Electrocardiographic Manifestations in Patients with Thyrotoxic Periodic Paralysis

Hsu, Yi-Chih; Lin, Yuh Feng; Chau, Tom; Liou, Jun-Ting; Kuo, Shi Wen; Lin, Shih Hua

doi:10.1097/00000441-200309000-00004

Cited by 64 publications

(52 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Electrocardiographic findings may be characteristic of hypokalemia, with increased P-wave amplitude, prolonged PR interval, widened QRS complexes, decreased T-wave amplitude, and U waves. Unlike hypokalemia from other causes, sinus tachycardia predominates in patients with TPP (17,18). Other electrocardiographic abnormalities include atrioventricular block, atrial fibrillation, ventricular fibrillation, and asystole (19).…”

Section: Managementmentioning

confidence: 99%

Thyrotoxic Periodic Paralysis

Re¹,

S²,

Walker³

2009

Encyclopedia of Neuroscience

View full text Add to dashboard Cite

Thyrotoxic periodic paralysis (TPP), a disorder most commonly seen in Asian men, is characterized by abrupt onset of hypokalemia and paralysis. The condition primarily affects the lower extremities and is secondary to thyrotoxicosis. It has been increasingly reported in the USA due to the rise in the immigrant population. Hypokalemia in TPP results from an intracellular shift of potassium induced by the thyroid hormone sensitization of Na + /K + -ATPase rather than depletion of total body potassium. Treatment of TPP includes prevention of this shift of potassium by using nonselective beta-blockade, correcting the underlying hyperthyroid state, and replacing potassium. TPP is curable once a euthyroid state is achieved. It is important for physicians to distinguish TPP from familial hypokalemic periodic paralysis, a more common cause of periodic paralysis in Caucasians. The absence of a family history of paralysis, male sex, presentation in the second to fourth decades of life, and signs of thyrotoxicosis like sinus tachycardia help in the diagnosis of this disorder. Early recognition of TPP is vital to initiating appropriate treatment and to avoiding the risk of rebound hyperkalemia that may occur if high-dose potassium replacement is given.T hyrotoxic periodic paralysis (TPP) is most common in Asian populations, with an incidence of approximately 2% in patients with thyrotoxicosis of any cause. It has been recognized in ais, Filipinos, Vietnamese, Koreans, Malaysians, Hispanics, African Americans, and Caucasians (1-5). TPP is characterized by acute onset of severe hypokalemia and profound proximal muscle weakness in patients with thyrotoxicosis (1).TPP is commonly misdiagnosed in western countries because of its similarities to familial periodic paralysis. Familial periodic paralysis is an autosomal dominant disorder caused by a defect in the gene coding for L-type calcium channel 1-subunit (CACNA1S) on chromosome 1q31-32 (2). e neuromuscular presentations of both are identical, and to enhance diagnosis of TPP, physicians need to look for subtle features of hyperthyroidism in the presence of hypokalemic periodic paralysis. Early diagnosis not only aids in definitive management with nonselective beta-blockers and correction of hyperthyroidism, but also prevents the risk of rebound hyperkalemia due to excessive potassium replacement. CASE REPORTA 33-year-old Hispanic man with a history of recurrent hypokalemia and muscle weakness presented to our emergency department with generalized muscle weakness more pronounced in his lower extremity. e patient's symptoms started in the early morning, and he was unable to walk to the bathroom. He had had similar episodes before and took potassium supplements sporadically. His initial episode of hypokalemia and paralysis had occurred 2 years earlier. He denied use of diuretics, laxatives, alcohol, or recreational drugs. He reported intermittent palpitations and diarrhea and had no family history of periodic paralysis.On physical examination, he had a mildly enlarged thyroid ...

show abstract

Section: Managementmentioning

confidence: 99%

Thyrotoxic Periodic Paralysis

Re¹,

S²,

Walker³

2009

Encyclopedia of Neuroscience

View full text Add to dashboard Cite

show abstract

“…Of note, one tracing demonstrated atrioventricular Wenckebach with 3:2 conduction (image not shown), which also has been reported in THPP. 5 The patient subsequently underwent a radioiodine uptake scan, which revealed an elevated 24-hour thyroid uptake at 79%, consistent with Graves disease. He was treated with radionuclide ablation of the thyroid with I-131, with no subsequent episodes of paralysis.…”

