Life-threatening hypokalemia associated with profound electrocardiographic manifestations in thyrotoxic periodic paralysis

Thyrotoxic periodic paralysis (TPP) is a rare muscular disorder, characterized by muscle weakness and hypokalemia triggered by thyrotoxicosis. In Asian populations, 2% of patients with thyrotoxicosis are affected, compared to only 0.1–0.2% of non-Asians. The vast majority of patients are male. Muscle weakness ranges in severity from very mild to life-threatening, due to respiratory compromise. We present a case of a previously healthy 39-year-old Hispanic male who presented with sudden quadriparesis and quickly recovered after being treated for hypokalemia and thyrotoxicosis. TPP, although unusual, is important to recognize as it is a potentially fatal condition that requires close monitoring and is readily reversible with appropriate therapy. Any cause of thyroid hormone excess can cause TPP, with Graves’ disease being the most common etiology. Acute treatment includes potassium repletion, while long-term management focuses on determining and treating the cause of thyrotoxicosis, since maintaining a euthyroid state will prevent further episodes of TPP.

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Thyrotoxic Periodic Paralysis—A Misleading Challenge in the Emergency Department

Diagnostics ◽

10.3390/diagnostics10050316 ◽

2020 ◽

Vol 10 (5) ◽

pp. 316 ◽

Cited By ~ 1

Author(s):

Stefana Bilha ◽

Ovidiu Mitu ◽

Laura Teodoriu ◽

Cristian Haba ◽

Cristina Preda

Keyword(s):

Clinical Signs ◽

Initial Therapy ◽

Periodic Paralysis ◽

The Other ◽

Motor Deficit ◽

Antithyroid Drugs ◽

Thyrotoxic Periodic Paralysis ◽

First Case ◽

Life Threatening ◽

Antithyroid Agents

Despite its’ life-threatening potential due to cardiac severe dysrhythmia in the context of severe hypokalemia, thyrotoxic periodic paralysis (TPP) often goes unrecognized. Although classically confined to young Asian men, it can occur irrespective of age, sex, and race. We report a short series of three cases of TPP as first presentation of Graves’ disease in a young Caucasian male and in two Caucasian elderly and middle-aged women, respectively. The first patient developed malignant ventricular arrhythmias due to severe hypokalemia and was defibrillated, with recovery after prompt potassium correction and administration of antithyroid agents and propranolol. The other two cases developed persistent hypokalemia despite adequate potassium chloride (KCl) repletion, with slow recovery of motor deficit and serum potassium normalization up to day 5. In the first case, long-term euthyroid state was achieved via total thyroidectomy due to the presence of a suspicious nodule that proved to be malignant. In the other two cases, medical treatment was the choice of therapy for thyrotoxicosis. None experienced recurrent TPP. Thyroid hormone evaluation is mandatory in the presence of hypokalemic paralysis, even in the absence of clinical signs of thyrotoxicosis. If TPP is confirmed, initial therapy should comprise antithyroid drugs and propranolol, besides hypokalemia correction.

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A Case of Nonfatal Ventricular Arrhythmia Due to Thyrotoxic Periodic Paralysis in a Saudi Patient as an Initial Presentation of Graves’ Disease

Clinical Medicine Insights Case Reports ◽

10.4137/ccrep.s34560 ◽

2016 ◽

Vol 9 ◽

pp. CCRep.S34560 ◽

Cited By ~ 1

Author(s):

Osamah Hakami ◽

Maswood M. Ahmad ◽

Naji Al Johani

Keyword(s):

Muscle Weakness ◽

Early Recognition ◽

Periodic Paralysis ◽

Graves Disease ◽

Thyrotoxic Periodic Paralysis ◽

Asian Populations ◽

Definitive Therapy ◽

Life Threatening ◽

Acute Paraparesis ◽

Saudi Male

Thyrotoxic periodic paralysis (TPP) is a potentially lethal complication of hyperthyroidism characterized by recurrent muscle weakness and hypokalemia. It has been commonly reported in non-Asian populations. Four cases were reported in Saudis so far, and one had a life-threatening arrhythmia. We describe an additional case of a 28-year-old apparently healthy Saudi male patient, who presented with acute paraparesis associated with hypokalemia (K: 2.0 mmol/L), complicated by ventricular tachycardia and cardiac arrest. He was successfully resuscitated and his hypokalemia was corrected. A diagnosis of Graves’ disease associated with TPP was made. He was initially treated with carbimazole and β-blockers and then given a definitive therapy with radioactive iodine, which showed a good response. This case highlights the importance of early recognition and prompt treatment of TPP as a differential diagnosis for muscle weakness. A brief review of TPP and associated arrhythmia is included.

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Disorders of potassium homeostasis

Oxford Textbook of Medicine ◽

10.1093/med/9780198746690.003.0474 ◽

2020 ◽

pp. 4748-4763

Author(s):

John D. Firth

Keyword(s):

