Abstract
I read with interest the report by Tracey Stover-Wall (“A Case Study in Metabolic Acidosis Induced by Inhalation,” March/April 2005) describing the case of a 15-year-old male who developed metabolic acidosis as a result of huffing carburetor cleaner.1Stover-Wall T A case study in metabolic acidosis induced by inhalation.Air Med J. 2005; 24: 66-69Abstract Full Text Full Text PDF PubMed Scopus (1) Google Scholar The author attributed the observed metabolic derangements to toluene poisoning from the inhalant abuse. However, in reviewing the data presented in the paper, it is apparent that methanol intoxication is a diagnosis that is more consistent with the history, clinical presentation, and laboratory abnormalities than is toluene intoxication. The patient presented with a significant partially compensated metabolic acidosis (HCO3 8 mEq/L) and acidemia (pH 7.25), though respiratory compensation was evident in the arterial blood gas analysis. The laboratory results also demonstrate a substantially elevated anion gap (35 mEq/L), while chloride and potassium determinations were normal (109 mEq/L and 4.1 mEq/L, respectively). The increased anion gap metabolic acidosis is classic for methanol intoxication and several other toxins; however, none of these other agents is typically present in carburetor cleaner. The elevated anion gap metabolic acidosis in methanol poisoning is the result of metabolic conversion of methanol to formate. The observed tachypnea/hyperpnea represents respiratory compensation of the metabolic acidosis. The laboratory picture surrounding toluene intoxication is quite different.2Streicher HZ Gabow PA Moss AH Kono D Kaehny WD Syndromes of toluene sniffing in adults.Ann Intern Med. 1981; 94: 758-762Crossref PubMed Scopus (196) Google Scholar Typically, toluene exerts its effects on acid-base balance at the kidney by causing a renal tubular acidosis (RTA). This condition results in a nonanion gap hyperchloremic metabolic acidosis. People who chronically huff toluene frequently complain of muscle weakness as a result of concomitant hypokalemia. Additionally, because of the increased loss of bicarbonate in the urine of RTA patients, urine pH also increases. Multiple reports exist of elevated blood methanol concentrations following huffing of carburetor cleaner.3Frenia ML Schauben JL Methanol inhalation toxicity.Ann Emerg Med. 1993; 22: 1919-1923Abstract Full Text PDF PubMed Scopus (42) Google Scholar, 4LoVecchio F Sawyers B Thole D Beuler MC Winchell J Curry SC Outcomes following abuse of methanol-containing carburetor cleaners.Hum Exp Toxicol. 2004; 23: 473-475Crossref PubMed Scopus (14) Google Scholar Occasionally, these patients become acidotic, though reports also exist of patients with significant blood methanol levels that do not develop classic laboratory signs of methanol toxicity.4LoVecchio F Sawyers B Thole D Beuler MC Winchell J Curry SC Outcomes following abuse of methanol-containing carburetor cleaners.Hum Exp Toxicol. 2004; 23: 473-475Crossref PubMed Scopus (14) Google Scholar This discrepancy may be the result of kinetic differences between ingested and inhaled methanol or the interaction of other components of the carburetor cleaner inhibiting metabolic conversion of methanol to its toxic acid metabolites. Even though some formulations of carburetor cleaner may contain both toluene and methanol, it is unlikely that toluene was the primary toxin in the present case. The slightly elevated creatinine (1.5 mg/dL) and modestly increased creatine phosphokinase (564 U/L) would likely respond to hydration and probably did not represent significant underlying renal pathology or renal risk due to rhabdomyolysis. In the absence of frank GI bleeding, the positive occult blood test may have simply represented gastric irritation from multiple episodes of vomiting. Additional therapeutic intervention, such as administration of a dose of the alcohol dehydrogenase inhibitor fomepizole to prevent progression of the acidosis, is also worthy of consideration. This case illustrates two key points that are frequently overlooked with respect to the appropriate management of poisoned patients. First, correct diagnostic tests must be performed and their results properly interpreted to correctly manage such a case; and, second, it is absolutely necessary to obtain the exact container(s) of substances believed to be involved in the toxic exposure and transport them to the hospital with the patient. Having the original containers available not only aids in focusing diagnostic testing and treatment but may also heighten suspicion for “hidden” toxins whose presence may not be initially apparent but whose toxic consequences may be catastrophic.
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