This is why diagnosis and subsequent treatment can sometimes be challenging, but it’s crucial to receive a proper and timely diagnosis to obtain the correct treatment. 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. An altered level of consciousness should prompt consideration of alternative diagnoses such as hypoglycaemia, seizures, sepsis, thiamine deficiency, or head injury. Arterial blood gas and biochemistry studies reveal a raised anion gap metabolic acidosis without evidence of lactic or diabetic ketoacidosis.
- Further, vitamin K administration in our patient resulted in normalization of his INR.
- Both steps require the reduction of nicotinamide adenine dinucleotide (NAD+) to reduced nicotinamide adenine dinucleotide (NADH).
- Alcoholic ketoacidosis occurs in patients with chronic alcohol abuse, liver disease, and acute alcohol ingestion.
- 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.
- Profound dehydration can culminate in circulatory collapse and/or lactic acidosis.
AKA patients usually present with abdominal pain and vomiting after abruptly stopping alcohol. 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 smell. 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.
Ethanol metabolism
DiscussionThis case highlights the importance of diagnosing patients with AKA and providing the appropriate treatment. With early diagnosis and appropriate treatment, patients improve rapidly and serious complications are prevented. Alcoholic ketoacidosis can develop when you drink excessive amounts of alcohol for a long period of time.
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. The patient received 4 liters of normal saline and was started on D5-1/2 NS prior to admission. He was given IV valium for alcohol withdrawal, and thiamine, folate, and phosphate were repleted. He was hospitalized for three days for management of AKA and alcohol withdrawal, then discharged once tolerating oral intake and in good condition. He was seen three weeks later in the emergency department for a similar presentation.
Symptoms and Signs of Alcoholic Ketoacidosis
The clinically relevant ketoacidoses to be discussed include diabetic ketoacidosis (DKA), alcoholic ketoacidosis (AKA), and starvation ketoacidosis. DKA is a potentially life-threatening complication of uncontrolled diabetes mellitus if not recognized and treated early. It typically occurs in the setting of hyperglycemia with relative or absolute insulin deficiency. The paucity of insulin causes unopposed lipolysis and oxidation of free fatty acids, resulting in ketone body production and subsequent increased anion gap metabolic acidosis.
If a person is already malnourished due to alcoholism, they may develop alcoholic ketoacidosis. This can occur as soon as one day after a drinking binge, depending on nutritional status, overall health status, and the amount of alcohol consumed. When your body burns fat for energy, byproducts known as ketone bodies are produced. If your body is not producing insulin, ketone bodies will begin to build up in your bloodstream. This buildup of ketones can produce a life-threatening condition known as ketoacidosis.
Differential Diagnosis
Lactic acidosis occurs when ethanol metabolism results in a high hepatic NADH/NAD ratio, diverting pyruvate metabolism towards lactate and inhibiting gluconeogenesis. In peripheral tissues, where NADH levels are lower, this lactate may be converted to pyruvate for metabolic needs. 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.
