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34
Complications in the Treatment of Spinal Trauma

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David J. Jacofsky, M.D. Bradford L. Currier, M.D. Choll W. Kim, M.D., Ph.D. Michael J. Yaszemski, M.D., Ph.D.

Treatment of spinal trauma has been described as early as the Hippocratic era. His famous extension bench, known as Scamnum when popularized by Celsius, was used frequently for realignment of a fractured or deformed spine. In ancient and medieval times, forceful and brisk maneuvers accompanied by immobilization were the mainstay of spinal trauma treatment. A patient would often lie prone while attendants would pull on his ankles and axillae and a physician would sit or press on prominences such as a gibbus or palpable fracture deformity. As recently as the late 1800s, Jean-Francis Calot and his contemporaries manipulated spinal deformities with their sts. In 1917, Hartmann (at the Accident Hospital for coal miners in Upper Silesia) treated a patient with a fracturedislocation of the thoracolumbar junction by having two assistants suspend the patient by the armpits and pelvis while he performed reduction by forceful manipulation from below with his sts. Later, through the rst 4 decades of the 20th century, methods of postural reduction by hyperextension were introduced. Davis, Rogers, and Bohlman were champions of such methods through the use of slings, frames, or similar devices.37 As one might imagine, such treatment led to unacceptably high rates of complications, including soft tissue breakdown, neurologic compromise, malunion, instability, and pulmonary compromise. Treatment of spinal trauma has changed signicantly over the last 2 decades. However, despite better imaging, better understanding, better access to treatment, and the availability of internal xation, challenging complications continue to exist today.

COMPLICATIONS OF NONOPERATIVE TREATMENT Halo Vest Immobilization

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Indications for use of the halo vest have evolved greatly since its description by Perry and Nickel in 1953. Initially
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described for postoperative immobilization of patients who had undergone cervical fusion for neck paralysis from poliomyelitis, Thompson and Freeman extended its use to the treatment of fractures. Complications of halo vest immobilization can be divided into those related to application of the device and those related to its use. Traditionally, the use of plaster-molded vests carried a risk of cast syndrome, pressure sores, and respiratory problems in patients with limited respiratory reserves. Prefabricated padded plastic vests have helped decrease the incidence of these complications, but at the expense of decreased rigidity and increased cost. However, patient compliance has improved and the incidence of pin loosening has decreased with these lightweight prefabricated vests. The pins themselves pose problems as well. Pin site infection is not uncommon but may be minimized with daily pin site care, including twice-daily application of a dilute hydrogen peroxide solution (50% in water). The reported incidence of pin site infection is approximately 30%.51 Oral antibiotics are usually effective, but if a pin is loose and infected, a new pin should be placed in a nearby hole in the halo ring. If the pins are incorrectly placed cephalad to the equator of the skull, halo slippage may occur (Fig. 341). The pins should be torqued to 8 in-lb in adults and 6 in-lb or less in children. In patients with osteoporosis or when the pins are inadvertently placed in the temporal areas, the skull can be perforated. Dural penetration has been reported.46 No orthosis can apply predictable and continuous traction to the cervical spine when the patient is not supine. When the patient is sitting or standing, a previously distracted cervical spine can become compressed by the force of gravity on the head and halo vest construct (Fig. 342). Such compression can lead to loss of reduction and possibly a new neurologic decit. Likewise, rotational forces are poorly constrained by a halo vest orthosis. Treatment of a unilateral facet dislocation, for example, may lead to persistent root compression and failure of therapy. Whitehill and colleagues78 described ve cases of loss of reduction in patients with facet dislocations immo-

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bilized in a halo vest. Glaser and associates32 and Bucholz and Cheung10 documented loss of reduction in 10% of all patients and in 37% of patients with facet subluxation and dislocation. Anderson and co-workers1 evaluated upright and supine lateral radiographs after halo immobilization in 42 patients with 45 noncontiguous levels of cervical spine injury. At noninjured levels, an average of 3.9 of angular change was found between adjacent levels from the occiput to C6. The greatest motion occurred more proximally (8.0 between the occiput and C1). No signicant translation was seen at the noninjured levels. At the injured level, sagittal-plane angulation averaged 7.0 and the average translation was 1.7 mm. Signicant fracture site motion was dened as greater than 3 of sagittal angulation or more than 1 mm of translation and occurred in 78% of the 45 injured levels. Three patients experienced loss of reduction that required reapplication of traction after vest removal. Asymptomatic malunion developed in 11 patients. One may postulate that it is this motion that contributes to such a high degree of nonunion in type II odontoid fractures treated in a halo vest. Residual kyphosis of a post-traumatic cervical spine can lead to a multitude of complications. Neural impairment can occur from compression of the spinal cord as it drapes over the apex of the deformity (Fig. 343). Late neck pain may be seen as a result of the modied mechanics of the paraspinous musculature that occurs when the lever arm of the muscles is altered by the deformity. Additionally, facet degeneration of adjacent segments can ensue from hyperextension of adjacent vertebral levels in an attempt to compensate for the loss of cervical lordosis in a kyphotic cervical spine.51 In properly chosen patients, halo immobilization is an excellent treatment option that is associated with frequent, but usually minor complications. However, nonunion and malunion can occur and should obviously be considered

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FIGURE 341. Failed halo pin sites. At follow-up, the halo pins of this gentleman had dislodged, and the vest and headpiece migrated proximally. His halo was removed and he was treated in a cervical collar for the remainder of treatment.

FIGURE 342. Poor axial immobilization by halo. Immobilization in the axial plane is difcult with all external xation systems, including the halo. In this patient with a fracture through a severely ankylosed cervical spine, the fracture is gapped open when supine (A) but compressed when upright (B).

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FIGURE 343. Failed external immobilization for cervical facet fractures. This patient was evaluated 112 years after nonoperative treatment of an initially nondisplaced C6 lateral mass fracture. He complained of neck pain and paresthesia down the lateral aspect of his arm. A, Flexion radiographs showed subluxation and kyphosis. B, Treatment included anterior cervical discectomy and fusion. Preoperative planning, however, included the possible need for circumferential fusion.

markers of treatment failure. In patients with nonexion injuries, the success rate of halo treatment approaches that of surgical fusion (87% vs. 95%).65 However, in the group of patients with posterior ligamentous injury, the failure rate increases to as high as 46%.11, 65

COMPLICATIONS OF OPERATIVE TREATMENT Patient Positioning

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Operative versus Nonoperative Treatment

In the age of modern medicine and modern implants, most clinicians intuitively believe that the risk of morbidity in patients with unstable spine fractures is higher in the nonoperative than the operative group. In the perioperative period, the risk of acute complications is no different. Rechtine and colleagues61 examined 235 patients with unstable thoracolumbar spine fractures who were given a choice of undergoing operative or nonoperative treatment. The groups were statistically similar in all respects. Although the length of stay in the hospital was 24 days greater in the nonoperative group, the incidence of complications (with the obvious exception of wound infection) was similar for decubitus ulcers, pneumonia, deep vein thrombosis, pulmonary embolism, and death. Polytrauma was a risk factor for increased complications, and the primary predictor of sacral decubitus ulcers was time on a spine board. Curry and Casady16 showed that a patient with spinal cord injury who is on a board for more than 8 hours is practically ensured of sacral skin breakdown. Admittedly, these studies have some inherent selection bias and are retrospective. However, it helps to show that aggressive nonoperative therapy can be as successful as operative management for properly chosen patients, and additionally it does not have the inherent risk of wound infection and iatrogenic injury.

