Difficult waters - treatment of alcoholic ketoacidosis

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http://www.emedicine.com/med/TOPIC102.HTM#section~Treatment

Medical Care

Treatment of AKA is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are:

Extracellular fluid volume depletion

Glycogen depletion

An elevated NADH/NAD+ ratio

In AKA, this goal can usually be achieved through the administration of dextrose and saline solutions.4 Carbohydrate and fluid replacement reverse the pathophysiologic derangements that lead to AKA by increasing serum insulin levels and suppressing the release of glucagon and other counterregulatory hormones. Dextrose stimulates the oxidation of NADH and aids in normalizing the NADH/NAD+ ratio. Fluids alone do not correct AKA as quickly as do fluids and carbohydrates together.

In alcoholics, thiamine (100 mg IV or IM) should be administered prior to any glucose-containing solutions in order to decrease the risk of precipitating Wernicke encephalopathy or Korsakoff syndrome.17

Phosphate depletion is also commonly present in alcoholics. The plasma phosphate concentration may be normal on admission; however, it typically falls to low levels with therapy as insulin drives phosphate into the cells. When present, severe hypophosphatemia may be associated with marked and possibly life-threatening complications, such as myocardial dysfunction, in these patients.

Bicarbonate therapy should be considered only in the face of severe, life-threatening acidosis (ie, pH <7.1) that is unresponsive to fluid therapy.

Evaluate the patient for signs of alcohol withdrawal syndrome, which may include tremors, agitation, diaphoresis, tachycardia, hypertension, tremors, agitation, seizures, or delirium. Exclude other causes of autonomic hyperactivity and altered mental status. If the diagnosis of alcohol withdrawal syndrome is established, consider the judicious use of benzodiazepines, which should be titrated to clinical response.