Eduovisual
Emergency & Toxicology
Isopropyl alcohol ingestion
— Rapidly absorbed from GI tract within 30 minutes; peak levels at 30–120 min
— Volume of distribution ~0.6 L/kg, similar to ethanol
— Metabolized by hepatic alcohol dehydrogenase (ADH) to acetone (not to acids)
— Acetone is further excreted via lungs and kidneys; half-life of acetone is long (~17–27 hr)
— Parent IPA half-life ~3–7 hours; roughly twice as intoxicating as ethanol on a molar basis
— Inebriated patient with profound CNS depression but NO metabolic acidosis and NO elevated anion gap
— Fruity/acetone breath (mimics DKA) without hyperglycemia or ketoacidosis
— Adolescents, alcoholics seeking substitute when ethanol unavailable, or accidental pediatric exposures (hand sanitizer in toddlers)
— Hemorrhagic gastritis with hematemesis after ingestion
— Psychiatric patients in detox settings, homeless populations, suicidal ingestions
— Osmolar gap: HIGH (IPA itself is osmotically active)
— Anion gap: NORMAL (no acid metabolites)
— Ketonemia/ketonuria: POSITIVE for acetone but serum glucose normal and bicarb preserved
Board pearl: The classic Step 3 vignette is a chronic alcoholic brought in obtunded with fruity breath, ketones in urine, normal glucose, normal pH, normal anion gap, and a wide osmolar gap — that is isopropyl alcohol until proven otherwise. Methanol and ethylene glycol both produce anion gap metabolic acidosis; IPA does not, because acetone is a ketone, not a carboxylic acid.
— CNS depression is the dominant feature — drowsiness, ataxia, slurred speech progressing to stupor, coma, and respiratory depression at high doses
— Onset within 30–60 minutes of ingestion; duration longer than ethanol intoxication of equivalent volume
— Hemorrhagic gastritis: nausea, vomiting (often coffee-ground or frank blood), abdominal pain, hematemesis — IPA is highly irritating to gastric mucosa
— Hypotension in severe cases from vasodilation and myocardial depression
— Hypothermia in prolonged exposure
— 0.5–1 mL/kg of 70% IPA → mild intoxication
— 2–4 mL/kg → severe toxicity, coma
— Lethal dose historically cited ~150–240 mL of 70% solution, but death has occurred at lower doses with comorbidity
— Access: hospital workers, cleaning staff, alcoholics in dry households, pediatric exposure to hand sanitizer bottles
— Co-ingestion of ethanol (very common — ask explicitly)
— Inhalational exposure (sponge baths in febrile children, industrial settings)
— Dermal absorption is minimal in adults but can be significant in infants under occlusive wraps
— Timing of last ingestion — critical for predicting peak and duration
— Suicidal intent → psychiatric evaluation mandatory after medical stabilization
— Polysubstance ingestion (benzos, opioids, acetaminophen) → broaden workup
— Pediatric ingestion of "just a sip" of hand sanitizer can produce hypoglycemia and CNS depression
Step 3 management: On initial encounter, simultaneously: (1) secure airway/IV/O₂/monitor, (2) draw labs including osmolality, electrolytes, glucose, lactate, ethanol level, salicylate, acetaminophen, and (3) obtain collateral history about substance, volume, and timing. Do not delay supportive care while awaiting confirmatory IPA level — many hospitals send it out, with turnaround >24 hours.
— Spectrum from mild ataxia and dysarthria → stupor → coma
— Depth of CNS depression is typically disproportionate to apparent ethanol-equivalent dose because IPA is roughly twice as potent and acetone itself is sedating
— Pupils usually normal or slightly miotic; nystagmus may be present
— Absent focal findings — focality should prompt CT head for alternate diagnosis (trauma, stroke, hemorrhage)
— Fruity, acetone-like breath — high-yield exam clue
— Aspiration risk is significant with hematemesis plus obtunded mental status — check gag reflex, threshold to intubate is low
— Respiratory depression in severe cases
— Epigastric tenderness from hemorrhagic gastritis
— Hematemesis, melena
— Occasional hemorrhagic tracheobronchitis or duodenitis
— Hypotension is the most concerning sign and signals severe toxicity — driven by peripheral vasodilation and direct myocardial depression
— Tachycardia (reflex or volume-depletion driven)
— Cardiovascular collapse portends mortality and is the leading cause of death in severe IPA poisoning
— Hypothermia from CNS-mediated thermoregulatory failure
— Hyporeflexia, flaccid tone
— No retinal findings (distinguishes from methanol) and no oxalate crystalluria or hypocalcemia (distinguishes from ethylene glycol)
Key distinction: Hypotension in an alcohol-poisoned patient who is not acidotic strongly favors isopropyl alcohol over ethanol; ethanol intoxication alone rarely produces hypotension unless complicated by GI bleed, sepsis, or hypothermia. Hypotensive IPA patients have mortality near 45% in case series — these patients need ICU admission and consideration for hemodialysis.
