Endocrine surgery is a subspecialty of general surgery that focuses predominantly on diseases of the thyroid, parathyroid, and adrenal glands. Understanding the pathophysiology of endocrine disease and its surgical management is important for providing optimal postoperative care.

I. THYROID AND PARATHYROID SURGERY

A. Thyroidectomy

1. The thyroid is a bilobed gland located in the anterior central neck, deep to the platysma, sternohyoid, and sternothyroid muscles. The two lobes are connected by a median isthmus that is usually anterior to the second to fourth tracheal rings. The primary functions of the thyroid are to produce thyroid hormone, an important metabolic hormone, and calcitonin, a regulatory hormone for calcium and phosphorus metabolism.

2. Indications for thyroid surgery include both benign (Graves’ disease, multinodular goiter) and malignant (papillary thyroid cancer, follicular thyroid cancer, medullary thyroid cancer, anaplastic thyroid cancer, and metastatic cancers) disease.

3. There are two main types of thyroid surgery: a hemithyroidectomy and isthmusectomy, where a unilateral lobe and the isthmus are resected, and a near or total thyroidectomy, where almost the entire gland is removed.

4. Depending on the indication, the thyroid resection may also be accompanied by lymph node dissection. This is most commonly performed in the central neck (Level VI), but modified radical neck dissections in the lateral compartments (Levels II, III, and IV) are done for lymph nodes that are clinically or radiographically positive for metastatic cancer.

5. Nearly all thyroid surgery and lymph node dissections can be performed through a single transverse cervical incision, but a separate lateral incision may be necessary for very high (Level II) lateral neck dissections.

B. Parathyroidectomy

1. The parathyroid glands are small glands that are typically closely associated with the posterior aspect or surgical capsule of the thyroid gland. There are usually two parathyroid glands on each side of the thyroid gland (superior and inferior), although ectopic (unexpected anatomical location) or supernumerary (more than four) glands can occur in 6% to 16% and 2.5% to 13% of patients, respectively. The parathyroid glands secrete parathyroid hormone (PTH), which regulates serum levels of calcium through effects on the bone, kidney, and intestines.

2. Indications for parathyroid surgery are usually primary hyperparathyroidism (HPT; autonomous oversecretion of PTH) from a parathyroid
adenoma (80% to 85% of patients with primary HPT), parathyroid hyperplasia (10% to 15% of patients), or rarely parathyroid carcinoma (<1% of patients with primary HPT). Operations for secondary HPT (physiologic increase in PTH secretion secondary to hypocalcemia) typically due to renal failure occur much less frequently since the development of calcimimetic therapies that increase the sensitivity of calcium-sensing receptors of the parathyroid glands.

3. Approaches to parathyroid surgery include standard bilateral exploration where all four glands are visualized or minimally invasive single-gland exploration that requires positive preoperative localization.

4. Parathyroid surgery is performed through either a single central or lateral transverse cervical incision.

C. Standard Postoperative Care

1. Recovery after thyroid and parathyroid surgery is usually rapid, and patients are typically provided a regular soft diet by the morning after surgery. Patients typically complain of throat pain with swallowing, but incisional pain is usually minimal because of disruption of the small cervical sensory nerves around the incision, and nausea can be well controlled with the use of antiemetics. Patients are monitored carefully for signs of recurrent laryngeal nerve (RLN) damage, hematoma, and hypocalcemia. Select patients may be suitable for outpatient surgery where they follow clear postoperative care pathways and are discharged home after a short period of monitoring in the postanesthesia care unit (typically around 4 hours of monitoring).

2. Hypothyroidism is expected following total thyroidectomy and can also occur in 15% to 50% of patients after hemithyroidectomy. Patients are usually given thyroid hormone replacement with levothyroxine at a dose of 1.4 to 1.8 µg/kg/day, with a slightly higher dose used in men and in patients with known malignancy to suppress thyroid-stimulating hormone.

II. COMPLICATIONS FOLLOWING THYROID AND PARATHYROID SURGERY

A. RLN Injury

1. RLN is a branch of the vagus nerve that innervates all intrinsic muscles of the larynx, with the exception of the cricothyroid muscle. As the RLN comes off the vagus, the right RLN travels down and courses behind the right subclavian artery and the left RLN courses behind the aortic arch before ascending in bilateral tracheoesophageal grooves and entering the larynx just under the inferior constrictor muscles.

2. Injury to the RLN may occur following thyroid surgery and, to a lesser extent, parathyroid surgery. Rates vary in the literature depending on the definition but typically average around 1% in large series.

3. The mechanism of injury to the RLN can vary from a transient stretch injury to inadvertent or deliberate transection of the nerve. Risk factors for RLN injury include invasive malignancy, nonidentification of the RLN, anterior displacement, excessive manipulation or dissection around the nerve resulting in traction or ischemia, and a reoperative field.

