Nonneural Complications of Thyroid and Parathyroid Surgery

Introduction

Thyroid and parathyroid operations rank among the most common procedures performed by endocrine surgeons and are generally considered low-risk procedures. Yet, complications occur even when surgery is performed by experienced surgeons. Endocrine neck surgery mandates adherence to certain core principles of surgery, such as absolute hemostasis, distinct identification and preservation of the relevant surrounding tissue, clear illumination and visualization of the operative field, and staying in the correct dissection plane. A firm understanding of embryology and anatomy are obligatory (see Chapter 31 , Principles in Thyroid Surgery). The importance of teamwork in preventing complications cannot be overemphasized. It is also essential that the modern-day endocrine surgeon stay abreast of ancillary technology that may assist the him or her with intraoperative decision making, such as intraoperative nerve monitoring or the use of immunofluorescence to assess the viability of parathyroid glands. These surgical adjuncts do not necessarily prevent complications from occurring but may help improve outcomes by providing the surgeon with actionable information at the point of care. Thyroid and parathyroid complications can be divided into two broad categories: neural complications and everything else. This chapter will address the latter category, nonneural complications.

Hypoparathyroidism

Permanent hypoparathyroidism is a devastating outcome after thyroid and parathyroid surgery and is associated with significant morbidity, reduction in quality of life, and increased risk of death. The true incidence is unknown as the definition of hypoparathyroidism varies around the world, but most authorities would agree that patients with an undetectable intact parathyroid hormone (PTH) level 6 months after surgery who require ongoing calcium supplementation can be classified as having permanent hypoparathyroidism. The signs and symptoms of hypocalcemia can be subtle and include perioral or digital paresthesias, muscle cramping, or anxiety. Furthermore, Chvostek sign, facial twitching when the facial nerve is tapped, and Trousseau sign, ischemia-induced carpal spasm, highlight the state of neuromuscular excitability during hypocalcemia. Importantly, Chvostek sign may be positive in up to 20% of normocalcemic individuals. More overt and alarming signs and symptoms include tetany, altered mental status, seizures, prolonged QT interval, heart failure, bronchospasm, and laryngospasm. Patients who experience tetany often describe the inability to move as nothing short of terrifying, leading to anxiety and in some extreme cases posttraumatic stress syndrome.

Identifying patients who are at increased risk for postoperative hypoparathyroidism before surgery is important because preventive measures can be undertaken to minimize the occurrence and/or clinical severity after surgery. For example, patients with Graves’ disease have a much higher incidence of temporary hypoparathyroidism after total thyroidectomy due to the increased vascularity and firm texture of the thyroid gland. These findings create challenges in preserving the blood supply of the parathyroid glands during parathyroid gland dissection. Moreover, the inherent hypermetabolic state of hyperthyroidism exacerbates postoperative hypoparathyroidism. Parathyroid gland preservation is also challenging in patients with Hashimoto’s thyroiditis due to the “woody” texture of the thyroid gland. Patients with thyroid cancer may require ipsilateral and/or bilateral level 6 and 7 central lymph node dissection, which may compromise parathyroid gland function after surgery due to a shared blood supply. In the era of routine ultrasound imaging before thyroid cancer surgery, the surgeon often has a good sense of who will require a central node dissection before the skin incision is made. For patients with hyperparathyroidism, four groups of patients have an increased risk of postoperative hypoparathyroidism: reoperative cases, familial cases (especially multiple endocrine neoplasia type 1 patients), pediatric patients (due to the high bone turnover and uniform hungry bone syndrome), and patients with secondary/tertiary hyperparathyroidism, all of whom require a multigland excision. The surgeon should consider commencing oral calcium supplementation with Rocaltrol 5 to 7 days before surgery in these patients.

The best treatment for hypoparathyroidism is prevention; a firm understanding of parathyroid blood supply is mandatory to minimize the risk of injury to the parathyroid blood supply. In most patients, the parathyroid glands derive their blood supply from small arteriolar branches from the inferior thyroid artery; collateral blood supply also arises from the superior thyroid artery, the thyroid ima, and other small neighboring vessels. During thyroidectomy, careful attention and the utmost care should be given when dissecting the parathyroid glands, taking every precaution to avoid dissection near the pedicle of the parathyroid gland. Many surgeons commence gland dissection with a top-down approach, gently sweeping the parathyroid glands from the thyroid gland in a posterolateral direction. Suction should be used judiciously, as parathyroid glands can easily be aspirated into the suctioning tubing.

