Intracellular Shift Of Potassium Research Articles

Thyrotoxic Periodic Paralysis after Surgery: A Case Report and Literature Review

Thyrotoxic periodic paralysis (TPP) is a rare but potentially life-threatening muscle disease in a thyrotoxic patient. Due to the lack of knowledge, the diagnosis is easily missed. Diagnosis of TPP is made by documentation of hypokalemia and hyperthyroidism in acute generalized muscle weakness. Hypokalemia is caused by an intracellular shift of potassium because of an increased Na-K-ATPase pump activity and the inhibition of the inward rectifying potassium (Kir) channels. The initial treatment aims to treat potentially life-threatening cardiac arrhythmias caused by severe hypokalemia. This can be done with potassium substitution and nonselective beta-blockers, being aware of the potential of rebound hyperkaliemia. Definitive treatment consists of avoiding triggers and correcting the hyperthyroid state with antithyroid drugs, radioactive iodine, or thyroidectomy. Once patients are, permanently euthyroid complete remission of the paralytic attacks usually occurs. We present a case of a 37-year-old male with diffuse muscle weakness after surgery. A new diagnosis of thyrotoxic periodic paralysis was made in the emergency department. This review summarizes the epidemiology, clinical manifestations, pathogenesis, diagnostics, and treatment of TPP.

FRI507 Thyrotoxic Periodic Paralysis: A Rare Occurrence Of Exogenous Thyroid Replacement

Abstract Disclosure: J. Case: None. D. Suravajjala: None. V. Eranki: None. Thyrotoxic periodic paralysis (TPP) occurs suddenly through excess thyroxine in tandem with insulin spurring an intracellular shift of potassium via increased activity of Na+/K+ ATPase pump leading to depletion of extracellular potassium with subsequent destabilization of cellular membranes and ensuing paralysis presenting with proximal muscle weakness of the legs. Common triggers involve vigorous exercise, infection, carbohydrate-rich meals, thyroiditis and graves' disease. Patients may be treated with IV potassium, non-selective beta blockers and treating the underlying cause. Exogenous thyroid hormone replacement causing iatrogenic hyperthyroidism as a cause of TPP is very rare. We present one such case below. A 61-year-old male with a history of primary hypothyroidism on thyroid replacement, atrial fibrillation, diabetes mellitus and hypertension, was admitted in September 2019 for lower extremity weakness at which time he was found with hypokalemia; he symptomatically improved following potassium replacement. He had a similar hospitalization in October, 2022 at which time he was found to have weakness alongside hypokalemia and hypomagnesemia, both of which were replaced with symptomatic improvement. He presented as an outpatient for follow up with likely etiology being TPP. Upon further review he had been taking both LT4 (Synthroid) 75mcg daily and T4/T3(Armour) 60mg daily; of note his TSH had been suppressed since 2019, three years prior to presentation. He was unsure why he had been on combination therapy. At our initial visit his labs were: TSH <0.005mIU/mL, free T4 1.38 ng/dL and T3 199 ng/dL. He was advised to stop all thyroid hormone replacement and experienced symptomatic improvement with normalization of potassium and magnesium. Repeat TFTs are pending for appropriate replacement dosing. Recognition of TPP and distinguishing from other etiologies of lower extremity weakness as well as other forms of periodic paralysis would aid in early resolution of an easily treatable, yet severe, condition given the implications of prolonged hypokalemia; earlier recognition of TPP in this patient as a sign of thyrotoxicosis may have prevented later hospitalizations and reduced risk of development of atrial fibrillation. This case also demonstrates the need for adequate monitoring and dosing of thyroid hormone supplement as well as potential complexities and risks of combination therapy in preventing an exogenously induced thyrotoxic state. Presentation: Friday, June 16, 2023

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

FRI550 Case Of Thyrotoxic Periodic Paralysis In African American Man With Cannabis Use

