Behavioral Health

Alcohol withdrawal: CIWA-Ar and CCS-style management

Clinical Overview and When to Suspect Alcohol Withdrawal

— Any hospitalized patient with >8 drinks/day, daily heavy use, or prior detox admissions

— Trauma, postoperative, or ICU patients who become tremulous, tachycardic, or diaphoretic 6–24 hours after last drink

— ED patients presenting with new seizure, hallucinations, or altered mental status plus known alcohol use disorder (AUD)

— Patients with AST:ALT >2, macrocytic anemia, elevated GGT, or unexplained thrombocytopenia

— 6–12 h: minor withdrawal — tremor, anxiety, insomnia, mild autonomic activation

— 12–24 h: alcoholic hallucinosis — visual/tactile, sensorium intact

— 24–48 h: withdrawal seizures — generalized tonic-clonic, usually single or brief cluster

— 48–96 h: delirium tremens (DTs) — confusion, severe autonomic storm, mortality 1–5% treated, up to 15% untreated

— Prior DTs or withdrawal seizures (strongest predictor)

— Sustained heavy use, older age, comorbid illness, electrolyte derangement, concurrent infection

— PAWSS score ≥4 identifies patients at high risk and should trigger scheduled (not symptom-triggered alone) prophylaxis

Board pearl: A patient with chronic AUD admitted for pancreatitis, pneumonia, or hip fracture who becomes tachycardic and tremulous on hospital day 2 has withdrawal until proven otherwise — do not anchor on sepsis or pain alone. CCS pearl: On day 1 of any AUD admission, order CIWA-Ar protocol, thiamine 100 mg IV, folate, MVI, and check Mg/Phos before symptoms escalate.

Definition: Alcohol withdrawal syndrome (AWS) is a constellation of autonomic, neuropsychiatric, and motor symptoms emerging after abrupt cessation or reduction of chronic ethanol intake, driven by GABA-A downregulation and NMDA upregulation during sustained drinking.

When to suspect — high-yield triggers:

Timeline (memorize cold):

Risk factors for severe withdrawal / DTs:

Presentation Patterns and Key History

— Mild: anxiety, irritability, tremor, headache, nausea, anorexia, insomnia, mild diaphoresis

— Moderate: prominent tremor, tachycardia >100, HTN, vomiting, vivid dreams, hyperreflexia

— Severe (DTs): disorientation, agitation, visual/tactile hallucinations, fever, marked autonomic instability

— Quantity/frequency: drinks per day, drinks per occasion, time of last drink (anchors timeline)

— Prior withdrawal episodes: any history of withdrawal seizures, DTs, or ICU admissions — kindling phenomenon means each episode is more severe than the last

— Co-ingestants: benzodiazepines, opioids, cocaine, methamphetamine — alter trajectory and treatment

— Comorbidities: cirrhosis, CHF, COPD, seizure disorder, head trauma, GI bleed — all worsen prognosis

— Nutrition/social: homelessness, food insecurity, IVDU — raise concern for Wernicke, refeeding, infection

— AUDIT-C (3 items, ≥4 men/≥3 women is positive) — USPSTF-endorsed primary care screen

— CAGE — older, less sensitive, still tested

— PAWSS (Prediction of Alcohol Withdrawal Severity Scale): 10 items; ≥4 = high risk for complicated withdrawal → start prophylactic benzodiazepines, not just symptom-triggered

Key distinction: Alcoholic hallucinosis (clear sensorium, isolated hallucinations, 12–24 h) vs DTs (clouded sensorium, global autonomic storm, 48–96 h). Mistaking hallucinosis for DTs leads to over-sedation; missing DTs is lethal. Step 3 management: Document CIWA-Ar score, PAWSS, last drink time, and prior DT history in every AUD admission note — these drive the order set.

Symptom clusters by severity:

History elements that change management:

Screening tools to know:

Collateral history: family/EMS reports often more reliable than patient self-report; ask specifically about eye-opener drinks, morning shakes, blackouts

Physical Exam Findings and Hemodynamic Assessment

— Tachycardia (HR >100) and HTN (SBP >140) are the earliest objective signs; trend Q1–2h

— Fever in withdrawal is usually low-grade; T >38.3°C should prompt infection workup (pneumonia, SBP, meningitis, UTI)

— Tachypnea with respiratory alkalosis is common; hypoxia is not from withdrawal alone — investigate

— Postural tremor (6–8 Hz), worse with arms outstretched

— Hyperreflexia, clonus, myoclonus

— Nystagmus, ophthalmoplegia, ataxia, confusion → Wernicke encephalopathy — give thiamine IV before glucose

— Pupils typically normal to mildly dilated; pinpoint suggests opioid co-ingestion

— Orientation, attention (serial 7s, months backward), and hallucination type (visual/tactile in withdrawal; auditory more typical of primary psychosis)