The potential for complications begins as early as or perhaps even before patient positioning on the operating table. Care must be taken to ensure that the airway is protected when the patient is transferred from a bed to the operating table, especially if the patient is also being turned from a supine to a prone position. In the prone position, the face must be padded evenly to avoid pressure ulceration. Prefabricated foam pads with holes for airway access are available and effective. Support devices with mirrored bases allow visual inspection of the facial structures throughout the operation. Direct pressure on the eye must be specically avoided to prevent catastrophic retinal artery occlusion and loss of vision.55, 83 Direct pressure applied to the scalp has been associated with alopecia, which is usually reversible but is occasionally permanent. Slight rotation of the patients head throughout the procedure, if not clinically contraindicated, helps prevent such complications. Meticulous padding of vulnerable areas, such as the elbows and knees, should help prevent neurapraxia or more serious nerve injuries to the ulnar and common peroneal nerves. The lateral femoral cutaneous nerves are easily injured by undue pressure at the proximal aspect of the thighs. The brachial plexus is at risk if the lateral decubitus or prone position is used. An axillary roll placed 5 to 10 cm distal to the axilla and avoidance of excessive abduction and forward exion of the arm will help reduce the incidence of brachial plexopathy. Venous return must be considered during patient

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positioning as well. The abdomen and chest should remain free of pressure to prevent vena cava obstruction. Low venous return can lead to loss of cardiac preload and subsequent hypotension. Obstruction of caval ow can produce increased venous pressure around the sinusoids of the spine and thereby cause unnecessary and often signicant increases in blood loss. The knee-chest position has been associated with reports of lower extremity compartment syndrome requiring fasciotomy.3 In the dependent position with the hips and knees exed, venous pooling occurs. Awareness of this potential postoperative complication is required for quick recognition should it occur.

Postoperative Deformity
Fixation failure, loss of reduction, and subsequent deformity are complications of spinal surgery for trauma. Flat back syndrome is due to loss of the normal lumbar lordosis. It is frequently the result of distraction instrumentation that ends caudally below L3 (Fig. 344). Although

solid arthrodesis may be achieved, the at back deformity can be problematic.19, 48 Muscular strain and chronic pain are often reported as patients attempt to maintain their lordosis. Additionally, compensatory hyperlordosis above and below the fusion levels often causes degenerative spondylosis and stenosis. Avoidance of overdistraction and the use of appropriately contoured segmental xation help prevent this complication. Flattening the lumbar lordosis facilitates decompression procedures by increasing the interlaminar distance, but if fusion is contemplated, lumbar lordosis must be maintained. Lumbar lordosis is increased by extension of the hips and decreased by hip exion, as occurs when patients are placed in the kneechest position or positioned on a four-post frame. Although hyperlordosis is much less common, it can lead to complications as well. Iatrogenic foraminal stenosis and nerve root impingement can occur secondary to excessive lordosis.71 The best treatment of iatrogenic deformity is avoidance, but if diagnosed early, it can be treated by realignment. Delay in diagnosis or treatment ultimately results in a more extensive procedure. Additionally, a patient who complains of pain in the presence of late iatrogenic deformity

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FIGURE 344. Post-traumatic at back deformity. This patient sustained an L3 burst fracture 11 years ago. Progressive bilateral lower extremity weakness, right leg pain, and early fatigue prompted the current medical evaluation. Standing radiographs show signicant sagittal imbalance and loss of lumbar lordosis (A). Treatment included anterior discectomy and interbody fusion, followed by removal of previous instrumentation, pedicle subtraction osteotomy, and instrumented fusion (B). Pedicle subtraction osteotomy is facilitated by the use of a hinged four-post frame (C), which allows gentle and gradual reduction of the osteotomy site (D). The inset shows the extent of bone resection for a pedicle subtraction osteotomy, which produces approximately 30 to 35 of correction.

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can be a diagnostic problem because it may be difcult to know whether it is the malalignment that is responsible for the patients symptoms.

have been performed to maximize fusion rates and avoid screw notching.

