Severe Hyperthyroidism Research Articles

SUN-522 A Case of Diabetic Ketoacidosis Associated with Thyroid Storm

Background: Thyrotoxic crisis is a rare complication of diabetic ketoacidosis (DKA). We herein report a case of DKA and subsequent thyroid storm which required emergent tracheostomy possibly due to large goiter and post-intubation obstruction.Clinical Case: A 26-year-old woman was admitted to our emergency department complaining fever (38.2℃) and palpitation. There was no history of autoimmune disease. Physiological examination revealed tachycardia (pulse rate 164/min), tachypnea (55/min), impaired consciousness with a GCS score of 13 (E3V4M6) and goiter. Endotracheal intubation was performed. Her laboratory tests showed metabolic acidosis (pH 7.255), marked high plasma glucose of 1,672 mg/dL, elevated HbA1c of 9.2%, elevated FT3 and FT4 with suppressed TSH. She scored 55 on the diagnostic criteria for thyroid storm of Burch & Wartofsky. Based on these findings, she was diagnosed as having DKA and thyroid crisis. The patient responded well to standard treatment which involves intravenous insulin infusion with pump, correction of electrolyte disturbances, use of methimazole, as well as propranolol. Meanwhile, the patient was positive for anti-glutamic acid decarboxylase (GAD) antibody, TSH receptor antibody, as well as thyroid stimulating antibody, indicating type 1 diabetes and Graves’ disease. She underwent extubation on day 5, however, she developed wheezing around day 30. Imaging analysis demonstrated remarkable tracheal stenosis that is possibly due to large goiter and airway injury by intubation. Emergent tracheostomy was performed on day 50, because the dyspnea became progressively worse. Later, she was successfully treated by tracheal stent placement. At the follow-up period, the patient was found to be doing well, with no severe hyperthyroidism or changes in bronchoscopic findings.Conclusion: Thyroid storm is a rare but serious complication of DKA. Our report highlights the importance of considering airway obstruction due to large goiter especially in patients with a past history of prolonged ventilation.

SAT-464 A Case of Impending Thyroid Storm in a Patient with Subacute Thyroiditis Following an Influenza Vaccine

Introduction: Thyroid storm is a rare, potentially fatal condition, affecting 1% of individuals with thyrotoxicosis. Although it can theoretically be seen in any cause of thyrotoxicosis, the most likely underlying etiology is Graves’ disease. The rarity of thyroid storm due to thyroiditis makes the diagnosis challenging as the clinical and biochemical features overlap Grave’s disease. Here we describe a rare case of severe thyrotoxicosis in a woman due to subacute thyroiditis that developed after receiving an influenza vaccine.Case report: A 30 year-old Caucasian female with no known past medical history presented to the ED with worsening sore throat, odynophagia and anterior neck pain. Symptoms began 4 weeks ago prior to presentation, 1 day after receiving an influenza vaccine. Other symptoms included loss of appetite, chills, fever, fatigue, malaise, abdominal pain, diarrhea, palpitations, heat intolerance and 5lbs weight loss. She was treated by her primary care provider for suspected pharyngitis with a course of corticosteroids and antibiotics. Two weeks later, given worsening symptoms, was referred to the emergency room. On exam, she appeared anxious and was tachycardic (124 beats per minute) and tachypneic (28 breaths per minute). She had no lid lag, stare, thyromegaly or thyroid bruit. However, there was significant tenderness on palpation of the anterior neck. Laboratory evaluation was notable for TSH <0.01 uIU/mL (0.39 - 4.0.8), free T4 5.19 ng/dL (0.58 - 1.64), free T3 10 pg/ml (2.53-3.87), ESR 95 mm/hr (0-20) and CRP 9.339 mg/dl (0.0-0.9) consistent with thyrotoxicosis. Given Burh-Wartofsky score of 45, there was a concern for impending thyroid storm. She received hydrocortisone, methimazole and beta blockers and was admitted to the intensive care unit. She responded dramatically to treatment and was discharged within 24 hours on prednisone and metoprolol. The 24-hour radioactive iodine uptake (RAIU) was 2.7% 2 weeks post admission, consistent with a diagnosis of subacute thyroiditis. TSI was negative. Family history was negative for autoimmune disease. She continued on beta blockers with a steroid taper for 8 weeks. Thyroid function tests and inflammatory markers normalized within 3 months.Conclusion:Aside from the described patient, only three other cases of thyrotoxic crisis due to subacute thyroiditis have been reported in the literature. This case underscores the importance of thoroughly investigating the etiology of severe thyrotoxcosis, given the management and prognosis varies depending on underlying cause. Thyroiditis should be considering in the differential diagnosis of thyroid storm in patients who do not have a personal or family history of autoimmunity and present with neck tenderness in the setting of a precipitating event. Subacute thyroiditis is very uncommon after influenza vaccine, there have been 4 reported cases.