— Agitation severity drives medication intensity

— Diaphoresis, flushing, spider angiomata, palmar erythema, jaundice, caput medusae → underlying cirrhosis

— Bruising, head lac, tongue bite → suspect unwitnessed withdrawal seizure or fall

— Persistent HR >120 or SBP >180 despite adequate benzodiazepines

— Hypotension — not typical of withdrawal; consider GI bleed, sepsis, adrenal insufficiency, dehydration

— Arrhythmia — check Mg, K, QTc; alcoholic cardiomyopathy may decompensate

Board pearl: The triad of confusion + ophthalmoplegia + ataxia = Wernicke; give thiamine 500 mg IV TID × 2–3 days for suspected Wernicke (not the 100 mg prophylactic dose). CCS pearl: Order fingerstick glucose immediately; if hypoglycemic, give thiamine before dextrose to avoid precipitating Wernicke in a chronic drinker.

Vital signs — the early warning system:

Neurologic exam:

Mental status:

Skin and general:

Hemodynamic red flags requiring escalation:

Diagnostic Workup — Initial Labs, Imaging, ECG

— CBC — macrocytosis (MCV >100), thrombocytopenia (marrow suppression or cirrhosis)

— CMP — AST:ALT >2, elevated bilirubin, low albumin, BUN/Cr for volume status

— Mg, Phos, Ca — hypomagnesemia is nearly universal and lowers seizure threshold; replete aggressively

— Glucose — hypoglycemia common in malnourished drinkers

— Lipase — alcoholic pancreatitis

— Ammonia if hepatic encephalopathy suspected (clinical diagnosis though)

— Coags (PT/INR) — synthetic liver function

— Lactate — elevated in shock, seizure, thiamine deficiency

— Ethanol level — withdrawal can begin while BAL still positive in heavy drinkers; a "normal" BAL does not exclude withdrawal

— Urine drug screen — co-ingestants change management (benzos, opioids, stimulants)

— Acetaminophen and salicylate levels if AMS or suicidal ideation

— Osmolar gap if AMS — methanol, ethylene glycol, isopropyl

— Blood cultures, UA, CXR if febrile, tachycardic out of proportion, or altered

— LP if meningismus, persistent fever, or AMS not explained by withdrawal

— Diagnostic paracentesis in any cirrhotic with ascites and AMS or fever (rule out SBP)

— QTc prolongation (electrolyte-driven), holiday heart (AF/SVT), ischemia from demand

— Non-contrast head CT for first-time seizure, focal deficit, head trauma, or AMS not improving with benzodiazepines

Step 3 management: In a withdrawing patient with new seizure, order head CT and check Mg, Na, glucose, BAL — but do not delay benzodiazepines waiting for imaging. Board pearl: Withdrawal seizures are generalized and brief; focal seizures or status epilepticus demand alternative diagnosis (structural lesion, hyponatremia).

Core labs on arrival:

Toxicology:

Infectious workup (low threshold):

ECG:

Imaging:

Diagnostic Workup — Advanced or Confirmatory Studies

— 10 items: nausea/vomiting, tremor, sweats, anxiety, agitation, tactile/auditory/visual disturbances, headache, orientation

— Max score 67; <8 mild, 8–15 moderate, >15 severe, >20 = high risk DTs

— Validated only in awake, communicative, English-speaking patients — do not use in intubated, demented, encephalopathic, or non-verbal patients

— RASS (Richmond Agitation-Sedation Scale) for ICU/intubated patients — goal RASS 0 to −2

— MINDS or Brief Alcohol Withdrawal Scale (BAWS) in some institutions

— Symptom-triggered vs scheduled dosing decision hinges on whether a valid scale can be applied

— CDT (carbohydrate-deficient transferrin) — most specific for heavy use in prior 2 weeks

— GGT — sensitive but nonspecific

— PEth (phosphatidylethanol) — direct ethanol metabolite, detects use over 3–4 weeks; increasingly used in transplant evaluation

— EtG/EtS urine — detects use in last 3–5 days

— MRI brain if Wernicke suspected and CT non-diagnostic — mammillary body, periaqueductal gray, thalamic enhancement

— EEG if seizures atypical, prolonged, or non-convulsive status considered

— If signs of CHF, holiday heart, or unexplained tachycardia — assess for dilated alcoholic cardiomyopathy

Key distinction: CIWA-Ar measures symptoms, not severity of underlying disease. A sedated patient may score low yet be in profound withdrawal — use RASS and clinical judgment. CCS pearl: On the CCS case, order CIWA-Ar q1h initially; once scores <8 for 8 hours, space to q2–4h, then discontinue protocol.