CCS pearl: On a CCS case, immediately order continuous cardiac monitoring, pulse oximetry, two large-bore IVs, isotonic crystalloid bolus 1–2 L for hypotension, and accucheck — hypoglycemia coexists in pediatric and malnourished alcoholic patients.
— BMP — electrolytes, BUN/Cr, glucose, bicarbonate; calculate anion gap
— Serum osmolality (measured by freezing point depression) — calculate osmolar gap
— Serum ethanol level — always co-occurs or is a key differential
— Acetaminophen and salicylate levels — mandatory in any unknown ingestion or suicide attempt
— VBG or ABG with lactate — to confirm absence of acidosis
— Serum ketones / β-hydroxybutyrate — acetone is detected, β-hydroxybutyrate is not elevated
— Urinalysis — ketonuria present, no calcium oxalate crystals (distinguishes from ethylene glycol)
— CBC, lipase, LFTs — for GI bleed, pancreatitis, hepatic comorbidity
— Pregnancy test in reproductive-age women
— Calculated osm = 2(Na) + glucose/18 + BUN/2.8 (+ ethanol/4.6 if ethanol present)
— Osmolar gap = measured − calculated; normal <10
— Each 100 mg/dL of IPA raises osmolar gap by ~16.6 mOsm/kg
— Estimate IPA level (mg/dL) ≈ osmolar gap × 6
— Should be normal (<12) in pure IPA — its presence suggests co-ingestion (methanol, ethylene glycol, salicylates) or shock/lactic acidosis from severe hypotension
— Usually unremarkable; sinus tachycardia common
— Look for QTc prolongation, signs of co-ingestion (TCAs widen QRS, etc.)
— CT head if depressed mentation does not match story, focal deficit, trauma, or fails to improve
— CXR if aspiration suspected
— Serum isopropanol and acetone levels by gas chromatography — definitive but slow turnaround; manage clinically while awaiting
Board pearl: The exam loves the triad — elevated osmolar gap + normal anion gap + ketosis without acidosis + normal glucose = isopropyl alcohol. If glucose is high → DKA. If anion gap is wide → methanol/ethylene glycol/AKA.
— Gas chromatography quantifies serum isopropanol and acetone; gold standard but not real-time
— Levels >400 mg/dL associated with coma; >450 mg/dL historically linked to higher mortality, though clinical status drives management more than level
— Acetone level can remain elevated for 24–48 hours after parent compound clears
— Methanol → wide anion gap, visual symptoms ("snowstorm" vision), retinal edema on fundoscopy, formic acid accumulation
— Ethylene glycol → wide anion gap, calcium oxalate crystalluria, hypocalcemia, AKI, possible Wood's lamp fluorescence of urine (unreliable)
— Propylene glycol (IV lorazepam infusions, antifreeze) → anion gap acidosis with elevated lactate and osmolar gap
— Alcoholic ketoacidosis → anion gap acidosis with β-hydroxybutyrate predominance, normal or low glucose
— DKA → hyperglycemia, anion gap acidosis, ketonemia
— Lactate — elevated lactate in IPA suggests shock, severe toxicity, or alternate diagnosis
— Lipase/amylase — IPA can precipitate hemorrhagic pancreatitis
— CK — rhabdomyolysis from prolonged immobilization
— Coagulation panel and type/crossmatch if hematemesis significant
— Drug screen — broaden differential
— Reserved for ongoing or massive hematemesis after stabilization; most hemorrhagic gastritis is self-limited
Key distinction: The dipstick urine ketone test detects acetoacetate well but acetone poorly with the nitroprusside reaction — yet IPA produces enough acetone that ketonuria is usually positive. β-hydroxybutyrate, the dominant ketone in DKA and AKA, is not detected by nitroprusside — so a patient with "trace" ketones but severe acidosis may still have DKA/AKA.
Step 3 management: Do not wait for the confirmatory IPA level to commit to supportive care, ICU triage for hypotension/coma, or dialysis consultation. Bedside calculation of the osmolar gap is your real-time diagnostic tool.
