Secondary hypokalemic myoplegias

Abstract

Objective:to investigate the features of clinical manifestations and course of secondary hypokalemic myoplegia (SHM) of various etiologies.Patients and methods. The investigation enrolled 10 patients with SHM. The patients' mean age was 39.5±16.2 years. The cause of SHM was hyperaldosteronism in 3 cases, thyrotoxicosis in 1, nontraumatic rhabdomyolysis in 2, and severe toxicosis and massive obstetric hemorrhage in 4.Results and discussion. The blood potassium level difference between days 7 and 1 of hospitalization in patients with hyperaldosteronism and thyrotoxicosis was 2.2±0.4 mmol/l; this indicator in the other patients was less (1.6±0.8 mmol/l). The dynamics of an increase in the blood potassium concentrations during the 7 days differed significantly in 4 pregnant women who had undergone a cesarean section for placental abruption, antenatal fetal death, or their severe toxicosis with suddenly developed neuromuscular disorders (2.1±0.8 mmol/l), and in other patients with SHM (1.4±0.2 mmol/l). SHM in Conn's syndrome and thyrotoxicosis was characterized by long-term (11.8±3.6-day) neuromuscular disorders, while in SHM of another etiology, there were shorter (5.8±4-day) muscle weakness episodes (p<0.05). The SHM duration was recorded to be shorter in 4 pregnant women (4.3±4 days) than that in the other patients (10.3±2.9 days) (p<0.05). In nontraumatic rhabdomyolysis, the duration of hypokalemic paralysis (HP) was significantly longer (9±1.4 days) than in pregnancy (4.3±3.9 days). The episodes of HP in thyrotoxicosis and aldosteroma turned out to be longer (495.8±331.5 days) (p<0.05) than those in the presence of electrolyte changes in pregnant women and in rhabdomyolysis (14±5.7 days). In patients without adrenal tumors, thyrotoxicosis, the SHM periods requiring urgent hospitalization were more prolonged in nontraumatic rhabdomyolysis (30±8.5 days) (p<0.05) than those in the presence with electrolyte disorders in pregnant women (11.2±3.7 days).Conclusion. The differential diagnostic algorithm for examining patients with acute flaccid paralysis of various etiologies due to hypokalemia has not been well elaborated, especially in endocrine disease and rhabdomyolysis. The differences in the rate of hypokalemia reversal in hyperaldosteronism, thyrotoxicosis, and rhabdomyolysis are likely to be associated with the multifactorial etiology of SHM. An incorrect assessment of the etiology of SHM is a common reason for its late diagnosis and inadequate treatment.