CIWA-Ar scale — the workhorse:

Alternatives when CIWA invalid:

Biomarkers of chronic use (not for acute management, but exam-relevant):

Advanced imaging:

Echocardiogram:

Risk Stratification and First-Line Management Logic

— PAWSS <4 and CIWA <8: outpatient management reasonable if reliable, sober support, no comorbidity, no prior DTs

— PAWSS ≥4 or CIWA 8–15: admit to medical floor, symptom-triggered benzodiazepines, monitor q1–2h

— CIWA >15, prior DTs/seizures, severe comorbidity, hemodynamic instability: stepdown or ICU

— DTs, refractory withdrawal, need for high-dose benzodiazepines, intubation, phenobarbital, or propofol: ICU

— Symptom-triggered (preferred when valid CIWA possible): lower total benzo dose, shorter LOS, fewer complications

— Fixed-dose scheduled taper: for high-risk patients (prior DTs, PAWSS ≥4), patients unable to communicate, or settings without trained nursing

— Front-loading: rapid escalation of diazepam 10–20 mg q1–2h until calm, then self-tapers due to long half-life — particularly useful in severe withdrawal

— Thiamine 100 mg IV daily × 3 days (500 mg TID if Wernicke suspected), then PO

— Folate 1 mg, multivitamin

— Magnesium repletion to >2.0; potassium, phosphate as needed

— IV fluids judiciously — many patients are euvolemic or overloaded despite appearance; avoid reflexive aggressive hydration

— NPO if seizure risk or vomiting; otherwise resume diet

— Fall precautions, seizure precautions, quiet environment, frequent reorientation

— Antipsychotics as monotherapy (lower seizure threshold, do not treat underlying GABA deficit)

— Restraints unless absolutely necessary

Step 3 management: The single most important early order is scheduled or symptom-triggered benzodiazepines plus thiamine, magnesium, and a valid monitoring scale — everything else is supportive.

Triage decisions driven by PAWSS, CIWA, and comorbidity:

Two dosing strategies:

Universal supportive measures (CCS order set):

Avoid:

Pharmacotherapy — First-Line Benzodiazepine Regimens

— Diazepam (Valium): long half-life (active metabolites), smooth self-taper, first choice in most adults; 10–20 mg IV/PO q1–2h symptom-triggered

— Lorazepam (Ativan): intermediate-acting, no active metabolites — preferred in cirrhosis, elderly, severe hepatic dysfunction; 2–4 mg IV/PO q1–2h

— Chlordiazepoxide (Librium): long-acting oral, useful for outpatient or mild inpatient taper; 50–100 mg q6h tapering over 3–5 days

— Oxazepam: short, hepatically conjugated only (no CYP), useful in liver disease but slower onset

— CIWA 8–15: diazepam 10 mg or lorazepam 2 mg

— CIWA 16–20: diazepam 20 mg or lorazepam 4 mg

— CIWA >20: escalate, reassess q1h, consider ICU

— Day 1: 50 mg q6h; Day 2: 50 mg q8h; Day 3: 25 mg q6h; Day 4: 25 mg q8h; Day 5: 25 mg qHS; PRN doses available

— Gabapentin 300–600 mg TID — useful for mild withdrawal, outpatient, and cravings post-detox

— Carbamazepine — anti-kindling, less sedating, used outside US more

— Clonidine/dexmedetomidine — control autonomic symptoms but do not prevent seizures or DTs — never replace benzos

— Beta-blockers — same caveat; mask tachycardia and obscure CIWA scoring

— Haloperidol — only for refractory agitation after adequate benzos; lowers seizure threshold

Board pearl: In cirrhosis or severe hepatic impairment, use lorazepam, oxazepam, or temazepam ("LOT") — they bypass CYP oxidation and avoid accumulation. CCS pearl: Always order PRN benzodiazepines alongside scheduled dosing and reassess CIWA q1h until stable.

Benzodiazepines are first-line — they treat the GABA deficit directly and prevent seizures and DTs.

Drug selection:

Symptom-triggered protocol example:

Fixed-dose taper example (chlordiazepoxide):

Adjuncts (never monotherapy):

Refractory Withdrawal — Phenobarbital, Propofol, Dexmedetomidine

— Acts on GABA-A (different site than benzos) and inhibits glutamate — covers both deficits

— Loading: 10 mg/kg IV over 30 minutes, or 130–260 mg IV q15–30 min titrated to sedation

— Long half-life (80–120 h) provides self-taper, reducing rebound

— Increasingly used as first-line in ED and ICU in some protocols (front-loaded phenobarbital + symptom-triggered benzos)

— Watch: respiratory depression, hypotension, oversedation — have airway ready

— For intubated patients with severe DTs unresponsive to benzos

— GABA-A agonist + NMDA antagonist; rapid titration

— Monitor for propofol infusion syndrome with prolonged high-dose use (metabolic acidosis, rhabdomyolysis, bradycardia)

— α2-agonist; controls autonomic symptoms and agitation without respiratory depression

— Adjunct only — does not prevent seizures or DTs; always continue benzos or phenobarbital

— Useful to reduce total benzodiazepine load and avoid intubation

— NMDA antagonist; emerging adjunct in refractory cases; not yet standard of care

— Inability to protect airway, refractory agitation, need for high-dose sedation, respiratory failure

— Use RSI with ketamine or etomidate; avoid succinylcholine if hyperkalemia suspected

— Flumazenil — can precipitate seizures in chronic benzo or alcohol users

— Physical restraints prolonged — rhabdomyolysis risk

Step 3 management: For DTs requiring escalating benzodiazepines, transfer to ICU, initiate phenobarbital loading or dexmedetomidine adjunct, and prepare for possible intubation. Board pearl: Phenobarbital + benzodiazepine combinations reduce ICU admission and intubation in severe withdrawal trials.

