Isopropyl Alcohol-induced Pseudo-azotemia: Taking Advantage of a Laboratory Error

A 46-year-old woman was found confused with a spilled bottle of rubbing alcohol. Initial vital signs were: blood pressure 101/64 mm Hg, respiration 16 breaths per minute, pulse 165 beats per minute, and oxygen saturation 85% on room air. The chemistries were: sodium 144 mmol/L, bicarbonate 22 mmol/L, blood urea nitrogen (BUN) 9 mg/dL, creatinine (Cr) 3.4 mg/dL, glucose 252 mg/dL, lactate 7.5 mmol/L, and osmolality 386 mOsm/kg. The anion gap was 18, and the osmolal gap was 81 mOsm/kg. The cardiac enzymes and electrocardiogram were normal. An arterial blood gas performed on 100% nonrebreather gave a pH of 7.44 and oxygen saturation 98%. Her tachycardia, hypotension, and lactic acidosis improved with hydration. A toxicology screen was pending. The dipstick urinalysis revealed 2+ acetone, and microscopy was bland. She had a baseline creatinine of 0.7 mg/dL 1 month earlier. Given the above data and assuming that the normal osmolal gap is 15 mOsm/kg, should she have undergone immediate hemodialysis?

In the presence of a high osmolal gap and possible alcohol overdose, we may have been tempted to dialyze the patient. However, careful analysis suggested that the patient could be managed conservatively. The patient had a mild anion gap acidosis that could be explained from a pure lactic acidosis resulting from tissue hypoxia instead of ethylene glycol and methanol ingestion. The abundance of acetone integrated with the history, physical, and laboratory findings of disproportionate BUN/Cr suggested isopropyl alcohol-induced pseudo-renal failure1 by applying Occam’s Razor. Thus, the next step was to account for the osmolal gap and estimate the concentrations of isopropyl alcohol and acetone.

First, the Jaffe-alkaline-picrate-colorimetric method, used on many automated chemistry instruments, can spuriously overestimate serum Cr level when acetone is abundant. For every 100 mg/dL of acetone, the serum creatinine is increased by 1 mg/dL.1, 2 Applying this approximation, we back-calculated the acetone level during presentation:

Acetone – (measured serum Cr − baseline serum Cr) * 100 = (3.4 − 0.7) * 100 = 270 md/dL

By knowing the concentration of any toxin, the osmolal gap can be calculated:

Because the molecular weight (MW) of acetone is 58, the estimated osmolal gap contribution is 47. Invoking the normal serum osmolal gap of 15, the estimated osmolal gap contribution from isopropyl alcohol is 81 − 47 − 15 = 19 mOsm/kg. Thus, the estimated isopropyl alcohol level (MW = 60) was 114 mg/dL. If we had neglected to back-calculate the acetone contribution, we may have thought the patient required hemodialysis (isopropyl alcohol level of 396 mOsm/kg).3 However, because the level of isopropyl alcohol was much less, we decided on conservative management. After 2 hours, the laboratory reported the serum levels of acetone and isopropyl alcohol as 284 mg/dL and 96 mg/dL, respectively. Our patient recovered uneventfully.

Although pseudo-azotemia after isopropyl alcohol intoxication has been reported,1 this knowledge has not been applied to patient management. We illustrated here that we could accurately estimate the concentration of isopropyl alcohol and avoid hemodialysis by taking advantage of a laboratory error.