SUN-513 Severe Hyperthyroidism in a Complete Molar Pregnancy

Hydatidiform mole (HM), a type of gestational trophoblastic disease (GTD), is a rare cause of clinical hyperthyroidism. The development of hyperthyroidism requires an elevation of HCG >100,000 mlU/mL for several weeks. Complete mole has a marked HCG elevation compared to partial mole thus presents with a higher incidence of thyrotoxicosis. Surgical uterine evacuation is the treatment of choice for HM. However, untreated hyperthyroidism can pose a risk for the development of thyroid storm and high-output cardiac failure in the perioperative period. To our knowledge, there are no specific guidelines for management at this time. We present a case of hyperthyroidism secondary to complete molar pregnancy successfully treated with propylthiouracil (PTU), potassium iodide (SSKI), and atenolol in the preoperative period.A 42-year-old female with history of migraines presented to her gynecologist with a 3-week history of lower abdominal cramping, vomiting, loss of appetite, and abnormal vaginal bleeding. She also endorsed a 6-pound weight loss, intermittent tachycardia, exertional dyspnea, and increased anxiety. Pregnancy test was positive, and ultrasound was concerning for GTD. Laboratory work up was significant for HCG 797,747 mIU/mL (< 5mlU/mL), TSH <0.005 mIU/mL (0.4-4.0 mlU/mL), Free T4 3.09 ng/dL (0.9-1.9 ng/dL), and Free T3 11.48 pg/dL (1.76-3.78 pg/dL). The patient was admitted to the hospital and started on PTU 100 mg Q6H, SSKI 200 mg TID following the first dose of PTU, and atenolol 25 mg daily. She underwent an uncomplicated D & C the next day. On post-op day 1, HCG decreased to 195,338 mIU/mL and Free T4 to 2.39 ng/dL. The patient was discharged on the aforementioned doses of PTU and atenolol. One-week follow-up labs showed HCG 8,917 mIU/mL and Free T4 1.22 ng/dL. Surgical pathology confirmed a complete hydatidiform mole. PTU was decreased to 50 mg TID. On post-op day 14, HCG had risen to 15,395 mIU/mL with onset of nausea and vomiting. Repeat Free T4 remained within reference range. Patient was taken back to surgery for a laparoscopic total hysterectomy with bilateral salpingectomy. Pathology confirmed an invasive hydatidiform mole. Two-week follow-up lab work showed HCG 155 mIU/mL, TSH 1.5 mIU/mL, and Free T4 1.19 ng/dL. PTU and atenolol were then discontinued.The development of hyperthyroidism in molar pregnancy is largely influenced by the level of HCG and usually resolves with treatment of GTD (1). However, it’s crucial to control thyrotoxicosis to avoid perioperative complications. This case also highlights the importance of monitoring HCG levels following a complete molar pregnancy due to an increased risk for invasive neoplasm.1. Walkington, L et al. “Hyperthyroidism and human chorionic gonadotrophin production in gestational trophoblastic disease.” British journal of cancer vol. 104,11 (2011): 1665-9. doi:10.1038/bjc.2011.139

