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Summary Table

Feature	Alcohol Intoxication	Alcohol Withdrawal
Risk Factors	Binge drinking, adolescents, college-age adults, chronic alcohol use disorder, concurrent sedative use	Chronic heavy drinker who abruptly stops or significantly reduces intake; history of prior withdrawal seizures; concurrent illness forcing cessation (hospitalization, trauma)
Etiology	Direct CNS depression by ethanol via GABA-A receptor potentiation and NMDA receptor inhibition	Loss of chronic ethanol-mediated GABA-A stimulation and unopposed NMDA/glutamate excitatory rebound
Patient Presentation	Slurred speech, ataxia, disinhibition, somnolence, stupor, or coma depending on severity	Tremulousness, agitation, anxiety, insomnia, nausea/vomiting, seizures, or florid delirium tremens
Classic Physical Exam	Nystagmus, conjunctival injection, smell of alcohol, depressed reflexes, hypothermia in severe cases	Tremor (especially hands), diaphoresis, tachycardia, hypertension, hyperthermia, agitation, visual/tactile hallucinations
Key Diagnostic Results	Elevated serum ethanol level, elevated osmolal gap, possible hypoglycemia, possible metabolic acidosis if co-ingestion	Clinical diagnosis using CIWA-Ar score; labs show hypomagnesemia, hypokalemia, elevated GGT, elevated MCV, possible thrombocytopenia
Management	Supportive care, airway protection, IV fluids, thiamine before glucose, monitor for aspiration and respiratory depression	Benzodiazepines (symptom-triggered using CIWA-Ar), thiamine, folate, electrolyte repletion, ICU for delirium tremens
Keywords	"Found down," "smells of alcohol," "unresponsive with depressed respirations," "elevated osmolal gap"	"Stopped drinking 2 days ago," "tremulous," "sees bugs on the wall," "seizure 48 hours after last drink," "diaphoretic and tachycardic"

1. Pathophysiology

Alcohol Intoxication

Ethanol is a small, water-soluble molecule that freely crosses the blood-brain barrier. Its primary mechanism of CNS depression involves two simultaneous actions: potentiation of GABA-A receptor activity (the brain's primary inhibitory system) and inhibition of NMDA glutamate receptors (the brain's primary excitatory system). The net result is global CNS depression that scales with blood alcohol concentration.

At low concentrations, ethanol preferentially suppresses cortical inhibitory circuits, which paradoxically produces disinhibition and euphoria. This is why mildly intoxicated patients appear talkative and impulsive rather than sedated. As levels rise, deeper brain structures are affected: the cerebellum (causing ataxia and dysarthria), the reticular activating system (causing stupor and coma), and ultimately the medullary respiratory centers (causing respiratory depression and death).

A critical biochemical consequence is that ethanol metabolism by alcohol dehydrogenase generates excess NADH, shifting the NAD+/NADH ratio. This drives several testable metabolic derangements: hypoglycemia (impaired gluconeogenesis), lactic acidosis (pyruvate shunted toward lactate), and hypertriglyceridemia. The excess NADH also explains why the osmolal gap is elevated: ethanol is an osmotically active substance that is measured by the osmometer but not accounted for in the calculated osmolality formula.

Alcohol Withdrawal

In the chronic drinker, the brain has adapted to the constant presence of ethanol. To maintain homeostasis against persistent GABA enhancement and NMDA suppression, the CNS downregulates GABA-A receptors and upregulates NMDA receptors and voltage-gated calcium channels. When ethanol is suddenly removed, this compensatory state is unmasked: the patient now has reduced inhibitory tone and dramatically increased excitatory tone. This produces a state of CNS hyperexcitability that manifests as tremor, autonomic hyperactivity, seizures, and potentially fatal delirium tremens.

The reason withdrawal can kill is straightforward: unopposed sympathetic and excitatory activity leads to hyperthermia, cardiovascular collapse, and refractory seizures. Delirium tremens carries a mortality rate of up to 37% if untreated, though with modern ICU care this drops to approximately 1 to 5%.

