Alcoholic Ketoacidosis: A Silent Killer

Posted on 2nd August 2019

Glucose stimulates insulin production, which stops lipolysis and halts further ketone formation. Glucose also increases oxidation of NADH to NAD, thereby further stopping ketone production. Once fluid and electrolyte losses are replaced, change fluids to 5% dextrose in half normal saline until oral intake is assured.1 Patients with alcoholic ketoacidosis are not hyperosmolar. Unlike treatment of diabetic ketoacidosis, cerebral edema is of little concern with large volumes of fluid administration. Even with vigorous fluid resuscitation, in our review of the literature, cerebral edema has not been reported among those being treated for alcoholic ketoacidosis.

What are the symptoms of alcoholic ketoacidosis?

  • Nausea and vomiting.
  • Abdominal pain.
  • Agitation, confusion.
  • Changed level of alertness, which may lead to coma.
  • Fatigue, slow movements.
  • Deep, labored, rapid breathing.
  • Loss of appetite.
  • Symptoms of dehydration, such as dizziness, lightheadedness, and thirst.

Alcoholic ketoacidosis should be differentiated from other alcohol ingestions. Methanol and ethylene glycol ingestions do not produce ketosis, and acidosis tends to be severe. Isopropyl alcohol ingestion results in production of ketones. The presence of a large osmolal gap suggests acute isopropyl, ethanol, methanol, or ethylene glycol ingestion. If the blood alcohol level is known, then its contribution to any osmolal gap can be calculated.

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A 1991 case series found that the most common symptoms among 74 patients presenting with AKA are nausea (76%), vomiting (73%), and abdominal pain (62%). These symptoms often develop one to two days before ketoacidosis and are due to other effects of alcohol, like gastritis. They may be the reason that patients abruptly stop drinking, triggering ketoacidosis. Though these abdominal complaints are common, they are less commonly accompanied by signs such as abdominal distension, hypoactive bowel sounds, or rebound tenderness.

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AKA can occur in adults of any age; it more often occurs in persons aged years who are chronic alcohol abusers. Rarely, AKA occurs after a binge in persons who are not chronic drinkers. Ingestion, alcoholic ketoacidosis produces an elevated osmol gap and an AGMA. The aim of this study was to identify risk factors suggestive of AKA when TA ingestion was the primary …

Inhaled industrial acetylene. A diabetic ketoacidosis mimic

Glucose levels are usually mildly elevated but are not generally above 250 mg/dl. The initial glucose levels are more likely to be in the normal range. Symptoms result not only from an anion gap metabolic acidosis but also from coexisting disorders, like withdrawal from alcohol and the acute effects of binge drinking. Laboratory testing reflects the combination of these disorders. Ethanol metabolism results in NAD depletion manifesting as a higher ratio of the reduced form of nicotinamide adenine dinucleotide to NAD.

Acetyl coenzyme A may be metabolized directly, resulting in ketoacid production; used as substrate for the Krebs cycle; or used for free fatty acid synthesis (Figure 226-1). People with this condition are usually admitted to the hospital, alcoholic ketoacidosis often to the intensive care unit . Medicines may be given to prevent alcohol withdrawal symptoms. AKA can occur in adults of any age; however, it most often develops in persons aged years who are chronic abusers of alcohol.

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Summarize the importance of collaboration and communication among the interprofessional team to enhance the delivery of care for patients affected by alcoholic ketoacidosis. Review the fluid and volume resuscitation and correction of electrolyte abnormalities used in the treatment of alcoholic ketoacidosis. Once you have decided to seek treatment, selecting the appropriate course will depend on your situation. If you have an alcohol use disorder and have drunk excessively over a long period of time, you may require medically supervised detoxification. Medically supervised detoxification can reduce the risk of severe withdrawal symptoms and the risk of relapse. Heavy alcohol use can also impair the liver’s ability to synthesize and release glucose. These two factors decrease the body’s normal levels of readily available energy, and it responds by breaking down fat and producing ketones.

alcoholic ketoacidosis

In a large cohort, coefficients from regression analyses estimating the contribution of glucose, urea, and ethanol were higher than 1.0. Our simplified formula to precisely calculate osmolarity yielded improved diagnostic accuracy for suspected toxic alcohol exposures than previously published formulas. The osmolal gap has been used for decades to screen for exposure to toxic alcohols.

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And, as it turns out, you need NAD+ to perform gluconeogenesis. With less NAD+, you cannot convert lactate into pyruvate , which is also why AKA patients often have hyperlactemia. So, the drinker doesn’t have glycogen to break down and cannot make sugar, but at least they can use fat to make fuel, right?. Normally when you are starving, you make the ketones acetoacetate, and to a lesser extent acetone and beta hydroxybutyrate . Acetoacetate is helpful because it can be converted to acetyl-coA and go through the Krebs cycle to make ATP. For it to generate ATP it first needs to be converted to acetoacetate which requires – you guessed it – NAD+ . Unfortunately, with less reduced NAD+, you favor the formation of BHB over acetoacetate.

  • The ketone which is present is mostly beta-hydroxybutyrate rather than acetoacetate resulting in only a weakly positive nitroprusside test.
  • Magnesium and phosphate levels should be measured and repleted if the serum levels are found low.
  • Symptoms ameliorated with glucose injection and fluid loading.
  • It is essential to administer thiamine before any glucose administration to avoid Wernicke’s encephalopathy preci[itation.
  • The next important step in the management of AKA is to give isotonic fluid resuscitation.

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