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C H A P T E Rz z z z z z z z z z z z z z z z z z z z z z z z z z z34

Complications in the Treatmentof Spinal TraumaComplications in the Treatmentof 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 asthe Hippocratic era. His famous extension bench, knownas ‘‘Scamnum’’ when popularized by Celsius, was usedfrequently for realignment of a fractured or deformedspine. In ancient and medieval times, forceful and briskmaneuvers accompanied by immobilization were the main-stay of spinal trauma treatment. A patient would often lieprone while attendants would pull on his ankles and axillaeand a ‘‘physician’’ would sit or press on prominences suchas a gibbus or palpable fracture deformity.

As recently as the late 1800s, Jean-Francis Calot and hiscontemporaries manipulated spinal deformities with theirfists. In 1917, Hartmann (at the Accident Hospital for coalminers in Upper Silesia) treated a patient with a fracture-dislocation of the thoracolumbar junction by having twoassistants suspend the patient by the armpits and pelviswhile he performed reduction by forceful manipulationfrom below with his fists. Later, through the first 4 decadesof the 20th century, methods of postural reduction byhyperextension were introduced. Davis, Rogers, and Bohl-man were champions of such methods through the use ofslings, frames, or similar devices.37

As one might imagine, such treatment led to unaccept-ably high rates of complications, including soft tissuebreakdown, neurologic compromise, malunion, instability,and pulmonary compromise. Treatment of spinal traumahas changed significantly over the last 2 decades. How-ever, despite better imaging, better understanding, betteraccess to treatment, and the availability of internal fixation,challenging complications continue to exist today.

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Halo Vest Immobilization

Indications for use of the halo vest have evolved greatlysince its description by Perry and Nickel in 1953. Initially

described for postoperative immobilization of patientswho had undergone cervical fusion for neck paralysis frompoliomyelitis, Thompson and Freeman extended its use tothe treatment of fractures. Complications of halo vestimmobilization can be divided into those related toapplication of the device and those related to its use.Traditionally, the use of plaster-molded vests carried a riskof cast syndrome, pressure sores, and respiratory problemsin patients with limited respiratory reserves. Prefabricatedpadded plastic vests have helped decrease the incidence ofthese complications, but at the expense of decreasedrigidity and increased cost. However, patient compliancehas improved and the incidence of pin loosening hasdecreased with these lightweight prefabricated vests.

The pins themselves pose problems as well. Pin siteinfection is not uncommon but may be minimized withdaily pin site care, including twice-daily application of adilute hydrogen peroxide solution (50% in water). Thereported incidence of pin site infection is approximately30%.51 Oral antibiotics are usually effective, but if a pin isloose and infected, a new pin should be placed in a nearbyhole in the halo ring. If the pins are incorrectly placedcephalad to the equator of the skull, halo slippage mayoccur (Fig. 34–1). The pins should be torqued to 8 in-lb inadults and 6 in-lb or less in children. In patients withosteoporosis or when the pins are inadvertently placed inthe temporal areas, the skull can be perforated. Duralpenetration has been reported.46

No orthosis can apply predictable and continuoustraction to the cervical spine when the patient is notsupine. When the patient is sitting or standing, a previ-ously distracted cervical spine can become compressed bythe force of gravity on the head and halo vest construct(Fig. 34–2). Such compression can lead to loss of reductionand possibly a new neurologic deficit. Likewise, rotationalforces are poorly constrained by a halo vest orthosis.Treatment of a unilateral facet dislocation, for example,may lead to persistent root compression and failure oftherapy. Whitehill and colleagues78 described five cases ofloss of reduction in patients with facet dislocations immo-

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bilized in a halo vest. Glaser and associates32 and Bucholzand Cheung10 documented loss of reduction in 10% of allpatients and in 37% of patients with facet subluxation anddislocation.

Anderson and co-workers1 evaluated upright and su-pine lateral radiographs after halo immobilization in 42patients with 45 noncontiguous levels of cervical spineinjury. At noninjured levels, an average of 3.9° of angularchange was found between adjacent levels from the occiputto C6. The greatest motion occurred more proximally (8.0°between the occiput and C1). No significant translationwas seen at the noninjured levels. At the injured level,sagittal-plane angulation averaged 7.0° and the averagetranslation was 1.7 mm. Significant fracture site motionwas defined as greater than 3° of sagittal angulation ormore than 1 mm of translation and occurred in 78% of the45 injured levels. Three patients experienced loss ofreduction that required reapplication of traction after vestremoval. Asymptomatic malunion developed in 11 pa-tients. One may postulate that it is this motion thatcontributes to such a high degree of nonunion in type IIodontoid fractures treated in a halo vest.

Residual kyphosis of a post-traumatic cervical spine canlead to a multitude of complications. Neural impairmentcan occur from compression of the spinal cord as it drapesover the apex of the deformity (Fig. 34–3). Late neck painmay be seen as a result of the modified mechanics of theparaspinous musculature that occurs when the lever armof the muscles is altered by the deformity. Additionally,facet degeneration of adjacent segments can ensue fromhyperextension of adjacent vertebral levels in an attempt tocompensate for the loss of cervical lordosis in a kyphoticcervical spine.51

In properly chosen patients, halo immobilization is anexcellent treatment option that is associated with frequent,but usually minor complications. However, nonunion andmalunion can occur and should obviously be considered

FIGURE 34–1. Failed halo pin sites. At follow-up, the halo pins of thisgentleman had dislodged, and the vest and headpiece migrated proxi-mally. His halo was removed and he was treated in a cervical collar forthe remainder of treatment.

FIGURE 34–2. Poor axial immobiliza-tion by halo. Immobilization in theaxial plane is difficult with all externalfixation systems, including the halo.In this patient with a fracture througha severely ankylosed cervical spine,the fracture is gapped open whensupine (A) but compressed when up-right (B).

1013CHAPTER 34 • Complications in the Treatment of Spinal Trauma


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

Operative versusNonoperative Treatment

In the age of modern medicine and modern implants, mostclinicians intuitively believe that the risk of morbidity inpatients with unstable spine fractures is higher in thenonoperative than the operative group. In the perioperativeperiod, the risk of acute complications is no different.Rechtine and colleagues61 examined 235 patients withunstable thoracolumbar spine fractures who were given achoice of undergoing operative or nonoperative treatment.The groups were statistically similar in all respects. Al-though the length of stay in the hospital was 24 daysgreater in the nonoperative group, the incidence of compli-cations (with the obvious exception of wound infection)was similar for decubitus ulcers, pneumonia, deep veinthrombosis, pulmonary embolism, and death. Polytraumawas a risk factor for increased complications, and theprimary predictor of sacral decubitus ulcers was time on aspine board. Curry and Casady16 showed that a patientwith spinal cord injury who is on a board for more than8 hours is practically ensured of sacral skin breakdown.Admittedly, these studies have some inherent selection biasand are retrospective. However, it helps to show thataggressive nonoperative therapy can be as successful asoperative management for properly chosen patients, andadditionally it does not have the inherent risk of woundinfection and iatrogenic injury.