Kindling is a tested concept: each successive episode of withdrawal sensitizes the brain, making future withdrawal episodes progressively more severe. A patient with a history of prior withdrawal seizures is at significantly higher risk for severe withdrawal.

2. Classification and Clinical Manifestation

Severity by Blood Alcohol Concentration

BAC (mg/dL)	Clinical Stage	Key Features
20 to 50	Mild euphoria	Relaxation, mild impairment of judgment, slight decrease in fine motor coordination
50 to 100	Impaired judgment	Emotional lability, impaired reaction time, legally impaired in most jurisdictions
100 to 200	Obvious intoxication	Ataxia, slurred speech, nystagmus, significant cognitive impairment
200 to 300	Severe intoxication	Marked ataxia, vomiting (aspiration risk), stupor, hypothermia
300 to 400	Stupor/Coma	Respiratory depression, loss of protective reflexes, risk of aspiration pneumonia
>400	Potentially lethal	Respiratory arrest, cardiovascular collapse, death (though chronic drinkers may tolerate much higher levels)

A chronic heavy drinker may be ambulatory and conversational at a BAC that would render a naive drinker comatose. The vignette will often specify "chronic alcohol use" to explain a seemingly paradoxical presentation.

Alcohol Withdrawal

Syndrome	Time After Last Drink	Clinical Features	Severity
Minor withdrawal (tremulousness)	6 to 12 hours	Anxiety, insomnia, tremor, mild tachycardia, mild hypertension, GI upset, intact sensorium	Mild
Alcoholic hallucinosis	12 to 24 hours	Visual, auditory, or tactile hallucinations with intact orientation and clear sensorium (patient knows the hallucinations are not real)	Moderate
Withdrawal seizures	12 to 48 hours	Generalized tonic-clonic seizures, typically brief and self-limited; may occur in clusters; no postictal focal deficits	Moderate to Severe
Delirium tremens (DT)	48 to 96 hours (peak at 72 hours)	Global confusion, profound autonomic instability (fever, tachycardia, hypertension, diaphoresis), agitation, hallucinations with loss of orientation, tremor	Life-threatening

The timeline is the single most important discriminator on the exam. When the vignette says "48 hours after admission for pneumonia, the patient becomes confused, diaphoretic, and tremulous," the answer is delirium tremens until proven otherwise.

3. Diagnostic Workup

Test	Intoxication	Withdrawal
Best Initial Test	Serum ethanol level	Clinical diagnosis using CIWA-Ar (Clinical Institute Withdrawal Assessment for Alcohol, revised)
Gold Standard	Serum ethanol level (also the best initial test)	Clinical assessment and CIWA-Ar scoring (no confirmatory lab test exists)
Key Labs	Serum ethanol, serum osmolality + calculated osmolal gap, blood glucose, BMP, ABG/VBG, serum ketones if acidotic	BMP (hypokalemia, hypomagnesemia, hypophosphatemia), CBC (macrocytosis, thrombocytopenia), hepatic panel (elevated AST > ALT, typically 2:1 ratio), GGT, lipase
Imaging	CT head if altered mental status to rule out subdural hematoma or other traumatic pathology	CT head if first seizure, focal neurological deficits, or persistent altered mental status to exclude structural pathology
Special Considerations	Always check serum osmolal gap; if anion gap metabolic acidosis is present, consider methanol or ethylene glycol co-ingestion	Always check magnesium (seizure threshold lowering); blood smear may show target cells or macrocytosis

For intoxication, the approach is predominantly supportive and the diagnostic goal is to rule out dangerous co-ingestants and traumatic injuries. The serum ethanol level confirms the diagnosis, but the osmolal gap is the more nuanced test point. Ethanol elevates the osmolal gap because it raises measured osmolality without affecting calculated osmolality. The formula for the osmolal gap is:

$$\text{Osmolal Gap} = \text{Measured Osmolality} - \text{Calculated Osmolality}$$

$$\text{Calculated Osmolality} = 2[\text{Na}^+] + \frac{\text{Glucose}}{18} + \frac{\text{BUN}}{2.8}$$

A normal osmolal gap is less than 10 mOsm/kg. In ethanol intoxication, the gap is elevated but the anion gap is typically normal. If you see an elevated osmolal gap with an elevated anion gap metabolic acidosis, think toxic alcohol ingestion (methanol or ethylene glycol), not simple ethanol intoxication. This is a classic exam pivot.

