AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

The term myxedema has been applied to several clinical entities and is often used interchangeably with severe hypothyroidism, the common clinical condition in which the thyroid gland produces abnormally low levels of hormones.

Myxedema also refers to 2 different dermatologic conditions. Pretibial myxedema, an uncommon skin disorder, occurs not in cases of hypothyroidism but in hyperthyroid states, including, most commonly, Graves disease. The term pretibial is somewhat misleading, because the condition can affect other areas of the body and could more accurately be called localized dermopathy.

The other skin condition, called myxedema, occurs in severe, long-standing hypothyroid states and is caused by the deposition of mucopolysaccharides within the dermis.

This article discusses myxedema coma, an uncommon but life-threatening form of untreated hypothyroidism with physiological decompensation.^{1, 2, 3} The condition occurs in patients with long-standing, untreated hypothyroidism and is usually precipitated by a secondary insult, such as climate-induced hypothermia, infection, or another systemic condition, or drug therapy. Patients with myxedema coma have changes in their mental status, including lethargy, stupor, delirium, or coma. A more appropriate term for myxedema coma is myxedema crisis; this article often uses the term myxedema coma/crisis.

Related eMedicine topics:
Graves Disease [Endocrinology]
Graves Disease [Pediatrics: General Medicine]
Hypothyroidism [Endocrinology]
Hypothyroidism [Pediatrics: General Medicine]
Hypothyroidism and Myxedema Coma
Pretibial Myxedema

Related Medscape topics:
Resource Center Hypothyroidism
Resource Center Thyroid Disease

Pathophysiology

Myxedema coma/crisis occurs most commonly in older women with long-standing, undiagnosed or undertreated hypothyroidism who experience an additional significant stress, such as infection, a systemic disease, certain medications, and exposure to a cold environment.

When hypothyroidism is long-standing, physiologic adaptations occur. Reduced metabolic rate and decreased oxygen consumption result in peripheral vasoconstriction, which maintains core temperature. The number of beta-adrenergic receptors is reduced, usually with preservation of alpha-adrenergic receptors and circulating catecholamines, causing beta/alpha-adrenergic imbalance, diastolic hypertension, and reduced total blood volume.

Myxedema coma/crisis is a form of decompensated hypothyroidism in which adaptations are no longer sufficient.⁴ Essentially, all organ systems are affected.

Metabolic

Thyroid hormones are critical for cell metabolism and organ function. With an inadequate supply, organ tissues do not grow or mature, energy production declines, and the action of other hormones is affected.

Although weight gain is common, severe obesity is rarely secondary to hypothyroidism alone. However, long-standing, untreated hypothyroidism may result in years of inactivity, eventually with a large increase in weight.

Because of decreased drug metabolism, overdoses of medications (eg, morphine, hypnotics, anesthetic agents, sedatives) can occur and can even precipitate myxedema crisis.

Neurologic

Although the condition is called myxedema coma, the absence of coma does not exclude the diagnosis of this disorder. The presenting mental status may be lethargy or stupor. The exact mechanisms causing changes in mental status are not known. Brain function is influenced by reductions in cerebral blood flow and oxygen delivery, a lack of thyroxine (T4) and triiodothyronine (T3), and reductions in oxygen and glucose consumption; all of these factors are probably involved. Hyponatremia brought on by renal dysfunction may be an additional cause of altered mental function.

Cardiovascular

The heart is profoundly depressed, with bradycardia and decreased contractility causing low stroke volume and cardiac output. These changes are caused by decreased production of myocyte contractile proteins and enzymes, including NA⁺/K⁺ adenosine triphosphatase (NA⁺/K⁺ ATPase), as a result of low levels of gene transcription in the absence of T3.

Increased systemic vascular resistance occurs; although the causes appear to be multifactorial, a study suggests that in many cases, the increase is secondary to decreased T3 levels.⁵ Nonspecific ST- and T-wave inversion changes, low voltage, and ventricular arrhythmias may be noted. Plasma volume is decreased, and capillary permeability is increased, leading to fluid accumulation in tissue and spaces and possibly causing pericardial effusions.

Pulmonary

Typically, the lungs are not severely affected. Respiratory muscle dysfunction may be compromised, and depressed ventilatory drive and increased alveolar-arterial oxygen gradient are common. Fluid accumulation may cause pleural effusions and decreased diffusing capacity. Ventilation-perfusion mismatch is common, contributing to hypercapnia. Dysfunction of other organ systems may have profound effects. Severe obesity, if present, causes decreased lung volumes, diffusion capacity, and flow rates and may be the primary cause of the hypoventilation, hypoxia, hypercarbia, and depressed respiratory drive that is often noted in these patients. However, hypothyroidism may also have a direct impact, because the condition can cause obstructive sleep apnea that resolves with thyroid replacement (even without weight loss).

