC: Common during first bag (flushing, urticaria, bronchospasm). Slow the rate, give antihistamines. Do NOT withhold NAC, it is lifesaving.

King’s College Criteria (Transplant Referral): pH < 7.3 after resuscitation, OR all three: INR > 6.5, Cr > 3.4, Grade III/IV encephalopathy.

Serotonin Syndrome vs NMS vs Malignant Hyperthermia

Feature	Serotonin Syndrome	Neuroleptic Malignant Syndrome (NMS)	Malignant Hyperthermia (MH)
Onset	Rapid (hours, within 24h)	Slow (days to weeks)	Acute (minutes to hours after anesthetic exposure)
Cause	Serotonergic drugs (SSRIs, MAOIs, tramadol, linezolid, MDMA)	Dopamine antagonists (haloperidol, metoclopramide) or dopamine withdrawal	Volatile anesthetics (sevoflurane, desflurane, isoflurane) and/or succinylcholine
Setting	Any setting (ward, ED, outpatient)	Any setting, often psychiatric patients	Operating room / post-anesthesia
Pathophysiology	Excess serotonin at 5-HT_1A & 5-HT_2A receptors	Central dopamine D₂ receptor blockade in hypothalamus & basal ganglia	Uncontrolled Ca²⁺ release from sarcoplasmic reticulum via RYR1 mutation
Neuromuscular	Clonus, hyperreflexia, myoclonus (lower extremities > upper)	Lead-pipe rigidity, hyporeflexia, bradykinesia	Generalized rigidity (masseter spasm first), no clonus
Pupils	Mydriasis	Normal	Normal
GI	Diarrhea, hyperactive bowel sounds	Normal/decreased bowel sounds	Not prominent
Temp	↑ (usually < 41°C)	↑↑ (can be > 41°C)	↑↑↑ (rapidly > 40°C, can exceed 43°C)
CK	Mildly elevated	Markedly elevated (> 1000, often > 10,000)	Massively elevated (> 10,000, can exceed 100,000)
Key Labs	Mild CK elevation, leukocytosis	CK ↑↑↑, WBC ↑, LFTs ↑, myoglobinuria	Hypercarbia (rising EtCO₂ is often earliest sign), mixed respiratory & metabolic acidosis, hyperkalemia, myoglobinuria
Mental Status	Agitation, confusion	Altered, stupor, catatonia	Patient under anesthesia (may have delayed emergence)
Autonomic	Tachycardia, HTN, diaphoresis	Tachycardia, labile BP, diaphoresis, sialorrhea	Tachycardia, arrhythmias (hyperkalemia-driven), tachypnea, mottled skin
Treatment	Stop serotonergic drug, cyproheptadine 12mg then 4mg q4h, benzos, cooling	Stop antipsychotic, dantrolene 1–2.5 mg/kg IV, bromocriptine 2.5mg TID, cooling	Stop volatile anesthetic & succinylcholine, dantrolene 2.5 mg/kg IV q5min (max 10 mg/kg), 100% O₂, aggressive cooling, treat hyperkalemia
Resolution	24–72 hours	Days to weeks (7–14 days typical)	Hours with dantrolene (recheck CK q6h × 36h, may recur)
Mortality	Low (< 1% if recognized)	5–20% (higher if unrecognized)	5–10% with dantrolene (was > 70% before dantrolene)
Genetic	No	No (idiosyncratic)	Yes, autosomal dominant RYR1 mutation, test with caffeine-halothane contracture test

Dantrolene is used in both NMS and MH but the mechanism differs. In MH it directly addresses the RYR1 calcium channel defect. In NMS it reduces muscle rigidity. Cyproheptadine (5-HT_2A antagonist) is specific to serotonin syndrome.

Hunter Criteria for Serotonin Syndrome: In the setting of a serotonergic agent, any ONE of: (1) spontaneous clonus, (2) inducible clonus + agitation/diaphoresis, (3) ocular clonus + agitation/diaphoresis, (4) tremor + hyperreflexia, (5) temp > 38°C + ocular or inducible clonus.

MH Early Warning Signs (OR): Unexplained rising EtCO₂ is often the FIRST sign. Then tachycardia, jaw rigidity after succinylcholine, generalized rigidity, rapid temperature rise. If suspected: immediately stop triggering agent, switch to IV anesthetics (propofol/opioids), hyperventilate with 100% O₂ on clean circuit, give dantrolene, and call MH hotline (1-800-644-9737).

