Clinical features and recovery pattern of secondary hypokalaemic paralysis

PurposeInformation regarding frequency, details of neurological signs and recovery patterns of patients with secondary hypokalaemic paralysis (HP) is limited. This study aimed to analyse the frequency, aetiology, clinical features and recovery patterns of patients with secondary HP.MethodsThe clinical and laboratory records of 18 consecutive patients with secondary HP aged & GE; 18 years admitted to our hospital between April 2011 and March 2022 were reviewed. Patients with inherited hypokalaemic periodic paralysis were excluded.ResultsOf the 18 patients, 16 had a common aetiology: chronic alcoholism, diarrhoea or an imbalanced diet. Initial symptoms, such as fatigue, were often atypical. Three patients had prominent asymmetric limb weakness and four had predominant upper limb weakness. On admission, the mean serum potassium and creatine kinase (CK) levels of the patients were 1.90 mmol/L and 4488 U/mL, respectively. Ten patients (56%) had decreased potassium levels after admission, despite potassium replacement treatment (rebound hypokalaemia). Twelve patients presented with increased CK levels even after 2-5 days (delayed hyperCKaemia). Low serum magnesium levels significantly correlated with rebound hypokalaemia.ConclusionsSecondary HP can be caused by a variety of conditions, but mainly occurs due to lifestyle conditions/disorders. Secondary HP often presents with atypical symptoms, and the initial symptoms can be non-specific. Rebound hypokalaemia and delayed hyperCKaemia are common in secondary HP, despite potassium replacement. As such, careful serial monitoring is needed for patients with secondary HP.

Automated summary

This study analyzed the frequency, etiology, clinical features, and recovery patterns of patients with secondary hypokalaemic paralysis. Lifestyle conditions/disorders such as chronic alcoholism, diarrhea, and imbalanced diet were the common causes. Initial symptoms were often atypical, and rebound hypokalaemia and delayed hyperCKaemia were common despite potassium replacement. Careful serial monitoring is needed for patients with secondary hypokalaemic paralysis.