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Abstract: SA-PO1011

An Unusual Case of Extensive Brain Infarction and Metabolic Acidosis

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports


  • Vasquez-Rios, George, University of Kentucky Medical Center, Lexington, Kentucky, United States
  • Alkhankan, Hani, University of Kentucky Medical Center, Lexington, Kentucky, United States
  • Sawaya, B. Peter Emile, University of Kentucky Medical Center, Lexington, Kentucky, United States
  • Neyra, Javier A., University of Kentucky Medical Center, Lexington, Kentucky, United States

Extensive CNS compromise is a rare complication of methanol intoxication that needs prompt recognition.


A 24-year-old man presented to the ED with a 2-day history of progressive lethargy, diffuse muscular rigidity, and fever. His medical history was relevant for schizophrenia, substance abuse, and essential hypertension. On arrival, his vitals were BP: 169/133 mmHg, HR: 123 beats/min, RR: 25 respirations/min, SatO2: 98% (FiO2: 50%) and T: 38.3 C. Neurological findings included GCS:7, bilateral mydriasis and symmetrical hypoactive reflexes. Laboratory studies revealed severe high anion gap metabolic acidosis (arterial pH 7.21, pO2 100 mmHg, pCO2 8 mmHg and HC03-: 5 mEq/L; anion gap: 36), leukocytosis, mild hyperkalemia, and elevated serum creatinine at 1.36 mg/dl (baseline: 0.96 mg/dl). Calculated and measured serum osmolality were: 302 mOsm/Kg and 297 mOsm/Kg respectively (osmolar gap: 5). After initial workup, sepsis, medication overdose, illicit substance abuse and toxic environmental exposure were excluded. Head CT scan showed extensive bilateral infarctions affecting the lenticular nuclei with hemorrhagic conversion on the right side, along with occipital lobe and cerebellar infarction. Ultimately, his serum methanol level was found to be 40 mg/dL confirming the diagnosis of acute methanol intoxication. Initially, he was aggressively treated with isotonic fluid resuscitation and bicarbonate replacement with mild improvement of his overall clinical status. A 4-hour hemodialysis treatment was administered (delivered single-pool Kt/V: 1.32) to enhance acid/toxic byproduct removal. Intravenous fomepizole (600 mg) and leucovorin (4 doses) were also administered. He was transitioned to continuous venous-venous hemofiltration (CVVH) with an effluent dose of 35 ml/kg/hr to prevent a potential rebound effect. Following 18-hour CVVH therapy, his serum methanol levels were down to 11 mg/dL. His clinical status progressively improved although residual visual impairment and motor deficits were noted upon discharge.


Extensive cerebral infarction is an unusual presentation of methanol intoxication and may cause a delay in reaching the final diagnosis in a patient with decreased mental status. Rapid recognition and treatment of methanol intoxication are pivotal for survival and attenuation of sequelae.