MON-445 A Fatal Case of Refractory Myxedema Coma with Multiorgan Failure

Background/Objective: Myxedema coma typically presents with decreased level of consciousness and hypothermia, often due to thyroid pathology. In central causes, normal thyroid-stimulating hormone (TSH) levels may delay diagnosis. The purpose of this report is to describe a patient with a history of head trauma who presented with myxedema coma as a manifestation of panhypopituitarism. Case Report: The admitted patient was a 52-year-old man who presented with mental and physical slowness, drowsiness, and weakness. He also had hypotension, hypoglycemia, and low oxygen saturation. Initial evaluation revealed severe pericardial and bilateral pleural effusions, plasma TSH of 2.42 mU/L (normal range 0.25-5.00 mU/L), and plasma adrenocorticotropic hormone (ACTH) of 7.1 pg/mL (normal range 5.2-40.3 pg/mL). Later, his condition deteriorated with anasarca and coma. Signs of improvement were noted after intravenous corticosteroid administration. A subsequent blood test was conducted, which showed a free thyroxine (FT4) level of 0.14 ng/dL (normal range 0.93-1.70 ng/dL). A cranial magnetic resonance scan revealed posttraumatic lesions. The patient's family later admitted head injuries at home. Treatment with intravenous levothyroxine was initiated, resulting in improvement and subsequent discharge in perfect alertness. Conclusion: Hypopituitarism should be suspected in patients with head trauma and symptoms of hormone deficiency. Advanced clinical forms, such as myxedema coma, may also occur. Pituitary hormone levels might be in the normal range, so target gland hormones should be assessed to reach a diagnosis. In the case of suspected central hypothyroidism, requesting only TSH levels may result in a missed diagnosis. For this reason, both TSH and FT4 levels should be measured when central hypothyroidism is suspected.

SUBMANDIBULAR SPACE AIRWAY OBSTRUCTION: A RARE PRESENTATION OF MYXEDEMA COMA

Disclosure: D. Krinsky: None. E. Krug: None. J.A. Mullally: None. Introduction: Myxedema coma is a rare endocrine emergency. The classic presentation is progressive worsening of hypothyroidism, over the course of months, usually in the setting of improper intake of levothyroxine. Here, we present a unique case in which a 91-year-old male presented with myxedema coma 3 weeks after resection of a non-functioning pituitary macroadenoma. Case Presentation: A 91-year-old male with history of hypertension and atrial fibrillation initially presented with progressive bitemporal hemianopsia due to an enlarging 2.4 cm pituitary macroadenoma with compression of the optic chiasm. Pre-operative pituitary labs, including thyroid function tests, were normal and he underwent transsphenoidal resection. Free T4 and cortisol levels were normal post-op day 3 and the patient did not require hormone replacement on discharge. 3 weeks later, the patient presented with hypotension and altered mental status. On admission, he was oriented to self only, able to follow simple commands, with dry oral mucosa, and bilateral non-pitting lower extremity edema. Laboratory studies indicated a normal TSH of 0.386 mlU/L (reference range 0.35-4.7). The following day, the patient became unresponsive, bradycardic, and had hypothermia to 30° C. His free T4 was found to be low at 0.4ng/dL (reference range 0.7-1.9) The diagnosis of myxedema coma was made, and intravenous levothyroxine was initiated after administration of intravenous hydrocortisone to prevent adrenal crisis. After initiation of treatment, the patient’s mental status improved, and he was discharged on long term thyroid hormone and glucocorticoid replacement. Discussion: Myxedema coma is a clinical diagnosis and requires urgent treatment as it has a mortality rate as high as 30-50%. This case was unusual because myxedema coma most often occurs in the setting of primary hypothyroidism with inadequate intake of thyroid hormone supplementation over the course of months. In contrast, our patient presented only 3 weeks after pituitary surgery, with a new diagnosis of central hypothyroidism and myxedema coma. Our case demonstrates central hypothyroidism and myxedema coma can develop quite rapidly after pituitary surgery. Clinical guidelines recommend checking a FT4 between 4-6 weeks after pituitary surgery. Our patient presented with severe biochemical hypothyroidism and myxedema coma only 3 weeks post-operatively despite having a normal FT4 3 days post-op. Based on our case, there may be a benefit to checking FT4 at an earlier post-op time point. Additionally, initially only a TSH was checked for our patient and was normal. When considering a diagnosis of myxedema coma in a patient with recent pituitary surgery, a FT4 must be checked as the TSH will not be reliable in central hypothyroidism. Clinicians should be aware of the potential for new central hypothyroidism and even myxedema coma within weeks of pituitary surgery. Presentation: 6/2/2024