During the course of surgery, parathyroid glands that appear to be devascularized should be reimplanted into neighboring musculature. This is recognized by a gland that becomes dusky or even black throughout the course of surgery. After thyroidectomy, a thorough examination of the surgical specimen should be undertaken to identify any parathyroid glands that have been inadvertently removed. Any glands that are identified should be considered for autoimplantation.

Autoimplantation is accomplished by sectioning the gland with a sharp scalpel into 1-mm pieces and placing it into a pocket of strap musculature or in the sternocleidomastoid muscle. Another technique involves suspending the tissue in saline and injecting it with a syringe and needle into the muscle. These maneuvers have been shown to decrease rates of permanent hypoparathyroidism.

Surgical adjuncts and point-of-care testing can assist the surgeon with intraoperative decision making. Immunofluorescence imaging and parathyroid gland angiography are relatively new techniques that can be used to assess gland viability during thyroid (and parathyroid) surgery. In a randomized control trial assessing the utility of indocyanine green (ICG) fluorescence in predicting parathyroid gland function after thyroid surgery, the authors demonstrated that ICG imaging can reliably predict postoperative gland function and obviate the need for laboratory testing and oral supplementation (see Chapter 31 , Principles in Thyroid Surgery). This technology can be extremely helpful in determining parathyroid remnant viability when performing subtotal parathyroidectomy in patients with known or suspected multigland disease (multiple endocrine neoplasia type 1 [MEN 1] and secondary/tertiary hyperparathyroidism). Intraoperative PTH testing has been shown to identify patients who are at risk for postoperative hypocalcemia. During thyroid surgery, rapid PTH levels less than 15 mg/dL correlate with a higher incidence of postoperative hypoparathyroidism.

Treatment for hypocalcemia is determined by its degree and duration. The goal is to maintain a low-normal calcium level, thereby controlling symptoms while stimulating gland function. The first line of treatment is oral calcium supplementation with or without calcitriol to improve calcium absorption. Oral calcium supplementation is commenced, administering 2 to 10 g daily in divided doses. It is important to note that different calcium preparations provide different levels of elemental calcium ( Table 44.1 ). Severe cases of symptomatic hypocalcemia are treated with intravenous calcium gluconate. Calcium chloride may be used when a central venous catheter is present.

Hypothyroidism

The requirement of levothyroxine after total or partial thyroidectomy is used to restore thyroid function or during suppressive hormone therapy. After partial, less-than-total thyroidectomy, clinically apparent hypothyroidism arises in 11% to 50% of patients. This wide variation in literature may be due to different definitions of hypothyroidism, and differences in follow-up, surgical techniques, and the timing of commencing levothyroxine supplementation among other reasons. As hypothyroidism after total thyroidectomy is a consequence and not a complication, we will discuss only the occurrence of hypothyroidism after partial thyroidectomy. The need of hormone therapy should be an important issue when deciding the best surgery for the patient because in some situations even partial or total thyroidectomy can be acceptable options. Many factors have been described as predictors for the development of postoperative hypothyroidism, such as age, gender, the presence of microsomal antibodies, thyroiditis, multinodular goiter, preoperative thyrotoxicosis, and a thyroid remnant volume measuring < 6 mL.

In a systematic review and meta-analysis of patients who underwent partial thyroidectomy, Verloop et al. showed that 1 in 5 patients will develop some form of hypothyroidism (subclinical or clinical, definite or transient) and 1 in 25 will have clinical hypothyroidism. In this study, as in many others, the most important preoperative predictors of hypothyroidism are thyroid-stimulating hormone (TSH) in the high-normal range and positive anti-thyroperoxidase (TPO) status. Generally, it is important to discuss with the patients preoperatively the possible eventual need for hormone replacement after partial thyroidectomy.

Thyrotoxic Storm

Thyrotoxic storm or crisis is a rare but life-threatening complication of thyroid surgery that is unfamiliar to most surgeons due to its infrequent occurrence. Typically, a precipitating event such as surgery, trauma, infection, myocardial infarction, and other systemic events will transform thyrotoxicosis into thyroid storm. Also, this can be precipitated with excess iodine intake such as with iodinated contrast agents or amiodarone exposure. The physiology surrounding this event is the sudden dissociation of thyroid hormone from its binding proteins. This increase in free thyroid hormone can then lead to the constellation of signs and symptoms as it affects the neurologic, cardiopulmonary, gastrointestinal, and other systems. Common signs and symptoms include fever, tachycardia, cardiac arrhythmias, and, in extreme cases, cardiovascular collapse, hepatic failure, and death.

