Thyrotoxicosis: an unusual cause of periodic paralysis (a case report from Tanzania)

¹The Aga Khan Hospital, Dar es Salaam, Tanzania

^&Corresponding author
Hussein Manji, The Aga Khan Hospital, Dar es Salaam, Tanzania

Introduction    

Thyrotoxic Periodic Paralysis (TPP) is a relatively rare presentation of patients to the Emergency Department, which involves muscle paralysis in a setting of acute hypokalemia in hyperthyroidism. There is no reported case of this disorder in Tanzania yet, and there is a paucity of reported cases of TPP in the African continent. This is a case of a 36-year-old gentleman who presented with a three-day history of weakness which progressed to paralysis of the limbs with no constitutional symptoms. He presented with normal vital signs and with diminished power and deep tendon reflexes in all limbs. The patient was found to have low potassium with elevated free T3 and low TSH. Thyroid ultrasound showed features consistent with diffuse autoimmune thyroiditis, likely Graves' disease. The patient was admitted with a diagnosis of electrolyte imbalance, specifically hypokalemia and hyperthyroidism. The patient was administered intravenous Potassium Chloride with an improvement of power in all extremities. Potassium therapy was continued, and antithyroid medications were also initiated. Patient had a resolution of all symptoms with regained power of 5/5 in all extremities and he regained his ability to walk. This case is reported to identify clues early for this rare but possible cause of paralysis, close the knowledge gap amongst physicians, and generate awareness on this diagnosis to allow appropriate management and definitive treatment to achieve a euthyroid state and ameliorate any major complications. The recognition will also contribute to the pool of cases and raise the index of suspicion amongst physicians.

Patient and observation     

A 36 years old Chinese gentleman presented to our accident and emergency department with generalized body weakness for three days that was insidious in onset and gradually progressive associated with an inability to walk and lift his upper limbs. He reported numbness and weakness in his lower limbs the previous day, which was initially distal and symmetrical and moved proximally, eventually involving upper limbs in the same pattern. He did not have any other constitutional symptoms or pertinent complaints. He was treated conservatively with IV fluids in a peripheral center before arrival to our hospital with no improvement. He is a chronic smoker but denied the use of alcohol. He did not have any associated comorbidities.

Clinical findings: vital signs on presentation included a respiratory rate of 20 breaths per minute with oxygen saturation of 98% on room air with a pulse rate of 140 beats per minute and blood pressure of 114/80 mmHg. The patient was conscious but restless with a Glasgow Coma score of 15/15. Physical examination revealed reduced power in the lower and upper extremities. Proximal muscles scored 0/5, and distal muscles had a score of 1/5. Deep tendon reflexes were diminished in all four limbs with preserved sensory function and a normal muscle tone. Meningeal irritation signs and upper motor neuron disorder signs were absent. There were no signs of goiter. Cardiovascular, abdominal and respiratory examinations were normal.

Diagnostic assessment: blood was drawn for lab investigations, and venous blood gas and ECG was done. The bedside blood glucose was 5.0 mmol/L. Venous Blood Gases (VBG) results showed pH of 7.3 with initial potassium of <2 mmol/l. The laboratory-confirmed a low potassium reading of 1.59 mmol/l. Thyroid function test results showed high free T3 of 34.83 pmol/l, T4 >100 pmol/l and low TSH < 0.005 uIU/ml. ECG (Figure 1) showed features of hypokalemia, i.e., flattened T waves, U-wave, and high QRS Voltage. Urine Electrolytes also showed a low potassium of 11.78 mmol/L (Table 1). Other lab results included a white blood cell count of 4.01 x 103 cells/mL, hemoglobin of 14.4g/dL and platelet count of 278000 cells/mL with an otherwise normal differential. Malaria was negative, Urinalysis was normal and C- reactive protein was 6.5. Renal function tests were within normal ranges with a blood urea nitrogen of 4.12 mmol/L and creatinine of 50.29 μmol/L. He had a sodium of 142.22, Chloride of 105.17, Magnesium of 0.81 and Calcium of 2.38. Thyroid ultrasound showed features consistent with diffuse autoimmune thyroiditis, likely Graves´ disease. He was given a provisional diagnosis of Thyrotoxicosis due to hyperthyroidism and electrolyte imbalance, specifically hypokalemia with differentials of Guillain-Barré syndrome, Transverse Myelitis and Poliomyelitis.