4. Signs and symptoms

a. Symptoms of unilateral RLN injury vary from being completely asymptomatic to dysphagia and voice compromise.

b. The most common symptom of unilateral RLN injury is dysphonia, or hoarseness. Other symptoms of unilateral RLN injury include
an increased risk of aspiration with thin liquids, dysphagia, and resulting dyspnea.

c. Bilateral RLN injury is a surgical emergency because it has the greatest impact on respiration and can present with stridor or respiratory distress because both vocal cords may be nearly closed.

5. Diagnosis

a. The gold standard for diagnosis of RLN injury is by fiberoptic laryngoscopy. Depending on practice patterns, this can be performed routinely or selectively following thyroid surgery.

b. RLN injury results in the cord lying in the paramedian position (Fig. 8.1). The most common explanation is the Wagner and Grossman theory, which states that injury to the RLN will lead to overrepresentation of the innervated cricothyroid muscle, which acts to adduct the cord.

c. The extent of vocal symptoms is usually related to the distance of the paralyzed cord from the midline.

d. Other diagnostic tools such as laryngeal electromyography and video stroboscopy are typically utilized in the later outpatient setting.

6. Management

a. Unilateral injury

1. Early management of a patient with identified RLN injury should be to maintain aspiration precautions. Postural strategies such as chin tuck when drinking thin liquids can help reduce the risk of aspiration. Patients should also be instructed to use more force when speaking.

2. Transient injury should resolve by 3 months postoperatively. If the patient’s voice or ability to swallow liquids has not fully recovered by then, the injury may be permanent, which can have a significant impact on the patient’s quality of life and ability to work. Therefore, patients with suspected permanent nerve injury should be referred to a laryngeal surgeon for laryngoscopy and likely vocal cord medialization (thyroplasty or vocal cord injection).

b. Bilateral injury

1. If the patient develops acute stridor and respiratory distress in the immediate postoperative period, bilateral RLN injury should be suspected and immediate fiberoptic laryngoscopy should be done to confirm the diagnosis.

2. Emergent reintubation or a surgical airway (cricothyrotomy or preferably tracheostomy) may be required.

7. Differentials

a. Alternative causes of postoperative hoarseness include superior laryngeal nerve injury, direct cricothyroid muscle injury, or intubation trauma leading to vocal fold injury or arytenoid dislocation.

B. Hypoparathyroidism

1. Hypoparathyroidism is the most common complication following thyroid and parathyroid surgery. The definition of postoperative hypoparathyroidism varies in the literature, but usually always involves the identification of low serum calcium levels after surgery. It is the most common cause of prolonged hospitalization following neck surgery and is the leading cause of readmission.

2. Hypoparathyroidism can be temporary or permanent, with the latter usually defined as no recovery of the parathyroid glands 6 months after surgery. Quoted rates of temporary hypoparathyroidism are 15% to 30%, with rates of permanent hypoparathyroidism being 1% to 2%.

3. The mechanism of hypoparathyroidism is due to either direct or indirect injury to the parathyroid glands. This can be due to excessive manipulation, inadvertent removal, or devascularization of one or more glands. Strategies such as parathyroid reimplantation into the sternocleidomastoid muscle are utilized intraoperatively to help reduce the incidence of permanent hypoparathyroidism. Injury to the parathyroids leads to an inadequate release of PTH to maintain calcium homeostasis with resulting hypocalcemia and its subsequent clinical manifestations.

4. Factors that increase the risk of postoperative hypoparathyroidism include more extensive surgery, central neck dissection (usually results in removal/ischemia of both inferior parathyroid glands), neck reoperation, and Graves’ disease.

5. Serum intact PTH levels may be drawn at the end of thyroid or parathyroid operations, with levels <15 pg/mL suggestive of increased risk of developing postoperative hypoparathyroidism.

6. Signs and symptoms

a. Acute hypocalcemia leads to neuromuscular irritability. The earliest symptoms of mild hypocalcemia include perioral or digital paresthesia and numbness as well as muscle cramping. It is important to differentiate digital paresthesia versus postanesthesia muscle cramping because of patient positioning or residual neuromuscular blockade. Unlike postanesthesia paresthesia, digital paresthesia secondary to hypocalcemia typically occurs in the fingers or toes bilaterally.

b. Historical signs of hypocalcemia included Chvostek’s sign (ipsilateral facial twitching elicited by tapping over the facial nerve, which is also present in up to 20% of normocalcemic individuals) and Trousseau’s sign (carpal spasm elicited by inflating a blood pressure cuff around the arm above systolic pressure for 3 minutes). These signs are not reliable and should not be used for diagnosis.