Abstract Disclosure: H. Al Jumaili: None. A. Mahaldar: None. S. Campbell: None. A. Gosmanova: None. Introduction: Recent changes in cannabis use (CU) laws led to growing interest in its use for recreational and therapeutic purposes. may have serious health problems such as hypokalemia, paralysis and rhabdomyolysis. Thyrotoxic Periodic Paralysis (TPP) is a rare and life-threatening complication of the thyrotoxicosis characterized by acute reversable painless muscle weakness or paralysis and hypokalemia due to massive intracellular shift of potassium. This condition is mainly seen males of Asian descent. Case: A 31-year-old African American man with Graves’ disease admitted to the hospital for upper and lower extremities weakness after Thanksgiving Day. He woke up with sudden inability to move any of his extremities with. He had high carbohydrate meal, on the evening. Patient reported having similar periodic episodes of paralysis, usually worse in the lower extremities for the last 2 years. This episode lasted longer than usual. On exam, he had enlarged thyroid gland and tachycardia. motor weakness, worse on lower extremities, hyporeflexia and intact sensation. Potassium was 1.8 mmol/l, magnesium 1.5 mg/dl, TSH <0.01 mIU/ml, FT4 4.3 ng/dl, FT3 18.3 ng/dl, anti-thyroid antibodies were elevated at 18 IU/L, and urine screen was positive for cannabinoid. Potassium was replaced, he was given propranolol and continued on methimazole. Patient's paralysis had improved in all four limbs, with serum potassium of 4.1 mmol/L. Discussion: TPP is a rarely seen condition in US but is known in an eastern Asian population, and in US the incidence rate was reported to be around 0.1 to 0.2%. American Indian are thought to be the higher risk. Underlying mechanism is imbalance in potassium homeostasis due to increased cellular Na-K ATPase pump activity with shift of potassium to the intracellular space. There are many theories regarding the cause of exaggerated intracellular potassium influx in TPP. Na-K ATPase activity is directly stimulated by thyroid hormone and insulin response to carbohydrate ingestion which promotes potassium uptake into muscle correlating with clinical observation that paralysis seen after a high carbohydrate meal. KCNJ18 gene mutations which alter the function of an inwardly rectifying potassium channel named Kir2.6 have been detected in some patients. In our patient, additional factor such as cannabis use potentiated intracellular potassium shift and hypokalemia. Recent evidence suggests that the CB1 receptor is expressed not only in the brain, but also found in lungs, heart, and skeletal muscle. Stimulation of (CB1) and activation of G protein-coupled inwardly rectifying potassium (GIRK) channels through intra-cellular signal cascades promotes hypokalemia and paralysis. Conclusion: This case raises awareness of TPP in non-Asian population and highlights the importance to consider cannabis as additional trigger for hypokalemia and paralysis. Presentation: Friday, June 16, 2023

A rare complication of a relatively common disease: periodic paralysis caused by thyrotoxicosis

Thyrotoxic periodic paralysis is a sporadic form of hypo-kalemic periodic paralysis and it is most commonly presents as sudden onset weakness in the proximal muscles. It is a disorder most commonly seen in Asian men which is characterised by abrupt onset of hypo-kalemia and paralysis and it is primarily affects lower extremities and is secondary to thyrotoxicosis. It is due to an intracellular shift of potassium induced by thyroid hormone sensitisation of Na/K ATPase rather than depletion of total potassium. The absence of a family history, male predilection and, presentation in second to fourth decade of life and signs of thyrotoxicosis and sinus tachycardia help in the diagnosis of the disorder. The age of onset is later and corresponded with age of incidence of thyrotoxicosis. It is very essential to diagnose TPP early and treat appropriately.

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: a presentation of hyperthyroidism increasing in frequency around the world

Thyrotoxic periodic paralysis (TPP) is a complication of hyperthyroidism commonly seen in Asian populations. It presents as sudden-onset muscle paralysis and hypokalaemia. Diagnosis is often delayed due to the rarity of the disease, the subtlety of the hyperthyroidism and the fleeting nature of the clinical presentation. With global expansion, physicians outside Asia should be aware of this disease for early recognition and treatment as severe cardiac arrhythmias, which may prove fatal, can occur. Several breakthroughs have been made in identifying the pathophysiological mechanism resulting in the severe hypokalaemia, including mutations in the Kir2.6 channel, an inwardly rectifying potassium channel, which results in a massive intracellular potassium shift. Treating the underlying hyperthyroidism is the definitive treatment; however, beta blockers and potassium supplementation are vital in acute management of this condition. This is a report of a case seen in Cape Town, South Africa with a review of the literature regarding the clinical features, pathophysiology and treatment.

