Case Of Thyrotoxic Periodic Paralysis Research Articles

A Rare Case of Thyrotoxic Periodic Paralysis in a Patient with Concomitant Methimazole-Induced Agranulocytosis

A Rare Case of Thyrotoxic Periodic Paralysis in a Patient with Concomitant Methimazole-Induced Agranulocytosis

7342 Thyrotoxic Periodic Paralysis

Abstract Disclosure: G. Arora: None. Case presentation: A 40 year old male with no significant past medical history presented to the emergency department with diffuse body weakness for one day. On the night prior to admission, his thighs started getting sore which in a matter of a few hours, progressed to weakness involving his entire body. He was unable to flex his hips, shoulders, and neck. He was unable to get up or move without assistance. He was found to have an irregular heartbeat two weeks prior to admission and had undergone a thyroid ultrasound which showed inflammation of the thyroid gland. He was not started on any new medications. He endorsed fatigue, palpitations, neck swelling, and 45 lbs unintentional weight loss over 6 months. No fever, chills, vision changes, congestion, chest pain, shortness of breath, cough, tingling, numbness or weakness. He denied alcohol or drug use. Physical examination was notable for blood pressure 151/80 mm Hg, heart rate 120 bpm, enlarged thyroid gland tender to palpation, and muscle weakness (motor strength 3/5 in flexors and extensors of hips and knees). Labs were notable for K 2.3 (3.5 - 5.1 mmol/L), ALP 218 (32 - 91 U/L), TSH <0.010 (0.400 - 4.300 mcIU/mL), Free T4 3.5 (0.6 - 1.6 ng/dL), CK 608 (49 - 397 U/L). Urine toxicology was negative. MRI spine did not show any acute abnormality except for thyromegaly. He received potassium supplementation which led to symptomatic improvement and was admitted to medical floor. Further tests revealed: TSI 39.50 (<=0.54 IU/L), TSH receptor antibody 26 (<=1.75 IU/L), thyroid microsomal antibody 773.3 (0.0 - 9.0 IU/mL), anti-thyroglobulin antibody 4 (<4 IU/mL). Thyroid ultrasound showed an enlarged, heterogenous, hypervascular thyroid without any nodules. He was started on Propranolol and Propylthiouracil, which led to symptom resolution and he was discharged. Discussion: Thyrotoxic periodic paralysis (TPP) is a rare muscle disorder, belonging to the family of diseases called channelopathies. Thyroid hormone increases tissue responsiveness to beta-adrenergic stimulation, which increases Na-K ATPase activity on the skeletal muscle membrane driving potassium into cells. This leads to hyperpolarization of the muscle membrane and relative inexcitability of the muscle fibers, especially in the presence of a trigger such as provocation with exercise, fasting state or a high carbohydrate meal (insulin stimulates Na-K ATPase pump). Furthermore, more than 95% of TPP cases occur in males. This predominance is due to androgen-induced Na-K ATPase sensitization, more pronounced hyperinsulinemia, comparatively higher sympathetic and catecholamine-induced Na-K ATPase activity and higher muscle mass in males. Given the life-threatening association of severe hypokalemia, TPP should be considered in all patients presenting with acute painless muscle weakness. Presentation: 6/3/2024

SAT478 A Rare Case of Thyrotoxic Periodic Paralysis in a Patient with Concomitant Methimazole-Induced Agranulocytosis