Benzodiazepine-resistant withdrawal: persistent CIWA >15 or RASS >+2 despite >40 mg diazepam-equivalent in 1 hour or escalating cumulative doses without improvement.

Phenobarbital:

Propofol:

Dexmedetomidine:

Ketamine:

When to intubate:

Avoid:

Special Populations — Elderly and Renal/Hepatic Impairment

— Higher risk for delirium, falls, oversedation, paradoxical agitation

— Use lorazepam (no active metabolites) at half typical doses (e.g., 0.5–1 mg)

— Beware polypharmacy — opioids, antihistamines, anticholinergics worsen delirium

— CIWA may underestimate severity in patients with baseline cognitive impairment — combine with clinical judgment

— Lower threshold for telemetry and inpatient admission

— Use "LOT" benzodiazepines — Lorazepam, Oxazepam, Temazepam — glucuronidation only, no CYP oxidation

— Avoid diazepam and chlordiazepoxide — long half-lives accumulate, precipitating hepatic encephalopathy

— Distinguish withdrawal from hepatic encephalopathy: asterixis, elevated ammonia, response to lactulose favor encephalopathy; tremor, autonomic storm, hallucinations favor withdrawal — often coexist

— Continue lactulose and rifaximin; check for GI bleed (variceal, gastritis)

— Avoid acetaminophen >2 g/day in active cirrhosis; avoid NSAIDs entirely

— Lorazepam active metabolite glucuronide can accumulate in ESRD with prolonged infusions — monitor sedation

— Phenobarbital renally cleared — reduce dose in CKD/ESRD

— Avoid propylene glycol toxicity with high-dose IV lorazepam infusions (>10 mg/h) — check osmolar gap, lactate

— Benzodiazepine respiratory depression riskier — titrate carefully, monitor SpO2/CO2

— Manage volume status carefully; avoid aggressive IVF in HFrEF

Key distinction: Hepatic encephalopathy and alcohol withdrawal can occur simultaneously; treating only one worsens the other. CCS pearl: For a cirrhotic in withdrawal, order lorazepam symptom-triggered, lactulose titrated to 3 BMs/day, rifaximin 550 mg BID, thiamine, and diagnostic paracentesis if ascites present.

Elderly (≥65):

Cirrhosis/hepatic impairment:

Renal impairment:

Heart failure / COPD:

Special Populations — Pregnancy, Adolescents, and Co-Occurring Disorders

— Alcohol withdrawal in pregnancy is a medical emergency — untreated withdrawal (seizures, DTs, hyperthermia) is far more harmful to fetus than benzodiazepine exposure

— Lorazepam preferred (shorter half-life, less fetal accumulation than diazepam)

— Monitor fetal heart tones; involve OB, MFM, addiction medicine, social work early

— Continue thiamine, folate, prenatal vitamins

— Screen for other substances (tobacco, opioids, stimulants) and IPV

— Counsel on FAS/FASD risk — alcohol is a teratogen with no safe threshold

— Postpartum: monitor neonate for neonatal abstinence if benzodiazepines used near delivery

— Less common but rising; lower thresholds for withdrawal due to binge patterns

— Screen with CRAFFT tool

— Confidentiality protections vary by state; know minor consent rules for substance use treatment

— Consider co-occurring mental health disorders (depression, anxiety, ADHD)

— Benzodiazepine + alcohol withdrawal: overlapping syndromes; longer taper, often phenobarbital-based

— Opioid + alcohol: treat both — buprenorphine or methadone for opioid withdrawal does not treat AWS

— Stimulant intoxication can mimic withdrawal — urine tox helps

— Mood/anxiety/PTSD common; defer definitive psychiatric diagnosis until 2–4 weeks of sobriety where possible

— Treat suicidal ideation acutely regardless

Board pearl: Withhold benzodiazepines from a pregnant patient in active withdrawal is never the right answer — untreated withdrawal causes fetal distress, miscarriage, and maternal mortality. Step 3 management: Engage MAT services, social work, and SBIRT counseling before discharge for every AUD patient — this is the longitudinal Step 3 expectation.