SUN-506 Hyperthyroidism Induced Hepatic Apoptosis

Background:Graves’ disease is commonly associated with abnormal liver function tests, most frequently ALP, but the exact mechanism is not fully understood. In vitro and in vivo animal studies have shown elevated T3 activity can induce hepatocyte apoptosis via a mitochondrial-mediated pathway. This case demonstrates a patient with elevated aminotransferases and hepatic apoptosis most likely secondary to severe hyperthyroidism.Clinical Case:50 year old female with a past medical history of migraines was seen by primary care for fatigue and 15 lb weight loss in one month. She was found to be hyperthyroid with TSH < 0.1 uIU/L (n=0.34-5.6), free T4 3.48 ng/dL (n=0.58-1.64) and mildly elevated aminotransferases of AST 77 IU/L (n=15-41), ALT 144 IU/L (n=12-63), which increased within a week to 159 IU/L and 309 IU/L respectively. ALP and bilirubin were within normal range. She was started on methimazole 20 mg twice daily by her PCP. The patient developed vomiting and stopped taking methimazole after 3-4 days. Upon initial presentation to endocrine clinic, found to be clinically hyperthyroid and as LFTs were improved but still elevated, she was re-challenged with methimazole at a lower dose as well as started on a beta blocker and cholestyramine. TT3 checked was elevated at 2.10 ng/mL (n 0.87-1.78). Graves’ disease was confirmed with elevated TSI as well as RAI uptake and scan showing increased homogenous uptake.She had extensive workup for another etiology by hepatology including autoimmune, which were negative. Her fibrosis score was stage F1-F2 (n=F0) and necroinflammatory activity grade A3 indicating severe activity (n=grade A0). Core needle biopsy of the liver showed focal lytic necrosis/apoptosis and abundant pigment-laden Kupffer cells signifying recent hepatocellular injury. Her AST and ALT down trended and normalized with repeat fibrosis score of F1 and necroinflammatory activity grade A0. She eventually had definitive therapy with RAI treatment. Conclusion: In most cases of hyperthyroid induced liver dysfunction, liver histology showed fatty infiltration, cytoplasmic vacuolization, nuclear irregularity and hyperchromatism.This case, without any other known causes that could explain her hepatic injury, indicates the possible role of hyperthyroidism in hepatic apoptosis.

Abstract #799405: Atypical Presentation of Severe Thyrotoxicosis in Early Pregnancy

Abstract #799405: Atypical Presentation of Severe Thyrotoxicosis in Early Pregnancy

Therapeutic Plasma Exchange in Refractory Hyperthyroidism

Introduction: Hyperthyroid patients who are unresponsive to medical treatment remain a challenging clinical problem. Objective: The goal of our study was to evaluate the use of therapeutic plasma exchange (TPE) in hyperthyroid patients and their outcome after TPE. Method: We retrospectively reviewed 22 patients who underwent TPE for refractory thyrotoxicosis in our institution: 13 with Graves’ disease, 7 with amiodarone-induced thyrotoxicosis (AIT), 1 with toxic goiter, and 1 pregnant patient with familial nonautoimmune thyrotoxicosis. Results: Before TPE, all patients had severe hyperthyroidism, and antithyroid drugs were either contraindicated or not sufficiently effective to restore euthyroidism promptly. After all the TPEs, free T₄ (fT4) decreased significantly by 48% (p = 0.001) and fT3 by 52% (p = 0.0001). The median number of TPE sessions per patient was 4 (range: 1–10). There were no complications during the 91 TPE sessions. Total thyroidectomy with no severe side effects was performed on 16/22 patients and 1 other patient was treated with radioactive iodine. One patient died from severe thyrotoxicosis during medical care. The remaining 4 patients were followed up without any radical treatment. For all 7 patients with AIT, iterative TPE led to a significant clinical improvement, and amiodarone was continued for 1 patient. Available treatments were continued between TPE sessions (cholestyramine for 13 patients [60%] and glucocorticoids for 16 patients [73%]). Conclusion: TPE allowed a safe decrease of 50% in thyroid hormone levels, and it should be considered for refractory hyperthyroid patients when medical treatments are contraindicated or have failed to restore euthyroidism, irrespective of the etiology of the thyrotoxicosis.

Thyroid Hormone Diseases and Osteoporosis.