A Severe Case of Hypokalemic Metabolic Alkalosis: A Quiz

A Severe Case of Hypokalemic Metabolic Alkalosis: A Quiz

ODP526 Thyrotoxic Periodic Paralysis in Graves’ Disease: A rare presentation in an African American male

Abstract INTRODUCTION: Thyrotoxic Periodic Paralysis is a rare but life-threatening manifestation of hyperthyroidism characterized by hypokalemia, acute flaccid paralysis, and signs of hyperthyroidism. Despite being commonly seen in East Asian males, TPP has been increasingly reported in other parts of the world including western countries. Early recognition and prompt treatment of TPP is essential in preventing its grave and potentially life-threatening consequences. CASE PRESENTATIONA 21-year-old African American male patient with past medical history significant for hypertension and untreated hyperthyroidism presented to the emergency department with sudden onset bilateral lower extremity weakness and difficulty walking for one day. Upon arrival to the emergency department, vitals were unremarkable. On examination, patient had a decreased muscle tone in bilateral lower extremities with depressed deep tendon reflexes. The thyroid gland was diffusely enlarged. The remainder of physical exam was normal. Electrolyte abnormalities were also present with decreased serum potassium level of 1.2 mEq/L (3.6-5.1 mEq/L) and magnesium of 1.7 mg/dL (1.8-2.5 mg/dL). A low TSH level of <0. 010 mIU/mL (0.350-4.940 mIU/mL) with elevated free T4 levels of 4.30 ng/dL (0.70-1.48 ng/dL) were noted. CT Head/ Brain without contrast and Chest X ray were unremarkable. Potassium replacement was initiated with oral and intravenous potassium chloride. He was also started on oral atenolol (25 mg daily) and methimazole (10 mg daily). The patient's symptoms resolved in few hours after the treatment was started. An ultrasound of the thyroid gland showed diffuse heterogeneity of the gland most consistent with thyroiditis or similar abnormality. No definite focal abnormalities were noted. TSH receptor antibodies were also elevated with levels at 10.70 IU/L (≤1.75 IU/L) making Graves’ disease the most likely diagnosis. The patient's condition significantly improved along his hospitalization with complete resolution of symptoms and electrolyte abnormalities. He was subsequently discharged on atenolol and methimazole with outpatient follow up at the endocrinology clinic. DISCUSSION TPP is an underreported yet possibly fatal medical complication of hyperthyroidism. Prevalence is higher in Asia, however, incidence in Western countries has been increasing. While the underlying pathophysiology is poorly understood, h ypokalemia in TPP results from an intracellular shift of potassium induced by an increased adrenergic sensitization of Na + /K + –ATPase pump. Genetic and environmental factors may possibly play a role. Treatment of TPP entails beta-blockade to prevent intracellular shift of potassium, replenishing potassium stores, as well as correcting the underlying hyperthyroid state. Immediate diagnosis and initiation of treatment prevents serious cardiopulmonary complications and increases the probability of full recovery of muscle weakness. Presentation: No date and time listed

RF25 | PMON113 Subarachnoid Hemorrhage Complicated by Nephrogenic and Central Diabetes Insipidus