— Asymptomatic with reliable history, small ingestion, normal vitals, normal mental status → observe 4–6 hours; if remains asymptomatic, medical clearance
— Mild–moderate intoxication (ataxia, drowsy but arousable, stable vitals) → admit to monitored bed, supportive care, serial reassessment
— Severe (coma, hypotension, GI hemorrhage, respiratory depression) → ICU, aggressive resuscitation, hemodialysis consideration
— Airway, breathing, circulation — intubate for GCS ≤8, loss of airway protection, or respiratory failure
— IV access, isotonic crystalloid for hypotension; vasopressors (norepinephrine) if fluid-refractory
— Antiemetics, PPI IV (pantoprazole 40 mg IV) for hemorrhagic gastritis
— Continuous cardiac monitoring, pulse oximetry, capnography in intubated patients
— Warming measures for hypothermia
— Glucose check and dextrose if hypoglycemic; thiamine 100 mg IV in alcoholics before glucose
— Do NOT give fomepizole or ethanol — IPA's metabolite (acetone) is not toxic in the way formate or oxalate are; ADH inhibition only prolongs IPA half-life and the obtundation
— Do NOT give activated charcoal — alcohols are poorly adsorbed; charcoal raises aspiration risk in an obtunded patient
— Do NOT perform gastric lavage — minimal benefit beyond ~30–60 minutes and risks aspiration; consider only for massive recent ingestion with protected airway
— Refractory hypotension despite fluids and vasopressors
— IPA level >400–500 mg/dL
— Prolonged coma threatening airway/ventilator-associated complications
— Hemodynamic instability with renal/hepatic impairment limiting clearance
Board pearl: The exam reflexively tests "fomepizole vs ethanol" for toxic alcohols — but for isopropyl alcohol the answer is NEITHER. Management is supportive ± hemodialysis. Fomepizole is for methanol and ethylene glycol only.
— 0.9% NaCl or LR boluses 500 mL–1 L, reassess; total 20–30 mL/kg if hypotensive
— Avoid over-resuscitation in elderly/CHF — titrate to MAP ≥65, urine output ≥0.5 mL/kg/hr
— Norepinephrine first-line for fluid-refractory hypotension, starting 0.05 µg/kg/min, titrate
— Vasopressin or epinephrine as second agents
— Dopamine reasonable but less preferred per current sepsis-extrapolated practice
— Pantoprazole 40 mg IV bolus then 8 mg/hr infusion or 40 mg IV q12h for hemorrhagic gastritis
— Transfuse PRBCs if Hgb <7 (or <8 in cardiac comorbidity), platelets/FFP as needed
— Ondansetron 4–8 mg IV for nausea
— Thiamine 100 mg IV before any glucose-containing fluids to prevent Wernicke's
— Folate 1 mg, multivitamin
— Dextrose 50% 25–50 mL IV if hypoglycemic
— Magnesium repletion (alcoholics frequently low)
— Avoid benzodiazepines unless absolutely needed — they compound CNS depression
— Use short-acting agents (propofol, dexmedetomidine) under controlled ventilation
— Empiric coverage if aspiration pneumonitis evolves into pneumonia (ceftriaxone ± metronidazole) — but most aspiration pneumonitis is chemical, not bacterial, in first 48 hr
— Once medically cleared, psychiatric evaluation for intentional ingestion, with 1:1 sitter and contraband search per hospital protocol
Step 3 management: Remember the mantra — ABCs, fluids, pressors, PPI, dialysis if severe, NO fomepizole, NO ethanol, NO charcoal. Acetone clearance is renal/pulmonary; supporting perfusion and ventilation accelerates recovery.
