Alcoholic Ketoacidosis: Etiologies, Evaluation, and Management

They can also reduce the amount of insulin your body produces, leading to the breakdown of fat cells and the production of ketones. Glucose comes from the food you eat, and insulin is produced by the pancreas. When you drink alcohol, your pancreas may stop producing insulin for a short time. Without insulin, your cells won’t be able to use the glucose you consume for energy. Efficient and timely management can lead to enhanced patient outcomes in patients with AKA.

Alcoholic ketoacidosis: clinical and laboratory presentation, pathophysiology and treatment

There may be a history of previous episodes requiring brief admissions with labels of “query pancreatitis” or “alcoholic gastritis”. alcoholic ketoacidosis (AKA) is a common reason for investigation and admission of alcohol dependent patients in UK emergency departments. Although well described in international emergency medicine literature, UK emergency physicians rarely make the diagnosis of AKA. There is increasing evidence that rather than being benign and self limiting, AKA may be a significant cause of mortality in patients with alcohol dependence. This literature review discusses the history, characterisation, pathophysiology, diagnosis, and management of AKA. One complication of alcoholic ketoacidosis is alcohol withdrawal.

Evaluation and management of the critically ill adult with diabetic ketoacidosis

If severe hypokalemia is present dextrose containing fluids can be held until potassium levels are normalized. Other electrolyte abnormalities concomitantly present with alcohol abuse and poor oral intake include hypomagnesemia and hypophosphatemia. Magnesium and phosphate levels should be measured and repleted if the serum levels are found low. Examination should reveal https://ecosoberhouse.com/ 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.

BOX 1 PRESENTING FEATURES OF AKA

Without insulin, most cells cannot get energy from the glucose that is in the blood. Cells still need energy to survive, so they switch to a back-up mechanism to obtain energy. Fat cells begin breaking down, producing compounds called ketones. Ketones provide some energy to cells but also make the blood too acidic (ketoacidosis).

The underlying pathophysiology is related to poor glycogen stores and elevated nicotinamide adenine dinucleotide and hydrogen. This results in metabolic acidosis with elevated beta-hydroxybutyrate levels. Patients with AKA most commonly present with a history of alcohol use (acute or chronic), poor oral intake, gastrointestinal symptoms, and ketoacidosis on laboratory assessment. Patients are generally dehydrated, and serum glucose can be low, normal, or mildly elevated. An anion gap metabolic acidosis with ketosis and electrolyte abnormalities are usually present on laboratory evaluation. Management includes fluid resuscitation, glucose and vitamin supplementation, electrolyte repletion, and evaluation for other conditions.

It most often occurs in a malnourished person who drinks large amounts of alcohol every day. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. 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. The toxicokinetics that are pertinent to the diagnosis of AKA include the rate of alcohol oxidation in the body. Ethyl alcohol oxidizes at a rate of 20 to 25 mg/dL per hour in most individuals.

• This test will provide information about your sugar levels to help determine whether you have diabetes.
• It also depends on how long it takes to get your body regulated and out of danger.
• Typical characteristics of the latter may include rhinophyma, tremulousness, hepatosplenomegaly, peripheral neuropathy, gynecomastia, testicular atrophy, and palmar erythema.
• As you might already know, those with type one diabetes are unable to produce enough insulin.
• This results in metabolic acidosis with elevated beta-hydroxybutyrate levels.

Typically, an alcohol binge leads to vomiting and the cessation of alcohol or food intake for ≥ 24 hours. During this period of starvation, vomiting continues and abdominal pain develops, leading the patient to seek medical attention. If you are diagnosed with alcoholic ketoacidosis, your recovery will depend on a number of factors.

• During this period of starvation, vomiting continues and abdominal pain develops, leading the patient to seek medical attention.
• This results in a decrease in circulating lactic acid and an increase in acetoacetate.
• If a person is already malnourished due to alcoholism, they may develop alcoholic ketoacidosis.
• Sudden death due to alcoholic ketoacidosis is common among those who binge drink on an empty stomach or lose nutrients through vomiting.
• Alcoholic ketoacidosis can develop when you drink excessive amounts of alcohol for a long period of time.
• Group meetings provide support for people trying to quit drinking.
• They provide some energy to your cells, but too much may cause your blood to become too acidic.

Lactic acid levels are often elevated because of hypoperfusion and the altered balance of reduction and oxidation reactions in the liver. Group meetings provide support for people trying to quit drinking. Meetings are widely available at little-to-no cost in most communities. Support groups can be a valuable source of support and can be combined with medication and therapy.

Clinical Features