Anatomy of the Sacrum

The sacrum is the most caudal fixed segment of the axial skeleton. The sacrum derives its name from the Greek hieron osteon (“sacred bone”). Use of this bone in religious sacrificial rites, and its role in protecting the genitalia, resulted in the word hieron being interpreted as “sacred” or “holy.” Through a direct translation into Latin, the term os sacrum was coined by the Romans and has come down to us unchanged today. The sacrum is a virtually motionless spinal segment that develops from five fused vertebrae. Each vertebra develops from three primary ossification centers, giving rise to the anterior and posterior elements. The fibrocartilaginous disk between the last two sacral vertebrae fuses at about 15 years of age; fusion continues in a cephalad direction until segmental fusion is complete at about 25 years of age. The sacrum sits like a keystone in the posterior arch of the pelvis and distributes load from the axial skeleton to the pelvis through the relatively immobile sacroiliac joints. Stability is enhanced by strong anterior and posterior ligamentous attachments between the sacrum and the pelvis. The sacrum lies at a 40-degree angle from the horizontal at the lumbosacral junction. Thus, axial loads promote rotational stresses that are counteracted by the sacrotuberous and sacrospinous ligaments, which attach opposite the S4 foramina. The first sacral foramen has the largest diameter: the diameter of the foramina in the sacrum decreases from proximal to distal from S1 to S4. The diameter of the nerve root also decreases from one third of the foraminal diameter proximally to one sixth of the foraminal diameter distally; therefore, foraminal entrapment is less likely at the lower sacral levels.

Pathophysiology and Classification of Sacral Fractures

In discussions of stability, the sacrum and pelvis are considered one unit. The pelvic ring is a relatively rigid structure whose disruption requires discontinuity in at least two places. Discontinuity can occur as either a fracture or a ligamentous disruption. Gunterberg and coworkers⁷ performed biomechanical studies of cadaveric specimens loaded to failure to evaluate pelvic stability after major amputation of the sacrum. Specimens resected below S2, sparing the sacroiliac joints, were stable. Specimens resected between S1 and S2 had one third of the sacroiliac joint resected, and stability was reduced 30%. Specimens resected 1 cm below the sacral promontory had half of the sacroiliac joint removed, and the load-to-failure strength was reduced 50%. Overall, the load to failure far exceeded the anticipated physiologic loads.

Bonnin’s original classification divided sacral fractures into six categories³: (1) juxtailiac marginal fractures; (2) fractures involving the S1 or S2 foramen with upward displacement of the lateral mass; (3) fractures through the sacral foramina, which separate the lateral mass from the body of the sacrum; (4) comminuted fractures of the upper sacrum; (5) avulsion fractures of the attachment of the sacrotuberous ligament; and (6) transverse fractures of the sacrum. Bonnin’s classification delineates common fracture types but does not correlate the fracture with the mechanism of injury or aid in clinical evaluation and prognosis. A number of classification systems for sacral fractures have been proposed since Bonnin’s time. The goals of these classification schemes have been to correlate the observed fracture with the mechanism of injury and the clinical findings and to aid in treatment planning. In 1984, Schmidek and coworkers⁶ proposed a classification based on the mechanism of injury and the resulting fracture pattern. They divided sacral fractures into those caused by direct trauma to the sacrum and those resulting from forces applied indirectly to the sacrum. Direct forces include penetrating injuries that result in open fractures, often accompanied by extensive pelvic visceral injuries. Penetrating injuries are usually stable if the sacrum and the sacroiliac joints above the S1 foramina are intact. Direct closed fractures are often caused by a hard fall onto the buttocks, causing low transverse-type fractures near the kyphos of the sacrum. Although such fractures usually occur through the foramina of S4, any of the lower three vertebrae can be involved. The distal fragment is often displaced anteriorly and may perforate the rectum in more severe cases. Because this part of the sacrum is not involved in the transmission of weight, these fractures are typically stable.

Transverse fractures accounted for 5% to 10% of all sacral fractures in the series by Schmidek and colleagues.⁶ Indirect trauma to the sacrum follows injuries to the pelvic ring or lumbar spine. The mechanism, usually a flexion injury from a position of hip flexion with knee extension, causes traumatic spondylolisthesis through the S1 or S2 foramina, with forward displacement of the upper spinal segment. Typically, this type of injury occurs in younger patients before intersegmental ossification is complete. One fourth of transverse sacral fractures resulting from falls also have an associated thoracolumbar burst fracture. Thus, lower extremity motor weakness must prompt the examiner to look for associated spinal injuries. Lumbosacral fracture-dislocations are caused by mechanisms similar to those underlying high transverse sacral fractures, and they usually involve fracture of the S1 facet, with resultant instability.