Abstract Introduction Diabetes insipidus (DI) is a rare complication of subarachnoid hemorrhage (SAH) and associated with worse prognosis and increased mortality. We present a case of combined nephrogenic and central DI together with osmotic diuresis as a result of SAH and discuss the pathophysiology. Case A 63-year-old female without significant past medical history was found unresponsive. CT head followed by angiography confirmed extensive SAH arising from a saccular anterior communicating artery (Acoma) aneurysm. She underwent emergent coil embolization and right frontal external ventriculostomy drain placement. Postoperatively, she developed polyuria (300-400 mL/hour) and hypernatremia (156 mEq/L) concerning for the development of DI. Serum osmolality was elevated at 316 mOsm/kg, urine osmolality inappropriately low relative to serum osmolality at 289 mOsm/kg but also unexpectedly high for complete DI, serum potassium 2.9 mEq/L and urine potassium elevated urine at 9 mEq/L. Serum copeptin was 6 pmol/L and inappropriately low for nephrogenic DI, suggesting a mixed central and peripheral process as well as contribution from osmotic diuresis. Intravenous (IV) desmopressin (DDAVP) only slightly reduced the polyuria. Management was complicated by adypsia and persistent hypokalemia requiring ongoing replacement. IV fluid, which had initially consisted of high-osmolality Plasma-Lyte (294 mOsm/L), matched to urine output, was switched to D5W, leading to a significant decrease in polyuria. On post-operative day 17, DDAVP was discontinued with normalization of sodium (137 mEq/L), potassium (3.8 mEq/L) and urine output. Three months post-operatively, she was asymptomatic with intact pituitary function and no hypokalemia. Discussion Hypokalemia in patients with SAH is thought due to acute intracellular shift of potassium caused by excessive β2-adrenergic activity generated endogenously by the sympathetic nervous system. In our patient, there was also likely contribution from distal tubular delivery of sodium from osmotic diuresis, leading to increased urinary potassium losses and hypokalemia-induced partial nephrogenic DI which was further complicated by partial central DI as suggested by the inappropriately low copeptin level for nephrogenic DI in face of a high serum osmolality and inappropriately low urine osmolality. As the vascular supply to anterior hypothalamus is derived from the Acoma, rupture may compromise perfusion affecting neuronal populations in the lamina terminalis that regulate thirst and AVP secretion in response to hyperosmolarity. Early detection of DI is critical because hypovolemia can predispose to cerebral vasospasm and worsen outcomes. This case also depicts the importance of careful consideration of sources of osmolar loads such as the composition of administered IV fluids, and aggressive potassium replacement to maintain DDAVP sensitivity. Conclusion DI should be considered in polyuria syndrome with hypernatremia after a neurosurgical event. Nephrogenic and central DI and adypsia can manifest following SAH, with sources of iatrogenic osmolar load further complicating the clinical picture. Early recognition and treatment may reduce morbidity and mortality. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m., Monday, June 13, 2022 1:12 p.m. - 1:17 p.m.

Thyrotoxic periodic paralysis mimicking hypokalemic periodic paralysis

Thyrotoxic periodic paralysis is a unique disorder that causes episodic proximal lower extremity muscle weakness in a patient who already has a hyperthyroid state and is not treated for the underlying disease state. The affected population mostly includes Asian in origin specifically the male gender (vs most thyroid disorder affects the women gender). Precipitating factors include in addition to a hyperthyroid state are strenuous exertion, a high-carbohydrate meal, and drugs like diuretics, insulin, high dose of steroids, antiretrovirals, and interferon therapy. Other genetic causes include the decreased activity of Kir2.6 mutation increased activity of Na+/K+ ATPase causing an intracellular shift of potassium that leads to hypokalaemia. The other challenging part for the physician is to differentiate it from Familial periodic paralysis an autosomal disorder seen in Caucasians and Western countries because both the disorders present similarly and differentiate between them by the presence of hyperthyroid state with hypokalaemia in Thyrotoxic periodic paralysis. The mortality is associated with respiratory paralysis hence the acute intervention includes giving nonselective beta-blockers followed by anti-thyroid medications. We present a case of an Indian adolescent who presented to us with lower muscle weakness with an underlying thyrotoxicosis state. This help physician with early diagnosis and appropriate treatment.  Â

