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Myxedema Coma or Crisis Treatment & Management

  • Author: Mohsen S Eledrisi, MD, FACP, FACE; Chief Editor: George T Griffing, MD  more...
 
Updated: Dec 15, 2015
 

Medical Care

Myxedema coma is a medical emergency that requires immediate attention. If the diagnosis is suspected, immediate management is necessary before confirming the diagnosis due to the high associated mortality rate. Patients with myxedema coma should be managed in an intensive care unit with continuous cardiac monitoring. Initial steps in management include the elements below.

Airway management

Maintenance of adequate airway is crucial, since most patients have depressed mental status along with respiratory failure. Mechanical ventilation is commonly required during the first 36-48 hours, but some patients require prolonged respiratory support for as long as 2-3 weeks.

Thyroid hormone replacement

The ideal mode of therapy and doses of thyroid hormone therapy in myxedema coma remain controversial due to the rarity of the condition and lack of clinical trials. Some clinicians favor the administration of levothyroxine (T4), while others prefer a combination of T4 and liothyronine (T3).[1, 2, 26, 27] The American Thyroid Association recommends combination therapy with T4 and T3.[28]

Because of reduced gastrointestinal absorption, intravenous thyroid hormone therapy is advised.

An intravenous loading dose of 300-600 micrograms of levothyroxine (T4) is followed by a daily intravenous dose of 50-100 micrograms.[2] Larger doses of T4 probably have no advantage and may be dangerous.[29]  The lower end of the dosing range is recommended in older patients, those at risk for cardiac complications such as myocardial infarction and arrhythmias, and in patients with coronary artery disease, since full-dose T4 therapy may worsen myocardial ischemia by increasing myocardial oxygen consumption.[28]

Because the rate of conversion of T4 to the active hormone T3 can be reduced in these patients, the addition of T3 along with T4 has been recommended.[28] T3 has a quicker onset of action than T4, as increases in body temperature and oxygen consumption has been reported to be faster with T3 therapy compared to T4.[2] T3 therapy is given as bolus of 5-20 micrograms intravenously and to be continued at a dosage of 2.5-10 micrograms every 8 hours depending on the patient's age and coexistent cardiac risk factors.[28]

Intravenous levothyroxine treatment in severely hypothyroid patients usually leads to improvement in cardiovascular, renal, pulmonary, and metabolic parameters within a week. Serum T4 and T3 concentrations may improve or normalize with a similar time frame, with more gradual improvement in serum TSH. Thus, the therapeutic endpoints in myxedema coma should be improved mental status, improved cardiac function, and improved pulmonary function.

Measurement of thyroid hormones every 1-2 days is suggested.[28] Failure of TSH to decrease or of thyroid hormone levels to increase suggests the need to increase doses of T4 and/or add T3.

The treatment is changed to the oral form once the patient is able to take medications by mouth.

Glucocorticoid therapy

Patients with primary hypothyroidism may have concomitant primary adrenal insufficiency while patients with secondary hypothyroidism may have associated hypopituitarism and secondary adrenal insufficiency. The other rationale for the treatment with corticosteroids is the potential risk of precipitating acute adrenal insufficiency caused by the accelerated metabolism of cortisol that follows T4 therapy.[2]

Stress doses of intravenous glucocorticoids should be administered until the possibility of adrenal insufficiency is excluded by a random serum cortisol, which is helpful only if very low, or, better, by an ACTH stimulation test.

Hydrocortisone at a dose of 50-100 mg every 8 hours is administered. An alternative is dexamethasone at a dose of 2-4 mg every 12 hours. Dexamethasone has the advantage of not affecting the serum cortisol concentration and can be used immediately without affecting the results of the ACTH stimulation test, which can be performed at any time. If the test is normal, corticosteroids can be stopped without tapering.

Supportive measures

Treat hypothermia with passive rewarming using ordinary blankets and a warm room. Active rewarming using external devices carries a risk of vasodilatation and worsening hypotension and should be avoided. The use of a rectal probe helps to determine the true core temperature and to monitor rewarming.