— IPA (MW 60 Da, low protein binding, small Vd ~0.6 L/kg) is highly dialyzable
— Acetone is also cleared, though more slowly
— HD can reduce IPA half-life from 3–7 hours to <2 hours
— Hemodynamic instability refractory to fluids and vasopressors
— Coma or respiratory depression requiring prolonged mechanical ventilation
— Serum IPA >400–500 mg/dL (level alone, with significant symptoms)
— Renal failure impairing clearance
— Concomitant severe metabolic derangement
— Place temporary dialysis catheter (right IJ or femoral) under ultrasound guidance with informed consent (or implied if life-threatening)
— Nephrology consult early — do not wait for confirmatory IPA level if clinical picture severe
— Typical session 4–6 hours; recheck level post-HD and clinically reassess
— CRRT acceptable if patient too unstable for intermittent HD, though clearance slower
— RSI with etomidate or ketamine (avoid further hypotension), succinylcholine or rocuronium
— Cuffed ETT given aspiration risk from hematemesis
— NG/OG decompression after intubation if significant gastric blood
— GI consultation for ongoing hematemesis after stabilization; usually self-limited and managed medically with PPI
— Dermal: remove clothing, copious water irrigation if topical exposure
— Inhalation: remove from source, O₂, bronchodilators if wheezing
— GI: no activated charcoal, no lavage in routine cases (alcohols poorly bound, risk > benefit)
CCS pearl: On CCS, the chain of orders for severe IPA poisoning runs: IV access → labs → ABG/osmolality → fluid bolus → intubate if obtunded → norepinephrine if hypotensive → nephrology consult for HD → ICU admission → psychiatry consult once stable. Forgetting nephrology in the hypotensive comatose patient is a common scoring miss.
— Reduced hepatic ADH activity prolongs IPA half-life; expect longer obtundation
— Higher baseline risk of aspiration, falls during intoxication, and rib fractures from prolonged immobilization
— Polypharmacy (benzodiazepines, opioids, antihypertensives) compounds CNS depression and hypotension
— Lower physiologic reserve → earlier ICU transfer threshold
— Increased GI bleeding risk if on anticoagulants/antiplatelets; reverse anticoagulation as indicated (4-factor PCC for warfarin, andexanet/PCC for DOACs per institutional protocol)
— Volume resuscitation must balance hypotension against CHF/diastolic dysfunction — consider POCUS for IVC and cardiac function
— Acetone clearance is partly renal — accumulation prolonged in CKD/AKI
— Lower threshold for hemodialysis, both for IPA removal and for managing volume/electrolytes
— Avoid nephrotoxic adjuncts (NSAIDs, contrast)
— Dose-adjust co-administered medications (e.g., enoxaparin for VTE prophylaxis once GI bleeding controlled)
— Cirrhotics have reduced ADH activity → slower IPA → acetone conversion, so parent compound persists longer
— Higher baseline coagulopathy increases GI hemorrhage severity; have FFP/cryoprecipitate available
— Increased risk of hepatic encephalopathy compounding CNS depression — check ammonia, treat with lactulose if appropriate
— Watch for concurrent alcoholic hepatitis (the population overlaps)
— Thiamine before glucose, screen for Wernicke-Korsakoff
— CIWA protocol initiation once IPA clears, since ethanol withdrawal may emerge
— Screen for cardiomyopathy, anemia, thrombocytopenia, electrolyte derangements (Mg, Phos, K)
Step 3 management: In an elderly cirrhotic with IPA ingestion, anticipate prolonged ICU course, early HD, aggressive thiamine/electrolyte repletion, and overlap with ethanol withdrawal management once IPA-mediated CNS depression resolves. Discharge planning should include social work and addiction medicine referral.
— Common scenario: toddler swallows hand sanitizer (60–70% ethanol or IPA-based) or mouthwash; or febrile child receives alcohol sponge bath
— Small body mass + immature hepatic ADH + low glycogen stores → profound hypoglycemia in addition to CNS depression
— Check fingerstick glucose immediately and treat with D10W 5 mL/kg or D25W 2 mL/kg
— Dermal absorption significant in infants — avoid alcohol sponging entirely
— Lower thresholds for ICU admission and HD in severe pediatric cases
— Mandatory: assess accidental vs. intentional ingestion, evaluate home safety (storage of cleaning products), consider child protective services if neglect suspected
— Recreational ingestion ("hand sanitizer challenges"), suicide attempts, substitute for ethanol
— Mandatory psychiatric evaluation; CRAFFT screening; involve parents/guardians per state minor consent laws
— Confidentiality: substance use disclosure to parents varies by state; understand local mature minor doctrine
— IPA crosses placenta; data limited but fetal CNS depression and possible miscarriage risk in massive ingestions
— Fetal monitoring continuous if viable gestation (≥23–24 weeks)
— Management mirrors non-pregnant adult: supportive care, fluids, vasopressors, HD if severe
— Fomepizole is NOT used for IPA, but if methanol/ethylene glycol co-ingestion is suspected, fomepizole is pregnancy category C and is given when life-threatening — maternal life takes precedence
— Left lateral decubitus positioning in 2nd/3rd trimester, OB consultation
— Postpartum: screen for postpartum depression, substance use disorder, intimate partner violence
Board pearl: A toddler with altered mental status after ingesting hand sanitizer needs glucose first, then supportive care — hypoglycemia is the under-recognized killer in pediatric alcohol ingestions, even more than CNS depression itself. Always order an accucheck before assuming intoxication is "just sedation."