Disclosure: K. Ho: None. E. Kabaswaga: None. K. Cano: None. J. Baskaran: None.Myxedema coma is a medical emergency with a high mortality rate that can result from poorly managed hypothyroidism. It can be challenging to manage when there are confounding factors. We report a case of a 68-year-old male to highlight the importance of prompt diagnosis and intervention. A 68-year-old man presented due to altered mental status and seizure-like activity. His past medical history included hypothyroidism and Parkinson’s disease with dementia. He was hypotensive, bradycardic, hypothermic, and observed to have a grand mal seizure in the hospital. TSH was 134 and free T4 was 0.19. A score of 80 on the diagnostic scale for myxedema coma confirmed the diagnosis. He was taken to the ICU, intubated, and started on vasopressors for his sepsis, as well as intravenous levothyroxine and hydrocortisone. Steroids were tapered once hemodynamically stable and adrenal insufficiency was ruled out. Neurology was consulted for new-onset seizures, with an EEG showing signs of a focal seizure. Vitals gradually normalized; IV levothyroxine was transitioned to a stable oral dose. He was discharged with new antiepileptic medication and optimized hypothyroidism medication. In this case, the diagnosis was confounded by the patient’s underlying dementia and abnormal movements, which could have been used to explain the patient’s general obtundation to be signs of his Parkinson’s. Due to his known hypothyroidism, clinical suspicion remained high for myxedema with seizures as a complication. Subsequently, the patient was managed appropriately with medication and consultation with neurology. Levothyroxine is the drug of choice since it has a slow onset and fewer side effects than T3, which is more potent, but can increase tissue oxygen consumption and strain the cardiovascular system, making it risky for elderly patients. TSH levels reflect the thyroid status over 6 weeks, thus response to therapy is determined by T4 levels, and clinical status. This case underscores the importance of quickly identifying and treating myxedema coma in patients, especially in those with confounding diagnoses, to improve outcomes. Myxedema coma has an estimated annual incidence of 0.22 cases per million in the United States. Although uncommon, it carries a high mortality rate ranging from 30% to 60%. It frequently manifests in individuals with untreated hypothyroidism and is commonly precipitated by a systemic illness with broad symptoms, which require elucidation to separate from confounding factors. Our patient developed myxedema due to his noncompliance with medications, with underlying Parkinson’s disease and dementia muddling the diagnosis, but after diagnosis, eventual management was successful. This case emphasizes the importance of quickly identifying and treating myxedema coma in patients, especially in those with confounding diagnoses, to improve outcomes.Presentation: Monday, July 14, 2025

Myxedema coma is a rare life-threatening disorder characterized by severe hypothyroidism leading to multiorgan failure and even death. This case also reminds clinicians that the misnomer “coma” is misleading, and the patient can present with less severe symptoms. We present a case of a 72-year-old female with a history of primary hypothyroidism who presented to the emergency department with progressively worsening confusion for three days. Laboratory results revealed thyroid-stimulating hormone (TSH) 402.0 µU/L and free thyroxine (T4) 0.22 ng/dL. The patient was compliant with the levothyroxine but she found to be malnourished on presentation. The patient was treated with intravenous levothyroxine and liothyronine. The patient’s mental status improved to the baseline, and she was discharged to a skilled nursing facility. Myxedema coma is a rare but life-threatening disorder that providers should be familiar with, including management and treatment. To the best of our knowledge, this is the highest TSH level ever reported so far, and the first case of myxedema coma precipitated due to malnutrition.

