Файл: NMS Surgery_booksmedicos.org.pdf

the lower pole of the thyroid, near the point of attachment of the thyrothymic ligament. In the other 50%, the inferior parathyroid glands are intimately associated with the thymus, either in the neck or in the superior mediastinum. (Reprinted with permission from

Edis AJ, Grant CS, Egdahl RH. Comprehensive Manuals of Surgical Specialties— Manual of Endocrine Surgery, 2nd ed. New York: Springer-Verlag; 1984:2.

)

Injury to the parathyroids during thyroid surgery usually occurs during total lobectomy or total thyroidectomy and results from disruption of the blood supply to the parathyroids. If this occurs, the consequence is either temporary or permanent hypoparathyroidism, unless the parathyroids can be successfully reimplanted (see III A ]).

C Abnormalities of thyroid descent

(see Chapter 18, III B )

Route of descent

Normal descent. The thyroid migrates downward from its point of origin at the foramen cecum at the base of the tongue. It descends to assume its normal position on either side of the trachea at the level of the thyroid and cricoid cartilages.

Abnormal descent of the thyroid may result in ectopic placement of thyroid tissue in the tongue, in the midline of the neck, or in the mediastinum.

Glottic (lingual) thyroid

Location. Glottic (lingual) thyroid occurs when the thyroid does not descend into the neck and remains at the base of the tongue. It may be the only functioning thyroid tissue in the individual.

Symptoms of obstruction or difficulty with speech are usually related to goiter formation in the lingual mass.

Diagnosis is by inspection or indirect laryngoscopy. A radioiodine thyroid scan should be performed to identify the mass as thyroid tissue.

Management

Suppression of thyroid -stimulating hormone (TSH) with thyroxine should be the first step in management because glottic thyroid tissue is usually hypofunctioning.

Surgical removal should be considered when a patient has obstructive symptoms, especially if hormonal therapy is ineffective.

P.314

Ectopic midline thyroid tissue

Location. A diagnosis of ectopic midline thyroid tissue should be considered when a midline mass is encountered below the hyoid bone.

Diagnosis. If there is no thyroid gland in the neck, the ectopic thyroid should be confirmed by radioiodine scan because removal of the ectopic tissue will leave the patient without functioning thyroid tissue.

Mediastinal thyroid (substernal goiter)

Location. Most aberrant thyroids in the mediastinum are located in the anterosuperior mediastinum. They may represent substernal extensions from an enlarged thyroid or normal thyroid tissue, resulting from aberrant embryologic descent of the thyroid into the mediastinum.

Normal functioning thyroid tissue will take up radioiodine and, thus, can be confirmed by a radioiodine scan of the mediastinum.

Substernal extensions of the thyroid may be caused by adenomatous hyperplasia and, as a result, may not take up radioiodine.

Substernal goiters usually occur in older age -groups.

They usually result in tracheoesophageal compression.

They do not respond to nonoperative attempts to relieve pressure symptoms by suppressing TSH with thyroxine.

Management. Operation is usually advised to relieve pressure symptoms or to diagnose an otherwise undiagnosed mediastinal mass. Substernal goiters can usually be removed through a cervical incision without the need for sternotomy because their blood supply is derived from the neck.

Thyroglossal duct cysts and sinuses

Location. Thyroglossal duct cysts usually present as midline masses located between the hyoid bone and the thyroid isthmus. They are always connected to the base of the tongue, traversing the center of the hyoid bone.

Signs or symptoms

They may be solid or cystic and may communicate with the skin, forming a sinus.

These lesions may present at any age, but most are found in children.

A history of redness and inflammation from infection in the cyst is present in one third of the cases.

Management. Treatment involves excising the cyst or sinus along with a portion of the hyoid bone and the proximal duct extending to the base of the tongue (Sistrunk procedure).

D Thyroid dysfunction requiring surgery

Thyroid hormones

Tri -iodothyronine and thyroxine. The follicular cells of the thyroid are derived primarily from the floor of the foregut. These cells produce the thyroid hormones triiodothyronine (T 3 ) and thyroxine (T 4 ; tetraiodothyronine).

Hormone synthesis and release

Iodine and tyrosine combine to form T 3 and T 4 .

Both of these hormones bind with thyroglobulin and are stored in the gland until released into the bloodstream.

