Myxedema Coma or Crisis Treatment & Management

  • Author: Elena Citkowitz, MD, PhD, FACP; Chief Editor: George T Griffing, MD   more...
 
Updated: Nov 23, 2011
 

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[10, 11] or high dose T4 or T3 replacement reduces mortality.[7]
  • In light of the possibility of adrenal insufficiency, stress steroid replacement after a cortisol level is obtained.[12]
  • 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 ischemia[13]
    • 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.
Next

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.
Previous
Next

Consultations

  • Endocrinologist
  • Critical care
  • Consultations with the following practitioners may be necessary, depending on complications:
    • Infectious disease specialists
    • Pulmonologists
    • Cardiologists
Previous
Next

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.

Previous
Next

Activity

Once stable, patients may progress to usual activity as their strength allows. Physical therapy may be useful for patients who are debilitated.

Previous
Proceed to Medication
 
 
Contributor Information and Disclosures
Author

Elena Citkowitz, MD, PhD, FACP  Clinical Professor of Medicine, Yale University School of Medicine; Director, Cholesterol Management Center, Director, Cardiac Rehabilitation, Department of Medicine, Hospital of St Raphael

Elena Citkowitz, MD, PhD, FACP is a member of the following medical societies: American College of Physicians, American Heart Association, National Lipid Association, and Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Stephanie L Lee, MD, PhD  Associate Professor, Department of Medicine, Boston University School of Medicine; Director of Thyroid Health Center, Associate Chief, 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, and Endocrine Society

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Salary Employment

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, and Endocrine Society

Disclosure: Nothing to disclose.

Mark Cooper, MBBS, PhD, FRACP  Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor 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, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

References
  1. Wall CR. Myxedema coma: diagnosis and treatment. Am Fam Physician. Dec 1 2000;62(11):2485-90. [Medline]. [Full Text].

  2. Fliers E, Wiersinga WM. Myxedema coma. Rev Endocr Metab Disord. May 2003;4(2):137-41. [Medline].

  3. Kwaku MP, Burman KD. Myxedema coma. J Intensive Care Med. Jul-Aug 2007;22(4):224-31. [Medline].

  4. Nicoloff JT, LoPresti JS. Myxedema coma. A form of decompensated hypothyroidism. Endocrinol Metab Clin North Am. Jun 1993;22(2):279-90. [Medline].

  5. 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].

  6. Mathew V, Misgar RA, Ghosh S, Mukhopadhyay P, Roychowdhury P, Pandit K, et al. Myxedema coma: a new look into an old crisis. J Thyroid Res. 2011;2011:493462. [Medline]. [Full Text].

  7. 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].

  8. Rehman SU, Cope DW, Senseney AD, et al. Thyroid disorders in elderly patients. South Med J. May 2005;98(5):543-9. [Medline].

  9. 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].

  10. 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].

  11. Hylander B, Rosenqvist U. Treatment of myxoedema coma--factors associated with fatal outcome. Acta Endocrinol (Copenh). Jan 1985;108(1):65-71. [Medline].

  12. Jordan RM. Myxedema coma. Pathophysiology, therapy, and factors affecting prognosis. Med Clin North Am. Jan 1995;79(1):185-94. [Medline].

  13. 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].

  14. 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].

  15. 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].

  16. 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.

  17. Wartofsky L. Myxedema coma. Endocrinol Metab Clin North Am. Dec 2006;35(4):687-98, vii-viii. [Medline].

Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.