Thyrotoxic Periodic Paralysis Research Articles

Abstract #1004259: An Unusual Case Of Severe Hypokalemic Periodic Paralysis

Thyrotoxic Periodic Paralysis (TPP) is a disorder characterized by abrupt onset of hypokalemia and typically lower extremity paralysis secondary to thyrotoxicosis. Despite a higher incidence of hyperthyroidism in women, over 95 percent of TPP cases occur in men, with onset between 20-40 years of age. TPP has been most widely reported in Asian populations, in which the incidence among patients with hyperthyroidism is 2 percent. In non-Asian populations, this incidence is 0.1-0.2 percent.

Hypokalemic periodic paralysis: an underestimated autosomal-dominant disease with variable phenotypic presentations

Periodic paralysis (PP) diseases are autosomal dominant disorders due to gene-mutations that manifests with episodic muscle weakness and/or paralysis. Their mutations result in faulty ion-leaks that result in sustained muscle depolarization and inexcitability. The group include; hyperkalemic PP, hypokalemic PP (HypoPP type I & II), normokalemic PP, thyrotoxic PP, Paramyotonia congenita and Andersen-Tawil syndrome. The hypoPP is the most common disorder yet is underestimated in prevalence due to missed diagnosis mimicking hysterical disorders and neurological diseases as well as the hypokalemic syndromes (Bartter, Gitelman and renal tubular acidosis). Moreover, and due to their considerable gene-penetrance, their phenotypic spectrum ranges from infrequent attacks to progressive muscular failure. In this case report we present a patient with missed diagnosis for years and describe the algorithm of his diagnosis and management.
 Keywords: chanellopathies, diagnosis, hypokalemia, periodic paralysis, treatment.

A case of thyrotoxic periodic paralysis induced by super-stimulation of na–k–atpase in a competitive bodybuilder with thyrotoxicosis factitia.

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Thyrotoxic periodic paralysis presenting in an adult male from Cambodia: a case report

Thyrotoxic periodic paralysis presenting in an adult male from Cambodia: a case report

Thyrotoxic Periodic Paralysis in Young Caucasian Male

Abstract Background: Thyrotoxic periodic paralysis (TPP) can be a medical emergency as delay in diagnosis can lead to life-threatening arrhythmia. Periodic paralysis is more prevalent in the Asian population. We report a case of thyrotoxic periodic paralysis in a young Caucasian male. Case: A 24-year-old male with a past history of Graves’ disease, hypertension, and asthma was brought to the hospital due to leg weakness and fall. He was initially diagnosed with Graves’ disease 2 years ago. The patient could not take methimazole or metoprolol due to the affordability issue for the last 18 months. On presentation, he fell on the floor while attempting to stand up from the couch. He could not stand up or pick his cell phone. He remained on the floor for 2-3 hrs. A review of the system was positive for palpitation and fatigue and negative for diarrhea, weight loss, anxiety, sleep problem, and dry eyes. On arrival, he had a pulse of 100/min, BP of 157/85 mmHg with rest of vitals signs normal. Motor strength on bilateral lower extremities were 2/5. Upper extremity strength was normal. No thyromegaly or thyroid bruit was noted in the exam. The rest of the physical exam was normal. Labs showed Potassium 1.9 with a normal reference range (RR) of 3.5 - 5.1 mmol/l. His TSH was < 0.01 (RR 0.35 - 5.00 MCU/ML), Free T4 was 5.0 (RR 0.6- 1.6 NG/DL), Total T3 was 425 (RR 87 - 180 NG/DL) and CK was 70 (RR 35- 232 U/L). EKG showed sinus rhythm at 90 bpm with no PR, T/ST, or QT abnormalities. He was given IV potassium and was also started on methimazole 10mg TID and metoprolol. His weakness and tachycardia were improved the next day. We discussed with him the options of medical management vs. surgery. He underwent a total thyroidectomy. Biopsy showed nodular hyperplasia consistent with graves’ disease. Discussion: Thyrotoxic periodic paralysis (TPP) is characterized by hypokalemia and episode of acute muscle weakness in lower extremities in the setting of hyperthyroidism. The pathophysiology of TPP remains uncertain. Hyperthyroidism is a hyperadrenergic state in which beta-2-adrenergic stimulation in muscle cells directly induces cellular K+ uptake by increasing cAMP, leading to activation of Na/K ATPase. The increase in the influx of intracellular K+ leads to hypokalemia and skeletal muscle weakness. Some studies show pathophysiology can be different in Caucasians compared to the Asian population that there could be abnormalities in Na and K channels other than Na/K ATPase. Potassium replacement should be done with caution as hypokalemia is due to intracellular shift and rebound hyperkalemia is common during the management. Beta-blocker may reverse adrenergic overstimulation of Na/K ATPase. It can help rapidly improve paralytic symptoms.

