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Table of Contents
CASE REPORT
Year : 2022  |  Volume : 13  |  Issue : 1  |  Page : 64-66

Acute flaccid quadriparesis: An uncommon presentation of common disease


1 Department of Medicine, Kasturba Medical College, MAHE, Manipal, Karnataka, India
2 Department of Infectious Disease, Kasturba Medical College, MAHE, Manipal, Karnataka, India

Date of Submission23-Jul-2021
Date of Decision21-Sep-2021
Date of Acceptance21-Sep-2021
Date of Web Publication19-Jan-2022

Correspondence Address:
Dr. B Nandakrishna
Department of General Medicine, Kasturba Hospital, Madhav Nagar, Manipal - 576 104, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/injms.injms_85_21

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  Abstract 


Acute flaccid quadriparesis is a common presentation to the emergency department with multiple etiologies such as paralytic snakebite, Guillain–Barre Syndrome, and periodic paralysis. Periodic paralysis is a rare entity where the patient presents with weakness, proximal more than distal. The cause for periodic paralysis may vary from hypokalemia to thyrotoxicosis. Thyrotoxicosis commonly presents with weight loss, heat intolerance, tachycardia, and nonspecific symptoms such as fatigue and diarrhea. Neurologic manifestations such as thyroid eye disease and proximal myopathy are commonly seen with Grave's disease. We present a case of 24-year-old male presenting with acute onset weakness of both lower limbs and found to have low potassium. Thyrotoxic periodic paralysis was diagnosed from clinical and investigation findings. Weakness improved with potassium supplementation. Hyperthyroidism was treated with carbimazole and propranolol.

Keywords: Grave's disease, periodic paralysis, quadriparesis


How to cite this article:
Sharma VC, Nandakrishna B, Vidyasagar S, Varma M. Acute flaccid quadriparesis: An uncommon presentation of common disease. Indian J Med Spec 2022;13:64-6

How to cite this URL:
Sharma VC, Nandakrishna B, Vidyasagar S, Varma M. Acute flaccid quadriparesis: An uncommon presentation of common disease. Indian J Med Spec [serial online] 2022 [cited 2022 Oct 2];13:64-6. Available from: http://www.ijms.in/text.asp?2022/13/1/64/335973




  Introduction Top


Thyrotoxic periodic paralysis (TPP) is a rare entity, presenting more commonly in males when compared to female patients. It can present with acute onset of proximal muscle weakness, with features of thyrotoxicosis such as palpitations and weight loss and has been associated with severe hypokalemia. Hence, it is important to look for the features of thyrotoxicosis in patients presenting with proximal muscle weakness to diagnose TPP as its management potentially reverses the weakness in the patients.


  Case Report Top


A 27-year-old male with no known premorbidities presented with complaints of acute onset progressive bilateral upper and lower limb weakness of 1-day duration. His vitals showed a pulse rate of 106 bpm with regular rhythm, blood pressure 132/78 mmHg, respiratory rate of 12/min, and SpO2 of 100% at room air. Motor power was 1/5 (Medical Research Council [MRC]) in the lower limbs and 3/5 MRC in the upper limbs. Cranial nerve examination was normal, and all deep tendon reflexes were elicited. Sensory system examination was normal. There was no respiratory muscle involvement. General physical examination revealed diffuse nontender thyroid swelling with no bruit as shown in [Figure 1]. Eye signs such as exophthalmos, lid lag, and swelling were absent.
Figure 1: Butterfly-shaped diffuse swelling of thyroid gland

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His serum potassium was low, 2.7 mmol/L. Renal function tests, liver function tests, venous bicarbonate, and hemogram were normal. Electrocardiogram (ECG) done showed PR prolongation and U waves suggestive of hypokalemia [Figure 2]. A diagnosis of hypokalemic paralysis was made. Considering clinical findings, a thyroid function test was done, which showed low serum TSH (0.013 micro IU/L) with raised free T3 and T4 (28.27 ng/ml and 7.77 mcg/ml, respectively) suggesting hyperthyroidism. A Tc99 thyroid scan revealed diffuse thyroid uptake suggestive of Grave's disease [Figure 3].
Figure 2: Electrocardiogram showing diffuse T-wave flattening and U waves (red arrow) suggestive of hypokalemia

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Figure 3: Tc-99 pertechnetate scan showing B/L diffuse uptake of the thyroid gland

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He was treated with oral and intravenous potassium replacements. Motor power normalized with it, and ECG changes reverted to normal as shown in [Figure 4]. Repeat potassium levels after the treatment was 3.8 mmol/L. He was treated with carbimazole 30 mg/day and propranolol for hyperthyroidism. He was discharged on potassium supplements and was advised regular follow-up.
Figure 4: Electrocardiogram showing normal T wave and disappearance of U wave after potassium correction

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  Discussion Top


It is important to keep hypokalemic paralysis in mind as a differential diagnosis when a patient comes with acute onset weakness of the limbs. Other causes for acute flaccid paralysis are Guillain-Barre Syndrome, neuroparalytic snake bite, and periodic paralysis. Guillain-Barre Syndrome is characterized by acute onset progressive ascending paralysis with absent reflexes. Facial nerve and respiratory muscle involvement may also be seen. Neuroparalytic snake bite typically presents with descending paralysis with ptosis being the first involvement. Hypokalemic paralysis is differentiated from these two by the absence of respiratory and ocular muscle involvement and preserved deep tendon reflexes. Hypokalemic paralysis can be inherited or acquired. The inherited form also called periodic paralysis typically presents from adolescence age. High carbohydrate diet or heavy exercise typically precipitates weakness. The acquired cause includes renal tubular acidosis, hyperthyroidism, and drug-induced hypokalemia.

