Niranjan Tachamo, MD*1;Bidhya Timilsina, MD1;Saroj Lohani, MD1;Salik Nazir, MD1;Elan Mohanty1;Noelle Juliano2 and Krysta Brown, DO3, (1)Reading Health System, West Reading, PA, (2)Reading Health System, Department of Medicine, West Reading, PA, (3)Reading Hospital & Medical Center, West Reading, PA

Meeting: Hospital Medicine 2017, May 1-4, 2017; Las Vegas, Nev.

Abstract number: 743

Categories: Adult, Clinical Vignette Abstracts

Keywords: ,

Case Presentation:

A 25 year-old male with no significant past medical history presented to the emergency department after he woke up with sudden onset weakness in his bilateral thighs and arms. He had history of heat intolerance, palpitations, dysphagia and weight loss of 40 pounds over last 3 months but denied any changes in skin, hair or bowel movements. He denied any diarrhea, vomiting, laxative or diuretic abuse. He denied any supplements, alcohol or drug abuse. History was negative for any recent contrast scans or thyroid disease in the family. He had similar episode one month ago sustaining a fall and was treated as dehydration without further work up. Vital signs included blood pressure of 105/54 mm Hg, pulse 106/minute, temperature 36.4 °C and respiratory rate 20/minute. Body mass index was 26.93 kg/m2. Physical examination revealed diffusely enlarged thyroid gland with bruit but no orbitopathy. Power, sensation and reflexes were intact. Rest of the examination was unremarkable. Pertinent labs included potassium 1.9 mEq/L, TSH <0.006 uIU/mL, free T4 3.71 ng/dL, free T320.1 pg/mL and calcium 10.5 mg/dL. Electrocardiogram revealed sinus tachycardia. Ultrasonography of neck revealed diffusely enlarged vascular thyroid gland suggestive of Grave’s disease. His symptoms were consistent with thyrotoxic periodic paralysis and he was treated with potassium repletion, atenolol and methimazole. His paralysis resolved completely and he was discharged home on atenolol and methimazole to follow up with outpatient endocrinology for further workup.


Thyrotoxic periodic paralysis (TPP) is characterized by episodes of abrupt onset hypokalemia and profound proximal muscle weakness associated with thyrotoxicosis. There may not always be preceding history or clinical manifestations of hyperthyroidism, thus posing diagnostic challenge. Massive intracellular influx of potassium due to increased Na-K-ATPase activity from hyperthyroidism causes hypokalemia. Attacks may last for hours to days and may be precipitated by strenuous exercise or high-carbohydrate meals. Though TPP is uncommon in Caucasians, it is increasingly seen in Western world due to population mobility. The prototypical patient is an Asian male of age 20s-30s. Intravenous potassium supplementation shortens the duration of attack but has risk of rebound hyperkalemia as total body potassium is normal. It is important to check thyroid function test even during first episode of periodic paralysis as both TPP and Familial hypokalemic periodic paralysis (FHPP) have similar clinical manifestations but differ significantly in management. In contrast to FHPP, potassium supplementation is ineffective to prevent recurrent attacks of TPP but can be prevented only by maintaining euthyroid state.


Thyrotoxic periodic paralysis is a rare but easily treatable condition which if missed, can be debilitating and fatal. It is crucial to differentiate TPP from FHPP as management differs significantly despite similar clinical manifestations.

To cite this abstract:

Tachamo, N; Timilsina, B; Lohani, S; Nazir, S; Mohanty, E; Juliano, N; Brown, K . PARALYSIS THAT EASILY REVERSES- AN UNCOMMON AND OVERLOOKED CONDITION!. Abstract published at Hospital Medicine 2017, May 1-4, 2017; Las Vegas, Nev. Abstract 743. Journal of Hospital Medicine. 2017; 12 (suppl 2). Accessed February 25, 2020.

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