Myxedema Coma Basics

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Myxedema coma is a complication of long-term, untreated or poorly-controlled hypothyroidism that causes an inability for the body to maintain homeostasis. Left untreated, myxedema coma can lead to respiratory failure, GI bleeding, myocardial infarction, sepsis, and death.

Myxedema coma physiology

The thyroid gland produces two important hormones, T3 (triiodothyronine) and T4 (thyroxine). Of the two, T3 is the most potent, and most of the body’s T4 is converted into T3 in the tissues. Thyroid hormones influence every cell in the body and have a significant influence on most of the body’s functions, which is why a patient in myxedema coma can have such a broad range of presenting symptoms. Myxedema coma is an extreme form of hypothyroidism and can occur without precipitating factors or when the body’s homeostatic mechanisms are overwhelmed by stressors such as infection, hypothermia, hypoglycemia, surgery, and even some medications.

Medications that have been known to cause hypothyroidism and myxedema coma are amiodarone, lithium, and phenytoin.

Now that you have some basic understanding of myxedema coma, let’s dive into this condition using the Straight A Nursing LATTE Method.

L: How does the patient LOOK?

Manifestations of myxedema coma are widespread simply because thyroid hormone influences most of the body’s functions. 

Temperature dysregulation – Hypothermia is a common clinical manifestation of myxedema coma, with temperatures typically measuring below 35.5° C or 95.9° F. The lower the patient’s body temperature, the worse the prognosis.

Neurological – Neurological manifestations include lethargy, confusion, decrease in intellectual function, decreased deep tendon reflexes, psychosis, and even coma. 

Respiratory – A patient with myxedema coma will have diaphragmatic weakness and a decreased ventilatory response to low PaO2 or elevated PaCo2. What you will observe in the patient is hypoventilation, with shallow and slow breaths. Edema of the tongue or pharynx can cause airway obstruction, which further impedes proper respiratory function. Hypercapnia, which is an elevated CO2 level, is thought to be the main cause of coma in these patients.

Cardiac – Initially the body attempts to compensate for hypoxia and hypothermia through peripheral vasoconstriction and the shunting of blood toward vital organs, which can cause an elevated diastolic blood pressure. However, as these compensatory mechanisms fail, the patient will become hypotensive. Hemodynamic stability is further reduced due to bradycardia and decreased cardiac output. Other cardiac manifestations include heart block, bundle branch blocks, low voltage EKG tracings, prolonged QT intervals, and even shock.

Hematologic – Decreased clotting factors place the patient at high risk for bleeding.

Immunologic dysfunction – Myxedema coma can impair the body’s ability to respond to infection due to its effect on essentially all body systems.

Gastrointestinal – Common GI manifestations include nausea and vomiting, ileus, abdominal distention, megacolon, abdominal pain, constipation and lack of appetite. In addition, GI bleeds can occur due to hematologic complications. 

Renal and electrolytes – Patients with myxedema coma typically have low GFR, urinary retention, and hyponatremia. Hyponatremia is due to decreased excretion of free water secondary to increased antidiuretic hormone and low GFR. A low sodium level is another leading cause of altered mental status and coma in these patients.

Physical appearance – The face of a patient with myxedema coma may appear puffy with periorbital edema. Other facial manifestations include ptosis, an enlarged tongue, and thinning hair. The patient may also have dry skin, nonpitting edema of the lower extremities and, in some cases, a goiter. A scar on the neck may indicate prior thyroidectomy which puts the patient at high risk for hypothyroidism and myxedema coma.

A: How do you ASSESS a patient with myxedema coma?

Because myxedema coma can manifest in so many ways and have such a wide range of complications, assessments will also be very generalized. Key things to assess include:

• Obtain a full set of VS – the patient is likely to have a low respiratory rate and be hypothermic, hypotensive, and bradycardic.
• Assess mental status and level of consciousness
• Assess for edema of the tongue and pharynx, both of which can put your patient at risk for airway obstruction
• Monitor for EKG changes and cardiac arrhythmias
• Auscultate bowel sounds which will be absent in cases of ileus
• Measure urine output which can be decreased due to an increase in antidiuretic hormone (ADH)
• Monitor for signs of bleeding, especially GI bleeding
• Look for signs of infection which can precipitate or complicate myxedema coma such as cloudy urine, a cough with thick sputum, or a wound with purulent drainage.

T: What TESTS are utilized?

