alcoholic ketoacidosis blood alcohol levels were present in two thirds of patients in whom alcohol levels were determined, and levels consistent with intoxication were seen in 40% of these patients. Electrolyte disorders including hyponatremia, hypokalemia, hypophosphatemia, hyperglycemia, hypocalcemia, and hypomagnesemia were common on presentation. The most common symptoms were nausea, vomiting, and abdominal pain. The most common physical findings were tachycardia, tachypnea, and abdominal tenderness. Altered mental status, fever, hypothermia, or other abnormal findings were uncommon and reflected other underlying processes. Therapy consists of both glucose administration and volume repletion (Table 226-3). Fluids alone do not correct the ketoacidosis as fast as fluids and glucose administered together.

He was admitted to the internal https://ecosoberhouse.com/ service for continued management. By hospital day two, the patient’s INR normalized to therapeutic range and his warfarin was restarted. On hospital day three, the patient was discharged home with outpatient services for his alcohol use disorder. 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.

Metabolism of ethanol

Review the fluid and volume resuscitation and correction of electrolyte abnormalities used in the treatment of alcoholic ketoacidosis. If you or someone you know has an alcohol use disorder, they may be at risk of developing alcoholic ketoacidosis. Seeking treatment sooner than later might prevent this life-threatening condition. Excessive drinking damages the pancreas, impacting insulin production.

Fat is broken down into ketones that can be used as an alternative fuel source. Two beneficiaries of this process are the heart and the brain (Stryer Biochemistry 5th edition. Section 30.2, Each Organ Has a Unique Metabolic Profile). Despite what Dunkin’ Donuts would lead you to think, the heart runs on fats and ketones . They brain does not have glycogen stores, so during a fast it relies on ketones.

Alcohol-induced ketoacidosis and hypoglycemia in alcohol-related emergencies

Selected aspects of the pathophysiology of metabolic acidosis in diabetes mellitus. With these tests, the doctor could find evidence of diabetes, which will require specialized treatment.

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.

Alcoholic Ketoacidosis: Symptoms, Causes, and Risks

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?.

The differential diagnosis includes other causes of an increased anion gap metabolic acidosis. In a patient with diabetes, there must also be a consideration of diabetic ketoacidosis . Symptoms often include abdominal pain, vomiting, agitation, a fast respiratory rate, and a specific “fruity” smell. Examination should reveal a clear level of consciousness, generalised abdominal tenderness , 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.