Emergent Treatment of Alcoholic Ketoacidosis: Overview, Prehospital Care, Emergency Department Care

Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurements. Leukocytosis can occur even in the absence of infection; bandemia more accurately predicts infection. One study showed that an elevated band count in persons with DKA had a sensitivity for predicting infection of 100 percent (19 out of 19 cases) and a specificity of 80 percent.26 Chest radiography and urine and blood cultures should be added for further evaluation of infection. An elevated hemoglobin level caused by dehydration may also exist.

Alcoholic ketoacidosis is usually triggered by an episode of heavy drinking. If you can’t eat for a day or more, your liver will use up its stored-up glucose, which is a type of sugar. When your liver uses up its stored glucose and you aren’t eating anything to provide more, your blood sugar levels will drop. The clinical and biochemical features of AKA are summarised in boxes 1 and 2.

Clinical ReviewsAlcoholic Ketoacidosis: Etiologies, Evaluation, and Management

Your doctor and other medical professionals will watch you for symptoms of withdrawal. Your doctor may also admit you to the intensive care unit (ICU) if you require ongoing care. The length of your hospital stay depends on the severity alcoholic ketoacidosis smell of the alcoholic ketoacidosis. It also depends on how long it takes to get your body regulated and out of danger. If you have any additional complications during treatment, this will also affect the length of your hospital stay.

alcoholic ketoacidosis treatment

AKA is a diagnosis of exclusion, and many other life-threatening alternative or concomitant diagnoses present similarly, and must be ruled out. Failure to https://ecosoberhouse.com/ make the diagnosis can result in severe metabolic abnormalities, acidosis, and shock. People who drink large quantities of alcohol may not eat regularly.


Not eating enough or vomiting can lead to periods of starvation. Laboratory analysis plays a major role in the evaluation of a patient with suspected alcoholic ketoacidosis. Patients are usually tachycardic, dehydrated, tachypneic, present with abdominal pain, and are often agitated.

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Larger studies by Fulop and Hoberman5 and Wrenn et al6 (24 and 74 patients, respectively) clarified the underlying acid base disturbance. Although many patients had a significant ketosis with high plasma BOHB levels (5.2–14.2 mmol/l), severe acidaemia was uncommon. In the series from Fulop and Hoberman, seven patients were alkalaemic. Patients can have a long-standing history of alcohol use and may also present following binges. Acetic acid is a product of the metabolism of alcohol and also a substrate for ketogenesis.

The syndrome of alcoholic ketoacidosis

Efficient and timely management can lead to enhanced patient outcomes in patients with AKA. However, after adequate treatment, it is equally essential to refer the patient to alcohol abuse rehabilitation programs to prevent recurrence and long-term irreversible damage from alcohol abuse. Figure 14,29 provides the treatment approach for DKA in adults, and Figure 224,30 provides the treatment approach for DKA in persons younger than 20 years. Both approaches are recommended by the American Diabetes Association. Specific issues for the adult patient are discussed in more detail below. For persons younger than 20 years, insulin should be administered gradually, and fluid and electrolyte replacement should be done cautiously because of limited data and concern for precipitating cerebral edema.

  • On physical exam, most of the patients with ketoacidoses present with features of hypovolemia from gastrointestinal or renal fluid and electrolyte losses.
  • Many patients with AKA were found to have extremely elevated concentrations of plasma free fatty acids, with mean levels much higher than reported in patients with diabetic ketoacidosis.3,4 Patients also had markedly raised cortisol and growth hormone, and relatively low plasma insulin levels.
  • Antiemetics such as ondansetron or metoclopramide may also be given to control nausea and vomiting.
  • The members of the interprofessional team should communicate to ensure that the patient is receiving the optimal standard of care.

On hospital day one, after continued fluid resuscitation with 5% dextrose in half-normal saline, the patient’s anion gap closed, his INR decreased to 5.9, and he did not require lorazepam for treatment of alcohol withdrawal. By hospital day two, the patient’s INR normalized to therapeutic range and his warfarin was restarted. On hospital day three, the patient was discharged home with outpatient services for his alcohol use disorder. Examination should reveal a clear level of consciousness, generalised abdominal tenderness (without peritoneal signs), and tachypnoea. There may be concomitant features of dehydration or early acute alcohol withdrawal. Bedside testing reveals a low or absent breath alcohol, normal blood sugar, metabolic acidosis, and the presence of urinary ketones, although these may sometimes be low or absent.

Diabetes self-management education (DSME) and diabetes self-management support (DSMS) are recommended at the time of diagnosis of prediabetes or diabetes and throughout the lifetime of the patient. DSMS is an individualized plan that provides opportunities for educational and motivational support for diabetes self-management. DSME and DSMS jointly provide an opportunity for collaboration between the patient and health care providers to assess educational needs and abilities, develop personal treatment goals, learn self-management skills, and provide ongoing psychosocial and clinical support. In AKA, transaminitis, and hyperbilirubinemia due to concurrent alcoholic hepatitis may also be present. The alcohol level itself need not be elevated as the more severe ketoacidosis is seen once the level falls, and the counter-regulatory response begins and shunts the metabolism towards lipolysis. Hypokalemia and increased anion-gap are usually seen with similar mechanisms to those seen in DKA.

alcoholic ketoacidosis treatment