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The Role and Timing of Decompression in Acute Spinal Cord Injury: What Do We Know? What Should We Do?

Fehlings, Michael G., MD, PhD, FRCS(C)*; Sekhon, Lali H.S., MB, BS, PhD, FRACS; Tator, Charles, MD, PhD, FRCS(C)*

Surgical Treatment of Acute and Chronic Spinal Cord Injury
Free
SDC

The management of acute spinal cord injury has traditionally concentrated on preventative measures as well as, for the better part of the previous century, conservative care. Pharmacologic interventions, in particular intravenous methylprednisolone therapy, have shown modest improvements in clinical trials and are still undergoing evaluation. More recent interest has focused on the role of surgical reduction and decompression, particularly “early” surgery. A review of the current evidence available in the literature suggests that there is no standard of care regarding the role and timing of surgical decompression. There are insufficient data to support overall treatment standards or guidelines for this topic. There are, however, Class II data indicating that early surgery (<24 hours) may be done safely after acute SCI. Furthermore, there are Class III data to suggest a role for urgent decompression in the setting of 1) bilateral facet dislocation and 2) incomplete spinal cord injury with a neurologically deteriorating patient. Whereas there is biologic evidence from experimental studies in animals that early decompression may improve neurologic recovery after SCI, the relevant time frame in humans remains unclear. To date, the role of decompression in patients with SCI is only supported by Class III and limited Class II evidence and accordingly can be considered only a practice option. Accordingly, there is a strong rationale to undertake prospective, controlled trials to evaluate the role and timing of decompression in acute SCI.

From the *Division of Neurosurgery, Toronto Western Hospital, University Health Network, and University of Toronto, Toronto, Ontario, Canada, and the

†Department of Neurosurgery, Royal North Shore and Dalcross Private Hospital, and the University of Sydney, Sydney, New South Wales, Australia.

Device status category: 1.

Conflict of interest category: 12.

Address correspondence to

Michael G. Fehlings, MD, PhD, FRCSC

Head, Spinal Program

University Health Network

University of Toronto

399 Bathurst Street, Suite 2-147

Toronto, Ontario, Canada M5T 2S8

E-mail: michael@uhnres.utoronto.ca

Spinal cord injury (SCI) occurs with an average annual incidence of 11,000 cases in North America and is an important cause of morbidity and mortality. 51,68,98 The main causes of acute SCI include motor vehicle collisions, sports and recreational activities, work-related accidents, falls, and violence. 51,68 Despite modest clinical benefits with methylprednisolone (MPSS), the neurologic prognosis for a patient with a severe SCI remains grim. 24–26,50 Moreover, the financial and social costs associated with acute SCI are staggering. 60,96 Kraus et al 68 estimated, based on 1975 data, an “annual cost to the United States for support and treatment of all persons with a SCI of two billion dollars.” In 1992, Harvey et al 61 estimated that this figure had risen to $4 billion annually. Given this background, it is appropriate to consider the evidence regarding decompression of acute SCIs, particularly given the frequency of this intervention in North America. 99,104

The biology of acute SCI involves both primary and secondary injury mechanisms. 2–4,6,7,50,62,98,100,105,115,116 Most traumatic cord injuries occur as result of rapid cord compression because of a fracture–dislocation or burst fracture. 30,64,94 Acute spinal cord distraction, acceleration–deceleration with shearing, and transection from penetrating injuries are additional mechanisms of trauma. 44,68 As reviewed by the senior author and others, 8,34,48,50,98 there is strong evidence that the primary initial injury initiates a series of events that include the following: 1) ischemia, impaired autoregulation, neurogenic shock, hemorrhage, microcirculatory disruption, vasospasm, and thrombosis 6,50,98; 2) ionic derangements, including increased intracellular calcium and sodium, and increased extracellular potassium 2–4,50; 3) accumulation of neurotransmitters, including serotonin, catecholamines, 82 and extracellular glutamate, 3 which contribute to cellular injury 50; 4) arachidonic acid release, free radical and eicosanoid production, and lipid peroxidation 8,9,41,58,62; 5) endogenous opioids 50; 6) edema 109; 7) inflammation; 8) loss of adenosine triphosphate-dependent cellular processes 8; and 9) apoptosis. 50 The development of these secondary injury events, which lead to tissue destruction during the first few hours after injury, is of relevance to the surgical and nonsurgical treatment of SCI. The severity of the pathologic changes and the degree of recovery are directly related to the duration of acute compression as demonstrated by studies in animal models in which longer periods of cord compression were associated with poorer neurologic recovery.

