2 Acute Trauma and Chronic Overuse (According to Region) Intracranial sequelae of trauma are of paramount concern, clinically and prognostically, when it comes to diagnostic imaging of acute traumatic brain injury. The diagnostic algorithm depends primarily upon the mechanism of the trauma (impact force, impact site) and upon the clinical findings. Conventional diagnostic radiography is only useful for examining the region of the facial bones. Otherwise, potential bony injuries of the skull should be evaluated with high-resolution multidetector CT. MRI can be complementary in certain clinical settings such as a subacute traumatic brain injury or brainstem lesion. Pathology. Depending on the type of force, cranial vault fractures may be linear, comminuted, segmental (often associated with fragment dislocation), or depressed. Variants include separation of the cranial sutures (diastatic fractures) in patients up to the age of 30 years and “ping-pong” fractures in infants, which resemble the elastic and reversible dents of a ping-pong (table tennis) ball. Complications include cerebrospinal fluid fistula (in some cases associated with pneumocephalus), brain contusions, and brain herniation. Temporal fractures often result in intracranial hemorrhage (middle meningeal artery, venous sinuses). In rare cases involving children, a leptomeningeal cyst may develop that presents as a “growing” skull fracture. Radiography. Conventional radiographs are obsolete for evaluating skull trauma as they may demonstrate fractures but not associated intracranial pathology. Furthermore, studies have shown that only approximately 50% of patients with intracranial hemorrhage also have a fracture. When radiographs are obtained, confusion can arise from normal variants that may simulate fractures including vascular grooves, sutures, synchondroses, and irregularities of the internal table. Fracture lines may cross these normal structures and their lack of sclerotic margins is often helpful in diagnosis ( Fig. 2.1). CT. Indications for obtaining a CT examination after head injury include impaired consciousness, persisting vomiting, retrograde amnesia, seizure, severe (penetrating) trauma, multiple injuries, or signs of a basilar skull fracture. Indirect signs of a fracture should be noted: opacification or air–fluid levels in the paranasal sinuses, the mastoid cells, and the middle ear cavity, or air in the subarachnoid space. US. Ultrasound is only used in children. Palpable cephalohematomas associated with skull contusions can be well assessed using ultrasound, as can possible skull fractures. In these cases it is important to distinguish between fractures and cranial sutures. An adjacent epidural or subdural hematoma must be excluded in the presence of a displaced or impacted skull fracture, if necessary with the use of a CT scan. MRI. MRI has little if any role in the diagnostic work-up of acute head injury. Special features in children. Strict criteria must be applied when considering the use of radiography in children, especially after mild head injury Guidelines on the use of imaging of children after mild head trauma are issued by national societies in many countries and should be consulted. Moderate and severe head injuries, however, require immediate diagnostic imaging with CT. Pathology. Basilar skull fractures commonly occur with head trauma. They preferentially involve the orbital roof, cribriform plate, petrous pyramid of the temporal bone, or the occipital bone. The central parts of the skull base are less frequently involved. These fractures may be associated with injuries to the neurovascular structures passing through this region (cranial nerve injuries, cerebrospinal fluid fistulas, carotid aneurysms, sinus cavernosus fistulas, etc.; Figs. 2.2 and 2.3). Lesions of the optic nerves or chiasm are common complications of injuries of the middle or anterior skull base. Posttraumatic cerebrospinal fluid fistulas are most commonly found in the region of the cribriform plate where the fractures typically course along the thin parts of the bone. Fractures of the posterior skull base often extend from elsewhere in the skull, but primary fractures in this region often result in a fatal brainstem injury. Radiography. Conventional radiographs have no role in evaluating this type of injury. CT. High-resolution multidetector CT with a slice thickness of 0.5 to 1.0 mm (with or without 3D reconstructions) is the standard imaging technique in this clinical scenario. The classification of fractures of the petrous bone into transverse and longitudinal fractures is somewhat arbitrary as many cases involve more than one fracture orientation. Longitudinal fractures of the petrous bone are more common, representing 