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Alcoholic Ketoacidosis in Pregnancy : Obstetrics & Gynecology

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In contrast to diabetic ketoacidosis, people with alcoholic ketoacidosis are usually alert and lucid despite the severity of the acidosis. Complete blood count – The white blood cell count , hemoglobin, and hematocrit levels may be elevated in a dehydrated patient. An elevated mean corpuscular volume is often seen in patients with chronic alcohol use disorder. Ketone production can be further stimulated in malnourished, vomiting patients or in those who are hypophosphatemic.6 Both conditions are seen commonly in alcoholic patients with alcoholic ketoacidosis.

alcoholic ketoacidosis

People usually do not present with high blood sugar or sugar in the urine. This can cause false negative results when testing urine ketones as they only measure acetoacetate. Ethanol level are often low or negative despite a chronic alcohol use history. Electrolyte disturbances may include hypokalemia or hypomagnesemia may also be present. AKA is a common disorder in the emergency department, more common than previously thought. The acid-base abnormalities are more diverse than just a wide-gap metabolic acidosis and often include a concomitant metabolic alkalosis, hyperchloremic acidosis, or respiratory alkalosis.

Ed Treatment/Procedures

In AKA, the increased ratio of NADH/NAD+ increases the proportion of beta hydroxybutyrate relative to acetoacetate. Alcoholic ketoacidosis should be differentiated from other alcohol ingestions. Methanol and ethylene glycol ingestions do not produce ketosis, and acidosis tends to be severe. 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. Each 100 milligrams/dL (21.7 mmol/L) of ethanol raises the osmolal gap by 22.

How do you fix alcoholic ketoacidosis?

Once the diagnosis of alcoholic ketoacidosis (AKA) is established, the mainstay of treatment is hydration with 5% dextrose in normal saline (D5 NS) to address the principal physiologic derangement, a lack of metabolic substrate (glucose).

Patients develop acidosis, which causes an increase in respiratory rate and fluid loss. The relative starvation state in AKA leads to excessive glucagon secretion and reduced peripheral insulin concentrations, which plays a key role in developing ketoacidosis. Metabolism of fats through lipolysis produces alcoholic ketoacidosis beta-hydroxybutyrate and acytyl-acetate . These ketones are utilized for cellular respiration to provide energy through adenosine triphosphate production, but add to the anion gap acidosis seen in AKA. Increased availability of free fatty acids, which provide the major substrate for ketone body formation.

Substance Use Treatment

These include acute pancreatitis, gastrointestinal bleeding, and alcohol withdrawal. Mortality specifically due to AKA has been linked to the severity of serum beta-hydroxybutyric acid in some studies. Metabolic Panel – The basic metabolic panel will likely be abnormal. Potassium levels can be normal or low, as dehydration and decreased oral intake frequently decrease the serum potassium level. Bicarbonate or HCO3 will likely be decreased with the presence of metabolic acidosis. The blood urea nitrogen to creatinine ratio may be elevated if the patient is dehydrated.

Why does alcoholism cause ketoacidosis?

Alcoholic ketoacidosis is caused by the combined effects of alcohol and starvation on glucose metabolism; it is characterized by hyperketonemia and elevated anion gap metabolic acidosis without significant hyperglycemia.

Warfarin overdose was also considered, although the patient repeatedly denied this and reports he did not have access to his medications. Further, vitamin K administration in our patient resulted in normalization of his INR. In general, the prognosis for a patient presenting with AKA is good as long as the condition is identified and treated early.

Critical Care

Hormone-sensitive lipase is normally inhibited by insulin, and, when insulin levels fall, lipolysis is up-regulated, causing release of free fatty acids from peripheral adipose tissue. One complication of alcoholic ketoacidosis is alcohol withdrawal. Your doctor and other medical professionals will watch you for symptoms of withdrawal.

  • This goal can usually be achieved through the administration of dextrose and saline solutions.
  • Alcoholic Ketoacidosis is a sample topic from the 5-Minute Emergency Consult.
  • These include acute pancreatitis, gastrointestinal bleeding, and alcohol withdrawal.
  • Although the underlying pathophysiology is complex, a proper comprehension greatly aids in the diagnosis and management of this condition.
  • Diagnosis is made by the criteria listed in Table 226-1, with metabolic acidosis, positive serum ketones, elevated anion gap, and a low or mildly elevated serum glucose level.
  • If your body is not producing insulin, ketone bodies will begin to build up in your bloodstream.

He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of theFOAMmovement (Free Open-Access Medical education) and is co-creator oflitfl.com, theRAGE podcast, theResuscitologycourse, and theSMACCconference. Altered mental status is less common in AKA than in DKA, as neurological manifestations in DKA are thought to be secondary to a rise in plasma osmolality due to hyperglycemia and consequent water loss. Symptoms of withdrawal, such as tremulousness, are less common.

Delayed presentation or diagnosis may result in end-organ damage such as acute renal failure with tubular necrosis. The long-term prognosis of patients diagnosed with AKA depends on the severity of their underlying alcohol abuse disorder rather than AKA itself. The major cause of morbidity and mortality in patients diagnosed with AKA is under-recognition of concomitant diseases .

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