Alcoholic Ketoacidosis Treatment & Management

Updated: Oct 05, 2022
  • Author: George Ansstas, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
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Approach Considerations

Treatment of alcoholic ketoacidosis (AKA) is directed toward reversing the three major pathophysiologic causes of the syndrome, which are:

  • Extracellular fluid volume depletion

  • Glycogen depletion

  • An elevated ratio of the reduced form of nicotinamide adenine dinucleotide (NADH) to nicotinamide adenine dinucleotide (NAD+)

This goal can usually be achieved through the administration of dextrose and saline solutions. [5]

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. Indeed, evidence-based guidelines by Flannery et al, on the management of intensive care unit patients with a chronic alcohol disorder, including symptoms that mimic or mask Wernicke encephalopathy, recommend that in cases of suspected AKA, dextrose-containing fluids be used in place of normal saline during the first day of admission. [28]

In alcoholics, thiamine (100 mg IV or IM) should be administered prior to any glucose-containing solutions. This will decrease the risk of precipitating Wernicke encephalopathy or Korsakoff syndrome. [13]

Phosphate depletion is also common 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.

Institute appropriate treatment for serious, coexisting, acute illnesses. These may include pancreatitis, hepatitis, heart failure, or infection.

Prevention of AKA involves the treatment of chronic alcohol abuse.

Transfer considerations

Patients generally do not need to be transferred to special facilities. Appropriately evaluate the patient for any life-threatening complications before a transfer is considered. Always assess the patient's stability for transfer.


Treatment of Severe Acidosis

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


Management of Alcohol Withdrawal Syndrome

Evaluate the patient for signs of alcohol withdrawal syndrome, which may include the following:

  • Tremors

  • Agitation

  • Diaphoresis

  • Tachycardia

  • Hypertension

  • Tremors

  • Agitation

  • Seizures

  • 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.



The underlying severity of the disease process and of the underlying diseases associated with AKA determines the role of the consultant. Patients with uncomplicated AKA may need nothing more than appropriate treatment and observation until their metabolic and systemic abnormalities are resolved. Patients with an acute abdomen need consultation with a surgeon. Patients with underlying medical problems may need to consult with the appropriate specialist.

If indicated, provide follow-up with AKA patients to assess the problem of alcohol abuse. Consider referral to a counselor at an alcohol treatment center.


Long-Term Monitoring

Arrange follow-up to evaluate patients after the resolution of symptoms, in order to detect other complications of chronic alcohol abuse. The patient may benefit from an alcohol rehabilitation program.