|Year : 2013 | Volume
| Issue : 3 | Page : 114-115
Thyrotoxicosis presenting first time as hypokalemic paralysis
ZD Sharma, VS Gokhale, N Chaudhari, AL Kakrani
Department of Medicine, Padm. Dr. D.Y. Patil Medical College and Research Hospital, Pimpri, Pune, India
|Date of Web Publication||6-Aug-2013|
Z D Sharma
Department of Medicine, Padm. Dr. D.Y. Patil Medical College and Research Hospital, Sant Tukaram Nagar, Pimpri, Pune - 18
Source of Support: None, Conflict of Interest: None
Thyrotoxicosis has varied manifestations, from its usual to rare presentations. Thyrotoxicosis presenting as acute quadriplegia is a very rare phenomenon and is attributed to hypokalemia. Thyrotoxic hypokalemic periodic paralysis is known but rare manifestation and as a first presentation is relatively unknown. Here, we present a case of young male in whom thyrotoxicosis presented for the first time as hypokalemic paralysis.
Keywords: Hyperthyroidism, hypokalemic periodic paralysis, thyrotoxicosis, quadriplegia
|How to cite this article:|
Sharma Z D, Gokhale V S, Chaudhari N, Kakrani A L. Thyrotoxicosis presenting first time as hypokalemic paralysis. Thyroid Res Pract 2013;10:114-5
|How to cite this URL:|
Sharma Z D, Gokhale V S, Chaudhari N, Kakrani A L. Thyrotoxicosis presenting first time as hypokalemic paralysis. Thyroid Res Pract [serial online] 2013 [cited 2022 Aug 18];10:114-5. Available from: https://www.thetrp.net/text.asp?2013/10/3/114/116132
| Introduction|| |
Thyrotoxicosis presenting first time as hypokalemic periodic paralysis (HPP) is a rare entity. It is much more common in patients of Asian descent as compared to western population. It may present as rapidly evolving quadriplegia and lead to a diagnostic dilemma for the physicians. Here, we report of case of thyrotoxicosis presenting first time as HPP in a young male who previously had no history of thyroid disease.
| Case Report|| |
A 27-year-old male patient resident of Maharashtra, India presented to the Emergency Department with complains of mild fever and weakness of all four limbs since 1 day. The fever was mild, continuous without chills, and rigors. The fever resolved on its own by evening. Next day at 4 am, patient tried to get up from sleep to pass urine and realized that he is not able to move his legs. He also could not move side to side in bed. At this time, patient could move his arms. This weakness progressed within hours, so that patient could not move his arms as well. There was no history of loss of consciousness, seizures, regurgitation of food, diplopia, facial deviation, and bladder or bowel involvement. There was no history of trauma or respiratory difficulty. Furthermore, there was no history of sensory symptoms in the patient. The patient gave no history of any addictions, or any major illness in the past.
On examination, the patient had tachycardia with pulse of 108/m, BP - 140/60 mmHg with pulse pressure of 80 mmHg. Respiratory rate was 20 breathes/min and patient was maintaining his oxygen saturation at room air. There was no neck swelling.
On neurological examination, the patient was conscious, oriented and normal higher mental functions. There was no cranial nerve involvement. Patient had hypotonia with power of 2/5 in all muscles groups at all joints. Deep tendon reflexes were diminished and superficial reflexes were present. Plantars were bilaterally flexors. There were no cerebellar signs or signs or raised intracranial tension. Cardiovascular examination revealed a pan systolic murmur at the apex. There were no other signs.
On investigations, the hemogram, Liver function tests LFT, renal function test RFT were normal. Serum potassium was found to be 2.6 meq/l, and serum sodium - 139 meq/l. Serum calcium and serum magnesium were found to be normal. Further, investigations were aimed at finding the cause of hypokalemia.
Urinary pH and electrolytes were normal, thus ruling out renal tubular acidosis as a cause. Thyroid function test revealed a low thyroid stimulating hormone TSH of <0.01 μIU/ml. T4 was found to be 11.92 μg/dl. T3 was normal at 1.04 ng/ml. Anti-thyroid peroxidase TPO antibody was found to be positive. From history gastrointestinal causes, familial hypokalemic paralysis and chronic diuretic use was excluded. The patient was negative for HIV and HbsAg. Chest X-ray and ultrasound of the abdomen did not reveal any abnormalities. ECG revealed sinus tachycardia.
