David J. Hernandez and Chad E. Galer Abstract
The boundaries of the neck dissection bring the surgeon in close proximity to a number of nerves that are important for facial symmetry, voice production, swallowing, tongue sensation and movement, and diaphragm contraction. Under most circumstances, injury to any of these nerves should be considered an unanticipated complication during a neck dissection and often results in reduced patient quality of life. Mastery of the anatomy and a keen awareness of the potential pitfalls are required to minimize complications during a neck dissection. Early recognition of complications allows the surgeon to manage them expediently, which often spares the patient further morbidity and potentially mortality. The surgeon must have a clear understanding of the cranial nerves, arteries, veins, and lymphatics of the neck and be able to utilize landmarks and maneuvers to removal nodal packet contents safely. Nevertheless, the only effective way to completely avoid complication is to not operate at all. Thus, surgeons must also be versed in the recognition and management of complications as well as appreciate when to seek consultation with other physicians or surgeons.
Keywords: complication, neck dissection, anatomy, infection, blowout, stroke, nerve injury, chyle leak, air embolism, pneumothorax, hypoparathyroidism, blindness
This chapter explores the various pitfalls encountered during neck dissections. A strong emphasis on mastering the anatomy will help avoid unnecessary morbidity. Every surgeon who performs neck dissections should be keenly aware of the potential complications he or she might face, be able to quickly diagnose them (especially if they are life threatening), and be capable of managing them to minimize further morbidity and potential mortality.
This chapter will focus on surgical complications specific to the neck dissection, and will not cover morbidity associated with primary tumor ablation (pharyngocutaneous fistula, thyroidectomy, etc.), reconstruction, and nonsurgical complications.
11.2 Wound Infection/Dehiscence
The excellent blood supply of the neck limits the rate of wound infection and dehiscence. In the absence of communication with the aerodigestive tract, neck dissection is a clean procedure and carries a wound infection rate of approximately 1%. This increases considerably when the aerodigestive tract is entered, with studies showing surgical site infection (SSI) rates (as strictly defined by the Centers for Disease Control and Prevention [CDC]) of between 3 and 41%.1.2 Antibiotic prophylaxis can decrease this risk to about 13%.1 Multiple antibiotic combinations have been tested, with the most common being cefa- zolin for clean procedures, and ampicillin-sulbactam for clean-contaminated. Clindamycin alone has been shown to be inferior to ampicillin-sulbactam, and it is recommended to add gram-negative coverage for patients who are allergic to penicillins.3,4 Duration of antibiotic prophylaxis longer than 24 hours does not correlate with improvement in SSI rate.5,6,7 Multiple factors have been shown to increase risk of SSI including medical (hypothyroidism, diabetes, smoking, methicillin-resistant Staphylococcus aureus colonization, hypoalbuminemia, history of previous radiation therapy) and surgical (operative time, operative blood loss, flap failure, operative takebacks, concomitant tracheostomy, osteocutaneous free flaps).8,9,10 When possible, these should be addressed to reduce the risk of infection.
Wound dehiscence is often closely related to wound infection; however, it can occur primarily. Careful attention to incision planning, particularly in the case of previous surgery or radiation, is critical to avoid flap loss and subsequent dehiscence. Avoiding trifurcated incisions when possible, gentle tissue handling, subplatysmal dissection, meticulous closure, and elimination of dead spaces are all technical considerations that reduce the risk of wound complications. Similarly, avoidance of excess tension on the skin—particularly if skin is resected with the specimen—is mandatory to avoid diminished vascularity and secondary tissue loss.
11.3 Vascular Complications
Bleeding complications after a neck dissection typically cause issues related to local compression, rather than loss of blood volume and resultant hemodynamic instability. Hematomas typically develop in the immediate postoperative time frame, but there are reports of patients presenting 1 week postoperatively with acute hematomas requiring surgical treatment. Most hematomas should be managed with exploration in the operating room with control of any offending vessels. The overall incidence of postoperative hematoma after neck surgery is estimated to be 1 to 1.7%.11
Patients may develop difficulty breathing when a hematoma expands, and causes venolymphatic obstruction that leads to supraglottic edema (Fig. 11.1). For this reason, once a hematoma is identified, it should be managed expediently, and, occasionally, bedside drainage is necessary to prevent upper airway obstruction if patients show signs of respiratory distress. The airway should be secured as soon as an expansile hematoma is identified.
Hematomas are best avoided by ensuring meticulous hemostasis during the dissection and prior to closing the wound. Many surgeons evaluate for bleeding using intraoperative Valsalva maneuver or Trendelenburg tilt. Several studies have shown that these maneuvers identify small bleeding points, but their use does not correlate with a reduction in hematoma formation.12.13
Numerous attempts have been made using specialized instruments (e.g., Harmonic scalpel) or hemostatic products to decrease intraoperative bleeding, and reduce rate of hematoma. Studies have shown some nonclinically significant improvement in intraoperative bleeding and postoperative drainage, but unfortunately are underpowered to detect differences in hematoma rates.220.127.116.11.18 Proper patient selection, meticulous surgical technique, and thorough hemostasis are still the best practices for preventing postoperative hematoma.
Arterial spasm may also deceive the surgeon intraoperatively. Thus, it is advisable to routinely examine the superior thyroid, occipital, transverse cervical, and facial arteries at the end of a case if the nodal packets near these vessels were dissected.
