Focus treatment on correcting electrolytes
Initial evaluation of a patient suspected of having THPP should include a complete blood count, TSH measurement, serum and urine electrolyte tests, and an ECG. Further work-up, including ultrasound and scan of the thyroid upon confirmation of thyrotoxicosis and hypokalemia, may be required. Physical examination may reveal thyromegaly. Exophthalmos and other hyperthyroidism symptoms often are absent.1
Diagnosis confirmed? Treat the hypokalemia first. Acute management of THPP centers on electrolyte correction. Total body stores of potassium in patients with THPP are usually normal, so the clinician must use care to avoid excessive potassium administration.1-5 Rebound hyperkalemia can occur in patients who receive > 90 mEq/L of potassium chloride within 24 hours.1
Definitive therapy may include antithyroid medication, radioactive iodine ablation (RIA), and/or thyroidectomy.1-5 All have the common goal of controlling the hyperthyroidism and preventing recurrent paralysis, which occurs in 62.2% of patients within the first three months following diagnosis.3 If antithyroid medications fail, then RIA is the next choice.1 Beta-blockers work by decreasing the Na+,K+-ATPase activity from the underlying hyperadrenergic state.1 Administration of acetazolamide—which is the primary treatment modality for FPP and idiopathic periodic paralysis—can precipitate THPP attacks and is contraindicated.1,5
If medical management is unsuccessful or the patient develops compression symptoms, then thyroidectomy should be considered.3 If the patient chooses thyroidectomy, medical optimization with antithyroid medications is indicated to mitigate the risks of anesthesia. When the thyroidectomy is performed by an experienced thyroid surgeon, the long-term results are excellent.
Case patient. Once this patient’s hypokalemia was corrected, she was successfully extubated. Despite appropriate medical therapy, her hyperthyroidism was poorly controlled. The endocrinologist believed that RIA was suboptimal for three reasons: 1) it might result in incomplete ablation, 2) it required a long treatment period to be effective, and 3) its prolonged course of treatment extended the time interval that the patient would be at risk for recurrent paralysis.
A surgeon was consulted for definitive treatment with thyroidectomy. The patient’s medications were changed to propylthiouracil (150 mg every 8 h) and propranolol (10 mg bid) until a euthyroid state was achieved and she could tolerate a general anesthetic without precipitating a thyroid storm. Two months later, she underwent total thyroidectomy without complication. Her postoperative course was normal.
THE TAKEAWAY
Thyrotoxic hypokalemic periodic paralysis is rare. Patients typically present with myalgia, cramping, and stiffness that progress to paralysis. Prompt electrolyte repletion is paramount for successful outcomes.1-5 Control of hyperthyroidism is the long-term goal.1-5 Definitive therapy can be achieved medically or surgically. Total thyroidectomy is a reasonable treatment option for medically refractory hyperthyroidism or when RIA is contraindicated. Long-term prognosis is excellent.
REFERENCES
1. Lin SH. Thyrotoxic periodic paralysis. Mayo Clin Proc. 2005;80:99-105.
2. Antonello IC, Antonello VS, de Los Santos CA, et al. Thyrotoxic hypokalemic periodic paralysis: a life-threatening syndrome. Eur J Emerg Med. 2009;16:43-44.
3. Lin YC, Wu CW, Chen HC, et al. Surgical treatment for thyrotoxic hypokalemic periodic paralysis: case report. World J Surg Oncol. 2012;10:21.
4. El-Hennawy AS, Nesa M, Mahmood AK. Thyrotoxic hypokalemic periodic paralysis triggered by high carbohydrate diet. Am J Ther. 2007;14: 499-501.
5. Chang CC, Cheng CJ, Sung CC, et al. A 10-year analysis of thyrotoxic periodic paralysis in 135 patients: focus on symptomatology and precipitants. Eur J Endocrinol. 2013;169:529-536.
6. Vijayakumar A, Ashwath G, Thimmappa D. Thyrotoxic periodic paralysis: clinical challenges. J Thyroid Res. 2014;2014:649502.
7. Ray S, Kundu S, Goswami M, et al. An unusual cause of muscle weakness: a diagnostic challenge for clinicians. BMJ Case Rep. 2012;2012.
8. Dassau L, Conti LR, Radeke CM, et al. Kir2.6 regulates the surface expression of Kir2.x inward rectifier potassium channels. J Biol Chem. 2011;286:9526-9541.
9. Ryan DP, da Silva MR, Soong TW, et al. Mutations in potassium channel Kir2.6 cause susceptibility to thyrotoxic hypokalemic periodic paralysis. Cell. 2010;140:88-98.