70 to 80% of all petrous bone fractures. They course along the longitudinal axis of the temporal bone and through the roof of the middle ear cavity, to end in the region of the tensor tympani muscle ( Fig. 2.4). The region around the geniculate ganglion is often involved (10–20% of these cases are associated with facial nerve injuries). They often result in dislocation of the ossicular chain and conductive hearing loss. These carry a risk of an associated ascending infection from the external auditory canal, found in 20% of all fractures of the petrous bone. Fig. 2.1 Typical linear skull fracture. Note the sharp contour of the fracture line and the absent marginal sclerosis in contrast with the cranial suture and the vascular channel. Fig. 2.3 Basilar skull fracture involving the cavernous sinus secondary to fracture of the lateral wall of the sphenoid sinus. The patient had exophthalmos on the right side. CT after contrast administration. Transverse fractures of the petrous bone begin at the posterior surface of the pyramid, traverse the roof of the internal auditory canal and also proceed toward the geniculate ganglion. They usually terminate in the musculotubal canal ( Figs. 2.5 and 2.6). Symptoms depend on the course of the fracture and may include sensorineural deafness and/or vertigo and spontaneous nystagmus. The facial nerve is injured in up to 50% of cases. CT. Using the data from axial thin-slice CT scanning, coronal reconstructions are usually helpful for assessing the course of the fracture. Indirect signs of a fracture are opacification of the mastoid cells and/or the tympanon. MRI. If hearing loss and/or facial nerve paralysis is present, MRI is indicated to directly evaluate the facial nerve and exclude a hematoma. Important findings. It is important to search particularly for fractures involving the labyrinth, the internal auditory canal, and the facial nerve as well as dislocation of the ossicular chain. A distinction is made between midfacial, orbital, and mandibular fractures. Facial bone fractures are primarily the result of motor vehicle accidents and, less commonly, physical altercations. High-resolution CT using a low-dose technique (if necessary with 3D reconstructions) is the standard imaging modality, especially for fractures of the midface and orbit. Mandibular fractures (usually multiple), dental fractures, etc. may be evaluated with conventional radiographs, orthopantomography, or low-dose CT. Typical direct fracture signs: • Interruption in contour (with or without step-off). • Double contour or increased density (fragment superimposition). • Radiolucent line. Typical indirect fracture signs: • Soft tissue swelling. • Opacification or air–fluid levels in the paranasal sinuses. • “Hanging drop” sign of an orbital floor fracture. • Intraorbital and/or intracranial air. Nasal fractures. This is the most common isolated fracture. Radiographs are not usually necessary. Lateral views of the nasal bone and possibly paranasal sinus views may be helpful in equivocal cases. Caution There is the risk of confusing fractures of the nose with normal sutures; fractures are usually situated more peripherally ( Fig. 2.7). Fracture of zygomatic arch. This is best visualized with the axial view (so called bucket-handle view) ( Fig. 2.8). More displaced fractures are of therapeutic relevance. In small children, the zygomatic arch should be assessed primarily by ultrasound. Fracture of the zygoma. A common injury is the tripod fracture, in which the bony connections of the zygoma with the adjacent bones are disrupted or fractured ( Figs. 2.9 and 2.10). Its depiction is achieved with paranasal sinus views and/or lateral views. CT is used in equivocal cases. Orbital fracture. Fractures of the thin orbital floor and the thin medial lamina papyracea are common. Herniation of orbital contents (fat, inferior rectus muscle) into the maxillary sinus may complicate this type of fracture ( Figs. 2.11–2.13). Typical indirect signs of a fracture include the “hanging drop” sign (see Figs. 2.11 and 2.12) and orbital emphysema. The term blow-in fracture is used when an orbital wall fracture results in bone being displaced into the orbit. Diagnostic imaging typically begins with orbital radiographs; a CT scan is indicated when a fracture has been detected (to search for other fractures, define the extent of the fracture, or assess for an associated hematoma) and in equivocal cases. Fig. 2.6 Transverse fracture of the petrous bone extending through the epitympanum. Shadowing prevents demarcation of the facial nerve. Dislocation of the ossicular chain is also evident. Fig. 2.8 Zygomatic arch fracture. (a) Loss of the physiological contour indicating the significant impression. (b) After