— Hypotension and cardiovascular collapse — leading cause of death in severe IPA poisoning
— Myocardial depression, vasodilation, decreased SVR
— Arrhythmias uncommon but possible from electrolyte shifts
— Coma, respiratory depression, aspiration
— Anoxic brain injury if airway not protected
— Prolonged sedation from acetone (long half-life)
— Hemorrhagic gastritis, esophagitis, duodenitis with hematemesis/melena
— Hemorrhagic pancreatitis — check lipase if abdominal pain persists
— Aspiration pneumonitis from emesis with depressed gag
— Aspiration pneumonia (delayed bacterial superinfection 48–72 hr)
— ARDS in severe cases
— Pre-renal AKI from hypotension
— Rhabdomyolysis from prolonged immobilization → pigment nephropathy
— Hypoglycemia (especially pediatric, malnourished, chronic alcoholic)
— Hypothermia
— Electrolyte derangements (hypokalemia, hypomagnesemia)
— Hemorrhage from gastritis; rarely DIC in severe shock
— Underlying SUD or depression unaddressed → recidivism
— Repeat ingestions, completed suicide on follow-up
— Catheter-related infections from dialysis access
— Ventilator-associated pneumonia in prolonged intubation
— Pressure injuries, DVT in prolonged immobilization → start mechanical VTE prophylaxis early, chemical prophylaxis once bleeding controlled
Key distinction: Unlike methanol (blindness, putaminal necrosis) and ethylene glycol (AKI, hypocalcemia, oxalate nephropathy), IPA's complications are driven by hypotension and GI hemorrhage rather than end-organ toxicity from a poisonous metabolite. This is why supportive care — and not antidote therapy — is the cornerstone.
Step 3 management: During admission, perform serial mental status checks, q4h vitals initially, daily CBC/BMP, monitor lipase if abdominal symptoms, and reassess for aspiration pneumonia at 48–72 hr if febrile or hypoxemic.
— GCS ≤12 or rapidly declining mental status
— Need for intubation/mechanical ventilation
— Hypotension requiring vasopressors
— Hemodynamic instability or arrhythmia
— Active GI hemorrhage requiring transfusion or endoscopy
— Serum IPA >400 mg/dL or osmolar gap >50 with clinical toxicity
— Receiving or anticipating hemodialysis
— Severe acid-base or electrolyte derangement
— Significant comorbidity (cirrhosis, CKD, CHF) with moderate toxicity
— Mild–moderate intoxication, hemodynamically stable, awake but ataxic
— No active hemorrhage
— Adequate airway protection
— Reliable for serial neuro checks
— Asymptomatic after 4–6 hours of observation post-ingestion
— Normal mental status, normal vitals, tolerating PO
— Reliable adult caregiver (especially for pediatric and intoxicated patients)
— Cleared by psychiatry if intentional ingestion
— Outpatient follow-up arranged
— Medical toxicology / Poison Control (1-800-222-1222) — early call, document recommendations
— Nephrology — for HD candidacy and access
— Psychiatry — for any intentional ingestion before discharge; involuntary hold (5150/equivalent state code) if imminent suicide risk
— Gastroenterology — significant or persistent hematemesis
— Social work / case management — substance use disorder resources, safe disposition, child welfare if applicable
— Addiction medicine — for chronic alcoholic substitution patterns
— Community hospital without HD capability → transfer to tertiary center for severe cases
— Pediatric cases → transfer to pediatric tertiary care
CCS pearl: "Move clock forward 4 hours" — reassess vitals, mental status, repeat osmolar gap and BMP. If improving, downgrade. If worsening, escalate. Document every escalation decision; do not let the CCS clock advance more than 4 hours without a reassessment in unstable patients.