Effect of Chronic and Acute Thyroid Hormone Reduction on Perioperative Outcome

Disclosure: B. Celik: None. D. Shelden: None. Introduction: Myxedema coma (MC) is a rare condition that is caused by severe hypothyroidism. It has an estimated incidence of 2.6 cases per million per year. MC can cause hypothermia, bradycardia, hypotension, and even shock. Here we present a patient with shock caused by MC.Clinical Case: An 86-year-old female with hypothyroidism presented with shortness of breath and lethargy. On the initial examination, heart rate was 45 beats per minute, blood pressure was 94/57 mmHg, and temperature was 93.2°F. The patient was lethargic, and her extremities were cold. Laboratory workup showed TSH of 34.6 mcIU/mL (n: 0.4 - 4.5 mcIU/mL), free T4 of 0.7 ng/dL (n: 0.7 – 1.5 ng/dL), undetectable free T3 (n: 1.7 – 3.7 pg/mL), and lactic acid of 3.8 mmol/L (n < 2 mmol/L). ECG showed sinus bradycardia, and chest X-ray showed bilateral pleural effusions. Myxedema coma score was 75. The patient was put on IV levothyroxine and solumedrol. Epinephrine, norepinephrine, and vasopressin infusions were started due to resistant hypotension. Hypotension persisted despite multiple high-dose vasopressors. The Fick formula showed decreased cardiac index and output. Dobutamine infusion was started, which resulted in decreased vasopressor requirements. Thoracentesis of pleural effusions was done, and fluid studies were consistent with a transudate. A transthoracic echocardiogram (echo) was done and showed preserved ejection fraction (EF). TSH improved to 8.14 mcIU/mL, and free T4 improved to 0.9 ng/dL. The patient’s mental status improved, hypotension resolved, and vasopressors were weaned off.Clinical lessons: MC is a rare diagnosis due to widespread use of thyroid function tests and early diagnosis of hypothyroidism, but it still has a very high mortality rate, up to 30%. Although the treatment of MC is well established, insufficient data exist regarding the management of cardiovascular complications associated with MC. Low intracellular T3 leads to depressed cardiac functions with decreased inotropism and chronotropism. Our patient presented with persistent bradycardia and hypotension requiring atropine use and multiple high-dose vasopressor infusions. Despite the Fick formula showing low cardiac index and output, echo showed preserved EF. This is most likely caused by dobutamine infusion, which started prior to the echo. Hormone replacement therapy with intravenous levothyroxine is the mainstay of treatment in MC. Studies show that with appropriate thyroid hormone treatment, cardiovascular function can be restored, but as observed in our case, this recovery can take time, and patients might need inotropic support in the meantime. Cardiac complications significantly increase the mortality rate of MC, up to 60%. Prompt recognition and management of cardiovascular dysfunction are crucial for improving outcomes. Physicians should not hesitate to obtain an early echo and use inotropic support if needed. Presentation: Saturday, July 12, 2025

Introduction: Myxedema coma is an endocrine emergency with a very high mortality rate. As per the American Thyroid Association, initial thyroid hormone replacement for myxedema coma should be intravenous levothyroxine (LT4). However, in India, the availability of intravenous LT4 is limited. Often, crushed LT4 tablets are given through the enteral route when parenteral therapy is unavailable. No data or protocol is available for the administration of oral LT4 in myxedema coma. The aim of this study was to assess the effectiveness of oral LT4 in patients diagnosed with myxedema coma and to formulate a protocol for oral LT4 that can be used to guide the treatment of patients when intravenous LT4 is unavailable. Methods: This retrospective observational study included patients diagnosed with myxedema coma between January 2010 and December 2019. The diagnosis of myxedema coma was based on the diagnostic scoring system for myxedema coma proposed by Popoveniuc et al. [Endocr Pract. 2014 Aug;20(8):808–17]. Dosing of oral LT4 was decided as per our institutional protocol. Results: Fourteen patients (11 males and 3 females) with a median age of 67.5 years (range 11–82) with myxedema coma were included. All patients had central nervous system manifestations, and sepsis was the most common precipitating factor. The median myxedema score was 72.5 (normal ≤25), and the median length of hospital stay was 12 days (range 3–18). The oral LT4 regimen consisted of a loading dose of 300–500 μg, followed by taper over the next 3–5 days. With this regimen, 13 patients survived, and only 1 patient died. Conclusion: Oral LT4 is an effective treatment option for myxedema coma when intravenous LT4 is unavailable.