A more detailed knowledge of the pathophysiology of acute SCI has led to clinically relevant neuroprotective approaches to attenuate the effects of the secondary injury. The NASCIS II study reported a modest beneficial effect of high-dose if given within 8 hours of injury in patients with complete and incomplete spinal cord injuries, 24,25 which emphasizes the importance of the timing of intervention. Moreover, the NASCIS III study provided suggestive evidence that treatment within 3 hours may be better than treatment initiated 3–8 hours after trauma. 26 These studies thus support the concept of targeting secondary SCI mechanisms in patients. It is unclear, however, whether the “time window” for MPSS can be applied to surgical decompression.

Although the National Acute Spinal Cord Injury Studies (NASCIS II and NASCIS III) 24–26 have shown modest improvements in recovery of patients with SCI with high-dose steroids, this therapy has had only a modest functional impact in these patients, and many practitioners are reluctant to use this drug given its potential toxicity. Accordingly, recent advances in the safety and efficacy of surgical decompression of the spinal cord offer considerable promise for repairing some of the neurologic injury caused by spinal trauma. 5,16,49,95,110 However, despite the widespread use of surgery in patients with acute SCI in North America, the role of this intervention in improving neurologic recovery remains controversial because of the lack of well-designed and executed randomized controlled trials. In this article we critically review the experimental and clinical evidence regarding the value of surgical decompression in acute, nonpenetrating SCI. Comparison with the results of conservative, nonoperative management of SCI is also made.

This work represents an updated and reformatted analysis of a previous study reported by our group. 51 In particular, the present article examines a number of recent studies 4,42,50,51,80,85,99,107 that were not included in our earlier report.

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Methods

An internet-based (PUBMED), computer-assisted MEDLINE search was undertaken of the experimental and clinical literature from 1966 to 2001 dealing with the role of decompression in SCI using the medical subject headings (MeSH) of “decompression” and “spinal cord injury.” Articles with English, German, and French abstracts were selected for review. This computerized literature review yielded a total of 922 studies, which were then pared down to 97 articles based on relevance to the issue of SCI management. This analysis was supplemented by a detailed examination of the reference lists from selected articles and standard spine textbooks. As summarized in Table 1, evidence from clinical trials was defined as Class I (well-designed and conducted randomized controlled trials), Class II (prospective cohort studies or controlled studies with well-defined comparison groups), or Class III (case series, retrospective reviews, and expert opinion). 113

Table 1

Table 1

A total of 66 articles (17 experimental studies in animal models and 49 clinical studies) were selected for detailed analysis (Tables 2–6). Of the clinical articles, 9 dealt with nonoperativemanagement, 28 with the role of surgical intervention in the early (<4 weeks) postoperative period (Tables 3 and4), 11 with the effect of closed reduction (Table 5), and 8 with the role of delayed decompression (Table 6). Based on this analysis, suggested evidence-based recommendations regarding the role of acute decompression in SCI were generated (Table 7).

Table 2

Table 2

Table 3

Table 3

Table 4

Table 4

Table 5

Table 5

Table 6

Table 6

Table 7

Table 7

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Results

Experimental Studies of Decompression in Acute SCI in Animal Models

There is compelling evidence from laboratory studies in animal models that persistent compression of the spinal cord is a potentially reversible form of secondary injury. The severity of SCI in animal models is related to the force of compression, duration of compression, displacement, impulse, and kinetic energy. 44,54,63,83,86,91 Numerous experimental studies of decompression after SCI have been performed in various animal models. 6,19,28,32,37,40,42,44,54,66,67,81,90–93,100 These studies have a wide range of species, including models in primates, dogs, cats, and rodents, and have consistently shown that neurologic recovery is enhanced by early decompression (Table 2).