Release is under the control of TSH from the pituitary and thyrotropin-releasing hormone (TRH) from the hypothalamus.

A feedback mechanism regulating T 3 and T 4 release is related to the levels of the circulating hormones.

Hormonal action

The thyroid hormones activate energy-producing respiratory processes, resulting in an increase in the metabolic rate and an increase in oxygen consumption.

Increased glycogenolysis results in an increase in blood sugar levels.

The thyroid hormones also enhance metabolic, circulatory, and somatic neuromuscular actions of catecholamines.

The result is an increase in the pulse rate, cardiac output, and blood flow.

P.315

Nervousness, irritability, muscular tremors, and muscle wasting can also occur.

These effects can be blocked by the use of β-blockers, such as propranolol.

Thyrocalcitonin. The parafollicular , or C, cells are derived from the ultimobranchial body. These cells are part of the amine precursor uptake and decarboxylation (APUD) cell system (see Chapter 17, II A ) and produce thyrocalcitonin.

Graves' disease (diffuse toxic non-nodular goiter)

Pathogenesis. Graves' disease is thought to be an autoimmune disease resulting from a defect in cell -mediated immunity.

A substance known as long -acting thyroid stimulator (LATS) is produced, which increases the size of the thyroid and its production of thyroid hormone.

A clinical syndrome of hypermetabolism with associated abnormal eye signs, and an unusual form of pretibial edema results.

Clinical presentation

Hypermetabolic state

Symptoms include palpitations, sweating, intolerance to heat, irritability, insomnia, nervousness, weight loss, and fatigue.

Signs include an audible bruit over the gland, tremors of the hands and tongue, cardiac arrhythmias, and a widening of the palpebral fissure of the eye.

Abnormal deposition of mucopolysaccharide and round cell infiltration in the tissues is characterized by exophthalmos, edema of the eyelids, chemosis, and pretibial edema.

Diagnosis

Graves' disease is confirmed by the presence of an increased total serum T 4 , an increase in the T 3 resin uptake (T 3 RU), and an increase in T 3 by radioimmunoassay.

An increase of the free thyroxine index (the T 3 RU value times the total serum T 4 ) and an

increase in radioiodine uptake distinguish this form of thyrotoxicosis from thyrotoxicosis without hyperthyroidism (caused by thyroiditis, factitious thyrotoxicosis, or struma ovarii).

A thyroid scan shows an enlarged thyroid with uniform uptake throughout.

The serum cholesterol level is decreased, and the blood sugar and alkaline phosphatase are increased.

Medical treatment. The preferred initial treatment is medical because the disease has a tendency to remit spontaneously after 1–2 years in adults or after 3–6 months in children.

Radioiodine (131 I) administered orally is simple, safe, and inexpensive.

It obviates the need for surgery and apparently does not increase the risk of carcinoma.

It has, however, several disadvantages.

It may produce hypothyroidism in the fetus if administered during pregnancy.

Because of its slow onset of effectiveness, concomitant use of antithyroid drugs may be necessary if the patient is severely symptomatic.

Antithyroid drugs are effective in about 50% of patients, especially those with symptoms of short duration and with a small gland. They are rapidly effective and can reverse symptoms in a short time.

These drugs act by altering various stages of iodine metabolism.

Propylthiouracil and methimazole act through competitive inhibition of peroxidase, blocking the oxidation of iodide to elemental iodine. Propylthiouracil also interferes with the peripheral conversion of T 4 to T 3 .

Iodine in high concentrations blocks the release of thyroid hormones by inhibiting proteolysis. However, glands treated with iodine suppression escape this therapeutic effect after 10–14 days of therapy.

Propranolol, a β-adrenergic blocker, reduces the secondary effects of hypermetabolism, such as tachycardia, without affecting the production of T 3 or T 4 .

Their main disadvantage is that the incidence of recurrence is high if the drugs are stopped, and prolonged therapy is required.

They must be discontinued if drug toxicity occurs, manifested by fever, rash, arthralgia, a lupuslike syndrome, or agranulocytosis.

Surgical treatment. The preferred operation for Graves' disease is bilateral subtotal thyroidectomy.

