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Management of Sacral Fractures
The sacrum is integral to the biomechanical and neuroprotective roles of the spinal column and pelvic ring. Although injuries to the sacrum have historically been relatively overlooked within the realm of spine trauma, sacral fractures may result in deformity, chronic pain, and loss of lower extremity, bowel, bladder, and sexual function. Treatment of sacral fractures must therefore address the sacrum’s structural and neurologic roles and requires a thorough understanding of neural decompression and skeletal reconstruction techniques. The severity of sacral fractures varies from lower-energy insufficiency fractures in osteopenic patients to complex, widely displaced fracture patterns caused by high-energy mechanisms. In either case, treatment must often account for associated injuries and underlying medical conditions. The evaluation and treatment of these injuries must take into consideration a number of factors beyond those relevant to the lumbar spine or pelvic ring alone. These factors are related to the complexity of the lumbosacral junction, challenges associated with fixation of the sacrum and posterior pelvic ring, and the relatively large forces that must be neutralized to achieve and maintain a reduction across the lumbosacral junction. Optimal results usually require multidisciplinary efforts among the spine surgeon, orthopedic traumatologist, trauma surgeon, internist, and rehabilitation medicine specialist.
Anatomic and Biomechanical Considerations
The sacrum is the foundation of the spinal column, providing an anchor for the mobile lumbar spine. Compared with the remainder of the lumbar spine, the lumbosacral articulation is inherently more stable than more cephalad lumbar motion segments because of the presence of additional ligamentous stabilizers in the form of (1) the iliolumbar ligaments that extend from the L5 transverse processes to the iliac crests and (2) the sacrolumbar ligaments that originate contiguously with the iliolumbar ligament and insert into the anterosuperior aspect of the sacrum and sacroiliac (SI) joint.
The sacrum has a forward inclination that is balanced by the usual lumbar lordosis, allowing a plumb line to normally extend from C7 to the posterior aspect of the L5–S1 intervertebral disc. The sacral inclination angle varies from 10 to 90 degrees and usually ranges between 45 and 60 degrees. , Pelvic incidence, which measures the orientation of the lumbosacral junction relative to the pelvis, can be a valuable method for determining sagittal alignment when treating sacral fractures and is usually approximately 50 degrees. Sacral fractures that significantly alter spinal sagittal alignment may result in difficulty with maintaining an erect posture, compensatory lumbar malalignment, and associated pain and functional deficits.
The sacrum also forms the posterior aspect of the pelvic ring and has therefore been described as the keystone of the pelvic ring because it maintains stability while transmitting forces from the lumbosacral articulation across the SI joints to the pelvis. This keystone function is particularly true in the pelvic outlet plane, in which the orientation of the sacrum relative to the ilium is such that axial forces lock the sacrum into the pelvic ring and further stabilize the SI articulation. However, in the pelvic inlet plane, the sacrum is shaped like a “reverse keystone,” which is more inherently unstable and therefore requires substantial intrinsic and extrinsic ligamentous stabilization of the SI joints while still permitting pelvic ring motion.
The osseous sacral anatomy is comprised of five kyphotically aligned, fused vertebral segments, with significant variability in upper sacral anatomy in the form of transitional vertebrae and sacral dysplasia. , Because upper sacral variability results in significant alteration in the relationships among the sacrum, pelvis, and spinal column relative to their adjacent neurovascular structures, these variations must be recognized, particularly if surgical treatment of sacral fractures is being considered.
The upper sacral body has the densest sacral cancellous bone, particularly adjacent to the superior S1 end plate. The ventral aspect of the upper S1 body that projects anteriorly and superiorly into the pelvis is termed the sacral promontory . The sacral ala, the lateral portion of the sacrum that articulates with the ilium through the SI joints, is largely cancellous and is formed by the coalescence of the sacral transverse processes. The cancellous alar bone is hypodense, particularly in older individuals, and an alar void is a consistent finding in middle-aged and older adults. , The relative difference in bone density between the upper and the lower sacral body predisposes this area to fracture. The hypodense ala is predisposed, particularly in older and osteopenic patients, to fracture line propagation. This problem is accentuated by the relative strength of the SI joint ligaments. Similarly, younger individuals injured before complete ossification of the sacrum are predisposed to disruption at the S1–S2 level because of relative weakness at that interval. The suboptimal alar bone density must be taken into consideration when planning reconstructive procedures.