The mechanism by which hyperthyroidism can produce hypokalemic periodic paralysis is not well understood. Thyroid hormone sensitizes sympathetic action on beta-adrenergic receptors of skeletal muscle. This drives potassium into the intracellular compartment through sodium-potassium ATPase receptors ensuing hyperpolarization of the muscle membrane and the onset of weakness.[1],[2]

While patients with thyrotoxic PP do not have the genetic mutations associated with familial hypokalemic PP, it has been suggested that individuals who are susceptible to thyrotoxic PP may have an ion channel defect, which, in the euthyroid state, is not sufficient to produce symptoms. In a study, it was found that patients with TPP have a mutation in the inward correcting potassium channel, Kir 2.6 which is regulated transcriptionally by thyroid hormone.[3] In another study, it was found that the expression of this gene was reduced during thyrotoxicosis and restored in euthyroid stated in patients with TPP.[4]

Hyperthyroidism commonly presents with weight loss and increased appetite, tremors, hair loss, and heat intolerance. Cardiac manifestations such as tachycardia, atrial fibrillation, and heart failure are common in elderly. Neurologic manifestations commonly seen are thyroid eye disease, and proximal myopathy is commonly seen with Grave's disease. TPP is a relatively rare entity seen only in 2% of cases in the Asian population as per studies.[5],[6] TPP is commonly seen in males, although most thyroid disorders are common in women.[7],[8] As reported in the literature, over 95% of thyrotoxic PP cases occur in men.[9]

In an acute setting, the correction of potassium levels by either oral or intravenous supplements usually reverses the paralysis. Rebound hyperkalemia should be kept in mind while correcting potassium which is due to the release of potassium from the cells and hence close monitoring of potassium levels is essential. Nonselective beta-blockers have been used to terminate the neuromuscular symptoms and prevention of further attacks as they reduce the intracellular shift of potassium. Achieving a euthyroid state is essential in preventing further attacks of periodic paralysis. Depending on the underlying etiology, patient should be put on antithyroid drugs or may require a radioiodine ablation or surgery. In patients of TPP secondary to Grave's disease, treatment with radioiodine ablation was found to be more effective in preventing relapses when compared to antithyroid drugs.[10]

In our case, patient presented with acute onset weakness of both upper and lower limbs, predominantly proximal muscles. Age of presentation and the absence of high carbohydrate intake preceding weakness were pointers against the inherited form of periodic paralysis. Clinical examination, thyroid function tests, and a thyroid scan confirmed Grave's disease. Potassium correction improved symptoms. He was treated with carbimazole and propranolol and potassium supplements and discharged on improvement.


  Conclusion Top


It is important to consider periodic paralysis as a differential when a patient presents with acute onset weakness as the correction of the underlying abnormality will drastically improve the symptoms and also prevents investigations which may not be required. Thyrotoxicosis as a cause for hypokalemia causing periodic paralysis should be kept in mind.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

None.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Rhee EP, Scott JA, Dighe AS. Case 4-2012: A 37-year-old man with muscle pain, weakness, and weight loss. N Engl J Med 2012;366:553-60.  Back to cited text no. 1
    
2.
Chan A, Shinde R, Chow CC, Cockram CS, Swaminathan R. In vivo and in vitro sodium pump activity in subjects with thyrotoxic periodic paralysis. BMJ 1991;303:1096-9.  Back to cited text no. 2
    
3.
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. 3
    
4.
Melo MC, de Souza JS, Kizys MM, Vidi AC, Dorta HS, Kunii IS, et al. Novel lincRNA susceptibility gene and its role in etiopathogenesis of thyrotoxic periodic paralysis. J Endocr Soc 2017;1:809-15.  Back to cited text no. 4
    
5.
Ober KP. Thyrotoxic periodic paralysis in the United States. Report of 7 cases and review of the literature. Medicine (Baltimore) 1992;71:109-20.  Back to cited text no. 5
    
6.
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. 6
    
7.
Vijayakumar A, Ashwath G, Thimmappa D. Thyrotoxic periodic paralysis: Clinical challenges. J Thyroid Res 2014;2014:649502.  Back to cited text no. 7
    
8.
Chaudhry MA, Wayangankar S. Thyrotoxic periodic paralysis: A concise review of the literature. Curr Rheumatol Rev 2016;12:190-4.  Back to cited text no. 8
    
9.
Ko GT, Chow CC, Yeung VT, Chan HH, Li JK, Cockram CS. Thyrotoxic periodic paralysis in a Chinese population. QJM 1996;89:463-8.  Back to cited text no. 9
    
10.
Chang RY, Lang BH, Chan AC, Wong KP. Evaluating the efficacy of primary treatment for Graves' disease complicated by thyrotoxic periodic paralysis. Int J Endocrinol 2014;2014:949068.  Back to cited text no. 10
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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