Another rare but potentially serious bleeding complication can arise during a neck dissection if the patient has a tortuous carotid artery that results in a laterally displaced segment of carotid artery.19 This can be particularly prominent in elderly patients (Fig. 11.2). Such a segment of distorted carotid artery is prone to injury when dissecting the lateral nodal contents off the transition point between the floor of the neck and the carotid sheath. Vascular injury in these cases may be avoided by routinely reviewing the preoperative CT scan. Injury to the carotid artery during a neck dissection may result in life-threatening blood loss and stroke.
Fig.11.1 Edematous false vocal folds and partially obstructed airway in a patient being intubated due to airway compromise caused by a neck hematoma.
11.3.2 Internal Jugular Vein Blowout
Internal jugular vein (IJV) blowout has been reported and is usually associated with circumferential dissection of the vessel, desiccation of the vessel adventitia, and/or a concomitant salivary fistula.20 This is a low-pressure system; therefore, bleeding is typically not florid, but it may be intermittent and associated with increased venous pressure as it occurs with coughing. At the time of surgical intervention, the carotid sheath should be carefully inspected, and consideration given to flap coverage in the context of a salivary fistula, as this situation also puts the carotid at risk of blowout.
11.3.3 Carotid Blowout Syndrome
This is defined as rupture of the carotid artery or branches caused by tumor involvement of the vessel, or as a result of late radiation toxicity. The level of severity is further subdivided into three clinical syndromes: threatened blowout, which refers to a clinically exposed vessel or radiologic evidence of tumor invasion to the vascular structure; impending blowout, when a herald bleed has settled spontaneously; and acute carotid blowout syndrome, with profuse, uncontrollable bleeding. When a carotid artery blowout is suspected, the surgeon typically has little time to act and mobilize resources. Radiation treatment and, particularly, re-irradiation place patients at increased risk of carotid blowout. Other contributing factors include a history of a neck dissection (particularly a radical neck dissection), fistula, devitalized soft tissue overlying the carotid, and cancer overlying or encasing the carotid.
Fig. 11.2 (a) A tortuous segment of internal carotid artery (white arrow) is noted after a left neck dissection. This knuckle of artery may be mistaken for a prominent lymph node if care is not taken. (b) CT angiogram of a different patient with a more extreme example of an ectatic internal carotid artery (white arrow) on the left. (Image b reproduced with permission of Agarwal G, Gupta A, Chaudhary V, Mazhar H, Tiwari S. Rare anatomical variant of the cervical internal carotid artery. Br J Oral Maxillofac Surg 2017;55:530-532.)
Since survival is not guaranteed after developing this severe complication, extreme measures must be employed in managing it. This typically involves placing constant digital pressure over the area of hemorrhage, mobilizing a code team to actively start resuscitation while transporting the patient to the operating room, or to the interventional radiology suite, to ligate, bypass, stent, or embolize the carotid artery. In the case of operative intervention, the finger is prepped into the field and continuous pressure is maintained while wide exposure is obtained. If available, vascular surgeons may be of great assistance in managing this complex surgical scenario. More recently, excellent results have been obtained using endovascular stenting of the carotid artery.21.22
In patients with a known substantial risk of carotid blowout (e.g., patient with unresectable carcinoma encasing the carotid, with contiguous disease involving the skin or pharynx), a frank discussion should be undertaken with the patient regarding this often-fatal complication and the potential role of prophylactic endovascular intervention. Advanced directives should be strongly encouraged for these patients.
11.4 Neurologic Complications
Stroke is a rare, but functionally devastating complication of neck dissection. The risk of stroke in older series ranged as high as 4.8%. These studies, however, were retrospective and did not account for variables such as smoking, which is also correlated with the risk of stroke.
In a systematic review of NSQIP (National Surgical Quality Improvement Program) data, Cramer et al reported an increased risk of stroke following a neck dissection in patients with at least two carotid artery stenosis (CAS) risk factors (age older than 65 years, smoking, diabetes mellitus, hypertension, congestive heart failure, renal failure, history of stroke or transient ischemic attack).23 The risk for such patients was measured at 2.86% for bilateral neck dissections, 0.41% for unilateral neck dissection, and 0.24% for no neck dissection. Additionally, stroke was significantly associated with 30-day mortality (7.4%). Another large database study from Canada showed a similar stroke rate in 30 days following surgery (0.7%) as compared to non-head and neck major surgery. Similar risk factors were identified, but the data were not reported separately for the high-risk group.24 Additionally, the authors found a significant decrease in incidence from 1995 to 2012 (1.1-0.3%).
In patients with carotid artery disease, or risk factors for CAS, extra care should be taken to avoid retraction of the carotid sheath, and unnecessary manipulation of the carotid. If a very high-grade stenosis is identified on imaging, consideration can be made for preoperative endarterectomy, with careful consideration of the risk in the oncologic context.
11.4.2 Spinal Accessory Injury
Spinal accessory nerve injuries are best avoided by understanding not only the anatomic relationships of the nerve within the neck, but also that many patients with shoulder dysfunction after a neck dissection have an anatomically intact nerve. While the rate of unintended transection of the spinal accessory nerve is exceedingly low in experienced hands, the rate of shoulder syndrome after radical neck dissection is estimated to be 47 to 100%.25 In addition, careful evaluation of shoulder function after neck dissection shows an approximately 20% reduction in function following a selective neck dissection, and up to 50% reduction following a modified radical neck dissection (with dissection of spinal accessory in level V as well). A program of physical therapy in the postoperative period is helpful in reversing weakness and postoperative pain, and it is routinely offered to patients after neck dissection at many institutions.26,27
Injury to the spinal accessory nerve during a neck dissection may result from excessive traction and/or devascularization of the nerve. Direct traction on the nerve with a retractor should be avoided at all times during the procedure. If needed, a retractor may be placed on the sternocleidomastoid muscle (SCM) immediately cranial or caudal to the insertion of the spinal accessory nerve. Devascularization of a segment of the nerve is often difficult to avoid during dissection of level IIB (in addition to level IIA).28 Bipolar electrocautery or cold techniques are best used near the nerve to avoid thermal injury as well. An additional area of concern for spinal accessory injury is in the posterior triangle of the neck, where the nerve is very superficial and can be injured while raising the skin flaps. Furthermore, in this area the nerve tends to be tortuous and may have a branching pattern, so meticulous attention to its meandering is critical to avoid injury.