The above tests along with clinical signs of a hyper-dynamic state confirmed the diagnosis of Thyrotoxicosis. With no past history this was the first presentation of the illness.
The patient was immediately started on intravenous potassium replacement. The patient gradually improved over next 12 h and regained full power in 24 h. The pulse pressure also normalized and the pan systolic murmur reduced in intensity. His potassium was 3.9 meq/dl at the time of discharge.
A final diagnosis of thyrotoxic hypokalemic periodic paralysis (THPP) was made and patient discharged on tablets carbimazole, propranolol, and potassium supplements.
| Discussion|| |
Thyrotoxic periodic paralysis (TPP) is a serious and potentially lethal complication of thyrotoxicosis. The first case of THPP was described by Rossenfield in 1902.  It is a rare disorder that mainly affects the skeletal muscles. Smooth muscles are rarely involved; however, in severe attacks respiration may be effected. THPP is found more in males of Asian/oriental descent. The overall incidence of TPP in Chinese and Japanese thyrotoxic patients is 1.8% and 1.9%, respectively.  In North America, the incidence of hypokalemic paralysis in thyrotoxicosis is 0.1-0.2%.  The exact incidence of THPP is not known in Indian population.
In a retrospective study done at Sanjay Gandhi Post Graduate Institute SGPGI Lucknow, 52 patients presented as hypokalemic paralysis in 11 years, out of which only 9 were diagnosed as thyrotoxic periodic paralysis. 
Patients are mostly young males in 20-40 years of age group although, sporadic cases of THPP have also been reported in adolescents.  The proximal muscles are more involved than distal muscles. The attacks are characterized by transient episodes of weakness which range from mild muscle fatigue to complete flaccid paralysis. An attack commonly involves the lower limb initially and proceeds to involve the girdle and upper limbs as well. There is no sensory involvement. Although, patients present with tetraparesis that resembles other conditions such as Gullain-Barre syndrome, transverse myelitis, and acute spinal cord compression or hysteria, bowel and bladder function are never affected. Patients may experience recurrent episodes of weakness that last from a few hours up to 72 h, with complete recovery in between the attacks. There may also be prodromal symptoms of aches, cramps, and stiffness of the affected muscles. In the majority of patients, deep tendon reflexes are markedly diminished or absent, although some patients may have brisk or normal jerks, even during paralysis. 
Attacks are commonly precipitated by ingestion of carbohydrate-rich meals or sweet snacks, alcohol, or strenuous exercise. In these patients the paralysis can be induced by a high glucose load, insulin infusion, and exercise test. The weakness does not occur during exercise but during the resting period after exercise and may be aborted by resumption of the exercise. 
It is important to know that even though in acute attacks serum potassium levels are low, the total body potassium remains normal.  Some genetic associations have been seen with THPP like HLA-DRw8 in Japanese population, ARBW22 and AW19B17 in Chinese, which may serve as a marker for the disease.
Definitive treatment consists of medical, surgical and radio-ablative therapy. During attacks potassium supplements are to be given with caution as in not to overcorrect. Heavy carbohydrate meals should be avoided. Beta blockers like propranolol can be used until patient reaches euthyroid state. Potassium sparing diuretics can also be used. Hyperthyroidism is usually subtle in these cases leading to delay in diagnosis and treatment. 
This article highlights the need of identification of THPP and testing patients for thyroid dysfunction in this clinical setting. Early testing and treatment can lead to better management and care for the patient and prevent future attacks, especially in Asian males presenting with periodic paralysis.
| References|| |
|1.||Paul B, Hirudayaraj P, Baig MW. Thyrotoxic periodic paralysis: An unusual presentation of weakness. Emerg Med J 2003;20:E7. |
|2.||Kung AW. Clinical review: Thyrotoxic periodic paralysis: A diagnostic challenge. J Clin Endocrinol Metab 2006;91:2490-5. |
|3.||Ober KP. Thyrotoxic periodic paralysis in the United States. Report of 7 cases and review of the literature. Medicine (Baltimore) 1992;71:109-20. |
|4.||Kalita J, Goyal G, Bhoi SK, Chandra S, Misra UK. Comparative study of thyrotoxic periodic paralysis from idiopathic hypokalemic periodic paralysis: An experience from India. Ann Indian Acad Neurol 2012;15:186-90. |
|5.||Balakrishnan RK, Chandran SR, Thirumalnesan G, Doraisamy N. Thyrotoxic periodic paralysis. Indian J Endocrinol Metab 2011;15:S147-149. |