Thyroid storm reflects an exacerbation of a thyrotoxic state; it is seen most often in Graves’ disease, but it occurs less commonly in patients with toxic adenoma or toxic multinodular goiter. Clinical manifestations and management of thyroid storm are discussed elsewhere in this text. Wound Hemorrhage Wound hemorrhage with hematoma is an uncommon complication reported in 0.3% to 1.0% of patients in most large series. However, it is a well-recognized and potentially lethal complication (52). A small hematoma deep to the strap muscles can compress the trachea and cause respiratory distress. A small suction drain placed in the wound is not usually adequate for decompression, especially if bleeding occurs from an arterial vessel. Swelling of the neck and bulging of the wound can be quickly followed by respiratory impairment.

Wound hemorrhage is an emergency situation, especially if any respiratory compromise is present. Treatment consists of immediately opening the wound and evacuating the clot, even at the bedside. Pressure should be applied with a sterile sponge and the patient returned to the operating room. Later, the bleeding vessel can be ligated in a careful and more leisurely manner under optimal sterile conditions with good lighting in the operating room. The urgency of treating this condition as soon as it is recognized cannot be overemphasized if respiratory compromise is present,

Injuries to the recurrent laryngeal nerve occur in 1% to 2% of thyroid operations when performed by experienced neck surgeons, and at a higher prevalence when thyroidectomy is done by a less experienced surgeon. They occur more commonly when thyroidectomy is done for malignant disease. Sometimes the nerve is purposely sacrificed if it runs into an aggressive thyroid cancer. Nerve injuries can be unilateral or bilateral and temporary or permanent, and they can be deliberate or accidental. Loss of function can be caused by transaction, ligation, clamping, traction, or handling of the nerve. Tumor invasion can also involve the nerve. Occasionally, vocal cord impairment occurs as a result of pressure from the balloon of an endotracheal tube as the recurrent nerve enters the larynx. In unilateral recurrent nerve injuries, the voice becomes husky because the vocal cords do not approximate one another. Shortness of breath and aspiration of liquids sometimes occur. Usually, vocal cord function returns within several months; it certainly returns within 9 to 12 months if it is to return at all. If no function returns by that time, the voice can be improved by operative means. The choice is insertion of a piece of Silastic to move the paralyzed cord to the midline; this procedure is called a laryngoplasty.

Bilateral recurrent laryngeal nerve damage is much more serious, because both vocal cords may assume a medial or paramedian position and cause airway obstruction and difficulty with respiratory toilet. Most often, tracheostomy is required. In the authors’ experience, permanent injuries to the recurrent laryngeal nerve are best avoided by identifying and carefully tracing the path of the recurrent nerve. Accidental transaction occurs most often at the level of the upper two tracheal rings, where the nerve closely approximates the thyroid lobe in the area of Berry’s ligament. If recognized, many believe that the transected nerve should be reapproximated by microsurgical techniques, although this is controversial. A number of procedures to later reinnervate the laryngeal muscles have been attempted with only limited success (62).

Injury to the external branch of the superior laryngeal nerve may occur when the upper pole vessels are divided (Fig. 6) if the nerve is not visualized (9). This injury results in impairment of function of the ipsilateral cricothyroid muscle, a fine tuner of the vocal cord. This injury causes an inability to forcefully project one’s voice or to sing high notes because of loss of function of the cricothyroid muscle. Often, this disability improves during the first few months after surgery.

In recent years many surgeons have sought to try to further diminish the low incidence of recurrent laryngeal nerve (RLN) injury by use of nerve monitoring devices during surgery. Although several devices have been utilized, all have in common some means of detecting vocal cord movement when the recurrent laryngeal nerve is stimulated. Many small series have been reported in the literature assessing the potential benefits of monitoring to decrease the incidence of nerve injury (63-65). Given the low incidence of RLN injury, it is not surprising that no study has shown a statistically significant decrease in RLN injury when using a nerve monitor. The largest series in the literature by Dralle reported on a multi-institutional German study of 29,998 nerves at risk in thyroidectomy (66). Even with this large of a study, no statistically significant decrease in rates of RLN injury could be showed with nerve monitoring.