The posterior surface of the sacrum is convex and is formed by the coalescence of posterior elements. The middle sacral crest corresponds to the spinous processes, the intermediate sacral crests correspond to the zygapophyseal joints, and the area between corresponds to the laminae. The lowest one or two sacral segments have incompletely formed bony posterior elements, resulting in an aperture into the sacral spinal canal known as the sacral hiatus. Enlargement of the sacral hiatus may weaken the sacrum and predispose it to fracture.
The dural sac typically ends at the S2 level, and the filum terminale attaches its caudal end to the coccyx. At the junction of the body and the sacral ala are four paired ventral and dorsal neuroforamina through which the ventral and dorsal rami of the sacral nerve roots pass. The relative space available to the sacral nerve roots in the ventral foramina is lowest at the S1 and S2 levels, where the nerve roots occupy one-third to one-fourth of the foraminal space, compared with the S3 and S4 levels, where the nerve roots occupy one sixth of the available foraminal space. The lower sacral roots are therefore less likely to be impinged upon in injuries involving displacement of the neuroforamina.
The dorsal nerve roots exit through their respective posterior neuroforamina to supply motor branches to the paraspinous muscles and cutaneous sensory branches that form the cluneal nerves. Anteriorly, the L5 nerve root passes underneath the inferior edge of the sacrolumbar ligament and drapes over the anterosuperior aspect of the sacral ala. It anastomoses with the L4 ventral ramus and is joined by the exiting ventral sacral nerve roots as it passes caudally along the sacral ala to form the sacral plexus. The dual innervation of the perineal structures from both the left and the right sacral plexus is protective of bowel, bladder, and sexual function. These functions are largely preserved in the event of unilateral transection of the sacral nerve roots, whereas bilateral transection causes complete loss of function.
The presacral area has an extensive and highly variable vascular network. The middle sacral artery typically courses ventrally along the midline of the L5 vertebral body and the sacrum after branching from the aorta at the common iliac bifurcation. The common iliac arteries subsequently give rise to the internal iliac arteries that lie anterior to the SI joints and give off both superior and inferior lateral sacral arteries. The superior lateral sacral artery courses caudally, just lateral to the sacral foramina, and supplies the spinal canal through the S1 and S2 ventral foramina, whereas the inferior lateral sacral artery traverses the inferior aspect of the SI joint before anastomosing with the middle sacral artery and giving off spinal arteries that pass through the S3 and S4 ventral foramina. The internal iliac veins lie posteromedial to the internal iliac arteries and course caudally. They are located medial to the SI joint directly adjacent to the sacral ala. The internal iliac veins give rise to an extensive presacral venous plexus, formed by anastomoses between the lateral and the middle sacral veins that communicate transforaminally with the epidural veins in the spinal canal. , , This extensive vascular network renders anterior exposures to the sacrum impractical and perilous.
Familiarity with the anatomy of the ilium is also important for accurate iliac screw placement in lumbopelvic fixation techniques. The ilium provides a continuous bony channel, the sciatic buttress, that extends between the posterior superior iliac spine and the anterior inferior iliac spine, with dimensions that readily accommodate iliac screws.
Classification
Historically, several sacral classification systems have been proposed to describe sacral fractures or subsets of sacral fracture. , Among these are the Denis classification, Roy-Camille classification as modified by Strange-Vognsen and Lebech, and the Isler classification. Despite having contributed to our understanding and treatment of sacral fractures, these classification systems remained too broad or simplistic to be universally applied to all fractures in a manner that could reliably help to guide their treatment. The recognized shortcomings of prior systems in describing the complex and heterogeneous patterns of sacral injuries have most recently led to the development of the more comprehensive AOSpine Sacral Fracture Classification System.