In a recent study, Dimar et al 42 used the New York University weight drop model to produce thoracic SCI in rats and an epidural spacer placed adjacent to the contusion to mimic the effect of persisting compression. The effect of decompression at 0, 2, 6, 24, and 72 hours after SCI was then assessed by quantitative analysis of locomotor recovery, lesion volume, and electrophysiology. Neurologic recovery was significantly dependent on time to decompression, with significant differences seen in all experimental groups. This study provides the strongest experimental evidence to date of a clear beneficial effect of spinal cord decompression after SCI.

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Role of Conservative Management in Acute SCI

To place the potential role of surgery in the management of SCI in an appropriate context, it is important to briefly examine the outcomes of conservative, nonoperative treatment. Guttmann advocated the use of postural techniques combined with bed rest to achieve reduction and spontaneous fusion of the spine. 55,56 Operative intervention was rarely undertaken because of a higher incidence of neurologic complications and poorer clinical outcomes with laminectomy. 11–13,34,55,56 For example, Frankel et al, 52 who followed the management principles of Guttmann, 55,56 reported on a cohort of 612 patients with “closed spinal injuries” who were managed conservatively. 52 Only four of these patients developed spinal instability and required fusion by surgical techniques. However, details regarding the fractures and the criteria for determining spinal instability or failure of a nonoperative approach were not described. Of note, 29% of Frankel A patients (with complete motor and sensory paralysis below the level of the injury) improved at least one grade during the course of their hospital stay. These data thus provide a benchmark against which other interventions can be judged.

The spontaneous improvement in neurologic status with nonoperative management has been also reported by a number of other authors. 11–13,35,43,97,111,114 Some investigators have even claimed that neither spinal surgery nor anatomic realignment of the spinal column improved neurologic outcome in patients with acute SCI with the possible exception of bilateral locked facets. 39,59 However, to date, the studies of conservative treatment are limited to noncontrolled, retrospective analyses of clinical databases (Class III evidence). Moreover, surgeons now recognize that laminectomy without fusion is contraindicated in most cases of acute SCI because of inadequate decompression of the cord and exacerbation of underlying traumatic instability. 23,49

Although careful, nonoperative management is key to the care of patients with SCI, modern surgical techniques have advanced considerably over the past two decades. Moreover, there is increasing evidence that an exclusive policy of nonoperative treatment of SCI can lead to high complication rates. For example, neurologic deterioration can occur in up to 10% of patients with incomplete cervical SCI who undergo an exclusively nonoperative approach. 65

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Role of Decompression in the Management of Acute SCI

Tables 3–6 summarize the clinical studies that have examined the role of decompression in the treatment of SCI. 14,15,17,21,38,45,46,69,71,73,74,76,77,79,84,88,89,104,108

The clinical uncertainty in the role and timing of surgical intervention in the setting of acute SCI is reflected by the wide variations in practice patterns seen across North America. This view is supported by a recent retrospective, multicenter study of SCI management in 585 cases undertaken by our group. 99 Although 65.4% of cases in North America were managed surgically in this cross-sectional study, there was no consensus as to timing of operative intervention: 23.5% of patients underwent surgery within 24 hours of SCI, whereas >40% of cases were managed by delayed surgery (>5 days).

Our literature review found nine prospective, controlled studies of surgical decompression in acute SCI 33,47,80,85,95,102,103,106,107 (Table 3). In a prospective, nonrandomized case–control study of 208 patients with acute spinal cord or cauda equina injury, Tator et al compared the results of surgery (56% of patients) with nonoperative management (44%). 95 Operative management was associated with a lower overall mortality rate (6.1%) than nonoperative treatment (15.2%) despite a higher rate of thromboembolic complications in the surgical group. Overall, there was no difference between operated and nonoperated patients in length of stay or neurologic recovery.