Thyroid hormones are essential for normal skeletal development and normal bone metabolism in adults but can have detrimental effects on bone structures in states of thyroid dysfunction. Untreated severe hyperthyroidism influences the degree of bone mass and increases the probability of high bone turnover osteoporosis. Subclinical hyperthyroidism, defined as low thyrotropin (TSH) and free hormones within the reference range, is a subtler disease, often asymptomatic, and the diagnosis is incidentally made during screening exams. However, more recent data suggest that this clinical condition may affect bone metabolism resulting in decreased bone mineral density (BMD) and increased risk of fracture, particularly in postmenopausal women. The main causes of exogenous subclinical hyperthyroidism are inappropriate replacement dose of thyroxin and TSH suppressive L-thyroxine doses in the therapy of benign thyroid nodules and thyroid carcinoma. Available data similarly suggest that a long-term TSH suppressive dose of thyroxin may decrease BMD and may induce an increased risk of fracture. These effects are particularly observed in postmenopausal women but are less evident in premenopausal women. Overt hypothyroidism is known to lower bone turnover by reducing both osteoclastic bone resorption and osteoblastic activity. These changes in bone metabolism would result in an increase in bone mineralization. At the moment, there are no clear data that demonstrate any relationship between BMD in adults and hypothyroidism. Despite these clinical evidences, the cellular and molecular actions of thyroid hormones on bone structures are not complete clear.

The role of therapeutic plasmapheresis in patients with hyperthyroidism

BackgroundHyperthyroidism is characterized by excess hormone secretion from the thyroid gland. Anti-thyroid drugs (ATDs), surgery, and radioactive iodine can be used in treatment. Plasmapheresis is a rapid and effective treatment option in cases where rapid euthyroidism is needed to be obtained due to complications of thyrotoxicosis and major adverse effects of ATDs. Material and methodWe present patients receiving plasmapheresis to provide immediate euthyroidism due to severe hyperthyroidism, adverse effects of ATDs, or non-thyroid surgery from January 2012 to December 2016. ResultsThis study included 18 patients. The etiology of hyperthyroidism was TDG in seven patients, TDMNG in two, TA in two, TMNG in four, and one patient had AIT. Plasmapheresis was performed to achieve euthyroidism before surgery in two patients. The mean plasmapheresis session was 5.35. The mean number of sessions needed for patients with TDG and TDMNG was 4, whereas it was 6.5 for patients with TA and TMNG (p = 0.07). The decrease of mean free thyroxine and free triiodothyronine were 57 % and 73 %, respectively (p < 0.001). After plasmapheresis, total thyroidectomy was performed in 14 patients. Euthyroidism was achieved with RAI in one patient and with medical therapy in three patients. ConclusionsPlasmapheresis therapy is a reliable and effective treatment option for patients who cannot use ATDs because of their adverse events and those with hyperthyroidism that does not resolve with these drugs, or to achieve euthyroidism before total thyroidectomy, RAI or non-thyroid emergency surgery. However, it cannot be used widely because it is expensive and invasive.

Long-term results of surgical treatment in patients with toxic goiter and severe thyrotoxicosis

Long-term results of surgical treatment in patients with toxic goiter and severe thyrotoxicosis

“Is there any reason to treat subclinical hypo and hyperthyroidism?”

Subclinical thyroid disease represents an early stage of thyroid dysfunction, which is usually asymptomatic and biochemically defined; its diagnosis can be performed thanks to the high sensitivity of the hypothalamic-pituitary-thyroid axis. The approach to this disorder requires correct diagnosis, clinical assessment and treatment. Cardiovascular diseases (e.g. atrial fibrillation, heart failure, and coronary heart disease), bone loss and fractures, and dementia represent the main adverse events of severe subclinical hyperthyroidism with undetectable TSH levels. Treatment of patients with subclinical hypothyroidism with a serum TSH level above 10 mIU/L is justified in order to reduce the risks of coronary heart disease and heart failure.

The potential markers involved in newly diagnosed graves' disease and the development of active graves' orbitopathy

