eMedicine Specialties > Endocrinology > Thyroid
Myxedema Coma or Crisis: Treatment & Medication
Updated: Aug 5, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
Myxedema crisis/coma is a life-threatening condition; therefore, patients with this disorder must be stabilized in an intensive care unit. The first 24-48 hours are critical. If the diagnosis is considered likely, immediate and aggressive administration of multiple interventions is necessary to lower an otherwise high rate of mortality. Initial priorities include the following:
- Mechanical ventilation if respiratory acidosis/hypercapnia/hypoxia is significant
- Immediate intravenous thyroid hormone replacement while awaiting confirmatory test results (T4 and TSH), even if the diagnosis of myxedema coma is only probable.
- Because GI absorption is compromised, intravenous therapy is mandatory. Whether to use T4 alone, combined T4 and T3, or T3 alone remains a subject of controversy. Deiodinase conversion of T4 to the active hormone T3 is reduced in these patients, and T3 administration may be advisable. However, T3, because of its more immediate action and short half-life, may be more likely to cause arrhythmias, particularly if myocardial function is compromised. The usual conversion to an intravenous dose of T4 is approximately one half to two thirds of the oral dose.
- An intravenous loading dose of 500-800 mcg of levothyroxine is followed by a daily intravenous dose of 50-100 mcg; the daily dose is administered until the patient is able to take medication by mouth. Use caution in elderly persons and in patients with coronary artery disease or myocardial infarction, because full-dose T4 therapy may worsen myocardial ischemia by increasing myocardial oxygen consumption.{Ref9}. Some authorities advocate the use of additional intravenous T3, at 10-20 mcg every 8-12 hours, especially in young patients with low cardiovascular risk.
- Because of the rarity of the condition, randomized trials comparing different treatment modalities are not available. Observational studies are not in agreement regarding whether low9,10 or high dose T4 or T3 replacement reduces mortality.6
- In light of the possibility of adrenal insufficiency, stress steroid replacement after a cortisol level is obtained.11
- After a baseline cortisol level is ascertained, initiate hydrocortisone at 5-10 mg/hr. Continue therapy unless the random cortisol level on admission indicates adrenal function without abnormalities, in which case, hydrocortisone may be stopped without tapering.
- Passive rewarming using ordinary blankets and a warm room (rapid and external rewarming are contraindicated)
- Treatment of associated infection
- Correction of severe hyponatremia (sodium level <120 mEq/L) with saline, free water restriction
- Broad-spectrum antibiotics with modification of the antibiotic regimen based on culture results
- Correction of hypoglycemia with intravenous dextrose
- Treatment of severe hypotension with cautious administration of 5-10% glucose in half-normal or normal saline (or hypertonic saline if severely hyponatremic, ie, <120 mEq/L)
- Dose adjustment of any medication to compensate for decreased renal perfusion, drug metabolism, etc
- Infection
- The precipitating event in myxedema coma/crisis is often overt or occult bacterial infection.
- Fever and elevated white blood cell (WBC) count are usually absent, although a left shift and/or bands may be observed.
- Pan-culture and initiate empiric broad-spectrum antibiotic treatment, which can be narrowed if the source of infection is identified.
- If culture results remain negative, antibiotics may be discontinued.
- Myocardial ischemia12
- Myocardial infarction may be the precipitating event in older patients, or it may subsequently occur.
- Serial CK determinations with fractionation assist in the diagnosis and treatment of an acute coronary event. CK levels are often elevated in myxedema coma/crisis but are usually of muscle origin.
- If ischemia or infarction is diagnosed, or if the patient has significant risk factors for coronary artery disease, institute thyroid replacement at low doses.
- Volume status
- Intravenous glucose and normal saline should be carefully administered, because patients are usually volume overloaded and prone to congestive heart failure from the reduced cardiac function of hypothyroidism. If severely hyponatremic (sodium level <120 mEq/L), consider administration of small amounts of hypertonic saline followed by intravenous furosemide to improve volume status.
- Generally, hypotension is resistant to the usual drugs until thyroid hormone and glucocorticoids (if insufficient) are administered. If hypotension does not improve with prudent fluid replacement, whole blood can be transfused. Finally, cautious administration of dopamine can be used.
Surgical Care
Stabilize patients in myxedema coma on T4 and glucocorticoids prior to surgical procedures. In life-threatening situations, administer a loading dose of T4 and glucocorticoids before induction of anesthesia. Careful cardiovascular monitoring with a Swan-Ganz catheter is required.
- Endotracheal intubation - Decreased ventilatory drive, CO 2 retention, and hypoxemia all necessitate mechanical respiratory assistance to prevent cardiovascular collapse and worsening of hypoxia and hypercapnia.