A Case of Thyrotoxic Periodic Paralysis

Introduction: Thyrotoxic periodic paralysis (TPP) is an uncommon disorder characterized by simultaneous thyrotoxicosis, hypokalemia, and paralysis. It is a rare complication of hyperthyroidism with a prevalence of 1 in 100,000. It has a higher prevalence in young Asian males, with much fewer cases reported in Hispanic patients. The majority of cases are seen in hyperthyroidism due to Grave’s disease, however other causes of thyrotoxicosis have been associated with TPP. Hypokalemia occurs when thyroid hormone stimulates the sodium-potassium-ATP pump by binding to the thyroid response elements upstream of the genes for this pump, increasing its activity and thereby causing a transcellular shift of potassium into the intracellular fluid. Attacks usually begin with proximal muscle weakness of the lower extremities and may progress to tetraplegia, with the degree of muscle weakness corresponding to serum potassium levels. Interestingly, no correlations with serum T3 or T4 levels have been found.Clinical Case: A 38-year-old Hispanic man with a history of GERD presented to the emergency department with an inability to move his extremities. Initial labs were significant for profound hypokalemia to 2.0 mEq/L (3.5-5) and hyperthyroidism, with TSH<0.05 uU/mL (0.3-4.2) and free T4 2.4 ng/dL (0.6-1.5). Additional workup revealed a positive thyroid stimulating immunoglobulin and a positive thyrotropin binding inhibitor, and thyroid ultrasound demonstrated a hyperemic thyroid with numerous subcentimeter hypoechoic nodules, all of which was suggestive of Grave’s disease. His symptoms resolved with potassium repletion, suggesting thyrotoxic periodic paralysis secondary to hyperthyroidism. Upon further evaluation, the patient endorsed several months of hyperthyroid symptoms such as tremors, heat intolerance, and weight loss. He also endorsed alcohol use, a high carbohydrate diet, and recent life stressors, a combination of which likely precipitated his thyrotoxic periodic paralysis. He was discharged on methimazole 10 mg daily and propranolol 40 mg BID, with a decrease in his free T4 and improvement in his symptoms. He has been educated to avoid alcohol consumption and high-carbohydrate meals to avoid precipitating another episode of periodic paralysis, and once his hyperthyroidism is under better control he plans to undergo radioactive iodine ablation (RAI) for definitive management.Conclusions: Thyrotoxic periodic paralysis is a rare but dangerous complication of hyperthyroidism, and should be considered in the differential diagnosis when young individuals present with otherwise unexplained hypokalemia and paralysis. Acute management is potassium repletion, long term management involves treatment of thyrotoxicosis and avoiding precipitating factors, and definitive therapy is RAI or thyroidectomy.

A Case of Recurrent Paralysis and Low Potassium: Is It the Thyroid?