Thyrotoxic periodic paralysis associated with Graves’ disease: a case series

SummaryThyrotoxic periodic paralysis (TPP) is a rare condition characterised by acute onset hypokalaemia and paralysis which most commonly affects men of Asian descent between the ages of 20 and 40 years (1, 2). It has been reported in approximately 2% of patients with thyrotoxicosis in China and Japan (1, 2, 3). Hypokalaemia in TPP results from a massive intracellular shift of potassium induced by the thyroid hormone sensitisation of Na+/K+-ATPase (4). Treatment of TPP includes prevention of this shift by using beta-blockade, rapid potassium replacement and treatment of the underlying hyperthyroidism. We present two cases of TPP with differing outcomes. In the first case, a 33-year-old Filipino gentleman presented to our emergency department (ED) with a 3-month history of recurrent proximal lower limb weakness. Serum potassium was 2.2 mmol/L (3.3–5.1) and he was given i.v. potassium replacement. Thyroid function tests (TFTs) and thyroid antibodies were consistent with Graves thyrotoxicosis. He was discharged home on carbimazole and remains well controlled on long-term medical therapy. In the second case, a 22-year-old Malaysian gentleman presented to our ED with new-onset bilateral lower limb painless paralysis. Serum potassium was 1.9 mmol/L with TFTs demonstrating Graves thyrotoxicosis. He was treated with i.v. potassium replacement and discharged home on carbimazole and propranolol. He represented to the hospital on two further occasions with TPP and was advised to consider total thyroidectomy given his refractory Graves’ disease. These cases highlight the importance of prompt recognition of this rare life-threatening complication of Graves’ disease, especially in patients of Asian descent.Learning pointsThyrotoxic periodic paralysis is a rare condition characterised by hypokalaemia and acute painless muscle weakness in the presence of thyrotoxicosis.The signs and symptoms of thyrotoxicosis can be subtle in these patients.It is most commonly seen in Asian males between the ages of 20 and 40 and is most frequently caused by Graves’ disease.Prompt recognition is essential as it is a life-threatening condition.Urgent i.v. potassium replacement and beta-blockade with a non-selective beta-blocker are the mainstays of treatment.i.v. potassium replacement should not be given in dextrose as this can potentiate hypokalaemia.

Caffeine-induced hypokalemia: a case report

BackgroundWith an increase in the global popularity of coffee, caffeine is one of the most consumed ingredients of modern times. However, the consumption of massive amounts of caffeine can lead to severe hypokalemia.Case presentationA 29-year-old man without a specific past medical history was admitted to our hospital with recurrent episodes of sudden and severe lower-extremity weakness. Laboratory tests revealed low serum potassium concentration (2.6–2.9 mmol/L) and low urine osmolality (100–130 mOsm/kgH2O) in three such prior episodes. Urinary potassium/urinary creatinine ratio was 12 and 16 mmol/gCr, respectively. The patient was not under medication with laxatives, diuretics, or herbal remedies. Through an in-depth interview, we found that the patient consumed large amounts of caffeine-containing beverages daily, which included > 15 cups of coffee, soda, and various kinds of tea. After the cessation of coffee intake and concomitant intravenous potassium replacement, the symptoms rapidly resolved, and the serum potassium level normalized.ConclusionsAn increased intracellular shift of potassium and increased loss of potassium in urine due to the diuretic action have been suggested to be the causes of caffeine-induced hypokalemia. In cases of recurring hypokalemia of unknown cause, high caffeine intake should be considered.

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 & 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 & 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 <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 & treatment prevents life threatening complications. Differential diagnosis of TPP includes familial periodic paralysis, Guillain-Barre Syndrome & 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.

Nebulized albuterol delivery is associated with decreased skeletal muscle strength in comparison with metered-dose inhaler delivery among children with acute asthma exacerbations.

ObjectiveAlbuterol is a β2‐agonist and causes an intracellular shift of potassium from the interstitium. Whole‐body hypokalemia is known to cause skeletal muscle weakness, but whether this occurs as a result of hypokalemia from the intracellular shift during albuterol treatment is unknown. We sought to determine if albuterol total dose or route of administration (nebulization and/or metered‐dose inhaler) is associated with skeletal muscle weakness.MethodsThis was a prospective observational study using convenience sampling. Skeletal muscle strength was measured before and after 1 hour of albuterol treatment using a hand‐grip dynamometer in participants aged 5–17 years with acute asthma exacerbation in the emergency department. We examined associations of albuterol dose and route of administration with changes in grip strength.ResultsAmong 50 participants, 10 received continuous albuterol by nebulizer and 40 received albuterol by metered‐dose inhaler. The median (interquartile range) in change of grip was ‐7.8% (interquartile range, ‐23.3, +5.1) for those treated with a nebulizer and +2.4% (interquartile range, ‐5%, +12.7%) for those treated with a metered‐dose inhaler (P = 0.036 for the difference). In a multiple linear regression model adjusted for the pretreatment Acute Asthma Intensity Research Score and age, participants treated with a nebulizer had a 12.9% decrease in skeletal muscle strength compared with those treated with a metered‐dose inhaler.ConclusionHigher doses of albuterol administered via nebulization result in decreased skeletal muscle strength in patients with acute asthma; whereas, albuterol administration via metered‐dose inhalers showed no effect on skeletal muscle strength.