- Cardiac monitoring in an intensive care unit
- Myxedema coma/crisis is a medical emergency and requires close monitoring and stabilization.
- Patients are at risk of myocardial ischemia.
- Central venous pressure or Swan-Ganz catheter monitoring - Hypotension signifies loss of blood volume from bleeding or vascular redistribution and must immediately be corrected.
- Temperature monitoring - This requires the use of a rectal probe to determine true core temperature and to monitor rewarming.
Consultations
- Endocrinologist
- Critical care
- Consultations with the following practitioners may be necessary, depending on complications:
- Infectious disease specialists
- Pulmonologists
- Cardiologists
Diet
Motility of the GI tract is usually decreased; therefore, withhold food until the patient is alert and extubated and normal bowel sounds are present; at that time, gradually introduce soft foods.
Activity
Once stable, patients may progress to usual activity as their strength allows. Physical therapy may be useful for patients who are debilitated.
Medication
The goals of pharmacotherapy are to increase thyroid hormone levels, reduce morbidity, and prevent complications.
Thyroid hormones
Immediate administration of intravenous levothyroxine is necessity if myxedema coma/crisis is considered likely. Controversy exists regarding whether additional treatment with T3 is necessary. When the patient is eating and ambulating, oral T4 may be substituted.
Levothyroxine (Synthroid, Levoxyl)
In active form, influences growth and maturation of tissues. Involved in normal growth, metabolism, and development. IV dosage form has a long half-life (may be administered qd and is the preferred route of administration in patients with myxedema coma/crisis because GI tract absorption may be compromised). Preferred by many authorities, because the onset of action is slow and sustained, making adverse effects less likely to occur and serum levels easier to monitor. Administering only T4 assumes normal conversion to T3 by deiodinase activity, which is usually compromised in severe illness. IV dose of T4 is approximately one half to two thirds of the PO dose. Lower doses recommended if patient has uncontrolled atrial arrhythmia or recent MI.
Adult
200-500 mcg IV loading dose, followed by 50-100 mcg/d IV; switch to 50-200 mcg/d PO when patient is ambulatory
Pediatric
Not established
Cholestyramine, antacids, sucralfate, and iron salts may decrease GI tract absorption; estrogens may decrease response to thyroid hormone therapy in patients with nonfunctioning thyroid glands; hepatic enzyme inducers (eg, phenytoin) may increase degradation; insulin, antidiabetic agents, theophylline, adrenocorticoids, digoxin, and anticoagulants may need dose adjustments; phenytoin IV may release thyroid hormone from thyroid-binding globulin; effect of anticoagulants is increased when administered with T4 or T3; activity of some beta blockers may decrease when patient is converted to euthyroid state
Documented hypersensitivity; untreated thyrotoxicosis; uncorrected adrenal insufficiency; acute MI uncomplicated by hypothyroidism
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Caution in patients who are elderly or who have renal insufficiency, hypertension, ischemia, angina, and other cardiovascular diseases; periodically monitor thyroid status
Liothyronine (Cytomel, Triostat)
Synthetic form of the natural thyroid hormone, T3, converted from T4. T3 is the active form, but because peripheral conversion of T4 to T3 is compromised in patients who are hypothyroid, some authorities suggest combined IV T4 and T3 in these patients. However, patients with cardiovascular disease are at greater risk of arrhythmia and infarction.
T3 has a short half-life and must be administered q8h. Because of concerns about abrupt onset and fluctuating concentrations in tissues, experts advise coadministration of T3 with T4.
Adult
10 mcg IV q8h
Pediatric
Not established
Hepatic enzyme inducers (eg, phenytoin) may increase degradation; insulin, antidiabetic agents, theophylline, adrenocorticoids, digoxin, and anticoagulants may need dose adjustments; phenytoin IV may release thyroid hormone from thyroid-binding globulin, effects of TCAs and sympathomimetics may be increased; cholestyramine may decrease absorption; estrogens may decrease response to thyroid hormone therapy in patients with nonfunctioning thyroid glands; activity of some beta blockers may decrease when patient is converted to euthyroid state; beta blockers may decrease the conversion of T3 to T4
Documented hypersensitivity; uncorrected adrenal insufficiency; acute MI uncomplicated by hypothyroidism; untreated thyrotoxicosis
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Caution in patients who are elderly or who have renal insufficiency, hypertension, ischemia, angina, and other cardiovascular diseases; periodically monitor thyroid status
Corticosteroids
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.
Hydrocortisone (Solu-Cortef, Hydrocortone)
DOC because of mineralocorticoid activity and glucocorticoid effects. Patients presenting with myxedema coma/crisis may have adrenal insufficiency, and stress doses of IV steroids must be administered along with initial thyroid replacement until adrenal function has been determined to be normal.
