Step 4. Adjust the protein intake, if necessary
C. Abnormal Thyroid Function Tests
Table 39.1 shows the expected changes in plasma free T4 and TSH levels in specific conditions.
1. Acute, non-thyroidal illness is associated with low plasma levels of free T3, which is the result of impaired conversion of T4 to T3 in non-thyroidal tissue (6). With increasing severity of illness, both free T3 and free T4 levels are depressed, which is the pattern reported in 30–50% of ICU patients (6,7). As mentioned earlier, plasma TSH levels are normal in a majority of patients with euthyroid sick syndrome.
2. Primary hypothyroidism is characterized by reciprocal changes in free T4 and TSH levels, while in secondary hypothyroidism (from hypothalamic-pituitary dysfunction), both free T4 and TSH levels are depressed.
III. THYROTOXICOSIS
Thyrotoxicosis is almost always the result of primary hyperthyroidism. Notable causes include autoimmune thyroiditis, and chronic therapy with amiodarone (11).
A. Clinical Manifestations
1. The principal manifestations of thyrotoxicosis are agitation, tachycardias (including atrial fibrillation), and fine tremors.
2. Elderly patients with hyperthyroidism can be lethargic rather than agitated; this condition is called apathetic thyrotoxicosis. The combination of lethargy and atrial fibrillation is a frequently cited presentation for apathetic thyrotoxicosis in the elderly.
3. Thyroid storm is an uncommon but severe form of hyperthyroidism that can be precipitated by acute illness or surgery.
a. This condition is characterized by hyperpyrexia (temp. can exceed 104°F), severe agitation or delirium, and tachycardia with high-output heart failure. Advanced cases are associated with obtundation or coma, generalized seizures, and hemodynamic instability.
b. If untreated, the outcome is uniformly fatal (11).
B. Diagnosis
1. The plasma TSH level is the most sensitive and specific diagnostic test for hyperthyroidism (11).
2. TSH levels are <0.01 mU/dL in mild cases of hyperthyroidism, and TSH levels are undetectable in most cases of overt thyrotoxicosis (11).
3. A normal TSH level excludes the diagnosis of hyperthyroidism (11).
C. Management
The acute pharmacologic management of thyrotoxicosis and thyroid storm is summarized in Table 39.2.
1. β-Receptor Antagonists
Treatment with β-receptor antagonists relieves the tachycardia, agitation, and fine tremors in thyrotoxicosis.
a. Propranolol has been the most widely used β-receptor antagonist in hyperthyroidism, but it is a non-selective β-receptor antagonist, which makes it less than ideal for patients with asthma or systolic heart failure.
b. Selective β-receptor antagonists like metoprolol (25–50 mg PO every 4 hours) can be used for thyrotoxicosis, but propranolol remains the drug of choice for thyroid storm (11).
c. The ultra-rapid-acting agent esmolol is an appealing choice for acute rate control in atrial fibrillation associated with hyperthyroidism. (See Table 13.1 for dosing recommendations.)
2. Antithyroid Drugs
Two drugs are used to suppress thyroxine production: methimazole and propylthiouracil (PTU).
Both are given orally.
a. Methimazole is preferred for the treatment of thyrotoxicosis, while PTU is favored for the treatment of thyroid storm (11).
b. Uncommon but serious side effects include cholestatic jaundice for methimazole, and fulminant hepatic necrosis or agranulocytosis for PTU (11).
3. Inorganic Iodine
In severe cases of hyperthyroidism, iodine (which blocks the synthesis and release of T4) can be added to antithyroid drug therapy. The iodine is given orally as a saturated potassium iodide solution (Lugol’s solution). In patients with an iodine allergy, lithium (300 mg orally every 8 hours) can be used as a substitute (12).
4. Special Concerns in Thyroid Storm
a. Aggressive volume resuscitation is often required in thyroid storm because of vomiting, diarrhea, and heightened insensible fluid loss.
b. Thyroid storm can accelerate glucocorticoid metabolism and create a relative adrenal insufficiency; as a result prophylactic hydrocortisone (300 mg IV as a loading dose, followed
by 100 mg IV every 8 hours) is recommended (11).
IV. HYPOTHYROIDISM
Symptomatic hypothyroidism is uncommon, with a prevalence of only 0.3% in the general population (13). Most cases are the result of chronic autoimmune thyroiditis (Hashi-moto’s thyroiditis), while less common causes include radioiodine or surgical treatment of hyperthyroidism, hypothalamic-pituitary dysfunction from tumors and hemorrhagic necrosis (Sheehan’s syndrome), and drugs (lithium, amiodarone).
A. Clinical Manifestations
1. The clinical manifestations of hypothyroidism are often subtle, and include dry skin, fatigue, muscle cramps, and constipation. Advanced cases can be accompanied by hyponatremia and a skeletal muscle myopathy, with elevated muscle enzymes (creatine kinase and aldolase), and an increase in the serum creatinine (from creatine released by skeletal muscle) in the absence of renal dysfunction (14).
2. Contrary to popular perception, obesity is not a consequence of hypothyroidism (13).
3. Hypothyroidism can be associated with pleural and pericardial effusions. The mechanism is an increase in capillary permeability, and the effusions are exudative in quality.
a. Pericardial effusions are the most common cause of an enlarged cardiac silhouette in patients with hypothyroidism (15). These effusions usually accumulate slowly and do not cause cardiac tamponade.
4. Advanced cases of hypothyroidism are accompanied by an edematous appearance known as myxedema. This condition is mistaken for edema, but is caused by the intradermal accumulation of proteins (16). Myxedema is also associated with hypothermia and depressed consciousness; the latter condition is called myxedema coma, although total unresponsiveness is uncommon (16).
B. Diagnosis
The changes in free T4 and TSH levels in hypothyroidism are shown in Table 39.1.
1. Serum T3 levels can be normal in hypothyroidism, but free T4 levels are always reduced (13).
2. Serum TSH levels are increased (often above 10 mU/dL) in primary hypothyroidism, and are depressed in hypothyroidism from hypothalamic-pituitary dysfunction.