LMP collaboration yields new POC test for determining ketoacidosis-related deaths Laboratory Medicine and Pathobiology

Initial IV fluids should contain added water-soluble vitamins and magnesium, with potassium replacement as required. Lactic acid levels are often elevated because of hypoperfusion and the altered balance of reduction and oxidation reactions in the liver. All chronic alcohol misusers attending the ED should receive intravenous B vitamins as recommended by The Royal College of Physicians.23 Strenuous efforts must be made to exclude concomitant pathology. Wrenn et al found altered mental status in 15% of patients, attributable in all but one case to hypoglycaemia, severe alcohol intoxication, or infection. Fever was seen in only two patients, both with other likely underlying causes. Neurologically, patients are often alcoholic ketoacidosis agitated but may occasionally present lethargic on examination.

Beta-hydroxybutyric acid–an indicator for an alcoholic ketoacidosis as cause of death in deceased alcohol abusers

During starvation, there is a decrease in insulin secretion and an increase in the production of counter-regulatory hormones such as glucagon, catecholamines, 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.

Symptoms and Signs of Alcoholic Ketoacidosis

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. Typically, an alcohol binge leads to vomiting and the cessation of alcohol or food intake for ≥ 24 hours. During this period of starvation, vomiting continues and abdominal pain develops, leading the patient to seek medical attention. Alcoholic ketoacidosis (AKA) is a common reason for investigation and admission of alcohol dependent patients in UK emergency departments. Although well described in international emergency medicine literature, UK emergency physicians rarely make the diagnosis of AKA. 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.

• An altered level of consciousness should prompt consideration of alternative diagnoses such as hypoglycaemia, seizures, sepsis, thiamine deficiency, or head injury.
• Although many patients had a significant ketosis with high plasma BOHB levels (5.2–14.2 mmol/l), severe acidaemia was uncommon.
• Diagnosis is by history and findings of ketoacidosis without hyperglycemia.

History and Physical

• Routine clinical assays for ketonemia test for AcAc and acetone but not for β-OH.
• Toxic metabolites of both substances result in severe metabolic acidosis with wide anion gap and wide osmolal gap.18 Neither, however, causes ketosis.
• 1, 2, 3  The diagnosis of AKA requires arterial blood gas (ABG) measurement and serum chemistry assays.

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.

Ethanol metabolism

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.

• All remaining papers were retrieved and the reference lists hand searched for any additional information sources.
• In contrast to diabetic ketoacidosis, the predominant ketone body in AKA is β-OH.
• With timely and aggressive intervention, the prognosis for a patient with AKA is good.
• Often, blood alcohol levels are no longer elevated when patients present with alcoholic ketoacidosis.
• Management is based around exclusion of serious pathology and specific treatment for AKA where it is present.

Patients who appear significantly ill and those Twelve-step program with positive ketones should have arterial blood gas and serum lactate measurements. Toxicity from 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.

• Several mechanisms are responsible for dehydration, including protracted vomiting, decreased fluid intake, and inhibition of antidiuretic hormone secretion by ethanol.
• The prognosis for alcoholic ketoacidosis is good as long as it’s treated early.
• Magnesium and phosphate levels should be measured and repleted if the serum levels are found low.
• 4 This finding can help to distinguish AKA from diabetic ketoacidosis (DKA).

Introducing medical students to the world of Lab Medicine: LMP launches The

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.