Late Deformity Instrumentation Failure

Loss of stabilization may result from error in surgical technique, improper preoperative planning, or poor implant selection. Systems using rods and hooks may fail from hook pull-out, hook-rod disengagement, or rod fracture. Hook pull-out may be due to improper placement or osseous fracture. Lamina fracture may be associated with aggressive laminotomy, osteoporotic bone, or overdistraction (Fig. 345). Hook dislodgment is the most commonly reported complication of posterior Harrington rod instrumentation after spinal trauma.7, 13, 25, 28, 31 Edwards and colleagues24 noted four factors that account for hook dislodgment: rigidity of xation, the anatomic level, hook design, and rod clearance. The rate of hook dislodgment depends on the spinal level, with the rate varying from 5% at L4 to 20% at S1.31, 76 In older, semirigid Harrington models, rod clearance greater than 1 cm was needed to prevent rod-hook disengagement during exion and rotation. The advent of segmental multihook xation has decreased the incidence of hook failure. However, care must be taken to fully tighten the hooks on the rod to prevent motion at this interface. The advent of pedicle screw xation has expanded the armamentarium of the spine surgeon for treating trauma. Though largely avoidable, the potential complications associated with pedicle screw use can be signicant. A short screw or a screw placed laterally has suboptimal xation, whereas a medially placed screw may violate the canal and cause a dural tear or neurologic injury. A screw that is excessively long may violate the anterior aspect of the vertebral body and can cause potentially life-threatening perforation of the great vessels (Fig. 346). Pedicle screws can fracture the pedicle on insertion and can potentially loosen, break, or pull out. Although a largerdiameter screw has greater biomechanical pull-out strength, judgment is needed to avoid pedicle blowout.82, 88 In a large series of 4790 pedicle screws in 875 patients, Lonstein and co-workers52 showed that in experienced hands, the rate of complications is quite low. In their series, reoperation was necessary for 11 screws (0.2%) because of nerve root irritation, and 25 (0.5%) screws were fractured at follow-up. More unusual complications of pedicle screw xation have been reported as well. Some surgeons insert markers or Kirschner wires into the pedicle holes to check position with a radiograph or image intensier before screw placement. At least one case of fatal cardiac tamponade from myocardial violation with a Kirschner wire has been reported. Fluoroscopy was used to conrm the position of the wire, and no evidence of complications was noted during the procedure itself.38 For many years, some surgeons have used translaminar or facet screws to facilitate fusion.45, 53 Although violation of the canal or nerve root is possible, the reported rate of complications is low. The screws should be placed only after decortication and cancellous packing of the facets Late and progressive deformity and chronic pain as a result of spinal trauma can lead to signicant disability. Although these sequelae can occur despite proper management, each injury pattern and each patient must be considered individually to minimize complications. Patient age, lifestyle, and preexisting deformity may all play a role, but the initial stability of the injury and its initial management are probably paramount in predicting future decompensation and deformity.54 The thoracolumbar junction is the most common site for acute fractures and the development of late posttraumatic deformity. The abrupt change between the more mobile lumbar spine and the more rigid thoracic spine with its stabilizing ribs and sternum places the thoracolumbar junction at high risk for decompensation. However, no area of the spine is immune to deformity, and decompensation is not limited to the sagittal plane; a complex threedimensional deformity may be located anywhere from the occiput to the sacrum. The most important aspect of managing spinal deformity is prevention, and to avert the development of such deformity, the initial injury must be well understood. Osseous destruction is only part of the equation; ligamentous injury and disc disruption must be evaluated as well. Andreychik and associates2 attributed an increase in postoperative kyphosis without an increase in vertebral body compression to structural failure of adjacent disc spaces resulting from the initial injury. Because fractures extending into the disc space may not be appreciated on routine supine radiographs, physiologic loading may be required to fully assess stability. Missed posterior ligamentous injury can cause subsequent progressive deformity. Burst fractures, for example, typically settle less than 10 before the kyphotic deformity is checkreined by the posterior ligamentous structures. However, if these structures are disrupted, severe deformity can ensue. Most clinicians agree that the goal of treatment is to restore normal alignment to an unstable spine for a period sufcient to allow healing through either spontaneous bony healing or surgical arthrodesis. Bedrest, casting, and bracing have all proved effective in the treatment of spine fractures in the proper injury and proper patient groups. If the injury, the patients compliance, and the potential for healing permit the use of nonoperative management, close follow-up is critical. Clinical evaluation and serial standing radiographs should be carried out early should a deformity begin to develop. The deleterious effects of laminectomy alone for neural decompression in the presence of spinal trauma are well documented (Fig. 347). Complete spondyloptosis and severe deformity have been reported.79 Malcolm and co-workers54 reported on 48 patients with post-traumatic kyphosis. Half of these patients had an isolated laminectomy at the time of injury, and detrimental effects were seen at all levels of the spine. In the thoracic spine, the kyphotic deformity was 15 greater in the group that underwent

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FIGURE 345. Hook failure. This patient has signicant osteoporosis contributing to fractures of the lamina at the site of the proximal (T10) hooks as shown on a lateral radiograph (A) and computed tomographic scan (B). Treatment included proximal extension of the fusion with pedicle screw instrumentation (C).

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FIGURE 346. Pedicle screw malposition. Pedicle screws that are too long may penetrate the anterior cortex of the vertebral body and place the great vessels at risk, as seen on this computed tomographic scan.

decompression with laminectomy. At the thoracolumbar junction, the deformity was 13 more severe, and in the lumbar spine, the difference in kyphosis was 35 for those who had undergone laminectomy and 24 for those who did not. Technical errors can precipitate deformity even in the face of posterior instrumentation. A fusion that is too short and does not span the zone of injury is more likely to lead to a junctional deformity, especially if the arthrodesis ends at the cervicothoracic or thoracolumbar junction or at the apex of the thoracic kyphosis (Fig. 348). Additionally, a short fusion that spans the defect but is placed posterior to destroyed anterior elements is more likely to fail unless the anterior column is restored (Fig. 349). Parker and others have developed and validated a classication scheme to help determine when an anterior strut graft is required to supplement a short posterior construct for thoracolumbar fractures.60 Clinical Features of Late Deformity. Symptoms attributable to deformity may be insidious in onset and may follow a painless period of indeterminate length. As many as 70% to 90% of patients experience some chronic pain at the region of the fracture regardless of the type of treatment or the degree of deformity.18, 43, 59, 86 As many as 20% may be permanently disabled, and 40% report functional limitations. Debilitating pain is often the initial symptom and is the most common cause of reconstructive surgery for post-traumatic deformity. Though challenging, the clinician must try to isolate the cause of the patients symptoms. Instability or nonunion is more amenable to surgical intervention than is mechanical back pain. Mechanical back pain in this setting is an activity-related pain that may be muscular, discogenic, or arthritic in nature. Alternatively, it may be due to stress fractures of adjacent vertebrae secondary to excessive loads caused by the deformity. No consensus has been reached on the specic severity

of kyphosis that leads to pain and symptoms. Farcy and co-workers26 showed that at the thoracolumbar junction, a threshold of 25 is tolerated before symptoms are likely to occur. The lumbar spine tolerated only 15 of deformity. However, Andreychik and co-workers2 did not nd any correlation between symptoms and the degree of deformity in their series of 55 burst fractures of the lumbar spine. Most authors, however, agree that more sedentary patients tolerate a greater degree of deformity than do active laborers or athletes, which is not surprising when one considers the muscular work involved in maintaining posture in the presence of deformity. In a paraplegic patient, poor sitting balance because of progression of deformity may be of more concern than pain. Altered sitting balance can lead to soft tissue complications at the gibbus and in the buttock region. It can also impair the ability to power a wheelchair with the upper part of the body and arms. Additionally, subtle deformity may rapidly overcome the ability of weakened paraspinal muscles in patients with higher neurologic compromise. Finally, some patients may be seen primarily with a progressive neurologic decit. Malcolm and coauthors reported that approximately 27% of patients had a progressive neurologic decit.54 The neurologic decit is a function of the degree of deformity and the amount of canal compromise secondary to retropulsed bone within the canal. Fidler27 showed that typically bone fragments in the canal are resorbed over time but that severe angular deformity and abnormal transmission of stress may alter this remodeling process. Additionally, hypertrophic remodeling from segmental instability and perhaps the development of a post-traumatic syrinx can increase the stenosis of a given level. The deformity of the spine may be quite complex and must be appreciated in three dimensions. Full-length standing (or sitting) radiographs should be obtained. In addition, bending lms can be used to assess exibility. If pseudarthrosis is suspected, exion and extension views may assist in the diagnosis of segmental instability. If the levels adjacent to the deformity are not exible enough to compensate for kyphosis, a crouched gait may develop and lead to exion contractures of the hips. These exion deformities of the lower extremities should be addressed before correction of the spinal deformity. Classication of Late Deformity. In 1993, Denis and Burkus proposed three types of post-traumatic deformity.19 Each type includes three subtypes. This classication helps in planning the surgical approach and instrumentation, but it does not distinguish deformities on the basis of their relative magnitudes (Table 341). Surgical Management of Late Deformity. Surgical indications for correction of deformity include incapacitating pain, progressive deformity, new or progressive neurologic decit, or failure of a signicant neurologic decit to improve in the face of residual deformity and neural compression. Because the risks of extensive surgical interventions are signicant, one should consider cosmetic deformity alone a relative indication for surgical intervention. For Denis and Burkus type IA deformities of less than 15 that meet the criteria for surgical intervention, posterior spinal fusion is indicated. If the overall sagittal balance of the spine is acceptable and the patients symptoms are