Always obtain a blood glucose in any intoxicated patient. Ethanol impairs hepatic gluconeogenesis, and hypoglycemia can mimic or compound the CNS depression of intoxication. CT head is indicated whenever the altered mental status is disproportionate to the measured ethanol level, or when there is any sign of head trauma, since chronic alcohol users are at high risk for subdural hematoma.

For withdrawal, there is no single confirmatory laboratory test. The diagnosis is clinical and graded by the CIWA-Ar scale, which scores ten domains: nausea/vomiting, tremor, paroxysmal sweats, anxiety, agitation, tactile disturbances, auditory disturbances, visual disturbances, headache, and orientation/clouding of sensorium. Scores range from 0 to 67:

CIWA-Ar Score	Severity	Action
< 10	Mild	Observation, no pharmacotherapy typically required
10 to 18	Moderate	Consider benzodiazepine administration
> 20	Severe	Aggressive benzodiazepine dosing, consider ICU admission

The CIWA-Ar protocol is the backbone of symptom-triggered therapy, which is the preferred approach over fixed-dose scheduling because it results in lower total benzodiazepine doses and shorter treatment duration.

Laboratory studies in withdrawal serve to identify complications and comorbidities: hypomagnesemia (lowers seizure threshold and must be corrected), hypokalemia (often refractory until magnesium is repleted), thrombocytopenia (direct marrow toxicity of ethanol), and the classic AST:ALT ratio greater than 2:1 that suggests alcoholic liver disease.

4. Management and Treatment

Setting	Intoxication	Withdrawal
Acute Stabilization	ABCs, airway protection, lateral decubitus position to prevent aspiration, IV access	Benzodiazepines guided by CIWA-Ar, IV fluids, continuous monitoring
First-Line Pharmacotherapy	Thiamine 100 mg IV before any glucose administration, then D50W if hypoglycemic	Chlordiazepoxide (mild/moderate, oral) or Diazepam/Lorazepam (severe, IV)
Adjunctive Therapy	IV normal saline, electrolyte repletion, antiemetics	Thiamine 500 mg IV x 3 days (if Wernicke suspected), folate 1 mg daily, magnesium 2 g IV, potassium repletion
Refractory Cases	Intubation and mechanical ventilation for respiratory failure; hemodialysis only in rare severe toxicity	Phenobarbital or propofol infusion in ICU for benzodiazepine-resistant DT
Long-Term	Brief intervention, motivational interviewing, referral to addiction medicine	Naltrexone 50 mg daily (or 380 mg IM monthly) or Acamprosate 666 mg TID for relapse prevention; Disulfiram 250 mg daily as aversion therapy

Alcohol Intoxication

The cornerstone is supportive care. Most intoxicated patients recover with time as the liver metabolizes ethanol at a roughly fixed rate of 15 to 20 mg/dL per hour. The critical steps are:

Airway protection is the priority. Position the patient in the lateral decubitus (recovery) position to reduce aspiration risk. Intubate if the gag reflex is absent or respiratory depression is present.
Thiamine 100 mg IV must be given before any glucose-containing fluids. This is one of the most tested management pearls in all of emergency medicine. Glucose administration in a thiamine-depleted patient can precipitate or worsen Wernicke encephalopathy by exhausting the remaining thiamine stores (thiamine is a cofactor for pyruvate dehydrogenase and other enzymes in glucose metabolism). The classic teaching: "banana bag" = thiamine first, then glucose.
Correct hypoglycemia with D50W (50 mL of 50% dextrose IV) after thiamine.
IV normal saline for volume repletion and to support renal clearance.
Check for co-ingestants and trauma. An intoxicated patient with a GCS that does not improve as the BAC falls needs CT imaging to exclude intracranial pathology.

