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 (see Hypothyroidism).

Myxedema also refers to two different dermatologic conditions. Pretibial myxedema, an uncommon skin disorder, occurs in hyperthyroid states, usually 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. The condition occurs in patients with long-standing untreated hypothyroidism and is usually precipitated by a secondary insult such as climate-induced hypothermia, infection, other systemic diseases, and drug therapies. Patients with myxedema coma have changes in their mental status, including lethargy, stupor, delirium, or coma. A more appropriate term is myxedema crisis, and this article often uses the term myxedema coma/crisis.

Pathophysiology

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

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 (Nicoloff, 1993) in which adaptations are no longer sufficient. 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.

While weight gain is common, severe obesity is rarely secondary to hypothyroidism alone. However, long-standing untreated hypothyroidism may result in years of inactivity with an eventual 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

In spite of the term coma, its absence does not exclude the diagnosis. The presenting mental status may be lethargy or stupor. The exact mechanisms causing changes in mental status are not known. Reductions in cerebral blood flow and oxygen delivery, reduced oxygen and glucose consumption, and the lack of thyroxine (T4) and triiodothyronine (T3) influence brain function, and all 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⁺ ATPase, caused by low levels of gene transcription in the absence of T3.

Increased systemic vascular resistance occurs and, while the causes appear to be multifactorial, a recent study suggests that almost half of the increase is secondary to decreased T3 levels (Diekman, 2001). 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 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 decrease intestinal motility. Patients with myxedema coma can present with gastric atony, megacolon, or paralytic ileus. Malabsorption has also been reported. Ascites, while uncommon, may be due to increased capillary permeability, congestive heart failure, or other mechanisms.

Frequency

United States

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

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 and 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 is unknown in these populations.

Mortality/Morbidity

Myxedema coma/crisis is a metabolic and cardiovascular emergency. If not promptly diagnosed and treated, mortality rates are 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 body temperature less than 93°F, persistent hypothermia unresponsive to 72 hours of therapy, advanced age, bradycardia (<44 beats per min), sepsis, myocardial infarction, and hypotension.

Race

No studies suggest a racial or ethnic predisposition 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. 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 pneumonia or other infection, cold environmental temperatures, overmedication, stroke, congestive heart failure, or trauma.



• 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 was recently reported in a woman presenting in labor.

Physical

• Hypothermia is usually present. 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:
• • Hypothermia
  
  
  
  • Decreased pulse pressure, normal systolic pressure, elevated diastolic pressure, slow pulse and respiration rates
  
  
  
  • Coarse or thinning hair; facial swelling or coarseness; periorbital nonpitting edema; macroglossia; enlargement of tonsils, nasopharynx, larynx
  
  
  
  • 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
  
  
  
  • Extremities - Cold, nonpitting edema of hands and feet
  
  
  
  • Skin/nails - Pale, dry, scaly, thickened skin; dry brittle nails; ecchymoses, purpura, sallowness due to carotenemia
  
  
  
  • Neuromuscular - Confusion, stupor, obtundation, coma, slow speech, seizures, reflexes with slow relaxation phase

Causes

Myxedema coma/crisis is a physiological decompensation of severe primary or secondary hypothyroidism usually caused by some additional physiological stress, as follows:

• Infection/systemic illness



• Cold environmental temperatures



• Trauma



• Burns



• Cerebrovascular accident



• Congestive heart failure



• Drugs
  
  
  • Tranquilizers
  
  
  
  • Sedatives
  
  
  
  • Anesthetics
  
  
  
  • Analgesics/narcotics
  
  
  
  • Amiodarone
     
  • Rifampin
  
  
  • Lithium
  
  
  • Phenytoin
     
• GI hemorrhage



• Hypoglycemia



• Carbon dioxide 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 thyrotropin (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: Levels are usually elevated because of decreased renal perfusion.



• Serum glucose: Hypoglycemia is common but may also suggest adrenal insufficiency.



• CBC with differential



• Creatine kinase (CK): CK levels are often elevated, and fractionation indicates skeletal (not cardiac) muscle injury unless a myocardial infarction was the precipitating event.



• CBC with differential: Bands and/or a left shift may be the only sign of infection.



• Arterial blood gases: Increased PCO₂ and decreased PO₂



• 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, 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 condition 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 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. Use caution in the patient with coronary artery disease or myocardial infarction because full-dose T4 therapy may worsen myocardial ischemia by increasing myocardial oxygen consumption.
  
  
  
  • An intravenous loading dose of 200-500 mcg of levothyroxine is commonly recommended, followed by a daily intravenous dose of 50-100 mcg. Lower doses are indicated for elderly patients and for those in whom myocardial ischemia is thought likely. Some authorities advocate additional intravenous T3 at 10 mcg every 8 hours in young patients with low cardiovascular risk.
     
• Steroid therapy: Initiate hydrocortisone at 100 mg every 8 hours after a baseline cortisol level is ascertained, and continue unless the random cortisol level on admission indicates adrenal function without abnormalities, in which case hydrocortisone may be stopped without tapering.



