Thyroid crisis is an emergency due to impaired thyroid function caused by various conditions, particularly infections such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that result in the dysfunction of various vital organs. We report a case of a 31-year-old Indonesian female with a 2-year history of hyperthyroidism with elevated thyroid-stimulating hormone (TSH) receptor antibodies. (TRAb) who developed thyroid crisis possibly in association with SARS-CoV-2 pneumonia, sepsis, and disseminated intravascular coagulation (DIC). Prior to admission, she was treated for her hyperthyroidism with propylthiouracil and had been in stable remission for a year. She was admitted to the Emergency Room with complaints of watery stools, icteric sclerae, jaundice, coughing, and shortness of breath. The physical examination showed a World Health Organization (WHO) performance score of 4, delirium, blood pressure within normal limits, tachycardia, tachypnea, axillary temperature of 36.7°C, icteric sclerae, jaundice, and exophthalmos. There was a 3 cm palpable nodule on the right side of the neck. Auscultation of the lungs revealed bilateral pulmonary rales. Abdominal examination noted a palpable liver and enlarged spleen. Laboratory tests showed thrombocytopenia, electrolyte imbalance, hypoalbuminemia and elevated transaminases. The thyroid function tests showed a suppressed TSH level with an elevated free thyroxine (FT4) level. The SARS-CoV-2 polymerase chain reaction (PCR) swab test was positive. Initial patient management was with supportive therapy that included favipiravir and anti-hyperthyroidism medication; however, despite these interventions, her condition continued to deteriorate and she died after a few hours. This case demonstrates no difference in therapy between patients with thyroid crises and COVID-19 or other infections. Proper and timely treatment is important for reducing mortality rates.
COVID-19 ; Thyroid Crisis ; Thyroid Crisis ; Thyrotoxicosis

Thyrotoxicosis is a well-recognized cause of myopathy, but rarely presents as acute flaccid quadriparesis. We report a 25-year-old female with underlying uncontrolled Graves’ disease who presented with thyroid storm and acute flaccid quadriparesis due to thyrotoxic myopathy. She showed marked clinical improvement with subsequent normalization of her thyroid parameters. Besides highlighting this rare association, this report underscores the importance of considering thyrotoxic myopathy in the evaluation of patients with acute flaccid quadriparesis.
Thyroid Crisis ; Quadriplegia

No abstract available.
Anesthesia ; Thyroid Crisis ; Thyroid Gland

Thyroid storm is a life-threatening condition with mortality rates reaching up to 20 to 30%. First-line treatment includes inhibition of thyroid hormone synthesis, prevention of release of preformed hormones, blocking of peripheral FT4 to FT3 conversion, enhancing hormone clearance, and definitive radioactive iodine ablation. However, in the presence of life-threatening adverse effects (e.g., agranulocytosis) and contraindications (e.g., fulminant hepatic failure), therapeutic plasma exchange (TPE) can be used to rapidly remove circulating thyroid hormones, antibodies, and cytokines in plasma; this is recommended by the American Society of Apheresis (ASFA) and the American Thyroid Association (ATA) as second-line treatment for thyroid storm. Here, we report a 49-year-old female with Graves' disease admitted in our emergency room for a 6-week history of fever, weight loss, jaundice, exertional dyspnea, palpitations, and diarrhea. Her initial thyroid hormone levels were: FT4 64.35 (NV 9.01-19.05 pmol/L), FT3 23.91 (NV: 2.89-4.88 pmol/L), and TSH 0.00000 (NV: 0.35-4.94 mIU/L) and we managed her as a case of thyroid storm (Burch-Wartofsky score 70) by initiating high dose propylthiouracil. However, her sensorium deteriorated and serum bilirubin continued to rise from 307.2 on admission to 561.6 umol/L on the 5th hospital day (NV: 3 - 22 umol/L). TPE was performed after consultation with the Division of Hematology. Over the treatment course, her thyroid hormones normalized: FT4 13.18 pmol/L, FT3 2.30 pmol/L. However, despite TPE, her symptoms worsened and she became comatose, had hypotension despite vasopressors and developed new-onset atrial fibrillation. She expired on her 7th hospital day from multiorgan failure. TPE is effective in decreasing circulating thyroid hormone levels. However, it had no effect on clinically important outcomes as our patient still deteriorated and eventually succumbed. We still wrote and submitted this case report since if only successful cases were reported, the true effectiveness rate of TPE could not be determined.Thyroid storm is a life-threatening condition with mortality rates reaching up to 20 to 30%. First-line treatment includes inhibition of thyroid hormone synthesis, prevention of release of preformed hormones, blocking of peripheral FT4 to FT3 conversion, enhancing hormone clearance, and definitive radioactive iodine ablation. However, in the presence of life-threatening adverse effects (e.g., agranulocytosis) and contraindications (e.g., fulminant hepatic failure), therapeutic plasma exchange (TPE) can be used to rapidly remove circulating thyroid hormones, antibodies, and cytokines in plasma; this is recommended by the American Society of Apheresis (ASFA) and the American Thyroid Association (ATA) as second-line treatment for thyroid storm. Here, we report a 49-year-old female with Graves' disease admitted in our emergency room for a 6-week history of fever, weight loss, jaundice, exertional dyspnea, palpitations, and diarrhea. Her initial thyroid hormone levels were: FT4 64.35 (NV 9.01-19.05 pmol/L), FT3 23.91 (NV: 2.89-4.88 pmol/L), and TSH 0.00000 (NV: 0.35-4.94 mIU/L) and we managed her as a case of thyroid storm (Burch-Wartofsky score 70) by initiating high dose propylthiouracil. However, her sensorium deteriorated and serum bilirubin continued to rise from 307.2 on admission to 561.6 umol/L on the 5th hospital day (NV: 3 - 22 umol/L). TPE was performed after consultation with the Division of Hematology. Over the treatment course, her thyroid hormones normalized: FT4 13.18 pmol/L, FT3 2.30 pmol/L. However, despite TPE, her symptoms worsened and she became comatose, had hypotension despite vasopressors and developed new-onset atrial fibrillation. She expired on her 7th hospital day from multiorgan failure. TPE is effective in decreasing circulating thyroid hormone levels. However, it had no effect on clinically important outcomes as our patient still deteriorated and eventually succumbed. We still wrote and submitted this case report since if only successful cases were reported, the true effectiveness rate of TPE could not be determined.

