Alcoholic Ketoacidosis: Causes, Symptoms, and Diagnosis

He denies a history of diabetes mellitus, ingestion of any toxic alcohols, or recent illness. 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.

  1. Alcoholic ketoacidosis is attributed to the combined effects of alcohol Alcohol Toxicity and Withdrawal Alcohol (ethanol) is a central nervous system depressant.
  2. All remaining papers were retrieved and the reference lists hand searched for any additional information sources.
  3. The patient should have blood glucose checked on the initial presentation.
  4. Whilst a decreased conscious level may have been expected, our patient was lucid enough to report drinking one to two bottles of wine per day for the past 30 years, with a recent binge the day prior to admission.

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.

Cells need glucose (sugar) and insulin to function properly. 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.

The doctor must exclude these other causes before diagnosing 15 of the best sobriety podcasts to listen to in recovery. 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.

The clinical and biochemical features of AKA are summarised in boxes 1 and 2. The classical presentation is of an alcoholic patient with abdominal pain and intractable vomiting following a significant period of increased alcohol intake and starvation. There may be a history of previous episodes requiring brief admissions with labels of “query pancreatitis” or “alcoholic gastritis”. Typically, an alcohol binge leads to vomiting and the cessation of alcohol or food intake for ≥ 24 hours.

Clinical studies of alcoholic ketoacidosis

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education. The remainder of the patient’s laboratory evaluation – including liver enzymes, amylase, and lipase – were within normal limits, and methanol, ethylene glycol, salicylate, and digoxin levels were negative. Of note in the table above, the patient’s INR was greater than 11, above the upper limit of the assay, and this was confirmed by repeating the test.

Symptoms of Alcoholic Ketoacidosis

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. 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.

How do doctors treat alcoholic ketoacidosis?

This case demonstrates the importance of considering AKA in the differential diagnosis of a patient presenting with non-specific symptoms, significant metabolic acidosis and a history of alcohol excess. It is essential to differentiate AKA from DKA to ensure that inappropriate insulin administration does not occur. The key tenants to management alcohol rehabilitation programs of AKA include fluid resuscitation and electrolyte correction. AKA can be an unrecognized cause of patients presenting with a severe metabolic acidosis, including the presence of ketones. It should be suspected in any patient who has a history of chronic alcohol dependency, malnutrition or recent episode of binge drinking [1].

The diagnosis is often delayed or missed, and this can have potentially fatal consequences. There are a variety of non-specific clinical manifestations that contribute to these diagnostic difficulties. In particular, cases of AKA can be misdiagnosed as diabetic ketoacidosis (DKA).

Lactic acidosis

Although the underlying pathophysiology is complex, a proper comprehension greatly aids in the diagnosis and management of this condition. 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. Emergency clinician knowledge of the evaluation and management of AKA is essential in caring for these patients.

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.

Diagnosis

These conditions have to be ruled out before a medical professional can diagnose you with alcoholic ketoacidosis. It most often occurs in a malnourished person who drinks large amounts of alcohol every day. Subsequent fluid resuscitation and monitoring were instituted.

To treat transactional writing: letters that heal, doctors give people thiamine (vitamin B1) by vein (intravenously) followed by intravenous saline and glucose solution. Other vitamins and minerals, such as magnesium, are added to the saline solution. Alcoholic ketoacidosis (AKA) is defined by metabolic acidosis and ketosis in a patient with alcohol use. This is a common presentation in the emergency department (ED) and requires targeted therapies.

Joining a local chapter of Alcoholics Anonymous may provide you with the support you need to cope. You should also follow all of your doctor’s recommendations to ensure proper nutrition and recovery. 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 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.

Alcohol dehydrogenase (ADH), a cytosolic enzyme, metabolizes alcohol to acetaldehyde in hepatocytes. Acetaldehyde is metabolized further to acetic acid by aldehyde dehydrogenase. Both steps require the reduction of nicotinamide adenine dinucleotide (NAD+) to reduced nicotinamide adenine dinucleotide (NADH). This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). Limiting the amount of alcohol you drink will help prevent this condition.

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