Among the problems of nerve monitoring technology are that the devices can malfunction so that the surgeon cannot depend on the device to always identify the nerve (67). Proponents of nerve monitoring suggest that the technology might be helpful even if a statistically significant decrease in the rate of RLN cannot be shown. Although some authors have suggested that RLN monitors may be most helpful in difficult reoperative cases when significant scar tissue is encountered, this has not been shown to be the case. At this time, nerve monitoring technology in thyroid surgery should not take the place of meticulous dissection. Surgeons may choose to use the technology, but the data do not support the suggestion that nerve monitors allow thyroid surgery to be performed in a safer fashion than that by a good surgeon utilizing careful technique.

Postoperative hypoparathyroidism can be temporary or permanent. The incidence of permanent hypoparathyroidism has been reported to be as high as 20% when total thyroidectomy and radical neck dissection are performed, and as low as 0.9% for subtotal thyroidectomy. Other excellent neck surgeons have reported a lower incidence of permanent hypoparathyroidism (68). Postoperative hypoparathyroidism is rarely the result of inadvertent removal of all of the parathyroid glands but is more commonly caused by disruption of their delicate blood supply. Devascularization can be minimized during thyroid lobectomy by dissecting close to the thyroid capsule, by carefully ligating the branches of the inferior thyroid artery on the thyroid capsule distal to their supply of the parathyroid glands (rather than ligating the inferior thyroid artery as a single trunk) (Fig. 16F), and by treating the parathyroids with great care. If a parathyroid gland is recognized to be nonviable during surgery, it can be autotransplanted after identification by frozen section. The gland is minced into 1 mm to 2 mm cubes and placed into pockets in the sternocleidomastoid muscle.

Postoperative hypoparathyroidism results in hypocalcemia, hyperphosphatemia, and a low parathyroid hormone (PTH) level. It is manifested by circumoral numbness, tingling of the fingers and toes, and intense anxiety occurring soon after surgery. Chvostek’s sign appears early, and carpopedal spasm can occur. Symptoms develop in most patients when the serum calcium level is less than 7.5 to 8 mg/dL. The parathyroid hormone is low or absent in hypoparathyroidism.

We measure the serum calcium level every 12 hours while the patient is in the hospital. Most patients are able to leave the hospital on the morning after surgery if they are asymptomatic and their serum calcium level is 7.8 mg/dL or above. Oral calcium pills are used liberally. Patients with symptomatic hypocalcemia are treated in the hospital with 1 g (10 mL) of 10% calcium gluconate infused intravenously over several minutes, and then 5 g of this calcium solution placed in each 500 mL intravenous bottle to run continuously, starting with about 30 mL/hour. Oral calcium, usually as calcium carbonate (1250 mg to 2500 mg four times per day), should be started. With this treatment regimen most patients become asymptomatic and their calcium and PTH levels become normal. The intravenous therapy is tapered and stopped as soon as possible, and the patient is sent home and told to take oral calcium pills. This condition is referred to as transient hypocalcemia or transient hypoparathyroidism.

Management of more persistent severe hypocalcemia requires the addition of a vitamin D preparation to facilitate the absorption of oral calcium. We prefer the use of 1,25-dihydroxyvitamin D (Calcitriol) because it is the active metabolite of vitamin D and has a more rapid action. Calcitriol (0.5 mcg to 1.0 mcg) with oral calcium carbonate therapy is given four times daily for the first several days, then this priming dose of vitamin D is reduced. The usual maintenance dose for most patients with permanent hypoparathyroidism is Calcitriol 0.25 to 0.5 μg daily, along with calcium carbonate, 500 mg Ca2+ several times daily, although some patients require larger doses. Serum calcium levels must be monitored carefully after discharge, and the dosage of the medications is adjusted promptly to prevent hypercalcemia as well as hypocalcemia. Finally, the serum PTH level should be analyzed periodically to determine whether permanent hypoparathyroidism is truly present, because the authors and others have seen cases of postoperative tetany, perhaps caused by “bone hunger,” that later resolved completely. In such cases, circulating PTH is normal and all therapy could be stopped. Remember that in bone hunger, both the serum calcium and phosphorus values are low, whereas in hypoparathyroidism, the serum calcium value is low but the phosphorus level is elevated.