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Patient Positioning

The potential for complications begins as early as orperhaps even before patient positioning on the operatingtable. Care must be taken to ensure that the airway isprotected when the patient is transferred from a bed to theoperating table, especially if the patient is also being turnedfrom a supine to a prone position. In the prone position,the face must be padded evenly to avoid pressure ulcera-tion. Prefabricated foam pads with holes for airway accessare available and effective. Support devices with mirroredbases allow visual inspection of the facial structuresthroughout the operation. Direct pressure on the eye mustbe specifically avoided to prevent catastrophic retinal arteryocclusion and loss of vision.55, 83 Direct pressure applied tothe scalp has been associated with alopecia, which isusually reversible but is occasionally permanent. Slightrotation of the patient’s head throughout the procedure, ifnot clinically contraindicated, helps prevent such compli-cations.

Meticulous padding of vulnerable areas, such as theelbows and knees, should help prevent neurapraxia ormore serious nerve injuries to the ulnar and commonperoneal nerves. The lateral femoral cutaneous nerves areeasily injured by undue pressure at the proximal aspect ofthe thighs. The brachial plexus is at risk if the lateraldecubitus or prone position is used. An axillary roll placed5 to 10 cm distal to the axilla and avoidance of excessiveabduction and forward flexion of the arm will help reducethe incidence of brachial plexopathy.

Venous return must be considered during patient

FIGURE 34–3. Failed external immobilization for cervicalfacet fractures. This patient was evaluated 11⁄2 years afternonoperative treatment of an initially nondisplaced C6lateral mass fracture. He complained of neck pain andparesthesia down the lateral aspect of his arm. A, Flexionradiographs showed subluxation and kyphosis. B, Treat-ment included anterior cervical discectomy and fusion.Preoperative planning, however, included the possible needfor circumferential fusion.

1014 SECTION II • Spine


positioning as well. The abdomen and chest should remainfree of pressure to prevent vena cava obstruction. Lowvenous return can lead to loss of cardiac preload andsubsequent hypotension. Obstruction of caval flow canproduce increased venous pressure around the sinusoidsof the spine and thereby cause unnecessary and oftensignificant increases in blood loss. The knee-chest positionhas been associated with reports of lower extremitycompartment syndrome requiring fasciotomy.3 In thedependent position with the hips and knees flexed, venouspooling occurs. Awareness of this potential postoperativecomplication is required for quick recognition should itoccur.

Postoperative Deformity

Fixation failure, loss of reduction, and subsequent defor-mity are complications of spinal surgery for trauma. Flatback syndrome is due to loss of the normal lumbarlordosis. It is frequently the result of distraction instrumen-tation that ends caudally below L3 (Fig. 34–4). Although

solid arthrodesis may be achieved, the flat back deformitycan be problematic.19, 48 Muscular strain and chronic painare often reported as patients attempt to maintain theirlordosis. Additionally, compensatory hyperlordosis aboveand below the fusion levels often causes degenerativespondylosis and stenosis. Avoidance of overdistraction andthe use of appropriately contoured segmental fixation helpprevent this complication. Flattening the lumbar lordosisfacilitates decompression procedures by increasing theinterlaminar distance, but if fusion is contemplated, lum-bar lordosis must be maintained. Lumbar lordosis isincreased by extension of the hips and decreased by hipflexion, as occurs when patients are placed in the knee-chest position or positioned on a four-post frame. Althoughhyperlordosis is much less common, it can lead to compli-cations as well. Iatrogenic foraminal stenosis and nerve rootimpingement 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 moreextensive procedure. Additionally, a patient who com-plains of pain in the presence of late iatrogenic deformity

FIGURE 34–4. Post-traumatic flat 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 significant sagittal imbalance and loss of lumbarlordosis (A). Treatment included anterior discectomy and interbody fusion, followed by removal of previous instrumentation, pedicle subtractionosteotomy, and instrumented fusion (B). Pedicle subtraction osteotomy is facilitated by the use of a hinged four-post frame (C), which allows gentle andgradual reduction of the osteotomy site (D). The inset shows the extent of bone resection for a pedicle subtraction osteotomy, which producesapproximately 30° to 35° of correction.



can be a diagnostic problem because it may be difficult toknow whether it is the malalignment that is responsible forthe patient’s symptoms.

Instrumentation Failure

Loss of stabilization may result from error in surgicaltechnique, improper preoperative planning, or poor im-plant selection. Systems using rods and hooks may failfrom hook pull-out, hook-rod disengagement, or rodfracture. Hook pull-out may be due to improper placementor osseous fracture. Lamina fracture may be associated withaggressive laminotomy, osteoporotic bone, or overdistrac-tion (Fig. 34–5). Hook dislodgment is the most commonlyreported complication of posterior Harrington rod instru-mentation after spinal trauma.7, 13, 25, 28, 31 Edwards andcolleagues24 noted four factors that account for hookdislodgment: rigidity of fixation, the anatomic level, hookdesign, and rod clearance. The rate of hook dislodgmentdepends on the spinal level, with the rate varying from 5%at L4 to 20% at S1.31, 76 In older, semirigid Harringtonmodels, rod clearance greater than 1 cm was needed toprevent rod-hook disengagement during flexion and rota-tion. The advent of segmental multihook fixation hasdecreased the incidence of hook failure. However, caremust be taken to fully tighten the hooks on the rod toprevent motion at this interface.

The advent of pedicle screw fixation has expanded thearmamentarium of the spine surgeon for treating trauma.Though largely avoidable, the potential complicationsassociated with pedicle screw use can be significant. Ashort screw or a screw placed laterally has suboptimalfixation, whereas a medially placed screw may violatethe canal and cause a dural tear or neurologic injury. Ascrew that is excessively long may violate the anterioraspect of the vertebral body and can cause potentiallylife-threatening perforation of the great vessels (Fig. 34–6).Pedicle screws can fracture the pedicle on insertion and canpotentially loosen, break, or pull out. Although a larger-diameter screw has greater biomechanical pull-outstrength, judgment is needed to avoid pedicle blow-out.82, 88 In a large series of 4790 pedicle screws in 875patients, Lonstein and co-workers52 showed that in experi-enced hands, the rate of complications is quite low. In theirseries, reoperation was necessary for 11 screws (0.2%)because of nerve root irritation, and 25 (0.5%) screws werefractured at follow-up. More unusual complications ofpedicle screw fixation have been reported as well. Somesurgeons insert markers or Kirschner wires into the pedicleholes to check position with a radiograph or imageintensifier before screw placement. At least one case offatal cardiac tamponade from myocardial violation with aKirschner wire has been reported. Fluoroscopy was used toconfirm the position of the wire, and no evidence ofcomplications was noted during the procedure itself.38

For many years, some surgeons have used translaminaror facet screws to facilitate fusion.45, 53 Although violationof the canal or nerve root is possible, the reported rate ofcomplications is low. The screws should be placed onlyafter decortication and cancellous packing of the facets

have been performed to maximize fusion rates and avoidscrew notching.