Humans ; Infant ; Male ; Thyroid Crisis ; diagnosis ; therapy

We report a case of a 40-year-old multiparous woman who underwent total abdominal hysterectomy due to massivevaginal bleeding from partial molar pregnancy. Post-operatively, she developed high-grade fever, profuse sweating andshortness of breath. Examination revealed tachycardia, hypertension, elevated jugular venous pressure, and crackleson both lower lung fields, with no palpable thyroid mass. Free thyroxine (FT4) and human chorionic gonadotropinβ-subunit(β-hCG) were markedly elevated, while thyroid stimulating hormone (TSH) was significantly suppressed. With a Burch and Wartofskyscore of 55, thyroid storm from the molar pregnancy was considered. She was givenpropylthiouracil (PTU), propranolol and hydrocortisone. Resolution of her signs and symptoms were noted 2 to 3 daysfollowing treatment.
Thyroid Crisis ; Pregnancy ; Hydatidiform Mole ; Hyperthyroidism

Thyrotoxicosis (thyroid crisis) is a known cause of sudden death; however, only a few cases of death resulting from thyrotoxicosis have been reported. Histopathologic examination and postmortem thyroid function tests may be helpful in postmortem diagnosis, but their usefulness seems to be limited. We report three autopsy cases associated with thyrotoxicosis.
Autopsy ; Death, Sudden ; Thyroid Crisis ; Thyroid Function Tests ; Thyrotoxicosis

Thyrotoxicosis autoimmune encephalopathy (TAE) and Hashimoto's encephalopathy (HE) are steroid responsive disorders of persistent or relapsing neurological or neuropsychological deficits associated with elevated serum concentrations of an antithyroid antibody. Most patients with TAE or HE are reported to have normal brain imaging findings at the time of presentation. We report here a rare case of TAE in whom brain MRI abnormalities were associated with clinical manifestations of thyroid storm.
Brain ; Humans ; Magnetic Resonance Imaging* ; Neuroimaging ; Neurologic Manifestations* ; Thyroid Crisis* ; Thyroid Gland* ; Thyrotoxicosis

We describe a case of thyroid storm due to thyrotoxicosis factitia, which was caused by the ingestion of excessive quantities of exogenous thyroid hormone for the purpose of reducing weight. An 18-year-old female was admitted to the hospital 24 hours after taking up to 50 tablets of synthyroid (1 tablet of synthyroid : levothyroxine 100 microgram). Because of her stuporous mental state and acute respiratory failure, she was intubated and treated in the intensive care unit. After reviewing her history carefully and examining plasma thyroid hormone levels, we diagnosed this case as a thyroid storm due to thyrotoxicosis factitia. Her thyroid function test revealed that T3 was 305 ng/dL, T4 was 24.9 microgram/dl, FT4 was 7.7 ng/dL, TSH was 0.05 micro IU/mL and TBG was 12.84 microgram/mL (normal range: 11.3 - 28.9). TSH receptor antibody, antimicrosomal antibody, and antithyroglobulin antibody were negative. She was recovered by treatment, namely, steroid and propranolol, and was discharged 8 days after admission. Thyroid storm due to thyrotoxicosis factitia caused by the ingestion of excessive thyroid hormone is rarely reported worldwide. Therefore, we now report a case of thyroid storm that resulted from thyrotoxicosis factitia caused by the ingestion of a massive amount of thyroid hormone over a period of 6 months.
Adolescent ; Factitious Disorders/*complications ; Female ; Human ; Thyroid Crisis/*etiology ; Thyroid Hormones/*poisoning ; Thyrotoxicosis/*complications

Rhabdomyolysis is defined as skeletal muscle injury with release of muscle cell constituents into the plasma. Trauma and drugs are important causes of rhabdomyolysis and not rarely it is associated with metabolic disorders such as diabetic coma, severe electrolyte disturbances and myxedema coma. There are a few reports about rhabdomyolysis developed in patient with thyroid storm. which is defined as a sudden, life threatening exacerbation of thyrotoxicosis. In this report, we described the case of thyroid storm complicated by rhabdomyolysis.
Coma ; Diabetic Coma ; Humans ; Muscle Cells ; Muscle, Skeletal ; Myxedema ; Plasma ; Rhabdomyolysis* ; Thyroid Crisis* ; Thyroid Gland* ; Thyrotoxicosis