BackgroundGraves' disease (GD) patients experience two major issues: one is the severe hyperthyroidism associated with newly diagnosed GD, and the other involves the disfiguring and dysfunctional features of active Graves' orbitopathy (GO). Therefore, the aim of our study was to identify potential markers involved in the initial phase of GD dysfunction and the development of active GO. MethodsSeventy-eight subjects were recruited: 40 with newly diagnosed GD, 20 with inactive GO and 18 with active GO. GO activity was evaluated by the clinical activity score (CAS, active GO = CAS ≥ 3), and severity was assessed according to the NOSPECS classification. Plasma selenium concentrations were determined by dual channel hydride generation atomic fluorescence photometry. A liquid chip assay was used to measure plasma Th1 cytokines IFN-γ and TNF-α; Th2 cytokines IL4, IL5 and IL6; Th17 cytokine IL23; Treg cytokines IL10 and TGF-β; and two chemokines, CCL2 (Th2 chemokine) and CXCL10 (Th1 chemokine). ResultsAmong the three groups, newly diagnosed GD patients showed significantly elevated plasma levels of CXCL10 and IL-23 (all p < 0.05). Both CXCL10 and IL23 were significantly correlated with hyperthyroidism severity, specifically, increasing FT3 and FT4 and decreasing TSH. Notably, a very strong positive relationship between IL23 and CXCL10 was revealed (adjusted R square = 0.795; p < 0.001).Moreover, the selenium level was lower, while that of CCL2 was higher, in active GO than in inactive GO (p = 0.007, p < 0.001, respectively). Likewise, we also discovered that increasing CCL2 levels and decreasing selenium levels were associated with high CAS. Remarkably, after adjusting for potential confounding factors, selenium (OR, 0.919) and CCL2 (OR, 1.042) were still independent predictors for the diagnosis of active GO, and similar conclusions were drawn by receiver operating characteristic (ROC) curve analysis. ConclusionPro-inflammatory cytokines, especially Th17-associated cytokines (e.g., IL23) and Th1 chemokines (e.g., CXCL10), appear to be involved in the initial phase of GD dysfunction. Moreover, we revealed for the first time that decreased plasma selenium levels and increased concentrations of Th2 chemokines (e.g., CCL2) may reflect GO disease activity, shedding light on the diagnosis and evaluation of active GO.

Thyrotoxicosis after massive triiodothyronine (LT3) overdose: a coast-to-coast case series and review.

Excessive exogenous thyroid hormone ingestion may lead to severe thyrotoxicosis and cause potential harm. We have reviewed the literature and suggested that thyroid hormone supplementation should not be used to alleviate nonspecific complaints in patients with normal endogenous thyroid function. Failure to do so may cause serious harm, as demonstrated in one of the cases described here. In addition, treatment based on symptom relief only without biochemical measure may lead to overmedication – as reported from academic hospitals both in Canada and the United States. Given the risk of severe thyrotoxicosis from potential compounding errors, pharmacies providing a compounding service should be subject to more rigorous monitoring by the food and drug administration. Clinicians should also use local biochemical markers when titrating thyroid hormone supplements even though the normal thyroid function reference range has its limitation, failure to do so may result in iatrogenic thyrotoxicosis.

Therapeutic Plasma Exchange as a Bridge to Total Thyroidectomy in Patients with Severe Thyrotoxicosis

Graves disease is the most common cause of thyrotoxicosis. Medical management is the first-line treatment but may be contraindicated or ineffective. In patients with severe, refractory thyrotoxicosis therapeutic plasma exchange (TPE) may be indicated as a bridge to thyroidectomy. We present 3 cases of thyrotoxicosis refractory to medical management that were successfully treated with TPE and subsequent total thyroidectomy, and provide an analysis of the response to therapy via a change in free thyroxine (fT4) levels throughout their treatment course. The average change in fT4 per liter of fluid exchanged was 0.37 ng/dL (SD = 0.08) and the average percentage change of fT4 after each treatment was 20.7% (SD = 8.28). The mean decrease in fT4 after 4 TPE treatments was 57.4%. All patients successfully underwent total thyroidectomy without complication and were discharged from the hospital. TPE should be considered for thyrotoxic patients with severe hyperthyroidism or thyroid storm refractory to medical management or contraindications to antithyroid drugs who need a bridge to total thyroidectomy. In these cases, TPE was a safe and effective treatment that enabled definitive management with thyroidectomy and may be considered in other patients with severe refractory hyperthyroidism or thyrotoxicosis.