There is no role for activated charcoal in alcohol intoxication (ethanol is absorbed too rapidly). There is no role for routine gastric lavage. Hemodialysis is technically effective at clearing ethanol but is reserved for extreme cases (BAC > 500 mg/dL with hemodynamic instability), which are rarely tested.

Alcohol Withdrawal

The management follows a graded, symptom-triggered protocol:

Benzodiazepines are first-line therapy. They work by directly substituting for ethanol's effect at the GABA-A receptor, counteracting the hyperexcitable state.

Drug	Route	Typical Dosing	Notes
Chlordiazepoxide	Oral	25 to 100 mg every 6 hours, tapered over 3 to 5 days	Preferred for mild to moderate withdrawal; long half-life provides smooth taper; avoid in liver failure
Diazepam	IV/Oral	5 to 20 mg IV every 5 to 15 minutes until CIWA < 10	Long-acting; active metabolites; preferred for rapid loading in severe withdrawal; avoid in liver failure
Lorazepam	IV/IM/Oral	2 to 4 mg IV every 15 to 20 minutes until CIWA < 10	Preferred in hepatic impairment (no active metabolites, glucuronidation only); preferred in elderly

The exam loves to test the choice between these: Lorazepam is the answer when the patient has liver disease, because chlordiazepoxide and diazepam undergo hepatic oxidation and produce active metabolites that can accumulate dangerously.

Thiamine repletion: 100 mg IV daily for prophylaxis. If Wernicke encephalopathy is suspected (confusion, ophthalmoplegia, ataxia), the dose is high-dose IV thiamine: 500 mg IV three times daily for 2 to 3 days, then 250 mg daily for 3 to 5 days.
Folate 1 mg daily for macrocytic anemia due to folate deficiency.
Magnesium sulfate 2 g IV: Critical because hypomagnesemia lowers the seizure threshold and makes hypokalemia refractory to potassium replacement.
For withdrawal seizures: Benzodiazepines are first-line. Phenytoin is not effective for alcohol withdrawal seizures and should not be used. This is a frequently tested point. The seizures are not due to an epileptic focus; they are due to global excitatory rebound, and GABA-ergic agents are the correct treatment.
Benzodiazepine-resistant delirium tremens: Defined as persistent symptoms despite adequate benzodiazepine dosing (some patients require hundreds of milligrams of diazepam equivalents). The next step is phenobarbital (a barbiturate that acts at a different site on the GABA-A receptor) or propofol infusion in the ICU setting with mechanical ventilation. Dexmedetomidine (an alpha-2 agonist) is an adjunct for controlling sympathetic hyperactivity but does not treat seizures.
Long-term relapse prevention (tested in outpatient management questions):
- Naltrexone (50 mg PO daily or 380 mg IM monthly): Opioid receptor antagonist that reduces the rewarding effects of alcohol. Contraindicated in patients on opioids or with acute hepatitis/liver failure.
- Acamprosate (666 mg PO three times daily): Modulates glutamate/NMDA activity to reduce cravings. Safe in liver disease but contraindicated in severe renal impairment (CrCl < 30 mL/min). The exam tests this contrast directly: liver disease = use acamprosate; kidney disease = use naltrexone.
- Disulfiram (250 mg PO daily): Inhibits aldehyde dehydrogenase, causing accumulation of acetaldehyde if alcohol is consumed (flushing, nausea, vomiting, hypotension). Requires informed, motivated, supervised patients. Not first-line.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Wernicke encephalopathy	Also presents in alcoholic patients with confusion and ataxia	Classic triad: ophthalmoplegia (lateral rectus palsy/nystagmus) + confusion + ataxia. The ataxia here is cerebellar gait ataxia, not simple intoxication stumbling. Responds to thiamine, not time.
Hepatic encephalopathy	Confusion and asterixis in an alcoholic patient	Look for stigmata of chronic liver disease (jaundice, ascites, spider angiomata), elevated ammonia, fetor hepaticus. Asterixis (flapping tremor) is the signature finding, not the fine tremor of withdrawal.
Hypoglycemia	Altered mental status, diaphoresis, confusion, and tachycardia overlap with both intoxication and withdrawal	Fingerstick glucose is low (< 70 mg/dL). Resolves immediately with glucose administration. Always check glucose in any altered patient.
Subdural hematoma	Alcoholic patients fall frequently; altered mental status may be attributed to intoxication	Mental status does not improve as BAC falls, or worsens. Focal neurological deficits, unilateral pupil dilation. CT shows crescent-shaped hyperdensity (acute) or hypodensity (chronic).
Meningitis/Encephalitis	Fever, altered mental status, possible seizures overlap with DT	Nuchal rigidity, positive Kernig/Brudzinski signs, CSF pleocytosis. DT patients are febrile from autonomic instability, not infection, but you cannot distinguish clinically without LP if in doubt.
Benzodiazepine or opioid intoxication	CNS depression, altered mental status, respiratory depression	Opioids: miotic (pinpoint) pupils, responds to naloxone. Benzodiazepines: responds to flumazenil (though flumazenil is rarely used due to seizure risk). Ethanol: no specific antidote, elevated osmolal gap.
Toxic alcohol ingestion (methanol, ethylene glycol)	Elevated osmolal gap, altered mental status in a "drunk-appearing" patient	Anion gap metabolic acidosis distinguishes toxic alcohols from ethanol. Methanol: visual complaints ("snowstorm vision"), retinal edema. Ethylene glycol: calcium oxalate crystals in urine, renal failure.
Thyroid storm	Tachycardia, fever, agitation, tremor, and diaphoresis overlap with DT	Look for goiter, exophthalmos, lid lag. TSH is suppressed with elevated free T4/T3. No history of alcohol cessation.
Neuroleptic malignant syndrome (NMS)	Fever, altered mental status, autonomic instability	"Lead-pipe" rigidity is the hallmark. History of recent antipsychotic use or dose change. Markedly elevated CK.
Serotonin syndrome	Fever, agitation, autonomic instability, tremor	Clonus (especially lower extremity), hyperreflexia, diarrhea. History of serotonergic medication use. Onset is rapid (within hours of medication change).