Late Deformity

Late and progressive deformity and chronic pain as a resultof spinal trauma can lead to significant disability. Althoughthese sequelae can occur despite proper management, eachinjury pattern and each patient must be considered indi-vidually to minimize complications. Patient age, lifestyle,and preexisting deformity may all play a role, but the initialstability of the injury and its initial management areprobably paramount in predicting future decompensationand deformity.54

The thoracolumbar junction is the most common sitefor acute fractures and the development of late post-traumatic deformity. The abrupt change between the moremobile lumbar spine and the more rigid thoracic spinewith its stabilizing ribs and sternum places the thoracolum-bar junction at high risk for decompensation. However, noarea of the spine is immune to deformity, and decompensa-tion is not limited to the sagittal plane; a complex three-dimensional deformity may be located anywhere from theocciput to the sacrum.

The most important aspect of managing spinal defor-mity is prevention, and to avert the development of suchdeformity, the initial injury must be well understood.Osseous destruction is only part of the equation; ligamen-tous injury and disc disruption must be evaluated as well.Andreychik and associates2 attributed an increase in post-operative kyphosis without an increase in vertebral bodycompression to structural failure of adjacent disc spacesresulting from the initial injury. Because fractures extend-ing into the disc space may not be appreciated on routinesupine radiographs, physiologic loading may be requiredto fully assess stability. Missed posterior ligamentous injurycan cause subsequent progressive deformity. Burst frac-tures, for example, typically settle less than 10° before thekyphotic deformity is checkreined by the posterior liga-mentous structures. However, if these structures are dis-rupted, severe deformity can ensue.

Most clinicians agree that the goal of treatment is torestore normal alignment to an unstable spine for a periodsufficient to allow healing through either spontaneousbony healing or surgical arthrodesis. Bedrest, casting, andbracing have all proved effective in the treatment of spinefractures in the proper injury and proper patient groups. Ifthe injury, the patient’s compliance, and the potential forhealing permit the use of nonoperative management, closefollow-up is critical. Clinical evaluation and serial standingradiographs should be carried out early should a deformitybegin to develop.

The deleterious effects of laminectomy alone for neuraldecompression in the presence of spinal trauma are welldocumented (Fig. 34–7). Complete spondyloptosis andsevere deformity have been reported.79 Malcolm andco-workers54 reported on 48 patients with post-traumatickyphosis. Half of these patients had an isolated laminec-tomy at the time of injury, and detrimental effects were seenat all levels of the spine. In the thoracic spine, the kyphoticdeformity was 15° greater in the group that underwent



FIGURE 34–5. Hook failure. This patient has significant osteoporosiscontributing to fractures of the lamina at the site of the proximal (T10)hooks as shown on a lateral radiograph (A) and computed tomographicscan (B). Treatment included proximal extension of the fusion withpedicle screw instrumentation (C).


decompression with laminectomy. At the thoracolumbarjunction, the deformity was 13° more severe, and in thelumbar spine, the difference in kyphosis was 35° for thosewho had undergone laminectomy and 24° for those whodid not.

Technical errors can precipitate deformity even in theface of posterior instrumentation. A fusion that is too shortand does not span the zone of injury is more likely to leadto a junctional deformity, especially if the arthrodesis endsat the cervicothoracic or thoracolumbar junction or at theapex of the thoracic kyphosis (Fig. 34–8). Additionally, ashort fusion that spans the defect but is placed posterior todestroyed anterior elements is more likely to fail unless theanterior column is restored (Fig. 34–9). Parker and othershave developed and validated a classification scheme tohelp determine when an anterior strut graft is required tosupplement a short posterior construct for thoracolumbarfractures.60

Clinical Features of Late Deformity. Symptomsattributable to deformity may be insidious in onset andmay follow a painless period of indeterminate length. Asmany as 70% to 90% of patients experience some chronicpain at the region of the fracture regardless of the type oftreatment or the degree of deformity.18, 43, 59, 86 As many as20% may be permanently disabled, and 40% reportfunctional limitations. Debilitating pain is often the initialsymptom and is the most common cause of reconstructivesurgery for post-traumatic deformity. Though challenging,the clinician must try to isolate the cause of the patient’ssymptoms. Instability or nonunion is more amenable tosurgical intervention than is mechanical back pain. ‘‘Me-chanical back pain’’ in this setting is an activity-related painthat may be muscular, discogenic, or arthritic in nature.Alternatively, it may be due to stress fractures of adjacentvertebrae secondary to excessive loads caused by thedeformity.

No consensus has been reached on the specific severity

of kyphosis that leads to pain and symptoms. Farcy andco-workers26 showed that at the thoracolumbar junction,a threshold of 25° is tolerated before symptoms are likelyto occur. The lumbar spine tolerated only 15° of deformity.However, Andreychik and co-workers2 did not find anycorrelation between symptoms and the degree of deformityin their series of 55 burst fractures of the lumbar spine.Most authors, however, agree that more sedentary patientstolerate a greater degree of deformity than do activelaborers or athletes, which is not surprising when oneconsiders the muscular work involved in maintainingposture in the presence of deformity.

In a paraplegic patient, poor sitting balance because ofprogression of deformity may be of more concern thanpain. Altered sitting balance can lead to soft tissue compli-cations at the gibbus and in the buttock region. It can alsoimpair the ability to power a wheelchair with the upperpart of the body and arms. Additionally, subtle deformitymay rapidly overcome the ability of weakened paraspinalmuscles in patients with higher neurologic compromise.

Finally, some patients may be seen primarily with aprogressive neurologic deficit. Malcolm and coauthorsreported that approximately 27% of patients had a progres-sive neurologic deficit.54 The neurologic deficit is a func-tion of the degree of deformity and the amount of canalcompromise secondary to retropulsed bone within thecanal. Fidler27 showed that typically bone fragments in thecanal are resorbed over time but that severe angular de-formity and abnormal transmission of stress may alter thisremodeling process. Additionally, hypertrophic remodelingfrom segmental instability and perhaps the development ofa post-traumatic syrinx can increase the stenosis of a givenlevel. The deformity of the spine may be quite complex andmust be appreciated in three dimensions. Full-lengthstanding (or sitting) radiographs should be obtained. Inaddition, bending films can be used to assess flexibility. Ifpseudarthrosis is suspected, flexion and extension viewsmay assist in the diagnosis of segmental instability. If thelevels adjacent to the deformity are not flexible enough tocompensate for kyphosis, a crouched gait may develop andlead to flexion contractures of the hips. These flexiondeformities of the lower extremities should be addressedbefore correction of the spinal deformity.