Introduction: Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism that is characterized by episodes of hypokalemia and acute weakness. Although hyperthyroidism is more common in females, over 95% of cases of TPP have been observed in males, especially in Asian males with an incidence of 2% among hyperthyroid patients. In non-Asian populations, the incidence in hyperthyroid patients is estimated to be around 0.1 to 0.2% [1]. We describe a case of TPP seen in a Hispanic male. Case Report: A 36-year-old Hispanic male with no past medical history presents with weakness in all extremities and difficulty breathing after consuming a carbohydrate heavy meal the night prior. He reports a recent, similar episode evaluated in another ER, which resolved after given potassium supplementation. He denied any vomiting, diarrhea, polyuria, diaphoresis, use of insulin or other medications, or any family history of paralysis.His labs were significant for hypokalemia of 1.9, TSH of <0.005 (0.358-3.740), free T4 of 2.22 (0.76-1.46), and total T3 of 2.7 (0.60-1.81). Thyroid stimulating immunoglobulin was 0.12 (0.0-0.55). His symptoms improved and potassium levels normalized following the administration of potassium chloride. He was discharged on propranolol and advised to follow up for further workup of his hyperthyroidism with radioactive iodine uptake scan. Discussion: Thyrotoxic periodic paralysis is a potentially life-threatening condition associated with cardiac arrhythmias and respiratory failure. Hyperthyroidism increases response to β-adrenergic stimulation, which increases activity of the sodium-potassium ATPase and causes hyperpolarization of skeletal muscle [2]. Hyperthyroid patients are prone to episodes of paralysis due to their increased susceptibility to the hypokalemic action of insulin, which activates the sodium-potassium ATPase pump, and epinephrine, which stimulates β-adrenoreceptors. Management of an acute attack of TPP includes potassium administration. In cases where paralysis and hypokalemia are not reversed, intravenous propranolol has been shown to resolve the attack by blocking the β-adrenergic receptors. Definitive treatment of TPP includes managing the hyperthyroid state with medical therapy, radioactive iodine therapy, or surgery. Until the euthyroid state is reached, a β-blocker can prevent episodes of acute paralysis. Avoidance of carbohydrate heavy meals, exercise, and stress are recommended as these factors can potentially exacerbate hypokalemia. In patient with acute paralysis, it is important to consider the diagnosis of TPP as this condition can be prevented once euthyroidism is achieved. Diagnosis and management will lead to prevention of morbidity and mortality associated with the hypokalemia.

Thyrotoxic Periodic Paralysis: A Rare Presentation of Graves’ Disease

Abstract Background: Thyrotoxic periodic paralysis (TPP) is a rare but serious thyroid emergency characterized by hypokalemia, acute onset flaccid paralysis &amp; thyrotoxicosis. Typically, seen in an Asian male with untreated hyperthyroidism symptoms, who awakens at night or in the early morning with flaccid ascending paralysis. This is precipitated by exercise, alcohol or carbohydrate rich meal. TPP is widely reported &amp; studied in Asian population. Its prevalence is about 2 % in Asian hyperthyroid patients. However, incidence is 0.1-0.2% in non-Asian hyperthyroid patients. Clinical Case: 33-year-old Caucasian male with celiac disease and no thyroid disease sought emergency care for complaints of sudden onset severe weakness in all extremities. He reported 20-pound unintentional weight loss, intermittent palpitations and low-grade fever. He noticed leg cramps with numbness and unable to move his extremities. At initial evaluation, he had acute flaccid paralysis and tachycardia. Initial laboratory studies showed potassium at 1.9 mmol/l, Magnesium at 1.8, suppressed TSH &amp;lt;0.005 uIU/ml with elevations in free T4 at 2.43 ng/dl and total T3 at 1.9 ng/ml. CT and MRI head were normal. Patient’s aldosterone level was normal. The patient’s paralysis and hypokalemia resolved after potassium replacement. Thyroid stimulating immunoglobulin was elevated and increased vascularity suggestive of Grave’s disease noted on thyroid Ultrasound. Methimazole and propranolol were initiated. His neurological workup was negative. After resolution of paralysis and hypokalemia he was discharged home. Since our patient presented with severe hypokalemia, flaccid paralysis and hyperthyroidism, that resolved promptly with potassium replacement, hence likely diagnosis of thyrotoxic periodic paralysis. Discussion: Thyrotoxic periodic paralysis is potentially reversible and mostly seen with Graves’ disease among Asian population. Early diagnosis &amp; treatment prevents life threatening complications. Differential diagnosis of TPP includes familial periodic paralysis, Guillain-Barre Syndrome &amp; acute intermittent porphyria. Diagnosis is based on family history, characteristic presentation, hyperthyroidism with low serum potassium level. Possible mechanism is increased sodium-potassium ATPase activity in the skeletal muscle membrane leading to intracellular shift of potassium causing hypokalemia and muscle inexcitability. Treatment includes potassium replacement, nonselective beta-blocker and definitive treatment of hyperthyroidism, to prevent further episodes.

