Journal of medical case reports · 2026
Pseudo-SAH in a patient with methanol poisoning: a case report.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
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Defaee Sahar, Ouspid Elham, Barahimi Elham, Sheybani-Arani MohammadHosein, Khajavi-Mayvan Fatemeh
Аннотация
BACKGROUND: Methanol is a toxic alcohol found in many industrial products. Ingestion can cause severe metabolic acidosis, optic nerve damage, and central nervous system depression. While bilateral putaminal necrosis is a typical radiologic finding, pseudo-subarachnoid hemorrhage (pseudo-SAH) is a rare and often misdiagnosed complication. Prompt recognition is essential to avoid unnecessary interventions.
CASE PRESENTATION: A 31-year-old Caucasian Iranian male presented unresponsive after consuming 1-2 L of homemade methanol. He experienced cardiac arrest upon arrival but was successfully resuscitated. Laboratory tests showed severe metabolic acidosis, acute kidney injury and hepatic enzymes elevation. Hemodialysis and supportive care were initiated. Despite treatment, the patient remained comatose. On day 3, neurological examination revealed fixed pupils and absent reflexes. Brain CT showed diffuse cerebral edema and hyperdensities initially misinterpreted as subarachnoid hemorrhage. Following neurology consultation, these findings were identified as pseudo-SAH, reflecting severe hypoxic-ischemic brain injury. The patient was declared brain dead following evidence of cerebral herniation.
CONCLUSION: Pseudo-SAH is a radiologic manifestation of severe cerebral edema rather than a primary cause of death. In methanol intoxication, it can mimic true subarachnoid hemorrhage on imaging and lead to diagnostic confusion. Clinicians should maintain a high index of suspicion for pseudo-SAH in patients with methanol poisoning and unexplained radiologic findings to ensure accurate diagnosis and appropriate management.
CASE PRESENTATION: A 31-year-old Caucasian Iranian male presented unresponsive after consuming 1-2 L of homemade methanol. He experienced cardiac arrest upon arrival but was successfully resuscitated. Laboratory tests showed severe metabolic acidosis, acute kidney injury and hepatic enzymes elevation. Hemodialysis and supportive care were initiated. Despite treatment, the patient remained comatose. On day 3, neurological examination revealed fixed pupils and absent reflexes. Brain CT showed diffuse cerebral edema and hyperdensities initially misinterpreted as subarachnoid hemorrhage. Following neurology consultation, these findings were identified as pseudo-SAH, reflecting severe hypoxic-ischemic brain injury. The patient was declared brain dead following evidence of cerebral herniation.
CONCLUSION: Pseudo-SAH is a radiologic manifestation of severe cerebral edema rather than a primary cause of death. In methanol intoxication, it can mimic true subarachnoid hemorrhage on imaging and lead to diagnostic confusion. Clinicians should maintain a high index of suspicion for pseudo-SAH in patients with methanol poisoning and unexplained radiologic findings to ensure accurate diagnosis and appropriate management.