Acute Hypokalemic Periodic Paralysis Presenting as Acute Quadriparesis in a 44-Year-old Female: A Case Report and Literature Review
Y. M. Bindhu
Department of Neurosurgery, Department of Pharmacy Practice, RGUHS, S.S. Institute of Medical Sciences and Research Centre (SSIMS and RC), Davangere, Karnataka, India.
B. B. Likhitha
*
Department of Neurosurgery, Department of Pharmacy Practice, RGUHS, S.S. Institute of Medical Sciences and Research Centre (SSIMS and RC), Davangere, Karnataka, India.
*Author to whom correspondence should be addressed.
Abstract
Background: Hypokalemic periodic paralysis (HPP) is a skeletal muscle channelopathy characterised by acute episodes of muscle weakness or paralysis associated with severe hypokalaemia. Primary HPP results from inherited ion-channel mutations, whereas secondary HPP is caused by transcellular potassium shifts into cells or potassium loss, including renal and gastrointestinal losses. We describe a case of HPP associated with severe gastrointestinal fluid loss and acute quadriparesis.
Case Presentation: A 44-year-old woman presented with rapidly progressive, symmetrical quadriparesis following several episodes of acute, non-projectile vomiting. Physical examination revealed marked motor weakness (power 2/5 in the upper and lower extremities; straight-leg-raising test, 0°), with preservation of cranial-nerve function, sensation, and bowel and bladder function. Investigations showed severe hypokalaemia (K, 1.66 mEq/L), with otherwise normal blood urea nitrogen, creatinine, blood glucose (106 mg/dL), and thyroid function (TSH, 0.85 µIU/mL). Electrocardiography showed a regular rate and rhythm with subtle U waves. Intravenous and oral potassium replacement increased the serum potassium level to 3.30 mEq/L by day 5. Motor strength and neurological function were fully restored to 5/5 in all four extremities.
Discussion: Rapid differentiation of secondary hypokalaemic quadriparesis from acute neuromuscular emergencies, including Guillain–Barré syndrome (GBS), acute ischaemic stroke, myasthenia gravis, and acute transverse myelitis, is essential to enable early electrolyte replacement and reverse neuromuscular blockade before life-threatening respiratory or cardiovascular dysfunction develops.
Conclusion: Several conditions may present with acute flaccid quadriparesis. Serum electrolytes should therefore be assessed promptly in patients with suspected hypokalemic periodic paralysis. Early testing enables rapid, readily available treatment and may avoid an unnecessary, time-consuming invasive work-up.
Keywords: Hypokalemic periodic paralysis, quadriparesis, flaccid paralysis, hypokalemia, potassium replacement, channelopathy