Introduction: Diabetic ketoacidosis (DKA) and thyroid storm are individually rare but potentially fatal endocrine crises in pregnancy. Each carries significant maternal and fetal morbidity, with mortality risk compounded when they occur concomitantly. Physiological and pharmacokinetic changes of pregnancy, combined with overlapping symptoms, necessitate urgent treatment strategies. Case: A 29-year-old G2P2 female at 29 weeks’ gestation, with poorly controlled type 2 diabetes mellitus (hemoglobin A1c 8.1%) on a basal–bolus insulin regimen and Graves’ disease managed with carbimazole, non-adherent to medications, presented with fever, vomiting, and dyspnea. On examination, she was tachycardic (HR 138 bpm), hypotensive (BP 94/60 mmHg), and hypoxic. Laboratory investigations revealed hyperglycemia (glucose 27.1 mmol/L), severe metabolic acidosis (pH 7.02, bicarbonate 4.9 mmol/L), and elevated serum ketones (4.6 mmol/L), consistent with DKA. Thyroid function tests showed suppressed thyroid-stimulating hormone (<0.005 mIU/L) and elevated free T4 (28.2 pmol/L), with a Burch–Wartofsky score of 70. Unfortunately, intrauterine fetal demise was confirmed upon the patient’s presentation to the emergency department. She was intubated and admitted to the intensive care unit, receiving fluid resuscitation judiciously according to the DKA regimen, with frequent assessment of volume status. Intravenous insulin and potassium supplements were commenced concurrently. Metabolic stabilization was achieved within 24 hours. Carbimazole, propranolol, Lugol’s iodine, and intravenous hydrocortisone were started for treatment of thyroid storm. A breech-assisted vaginal delivery was performed, and her postpartum course was uneventful. Conclusion The case reveals the catastrophic potential of concurrent DKA and thyroid storm in pregnancy, where rapid maternal deterioration and poor fetal outcomes can occur despite timely intervention. High clinical suspicion, early biochemical confirmation, and coordinated multidisciplinary management are vital. Precipitating factors, particularly medication non-adherence, must be addressed through intensive patient education and structured follow-up to prevent recurrence.
Female ; Pregnancy ; Diabetic Ketoacidosis ; Thyroid Crisis

Introduction: Hurthle cell adenoma is a rare benign thyroid neoplasm that can only be diagnosed through histopathological examination. Hurthle cell neoplasm typically presents as nonfunctioning cold nodule on thyroid scintigraphy. We report a rare case of Hurthle cell adenoma presenting with thyroid storm, with unusual findings of “cold” within “hot” thyroid nodule on scintigraphy. Case: A 73-year-old male with hypertension, chronic kidney disease, coronary artery disease, and Parkinson’s disease presented to the emergency department with fever and diarrhea. His temperature was 38.4°C, heart rate 106 bpm, and blood pressure 138/75 mmHg, with atrial fibrillation and signs of heart failure. The Burch-Wartofsky score was 50, consistent with thyroid storm. Laboratory tests revealed free thyroxine 4 37.8 pmol/L (NR 11.5–22.7), free thyroxine 3 5.6 pmol/L (NR 3.5–6.5), and thyroid-stimulating hormone <0.01 mIU/L (NR 0.55– 4.78). Thyroid autoantibodies, including anti-thyroid peroxidase, anti-thyroglobulin, and thyroid-stimulating immunoglobulins, were negative (<0.10 IU/L). The thyroid storm was precipitated by invasive Klebsiella syndrome with endophthalmitis and lung and liver abscess. He was treated with Lugol’s iodine, corticosteroid, antibiotics, and carbimazole. Ultrasound thyroid revealed a mixed cystic-solid nodule in the left thyroid lobe, measuring 2.3 × 3.3 × 4.3 cm (TIRADS category 3). Technetium-99m thyroid scintigraphy demonstrated a hyperfunctioning left thyroid nodule with a focal intranodular cold spot measuring 5.0 × 3.7 cm. Fine needle aspiration cytology of the nodule was benign follicular cells. Following stabilization with anti-thyroid treatment, he underwent left hemithyroidectomy. Histopathology examination revealed a Hurthle cell adenoma without capsular or vascular invasion. Postoperatively, he remained clinically euthyroid. Surveillance ultrasound performed 8 months later showed a normal right thyroid lobe, and lifelong surveillance was planned. Conclusion This case illustrates a rare and unusual presentation of thyroid storm caused by a toxic Hurthle cell adenoma containing an intranodular cold spot on scintigraphy. To our knowledge, only one similar case has been reported in the literature, and our case is the first to present with thyroid storm.
Oxyphil Cells ; Thyroid Crisis ; Adenoma