Skin Deep: A Rare Case of Thyrotoxic Periodic Paralysis in an African American Patient

Background: Thyrotoxic Periodic Paralysis (PP) is a rare form of hypokalemic PP that occurs in association with hyperthyroidism, especially Grave’s disease. This disease is frequently seen in males and is particularly prevalent among Asians with an incidence rate of 2%. In non-Asian populations, the incidence among those with hyperthyroidism is even lower at 0.1 - 0.2% and therefore significantly rare in African populations. Inability to recognize this emergency in the non-Asian population can therefore result in potentially fatal outcomes. Case Presentation: A 27 year old African American male with a history of Grave’s disease presented to the emergency department (ED) with the inability to move his muscles. Patient was initially diagnosed with Grave’s disease in 2017 when he was found to have suppressed TSH with elevated TSI and started on methimazole 40mg daily. The patient ran out of methimazole about 2 weeks prior to presentation and woke up on the day of admission with extreme muscle weakness. At the outside hospital, he was found to have potassium of 1.5mEq/L,TSH of < 0.1uL/ml and Free T4 of 3.4 ng/dL. He was given 1000 mg Propylthiouracil, stress dose hydrocortisone, propranolol and potassium replacement and then transferred to our ED for Endocrine evaluation. On assessment, he complained of nausea, vomiting, full body muscle weakness, tingling in his extremities and irritability. He denied any recent illnesses. On physical exam, Temperature 97.4 F, Respiration 18, Pulse 84, BP 157/72, O2 saturation 99%. His thyroid gland was enlarged however non-tender and without bruit. He had normal respiratory and cardiac exam. He was lying flat in bed and unable to raise his limbs against gravity and also unable to hold up his limbs when raised. He lacked his patellar and ankle jerk reflexes bilaterally. He was otherwise alert and oriented x 3. On labs, TSH was 0.004 uL/ml, Total T3 was 294 ng/dL, Free T4 of 3.01 ng/dL, Potassium was 2.1 mEq/L. His potassium was cautiously replaced and improved to 4.7 mEq/L later in the day, at which time, the patient was able move and sit up in bed. He was restarted on Methimazole 40mg daily for his thyroid disease and arranged for outpatient follow up. Discussion: Thyrotoxic PP is seen in a male-to-female ratio ranging from 17:1 to 70:1 and occurs at an average age of 20-40 years. Thyrotoxic PP is especially rare in the non-Asian population at an incidence rate of 0.1 - 0.2%. Nevertheless, in setting of ever-growing diversity due to immigration and inter-race relationships, it is difficult to predict one’s genetics based on the color of their skin. It is possible that our African American patient may have an Asian ancestor unbeknownst to him. Therefore, we must keep a broad differential regardless of one’s race so as to not miss timely diagnosis of medical emergencies which can result in reduced muscle strength, flaccid paralysis, respiratory failure, cardiac arrhythmias and eventual death.