Abstract Disclosure: K.S. Wei: None. S.M. Cannon: None. T.E. Angell: None. Introduction: Thyrotoxic state may precipitate sudden-onset unilateral or bilateral extremity weakness brought on by transient hypokalemia requiring specific management. Clinical Case: A 48-year-old woman presented to our hospital with fevers, sore throat, and sudden-onset bilateral leg weakness. Ten weeks prior, she was started on methimazole 20mg daily for a new diagnosis of Graves’ disease. Two days prior to presentation, she had consumed a carbohydrate-heavy meal and that night experienced acute-onset lower extremity weakness rendering her unable to walk. She also had been experiencing sore throat, odynophagia, and intermittent fevers. On admission, the patient was found to be febrile, tachycardic, and in shock with WBC <0.5 (ref: 4.5-10 K/cumm), potassium 2.6 (3.5-5.1 mmol/L), lactate 4.1 (0.5-2.2 mmol/L), TSH <0.01 (0.27-4.2 uIU/mL), fT4 4.04 (0.93-1.7 ng/dL) and was admitted to the ICU for neutropenic fever and septic shock. Computed tomography (CT) imaging of the thorax showed right lung consolidation suggesting pneumonia. Magnetic resonance imaging of the spine and CT head did not demonstrate an etiology for her weakness. She was diagnosed with thyrotoxic periodic paralysis (TPP) and treated with potassium. For severe hyperthyroidism with methimazole contraindication, she received broad spectrum antibiotics, lithium 300mg orally every 8 hours, and propranolol 10-20mg every 8 hours. Given minimal improvement in both weakness and hypokalemia after 48 hours of therapy, she was also diagnosed with refeeding syndrome and potassium repletion was intensified. The patient’s shock resolved, with slow improvement of lower extremity weakness over a two-week period and resolution of agranulocytosis and fevers. Conclusion: This rare presentation offers several distinct points regarding the patient’s care. Firstly, TPP is a rare hyperthyroidism-related hypokalemia that can cause weakening of the extremities due to a rapid intracellular shift of potassium (1) and is an important syndrome to consider on the differential for any thyrotoxic patient presenting with sudden-onset weakness. Secondly, gentle potassium repletion is recommended to prevent rebound hyperkalemia. However, our patient had both total body loss of potassium from refeeding syndrome and intracellular shift from TPP, requiring more aggressive potassium repletion to treat her paralysis than is typical for TPP alone. In settings where weakness and hypokalemia do not improve with beta blockade and gentle potassium repletion, it is important to investigate other causes of hypokalemia and consider concurrent overlapping diagnoses. Lastly, patients with methimazole-induced agranulocytosis may require alternative treatments, such as lithium to control hyperthyroidism. 1) Lin, Shih-Hua. Thyrotoxic Periodic Paralysis. Mayo Clin Proc. 2005;80(1):99-105. Presentation Date: Saturday, June 17, 2023

SAT507 New Onset Graves’ Thyrotoxicosis Complicated by Hypokalemic Periodic Paralysis: A Late Sequela of COVID- 19 Infection

Abstract Disclosure: E. Askar: None. H. Basharat: None. L. Lotfi: None. Y. Jamal: None. Background: Thyrotoxic periodic paralysis (TPP)is a rare endocrine emergency identified by hypokalemia and ascending symmetrical paralysis of extremities. If left untreated, it can lead to cardiopulmonary collapse. There are cases in the literature highlighting that Covid-19 infection or Covid vaccination can cause hypokalemic periodic paralysis with or without thyroid dysfunction. To our knowledge, four cases of Covid induced TPP and three cases of TPP after Covid vaccination have been reported in the literature. In all cases, the patients developed TPP soon after (within two months) Covid-19 infection or vaccination. However, we describe a case of a young, healthy euthyroid male who developed TPP as an initial manifestation of new-onset Graves' disease after five months of Covid infection. Even though Covid-19 infection has been known to cause thyroid dysfunction, especially subacute thyroiditis, there have only been a few case reports of Covid induced Graves' disease presenting as TPP at initial diagnosis. Clinical Case: A 37-year-old Asian male with no past medical history presented to the emergency department with lower extremity paralysis, palpitations, tremors and diaphoresis one day prior to presentation. He was diagnosed with mild COVID 19 infection, five months prior to presentation. Since then, he has been having intermittent palpitations but did not have any other symptoms. Vital signs on admission revealed heart rate of 100 beats/min, respiratory rate of 16 breaths/min, blood pressure of 131/66 mmHg, temperature of 97.5°F and oxygen saturation of 98% on room air. Physical examination was significant for an anxious young male with tender enlarged thyroid gland. There was positive thyroid bruit. Pemberton sign was negative. Muscle strength of 1/5 in bilateral lower extremities with brisk deep tendon reflexes and tremors in both hands were noticed. Laboratory studies showed white blood cell count of 13.07 (3.80-10.50 x 109/L), serum potassium of 1.4 mmol/L (3.5-5.3) and thyroid stimulating hormone of <0.01 mIU/L (0.358-3.74), free thyroxine of 5.5 ng/dl (0.9-1.8), total Triiodothyronine of 438 ng/dl (80-200) and positive thyroid stimulating immunoglobin of 4.22 IU/l (0.00-0.55) confirming Graves' disease as a diagnosis causing thyrotoxicosis with periodic paralysis. Patient did not have any history of thyroid disease with no available previous thyroid function tests. Patient was admitted to intensive care unit. Judicious repletion of potassium was done and he was started on propranolol 40 mg daily and methimazole 30 mg daily that lead to resolution of his paralysis and hyperthyroid symptoms. Conclusion: Here we report a case of new onset Graves' disease with TTP after COVID 19 increasing the likelihood that Covid 19 is a direct cause of new onset autoimmune thyroid illness. More studies are required to identify the mechanism and to confirm if the relationship is causal. Presentation Date: Saturday, June 17, 2023

Code Pseudo Stroke - A Case of Hypokalaemic Periodic Paralysis Mimicking Stroke.

