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| CASE REPORT |
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| Year : 2019 | Volume
: 9
| Issue : 4 | Page : 199-202 |
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A rare case of hypokalemic ventricular tachycardia in a patient with thyrotoxic periodic paralysis
Bader Abu Ghalyoun1, Ibrahim Khaddash1, Dema Shamoon1, Hamid Shaaban2, Michael Hanna1, Satish Tiyyagura1, Mourad Ismail3
1 Department of Cardiology, St. Joseph's Regional Medical Center, Affiliate of New York Medical College of Medicine, Paterson, Newark, NJ, USA
2 Department of Internal Medicine, St. Michael's Medical Center, Affiliate of New York Medical College of Medicine, Newark, NJ, USA
3 Department of Critical Care, St. Joseph's Regional Medical Center, Affiliate of New York Medical College of Medicine, Paterson, Newark, NJ, USA
| Date of Submission | 31-May-2017 |
| Date of Decision | 14-Aug-2019 |
| Date of Acceptance | 20-Sep-2019 |
| Date of Web Publication | 11-Dec-2019 |
Correspondence Address:
Dr. Hamid Shaaban
111 Central Avenue, Newark, NJ
USA
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/IJCIIS.IJCIIS_39_17
 Abstract | | |
Thyrotoxic periodic paralysis (TPP) is a potentially fatal complication of hyperthyroidism, characterized by recurrent muscle paralysis and hypokalemia. We present a case of a 32-year-old apparently healthy male patient, who presented with acute paraparesis associated with hypokalemia (K: 1.6 mmol/L), complicated by ventricular tachycardia (VT). Advanced cardiac life support was initiated with an amiodarone infusion, and eventually QRS complex narrowed and wide complex tachycardia resolved. Intravenous potassium chloride (KCl) 40 mEq over 2–3 h and oral KCL 40 mEq were administered to treat the electrolyte imbalance. Patient paralysis was quickly reversed; motor function was regained with movement of the lower extremities. This case highlights the importance of early recognition and prompt treatment of TPP as a differential diagnosis for muscle weakness, especially in the setting of severe hypokalemia. It is important to pay attention to the possibility of the development of lethal VT associated with hypokalemia in the setting of hyperthyroidism and thyrotoxic paralysis.
Keywords: Hypokalemia, paralysis, thyrotoxicosis, ventricular tachycardia
How to cite this article:
Ghalyoun BA, Khaddash I, Shamoon D, Shaaban H, Hanna M, Tiyyagura S, Ismail M. A rare case of hypokalemic ventricular tachycardia in a patient with thyrotoxic periodic paralysis. Int J Crit Illn Inj Sci 2019;9:199-202 |
How to cite this URL:
Ghalyoun BA, Khaddash I, Shamoon D, Shaaban H, Hanna M, Tiyyagura S, Ismail M. A rare case of hypokalemic ventricular tachycardia in a patient with thyrotoxic periodic paralysis. Int J Crit Illn Inj Sci [serial online] 2019 [cited 2023 Mar 25];9:199-202. Available from: https://www.ijciis.org/text.asp?2019/9/4/199/272767 |
| Introduction | |  |
Thyrotoxic periodic paralysis (TPP) is a condition that appears at an incidence of 2% in patients with thyrotoxicosis, commonly in males of Asian descent, yet not limited to these ethnic groups.[1],[2] It occurs as acute episodes of muscle weakness associated with hypokalemia, which resolves once the hypokalemia is treated and is usually precipitated by exercise, carbohydrate load, or stress. In addition to the paralysis, complications resulting from TPP include arrhythmias, respiratory problems, especially hypercapnic respiratory failure, and death.[2] A dangerous risk factor that leads to ventricular tachycardia (VT) is hypokalemia and must be corrected immediately.[3],[4],[5],[6] Hypokalemia prolongs repolarization and increases the slope of diastolic depolarization of automatic cells leading to tachycardia.[5] In patients with hyperthyroidism, an increase in thyroid hormones influences catecholamine binding and decreases activation at the tissue receptor site.[2] Although the pathophysiology of TPP is multifactorial and unclear, hypokalemia contributes to the development of paralysis in addition to VT.[4],[5],[6] In this case report, we discuss a patient with hyperthyroidism that presented with acute paralysis and VT due to profound hypokalemia.