Denis Classification
Although several sacral fracture classification systems have previously been proposed, none was widely adopted until 1988, when Denis et al. described an anatomic classification that correlated fracture location relative to the sacral foramen with the presence of neurologic injury. This classification divides the sacrum into three zones ( Fig. 164.1 ). Zone I (alar zone) fractures remain lateral to the neuroforamina. Zone II (foraminal zone) fractures involve one or more neuroforamina while remaining lateral to the spinal canal. Zone III (central zone) fractures involve the spinal canal. A greater likelihood of neurologic injury was observed as fractures occurred more medially. In this series, zone I fractures had a 5.9% incidence of neurologic injury, primarily to the L5 nerve root as it courses over the ala. Zone II fractures had a 28.4% incidence of neurologic injury due to either foraminal displacement, and resulting impingement on the exiting nerve root, or “traumatic far-out syndrome,” in which the L5 nerve root is caught between the L5 transverse process and the displaced sacral ala. Zone III fractures had a 56.7% incidence of neurologic deficits resulting from injury within the spinal canal, with 76.1% of these individuals having bowel, bladder, and sexual dysfunction. Although Denis et al. noted a broad spectrum of zone III sacral fracture–dislocations, including the presence of both transverse and longitudinal fracture line orientations, zone III sacral fractures would be more formally characterized in subsequent studies and classification systems. It should be noted that more recent studies have demonstrated a far lower likelihood of neurologic injury. Khan and coauthors recently reported an overall neurologic injury rate of 3.5%, compared with 21.6% in the series by Denis. They categorized their neurologic injury rate according to the Denis zone of injury as: zone 1—1.9% versus 5.9% in the series by Denis; zone II—5.8% versus 28.4%; and zone III—8.6% versus 56.7%.
Gibbons et al. studied 44 cases of sacral fracture according to the Denis classification system to describe the patterns of neurologic injury. With an overall 34% incidence of neurologic injury, they used these results as a basis for classifying neurologic injury caused by sacral fractures: (1) no neurologic injury; (2) paresthesias only; (3) motor loss with retained bowel and bladder function; and (4) bowel and/or bladder dysfunction. They reported neurologic injury in 24% of zone I injuries, 29% of zone II injuries, and 58% of patients with zone III injuries. Neurologic deficits with zone I and II injuries involved primarily the L5 and S1 roots. No patient with zone I or II injuries had bowel or bladder dysfunction, whereas 6 of the 12 patients with zone III injuries and neurologic deficits had bladder dysfunction.
One recognized shortcoming of this classification is that the Denis classification does not further differentiate zone III fractures, which can vary from nondisplaced sagittal plane fractures to highly unstable fractures with combined transverse and longitudinal components. In contrast to transverse Denis zone III sacral fractures, midline longitudinal Denis zone III sacral fractures, in which the sacrum is disrupted through the sagittal plane, have a low incidence of neurologic injury ( Fig. 164.2 ). This injury, was originally reported by Wiesel et al. in 1979, who suggested that the lower incidence of neurologic injury compared with transverse fractures is the result of nerve roots being subjected to a lateral displacement force rather than a shear force. Bellabarba et al. subsequently described this injury as a variant of the anteroposterior compression type pelvic ring injury, in which none of the patients with midline sagittal fractures in the case series had neurologic deficits, in contrast to the high incidence of neurologic injury reported in patients with predominantly transverse sacral fractures involving the spinal canal.
Transverse Sacral Fractures and the Roy-Camille Classification
Early case reports often characterized the zone III injury pattern as solely a transverse fracture, possibly because of imaging limitations. Computed tomography (CT) demonstrates that most transverse fractures of the upper sacrum have complex, three-dimensional fractures patterns. The majority of these injuries are currently understood to consist of a transverse fracture of the sacrum with associated “longitudinal” or “vertical” transforaminal and/or alar fractures that extend rostrally to the lumbosacral junction to form the so-called U fracture and its variations (e.g., H, Y, and lambda fracture patterns) ( Fig. 164.3 ). These fractures are also characterized by a high incidence of L5 transverse process fractures, indicating disruption of the iliolumbar ligament.
Roy-Camille et al. reported a series of 13 patients with transverse sacral fractures, which they classified as type 1, flexion deformity of the upper sacrum (angulation alone); type 2, flexion deformity with posterior displacement of the upper sacrum (angulation and posterior translation); and type 3, anterior displacement of the upper sacrum without angulation (anterior translation alone). Based on cadaveric studies, they hypothesized that types 1 and 2 were caused by impact with the lumbar spine in flexion, whereas type 3 fractures were caused by impact with the lumbar spine and hips in extension. Strange-Vognsen and Lebech added the type 4 injury, theorizing that comminution of the upper sacrum without significant angulation or translation was caused by impact with the lumbar spine in the neutral position ( Fig. 164.4 ). A type 5 direct impalement–type injury has more recently been proposed by Schildhauer et al. Recognition of these described variations have implications for fracture stability and fracture fixation strategy.