Most fractures produced by indirect forces are vertical fractures of the sacrum, which almost always occur in conjunction with pelvic fractures. Schmidek and coworkers⁶ classified these fractures into four fracture patterns: (1) lateral mass fractures (extending from the sacral notch through the ventral foramina), (2) juxtaarticular fractures (lateral sacral mass fractures with fragments dissociated from the body of the sacrum), (3) cleaving fractures (vertically oriented fractures from the sacral notch through the sacrococcygeal region), and (4) avulsion fractures (along the convex margin of the sacrum at the attachments of the sacrotuberous and sacrospinous ligaments). Combination fractures, with features of more than one pattern, may also occur. Although this scheme categorizes the different types of sacral fractures, it is cumbersome to remember and apply. In 1988, Denis and colleagues¹ published a series of 236 sacral fractures and proposed a simplified classification scheme that categorizes sacral fractures based on the sacrum’s division into three anatomic zones: zone I (alar region), zone II (foraminal region), and zone III (region of the central sacral canal). A zone II fracture can involve zone I but cannot extend into zone III, whereas a zone III fracture can involve zones I and II. In addition to being simple, this classification is relevant to the biomechanical forces applied to the sacrum and the probability of neural injury, and it aids in choosing among treatment options.

Zone I fractures pass through the ala without damaging the foramina or central canal (Fig. 320-1). They are usually caused by lateral compression of the pelvis during pedestrian accidents in which the posterior sacroiliac ligaments remain intact and a portion of the ala is compressed anteriorly. Zone I fractures are stable by virtue of the intact posterior ligaments. Vertical shear injuries of the pelvis can produce more severe zone I fractures, with superior displacement of the ala and compression of the L5 nerve root between the fracture fragment and the L5 transverse process (Fig. 320-2). Wiltse and colleagues named this mechanism of L5 root injury the traumatic far-out syndrome.⁸ Zone I fractures also include avulsion fractures at the bulbous enlargement of the sacrum adjacent to the S4 foramen, which is the point of attachment of the sacrospinous and sacrotuberous ligaments. A substantial degree of pelvic disruption occurs with avulsion fractures; therefore, the pelvis is often unstable.

FIGURE 320-1 Zone I fracture (Denis classification) through the ala of the sacrum.

FIGURE 320-2 Zone I fracture (Denis classification) through the ala of the sacrum with upward displacement of the fracture fragment, trapping the L5 nerve root against the transverse process of L5 (traumatic far-out syndrome).

Zone II fractures involve one or several sacral foramina, but not the sacral canal (Fig. 320-3). They are often vertical shear fractures sustained by passengers involved in high-speed motor vehicle crashes, but they may also occur after lateral pelvic compression injuries such as those occurring in zone I fractures. Vertical shear injuries often involve zone II but may also involve zone III. Usually, they are part of an anterior-posterior vertical fracture (double vertical fracture) of the pelvis. These fractures result from a significant transmission of force through one leg or on one side of the pelvis. Vertical shear injuries are uniformly unstable, and the degree of disruption of the sacroiliac joint correlates with both the degree of pelvic instability and the likelihood of neurological deficit.⁶ Neurological injuries occur in 28% to 54% of zone II fractures.

FIGURE 320-3 Zone II fractures (Denis classification) through the sacral foramina may involve one or several foramina.

Zone III fractures involve the sacral canal medial to the foramina and may involve zones I and II (Fig. 320-4). This group includes vertical shear injuries, high and low transverse fractures, and traumatic lumbosacral fracture-dislocations (or traumatic spondylolisthesis of L5 on S1). The transverse sacral fracture, also called the suicidal jumper’s fracture,⁹ commonly follows a fall from a height. This fracture typically crosses S2-3, just below the level of the sacroiliac joints, with anteroinferior displacement of the upper sacral segment.

FIGURE 320-4 A, Zone III oblique fracture. B, Zone III transverse fracture. Zone III fractures involve the sacral canal medial to the foramina and can involve zones I and II. They include vertical shear fractures, high and low transverse fractures, and traumatic lumbosacral fracture-dislocations.

