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Critical Consideration of Myxedema Coma in the Postoperative Setting: A Case Report

Tran, Minh MBBS*; Vincent, Lauren MD; Ho, Gordon MD; Kelly, Kaitlyn MD§; Bouvet, Michael MD§; Meier, Angela MD, PhD

doi: 10.1213/XAA.0000000000000864
Case Reports

Myxedema coma is a rare but highly fatal condition with reported mortality >40%–50%. Early recognition and prompt treatment are critical for survival. Here we describe a case of possible postoperative myxedema coma after subacute neck hematoma evacuation after hemithyroidectomy in a patient on concurrent amiodarone therapy. Symptoms included somnolence, hypothermia, and prolonged QTc with torsades de pointes resistant to magnesium therapy requiring defibrillation and overdrive pacing. Consideration of the possible diagnosis of myxedema coma resulted in prompt therapy and symptom resolution within 48 hours. Thyroid disorders, although rare, should be considered in the postoperative setting.

From the *Department of Anesthesiology

Department of Medicine

Department of Medicine, Division of Cardiology

§Department of Surgery

Department of Anesthesiology, Division of Critical Care, University of California San Diego, San Diego, California.

Accepted for publication June 18, 2018.

Funding: None.

Conflicts of Interest: See Disclosures at the end of the article.

Address correspondence to Angela Meier, MD, PhD, Department of Anesthesiology, University of California San Diego, 200 W Arbor Dr, San Diego, CA 92103. Address e-mail to

Myxedema coma from severe hypothyroidism was first described in 1879 in London1 and was named for the mucin deposits or myxedema that accumulates in tissues with this disorder. Severe hypothyroidism culminating in myxedema coma has an incidence of 0.22 per million,2 can be precipitated by acute illness or physiological stress, and has a high mortality rate, especially if unrecognized.3,4 Amiodarone therapy is known to cause both hyperthyroidism and hypothyroidism in some patients with only 6 reported cases of amiodarone-induced myxedema coma in the literature.5 Here we describe a unique case of postoperative myxedema coma precipitated by neck hematoma after a hemithyroidectomy in the setting of amiodarone administration.

The patient provided written informed consent to publish health data without identifying information.

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A 63-year-old woman, body mass index 28.2, with multiple comorbidities including hyperlipidemia, asthma, left hemiplegia from previous stroke, right hemithyroidectomy >40 years ago, and type 2 diabetes mellitus with severe nephropathy underwent an elective right arm brachiobasilic arteriovenous fistula formation under general anesthesia. Her course was complicated by negative-pressure pulmonary edema postextubation (Figure A, i) from a previously undiagnosed large goiter (Figure A, ii and iii) causing external tracheal compression. After reintubation and within 24 hours of admission to the intensive care unit, she was started on amiodarone therapy for atrial fibrillation with rapid ventricular response associated with hypotension requiring cardioversion direct current cardioversion). Her thyroid function was in the normal range at this time (thyroid stimulating hormone [TSH], 0.44 μIU/mL). Three days later, she underwent a left hemithyroidectomy with a thyroid lobectomy specimen weighing 416 g (Figure A, iii). Her pathology report revealed a multinodular goiter with an underlying follicular adenoma. After transfer to step down level care, intermittent hemodialysis was initiated in the setting of worsening renal function, and warfarin anticoagulation was commenced for stroke prevention. Five days after transfer to lower level care, while having dinner, our patient developed acute difficulty swallowing, difficulty breathing, and rapid neck swelling with associated agitation before becoming apneic. Apneic hypoxia progressed to severe bradycardia and pulseless electrical activity arrest requiring cardiopulmonary resuscitation for 1 minute, 1 mg of epinephrine, and bedside release of the neck hematoma (yielding approximately 300 mL of blood clot). She was reintubated and vocal cord edema was noted. Her medication-induced coagulopathy (international normalized ratio 2.5) was treated with 2 units of fresh frozen plasma before emergency transfer to the operating room for definitive hematoma evacuation (further 200 mL) and transfusion of packed red blood cells. Postoperatively, she was transferred intubated and ventilated to the intensive care unit. On arrival, she was noted to be hypothermic 94°F/34.4°C, in sinus bradycardia with intermittent junctional rhythms at 49–52 bpm, and prolonged QTc (700 milliseconds) with associated somnolence. She was externally warmed with a forced air warming system, and all hypnotics and QT-prolonging medications including amiodarone were discontinued. She subsequently developed torsades de pointes with polymorphic ventricular tachycardia requiring magnesium therapy (2 g intravenous [IV] twice) and cardiac defibrillation for hemodynamic instability. An urgent endocrinology consult was placed for suspected myxedema coma. An isoproterenol infusion with transvenous overdrive pacing was initiated after consultation with cardiology (Figure B, ii). Myxedema coma treatment was started empirically and consisted of stress dose steroids (hydrocortisone 100 mg every 6 hours) and IV levothyroxine (400–200 μg IV, liothyronine 20 μg orally once, followed by 5 μg orally every 8 hours with daily free thyroxine [FT4] and free triiodothyronine [FT3] levels). Elevated TSH levels to 36 (0.27–4.2 μIU/mL) with low FT4 0.43 (0.93–1.7 ng/dL) and T3 <0.2 (0.8–2 ng/mL) within 24 hours confirmed suspicion of severe hypothyroidism (Figure B, i) with suspected myxedema coma. Within 48 hours of treatment initiation, no further episodes of torsades de pointes were noted and her QTc normalized to 424 milliseconds. Her mental status improved markedly. Her pacing was discontinued, and she was extubated within 72 hours. Her mental status returned to baseline, and she was discharged to a rehabilitation hospital approximately 2.5 weeks later on daily levothyroxine.

