It should be used as an indicator of the severity of the disease.13 Identifying these high-risk patients can help set the intensity of monitoring required for the patient to ensure optimal patient outcomes are achieved. Alcoholic ketoacidosis (AKA) is a condition seen commonly in patients with alcohol use disorder or after a bout of heavy drinking. It is a clinical diagnosis with patients presenting with tachycardia, tachypnea, dehydration, agitation, and abdominal pain. This activity illustrates the evaluation and treatment of alcoholic ketoacidosis and explains the role of the interprofessional team in managing patients with this condition. In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), blood urea nitrogen (BUN) and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured.
Treatments for Alcohol Use Disorder
It happens when the body cannot produce enough insulin, leading to high blood sugar levels. The body starts breaking down fat for energy, producing ketones as a byproduct. Alcoholic Ketoacidosis (AKA) occurs in individuals with chronic alcohol use, especially after a period of heavy drinking followed by vomiting and lack of food intake. Lactic acidosis occurs when ethanol metabolism results in a high hepatic NADH/NAD ratio, diverting pyruvate metabolism towards lactate and inhibiting gluconeogenesis. In peripheral tissues, where NADH levels are lower, this lactate may be converted to pyruvate for metabolic needs. Pyruvate and lactate are then maintained in steady state at much higher levels than normal.
Deterrence and Patient Education
- Larger studies by Fulop and Hoberman5 and Wrenn et al6 (24 and 74 patients, respectively) clarified the underlying acid base disturbance.
- Alcohol withdrawal, in combination with nausea and vomiting, makes most patients agitated.
- The next important step in the management of AKA is to give isotonic fluid resuscitation.
- Decreased insulin and elevated glucagon, cortisol, catecholamine, and growth hormone levels can increase the rate of ketogenesis.
- The toxicokinetics that are pertinent to the diagnosis of AKA include the rate of alcohol oxidation in the body.
- Going on a drinking binge when your body is in a malnourished state may cause abdominal pain, nausea, or vomiting.
The greatest threats to patients with alcoholic ketoacidosis are marked contraction in extracellular fluid volume (resulting in shock), hypokalaemia, hypoglycaemia, and acidosis. The clinical and biochemical features of AKA are summarised in boxes 1 and 2. The classical presentation is of an alcoholic patient with abdominal pain and intractable vomiting following a significant period of increased alcohol intake and starvation. There may be a history of previous episodes requiring brief admissions with labels of “query pancreatitis” or “alcoholic gastritis”. Most cases of AKA occur when a person with poor nutritional status due to long-standing alcohol abuse who has been on a drinking binge suddenly decreases energy intake because of abdominal pain, nausea, or vomiting. In addition, AKA is often precipitated by another medical illness such as infection or pancreatitis.
How Can Alcoholic Ketoacidosis Be Prevented?
Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Alcoholic ketoacidosis is a recognised acute complication in alcohol dependent patients. Given the frequency with which the condition is seen in other countries, the possibility exists that many cases may be unrecognised and misdiagnosed in UK EDs. AKA should be included in the differential diagnosis of alcohol dependent patients presenting with acute illness. Management is based around exclusion of serious pathology and specific treatment for AKA where it is present.
BOX 3 MANAGEMENT OF AKA
During starvation, there is a decrease in insulin secretion and an increase in the production of counter-regulatory hormones such as glucagon, catecholamines, alcoholic ketoacidosis cortisol, and growth hormone. Hormone-sensitive lipase is normally inhibited by insulin, and, when insulin levels fall, lipolysis is up-regulated, causing release of free fatty acids from peripheral adipose tissue. In general, the prognosis for a patient presenting with AKA is good as long as the condition is identified and treated early.
- These include acute pancreatitis, gastrointestinal bleeding, and alcohol withdrawal.
- Elevated cortisol levels can increase fatty acid mobilization and ketogenesis.
- Patients with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated hemoglobin (HbA1C).
- In addition, AKA is often precipitated by another medical illness such as infection or pancreatitis.
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. Patients are usually tachycardic, dehydrated, tachypneic, present with abdominal pain, and are often agitated. 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 25 mg/dL per hour in most individuals. The accompanying lack of alcohol in the patient’s body and the fact that for some time, the only source of calories that a patient has is ethanol both contribute to the clinical syndrome that we see.
Ketoacidosis and lactic acidosis–frequent causes of death in chronic alcoholics?
Often, blood alcohol levels are no longer elevated when patients present with alcoholic ketoacidosis. Free fatty acids are either oxidized to CO2 or ketone bodies (acetoacetate, hydroxybutyrate, and acetone), or they are esterified to triacylglycerol and phospholipid. Carnitine acyltransferase (CAT) transports free fatty acids into the mitochondria and therefore regulates their entry into the oxidative pathway. The decreased insulin-to-glucagon ratio that occurs in starvation indirectly reduces the inhibition on CAT activity, thereby allowing more free fatty acids to undergo oxidation and ketone body formation. Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia.
- There is increasing evidence that rather than being benign and self limiting, AKA may be a significant cause of mortality in patients with alcohol dependence.
- All alcoholic patients presenting with acute illness should be offered contact with addiction services prior to or following discharge wherever possible.
- Efficient and timely management can lead to enhanced patient outcomes in patients with AKA.
Treatment of Alcoholic Ketoacidosis
Support groups can be a valuable source of support and can be combined with medication and therapy. The majority of papers detected by this search focus primarily on diabetes mellitus and its complications, and were excluded. General literature reviews, single case reports, and letters were also excluded. All remaining papers were retrieved and the reference lists hand searched for any additional information sources.
Although many patients had a significant ketosis with high plasma BOHB levels (5.2–14.2 mmol/l), severe acidaemia was uncommon. In the series from Fulop and Hoberman, seven patients were alkalaemic. 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.
Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurements. Toxicity from Oxford House methanol or ethylene glycol is an important differential diagnosis. Toxic metabolites of both substances result in severe metabolic acidosis with wide anion gap and wide osmolal gap.18 Neither, however, causes ketosis.