Pregnancy:

Adolescents:

Co-occurring substance use:

Co-occurring psychiatric illness:

Complications and Adverse Outcomes

— Generalized tonic-clonic, typically 12–48 h after last drink

— Usually single or brief cluster; status epilepticus is rare and suggests alternative etiology (structural, metabolic)

— Treat acute seizure with lorazepam 2–4 mg IV; do not start chronic antiepileptics for isolated withdrawal seizure

— Mortality 1–5% treated, up to 15–20% untreated

— Hyperthermia, severe autonomic instability, profound agitation

— Causes of death: arrhythmia, aspiration, hyperthermia, trauma, intercurrent infection

— Wernicke: acute, reversible — confusion, ophthalmoplegia, ataxia; treat with high-dose IV thiamine (500 mg IV TID × 2–3 days)

— Korsakoff: chronic, often irreversible — anterograde amnesia, confabulation

— Always give thiamine before glucose in chronic drinker

— Holiday heart (AF, atrial flutter) — usually resolves with abstinence and rate control

— Demand ischemia, takotsubo, QT prolongation, sudden cardiac death

— Hypomagnesemia, hypokalemia, hypophosphatemia (refeeding), hypoglycemia

— Alcoholic ketoacidosis — anion gap acidosis, elevated β-hydroxybutyrate, treat with dextrose + saline + thiamine

— Oversedation, respiratory depression, delirium from excessive benzos

— Propylene glycol toxicity from high-dose lorazepam infusions

— Missed alternative diagnoses (sepsis, ICH, meningitis) anchored on withdrawal

CCS pearl: In a withdrawing patient who develops fever and AMS despite adequate benzos, broaden — order blood/urine cultures, CXR, LP if no contraindication, and consider empiric antibiotics. Anchoring kills.

Withdrawal seizures:

Delirium tremens:

Wernicke-Korsakoff:

Cardiovascular:

Electrolyte and metabolic:

Aspiration pneumonia, rhabdomyolysis, trauma (falls, MVCs), pressure injuries from prolonged immobility

Iatrogenic:

When to Escalate — ICU, Consult, and Triage Decisions

— CIWA >25 or refractory to escalating benzodiazepines (>40 mg diazepam-equivalent/hour without response)

— Need for phenobarbital loading, dexmedetomidine infusion, propofol, or intubation

— Hemodynamic instability — SBP <90 or >200, HR >140, arrhythmia

— Hyperthermia >39°C, severe metabolic derangement

— Active DTs with severe agitation or confusion

— Concurrent critical illness (pancreatitis, sepsis, GI bleed, ACS)

— Airway compromise or aspiration

— CIWA 15–25 with adequate response to benzos

— Prior DTs/seizure history, significant comorbidity

— Need for q1h monitoring not feasible on general floor

— CIWA <15, stable vitals, responsive to symptom-triggered dosing, no high-risk features

— Mild withdrawal (CIWA <10), no prior complications, reliable support, no comorbidity, daily follow-up available

— Provide chlordiazepoxide or gabapentin taper, thiamine, folate, MVI, follow-up in 24–48 h

— Addiction medicine/psychiatry — every AUD patient before discharge

— Social work — housing, insurance, transportation to rehab

— Hepatology if cirrhosis; cardiology if holiday heart with hemodynamic compromise

— Neurology if atypical seizures or persistent deficits

— Critical-access hospital without ICU capability → arrange transfer before decompensation

— Document EMTALA-compliant transfer with accepting physician

Step 3 management: Decision to admit, transfer, or discharge hinges on PAWSS, CIWA trajectory, comorbidity, and social support — not on a single snapshot vital sign. Board pearl: Prior DTs or withdrawal seizure is an automatic admission criterion even if currently asymptomatic.

ICU admission criteria:

Stepdown/telemetry:

Medical floor:

Outpatient detox candidates:

Consults to consider:

Transfer considerations:

Key Differentials — Other Substance Withdrawal and Intoxications

— Similar autonomic and seizure profile but longer onset (1–7 days depending on agent half-life)

— Treatment: long-acting benzodiazepine taper (diazepam or chlordiazepoxide), phenobarbital adjunct

— History of prescribed benzos, often for anxiety or insomnia

— Rare now; similar mechanism; can be lethal; phenobarbital-based taper

— Not life-threatening in healthy adults (unlike alcohol)

— Yawning, lacrimation, rhinorrhea, piloerection, mydriasis, abdominal cramping, diarrhea

— COWS scale; treat with buprenorphine (after mild withdrawal established) or methadone, plus clonidine, loperamide, ondansetron

— Crash → fatigue, hypersomnia, depression, increased appetite

— Supportive only; watch for suicidal ideation

— Irritability, anxiety, sleep disturbance, decreased appetite; supportive care

— Severe, mimics alcohol/benzo withdrawal; benzo + phenobarbital

— Sympathomimetic toxidrome — overlaps with withdrawal vitals but pupils dilated, agitation acute, history differs

— "Mad as a hatter, red as a beet, dry as a bone, hot as a hare, blind as a bat" — dry skin (vs diaphoretic withdrawal), urinary retention

— Clonus, hyperreflexia (serotonin); rigidity, hyperthermia, leukocytosis (NMS); medication history is key

Key distinction: Alcohol withdrawal patients are diaphoretic with tremor; anticholinergic toxidrome patients are dry and flushed — touching the skin distinguishes them at the bedside.