6. Traps and High-Yield Pearls

The most common way students lose points on alcohol questions is by failing to respect the timeline of withdrawal. A vignette describing a hospitalized patient who becomes agitated and confused on hospital day 3 is not describing "ICU delirium" or "sundowning" if the patient has a known history of heavy drinking. The answer is delirium tremens. Exam writers deliberately embed the alcohol history earlier in the vignette (sometimes in the social history section that students skim past) and present the withdrawal complication as if it were a new problem.

The second classic trap is phenytoin for alcohol withdrawal seizures. Phenytoin works by stabilizing sodium channels and is effective for structural epilepsy, but alcohol withdrawal seizures arise from GABA/glutamate imbalance, not a focal seizure disorder. Phenytoin does not prevent or treat these seizures. The correct answer is always benzodiazepines. If the student sees "seizure" and reflexively picks phenytoin, they have fallen for the distractor.

The third recurring trap involves Wernicke encephalopathy. The vignette will describe a malnourished alcoholic patient who is brought in with confusion and is given IV dextrose. The patient then deteriorates. The question asks what should have been done differently. The answer: thiamine must be administered before glucose. This is non-negotiable and tested repeatedly.

The fourth trap is the choice of benzodiazepine in liver disease. A patient with known cirrhosis or significantly impaired hepatic function who is in withdrawal must receive lorazepam (or oxazepam), not diazepam or chlordiazepoxide. The active metabolites of the longer-acting agents accumulate and cause prolonged, dangerous sedation.

Finally, for long-term pharmacotherapy, the exam tests whether you can match the drug to the patient's comorbidities: naltrexone for the patient with intact liver but kidney issues; acamprosate for the patient with liver disease but intact kidneys. If you see "elevated LFTs" or "cirrhosis" in the stem, the relapse prevention drug is acamprosate. If you see "CKD" or "creatinine 3.5," the answer is naltrexone.

The core competency being tested across all alcohol questions is pattern recognition under time pressure: identifying the correct syndrome on the intoxication-withdrawal spectrum, applying the right timeline, choosing the right agent for the right patient, and never forgetting to give thiamine first.

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