Published - Fri, 11 Nov 2022
Alcoholic ketoacidosis is usually seen in alcoholic patients who are forced to abruptly cease drinking alcohol after a drinking binge, but it may also be seen in first-time drinkers. Diabetes mellitus does not exist in these patients.
PATHOGENESIS: The pathogenesis is uncertain. It is related to low insulin levels, reduction of available nicotinamide adenine dinucleotide, and increased ketone formation.
1. Patient history: The patient has recently stopped or limited alcohol consumption because of abdominal pain, nausea, and vomiting, not from a desire to stop drinking.
a) Diffuse abdominal pain is typically present. Pancreatitis, gastritis, and hepatitis, for example, are diseases linked to alcoholism that can induce abdominal discomfort. Other conditions unrelated to alcoholism might also produce abdominal pain (e.g., sepsis, pneumonia, pyelonephritis).
b) There may be signs of alcohol withdrawal or delirium tremens.
3. Physical examination findings
a) Hydration status: Dehydration occurs secondary to vomiting, diaphoresis, and decreased oral intake. The patient has tachycardia and hypotension and is critically unwell.
b) Vital signs: Kussmaul respirations may be present, and the temperature may be elevated or normal.
c) The range of mental states includes normal and comatose.
d) Alcoholism stigmata, such as spider angiomata, may be seen.
DIFFERENTIAL DIAGNOSES: An anion gap acidosis-causing condition needs to be ruled out. The most important conditions to take into account include isopropyl alcohol intoxication, hyperemesis gravidarum, hunger, cyanide poisoning, and diabetic ketoacidosis.
1. Serum biochemical profile will establish the presence of an anion gap acidosis. A mixed disorder could also exist (e.g., metabolic ketoacidosis may occur from vomiting and respiratory alkalosis may occur from fever, sepsis, or alcohol withdrawal).
2. Ketone studies: β-hydroxybutyric acid is the predominant ketone formed in alcoholic ketoacidosis. The nitroprusside test has limited use in individuals with alcoholic ketoacidosis since it only detects acetoacetate and not -hydroxybutyrate. Acetoacetate levels rise during treatment, giving the ketoacidosis a fictitious appearance of deteriorating.
3. Bedside glucose determination: The level of blood sugar may be low, normal, or only slightly higher. Most individuals' blood glucose levels range from normal to elevated.
THERAPY: Ketoacidosis can be reversed in 12 to 18 hours.
1. Dehydration is treated with saline solutions containing glucose and thiamine. The clinical response appears to be enhanced by glucose. If inadequate oral intake is suspected, magnesium and vitamin supplements should be administered.
2. Insulin: Administration of insulin is not indicated unless the patient has concomitant diabetes mellitus.
3. Bicarbonate: Bicarbonate administration is under question. Most people recommend only giving bicarbonate in cases of cardiac arrest with known severe acidosis.
1. Admission: Patients with severe metabolic acidosis or those who are unable to tolerate oral fluids should be hospitalised. Prior to discharge, underlying or precipitating illnesses, as well as abdominal pain, must be assessed. Patients often react to therapy in 12 to 24 hours, at which point they may be released.
2. Discharge: The patient might be released from the emergency room if the therapy goes well. It is crucial to closely monitor patients and refer them for alcoholism treatment.
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