Complications of Surgery for Decompression of Spinal Stenosis and Disc Disease

Epidemiology

Clinical Presentation

Nonfusion of the operated level can present as chronic pain. In the series of Bolesta and coworkers, the 8 patients who did not have complete fusion manifested no pain (4 patients), pain without need for further surgery (1 patient), and pain severe enough to require additional surgery (3 patients, with pain relief in 2 of the 3).

Pathophysiology

Arthrodesis may require months to years to achieve the maximum degree of bone fusion. Multiple factors contribute to the rapidity and success of complete bone fusion, including adequate bone graft substrate, immo-bilization of the region being fused, and many hostrelated factors. Factors that predispose to nonunion include excessive motion/trauma at the operated level, smoking, diabetes, malnutrition, corticosteroid usage, and osteoporosis.

Imaging

Radiographic signs of successful fusion include (1) continuity of bone density and bony trabeculae across the interspace; (2) minimal loss of height at the operated disc space; (3) less than 3 degrees of movement at the operative site on flexion-extension series; (4) presence of a sclerotic line between the graft and the vertebral bone indicating bone remodeling with new bone formation at the junction; (5) absence of any lucent “halo” or periprosthetic lucency around the implant(s); and (6) integrity of the construct with no screw fracture, pullout, or plate buckling. At times, there may also be resorption of anterior osteophytes (see Figs. 25-1 and 25-2 ).

Epidemiology

In 42 patients with single-level ACD, ACDF, or ACDFP, the extent of cervical lordosis from C2 to C7 did not change after ACD, ACDF, or ACDFP. Kyphosis was seen at the operative level at 2 years in 75% of patients treated by simple ACD but in none of those treated by ACDF or ACDF with instrumentation. In 25 patients with three-level and four-level ACDF and complete fusion, a lordotic curvature was achieved in 84%. In 26 patients with four- and five-level surgeries, follow-up showed successful reconstruction of a lordotic curve in 20 (76.9%), a hypolordotic curve in 4 (15.4%), and a kyphotic curve in 2 (7.7%).

Patient Presentation

Postoperative cervical kyphosis typically presents as axial or radicular pain but sometimes as head drop.

Pathophysiology

Initial resection of bone plus later resorption of the host bone and the interbody graft may lead to settling and angulation of the construct, with kyphosis.

Imaging

Plain radiographs, reformatted sagittal CT scans, and MR images display the overall curvature of the spine and enable precise measurements of the angle across the operative level ( Fig. 25-4 ).

Epidemiology

Among 42 consecutive patients treated by single-level ACD, ACDF, or ACDFP, radicular symptoms developed at a level adjacent to the site of surgery in 17% of all cases, specifically ACD, 17%; ACDF, 20%; and ACDFP, 20%. Among 26 patients with long (four- or five-level) anterior cervical constructs, adjacent level disc degeneration developed in 19 (73%).

Patient Presentation

Adjacent level disease may become symptomatic in as many as 15% of patients undergoing multilevel surgeries and may progress in 12%. Ultimately, 2 (7.7%) of 26 patients undergoing four- and five-level procedures required surgery at levels adjacent to the index construct.

Pathophysiology

Successful fusion of one or more spinal levels increases the biomechanical load on the adjoining levels. The increased load may lead to excessive motion at the adjoining levels, accelerated degeneration of the discs, stretching or damage to the ligaments, and new or more severe compression of emerging or traversing nerve roots.

Imaging

Serial imaging studies can assess the extent to which surgical hardware impinges on and distorts adjacent bony elements ( Fig. 25-5 ). Serial studies document whether the levels adjoining the surgical site develop narrowing of the interspaces, spondylotic spurs, and subluxations of the vertebral bodies and posterior elements with flexion and extension. They also display any impingement of the surgical hardware on bone.