Serum Potassium ◽

Potassium Concentration ◽

Periodic Paralysis ◽

Electrolyte Disorders ◽

Thyrotoxic Periodic Paralysis ◽

Serum Potassium Concentration ◽

Intravenous Insulin ◽

Nebulized Salbutamol ◽

Life Threatening ◽

Electrocardiogram Ecg

Hypokalaemia is defined as a serum potassium concentration lower than 3.5 mmol/litre and is the most common electrolyte abnormality seen in clinical practice, found in about 20% of hospital inpatients. Clinical features and investigation—mild hypokalaemia is asymptomatic, but nonspecific symptoms develop with more severe disturbance, and serious neuromuscular problems sometimes arise at serum potassium concentrations lower than 2.5 mmol/litre. Emergency management is rarely required, but intravenous infusion of potassium should be given in the rare circumstances of life-threatening cardiac arrhythmia or muscular paralysis. There are a very large number of possible causes of hypokalaemia, the most common causes being diuretics (particularly thiazides), vomiting, and diarrhoea. The most common genetic cause is Gitelman’s syndrome. Management is with potassium and magnesium supplements. Other causes of tubular wasting of potassium include Bartter’s syndrome and mineralocorticoid excess. There are several rare conditions in which hypokalaemia is associated with episodes of extreme weakness/paralysis, including thyrotoxic periodic paralysis and familial hypokalaemic periodic paralysis. Hyperkalaemia, defined as a serum potassium concentration of greater than 5.0 mmol/litre, is asymptomatic, and severe hyperkalaemia (>7 mmol/litre) is the most serious of all electrolyte disorders because it can cause cardiac arrest. The electrocardiogram (ECG) is the best guide to the significance of hyperkalaemia in any particular individual. Patients with ECG manifestations more severe than tenting of the T waves should be given intravenous calcium gluconate (10 ml of 10%) followed by intravenous insulin and glucose, or nebulized salbutamol. There are many causes of hyperkalaemia, but by far the most common are renal failure and/or drugs. Other causes include exhaustive exercise, acidosis, drugs, and hyperkalaemic periodic paralysis (very rare).

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Thyrotoxic periodic paralysis complicated by life-threatening acute hypercapnic respiratory failure in a Chinese male with painless thyroiditis

The American Journal of Emergency Medicine ◽

10.1016/j.ajem.2018.11.010 ◽

2019 ◽

Vol 37 (2) ◽

pp. 379.e1-379.e3 ◽

Cited By ~ 1

Author(s):

Yan-Ying Qian ◽

Zhi-Juan Dai ◽

Cong Zhu ◽

Yao-Xin Zhu ◽

Chao-Ming Wu

Keyword(s):

Respiratory Failure ◽

Periodic Paralysis ◽

Thyrotoxic Periodic Paralysis ◽

Hypercapnic Respiratory Failure ◽

Life Threatening ◽

Acute Hypercapnic Respiratory Failure ◽

Painless Thyroiditis ◽

Chinese Male

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Upper extremity deep venous thrombosis secondary to thyrotoxic periodic paralysis with accompanying hyperphosphatemia and severe hypomagnesemia

The Southwest Respiratory and Critical Care Chronicles ◽

10.12746/swrccc.v9i41.927 ◽

2021 ◽

Vol 9 (41) ◽

pp. 47-49

Author(s):

Jasmin Rahesh ◽

Layan Al-Sukhni ◽

Baseer Quraishi ◽

Tarek Naguib

Keyword(s):

Venous Thrombosis ◽

Deep Venous Thrombosis ◽

Upper Extremity ◽

Periodic Paralysis ◽

Central Catheter ◽

Thyrotoxic Periodic Paralysis ◽

Vein Thrombosis ◽

Life Threatening ◽

Characteristic Features ◽

Deep Vein

Thyrotoxic periodic paralysis is a rare but life-threatening complication of hyperthyroidism. Characteristic features involve thyrotoxicosis, acute paralysis, and hypokalemia. Mild hypomagnesemia and hypophosphatemia are also present in most cases due to the resulting transcellular shift of electrolytes. Complications of thyrotoxic periodic paralysis reported in the literature have included cerebral venous thrombosis as well as lower extremity deep venous thrombosis. We present a patient with an unusual presentation of thyrotoxic periodic paralysis as reflected by hyperphosphatemia, upper extremity deep venous thrombosis and severe hypomagnesemia. This is the first reported case of upper extremity deep vein thrombosis in association with a peripherally inserted central catheter line secondary to thyrotoxicosis.

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Evaluating the Efficacy of Primary Treatment for Graves’ Disease Complicated by Thyrotoxic Periodic Paralysis

International Journal of Endocrinology ◽

10.1155/2014/949068 ◽

2014 ◽

Vol 2014 ◽

pp. 1-6 ◽

Cited By ~ 4

Author(s):

Rita Yuk-Kwan Chang ◽

Brian Hung-Hin Lang ◽

Ai Chen Chan ◽

Kai Pun Wong

Keyword(s):

Radioactive Iodine ◽

Primary Treatment ◽

Periodic Paralysis ◽

Antithyroid Drugs ◽

Graves Disease ◽

Thyrotoxic Periodic Paralysis ◽

Term Efficacy ◽

Life Threatening ◽

Life Threatening Complication

Objective. Thyrotoxic periodic paralysis (TPP) is a potentially life-threatening complication of Graves’ disease (GD). The present study compared the long-term efficacy of antithyroid drugs (ATD), radioactive iodine (RAI), and surgery in GD/TPP.Methods. Sixteen patients with GD/TPP were followed over a 14-year period. ATD was generally prescribed upfront for 12–18 months before RAI or surgery was considered. Outcomes such as thyrotoxic or TPP relapses were compared between the three modalities.Results. Eight (50.0%) patients had ATD alone, 4 (25.0%) had RAI, and 4 (25.0%) had surgery as primary treatment. Despite being able to withdraw ATD in all 8 patients for 37.5 (22–247) months, all subsequently developed thyrotoxic relapses and 4 (50.0%) had ≥1 TPP relapses. Of the four patients who had RAI, two (50%) developed thyrotoxic relapse after 12 and 29 months, respectively, and two (50.0%) became hypothyroid. The median required RAI dose to render hypothyroidism was 550 (350–700) MBq. Of the 4 patients who underwent surgery, none developed relapses but all became hypothyroid.Conclusion. To minimize future relapses, more definitive primary treatment such as RAI or surgery is preferred over ATD alone. If RAI is chosen over surgery, a higher dose (>550 MBq) is recommended.

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