| • Methanol (windshield washer fluid, moonshine, antifreeze additive): | ||||
| — Wide anion gap metabolic acidosis from formic acid | ||||
| — Visual disturbances ("snowstorm," central scotoma), retinal edema, optic disc hyperemia | ||||
| — Treat: fomepizole (15 mg/kg load, then 10 mg/kg q12h), folate/folinic acid, hemodialysis | ||||
| — Putaminal hemorrhage/necrosis on CT | ||||
| • Ethylene glycol (antifreeze): | ||||
| — Wide anion gap metabolic acidosis from glycolic/oxalic acids | ||||
| — Calcium oxalate crystalluria, hypocalcemia, AKI, possible QT prolongation | ||||
| — Treat: fomepizole, thiamine and pyridoxine cofactors, hemodialysis | ||||
| • Propylene glycol: | ||||
| — Found in IV lorazepam, diazepam, phenytoin formulations and antifreeze | ||||
| — Anion gap acidosis with elevated lactate and elevated osmolar gap | ||||
| — Stop infusion; supportive; HD in severe cases | ||||
| • Ethanol: | ||||
| — CNS depression similar but milder per molar dose | ||||
| — No osmolar gap surprise (calculated correction available) | ||||
| — May coexist with IPA — measure level | ||||
| • Alcoholic ketoacidosis (AKA): | ||||
| — Chronic alcoholic, recent binge then abstinence with vomiting | ||||
| — Anion gap acidosis, ketosis (β-hydroxybutyrate predominant), often hypoglycemia | ||||
| — Treat: dextrose + saline + thiamine | ||||
| • Diabetic ketoacidosis (DKA): | ||||
| — Hyperglycemia, anion gap acidosis, ketonuria, dehydration | ||||
| — Treat: insulin, fluids, potassium | ||||
| Key distinction table: | ||||
| Toxin | Anion gap | Osmolar gap | Glucose | Hallmark |
| IPA | Normal | High | Normal | Acetone breath, no acidosis |
| Methanol | High | High | Normal | Vision changes |
| Ethylene glycol | High | High | Normal | Oxalate crystals, AKI |
| AKA | High | Normal | Low/normal | Recent binge + vomiting |
| DKA | High | Normal | High | Hyperglycemia |
| Ethanol | Normal | High (early) | Normal | Slurred speech |
| Board pearl: High osmolar gap + normal anion gap + normal glucose + ketonuria = isopropyl alcohol. Memorize this string — it appears almost verbatim in vignettes. |
— Miosis, respiratory depression, decreased bowel sounds
— Naloxone 0.04–2 mg IV/IM/IN reverses
— No osmolar gap, no ketosis
— CNS depression with relatively preserved vitals
— Flumazenil rarely used (seizure risk)
— Often co-ingested with alcohol
— Profound CNS depression, often resolves spontaneously
— Always check fingerstick — reversible coma cause
— D50 1 amp IV, repeat as needed
— Especially in psychogenic polydipsia, MDMA use, beer potomania
— Check sodium; correct cautiously
— Asterixis, fetor hepaticus (mimics fruity breath but is sulfurous), elevated ammonia
— BUN markedly elevated, asterixis; dialysis indicated
— Headache, multiple victims, cherry-red skin (rare), elevated COHb on co-oximetry
— Meningitis, encephalitis — fever, meningismus; LP indicated
— Stroke, ICH, SDH (especially in alcoholics with falls)
— CT head for focal deficits or unexplained coma
— Consider EEG if not awakening
— Confusion, ophthalmoplegia, ataxia in alcoholic — thiamine 500 mg IV TID for treatment dose
— Fever, hypotension, leukocytosis, lactate
Step 3 management: The "coma cocktail" mindset — glucose, naloxone, thiamine, O₂ — remains a useful rapid-fire approach in undifferentiated altered mental status while specific labs return. Add a CT head and broaden workup if no rapid improvement.
CCS pearl: Order fingerstick glucose, ABG with co-oximetry, naloxone trial in suspected opioid, ammonia in cirrhotic, CT head if focal or persistent coma — these orders run in parallel, not in series.