Tests utilized in the evaluation of a patient with confirmed or suspected myxedema coma include:

• Thyroid hormone – TSH will be elevated while T4, free T4 and free T3 will be low or undetectable
• CBC – the patient may be anemic and have a low WBC count (leukopenia)
• Glucose – hypoglycemia can occur due to decreased metabolism
• Sodium – hyponatremia is common
• Cortisol – hypothyroidism can mask adrenal insufficiency
• Creatinine – likely to be elevated due to impaired renal function
• ABG – an arterial blood gas may reveal hypoxia, hypercapnia and respiratory acidosis
• Lumbar puncture – may show elevated pressure and high protein count due to increased permeability of the meninges and decreased metabolism (often done to rule out other causes for neurological deterioration)
• EKG – continuous EKG monitoring is important since arrhythmias and significant bradycardia can occur

T: How is myxedema coma TREATED?

Patients with myxedema coma will require ICU admission and continuous monitoring for complications. 

The mainstay of treatment is thyroid hormone replacement in the form of intravenous T4 and T3.

• Levothyroxine (Synthroid) is the synthetic form of T4, which must be converted into T3 in the body. A dose between 200 to 400 mcg is initially administered as a slow IV bolus, followed by daily doses in the 50 to 100 mcg range until the patient is able to take PO medication. 
• Liothyronine (Cytomel) is the synthetic form of T3 and is given concurrently with T4. Though you may see some cases where only T4 is administered, recent recommendations state that administration of both hormones is beneficial due to the greater biologic activity and more rapid onset of T3. In addition, in hypothyroidism the conversion of T4 to T3 is impaired. However, it is important to note that high doses of T3 should be avoided. A typical initial dose is 5 to 20 mcg and follow-up doses range from 2.5 to 10 mcg every eight hours until the condition improves.
• Glucocorticoids. Administration of thyroid hormone increases cortisol metabolism, which can be devastating for a patient with adrenal insufficiency. For this reason, glucocorticoids (hydrocortisone) are often given prior to thyroid hormone and then stopped or decreased once the cortisol level has been obtained.

Supportive therapies are aimed at addressing and preventing complications. These include: 

• Warming – Patients with myxedema coma are passively rewarmed with warming blankets since more aggressive warming therapies can cause vasodilation and worsen hypotension
• Mechanical ventilation – In some cases, mechanical ventilation may be necessary for severe hypoventilation, airway obstruction, or airway maintenance in a comatose patient
• Fluid and electrolyte replacement as needed for hypotension and hyponatremia (or any other electrolyte abnormality)
• Dextrose – Hypoglycemia is treated with IV dextrose
• Treat underlying cause – A common underlying cause is infection, so antibiotics may be initiated while infection is investigated
• Vasopressors – If fluids are not effective in treating hypotension, vasopressors may be utilized until the thyroid hormone has had time to take effect. (note this can increase the risk of cardiac arrhythmias so careful monitoring is vital)

E: What EDUCATION will be provided?

The main thing to teach your patient about myxedema coma is prevention. This is generally through adherence to thyroid hormone supplementation and how to recognize the signs of hypothyroidism which could indicate they need their dose adjusted. They should also have their thyroid function monitored regularly with lab tests such as TSH. 

Did you find this LATTE framework helpful? Download your very own LATTE Method Template here!

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References:

Arif, A., Mukhtar, S., Naseem, S., Hashm, H., Malik, A., Shoaib, I., Grabau, G. M., & Khan, T. A. (2020). SAT-496 Acute GI Bleed Associated with Myxedemic Coma: Yes It Still Exists! Journal of the Endocrine Society, 4(Supplement_1), SAT-496. https://doi.org/10.1210/jendso/bvaa046.001

Elshimy, G., Chippa, V., & Correa, R. (2024). Myxedema. In StatPearls. StatPearls Publishing. http://www.ncbi.nlm.nih.gov/books/NBK545193/

Pennant, M., & Kim, Y. K. (2022). Abstract #1169776: Hypothyroidism Secondary to Hashimoto’s Thyroiditis Presenting After Acute Phenytoin Overdose. Endocrine Practice, 28(5, Supplement), S133–S134. https://doi.org/10.1016/j.eprac.2022.03.312

Ross, D. S. (n.d.). Myxedema Coma. UpToDate.

Saraiva, M., Maia, A., Assunção, G., Freitas, C., & Couto de Carvalho, A. (2023). Myxedema coma following rifampicin – A clinical case and literature review. Annales D’endocrinologie, 84(1), 81–82. https://doi.org/10.1016/j.ando.2022.09.019

Wall, C. R. (2000). Myxedema Coma: Diagnosis and Treatment. American Family Physician, 62(11), 2485–2490. https://www.aafp.org/pubs/afp/issues/2000/1201/p2485.html

Last Updated on March 5, 2025 by Maureen Osuna, MSN, RN