Thyroid Disease in the Intensive Care Unit

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Chapter 53 Thyroid Disease in the Intensive Care Unit

Annis Marney, MD, MSCI

1 What thyroid conditions require intensive care?

Thyroid storm: Life-threatening thyrotoxicosis (accounts for 1%-2% of admissions for thyrotoxicosis and carries 20%-30% mortality)

Myxedema coma: Life-threatening hypothyroidism (approximately 20% mortality)

Note: Nonthyroidal illness syndrome (NTIS), formerly known as euthyroid sick syndrome, is not life threatening.

2 How do you diagnose thyroid storm?

Thyroid storm often occurs in people with Graves disease who have stopped medication or whose condition is undiagnosed. In addition, a precipitating factor often exists such as severe infection, diabetic ketoacidosis, myocardial infarction (MI), cerebrovascular accident (CVA), heart failure, trauma, amiodarone therapy (short or long term), or a recent test involving iodinated contrast load (less than 6 weeks before presentation). It shares laboratory findings with thyrotoxicosis but is different from simple thyrotoxicosis in that it involves fever.

Clinical symptoms include the following:

Fever >102° F (38.9° C) (hallmark): most consider this the sine qua non of thyroid storm

Blood pressure not necessarily high or low

Cardiac arrhythmias, heart failure, and/or ischemia: common

Nausea, vomiting, diarrhea

Agitation, tremulousness, delirium

Jaundice: a particularly worrisome sign

Laboratory findings include suppressed (undetectable, not just low) thyroid-stimulating hormone (TSH) and elevated serum total thyroxine (T₄) (TT₄), free T₄ (FT₄), total triiodothyronine (T₃) (TT₃), and free T₃ (FT₃).

3 How do you treat thyroid storm?

Use common sense. First, support the patient as you would any critically ill patient and be sure to initiate cardiac monitoring. Next, reduce thyroid hormone production with thioureas. Finally, stop release of preformed hormone by adding iodide. Simultaneously with these measures give β-blockade to slow heart rate and reduce conversion of T₄ to T₃ (see Table 53-1).

^{Table 53-1} Supportive Care and Specific Medications for Thyroid Storm

Intervention and mechanism of action	Dose	Route
Supportive care
Isotonic fluids	Patient specific	IV
Oxygen	Patient specific	Nasal cannula if stable enough
Cooling blanket		Topical
Acetaminophen or other antipyretics	Adult dosing	Oral, rectal, or NG
Thioureas: reduce thyroid hormone production
Propylthiouracil	150 mg every 6 hr	Oral, rectal, or NG
Methimazole (Tapazole)	20 mg every 8 hr	Oral, rectal, or NG
Iodide: reduce hormone production and T₄ to T₃ conversion 2-4 hr after starting thioamide (above)
Saturated solution of potassium iodide	5 drops (250 mg) twice daily	Oral
Iopanoic acid	0.5 g twice daily	Oral or IV
Iohexol	0.6 g (2 mL of Omnipaque 300) twice daily	IV
β-Blockade: reduce heart rate and reduce conversion of T₄ to T₃
Propranolol	40-80 mg every 6 hr	Oral
Propranolol	0.5-1.0 mg over 10 min every 3 hr	IV
Esmolol (especially if patient has asthma and needs β₁-selective agent)	0.25-0.5 mg/kg bolus followed by 0.05-0.1 mg/kg/min infusion	IV
Glucocorticoids: support circulation, supplement glucocorticoid reserve because of increased metabolism and reduced half-life with thyrotoxicosis, and reduce T₄ to T₃ conversion
Dexamethasone	2 mg every 6 hr × 48 hr, then taper dose rapidly	Oral or IV
Hydrocortisone	100 mg every 8 hr × 48 hr, then taper dose rapidly	IV
Resin binders: remove T₄ in the gut to reduce enterohepatic circulation of free T₄
Cholestyramine or colestipol	20-30 g daily	Oral or NG

IV, Intravenous; NG, nasogastric.

4 How do you diagnose myxedema coma?

Myxedema coma often occurs in people with undiagnosed or untreated hypothyroidism and is the end stage of a process that takes days to weeks. Often these people have had a precipitating event such as MI, CVA, acute infection, trauma, or hemorrhage. There may be a history of previous thyroid surgery or radioactive iodine ablation for hyperthyroidism, but because of mental status changes you may not get that history. Always look for an anterior neck scar for previous thyroid surgery.

Clinical symptoms include the following:

Altered mental status (coma not strictly necessary, but altered mental status is)

Hypothermia (as low as 75° F [23.9° C] has been reported)

Dry, coarse skin

Gravelly, hoarse voice

Thin scalp and eyebrow hair

Pleural and cardiac effusions

Delayed relaxation time of reflexes (Achilles = most sensitive)

Laboratory findings include elevated TSH with low or low-normal serum TT₄, FT₄, TT₃, and FT₃.

5 How do you treat myxedema coma?

Again, use common sense. First, support the patient as you would any critically ill patient and be sure to initiate cardiac monitoring and ventilatory support and secure intravenous access (avoid oral or nasogastric medications because of possible ileus, which is common in myxedema coma). Next, administer glucocorticoids. Thyroid hormone speeds metabolism throughout the body, including metabolism of glucocorticoids. If the patient has underlying or undiagnosed adrenal insufficiency (autoimmune, typically), administration of thyroid hormone with a backdrop of adrenal insufficiency can precipitate adrenal crisis and is avoidable. Not every patient requires this, but it is impossible to differentiate acutely who does and who does not; therefore everyone should get it. You can taper quickly once you determine who needs steroids. Finally, give a parenteral thyroid hormone (see Table 53-2).