Adult
100 mg IV q8h
Pediatric
Not established
Corticosteroid clearance may decrease with estrogens; may increase digitalis toxicity secondary to hypokalemia
Documented hypersensitivity; viral, fungal, or tubercular skin infections
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in hyperthyroidism, osteoporosis, peptic ulcer, cirrhosis, nonspecific ulcerative colitis, diabetes, and myasthenia gravis
More on Myxedema Coma or Crisis |
| Overview: Myxedema Coma or Crisis |
| Differential Diagnoses & Workup: Myxedema Coma or Crisis |
Treatment & Medication: Myxedema Coma or Crisis |
| Follow-up: Myxedema Coma or Crisis |
| References |
| Further Reading |
| « Previous Page | Next Page » |
References
Wall CR. Myxedema coma: diagnosis and treatment. Am Fam Physician. Dec 1 2000;62(11):2485-90. [Medline]. [Full Text].
Fliers E, Wiersinga WM. Myxedema coma. Rev Endocr Metab Disord. May 2003;4(2):137-41. [Medline].
Kwaku MP, Burman KD. Myxedema coma. J Intensive Care Med. Jul-Aug 2007;22(4):224-31. [Medline].
Nicoloff JT, LoPresti JS. Myxedema coma. A form of decompensated hypothyroidism. Endocrinol Metab Clin North Am. Jun 1993;22(2):279-90. [Medline].
Diekman MJ, Harms MP, Endert E, et al. Endocrine factors related to changes in total peripheral vascular resistance after treatment of thyrotoxic and hypothyroid patients. Eur J Endocrinol. Apr 2001;144(4):339-46. [Medline]. [Full Text].
Rodríguez I, Fluiters E, Pérez-Méndez LF, et al. Factors associated with mortality of patients with myxoedema coma: prospective study in 11 cases treated in a single institution. J Endocrinol. Feb 2004;180(2):347-50. [Medline]. [Full Text].
Rehman SU, Cope DW, Senseney AD, et al. Thyroid disorders in elderly patients. South Med J. May 2005;98(5):543-9. [Medline].
Sheu CC, Cheng MH, Tsai JR, et al. Myxedema coma: a well-known but unfamiliar medical emergency. Thyroid. Apr 2007;17(4):371-2. [Medline].
Yamamoto T, Fukuyama J, Fujiyoshi A. Factors associated with mortality of myxedema coma: report of eight cases and literature survey. Thyroid. Dec 1999;9(12):1167-74. [Medline].
Hylander B, Rosenqvist U. Treatment of myxoedema coma--factors associated with fatal outcome. Acta Endocrinol (Copenh). Jan 1985;108(1):65-71. [Medline].
Jordan RM. Myxedema coma. Pathophysiology, therapy, and factors affecting prognosis. Med Clin North Am. Jan 1995;79(1):185-94. [Medline].
Taguchi T, Iwasaki Y, Asaba K, et al. Myxedema coma and cardiac ischemia in relation to thyroid hormone replacement therapy in a 38-year-old Japanese woman. Clin Ther. Dec 2007;29(12):2710-4. [Medline].
Dutta P, Bhansali A, Masoodi SR, et al. Predictors of outcome in myxoedema coma: a study from a tertiary care centre. Crit Care. 2008;12(1):R1. [Medline]. [Full Text].
Rimar D, Kruzel-Davila E, Dori G, et al. Hyperammonemic coma--barking up the wrong tree. J Gen Intern Med. Apr 2007;22(4):549-52. [Medline]. [Full Text].
Brent GA, Larsen PR, Davies TF. Hypothyroidism thyroiditis. In: Kronenberg HM, Melmed S, Polonsky KS, et al, eds. Williams Textbook of Endocrinology. 11th ed. Philadelphia, Pa: Saunders/Elsevier; 2008.
Wartofsky L. Myxedema coma. Endocrinol Metab Clin North Am. Dec 2006;35(4):687-98, vii-viii. [Medline].
Further Reading
Related eMedicine topics:
Graves Disease [Endocrinology]
Graves Disease [Pediatrics: General Medicine]
Hypothyroidism [Endocrinology]
Hypothyroidism [Pediatrics: General Medicine]
Hypothyroidism and Myxedema Coma
Pretibial Myxedema
Keywords
myxedema coma, myxedema crisis, hypothyroidism, severe hypothyroidism, decompensated hypothyroidism, pretibial myxedema, Graves disease, Graves' disease, localized dermopathy, thyroid hormones, autoimmune thyroid disease, thyroid ablation therapy, iodine deficiency, thyroxine, T4, triiodothyronine, T3, thyroid-stimulating hormone, TSH, thyrotropin
Treatment & Medication: Myxedema Coma or Crisis