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FIGURE 347. Postlaminectomy cervical kyphosis. A, This patient sustained posterior element fractures of the lower cervical spine and had an incomplete spinal cord injury. Advanced imaging studies showed canal compromise from the posterior element fractures. He was treated with laminectomy of C5 and C6 and halo immobilization. B, C, Serial radiographs showed gradual loss of reduction, with the development of kyphosis. The patient was eventually treated with corpectomy and fusion.

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FIGURE 348. Junctional kyphosis after an L2 burst fracture treated with anterior L1L3 instrumented fusion. Kyphosis developed at the thoracolumbar junction from an osteoporotic compression fracture adjacent to the fused segment.

located at the apex of the deformity, a short fusion with instrumentation will probably sufce, especially if pseudarthrosis or limited segmental instability is the source of the pain. As the magnitude of the deformity increases, an anterior procedure preceding the posterior fusion assists in correction of the deformity. However, Edwards and Rhyne23 demonstrated that late correction of up to 30 of kyphosis is feasible through a posterior approach in the absence of an anterior bony bridge. These authors apply three-point loading through posterior constructs to cause viscoelastic relaxation of the anterior scar and ligaments. An osseous bridge anteriorly would require a limited anterior release before correction posteriorly. In the thoracic spine, assuming that infection has been eliminated from the differential diagnosis, a posterior compression construct will usually be adequate to repair a pseudarthrosis. In the presence of neurologic compromise (type IC), it may be possible to decompress the neural elements by correcting the deformity from a posterior approach if the deformity and compression are mild. This approach requires a longer construct with multiple attachment sites. However, compression from larger deformities or retropulsed bone in the canal mandates anterior decompression before a posterior approach. Regardless of the approach, the goal is restoration of 40 or less of kyphosis from T2 through T12, which may necessitate the use of a longer posterior construct in patients with type IB deformities. If correction of kyphosis cannot be fully achieved through combined anterior and posterior approaches, wedge-type osteotomies, such as an eggshell or pedicle subtraction osteotomy, may be performed (typically in the lumbar spine below the level of the conus medullaris). Ending a fusion at a level of disc disease or instability should be avoided during the selection of fusion levels. The thoracolumbar junction deserves special attention. Small deformities (e.g., less than 20) with no

neurologic decit (type IIA) can be treated with a short posterior construct that preserves lumbar motion segments. In type IIB deformities with associated hyperkyphosis of the thoracic spine, the construct must be extended and may require either a limited anterior release for a exible deformity or a more extensive release if the upper thoracic deformity is xed. Type IIC deformities with neurologic decit and canal compromise of more than 25% require anterior decompression. Occasionally, shortsegment decompression with a strut graft and anterior instrumentation may obviate the need for a posterior construct, but any residual posterior instability or the absence of a stable anterior reconstruction would mandate a staged procedure. The use of an anterior strut, however, may allow one to preserve lower lumbar motion segments. McBride and Bradford58 reported on their series of six patients with a mean thoracolumbar junctional kyphosis of 38 and a range of 20 to 83. Five of the six had a neurologic decit, and all had canal encroachment of 25% to 57%. All patients were treated by transthoracic vertebrectomy and an allograft strut augmented with a vascularized pedicle 10th rib graft. The mean correction was 26, or 68%. All neurologically incomplete patients improved, and although one patient required revision for graft displacement, no pseudarthroses were reported. The authors note that such treatment requires a competent posterior osteoligamentous complex or the addition of either solid anterior instrumentation or a staged posterior construct. In the lumbar spine, true kyphosis is rarely seen. Rather, kyphosis typically refers to the loss of lordosis, also called at back deformity or hypolordosis. The rst report of osteotomy of the spine for kyphosis was made by Smith-Petersen and colleagues.71 Distraction and deformity of neural and vascular structures and subsequent complications led to investigation of alternative corrective procedures. The method preferred today is an eggshell osteotomy, also called a pedicle subtraction osteotomy. This technique shortens rather than lengthens the vertebral column.49, 73, 75 This osteotomy involves transpedicular xation above and below the level to be osteotomized, usually at the apex of the deformity, and correction of the deformity through removal of cancellous bone from the vertebral body. Asymmetric decancellation can correct both coronal and sagittal deformities. Up to 50 of sagittal correction and 40 of coronal correction can be achieved. The osteotomy is started only after instrumentation is completed because the blood loss from the procedure can be severe and may necessitate expeditious closure of the bony osteotomy site. The osteotomy is closed by extension bending at the decancellation site, which is accomplished by extending the table. Reduction can be facilitated by positioning the patient on a hinged frame so that the table can be extended to help close the osteotomy (see Fig. 344). Adjacent nerve roots above and below the osteotomy then share a common foramen created by removal of the pedicle. Meticulous care must be used to avoid entrapment of nerve roots or dura. This procedure should be effective for most type III deformities.62 In the cervical spine, Vaccaro and colleagues74 showed that long anterior reconstructions with static plates have an

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FIGURE 349. Failure of the anterior column. A, This patient suffered a C6C7 fracture-dislocation resulting in damage to the superior end-plate of C7. B, Reduction was readily accomplished with traction. C, An attempt at posterior fusion with instrumentation and halo immobilization was inadequate because of a lack of anterior column support. D, Subsequent treatment with anterior C6 corpectomy and instrumented fusion restored proper alignment and resulted in solid fusion.