Therapeutic intervention: he was initiated on pharmacologic intervention and started on intravenous Potassium Chloride at ten mEq per hour. After 1 hour of treatment, the power in all extremities improved to 3/5. The patient was admitted to the Intensive Care Units (ICU) under the care of the Internal Medicine team.

Follow-up and outcomes: after admission, the patient was initiated on oral potassium chloride 40 mEq STAT dose and continued on intravenous potassium chloride at 10mEq per hour. After 9 hours, serum potassium levels reached 5.5 mmol/l. The patient had a resolution of all symptoms with regained power of 5/5 in all extremities and a regained ability to walk. Anti-thyroid medication was started with Propanol 40mg per oral daily and Carbimazole 20mg per oral twice daily. On the third day, the patient was transferred to the ward for further management but decided to leave against medical advice due to resolution of symptoms but complied to continue with propanol and carbimazole and attend the outpatient clinic for follow-up. He was discharged with a final diagnosis of TPP secondary to Graves´ disease. On discharge, there was resolution of serum potassium and urine potassium (Table 2).

Discussion     

This case report highlights TPP, which is often a missed diagnosis and the failure to recognize it leads to improper management of this condition. The strength of this case report is it helps detect a novelty diagnosis in our setting and provides a deeper and narrative understanding of an often missed and underappreciated diagnosis. The limitations include the lack of generalizability and focus on a relatively rare cause of lower limb paralysis with the risk for over-emphasizing the same diagnosis [1].

These patients often do not have obvious symptoms. Hence, clues are used collectively to attain this diagnosis, including the presentation in a male adult with no family history of paralysis, tachycardia, signs of hyperthyroidism, features and investigations suggestive of hypokalemia and typical acid-base and electrolyte findings such as normal blood acid-base state, hypokalemia with low urinary potassium excretion, hypophosphatemia associated with hypophosphaturia, and hypercalciuria [2].

One theory suggests that the 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. Following the reduction in extracellular potassium, the sarcolemma membrane depolarizes rather than hyperpolarizes. This paradoxical effect leads to the inactivation of sarcolemma sodium channels, causing the pathognomonic paralysis of skeletal muscles [1]. Another theory revolves around the loss of function mutations of the skeletal muscle-specific inward rectifying K+ (Kir) channel, Kir2.6 causing a vicious cycle of hypokalemia and paradoxical depolarization causing muscle paralysis [3].

There is global reporting of TPP with prevalence in the Asian community. Population mobility has contributed to the reported incidence in different countries all over the world and it is increasingly being seen in Western countries [4,5]. There is a paucity of such cases reported in Africa, although there have been incidences of TPP occurring amongst African Americans or native Africans too, as seen in cases reported in Senegal [6] and Somalia [7]. 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 [8].

Conclusion     

TPP typically occurs in a young Asian male patient though variations to this have been noted. Due to the paucity of cases in Africa and this being the first case reported in Tanzania, it is crucial to identify the clues early and close the knowledge gap amongst physicians and generate awareness on this diagnosis to allow appropriate management and definitive treatment to achieve a euthyroid state and ameliorate any major complications. Given that thyrotoxicosis is an established but relatively rare and underdiagnosed cause of paralysis; the recognition of this disease will contribute to the pool of cases and raise the index of suspicion amongst physicians.

Competing interests     

The authors declare no competing interests.

Authors' contributions     

Hussein Manji and Martin Ngonyani were both involved in the care of the patient directly with Martin Ngonyani attending to the patient and Hussein Manji supervising and overseeing the care. Both authors drafted the manuscript, contributed to the conception and design of this report. Martin Ngonyani developed the theoretical write-up and collected the information from the patient's records. Hussein Manji drafted and edited the manuscript and performed the critical revision of the report for publication purposes. Both authors were involved in the final approval for publication.

Tables and figure     

Table 1: laboratory results on initial presentation

Table 2: laboratory results on discharge

Figure 1: electrocardiogram (ECG) 12- lead

References