Adrenal and Thyroid Dysfunction
This chapter describes the spectrum of adrenal and thyroid disorders that occur in critically ill patients, and how to identify and manage each of these disorders.
I. Adrenal Insufficiency
A. Adrenal Suppression in Critical Illness
Adrenal insufficiency is common in critically ill patients. The overall prevalence is 10–20% (1), but rates as high as 60% have been reported in patients with severe sepsis and septic shock (2).
The adrenal suppression in critically ill patients is often reversible, and is called critical illness-related corticosteroid insufficiency (CIRCI) (3).
The mechanisms involved in CIRCI are complex, and not fully elucidated; Figure 39.1 shows some of the known mechanisms (1,2,3,4). As indicated, the systemic inflammatory response plays a major role in CIRCI.
Systemic sepsis and septic shock are the leading causes of adrenal suppression in critically ill patients, and most cases involve suppression at the hypothalamic-pituitary level (2).
B. Clinical Manifestations
Adrenal suppression should be suspected in any ICU patient with unexplained or refractory hypotension.
A random plasma cortisol level that is 35 μg/dL or higher is evidence of normal adrenal function in critically ill (stressed) patients, while a random plasma cortisol level below 10 μg/dL is evidence of adrenal insufficiency (1,3).
If the random plasma cortisol level is indeterminate (10–34 μg/dL), a rapid ACTH stimulation test can be performed. A blood sample is obtained for a baseline plasma cortisol level, and the patient is given an IV injection of synthetic ACTH (250 μg), followed 60 minutes later by a repeat plasma cortisol level.
An increment in plasma cortisol of less than 9 μg/dL is evidence of primary adrenal insufficiency (1,3).
However, a larger increment in plasma cortisol (≥9 μg/dL) does not eliminate the possibility of secondary adrenal insufficiency from hypothalamic-pituitary dysfunction (which is common in septic shock, as mentioned earlier).
In patients with septic shock, plasma cortisol levels are not considered necessary for identifying patients who might benefit from corticosteroid therapy; in these patients, corticosteroid
therapy is sanctioned when hypotension is refractory to volume resuscitation, and requires a vasopressor drug (5). (See Chapter 9, Section II-D, for more information on steroid therapy in septic shock.)
The treatment of CIRCI is intravenous hydrocortisone, 200-300 mg daily, in 3 divided doses (1), or by continuous infusion in septic shock (5).
The addition of a mineralocorticoid (i.e., fludrocortisone, 50 μg orally once daily) is considered optional (1), because hydrocortisone has excellent mineralocorticoid activity.
Hydrocortisone can be discontinued after satisfactory resolution of the predisposing condition. If the period of hydrocortisone therapy exceeds 7–10 days, a gradual taper of the dosage is recommended (1).
II. Evaluation of Thyroid Function
Laboratory tests of thyroid function can be abnormal in up to 90% of critically ill patients (6). In most cases, the abnormality is a consequence of non-thyroidal illness (i.e., euthyroid sick syndrome), and is not a sign of thyroid disease (6,7). This section describes the laboratory evaluation of thyroid function, and how to distinguish non-thyroidal illness from thyroid disease.
A. Thyroxine and Triiodothyronine
Thyroxine (T4) is the principal hormone secreted by the thyroid gland, but the active form is triiodothyronine (T3), which is formed by deiodination of thyroxine in extrathyroidal tissues.
T3 and T4 are extensively bound to plasma proteins, and less than 1% of either hormone is present in the free, or biologically active form (8).
Because of the potential for alterations in plasma proteins and protein binding in acute illness, free T4 levels are used to evaluate thyroid function in acutely ill patients. (Free T3 levels are not routinely available.)