These transverse fractures account for 5% to 10% of sacral fractures and are frequently accompanied by neurological injury.⁶ Fractures in zone III are associated with a high incidence of bilateral nerve root damage and cauda equina dysfunction. Certain features correlate with a high risk for instability: sacroiliac joint disruption, sacrospinous and sacrotuberous avulsion fractures, high transverse and bilateral sacral fractures, and vertical shear fractures. In contrast, lumbosacral fracture-dislocations are highly unstable during flexion.

Sacral Insufficiency Fractures

Occult fractures of the sacrum in older osteoporotic patients have been reported as a cause of back pain. These fractures can occur with minimal trauma or without a history of trauma; they are for the most part radiographically occult. The use of bone scintigraphy has allowed the detection of these fractures in suspected patients with risk factors. The typical appearance on bone scan is an H-shaped hyperfixation of the tracer; however, most patients display tracer accumulation only at the site of the fracture. Sacral insufficiency fractures typically occur in zone II and are oriented vertically.

Besides osteopenia in the postmenopausal woman, other conditions like local radiation therapy, chronic steroid use, and rheumatoid arthritis can predispose patients to having sacral insufficiency fractures. Sacral insufficiency fractures are often found in patients with other associated fractures of the spine and pelvis. Pubic fractures are most frequently associated with sacral fractures; discovery of one should prompt the examiner to look for the other.

Clinical Presentation

Clinical suspicion is essential for an early diagnosis of sacral fracture. Sacral fractures can produce neurological deficits, which may be easily overlooked in patients with multiple traumatic injuries. The high incidence of sacral fractures associated with pelvic injuries should prompt a search for their presence when there is significant pelvic pathology.

Posterior pelvic fractures are associated with an increased risk for uncontrolled hemorrhage and death. Thus, these fractures are often immobilized and stabilized urgently to control pain and bleeding, typically by external fixation techniques performed after initial resuscitation.

In hemodynamically stable patients, the presence of pain, swelling, ecchymosis, open wounds, tenderness to palpation over the sacrum, or a palpable deformity should alert the examiner to the possibility of sacral injury. Deficits in lower extremity motor function may be observed—namely, weakness in eversion and plantarflexion of the foot (S1) and hip extension (S2). Motor deficits associated with isolated sacral fractures are usually minor because most lower extremity motor control arises cephalad to sacral fractures. The superior gluteal nerve can be injured, causing weakness of hip abduction and internal rotation. Much of the sacral innervation is associated with urogenital and anal sphincter control as well as with perineal sensation. The second through fifth sacral roots innervate the muscles responsible for anal sphincter tone, anal wink, and bulbocavernosus reflex and also provide the parasympathetic input to the inferior hypogastric plexus. S2 is the main constituent of the pudendal nerve, which, with S3 and S4 branches, supplies the striated muscles of the internal and external anal sphincters. Parasympathetic innervation through pelvic splanchnic afferent nerves carries sensation for the awareness of bladder filling, and efferent fibers control both bladder detrusor and rectal contractions. Sympathetic innervation from S2 and S3 sympathetic ganglia controls contraction of the urethral and anal sphincters.

The incidence of neural injury in an unselected series of pelvic fractures was 0.75% to 11%. In Denis and coworkers’ series of 236 sacral fractures, 49 patients (21%) had neurological deficits. Five patients with deficits also had associated thoracolumbar fractures with paraparesis. The likelihood of neurological injury is increased in unstable pelvic and sacral fractures. In addition to immediate neurological deficits, delayed neurological injuries can follow callus formation and untreated spinal instability. Some patients with cauda equina syndrome may recover bowel and bladder function if the S2 and S3 nerve roots are preserved unilaterally.