surgical reduction. Fig. 2.10 Classic tripod fracture. Fractures are marked by arrows. Surface reconstruction using CT data set. Fig. 2.11 Orbital floor fracture. (a) Typical shadowing of the cranial part of the maxillary sinus. (b) The fracture is better seen on CT scan, unobscured by overlying structures. Severe facial trauma often results in complex transfacial injuries that are difficult to define and classify. The Le Fort classification system has proven useful in this regard ( Fig. 2.14): • Le Fort I: Separation of the alveolar process from the rest of the maxilla (floating palate). All the walls of the maxillary sinuses are fractured. • Le Fort II: Pyramid-shaped fracture (“pyramidal fracture”) with separation of the central midface. The fracture line courses through the root of the nose, the medial orbital wall, and the orbital floor. The medial wall of the maxillary sinus is preserved. • Le Fort III: This fracture results in separation of the face from the skull. The fracture line courses bilaterally through the root of the nose, medial orbital wall, orbital floor, and lateral orbital wall. There are additional fractures of the zygomatic arches. The common feature of all Le Fort fractures is involvement of the pterygoid processes ( Fig. 2.15). It is very common to find combinations of different (Le Fort) fracture types in one or even both halves of the midface ( Fig. 2.16). Particular attention should be paid to possible associated injuries (anterior skull base, mandible, etc.). CT. High-resolution CT is the modality of choice for suspected complex midfacial injuries. 3D reconstructions are often helpful for providing better visualization. MRI. When associated cranial nerve injury and/or brain injury are suspected, MRI is indicated. Mandibular fractures are commonly multiple (50–60% of cases). Fractures that course through the dental alveolus are regarded as open fractures. A differentiation is made between fractures of the mandibular body, the mandibular angle, and the mandibular ramus as well as those that involve the mandibular joint. Radiography. Standard radiographs are typically obtained. An orthopantomogram may be helpful. CT. CToffers the most exact fracture depiction, which is oftenessential for an optimal treatmentoutcome ( Fig. W2.1). In addition to 3D reconstructions ( Fig. W2.2), orthopantomograms can also be generated from the CT data set. A more recent technique, known as cone beam CT, is also proving to be useful ( Fig. W2.3). Fig. 2.15 Fracture involving the pterygoid process of the sphenoid. All Le Fort fractures involve the pterygoid process. Anatomy. See Chapter 2.2.1 and Fig. W2.4. Radiography. Radiographs are still commonly used for screening in cases of mild spinal trauma. The lateral view is the most important. It should be performed without repositioning the patient. Severe spinal injuries should be immediately investigated with CT because the extent of injury is often underestimated on conventional radiographs. The need for lateral and swimmer oblique views, and above all functional studies, should be assessed critically with regard to their diagnostic value. If a multislice CT unit is available, then conventional radiographs of the spine should be dispensed with in the patient who has sustained significant trauma. Apart from evidence of fracture lines and/or fragments, indirect signs of spinal injury include: • Loss of vertebral height. • Widening or deformity of the vertebral body. • Linear sclerosis within a vertebral body. • Irregularity or interruption of reference lines ( Figs. 2.17 and 2.18). • Segmental malalignment (this is best recognized by observing the posterior vertebral line; segmental fanning of the facet joints and spinal processes is a very helpful sign of significant injury ( Fig. 2.19). • Widening or narrowing of an intervertebral disk space relative to adjacent levels. • Widened prevertebral soft tissues (in the cervical spine this should not exceed 7 mm in adults at the level of the inferior margin of C2) ( Fig. 2.20; see also Fig. 2.17). However, a normal appearance of the prevertebral soft tissues does not exclude significant underlying bone or ligament injury. Attention should also be paid to any displacement of the prevertebral fat stripe or contour of the trachea. Fig. 2.17 Criteria for assessing the lateral view of the cervical spine. (a) Reference lines for assessing alignment and physiological width of the prevertebral soft tissue shadow. (b) Physiological width of the atlantodental interval. Fig. 2.18 Disruption of all three reference lines in the presence of anterior subluxation of C5. The disruption is secondary to discoligamentous rupture and bilateral facet joint dislocation (flexion–distraction