What question did this study set out to answer?

To examine the rare coexistence of severe hypokalemia, Wernicke’s encephalopathy, and hypoxic–ischemic brain injury in pregnancy.

April 23, 2026Open Access

Severe Hypokalemia Complicated by Wernicke’s Encephalopathy and Hypoxic–Ischemic Brain Injury in Pregnancy: A Case from a Resource-Limited ICU

Key Points

To examine the rare coexistence of severe hypokalemia, Wernicke’s encephalopathy, and hypoxic–ischemic brain injury in pregnancy.
Case report of a pregnant woman at 18 weeks gestation with severe hypokalemia and neurological symptoms.
Utilized laboratory evaluations and brain MRI for diagnosis and monitoring of the conditions.
Administered high-dose thiamine and provided mechanical ventilation and rehabilitation.
Severe hypokalemia led to acute kidney injury and respiratory failure.
Patient showed fluctuating mental status and ophthalmoplegia consistent with Wernicke’s encephalopathy.
Partial neurological recovery achieved after prolonged ventilatory support with ongoing rehabilitation needs.

Abstract

Introduction: Pregnancy is a metabolically vulnerable state in which electrolyte disturbances, nutritional deficiencies, and hypoxic events can rapidly lead to severe neurological complications. Wernicke’s encephalopathy and hypoxic–ischemic brain injury are uncommon but potentially devastating conditions that are frequently underdiagnosed, particularly in resource-limited intensive care settings. To our knowledge, the coexistence of profound hypokalemia, Wernicke’s encephalopathy, and hypoxic–ischemic brain injury during pregnancy has been rarely reported, particularly from resource-limited intensive care settings. Case Presentation: We report the case of a 22-year-old previously healthy pregnant woman at 18 weeks’ gestation who presented with prolonged vomiting, progressive lower-limb weakness, and acute respiratory failure requiring mechanical ventilation. Laboratory evaluation revealed severe hypokalemia with associated acute kidney injury. Despite correction of electrolyte abnormalities, she developed persistent neuromuscular weakness, recurrent respiratory failure, and hemodynamic instability. Fluctuating mental status and ophthalmoplegia raised suspicion for Wernicke’s encephalopathy, and high-dose parenteral thiamine was initiated. Brain magnetic resonance imaging later demonstrated hypoxic–ischemic changes. Her clinical course was further complicated by rhabdomyolysis, hepatic dysfunction, thrombocytopenia, and intrauterine fetal demise. Following prolonged ventilatory support and tracheostomy, she achieved partial neurological recovery and was discharged with ongoing rehabilitation needs. Conclusion: This case highlights the complex interplay between severe electrolyte disturbances, thiamine deficiency, and hypoxic brain injury during pregnancy. Early recognition of nutritional and metabolic causes of neurological deterioration, prompt empiric thiamine therapy, and aggressive prevention of hypoxic events are critical to improving maternal outcomes, particularly in resource-limited settings. Keywords: pregnancy, hypokalemia, Wernicke’s encephalopathy, hypoxic–ischemic brain injury, resource-limited ICU, quadriparesis

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