In an analysis of the NASCIS II database (Class II evidence), Duh et al 47 reported that patients undergoing acute surgery (<25 hours after injury) had improved (although not statistically significant) outcomes (mean neurologic change score of 17.8) when compared with a control cohort treated nonoperatively (mean change score of 13.2). Interestingly, results of surgery were similar in the early (<25 hours) and delayed (>200 hours) groups. In contrast, in a series of prospective studies Vale et al, 103 Vaccaro et al, 102 and Waters et al 106 could not document a beneficial effect of surgical decompression. It is noteworthy, however, that all patients underwent delayed operative management in the study by Waters et al. 106 Moreover, although the study by Vaccaro et al 102 was a prospective, randomized trial, 20 of the 62 patients were lost to follow-up and “early” surgery was defined as being within 72 hours after SCI. In view of the large number of patients lost to follow-up, we have considered the study by Vaccaro et al 102 to provide Class II evidence. More recently, Chen et al 33 evaluated 37 patients with cervical spondylosis and incomplete cord injury to assess surgical versus nonsurgical outcomes. They suggested that 13 of 16 patients treated surgically improved within 2 days of surgery and, overall, showed faster recovery of neurologic function, better long-term neurologic outcome, shorter hospital stays, and fewer complications than the nonoperative group. Because of the lack of randomization, this study was classified as Class II evidence.

A number of authors have advocated early operative intervention in patients with acute SCI. For example, Aebi et al, 1 Wiberg and Hauge, 109 Hadley et al, 57 and Wolf et al 112 recommended early reduction (4–10 hours) and operative fixation of spinal fractures associated with SCI. Some evidence is presented in these studies, which suggests that early decompression may enhance neurologic recovery in selected patients with SCI. However, these studies lack randomization or appropriate controls and thus represent Class III evidence only. Thus, the benefits of surgical intervention need to be weighed against the spontaneous recovery that may occur in nonoperatively managed patients with acute SCI. 52,65

The clinical benefits of early reduction of fracture–dislocations of the spine by closed techniques or open surgery are difficult to assess in the absence of Class I data (Tables 3–5). 1,29,36,53,78,80,88,89,108 Reports of significant neurologic improvement in some cervical cases decompressed early by traction are encouraging but do not provide convincing, clinical evidence to support standards or overall guidelines. 29 Moreover, a number of studies have not found any neurologic benefit to reduction 39,59,106 with the possible exception of patients with bilateral facet dislocation. 10 Of particular relevance to this patient population is the study by Burke and Berryman 31 in which 76 patients with unilateral or bilateral dislocations of the cervical spine were treated with closed reduction under general anesthesia. Fifty percent of the patients were admitted to their center within 8 hours. These authors concluded that early reduction improved the neurologic recovery of patients with incomplete SCI. Based on these data and a limited number of other Class II studies (Table 5), there are thus limited data to support a recommendation for urgent reduction of bilateral locked facets in a patient with incomplete tetraplegia.

Despite the potential appeal of aggressive, closed reduction of locked cervical facets, our multicenter, cross-sectional study in 585 cases documented an 8.1% rate of neurologic deterioration with attempts at closed reduction. 99 These data are sobering and emphasize the difficulty in interpreting accounts of the beneficial effects of rapid closed reduction by traction in the absence of Class I data.

Aebi et al 1 undertook a retrospective review of 100 patients with cervical spine injuries and attempted to find an association between neurologic recovery and the timing of fracture reduction by closed or open techniques. A manual or surgical reduction was performed within the first 6 hours after the accident in only 25% of the cases, and within the first 24 hours in 57%. Overall, 31% of the 100 patients recovered, and 75% of the recoveries were in patients reduced within the first 6 hours (Table 5).

Cotler et al examined the safety and efficacy of early reduction and undertook a prospective study of early reduction by traction in 24 patients (Class II evidence). 36 They found no neurologic deterioration in any of the patients, most of whom were successfully reduced by closed techniques within 24 hours of injury, although the exact interval in hours between injury and reduction was not given. Mirza et al 78 retrospectively reviewed 30 patients with cervical spine injuries who underwent surgical decompression and stabilization either before or after 72 hours. These authors suggested that the early group had improved neurologic recovery immediately after surgery, without an increase in associated morbidity.