injury). Fig. 2.19 Segmental interspinous gaping and widening of the dorsal intervertebral space at C5/C6 after a flexion–distraction injury. It should always be kept in mind that any attempt to classify an injury on the basis of radiographs alone should be done with the utmost caution since high-grade, unstable injuries can be easily underestimated with radiographs and may even be present despite an unremarkable radiographic series. CT. CT of the spine has become the imaging modality of choice for evaluating patients after significant trauma (e.g., high-speed motor vehicle accident, fall from a height, and the like). The use of CT is obligatory for possible unstable fractures detected with radiography and in cases with suspected canal compromise due to displaced fragments or hematoma. MRI. The advantages of MRI are its ability to display discoligamentous injuries (especially in an obtunded patient), spinal cord injuries (edema, hematomyelia, transection, vascular occlusion), and bone bruises. Its use is indicated in all patients who present with neurologic findings. Pathology. Fractures, dislocations, and soft tissue injuries are most commonly located at the level of the lower cervical spine and the thoracolumbar junction. In many cases clinical signs and symptoms together with radiographic findings will allow a prompt and correct diagnosis. However, factors such as poor-quality radiographs (portable technique, overlying structures, especially in the lower cervical and upper thoracic regions) or inexperience of the imager result in a relatively high rate of radiologically unrecognized spinal injuries (~ 15–30 %). As well as the use of anatomical aspects (such as the location within the spine), spinal injuries are classified according to the type of forces involved: • Compression. • Flexion. • Extension. • Rotation. • Translation (shearing). One of the most commonly used classification systems for spinal injuries is that of Magerl, which is based on the current AO classification system ( Fig. 2.21). It also attempts to take into consideration discoligamentous injury patterns as evident on MRI scans. With the Magerl classification, the severity of the injury increases from Types A through C as well as within the types from groups 1 through 3. Type A and Type B injuries are often combined. In the United States, the Thoracolumbar Injury Classification and Severity Score (TLICS), published in 2005 by A. R. Vaccaro et al. is currently used ( see references in Chapter 2.2.2). Fig. 2.20 Widening of the prevertebral shadow should raise concern for injury. (a) Because it was not possible to evaluate the lower cervical spine adequately on radiographs due to superimposition of the shoulder girdle, clarification must be achieved using sectional imaging. (b) MRI reveals an (unstable) C6/C7 flexion injury as the cause of the prevertebral hematoma. Compression injuries result from vertical forces impacting on the vertebra from a cranial or caudal direction. The fracture is usually located in the thoracolumbar region and characterized by widening of the vertebral body and loss of vertebral height as well as by disruption of the vertebral cortex. The Type A1 lesion ( Fig. 2.21) is a failure of the anterior column resulting in an isolated vertebral body injury. Subgroups of A1 fractures include • A1.1: a pure impact fracture of the superior end plate. • A1.2: a wedge type fracture. • A1.3: a vertebral body collapse. A1.3 fractures are typical osteoporotic compression fractures that result in compression of both end plates with an intact posterior wall (the so-called “fish” or “fish mouth” vertebra). Whereas A1 and A2 fractures are usually stable injuries ( Figs. 2.21 and 2.22), A3 burst fractures ( Figs. 2.23 and 2.24) are often considered to be unstable due to involvement of the posterior wall and contiguous intervertebral disks and in some cases may require surgical stabilization, especially when the burst fracture is complete (A3.3) (see Fig. 2.24). Comminuted fractures with displacement fracture fragments in the spinal canal often result in associated neurologic complications. If the neurologic deficit does not correlate with the extent of the spinal canal stenosis, then a search should be made for an associated epidural hematoma, intervertebral disk protrusion or spinal cord injury, in which case an MRI scan is the diagnostic modality of choice. CT myelography is an alternative for a patient with a contraindication for MRI or if MR scanning is unavailable. Caution Widening of the interspinous distance and/or fractures of the posterior spinal segments are indications of a higher-grade injury ( Fig. 2.25); it is imperative that these structures are assessed on the radiographic examination, and CT