EtOH intoxication

Ethanol is the one of the most commonly abused drug in the world. Mishaps generally happen due to secondary injuries after intoxication. We all see frequent attenders in ED who visit us almost every weekend and it is easy to miss underlying potentially life-threatening diseases if we fail to follow a systematic way to evaluate them.

Alcohol Metabolism

Ethanol is a CNS depressant that enhances the inhibitory neurotransmitter GABA receptors and blockade of excitatory NMDA receptors. Because of the phenomenon of tolerance, blood ethanol levels correlate poorly with degree of intoxication.  At low concentrations, ethanol metabolism follows first-order kinetics, but as concentrations rise, metabolism switches to zero-order kinetics i.e. a fixed amount is metabolised per unit of time. Rates of elimination from the blood vary between 20-30 milligrams/dL/h.

The legal limit to drive a vehicle varies in different countries. UK, Canada and the United States state 80 mg/dL as the legal definition of intoxication for the purposes of driving motor vehicles whereas in India, the limit is 30mg/dL. 

 Clinical Presentation

Lethargy, Drowsiness, Disinhibition, Euphoria, Agitation and Combativeness are classical clinical features. However, severe intoxication may present with slurred speech, nystagmus, ataxia, and decreased motor coordination and this can be hard to differentiate from Wernicke’s. Treat them with fluids if they are tachycardic (reflex tachycardia due to peripheral vasodilatation). Fever should prompt workup for sepsis and possible Delirium Tremens. Ethanol ingestion may also cause hypoglycemia, due to poor glycogen reserve, poor oral intake and reduced gluconeogenesis.

Potential Mimics and co-existing conditions

• Encephalopathy (Hepatic, Uremic, Septic)
• Hypoglycaemia
• Traumatic Brain Injury (Subdural)
• Stroke
• Seizure
• Wernickes
• Concomittant drug ingestions
• Dyselectrolytemia (HypoNa, HyperNa, HyperCa)
• Alcoholic Ketoacidosis
• Hypothermia
• DKA
• Myxoedema
• Psychosis
• Alcoholic Hepatitis and Pancreatitis

ED Management

Performing a detailed physical examination is paramount (Speech, Cranial Nerves, Gait, Nystagmus, GCS, Cerebellum, Evidence of trauma, Abdomen exam) to avoid missing co-existing conditions. Fill the gaps in your history via paramedics, by standers. Usually, uncomplicated intoxication improves within a few hours but if they don’t get sober or worsen then begin evaluation for other causes of altered mental status.

If history and exam are benign then investigations are of limited benefit. At least, obtain a bedside glucose level or a venous blood gas. Acute intoxication may be associated with mild metabolic acidosis, but a significant HAGMA suggests the presence of lactic acidosis, ketoacidosis, or methanol or ethylene glycol toxicity. Ethanol blood levels are not required unless there is a diagnostic dilemma but many prefer to do it anyways to ensure documentation. 

Most physicians agree that observation is the way to go until they are sober. Manage symptoms and beware of hypoglycemia. The classical teaching of Wernicke’s encephalopathy being precipitated by prolonged sustained administration of IV carbohydrate does not hold true and currently there is no evidence that a single dose of IV glucose can cause Wernicke’s.  Otherwise, majority of them do NOT need Pabrinex but administer if you suspect Wernicke’s. Additionally, bolus IV fluids do not help to attain sobriety any earlier. Metadoxine is used in some countries to enhance the metabolism of ethanol and accelerate recovery.

Take Home:

Simple ethanol intoxication needs ED observation until sober. Admit if they are suicidal, homicidal or psychotic. Always try and arrange appropriate transport for them and discharge in the care of a responsible companion.

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic