Myxedema coma

Myxedema coma is an extreme or decompensated form of hypothyroidism and while uncommon, is potentially lethal.[1][2][3] A person may have laboratory values identical to a "normal" hypothyroid state, but a stressful event (such as an infection, myocardial infarction, or stroke) precipitates the myxedema coma state, usually in the elderly. Primary symptoms of myxedema coma are altered mental status and low body temperature. Low blood sugar, low blood pressure, hyponatremia, hypercapnia, hypoxia, slowed heart rate, and hypoventilation may also occur.[4] Myxedema, although included in the name, is not necessarily seen in myxedema coma. Coma is also not necessarily seen in myxedema coma,[5] as patients may be obtunded without being comatose.[2]

Myxedema coma
SpecialtyEndocrinology Edit this on Wikidata
Symptomsdeterioration of the patient's mental status[1]
Causesinfections (especially pneumonia and urosepsis), certain medications, failure to reinstate thyroid replacement therapy[1]
Treatmentadmission to the intensive care unit, correct hypovolemia and electrolyte abnormalities, mechanical ventilation if needed, thyroid hormone replacement[1]

According to newer theories, myxedema coma could result from allostatic overload in a situation where the effects of hypothyroidism are amplified by nonthyroidal illness syndrome.[6]

Causes

Myxedema coma represents an extreme or decompensated form of hypothyroidism. Most cases occur in patients who have been previously diagnosed with hypothyroidism, yet in some cases, hypothyroidism may not have been previously identified. [1][2][3]

Common precipitating factors of myxedema coma include:

Other precipitating factors include:

Pathophysiology

The thyroid gland is responsible for regulating whole-body metabolism through the production of two major hormones: thyroxine (T4) and triiodothyronine (T3). Of the metabolically active thyroid hormones, 93% is T4 and 7% is T3. T3 is four times more potent than T4 and most T4 is converted to T3 in the tissues. Iodine is necessary for adequate hormone production. Thyroid-stimulating hormone (TSH) is a circulating or serum hormone from the pituitary gland that stimulates the thyroid gland to produce T3 and T4. Hypothyroidism occurs when the thyroid gland does not produce enough T3 and T4.[3]

The most common cause of hypothyroidism worldwide is too little dietary iodine. Hashimoto's thyroiditis is the most common cause of hypothyroidism in countries with sufficient dietary iodine. With the cessation of the production of thyroid hormone, the thyroid gland contains enough reserve T3 and T4 to last 2 to 3 months.[3]

The thyroid hormones T3 and T4 influence the production by virtually all cells in the body of hundreds of new intracellular proteins and enzymes. This influence includes the expression of the calcium ATPase, regulation of ion channels, oxidative phosphorylation, increased Na-K-ATPase activity, increased carbohydrate metabolism, increased free fatty acids, increased vitamin requirements, and increased overall metabolism. The absence of the thyroid hormones T3 and T4 are responsible for many bodily functions at the genetic and cellular level and an absence of these thyroid hormones as seen in myxedema coma has very serious consequences including a broad spectrum of symptoms and a high mortality rate.[3]

Diagnosis

Clinical features of myxedema coma:[1][2][3]

Laboratory features in myxedema coma:[1][2][3]

  • Anemia
  • Elevated creatine kinase (CPK)
  • Elevated creatinine
  • Elevated transaminases
  • Hypercapnia
  • Hypercholesterolemia (elevated LDL)
  • Hyperlipidemia
  • Hypoglycemia
  • Hyponatremia
  • Hypoxia
  • Leukopenia
  • Respiratory acidosis

Epidemiology

Hypothyroidism is four times more common in women than men. The incidence of myxedema coma has been reported to be 0.22 per 1000000 per year but the data is limited and especially lacking in countries outside the western world and countries along the equator. Myxedema coma is most common in people 60 years old and older and is most common in the winter months when hypothermia is more common.[1][2][3]

See also

References
  1. Wall, Cristen Rhodes (2000-12-01). "Myxedema Coma: Diagnosis and Treatment". American Family Physician. 62 (11): 2485–2490. ISSN 0002-838X. PMID 11130234.
  2. Mathew, Vivek; Misgar, Raiz Ahmad; Ghosh, Sujoy; Mukhopadhyay, Pradip; Roychowdhury, Pradip; Pandit, Kaushik; Mukhopadhyay, Satinath; Chowdhury, Subhankar (2011-09-15). "Myxedema Coma: A New Look into an Old Crisis". Journal of Thyroid Research. 2011: 493462. doi:10.4061/2011/493462. PMC 3175396. PMID 21941682.
  3. Elshimy, Ghada; Correa, Ricardo (2022). "Myxedema". StatPearls. StatPearls Publishing. PMID 31424777.
  4. Van den Berghe, Greet, ed. (2008). Acute endocrinology: From Cause to Consequence (1 ed.). New York: Humana Press. pp. 29–44. ISBN 978-1-60327-176-9.
  5. Gardner, David G., Shoback, Dolores M., Greenspan, Francis S. (2017). Greenspan's basic & clinical endocrinology (10th ed.). McGraw-Hill Education. p. 783. ISBN 978-1259589294. OCLC 1075522289.{{cite book}}: CS1 maint: multiple names: authors list (link)
  6. Chatzitomaris, Apostolos; Hoermann, Rudolf; Midgley, John E.; Hering, Steffen; Urban, Aline; Dietrich, Barbara; Abood, Assjana; Klein, Harald H.; Dietrich, Johannes W. (20 July 2017). "Thyroid Allostasis–Adaptive Responses of Thyrotropic Feedback Control to Conditions of Strain, Stress, and Developmental Programming". Frontiers in Endocrinology. 8: 163. doi:10.3389/fendo.2017.00163. PMC 5517413. PMID 28775711.
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