Technically, the nerve is easily identified in the carotid triangle by slowly unwrapping the fascia of the SCM. The tendinous portion of the SCM is superficial to the nerve. The occipital perforating vessels supplying the upper portion of the SCM are found immediately superficial to the nerve (Fig. 11.3). The bony landmark for the point where the nerve intersects with the IJV is the transverse process of the atlas, or C1.29 Typically, the nerve traverses the IJV superficial—or lateral—to the vein (40-96%).30 Occasionally, the nerve crosses deep—or medial—to the nerve (3-57%), and, rarely, the nerve courses through a fenestrated or bifurcating vein (Fig. 11.3). There is even a report of the nerve splitting around the vein.27 Given the variable relationship between the spinal accessory nerve and the IJV, it is prudent that surgeons be aware of this variability to avoid unnecessary injury to the IJV or spinal accessory nerve.
Dissection of level V places the nerve at increased risk due to its superficial course in this location. A firm grasp of the surgical planes and the course of the nerve in the posterior triangle is key to avoid injury. Identifying the anterior border of the trapezius is most helpful, since the nerve typically courses 1 to 2 cm inferior and parallel to this landmark. The nerve typically enters the anterior surface of the trapezius 2 to 5 cm superior to the clavicle. Along the posterior border of the SCM, the spinal accessory nerve is located typically within 1 cm superior to Erb’s point.29
11.4.3 Marginal Mandibular Nerve Injury
The marginal mandibular nerve (MMN) is most relevant during a level I neck dissection, and to a lesser extent during access to the superior limit of level II. This branch of the facial nerve is responsible for innervating the depressors of the lower lip: the depressor anguli oris and depressor labii inferioris muscles. The consequence of the injury is an asymmetric smile, as well as some perceived difficulty with drinking and eating.31
Fig. 11.3 (a) Right spinal accessory nerve identified immediately deep to the perforating occipital vessels supplying the superior sternocleidomastoid muscle. (b) Rare example of a spinal accessory nerve traversing between a fenestrated internal jugular vein. (Reproduced with permission of Tatla T, Kanagalingam J, Majithia A, Clarke PM. Upper neck spinal accessory nerve identification during neck dissection. J Laryngol Otol 2005;119:906-908.)
Using the traditional House-Brackmann scale to assess lower domain facial nerve function, Moller et al reported a 14% rate of weakness at 2 weeks post-op, which had decreased to about 4% on long-term follow-up.32 In another study by Batstone et al, up to a 23% incidence of weakness, 31% initially and decreasing to 13% between 1 and 2 years, was identified.31 A subgroup of patients experience significant distress over this.
Transient lower lip weakness often develops after a neck dissection due to the disruption of the cervical branch of the facial nerve, which innervates the platysma. The weakness of the lower lip due to loss of platysmal function is self-limiting when the MMN is left intact.33 The key to avoiding injury to the MMN — as is the case with avoiding injury to any other nerve—is having a firm grasp of the anatomy.
The MMN may actually consist of more than one nerve branch. It typically crosses the facial artery 1.73 mm inferior to the lower border of the mandible.34 Thus, the facial notch is a very reliable landmark when identifying the MMN. Subplatys- mal flap elevation will avoid injury to the MMN since the nerve lies in a fascial layer deep to the platysma. The nerve is found superficial to the facial artery and vein. The Hayes Martin maneuver consists in ligating the facial vein inferior to the mandible (approximately at the level of the inferior border of the submandibular gland) retracting the superior vein stump superiorly. This protects the nerve in the fascial plane, superficial to the facial vein, without definitively identifying it. However, whenever perifacial node dissection is necessary, the MMN must be skeletonized and retracted above the level of the mandible. It is recommended that careful dissection of the nerve begin at the level of the facial notch, as this is a consistent landmark as noted earlier. Once the nerve is identified at the facial notch, it should be dissected anteriorly and posteriorly until it may be retracted above the level of the mandible.
Unilateral MMN paralysis may result in an asymmetric smile, asymmetry during expression of certain facial emotions, oral incompetence, drooling, and lip biting.35 Treatment of a unilateral MMN injury, should it prove to be a permanent paralysis, is centered on restoring symmetry to the lower lip. This may be accomplished in a number of methods aimed at either restoring mobility to the lip on the unilateral side or paralyzing the contralateral lower lip. The contralateral lower lip depressors may be paralyzed temporarily with injection of botulinum toxin33 or by resecting the contralateral depressor labii inferioris muscle.35 Alternatively, procedures aimed at restoring movement of the paralyzed lower lip include the anterior belly digastric muscle flap33.36 and the extensor digitorum brevis free flap.33
11.4.4 Vagus Nerve Injury
The vagus nerve is at greatest risk for injury when a radical neck dissection is performed. On occasion, the neck disease may directly involve the vagal nerve as it may involve the IJV and the carotid artery. During sacrifice of the IJV, it is prudent to ensure that the vagus nerve is not inadvertently ligated. This is best avoided by carefully dissecting the IJV circumferentially in order to exclude the vagal nerve. If possible, visually confirming the location of the vagal nerve within the carotid sheath should also reassure the surgeon that it is not injured during dissection within the carotid sheath.
