Clinical and Aetiological Spectrum of Hypokalemic Flaccid Paralysis in Western Odisha

Biranchi Narayan Mohapatra, Sujit Kumar Lenka, Manoranjan Acharya, Chakradhar Majhi, Gouri Oram, Khetra Mohan Tudu
Journal of the Association of Physicians of India 2016, 64 (5): 52-58

OBJECTIVE: To study the clinical profile of hypokalemic flaccid paralysis (HKFP) and to evaluate its causes.

METHODS: Fifty cases of hypokalemic flaccid paralysis (HKFP) admitted between November 2012 to October 2014 were taken up in the study. Serum potassium level < 3.5 mmol/ltr has been taken as hypokalemia. All cases were studied for spot and/or 24 hour urinary sodium / potassium, serum potassium / calcium / magnesium. Hypokalemic periodic paralysis (HPP) were diagnosed if there was spot/24 hour urine potassium excretion < 20mmol/ltr in presence of hypokalemia and flaccid weakness without other causes. EMG and nerve conduction study were done to exclude polyneuropathy and myopathic cases.

RESULTS: Out of 50 cases of HKFP, male gender predominated (88%). Maximum number of cases (70%) occurred in 21 to 40 years of age. It occurred in all seasons but more in summer (58%). The precipitating factors were present in 76% of cases out of which high carbohydrate meal (28%), vomiting (16%), excessive sweating (8%), diarrhea (8%) and increased urination (12%) were present. Twenty percent of cases had recurrence (2 to 3 episodes most often) and 6% of cases had family history. Quadriparesis was seen in (54%), paraparesis (36%), hemiparesis (10%) and neck muscle weakness (32%). No case was present with respiratory paralysis or cranial nerve palsy. Twenty-one cases (42%) have very low potassium < 2.5 mmol/ltr, 11 cases (22%) with potassium level between 2.5 to 2.9 mmol/ltr and 18 cases (36%) with 3 to 3.5 mmol/ltr. There was no correlation between severity weakness and potassium level. Eleven cases (22%) had thyrotoxicosis and 3 cases (6%) were hypothyroid. Thirteen cases (26%) have excess urinary loss of potassium (≥20 mmol/ltr) of which 5 cases (10%) were distal renal tubular acidosis (dRTA), four cases (8%) were Gitelman's syndrome (GS) and in 4 cases exact cause could not be diagnosed. Non-renal / prior renal loss of potassium like diarrhea and excessive sweating was responsible in 8% cases each and vomiting in 10% of cases. One unique case of hypernatraemic hypokalemic paralysis (HHP) was found. Only 9 (18%) cases are hypokalemic periodic paralysis (HPP).

CONCLUSIONS: HKFP is a hetergenous group of disease of which a significant number of patients had thyroid disorders mostly in the form of thyrotoxicosis followed by renal tubular dysfunctions like dRTA and GS; non-renal and prior renal loss of potassium like diarrhea, excessive sweating and vomiting respectively. Early recognition and prompt management of these conditions will give gratifying result and prevent further attacks in some cases.


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