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Summarized from Maurya P, Kalita J, Misra U. Spectrum of hypokalaemia periodic paralysis in a tertiary care centre in India. Postgrad Med J 2010; 86: 692-95
Hypokalemia, one of the most common electrolyte disturbances, is diagnosed if plasma potassium concentration is less than 3.5 mmol/L. Mild hypokalemia (plasma potassium 3.0-3.5 mmol/L) is usually asymptomatic, but greater degree of hypokalemia can result in signs and symptoms that reflect the fundamental role of potassium in neuromuscular transmission.
Severe hypokalemia (plasma potassium <2.5 mmol/L) is usually associated with acute flaccid paralysis that can range from mild muscle weakness to severe paralysis. Involvement of cardiac or respiratory muscle can result in life-threatening arrhythmia or respiratory failure.
A recently published study sought to report the clinical features, underlying cause and outcome for 30 consecutive patients (age 17-52 years) presenting with hypokalemic paralysis at an Indian tertiary-care, teaching hospital. Median plasma potassium was 2.2 mmol/L (range 1.0-3.4). Seven patients had mild hyperkalemia (in the range of 3.0-3.5 mmol/L).
Eleven patients had a history of recurring muscle weakness. All patients had quadraparesis (muscle weakness in all four limbs); in 10 patients the weakness was severe. Six patients had respiratory failure, one requiring mechanical ventilation for 2 days. ECG changes, typical of hypokalemia, were evident in seven patients. A secondary cause for hypokalemic paralysis was identified in 13 (43.3 %) patients.
The remaining 17 were categorized as suffering primary (idiopathic) hypokalemic paralysis. The underlying causes of secondary hypokalemia were: renal tubular acidosis (four cases); Gitelman syndrome (four cases) and thyrotoxicosis (five cases).
Hypokalemia was significantly less severe in those with idiopathic hypokalemic paralysis; all those with mild hypokalemia were in this group and results indicate that the finding of plasma potassium <2.0 mmol/L strongly suggests a secondary cause.
All patients improved quickly with potassium supplementation (delivered orally for those with mild to moderate hypokalemia and intravenously for those with potassium <2.0 mmol/L). Additionally, those with renal tubular acidosis were prescribed sodium bicarbonate and those with thyrotoxicosis, carbimazole and propanalol. None of the patients died during 15 months of follow-up, but one suffered a recurrence of hypokalemic paralysis.
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