may be needed for complete evaluation. Extension injuries are less common than those related to flexion but are frequently overlooked or underestimated due to the often subtle associated radiographic findings. They result in neurologic damage less commonly than do flexion injuries. They often occur in older patients who sustain a ground-level fall, striking their head, producing hyperextension of the cervical spine. The cervical spine is particularly susceptible to hyperextension injuries due to its exposed position and its high degree of sagittal mobility with the center of rotation at the level of the articular processes. Vertebral alignment, including the spinolaminar line, may be normal after injury. Caution Any (segmental) widening of an intervertebral space is highly suspect of a hyperextension injury; a segmentally widened intervertebral space is never a normal finding! Extension teardrop fracture. A hyperextension injury (typical case: a dive head-first into shallow water) results in a genuine avulsion of bone at the attachment of the anterior longitudinal ligament ( Figs. 2.26–2.28). Typical levels of injury include the lower cervical spine (often in young patients) as well as in the C2 region (especially in older patients). An important point is the fact that the teardrop fragment represents the fixed point because it has remained firmly attached to the anterior longitudinal ligament, while the associated vertebral body has torn away, resulting in a triangular fragment along the anterior inferior margin of the involved vertebra on radiographs. However, neither radiography nor CT reflects the full degree of soft tissue pathology associated with such injuries, and MR imaging is indicated in these cases to identify ligamentous and spinal cord injuries. Fig. 2.22 Magerl Type A1 compression fracture. (a) Anterior reduction of height (arrows) as compared with the adjacent vertebrae. (b) The CT scan shows that only the anterior parts of the vertebra are involved. Fig. 2.23 Partial burst fracture (Type A3.1 compression fracture). (a) The cranial part of the vertebral body has burst; the inferior end plate is intact. (b) Spinal canal stenosis secondary to dorsal displacement of a posterior fragment. Fig. 2.24 Complete burst fracture (Type A3.3 compression fracture). (a) Inferior and superior end plates are fractured. (b) The vertebral body has multiple fracture lines running through it. Fig. 2.25 Higher-grade injury? Always look at the posterior parts of the vertebra! (a) The radiograph shows a compression fracture of L1 with involvement of the posterior margin (most likely Type A3.1), but the spinous processes have been cropped from the film. (b) A bony avulsion of the interspinous ligament at T12 (arrow) is apparent on this CT image; this confirms an (unstable!) Type B1 flexion injury. Posterior subluxation/dislocation. Rupture of the anterior and (rarely) the posterior longitudinal ligaments as well as the intervertebral disk, combined with dislocation/subluxation of the facet joints and, in some cases, additional fractures through the neural arches results in transient posterior translation of the vertebra ( Fig. 2.29). This injury is highly unstable and is associated with severe neurologic deficits. It most often occurs in the mid-cervical region (C4–C6) and at the thoracolumbar junction. Because the vertebra frequently reduces spontaneously, spinal alignment may appear normal on radiographs. Indirect, often subtle, findings such as anterior soft tissue swelling or anterior widening of a disk space should prompt further evaluation with MRI to assess the degree of ligamentous and spinal cord injury. Such hyperextension injuries are particularly common in older patients with degenerative spines in whom the canal is already narrowed by osteophytes and redundant ligaments (Chapter 2.2.4). These patients often present with a central cord syndrome in which the neurologic symptoms are more pronounced in the upper than in the lower extremities. Flexion injuries are the most commonly encountered in the spine. They are the result of excessive flexion of the spine in which the axis of rotation is usually at the level of the dorsal third of the intervertebral disk space. The anterior vertebral segments are maximally compressed, while the posterior are distracted. Typical compression/distraction injuries can develop as a result of this mechanism such as transverse disruption of the posterior ligamentous complex (Type B1 injury) or transverse bony disruption (spinous processes, pedicles, pars interarticularis; Type B2) ( Figs. 2.30–2.33). With high-velocity flexion loading, subluxation/dislocation of the facet joints occurs, resulting in some cases in complete bilateral dislocation and