Renal

Kidney function may be severely compromised, partly because of low cardiac output and vasoconstriction that causes a low glomerular filtration rate. Reduced levels of NA⁺/K⁺ ATPase decrease sodium reabsorption and impair free water excretion, resulting in hyponatremia, which is usually present in myxedema coma.

Gastrointestinal

Severe or even mild hypothyroidism decreases intestinal motility. Patients with myxedema coma can present with gastric atony, megacolon, or paralytic ileus. Malabsorption has also been reported. Ascites, while uncommon, may occur due to increased capillary permeability, congestive heart failure, or other mechanisms.

Frequency

United States

Hypothyroidism is a common disorder in the older population; in the United States, the condition is present in 8% of women and 2% of men older than 50 years. Myxedema coma is a rare consequence of untreated hypothyroidism.

International

In areas in which the population ingests sufficient iodine, the most common cause of hypothyroidism is autoimmune thyroid disease and thyroid ablation therapy, with a prevalence of approximately 8% of women aged 50 years or older.

In regions where not enough iodine is ingested, the most common cause of hypothyroidism is iodine deficiency, with the prevalence of hypothyroidism correlating with the iodine content of the diet. Severe hypothyroidism (neonatal thyrotropin [TSH] >5 mU/L in >40% of births) and cretinism are observed with severe iodine deficiency (<20 mcg/dL). Iodine deficiency of this magnitude is generally observed only in isolated, mountainous regions of South America, Africa, and Asia. The prevalence of myxedema coma/crisis in the populations of these areas is unknown.

Mortality/Morbidity

Myxedema coma/crisis is a metabolic and cardiovascular emergency. If the condition is not promptly diagnosed and treated, the mortality rate is approximately 50% or more. Even with immediate recognition and appropriate medical intervention, mortality rates of up to 25% are observed. Factors suggesting a poor prognosis are a body temperature of less than 93° F, persistent hypothermia that is unresponsive to 72 hours of therapy, advanced age, bradycardia (<44 beats per min), sepsis, myocardial infarction, and hypotension. In addition, a study found that the patient's admission level of consciousness, as well as his/her score on the Glasgow Coma Scale and on the Acute Physiology and Chronic Health Evaluation (APACHE) II, were most predictive of survival.⁶

Race

No studies suggest a race or ethnic predilection to myxedema coma/crisis.

Sex

Myxedema coma/crisis is approximately 4-8 times more common in women than in men, corresponding to the increased incidence of hypothyroidism in women.

Age

The incidence of hypothyroidism increases with age; the physiological decompensation of severe hypothyroidism, myxedema coma/crisis, occurs primarily in the elderly.⁷ However, this condition should not be automatically ruled out in young adults.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Although most patients with myxedema coma/crisis have a long history of hypothyroidism, undiagnosed or undertreated myxedema coma/crisis may be the initial manifestation of a hypothyroid state.
• A history of generalized fatigue, cold intolerance, constipation, and dry skin (common features of long-standing hypothyroidism) are usually present. These features slowly progress to lethargy, delirium, or coma.
• Faster progression may occur, precipitated by overmedication, stroke, congestive heart failure, trauma, exposure to cold environmental temperatures, or an infection, such as pneumonia.
• Relatives or friends who know the patient may be able to report a history of long-standing fatigue, weight gain, hair and skin changes, edema, constipation, and cold intolerance.
• Most cases of myxedema coma/crisis occur during the winter in women aged 60 years or older, although a case of a woman presenting in labor has been reported.

Physical

• Hypothermia is usually present in myxedema coma/crisis. If mercury thermometers are used, the degree of hypothermia may not be recognized unless the temperature of the thermometer is lowered before checking the patient's temperature. Moreover, use of special thermometers that record well below 90°F may be necessary in order to determine the patient's actual temperature and to monitor rewarming.
• Absence of fever in the presence of infection can be expected.
• The following features are extremely common, although some are not invariably present:
• • Hypotension/shock
  • Hypothermia
  • Decreased pulse pressure, normal systolic pressure, elevated diastolic pressure, slow pulse and respiration rates
  • Periorbital, nonpitting edema; facial swelling or coarseness; macroglossia; enlargement of the tonsils, nasopharynx, and larynx; coarse or thinning hair⁸
  • Thyroid - Enlarged, not palpable, scar suggesting previous thyroidectomy
  • Lungs - Slow respiration rate, hypoventilation, congestion, pleural effusions, consolidation
  • Heart - Soft or distant heart sounds, diminished apical impulse, bradycardia, enlarged heart, pericardial effusion
  • Abdomen - Distension secondary to ileus and/or ascites, diminished or absent bowel sounds
  • Bladder distension
  • Extremities - Cold, nonpitting edema of the hands and feet
  • Skin/nails - Cool, pale, dry, scaly, thickened skin; dry, brittle nails; ecchymoses, purpura, sallowness due to carotenemia
  • Neuromuscular - Confusion, stupor, obtundation, coma, slow speech, seizures, reflexes with a slow relaxation phase