The vagal nerve is situated posteriorly within the carotid sheath, between the IJV and the carotid artery, and the most common clinical manifestation in case of an injury is ipsilateral vocal cord paralysis. Depending on the location of injury, vagal nerve fibers that supply the superior vagal nerve may also be affected, which may affect laryngeal sensation and contribute to aspiration. Dysphagia may also result from a high vagal nerve injury, due to the vagal nerve branches that innervate the pharyngeal constrictors and other muscles involved with deglutition.
Immediate neurography should be performed after a vagal nerve injury is identified, while an interposition nerve graft should be attempted if there is anatomical discontinuity of the nerve. When the nerve is injured, patients will acutely present with a hoarse, breathy voice in the immediate postoperative period. Since aspiration is a common associated feature, a formal evaluation of swallowing is recommended prior to resuming oral diet. The management of the vocal cord paralysis will depend on the nature of the injury, and the prognosis for full recovery. A temporary vocal cord medialization can provide significant symptomatic relief while allowing time to observe for nerve regeneration. If the functional prognosis is estimated to be poor—or if the patient has failed to improve—more definitive approaches such as a type I thyroplasty are indicated. Involving a laryngologist early after the injury can be very helpful to inform these decisions.
11.4.5 Phrenic Nerve Injury
The phrenic nerve is derived from the third, fourth, and fifth cervical nerves. It takes a slightly lateral-to-medial course in the neck, along the anterior surface of the anterior scalene muscle (Fig. 11.4). It is at greatest risk to injury during dissection of levels III and IV. The phrenic nerve lies immediately deep to the fascia overlying the anterior scalene muscle (prevertebral fascia), which comprises part of the floor of the neck. During a neck dissection, phrenic nerve injury is avoided by carefully preserving this fascial layer while detaching the contents of levels III and IV from the floor of the neck. It is also necessary to be prudent with the use of electrocautery in this area, particularly in the event of an injury to the transverse cervical vessels.
Fig. 11.4 Following a right neck dissection, the phrenic nerve (black arrow) is seen coursing from lateral to medial overlying the anterior scalene muscle. The transverse cervical artery (white arrow), the internal jugular vein (blue arrow), and cervical rootlets are pictured as well. The sternocleidomastoid muscle is retracted laterally.
Injury to the phrenic nerve results in hemidiaphragm paralysis. Hemidiaphragm paralysis can also occur with an intact phrenic nerve if the branches from the third to fifth cervical nerves are damaged near the cervical plexus. This diagnosis may be suspected on chest X-ray, but the more confirmatory diagnostic would be chest fluoroscopic radiography in which a patient is asked to sniff or inspire forcefully. The affected diaphragm fails to depress during this maneuver when it is paralyzed. This complication is typically not accompanied by long-term respiratory insufficiency as long as the other phrenic nerve is intact, provided that the patient’s respiratory function is not marginal at baseline. It can lead to exertional dyspnea, however. Bilateral phrenic nerve paralysis is more likely to require artificial respiratory support. Plication of the paralyzed diaphragm is a potential treatment option for a paralyzed diaphragm.
11.4.6 Hypoglossal Nerve
The hypoglossal nerve is typically not in great danger of injury during a neck dissection, except during a radical or extended neck dissection with disease involving the nerve. The hypoglossal nerve is deep to the ranine veins, which are encountered just deep and inferior to the posterior belly of the digastric muscle. The proximal nerve is located posterior to the carotid artery and distally it is found on the lateral surface of the hyoglossus muscle. Dissecting superficial to the ranine veins and keeping these vessels intact will ensure the hypoglossal nerve is not injured and prevent the nuisance bleeding that may be encountered from these veins. Anecdotally, it is during attempts to control bleeding from ranine veins that accidental injury to the hypoglossal nerve may result. Thus, the ranine veins are not necessarily ligated during a neck dissection. The hypoglossal nerve should also be routinely identified prior to ligating the facial artery in level IB, as the proximal segment of the hypoglossal nerve often runs parallel to and has a similar caliber to the facial artery.
11.4.7 Lingual Nerve
The lingual nerve is encountered during dissection of the submandibular triangle, in the context of either level IB neck dissection or submandibular gland excision. While there is a paucity of data regarding lingual nerve injury in neck dissection, the incidence has been reported between 0 and 4.4% in submandibular gland excision. Generally, unless involved by tumor, the lingual nerve is robust and easily identified during the procedure. However, care must be taken while dividing the submandibular ganglion to place clamps far enough from the “elbow” of the lingual nerve to avoid crush injury.
11.4.8 Brachial Plexus
The brachial plexus is located between the anterior and middle scalene muscles. It is identified in level IV and V dissections. As with the phrenic nerve, it is deep to the prevertebral fascia, so careful dissection superficial to this plane will prevent injury. Fortunately, this nerve complex is rarely injured during neck dissection although it has been reported in the literature.
11.4.9 Sympathetic Chain
The sympathetic chain and ganglion lie posterior to the carotid artery. Injury will result in ipsilateral Horner’s syndrome (miosis, ipsilateral ptosis, and anhidrosis). To avoid encountering the sympathetic chain, the surgeon must remember to “climb the mountain” and transition from dissecting along the preverte- bral fascia laterally to coming over the great vessels medially.