Isler Classification
Isler demonstrated that, even in the absence of a transverse fracture line, sacral fractures can be associated with spinal column instability. He described variations of longitudinal sacral fractures through the S1 and S2 neuroforamina that result in L5–S1 instability because of facet joint disruption ( Fig. 164.5 ). Injuries with the fracture line lateral to the S1 articular process are not associated with instability of the lumbosacral articulation, because the L5–S1 articulation remains continuous with the stable component of the sacrum. However, fractures that extend into or medial to the S1 articular process may disrupt the associated facet joint and potentially destabilize the lumbosacral junction. Complete displacement of the facet joint can cause a locked facet joint, making sacral fracture reduction difficult with closed methods alone. Facet disruption may also cause posttraumatic arthrosis and late lumbosacral pain.
Lumbosacral Injury Classification System
The importance of factors other than fracture pattern in guiding the treatment and determining outcomes of sacral fractures was first introduced as part of a new classification system in 2012 called the lumbosacral injury classification system, which was based on three injury characteristics: injury morphology, posterior ligamentous complex integrity, and neurologic status. An overall injury severity score was calculated by adding a weighted score from each category, allowing patients to be stratified into surgical and nonsurgical treatment groups. Modifiers to determining appropriate selection for operative treatment include systemic injury load and physiologic status of the polytraumatized patient, status of the soft tissues, and expected time to mobility. An algorithm was also developed to determine the recommended operative technique based on the previously out lined injury characteristics.
Aospine Sacral Fracture Classification System
To develop a straightforward hierarchal classification system progressing from least to most stable sacral fracture and capturing involvement of the lumbar spine and/or pelvis, the AOSpine Sacral Fracture Classification System was developed by a collaborative effort involving an international group of spine and pelvis trauma surgeons ( Fig. 164.6 ). This classification has focused on categorizing sacral fractures based on issues pertaining to treatment and prognosis.
Most broadly, injuries are classified into type A lower sacrococcygeal injuries below the SI joints with no impact on pelvic or spinopelvic instability, type B posterior pelvic injuries with primary impact on posterior pelvic ring stability, and type C spinopelvic injuries with implications of spinopelvic instability. Type A injuries are further subclassified into type A1 coccygeal or compression injuries including ligamentous avulsion fractures, A2 nondisplaced transverse fractures distal to the SI joint, and A3 displaced transverse fractures below the SI joint. Of note, although type A1 avulsion fractures may not impact sacral stability, they may indicate a disruption of the sacrotuberous and sacrospinous ligaments in association with a pelvic ring disruption. Type B injuries are unilateral longitudinal sacral injuries without a transverse component, in which the ipsilateral superior S1 facet remains contiguous with the medial portion of the sacrum. These are further classified based on their relation to the sacral foramen. Importantly, this type B category, to classify the vertical sacral fractures in increasing order of severity, departs from the convention used by Denis and coauthors by classifying vertical fractures medial to the foramina (central sacral fractures) as the least severe (B1), followed by alar fractures entirely lateral to the foramina (B2), followed by fractures which involve the foramina (B3), which were classified as most severe. This was based on both objective data and expert opinion that, when considering vertical fracture patterns only and excluding the complex multiplanar sacral fractures that do not constitute type B fractures in the AO classification, fractures medial to the foramina have the lowest likelihood of neurologic injury and are likely the most stable. Type C spinopelvic injuries are divided into C0 nondisplaced to minimally displaced sacral U-type insufficiency fractures, C1 longitudinal fractures in which the ipsilateral superior S1 facet is discontinuous with the medial portion of the sacrum, C2 fractures with bilateral type B fractures without a transverse component, and C3 displaced sacral U type fractures. A patient’s neurologic status is captured with the same neurologic injury designation that is consistently used across all AOSpine classification systems: Nx, patient who cannot be examined; N0, without neurologic deficits; N1, with transient neurologic injury; N2, with nerve root injury; and N3 with cauda equina syndrome. Because there is no possibility for injury to the spinal cord at such a caudal level, use of the N4 neurologic injury designation for complete SCI is not appropriate for sacral fractures. Patient specific clinical modifiers that may affect the treatment course are included: M1, significant soft tissue injury—whether an open injury or closed degloving injury; M2, metabolic bone disease; M3, associated anterior pelvic ring injury; and M4, associated SI joint injury.
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