Benzodiazepine withdrawal:

Barbiturate withdrawal:

Opioid withdrawal:

Stimulant withdrawal (cocaine, methamphetamine, amphetamines):

Cannabis withdrawal:

GHB withdrawal:

Stimulant or hallucinogen intoxication:

Anticholinergic toxidrome:

Serotonin syndrome / NMS:

Key Differentials — Other-Category Causes of AMS in the Drinker

— Always on the differential in any AUD patient with AMS; fever may be absent

— Low threshold for blood cultures, UA, CXR, LP, empiric antibiotics ± acyclovir

— Asterixis, elevated ammonia (supportive, not diagnostic), precipitants (GI bleed, infection, constipation, electrolytes, sedatives)

— Treat with lactulose, rifaximin, address precipitant

— Subdural hematoma — falls common in drinkers; chronic SDH may present with subacute confusion

— SAH, ischemic stroke, ICH — focal deficit, headache, neck stiffness

— Low threshold for non-contrast head CT in any AUD patient with AMS, head trauma, or focal exam

— Hypoglycemia — fingerstick at bedside

— Hyponatremia — beer potomania (low solute intake + high fluid) → severe symptomatic hyponatremia; correct slowly to avoid osmotic demyelination

— Alcoholic ketoacidosis — anion gap, ketones, normal-low glucose

— Uremia, hypercapnia, hypoxia

— Methanol — visual changes, anion gap, osmolar gap → fomepizole, dialysis

— Ethylene glycol — calcium oxalate crystals, renal failure → fomepizole, dialysis

— Isopropyl — ketosis without acidosis

— Primary psychosis, mania — auditory hallucinations more typical, clear sensorium, no autonomic storm

Board pearl: Severe hyponatremia in a heavy beer drinker = beer potomania; correct sodium <8–10 mEq/L per 24 h to prevent osmotic demyelination. CCS pearl: Always order fingerstick glucose, head CT, and basic labs before attributing AMS solely to withdrawal.

Sepsis / meningitis / encephalitis:

Hepatic encephalopathy:

Intracranial pathology:

Metabolic:

Toxic alcohols:

Wernicke encephalopathy (see Chunk 11)

Post-ictal state from unwitnessed seizure

Psychiatric:

Secondary Prevention — Discharge Medications and Long-Term Plan

— Naltrexone (oral 50 mg daily or IM 380 mg monthly) — first-line; reduces heavy drinking days and cravings; avoid in active opioid use, acute hepatitis, or LFTs >5× ULN

— Acamprosate 666 mg TID — modulates glutamate; best for abstinence maintenance; renally dosed, avoid in CrCl <30; safe in liver disease

— Disulfiram 250 mg daily — aversive agent; requires motivated patient and witnessed dosing; avoid in CAD, severe liver disease, psychosis

— Gabapentin 300–600 mg TID — cravings, sleep, mild withdrawal symptoms

— Topiramate — reduces heavy drinking; cognitive side effects

— Baclofen — used in cirrhosis where naltrexone/acamprosate not ideal

— Thiamine 100 mg PO daily, folate 1 mg, multivitamin for ≥30 days

— Brief intervention (SBIRT model) at discharge

— Naloxone if any opioid co-use

— Vaccinations: hepatitis A and B if not immune, pneumococcal, influenza

— Cancer screening per USPSTF (alcohol increases breast, colorectal, hepatocellular, head/neck cancer risk)

— Motivational interviewing, CBT, contingency management

— AA/SMART Recovery/community supports

— Outpatient counseling, intensive outpatient (IOP), partial hospitalization (PHP), residential rehab — match level to severity

— Depression, anxiety, PTSD — treat after 2–4 weeks of sobriety where possible

— Hepatitis C screening, HIV screening

— Cardiovascular risk factors, osteoporosis

Step 3 management: Start naltrexone or acamprosate before discharge — initiation in hospital improves uptake versus deferred outpatient prescribing. Board pearl: Naltrexone is contraindicated with any opioid use in last 7–10 days due to precipitated withdrawal.

