Introduction
The accumulation of ketones in the blood due to alcohol use is known as alcoholic ketoacidosis (AKA). A particular chemical compound called ketone is produced when the body breaks down fat for energy. It is a severe case of metabolic acidosis, in which the body fluid contains excessive amounts of acid. AKA is more frequent among long-term alcoholics than binge drinkers. Onset usually occurs a few days after a drop in appetite. Symptoms are typically the basis for diagnosis. Blood sugar levels are frequently normal or very slightly elevated. Other high anion gap metabolic acidosis causes, such as diabetic ketoacidosis, which may also manifest similarly.
What Causes Alcoholic Ketoacidosis?
Alcoholic ketoacidosis is brought on by a complex physiology that develops due to chronic, high alcohol consumption, frequently in conjunction with malnutrition. Chronic alcohol consumption can reduce the amount of glycogen in the liver, and ethanol metabolism further reduces gluconeogenesis. This may result in a decrease in glucose availability, hypoglycemia, and an increased reliance on fatty acid and ketone metabolism. An additional stressor like vomiting event dehydration can increase the levels of counterregulatory hormones like glucagon, cortisol, and growth hormone, which may further boost the release of free fatty acids and the synthesis of ketone bodies. The ethanol metabolism can also raise blood levels of lactic acid, which may also cause metabolic acidosis.
What Are the Signs and Symptoms Associated With Alcoholic Ketoacidosis?
Frequently observed symptoms are:
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Nausea.
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Vomiting.
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Abdominal discomfort.
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Tachypnea.
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Tachycardia.
Alcoholic ketoacidosis differs from diabetic ketoacidosis in that patients are typically alert and conscious despite the severity of the acidosis.
What Is the Pathophysiology of Alcoholic Ketoacidosis?
Patients who have consumed a lot of alcohol arrive in a dehydrated state and then continue to have oral intake problems. Poor oral administration intake lasts for one to three days during this time. Low glycogen levels and a lack of oral meal intake are the first steps in the pathophysiology of alcoholic ketoacidosis, which causes the metabolism to switch from carbohydrates to fats and lipids. Reduced oral consumption results in lower insulin levels and higher amounts of hormones that regulate metabolism, including cortisol, glucagon, and epinephrine. Hormone-sensitive lipase is able to function more actively due to the absence of insulin. As ethanol is converted into acetaldehyde and acetyl-CoA, increasing the NADH/NAD+ ratio, these effects are further amplified. Lipid metabolism is subsequently boosted by the increasing NADH/NAD+ ratio.
How Is Alcoholic Acidosis Diagnosed?
Symptoms are typically used to make a diagnosis. Laboratory findings also help confirm the diagnosis.
Laboratory Findings Are:
1. Complete Blood Count - In a dehydrated patient, the WBC (white blood cells), hemoglobin, and hematocrit levels may be raised. In patients with chronic alcohol use disorder, a higher mean corpuscular volume (MCV) is frequently observed.
2. Metabolic Panel - The fundamental metabolic panel will probably be off. Potassium levels can range from normal to low because dehydration and a reduction in oral intake typically cause the serum potassium level to drop. With the presence of metabolic acidosis, bicarbonate or HCO3 levels would likely fall. If the patient is dehydrated, the blood urea nitrogen (BUN) ratio to creatinine may increase. Glucose levels are often raised but seldom exceed 250 milligrams per deciliter. The chances of the first glucose levels falling within the normal range are higher.
3. Betahydoxy Butyrate - There will be a considerable increase in beta-hydroxybutyrate serum (B-OH). Beta-hydroxybutyrate levels will be elevated to a much greater extent than lactate levels. A different source of acidosis should be considered if the lactate is more than four millimoles per liter. Often, there are no or very low serum alcohol levels.
4. Arterial Blood Gas - Most likely the blood gas analysis will show a low or normal pH. With a lower hydroxy bicarbonate level, metabolic acidosis will be present. If the patient is capable, the patient will mount a respiratory alkalosis. Given that severe vomiting can result in metabolic alkalosis, the existence of a mixed condition may also be present.
5. Urinalysis - A urine analysis may reveal an elevated specific gravity due to the patient's typical dehydration. If the patient has consumed enough liquids recently for antidiuretic hormone (ADH) inhibition to still be in effect, and if the patient has been capable of withstanding oral fluids for the past 24 hours without consuming any significant solid food, the specific gravity of the urine may be within the normal range.
6. Nitroprusside Test - By detecting acetoacetate, the nitroprusside test can be used to prove ketonuria. As the urine nitroprusside test may greatly underestimate the presence of beta-hydroxybutyrate, which is the main ketoacid found in alcoholic ketoacidosis, it is possible that it will test faintly positive despite the presence of severe ketosis.
Other Tests:
A dehydrated patient with a persistent alcohol use disorder and alcoholic ketoacidosis may exhibit atrial fibrillation or atrial flutter, while the EKG (electrocardiogram) is likely to show sinus tachycardia. Typically, the initial chest X-ray is negative.
What Is the Treatment Plan For Managing Alcoholic Acidosis?
A clinical diagnosis of alcoholic ketoacidosis should be made. Patients require fluid resuscitation, careful electrolyte monitoring, and treatment to avoid alcohol withdrawal.
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On the first visit, the patient's blood sugar level should be checked.
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Administration of isotonic fluid resuscitation is the next critical step in the therapy of alcoholic ketoacidosis. Standard saline with dextrose is the fluid of choice.
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To break the cycle of ketogenesis and release more insulin, dextrose is necessary. To boost glycogen reserves and lowering levels of hormones that regulate metabolism.
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Thiamine must be administered before any glucose treatment to prevent Wernicke's encephalopathy precipitation.
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Until potassium levels return to normal, dextrose-containing fluids might be withheld in cases of severe hypokalemia.
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Hypomagnesemia and hypophosphatemia are two further disorders of the electrolytes that can coexist with alcohol consumption and inadequate oral nutrition.
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Magnesium and phosphate levels should be checked and replenished if serum levels are found to be low.
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Based on the possibility of seizures brought on by approaching alcohol withdrawal, intravenous benzodiazepines may be given.
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Antiemetics such as Metoclopramide or Ondansetron may also be used to prevent nausea and vomiting.
Conclusion
Alcohol use disorder patients frequently experience alcoholic ketoacidosis. Patients who report tachycardia (a fast regular, or irregular heartbeat), tachypnea (unusually rapid breathing), dehydration, agitation, and stomach pain have this clinical diagnosis. The management of patients with alcoholic ketoacidosis is explained, along with the evaluation and therapy of the illness, in this activity. Alcoholic ketoacidosis is brought on by a complicated physiology brought on by extended and severe alcohol consumption, typically in conjunction with inadequate nutrition. The frequency of alcohol abuse in a community and prevalence are correlated. With treatment, outcomes are mostly positive. However, 10 percent of patients may experience cardiac arrest. Although the actual prevalence is unknown, it is suggested that alcoholic ketoacidosis is a substantial cause of death among those with chronic alcoholism. Due to the difficulties in making a diagnosis and the presence of numerous illnesses at presentation, it is difficult to estimate the prevalence and outcomes of the disease.