Epidemiology

Lowery and associates found hardware failure in 35% of anterior cervical plate fixations. Fountas and coworkers reported a 0.1% rate of instrumentation failure for first ACDF. With long-segment (four- or five-level) anterior cervical constructs, the fixation plate may impinge on adjacent levels either primarily (11.5%) or secondarily (owing to settling of the construct with telescoping at the end of a long construct) (15.4%) (total: 27%). The geometry of long-segment constructs often changes over time but typically does not undergo catastrophic failure. In patients treated with corpectomy and strut grafting, the incidence of graft migration increases with the number of levels treated, that is, with the length of the strut graft ( Table 25-3 ).

Clinical Presentation

In Lowery and coworkers' series, the hardware failure did not endanger the patient. However, mechanical failure has led to significant injury to the prevertebral tissue in other series.

Pathophysiology

Hardware failure may cause, or result from, failed fusion, destabilization of the construct, and erosion of prevertebral soft tissue structures. (See Esophageal Perforation, later.)

Imaging

Plain radiographs and CT scans with reformatted 2D and 3D images depict the integrity or disruption of the hardware, misplacement or loosening of the fixation screws, and collapse/angulation of the construct ( Figs. 25-6 to 25-8 ).

Epidemiology

Fountas and coworkers reported cord contusions in 2 patients (0.2% of >1000 cases).

Clinical Presentation

Both of the reported patients in Fountas and coworkers' series presented with postoperative worsening of preexisting myelopathy. In both patients there was gradual improvement over the next 6 weeks after intensive physical therapy and they returned to their preoperative functional level 12 weeks after the procedure. Neither showed neurologic deficits or myelopathic signs at the 12-month follow-up evaluation.

Imaging

In Fountas and coworkers' patients there was evidence on MR images of cord contusion. Seichi and associates studied the incidence and significance of postoperative “expansion” of preexisting areas of T2 prolongation (high T2 signal intensity) in 114 patients with stenotic cervical myelopathy ( Fig. 25-9 ). They found abnormal postop-erative expansion of the high intensity zone in 7/114 (6.1%) patients. Four of these 7 patients were symptomatic; 3 were not. After surgery, 9 patients (7.9%) suffered unilateral upper motor paresis with sparing of the lower extremity. Five of these 9 (56%) exhibited expansion of the high signal zone, correlating with distal paresis arising immediately after surgery (3 patients) or diffuse paresis (2 patients). Four of the 9 (44%) showed no expansion of the zone. These 4 had solely unilateral proximal deltoid, biceps, and brachialis palsy first arising 4 to 6 days postoperatively.

Pathophysiology

After reviewing 10 cases, Kraus and Stauffer suggested that the risk of spinal cord injury is increased by advancing instruments, such as nerve hooks, into the spinal canal to remove posterior osteophytes.

Epidemiology

Temporary dysphagia is found in up to 60% of patients after anterior cervical discectomy. It persists for more than 12 months in up to 12% of patients. Fountas and coworkers found mild to moderate postoperative dysphagia in 9.5% of 1015 first ACDFs. Ninety-five percent of these cases cleared completely within 2 to 7 days postoperatively. The rest improved slowly over 2 to 4 weeks after surgery. In 310 patients undergoing ACD, Lee and coworkers found dysphagia in 54.0% at 1 month, 33.6% at 2 months, 18.6% at 6 months, 15.2% at 12 months, and 13.6% at 24 months after surgery. Risk factors for postoperative dysphagia that persists for at least 24 months include female gender (18.3% vs. 9.9% for males), revision surgery (27.7% vs. 11.3% primary surgery), and multilevel surgery (three or more levels) (19.3% vs. 9.7% for one- or two-level surgery). Dysphagia is also more common in elderly patients versus young patients. In Lee and colleagues' series, the prevalence of dysphagia did not increase with use of instrumentation or with corpectomy versus discectomy.

