Alcoholic ketoacidosis (AKA) is a clinical syndrome seen mostly in chronic alcoholics and frequently seen in patients who binge drink. Typical patients are usually chronic drinkers who are unable to tolerate oral nutrition for a 1 to 3 day period. Patients often have a recent bout of heavy drinking before the period of relative starvation, with persistent vomiting and abdominal pain contributing to their inability to tolerate PO intake.
The etiology of Alcoholic ketoacidosis stems from the patient's inability to ingest, absorb and utilize glucose from their diet. The vomiting and nausea prevent the patient from keeping foodstuffs in the GI tract that can cross over and provide nourishment. The alcohol further depressed gluconeogenesis in the body and keeps blood sugar levels low. An anxiety state and alcohol withdrawal further exacerbate the patient's ability to eat. The lack of nutrients other than alcohol causes the creation of ketones and an elevated gap ketoacidosis in the absence of diabetes.
The prevalence correlates with the incidence of alcohol abuse in a community. No racial or sexual differences in incidence are noted. AKA can occur in adults of any age; it more often occurs persons aged 20-60 years who are chronic alcohol abusers. Rarely, AKA occurs after a binge in persons who are not chronic drinkers.
Patients present in a dehydrated state after a bout of heavy drinking and then an ongoing lack of oral intake. This period of poor PO intake lasts from 1 to 3 days. The pathophysiology of AKA starts with low glycogen stores and a lack of oral food intake, which shifts the metabolism from Carbohydrates to fats and lipids. The decreased PO intake causes decreased insulin levels and an increase in counterregulatory hormones, Cortisol, Glucagon, and Epinephrine. The lack of insulin also allows an increase in the activity of hormone sensitive lipase. These changes are further enhanced, for as Ethanol is metabolized to Acetaldehyde and AcetylCOA, the NADH/NAD+ ratio increase. The resultant increased NADH/NAD+ ratio increases lipid metabolism. All of these changes increase the breakdown of lipids to Ketoacids. The elevated NADH/NAD+ ratio further encourage the conversion of Acetoacetate to Beta-Hydroxybutyrate. Beta-hydroxybutyrate is the predominate ketoacid in AKA. Ketoacids further accumulate as dehydration and decreased renal perfusion limit the removal of ketoacids. The differential diagnosis includes other causes of increased anion gap metabolic acidosis. In a patient with diabetes, there must also be a consideration of DKA. A hemoglobin A1C may help in that consideration
The toxicokinetics that are pertinent to the diagnosis of AKA include the rate of alcohol oxidation in the body. Ethyl alcohol oxidizes at a rate of 20 to 25mg/dl per hour in most individuals. The accompanying lack of alcohol in the patient's body and the fact that for sometime the only source of calories that a patient has is ethanol both contribute to the clinical syndrome that we see.
Diagnosis of AKA is made on a clinical basis. Patients are usually tachycardic, dehydrated, tachypneic, present with abdominal pain and are often agitated. Most patients will often have a ketone odor on their breath.
Neurologically, patients are often agitated, but may occasionally present lethargic on examination. Alcohol withdrawal, in combination with nausea and vomiting, makes most patients agitated. However, if an AKA patient is lethargic or comatose, an alternative cause should be sought.
Laboratory findings are as follows:
Diagnosis of the condition of AKA is the first step in treatment. The patient should have an accucheck, or bedside POC testing was done on initial presentation. The patients need to be treated with fluid and volume resuscitation. The patient will need IV normal saline volume replacement. If the initial blood glucose level is normal or low, five%dextrose should be added to the IV fluids. The patient will need volume replacement to replenish circulating volume and to increase the elimination of ketoacids. Dextrose will increase glycogen stores, diminish counterregulatory hormones and increase insulin secretion. Dextrose will help to suppress and eliminate ketoacid formation. Hypokalemia needs to be treated, and dextrose containing fluids can be held until potassium levels are normalized. Intravenous saline will also diminish serum potassium levels. Thiamine administration should proceed with the IV fluids. Magnesium and Phosphate can be repleted if the serum levels are found to be low. Intravenous Benzodiazepines should be given for seizure prophylaxis and to prevent full blown alcoholic withdrawal. An antiemetic such as Ondansetron or Metoclopramide may also be given to control nausea and vomiting.
AKA should be diagnosed clinically. The patients need fluid resuscitation, close monitoring of electrolytes and treatment to prevent alcohol withdrawal. They also need to have a complete history and physical for complete differential diagnosis.
Starvation ketosis is more common than AKA, In addition, but starvation ketosis is not often complicated by acidosis. Diabetic ketoacidosis can be confused with AKA. The glucose levels in AKA are rarely above 250mg/dl. In a hyperglycemic patient, Hemoglobin A1C can also be ordered to assess for the presence of prolonged hypeAlso, in AKA, the Betahydroxybutyrate to acetoacetate ratio will be much higher with ratios of up to 8: 1, whereas DKA B-OH to acetoacetate ratios are a 3: 1 ratio. The B-OH levels are higher in AKA.
Other diagnoses that need to be considered are toxic alcohol ingestions. Methanol and Ethylene Glycol ingestions can cause GI upset and an overwhelming acidosis. Adding to the difficulty, the patient is often a chronic alcoholic. Elevation of the osmolar gap < 20mOsm/kg is not often present in AKA but is present in ingestions of the toxic alcohols. Always correct for the ethanol level in the osmolar gap calculation by dividing the ethanol level by 4.6.