11.4.10 Cervical Rootlets
Another consideration to be made during a neck dissection is to the preservation of the cervical root branches. Garzaro et al reported significantly improved shoulder mobility and quality of life in patients who preserved cervical root branches compared to patients who had these nerves transected during their neck dissection.37 There was also significantly less loss of cutaneous sensation in the preservation group. Another study also noted lower pain scores and less head and neck pain when the spinal accessory nerve was spared during a neck dis- section.38 This study also found that dissection of level V, which typically involves sacrifice of the cervical rootlets, is associated with worse pain and quality of life, even when the spinal accessory nerve is spared. Thus, cervical root branches should be spared during a selective neck dissection, especially when performed in the context of an N0 neck, to minimize perioperative morbidity.
11.5 Chyle Leak
Dissection of the left level IV nodal packet should always be done cautiously and with attention to the area of the thoracic duct. While encountering and injuring the thoracic duct itself is not a serious complication, an unidentified thoracic duct injury that is not addressed intraoperatively may result in a postoperative chylous fluid leak, or chyle leak. This complication often presents as turbid, opaque, and often milky fluid drainage that shows up in the bulb of a closed suction drain, particularly after the patient begins to eat (Fig. 11.5). Thus, it may present somewhat delayed if the patient’s enteral nutrition is restricted in the immediate postoperative period. The thoracic duct transports chyle, which consists of lymph and free fatty acids (emulsified fats), from the abdomen to the left neck. It empties into the systemic circulation at the junction between the left IJV and the left subclavian vein (Fig. 11.5). It is the largest lymphatic duct in the body. The right lymphatic duct empties in a similar location in the right neck. While we often think of chyle leaks occurring in the left level IV neck, approximately 25% of the time chyle leaks occur on the right,39 but these tend to be self-limited and can be managed conservatively. The overall incidence of chyle leaks is around 3%, although estimates range up to 5.7%.
Intraoperatively, it is prudent to always inspect level IV after a lateral neck dissection, to look for any frank chyle fluid. Most clinically significant chyle leaks are first identified intraopera- tively. A Valsalva maneuver may help identify and localize a lymphatic leak, as the increased intrathoracic pressure acts to advance chyle within the thoracic duct. If a chyle leak is identified intraoperatively, it should be clipped, tied, or suture ligated. If possible, the duct should be ligated with some associated soft tissue, as the thin wall is easily torn. A Valsalva maneuver should be repeated after the repair to ensure the leak has been addressed. In these cases, the suction drain output should be watched closely postoperatively.
Fig. 11.5 (a) Illustration of the thoracic duct as it empties into the junction of the left internal jugular vein and subclavian vein. (Adapted from Delaney et al.41) (b) Post-op day 1 picture of a patient with a bulb suction drain collecting fluid consistent with a chylous leak.
If a chyle leak is suspected in the postoperative setting, conservative measures should be taken initially. The patient should be started on a medium chain fatty acid diet or enteral feeding depending on the circumstances. Fluids and electrolytes should be monitored and repleted as needed. The head of bed should be elevated, activity should be restricted, and stool softeners should be given. These measures reduce the flow of chyle fluid in the thoracic duct by limiting increases in intrathoracic pressure. At times, pressure dressings are utilized, but many surgeons find them ineffective and risk pressure necrosis of the skin flaps. Close monitoring of the drain output can be used to assess the patient’s progress.
Octreotide is a synthetic formulation of somatostatin, which is a neuroendocrine hormone that inhibits the release of a variety of gastrointestinal hormones that regulate digestion and absorption. It reduces the production of chyle, and decreases the flow of lymphatic and chylous fluid. This medication has proven to be an important adjunct in the armamentarium against chyle leaks.40,41
Historically, chyle leaks have been divided into low- and high-output leaks depending on the amount of chyle collected from the drain, with the arbitrary cutoff value of typically 500 mL/d. More important than focusing on a value of drain output is assessing the response to conservative treatment. Persistent chyle leaks should be managed more aggressively. This may entail transcervical exploration with ligation of any identifiable offensive lymphatic channels. Additionally, consideration should be made to rotating some muscle into the area of the leak and/or applying a topical agent such as a cyanoacrylate adhesive, fibrin glue, or polyglactin mesh.42.43 Other interventions reserved for the most recalcitrant chyle leaks include embolization and thoracoscopic thoracic duct liga- tion.41.44 Total parenteral nutrition (TPN) may also be utilized in cases refractory to conservative measures; however, the risks of TPN—such as infection—must be weighed heavily prior to pursuing this approach.
11.6 Venous Air Embolus
This is a rare but potentially fatal complication that merits attention. A venous air embolism may occur when atmospheric air is exposed to a large vein, such as the IJV, and there exists a gradient for air to enter the systemic venous circulation, which may occur if the neck is slightly elevated above the heart. This complication may present with a sudden drop in end-tidal CO2 and arterial blood pressure. A “mill-wheel” murmur may be heard over the precordial area. If this complication is suspected, local pressure with a moist lap should be applied to the neck or the bleeding should be controlled quickly. The patient should then be placed in the left lateral decubitus (Durant’s maneuver) and simultaneously in the Trendelenburg position. This maneuver lodges the air bubble in the apex of the right ventricle and prevents its propagation into the pulmonary arteries, which may result in right ventricular outflow obstruction. In severe or extreme cases, a central venous catheter should be used to aspirate the air from the right atrium. Advanced cardiac life support (ACLS) protocol should be followed as necessary. The definitive treatment of venous air emboli, as is the treatment of decompression syndrome, is hyperbaric oxygen.45
Dissection that involved levels IV and V, particularly level VB or the supraclavicular nodes, potentially places the lung apices at risk for pleural violation. This rare complication is avoided by properly demarcating the dissection inferiorly. The clavicle and transverse cervical vessels are useful landmarks to avoid dissection beyond the inferior limits of a level IV and V neck dissection. In certain patients, superiorly displaced lung apices may redispose to this injury. Patients with bulky level IV and V nodal disease are also at increased risk of pneumothorax.
