Alcoholic Ketoacidosis: Etiologies, Evaluation, and Management Journal of Emergency Medicine

Several mechanisms are responsible for dehydration, including protracted vomiting, decreased fluid intake, and inhibition of antidiuretic hormone secretion by ethanol. Volume depletion is a strong stimulus to the sympathetic nervous system and is responsible for elevated cortisol and growth hormone levels. Generally, the physical findings relate to volume depletion and chronic alcohol abuse. Typical characteristics of the latter may include rhinophyma, tremulousness, hepatosplenomegaly, peripheral neuropathy, gynecomastia, testicular atrophy, and palmar erythema. The patient might be tachycardic, tachypneic, profoundly orthostatic, or frankly hypotensive as a result of dehydration from decreased oral intake, diaphoresis, and vomiting.

  • Group meetings provide support for people trying to quit drinking.
  • Glucose comes from the food you eat, and insulin is produced by the pancreas.
  • Prolonged vomiting leads to dehydration, which decreases renal perfusion, thereby limiting urinary excretion of ketoacids.
  • However, after adequate treatment, it is equally essential to refer the patient to alcohol abuse rehabilitation programs to prevent recurrence and long-term irreversible damage from alcohol abuse.
  • If not treated quickly, alcoholic ketoacidosis may be life-threatening.

History and Physical

Patients improved rapidly (within 12 hours) with intravenous glucose and large amounts of intravenous saline, usually without insulin (although small amounts of bicarbonate were sometimes used). 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+). 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.

  • If indicated, provide follow-up with AKA patients to assess the problem of alcohol abuse.
  • If you or someone else has symptoms of alcoholic ketoacidosis, seek emergency medical help.
  • Exclude other causes of autonomic hyperactivity and altered mental status.
  • Efficient and timely management can lead to enhanced patient outcomes in patients with AKA.
  • Jenkins et al2 suggested that alcohol induced mitochondrial damage might account for AKA.
  • Cirrhosis of the liver can cause exhaustion, leg swelling, and nausea.

Alcoholic Ketoacidosis Treatment & Management

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.

What Are the Symptoms of Alcoholic Ketoacidosis?

alcoholic ketoacidosis is the buildup of ketones in the blood due to alcohol use. Ketones are a type of acid that form when the body breaks down fat for energy. The absence of hyperglycemia makes diabetic ketoacidosis improbable. Patients with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated hemoglobin (HbA1C).

alcoholic ketoacidosis

Metabolism of ethanol

alcoholic ketoacidosis

Clinical Features

  • If a person is already malnourished due to alcoholism, they may develop alcoholic ketoacidosis.
  • This literature review discusses the history, characterisation, pathophysiology, diagnosis, and management of AKA.
  • 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+).
  • Support groups can be a valuable source of support and can be combined with medication and therapy.

What are the complications of alcoholic ketoacidosis?

alcoholic ketoacidosis

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