Thyroid and Adrenal Disorders in the Intensive Care Unit

Chapter 85


Thyroid and Adrenal Disorders in the Intensive Care Unit



Abnormalities in thyroid and adrenal function tests are commonly seen in critically ill patients in the intensive care unit (ICU). These may reflect endocrine dysfunction that requires intervention or a physiologic adaptation to illness.




The Nonthyroidal Illness Syndrome


The nonthyroidal illness syndrome (NTIS) is an alteration in thyroid function tests seen in patients with acute or chronic illness with no prior history of thyroid dysfunction. Low serum T3 is the most common abnormality in NTIS; however, decreases in TSH and T4 are seen in more prolonged or severe illness. Elevations in reverse T3 (rT3) may also be evident (Figure 85.1).




Epidemiology and Etiology


NTIS is seen in up to 75% of hospitalized patients. Whether NTIS represents a physiologic adaptation as the body attempts to reduce energy expenditure or a true pathologic state is uncertain. The decrease in physiologically active T3 results from decreased peripheral monodeiodination of T4. A form of central hypothyroidism also likely exists because of reduced hypothalamic production of thyrotropin-releasing hormone (TRH) with resultant decrease in TSH.


Drugs used in the ICU can also affect both thyroid function and thyroid function tests. Corticosteroids and dopamine decrease both basal TSH secretion and pituitary response to TRH. Corticosteroids also decrease the peripheral conversion of T4 to T3. A number of other drugs commonly used in the ICU can affect the thyroid function or the interpretation of thyroid function tests. Drugs that can cause hypothyroidism include lithium, intravenous (IV) iodinated radiographic contrast agents, amiodarone, aminoglutethamide, thalidomide, interferon alpha, and interleukin-2. Drugs that can cause hyperthyroidism include iodine and amiodarone, interferon alpha, denileukin diftitox, and interleukin-2.



Diagnosis


TSH is usually suppressed, necessitating differentiation from hyperthyroidism. TSH is low enough to be undetectable in only 7% of NTIS patients (usually those who have received corticosteroids or dopamine). An undetectable TSH therefore suggests hyperthyroidism. Assessment of T4 and T3 levels differentiates between the two conditions, as these will be elevated only in hyperthyroidism (Figure 85.2).



Differentiating between NTIS and hypothyroidism is more challenging. An elevation in TSH as high as 20 mIUu/L may be seen during the recovery phase of NTIS. Elevations above 20 mIUu/L occur in only 3% of patients with NTIS and therefore suggest underlying hypothyroidism.


Studies suggest levels of T4 < 4 mcg/dL are associated with mortality risk of 50%, which increases to 80% if levels decrease to 2 mcg/dL. Whether NTIS contributes to this high mortality or merely reflects the severity of underlying illness remains debated. Efforts to supplement T4 and T3 in critically ill patients do not improve outcomes and may be detrimental. Currently no evidence supports thyroid hormone replacement in patients with NTIS. Patients diagnosed with NTIS in the ICU should have an assessment of thyroid function after recovery from their critical illnesses to ensure normalization.



Thyrotoxicosis



Etiology


Thyrotoxicosis may result from excessive serum concentrations of T4, T3, or both. Primary hyperthyroidism, the usual underlying diagnosis, causes both increased production and release of thyroid hormones; etiologies include Graves disease (diffuse toxic goiter), and functioning thyroid nodule(s) (toxic adenoma or toxic multinodular goiter). Alternatively, hyperthyroidism may result solely from the excessive release of stored thyroid hormone in conditions such as silent thyroiditis, postpartum thyroiditis, and subacute or granulomatous thyroiditis).


Secondary hyperthyroidism is rare and caused by the excessive production of TSH from a pituitary adenoma. In this condition, the thyroid hormone levels are elevated but TSH is elevated or inappropriately normal.


Other causes of hyperthyroidism include excessive consumption of exogenous thyroid hormone which may be surreptitious. Amiodarone may also cause hyperthyroidism, either by increased thyroid hormone production or a destructive thyroiditis. Additional causes of hyperthyroidism are listed in Table 85.1.



