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. Several mechanisms are responsible for dehydration, including protracted vomiting, decreased fluid intake, and inhibition of antidiuretic hormone secretion by ethanol.
Signs and symptoms
Alcohol withdrawal, in combination with nausea and vomiting, makes most patients agitated. However, if an AKA patient is lethargic or comatose, an alternative cause should be sought. The prevalence of AKA in a given community correlates with the incidence and distribution of alcohol abuse in that community. This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). The majority of papers detected by this search focus primarily on diabetes mellitus and its complications, and were excluded.
What Are the Symptoms of Alcoholic Ketoacidosis?
- Similar symptoms in a person with alcohol use disorder may result from acute pancreatitis, methanol (wood alcohol) or ethylene glycol (antifreeze) poisoning or diabetic ketoacidosis.
- If you or someone else has symptoms of alcoholic ketoacidosis, seek emergency medical help.
- When you drink alcohol, your pancreas may stop producing insulin for a short time.
- This case demonstrates the importance of considering AKA in the differential diagnosis of a patient presenting with non-specific symptoms, significant metabolic acidosis and a history of alcohol excess.
- The long-term prognosis for the patient is influenced more strongly by recovery from alcoholism.
Volume depletion is a strong stimulus to the sympathetic nervous system and is responsible for elevated cortisol and growth hormone levels. The prognosis for alcoholic ketoacidosis is good as long as it’s treated early. However, the long-term prognosis depends on the severity of the underlying alcohol abuse disorder. We present a 64-year-old female who presented with generalized abdominal pain, nausea, vomiting and shortness of breath.
- But it can happen after an episode of binge drinking in people who do not chronically abuse alcohol.
- Ketones are a type of acid that form when the body breaks down fat for energy.
- Magnesium and phosphate levels should be measured and repleted if the serum levels are found low.
- If history does not rule out toxic alcohol ingestion as a cause of the elevated anion gap, serum methanol and ethylene glycol levels should be measured.
BOX 3 MANAGEMENT OF AKA
The greatest threats to patients with alcoholic ketoacidosis are marked contraction in extracellular fluid volume (resulting in shock), hypokalaemia, hypoglycaemia, and acidosis. Arrange follow-up to evaluate patients after the resolution of symptoms, in order to detect other complications of chronic alcohol abuse. The patient may benefit from an alcohol rehabilitation program. Alcoholic ketoacidosis is a complication of alcohol use and starvation that causes excess acid in the bloodstream, resulting in vomiting and abdominal pain. Elevated cortisol levels can increase fatty acid mobilization and ketogenesis.
Related MedlinePlus Health Topics
Larger studies by Fulop and Hoberman5 and Wrenn et al6 (24 and 74 patients, respectively) clarified the underlying acid base disturbance. Although many patients had a significant ketosis with high plasma BOHB levels (5.2–14.2 mmol/l), severe acidaemia was uncommon. In the series from Fulop and Hoberman, seven patients were alkalaemic. Alcoholic ketoacidosis most commonly happens in people who have alcohol use disorder and chronically drink a lot of alcohol. But it can happen after an episode of binge drinking in people who do not chronically abuse alcohol. Alcoholic ketoacidosis doesn’t occur more often in any particular race or sex.
What are the symptoms of alcoholic ketoacidosis?
Although AKA can cause a modest elevation in serum glucose, significant hyperglycaemia in patients with metabolic acidosis, the presence of ketones and a suggestive history would make DKA the more likely diagnosis. The clinical importance in recognizing AKA from DKA is demonstrated by cases of patients who were treated as DKA and developed severe hypoglycaemia as a result of inappropriate insulin administration [8]. The key differential diagnosis to consider, and exclude, in these patients is DKA. Although DKA can also present with a severe metabolic acidosis, with a raised anion gap and the presence of ketones, the history and examination are quite distinct from that of someone presenting with AKA (Table 1).
Subsequent mismanagement can lead to increasing morbidity and mortality for patients. AKA typically presents with a severe metabolic acidosis with a raised anion gap and electrolyte abnormalities, which are treatable if recognized early and appropriate management instituted. Given the increasing epidemic of alcohol-related healthcare admissions, this is an important condition to recognize and we aim to offer guidance on how to approach similar cases for the practising clinician. The presence of a high anion gap, although not specific, is suggestive of AKA in a patient with an appropriate clinical history [9]. Additional measurements that may help determine the diagnosis of AKA include beta-hydroxybutyrate levels (high in AKA, low in DKA) and serum alcohol concentration (typically low or undetectable) [8].
Exclude other causes of autonomic hyperactivity and altered mental status. If the diagnosis of alcohol withdrawal syndrome is established, consider the judicious use of benzodiazepines, which should be titrated to clinical response. Following resuscitation, alcoholic ketoacidosis our patient had plasma electrolyte levels corrected, nutritional supplementation provided and completed an alcohol detoxification regimen. Given the early recognition of AKA and concurrent management, our patient had a good outcome.
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