Pharmacotherapy for AUD (FDA-approved):

Off-label adjuncts:

Universal discharge bundle:

Behavioral interventions:

Address comorbidities:

Follow-Up, Monitoring, and Rehab/Counseling

— Within 7 days of discharge with PCP or addiction medicine — early follow-up reduces relapse and readmission

— Phone check-in within 24–48 h if available (transitions-of-care best practice)

— Outpatient counseling within 1–2 weeks

— LFTs at baseline and every 4–12 weeks on naltrexone (especially first 6 months)

— Renal function on acamprosate

— CBC, MCV trends as biomarker of ongoing use (MCV declines with abstinence over months)

— GGT, AST/ALT, PEth if monitoring sobriety (e.g., transplant evaluation, employment, custody)

— Blood pressure — often improves significantly with abstinence

— Reinforce that AUD is a chronic, relapsing disease, not a moral failing

— Use non-stigmatizing language ("person with AUD" not "alcoholic")

— Discuss harm reduction if abstinence not yet a goal — reducing quantity still improves outcomes

— Identify triggers, high-risk situations, coping strategies

— Outpatient → IOP (9+ hours/week) → PHP (20+ hours/week) → residential → medically managed inpatient

— Engage family with consent; offer Al-Anon resources

— Address housing, employment, legal issues, transportation — these predict relapse

— Tobacco use (highly comorbid; brief tobacco cessation counseling)

— Insomnia (non-benzodiazepine strategies; sleep hygiene, trazodone, melatonin)

— Chronic pain (avoid opioids; consider gabapentin, duloxetine, PT)

CCS pearl: "Schedule follow-up appointment with PCP in 1 week" and "refer to outpatient addiction services" are nearly always correct CCS actions for AUD discharge. Board pearl: Early outpatient contact is the single strongest predictor of sustained engagement in AUD treatment.

Post-discharge follow-up cadence:

Monitoring parameters:

Counseling content:

Level-of-care matching (ASAM criteria):

Family and social:

Screen for and treat:

Ethical, Legal, and Patient Safety Considerations

— Acute intoxication and withdrawal impair decision-making capacity — capacity is decision-specific and time-specific

— A patient may lack capacity to refuse treatment for withdrawal but regain it as symptoms resolve

— Document the four elements: understand, appreciate, reason, express choice

— Against medical advice (AMA) discharge during active withdrawal: assess capacity carefully; if patient lacks capacity, may need to hold under medical/psychiatric authority (state-specific)

— Many states have statutes (e.g., "Marchman Act," "Section 35") allowing involuntary commitment for severe substance use disorder posing imminent danger

— Know your state's framework; engage social work, psychiatry, and legal early

— Impaired professionals (pilots, physicians, commercial drivers) — state-specific reporting obligations

— Child endangerment — intoxication while caring for minors triggers CPS reporting in many states

— Intimate partner violence screening — offer resources; mandatory reporting varies by state

— 42 CFR Part 2 provides heightened protection for substance use treatment records — separate consent often required for release

— Document carefully; do not share SUD information without explicit consent

— Medication reconciliation at discharge — verify naltrexone/acamprosate, thiamine, no benzodiazepines prescribed without addiction-medicine oversight

— Avoid prescribing benzodiazepines or opioids at discharge — high overdose and relapse risk

— Provide written instructions, follow-up appointments, and contact numbers

— Confirm pharmacy access, insurance coverage, transportation

— Recognize that stigma worsens outcomes; use trauma-informed, non-judgmental care

— Equal access to pain management, organ transplantation, and other care regardless of AUD history

Step 3 management: Before discharging an AUD patient, perform medication reconciliation, schedule 7-day follow-up, prescribe naltrexone or acamprosate, and provide naloxone if any opioid co-use — this bundle is the transition-of-care standard.

Capacity assessment:

Involuntary commitment:

Mandatory reporting:

Confidentiality:

Transition-of-care safety:

Stigma and bias:

High-Yield Associations and Rapid-Fire Clinical Facts

— Minor symptoms 6–12 h, hallucinosis 12–24 h, seizures 24–48 h, DTs 48–96 h

Board pearl: A binge drinker presenting with palpitations and an irregular rhythm after a weekend bender has holiday heart — rate control, anticoagulation per CHA2DS2-VASc, and counsel abstinence.

Timing — memorize:

DT mortality: 1–5% treated, 15–20% untreated

Strongest predictor of severe withdrawal: prior history of DTs or withdrawal seizures (kindling)

PAWSS ≥4 → prophylactic benzodiazepines

CIWA-Ar: validated only in awake, communicative patients

Thiamine before glucose in chronic drinkers — prevents Wernicke

Wernicke triad: confusion, ophthalmoplegia, ataxia (only ~10% have all three; treat empirically)

"LOT" benzos in liver disease: Lorazepam, Oxazepam, Temazepam

AST:ALT >2 suggests alcoholic liver disease; "scotch and tonic" mnemonic (AST > ALT)

MCV >100 + thrombocytopenia + GGT elevation = chronic alcohol use

Holiday heart: atrial fibrillation after binge drinking; usually resolves with abstinence

Alcoholic ketoacidosis: anion gap, β-hydroxybutyrate predominant, treat with D5NS + thiamine

Beer potomania: hyponatremia from low solute + high water; correct slowly

Naltrexone: avoid with opioid use, hepatitis flare

Acamprosate: renally dosed; safe in liver disease

Disulfiram: flushing, vomiting, hypotension with alcohol; requires motivation; avoid in CAD

