Thyrotoxic Periodic Paralysis Presenting with Hypokalemia: A Case Report

Background: Thyrotoxic periodic paralysis (TPP), a serious complication of hyperthyroidism, is a common etiology of secondary hypokalemic periodic paralysis (HPP). In this study, we present a case report of a patient who presented to our ED with weakness and hypokalemia and was found to have severe hyperthyroidism. Case presentation: A 29-year-old Chinese man presented to our Emergency Department complaining of feeling very weak and tired for 8 hours. The weakness was limited to his four limbs. On physical examination, he was conscious and oriented to place, persons, and time. Upper and lower limb exams showed a power of 4/5 with normal sensation and an absence of Babinski signs. The initial blood work was normal, except for mild hypokalemia; therefore, the initial plan was to start him on one liter of IV normal saline mixed with 40 mEq KCl over 4 hours before repeating the laboratory investigations. The repeated blood work showed a drop in his potassium level to 2.2 mmol/L, indicating the need for further potassium replacement and extensive blood work, including a thyroid function test, which showed severe hyperthyroidism. The patient was admitted to the critical care unit, where his vital signs were monitored continuously, and he received KCl replacement and began propranolol and carbimazole treatment. Conclusions: TPP should be a differential diagnosis for patients with unexplained hypokalemia and weakness, even in the absence of clinical features of hyperthyroidism.

exams were normal. Upper and lower limb exams showed a power of 4/5 with normal sensation and an absence of Babinski signs.
The initial blood work was normal, except for mild hypokalemia (Table 1); therefore, the initial plan was to start him on one liter of IV normal saline mixed with 40 mEq KCl over 4 hours before repeating the laboratory investigations, at which point he was to be discharged home if his potassium level had normalized.
The repeated blood work showed a drop in his potassium level to 2.2 mmol/L, which indicated the need for further potassium replacement and extensive blood work, including a thyroid function test, which showed severe hyperthyroidism. The patient was referred to critical care and endocrinology for further management of hypokalemia and thyrotoxicosis. The patient was admitted to the critical care unit, where his vital signs were monitored continuously, and he received KCl replacement and was started on propranolol and carbimazole. His weakness and potassium level improved over the course of his admission to the critical care unit, and he was discharged in excellent condition with follow-up appointment with the Endocrinology Department.

Discussion
In thyrotoxicosis, Na/K-ATPase overactivity plays a primary role in inducing muscle weakness and hypokalemia through intracellular potassium shifts that are aggravated by stress, catecholamine, and high levels of insulin that are released after consuming a meal rich in carbohydrates [1]. TPP can induce HPP; therefore, all patients with HPP should be investigated for TPP. In a retrospective study by Kalitha et al. [2], a review of 52 patients with HPP found that TPP accounts for approximately 17.3% of HPP, and there are no differences in demographic, clinical, biochemical and outcome profiles between idiopathic HPP and TPP. The diagnosis of TPP can be challenging because two-thirds of TPP patients have subclinical thyrotoxicosis at the time of presentation. Hegde et al. [3] reported a patient known to have Graves' disease who came to their ED with the clinical profile of HPP without the signs and symptoms of thyrotoxicosis. TTP and hypokalemia can be the initial presentation of thyrotoxicosis and Graves' disease [4][5][6]. Rebound hyperkalemia is a known complication during the treatment of TTP and HPP. In their review study, of the 52 HPP patients, 8 experienced rebound hyperkalemia; it is crucial to monitor the serum potassium level during treatment to avoid such complications [2]. The serum potassium level can be very low in patients with TPP [4,7].
However, normal potassium levels during paralytic attacks does not exclude the diagnosis of TPP. Several studies reported patients with TTP who presented at the ED with normokalemia and muscle paralysis. Serial monitoring of potassium levels is indicated to enable the observation of any progressive drop in serum potassium levels following admission [8,9]. In a study of 23 HPP patients by Jandhyala et al. [10], 13 (57%) had primary HPP, and 10 (43%) had secondary HPP. Men were predominantly affected [10]. Diarrhea, fever, strenuous activity, a meal rich in carbohydrates, and febrile illness are common precipitating factors [11][12][13][14]. In another study of 31 patients by Rao et al. [15], the secondary causes of HPP were analyzed; 13 patients were diagnosed with renal tubular acidosis, and two were diagnosed with TTP. Of the 31 patients, 19 were men [15]. Although hyperthyroidism is more common in females, TPP with secondary HPP occurs relatively more frequently in males [10,15,16].

Conclusions
TPP should be one of the differential diagnoses of patients with unexplained hypokalemia and weakness, even in the absence of clinical features of hyperthyroidism.