AN INTERESTING CASE OF ACUTE FLACCID PARALYSIS: A DIAGNOSTIC CHALLENGE

Abstract

Acute Flaccid Paralysis (AFP) is a complex, neurological clinical syndrome characterized by the rapid onset of profound muscle weakness, hypotonia, and diminished or absent deep tendon reflexes. The progression of weakness can be aggressive, occasionally leading to devastating complications such as bulbar palsy, acute respiratory failure, and death if not promptly identified and managed. While it is not a single disease entity, AFP serves as a critical red-flag presentation in emergency medicine and neurology, necessitating an immediate and systematic diagnostic approach to prevent irreversible morbidity. Hypokalemic periodic paralysis is a condition characterized by transient attacks of flaccid muscle weakness. It can be broadly classified into primary (familial) and secondary (acquired) forms. Familial cases are typically due to genetic channelopathies affecting skeletal muscle sodium or calcium channels. Secondary hypokalemic paralysis, on the other hand, arises from a massive intracellular shift of potassium (as seen in thyrotoxic periodic paralysis) or severe depletion of total body potassium due to gastrointestinal or renal losses.