Quick Differentiator: Clonus = Serotonin Syndrome. Lead-pipe rigidity + slow onset = NMS. OR setting + rising EtCO₂ + rigidity = MH. All three cause hyperthermia and elevated CK, but the clinical context and neuromuscular exam distinguish them.

↗ See full NMS vs Serotonin Syndrome topic (Neurology) →

Workup

APAP level (4h post-ingestion), salicylate level, ethanol
BMP, ABG, AG, osmolar gap, lactate, LFTs, coags
ECG (QRS width, QTc)
Urine drug screen (limited utility)

Management

Antidote Reference

Toxin	Antidote	Dose
Acetaminophen	NAC	150/50/100 mg/kg over 21h IV
Opioids	Naloxone	0.04–0.4mg IV titrate
TCA	Sodium bicarbonate	1–2 mEq/kg IV bolus
Beta-blockers	Glucagon	3–5mg IV
CCB	High-dose insulin	1u/kg/hr + D10W
Methanol/EG	Fomepizole	15mg/kg IV load
Organophosphates	Atropine + Pralidoxime	Atropine 2mg IV q5min
Digoxin	DigiFab	Based on level or empiric 10–20 vials if acute, life-threatening
Benzodiazepines	Flumazenil	0.2mg IV over 30s, then 0.3mg, then 0.5mg q1min (max 3mg). Only for iatrogenic oversedation in benzo-naive patients
Local anesthetic toxicity	Lipid emulsion (Intralipid)	20% lipid emulsion 1.5 mL/kg IV bolus, then 0.25 mL/kg/min infusion
Cyanide	Hydroxocobalamin	5g IV over 15 min (Cyanokit). Smoke inhalation with lactic acidosis
Iron	Deferoxamine	15 mg/kg/hr IV (max 6g/day). Rose-colored urine = vin rosé sign
Warfarin / Coagulopathy	Vitamin K + FFP/PCC	Vitamin K 10mg IV; 4-factor PCC (KCentra) 25–50 u/kg for life-threatening bleed
Isoniazid	Pyridoxine (B6)	Gram-for-gram (5g IV if unknown amount). INH seizures refractory to benzos

