If they can’t use glucose because there’s not enough insulin, your body switches to another method to get energy — breaking down fat cells. Read about the differences between alcohol abuse and alcoholism. Despite the similarity in name, ketosis and ketoacidosis are two different things. If you develop any of these symptoms, seek emergency medical attention.

Medically supervised detox is part of a general approach to addiction treatment called medically-assisted treatment . MAT is supported by the scientific community to successfully treat alcohol and other drug addiction and involve supervised detoxification, treatment planning, and counseling.


Alcoholic ketoacidosis can be a fatal outcome of initial high alcohol intake or binge drinking, followed by a lack of food or water for more than 24 hours. It differs from alcohol poisoning in that the BAC may be low or even zero. These are examples of when calculating alcohol consumption isn’t always straightforward. They are important, however, when making distinctions between normal and excessive levels of alcohol consumption. Someone may think they are consuming 3-4 drinks a day when, in actuality, they are consuming closer to 6 or more.

alcoholic ketoacidosis

The accompanying lack of alcohol in the patient’s body and the fact that for some time, the only source of calories that a patient has is ethanol both contribute to the clinical syndrome that we see. Typically the postmortem forensic toxicology in cases of AKA reveal a normal or low blood sugar level, very high acetone concentrations , and a negative or low blood alcohol concentration. Four patients were treated with insulin and four with NaHCO3 solutions. In retrospect, the need for either of these treatments was not clear. Two of the twenty-four patients died, one from circulatory failure secondary to hemorrhage and the other from pulmonary edema, but no patient died because of ketoacidosis per se. Alcohol specifically contributes to ketoacidosis in many ways. This leads to depleted levels of both carbohydrates and protein.

How is alcoholic ketoacidosis treated?

The toxicokinetics that are pertinent to the diagnosis of AKA include the rate of alcohol oxidation in the body. Ethyl alcohol oxidizes at a rate of 20 to 25 mg/dL per hour in most individuals.

We present a 64-year-old female who presented with generalized abdominal pain, nausea, vomiting and shortness of breath. Arterial blood gas analysis showed significant acidaemia with a pH of 7.10, bicarbonate of 2.9 mmol/l and lactate of 11.7 mmol/l. Ethanol metabolism results in NAD depletion manifesting as a higher ratio of the reduced form of nicotinamide adenine dinucleotide to NAD. When glycogen stores are depleted in a patient stressed by concurrent illness or volume depletion, insulin secretion is also suppressed. Under these same conditions, glucagon, catecholamine, and growth hormone secretion are all stimulated.

Signs and Symptoms

The resultant increased NADH/NAD+ ratio increases lipid metabolism. All of these changes increase the breakdown of lipids to ketoacids. The elevated NADH/NAD+ ratio further alcoholic ketoacidosis encourages the conversion of acetoacetate to beta-hydroxybutyrate. Ketoacids further accumulate as dehydration and decreased renal perfusion limit the removal of ketoacids.

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  • After these test results are in, they can confirm the diagnosis.
  • For it to generate ATP it first needs to be converted to acetoacetate which requires – you guessed it – NAD+ .
  • Diagnosis is confirmed if the patient history meets the DSM-V criteria for AUD.

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.

How Is Alcoholic Ketoacidosis Treated?

A degree of alcohol withdrawal and agitation are likely to be present, resulting in an increased heart rate as well. Patients are usually tachycardic, dehydrated, tachypneic, present with abdominal pain, and are often agitated. AUD is a clinical diagnosis, and laboratory tests are not usually required, although they may provide evidence of problematic alcohol use in patients who cannot provide a conclusive history. It should be noted that ketoacidosis is very rare9 and not a significant risk factor for AKA unless someone is also chronically abusing alcohol. This is not AKA, but simply an example of how it is the NADH/NAD ratio that is the problem, regardless of how the elevated ratio is produced. Ethanol also does a couple other things to cause hypoglycemia, including impairing release of alanine from skeletal muscle catabolism.

  • The alcohol further depresses gluconeogenesis in the body and keeps blood sugar levels low.
  • If they can’t use glucose because there’s not enough insulin, your body switches to another method to get energy — breaking down fat cells.
  • AlcoholicsAnonymous.com is a referrer service that provides information about addiction treatment practitioners and facilities.
  • The presence of a large osmolal gap suggests acute isopropyl, ethanol, methanol, or ethylene glycol ingestion.
  • Acetoacetic acid is the acid detected by several diagnostic tests for AKA, like the nitroprusside test, so false negatives may result.

Sodium bicarbonate is not indicated unless patients are severely acidemic, with a pH . Severe acidemia is unlikely to be explained by alcoholic ketoacidosis alone. 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. In 1940, Dillon and colleagues first described alcoholic ketoacidosis as a distinct syndrome. 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.

Summarize the importance of collaboration and communication among the interprofessional team to enhance the delivery of care for patients affected by https://ecosoberhouse.com/. 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