ИНТЕГРАЛЬНАЯ ОЦЕНКА СТЕПЕНИ ТЯЖЕСТИ ТИРЕОТОКСИКОЗА

Introduction. Estimate thyrotoxicosis severity considering proposed integral index based on a medical history, the main clinical, laboratory and instrumental methods of research Purpose. A study of 37 patients with toxic goiter using the proposed thyrotoxicosis severity integrated estimation was conducted. 23 (62.1%) were diagnosed with diffuse toxic goiter (DTZ), and 14 (37.8%) had multinodular toxic goiter (MTZ). There were 31 women (83.7%) and 6 men (16.2%). Results. Using our integrated thyrotoxicosis severity estimation 11 people (29.7%) were diagnosed with mild thyrotoxicosis, 25 people (67.5%) - moderate severity, 1 man (2.7%) - severe thyrotoxicosis. Compared with the classification specified in the Federal Clinical Recommendations (2014), 1.6 times more cases of mild thyrotoxicosis and 6 times less cases of severe thyrotoxicosis were detected. Conclusion. The proposed thyrotoxicosis severity integral estimation index is simple and affordable for clinical practice usage, it allows to more accurately estimate patient’s condition severity, suggests a personalized approach not only to thyrotoxicosis severity estimation, but also to determine further treatment tactics.

Early diagnosis and prompt treatment of severe thyrotoxicosis in patients with congestive cardiac failure is critical: lessons from a case of type 1 amiodarone induced severe thyrotoxicosis

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

Thyrotoxicosis in a Pediatric Patient with Supraventricular Tachycardia and Borderline Features of Thyroid Storm

The objective of this report was to emphasize the early recognition of thyrotoxicosis in the assessment of a pediatric patient with tachycardia. We present here the case of a 17-year-old female who presented with supraventricular tachycardia and was found to be in a state of severe thyrotoxicosis with borderline features of a thyroid storm. A 17-year-old African American female presented to the hospital with complaints of nausea, vomiting, and diarrhea associated with palpitations for 1 week. Initial workup included electrocardiogram, total blood count, lipase, basic metabolic panel, and thyroid function tests. Initial vital signs were significant for a temperature of 100.1°F, and tachycardia with a heart rate (HR) of 180 beats per minute (bpm). Initial telemetry was significant for supraventricular tachycardia with a HR of 180 bpm. Vagal maneuvers including carotid sinus massage were attempted first followed by 6 mg intravenous (IV) push and then 12 mg IV push of adenosine. However, the patient remained tachycardic with a HR in the 150s. Laboratory evaluation confirmed the presence of thyrotoxicosis with a thyroid-stimulating hormone of 0.17 μIU/mL (normal, 0.5 to 4.7 μIU/mL) with a free thyroxine of 4.90 ng/dL (normal, 0.8 to 2.0 ng/dL) and free triiodothyronine >20 pg/mL (normal, 1.95 to 5.85 pg/mL). She was subsequently treated with propranolol, methimazole, and hydrocortisone, which resolved her symptoms in a few hours. Due to high mortality rates, severe thyrotoxicosis needs to be recognized and treated early. This case report highlights the importance of early recognition of thyrotoxicosis in the initial management of tachycardia in the pediatric population.

5207Bilateral cardiac sympathetic denervation in structural heart disease

Abstract Background Left cardiac sympathetic denervation (LCSD) is an established therapy for refractory ventricular arrhythmias (VAs) in channelopathies. A multicentric American and Indian case series suggested a greater efficacy of bilateral denervation (BCSD) in patients with structural heart disease (SHD). Purpose To describe our single-center experience with BCSD in SHD. Methods Nine patients (78% male, mean 55±18 yrs, mean LVEF 31±14%) with SHD and refractory VAs underwent BCSD. All had a Video-Assisted Thoracoscopic Surgery (VATS), in 2 cases associated with the robotic technique. The underlying cardiomyopathy (CMP) was non-ischemic (NICMP) in most cases (n=5, 55%), ischemic in 2 cases, arrhythmogenic right ventricular (ARVC) in one and related to lamin A/C deficiency in one. All patients had an ICD, 44% (n=4) a CRT-D. NYHA functional class I was present in 4 patients, the rest were in NYHA class II (n=3) or III (n=2). Three patients were candidates to heart transplant/LV assistance device. The arrhythmic burden pre BCSD included in 7 pts (78%) a history of electrical storm (ES); the median number of shocks/patient in the 12 months before BCSD was 5 (IQ range 3–18). Except for 2 patients with previous thyrotoxicosis, the remaining were either on amiodarone (n=6) or on sotalol (n=1) before BCSD. Main BCSD indications were represented by drug refractory fast VT in 7 pts (cycle &lt;250 msec) and by recurrent monomorphic VT episodes (mean cycle 351 msec) after endocardial VT ablation in 2 patients. Results No major complication occurred. One patient (NICMP, NYHA II), has an uneventful follow up (FU) of less than 1 month and was excluded from the efficacy analysis. The median FU in the remaining 8 patients is 10 months (IQ range 6–19), during which the median number of shocks/patients was 0.5 (IQ range 0–3). Overall, 4 patients (50%) had ICD shock recurrences. Two cases (mean LVEF 17.5%, NYHA class III) had an ES during severe hemodynamic instability and subsequently died because of cardiogenic shock respectively 1 and 7 months after BCSD. One case had three, not consecutive ICD shocks 20 months after BCSD in the setting of severe amiodarone-induced thyrotoxicosis. Finally, one patient received a single intra-hospital ICD shock 5 days after BCSD before reintroduction of full-dose beta-blockers. The figure summarizes ICD shocks burden in the 6 months before and after BCSD. Among the 5 patients with NICMP/ARVC (4 in NYHA class I), only 1 had a single ICD shock recurrence. ICD shocks pre versus post BCSD, n=8 Conclusions Our case series, although numerically small, has a good follow-up and is the first reported in Europe. The results are in agreement with the suggested remarkable efficacy of BCSD in patients with good functional capacity and fast VAs. Therefore, cardiac sympathetic denervation should always be considered in patients with SHD and refractory ventricular tachyarrhythmias, especially in case VT ablation is either not indicated or fails.