Myxedema coma is a rare and life-threatening medical condition. We present a case of poorly controlled hypothyroidism that initially caused myxedema coma and then led to acute coronary syndrome (ACS).A 57-year-old woman with a history of Hashimoto's thyroiditis and coronary artery bypass grafting (CABG) came in with fatigue and worsening left-sided chest pain that occurred even at rest for the past 12 hours. She has not been taking her levothyroxine as prescribed and has not been seeing her endocrinologist for follow-up. When she arrived, her vitals showed that she had a heart rate of 53 beats per minute (sinus bradycardia), but otherwise, she was stable.The laboratory tests showed elevated levels of high sensitivity troponin T at 42 ng/L (normal value: <14 ng/L), a thyroid stimulating hormone level of 408 mIU/L (normal value: 0.5-2.5 mIU/L), a free thyroxine level of 0.4 (normal range: 0.8-1.8 ng/mL), and a decreased glomerular filtration rate of 71 mL/min/1.73 m2 (normal range: 90-120 mL/min/1.73 m2). Although the electrocardiogram did not show ST-T wave changes, the thrombolysis in myocardial infarction (TIMI) risk score was five. Additionally, there was a new onset decrease in ejection fraction to 40% and mild hypokinesia of the left ventricle on the echocardiogram.She was started on a heparin drip in the emergency department and subsequently underwent cardiac catheterization with drug-eluting stent (DES) placement. Myxedema coma score was 40 suggestive of coma risk myxedema and eventually, she was admitted to the intensive care unit. Her condition was managed using intravenous levothyroxine, liothyronine, and hydrocortisone. After her symptoms subsided, she was discharged with a prescription for dual antiplatelet agents and levothyroxine.Due to its rarity and high mortality rate, it is crucial for physicians to maintain a high level of suspicion for myxedema coma and promptly initiate treatment. This is especially important when a patient with a history of hypothyroidism presents with cardiac issues such as ACS or bradycardia that do not entirely align with the clinical picture.

Background: Hashimoto thyroiditis (HT) is uncommon in infancy, and myxedema coma (MC) is even less common. While prior reports have documented these entities separately, to our knowledge, MC in combination with HT has not been reported before in this age group. Methods/Results: A 10-month-old female presented with ptosis, lethargy, dysphagia, and failure to thrive (FTT). She developed hypotension, bradycardia, hypothermia, and apnea requiring intubation. Initial thyroid-stimulating hormone was 422 μIU/mL, and free thyroxine was < 0.5 ng/dL, despite the presence of a normal thyroid newborn screen (NBS). Of note, sepsis workup was unremarkable. With the diagnosis of MC, treatment with intravenous levothyroxine was initiated, although after hydrocortisone administration to avert the possibility of an adrenal crisis, despite a random cortisol of 16.4 μg/dL. Based on positive thyroid antibodies suggesting HT, autoimmune workup later revealed positive acetylcholinesterase antibodies consistent with a diagnosis of ocular myasthenia gravis. Conclusion: MC may be a cause of altered mental status in infancy and may simultaneously be associated with FTT on presentation. With the presence of a normal thyroid NBS, autoimmunity should be entertained as the etiology of profound hypothyroidism, as positive thyroid antibodies may prompt an exploration for coexisting diseases which may explain other presenting features.

Introduction Amiodarone is widely used as a rhythm-conversion agent in atrial fibrillation. It’s low negative inotropic activity and low risk of ventricular arrhythmia makes it an advantageous agent for atrial arrhythmia. One of the major limiting factors in the use of amiodarone can be its thyroid toxicity leading to thyroid-dysfunction; ranging from thyrotoxicosis to myxedema coma. Myxedema coma, although rare, is a deadly complication of hypothyroidism with a mortality rate as high as 60%. It is considered an endocrinologic emergency that requires prompt attention and treatment. We present a case of myxedema coma in the setting of chronic amiodarone intake.Case Presentation A 75-year-old female with a past medical history significant for atrial fibrillation, hypothyroidism, end stage renal disease from diabetic nephropathy on hemodialysis, Hepatitis C, hypertension, and hyperlipidemia was admitted to the hospital for evaluation of generalized weakness. Her medications included amiodarone 200mg/day among others. The next day, the rapid response team was called when the patient became hypotensive, bradycardic and unresponsive. She was transferred to the ICU and intubated immediately. On exam, her skin was dry and cold. Her laboratory findings revealed a markedly elevated TSH level of 185uIU/mL. Her most recent TSH level was 9.044uIU/mL from a year back. Other laboratory tests revealed WBC count of 9.0k/mm cu, hemoglobin 13.7 g/dL, platelet count 48 k/mm cu. A diagnosis of myxedema coma was made based on her presentation and lab findings. The patient was started on intravenous levothyroxine 100mg daily with intravenous hydrocortisone 100mg every 8 hours. T4 levels were 0.38ng/dL, T3 levels were 1.83pg/mL and TPO antibodies were negative. A decision was made not to administer intravenous T3 because of the patient’s advanced age and underlying atrial fibrillation. Over the course of the hospitalization, the patient was showing signs of clinical improvement and attempts were being made to wean her off the ventilator. However, later she died due to hemorrhagic shock.Conclusion Myxedema coma may manifest nonspecifically as lethargy and altered mental status and can present without the more specific symptoms of skin changes or myxedematous soft tissue changes. It is therefore, very important for physicians to consider myxedema coma as one of the differential diagnoses in patients on amiodarone with underlying thyroid disease. Administering amiodarone for elderly patients with underlying thyroid problems warrants attention to polypharmacy. The treatment guidelines for myxedema coma are yet to be established. While intravenous levothyroxine with intravenous hydrocortisone remains the mainstay of therapy, there are no consensus on T3 administration.

