A 58 year old woman is transferred to our Intensive Care Unit for septic shock, acute renal failure, and acidemia. She was well until 3 days ago where she was weak, had nausea and vomiting, as well as shortness of breath, exertional dyspnea, and generalized fatigue.
She has chronic pain for which she has been taking 2 grams of ibuprofen daily for the past week. She works at a Humvee factory stripping paint and installing rubber equipment. She does not use a respirator mask.
Vitals are 70/49, pulse oximetry of 99% on non‐invasive positive pressure ventilation. Temperature is 101 degrees Farenheit, heart rate 108 beats per minute, respirations 15 breaths per minute. She is arousable but somnolent, able to answer simple questions but not complex ones. There are basilar crackles.
Initial laboratories reveal: potassium 2.6md/dL, creatinine 5.2mg/dL, BUN 65mg/dL, calcium 7.2 and phosphorus 5.0. Her albumin is 1.9mg/dL and total protein 5.6mg/dL. Urinalysis reveals 3+protein, 2+blood, many white and red blood cells, no casts. Urine electrolytes are creatinine 9.2, potassium 43.3, sodium 88, chloride 81. Serum anion gap is 25. Urine anion gap is 50, and the urine pH is 5.5. Arterial blood gas showed pH‐7.059, PC02‐20.8, and P02‐ 110 on 50%‐FiO2. Lactate, salicylates, aspirin, blood alcohol, acetaminophen, isopropyl alcohol, acetone, and her urine drug screen were all negative. Blood cultures are positive for E.Coli bacteremia and chest x‐ray shows bilateral infiltrates. Toluene level is 8mg/dL. Hippurate levels were not measured.
The main clinical presentation of acute Toluene toxicity is weakness associated with hypokalemia, severe metabolic acidosis, and, on occasion, renal tubular acidosis. Most cases occur in acute exposure to elicit use such as “huffing.” This patient represents an unintentional acute Toluene exposure superimposed on sepsis. Toleune is metabolized to hippurate, which is excreted in the urine. The excretion of hippurate in the urine necessitates loss of cations, sodium and potassium. However, when hippurate cannot be excreted, it accumulates. This patient had multi‐factorial renal failure; a distal RTA, hypotension, and NSAID use. A fall in the glomerular filtration rate can transform the normal anion gap type of metabolic acidosis into one with a high anion gap as hippurate accumulates.
She was already hypotensive as a product of her sepsis. Profound acidemia worsens cardiac output, arterial tone, and efficacy of vasopressors, and constitutes a medical emergency. Correction of the underlying cause of acidemia is crucial. Initial support with intravenous sodium bicarbonate infusion is preferred. Emergent hemodialysis can be initiated. Because Toluene is a send‐out test, it cannot be used to drive medical decision making. Instead, clinical suspicion must be generated from profound anion gap acidosis in the absence of other causes of anion gap acidosis, the profound hypokalemia, and evidence of a distal renal tubular acidosis.
This case represents an atypical presentation of an atypical intoxication