What are the criteria for diagnosing alcohol poisoning?

Diagnosis of Alcohol Poisoning

Alcohol poisoning is diagnosed clinically based on a history of acute alcohol ingestion combined with progressive neurological impairment ranging from slurred speech and ataxia to coma and respiratory depression, with blood alcohol concentration (BAC) measurement serving to confirm the diagnosis rather than define it. 1

Clinical Presentation and Diagnostic Criteria

The diagnosis of acute alcohol intoxication relies on recognizing a spectrum of clinical manifestations that correlate with the severity of exposure:

Neurological Manifestations

• Mild to moderate intoxication: slurred speech, ataxia, incoordination, and behavioral changes 2
• Severe intoxication: progressive obtundation leading to coma, respiratory depression, autonomic dysfunction, and potential cardiac arrest 1
• Global neurological impairment distinguishes poisoning from simple intoxication and represents a medical emergency 1

Blood Alcohol Concentration Thresholds

The relationship between BAC and clinical severity varies significantly based on tolerance:

• Alcohol-naive adults and children: severe toxicity may occur at BAC <100 mg/dL (0.1%) 2
• General population: coma risk typically begins at BAC >250 mg/dL (0.25%) 2
• Chronic alcoholics: may demonstrate significant impairment only at concentrations >300 mg/dL (0.3%) due to tolerance 2

Critical caveat: BAC levels should never be used in isolation to determine clinical severity, as tolerance creates wide variability in clinical presentation at any given concentration 2. A chronic drinker may appear relatively functional at levels that would render an alcohol-naive person comatose.

Diagnostic Evaluation

Essential Initial Assessment

Upon presentation of suspected alcohol poisoning, the diagnostic approach should include:

• Cardiovascular and respiratory stabilization as the immediate priority 2
• BAC measurement to confirm exposure and provide medicolegal documentation 1
• Thiamine administration (before dextrose) to prevent Wernicke encephalopathy 2
• Dextrose administration after thiamine to address potential hypoglycemia 2

Differential Diagnosis Considerations

A critical pitfall is attributing all altered mental status to alcohol when other life-threatening conditions may coexist 2. Alternative etiologies must be systematically excluded:

• Head trauma (common in intoxicated patients with falls) 3
• Hypoglycemia 2
• Toxic alcohol ingestion (methanol, ethylene glycol, isopropanol) 4
• Concurrent drug ingestion 1
• Metabolic derangements 3
• Infectious processes (meningitis, encephalitis) 3

Laboratory Evaluation

Beyond BAC, additional testing should assess for:

• Comprehensive metabolic panel: to identify electrolyte abnormalities, renal dysfunction, and acid-base disturbances 3
• Anion gap calculation: an elevated anion gap suggests toxic alcohol ingestion rather than ethanol alone 5, 4
• Liver function tests: AST, ALT, GGT, bilirubin to assess for underlying alcoholic liver disease 6
• Complete blood count: to evaluate for infection, anemia, or thrombocytopenia 7

Distinguishing Ethanol from Toxic Alcohols

A wide anion gap metabolic acidosis in a patient with suspected alcohol poisoning should immediately raise concern for methanol or ethylene glycol ingestion, which carry significantly higher morbidity and mortality 5, 4:

• Methanol poisoning: associated with visual disturbances, basal ganglia abnormalities on neuroimaging, and poor neurologic outcomes in 24% of cases 5
• Ethylene glycol poisoning: causes renal failure and may show basal ganglia involvement but less commonly results in persistent neurologic deficits 5
• Anion gap ≥28 mmol/L in methanol toxicity independently predicts poor outcome with no favorable recoveries observed 5

Clinical Context and Screening

Identifying Underlying Alcohol Use Disorder

Acute alcohol poisoning should be recognized as a sentinel event for chronic alcohol abuse 1, 3. During or after stabilization:

• Screen systematically using AUDIT questionnaire: score ≥8 for men (≥4 for women/elderly) indicates problematic alcohol use 8
• Obtain drinking history: type of beverage, quantity consumed, weekly frequency, and duration of drinking 6
• Calculate average daily alcohol intake: [amount (mL) × alcohol by volume (%) × 0.785 × drinking days per week] ÷ 7 6
• Recognize underreporting: patients routinely deny or minimize alcohol consumption; obtain collateral history from family members 6

Physical Examination Findings

While nonspecific, certain findings suggest chronic alcohol use and may contextualize acute poisoning:

• Tender hepatomegaly, jaundice, spider angiomata 6
• Parotid gland hypertrophy, Dupuytren's contracture 6
• Signs of advanced liver disease: ascites, lower extremity edema, hepatic encephalopathy 6

Metabolism and Expected Recovery

• Ethanol metabolism rate: approximately 15 mg%/hour (15 mg/dL/hour) in non-dependent adults 2
• Withdrawal risk: ethanol-dependent patients may experience withdrawal symptoms within 8 hours of last drink, even with BAC >200 mg/dL 2
• Withdrawal manifestations: tremor, nausea/vomiting, hypertension, tachycardia, paroxysmal sweats, anxiety 2

Treatment Implications

There are no agents available for clinical use that reverse the acute effects of ethanol 2. Management consists of:

• Supportive care with close observation until BAC decreases to non-toxic levels 2
• Metadoxine administration to accelerate ethanol metabolism and elimination 1, 3
• Hemodialysis consideration in severely ill children or comatose adults 2
• Referral to alcohol treatment unit for all patients presenting with acute intoxication to address underlying alcohol use disorder 1, 3