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unacceptably high failure rate. In a retrospective, multicenter study examining the use of an anterior cervical locking plate and strut graft for a three-level corpectomy, the failure rate was 50% when a posterior construct was not used, as opposed to a 9% rate of graft or plate dislodgment when a two-level corpectomy was fused in a similar fashion. A higher incidence of graft failure was seen with increased age, failure to lock the screws into the plate, and the use of a peg-in-hole bone graft construct. The type of postoperative immobilization and violation of endplates with screws had no statistically signicant effect on failure rates. However, no comparison was made between traumatic and nontraumatic etiologies, and therefore it is unclear whether subclinical posterior ligamentous injury may increase the risk of failure. McAfee and Bohlman57 reviewed the results of 15 patients with multiple-level cervical corpectomies and an

TABLE 341

Classication of Late Deformity

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Neurologic Decit No No Yes No No Yes No No Yes Distant Kyphotic Deformity No Yes Yes No Yes Yes No Yes Yes

Type IA IB IC IIA IIB IIC IIIA IIIB IIIC

Level Cephalad to T11 Cephalad to T11 Cephalad to T11 T12L1 T12L1 T12L1 L2L4 L2L4 L2L4

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Source: Denis, F.; Burkus, J.K. Semin Spine Surg 5:187198, 1993.

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anterior-posterior cervical fusion with instrumentation. No patient in their series had dislodgment of either the instrumentation or graft material. It seems logical that a posterior tension band construct would help decrease the bending moment experienced by the anterior plate and strut graft, but further study into such biomechanics is still needed before recommendations regarding the best construct can be made.

Adjacent-Segment Disease
Adjacent-segment disease should be a concern for all surgeons who perform spinal fusions. Many reports have highlighted the accelerated degeneration that occurs above and below the level of a rigid fusion.42, 47 Additionally, it seems that instrumented fusions are even more prone to this phenomenon than are fusions without instrumentation. The etiology of this disease is still somewhat unclear, but it may be due to direct impingement of instrumentation on the facet joints. Some believe that denervation of the surrounding tissues, especially the facet capsule if injured, leads to neuropathic destruction of the facet. One can minimize this degeneration by protection of the facet capsule in joints outside the region of the fusion and by

attempting to never terminate a fusion in a region of stenosis, spondylolisthesis, posterior column deciency, or an abnormal disc. This type of preoperative planning, however, is less feasible in the setting of trauma than in the setting of elective fusion for degenerative disease. Extending a fusion to a normal level may decrease the incidence of one complication in exchange for a further decrease in mobility of the spine. Several studies have reported stress fractures of the pelvis in patients with long lumbosacral fusions.36, 84 This phenomenon is most likely to occur in older osteoporotic women. The fracture typically occurs on the side from which bone graft is harvested and is probably due to a stress riser created in the ilium at graft acquisition (Fig. 3410). Symptoms of stress fractures are usually seen in the rst few months after surgery, and protected weight bearing is generally adequate for resolution of the symptoms.

Pseudarthrosis
Pseudarthrosis is a complication of both instrumented and noninstrumented fusions and refers to failure of arthrodesis after an attempt at bony fusion. Rates of

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FIGURE 3410. Pelvic fracture during iliac crest bone graft harvesting. In the setting of osteoporosis, aggressive bone graft harvesting may lead to fracture of the ilium. A, This 72-year-old woman with rheumatoid arthritis underwent bone graft harvest from the iliac crest. B, Pain developed in her hip area. Radiographs revealed a fracture at the bone graft site (C) with subsequent pelvic instability.

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pseudarthrosis after posterior spinal fusion vary widely in the literature, from as low as 0% to as high as 30%.4, 77 The major sequela of pseudarthrosis is pain, but the diagnosis of pseudarthrosis can be challenging in a patient with pain after fusion. Instrumentation often obscures radiographic evaluation, and back pain may be a mechanical phenomenon in a patient with a solid fusion. Implant failure is a strong indicator of fusion failure, and radiolucency about the xation (e.g., pedicle screws) can support this diagnosis as well. Most orthopaedic surgeons agree that a change of more than 5 at a single functional spinal unit on exion-extension radiographs is worrisome for pseudarthrosis. The rate of pseudarthrosis increases with the number of levels being fused.12 Additionally, advanced age, malnutrition, obesity, and the use of nonsteroidal anti-inammatory medications have been associated with decreased rates of fusion. Brown and associates9 showed that tobacco smoking decreases rates of fusion. In a comparison of patients undergoing lumbar laminectomy and fusion, pseudarthrosis developed in 40% of smokers, whereas nonunion developed in only 8% of nonsmokers. Recently, Glassman and colleagues showed that if patients stop smoking for at least 6 months after lumbar fusion surgery, the rate of nonunion is comparable to that of nonsmokers.33 For smokers who did not stop smoking, the nonunion rate was 26.5%, whereas nonsmokers had a nonunion rate of 14.2%.33 Similarly, Rogozinski and co-workers66 looked at fusion rates in nonsmokers, preoperative smokers, and postoperative smokers. Although the fusion rate in the postoperative smoker group was less than 60%, the study indicated that nonsmokers and preoperative smokers had nearly the same rate of fusion. The negative impact of tobacco smoking on spinal arthrodesis has also been shown in the cervical spine.39 In the setting of trauma, it is impossible to ask patients to stop smoking before surgery, but cessation of smoking after arthrodesis seems to confer a benet. Autograft in some studies has also been shown to be superior to allograft as fusion material.1 However, although autograft is generally incorporated more quickly, the rate of successful fusion is no different with the use of allograft in single-level anterior fusions in the cervical spine.87 The incidence of pseudarthrosis in the setting of trauma seems to be lower than that in the setting of degenerative disease or deformity. In 1979, Bohlman8 reported on a large series of cervical spine fractures treated operatively without a single pseudarthrosis. Flesch and associates28 reported only 1 nonunion in 40 patients with thoracolumbar spine fractures treated with Harrington instrumentation and fusion. Edwards and Levine22 reported a 2% pseudarthrosis rate in 200 injuries of the thoracolumbar spine; the rate was almost four times higher at the lumbosacral junction. They noted that many of these pseudarthroses were due to technical error. Fusion rates can be enhanced with meticulous decortication of the transverse processes while trying to avoid fracture of these processes. Copious application of autograft and placement of graft beneath the posterior implants are recommended. Many spine surgeons favor the use of a gouge over the use of a bur for decortication because of the belief that thermal necrosis of bone occurs with bur decortication.

