Myxedema coma medical therapy: Difference between revisions
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==Overview== | ==Overview== | ||
All the patients with myxedema coma should be shifted to ICU and treatment should be started as quickly as possible. Given the clinical suspicion of myxedema coma, initiate replacement therapy without waiting for results of endocrine laboratory. The empirical use of glucocorticoids should be part of the initial therapeutic protocol, in view of the observations which indicate that severe hypothyroidism induces a lower adrenal response to stress. This is independent of whether or not there is simultaneous adrenal insufficiency. Since thyroid hormone speeds up metabolism of cortisol and its plasma levels may be decreased in the presence of adrenal insufficiency, the glucocorticoids should always be given prior to thyroid replacement because otherwise they could precipitate an adrenal crisis. Hydrocortisone will be given in doses of stress, 50- 100 mg intravenously (IV) every 6-8 h for 7 to 10 days or until hemodynamically stabilizes the patient. Suspend if laboratory commitment is discarded of the adrenal axis. Identify and properly treat the precipitating factor | |||
==Medical Therapy== | ==Medical Therapy== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
All the patients with myxedema coma should be shifted to ICU and treatment should be started as quickly as possible. Given the clinical suspicion of myxedema coma, initiate replacement therapy without waiting for results of endocrine laboratory. The empirical use of glucocorticoids should be part of the initial therapeutic protocol, in view of the observations which indicate that severe hypothyroidism induces a lower adrenal response to stress. This is independent of whether or not there is simultaneous adrenal insufficiency. Since thyroid hormone speeds up metabolism of cortisol and its plasma levels may be decreased in the presence of adrenal insufficiency, the glucocorticoids should always be given prior to thyroid replacement because otherwise they could precipitate an adrenal crisis. Hydrocortisone will be given in doses of stress, 50- 100 mg intravenously (IV) every 6-8 h for 7 to 10 days or until hemodynamically stabilizes the patient. Suspend if laboratory commitment is discarded of the adrenal axis. Identify and properly treat the precipitating factor
Medical Therapy
Treatment of myxedema coma should be performed in an Intensive Care Unit (ICU) and start with as quickly as possible. Given the clinical suspicion of myxedema coma, initiate replacement therapy without waiting for results of endocrine laboratory. The empirical use of glucocorticoids should be part of the initial therapeutic protocol, in view of the observations which indicate that severe hypothyroidism induces a lower adrenal response to stress. This is independent of whether or not there is simultaneous adrenal insufficiency. Since thyroid hormone speeds up metabolism of cortisol and its plasma levels may be decreased in the presence of adrenal insufficiency, the glucocorticoids should always be given prior to thyroid replacement because otherwise they could precipitate an adrenal crisis. Hydrocortisone will be given in doses of stress, 50- 100 mg intravenously (IV) every 6-8 h for 7 to 10 days or until hemodynamically stabilizes the patient. Suspend if laboratory commitment is discarded of the adrenal axis. Identify and properly treat the precipitating factor.[1][2][3][4]
Replacement Therapy
- Preferred regimen (1)-levothyroxine (LT4)200-400 μg in IV bolus in the first 48 hours, followed by one dose more physiological 50-100 μg IV daily until you can administer orally.
- Note-some propose to start with larger doses of 300-500 μg
- Note-To avoid the risk of cardiac complications continuous cardiac monitoring with dose reduction of thyroid hormone to see ischemic changes or arrhythmias.
- Preferred regimen (1)-levothyroxine (LT4)200-400 μg in IV bolus in the first 48 hours, followed by one dose more physiological 50-100 μg IV daily until you can administer orally.
- Alternative regimen (1)-10 μg of LT3 in IV bolus with the dose of LT4 and continue with 10 μg every 8-12 hs along the LT4 until recovery.OR
- Alternative regimen (2)-(LT4 + LT3) 5-20 μg IV bolus as loading dose, followed by 2.5-10 μg every 8 h
Supportive
Broad spectrum antibiotics should be started immediately given the high incidence of infections. Ventilation mechanics to reduce CO2 retention and respiratory acidosis. Hypothermia using passive methods(blankets), since they can generate greater vasodilation. The treatment of hypotension should be energetic by evaluating the best option, either volume replenishment or drug pressures, preferably with dynamic monitoring. Need to administer electrolytes and dextrose to correct hyponatremia and possible hypoglycaemia. Appropriate management of hyponatremia requires low hypertonic saline solution (50-100 ml ClNa al 3%), sufficient to increase the sodium concentration at about 2 mEq / l in the initial course of treatment, followed by an IV bolus of furosemide 40 to 120 mg for promote watery diuresis. A quick correction of the Hyponatremia can cause a complication of extreme severity as the osmotic demyelination syndrome (central pontine myelinolysis). After reaching a sodium level greater than 120 mEq / l, the water restriction is sufficient to completely normalize the natremia. Another therapeutic option (not available in Argentina), is to administer an antidiuretic hormone antagonist such as tolvaptan or conivaptan. Both drugs are approved in the United States for the treatment of patients with hyponatremia due to secretion syndrome inappropriate antidiuretic hormone, hypothyroidism, adrenal insufficiency and pneumopathies.
| Condition | Management |
|---|---|
| Hypocortisolemia | iv hydrocortisone 200-400 mg daily |
| Hypoventilation | Intubation and mechanical ventilation |
| Hypothermia | Blankets(no active rewarming) |
| Hyponatremia | Fluid restriction |
| Hypotension | volume expansion with crystalloid or whole blood |
| Hypoglycemia | glucose administration |
References
- ↑ Jordan RM (1995). "Myxedema coma. Pathophysiology, therapy, and factors affecting prognosis". Med. Clin. North Am. 79 (1): 185–94. PMID 7808091.
- ↑ Kwaku MP, Burman KD (2007). "Myxedema coma". J Intensive Care Med. 22 (4): 224–31. doi:10.1177/0885066607301361. PMID 17712058.
- ↑ Wall CR (2000). "Myxedema coma: diagnosis and treatment". Am Fam Physician. 62 (11): 2485–90. PMID 11130234.
- ↑ Rizzo L, Mana DL, Bruno OD, Wartofsky L (2017). "[Myxedema coma]". Medicina (B Aires) (in Spanish; Castilian). 77 (4): 321–328. PMID 28825577. Vancouver style error: initials (help)