Classification of Late Deformity. In 1993, Denis andBurkus proposed three types of post-traumatic defor-mity.19 Each type includes three subtypes. This classifica-tion helps in planning the surgical approach and instru-mentation, but it does not distinguish deformities on thebasis of their relative magnitudes (Table 34–1).

Surgical Management of Late Deformity. Surgicalindications for correction of deformity include incapacitat-ing pain, progressive deformity, new or progressive neuro-logic deficit, or failure of a significant neurologic deficit toimprove in the face of residual deformity and neuralcompression. Because the risks of extensive surgical inter-ventions are significant, one should consider cosmeticdeformity alone a relative indication for surgical inter-vention.

For Denis and Burkus type IA deformities of less than15° that meet the criteria for surgical intervention, poste-rior spinal fusion is indicated. If the overall sagittal balanceof the spine is acceptable and the patient’s symptoms are

FIGURE 34–6. Pedicle screw malposition. Pedicle screws that are too longmay penetrate the anterior cortex of the vertebral body and place thegreat vessels at risk, as seen on this computed tomographic scan.



FIGURE 34–7. Postlaminectomy cervical kyphosis. A, This patient sus-tained posterior element fractures of the lower cervical spine and had anincomplete spinal cord injury. Advanced imaging studies showed canalcompromise from the posterior element fractures. He was treated withlaminectomy of C5 and C6 and halo immobilization. B, C, Serialradiographs showed gradual loss of reduction, with the development ofkyphosis. The patient was eventually treated with corpectomy and fusion.



located at the apex of the deformity, a short fusion withinstrumentation will probably suffice, especially if pseudar-throsis or limited segmental instability is the source of thepain. As the magnitude of the deformity increases, ananterior procedure preceding the posterior fusion assistsin correction of the deformity. However, Edwards andRhyne23 demonstrated that late correction of up to 30° ofkyphosis is feasible through a posterior approach in theabsence of an anterior bony bridge. These authors applythree-point loading through posterior constructs to causeviscoelastic relaxation of the anterior scar and ligaments.An osseous bridge anteriorly would require a limitedanterior release before correction posteriorly. In the tho-racic spine, assuming that infection has been eliminatedfrom the differential diagnosis, a posterior compressionconstruct will usually be adequate to repair a pseudarthro-sis. In the presence of neurologic compromise (type IC), itmay be possible to decompress the neural elements bycorrecting the deformity from a posterior approach if thedeformity and compression are mild. This approach re-quires a longer construct with multiple attachment sites.However, compression from larger deformities or retro-pulsed bone in the canal mandates anterior decompressionbefore a posterior approach.

Regardless of the approach, the goal is restoration of40° or less of kyphosis from T2 through T12, which maynecessitate the use of a longer posterior construct inpatients with type IB deformities. If correction of kyphosiscannot be fully achieved through combined anterior andposterior approaches, wedge-type osteotomies, such as aneggshell or pedicle subtraction osteotomy, may be per-formed (typically in the lumbar spine below the level ofthe conus medullaris). Ending a fusion at a level of discdisease or instability should be avoided during theselection of fusion levels.

The thoracolumbar junction deserves special atten-tion. Small deformities (e.g., less than 20°) with no

neurologic deficit (type IIA) can be treated with a shortposterior construct that preserves lumbar motion seg-ments. In type IIB deformities with associated hyperkypho-sis of the thoracic spine, the construct must be extendedand may require either a limited anterior release for aflexible deformity or a more extensive release if the upperthoracic deformity is fixed. Type IIC deformities withneurologic deficit and canal compromise of more than 25%require anterior decompression. Occasionally, short-segment decompression with a strut graft and anteriorinstrumentation may obviate the need for a posteriorconstruct, but any residual posterior instability or theabsence of a stable anterior reconstruction would mandatea 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 sixpatients with a mean thoracolumbar junctional kyphosisof 38° and a range of 20° to 83°. Five of the six had aneurologic deficit, and all had canal encroachment of 25%to 57%. All patients were treated by transthoracicvertebrectomy and an allograft strut augmented with avascularized pedicle 10th rib graft. The mean correctionwas 26°, or 68%. All neurologically incomplete patientsimproved, and although one patient required revision forgraft displacement, no pseudarthroses were reported. Theauthors note that such treatment requires a competentposterior osteoligamentous complex or the addition ofeither solid anterior instrumentation or a staged posteriorconstruct.

In the lumbar spine, true kyphosis is rarely seen.Rather, kyphosis typically refers to the loss of lordosis, alsocalled flat back deformity or hypolordosis. The first reportof osteotomy of the spine for kyphosis was made bySmith-Petersen and colleagues.71 Distraction and defor-mity of neural and vascular structures and subsequentcomplications led to investigation of alternative correctiveprocedures.

The method preferred today is an eggshell osteot-omy, also called a pedicle subtraction osteotomy. Thistechnique shortens rather than lengthens the vertebralcolumn.49, 73, 75 This osteotomy involves transpedicularfixation above and below the level to be osteotomized,usually at the apex of the deformity, and correction of thedeformity through removal of cancellous bone from thevertebral body. Asymmetric decancellation can correctboth coronal and sagittal deformities. Up to 50° of sagittalcorrection and 40° of coronal correction can be achieved.The osteotomy is started only after instrumentation iscompleted because the blood loss from the procedure canbe severe and may necessitate expeditious closure of thebony osteotomy site. The osteotomy is closed by extensionbending at the decancellation site, which is accomplishedby extending the table. Reduction can be facilitated bypositioning the patient on a hinged frame so that the tablecan be extended to help close the osteotomy (see Fig.34–4). Adjacent nerve roots above and below the os-teotomy then share a common foramen created by removalof the pedicle. Meticulous care must be used to avoidentrapment of nerve roots or dura. This procedure shouldbe effective for most type III deformities.62

In the cervical spine, Vaccaro and colleagues74 showedthat long anterior reconstructions with static plates have an

FIGURE 34–8. Junctional kyphosis after an L2 burst fracture treated withanterior L1–L3 instrumented fusion. Kyphosis developed at the thora-columbar junction from an osteoporotic compression fracture adjacent tothe fused segment.



unacceptably high failure rate. In a retrospective, multi-center study examining the use of an anterior cervicallocking plate and strut graft for a three-level corpectomy,the failure rate was 50% when a posterior construct wasnot used, as opposed to a 9% rate of graft or platedislodgment when a two-level corpectomy was fused in asimilar fashion. A higher incidence of graft failure was seenwith increased age, failure to lock the screws into the plate,and the use of a peg-in-hole bone graft construct. The typeof postoperative immobilization and violation of end-plates with screws had no statistically significant effect onfailure rates. However, no comparison was made betweentraumatic and nontraumatic etiologies, and therefore it isunclear whether subclinical posterior ligamentous injurymay increase the risk of failure.