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.

Hypokalemia in peritoneal dialysis patients in Thailand: the pivotal role of low potassium intake.

Hypokalemia is highly prevalent in chronic peritoneal dialysis (PD) patients worldwide, particularly in Thailand. This study aims to investigate the major determinants of hypokalemia in Thai PD patients. A cross-sectional study was performed in chronic PD patients at 4 PD centers in Bangkok, Thailand. Hypokalemia was defined if the average serum potassium level during the last 3 consecutive visits was < 3.5mEq/L. Patients and/or their caregivers were asked to perform a 3-day dietary food record and take pre- and post-meal pictures following the instructed protocol. Daily dietary nutrients, including potassium, were estimated by a single dietician using INMUCAL-N software. Total potassium excretion was determined by 24-h PD effluents and urine collection. Intracellular and extracellular water values (ICW and ECW, respectively) were measured by electrical bioimpedance assay (BIA) to indirectly explore the role of intracellular potassium shift in hypokalemia. Among 60 eligible PD patients, 19 (31%) had hypokalemia. Hypokalemic patients had significantly lower dietary potassium intake (24.4 ± 11.1 vs. 30.5 ± 9.4mEq/day, p = 0.031) and lower total potassium excretion (28.5 ± 8.4 vs. 36.7 ± 11.2mEq/day, p = 0.006) compared to normokalemic patients. Both groups had comparable values of ICW and ECW. On logistic regression, there was no significant correlation between hypokalemia and daily PD exchange volume, total Kt/Vurea, residual renal function, concurrent medications (insulin, diuretics, renin-angiotensin-aldosterone inhibitor, and beta-blockers) or ICW. Low dietary potassium was an independent risk factor for hypokalemia. Low dietary potassium intake, rather than increased potassium excretion or intracellular shift, is the major contributing factor of hypokalemia in Thai chronic PD patients. Dietary intervention or potassium supplement protocol should be implemented.

Hypokalaemic Paralysis - A double trouble from concurrent Thyrotoxicosis and Gitelman syndrome: A report of two cases

Background Hypokalaemic paralysis is a rare group of disorders with concomitant muscle weakness and hypokalaemia. Thyrotoxicosis is a recognized and a common cause for hypokalaemic paralysis among Asians, in which intracellular shift of potassium is enhanced. Gitelman syndrome, an autosomal recessive renal salt loosing condition is characterized by hypokalaemia, hypocalciuria and hypomagnesaemia. Concurrence of these two conditions is very rarely reported. Case Presentation We report two genetically unrelated Sri Lankan patients who presented with concurrent thyrotoxicosis and Gitelman syndrome. Both of them presented with symptomatic hypokalaemia and detected to have thyrotoxicosis. One had Grave’s disease, while the other patient had toxic multinodular goiter. They were initially managed symptomatically for thyrotoxic hypokalaemic paralysis. Despite rendering euthyroidism with medical management, they persisted to have symtomatic hypokalaemia. On evaluation for a second pathology, we detected them to have Gitelman syndrome, which is a rare concurrence. Conclusion Elevated thyroid hormone levels can precipitate a paralytic episode in a patient with subclinical chronic hypokalaemia due to an additional underlying disease. Gitelman syndrome is such a disease which should be considered and actively looked for in a patient with persistent hypokalaemia following rendering euthyroidism.