The best treatment of thyroid storm is prevention. Antithyroid medications are administered before surgery, and beta-blockade is commonly used to control the systemic cardiac effects. In those with poorly controlled thyrotoxicosis requiring urgent thyroidectomy, preoperative iopanoic acid (500 mg bid), dexamethasone (1 mg bid), propylthiouracil or methimazole, and beta-blockade have been shown to decrease the likelihood of thyroid storm. In spite of these preventive measures, a small number of patients will develop thyroid storm. Treatment involves decreasing thyroid hormone synthesis, decreasing its release from the thyroid gland, preventing conversion of Tetraiodothyronine (T4) to Triiodothyronine (T3), managing systemic effects, and supportive care. When recognized intraoperatively, manipulation of the thyroid gland should cease and the operation terminated. First-line pharmaceutical treatment includes beta-blockade and administration of corticosteroids. Propranolol (4 to 10 mg/kg) is administered to reduce sympathetic activity and to block peripheral conversion of T4 to T3. Hydrocortisone (100 to 300 mg) ameliorates the toxicity associated with thyrotoxicosis by reducing fever, iodine uptake, TSH levels, and the inhibition of the peripheral converseion of T4 to T3. Thioamides such as methimazole are also used acutely to block thyroid hormone synthesis, and propylthiouracil inhibits the peripheral conversion of T4 to T3. Sodium iodine (1.0 to 2.5 g) also reduces thyroid hormone synthesis and release. Temperature reduction is achieved with cooling blankets and acetaminophen.

Postoperatively, the thyrotoxic storm patient may have altered mentation including confusion, agitation, and anxiety in addition to fever and tachycardia. Early recognition and prompt intervention are required to prevent cardiovascular and hepatic decompensation. Thyrotoxic storm is rare but potentially lethal, and its successful management relies on early diagnosis and prompt appropriate therapy.

Hemorrhage and Hematoma

Hemorrhage and hematoma formation after thyroid and parathyroid surgery can be life threatening. Fortunately, these complications occur in less than 2% of thyroid and parathyroid surgeries in developed countries, but some studies show an incidence up to 4.39%. Recently, there has been a trend for outpatient surgery in which the risk of postthyroidectomy hemorrhage will increase hospital stay and medical expenses and even threaten life in patients discharged. Predicting those patients who are at risk for these complications is difficult. Liu et al., in a recent meta-analysis, pointed out that older age, male sex, Graves’ disease, antithrombotic agent use, bilateral operation, neck dissection, and previous thyroid surgery are significant risk factors for postthyroidectomy hemorrhage. Suzuki et al. include the risk factors of obesity and blood transfusion on the day of surgery. Multiple studies have shown that postoperative hemorrhage and hematoma rates are equivalent in patients who have and have not undergone wound drainage. Therefore the need for wound drainage should be determined by the surgeon on a case-by-case basis, and a drain should not be relied on to prevent hematoma formation.

Prevention of hematoma begins preoperatively with attention to native and acquired coagulopathies, although routine coagulation studies are not performed. A detailed history of personal or familial bleeding should be ascertained. Additionally, the use of prescription and over-the-counter medicines, including herbal supplements, that may promote hemorrhage, should be ascertained and discontinued before surgery.

Intraoperatively, meticulous hemostasis should be maintained. Any bleeding encountered near the recurrent laryngeal nerve should be treated with judicious use of bipolar electrocautery. Additionally, fibrin sealants, cellulose-based hemostatic agents, or microfibrillar collagen may be useful adjuncts when electrocautery is deemed unsafe, although the efficacy of these hemostatic agents is still controversial in the literature. At present, newer vessel-sealing devices have not been shown to decrease hematoma rates, although more recent studies have shown a decrease in surgical time and intraoperative bleeding.