McAfee and Bohlman57 reviewed the results of 15patients with multiple-level cervical corpectomies and an

FIGURE 34–9. Failure of the anteriorcolumn. A, This patient suffered aC6–C7 fracture-dislocation resultingin damage to the superior end-plate ofC7. B, Reduction was readily accom-plished with traction. C, An attempt atposterior fusion with instrumentationand halo immobilization was inade-quate because of a lack of anteriorcolumn support. D, Subsequent treat-ment with anterior C6 corpectomyand instrumented fusion restoredproper alignment and resulted in solidfusion.

TABLE 34–1z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z

Classification of Late Deformity

Type LevelNeurologicDeficit

DistantKyphoticDeformity

IA Cephalad to T11 No NoIB Cephalad to T11 No YesIC Cephalad to T11 Yes YesIIA T12–L1 No NoIIB T12–L1 No YesIIC T12–L1 Yes YesIIIA L2–L4 No NoIIIB L2–L4 No YesIIIC L2–L4 Yes Yes

z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z zSource: Denis, F.; Burkus, J.K. Semin Spine Surg 5:187–198, 1993.



anterior-posterior cervical fusion with instrumentation. Nopatient in their series had dislodgment of either theinstrumentation or graft material. It seems logical that aposterior tension band construct would help decrease thebending moment experienced by the anterior plate andstrut graft, but further study into such biomechanics is stillneeded before recommendations regarding the best con-struct can be made.

Adjacent-Segment Disease

Adjacent-segment disease should be a concern for allsurgeons who perform spinal fusions. Many reports havehighlighted the accelerated degeneration that occurs aboveand below the level of a rigid fusion.42, 47 Additionally, itseems that instrumented fusions are even more prone tothis phenomenon than are fusions without instrumenta-tion. The etiology of this disease is still somewhat unclear,but it may be due to direct impingement of instrumenta-tion on the facet joints. Some believe that denervation ofthe surrounding tissues, especially the facet capsule ifinjured, leads to neuropathic destruction of the facet. Onecan minimize this degeneration by protection of the facetcapsule in joints outside the region of the fusion and by

attempting to never terminate a fusion in a region ofstenosis, spondylolisthesis, posterior column deficiency, oran abnormal disc. This type of preoperative planning,however, is less feasible in the setting of trauma than in thesetting of elective fusion for degenerative disease. Extend-ing a fusion to a ‘‘normal’’ level may decrease the incidenceof one complication in exchange for a further decrease inmobility of the spine.

Several studies have reported stress fractures of thepelvis in patients with long lumbosacral fusions.36, 84

This phenomenon is most likely to occur in older osteo-porotic women. The fracture typically occurs on theside from which bone graft is harvested and is probablydue to a stress riser created in the ilium at graft acquisi-tion (Fig. 34–10). Symptoms of stress fractures are usuallyseen in the first few months after surgery, and protectedweight bearing is generally adequate for resolution of thesymptoms.

Pseudarthrosis

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

FIGURE 34–10. Pelvic fracture during iliac crest bone graft harvesting. Inthe setting of osteoporosis, aggressive bone graft harvesting may lead tofracture of the ilium. A, This 72-year-old woman with rheumatoidarthritis underwent bone graft harvest from the iliac crest. B, Paindeveloped in her hip area. Radiographs revealed a fracture at the bonegraft site (C) with subsequent pelvic instability.



pseudarthrosis after posterior spinal fusion vary widely inthe literature, from as low as 0% to as high as 30%.4, 77 Themajor sequela of pseudarthrosis is pain, but the diagnosisof pseudarthrosis can be challenging in a patient with painafter fusion. Instrumentation often obscures radiographicevaluation, and back pain may be a mechanical phenome-non in a patient with a solid fusion. Implant failure is astrong indicator of fusion failure, and radiolucency aboutthe fixation (e.g., pedicle screws) can support this diagno-sis as well. Most orthopaedic surgeons agree that a changeof more than 5° at a single functional spinal unit onflexion-extension radiographs is worrisome for pseudar-throsis.

The rate of pseudarthrosis increases with the number oflevels being fused.12 Additionally, advanced age, malnutri-tion, obesity, and the use of nonsteroidal anti-inflammatorymedications have been associated with decreased rates offusion. Brown and associates9 showed that tobacco smok-ing decreases rates of fusion. In a comparison of patientsundergoing lumbar laminectomy and fusion, pseudarthro-sis developed in 40% of smokers, whereas nonuniondeveloped in only 8% of nonsmokers. Recently, Glassmanand colleagues showed that if patients stop smoking for atleast 6 months after lumbar fusion surgery, the rate ofnonunion is comparable to that of nonsmokers.33 Forsmokers who did not stop smoking, the nonunion rate was26.5%, whereas nonsmokers had a nonunion rate of14.2%.33 Similarly, Rogozinski and co-workers66 looked atfusion rates in nonsmokers, preoperative smokers, andpostoperative smokers. Although the fusion rate in thepostoperative smoker group was less than 60%, the studyindicated that nonsmokers and preoperative smokers hadnearly the same rate of fusion. The negative impact oftobacco smoking on spinal arthrodesis has also been shownin the cervical spine.39 In the setting of trauma, it isimpossible to ask patients to stop smoking before surgery,but cessation of smoking after arthrodesis seems to confer abenefit. Autograft in some studies has also been shown tobe 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 ofallograft in single-level anterior fusions in the cervicalspine.87

The incidence of pseudarthrosis in the setting of traumaseems to be lower than that in the setting of degenerativedisease or deformity. In 1979, Bohlman8 reported on alarge series of cervical spine fractures treated operativelywithout a single pseudarthrosis. Flesch and associates28

reported only 1 nonunion in 40 patients with thoracolum-bar spine fractures treated with Harrington instrumenta-tion and fusion. Edwards and Levine22 reported a 2%pseudarthrosis rate in 200 injuries of the thoracolumbarspine; the rate was almost four times higher at thelumbosacral junction. They noted that many of thesepseudarthroses were due to technical error. Fusion ratescan be enhanced with meticulous decortication of thetransverse processes while trying to avoid fracture of theseprocesses. Copious application of autograft and placementof graft beneath the posterior implants are recommended.Many spine surgeons favor the use of a gouge over the useof a bur for decortication because of the belief that thermalnecrosis of bone occurs with bur decortication.

VASCULAR AND SOFTTISSUE COMPLICATIONSz z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z

Cervical Spine

Injuries to the vascular and soft tissues in the cervical spineusually occur during operative treatment of an injury.However, injuries to these structures as a direct result oftrauma can occur as well. The common carotid artery andthe contents of the carotid sheath are at risk duringanterior exposure of the cervical spine. Blunt fingerdissection and repeated, but gentle, palpation of thecarotid artery to assess its location help decrease thelikelihood of injury. Likewise, palpation of the nasogastrictube can identify the location of the esophagus. Mobiliza-tion of the longus colli muscles off the anterolateralvertebral bodies before placement of deep retractors alsohelps minimize vessel damage. Checking the temporalartery pulse of the patient during the procedure helps toassess whether excessive retraction is causing occlusion ofthe carotid artery. Carotid artery laceration, division, andthrombosis have been reported during anterior spinalfusion.40 Some approaches to the cervical spine risk injuryto either the internal or external jugular vein. Although inmost circumstances these vessels can be ligated unilaterallywith little clinical consequence, venous injury can lead toair embolism, which may cause pulmonary compromise,blindness, or death.