When Your Thyroid Causes Muscle Paralysis

Background: Periodic paralysis represents a spectrum of disorders characterized by ion channel dysfunction, mainly Na-K-ATPase channels. Thyrotoxic periodic paralysis (TTP) is defined by the presence of hypokalemia and diffuse muscular paralysis in a pre-existing hyperthyroid state. Diagnosis can be challenging, especially in cases of undiagnosed hyperthyroidism due to the non-specific presentation of this illness. We present a case of a young male who presented with recurrent, spontaneous paralysis found to have Graves’ disease. Clinical Case: A 38-year-old Asian male presented with sudden onset diffuse weakness, numbness, and tingling. The weakness was so severe that he could barely walk more than a few steps. However, his symptoms resolved in less than 24 hours without any intervention. Five months later, the patient experienced a recurrent episode of this similar constellation of diffuse muscle weakness and paresthesia. The patient was taken to a nearby hospital, where he was provided with intravenous fluid resuscitation. Initial laboratory workup was notable for hypokalemia to 1.4 mmol/L (n: 3.6 - 5.3 mmol/L), hypophosphatemia to 0.6 mmol/L (n: 2.4 – 4.8 mmol/L), and elevated creatinine kinase to 807 U/L (n: 22 – 198 U/L). Additionally, TSH was <0.001 mU/L (n: 0.45 – 4.5 mU/L) along with free T4 3.4 ng/dL (n: 0.80 – 1.70 ng/dL. The patient denied any other symptoms or a family history of similar symptoms. Lumbar puncture and brain/spine MRIs were unremarkable. Symptoms gradually improved throughout hospitalization with fluid and electrolyte repletion. Hyperthyroidism was treated with methimazole 5mg twice daily, later changed to PTU 50mg every eight hours due to recurrent headaches. Thyroid uptake scan showed diffuse bilateral uptake to 39.11% at 4 hours and 61.8% at 24 hours. Follow up labs revealed: TSH 0.3 mU/L, free T4 1.44 ng/dL, free T3 3.5 pg/mL (n: 2.3 – 4.1 pg/mL). Patient denied recurrent episodes of weakness or paresthesia. Definitive hyperthyroidism treatment with RAI was planned. Conclusions: The prevalence of TPP is higher in Asian males compared to other ethnic groups. TPP manifests as a sporadic onset of muscle weakness ranging from mild weakness to flaccid paralysis. It has been described that thyroid hormone itself augments the activity of the Na-K-ATPase channel and increases its responsiveness to beta-adrenergic stimulation. In addition, hyperthyroidism is associated with insulin resistance leading to hyperinsulinemia. Both beta-agonism and insulin promote potassium to be driven into cells resulting in hypokalemia. As such, activities which increase beta adrenergic stimulation, like stress and exercise, and promote the secretion of insulin, such as heavy carbohydrate intake, are well described triggers of TPP. Treatment revolves around acutely treating hypokalemia followed by preventing subsequent attacks via regulation of the altered thyroid state.

Thyrotoxic Periodic Paralysis- An Uncommon Disease in the Western World: A Case Report

Thyrotoxic Periodic Paralysis (TPP) is a rare diagnosis in the western world; however, its incidence has been rising in recent years due to globalization. This condition has the potential to be deadly if not detected and treated in a time appropriate manner. This case discusses our management of a patient who came into our hospital with complaints of total body numbness and weakness for several hours. He was subsequently diagnosed with TPP and was treated with Methimazole and aggressive potassium supplementation and had an overall good outcome. This case report highlights an unusual disease that needs to be considered as a differential when a young man reports numbness and weakness to the clinician.

A 29-year-old Bodybuilder with Liothyronine-induced Thyrotoxic Hypokalaemic Periodic Paralysis.

In patients with bouts of muscle weakness and hypokalaemia, thyrotoxic hypokalaemic periodic paralysis should be suspected and thyroid function should be evaluated.In bodybuilders and strength athletes, undisclosed abuse of performance and image-enhancing drugs, including thyroid hormone, should be suspected.

Thyrotoxic Periodic Paralysis with Thyroid Storm as the First Presentation of Graves' disease; a Case Report.

Thyrotoxic periodic paralysis is a rare endocrine emergency that manifests as acute onset muscle weakness and hypokalaemia secondary to thyrotoxicosis. It mainly occurs due to rapid and dramatic intracellular shift of potassium resulting in hypokalaemia and acute flaccid paralysis. This condition predominantly affects males of Asian descent, and presentation can range from mild generalized weakness to complete quadriplegia, as seen in our case. We herein report a case of a 40-year-old female, who presented to us with acute onset flaccid quadriplegia and thyroid storm, which is the first ever manifestation of previously undiagnosed Grave’s disease. Liver abscess was found to be the underlying trigger for thyrotoxic paralysis and thyroid storm.

HYPERTHYROIDISM: LOOKING BEYOND PHYSICIAN'S PERSPECTIVE

Hyperthyroidism with its excess circulatory thyroid hormones commonly presents with systemic features like palpitation, weight loss and heat intolerance. This hyperadrenergic, hypermetabolic state with its peripheral and central nervous system affection produces protean neurological manifestations which are generally overlooked by internist. Features of neuropsychiatric nature, cognitive impairment, and dementia movement disorder like tremors or chorea may be presentation of undetected hyperthyroidism. Affliction for muscles presents with proximal myopathy with or without myalgia in 50-70% of long standing hyperthyroid state. Similarly thyrotoxic periodic paralysis due to low serum potassium in adult male is often misdiagnosed as Guillain-Barré syndrome, however replacement of potassium drastically reverse the condition. There is a strong association between autoimmune thyroiditis and ocular myesthenia which post difficulties in clinical diagnosis. Despite of so much variability in clinical presentation attainment of euthyroid state coupled with beta blocker in many situations is helpful to resolve most of the issues. Keywords: Hyperthyroidism, Grave's, Tremors, Myopathy, Periodic paralysis.