VASCULAR AND SOFT TISSUE COMPLICATIONS Cervical Spine

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Injuries to the vascular and soft tissues in the cervical spine usually occur during operative treatment of an injury. However, injuries to these structures as a direct result of trauma can occur as well. The common carotid artery and the contents of the carotid sheath are at risk during anterior exposure of the cervical spine. Blunt nger dissection and repeated, but gentle, palpation of the carotid artery to assess its location help decrease the likelihood of injury. Likewise, palpation of the nasogastric tube can identify the location of the esophagus. Mobilization of the longus colli muscles off the anterolateral vertebral bodies before placement of deep retractors also helps minimize vessel damage. Checking the temporal artery pulse of the patient during the procedure helps to assess whether excessive retraction is causing occlusion of the carotid artery. Carotid artery laceration, division, and thrombosis have been reported during anterior spinal fusion.40 Some approaches to the cervical spine risk injury to either the internal or external jugular vein. Although in most circumstances these vessels can be ligated unilaterally with little clinical consequence, venous injury can lead to air embolism, which may cause pulmonary compromise, blindness, or death. The vertebral artery is at risk from both anterior and posterior approaches to the cervical spine, especially in C1C2 transarticular arthrodesis. In a review by Golnos and colleagues35 of 1215 cases, these injuries occurred in 1 case from retraction of soft tissues, in 1 case during screw tapping, and in 2 cases from lateral decompression. Most authors agree that the vertebral artery should not be repaired, but rather packed with thrombin-soaked absorbable gelatin sponges to achieve hemostasis through tamponade. When transarticular screw xation is used, the contralateral side should not be instrumented if vertebral artery injury is suspected. In the rare case in which ligation is required for hemostasis, intraoperative angiography may be performed to assess the ability of the patient to tolerate such a procedure. However, in these cases, such studies are probably impractical, and furthermore, some evidence indicates that sacrice of one vertebral artery will not lead to permanent neurologic sequelae in most patients.68 The ability of a patient to tolerate unilateral vertebral artery ablation is supported by a study of nine patients with traumatic occlusion of the vessel. In two of the nine, neurologic sequelae developed, but the ndings were transient. However, Smith and associates70 reported that in three of seven cases of vertebral artery ligation, symptomatic vertebrobasilar symptoms such as syncope, nystagmus, dizziness, and Wallenbergs syndrome developed. They supported repair of an injured vertebral artery whenever possible. As the use of lateral mass screw xation expands, the number of vertebral artery injuries may increase. This complication from the placement of screws into the transverse foramen is best prevented by a knowledge of anatomy and bony landmarks.

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Esophageal perforation after anterior spinal trauma or surgery is uncommon, but well recognized. The largest series of esophageal perforations to date was reported by Gaudinez and coauthors30 from The Rocky Mountain Regional Spinal Injury Center. Over a 25-year period, 44 patients with esophageal perforation were treated at that institution. Although most pharyngoesophageal perforations occur in the early postoperative period, delayed perforations in patients who had fully convalesced from the acute postoperative period have been reported.44 The most frequently occurring symptoms are neck and throat pain, odynophagia, dysphagia, hoarseness, and aspiration. In the series by Gaudinez and colleagues,30 cervical osteomyelitis or cervical abscess developed in half the patients. Clinical ndings may include fever, cervical tenderness and induration, weight loss, tachycardia, crepitus from emphysema, and hematemesis. Though far less common, expectoration of necrotic bone has been reported as well. A high index of suspicion is required because diagnostic imaging often yields negative results. In addition, they showed that 22.7% of patients had false-negative results from imaging studies. Endoscopy was 63.6% sensitive for denitive diagnosis in the 40 patients who underwent the procedure.30 Though not specically mentioned in the aforementioned series, a combination of direct visualization and a swallow study is regarded by most to have the highest diagnostic yield. Management of esophageal perforation is variable. Conservative management includes observation, intravenous nutrition, a feeding tube or gastrostomy, appropriate antibiotic coverage, and aspiration precautions. These techniques may be effective for small, uncomplicated perforations. However, the literature suggests high morbidity and mortality with nonsurgical management of all but the smallest of perforations, especially with tears of the lower part of the esophagus. Consultation with a thoracic or esophageal surgical specialist is recommended in all cases. Prompt recognition of symptoms and pathology is paramount because a delay in diagnosis can lead to death. The esophagus should be examined carefully after any anterior cervical spinal operation, and any esophageal injury noted in the operative suite should be aggressively addressed with repair by an experienced surgeon. The repair can be augmented, when necessary, with a muscle ap, such as a proximally based medial pectoralis major rotational ap.

Thoracolumbar Spine
Anterior thoracolumbar surgery has a multitude of potential complications, including pneumothorax, hemothorax, and chylothorax. Massive hemothorax may occur from profuse vertebral body bleeding and can cause hemodynamic instability. It may require surgical tamponade of venous sinuses in the vertebral body with bone wax or ligation of bleeding segmental arteries.60 Hemorrhage from a thoracic fracture causing persistent hemothorax has been reported in a patient with a complete neurologic injury induced by the fracture.17 After more than 7 days of recurrent hemothorax, the patient underwent operative reduction and stabilization of the fracture, which led to the

cessation of bleeding. This scenario denes an additional indication for early xation of a high-energy thoracic vertebral fracture in patients with complete neurologic compromise. The presence of a thoracic fracture should also alert the physician to the possibility of thoracic duct injury. The incidence of chylothorax in association with rib and thoracic fractures is increasing because of escalating numbers of vehicular accidents and nonpenetrating trauma. At least 13 patients with chylothorax secondary to thoracic fractures have been reported, and at least 2 of them died of the sequelae of the chylothorax itself, 1 from tension chylothorax.85 Although most cases of traumatic chylothorax can be managed nonoperatively, the need for surgical intervention in the subset of patients with associated thoracic fractures is higher and approaches 50%. Delayed appearance of a patient with chylothorax is a result of the formation of a mediastinal chyloma, which then ruptures into a pleural cavity, usually 7 to 10 days after the injury. Once suspected, diagnostic thoracentesis and tube thoracostomy should be undertaken. Oral intake should be discontinued because even low-fat, clear liquids markedly increase chyle ow.34 Traditionally, continued chylous chest drainage despite 6 weeks of nonoperative therapy is an indication for surgical intervention. However, more recently, some authors have become more aggressive in preventing ongoing protein and lymphocyte losses and thereby minimizing the risk of infection. Some authors now recommend surgery if nonoperative management is unsuccessful after 2 weeks.69 Most agree that a more aggressive approach is preferred in a patient with concomitant spinal fractures because of the high immunologic and nutritional cost of prolonged chest tube drainage.69 Rare reports of iatrogenic chyle leaks after anterior thoracolumbar surgery have appeared. Most, however, agree that microlymphatic disruption is inevitable, and it seems likely that clinically insignicant chyle leaks are undiagnosed and heal spontaneously. Diaphragmatic rupture or herniation may occur after thoracolumbar exposure or after the crus of the diaphragm is taken down and repaired to improve exposure at the thoracolumbar region. The ureters and great vessels are at risk during retroperitoneal dissection, especially in the revision setting. Consideration should be given to preoperative ureteral stenting in these revision procedures. Injury to the sympathetic plexus overlying the anterior aspect of the lower lumbar and upper sacral vertebrae may cause retrograde ejaculation. Traditionally, much attention has been paid to the segmental blood supply of the thoracic cord. Specically, the artery of Adamkiewicz is considered to be vital to cord perfusion. The transthoracic approach to the spine usually requires mobilization of the segmental vessels over a multitude of levels. Dwyer and Schafer,21 however, have shown that ligation of multiple ipsilateral segmental arteries can be performed without neurologic compromise. DiChiro and colleagues20 demonstrated in monkeys that even the arteria magna could be ligated without sequelae. However, if both this vessel and the anterior spinal artery were disrupted, paraplegia resulted. Much of the work and the case reports of neurologic compromise in the face of segmental artery disruption have been related to surgical