The vertebral artery is at risk from both anterior andposterior approaches to the cervical spine, especially inC1–C2 transarticular arthrodesis. In a review by Golfinosand colleagues35 of 1215 cases, these injuries occurred in1 case from retraction of soft tissues, in 1 case during screwtapping, and in 2 cases from lateral decompression. Mostauthors agree that the vertebral artery should not berepaired, but rather packed with thrombin-soaked absorb-able gelatin sponges to achieve hemostasis through tam-ponade. When transarticular screw fixation is used, thecontralateral side should not be instrumented if vertebralartery injury is suspected.

In the rare case in which ligation is required forhemostasis, intraoperative angiography may be performedto assess the ability of the patient to tolerate such aprocedure. However, in these cases, such studies areprobably impractical, and furthermore, some evidenceindicates that sacrifice of one vertebral artery will not leadto permanent neurologic sequelae in most patients.68 Theability of a patient to tolerate unilateral vertebral arteryablation is supported by a study of nine patients withtraumatic occlusion of the vessel. In two of the nine,neurologic sequelae developed, but the findings weretransient. However, Smith and associates70 reported that inthree of seven cases of vertebral artery ligation, sympto-matic vertebrobasilar symptoms such as syncope, nystag-mus, dizziness, and Wallenberg’s syndrome developed.They supported repair of an injured vertebral arterywhenever possible. As the use of lateral mass screw fixationexpands, the number of vertebral artery injuries mayincrease. This complication from the placement of screwsinto the transverse foramen is best prevented by a knowl-edge of anatomy and bony landmarks.



Esophageal perforation after anterior spinal trauma orsurgery is uncommon, but well recognized. The largestseries of esophageal perforations to date was reported byGaudinez and coauthors30 from The Rocky MountainRegional Spinal Injury Center. Over a 25-year period, 44patients with esophageal perforation were treated at thatinstitution. Although most pharyngoesophageal perfora-tions occur in the early postoperative period, delayedperforations in patients who had fully convalesced from theacute postoperative period have been reported.44 The mostfrequently occurring symptoms are neck and throat pain,odynophagia, dysphagia, hoarseness, and aspiration. In theseries by Gaudinez and colleagues,30 cervical osteomyelitisor cervical abscess developed in half the patients. Clinicalfindings may include fever, cervical tenderness and indura-tion, weight loss, tachycardia, crepitus from emphysema,and hematemesis. Though far less common, expectorationof necrotic bone has been reported as well. A high index ofsuspicion is required because diagnostic imaging oftenyields negative results. In addition, they showed that22.7% of patients had false-negative results from imagingstudies. Endoscopy was 63.6% sensitive for definitivediagnosis in the 40 patients who underwent the proce-dure.30

Though not specifically mentioned in the aforemen-tioned series, a combination of direct visualization and aswallow study is regarded by most to have the highestdiagnostic yield. Management of esophageal perforation isvariable. Conservative management includes observation,intravenous nutrition, a feeding tube or gastrostomy, ap-propriate antibiotic coverage, and aspiration precautions.These techniques may be effective for small, uncompli-cated perforations. However, the literature suggests highmorbidity and mortality with nonsurgical management ofall but the smallest of perforations, especially with tears ofthe lower part of the esophagus. Consultation with athoracic or esophageal surgical specialist is recommendedin all cases. Prompt recognition of symptoms and pathol-ogy is paramount because a delay in diagnosis can lead todeath. The esophagus should be examined carefully afterany anterior cervical spinal operation, and any esophagealinjury noted in the operative suite should be aggressivelyaddressed with repair by an experienced surgeon. Therepair can be augmented, when necessary, with a muscleflap, such as a proximally based medial pectoralis majorrotational flap.

Thoracolumbar Spine

Anterior thoracolumbar surgery has a multitude of poten-tial complications, including pneumothorax, hemothorax,and chylothorax. Massive hemothorax may occur fromprofuse vertebral body bleeding and can cause hemody-namic instability. It may require surgical tamponade ofvenous sinuses in the vertebral body with bone wax orligation of bleeding segmental arteries.60 Hemorrhage froma thoracic fracture causing persistent hemothorax has beenreported in a patient with a complete neurologic injuryinduced by the fracture.17 After more than 7 days ofrecurrent hemothorax, the patient underwent operativereduction and stabilization of the fracture, which led to the

cessation of bleeding. This scenario defines an additionalindication for early fixation of a high-energy thoracicvertebral fracture in patients with complete neurologiccompromise.

The presence of a thoracic fracture should also alert thephysician to the possibility of thoracic duct injury. Theincidence of chylothorax in association with rib andthoracic fractures is increasing because of escalating num-bers of vehicular accidents and nonpenetrating trauma. Atleast 13 patients with chylothorax secondary to thoracicfractures have been reported, and at least 2 of them died ofthe sequelae of the chylothorax itself, 1 from tensionchylothorax.85 Although most cases of traumatic chylotho-rax can be managed nonoperatively, the need for surgicalintervention in the subset of patients with associatedthoracic fractures is higher and approaches 50%.

Delayed appearance of a patient with chylothorax is aresult of the formation of a mediastinal chyloma, whichthen ruptures into a pleural cavity, usually 7 to 10 daysafter the injury. Once suspected, diagnostic thoracentesisand tube thoracostomy should be undertaken. Oral intakeshould be discontinued because even low-fat, clear liquidsmarkedly increase chyle flow.34 Traditionally, continuedchylous chest drainage despite 6 weeks of nonoperativetherapy is an indication for surgical intervention. However,more recently, some authors have become more aggressivein preventing ongoing protein and lymphocyte losses andthereby minimizing the risk of infection. Some authorsnow recommend surgery if nonoperative management isunsuccessful after 2 weeks.69 Most agree that a moreaggressive approach is preferred in a patient with concom-itant spinal fractures because of the high immunologic andnutritional cost of prolonged chest tube drainage.69 Rarereports of iatrogenic chyle leaks after anterior thoracolum-bar surgery have appeared. Most, however, agree thatmicrolymphatic disruption is inevitable, and it seemslikely that clinically insignificant chyle leaks are undiag-nosed and heal spontaneously.