Genome-wide meta-analysis reveals novel susceptibility loci for thyrotoxic periodic paralysis.

Thyrotoxic periodic paralysis (TPP) is a rare and potentially fatal complication of hyperthyroidism. By meta-analysis of genome-wide association studies, we aim to discover novel susceptibility loci and understand the pathogenesis of TPP. This meta-analysis comprised 319 TPP cases and 3516 healthy controls from three independent cohorts (two from Hong Kong; one from Shanghai). Genetic variants in each cohort were separately genotyped, imputed and analyzed for association with TPP. Fixed-effect meta-analysis was performed to combine the data. Using the three independent genome-wide significant variants, a weighted genetic risk score (GRS) was developed. Of 7 077 246 variants tested for association with TPP, 260 variants reached genome-wide significance and were represented by independent variants from four distinct genomic loci, but a risk locus for Graves' disease at 6p21.33-p21.22 was excluded from subsequent analyses. Two novel loci near TRIM2 (4q31.3; rs6827197: OR = 4.075; P = 3.46 × 10-9) and AC140912.1 (16q22.3; rs6420387: OR = 1.861; P = 2.66 × 10-8) were identified. Together with previously reported KCNJ2 (17q24.3; rs312743: OR = 2.564; P = 1.15 × 10-21), the three susceptibility variants explained 4.36% of the genetic liability. Expression quantitative trait loci analyses showed the variants altered expression of TRIM2 in nerve and KCNJ2 in skeletal muscle. The weighted GRS had an area under curve of 0.827 and 0.682 in the derivation and validation cohorts in Hong Kong. We identified two novel TPP risk loci near TRIM2 and AC140912.1. While rare mutations in TRIM2 and KCNJ2 were implicated in monogenic disorders characterized by muscle paralysis, our study suggested common variants near these genes might dysregulate gene expression and lead to milder phenotypes.

A NOT SO SIMPLE THYROID CAUSE OF ST DEPRESSION: THYROTOXIC HYPOKALEMIC PERIODIC PARALYSIS

SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Thyrotoxic hypokalemic periodic paralysis (THPP) is a rare and reversible endocrine emergency. The excess of thyroid hormone increases the sensitivity of the Na-K-ATPase channels, shifting potassium from the extracellular to the intracellular space. CASE PRESENTATION: A previously healthy 53 year-old man presented with one day of generalized weakness. Associated symptoms included lower extremities paresthesias, headaches, nausea and vomiting in addition to 5 months of fatigue, weight loss and tremors. Physical findings were significant for a heart rate of 117bpm and a blood pressure of 140/65mmHg. Extremities were warm, clammy and well perfused. A fine hand tremor, diffuse weakness and hypotonia were present. EKG showed sinus tachycardia, diffuse ST depression and QT interval prolongation (figure 01). Laboratory showed a critical hypokalemia (at 1.63mEq/L), a suppressed TSH (<0.005µIU/mL) and an elevated T4L (4,03ng/dL). Intravenous potassium chloride was administered. EKG after KCl infusion (Figure 02) showed resolution of the repolarization changes. His muscular weakness also resolved. Patient was discharged with propranolol and methimazole for outpatient follow up. DISCUSSION: THPP is more common in men in between the age of twenty to forty Hypokalemia results in slowed conduction, delayed ventricular repolarization, shortened refractory period and increased automaticity. ECG changes include flattening and inversion of T waves in mild hypokalemia, Q-T interval prolongation and mild ST depression in more severe hypokalemia. Severe hypokalemia can cause torsades de pointes and ventricular tachycardia. Importantly ST depression as in our case is not common and should raise the concern for ischemia if not resolved with potassium reposition. CONCLUSIONS: THPP is a rare cause of hypokalemia which can cause malignant arrythmias. Severe hypokalemia is an unusual cause of ST segment depression, ventricular tachycardia and QT prolongation, being an important differential for ischemic heart disease. Reference #1: Lin YC, Wu CW, Chen HC, Chen HY, Lu IC, Tsai CJ, Kuo WR, Chiang FY. Surgical treatment for thyrotoxic hypokalemic periodic paralysis: case report. World jorunal of surgical oncology. 2012;10(1):21. Reference #2: Osadchii OE. Mechanisms of hypokalemia-induced ventricular arrhythmogenicity. Fundam Clin Pharmacol. 2010; 24:547–59. DISCLOSURES: No relevant relationships by RAIMUNDO BARROS, source=Web Response no disclosure on file for Lucia Belem; No relevant relationships by Ingrid Freitas, source=Web Response No relevant relationships by Simran Kenth, source=Web Response No relevant relationships by Neiberg de Alcantara Lima, source=Web Response No relevant relationships by Danielli Lino, source=Web Response No relevant relationships by José Silva, source=Web Response