— Mental status returned to baseline
— Stable vitals, tolerating PO, ambulating safely
— GI bleeding resolved or controlled with stable Hgb
— Electrolytes corrected
— No outstanding ICU-level needs
— PPI (omeprazole 20–40 mg PO daily) × 4–8 weeks if hemorrhagic gastritis was documented
— Thiamine 100 mg PO daily, folate 1 mg PO daily, multivitamin in chronic alcoholics
— Naltrexone 50 mg PO daily or acamprosate 666 mg PO TID for alcohol use disorder if patient consents and no contraindication (avoid naltrexone in opioid users or severe liver disease)
— Avoid disulfiram in non-adherent or impulsive patients
— Continue home meds, reconcile carefully — hold sedatives until stable
— Brief intervention and motivational interviewing in ED/inpatient setting
— Referral to outpatient addiction medicine, SAMHSA-funded programs, Alcoholics Anonymous
— Consider medication-assisted treatment for AUD
— Naloxone rescue kit if any concurrent opioid use
— Inpatient psychiatric admission if active suicidality, plan, or inadequate outpatient support
— Safety plan, lethal means restriction (lock up household alcohols, hand sanitizers, medications)
— Outpatient psychiatry follow-up within 7 days
— Crisis hotline numbers (988 Suicide & Crisis Lifeline)
— Pediatric: child-resistant caps, store hand sanitizer/cleaning products out of reach, poison control number on fridge
— Adults: remove access to substitute alcohols, engage household
— Update tetanus, hep A/B (alcoholics), influenza, pneumococcal as indicated
Board pearl: USPSTF recommends screening all adults for unhealthy alcohol use and providing brief behavioral counseling — the ED visit is a high-yield "teachable moment." Document the SBIRT (Screening, Brief Intervention, Referral to Treatment) intervention in the chart.
— Primary care visit within 1–2 weeks of discharge — reconcile meds, screen for complications, reinforce sobriety plan
— Psychiatry within 7 days if intentional ingestion or new diagnosis of depression/SUD
— Addiction medicine within 1–2 weeks for MAT initiation/titration
— GI follow-up at 4–6 weeks if significant hemorrhagic gastritis; consider outpatient EGD if symptoms persist
— CBC at 1–2 weeks if GI bleeding occurred — confirm Hgb stability
— LFTs, BMP for chronic alcoholics — baseline and trend
— Mental status, mood, suicidality at each visit (PHQ-9, AUDIT-C)
— Adherence to PPI, MAT, vitamins
— Lethal means restriction — single most effective suicide prevention
— Substance use disorder education — IPA is not a safe alcohol substitute despite myths; explain toxicity profile
— Relapse prevention strategies, identify triggers
— Engage family/support system with patient consent
— Address comorbid depression, anxiety, PTSD
— Intensive outpatient programs (IOP), partial hospitalization (PHP), or inpatient rehab based on severity (ASAM criteria)
— Peer support: AA, SMART Recovery
— Vocational rehabilitation and housing support if needed (social work)
— Note SBIRT intervention, harm reduction counseling, MAT discussion
— Provide written aftercare instructions and resource numbers
Step 3 management: Build the longitudinal plan before discharge, not after. Schedule the PCP and psych appointments from the inpatient team using care coordinators — patients with SUD have notoriously poor self-arranged follow-up. Warm hand-offs cut readmission and completed suicide rates.
Board pearl: Single most effective discharge intervention for intentional ingestion isn't a medication — it's lethal means counseling and removing access at home. Document explicitly.
— Acutely intoxicated patient cannot consent to procedures (HD catheter, intubation) — invoke emergency exception/implied consent for life-threatening interventions
— Once intoxication resolves, re-discuss any ongoing treatments and document capacity
— Surrogate decision-maker (spouse, adult child, designated POA) if patient remains incapacitated and non-emergent decision arises
— Intentional ingestion mandates psychiatric evaluation
— If patient meets criteria (danger to self/others, grave disability), invoke state-specific involuntary hold (e.g., 5150 in CA, Section 12 in MA, Baker Act in FL)
— Document the specific behaviors and statements supporting the hold
— Child neglect/endangerment if pediatric IPA exposure reflects unsafe storage or parental impairment — report to CPS per state law
— Elder abuse/neglect in vulnerable adult cases
— Intimate partner violence screening; offer resources but reporting varies by state
— Substance use disorder records protected under 42 CFR Part 2 — stricter than HIPAA; explicit consent required for release
— Adolescent confidentiality varies by state; balance with safety
— Highest-risk window for suicide is first 30 days after discharge from psychiatric or medical admission for intentional ingestion
— Ensure warm hand-off to outpatient provider with appointment in hand
— Medication reconciliation: avoid discharging with large supplies of sedatives/opioids
— Provide naloxone kit and 988 hotline information
— Capacity is clinical, decision-specific, and assessed by treating physician
— Document the four pillars: understanding, appreciation, reasoning, choice
— 1:1 sitter for suicidal patients, contraband search, paper gown protocol, removal of cords/sharps from room
— Fall precautions for intoxicated patients
— Identification banding to prevent wrong-patient errors
Board pearl: A common Step 3 vignette: an intoxicated patient refuses care and tries to leave. Answer — the intoxicated patient lacks capacity; you may detain and treat under emergency exception until sober and capacity reassessed. Refusing AMA discharge to an intoxicated person is appropriate medical and legal practice.
