Thyroid disease





A 30-year-old woman presented for thyroidectomy. She had a history of anxiety, palpitations, heat intolerance, and weight loss. Her blood pressure was 150/90 mm Hg, and her pulse rate was 100 beats per minute. Her medications at home included methimazole and metoprolol. On physical examination, there was a fullness of her neck.





How are thyroid hormones produced?


Thyroid hormones affect metabolic function by facilitating biochemical reactions that increase heat production and oxygen consumption. They also contribute to upregulation of β-adrenergic receptors and in that way enhance catecholamine effects. Their synthesis originates in the hypothalamus, which produces thyrotropin-releasing hormone that stimulates the anterior pituitary to secrete thyroid-stimulating hormone (TSH). TSH allows iodine absorption into the thyroid, where triiodothyronine (T 3 ) and thyroxine (T 4 ) are produced. T 4 is altered by other tissues to make T 3 . T 3 is substantially more potent than T 4 . Both T 3 and T 4 are highly protein bound. Only the unbound portion is physiologically active. TSH levels are good screening tests for thyroid function. TSH is low in thyrotoxicosis and high in hypothyroidism.





Describe the classic presentation of thyrotoxicosis.


Thyrotoxicosis is a state of increased metabolic rate. Classically, patients present with nervousness, weight loss, and heat intolerance. The history also includes insomnia, fatigue, tremors, copious perspiration, and muscle weakness. Typical cardiovascular signs include sinus tachycardia and hypertension. High-output cardiac failure and ischemia may also be seen. Ophthalmic problems are associated with Graves disease–related hyperthyroidism ( Box 27-1 ).



BOX 27-1

Problems Associated with Thyroid Disease





  • Hyperthyroidism




    • Nervousness/anxiety



    • Weight loss



    • Tremor



    • Atrial fibrillation



    • Congestive heart failure



    • Myocardial ischemia



    • Thrombocytopenia




  • Medullary cancer




    • Multiple endocrine neoplasms—pheochromocytoma








How does thyroid storm differ from thyrotoxicosis?


The transition between thyrotoxicosis and thyroid storm is usually blurred. Thyroid storm is a state of decompensation from thyrotoxicosis. It can be precipitated by physiologic or pharmacologic stresses. Examples include surgery, trauma, large amounts of iodine, cessation of antithyroid medications, diabetic ketoacidosis, myocardial infarction, and cerebrovascular accident. It can occur intraoperatively or up to 18 hours postoperatively. Signs and symptoms include fever (>38.5° C), severe tachycardia, atrial fibrillation, congestive heart failure, hypertension, agitation, altered mentation, nausea, vomiting, diarrhea, and liver failure. Fluid losses from perspiration, nausea, vomiting, and diarrhea predispose to hypovolemic hypotension. Heart failure can also produce hypotension. Without treatment, mortality rates can reach 90%. The accompanying fever could result in hypovolemia, tachycardia, congestive heart failure, shock, and coma. The differential diagnosis of thyroid storm includes malignant hyperthermia, neuroleptic malignant syndrome, sepsis, hemorrhage, pheochromocytoma, and transfusion reaction.





Describe the treatment of thyroid storm.


Treatment of thyroid storm revolves around three principles: (1) Block thyroid hormone production and secretion. (2) Stop the conversion of T 4 to T 3 . (3) Antagonize the β-adrenergic effects of thyroid hormones. Propylthiouracil (PTU) and methimazole are the classic antithyroid drugs for hyperthyroidism. They inhibit thyroid hormone synthesis but require several weeks to reduce thyroid hormone levels toward normal. PTU offers the added benefit of reducing conversion of T 4 to T 3 . After thyroid hormone production is reduced with antithyroid medications for several hours, thyroid hormone secretion can be addressed. High-dose iodine in the form of Lugol solution, saturated solution of potassium iodide, or iopanoic acid reduces thyroid hormone release from the gland. Unless thyroid hormone synthesis has already been blocked, high-dose iodine therapy enhances hormone production and exacerbates thyroid storm. For patients with iodine allergies, lithium carbonate can be substituted for high-dose iodine preparations. Conversion of T 4 to T 3 is reduced with glucocorticoids. PTU and iopanoic acid also share this property.


β-Adrenergic blockade is the primary method of controlling catecholamine-like symptoms. When immediate cardiovascular control is required, esmolol is preferred. If β blockade is contraindicated, calcium-channel blockers, such as diltiazem, might be helpful. Table 27-1 outlines the treatment of thyroid storm.



TABLE 27-1

Therapy for Thyroid Storm





























































Block thyroid hormone production
PTU 200-400 mg PO every 6-8 hours
Methimazole 20-25 mg PO every 6 hours
Block thyroid hormone release
Lugol solution 4-8 drops PO every 6-8 hours
SSKI 5 drops PO every 6 hours
Iopanoic acid 1 g PO every 8 hours for 1 day, then 500 mg PO every 12 hours
Lithium carbonate 300 mg PO every 8 hours
Block T 4 to T 3 conversion
Hydrocortisone 100 mg IV every 8 hours
Block adrenergic-like effects
Propranolol 1-2 mg IV every 10-15 min or
20-120 mg PO every 4-6 hours
Esmolol 50-100 μg/kg/min
Diltiazem 5-10 mg/hour IV or
60-120 mg PO every 6-8 hours
Supportive therapy
Fluids
Cooling
Meperidine to inhibit shivering 12.5 mg IV every 10 min × 2
Acetaminophen 650 mg PO every 4-6 hours

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Jul 14, 2019 | Posted by in ANESTHESIA | Comments Off on Thyroid disease
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