Alcoholic Ketoacidosis: Practice Essentials, Pathophysiology, Etiology

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. Free fatty acids are either oxidized to CO2 or ketone bodies , or they are esterified to triacylglycerol and phospholipid. Carnitine acyltransferase transports free fatty acids into the mitochondria and therefore regulates their entry into the oxidative pathway.

  • In addition to isotonic fluid replacement, dextrose-containing intravenous fluids are needed.
  • When your fat cells break down, they release ketones, which are a type of acid that provides your cells with some energy.
  • Rarely, AKA occurs after a binge in persons who are not chronic drinkers.
  • If you don’t eat for a day or longer, then your liver will use up the glucose it’s stored up to give your cells energy.

The elevated L/P ratio also explains why lactate levels rise in AKA, just as they do in DKA. Both conditions are characterized by lipolysis and high NADH/NAD ratios, and in both conditions, hyperlactatemia is expected. In fact, just drinking a few beers can raise arterial lactate levels significantly without acidemia, just from raising your NADH/NAD ratio from ethanol metabolism,.

Ethanol metabolism

AKA is characterized by metabolic acidosis with an elevated anion gap, elevated serum ketone levels, and a normal or low glucose concentration. The diagnosis of AKA requires arterial blood gas measurement and serum chemistry assays. Severe derangements of potassium and/or magnesium may be implicated in the sudden deaths of some alcoholic patients, but not all. alcoholic ketoacidosis 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.

Mildly elevated osmolal gaps can exist, but it is important to consider co-ingestions, or other causes of anion gap acidosis, if the gap fails to close with ongoing fluid and carbohydrate treatment. Hypophosphatemia is common in alcoholics and can retard the resolution of acidosis because phosphorus is necessary for mitochondrial utilization of glucose for oxidation of NADH. A 49-year-old male with a history of alcohol abuse presents 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. Laboratory studies show a serum bicarbonate of 10 mEq/L, an anion gap of 30, a serum glucose of 95 mg/dL, a lactic acidosis with pH 7.2, hypophosphatemia, and trace ketonuria.

Ed Treatment/Procedures

Hypoalbuminemia can develop due to malnutrition or other health conditions. Find out how you can help and be a positive influence in their journey to be alcohol-free. What happens to your body after you take your first sip of alcohol? Learn the effects of drinking on your body and mental well-being. Your prognosis will be impacted by the severity of your alcohol use and whether or not you have liver disease. Prolonged used of alcohol can result in cirrhosis, or permanent scarring of the liver.

Does ketoacidosis go away on its own?

Yes, if left untreated, diabetes-related ketoacidosis results in death. Because of this, it's essential to treat DKA as soon as possible. Call your healthcare provider immediately or go to the nearest emergency room if you experience symptoms.

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