Hypokalaemic periodic paralysis is an acute flaccid paralysis secondary to hypokalaemia, triggered by hyperthyroidism, environmental elements such as a high carbohydrate intake or rest after intense exercise, and an underlying genetic component with mutations in the muscle ion channels.The pursuit of code stroke protocol in the in-patient setting must bear in mind reversible but potentially fatal and disabling alternative diagnoses such as stroke mimics including hypokalaemic periodic paralysis.Stroke mimics defined as acute onset neurological deficits that are not related to vascular cause are a true challenge, multiple scales have been created to distinguish them from an actual stroke, such as the Recognition of Stroke in the Emergency Room (ROSIER) scale.

Thyrotoxic Periodic Paralysis: An Under-Recognized Cause of Paralysis in Young Hispanic Men

BackgroundPatients presenting to the emergency department with paralysis can have a wide differential diagnosis. Thyrotoxic periodic paralysis (TPP) is a rare disorder causing transient flaccid paralysis in the setting of thyrotoxicosis and hypokalemia. It has been reported in Asian male populations predominantly, and the diagnosis is rarely considered in non-Asian populations. Recent research has identified cases in patients with diverse ethnic backgrounds, although epidemiologic data from the United States are very limited. ObjectiveOur aim was to report our experience with TPP at a tertiary care center in the United States. MethodsA retrospective chart review was conducted between January 2006 and February 2022 to identify cases of TPP and determine their demographic and clinical characteristics. Prevalence of TPP was estimated using the institutional hyperthyroidism registry. ResultsThirty-three patients with TPP were identified. All of the patients were male; median age was 28 years, and 85% were Hispanic. All patients had hypokalemia at presentation and 23% had rebound hyperkalemia after treatment. Prevalence of TPP in our population of patients with hyperthyroidism was approximately 0.5%. ConclusionsYoung Hispanic men presenting with paralysis should be evaluated for TPP, as the prevalence in this population may be higher than estimated previously. Management of TPP involves treatment of underlying hyperthyroidism and cautious potassium repletion, with an initial dose of no more than 60 mEq/L of potassium chloride to avoid rebound hyperkalemia.

Thyrotoxic Periodic Paralysis in the Post-COVID Era: A Case Report with Literature Review

Thyrotoxic Periodic Paralysis (TPP) is an acute potentially lethal emergency in patients with hyperthyroidism who present with sudden muscle weakness and hypokalemia. It is commonly precipitated by high carbohydrate or high salt content meals, strenuous exercise, stress, trauma, glucocorticoids, epinephrine, alcohol, or respiratory infections. COVID-19 infection or vaccination may represent a novel trigger for TPP. Furthermore, COVID-19 infection or vaccination may incite inflammatory processes leading to thyrotoxicosis, which can manifest as TPP. While COVID-19 causing subacute thyroiditis, euthyroid sick syndrome, Hashimoto’s disease, or Graves’ disease have been well documented in the literature; there have only been six case reports of post-COVID-19 TPP. Notably, all cases thus far have been restricted to male patients, and there is paucity of literature from North America. The purpose of this paper is to outline the first case of post-COVID-19 TPP in a female patient, who presented to the emergency department with acute paralysis and severe hypokalemia (2.2 mmol/L) three months after COVID-19 infection. Investigations in the emergency department showed thyrotoxicosis. She was treated with potassium replacement, which improved her paralysis. Subsequent investigations revealed severe hyperthyroidism from Graves’ disease, which is currently managed with metoprolol and methimazole. Her hyperthyroidism improved without recurrent hypokalemia or paralysis. In addition, we outline the epidemiology, pathophysiology, precipitants, and management of TPP, with a particular focus on COVID-19 infection or vaccination precipitating TPP. We discuss post-COVID-19 TPP cases thus far described in the literature. Knowing that North American COVID-19 infection waves lagged Asia, we could anticipate additional future TPP cases.

