A 34-year-old man is brought to the emergency department after being found confused in a retail parking lot. The patient is somnolent, disoriented, and unable to provide meaningful history but reports pain over the bilateral flanks. Temperature is 36.8 C (98.2 F), blood pressure is 110/70 mm Hg, and pulse is 110/min. The patient appears disheveled. Pupils are normal and reactive to light. Funduscopic examination shows no abnormalities. The lungs are clear on auscultation, and no heart murmurs are present. There is mild bilateral costovertebral angle tenderness. The patient moves all extremities equally to painful stimuli. Laboratory results are as follows:
| Sodium | 136 mEq/L |
| Potassium | 3.6 mEq/L |
| Chloride | 100 mEq/L |
| Bicarbonate | 12 mEq/L |
| Blood urea nitrogen | 34 mg/dL |
| Creatinine | 2.8 mg/dL |
| Calcium | 7.0 mg/dL |
| Glucose | 80 mg/dL |
| Plasma lactate | 2.3 mEq/L (normal: <2) |
| Serum ketones | negative |
| Prothrombin time | 11 sec (normal: 11-15) |
Urinary catheterization yields a small amount of bloody urine, analysis of which reveals numerous oxalate crystals. Which of the following would be most effective in management of this patient's current condition?
Toxic alcohol ingestion (methanol or ethylene glycol) | |
Typical sources |
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Clinical features |
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Management |
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ADHase = alcohol dehydrogenase; AKI = acute kidney injury; IV = intravenous. | |
This patient with encephalopathy (eg, somnolence, disorientation) and bilateral flank pain has a significantly decreased serum HCO3− consistent with metabolic acidosis. An elevated anion gap of 24 mEq/L indicates an anion gap metabolic acidosis (AGMA). These findings, in conjunction with acute kidney injury (AKI), urinary calcium oxalate crystals, and hypocalcemia (due to calcium oxalate formation) should raise suspicion for ethylene glycol toxicity.
Ethylene glycol is a toxic alcohol commonly found in antifreeze and brake fluid. When ingested, it mimics ethanol intoxication. Ethylene glycol is metabolized by alcohol dehydrogenase into the toxic compounds glycolic acid and oxalic acid. Accumulation of these organic acids causes AGMA and organ damage, including nephrolithiasis (ie, calcium oxalate crystals) and AKI (ie, direct nephrotoxicity). Treatment primarily involves the following 3 components:
Alcohol dehydrogenase inhibition to prevent the formation of toxic organic acids; the preferred antidote for ethylene glycol (and methanol) toxicity is fomepizole, but ethanol can be used if fomepizole is unavailable
Correction of acidemia via administration of intravenous sodium bicarbonate to decrease tissue penetration of toxic organic compounds
Hemodialysis to rapidly remove preformed toxic organic acids and parent alcohols, particularly in the presence of AGMA or end-organ damage
(Choice A) Antibiotics are indicated for treatment of acute pyelonephritis, which typically presents with unilateral costovertebral angle tenderness and fever. This patient has bilateral tenderness and no fever, making pyelonephritis unlikely.
(Choice C) Hydroxocobalamin is the antidote for cyanide poisoning, which is generally seen secondary to fires and occupational exposure (eg, mining, pest control). Although cyanide poisoning can cause AKI, a markedly elevated lactate level (eg, >10 mEq/L) would be expected.
(Choice D) Methylene blue is the treatment for methemoglobinemia, which develops following ingestion of certain medications (eg, dapsone) or anesthetic agents. Methemoglobinemia can cause AGMA due to tissue hypoxia and markedly increased lactic acid production; this patient's lactic acid level is only slightly elevated, and methemoglobinemia is not expected to cause nephrolithiasis.
(Choice E) N-acetylcysteine is the antidote for acetaminophen toxicity, which can cause liver failure (eg, jaundice, elevated prothrombin time) that is not present in this patient. Acetaminophen toxicity only rarely causes AGMA (ie, pyroglutamic acidosis); AKI and urinary oxalate crystals would not be expected.
Educational objective:
Ethylene glycol is metabolized by alcohol dehydrogenase to glycolic acid and oxalic acid, which cause anion gap metabolic acidosis and organ injury (eg, acute kidney injury). Fomepizole inhibits alcohol dehydrogenase and is the preferred antidote. Sodium bicarbonate and hemodialysis are indicated when there is evidence of acidemia and end-organ damage.