A CASE OF THYROTOXIC PERIODIC PARALYSIS IN AN AFRICAN AMERICAN MALE REQUIRING MECHANICAL VENTILATION AND HEMODIALYSIS

SESSION TITLE: Medical Student/Resident Critical Care SESSION TYPE: Med Student/Res Case Report PRESENTED ON: October 18-21, 2020 INTRODUCTION: Thyrotoxic periodic paralysis (TPP) represents a rare, acquired form of hypokalemic periodic paralysis characterized by acute onset muscle weakness and hypokalemia. We report a severe presentation requiring mechanical ventilation and hemodialysis (HD). CASE PRESENTATION: A 25 year old African American male presented with bilateral lower extremity weakness and hypokalemia at 1.6 mmol/L with characteristic hypokalemic ECG changes. After receiving 40 mEq IV potassium chloride, his hypokalemia worsened to 1.1. Given acute progression of ascending paralysis to complete paraplegia, 3/5 strength in upper extremities and concern for impending diaphragmatic weakness, he was intubated. Despite an additional 170 mEq of potassium, his repeat K+ was 1.5 with progressive EKG changes. He also had a metabolic acidosis with pH of 7.208 and a lactic acid of 8.7. Given refractory hypokalemia and concern that bicarbonate therapy for acidosis would worsen the hypokalemia, the patient was initiated on HD with a high potassium bath. The team confirmed suspicion of TPP upon return of TSH level <0.015 mU/L and administered 3 doses of 1 mg IV Propranolol during which he exhibited spontaneous extremity movements. Serial labs then revealed a rebound hyperkalemia up to 7.4 mmol/L with characteristic hyperkalemic ECG changes. He received usual stabilizing treatments and a second session of emergent HD to correct the up trending hyperkalemia. Diagnosis and recovery was confirmed after stable potassium levels, resolved acidosis, complete recovery of his neurological exam and notably elevated T4 and T3 levels. He was extubated without complication and discharged home on Propylthiouracil with instructions to follow-up with endocrinology for further evaluation of his hyperthyroidism. DISCUSSION: As compared to prior published cases of TPP most often amongst Asian males, management of this African American patient differed with the use of mechanical ventilation for airway protection due to rapidly progressive ascending paralysis and down trending negative inspiratory forces and vital capacities. It also necessitated the use of hemodialysis to correct both the refractory hypokalemia and concomitant acidosis. It is believed that a thyrotoxic-mediated beta-adrenergic response drives potassium into cells hyperpolarizing muscle fibers, causes an extracellular shift of hydrogen and increases conversion of pyruvate to lactate resulting in acidosis. The concern with addressing this with a bicarbonate drip was that a secondary alkalosis would further intracellularly shift potassium. Fortunately, already having a HD catheter in place allowed for more rapid treatment of the severe rebound hyperkalemia. CONCLUSIONS: Initial suspicion of TPP on the differential for ascending paralysis and earlier use of IV propranolol can prevent progression of paralysis, rebound hyperkalemia, lactic acidosis and life-threatening cardiac arrhythmias. Reference #1: Younis AA. Thyrotoxic Periodic Paralysis as a Presentation of Thyrotoxicosis: A Case Report and review of the literature. Mediterr J Rheumatol. 2018;29(1):46–48. Reference #2: Wong P. Hypokalemic thyrotoxic periodic paralysis: a case series. CJEM. 2003;5(5):353–355. Reference #3: Tassone H, Moulin A, Henderson SO. The pitfalls of potassium replacement in thyrotoxic periodic paralysis: a case report and review of the literature. J Emerg Med. 2004;26(2):157–161. DISCLOSURES: No relevant relationships by Firth Bowden, source=Web Response No relevant relationships by Uday Gulati, source=Web Response No relevant relationships by Asma Qayyum, source=Web Response No relevant relationships by samson zarbiv, source=Admin input