Introduction: Long-term antithyroid drug (LT-ATD) has emerged as a feasible treatment strategy for patients who decline radioactive iodine (RAI) or thyroidectomy for relapsed or refractory Graves’ disease (GD). Benefits include faster achievement of euthyroidism, lower risk of hypothyroidism, a more favorable cardiovascular profile, and avoidance of surgical risks. Although fluctuations in thyroid status may occur despite good compliance, thyroid storm is exceedingly rare in patients on LT-ATD. While there is no specific data on the incidence of thyroid storm in this cohort, surveys suggest an overall low incidence (0.2–0.76 cases per 100,000 annually). We report a patient with stable GD who developed a thyroid storm despite more than 10 years of LT-ATD. Case: A 40-year-old female was diagnosed with GD 11 years earlier during pregnancy. Treatment was stopped at 25 weeks’ gestation, but she relapsed at 7 months postpartum and was started on carbimazole. She declined RAI or surgery following a relapse and remained on carbimazole 5–10 mg daily, with good compliance. She presented with a 1-day history of fever, cough, rhinorrhea, diarrhea, and palpitations. She was compliant with carbimazole 5 mg daily. On presentation, BP was 132/70 mmHg, HR 140 bpm, temperature 38.5°C, and SpO2 98% on air. She was alert without agitation, had a diffuse goiter, mild proptosis, and conjunctival injection, with otherwise normal findings. Electrocardiogram showed sinus tachycardia. Laboratory investigations demonstrated mild transaminitis, leukocytosis, markedly elevated free T4 (>154 pmol/L), suppressed thyroid-stimulating hormone (<0.008 mIU/L), and elevated thyroid-stimulating immunoglobulin (2.25 IU/L, reference <0.55). Thyroid function tests 1 month ago was normal. Her Burch-Wartofsky score was 60, consistent with thyroid storm, likely precipitated by upper respiratory tract infection. She improved with treatment and was discharged with carbimazole 30 mg daily with planned tapering, subsequently agreeing to RAI as definitive treatment. Conclusion Infection may trigger thyroid storm despite good compliance with LT-ATD. Patients should be counselled regarding this risk and advised to seek early medical attention if thyrotoxic symptoms recur.
Antithyroid Agents ; Thyroid Crisis

Introduction: Thyroid storm is a life-threatening endocrine emergency with a mortality rate of 8–25% despite optimal therapy. Some patients exhibit a refractory phenotype characterized by rapid clinical deterioration and failure of conventional treatment, necessitating early escalation. Therapeutic plasmapheresis and lithium represent adjunctive therapies targeting different aspects of thyroid hormone physiology, yet their combined use remains underexplored. Case: A 55-year-old male with Graves’ disease, non-adherent to treatment since 2020, presented with fever, palpitations, and dyspnea for 2 days. He recently started on carbimazole 30 mg daily and propranolol 1 week prior. On examination, blood pressure was 158/74 mmHg, heart rate 180 bpm, Glasgow Coma Scale 15/15 with bibasal crepitations. Electrocardiogram showed atrial fibrillation at 168 bpm. His Burch-Wartofsky score was 95, consistent with thyroid storm. Standard therapy with propylthiouracil 250 mg QID, Lugol’s iodine, intravenous hydrocortisone 100 mg TDS, and carvedilol was commenced. However, after 3 days of treatment, he developed acute confusion and persistent fast atrial fibrillation requiring cardioversion. Liver function remained normal. Plasmapheresis was initiated on day 4 for six sessions. Propylthiouracil was switched to methimazole due to a declining white cell count from (5.5– 3.2 ×10⁹/L). Lithium 300 mg BD was added on day 13 due to inadequate free thyroxine 4 (FT4) reduction. After 1 week of combined therapy, FT4 decreased from 70 to 35 pmol/L. Conclusion Early recognition of refractory disease and timely escalation are critical as refractory thyroid storm carries high mortality, especially with cardiovascular and neurological involvement. When conventional therapy fails, plasmapheresis facilitates rapid clearance of circulating thyroid hormones and inflammatory mediators, while lithium inhibits thyroid hormone release, providing an alternative mechanism when thionamides alone are insufficient. Their combined use offers a synergistic approach and targets both circulating and intrathyroidal hormone pools, suggesting that early dual-modality intervention is essential to overcome therapeutic resistance and improve overall outcomes in refractory disease.
Lithium ; Thyroid Crisis ; Plasmapheresis