mentioning

confidence: 95%

“…1 Important ECG features that suggest a diagnosis of THPP center on the triad of resting sinus tachycardia attributable to the hyperadrenergic state, prolonged QT-U intervals attributable to hypokalemia, and a paradoxically prolonged PR interval that might be attributable to thyrotoxicosis (sinus tachycardia is usually associated with relatively short PR intervals). [3][4][5] Increased QRS voltage also has been reported in association with THPP, but it is a relatively nondiagnostic finding in young adult men. 5 Early recognition of these ECG markers in conjunction with the presentation of weakness may provide a valuable clue to the diagnosis of THPP before obtaining serum chemistries.…”

mentioning

confidence: 96%

“…[3][4][5] Increased QRS voltage also has been reported in association with THPP, but it is a relatively nondiagnostic finding in young adult men. 5 Early recognition of these ECG markers in conjunction with the presentation of weakness may provide a valuable clue to the diagnosis of THPP before obtaining serum chemistries. In this way, the ECG can prevent a key error in the management of THPP-namely, the overly aggressive repletion of potassium that can lead to rebound hyperkalemia and potentially fatal conduction disturbances.…”

mentioning

confidence: 96%

See 1 more Smart Citation

An Electrocardiogram Triad in Thyrotoxic Hypokalemic Periodic Paralysis

Goldberger

2007

Circulation

View full text Add to dashboard Cite

A 37-year-old Asian man presented to the emergency department with acute onset of bilateral lower-extremity weakness. Physical examination was notable for marked reduction in proximal muscle strength, with decreased deep tendon reflexes. Initial laboratory tests showed a potassium level of 1.3 mEq/L (normal range, 3.7 to 5.2 mEq/L), thyroid-stimulating hormone level Ͻ0.03 IU/mL (normal range, 0.4 to 5.0 IU/mL), total thyroxine of 21.8 g/dL (normal range, 4.8 to 10.8 g/dL), and free thyroxine level of 5.7 ng/dL (normal range, 0.8 to 1.8 ng/dL). The 12-lead ECG taken immediately after presentation was notable for sinus tachycardia, first-degree atrioventricular conduction delay, ST depressions, and prolonged T/U segments ( Figure 1).The patient was given 40 mEq of intravenous potassium chloride along with 60 mEq of oral potassium. Shortly afterward, his potassium was noted to be 6.7 mEq/L. The repeat ECG at that time showed peaked T waves in leads V 2 and V 3 . The potassium level normalized with the administration of sodium polystyrene.Thyrotoxic hypokalemic periodic paralysis (THPP) is characterized by transient, reversible episodes of muscle weakness and often profound hypokalemia. The disease is relatively uncommon in the United States and is reported primarily in men of Asian descent. 1,2 Hypokalemia is attributable to large shifts of potassium from the extracellular to the intracellular compartment that are presumably caused by increased Na/K ATPase pump activity associated with the hyperadrenergic, hyperthyroid state. 1 Important ECG features that suggest a diagnosis of THPP center on the triad of resting sinus tachycardia attributable to the hyperadrenergic state, prolonged QT-U intervals attributable to hypokalemia, and a paradoxically prolonged PR interval that might be attributable to thyrotoxicosis (sinus tachycardia is usually associated with relatively short PR intervals). [3][4][5] Increased QRS voltage also has been reported in association with THPP, but it is a relatively nondiagnostic finding in young adult men. 5

show abstract

“…Findings supportive of a diagnosis of TPP are sinus tachycardia, elevated QRS voltage and firstdegree AV block (sensitivity 97%, specificity 65%). 3 The exact pathophysiology of TPP is unknown. Thyroid hormone itself has a direct effect in stimulating the sodiumpotassium-adenosinetriphophatase (Na-K-ATPase) pump.…”

mentioning

confidence: 99%

Acute generalized weakness due to thyrotoxic periodic paralysis

Barnabé

2005

Canadian Medical Association Journal

View full text Add to dashboard Cite

Electrocardiographic Manifestations in Patients with Thyrotoxic Periodic Paralysis

Cited by 64 publications

References 27 publications

Thyrotoxic Periodic Paralysis

Thyrotoxic Periodic Paralysis

An Electrocardiogram Triad in Thyrotoxic Hypokalemic Periodic Paralysis

Acute generalized weakness due to thyrotoxic periodic paralysis

Contact Info

Product

Resources

About