Severe Myxedema After Cardiopulmonary Bypass

Introduction Myxoedema coma is an uncommon, life-threatening form of longstanding, neglected, untreated hypothyroidism.It is precipitated by an acute illness such as infections, myocardial infarction, cold exposure, or use of sedative drugs. It is characterized by lethargy, myxedematous manifestations and altered sensorium. We are presenting a case of myxedema associated with large unilateral pleural effusion and tachycardia. Case Presentation A 74 years old female with history hypothyroidism not in thyroid replacement for the past two years presented with urinary incontinence, progressive dyspnea, generalized weakness, confusion, anorexia, and constipation for the past two months. She was found to be somnolent, hypothermic, hypoxic, tachycardic with mild enlargement of thyroid gland, pretibial edema and delayed deep reflexes response. Chest x-ray showed a large right sided pleural effusion. Labs revealed macrocytic anemia, leukopenia, thrombocytopenia, TSH 214 micro IU/ml, free T4 0.14 ng/dl and free T3 less than 50 pg/dl. Urinalysis showed pyuria. Pleural fluid revealed transudate.Initially she was treated with ceftriaxone for UTI and intravenous Levothyroxine, Liothyronine, hydrocortisone for the myxedema. Despite initiation of treatment worsening hypoxemia and hypercapnia led to noninvasive ventilation and further intubation . She was extubated and continued on oral thyroid replacement therapy. Discussion Myxoedema coma has an incidence rate of 0.22 per million per year. The syndrome is more commonly seen in elderly women with longstanding hypothyroidism.Serious effusions, including pleural and pericardial, occur concomitantly with myxedema coma. There are cases on literature that describe myxedema associated with minimal pleural effusions but in our case patient had a large unilateral pleural effusion.The pathogenesis of pleural effusion is hypothesized to be related to increased capillary permeability. On our case patient was tachycardic which is unusual for myedematous patient who can not develop tachycardia in response to infection and stress. Myxoedema coma as a true medical emergency requires a multifaceted approach to treatment in critical care settings for mechanical ventilation, cautious warming and treatment of infections. Intravenous thyroid hormone replacement is the mainstay therapy and cortisone until adrenal insufficiency is excluded. Early recognition and therapy of myxedema coma are essential due to high mortality rate approximately 50% despite adequate treatment and it should be initiated even without laboratory confirmation if clinical suspicion remains high.

Development of an objective tool for the diagnosis of myxedema coma

Myxedema coma, a rare entity, with a reported 25%–65% mortality had no objective criteria for making the diagnosis when we began our study. We developed an objective screening tool for myxedema coma to more easily identify patients and examine the best treatment method in future prospective studies to reduce the mortality of this entity. We conducted a retrospective chart review to find all patients aged ≥18 years admitted with myxedema coma from January 1, 2005 through June 13, 2010 at Indiana University Health Methodist Hospital. On the basis of both our retrospective chart review and on literature accounts, we identified 6 criteria to diagnose myxedema coma. We identified 10 patients initially diagnosed with myxedema coma and established a control group consisting of 13 patients identified with altered mental status and increased thyroid-stimulating hormone (TSH) levels. The 6 variables we created for the screening tool were heart rate, temperature, Glasgow coma scale, TSH, free thyroxine, and precipitating factors. The screening tool has a sensitivity and specificity of about 80%. We ran a logistic regression model using the 10 study patients and 13 controls with the 6 variables. No variables alone significantly contributed to the model. However, the overall model was highly significant ( P = 0.012), providing strong support for a scoring system that uses these variables simultaneously. This screening tool enables physicians to rapidly diagnose myxedema coma to expedite treatment. A more refined diagnostic tool may be used in future clinical studies designed to determine the optimal treatment.