Clinical Presentation

Postoperative dysphagia manifests as pain with swallowing, difficulty in swallowing, coughing or choking with swallowing, new onset of heartburn, regurgitation of old food, feeling of throat blockage, and/or frequent throat clearing. Typically, the dysphagia is more severe with solid food than with liquids.

Pathophysiology

Postoperative dysphagia may result from pressure by the retractor blades against the gut wall. In 31 patients undergoing ACDF, Heese and associates showed that the mean pressure of the open retractor blades against the pharynx exceeded both the mean arterial pressure and the mean mucosal perfusion pressure of the pharynx. In open position, therefore, retractors may reduce mucosal perfusion and cause local ischemia.

Imaging

Barium swallow studies may show luminal narrowing, delayed transit, and/or laryngeal penetration/aspiration.

Epidemiology

Esophageal perforation is a rare complication of ACDF, with a reported incidence between 0% and 1.62%. Several recent large series (>1000 patients each) have found an incidence between 0.1% and 0.4%.

Clinical Presentation

The perforation may present acutely in the intraoperative period (27%), shortly postoperatively (27%), or weeks to months (even years) later (45%). Patients may present with progressive dysphagia, fever/sepsis, mediastinitis, and/or wound drainage, swelling, crepitus, or abscess. The diagnosis may be confirmed with a Gastrografin swallowing study. Although nonoperative management has been used selectively with success, the treatment generally involves surgical repair. When all causes of esophageal perforation were analyzed, there is some evidence suggesting that earlier treatment may lead to a better outcome. The mortality rate was 20% when treatment was instituted less than 24 hours from diagnosis and 50% when it occurred in a more delayed fashion, but this was not a randomized study.

Pathophysiology

Inadvertent perforation during surgery typically leads to immediate leak. Recognition of the perforation allows primary repair and, if needed, interposition of vital tissue. Such immediate repair may permit complete healing. Unrecognized perforations can lead to esophagocutaneous fistula and/or potentially fatal mediastinitis. Alternatively, a leak can present in a delayed fashion, sometimes from erosion of instrumentation into the esophagus. Loosening of cervical fixation screws and/or plates, for example, may allow the displaced hardware to erode into the cervical esophagus (0.8%). Extruded hardware that erodes into the esophagus has been reported to traverse the gastrointestinal tract and to exit orally or rectally, so the imager must be alert to the absence of any screws and should search for any “missing screw” whenever esophageal perforation occurs in the postsurgical patient. Treatment of chronic esophageal perforation is difficult, may necessitate multiple surgical procedures over years, and may require sternocleidomastoid myoplasty and deliberate creation of an external fistula ( Fig. 25-10B ).

Imaging

CT and MRI with contrast enhancement may demonstrate paraesophageal abscess or air in the surgical bed ( Figs. 25-10 to 25-12 ). However, air in the surgical field is normal in the early postoperative field. Increasing air on interval imaging should raise the suspicion for esophageal perforation. Both CT and MRI may be hard to interpret owing to postsurgical changes and instrumentation artifact (when present).

Epidemiology

Sagi and associates reported airway complications in 6% of more than 300 anterior cervical procedures. These required emergency re-intubation of the just-operated neck (with all attendant risks) in one third of cases (2%) and led to death in 0.3%. Terao and coworkers encountered airway complications in 1.8% of anterior surgeries, 1.1% of posterior surgeries, and 70% of combined anteroposterior (360-degree procedures). Risk factors for cervical edema include prolonged/difficult surgery involving high cervical exposures (C2, C3, or C4), exposure of more than three vertebral levels, combined anteroposterior surgery at the same time, operative time more than 5 hours, blood loss greater than 300 mL, and increased volume of crystalloid replacement. Histories of myelopathy, spinal cord injury, pulmonary problems, smoking, and anesthetic risk factors do not correlate with airway complications.