| Case Report | | |
A 32-year-old male without any significant medical history presented to the emergency department (ED) with complaints of lower back pain, weakness in the legs, and gait disturbance. The weakness was gradual, started 3 h before coming to the hospital, and ascended to involve bilateral upper extremities. He also had four episodes of nonbloody, nonbilious emesis. The patient denied any similar previous events. Upon further questioning, he reported a 15 pound unintentional weight loss since he did landscaping a month ago. Vitals on presentation showed a blood pressure of 148/70 and heart rate of 107 beats/min. The patient had a body mass index of 28.72 kg/m2. On physical examination, motor strength was 2/5 in both upper and lower extremities, and the patient was only able to move the digits of the hands and feet. Sensory examination was benign, upper extremities deep-tendon reflexes (DTR) were 1/4 bilaterally, knee DTRs were 1/4, and ankle DTRs were 0/4. On cardiovascular examination, the patient was tachycardic but regular without murmurs or gallops and cranial nerves were intact without facial muscle weakness. He denied any dyspnea, chest pain, palpitations, diaphoresis, and heat intolerance. He did not have a previous illness or gastrointestinal symptoms before the episodes. Past medical, family, and social history were unremarkable.
Initially, in the ED, orthopedics was consulted, and a magnetic resonance imaging of the lumbar spine was completed; the results were not significant. Due to the progression in the weakness, neurology was also consulted for a possible workup of Guillain–Barre syndrome.
Electrocardiography (ECG) [Figure 1] showed a wide complex tachycardia consistent with VT. Advanced cardiac life support was initiated with an amiodarone infusion, and eventually QRS complex narrowed [Figure 2] and wide complex tachycardia resolved. Laboratory values revealed a potassium level of 1.6 mEq/L (reference range: 3.5–5.0 mEq/L), phosphorus level of 1.7 mg/dL (reference range: 2.5–5.0 mg/dL), and magnesium level of 1.6 mg/dL (reference range: 1.7–2.5 mg/dL). Critical care team was consulted, and the patient was admitted to the intensive care unit. Intravenous potassium chloride (KCl) 40 mEq over 2–3 h and oral KCL 40 mEq were administered to treat the electrolyte imbalance. Patient paralysis was quickly reversed; motor function was regained with movement of the lower extremities. Electrocardiogram was repeated [Figure 3]. The patient was able to ambulate on his own and with assistance of physical therapy, his strength was 5/5 in all extremities, and he regained normal DTR. | Figure 1: First electrocardiogram on arrival showing ventricular tachycardia, spontaneously resolved in a few minutes though amiodarone was given
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 | Figure 2: Second electrocardiogram: K+ is 1.6 after the resolution of the ventricular tachycardia, showing the findings of hypokalemia
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 | Figure 3: Third electrocardiogram after the correction of the hypokalemia and resolution of the paralysis
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Thyroid profile revealed that the patient had hyperthyroidism with a thyroid-stimulating hormone of 0.018 micro-international units/mL (reference range: 0.35–5.60 micro international units/mL); thyroxin (T4) level of 18.4 μg/dL (reference range: 4.5–10.9 μg/dL); and triiodothyronine (T3) of 2.52 ng/mL (reference range: 0.60–1.81 ng/mL). After the correction of the hypokalemia and paralysis and obtaining the results of the thyroid profile, the patient was started on methimazole 20 mg BID, propranolol 20 mg BID, and decadron 2 mg Q8 h; however, his potassium was overcorrected to 6.1. The patient was eventually stabilized and discharged home on medical therapy with planned outpatient follow-up.
