Clinical biochemistry · 2026
Silent electrolyte imbalance unmasked by paralysis: a case of hypokalemia in a middle-aged woman.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Ошибки и ограничения
История · было → стало
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Advani Aman, Ahmed Hassan, Shabbir Muhammad Ahsan, Ahmed Maaz, Khan Tauqeer
Аннотация
BACKGROUND: Hypokalemic periodic paralysis is a rare autosomal dominant muscle channelopathy often misdiagnosed due to its atypical presentation. It is characterized by episodic flaccid paralysis with low serum potassium levels and may be triggered by factors such as high carbohydrate intake, infections, or medications.
CASE PRESENTATION: We report the case of a 25-year-old female who presented with acute ascending flaccid paralysis and was initially misdiagnosed with Guillain-Barré syndrome. Despite biochemical and electrocardiographic evidence of hypokalemia (serum K+: 2.7 mEq/L; electrocardiogram showing U waves and flattened T waves), potassium correction was not initiated. The patient rapidly deteriorated, required mechanical ventilation, and ultimately succumbed to her condition. Thyroid function testing was not performed despite clinical red flags, including a history of anxiety and depression, raising suspicion for thyrotoxic periodic paralysis.
DISCUSSION: This case highlights the diagnostic challenges of hypokalemic paralysis, particularly when presenting as a neurological emergency without classic features. The failure to promptly correct hypokalemia and investigate its underlying etiology contributed to a preventable fatal outcome. A systematic "hypokalemia-first" approach is recommended to avoid such diagnostic delays in similar clinical settings.
CONCLUSION: Timely recognition and correction of hypokalemia, alongside targeted evaluation of underlying causes such as thyrotoxicosis, are critical in patients presenting with acute flaccid paralysis. Standardized emergency protocols could significantly improve outcomes and prevent avoidable fatalities.
CASE PRESENTATION: We report the case of a 25-year-old female who presented with acute ascending flaccid paralysis and was initially misdiagnosed with Guillain-Barré syndrome. Despite biochemical and electrocardiographic evidence of hypokalemia (serum K+: 2.7 mEq/L; electrocardiogram showing U waves and flattened T waves), potassium correction was not initiated. The patient rapidly deteriorated, required mechanical ventilation, and ultimately succumbed to her condition. Thyroid function testing was not performed despite clinical red flags, including a history of anxiety and depression, raising suspicion for thyrotoxic periodic paralysis.
DISCUSSION: This case highlights the diagnostic challenges of hypokalemic paralysis, particularly when presenting as a neurological emergency without classic features. The failure to promptly correct hypokalemia and investigate its underlying etiology contributed to a preventable fatal outcome. A systematic "hypokalemia-first" approach is recommended to avoid such diagnostic delays in similar clinical settings.
CONCLUSION: Timely recognition and correction of hypokalemia, alongside targeted evaluation of underlying causes such as thyrotoxicosis, are critical in patients presenting with acute flaccid paralysis. Standardized emergency protocols could significantly improve outcomes and prevent avoidable fatalities.