Medications

Detailed Dosing

Drug	Dose	Notes
NAC IV	150mg/kg in D5W/1h, 50mg/kg/4h, 100mg/kg/16h	Anaphylactoid reactions common first bag
Naloxone	0.04mg → 0.4mg → 2mg titrate. Drip: 2/3 bolus/hr	Short t1/2; re-dosing needed for long-acting opioids
Glucagon	3–5mg IV bolus, infusion 2–5mg/hr	BB OD. Causes vomiting (aspiration risk)
Insulin HIE	1u/kg bolus then 1u/kg/hr + D10W	CCB OD. Monitor glucose q15min, K q1h
L-carnitine (Carnitor)	100 mg/kg IV load (max 6 g) over 30 min, then 15 mg/kg IV q4h until ammonia normalizes and clinical improvement	Valproate toxicity / VPA-induced hyperammonemia. Reverses carnitine depletion driving omega-oxidation and ammonia accumulation. Continue until ammonia < 60 and patient awake.
Sodium bicarbonate	1–2 mEq/kg IV bolus, then 150 mEq in 1 L D5W at 200 mL/hr	TCA toxicity (target QRS < 100, pH 7.45–7.55) and salicylate alkalinization (urine pH 7.5–8).
Fomepizole (Antizol)	15 mg/kg IV load → 10 mg/kg q12h × 4, then 15 mg/kg q12h. Dose q4h during HD.	Methanol / ethylene glycol. Inhibits alcohol dehydrogenase. Add thiamine + pyridoxine.
Atropine	2 mg IV, double q3–5 min until secretions dry	Organophosphate / carbamate / nerve agent. No upper-limit dose. Titrate to lung exam.
Pralidoxime (2-PAM)	1–2 g IV over 15–30 min, then 500 mg/hr infusion	Reactivates AChE before "aging" (12–48h). Best within 6h of organophosphate exposure.
Flumazenil (Romazicon)	0.2 mg IV q1 min (max 3 mg)	Benzo reversal. Avoid in chronic users, TCA / proconvulsant co-ingestion, or unknown OD.
DigiFab	Empiric 10–20 vials acute OD; calc # vials = (level × weight kg) / 100	Digoxin toxicity. Indications: K⁺ > 5, dysrhythmia, level > 10 (acute) or > 6 (chronic).
Vitamin K (phytonadione)	10 mg IV slow over 30 min; can also give PO/SC	Warfarin / superwarfarin. Onset 6–24h. Pair with 4F-PCC for active bleeding.
4-factor PCC (Kcentra)	25–50 units/kg IV based on INR	Reverses warfarin INR within minutes. Preferred over FFP for life-threatening bleed.
Intralipid 20%	1.5 mL/kg IV bolus, then 0.25 mL/kg/min for 10 min after stability	Local anesthetic systemic toxicity (LAST), refractory TCA / CCB / BB toxicity. Lipid sink.
Methylene blue	1–2 mg/kg IV over 5 min	Methemoglobinemia (SpO2 ~85% despite O2, chocolate blood). Avoid in G6PD deficiency (paradoxical hemolysis).
Hydroxocobalamin (Cyanokit)	5 g IV over 15 min; repeat 5 g if severe	Cyanide poisoning (smoke inhalation + AMS + lactate > 8). Turns urine/skin red. Interferes with co-oximetry.
Deferoxamine	15 mg/kg/hr IV, max 6 g/24h	Iron poisoning (level > 500 mcg/dL or symptomatic). "Vin rose" urine = active chelation.
Cyproheptadine	12 mg PO load, then 2 mg q2h until improvement (max 32 mg/24h)	Serotonin syndrome (5-HT2A antagonist). Adjunct to benzos and active cooling.
Dantrolene	2–3 mg/kg IV bolus, repeat to 10 mg/kg total	NMS, malignant hyperthermia. Direct skeletal muscle relaxant.

On Rounds

Why is intubating a salicylate patient so dangerous?

They hyperventilate to compensate for metabolic acidosis. During intubation, apnea → CO2 rises → sudden acidemia → salicylate moves into CNS → cardiac arrest. If you must intubate, pre-push bicarb and set vent RR 20–24.

Why is flumazenil contraindicated in TCA overdose?

TCAs lower seizure threshold. Benzos raise it (protective). Flumazenil reverses benzo protection → refractory seizures → worsening acidosis → death.

How do you differentiate sympathomimetic from anticholinergic toxidrome?

Both present with mydriasis, tachycardia, and agitation. The key differentiator is skin: sympathomimetic patients are diaphoretic (wet), while anticholinergic patients are dry (anhidrotic). Anticholinergic also has urinary retention, absent bowel sounds, and flushed skin. Mnemonic: “dry as a bone, red as a beet, hot as a hare, blind as a bat, mad as a hatter.”

A patient presents with elevated osmolar gap but normal anion gap after ingesting an unknown alcohol. What did they drink?

Isopropanol (rubbing alcohol). It is metabolized to acetone (a ketone, not an acid), so it causes an elevated osmolar gap and ketonemia/ketonuria without metabolic acidosis. Methanol and ethylene glycol both cause elevated osmolar gap AND anion gap (as their metabolites are acids: formic acid and glycolic/oxalic acid respectively).

When should you draw an APAP level, and what level mandates NAC?

Draw APAP level at 4 hours post-ingestion (levels before 4h are unreliable). Plot on the Rumack-Matthew nomogram. The treatment line begins at 150 mcg/mL at 4 hours. Any level above the line mandates NAC. If ingestion time is unknown or staggered, start NAC empirically if APAP is detectable (> 10 mcg/mL) or transaminases are elevated.

How do you distinguish serotonin syndrome from NMS at the bedside?

Onset: serotonin syndrome develops within hours; NMS over days to weeks. Neuromuscular: serotonin syndrome has clonus and hyperreflexia; NMS has lead-pipe rigidity and hyporeflexia. CK: mildly elevated in SS vs markedly elevated (> 10,000) in NMS. Treatment: SS responds to cyproheptadine; NMS to dantrolene and bromocriptine.

What are the indications for dialysis in toxic alcohol ingestion?