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treatment of deformity. The effect of deformity, especially if congenital, on the blood supply to the cord is unclear. In a polytrauma patient, cross-clamping of the aorta results in disruption of the segmental blood ow to the cord bilaterally, which may result in paralysis. Trauma to the cord and associated edema may make the spinal cord far more sensitive to the effects of mild ischemia. The anterior approach to the lumbar spine for the operative treatment of spinal trauma is usually performed through the retroperitoneal or, less commonly, the transperitoneal approach. If the pathologic condition does not dictate the side, most surgeons prefer the left because the aorta is more forgiving and easier to mobilize than the vena cava. The left common iliac vein is the vessel most at risk during left-sided retroperitoneal and transperitoneal exposures. Regardless of the approach, instrumentation should be placed on the lateral side of the vertebral body and not in contact with the great vessels. Vascular complications during posterior lumbar spine surgery are usually secondary to discectomy. Vascular injury during discectomy is most common at the L4L5 level. Freeman29 showed that the pituitary rongeur is the most frequent culprit. In the setting of trauma, one must be keenly aware of any disruption of the anterior longitudinal ligament. Incompetence of this ligament makes perforation of the great vessels more difcult to avoid. Unless acute hypotension occurs intraoperatively, these injures may initially go unnoticed. Late abdominal rigidity, abdominal pain, tachycardia, and anemia should alert the physician to this complication, which may be avoided by limiting the depth of insertion of the pituitary rongeur during discectomy. The lateral extracavitary approach to the thoracolumbar spine deserves special mention. This approach, which is used to replace a two-incision front-back procedure, allows ventral decompression and dorsal xation. The technique is technically demanding. Resnick and Benzel63 reported a 55% incidence of morbidity in a series of 33 patients with acute fractures. The most common complication was hemothorax or effusion requiring tube thoracostomy, followed by pneumonia, which occurred in seven patients. Other authors have noted pseudohernias caused by sacrice of the intercostal nerves. Although the morbidity associated with this procedure may be high, its risks should be weighed against the combined risk of a two-stage procedure.

Postoperative Infection
Postoperative infections may result from inoculation during the index procedure or from hematogenous seeding. The postoperative infection rate in the spine is 2% to 3%. Simple lumbar discectomy has less than a 1% infection rate, whereas combined fusion and instrumentation are associated with rates between 4% and 8%. Risk factors include increased age, obesity, diabetes, smoking, immunosuppression, duration of preoperative hospitalization, spinal dysraphism, myelodysplasia, revision surgery, operative time, and the use of instrumentation, bone graft, or methyl methacrylate.14, 15, 41, 50, 56, 67, 72, 81 The use of perioperative prophylaxis to prevent infec-

tion is widespread. Patients with instrumented fusions have a decreased infection rate with the use of prophylaxis when compared with those undergoing surgery without prophylaxis. Commonly, the antibiotic is administered before the incision and for 24 hours postoperatively, although some surgeons prefer to administer antibiotics until suction drains or catheters are removed. The choice of antibiotic is guided by consideration of multiple factors, including host immunocompetence, the bacterial ora common in the region, the type of procedure, cost, and the side effect prole. Most commonly, a cephalosporin is used. Because of increasing concern regarding the development of bacterial resistance, drugs such as vancomycin should be discouraged for prophylaxis and reserved only for patients at increased risk of methicillin-resistant staphylococcal infections. Such patients include those with lymphopenia, recent or current hospitalization, postoperative wound drainage, and alcohol abuse. Once the diagnosis of postoperative infection is made clinically, early surgical intervention is necessary because medical management is likely to fail. Debridement should proceed in a systematic fashion. Each layer is debrided and cultured before advancing deeper with the dissection. If gross deep drainage or purulence is encountered with subfascial aspiration, deep debridement is performed. Although solidly xed instrumentation is typically left in place in the early postoperative period, all other foreign bodies such as bone wax and Gelfoam must be removed. Any hematoma should be thoroughly evacuated. Many authors retain bone grafts, especially if they are adherent. Others recommend removal of loose grafts and washing before replacement. If the graft is grossly purulent or necrotic, it should be discarded and another bone grafting procedure performed at a later debridement when the local infection is controlled. Hemostasis must be meticulous to prevent re-formation of a hematoma seeded with bacteria. Dead space must be obliterated, and the use of a rotation ap should be considered for dead space management. Primary wound closure over drains, often with retention sutures to prevent dehiscence, is favored when possible. Depending on the amount of devitalized tissue, routine serial debridement is often required. Simple wound infections may be packed open and allowed to close by secondary intention. More complex wound infections may require musculocutaneous aps. Postoperatively, antibiotic therapy is required for at least 10 to 14 days for straightforward soft tissue wound infections. Six weeks of parenteral antibiotic treatment is preferred in cases of bone involvement, deep infection, or retained foreign bodies (e.g., metal or graft). In all cases, nutritional assessment and repletion are of paramount importance. Up to 35% of hospitalized patients have evidence of protein-calorie malnutrition. Weight loss of more than 10%, a serum transferrin level less than 1.5 g/L, anergy, a serum albumin concentration less than 3 g/dL, or a total lymphocyte count less than 1200 should raise suspicion of malnutrition. Protein-calorie malnutrition causes decreased cardiac output and peripheral oxygen tension as well as impaired pulmonary defenses, wound healing, and cell-mediated immune defenses. In addition to the treatment of malnutrition, its prevention must be considered in all hospitalized patients,

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SECTION II Spine

especially those with increased metabolic demands because of fever, trauma, or surgery.

longevity and quality of life of persons with spinal cord injury.