| Discussion | | |
TPP, a state in which proximal, symmetrical ascending muscle weakness in lower extremities occurs in hyperthyroid patients, is a multifactorial condition that involves hypokalemia and a hyperadrenergic state.[1],[2],[7] Pathogenesis still remains unclear, but it is known that a high amount of thyroid hormone present in the body leads to an increased activation and stimulation of channels and genes on the myocardium. Thyrotoxicosis leads to more binding and decreased inactivation of hormones at receptor sites located on tissues, commonly beta-2 adrenergic receptors on muscle cells.[2] Due to an increased activation of catecholamines, the Na+/K+-ATPase activity is over stimulated, leading to a state of low potassium from intracellular shift. Muscles are unable to depolarize and function properly, leading to a state of transient muscle weakness. Na+/K+-ATPase is affected by thyroid hormones as well as insulin. Therefore, symptoms are usually seen in the morning hours or at rest while after an intense work out and a high-carbohydrate meal.[1] Multiple differential diagnoses for weakness could be neuromuscular junction diseases such as myasthenia gravis and botulism, spinal cord diseases such as poliomyelitis, polyneuropathies like Guillain–Barre syndrome, and primary acute myopathies such as electrolyte abnormalities, myoglobinuria, and alcoholic myopathy.[2]
It has been shown that with a new onset of hyperthyroidism that presents with paralytic attacks, it is rarely associated with the typical findings normally seen with hyperthyroidism.[1],[7] In the patient presented, typical hyperthyroid symptoms such as palpitations, diarrhea, and heat intolerance were not evident, allowing TPP to be overlooked. Instead, muscle weakness and emesis were the first symptoms of a newly diagnosed hyperthyroidism.
Laboratory values that can be typically seen in a patient with TPP are hypokalemia, hypophosphatemia, and hypomagnesemia.[8],[9],[10],[11] In a study by Manthri, he evaluated the incidence and prevention of TPP in patients who were undergoing radioiodine therapy for hyperthyroidism. Forty-four patients of 100 hyperthyroid patients that did not receive potassium supplementation presented with generalized muscle weakness and one patient died from ventricular arrhythmia with ECG changes consistent with hypokalemia.[7]
VT presenting in patients with hyperthyroidism is a dangerous complication that is not commonly reported in literature. The coupling of cardiac arrhythmias and thyrotoxicosis is more so seen in patients with preexisting cardiac disease.[4] Cases that have been reported include a 4-year-old boy with febrile convulsions,[12] a 34-year-old woman presenting with thyrotoxicosis and cardiac arrest after VT,[12] a patient developing thyroid storm associated VT during surgery,[12] and a 57-year-old female with sustained VT due to hyperthyroidism secondary to iodine overload.[12]
Physiologically, thyroid hormones, T3 and T4, affect regulatory and structural genes in cardiac myocytes, and more importantly, binding of T3-receptor complexes to DNA regulates gene expression of calcium cycling to control cardiac myocyte contraction.[5] In addition, thyroid hormones regulate calcium uptake into the sarcoplasmic reticulum during diastole through the sarcoplasmic reticulum Ca2+-ATPase and phospholamban.[5] Although thyroid hormones play an important role in the action potential and repolarization of cardiac myocytes, the predilection to tachyarrhythmias is multifactorial and is still suspected to be due to a hyperadrenergic and hypokalemic state.[8],[9],[10],[11]
Hypokalemia can be the cause of torsades de pointes or polymorphic VT, a form of VT, which leads to ventricular fibrillation and death if untreated.[4] As stated before, hypokalemia delays repolarization and increases diastolic depolarization of pacemaker fibers, leading to tachycardia, increasing the likelihood of ectopic beat formation.[5] It increases the resting membrane potential as well as the duration of the action potential and the refractory period.[13] The increase in automaticity predisposes the myocardium to arrhythmias.[13] The typical electrocardiographic pattern of hypokalemia consists of prominent U-waves >1 mm and U-waves greater than T-waves in the same lead with associated ST-segment depression (sometimes with inversion of T-waves).[5],[13] However, when potassium levels are dangerously low, hypokalemic ECG findings can be missed. In our patient, a wide complex tachycardia was the initial ECG finding. Immediate defibrillation is required in life-threatening, unstable VT; however, in stable patients, the therapy is to correct the underlying cause. Rebound hyperkalemia is an important complication in TPP treatment and requires a slow rate of potassium correction and close monitoring of serum levels.
| Conclusion | | |
We present a patient with hyperthyroidism and hypokalemia both contributing to the development of a wide complex tachycardia. The treatment of hyperthyroid-associated VT is with beta-blockers and antiarrhythmic medications. Perchlorate can be used in cases of iodine overload. This case illustrates the association among hypokalemia, hyperthyroidism, and cardiac arrhythmias.
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. The authors followed applicable EQUATOR Network (http://www.equator-network.org/) guidelines during the preparation of this report.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]
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