A Case of Thyrotoxic Periodic Paralysis and Graves’ Ophthalmopathy Patient in Coincidence with Chronic Hepatitis B Infection

Graves' disease is an autoimmune thyroid disease with several characteristic symptoms and signs. Graves' ophthalmopathy, an inflammatory disease in the orbital area, is the main extrathyroid manifestation of Graves' disease. About 5% of Graves' ophthalmopathy patients have moderate to severe severity requiring high doses of systemic corticosteroid therapy. Graves' disease also has few complications, one of which is thyrotoxic periodic paralytic characterized by hypokalemia and muscle paralysis. Chronic hepatitis B virus infection has the potential to be co-incidence with other diseases (eg Graves ophthalmopathy). The need of high dose of corticosteroid therapy in treating Graves’ ophthalmopathy is a risk of reactivation in hepatitis B infection patient. This paper presented a Graves' disease patient complicated with Graves’ ophthalmopathy who developed limb muscle weakness. Patient will receive high doses of corticosteroids and prophylactic lamivudine therapy to prevent hepatitis B virus reactivation.

Sudden weakness due to thyrotoxic periodic paralysis: a case report

Thyrotoxic periodic paralysis (TPP) is a complication of hyperthyroidism. Lead to sudden hypokalemia and muscle weakness. In most cases, it is found mainly in young adult males of the Asian race. The paralysis is temporary and will return with potassium correction. There are very few cases reported in Indonesia regarding these cases of TPP. In our case, a 44-year old man complained of weakness that started later in the limbs but quickly improved. This case was diagnosed late at first, and uncorrected potassium levels led to recurrent paralysis. Laboratory test results showed severe hypokalemia (potassium level 1.81 mmol/L). The thyroxine level (T4) was 44.12 pmol/L and low serum thyroid-stimulating hormone (TSH) <0.0025 IU/mL.

Thyrotoxic periodic paralysis with normokalemia: a rare case report

Thyrotoxic periodic paralysis (TPP) is a rare etiology for muscle paralysis. It is frequently seen in Asian men. Apart from paralysis, most of them are asymptomatic and are devoid of other clinical features of hyperthyroidism. Due to the rarity of this condition, it is often missed and hence fatal. The metabolic derangement seen in TPP is hypokalemia and is thought to be the pathogenesis of the muscle paralysis. Although in rare clinical encounters, patients with TPP may present with normokalemia. The disorder usually presents in the 3rd decade. The cause for mortality in patients with TPP may be due to respiratory muscle paralysis leading to compromise of the respiratory function or refractory arrhythmias due to hypokalemia. Here we report a rare case of TPP with normokalemia.

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.

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)

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.

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 &amp;lt; 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 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.

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

SUN-514 Thyrotoxic Periodic Paralysis in Adolescence Patient a Case Report and Literature Review

BACKGROUND: Thyrotoxic periodic paralysis (TPP) is an uncommon disorder characterized by acute flaccid paralysis due to hypokalemia. It is diagnosed primarily in Asian adult males and is rare in children and adolescents. Here we report an adolescent male patient of Vietnamese descent who presented to the emergency department with an episode of syncope, muscle weakness, and shortness of breath one day after the initiation of methimazole treatment for Graves’ disease. The laboratory revealed significant hypokalemia. In this report we also included and summarized the reported cases of TPP in adolescent patients since 1997. Clinical Case: A 17-year-old Vietnamese American male who was recently diagnosed with Graves’ disease presented to the emergency department after an episode of syncope, muscle weakness, and difficulty breathing. Two months previously, he began having episodes of tachycardia. He was diagnosed with hyperthyroidism with a TSH of 0.007 mIU/mL and free T 4 > 7 ng/dL (0.8-1.9). He was subsequently evaluated by Cardiology and started on atenolol. He was then seen by Endocrinology 5 days after and started on methimazole 15 mg twice daily. On the next morning after starting methimazole, he reported feeling weak and passed out. His father had found him on the floor, weak and unable to move, approximately 30 minutes after his father “heard a thud upstairs”. The patient recalled that his legs gave out and he “hitting his face on a table”. In the emergency department, he was tachycardic at 116 bpm, widened pulse blood pressure of 131/50 mmHg with normal respiratory rate 24 BR/min. He had diffused and significant muscle weakness on his all extremities including grip strength.His potassium was 1.6 mmol/L (3.5 - 5.2) and magnesium 1.6 mmol/L (1.6-2.3). The rest of his chemistry panel was unremarkable. He had EKG changes consistent with hypokalemia with U waves, also revealing atrial rhythm with first degree AV block, intraventricular conduction delay, and QTc prolongation at 588 (<450). His chest x-ray was normal. Normal saline was administered, and potassium replacement was given with 40 mEq of KCl followed by D5 NS with 40 meq/L KCl at maintenance. He continued taking atenolol and methimazole. He was also given an IV dose of magnesium. His muscle strength returned completely and potassium level returned to normal range at 4.6 mmol/L after 24 hours of treatment. Conclusion: TPP is a rare cause of acute paralysis and can lead to cardiac arrhythmia and death without accurate diagnosis and prompt treatment. Our case should raise awareness of this disorder among pediatricians, emergency department physicians and endocrinologists. Acute paralysis with hypokalemia should also prompt the physician to consider evaluating thyroid function as a differential diagnosis in young Asian men.

