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CASE SNIPPET
Year : 2012  |  Volume : 58  |  Issue : 1  |  Page : 60-61

Paralysis caused by a large carbohydrate meal


1 Department of Medicine, Digestive Diseases Section, Yale University School of Medicine, New Haven, CT, USA
2 Department of Medicine, Pulmonary and Critical Care Section, Yale University School of Medicine, New Haven, CT, USA

Date of Web Publication25-Feb-2012

Correspondence Address:
M D Siegel
Department of Medicine, Pulmonary and Critical Care Section, Yale University School of Medicine, New Haven, CT
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0022-3859.93255

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How to cite this article:
Vilarinho S, Siegel M D. Paralysis caused by a large carbohydrate meal. J Postgrad Med 2012;58:60-1

How to cite this URL:
Vilarinho S, Siegel M D. Paralysis caused by a large carbohydrate meal. J Postgrad Med [serial online] 2012 [cited 2020 Oct 25];58:60-1. Available from: https://www.jpgmonline.com/text.asp?2012/58/1/60/93255


A 24-year-old Caucasian gentleman recently diagnosed with Graves' Disease presented to the emergency department (ED) complaining of sudden upper and lower extremities' paralysis. This episode coincided with the ingestion of a large carbohydrate meal the night before. In the ED, the patient's vital signs were within normal limits except for sinus tachycardia at 140 beats per min. He was mildly diaphoretic with mild left eye proptosis. There was no goiter. Blood work revealed a potassium concentration of 2.2 mmol/L, phosphorus 1.6 mg/dL, thyroid-stimulating hormone less than 0.04 uU/mL, and elevated total T4, free T4 and total T3 at 12.2 mcg/dL, 2.7 ng/dL and 266 ng/dL, respectively. The patient received 1.5 liters of normal saline, 2 mg of propranolol intravenously and 60 mEq of KCl with rapid improvement in muscle strength. The potassium level increased from 2.2 to 4.7 mmol/L. After 24 h of observation, he was discharged home on methimazole 10 mg twice a day and long-acting propranolol 120 mg daily, and was cautioned to avoid strenuous activity and large carbohydrate meals. Three months later, the patient underwent elective thyroidectomy and pathology analysis showed a diffusely hyperplastic thyroid gland with extensive papillary hyperplasia consistent with treated Graves' Disease.

This gentleman suffered from thyrotoxic periodic paralysis (TPP), which is an uncommon complication of thyrotoxicosis characterized by acute and reversible episodes of muscle weakness secondary to severe acute hypokalemia. TPP occurs in 0.1-0.2% of the hyperthyroid population in North America, [1],[2] and it is not related to the etiology, severity or duration of hyperthyroidism. Despite a higher incidence of thyrotoxicosis in women, TPP is most commonly observed in men, and unlike familial periodic paralysis, familial cases are thought to be extremely rare. TPP was initially described in the English language at the Mayo Clinic 80 years ago, [3] but its pathophysiology remains obscure. It is well accepted that hypokalemia is not caused by a total body deficiency of potassium, but by rapid and exaggerated potassium influx in myocytes. The factor(s) predisposing certain individuals to hypokalemia remain(s) poorly understood. Thyroid hormone, ί-adrenergic stimulation, and insulin surge (e.g., a high-carbohydrate meal as described in our patient), can increase Na-K ATPase activity, intracellular potassium shift and hypokalemia [Figure 1]. Mutations in potassium channel Kir2.6, which alter muscle membrane excitability leading to paralysis, have been also recently identified in a significant number of unrelated TPP patients and are thought to increase predisposition to TPP in hyperthyroid patients. [4]
Figure 1: Schematic illustration of how thyroid hormone, beta‑adrenergic stimulation and hyperinsulinemia (strenuous exercise, fasting and high‑carbohydrate load) can increase Na‑K ATPase activity and causehypokalemia

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TPP is an uncommon complication of hyperthyroidism, but it should be considered in patients with profound muscular weakness and hypokalemia. The immediate therapeutic goal is to increase the serum potassium concentration. As illustrated by this case, relatively little exogenous potassium supplementation is necessary when compared to hypokalemia that occurs with total body losses. [5] The medium and long-term therapeutic goal is to achieve a permanent euthyroid state. We believe that greater awareness and understanding of TPP amongst clinicians will result in early and accurate diagnosis and treatment, and promote further research to better understand the etiology and treatment of this disorder.

 
 :: References Top

1.Ober KP. Thyrotoxic periodic paralysis in the United States - report of 7 cases and review of the literature. Medicine 1992;71:109.  Back to cited text no. 1
[PUBMED]    
2.Kelley DE, Gharib H, Kennedy FP, Duda RJ Jr, McManis PG. Thyrotoxic periodic paralysis - report of 10 cases and review of electromyographic findings. Arch Intern Med 1989;149:2597-600.  Back to cited text no. 2
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3.Dunlap HF, Kepler EJ. A syndrome resembling familial periodic paralysis occurring in the course of exophthalmic goiter. Endocrinology 1931;15:541-6.  Back to cited text no. 3
    
4.Ryan DP, da Silva MR, Soong TW, Fontaine B, Donaldson MR, Kung AW, et al. Mutations in potassium channel Kir2.6 cause susceptibility to thyrotoxic hypokalemic periodic paralysis. Cell 2010;140:88-98.  Back to cited text no. 4
    
5.Manoukian MA, Foote JA, Crapo LM. Clinical and metabolic features of thyrotoxic periodic paralysis in 24 episodes. Arch Intern Med 1999;159:601-6.  Back to cited text no. 5
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