Before closing the wound, the Valsalva maneuver can be performed repetitively or the patient can be placed in the Trendelenburg position, and any identified bleeding sites can be identified and controlled. Cervical pressure dressings, such as the Queen Anne dressing, have been advocated in the past. These dressings, however, are cumbersome and may delay the recognition of a hematoma. These dressings do not prevent hematoma formation and therefore are not recommended. The patient should be awakened from anesthesia in a manner to avoid coughing. Recent studies has shown that the use of prophylactic dexamethasone before induction of anesthesia can reduce the incidence of postoperative nausea and vomiting in thyroidectomies. Perioperative antiemetics are also used to decrease the risk of emesis, but they have not been shown to affect hematoma rates. Taking these precautions and using meticulous surgical technique will decrease the risk of hemorrhage.

The timing of postoperative hematomas can range from immediate to several days postoperatively. The majority of hematomas, however, occur within the first 24 hours of surgery. The signs and symptoms of hematomas include neck swelling, pain, oozing from the suture line, ecchymosis, dysphagia/odynophagia, stridor, and respiratory distress. Hematomas are classified as superficial or deep depending on their relationship to the strap muscles. Deep hematomas are thought to cause respiratory distress and airway compromise by causing venous congestion and subsequent laryngopharyngeal edema. Time is essential as the longer the hematoma is present, the greater the resultant airway edema and difficulty in intubation. It has been advocated that the strap muscles be reapproximated loosely or incompletely to allow for egress of any accumulating deep neck hematoma.

When recognized, symptomatic hematomas should be decompressed immediately ( Figure 44.1 ). The wound is opened and the hematoma is evacuated. The airway should be controlled in cases with respiratory distress. Endotracheal intubation may be difficult depending on the degree of laryngopharyngeal edema. Therefore emergent tracheostomy may be necessary. Tracheotomy access is usually straightforward because of the ease of accessing the exposed trachea. Once the airway is secure, the patient is returned to the operating room for a formal wound exploration and control of hemorrhage. The wound is irrigated and closed as described previously.

Postoperative bleeding complications are rare but potentially life threatening and are associated with increased economic burden and resource utilization. Standard techniques are used to control any bleeding at the time of surgery, paying careful attention to any mediastinal vessels that are in the field. Hematomas are often discovered by floor nurses who are educated on the signs and symptoms of a cervical hematoma. A protocol for the management of this complication should be written and widely available to all members of staff responsible for the patient’s postoperative care. A regular examination of the neck (palpation and visualization) should be performed postoperatively at regular intervals.

Hypertrophic Scar

A scar is not typically classified as a complication; however, the negative effect of hypertrophic scars and keloid formation on a patient’s well-being cannot be underestimated. To expand on this concept, the psychosocial consequences of scar formation is a challenging outcome measure to study due to the wide variation in validated methodology (surveys and scar scores), heterogeneous patient populations, and differing cultural bias. It is safe to say that no patient desires an unfavorable scar on his or her neck.

The surgeon can undertake certain strategies to minimize or disguise scar formation. Placing the incision in a natural skin crease can help hide a scar. The length of a scar can be minimized by placing the incision in the higher skin crease; by doing so, the relatively fixed superior pole vessels can be divided early in the procedure, permitting the surgeon to elevate the relatively mobile inferior pole through the incision. Energy devices and/or excessive traction can lead to an abrasion or burn of the skin edge, which can exacerbate scar formation. If the skin edges are traumatized during the operation, reexcision of the skin edge should be considered before closure. Remote access endoscopic thyroid and parathyroid surgery, including the transaxillary, breast and transoral approaches, avoid a scar on the neck altogether by strategically placing the incision(s) in a remote location (see Chapter 32 and Extra Cervical Approaches to the Thyroid and Parathyroid Glands). Out of these options, the transoral route provides the most inconspicuous scar as the incisions are placed in the oral vestibule where the oral mucosa rapidly heals in a genuinely hidden location (see Chapter 33 Transoral Thyroidectomy).

Several precautions in the postoperative period will reduce hypertrophic scarring and keloid formation. If permanent skin sutures are used, the sutures should be removed in a timely fashion to avoid permanent markings. The wound at that point can be reinforced with Steri-strips. Over-the-counter wound products may help minimize scar formation. Additionally, the patient is counseled to avoid sun exposure, which may cause scar pigmentation. In women, breast support is encouraged to avoid any undue tension on the healing wound. Despite these measures, some patients will develop hypertrophic scars or form keloids. Initial management consists of intralesional steroid injection with triamcinolone acetonide. If this fails, scar revision can be performed. Importantly, keloid scar revision can lead to a worse outcome. Recently, laser therapy for the prevention of thyroidectomy scars has been studied and found to be efficacious.