If the pleural space is violated during a neck dissection, the pleura should be repaired primarily with suture whenever possible, and rarely requires any further intervention if identified and repaired promptly. When this complication is not identified immediately, the patient may develop tachycardia, hypotension, hypercapnia, and hypoxia. This may occur intraoperatively or in the postanesthetic care unit. If the patient is awake and conscious, they may complain of chest pain. If these symptoms and/or signs develop, a tension pneumothorax should be suspected and requires immediate treatment. This can be confirmed by auscultation of breath sounds and confirmed with a chest X-ray. However, when emergent intervention is required, the patient should be intubated (if not already) and a chest tube should be placed immediately. Conversely, if a small pneumothorax is identified on chest X-ray in a stable, asymptomatic patient who is spontaneously breathing via his or her native airway, it can likely be followed clinically and radiographically with serial chest X-rays. These pneumothoraxes normally resorb spontaneously. If this same patient were receiving positive pressure ventilation, a chest tube would likely be required. Typically, consultation with a thoracic surgeon is prudent to ensure proper management of this rare complication.
11.8 Hypoparathyroidism/ Hypocalcemia
The risk of hypocalcemia as a result of surgical hypoparathyroidism is not only associated with endocrine surgery, but may also develop following procedures involving central neck compartments such as total laryngectomy. In the literature, the rate of transient hypoparathyroidism and hypocalcemia has been reported at greater than 50% when a bilateral central neck dissection is performed in addition to the thyroidectomy.46.47 The rate of permanent hypoparathyroidism and hypocalcemia after this procedure has been reported at 12 to 16%.48.49
The keys to avoid this complication are proper patient selection and judicious indication of bilateral central neck dissections. Updated ATA (American Thyroid Association) guidelines50 recommend against prophylactic central neck dissection for T1-T2, noninvasive, clinically node-negative papillary thyroid carcinoma, and most follicular cancers. In fact, according to these guidelines, only a weak recommendation could be made for considering a prophylactic central neck dissection: (1) nodenegative T3-T4 papillary thyroid cancer, (2) presence of metastatic lateral neck nodes, or (3) gather information that will aid for further treatment planning.
When deciding on the need for an elective dissection of the central compartment in the context of squamous cell carcinoma of the hypopharynx, it is relevant to know the risk of central nodal disease based on the subsite of the primary. Joo et al reports the rate of paratracheal—or central neck nodal disease— for postcricoid, piriform sinus, and posterior pharyngeal wall cancers at 58, 20, and 8%, respectively.51
In terms of surgical technique, prevention of hypoparathyroidism depends on properly identifying parathyroids and preserving their blood supply during a central neck dissection. Any overtly devascularized parathyroid glands should be reimplanted in a well-vascularized muscle, after previous confirmation of histology on frozen section analysis. While the superior parathyroid glands are typically located dorsal to the recurrent laryngeal nerve, and the inferior parathyroids are generally ventral to the nerves, the location of parathyroid glands is highly variable, and the glands may be intrathyroidal, in nonstandard locations in the neck, or within the mediastinum.
11.9 Cerebral Edema/Blindness
Ligation of bilateral IJVs may result in severe facial edema and increased intracranial pressure (ICP). The elevated ICP is typically accompanied by systemic hypertension as a result of Cushing’s reflex. This may manifest in altered mental status in addition to the obvious facial edema. Even when only unilateral ligation of the IJV is performed, thrombosis of the contralateral IJV may result in this complication. In general, performing bilateral IJV ligation should be avoided whenever possible. It is worthwhile being aware that even when an IJV is preserved, postoperative thrombosis may occur, but this risk is minimized by preventing desiccation of the vessel and minimizing surgical trauma. It should also be noted that performing unilateral neck dissection may result in elevated ICP if the contralateral neck has been previously dissected or treated with radiation. Thus, whenever possible, preservation of the superficial venous drainage such as external jugular veins should be attempted. The management of this complication includes head of bed elevation, fluid restriction, corticosteroids, mannitol, and hyperventilation. The ICP normalizes within 24 hours usually.
Another rare but devastating complication to consider is blindness. Typically, blindness is associated with bilateral radical neck dissections, but reports have been made of this occurring following less radical surgery. The blindness is described as nonarteritic anterior (or posterior) ischemic optic neuropathy. The etiology of this complication is likely multifactorial and is associated with hypotension, anemia, and increased intracranial venous pressure, which is likely to occur after bilateral IJV sacrifice. The blindness presents postoperatively and is typically bilateral. If the IJVs were resected or ligated, the prognosis is poorer and typically permanent. If vision loss or blindness occurs in the setting of at least one preserved IJV, the prognosis is improved for recovery of vision. In addition to ophthalmologic consultation, steroids and diuretics may be given empirically, but this has not been proven to be very effective.52
Neck dissection is an essential part of the treatment of many head and neck cancers. In experienced and vigilant hands, nodal clearance can be successfully performed with acceptable morbidity. Many pitfalls await the unwary.