In contrast to the aforementioned studies of early decompression, Larson et al 70 advocated operating a week or more after SCI to allow medical and neurologic stabilization of the injured patient (Table 6). This remains the practice in many institutions, particularly in light of early reports suggesting an increased rate of medical complications with early surgery (<5 days after SCI). 75 Interestingly, a number of authors (summarized in Table 6) have documented recovery of neurologic function after delayed decompression of the spinal cord (months to years) after the injury. 10,18,20,22,27,70,101 Although these studies are retrospective in design, the improvement in neurologic function with delayed decompression in patients with cervical or thoracolumbar SCI who have plateaued in their recovery is noteworthy and suggests that compression of the cord is an important contributing cause of neurologic dysfunction.

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Effect of Surgery on Complications and the Length of Stay After SCI

The issue of whether surgery, especially early surgery, increases the rate of complications in patients with SCI has been one that has generated considerable controversy and debate. Many patients with SCI with high tetraplegia or significant associated systemic injuries are critically ill because of cardiorespiratory compromise. Early investigators such as Guttman 55,56 and Bedbrook and Sakae 12 and, more recently, Wilmot and Hall 111 and Marshall et al, 75 have argued against surgery, especially early intervention in these critically ill patients. However, modern techniques of critical care and neuroanesthesia 72,87,103 have allowed these patients to undergo surgery with minimal differences in complication rates between operative and nonoperative cases. 95,110 Indeed, an analysis of the NASCIS II database by Duh et al showed that those operated on in the first 24 hours had a lower rate of complications than those undergoing operative intervention at later timepoints. 47 In a study from our unit, the only difference in morbidity between the surgical and nonsurgical cases was a slight increase in the incidence of deep venous thrombosis in the operated group. 95 Furthermore, the length of stay in the two groups did not differ. 95 In the prospective, randomized trial of the timing of surgery by Vaccaro et al, 102 there was no significant difference in length of acute postoperative intensive care stay or length of inpatient rehabilitation between the early and late groups. This was reiterated by Mirza et al 78 and Chen et al. 33 Moreover, in a prospective study of 2204 cases, Waters et al 106,107 found that there was no difference in the complication rates of cases managed by nonoperative or surgical techniques. Accordingly, there is Class II evidence to support the safety of surgery, including operative treatment within the first 24 hours.

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Conclusion

There is strong experimental evidence from animal models that decompression of the spinal cord improves recovery after SCI (Table 2). However, it is difficult to determine a time window for the effective application of decompression in the clinical setting from these animal models. Studies of secondary injury mechanisms including ischemia, free radical-mediated lipid peroxidation, and calcium-mediated cytotoxicity suggest that early intervention within hours after SCI is critical to attain a neuroprotective effect. Whether the same time window applies to surgical treatment is as yet unclear. To date, the clinical studies that have examined the role of surgical decompression in SCI are limited to Class II and III evidence, except for one study of the timing of decompression. Surgery remains a valid practice option, although there are no conclusive data showing a benefit over conservative management approaches. There is Class II evidence suggesting that either early (<25 hours) or delayed (>200 hours) surgical intervention is safe and equally effective. Clearly, to better define the role of surgery in the management of acute SCI, randomized, controlled prospective trials are required.

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Key Points

  • There is a strong biologic rationale, based on experimental evidence in animal models, to support the concept that early decompression may improve outcome after acute SCI.
  • There are Class III data to suggest a role for urgent decompression in the setting of 1) bilateral facet dislocation and 2) incomplete spinal cord injury with a neurologically deteriorating patient (option).
  • There is Class II evidence that early (<24 hours) surgery does not increase the complication rate after acute SCI (guideline).
  • Based on a comprehensive review of the available literature, decompressive surgery for SCI can overall only be recommended as a practice option (Class III evidence).
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Keywords:

spinal cord injury; timing; surgery; decompression]Spine 2001;26:S101–S110

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