Primary Hypokalemic Paralysis Research Articles

Clinical and biochemical features of hypokalemic paralysis: a study from rural Eastern India

BackgroundHypokalemic paralysis is characterized by episodic attacks of flaccid muscle weakness of variable duration and severity associated with hypokalemia. Overall, there is a scarcity of data regarding hypokalemic paralysis from Indian subcontinent particularly from rural areas.MethodsA total of 50 consecutive patients of hypokalemic paralysis who were admitted in our hospital were recruited in this study.ResultsFifty patients of hypokalemic paralysis were admitted to our department over a period of 4 years. Forty-two (84%) patients presented with classic acute onset quadriparesis, while eight patients had atypical presentation. Five patients had paraparesis, two had hemiparesis and one patient presented with isolated neck muscle weakness without any limb weakness. Thirty-two patients had primary hypokalemic periodic paralysis (HoPP) and 18 had secondary hypokalemic paralysis. There was no significant difference in severity of weakness (p = 0.53), number of episodes of weakness (p = 0.66) and serum CPK levels (p = 0.36) between primary and secondary hypokalemic paralysis. Secondary cases required significantly prolonged time for recovery as well as higher potassium supplements as compared to the primary HoPP. The severity of weakness of proximal muscles measured in MRC grading showed a significant correlation with serum potassium levels (p = 0.010), but did not show any correlation with CPK Levels (p = 0.86).ConclusionHypokalemic paralysis is an important cause of acute flaccid paralysis in the Emergency Room that often improves dramatically with potassium supplements. While secondary cases often require treatment of underlying etiology, primary hypokalemic paralysis often requires chronic treatment with acetazolamide and/or potassium-sparing diuretics.

Clinical and Etiological Spectrum of Hypokalemic Periodic Paralysis in a Tertiary Care Hospital in Pakistan.

IntroductionHypokalemic periodic paralysis (HPP) is characterized by muscle weakness secondary to low serum potassium levels. It may be primary in origin or there may be secondary causes like thyrotoxic periodic paralysis, renal or suprarenal causes, or non-renal causes like gastroenteritis.AimTo study the etiology, clinical manifestations, and outcome after therapy of patients with hypokalemic paralysis.MethodologyThe study was conducted from January 2016 to December 2016. Patients fulfilling the diagnostic criteria for hypokalemic paralysis, i.e., flaccid muscle weakness involving two or more limb muscles due to serum potassium < 3.5 mmol/L and with no objective sensory signs were included in the study. Relevant investigations were done. Those with other causes of flaccid weakness or on diuretic therapy were excluded from the study. Data was analyzed using SPSS Version 20.0 (IBM Corp., Armonk, NY).ResultsIn our study, 14 patients out of a total of 18 (14/18, i.e., 77.78%) were male and 4/18 (22.22%) were female [Male: Female ratio: 3.5:1]. The mean age of onset of HPP in males (29.5±10.14 yrs.) was lesser than that of females (41±10.8 yrs.), but this difference was statistically not significant (p<0.066). In the entire sample there were 15/18 cases (83.33%) of primary and 3/18 (16.67%) cases of secondary HPP [2/3 had thyrotoxic periodic paralysis and 1/3 had gastroenteritis]. Furthermore, 12/18 patients (66.66%) had symmetrical weakness (five cases of paraparesis and all were male; seven cases of quadriparesis: six males and one female) and 6/18 (33.33%) had asymmetrical weakness (two paraparesis: one male, one female; four quadriparesis: two males, two females). Statistically, no significant difference (p<0.709) was seen in those with symmetrical versus those with asymmetrical weakness. In this study 7/18 (38.89%) cases had absent, 1/18 (5.55%) had diminished, and 10/18 (55.55%) cases had intact deep tendon reflexes. None of the cases had cranial, bulbar, or respiratory involvement. The mean serum potassium of sample was 3.18±0.5 standard deviation (SD). The reduction in serum potassium was moderate (2.5-3.5 mmol/L) in primary and severe (<2.5 mmol/L) in secondary HPP. Those with quadriparesis had severe hypokalemia with a mean serum potassium of 2.1 mmol/L. Only 3/18 patients had concomitant magnesium deficiency. Patients given intravenous potassium replacement (except one with moderate hypokalemia and given oral replacement) recovered dramatically. The mean recovery time was 38.6±20.3 hours. The recovery time in quadriparesis was about 24 hours and in paraparesis was 12 hours. Only one patient with thyrotoxic periodic paralysis (TPP) and with severe serum potassium deficiency (0.9 meq/L) died due to cardiac arrhythmia. No atypical presentation was seen.ConclusionHPP has male preponderance. The age of onset of HPP is earlier in males than in females. Moreover, males are more prone to have symmetrical weakness. Asymmetrical weakness has almost an equal gender distribution. Primary hypokalemic paralysis is more frequent than secondary. Thyrotoxic periodic paralysis is the commonest cause of secondary periodic paralysis. The recovery time in quadriparesis is almost double the recovery time in paraparesis. Respiratory involvement is rare. HPP is an important differential in the diagnosis of acute flaccid muscle weakness. It should be promptly addressed to prevent recurrence of paralysis.

Apparently Persistent Weakness After Recurrent Hypokalemic Paralysis: A Tale of Two Disorders

A 19-year-old woman presented with recurrent hypokalemic paralysis, followed by apparently persistent symptoms due to coexisting osteomalacia. Distal renal tubular acidosis type 1 (dRTA1) linked the metabolic abnormalities and occurred as an extraglandular feature of Sjögren syndrome (SS). This case highlights the fact that in the setting of recurrent hypokalemia, apparently progressive weakness should be distinguished from primary hypokalemic paralysis and evaluated for dRTA1, as the metabolic alterations are potentially treatable. Further dRTA1 may precede the occurrence of sicca syndrome in SS.