Clinical Presentation

Airway dysfunction typically presents as shortness of breath, decreased oxygen saturation, hypercapnia, and/or stridor. Acute airway obstruction nearly always results from pharyngeal edema, but hematoma, laryngeal obstruction (see later), and hardware slippage must be excluded. Normal postoperative soft tissue swelling increases markedly on the second day, is maximal at days 2 to 3, and gradually reduces from day 4 onward ( Tables 25-4 and 25-5 ). Therefore, extubation on postoperative day 1 and discharge to home may occur before maximal swelling. Epstein and associates recommended keeping patients intubated overnight and having the anesthesiologist remove the endotracheal tube to reduce the risk of such airway complications.

Pathogenesis

For procedures cephalic to C5 the swelling is most marked at C2-C3. There is no difference in the degree of soft tissue swelling between one-level and two-level surgeries.

Imaging

Plain lateral cervical radiographs are often obtained postoperatively to assess vertebral alignment, instrument position, and airway patency. Tables 25-4 and 25-5 give the expected thickness of the prevertebral soft tissue in the postoperative period.

Epidemiology

The recurrent laryngeal nerve is injured in 0.07% to 11% of ACDs, leading to transient (80%-90%) or permanent (10%-20%) dysfunction. In two series totaling more than 1300 patients, symptomatic dysfunction of the recurrent laryngeal nerve was seen in 3%. It develops equally frequently with left-sided versus right-sided surgical approaches. Actual paralysis of the recurrent laryngeal nerve is reported in 0.6% of patients.

Clinical Presentation

Postoperative unilateral recurrent laryngeal nerve dysfunction manifests clinically as a wet quality of the voice and/or new postoperative hoarseness. In Fountas and coworkers' series, all patients were treated conservatively and all showed spontaneous resolution of their symptomatology within a 12-week period. Other series, however, show that the dysfunction may be permanent.

Pathogenesis

Review of recurrent laryngeal nerve dysfunction in 900 consecutive patients coming to anterior cervical spine surgery over 12 years disclosed that vocal cord dysfunction results in part from pressure on the nerve by the endotracheal tube and the retractors. The retractors displace the larynx against the shaft of the endotracheal tube, leading to compression of the nerve. Monitoring of cuff pressure in the endotracheal tube and periodic relaxation of the retractors to permit re-perfusion of the nerve have been reported to decrease the rate of transient vocal cord paralysis from 6.4% to 1.7%. A more recent randomized study, however, found that cuff deflation did not affect the rate of transient laryngeal nerve dysfunction seen on laryngoscopy (about 15% in each group).

The course of the recurrent laryngeal nerve is different on the two sides. On the right side, the recurrent laryngeal nerve separates from the main trunk of the vagus nerve, passes anterior to and then beneath the subclavian artery, and then ascends in the tracheoesophageal groove. It frequently bifurcates before entering the larynx. On the left side, the recurrent laryngeal nerve descends parallel to the carotid artery, passes anterior to, under, and then posterior to the aortic arch at the ligamentum arteriosum, and then ascends within the tracheoesophageal groove (where it lies a little more medial than on the right side).

In a small minority of patients, the laryngeal nerve follows a variant course and is designated the “nonrecurrent” or “direct” laryngeal nerve. On the right, a direct inferior laryngeal nerve is reported in about 1% of patients and is often associated with aberrant subclavian artery. On the left, a direct left inferior laryngeal nerve is rare and is mostly associated with right aortic arch. These variants present unexpected risks to the operating surgeon.

Imaging

In addition to the usual information as to level, extent, and so on of cervical spondylosis and stenosis, preoperative assessment of patients for anterior cervical surgery should include review and specific reporting of (1) any preexisting laryngeal paralysis and (2) any anomalies of the aortic arch and great vessels that might raise concern about anomalous “direct” laryngeal arteries.

