Alcoholic ketoacidosis (AKA) is an acute metabolic acidosis seen in persons with a recent history of binge drinking and little or no nutritional intake.
Alcoholic ketoacidosis is characterized by high serum ketone levels and an elevated anion gap (see the Anion Gap calculator). A concomitant metabolic alkalosis is also common, resulting from vomiting and volume depletion. Although AKA most commonly occurs in adults with alcoholism, alcoholic ketoacidosis has been reported in less-experienced drinkers of all ages. [1, 2]
Assess the patient's airway and manage as clinically indicated. Administer oxygen as indicated.
Obtain intravenous access and administer fluid resuscitation for volume depletion and/or hypotension. Consider and treat hypoglycemia. 
Note information about the patient's social situation and the presence of intoxicating agents besides alcohol.
Emergency Department Care
Suspect alcoholic ketoacidosis in any patient with recent binge drinking and an elevated anion gap. A history of alcoholism is not necessary for the development of alcoholic ketoacidosis. One episode of heavy alcohol intake combined with inadequate carbohydrate intake is sufficient to generate this disease state. Presenting symptoms may include nausea & vomiting, malaise, abdominal pain, dizziness, tremulousness, tachypnea, tachycardia, and hypotension. 
Urine tests for ketones may be falsely negative or only trace positive in alcoholic ketoacidosis. This is because the relative excess of NADH to NAD+ created by the oxidative metabolism of ethanol creates a reducing environment. The ketoacids beta-hydroxybutyrate and alpha-ketoglutarate exist in dynamic equilibrium with one another; a reducing environment skews the proportions of these compounds towards an excess of beta-hydroxybutyrate, which may not be detected by routine assays for ketones. 
Although patients with alcoholic ketoacidosis have depleted glycogen stores, their serum glucose level is often within the normal range. An elevated lactic acid level and elevated osmolar gap due to acetone are typically seen. Significant lactic acidosis may be seen because of a combination dehydration and a metabolic redox state which favors pyruvate over lactate. 
An elevated osmole gap, though non-specific, should raise suspicion for toxic alcohol ingestion such as with methanol or ethylene glycol. If the anion gap (see the Anion Gap calculator) fails to close as resuscitation continues, it is important to consider other causes of an anion gap acidosis, such as methanol or ethylene glycol ingestion (co-ingestion). Although alcoholic ketoacidosis alone may increase the osmole gap, maintain a low threshold to treat suspected toxic alcohol ingestion with the alcohol dehydrogenase inhibitor, fomepizole. [7, 8] When considering other co-ingestants, note that alcoholic ketoacidosis can cause a mildly elevated osmolar gap (approximately 20 mmol/kg). 
Evaluate the patient for signs of alcohol withdrawal syndrome, which may include tremors, agitation, diaphoresis, tachycardia, hypertension, seizures, or delirium. Exclude other causes of autonomic hyperactivity and altered mental status. If the diagnosis of alcohol withdrawal syndrome is established, consider the judicious use of benzodiazepines, which should be titrated to clinical response.
Assess for clinical signs of thiamine deficiency (Wernicke-Korsakoff syndrome). Specifically look for nystagmus, confusion, ataxia, confabulation, and restriction of extraocular movements. Strongly consider providing thiamine supplementation to patients with alcohol dependence even without signs of thiamine deficiency.
Once the diagnosis of alcoholic ketoacidosis (AKA) is established, the mainstay of treatment is hydration with 5% dextrose in normal saline (D5 NS) to address the principal physiologic derangement, a lack of metabolic substrate (glucose). Carbohydrate and fluid replacement reverse this process by increasing serum insulin levels and suppressing the release of glucagon and other counterregulatory hormones and by providing metabolic substrate. Dextrose stimulates the oxidation of the reduced form of nicotinamide adenine dinucleotide (NADH) and aids in normalizing the ratio of NADH to nicotinamide adenine dinucleotide (NAD+).
Fluids alone do not correct AKA as quickly as fluids and carbohydrates together. Thiamine supplementation should also be given upon initiation of dextrose. Patients who can tolerate oral nutrition should be fed.
In general, exogenous insulin is contraindicated in the treatment of AKA, because it may cause life-threatening hypoglycemia in patients with depleted glycogen stores. In most cases, the patient's endogenous insulin levels rise appropriately with adequate carbohydrate and volume replacement. Insulin may be required in patients with diabetes who have AKA. If the patient's blood glucose level is significantly elevated, AKA may be indistinguishable from diabetic ketoacidosis (DKA). The disorders also may coexist.
As rehydration progresses and adequate renal function is established, consider electrolyte replacement, giving particular attention to potassium and magnesium.
Bicarbonate therapy should be considered only in the face of severe, life-threatening acidosis (ie, pH < 7.1) that is unresponsive to fluid therapy.
Associated disease states
Patients with alcoholic ketoacidosis (AKA) may have various coexisting illnesses, especially those commonly associated with chronic alcohol abuse. A thorough history and physical examination must be obtained. Associated conditions include pancreatitis, hepatitis, cirrhosis, coagulopathy, gastritis, GI bleeding, pneumonia, cardiomyopathy, alcohol withdrawal, infection, anemia, seizures, cerebrovascular accident (CVA), myopathy, rhabdomyolysis, neuropathy, arrhythmias, vitamin deficiency (Wernicke-Korsakoff syndrome), and intoxication with alcohol or other substances. These associated illnesses and conditions may be a significant source of morbidity and mortality if not properly addressed.
Admit patients for continued treatment. Restoration of volume status and correction of the acidosis may be difficult to accomplish in the emergency department (ED).
Counseling and/or therapy for alcohol abuse should be part of the patient's treatment regimen and should continue following discharge.
A requirement for any medications other than D5 NS and thiamine are uncommon. Fluid resuscitation, carbohydrate administration, and thiamine supplementation are the mainstays of treatment in alcoholic ketoacidosis (AKA). Fundamentally however, the patient must eat!
The need to correct pH actively depends on the severity of the pH imbalance, the compensatory capabilities of the patient, the patient's overall clinical condition, and the potential harm caused by alkali administration. Sodium bicarbonate and other comparable solutions are usually unnecessary with adequate carbohydrate and fluid replacement. 
This is indicated to correct a thiamine deficiency.
These agents are rarely used for the management of severe metabolic acidosis.