^{Table 53-2} Supportive Care and Specific Medications for Myxedema Coma

Intervention	Dose	Route
Supportive care
Isotonic fluids but avoid overloading because of hyponatremia	Patient specific	IV
Oxygen	Patient specific	Nasal cannula if stable enough
Thyroid hormone replacement therapy
Levothyroxine (T₄)	300-400 mcg loading dose then 50-100 mcg daily (based on weight)	IV
Liothyronine (T₃) (controversial)	10 mcg every 8 hr × 48 hr	IV
Glucocorticoid therapy: support circulation, supplement glucocorticoid reserve because of possible adrenal insufficiency
Dexamethasone	2 mg every 6 hr × 48 hr, then taper dose rapidly	IV
Hydrocortisone	100 mg every 8 hr × 48 hr, then taper dose rapidly	IV

IV, Intravenous.

Different schools of thought exist about T₃ therapy. It increases cardiac metabolic demands acutely and so can be unwise in elderly patients already acutely ill. Many practitioners believe that patients can convert T₄ to T₃ on their own and thus administering T₃ is unnecessary and potentially dangerous.

6 How do you diagnose NTIS?

NTIS, formerly known as euthyroid sick syndrome, often occurs in patients who have severe, prolonged critical illness and is essentially a laboratory abnormality to be monitored. It is not a primary thyroid disorder but instead results from a resetting of the hypothalamic-pituitary-thyroid axis, as well as changes in peripheral thyroid hormone metabolism and transport induced by nonthyroidal illness. The laboratory abnormalities occur sequentially as follows:

Serum TT₃ and FT₃ levels are low (decreased conversion of T₄ to T₃ in peripheral tissues).

TT₃ and FT₃ levels are even lower. FT₄ level may be normal, decreased, or increased. TSH level is normal or slightly decreased.

FT₄ level is low and TSH is high (may transiently be significantly elevated in the teens and 20s). This is the recovery phase and can be prolonged. Normalization of laboratory values can take weeks to months.

7 Could these laboratory values be confused with central hypothyroidism or pituitary dysfunction, and how can you tell the difference?

The laboratory results can be confusing, and you do have to take a careful history to be sure the patient has not had pituitary surgery or radiation therapy. Also, pituitary apoplexy could present with similar laboratory values, but the patient would have symptoms of severe headache and adrenal insufficiency as well. Only in cases where patients have symptoms concerning for apoplexy or a mass do you need to do magnetic resonance imaging (e.g., visual disturbance). Yes, sex hormones and insulin-like growth factor–1 levels may also be low, but this is likely the body’s adaptive function and does not require therapy (also therapy with sex steroids and growth hormone have been proved not to help). Adrenal insufficiency that is clinically significant will cause symptoms, and testing for it can be tricky but may be necessary (see Chapter 52 on the adrenal gland).

8 How do you treat NTIS?

Most often, you do not. There is a great deal of controversy in this area, however. The few studies that have been done show no benefit to giving T₄ in these patients. The recommendation is to recheck thyroid laboratory results in 4 to 6 weeks. It is possible that in cases of severely low T₄ and T₃ some patients may benefit from levothyroxine therapy, especially those with cardiac failure, but the evidence is far from conclusive.

Key Points Thyroid Disorders

1. Thyroid storm is life-threatening thyrotoxicosis that often presents with a precipitating factor and carries a high mortality rate if not treated promptly and appropriately.

2. When thyroid storm is diagnosed or suspected, give appropriate supportive care and treat with antithyroid drugs, cold iodine, β-blockers, and stress doses of glucocorticoids, along with management of any precipitating factors.

3. Myxedema coma is life-threatening hypothyroidism that often has an identifiable precipitating cause and has a high mortality rate if not promptly and adequately treated.

4. When myxedema coma is diagnosed or suspected, first treat with stress doses of glucocorticoids followed by rapid repletion of the thyroid hormone and treatment of any precipitating causes.

5. NTIS is not a thyroid disorder but rather laboratory changes in serum TSH, T₄, and T₃ resulting from cytokines and inflammatory mediators produced in patients with nonthyroidal illnesses and generally does not require treatment.

1 DeGroot L. “Non-thyroidal illness syndrome” is functional central hypothyroidism, and if severe, hormone replacement is appropriate in light of present knowledge. J Endocrinol Invest. 2003;26:1162.

2 Farwell A.P. Thyroid hormone therapy is not indicated in the majority of patient with sick euthyroid syndrome. Endocr Pract. 2008;14:1180–1187.

3 Goldberg P.A., Inzucchi S.E. Critical issues in endocrinology. Clin Chest Med. 2003;24:583–606.

4 Kwaku M.P., Burman K.D. Myxedema coma. J Intensive Care Med. 2007;22:224–231.

5 Warner M.H., Beckett G.J. Mechanisms behind the non-thyroidal illness syndrome: an update. J Endocrinol. 2010;205:1–13.

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