• Rewarming using ordinary blankets and a warm room (rapid and external rewarming are contraindicated)



• In light of the possibility of adrenal insufficiency, stress steroid replacement after obtaining a cortisol level



• Treatment of associated infection



• Correction of severe hyponatremia (sodium level £120 mEq/L)



• Broad-spectrum antibiotics with modification of the antibiotic regimen based on culture results



• Correction of hypoglycemia with intravenous glucose



• 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 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 ischemia
  
  
  • Myocardial infarction may be the precipitating event in older patients, or it may occur subsequently.
  
  
  
  • Serial CK determinations with fractionation assist in 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 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, carbon dioxide 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 be corrected immediately.



• Temperature monitoring requires 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, extubated, and normal bowel sounds are present, at which 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

Drug Category: Thyroid hormones

Immediate administration of intravenous levothyroxine is a 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 Name	Liothyronine (Cytomel, Triostat)
Description	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 Dose	10 mcg IV q8h
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; uncorrected adrenal insufficiency; acute MI uncomplicated by hypothyroidism; untreated thyrotoxicosis
Interactions	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
Pregnancy	A - Safe in pregnancy
Precautions	Caution in patients who are elderly or who have renal insufficiency, hypertension, ischemia, angina, and other cardiovascular diseases; periodically monitor thyroid status

Drug Category: Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. 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 levels are within reference ranges and 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 precipitants of 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 discharge 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 or who have 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

• Myxedema coma/crisis occurs in the setting of untreated or undertreated hypothyroidism and is precipitated by some additional insult (eg, cold environmental temperature, infection).



• Assuming the absence of other medical conditions that cause significant morbidity and that the patient can be maintained in a euthyroid state, the prognosis is excellent.



• A study of 11 patients with myxedema coma in which 7 survived classified factors that were and were not clinically significant in determining survival (Rodriguez, 2004).
  
  
  • Statistically significant factors correlated with survival
    
    
    • Coma on entry
    
    
    
    • Glasgow score
    
    
    
    • Apache II score  
       
  • Factors not significantly correlated with survival
    
    
    • Age
    
    
    
    • Body temperature
    
    
    
    • Heart rate
    
    
    
    • Free T4, TSH

Patient Education

• Patients must be counseled regarding the necessity of taking daily thyroid hormone replacement and being monitored on a regular basis so that the TSH level remains within the normal range.  



• Patients with a history of Hashimoto thyroiditis or those who have undergone thyroid irradiation or resection should be counseled that hypothyroidism might occur in the future. They should be familiarized with the symptoms suggestive 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

• Missing the diagnosis of myxedema coma/crisis is a major cause of increased mortality. 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 both 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 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 drugs with a narrow therapeutic margin.

• For patients already 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

• 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].
• Fred HL. Curable conspicuous ascites: the forgotten four. Hosp Pract (Off Ed). Oct 15 1999;34(11):98-100. [Medline].
• Gavin LA. Thyroid crises. Med Clin North Am. Jan 1991;75(1):179-93. [Medline].
• Jordan RM. Myxedema coma. Pathophysiology, therapy, and factors affecting prognosis. Med Clin North Am. Jan 1995;79(1):185-94. [Medline].
• Mazzaferri EL, Surks MI. Recognizing the faces of hypothyroidism. Hosp Pract (Off Ed). Mar 15 1999;34(3):93-6, 101-5, 109; discussion 109-10. [Medline].
• Nicoloff JT, LoPresti JS. Myxedema coma. A form of decompensated hypothyroidism. Endocrinol Metab Clin North Am. Jun 1993;22(2):279-90. [Medline].
• Pimentel L, Hansen KN. Thyroid disease in the emergency department: a clinical and laboratory review. J Emerg Med. Feb 2005;28(2):201-9. [Medline].
• Rehman SU, Cope DW, Senseney AD, Brzezinski W. Thyroid disorders in elderly patients. South Med J. May 2005;98(5):543-9. [Medline].
• Reinhardt W, Mann K. [Incidence, clinical picture and treatment of hypothyroid coma. Results of a survey]. Med Klin. Sep 15 1997;92(9):521-4. [Medline].
• Ringel MD. Management of hypothyroidism and hyperthyroidism in the intensive care unit. Crit Care Clin. Jan 2001;17(1):59-74. [Medline].
• Rodriguez I, Fluiters E, Perez-Mendez LF, Luna R, Paramo C, Garcia-Mayor RV. 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].
• Smallridge RC. Metabolic and anatomic thyroid emergencies: a review. Crit Care Med. Feb 1992;20(2):276-91. [Medline].
• Turhan NO, Kockar MC, Inegol I. Myxedematous coma in a laboring woman suggested a pre-eclamptic coma: a case report. Acta Obstet Gynecol Scand. Nov 2004;83(11):1089-91. [Medline].
• Wall CR. Myxedema coma: diagnosis and treatment. Am Fam Physician. Dec 1 2000;62(11):2485-90. [Medline].
• Wartofsky L. Myxedema coma. In: Werner SC, Ingbar SH, Braverman LE, Utiger RD, eds. Werner & Ingbar's the Thyroid: A Fundamental and Clinical Text. Lipincott:2000:843-847.
• Werner SC, Ingbar SH, Braverman LE, et al. Organ system manifestations of hypothyroidism (Section C). In: Werner and Ingbar's the Thyroid: A Fundamental and Clinical Text. 8th ed. Philadelphia, Pa:. Lipincott Williams & Wilkins;2000:774-847.

Article Last Updated: Jul 10, 2006