P.316

Indications. Thyroidectomy is indicated for Graves' disease under the following circumstances:

(1) When medical therapy has failed because remission has not occurred after treatment for 1 year in adults or for 3 months in children, (2) because the patient refuses to take the medication, or (3) because the patient develops an adverse reaction to the antithyroid drugs

When radioiodine therapy is not advisable because the patient is pregnant or the patient refuses radioiodine therapy

Objectives of surgery are to remove enough thyroid tissue to correct the hyperthyroidism.

In the past, many endocrinologists and surgeons recommended bilateral subtotal thyroid lobectomy. Approximately 4–5 gm of tissue was left in situ in the hopes of rendering the patient euthyroid while minimizing the risk of hypoparathyroidism and nerve injury.

However, as many as 40% of patients developed hypothyroidism postoperatively and required thyroid hormone supplementation. Another 40% of patients remained hyperthyroid to some extent and thus sometimes required further medical treatment of their disease.

Currently, most experts recommend performing either a near total thyroidectomy (total lobectomy on one side and a subtotal lobectomy on the other) or total thyroidectomy. Patients require supplementation thyroid hormone postoperatively, but the risk of persistent hyperthyroidism is greatly reduced.

Preoperative preparation. To minimize the risk of thyroid storm (see I D 2 e [4] [a]), the patient should be euthyroid before operation.

Antithyroid drugs are usually given until the patient is euthyroid, and then Lugol's solution or saturated potassium iodide is given for 7–10 days before surgery.

This reduces the risk of thyroid storm both during and after surgery. It also reduces the size and vascularity of the thyroid gland, which increases the technical ease of surgery.

However, it takes several weeks or longer to achieve the euthyroid state. Moreover, in a pregnant woman, thyroid drugs can cross the placenta and cause fetal goiter.

Propranolol can be given in conjunction with Lugol's solution if patients have had adverse reactions to antithyroid drugs.

This is effective in rapidly restoring the euthyroid state and in reducing thyroid size and vascularity. Moreover, it is not known to cause any fetal abnormalities if the patient is pregnant.

Propranolol must be given for 4–5 days postoperatively to prevent thyroid storm

because the half -life of circulating thyroid hormone is 5–10 days.

Complications of thyroidectomy (Note: These complications are not unique to the management of Graves' disease. They may occur during thyroidectomy for other thyroid conditions as well.)

Thyroid storm is a severe hypermetabolic state that causes hyperpyrexia and tachyarrhythmias due to uncontrolled hyperthyroidism.

Thyroid storm is rarely found when the patient is adequately prepared preoperatively. It occurs most often when a patient has undiagnosed hyperthyroidism and has surgery for some unrelated emergency.

Treatment is with large doses of antithyroid drugs, iodine, and propranolol.

Hemorrhage is possible due to increased vascularity in a hyperactive thyroid gland.

Postoperative hemorrhage can cause airway obstruction due to tracheal compression and laryngeal edema.

Treatment is by opening the wounds, evacuating the clot, and controlling the bleeding.

Hypoparathyroidism usually develops within the first 24 hours after surgery and results in a subnormal serum calcium concentration.

Symptoms of hypocalcemia include numbness and tingling periorally or in the fingers and toes, nervousness, and anxiety. Increased neuromuscular transmission is evidenced by positive Chvostek's and Trousseau's signs.

P.317

Treatment is with intravenous calcium gluconate, followed by oral calcium and vitamin D therapy after several days if hypocalcemia persists.

Serum calcium levels should be checked daily for at least 3 days after thyroidectomy.

Recurrent laryngeal nerve injury produces vocal cord paralysis.

Unilateral injury is usually manifested by hoarseness. If the nerve is intact, the patient usually recovers a normal voice in 3 weeks to 3 months postoperatively.

If the injury is bilateral, airway obstruction results due to paralysis of the vocal cords in the midline adducted position. This requires emergency intubation or tracheostomy. If the nerves are intact and the injury is temporary, recovery usually occurs in 3–6 months. If the injury is permanent, it will require either a permanent tracheostomy or lateral fixation of the arytenoid cartilages.

Injury to the external branch of the superior layrngeal nerve causes voice fatigue and a loss of timbre and projection.

This nerve is motor to the cricothyroid muscle and can be injured during ligation of the branches of the superior thyroid artery.