Dialysis is indicated for methanol or ethylene glycol when: pH < 7.25, renal failure, visual disturbance (methanol), serum level > 50 mg/dL, or deterioration despite fomepizole. Dialysis removes both the parent alcohol and toxic metabolites. Always give fomepizole while awaiting dialysis.

Why do you start naloxone at a low dose (0.04mg) rather than the full 2mg?

In chronic opioid users, high-dose naloxone precipitates acute withdrawal, severe agitation, vomiting (aspiration risk), sympathetic surge (hypertension, tachycardia, pulmonary edema). Goal is to restore respiratory drive, not full consciousness. Start at 0.04–0.4mg IV and titrate to RR > 12. Use a naloxone drip (2/3 of effective bolus/hr) for long-acting opioids.

Clinical Examples

📋 Case 1, Acetaminophen Overdose with NAC Protocol

Patient: 22F presents 6 hours after intentional ingestion of ~30g acetaminophen (60 tablets of 500mg). Nausea, vomiting, RUQ discomfort. VS: HR 92, BP 118/72, afebrile.

Labs: APAP level 220 mcg/mL at 6h post-ingestion, above treatment line on Rumack-Matthew nomogram. AST 45, ALT 38, INR 1.1, Cr 0.9.

Management:

Start NAC immediately: 150 mg/kg IV over 1h → 50 mg/kg over 4h → 100 mg/kg over 16h
Patient develops flushing and urticaria during first bag → anaphylactoid reaction. Slow infusion, diphenhydramine 50mg IV. Do NOT stop NAC
Monitor: APAP level, AST/ALT, INR q6h. At 24h: APAP undetectable, AST peaked at 1,200 then trending down, INR 1.3
NAC stop criteria met: APAP undetectable + AST trending down + INR < 2 + clinical improvement
Psychiatry consult for intentional ingestion before discharge

Key lesson: NAC is most effective within 8h but still beneficial up to 24–72h. Never withhold NAC for anaphylactoid reactions.

📋 Case 2, Toxic Alcohol Ingestion (Ethylene Glycol)

Patient: 48M found confused with empty antifreeze container. GCS 12. VS: HR 110, BP 100/60, RR 28, SpO2 96%.

Labs: Na 140, K 4.2, Cl 100, HCO3 8, BUN 28, Cr 2.4. AG = 32. Measured Osm 340, calculated 290 → osmolar gap = 50. Lactate 6.2. UA: calcium oxalate crystals. EtOH undetectable.

Clinical reasoning: Elevated osmolar gap + elevated AG + AKI + Ca oxalate crystals = ethylene glycol poisoning.

Management:

Fomepizole 15 mg/kg IV load immediately (blocks alcohol dehydrogenase)
Emergent hemodialysis: pH 7.18, Cr 2.4, multiple indications. Increase fomepizole dosing during HD (q4h)
Thiamine 100mg IV + pyridoxine 50mg IV (shunt metabolism away from toxic metabolites)
IV bicarb drip to correct severe acidosis (target pH > 7.2)
After 2 HD sessions: AG normalized, Cr trending down, osmolar gap closed

Key lesson: Osmolar gap and AG are inversely related over time. Early = high osmolar gap; late = high AG. Normal osmolar gap does NOT exclude toxic alcohol.

📋 Case 3, Serotonin Syndrome

Patient: 35M on sertraline 200mg daily, started tramadol 2 days ago. Presents with agitation, diaphoresis, fever 39.2°C, HR 124, BP 158/92.

Exam: Mydriasis, bilateral lower extremity clonus (spontaneous, > 3 beats), hyperreflexia, tremor, hyperactive bowel sounds, diarrhea. CK 680.

Clinical reasoning: Serotonergic agents (SSRI + tramadol) + rapid onset + clonus + hyperreflexia + diaphoresis. Hunter Criteria met (spontaneous clonus with serotonergic agent).

Why NOT NMS: Rapid onset (hours not days), clonus (not rigidity), hyperreflexia (not hyporeflexia), diarrhea (not constipation), CK only 680 (not > 10,000).