— MUDPILES for anion gap acidosis (M-methanol, U-uremia, D-DKA, P-propylene glycol/paraldehyde, I-iron/INH/isoniazid, L-lactate, E-ethylene glycol, S-salicylates)
— IPA is NOT in MUDPILES — it doesn't cause AGMA
— Acetone is also produced in DKA and starvation ketosis — fruity breath is shared
— IPA → acetone is the only common toxic alcohol where the metabolite is a ketone, not a carboxylic acid
— IPA causes the highest osmolar gap per mg/dL among toxic alcohols (smallest MW after methanol)
— Gap can be normal late in methanol/ethylene glycol poisoning (parent metabolized to acid)
— FDA-recommended: 60–95% ethanol or 70–91.3% isopropanol
— Pandemic-era surge in pediatric and prison-population ingestions
— 70% IPA (most common rubbing alcohol concentration)
— 91–99% IPA in higher-purity products — small volumes can be toxic
— Printing, electronics manufacturing, healthcare cleaning
— OSHA PEL 400 ppm 8-hr TWA
— Hypoglycemia is the underrecognized lethal complication
— Dermal absorption in infants under occlusive wraps — never use IPA sponge baths
— Acetone interferes with creatinine measurement (Jaffe reaction) — may falsely elevate Cr
— Acetone gives positive urine ketone dipstick (nitroprusside)
— Hypotension on presentation, coma duration, IPA level >400 mg/dL, comorbidities
Step 3 management: When the vignette mentions a chronic alcoholic with "fruity breath, ketonuria, normal glucose, and an osmolar gap of 35," reflex answer: isopropyl alcohol ingestion — manage with supportive care and dialysis if severe; no fomepizole.
— "A 47-year-old man with chronic alcoholism is brought to the ED obtunded. Vitals: BP 128/76, HR 96. Breath has a fruity odor. Labs: Na 140, Cl 103, HCO₃ 24, glucose 96, BUN 12, Cr 1.0. Measured osmolality 320 (calculated 290). UA: ketones 3+. What is the most likely diagnosis?"
— Answer: Isopropyl alcohol ingestion
— Trap distractors: DKA (glucose normal), methanol (no AGMA, no visual symptoms), ethylene glycol (no AGMA, no crystals), AKA (no AGMA)
— Same vignette, now BP 82/50 and obtunded. Best next step?
— Answer: IV fluids, intubation, nephrology consult for hemodialysis — NOT fomepizole, NOT ethanol, NOT charcoal
— "A 3-year-old is found lethargic after ingesting an unknown amount of hand sanitizer. Glucose 42, breath fruity, normal pH. Most immediate next step?"
— Answer: D25W 2 mL/kg IV (hypoglycemia trumps all in pediatric alcohol ingestion)
— "Which finding most reliably distinguishes IPA from methanol/ethylene glycol?"
— Answer: Normal anion gap with elevated osmolar gap (or "absence of metabolic acidosis")
— Asymptomatic 4 hours post-ingestion with normal vitals and labs — discharge after psychiatric clearance if intentional
— Comatose with hypotension — ICU + HD
— Intentional ingestion + active suicidality → psychiatric admission, not outpatient
— Chronic alcoholic → SBIRT, thiamine, naltrexone discussion, addiction medicine referral
— "Why would fomepizole be inappropriate here?" → IPA metabolizes to acetone, a non-toxic ketone; blocking ADH only prolongs sedation
— Intoxicated patient demanding discharge → refuse AMA, treat under implied consent, reassess capacity when sober
Board pearl: When the answer choices include "fomepizole" and "ethanol" alongside "supportive care + hemodialysis," and the vignette has no anion gap acidosis, the answer is almost always the supportive option. Anion gap status is the single most discriminating data point on these stems.
Isopropyl alcohol ingestion produces profound CNS depression with elevated osmolar gap, normal anion gap, ketosis without acidosis, and normal glucose — managed with supportive care, GI protection, and hemodialysis for severe or hemodynamically unstable cases, but NEVER with fomepizole or ethanol.
Board pearl: If you remember one teaching point: isopropyl alcohol is the toxic alcohol that does NOT cause an anion gap acidosis — and that single fact unlocks both the diagnosis and the correct management on virtually every Step 3 stem.