Treat associated infection. Given the severity of the condition, infection should always be considered and empiric broad-spectrum of antibiotics be considered until appropriate cultures are proven negative.

Correct severe hyponatremia with saline and free water restriction.

Correct hypoglycemia with intravenous dextrose.

Hypotension is usually corrected with thyroid hormone therapy. If blood pressure continues to be low, cautious use of intravenous fluids with normal saline is advised. Refractory hypotension can be treated with vasopressors such as dopamine, but patients should be weaned off the vasopressor as soon as possible because of the risk of pressor-induced ischemic event.[2]

Patients who are awake, no longer dependent on a ventilator, and medically stable may be transferred from the intensive care unit to a medical ward. 

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Surgical Care

Patients with myxedema coma who require surgical intervention are considered high risk for complications of anesthesia as well as intraoperative and postoperative complications. Stabilization of these patients before proceeding to surgery is preferred unless the procedure is urgent.

In life-threatening situations, the loading dose of T4 and glucocorticoids are administered before induction of anesthesia. Careful administration of anesthetic agents with consideration of using lower doses should be exercised given the decreased metabolism of these agents in patients with myxedema coma.

Close monitoring during surgery and in the postoperative period in a critical care unit is imperative. Monitoring includes respiratory, cardiac, and volume and temperature status.

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Consultations

Consultations include endocrinologists and critical care specialists. Depending on complications, consultations with pulmonologists and/or cardiologists may be appropriate.

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Diet

Most patients will be initially ill and will not be given any food by mouth. Many patients require nasogastric feeding, and if mechanical ventilation is prolonged, total parenteral nutrition may be required. 

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Activity

Once stable, patients may progress to usual activity as their strength allows. Physical therapy may be needed for incapacitated patients. 

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Prevention

Patients with a history of thyroid resection or ablation for hyperthyroidism and persons with a history of Hashimoto thyroiditis are at risk for developing hypothyroidism, and the TSH level should be monitored yearly. Such patients should be informed that hypothyroidism could occur in the future. They should understand the symptoms that signal the condition and the need to seek medical attention for appropriate testing.

In cold climates, inadequately heated residences are a significant cause of myxedema coma/crises in patients with undiagnosed or inadequately treated hypothyroidism.

Thyroid function tests should be monitored regularly in patients with hypothyroidism until the appropriate dose of levothyroxine is reached. Adherence to thyroid hormone therapy should be assessed regularly and to ensure maintenance of euthyroid state. Patients who are deemed nonadherent or have issues that may hinder adherence should have their thyroid function closely monitored.

Patients are advised to report to their physicians if they are prescribed any new medications since some drugs may interfere with the absorption, production, secretion, or clearance of thyroid hormone therapy. Patients should also contact their health care provider if symptoms of inadequately-treated hypothyroidism persist. 

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Long-Term Monitoring

Follow-up care after discharge is necessary to ensure adherence with thyroid hormone replacement.

If primary hypothyroidism was diagnosed, TSH levels are assessed every 4-6 weeks, and the dose of T4 is adjusted accordingly.

If hypothyroidism is secondary to pituitary dysfunction, free T4 levels are monitored. TSH level is not an accurate measure of thyroid function in this setting. 

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Contributor Information and Disclosures
Author

Mohsen S Eledrisi, MD, FACP, FACE Senior Consultant, Department of Medicine/Endocrinology, Hamad Medical Corporation, Qatar

Mohsen S Eledrisi, MD, FACP, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, Endocrine Society, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD Professor Emeritus of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, International Society for Clinical Densitometry, Southern Society for Clinical Investigation, American College of Medical Practice Executives, American Association for Physician Leadership, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical and Translational Research, Endocrine Society

Disclosure: Nothing to disclose.

Additional Contributors

Stephanie L Lee, MD, PhD Associate Professor, Department of Medicine, Boston University School of Medicine; Director of Thyroid Health Center, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Fellow, Association of Clinical Endocrinology

Stephanie L Lee, MD, PhD is a member of the following medical societies: American College of Endocrinology, American Thyroid Association, Endocrine Society

Disclosure: Nothing to disclose.

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