Postoperatively, three simple signs reliably identify vocal cord paralysis: (1) dilatation of the ipsilateral pyriform sinus, (2) thickening and medialization of the ipsilateral aryepiglottic fold, and (3) dilatation of the ipsilateral laryngeal ventricle ( Fig. 25-13 ). These findings should be sought and specifically commented on in each report on the postoperative patient. In rare patients with preexisting unilateral vocal cord paralysis, anterior cervical spine surgery may lead to bilateral vocal cord paralysis and require permanent tracheostomy. Manski and colleagues advocate preoperative assessment of the vocal cords to avoid inducing bilateral paralysis.

Epidemiology

The vertebral artery is injured in 0.2% to 0.5% of ACDs, with an estimated incidence of 0.25% among 12,205 cervical spine procedures (0.25%). Lacerations may occur at any spinal level. Vertebral artery injury occurs more frequently with ACC (81% of vertebral artery lacerations) than with ACDF (19%).

Pathogenesis

Causes of vertebral artery injury include excessive lateral drilling (which can occur from intraoperative loss of midline landmarks, especially with pathologic anatomy), excessive removal of lateral bone and disc, excessive lateral placement of hardware, and/or pathologic softening of bone by tumor or infection. It is generally considered safe to resect bone laterally up to the medial margin of the uncinate process (uncovertebral joint of Luschka). However, there is a less than 6-mm distance between the medial border of the uncinate process and the medial margin of the foramen transversarium. When the vertebral bodies are distracted, a “window” of approximately 6 mm opens between the uncinate process and the next-superior vertebra, exposing the vertebral artery to potential injury by drill, Kerrison punch, or curet.

In addition, the course of the vertebral artery alters subtly as it ascends in the neck. From C6 to C3 the vertebral artery (1) courses medially at an angle of approximately 4 degrees to the midline and (2) passes progressively farther posteriorly. Therefore, the extent of lateral resection must be adjusted level by level during surgery. At C6-C7, the vertebral artery typically runs between the transverse process of C7 and the longus colli before entering the foramen transversarium at C6. Therefore, the longus coli should be retracted at the level of C6 and care taken to avoid extensive lateral dissection at C6-C7.

The vertebral artery shows variable entry into the foramina transversaria ( Table 25-6 ). Imaging studies of 500 vertebral arteries showed that atypical entries are mostly unilateral (12.4% of patients) and rarely bilateral (0.8% of patients); are more common in women (66.7%) than in men (33.3%); and are nearly as frequent on the right (48.6%) as on the left (51.4%) sides. In case of high entry, the vertebral artery ascends anterior to the transverse processes, just posterior to the longus colli, unprotected by bone. Separate origin of the left vertebral artery from the aortic arch between the left common carotid artery and the left subclavian artery is found in 2.4% to 5.8% of cases. In such cases, the vertebral artery nearly always enters the foramen transversarium at C5.

A major cause of vascular injury is the anomalous course of the vertebral artery. The vertebral artery makes a prominent medial loop in 2.0% to 2.7% of cases. In Curylo and coworkers' series of seven medial loops, the loops were unilateral and were at C3 (three of seven), at C4 (three of seven), and at two levels (both C3 and C7). The medial deviation of the arterial loop may take two forms. The vertebral artery may loop into a medially enlarged foramen transversarium (1.2% of patients). In such a case the greatest medial deviation of the loop is at the level of the midbody of the vertebra, with normal position of the artery at the disc levels above and below. Alternatively, the artery may loop into the proximal portion of the intervertebral foramen close to the point of emergence of the nerve roots (0.8% of patients). For these reasons, the vertebral artery may course medial to the uncovertebral joint, usually at C3, C4, or C5. These anomalies may thin the pedicle and bring the vertebral artery medial to, or less than 1.5 mm from, the uncovertebral joint. In such cases, the “5.5-mm distance rule” from the uncinate process may not be applicable, leading to potential for injury. Such medially placed vertebral arteries are at risk of injury during surgery. In rare cases, the vertebral artery itself may be the cause of the radiculopathy. Anterior cervical surgery with prolonged retraction of the carotid sheath may lead to internal carotid artery thrombosis with hemispheric infarction.