THE PERFECT STORM: A CASE OF THYROID STORM AND RAPIDLY FATAL RHABDOMYOLYSIS SECONDARY TO INFLUENZA PNEUMONIA

SESSION TITLE: Wednesday Fellows Case Report Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Life-threatening end-organ damage secondary thyroid storm and rhabdomyolysis is often recognized late in patients presenting with sepsis. We present a case of rapidly fatal and refractory rhabdomyolysis and thyroid storm in a patient with influenza pneumonia. CASE PRESENTATION: A 41 year old male non-adherent to medical therapy for hyperthyroidism presented to the emergency department (ED) with chest pain and viral prodrome of one day duration. Vitals were remarkable for pulse of 127. A CXR (Figure 1) demonstrated bilateral pulmonary infiltrates, influenza swab was negative and labs were notable for a low serum bicarbonate (HCo3) level, elevated creatinine and liver function tests, bandemia, and an undetectable TSH. IV fluids and broad spectrum antimicrobials for presumed bacterial pneumonia were initiated. On hospital day 2, his labs were suggestive of worsening acidosis and rapidly progressive renal failure. The patient developed acute respiratory distress requiring emergent intubation and was transferred to the medical intensive care unit (MICU) where he suffered a PEA arrest upon arrival. ROSC was achieved followed by initiation of renal replacement therapy (RRT) along with methimazole, stress dose steroids, and lugol’s iodine solution for presumed thyroid storm. Empiric oseltamivir was added. Creatine kinase (CK) was 742,150. Over the course of 24 hours, his hyperkalemia continued to worsen requiring simultaneous use of two CRRT machines and therapeutic plasma exchange (TPE). Emergent thyroidectomy was considered, however the patient was deemed too unstable. An extended virus respiratory NAAT confirmed influenza-A. His hyperkalemia and thyroid hormone levels remained refractory to maximal medical management. On hospital day 3 he sustained another PEA arrest and died. DISCUSSION: Thyroid storm is a life-threatening condition with mortality nearing 100% in untreated individuals. The diagnosis is made clinically utilizing biochemical evidence of a hyperthyroid state and the Burch and Wartosky criteria, usually in the background of an inciting event such as influenza pneumonia as in this patient. Beyond standard interventions aimed at reducing production, secretion or peripheral conversion of thyroid hormone, this patient underwent TPE. We also highlight the relative insensitivity (∼80%) of nasopharyngeal influenza testing and the importance of empiric therapy when clinical equipoise and pre-test probability are high. CONCLUSIONS: Clinicians must maintain a high index of suspicion for influenza infection despite negative viral testing in the correct clinical setting maintaining a low threshold to initiate empiric oseltamivir. Thyroid storm, if suspected, should likewise be treated empirically before awaiting biochemical confirmation. This case highlights multi-organ failure and severe refractory metabolic derangements that occur in such a scenario. Reference #1: Carroll R, Matfin G. Endocrine and metabolic emergencies: thyroid storm. Ther Adv Endocrinol Metab. 2010;1(3):139-45. Reference #2: Karanikolas M, Velissaris D, Karamouzos V, Filos KS. Thyroid storm presenting as intra-abdominal sepsis with multi-organ failure requiring intensive care. Anaesth Intensive Care. 2009 Nov;37(6):1005-7. PubMed PMID: 20014610. Reference #3: Ba JH, Wu BQ, Wang YH, Shi YF. Therapeutic plasma exchange and continuous renal replacement therapy for severe hyperthyroidism and multi-organ failure: A case report. World J Clin Cases. 2019 Feb 26;7(4):500-507. DISCLOSURES: No relevant relationships by Mark Barash, source=Web Response No relevant relationships by Toni-Denise Espina, source=Web Response No relevant relationships by Kristi Maso, source=Web Response no disclosure on file for Tyler Qiu