Introduction: Therapeutic plasma exchange (TPE) has emerged as a rescue therapy in thyroid storm. Multiple cycles are often required to achieve adequate reduction in circulating thyroid hormone levels. We report a case of thyroid storm with multiorgan failure successfully managed with only two cycles of TPE, followed by carbimazole. : A 43-year-old female with no significant past medical history presented with a 5-month history of altered bowel habits. She has a small goiter, which was not investigated before. She underwent elective esophagogastroduodenoscopy and colonoscopy at a private centre, both of which were unremarkable. Post-procedure, she developed unstable tachyarrhythmia and cardiac arrest. Return of spontaneous circulation was achieved after three cycles of cardiopulmonary resuscitation, and she was transferred to the intensive care unit. Biochemical evaluation revealed severe thyrotoxicosis (thyroid-stimulating hormone [TSH] <0.008 mIU/L, free thyroxine 4 [FT4] >100 pmol/L). BurchWartofsky Point Scale was 90. Her clinical course was complicated by multiorgan failure, including ischemic hepatitis with coagulopathy and oliguric acute kidney injury requiring continuous venovenous hemodialysis. Lugol’s iodine and corticosteroids were initiated as thionamides were contraindicated due to severe hepatic dysfunction. She developed refractory tachyarrhythmia despite electrical cardioversion. Following a multidisciplinary discussion, TPE was initiated due to the limited choice of antithyroid medication. After two TPE sessions, thyroid function improved markedly (TSH 0.01 mIU/L, FT4 26.2 pmol/L), accompanied by improvement in hepatic and renal function, allowing safe commencement of carbimazole. Thyroid function remained stable with FT4 of 19.3 pmol/L 1 week post TPE. Echocardiography demonstrated mildly reduced left ventricular ejection fraction (45–50%) with bi-atrial dilatation. Conclusion This case highlights the role of limited-cycle TPE as an effective rescue therapy and bridging strategy to definitive treatment in severe thyroid storm with multiorgan failure. Timely TPE initiation may improve biochemical control and clinical outcomes in critically ill patients.
Plasma Exchange ; Thyroid Crisis

BACKGROUND

Thyroid storm (TS) continues to be a diagnostic and therapeutic challenge. It is a life-threatening severe thyrotoxicosis characterized by organ decompensation. This study aims to determine if there are any changes in this present century about TS diagnosis and management. Furthermore, it aims to describe the clinical profile, precipitants, and outcomes of patients with TS seen at the University of Santo Tomas Hospital (USTH) and assess the association of patient characteristics with mortality.

This is a retrospective cohort analysis of patients with TS admitted at USTH from 2009 through 2018. Logistic regression analysis was used to determine the association of age, Burch Wartofsky-Point Scale (BWPS) score, clinical manifestations, and precipitating factor with mortality.

A total of 21 cases were identified. Majority of the patients were female (90.48%) with a mean age of 42.90 years old. The overall mean BWPS was 49.52 (16.35) while those who expired had higher mean score of 61.67 (5.77). TS as the first clinical presentation was seen in only one patient (4.7%) while majority were previously diagnosed with hyperthyroidism, (95.24%). Graves’ disease (90.48%) was the most common etiology of thyrotoxicosis. Cardiac manifestations were predominant and tachycardia was the most common clinical manifestation (80.95%) with thyrotoxic heart disease as a comorbidity (23.81%). The most common precipitant was infection (52.38%) followed by noncompliance with treatment. The mean hospital length of stay was four days with two patients needing intubation, and both expired afterward. There were three mortalities (14.29%) due to multiple organ dysfunction and fatal arrythmia.

TS remains a life-threatening condition. Aggressive treatment is justified once with suspicion of TS. Age, BWPS on admission, clinical manifestation and precipitants did not predict the likelihood of mortality. Since predictive features are still not thoroughly identified due to its infrequency, it remains for us to be vigilant and not delay crucial treatment to improve the morbidity and mortality associated with TS.

Humans ; Multiple Organ Failure ; Plasma Exchange ; Respiratory Insufficiency/therapy* ; Thyroid Crisis/therapy*

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.

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