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Myxedema coma is not a common differential in the postoperative or intensive care setting. Only a few case reports are noted in the literature.6–8 We hereby report a complex case of probable myxedema coma based on clinical suspicion with recent thyroid hormones that were in the normal ranges highlighting the need for vigilance.

While “coma” in the context of myxedema coma is considered a misnomer because patients may not actually be comatose, the diagnostic features of myxedema coma include altered mental state ranging from disorientation, lethargy and possibly coma, hypothermia, or the absence of fever, and a precipitating event such as infection, trauma, surgery, or heart failure.4 It is almost exclusively seen in elderly women >60 years of age.2

Other typical symptoms of myxedema coma may include agitation (“myxedema madness”), seizures or confusion,1,9 hyponatremia, hypothermia, hypoventilation and hypoglycemia, bradycardia, low cardiac output, and hypotension (late finding).10 In addition, nonpitting edema, tongue edema, and a thickened nose may be present as a result of the abnormal deposition of mucin and albumin in soft tissues ensuing in this syndrome named “myxedema.”

Examples of drugs inducing myxedema coma include lithium or amiodarone,11 and it is possible that amiodarone could have contributed to the likely picture of myxedema coma for this patient.

Although the patient’s somnolence may have been explained by her hypoxic arrest, her recent surgery with hypnotic usage (propofol, sevoflurane), her hypothermia may have stemmed from intraoperative redistribution of heat, and her arrhythmia may have been due to low body temperature (although warming at that time) and amiodarone administration, the combination of her symptoms lead to consideration of this clinical diagnosis and treatment resulted in resolution of this picture.

If myxedema coma is suspected, treatment should immediately be initiated before definite test results such as TSH, T4, FT4, and T3 are available. Treatment includes replacement of thyroid hormones, administration of glucocorticoids (until coexisting adrenal disease has been excluded), and supportive measures such as forced air warming and electrolyte replacement.12 While experts agree on immediate treatment with thyroid hormone, some favor treatment with T3 and T4, while others recommend T4 alone.13–15 In myxedema coma, the conversion of T4 to T3 can be affected; however, T3 replacement can precipitate heart failure and impose an increased risk of myocardial infarction. A fine balance needs to be reached; hence, collaboration with endocrinology is crucial for safe treatment.

Despite treatment, mortality rates are reported to be as high at 30%–50%12 with cardiac symptoms, higher degree of hypothermia, and altered consciousness being associated with worse outcomes.16 Although our patient displayed several of these factors, early recognition and prompt treatment outlined above in the intensive care unit resulted in complete reversal of her symptoms.

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Although this is a complex case, it highlights the need to consider the possibility of myxedema coma in the postoperative and intensive care setting. Because acute illness, drugs (eg, amiodarone), stress such as trauma or surgery can precipitate myxedema coma, this syndrome can occur in such a setting. At the same time, this setting may obscure symptoms that can easily be attributed to other factors such as lingering anesthetics or other drug effects and confound the diagnosis. Failure to recognize this rare clinical syndrome can be fatal, and immediate treatment is lifesaving. We therefore aim to heighten the awareness of this syndrome that may occur in the postoperative setting.

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Name: Minh Tran, MBBS.

Contribution: This author helped write the manuscript and assemble/edit the figure.

Conflicts of Interest: None.

Name: Lauren Vincent, MD.

Contribution: This author helped provide input to the manuscript.

Conflicts of Interest: None.

Name: Gordon Ho, MD.

Contribution: This author helped provide material for the figure and input to the manuscript.

Conflicts of Interest: None.

Name: Kaitlyn Kelly, MD.

Contribution: This author helped provide input to the manuscript.

Conflicts of Interest: None.

Name: Michael Bouvet, MD.

Contribution: This author helped provide material for the figure and input to the manuscript.

Conflicts of Interest: None.

Name: Angela Meier, MD, PhD.

Contribution: This author helped write the manuscript and edit the figure.

Conflicts of Interest: Angela Meier received the mentored research training grant from the IARS unrelated to this work, and previously received consulting fees from Millennium Health unrelated to this work.

This manuscript was handled by: BobbieJean Sweitzer, MD, FACP.

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