Causes

Myxedema coma/crisis is a physiologic decompensation of severe primary or secondary hypothyroidism that is usually caused by additional physiologic stress. Specific types of such stress are as follows:

• Infection/systemic illness
• Cold environmental temperatures
• Trauma
• Burns
• Decreased cerebral blood flow/cerebrovascular accident
• Decreased cardiac output/congestive heart failure
• Respiratory acidosis (increased P_CO2, decreased P_O2)
• Drugs
• • Tranquilizers
  • Sedatives
  • Anesthetics
  • Analgesics/narcotics
  • Amiodarone
  • Rifampin
  • Beta blockers
  • Lithium
  • Phenytoin
  • Diuretics
• GI hemorrhage
• Hypoglycemia
• CO₂ retention

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Cerebrovascular accident

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

Laboratory values are essential for the workup of myxedema coma/crisis; however, if the condition is suspected, treatment must be initiated immediately without waiting for the results.

• Free T4 and TSH
• • Free T4 and T3 levels are low or undetectable.
  • The TSH level may be elevated, indicating a primary thyroid disorder.
  • A low or normal TSH level with low levels of T4 and T3 may indicate central (pituitary) hypothyroidism or the suppression of TSH production by severe illness or drugs, such as dopamine or high-dose glucocorticoids. A serum cortisol level should be determined before beginning intravenous steroids.
• Serum electrolytes and serum osmolality - Hyponatremia with low serum osmolality is common.
• Serum creatinine - Because of decreased renal perfusion, the levels are usually elevated.
• Serum glucose - Hypoglycemia is common but may also suggest adrenal insufficiency.
• Complete blood count (CBC) with differential - Bands and/or a left shift may be the only sign of infection.
• Creatine kinase (CK) - CK levels are often elevated, and fractionation indicates skeletal (not cardiac) muscle injury unless a myocardial infarction was the precipitating event.
• Arterial blood gases - Increased P_CO2 and decreased P_O2 are found.
• Pan-culture for sepsis

Imaging Studies

• Chest radiographs - Obtain chest radiographs for all patients. Cardiomegaly, pericardial effusion, congestive heart failure, and/or pleural effusion are observed.

Other Tests

• Electrocardiogram - Sinus bradycardia, low-amplitude QRS complexes, a prolonged QT interval, and flattened or inverted T waves are noted.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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 low^{9, 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, CO₂ 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

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The goals of pharmacotherapy are to increase thyroid hormone levels, reduce morbidity, and prevent complications.

Drug Category: 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.

Drug Category: Corticosteroids

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body's immune response to diverse stimuli.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Closely monitor vital signs, electrolytes, and glucose until the levels are within reference ranges and the patient is alert.
• Substitute oral medications for intravenous ones in patients who are extubated and eating.
• Watch for signs of infection, myocardial ischemia, and congestive heart failure.
• Patients who, before hospitalization, did not take their thyroid medication regularly must be evaluated to determine whether they require assistance in taking their thyroid hormone replacement every day.
• Institute physical therapy to assist in strength training and reconditioning.

Further Outpatient Care

• Follow-up care is necessary to ensure compliance with thyroid hormone replacement.
• If primary hypothyroidism was diagnosed, assess the TSH level every 6 weeks and adjust the T4 dose. Once a normal TSH level is obtained, it may be monitored yearly. If compliance is an issue, check the patient every 3-6 months.
• In hypothyroidism secondary to pituitary dysfunction, monitor free T4 levels. The TSH level is not an accurate measure of thyroid function.
• Obtain assurance that the precipitants of the initial presentation will not recur.

In/Out Patient Meds

• Oral levothyroxine is taken daily at least 1 hour before meals.
• If adrenal insufficiency or pituitary dysfunction has been diagnosed, replacement hormones must be taken as appropriate.

Transfer

• Patients who are awake, no longer dependent on a ventilator, and medically stable may be transferred from the intensive care unit to a medical floor. Before the patient is discharged to return home, transfer to a skilled-care nursing facility for further care and rehabilitation may be necessary.