TABLE 85.1


Causes of Hyperthyroidism



































































Common Causes Underlying Etiology Diagnostic Features
Graves disease Thyroid-stimulating immunoglobulin (TSI) binds to and stimulates the thyroid Increased thyroid radioactive iodine uptake with diffuse uptake on scan, positive thyroperoxidase antibodies; raised serum thyroid-stimulating immunoglobulin; diffuse goiter; ophthalmopathy may be present
Toxic adenoma Monoclonal autonomously secreting benign; thyroid tumor Normal to increased thyroid radioactive iodine uptake with all uptake in the nodule on scan; thyroperoxidase antibodies absent
Toxic multinodular goiter Multiple monoclonal autonomously secreting benign thyroid tumors Normal to increased thyroid radioactive iodine uptake with focal areas of increased and reduced uptake on scan; thyroperoxidase antibodies absent
Exogenous thyroid hormone Excess exogenous thyroid hormone Low to undetectable thyroid radioactive iodine uptake; low serum thyroglobulin values
Painless postpartum lymphocytic thyroiditis Autoimmune lymphocytic infiltration of thyroid with release of stored thyroid hormone Low to undetectable thyroid radioactive iodine uptake; thyroperoxidase antibodies present; occurs within 6 months after pregnancy
Painless sporadic thyroiditis Autoimmune lymphocytic infiltration of thyroid with release of stored thyroid hormone Low to undetectable thyroid radioactive iodine uptake; thyroperoxidase antibodies present
Subacute thyroiditis Thyroid inflammation with release of stored thyroid hormone; possibly viral Low to undetectable thyroid radioactive iodine uptake; low titer or absent thyroid peroxidase antibody (TPO Ab)
Iodine-induced hyperthyroidism Excess iodine Low to undetectable thyroid radioactive iodine uptake
Drug-induced thyrotoxicosis Lithium, interferon alpha; induction of thyroid autoimmunity (Graves disease) or inflammatory thyroiditis Thyroid radioactive iodine uptake elevated in Graves disease or low to undetectable in thyroiditis
Amiodarone-induced thyrotoxicosis Iodine-induced hyperthyroidism (type I) or inflammatory thyroiditis (type II) Low to undetectable thyroid radioactive iodine uptake
Thyroid-stimulating hormone (TSH) secreting pituitary adenoma Pituitary adenoma Raised serum thyroid-stimulating hormone and alpha-subunit with raised peripheral serum thyroid hormones
Gestational thyrotoxicosis Stimulation of thyroid gland thyroid-stimulating hormone receptors by human chorionic gonadotropin Thyroid radioactive iodine uptake contraindicated in pregnancy; first trimester, often in setting of hyperemesis or multiple gestation
Molar pregnancy Stimulation of thyroid gland thyroid-stimulating hormone receptors by human chorionic gonadotropin Molar pregnancy
Struma ovarii Ovarian teratoma with differentiation primarily into thyroid cells Low to undetectable thyroid radioactive iodine uptake (raised uptake of radioactive iodine in pelvis)
Widely metastatic functional follicular thyroid carcinoma Thyroid hormone production by large tumor masses Differentiated thyroid carcinoma with bulky metastases; tumor radioactive iodine uptake visible on whole-body scan

Adapted from Pearce EN: Diagnosis and management of thyrotoxicosis. Br Med J 332:1369-1373, 2006.




Diagnosis


Thyrotoxic patients have a decreased TSH (often undetectable) and increases in serum T4 and/or T3. Approximately 1% of patients will have isolated T3 thyrotoxicosis. A 24-hour radioactive iodine (RAI) thyroid uptake/scan or a pertechnetate scan will differentiate hyperthyroidism caused by increased hormone production from increased hormone release or exogenous intake. In the former, uptake will be elevated or normal, whereas in the latter, uptake will be low. RAI uptake may be falsely low in patients who have recently received iodinated contrast or amiodarone. Alternatively, pertechnetate scanning provides qualitative results in a few hours and an intense uptake of pertechnetate is indicative of increased thyroid hormone production. Either method must be interpreted with concurrent thyroid function tests.

< div class='tao-gold-member'>

Related posts:

Default ThumbnailIleus Default ThumbnailHematologic Default ThumbnailRespiratory Default ThumbnailSurgical-Specialized Default ThumbnailPractice Liberation and Weaning from Mechanical Ventilation and Extubation
Tags:
Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Thyroid and Adrenal Disorders in the Intensive Care Unit

Full access? Get Clinical Tree
Get Clinical Tree app for offline access