Alcoholic Ketoacidosis: Causes, Symptoms, and Diagnosis

Intravenous benzodiazepines can be administered based on the risk of seizures from impending alcohol withdrawal. Antiemetics such as ondansetron or metoclopramide may also be given to control nausea and vomiting. Your prognosis will be impacted by the severity of your alcohol use and whether or not you have liver disease.

Those with mild hyperglycemia may have underlying diabetes mellitus Diabetes Mellitus (DM) Diabetes mellitus is impaired insulin secretion and variable degrees of peripheral insulin resistance leading to hyperglycemia. Early symptoms are related to hyperglycemia and include polydipsia… Read more , which may be recognized by elevated levels of glycosylated hemoglobin (HbA1C).

Possible Complications of Alcoholic Ketoacidosis

Dextrose is required to break the cycle of ketogenesis and increase insulin secretion. The dextrose will also increase glycogen stores and diminish counterregulatory https://ecosoberhouse.com/ hormone levels. It is essential to administer thiamine before any glucose administration to avoid Wernicke’s encephalopathy preci[itation.

In general, the prognosis for a patient presenting with AKA is good as long as the condition is identified and treated early. The major cause of morbidity and mortality in patients diagnosed with AKA is under-recognition of concomitant diseases (that may have precipitated the AKA, to begin with). These include acute pancreatitis, gastrointestinal bleeding, and alcohol withdrawal. Mortality specifically due to AKA has been linked to the severity of serum beta-hydroxybutyric acid in some studies.

What are the symptoms of alcoholic ketoacidosis?

Patients are usually tachycardic, dehydrated, tachypneic, present with abdominal pain, and are often agitated. Most patients will often have a ketone odor on their breath. The toxicokinetics that are pertinent to the diagnosis of AKA include the rate of alcohol oxidation in the body.

• This test will provide information about your sugar levels to help determine whether you have diabetes.
• If you develop any of these symptoms, seek emergency medical attention.
• This drop in blood sugar causes your body to decrease the amount of insulin it produces.
• If history does not rule out toxic alcohol ingestion as a cause of the elevated anion gap, serum methanol and ethylene glycol levels should be measured.

Intravenous dextrose-containing fluid infusions should be stopped once the bicarbonate levels have reached mEq/L and the patient is tolerating oral intake. This typically occurs 8 to 16 hours after the initiation of treatment.2 Alcohol withdrawal in these patients should be aggressively managed with intravenous benzodiazepines. A 49-year-old male with a history of alcohol abuse presents alcoholic ketoacidosis symptoms to the ED with complaints of generalized abdominal pain and vomiting for the last 36 hours. The patient is well-known to the department for alcohol-related visits and continues to drink daily. On arrival, he is tachycardic and tachypneic, and physical examination findings include dry mucous membranes, decreased sakin turgor, epigastric tenderness, and a tremor in both hands.

Pathophysiology of Alcoholic Ketoacidosis

Support groups can be a valuable source of support and can be combined with medication and therapy.

• Read more , which may be recognized by elevated levels of glycosylated hemoglobin (HbA1C).
• Alcoholic ketoacidosis doesn’t occur more often in any particular race or sex.
• The patient is well-known to the department for alcohol-related visits and continues to drink daily.
• In addition to isotonic fluid replacement, dextrose-containing intravenous fluids are needed.
• Prolonged used of alcohol can result in cirrhosis, or permanent scarring of the liver.
• The dextrose will also increase glycogen stores and diminish counterregulatory hormone levels.

Pyruvate and lactate are then maintained in steady state at much higher levels than normal. This results in a decrease in circulating lactic acid and an increase in acetoacetate. Carbohydrate and fluid replacement reverse this process by increasing serum insulin levels and suppressing the release of glucagon and other counterregulatory hormones and by providing metabolic substrate. Dextrose stimulates the oxidation of the reduced form of nicotinamide adenine dinucleotide (NADH) and aids in normalizing the ratio of NADH to nicotinamide adenine dinucleotide (NAD+). The reversal of ketosis and vigorous rehydration are central in the management of AKA. In addition to isotonic fluid replacement, dextrose-containing intravenous fluids are needed.

Patients & Visitors

People who go on a major alcohol binge often vomit repeatedly and stop eating. If the vomiting and starvation go on for a day or more, the liver’s normal stores of sugar (glucose) decrease. The low glucose stores combined with lack of food intake cause low blood glucose levels. 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.

This can be caused by overdosing on aspirin and similar painkillers, by kidney disease, starvation, diabetes, or even by severe shock. The majority of papers detected by this search focus primarily on diabetes mellitus and its complications, and were excluded. General literature reviews, single case reports, and letters were also excluded. All remaining papers were retrieved and the reference lists hand searched for any additional information sources.