Gabapentin useful for outpatient mild withdrawal and craving reduction

Phenobarbital for benzo-resistant withdrawal

Flumazenil contraindicated in chronic alcohol/benzo users (seizure risk)

42 CFR Part 2 governs SUD record confidentiality

USPSTF: screen all adults for unhealthy alcohol use with AUDIT-C or single-question screen

Pregnancy: no safe level of alcohol; FAS = growth restriction, facial dysmorphism (smooth philtrum, thin upper lip, small palpebral fissures), CNS abnormalities

Alcohol-associated cancers: breast, colorectal, hepatocellular, oropharyngeal, esophageal

Board Question Stem Patterns

— Post-op or post-trauma patient becomes tremulous, tachycardic, anxious 24–36 h after admission

— Answer: alcohol withdrawal — start CIWA protocol, benzodiazepines, thiamine

— Differentiate hepatic encephalopathy (asterixis, ammonia, lactulose response) from withdrawal (tremor, autonomic storm, hallucinations); may coexist

— Use lorazepam for withdrawal, lactulose/rifaximin for HE

— Chronic drinker, last drink 36 h ago, generalized tonic-clonic seizure

— Treat with lorazepam; check Mg, glucose, Na; CT head; do not start chronic AED for isolated withdrawal seizure

— Chronic drinker given IV dextrose in ED, develops confusion and ophthalmoplegia

— Answer: high-dose IV thiamine 500 mg TID

— CIWA >20 despite cumulative high-dose diazepam

— Next step: phenobarbital loading and ICU transfer

— Stable AUD patient ready for discharge

— Best next step: naltrexone (or acamprosate if opioid use or hepatitis), follow-up within 1 week, counseling referral

— Pregnant patient in withdrawal; correct answer is lorazepam treatment, never withholding therapy

— Heavy beer drinker, Na 112, asymptomatic or mildly confused

— Correct slowly (<8–10 mEq/24 h) to avoid osmotic demyelination

— New AF after weekend binge in a young patient

— Rate control, anticoagulation by CHA2DS2-VASc, abstinence counseling

— Patient on chronic opioids for pain or recent heroin use → use acamprosate instead

— Assess capacity; if impaired by active withdrawal, may justify continued treatment

CCS pearl: On CCS withdrawal cases, the highest-yield orders are CIWA-Ar protocol, lorazepam/diazepam PRN, thiamine IV, magnesium, folate, MVI, fingerstick glucose, telemetry, fall precautions, and addiction medicine consult — in roughly that order.

Stem 1 — The trauma patient on hospital day 2:

Stem 2 — The cirrhotic with AMS:

Stem 3 — The new-onset seizure:

Stem 4 — Wernicke encephalopathy:

Stem 5 — Benzodiazepine-resistant withdrawal:

Stem 6 — Discharge planning:

Stem 7 — The pregnant drinker:

Stem 8 — Beer potomania:

Stem 9 — Holiday heart:

Stem 10 — Naltrexone contraindication:

Stem 11 — AMA discharge in withdrawal:

One-Line Recap

Alcohol withdrawal is a GABA-NMDA imbalance syndrome that progresses predictably from tremor at 6–12 hours through hallucinosis, seizures, and delirium tremens by 48–96 hours, managed with risk-stratified benzodiazepines (lorazepam in hepatic disease, diazepam otherwise), thiamine before glucose, electrolyte repletion, escalation to phenobarbital or ICU for refractory cases, and discharge with naltrexone or acamprosate plus structured follow-up within one week.

Board pearl: The Step 3 examiner rewards the candidate who treats alcohol withdrawal as both an acute neurologic emergency and a chronic relapsing disease — order the benzodiazepine and the naltrexone, schedule the follow-up, screen for comorbid conditions, and document capacity. CCS pearl: Every AUD admission ends with the same five-item discharge bundle: MAT initiated, thiamine continued, 7-day follow-up booked, naloxone if any opioid risk, and addiction counseling referral placed.

Recognize early: PAWSS ≥4 or prior DTs/seizures = prophylactic benzodiazepines, not symptom-triggered alone; CIWA-Ar only valid in awake, communicative patients.

Treat the deficit: Benzodiazepines are first-line — diazepam for most, lorazepam in liver disease, elderly, or pregnancy; phenobarbital for refractory cases; never use clonidine, beta-blockers, or antipsychotics as monotherapy.

Prevent Wernicke and miss-anchoring: Thiamine 100 mg IV (500 mg TID if Wernicke suspected) before glucose; always rule out infection, head injury, hepatic encephalopathy, electrolyte derangement, and toxic alcohols before attributing AMS solely to withdrawal.

Close the loop: Initiate naltrexone or acamprosate before discharge, schedule follow-up within 7 days, engage addiction medicine and social work, provide thiamine/folate/MVI, avoid benzodiazepine and opioid prescriptions at discharge, and use non-stigmatizing, trauma-informed language throughout.