O2-005 Acase of thyrotoxic periodic paralysis in which exercise stress conduction test was effective for pathophysiological evaluation

O2-005 Acase of thyrotoxic periodic paralysis in which exercise stress conduction test was effective for pathophysiological evaluation

Impact of first-line treatment choice on long-term outcomes of hyperthyroid Graves’ disease patients with thyrotoxic periodic paralysis

BackgroundThyrotoxic periodic paralysis (TPP) is a unique manifestation of Graves’ disease. While it is uncommon in Asian, it is extremely rare in Caucasian patients (0.1–0.2%). Previous studies suggested that TPP indicate more severity of Graves’ disease and definitive treatments should be used to prevent relapses. AimTo describe clinical features and impact of first-line treatment on long-term outcomes of TPP patients. MethodA retrospective cohort study over 35 years (1985–2019) of TPP from Graves’ disease patients was conducted. All cases were analyzed and their clinical courses were compared between those who received anti-thyroid drugs (ATD) versus radioactive iodine (RAI) as a primary treatment. None of them underwent surgery. ResultsA total of 2964 hyperthyroid Graves’ disease patients were treated and followed-up at least 3 months over the study period. TPP was identified in 63 cases (2.1%) of all patients. There were 60 males and only 3 females with age at presentation of 35.0 ± 8.2 years. TPP was the first presentation of hyperthyroid Graves’ disease in 82.5% of them. During the acute attack of TPP, all patients presented with bilateral lower limb flaccid weaknesses with median serum potassium of 2.1 mmol/L. No fatal TPP cases were found. RAI was selected as primary treatment in 27 patients (42.9%). Nearly all RAI-treated patients rendered hypothyroidism with the median RAI dose at 15 mCi. No patients who were in remission after RAI treatment developed recurrent attack of TPP. In the remaining 36 ATD-treated patients with mean follow-up time at 9.1 years, relapse was found in 10 patients (27.8%) after the drug discontinuation and 6 patients suffered recurrent TPP. Only 8 ATD-treated TPP patients (22.2%) went into remission. ConclusionsTPP is a rare complication of hyperthyroid Graves’ disease. Definitive treatment with RAI or thyroidectomy should be employed to prevent relapse and further attacks of TPP.

A Literature Review on Thyrotoxic Periodic Paralysis.

Thyrotoxic periodic paralysis (TPP) is a rare disease of the muscles that presents with painless weakness of the muscles. The patients usually have hypokalemia and hyperthyroidism with elevations in the level of triiodothyronine (T3) and thyroxine (T4). The muscle weakness is usually transient, and the patients in many cases suffer from recurrent episodes of muscle paralysis. This flaccid muscle paralysis predominantly affects the proximal and lower extremities group of muscles more than the distal and upper extremity muscles. This condition is one of the drastic complications of Graves's disease and, unfortunately, may require admission and treatment in the critical care units. It is often not recognized during the initial attack in the American population as the prevalence is very low among the Caucasian population and people from North America. However, while the prevalence is extremely low in the Caucasian population, it is known to be 10 times more common among the Asian population when compared with the Caucasian population. Furthermore, while the diseases of the thyroid gland are more common in females, this rare disease predominantly affects male sex. It is treated by reversing the hypokalemia, which can in itself prove to be fatal if not corrected quickly, and this is followed by treatment to restore the euthyroid state. A literature review on this reversible cause of muscle weakness is very important to better understand this disease.