Alcoholic ketoacidosis doesn’t occur more often in any particular race or sex. Alcoholic ketoacidosis is usually triggered by an episode of heavy drinking. If you can’t eat for a day or more, your liver will use up its stored-up glucose, which is a type of sugar.
- Increased ketogenesis secondary to the utilization of hepatic glycogen stores, with subsequently increased lipolysis and a decreased insulin-to-glucagon ratio, causes starvation ketosis.
- The classic laboratory findings in patients with AKA include an elevated anion gap metabolic acidosis and an elevated lactate.
- It’s important to note that AKA treatment also includes addressing any underlying issues, such as alcohol use disorder, and may involve a multidisciplinary approach including medical, nutritional, and psychological support.
- Initial steps include checking blood glucose levels and administering isotonic fluids, typically normal saline with dextrose, to halt ketogenesis and boost insulin secretion.
- The clinical assessment for Alcoholic Ketoacidosis (AKA) involves a comprehensive evaluation of patient history, physical examination, and laboratory findings.
- This buildup of ketones can produce a life-threatening condition known as ketoacidosis.
Table 1 Metabolic factors affecting acid base balance in AKA .
You can learn how to reduce your alcohol intake or eliminate it altogether. Joining a local chapter of Alcoholics Anonymous may provide you with the support you need to cope. You should also follow all of your doctor’s recommendations to ensure proper nutrition and recovery. Your doctor and other medical professionals will watch you for symptoms of withdrawal. If a person is already malnourished due to alcoholism, they may develop alcoholic ketoacidosis.
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- 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.
- During physical examination, healthcare professionals look for signs that are consistent with AKA, such as signs of dehydration and an alcoholic odor on the breath.
- Together, EtOH-mediated depletion of hepatic glycogen in diabetic (present study) or nondiabetic state (23, present study) is attributable in part to its inhibitory effect on the allosteric activation of GS.
Wrenn et al found altered mental status in 15% of patients, attributable in all but one case to hypoglycaemia, severe alcohol intoxication, or infection. Fever was seen in only two patients, both with other likely underlying causes. Alcohol abuse treatment programs teach people how to move into an alcohol-free lifestyle while teaching them healthy coping marijuana addiction strategies.
BOX 2 BIOCHEMICAL FEATURES OF AKA
Pyruvate and lactate are then maintained in steady state at much higher levels than normal. This results in a decrease in circulating lactic acid and an increase in acetoacetate. In 1940, Dillon et al1 described a series of nine patients who had episodes of severe ketoacidosis in the absence of diabetes mellitus, all of whom had evidence of prolonged excessive alcohol consumption. It was not until 1970 that Jenkins et al2 described a further three non‐diabetic patients with a history of chronic heavy alcohol misuse and recurrent episodes of ketoacidosis. This group also proposed a possible underlying mechanism for this metabolic disturbance, naming it alcoholic ketoacidosis. This condition is characterized by the presence of high levels of ketones in the blood, which are acidic by-products of fat metabolism.
What Are the Symptoms of Alcoholic Ketoacidosis?
- Antiemetics such as ondansetron or metoclopramide may also be given to control nausea and vomiting.
- Ethyl alcohol oxidizes at a rate of 20 to 25 mg/dL per hour in most individuals.
- First, alcohol contains empty calories, which deplete the diet of critical elements.
- Acetaldehyde is metabolized further to acetic acid by aldehyde dehydrogenase.
- Your doctor may also admit you to the intensive care unit (ICU) if you require ongoing care.
Conversely, when ketoacidosis is identified, but its origin is unrelated to alcohol, medical professionals may explore other diagnostic possibilities. This may involve conducting tests to rule out conditions such as starvation ketosis. However, if an individual presents with symptoms of ketoacidosis but is not found to be in a state of ketoacidosis, healthcare providers will investigate alternative conditions like alcohol poisoning. Elevated cortisol levels can increase fatty acid mobilization and ketogenesis.
What are the symptoms of alcoholic ketoacidosis?
Your doctor may also admit you to the intensive care unit (ICU) if you require ongoing care. The length of your hospital stay depends on the severity of the alcoholic ketoacidosis. It also depends on how long it takes to get your body regulated and out of danger. If you have any additional complications during treatment, this will also affect the length of your hospital stay.
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. Patients with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated hemoglobin (HbA1C). This drop in blood sugar causes your body to decrease the amount of insulin it produces. 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.
Dehydration and volume constriction directly decrease the ability of the kidneys to excrete ketoacids. Profound dehydration can culminate in circulatory collapse and/or lactic acidosis. The resulting increase in the NADH/NAD+ ratio inhibits hepatic gluconeogenesis and elevates the ratio of hydroxybutyric acid to acetoacetic acid. Acetic acid (an acyl group carrier) is linked with coenzyme A (a thiol) to produce Acetyl-CoA. It most often occurs in a malnourished person who drinks large amounts of alcohol every day. A 45 year old male presents intoxicated, smelling of alcohol and appears disheveled with vomit on his clothes.
How Can Alcoholic Ketoacidosis Be Prevented?
In general, the prognosis for a patient presenting with AKA is good as long as the condition is identified and treated early. The major cause of morbidity and mortality in patients diagnosed with AKA is under-recognition of concomitant diseases (that may have precipitated the AKA, to begin with). 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. It should be used as an indicator of the severity of the disease.13 Identifying these high-risk patients can help set the intensity of monitoring required for the patient to ensure optimal patient outcomes are achieved.
Ketones provide some energy to cells but also make the blood too acidic (ketoacidosis). This ketoacidosis is similar to the ketoacidosis that occurs in diabetes except that, unlike in diabetic ketoacidosis, blood glucose levels are low. Energy (caloric) restriction secondary to abdominal pain, nausea, or vomiting usually occurs prior to the onset of AKA. 7 Under conditions of starvation, the liver increases etoh ketoacidosis the production of ketones from fatty acids to supply the brain, kidney, and other peripheral tissues with a metabolic fuel that can replace glucose.
