Management of acute ethanol intoxication consists of observation until clinical sobriety is attained and attending to associated injuries or medical illness. A careful examination should be performed to evaluate for complicating injuries or medical conditions. Ethanol levels are not necessarily required for mild or moderate intoxication where no other abnormality is suspected, but many institutions offer a blood alcohol screening panel that tests for ethanol, methanol, and isopropanol. One advantage of the alcohol screening panel is the detection of otherwise unsuspected isopropanol or methanol. The assays for each alcohol are specific and do not cross-react with each other. Hypoglycemia should be excluded by a bedside glucose determination. Ethanol does not bind to activated charcoal, so it is not needed unless other adsorbable substances have been ingested. Any alcoholic with severe CNS depression, even if apparently attributable to intoxication, should receive thiamine. Because nutritional status is often wanting, folate and other vitamin supplements are often added to the intravenous solution. Patients with mild to moderate intoxication do not necessarily require intravenous line placement, treatment with vitamin supplements other than thiamine, or intravenous fluid administration unless clinical signs of volume depletion are present. The IV solution should be 5% D/0.9% NaCl since alcoholics are often glycogen depleted. Careful and serial observation is crucial, as deterioration in mental status should be considered secondary to causes other than ethanol and managed accordingly. Unhabituated patients eliminate ethanol from the bloodstream at a rate of 15 to 20 mg/dL per hour, while alcoholics average 25 to 35 mg/dL per hour. Most patients with central nervous system depression secondary to ethanol ingestion improve within a few hours of emergency department arrival at the ED. Respiratory depression may result in hypoventilation and carbon dioxide retention, which, if severe, may rarely require advanced airway management.

Alcoholics should be questioned about concomitant drug use. In the past, ethylene glycol or methanol was occasionally substituted for or combined with ethanol. Today cocaine has clearly become the most common concomitant drug used by alcoholics. The attraction of abusing these drugs together may relate to the formation of a metabolite, cocaethylene, which has 40 times the affinity for cocaine receptors of cocaine itself6 and is thus an extremely potent intoxicant. The risk of sudden death among users of both drugs simultaneously may be as high as 20 times that with cocaine alone. Ethanol is the most common cause of an osmolal gap (Table

160:1), which also characterizes isopropanol, methanol, and ethylene glycol poisoning. However, a distinguishing feature of methanol and ethylene glycol is the wide-anion-gap metabolic acidosis. It is seductive to attribute the metabolic acidosis to the presence of ethanol. This can lead to missing or a significantly delay in establishing the correct diagnosis. Indeed, metabolism of alcohol in the liver leads to the formation of ketoacids, relatively depleting NAD while increasing NADH. As a consequence, high NADH diverts pyruvate, destined for glucose formation, to lactate, resulting in acidosis and hypoglycemia. However, the presence of significant acidosis should never be ascribed to alcohol intoxication alone. An alternate cause must be sought expeditiously and will invariably be found. For a discussion on other issues related to the ethanol-intoxicated patient, see Chap 299.

Beat The Battle With The Bottle

Beat The Battle With The Bottle

Alcoholism is something that can't be formed in easy terms. Alcoholism as a whole refers to the circumstance whereby there's an obsession in man to keep ingesting beverages with alcohol content which is injurious to health. The circumstance of alcoholism doesn't let the person addicted have any command over ingestion despite being cognizant of the damaging consequences ensuing from it.

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