Thyroid emergencies.

Myxedema coma and thyroid storm are among the most common endocrine emergencies presenting to general hospitals. Myxedema coma represents the most extreme, life threatening expression of severe hypothyroidism with subjects presenting with deteriorating mental status, hypothermia, and multiple organ system abnormalities. It typically appears in patients with pre-existing hypothyroidism via a common pathway of respiratory decompensation with CO2 narcosis leading to coma. Without early and appropriate therapy, there is often a fatal outcome. It is a clinical diagnosis based on history and physical findings at presentation and not on any objective thyroid laboratory tests. Clinically based scoring systems have been proposed to aid in the diagnosis. While a relatively rare syndrome, the typical patient is an elderly woman (thyroid hypofunction being much more common in women) who may or may not have a history of previously diagnosed or treated thyroid dysfunction. Thyrotoxic storm or thyroid crisis also is a rare condition and it too reflects a clinical diagnosis. Diagnosis is based upon the appearance of severe hyperthyroidism accompanied by elements of systemic decompensation. Based upon the prospect of high mortality without aggressive treatment, therapy must be initiated as early as possible in a critical care setting. There are no clues to diagnosis based upon laboratory tests alone, but several scoring systems have been developed to aid in diagnosis. The usual clinical signs and symptoms of hyperthyroidism will be present along with more exaggerated clinical manifestations affecting the cardiovascular, gastrointestinal, and central nervous systems. A multi-pronged treatment approach has been recommended and has been associated with improved outcomes.

Cardiothyreosis: Prevalence and risk factors

Cardiothyreosis (CT) or thyrotoxic heart disease is associated with higher morbidity and mortality than the other forms of hyperthyroidism. Its risk factors have been analyzed in a limited number of studies. The aims of our study were to investigate the prevalence of CT and its risk factors in patients with hyperthyroidism. MethodsWe identified 538 patients with a hospital discharge diagnosis of hyperthyroidism from January 2000 to December 2015. Among them, 35 patients were diagnosed as having CT. Their demographic, clinical and biological characteristics were studied and compared with those of 72 controls (patients admitted for hyperthyroidism without CT) randomly selected using univariate and multivariate analysis. ResultsThe prevalence of CT in patients hospitalized with overt hyperthyroidism was 6.5%. The cardiac complications seen were atrial fibrillation (AF) in 33 cases (6.1%) and cardiac heart failure (CHF) in 11 cases (2%). The risk factors of CT were age greater than 50 years (OR=13.1; 95% CI [4.9–34.4]), low socioeconomic status (OR=2.8; 95% CI [1.2–6.7]), low educational level (OR=3.1; 95% CI [1.2–8.3]), personal history of hypertension (OR=3.5; 95% CI [1.1–11.2]) and a multinodular toxic goiter as the etiology of hyperthyroidism (OR=4.6; 95% CI [1.6–13.9]). After multivariate analysis, age greater than 50 years was the only independent risk factor of CT (adjusted OR=11.6; 95% CI [2.7–49.5]). Severe biological hyperthyroidism (FT4 >3 times normal) was associated with a lower risk of CT (adjusted OR=0.2; 95% CI [0.1–0.9]). ConclusionsThe prevalence of CT in patients with overt hyperthyroidism was relatively low. Cardiac complications were AF and CHF with a clear predominance of AF. Advanced age was the only independent risk factor of CT. Cardiac complications may be seen even if hyperthyroidism is not biologically severe.