The Denis three-zone classification system can be useful in anticipating neurological deficits associated with sacral fractures. Zone I fractures are rarely associated with neurological injuries. In the series by Denis and coworkers, 5.9% of patients with zone I fractures presented with neurological deficits.¹ Of these patients, 86% had L5 root lesions due to proximal displacement of the ala. Some patients with zone I injuries were impotent from pelvic or pudendal nerve injuries associated with bladder or urethral tears. In patients with zone II fractures, nerve root injuries can be expected if displacement is present. Denis and coworkers found that 28% of fractures of this type were associated with neurological deficits.¹ Neurological deficits in zone II fractures correlate strongly with ipsilateral disruption of the sacroiliac joint.⁶ In displaced zone I and II fractures, the traumatic far-out syndrome, with L5 nerve root injury caused by cephalad displacement of the lateral mass of the sacrum and L5 nerve root compression against the L5 transverse process, may be a cause of radicular deficits. Fifty-seven percent of patients with zone III fractures had associated neurological deficits; of these patients, 76% had bowel or bladder impairment or both.¹

Diagnostic Imaging

The sacrum is poorly visualized on standard anteroposterior radiographs of the pelvis because of the orientation of the sacrum at the lumbosacral junction. In one series,¹⁰ 49% of sacral fractures were not diagnosed during the initial hospitalization, including 24% of patients with neurological deficits referable to these fractures. Only 30% had appropriate radiographic studies that confirmed the fracture and explained the neurological deficit.¹ Therefore, unless a high degree of clinical suspicion is entertained, many sacral fractures will be missed on initial trauma radiographs. Certain findings on anteroposterior pelvic radiographs should arouse suspicion: (1) fracture of a lower lumbar transverse process, (2) significant anterior pelvic ring fracture without an identifiable posterior pelvic lesion, (3) asymmetry of the sacral notch, (4) clouding of the radiating trabecular pattern in the lateral sacral mass, or (5) irregularity of the arcuate lines of the upper three sacral foramina.

For patients with clinical signs of sacral injury or suspicious findings of anteroposterior pelvic films, or both, an appropriate imaging protocol includes a true anteroposterior sacral radiograph, performed with the x-ray beam directed 30 degrees cephalad (Ferguson’s view), and a lateral sacral radiograph that includes the entire coccyx. Thin-cut computed tomography (CT) scanning of the sacrum with reformatting is the most useful modality for evaluating complex sacral fractures and patients with neurological injuries.¹⁰ Sagittal CT reconstructions are especially helpful for diagnosing transversely oriented fractures and for evaluating the sacroiliac joint.

Myelography can be useful for evaluating an injury at S1 and lumbosacral dislocation. This modality can show nonfilling of the nerve roots associated with transverse fractures and cauda equina nerve root avulsions associated with traumatic meningoceles. Myelography, however, is of limited use in evaluating neurological deficits caused by sacral fractures because the thecal sac ends at S2 and because the incidence of associated foraminal and extraforaminal nerve root injuries is high.

The value of magnetic resonance imaging (MRI) in the evaluation of sacral fractures with neural injury has not been well defined. Many patients with multiple traumatic injuries are not candidates for MRI because they are hemodynamically unstable or need mechanical ventilation. In addition, the external fixators used to stabilize pelvic fractures can cause a metallic artifact that obscures visualization of the neural elements. Sacral insufficiency fractures are even less frequently diagnosed, owing to the lack of an adequate history of trauma, minimal displacement of fracture fragments, and technical difficulties associated with interpreting radiographs of osteopenic bone. In such cases, radionuclide bone scanning is a sensitive test and produces a characteristic H-shaped pattern of uptake.

Management

The management of sacral fractures remains controversial, despite an improved understanding of the anatomy and mechanisms of injury. No controlled study of treatment protocols has been undertaken, and the available information comes from case reports and small series. A sacral fracture, however, needs to be managed in the context of the patient’s general condition. The associated life-threatening injuries often encountered in patients with sacral fractures take precedence during early management. Therefore, early operative intervention for a sacral fracture can be constrained by these considerations. Loss of stability and the presence of neurological deficits are the primary considerations in the decision to operate. Sometimes, reduction and stabilization of an unstable pelvis (including the sacrum) may be a priority during resuscitation in an effort to control retroperitoneal hemorrhage and pain. Presacral or retroperitoneal bleeding occurs from injury to the internal iliac vessels and the presacral venous plexus.

Early treatment in patients with suspected sacral and pelvic fractures includes immobilization and military antishock trousers applied acutely. During transportation, intravascular volume resuscitation, external pelvic fixation, and fracture reduction should be instituted. Evacuation of retroperitoneal hematoma and pelvic exploration are contraindicated unless continuing and exsanguinating hemorrhage is present. An intra-abdominal or anterior approach to fresh sacral fractures, with evacuation of tamponading retroperitoneal blood, is fraught with the risk for causing uncontrollable hemorrhage.