locked facets. This may result from pure discoligamentous disruptions without an associated fracture (see Fig. 2.33). Unilateral facet joint dislocations or fractures occur when there is an additional rotational force, which is often underestimated on radiographs. Spontaneous fracture reduction can occur with the patient in a supine position. Pure anterior compression fractures are stable, whereas all flexion–distraction injuries are potentially unstable. Anterior wedge fracture. The mildest form of flexion injury involves anterior compression of the vertebral end plate, which remains intact posteriorly. A stronger force produces more extensive compression with more marked formation of a wedge-shaped vertebra and possible involvement of the posterior body (middle column). A wedge-shaped vertebra can develop not only anteriorly but also laterally. The osteoporotic wedge-shaped vertebra will be discussed in Chapter 8. Note In general, care should be taken not to exclude middle column involvement in a compression injury on the basis of conventional radiographs. With wedging of more than 15 to 20° relative to the opposite end plate, involvement of the middle column should certainly be excluded by CT. Fig. 2.27 Teardrop injury, at a typical site in the upper cervical spine. (a) Triangular fragment arising from the anterior inferior margin of C3. Alignment maintained; no interspinous gaping. (b) No spinal cord injury. On the whole, the findings are most compatible with a (stable) extension injury. Fig. 2.29 Posterior subluxation. (a) Posterior teardrop fragment of C7. (b) Anterior discoligamentous detachment of the anulus fibrosus. Fig. 2.30 Flexion injury. The posterior margin of the wedge-shaped fractured thoracic vertebra is disrupted, and widening of the interspinous distance one segment higher is evidence of an unstable Type B1 injury. Fig. 2.31 Flexion injury in the presence of cervical spine degeneration. (a) Typical dorsal interspinous widening with avulsion of the anterior osteophyte. (b) MRI demonstrates complete discoligamentous disruption, indicating a high-grade unstable flexion–distraction injury. Fig. 2.32 Lumbar Type B1 injury. Disruption of the dorsal ligamentous structures (ligamenta flava and ligamentum supraspinale) with concomitant anterior compression fracture. Flexion teardrop fracture. In this type of fracture flexion has resulted in separation of a triangular, or “teardrop,” fragment from the anteroinferior corner of the vertebral body ( Fig. 2.34; see also Figs. 2.26 and 2.35). The vertebral body is split in the coronal plane, with the posterior fragment protruding into the spinal canal. The fracture is most frequently located at the lower cervical spine (70% at C5). The most important feature of this injury, however, is that it results in disruption of the posterior longitudinal ligament and is therefore extremely unstable. It also commonly results in spinal cord injury. Chance fracture. A flexion injury with the center of rotation moved to the anterior abdominal wall (as is seen with a lap seatbelt) results in significantly magnified tensile forces in the spine and a horizontally orientated disruption of the vertebral column. These fractures most commonly involve the mid-thoracic to mid-lumbar vertebra with fractures involving not only the vertebral body but also the pedicle and other posterior elements, rendering these highly unstable ( Figs. 2.35 and 2.36). Of note, the disruption may predominantly involve the soft tissues (disk, ligaments) which will be best evaluated with MR imaging. These fractures may also be associated with anterior vertebral compressions (Type A fracture) and angular hyperkyphosis. Anterior subluxation/dislocation. This is a severe form of flexion–distraction injury that is characterized by disruption of the posterior ligamentous complex together with a tear of the posterior longitudinal ligament. The intervertebral disk is also commonly involved (discoligamentous disruption). This injury is highly unstable. Rupture of the posterior anulus fibrosus can in rare cases result in traumatic disk extrusion. This results in anterior tilting of the vertebra over the underlying vertebra with fanning of the spinous processes, incomplete articulation of the facet joints, and anterior displacement of the subluxed vertebra by more than 50%. In marked cases, unilateral or bilateral facet dislocation can also develop (known as locked facets; Fig. 2.37). This is found predominantly at the lower cervical spine. It involves the tip of the dislocated inferior articular facet (superior vertebral body) being locked in front of the superior facet of the inferior vertebral body. A pure unilateral facet dislocation is a relatively stable injury as a result