SUN-LB88 Thyrotoxic Periodic Paralysis in Hispanic Patients

BACKGROUND: Thyrotoxic periodic paralysis (TPP) presents as acute intermittent attacks of weakness related to hypokalemia, commonly reported in Asians and rare in Hispanics(1). Patients with TPP will have triiodothyronine (T3) triggered increased Na+/K+ ATPase pump activity and transcription of the KCNJ18 gene that encodes for the Kir2.6 channel(2). This permits insulin, catecholamines, stress and alcohol(3) to increase cellular intake of potassium, which causes depolarization and leads to weakness and paralysis. We report a case of TPP in a young Hispanic man who presented with lower extremity weakness and falls. CASE PRESENTATION: A 34-year-old Hispanic man with Graves’ disease, non-adherent to medications presented with generalized weakness, more pronounced in legs, and recurrent falls. Physical examination was unremarkable except for mild enlargement of thyroid gland and abnormal gait due to weakness. Laboratory data showed hypokalemia of 1.8 mmol/L (3.7-5.1 mmol/L) and a TSH level of <0.004 mIU/L (0.34-5.6 mIU/L). Free T4 3.74 ng/dL (0.6-1.6 ng/dL), free T3 597 pg/dL (230-420 Pg/dL), thyroid stimulating Ig 148 (<130). Electrocardiogram did not show U waves. Radio iodine 123 scan of thyroid revealed diffusely increased 24-hour radioactive uptake of 66.5% (10-30%). The patient was diagnosed with TPP and supplemented with three doses of potassium 40 mEq IV infusion. Methimazole and metoprolol were started. He made a good clinical recovery within days. After discharge, he was treated with I-131 (13 mci) and developed postablative hypothyroidism on long term. He was euthyroid on levothyroxine. He did not have any recurrence of weakness at 7-year follow-up. CONCLUSION: TPP is uncommonly seen in Hispanics patients as opposed to Asians(3). Physicians should consider TPP as part of the differential diagnosis in young hyperthyroid Hispanic men presenting with weakness or paralysis, as early recognition and treatment can reduce recovery time and potentially prevent tachyarrhythmia or death. REFERENCES: 1. Matta A, Koppala J, Gossman W. Thyrotoxic hypokalaemic periodic paralysis: a rare presentation of Graves’ disease in a Hispanic patient. BMJ Case Rep. 2014;2014. 2. Ryan DP, Ptacek LJ. Mutations in Potassium Channel Kir2.6 Cause Susceptibility to Thyrotoxic Hypokalemic Periodic Paralysis. Cell, 140(1), pp.88-98. 3. Amblee, A. and Gulati, S. (2016). Thyrotoxic Periodic Paralysis: Eight Cases in Males of Hispanic Origin from a Single Hospital. AACE Clinical Case Reports, 2(1), pp.e58-e64.

The three cases of Thyrotoxic periodic paralysis

The three cases of Thyrotoxic periodic paralysis

Thyrotoxic Periodic Paralysis with Sensory Deficits in Young African American Male: A Case Report and Literature Review.

Thyrotoxic periodic paralysis is a sporadic entity characterized by hypokalemia and paralysis in the setting of hyperthyroidism. TPP is most commonly described in young Asian males. Studies have shown an association with mutations affecting inward rectifying potassium channels. The pathophysiology involves Na+-K+- ATPase channel causing an increased intracellular shift of potassium ions in the hyperthyroid state and in the presence of another precipitating condition. Most cases of thyrotoxic periodic paralysis are defined in young Asian males of 20–40 years of age, here we present an interesting case of thyrotoxic periodic paralysis in 32-year-old African American male, who presented with sudden onset weakness in the bilateral lower extremity and left upper extremity. Interestingly, the patient also has sensory deficits, a feature not known to be associated with thyrotoxic periodic paralysis.