Stability of sacral fractures can be defined crudely as the ability of the fractured sacrum to bear physiologic loads without further displacement. Certain fracture patterns are more likely to be associated with instability: disruption and displacement of the sacroiliac joints; vertical sacral fractures, especially those associated with shear; and sacrotuberous and sacrospinous ligamentous rupture or avulsion. Many sacral fractures can be successfully managed conservatively with bed rest and pelvic immobilization. Most surgical approaches involve posterior neural decompression with skeletal reduction and internal fixation.

Sacral fractures without prior trauma are a common source of lower back pain in elderly osteopenic women. In their early stages, these fractures are difficult to detect radiologically. Bone scans can detect such fractures and should be obtained when there is a high degree of suspicion. Sacral insufficiency fractures in zone II are oriented vertically, paralleling the sacroiliac joints. They are managed conservatively with bed rest and treatment of the osteoporosis.

Most zone I fractures are stable and cause no neurological injury. They are treated symptomatically, and early mobilization is possible. If the fracture is unstable and associated with an anterior pelvic fracture or disruption, anterior pelvic fixation or plating is required. When a vertical shear pattern of injury involves zone I, II, or III with proximal and posterior migration of the hemipelvis, the pelvic injury is life threatening and requires emergent treatment. Skeletal traction and external pelvic fixation reduce hemorrhage and facilitate the patient’s management, but no external frame or anterior plate fixation adequately stabilizes a displaced posterior injury. In patients with L5 nerve root injuries caused by trapping from a superiorly displaced lateral mass of the sacrum, reduction of the fracture may decompress the nerve root adequately. For vertical shear injuries that are inherently unstable, early traction on the ipsilateral leg with or without manipulation may reduce the fracture. Reduction may be difficult to achieve if displacement is greater than 2 cm and the deformity has been present for more than 72 hours. In such cases, open reduction and internal fixation should be performed.

Posterior fixation of the sacrum is performed indirectly by stabilizing the posterior pelvis, and reduction of the sacral pelvic injury may decompress the neural elements. Posterior tension banding using double cobra plates or threaded rod assemblies connects the posterior iliac crests posterior to the sacrum, providing immediate stability; this method may be used in conjunction with anterior fixation or plating.

For patients with zone II injuries and radiculopathy caused by foraminal stenosis, bed rest has been recommended as the first line of treatment. Foraminal compression of the L5 root with the lateral far-out syndrome, with ankle dorsiflexion weakness and persistent sciatic pain or plantarflexion weakness due to trapping of the S1 nerve root, may require early nerve root decompression. Sacral laminectomy and foraminotomy of the involved roots are the procedures of choice. If the fracture is stable with sciatic pain but without neurological deficit, bed rest for 1 month is the treatment of choice. If the radiculopathy fails to resolve after 1 month or recurs and foraminal stenosis persists, the patient should be offered the option of surgery. If the fracture is unstable and the patient is in pain, an anterior external fixator may provide relief.

By definition, zone III fractures are vertical or transverse sacral fractures and often involve the central canal, with a higher incidence of neurologic deficits. Low transverse fractures commonly occur through the S4 sacral segment and do not compromise spinal or pelvic stability. Consequently, they are treated symptomatically. High transverse fractures and vertical sacral fractures through zone III are usually unstable and require internal or external stabilization. Decompression of the sacral canal and nerve roots, with or without reduction of the displaced fragments and fixation, may be indicated in the presence of neurological deficits.

Simple transverse fractures can compress the roots of the cauda equina at the level of the fracture; high-resolution CT with reformatting is necessary to identify the level of compression. We recommend early decompression of the sacral canal in patients with cauda equina injury in an effort to restore neurological function to the bowel, bladder, and sexual organs. Although severely displaced fractures can crush or lacerate the nerve roots beyond recovery, we recommend exploration and decompression because even unilateral preservation of the S2-4 roots permits the restoration of function.

Conclusion

Sacral fractures are a poorly understood and inadequately treated condition, despite their common occurrence in patients with multiple traumatic injuries and patients with osteopenia. Diagnosis is difficult, owing to their poor visualization on radiographs. A high degree of suspicion in multitrauma patients and in patients with osteopenia and undiagnosed low back pain will lead to detection of these fractures. No standard treatment options have been established; therefore, careful neurologic assessment and decisions regarding treatment have to be made on an individual basis.