Clinical Geriatrics

Introduction

The Substance Abuse & Mental Health Services Administration (SAMHSA) reported that substance abuse among adults age 60 years and older is a rapidly growing health problem. The report also stated that in 2000, 17% of Americans age 65 and older had problems with prescription drug and alcohol abuse.1 Most elderly people with alcohol abuse problems have a history of early-life alcohol abuse. However, a significant proportion start drinking later in life in response to traumatic life events such as the death of a loved one, loneliness, pain, insomnia, and retirement. This subset often experiences periods of binge drinking with little or no food intake. Alcoholic ketoacidosis (AKA) is an acute anion gap metabolic acidosis that typically occurs in people with a recent history of binge drinking and little or no nutritional intake. Some patients with AKA also have intractable vomiting and dehydration, and in these cases there is a concomitant metabolic alkalosis.

Case Presentation

An 86-year-old female, who had been a widow for the past 20 years, presented to the hospital with complaints of nausea, epigastric discomfort, and breathlessness for 2 days. She confessed to a history of alcohol abuse starting shortly after her husband’s death and to regularly consuming a pint of hard liquor each day. She had been on an alcohol binge for 4-5 days without eating any food, but she had stopped consuming alcohol because of nausea for 2 days prior to presentation. Although the patient was depressed and admitted to suicidal ideation, she denied ingestion of antifreeze, methanol-containing solvents, rubbing alcohol, or salicylates. Physical examination was remarkable for only signs of dehydration and epigastric tenderness. Fundoscopy did not reveal any retinal changes. On admission, the following levels were found: serum sodium, 142 mEq/L; potassium, 4.8 mEq/L; chloride, 101 mEq/L; bicarbonate, 6 mEq/L; anion gap, 35 mEq/L; blood urea nitrogen, 16 mg/dL; glucose, 117 mg/dL; blood ethyl alcohol, 0 mg/dL; arterial pH, 7.14; PCO2, 16 mm Hg; and PO2, 130 mm Hg. The serum osmolality was 341 mOsm/kg, as compared with a calculated value of 296.2 mOsm/kg, indicating an elevated osmolal gap of 44.8 mOsm/kg. The serum acetone concentration was 84 mg/dL (16.8 mmol/L); serum lactate, 2.3 mmol/L; amylase, 954 U/L; and lipase, 210 U/L. The urinalysis, including microscopy, was negative, except for the presence of ketones.

A provisional diagnosis of AKA was made, as the patient had a characteristic clinical presentation preceded by an alcohol binge that was terminated by nausea, with the last alcohol intake being 2 days before coming to hospital. Moreover, serum and urinary ketones were strongly positive. However, there was a diagnostic dilemma, as the patient presented with high anion gap and high osmolal gap metabolic acidosis, which also raised the concern of simultaneous toxic alcohol ingestion (methyl alcohol or ethylene glycol). There were also no other clinical features such as fundus changes or oxalate crystals on urinalysis to support the diagnosis of toxic alcohol ingestion. In spite of this, it was difficult to exclude simultaneous toxic alcohol ingestion in the emergency setting, especially with an unreliable history. The patient was vigorously hydrated and promptly dialyzed in view of very high osmolal gap.

The blood ethylene glycol, methyl alcohol, and isopropyl alcohol returned negative 3 days later from the reference laboratory. Therefore, the patient’s physicians retrospectively concluded that the high anion gap and osmolal gap in the patient was secondary to AKA.