Management:

Stop all serotonergic agents (sertraline and tramadol)
Cyproheptadine 12mg PO/NG load, then 4mg q4–6h
Benzodiazepines (lorazepam 2mg IV PRN) for agitation and muscle rigidity
Aggressive cooling if temp > 41°C. Antipyretics ineffective (fever from muscle activity)
IV fluids for rhabdomyolysis prevention, monitor CK and renal function
Symptoms improved within 24h. Full resolution by 72 hours

Key lesson: Serotonin syndrome is a clinical diagnosis (Hunter Criteria). Clonus is the hallmark. Rapid onset and rapid resolution once offending agents stopped.

Monitoring by Toxin

Toxin	Key Monitoring
APAP	AST/ALT q6–12h, INR, APAP level, lactate
Salicylate	Serial levels q2h, ABG, urine pH hourly
TCA	Continuous telemetry, serial ECG QRS width
BB/CCB	HR, BP, glucose q15min, K q1h, lactate

Summary

5 Toxidromes

Sympathomimetic (cocaine/meth), anticholinergic (DPH/TCA), cholinergic/SLUDGE (organophosphate), opioid (fentanyl), sedative-hypnotic (benzo). Plus serotonin syndrome (clonus, hyperreflexia).

Universal Workup

Fingerstick glucose, ECG (QRS/QTc), APAP + salicylate level, ethanol, BMP + AG, lactate, VBG. Coingestants are common.

APAP

NAC 150/50/100. Rumack-Matthew at 4h. LFTs may be normal early. Effective > 24h.

Salicylate

Alkalinize urine, target pH 7.5–8. NEVER intubate unless necessary. Dialysis if > 90 or severe symptoms.

TCA

Wide QRS or R in aVR > 3 mm → sodium bicarb. No flumazenil. Lipid for refractory.

BB / CCB

BB: glucagon. CCB: high-dose insulin (HIE) + calcium + D10W. Lipid for refractory.

Toxic Alcohol

Fomepizole 15 mg/kg load + thiamine + pyridoxine. Dialysis if pH < 7.25, AKI, visual symptoms, level > 50.

Valproate

L-carnitine 100 mg/kg load → 15 mg/kg q4h. Dialysis if level > 850. Check ammonia even with normal LFTs.

Decontamination

Activated charcoal < 1–2h, intact airway. WBI for sustained-release / iron / lithium / body packers.

Call Poison Control

1-800-222-1222. Always. Free expert consultation, tracks outcomes.

📄 One Pager

Emergency / Toxicology · One Pager

Toxicology & Overdose

5 toxidromes. APAP + salicylate + ECG on every overdose. Poison Control: 1-800-222-1222. NAC for acetaminophen. Naloxone for opioids. Treat the patient, not the poison.

🧪 5 Toxidromes

Sympathomimetic (cocaine): mydriasis, HTN, diaphoresis. Anticholinergic (DPH/TCA): mydriasis, dry, hot. Cholinergic (organophosphate): SLUDGE, miosis. Opioid: miosis, RD, CNS depression. Sedative-hypnotic: CNS depression, normal pupils. Plus serotonin syndrome: clonus + hyperreflexia + diaphoresis.

🚨 Universal Workup

Fingerstick glucose, ECG (QRS/QTc), APAP level, salicylate level, ethanol, BMP, lactate, VBG. Call Poison Control on EVERY case: 1-800-222-1222.

💊 Key Antidotes

NAC (APAP). Naloxone (opioids). Fomepizole (toxic alcohol). Atropine + pralidoxime (organophosphate). DigiFab (digoxin). Vitamin K + 4F-PCC (warfarin). L-carnitine (valproate). Lipid emulsion (LAST, refractory cardiotox).

💊 Key Drugs

NAC150 mg/kg → 50 mg/kg/4h → 100 mg/kg/16h

Naloxone0.04–2 mg IV titrate to RR

Fomepizole15 mg/kg IV load

L-carnitine100 mg/kg load → 15 mg/kg q4h

Activated charcoal1 g/kg PO (< 1–2h, airway intact)

⚠️ Pitfalls

Not checking APAP/ASA levels (coingestants common)
Under-dosing naloxone for fentanyl analogs (may need 2–10+ mg)
Flumazenil in chronic benzo users or TCA co-ingestion (seizures)
Intubating a salicylate patient (sudden acidemia → arrest)
Missing serotonin syndrome (clonus, hyperthermia, agitation)
Calcium in dig toxicity ("stone heart", use DigiFab)