SUN-496 A Challenging Diagnosis of Thyrotoxic Periodic Paralysis

Thyrotoxic Periodic Paralysis (TPP) is a rare but potentially lethal manifestation of hyperthyroidism which is characterized by muscular weakness due to intracellular shift of potassium and subsequent hypokalemia. The muscular weakness may range from mild weakness to complete flaccid paralysis. It is predominantly seen in Asian young men. Graves’ disease has been described as the most common cause of TPP. Other rare causes of hypokalemic periodic paralysis include inherited disorders and acquired cases due to drug abuse, specifically cocaine. It is important to recognize and diagnose TPP to provide appropriate treatment and prevent serious cardiopulmonary complications.A 26 year old Hispanic male with past medical history of cocaine abuse presented to the emergency department with profound lower extremity weakness since that morning. Laboratory studies on initial evaluation revealed hypokalemia. He was admitted to the intensive care unit (ICU) for IV potassium replacement and cardiac monitoring. Upon obtaining further history, the patient had suffered a similar episode of weakness and hypokalemia two months prior. At the time, he had a positive urine toxicology for cocaine. He was treated with IV potassium with resolution of his weakness and was told the reason for the episode was cocaine induced periodic paralysis. No further work up was done due to patient leaving Against Medical Advice. The patient stopped recreational drug abuse after this diagnosis.During current hospitalization, further laboratory studies revealed hyperthyroidism. TSI and TPO antibodies were elevated and thus patient was diagnosed with Graves’ disease. On questioning, patient was asymptomatic and clinically euthyroid. He was treated with IV potassium, methimazole and propranolol with quick resolution of weakness. He has been followed in an out-patient basis and he has had no further exacerbations.In this case, we present a case of TPP that was initially diagnosed as cocaine induced periodic paralysis which is an extremely rare disorder with only a couple of described cases in the literature. Diagnosis was initially missed as the patient was clinically euthyroid and had history of recreational drug abuse. Restoration of euthyroidism eliminates attacks of TPP. It is important to recognize and diagnose these patient to prevent further attacks.

An unusual cause of periodic weakness

Sir, Thyrotoxicosis is a rare cause of periodic paralysis. It is a rare endocrine disorder found mainly in men of Asian origin. We report the case of a 32-year-old male patient who came with repeated episodes of bilateral lower limb weakness for the last 2 months. The weakness episodes were mostly early morning lasting from few hours to occasionally a day. The patient had difficulty walking, climbing stairs, and getting up from the squatting position. Weakness used to improve with rest. There was no history of preceding high-carbohydrate diet or exertion. He also gave a history of heat intolerance, palpitations, and weight loss for the last 1 year. There was no significant past illness or family history. On physical examination, he had tachycardia with normal blood pressure. There was no exophthalmos or goiter. Neurological examination revealed hypotonia in bilateral lower limbs. He had a proximal weakness (Grade 3/5) in bilateral lower limbs while distal motor strength was normal. There was generalized hyporeflexia. Plantar responses were bilaterally flexor. The rest of the neurological examination was unremarkable. Laboratory studies revealed hypokalemia (serum potassium – 2.8 mmol/l), thyroid-stimulating hormone <0.001 mU/l, and free T4 56.8 pmol/l (normal range 9–21 pmol/l). Antithyroid peroxidase levels were high (1630 U/ml; normal range 0–50 U/ml). Electrocardiogram was normal. The patient was managed with oral potassium supplementation. He was started on carbimazole and propranolol therapy. The patient gradually improved and discharged. Thyrotoxic periodic paralysis (TPP) is a rare syndrome, predominantly found in young men of Asian origin. Various precipitating factors, including a high-carbohydrate meal, warm weather, and increased physical exertion, have been identified.[1] It mainly affects the proximal group of muscles without any cranial nerve or sensory involvement. Patients can rarely have respiratory failure or cardiac arrhythmias.[23] In TPP, the primary defect is an intracellular accumulation of potassium.[4] Thyroid hormones increase the activity of Na-K-ATP pump, which changes the permeability of the plasma membrane to potassium.[5] Other mechanisms have also been proposed which cause intracellular shift of potassium. Patients suspected of having TPP should be kept under cardiac monitoring to check for arrhythmias. Furthermore, arterial blood gas pressures and spirometric assessment required to monitor respiratory function.[1] Potassium levels should be monitored. Potassium correction is the cornerstone in the emergency management of TPP. Primary illness has to be treated with antithyroid drugs. Furthermore, beta-blockers should be added to manage the peripheral effects of thyrotoxicosis. In conclusion, young men presenting with periodic paralysis should be evaluated for thyrotoxicosis. Early diagnosis and prompt treatment can prevent fatal complications. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.