of interlocking of the dislocated facet joints and neurologic symptoms are uncommon. Nevertheless, the rotatory malalignment requires correction. The reverse hamburger-bun sign and the headphone sign on axial images are helpful imaging findings in these cases ( Fig. 2.38). Bilateral facet dislocation commonly results in traumatic spinal canal stenosis with neurologic deficits, which can occasionally develop after some delay. Fig. 2.34 Flexion injury of the upper thoracic spine. Fractures of the spinous processes with disruption of the posterior ligamentous complex. Additional vertical fracture of the anterior third of T2 (large flexion tear-drop fragment). Fig. 2.35 Chance fracture. Fracture with disruption of the posterior bony vertebral elements as well as compression of the anterior vertebra with a flexion tear-drop. Fig. 2.36 Chance fracture. (a) Dorsal bony disruption is evident on this CT scan. (b) The MRI scan also demonstrates the anterior bony disruption. Fig. 2.38 Typical findings of a dislocation injury of the cervical spine as demonstrated on axial imaging. Depiction of unilateral facet dislocation secondary to a rotational injury. Headphone sign: uncovertebral dislocation and step-off; reverse hamburger bun sign: loss of the regular facet contact; in each case empty joint surfaces are positioned “back to back.” Sites of predilection for typical rotational injuries are found at the atlantoaxial level and the thoracolumbar junction. Rotational injuries usually originate from severe flexion trauma combined with a torsional vector that leads to rupture of the posterior ligamentous and/or discoligamentous complex and/or fracture of the facet joints, resulting in rotational malalignment of the spinal axis. The discoligamentous involvement produces unstable spinal injuries that are associated with a high incidence of concomitant spinal cord injuries. The findings of asymmetrical dislocation or fracture of the facet joints and/or juxta-articular neural arch fractures point to a rotational component ( Fig. 2.39). Furthermore, fractures of the proximal parts of the ribs, transverse processes, and spinous processes are indirect signs of a rotational injury. Because of the risk of long-term rotatory and translational malalignment it is imperative to carefully assess images of spinal injuries (burst fractures in particular) for rotational malalignments. Rotational injuries—albeit uncommon—tend to be underestimated and underdiagnosed in multiply injured patients. Unilateral facet dislocation occurs as a result of a combination of hyperflexion with rotation and is found predominantly in the lower cervical spine (see Fig. 2.39). In only one-third of cases is it associated with a fracture of an articular process. There is often neurologic compromise due to associated foraminal narrowing. Caution MRI should be performed before treatment of unilateral facet dislocation to exclude disk injury. Any manipulation to reduce the dislocated facet joint can result in posterior displacement of an existing disk protrusion leading to neurologic complications. These injuries are the result of enormous horizontal or oblique forces. Usually the lower half of the body is fixed while the upper segment moves relative to it. The ligaments are always disrupted, even without associated fracture, if the superior spinal components are displaced dorsally. The vertebroligamentous injury pattern is complex. These are usually Grade C3 injuries according to the AO Classification (see Fig. 2.21), even though the rotational component is not always apparent (effect of positioning, spontaneous reduction in immobilization devices; Figs. 2.40 and 2.41). These injuries are often associated with severe neurologic symptoms, and multilevel injuries are commonly found in the rigid spine (Chapter 2.2.4). Transverse process fracture. Fractures of the lumbar transverse processes are predominantly the result of direct blows and usually of no clinical relevance. However, they are important as warning signs because these fractures are often associated with concomitant injuries such as other spinal injuries (possibly at a significant distance), and especially injuries to abdominal and retroperitoneal organs (e.g., renal lacerations) ( Fig. 2.42). Clay-shoveler’s fracture. This fracture of the tip of a spinous process occurs as a result of an abrupt flexion of the head and neck relative to the tight nuchal ligaments. It is a bony avulsion fracture at the attachment of the supraspinatus ligament at the cervicothoracic junction level, such that both this ligament and the posterior longitudinal ligament remain intact. The line of fracture is usually vertical through the dorsal portion of the spinous process and it is often a