Metabolic Changes
As a result of inactivity and changes in body composition, most patients with chronic spinal cord injury undergo important metabolic changes. Glucose intolerance occurs more frequently in these patients than in the general population. Baumann and Spungen5, 6 performed a 75-g oral glucose tolerance test on 100 veterans (50 with paraplegia and 50 with quadriplegia) and 50 able-bodied veteran controls. In the spinal cordinjured group, 22% of the subjects were diabetic by criteria established by the World Health Organization as compared with 6% in the control group. Normal oral glucose tolerance was noted in 82% of the controls, 50% of the paraplegics, and 38% of the quadriplegics. Insulin levels were lower in controls, thus indicating insulin resistance in the spinal cordinjured patients. This hyperinsulinemia may well play a role in the increased concentration of triglycerides and the decreased concentration of high-density lipoprotein cholesterol in spinal cordinjured patients. All these changes, coupled with inactivity, play a role in the high incidence of atherosclerosis seen in this group. Spinal cord injury leads to unloading of the skeleton, and hypercalcemia and hypercalciuria ensue quickly. Restriction of dietary calcium does not treat the cause of the derangement, which is initially due to increased osteoclastic activity within the rst 3 to 5 days and later involves a lifetime of decreased osteoblastic activity. Osteoporosis may lead to insufciency or traumatic fractures, but these fractures may be markedly underdiagnosed and manifested as little more than swelling. Hypercalciuria may result in early nephrolithiasis and the recommendation that dietary calcium be forever avoided. However, such restriction often leads to deciency and worsening of osteoporosis later in life, after the acute period of marked bone loss subsides, usually within 14 months.64 Although their role still remains to be dened, bisphosphonates may be the best agent for management of this condition.5, 64 Some evidence supports the depression of endogenous anabolic hormones in spinal cordinjured patients. Decreased levels of serum testosterone, growth hormone, and insulin-like growth factor type I may exacerbate the body composition changes seen in these patients. In addition, exercise tolerance and strength may be decreased. Thyroid dysfunction is seen as well. Depressed levels of triiodothyronine (T3) and reverse T3 have been demonstrated, and this effect may also contribute to fatigue and an increase in adiposity. However, some believe that it is due to associated illness and metabolic derangement, and as such, the use of replacement therapy for this type of deciency in the presence of normal thyroid tissue is controversial. Although the medical management of each of these metabolic derangements is beyond the scope of this chapter, the orthopaedic surgeon must be cognizant that such medical issues exist and must use an appropriate team to minimize the late sequelae of these abnormalities. Amelioration of these abnormalities promises to improve the

Dural Tear
It is difcult, if not impossible, to know the true incidence of dural tears as a result of trauma. In patients with high-energy injuries and complete paraplegia of the thoracic spine, actual severance of the cord and dural sac is possible. Likewise, a gunshot wound to the spine may cause disruption of the dura. Iatrogenic dural tears also occur, especially during attempted posterolateral decompression. Cerebrospinal uid (CSF) leaks may lead to positional headache, wound complications, meningitis, arachnoiditis, and pseudomeningocele. The diagnosis of iatrogenic CSF leakage is fairly straightforward. Obvious egress of uid from a visible tear in the dura is diagnostic. As the thecal sac decompresses because of a leak, the local pressure about the epidural veins decreases, and an increase in venous bleeding from the epidural space may be the rst indication of a dural tear. Additionally, when the dural sac is decompressed, especially when reducing a kyphotic deformity, leakage may occur from a tear. Postoperatively, one must be alert for signs of clear drainage from the wound or the presence of a subcutaneous uid collection. Severe headache exacerbated by an upright posture may be noted. Large volumes of uid may be seen inasmuch as the choroid plexus produces over 20 mL of CSF hourly. If it is unclear whether the uid is CSF testing for 2-transferrin can be useful. A , pseudomeningocele may develop if a dural tear occurs and is not repaired in watertight fashion. It may occur days to months postoperatively. Dural tears may be classied as dorsal, lateral, or ventral. Although the best treatment is prevention, most tears can be repaired primarily if they do occur. However, massive defects may be irreparable. The rst step in repair is complete exposure of the dural rent. Magnication and adequate lighting are required. Dural elements must be returned to their intrathecal location and should not be incorporated into the repair inadvertently. The goal is a watertight repair that is free of tension. Usually, this objective can be accomplished with 60 polypropylene (Prolene) suture placed in a running locking stitch. The recommended location of the suture is 2 mm from the dural edge with 3 mm between sutures. A Valsalva maneuver may be simulated by the anesthesiologist after repair to assess for residual leak. If leakage occurs after repair, augmentation with additional suture, gelatin sponge, autogenous fat, or brin glue is required. More complex tears may require grafting with fascia lata or with commercially available dural patches. Meticulous watertight fascial closure is as important as the dural repair itself because the fascial barrier is relied on to prevent durocutaneous stulas. Most surgeons avoid the use of intramuscular drains in the presence of a dural tear because negative pressure may encourage a persistent leak. During a posterior approach, most posterior and lateral dural tears can be exposed directly. Below the level of the conus, an anterior tear may be approached through a posterior durotomy and gentle retraction of nerve roots to

Copyright 2003 Elsevier Science (USA). All rights reserved.

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allow access to the anterior aspect of the dural tube. However, anterior tears during posterior exposure at cord levels may need to be treated indirectly. Indirect repair is most commonly performed with brin glue, which is formed by mixing thrombin and cryoprecipitate that has been screened for human immunodeciency and hepatitis virus. It forms a biologic glue with biomechanical patchlike properties, and it can seal tears that cannot be fully exposed for repair or it can be used to augment tenuous repairs. Cooling the individual components before mixing may improve the biomechanical strength of the product.80 In addition to repair, diversion of CSF through a subarachnoid drain for 4 to 5 days may allow the dura, fascia, and surgical incision to heal.

SUMMARY

zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz The complications of spinal trauma are numerous and challenging. They may occur as a direct result of the injury, because of a lack of appreciation of the injury and subsequent improper treatment, or as a result of the inherent risk of the treatment itself. Successful treatment of these complications relies on prompt recognition. Complications that occur as a result of spinal trauma are often related to immobilization. Prolonged bedrest leads to deconditioning, poor pulmonary function, and decubitus ulcers. Vigilance must be paid to these mundane, but clinically important issues, and proper understanding of the injury pattern provides another avenue by which to avoid complications. Spinal stability must be scrutinized with an eye toward potential deformity. Whether external or internal immobilization is used, all fractures should be monitored closely so that loss of reduction can be discovered early and treated expeditiously. Inadequate xation techniques, neglecting to support the anterior column, and failing to restore normal alignment are the causes of most iatrogenic deformities. Meticulous attention to detail during all phases of treatment, combined with attentive medical care, will prevent most of the complications associated with spinal trauma.
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