Lactic Acidosis: Causes, Symptoms, Treatment, and More

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. 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. 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.

Alcoholic Ketoacidosis: Mind the Gap, Give Patients What They Need

The metabolism of alcohol itself is a probable contributor to the ketotic state. Alcohol dehydrogenase (ADH), a cytosolic enzyme, metabolizes alcohol to acetaldehyde in hepatocytes. Acetaldehyde is metabolized further to acetic acid by aldehyde dehydrogenase.

• Typically, an alcohol binge leads to vomiting and the cessation of alcohol or food intake for ≥ 24 hours.
• Other symptoms may be present depending on the underlying cause and severity of the acidosis.
• In addition, AKA is often precipitated by another medical illness such as infection or pancreatitis.

What are the symptoms of alcoholic ketoacidosis?

In 1940, Dillon et al1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption. It was not until 1970 that Jenkins et al2 described a further three non‐diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis. Triglycerides stored in adipose tissue undergo lipolysis and are released into the circulation as free fatty acids bound ionically to albumin. Free fatty acids are removed by the liver, where they primarily undergo oxidation to hydroxybutyric acid and acetoacetate and subsequently are reesterified to triglyceride. Decreased insulin and elevated glucagon, cortisol, catecholamine, and growth hormone levels can increase the rate of ketogenesis.

BOX 1 PRESENTING FEATURES OF AKA

Metformin works in the liver and gut to lower blood sugar levels, but it can also increase lactic acid levels in the bloodstream by blocking energy production in the liver. 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. Generally, the physical findings relate to volume depletion and chronic alcohol abuse.

Signs and symptoms of alcoholic ketoacidosis

There may be a history of previous episodes requiring brief admissions with labels of “query pancreatitis” or “alcoholic gastritis”. Most cases of AKA occur when a person with poor nutritional status due to long-standing alcohol abuse who has been on a drinking binge suddenly decreases energy intake because of abdominal pain, nausea, or vomiting. In addition, AKA is often precipitated by another medical illness such as infection or pancreatitis.

Symptoms of Alcoholic Ketoacidosis

Lactic acidosis is characterized by increased lactate levels, an acidic product of anaerobic (without oxygen) metabolism. High lactate levels may occur with lactate overproduction, decreased lactate clearance, or both. The greatest threats to patients with alcoholic ketoacidosis are marked contraction in extracellular fluid volume (resulting in shock), hypokalaemia, hypoglycaemia, and acidosis. Regarding a diagnosis, lactic acidosis requires blood tests that measure the lactate level and evaluate for acidity in the bloodstream.

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. Laboratory studies show a serum bicarbonate of 10 mEq/L, an anion gap of 30, a serum glucose of 95 mg/dL, alcoholic ketoacidosis smell a lactic acidosis with pH 7.2, hypophosphatemia, and trace ketonuria. He denies a history of diabetes mellitus, ingestion of any toxic alcohols, or recent illness. Often, blood alcohol levels are no longer elevated when patients present with alcoholic ketoacidosis. In general, the prognosis for a patient presenting with AKA is good as long as the condition is identified and treated early.

Alcoholic ketoacidosis (AKA) is a condition seen commonly in patients with alcohol use disorder or after a bout of heavy drinking. It is a clinical diagnosis with patients presenting with tachycardia, tachypnea, dehydration, agitation, and abdominal pain. This activity illustrates the evaluation and treatment of alcoholic ketoacidosis and explains the role of the interprofessional team in managing patients with this condition. Toxicity from methanol or ethylene glycol is an important differential diagnosis.

• These include acute pancreatitis, gastrointestinal bleeding, and alcohol withdrawal.
• Management is based around exclusion of serious pathology and specific treatment for AKA where it is present.
• Larger studies by Fulop and Hoberman5 and Wrenn et al6 (24 and 74 patients, respectively) clarified the underlying acid base disturbance.
• Further, vitamin K administration in our patient resulted in normalization of his INR.

If you have any additional complications during treatment, this will also affect the length of your hospital stay. While there is no foolproof strategy to prevent lactic acidosis, practicing healthy lifestyle behaviors can help maintain the integrity of your liver and kidneys, which are crucial for lactate clearance. Moreover, a healthy lifestyle may help prevent specific underlying causes of lactic acidosis, like infection or cancer. Cardiogenic shock, which develops due to the heart malfunctioning, can also cause type A lactic acidosis. With cardiogenic shock, the heart fails to pump blood to vital organs.

Not eating enough or vomiting can lead to periods of starvation. They provide some energy to your cells, but too much may cause your blood to become too acidic. Types of shock include septic (widespread infection), hypovolemic (loss of blood/fluid), and cardiogenic (heart malfunctioning) shock.