Diaphragmatic rupture or herniation may occur afterthoracolumbar exposure or after the crus of the diaphragmis taken down and repaired to improve exposure at thethoracolumbar region. The ureters and great vessels are atrisk during retroperitoneal dissection, especially in therevision setting. Consideration should be given to preop-erative ureteral stenting in these revision procedures.Injury to the sympathetic plexus overlying the anterioraspect of the lower lumbar and upper sacral vertebrae maycause retrograde ejaculation.

Traditionally, much attention has been paid to thesegmental blood supply of the thoracic cord. Specifically,the artery of Adamkiewicz is considered to be vital to cordperfusion. The transthoracic approach to the spine usuallyrequires mobilization of the segmental vessels over amultitude of levels. Dwyer and Schafer,21 however, haveshown that ligation of multiple ipsilateral segmentalarteries can be performed without neurologic compromise.DiChiro and colleagues20 demonstrated in monkeys thateven the arteria magna could be ligated without sequelae.However, if both this vessel and the anterior spinal arterywere disrupted, paraplegia resulted. Much of the work andthe case reports of neurologic compromise in the face ofsegmental artery disruption have been related to surgical



treatment of deformity. The effect of deformity, especially ifcongenital, on the blood supply to the cord is unclear. Ina polytrauma patient, cross-clamping of the aorta results indisruption of the segmental blood flow to the cordbilaterally, which may result in paralysis. Trauma to thecord and associated edema may make the spinal cord farmore sensitive to the effects of mild ischemia.

The anterior approach to the lumbar spine for theoperative treatment of spinal trauma is usually performedthrough the retroperitoneal or, less commonly, thetransperitoneal approach. If the pathologic condition doesnot dictate the side, most surgeons prefer the left becausethe aorta is more forgiving and easier to mobilize than thevena cava. The left common iliac vein is the vessel most atrisk during left-sided retroperitoneal and transperitonealexposures. Regardless of the approach, instrumentationshould be placed on the lateral side of the vertebral bodyand not in contact with the great vessels.

Vascular complications during posterior lumbar spinesurgery are usually secondary to discectomy. Vascularinjury during discectomy is most common at the L4–L5level. Freeman29 showed that the pituitary rongeur is themost frequent culprit. In the setting of trauma, one must bekeenly aware of any disruption of the anterior longitudinalligament. Incompetence of this ligament makes perforationof the great vessels more difficult to avoid. Unless acutehypotension occurs intraoperatively, these injures mayinitially go unnoticed. Late abdominal rigidity, abdominalpain, tachycardia, and anemia should alert the physician tothis complication, which may be avoided by limitingthe depth of insertion of the pituitary rongeur duringdiscectomy.

The lateral extracavitary approach to the thoracolumbarspine deserves special mention. This approach, which isused to replace a two-incision front-back procedure, allowsventral decompression and dorsal fixation. The techniqueis technically demanding. Resnick and Benzel63 reported a55% incidence of morbidity in a series of 33 patients withacute fractures. The most common complication washemothorax or effusion requiring tube thoracostomy, fol-lowed by pneumonia, which occurred in seven patients.Other authors have noted pseudohernias caused by sacri-fice of the intercostal nerves. Although the morbidityassociated with this procedure may be high, its risks shouldbe weighed against the combined risk of a two-stageprocedure.

Postoperative Infection

Postoperative infections may result from inoculation dur-ing 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% infectionrate, whereas combined fusion and instrumentation areassociated with rates between 4% and 8%. Risk factorsinclude increased age, obesity, diabetes, smoking, immu-nosuppression, duration of preoperative hospitalization,spinal dysraphism, myelodysplasia, revision surgery, oper-ative time, and the use of instrumentation, bone graft, ormethyl methacrylate.14, 15, 41, 50, 56, 67, 72, 81

The use of perioperative prophylaxis to prevent infec-

tion is widespread. Patients with instrumented fusionshave a decreased infection rate with the use of prophylaxiswhen compared with those undergoing surgery withoutprophylaxis. Commonly, the antibiotic is administeredbefore the incision and for 24 hours postoperatively,although some surgeons prefer to administer antibioticsuntil suction drains or catheters are removed. The choice ofantibiotic is guided by consideration of multiple factors,including host immunocompetence, the bacterial floracommon in the region, the type of procedure, cost, and theside effect profile. Most commonly, a cephalosporin is used.Because of increasing concern regarding the developmentof bacterial resistance, drugs such as vancomycin should bediscouraged for prophylaxis and reserved only for patientsat increased risk of methicillin-resistant staphylococcalinfections. Such patients include those with lymphopenia,recent or current hospitalization, postoperative wounddrainage, and alcohol abuse.

Once the diagnosis of postoperative infection is madeclinically, early surgical intervention is necessary becausemedical management is likely to fail. Debridement shouldproceed in a systematic fashion. Each layer is debrided andcultured before advancing deeper with the dissection. Ifgross deep drainage or purulence is encountered withsubfascial aspiration, deep debridement is performed.

Although solidly fixed instrumentation is typically leftin place in the early postoperative period, all other foreignbodies such as bone wax and Gelfoam must be removed.Any hematoma should be thoroughly evacuated. Manyauthors retain bone grafts, especially if they are adherent.Others recommend removal of loose grafts and washingbefore replacement. If the graft is grossly purulent ornecrotic, it should be discarded and another bone graftingprocedure performed at a later debridement when the localinfection is controlled. Hemostasis must be meticulous toprevent re-formation of a hematoma seeded with bacteria.Dead space must be obliterated, and the use of a rotationflap should be considered for dead space management.Primary wound closure over drains, often with retentionsutures to prevent dehiscence, is favored when possible.Depending on the amount of devitalized tissue, routineserial debridement is often required. Simple woundinfections may be packed open and allowed to close bysecondary intention. More complex wound infections mayrequire musculocutaneous flaps.

Postoperatively, antibiotic therapy is required for atleast 10 to 14 days for straightforward soft tissue woundinfections. Six weeks of parenteral antibiotic treatment ispreferred in cases of bone involvement, deep infection, orretained foreign bodies (e.g., metal or graft).

In all cases, nutritional assessment and repletion are ofparamount importance. Up to 35% of hospitalized patientshave evidence of protein-calorie malnutrition. Weight lossof more than 10%, a serum transferrin level less than 1.5g/L, anergy, a serum albumin concentration less than3 g/dL, or a total lymphocyte count less than 1200should raise suspicion of malnutrition. Protein-caloriemalnutrition causes decreased cardiac output and periph-eral oxygen tension as well as impaired pulmonary de-fenses, wound healing, and cell-mediated immune de-fenses. In addition to the treatment of malnutrition, itsprevention must be considered in all hospitalized patients,



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

Metabolic Changes

As a result of inactivity and changes in body composition,most patients with chronic spinal cord injury undergoimportant metabolic changes. Glucose intolerance occursmore frequently in these patients than in the generalpopulation. Baumann and Spungen5, 6 performed a 75-goral glucose tolerance test on 100 veterans (50 withparaplegia and 50 with quadriplegia) and 50 able-bodiedveteran controls. In the spinal cord–injured group, 22% ofthe subjects were diabetic by criteria established by theWorld Health Organization as compared with 6% in thecontrol group. Normal oral glucose tolerance was noted in82% of the controls, 50% of the paraplegics, and 38% ofthe quadriplegics. Insulin levels were lower in controls,thus indicating insulin resistance in the spinal cord–injuredpatients. This hyperinsulinemia may well play a role in theincreased concentration of triglycerides and the decreasedconcentration of high-density lipoprotein cholesterol inspinal cord–injured patients. All these changes, coupledwith inactivity, play a role in the high incidence ofatherosclerosis seen in this group.