 Jain U, Somerville J, Saha S, et al. Oropharyngeal contamination predisposes to complications after neck dissection: an analysis of 9462 patients. Otolaryngol Head Neck Surg. 2015; 153(1):71-78
 Cannon RB, Houlton JJ, Mendez E, Futran ND. Methods to reduce postoperative surgical site infections after head and neck oncology surgery. Lancet Oncol. 2017; 18(7):e405-e413
 Weber RS, Raad I, Frankenthaler R, et al. Ampicillin-sulbactam vs clindamycin in head and neck oncologic surgery. The need for gram-negative coverage. Arch Otolaryngol Head Neck Surg. 1992; 118(11):1159-1163
 Pool C, Kass J, Spivack J, et al. Increased surgical site infection rates following clindamycin use in head and neck free tissue transfer. Otolaryngol Head Neck Surg. 2016; 154(2):272-278
 Mitchell RM, Mendez E, Schmitt NC, Bhrany AD, Futran ND. Antibiotic prophylaxis in patients undergoing head and neck free flap reconstruction. JAMA Otolaryngol Head Neck Surg. 2015; 141(12):1096-1103
 Cohen LE, Finnerty BM, Golas AR, et al. Perioperative antibiotics in the setting of oropharyngeal reconstruction: less is more. Ann Plast Surg. 2016; 76 (6):663-667
 Khariwala SS, Le B, Pierce BH, Vogel RI, Chipman JG. Antibiotic use after free tissue reconstruction of head and neck defects: short course vs long course. Surg Infect (Larchmt). 2016; 17(1):100-105
 Benatar MJ, Dassonville O, Chamorey E, et al. Impact of preoperative radiotherapy on head and neck free flap reconstruction: a report on 429 cases. J Plast Reconstr Aesthet Surg. 2013; 66(4):478-482
 Cannady SB, Hatten KM, Bur AM, et al. Use of free tissue transfer in head and neck cancer surgery and risk of overall and serious complication(s): an American College of Surgeons-National Surgical Quality Improvement Project analysis of free tissue transfer to the head and neck. Head Neck. 2017; 39(4):702-707
 Penel N, Lefebvre D, Fournier C, Sarini J, Kara A, Lefebvre JL. Risk factors for wound infection in head and neck cancer surgery: a prospective study. Head Neck. 2001; 23(6):447-455
 Matory YL, Spiro RH. Wound bleeding after head and neck surgery. J Surg Oncol. 1993; 53(1):17-19
 Tokaç M, Dumlu EG, Bozkurt B, et al. Effect of intraoperative valsalva maneuver application on bleeding point detection and postoperative drainage after thyroidectomy surgeries. Int Surg. 2015; 100(6):994-998
 Moumoulidis I, Martinez Del Pero M, Brennan L, Jani P. Haemostasis in head and neck surgical procedures: Valsalva manoeuvre versus Trendelenburg tilt. Ann RColl Surg Engl. 2010; 92(4):292-294
 Bajwa MS, Tudur-Smith C, Shaw RJ, Schache AG. Fibrin sealants in soft tissue surgery of the head and neck: a systematic review and meta-analysis of randomised controlled trials. Clin Otolaryngol. 2017;42(6):1141-1152
 Ren ZH, Xu JL, Fan TF, Ji T, Wu HJ, Zhang CP. The harmonic scalpel versus conventional hemostasis for neck dissection: a meta-analysis of the randomized controlled trials. PLoS One. 2015; 10(7):e0132476
 Lin WJ, Wang CC, Jiang RS, Huang YC, Ho HC, Liu SA. A prospective randomised trial of LigaSure Small Jaw® versus conventional neck dissection in head and neck cancer patients. Clin Otolaryngol. 2017; 42(2):245-251
 Fritz DK, Matthews TW, Chandarana SP, Nakoneshny SC, Dort JC. Harmonic scalpel impact on blood loss and operating time in major head and neck surgery: a randomized clinical trial. J Otolaryngol Head Neck Surg. 2016; 45(1):58
 Shin YS, Koh YW, Kim S-H, Choi EC. The efficacy of the harmonic scalpel in neck dissection: a prospective randomized study. Laryngoscope. 2013; 123 (4):904-909
 Pfeiffer J, Becker C, Ridder GJ. Aberrant extracranial internal carotid arteries: new insights, implications, and demand for a clinical grading system. Head Neck. 2016; 38 Suppl 1:E687-E693
 Cleland-Zamudio SS, Wax MK, Smith JD, Cohen JI. Ruptured internal jugular vein: a postoperative complication of modified/selected neck dissection. Head Neck. 2003; 25(5):357-360
 Manzoor NF, Rezaee RP, Ray A, et al. Contemporary management of carotid blowout syndrome utilizing endovascular techniques. Laryngoscope. 2017; 127(2):383-390
 Bond KM, Brinjikji W, Murad MH, Cloft HJ, Lanzino G. Endovascular treatment of carotid blowout syndrome. J Vasc Surg. 2017; 65(3):883-888
 Cramer JD, Patel UA, Maas MB, Samant S, Smith SS. Is Neck Dissection Associated with an Increased Risk of Postoperative Stroke? Otolaryngol Head Neck Surg. 2017; 157(2):226-232
 Thompson SK, Southern DA, McKinnon JG, Dort JC, Ghali WA. Incidence of perioperative stroke after neck dissection for head and neck cancer: a regional outcome analysis. Ann Surg. 2004; 239(3):428-431
 van Wilgen CP, Dijkstra PU, van der Laan BF, Plukker JT, Roodenburg JL. Shoulder complaints after neck dissection; is the spinal accessory nerve involved? BrJ Oral Maxillofac Surg. 2003; 41(1):7-11
