If severe hypokalemia is present dextrose containing fluids can be held until potassium levels are normalized. Other electrolyte abnormalities concomitantly present with alcohol abuse and poor oral intake include hypomagnesemia and hypophosphatemia. Magnesium and phosphate levels should be measured and repleted if the serum levels are found low. Alcoholic ketoacidosis (AKA) is a condition that presents with a significant metabolic acidosis in patients with a history of alcohol excess. The diagnosis is often delayed or missed, and this can have potentially fatal consequences. There are a variety of non-specific clinical manifestations that contribute to these diagnostic difficulties.
BOX 1 PRESENTING FEATURES OF AKA
Efficient and timely management can lead to enhanced patient outcomes in patients with AKA. However, after adequate treatment, it is equally essential to refer the patient to alcohol abuse rehabilitation programs to prevent recurrence and long-term irreversible damage from alcohol abuse. Following resuscitation, 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.
Differential Diagnosis
Despite the frequency of abdominal symptoms, objective findings other than tenderness were infrequent. Both Wrenn et al6 and Fulop and Hoberman5 found evidence of alcoholic hepatitis to be common, with frequent elevations in serum transaminase activities and bilirubin. You can prevent alcoholic ketoacidosis by limiting your alcohol intake. 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.
Signs and symptoms of alcoholic ketoacidosis
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). The main differential diagnoses for ketosis in our patient included AKA, starvation/fasting ketosis and DKA. In starvation ketosis, a mild ketosis is noted to develop in most after 12–24 h of fasting. Therefore, only a mild acidosis is observed in starvation ketosis. Alcoholic ketoacidosis is a recognised acute complication in alcohol dependent patients.
- Excessive alcohol consumption often causes malnourishment (not enough nutrients for the body to function well).
- Both steps require the reduction of nicotinamide adenine dinucleotide (NAD+) to reduced nicotinamide adenine dinucleotide (NADH).
- Free fatty acids are either oxidized to CO2 or ketone bodies (acetoacetate, hydroxybutyrate, and acetone), or they are esterified to triacylglycerol and phospholipid.
- Catecholamines, particularly epinephrine, increase fatty acid release and enhance the rate of hepatic ketogenesis.
- Fever was seen in only two patients, both with other likely underlying causes.
She was discharged home and has been well on follow-up appointments. Further biochemical investigation after treatment showed a rapid decline in the level of ketones and normalization of pH. 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.
Critical Care
Acetic acid (an acyl group carrier) is linked with coenzyme A (a thiol) to produce Acetyl-CoA. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. If you develop any of these symptoms, seek emergency medical attention. Laboratory analysis plays a major role in the evaluation of a patient with suspected alcoholic ketoacidosis. Patients are usually tachycardic, dehydrated, tachypneic, present with abdominal pain, and are often agitated.
alcoholic ketoacidosis smell is a problem caused by drinking a lot of alcohol without eating food. In contrast to diabetic ketoacidosis, the predominant ketone body in AKA is β-OH. Routine clinical assays for ketonemia test for AcAc and acetone but not for β-OH. Clinicians underestimate the degree of ketonemia if they rely solely on the results of laboratory testing. This drop in blood sugar causes your body to decrease the amount of insulin it produces. Your cells need insulin to use the glucose in your blood for energy.
Symptoms of Alcoholic Ketoacidosis
If you have any additional complications during treatment, this will also affect the length of your hospital stay. If your blood glucose level is elevated, your doctor may also perform a hemoglobin A1C (HgA1C) test. This test will provide information about your sugar levels to help determine whether you have diabetes.
If the vomiting and starvation go on for a day or more, the liver’s normal stores of sugar (glucose) decrease. The low glucose stores combined with lack of food intake cause low blood glucose levels. Without insulin, most cells cannot get energy from the glucose that is in the blood. Cells still need energy to survive, so they switch to a back-up mechanism to obtain energy.
