Alcoholic ketoacidosis is a recognised acute complication in alcohol dependent patients. Given the frequency with which the condition is seen in other countries, the possibility exists that many cases may be unrecognised and misdiagnosed in UK EDs. AKA should be included in the differential diagnosis of alcohol dependent patients presenting with acute illness. Management is based around exclusion of serious pathology and specific treatment for AKA where it is present. A possible link between AKA and sudden death in chronic alcoholism has been proposed but remains unconfirmed. Breathing tends to become deep and rapid as the body attempts to correct the blood’s acidity.
Complications
Your cells need insulin to use the glucose in your blood for energy. 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. The greatest threats to patients with alcoholic ketoacidosis are marked contraction in extracellular fluid volume (resulting in shock), hypokalaemia, hypoglycaemia, and acidosis.
- Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia.
- Typically, an alcohol binge leads to vomiting and the cessation of alcohol or food intake for ≥ 24 hours.
- Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism.
- Generally, the physical findings relate to volume depletion and chronic alcohol abuse.
- There is increasing evidence that rather than being benign and self limiting, AKA may be a significant cause of mortality in patients with alcohol dependence.
Differential diagnosis
When you drink alcohol, your pancreas may stop producing insulin for a short time. Without insulin, your cells won’t be able to use the glucose you consume for energy. After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education. Jenkins et al2 suggested that alcohol induced mitochondrial damage might account for AKA.
Possible Complications of Alcoholic Ketoacidosis
The metabolism of alcohol itself is a probable contributor to the ketotic state. Alcohol dehydrogenase (ADH), a cytosolic enzyme, metabolizes alcohol to acetaldehyde in hepatocytes. Acetaldehyde is metabolized further to acetic acid by aldehyde dehydrogenase. Both steps require the reduction of nicotinamide adenine dinucleotide (NAD+) to reduced nicotinamide adenine dinucleotide (NADH). He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.
This buildup of ketones can produce a life-threatening condition known as ketoacidosis. If you or someone else has symptoms of alcoholic ketoacidosis, seek emergency medical help. It most often occurs in a malnourished person who drinks large amounts of alcohol every day.
What to Know About Alcoholic Ketoacidosis
Diagnosis is by history and findings of ketoacidosis without hyperglycemia. A person who isn’t eating properly and getting the nutrition the body needs from food because they’re drinking heavy amounts of alcohol instead, starts to get a buildup of excessive amounts of ketones in the body. Toxicity from methanol or ethylene glycol is an important differential diagnosis. Toxic metabolites of both substances result in severe metabolic acidosis with wide anion gap and https://ecosoberhouse.com/article/why-does-alcohol-cause-bruising/ wide osmolal gap.18 Neither, however, causes ketosis.
Volume depletion is a strong stimulus to the sympathetic nervous system and is responsible for elevated cortisol and growth hormone levels. During starvation, there is a decrease in insulin secretion and an increase in the production of counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone. 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.
This can occur as soon as one day after a drinking binge, depending on nutritional status, overall health status, and the amount alcoholic ketoacidosis of alcohol consumed. When your body burns fat for energy, byproducts known as ketone bodies are produced. If your body is not producing insulin, ketone bodies will begin to build up in your bloodstream.
How can I prevent alcoholic ketoacidosis?
There is increasing evidence that rather than being benign and self limiting, AKA may be a significant cause of mortality in patients with alcohol dependence. This literature review discusses the history, characterisation, pathophysiology, diagnosis, and management of AKA. Elevated cortisol levels can increase fatty acid mobilization and ketogenesis. Growth hormone can enhance precursor fatty acid release and ketogenesis during insulin deficiency. Catecholamines, particularly epinephrine, increase fatty acid release and enhance the rate of hepatic ketogenesis.
- The clinical and biochemical features of AKA are summarised in boxes 1 and 2.
- Alcoholic ketoacidosis is a condition that can happen when you’ve had a lot of alcohol and haven’t had much to eat or have been vomiting.
- The doctor must exclude these other causes before diagnosing alcoholic ketoacidosis.
- Neurologically, patients are often agitated but may occasionally present lethargic on examination.
Treatment of Alcoholic Ketoacidosis
Alcohol produces structural changes in human liver mitochondria within days. Fulop and Hoberman5 argued that a functional abnormality is more likely to be responsible, as even severe AKA usually improves rapidly with treatment. They attributed this to the administration of therapy (intravenous dextrose) rather than the withdrawal of the toxin, ethanol. The condition is an acute form of metabolic acidosis, a condition in which there is too much acid in body fluids. Prolonged vomiting leads to dehydration, which decreases renal perfusion, thereby limiting urinary excretion of ketoacids. Moreover, volume depletion increases the concentration of counter-regulatory hormones, further stimulating lipolysis and ketogenesis.