Spinal cord injury leads to unloading of the skeleton,and hypercalcemia and hypercalciuria ensue quickly. Re-striction of dietary calcium does not treat the cause of thederangement, which is initially due to increased osteoclas-tic activity within the first 3 to 5 days and later involves alifetime of decreased osteoblastic activity. Osteoporosismay lead to insufficiency or traumatic fractures, but thesefractures may be markedly underdiagnosed and manifestedas little more than swelling. Hypercalciuria may result inearly nephrolithiasis and the recommendation that dietarycalcium be forever avoided. However, such restrictionoften leads to deficiency and worsening of osteoporosislater in life, after the acute period of marked bone losssubsides, usually within 14 months.64 Although their rolestill remains to be defined, bisphosphonates may be thebest agent for management of this condition.5, 64

Some evidence supports the depression of endogenousanabolic hormones in spinal cord–injured patients. De-creased levels of serum testosterone, growth hormone,and insulin-like growth factor type I may exacerbate thebody composition changes seen in these patients. Inaddition, exercise tolerance and strength may be de-creased. Thyroid dysfunction is seen as well. Depressedlevels of triiodothyronine (T3) and reverse T3 have beendemonstrated, and this effect may also contribute tofatigue and an increase in adiposity. However, some believethat it is due to associated illness and metabolic derange-ment, and as such, the use of replacement therapy for thistype of ‘‘deficiency’’ in the presence of normal thyroidtissue is controversial.

Although the medical management of each of thesemetabolic derangements is beyond the scope of this chap-ter, the orthopaedic surgeon must be cognizant that suchmedical issues exist and must use an appropriate team tominimize the late sequelae of these abnormalities. Amelio-ration of these abnormalities promises to improve the

longevity and quality of life of persons with spinal cordinjury.

Dural Tear

It is difficult, if not impossible, to know the true incidenceof dural tears as a result of trauma. In patients withhigh-energy injuries and complete paraplegia of the tho-racic spine, actual severance of the cord and dural sac ispossible. Likewise, a gunshot wound to the spine maycause disruption of the dura. Iatrogenic dural tears alsooccur, especially during attempted posterolateral decom-pression. Cerebrospinal fluid (CSF) leaks may lead topositional headache, wound complications, meningitis,arachnoiditis, and pseudomeningocele.

The diagnosis of iatrogenic CSF leakage is fairly straight-forward. Obvious egress of fluid from a visible tear in thedura is diagnostic. As the thecal sac decompresses becauseof a leak, the local pressure about the epidural veinsdecreases, and an increase in venous bleeding from theepidural space may be the first indication of a dural tear.Additionally, when the dural sac is decompressed, espe-cially when reducing a kyphotic deformity, leakage mayoccur from a tear. Postoperatively, one must be alert forsigns of clear drainage from the wound or the presence of asubcutaneous fluid collection. Severe headache exacer-bated by an upright posture may be noted. Large volumesof fluid may be seen inasmuch as the choroid plexusproduces over 20 mL of CSF hourly. If it is unclear whetherthe fluid is CSF, testing for β2-transferrin can be useful. Apseudomeningocele may develop if a dural tear occurs andis not repaired in watertight fashion. It may occur days tomonths postoperatively.

Dural tears may be classified as dorsal, lateral, orventral. Although the best treatment is prevention, mosttears can be repaired primarily if they do occur. However,massive defects may be irreparable. The first step in repairis complete exposure of the dural rent. Magnification andadequate lighting are required. Dural elements must bereturned to their intrathecal location and should not beincorporated into the repair inadvertently. The goal is awatertight repair that is free of tension. Usually, thisobjective can be accomplished with 6–0 polypropylene(Prolene) suture placed in a running locking stitch. Therecommended location of the suture is 2 mm from thedural edge with 3 mm between sutures. A Valsalva maneu-ver may be simulated by the anesthesiologist after repair toassess for residual leak. If leakage occurs after repair,augmentation with additional suture, gelatin sponge, au-togenous fat, or fibrin glue is required. More complex tearsmay require grafting with fascia lata or with commerciallyavailable dural patches. Meticulous watertight fascial clo-sure is as important as the dural repair itself because thefascial barrier is relied on to prevent durocutaneous fistu-las. Most surgeons avoid the use of intramuscular drains inthe presence of a dural tear because negative pressure mayencourage a persistent leak.

During a posterior approach, most posterior and lateraldural tears can be exposed directly. Below the level of theconus, an anterior tear may be approached through aposterior durotomy and gentle retraction of nerve roots to



allow access to the anterior aspect of the dural tube.However, anterior tears during posterior exposure at cordlevels may need to be treated indirectly.

Indirect repair is most commonly performed withfibrin glue, which is formed by mixing thrombin andcryoprecipitate that has been screened for human immu-nodeficiency and hepatitis virus. It forms a biologic gluewith biomechanical ‘‘patchlike’’ properties, and it canseal tears that cannot be fully exposed for repair or itcan be used to augment tenuous repairs. Cooling theindividual components before mixing may improve thebiomechanical strength of the product.80 In addition torepair, diversion of CSF through a subarachnoid drain for4 to 5 days may allow the dura, fascia, and surgicalincision to heal.

SUMMARYz z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z z

The complications of spinal trauma are numerous andchallenging. They may occur as a direct result of the injury,because of a lack of appreciation of the injury andsubsequent improper treatment, or as a result of theinherent risk of the treatment itself. Successful treatment ofthese complications relies on prompt recognition. Compli-cations that occur as a result of spinal trauma are oftenrelated to immobilization. Prolonged bedrest leads todeconditioning, poor pulmonary function, and decubitusulcers. Vigilance must be paid to these mundane, butclinically important issues, and proper understanding ofthe injury pattern provides another avenue by which toavoid complications. Spinal stability must be scrutinizedwith an eye toward potential deformity. Whether externalor internal immobilization is used, all fractures should bemonitored closely so that loss of reduction can be discov-ered early and treated expeditiously. Inadequate fixationtechniques, neglecting to support the anterior column, andfailing to restore normal alignment are the causes of mostiatrogenic deformities. Meticulous attention to detail dur-ing all phases of treatment, combined with attentivemedical care, will prevent most of the complicationsassociated with spinal trauma.

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