Deterrence/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.

• Patients who are likely to be noncompliant with medication regimens must have their thyroid function closely monitored.

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

Complications

• Adrenal crisis is a major complication if patients presenting with myxedema coma/crisis also have adrenal insufficiency and are not treated concomitantly with stress doses of intravenous corticosteroids.
• Myocardial infarction can cause myxedema coma/crisis but may also be a complication of intravenous treatment with thyroid replacement hormones in patients whose myocardial function is already precarious.

Prognosis

Observational studies have analyzed the predictors of survival for patients presenting with myxedema coma.

• In a study of 11 patients with myxedema coma in which 7 survived, statistically significant factors correlated with survival included the following⁶:
• • Coma on entry
  • Lower Glasgow Coma Scale
  • High APACHE II score 
•  The following factors were not significantly correlated with survival:
• • Age
  • Body temperature
  • Heart rate
  • Free T4, TSH
• In a study of 23 consecutive patients presenting with myxedema coma, 11 of whom survived, statistically significant predictors of mortality included the following¹³:
• • Hypotension and bradycardia at presentation
  • Need for mechanical ventilation
  • Hypothermia that is not responsive to treatment
  • Sepsis
  • Intake of sedatives
  • Lower Glasgow Coma Scale
  • High APACHE II score
  • High Sequential Organ Failure Assessment (SOFA) score.  The SOFA score at baseline was most predictive, and a day 3 score of more than 6 was highly predictive of a poor outcome.

Patient Education

• Patients must be counseled regarding the necessity of taking daily thyroid hormone replacement and of being monitored on a regular basis so that their TSH level remains within the normal range.  
• Patients with a history of Hashimoto thyroiditis or who have undergone thyroid irradiation or resection should be counseled that hypothyroidism might occur in the future. They should be familiarized with the symptoms that suggest the presence of hypothyroidism and should understand the necessity of seeking prompt medical attention for appropriate testing.
• For excellent patient education resources, visit eMedicine's Endocrine System Center. Also, see eMedicine's patient education articles Thyroid Problems and Myxedema Coma.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Before presentation, many patients may have been treated with diuretics for edematous states, which may mask the manifestations of myxedema and cause a delay in diagnosis.¹³
• Missing the diagnosis of myxedema coma/crisis is a major cause of increased mortality.¹⁴ In patients presenting with lethargy, bradycardia, hypothermia, and respiratory depression, myxedema coma/crisis should be considered. Tests for thyroid and adrenal function must be drawn immediately, and treatment should be initiated with levothyroxine and hydrocortisone before test results are available.
• Even if myxedema coma/crisis is treated appropriately with thyroid replacement, failure to include stress doses of intravenous steroids can cause adrenal crisis in patients who have adrenal insufficiency on presentation.
• Signs of infection may be subtle in patients with myxedema coma/crisis. Patients are hypothermic, and leukocytosis is not common. A WBC differential may be one of the few clues to the presence of infection or sepsis. Pan-cultures should be obtained as part of the initial workup.
• In patients who have coronary artery disease, myocardial ischemia/infarction may be either a precipitant of myxedema coma/crisis or a consequence of rapid thyroid hormone replacement. Cardiac enzyme assays are a necessary part of the initial workup and management of these patients. Older patients should receive lower doses of thyroid hormone and should be closely monitored for signs of ischemia.

• Late intubation is a risk for increased mortality from myxedema coma. Respiratory support should be instituted if hypercapnia is detected.

• Administration of all medications must be adjusted for the reduction in drug metabolism and clearance that occurs with myxedema coma/crisis. Extremely careful oversight is necessary in order to avoid overmedication, especially of anesthetics and of drugs with a narrow therapeutic margin.

• For patients who have already been anticoagulated with warfarin, correction of hypothyroidism may necessitate a decrease in the dose of warfarin needed to maintain a therapeutic level of anticoagulation. The international normalized ratio (INR) should be closely monitored during thyroid hormone repletion.

Special Concerns

• Geriatric patients and patients with risk factors for coronary artery disease should be carefully monitored to ensure that an acute ischemic event is neither a precipitant of myxedema coma/crisis nor a consequence of treatment.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

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12. 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].
13. 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].
14. 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].
15. Brent GA, Larsen PR, Davies TF. Hypothyroidism thyroiditis. In: Kronenberg HM, Melmed S, Polonsky KS, et al, eds. Williams Textbook of Endocrinology. 11^th ed. Philadelphia, Pa: Saunders/Elsevier; 2008.
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Article Last Updated: Aug 5, 2008