 Eickmeyer SM, Walczak CK, Myers KB, Lindstrom DR, Layde P, Campbell BH. Quality of life, shoulder range of motion, and spinal accessory nerve status in 5-year survivors of head and neck cancer. PM R. 2014; 6(12):1073-1080
 McNeely ML, Parliament MB, Seikaly H, et al. Effect of exercise on upper extremity pain and dysfunction in head and neck cancer survivors: a randomized controlled trial. Cancer. 2008; 113(1):214-222
 Cappiello J, Piazza C, Nicolai P. The spinal accessory nerve in head and neck surgery. Curr Opin Otolaryngol Head Neck Surg. 2007; 15(2):107-111
 Durazzo MD, Furlan JC, Teixeira GV, et al. Anatomic landmarks for localization of the spinal accessory nerve. Clin Anat. 2009; 22(4):471-475
 Taylor CB, Boone JL, Schmalbach CE, Miller FR. Intraoperative relationship of the spinal accessory nerve to the internal jugular vein: variation from cadaver studies. Am J Otolaryngol. 2013; 34(5):527-529
 Batstone MD, Scott B, Lowe D, Rogers SN. Marginal mandibular nerve injury during neck dissection and its impact on patient perception of appearance. Head Neck. 2009; 31(5):673-678
 M0ller MN, S0rensen CH. Risk of marginal mandibular nerve injury in neck dissection. Eur Arch Otorhinolaryngol. 2012; 269(2):601-605
 Tulley P, Webb A, Chana JS, et al. Paralysis of the marginal mandibular branch of the facial nerve: treatment options. BrJ Plast Surg. 2000; 53(5):378-385
 Balagopal PG, George NA, Sebastian P. Anatomic variations of the marginal mandibular nerve. Indian J Surg Oncol. 2012; 3(1):8-11
 Hussain G, Manktelow RT, Tomat LR. Depressor labii inferioris resection: an effective treatment for marginal mandibular nerve paralysis. BrJ Plast Surg. 2004; 57(6):502-510
 Tan ST. Anterior belly of digastric muscle transfer: a useful technique in head and neck surgery. Head Neck. 2002; 24(10):947-954
 Garzaro M, Riva G, Raimondo L, Aghemo L, Giordano C, Pecorari G. A study of neck and shoulder morbidity following neck dissection: the benefits ofcervi- cal plexus preservation. Ear Nose Throat J. 2015; 94(8):330-344
 Terrell JE, Welsh DE, Bradford CR, et al. Pain, quality of life, and spinal accessory nerve status after neck dissection. Laryngoscope. 2000; 110(4):620-626
 Smith ME, Riffat F, Jani P. The surgical anatomy and clinical relevance of the neglected right lymphatic duct: review. J Laryngol Otol. 2013; 127(2):128-133
 Jain A, Singh SN, Singhal P, Sharma MP, Grover M. A prospective study on the role of octreotide in management of chyle fistula neck. Laryngoscope. 2015; 125(7):1624-1627
 Delaney SW, Shi H, Shokrani A, Sinha UK. Management of chyle leak after head and neck surgery: review of current treatment strategies. Int J Otolaryngol. 2017; 2017:8362874
 Kim HK, Kim SM, Chang H, et al. Clinical experience with n-butyl-2-cyanoa- crylate in performing lateral neck dissection for metastatic thyroid cancer. Surg Innov. 2016; 23(5):481-485
 Cheng L, Lau CK, Parker G. Use of TissuePatch™ sealant film in the management of chyle leak in major neck surgery. BrJ Oral Maxillofac Surg. 2014; 52 (1):87-89
 Wilkerson PM, Haque A, Pitkin L, Soon Y. Thoracoscopic ligation of the thoracic duct complex in the treatment for high-volume chyle leak following modified radical neck dissection: safe, feasible, but underutilised. Clin Otolaryngol. 2014; 39(1):73-74
 Moon RE. Hyperbaric oxygen treatment for air or gas embolism. Undersea Hyperb Med. 2014; 41(2):159-166
 McMullen C, Rocke D, Freeman J. Complications of bilateral neck dissection in thyroid cancer from a single high-volume center. JAMA Otolaryngol Head Neck Surg. 2017; 143(4):376-381
 Cavicchi O, Piccin O, Caliceti U, De Cataldis A, Pasquali R, Ceroni AR. Transient hypoparathyroidism following thyroidectomy: a prospective study and multivariate analysis of 604 consecutive patients. Otolaryngol Head Neck Surg. 2007; 137(4):654-658
 Giordano D, Valcavi R, Thompson GB, et al. Complications of central neck dissection in patients with papillary thyroid carcinoma: results of a study on 1087 patients and review of the literature. Thyroid. 2012;22(9):911-917
 Roh JL, Kim JM, Park CI. Lateral cervical lymph node metastases from papillary thyroid carcinoma: pattern of nodal metastases and optimal strategy for neck dissection. Ann Surg Oncol. 2008; 15(4):1177-1182
 Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid. 2016; 26(1):1-133
 Joo YH, Sun DI, Cho KJ, Cho JH, Kim MS. The impact of paratracheal lymph node metastasis in squamous cell carcinoma of the hypopharynx. Eur Arch Otorhinolaryngol. 2010; 267(6):945-950
 Pazos GA, Leonard DW, Blice J, Thompson DH. Blindness after bilateral neck dissection: case report and review. Am J Otolaryngol. 1999; 20(5):340-345