chronic, incidental finding (evidenced by sclerotic margins with or without associated calcification of the nuchal ligament; Fig. 2.43). However, clay-shoveler’s fractures must not be confused with an oblique Chance fracture of the spinous process or with fractures of the spinous process, which are indication of a severe dorsal distraction injury. Fractures of the sacrum. These are usually the result of a direct trauma (fall). The majority occur in combination with pelvic fractures. Denis distinguishes three types: • Type I: Lateral to the neural foramina, no neurologic symptoms. • Type II: Transforaminal sacral fractures, commonly associated with neurologic symptoms ( Fig. 2.44). • Type III: Central fractures involving the sacral canal; neurologic symptoms are common. Fig. 2.39 Rotational injury of the thoracolumbar junction. (a) Obvious segmental angulation. (b) Concave fracture of the facet joint: “empty” facet joint on the convex side (arrow), indicating facet dislocation. Fig. 2.40 Translational shear-type injury of the thoracolumbar junction. (a) Complete osteoligamentous disruption with lateral subluxation. (b) Prominent distraction with dorsal dislocation. Fig. 2.41 A rare case of discontinuous and considerably separated thoracic and thoracolumbar fractures/dislocations with bony avulsion of the anterosuperior margin of T12. The corresponding axial slices (not shown here) illustrated slight rotatory malalignment of the involved segments. Fig. 2.42 Fracture of the transverse process (arrow). In itself it is of no clinical significance, but is often an important indicator of associated injuries. Fractures of the coccyx. Radiographic assessment of the sacrococcygeal region is difficult due to the wide range of individual anatomical variability. Ventral angulation at the sacrococcygeal junction is an extremely common variant. A fracture may be identified using sectional imaging modalities (CT, MRI), but this rarely results in a change in subsequent management. Even so, chronic posttraumatic coccydynia may develop in some cases. The Magerl classification system (based on the AO system) is used for classifying fractures of the subaxial cervical, thoracic, and lumbar spine (the latter two may also be classified according to the TLICS system, see Chapter 2.2.2). Other classification systems have been developed for the upper cervical region (from the craniocervical junction to C2). Fractures of the occipital condyles are rare and are usually the result of axial blows to the head; they are best classified using the Anderson and Montesano system: • Type I: Compression fracture of the occipital condyles. • Type II: Basilar skull fracture that extends to involve the occipital condyle region. These fractures are usually stable and only identified on appropriate CT scan sections ( Fig. 2.45). • Type III: Avulsion fractures with bony ligamentous avulsions (alar and cruciform ligaments of the atlas) on the inner surface of the condyles; these injuries are potentially unstable. They often occur in combination with brainstem injuries and are the result of severe trauma. The often subtle avulsion fragments must be carefully looked for on multiplanar CT images since they are often the only signs of severe craniocervical ligament disruption ( Fig. 2.46). MRI may be used to assess associated ligamentous and/or cord injury. The infrequently encountered disruption of all ligaments at the craniocervical junction represents the ultimate form of craniocervical dissociation. This injury is seen after high-velocity trauma from considerable whiplash movement of the head with the body restrained; it is especially common in children owing to their large head-to-body ratio and lax craniocervical ligaments. (see the subsection “Special features of pediatric cervical spine injuries”). This injury is almost always fatal due to severe spinal cord damage, and if the patient does survive it is typically with a severe neurologic deficit. The angled position of the occipital condyles and atlantoaxial articular surfaces as well as the ring configuration of the atlas predispose the atlas to a burst fracture of its arch during axial compression (the so-called burst effect). Isolated fractures of the anterior and posterior arch of the atlas, on the other hand, are caused by hyperextension injuries. Neurologic deficits are rather rare with fractures of the atlas since they tend to result in enlargement of the diameter of the spinal canal. The following modified fracture classification system according to Jefferson is currently in use: • Type I: Fracture of the anterior ring of the atlas; there is often an additional fracture of the dens. Extension mechanism, usually stable. • Type II: Fracture of the posterior ring of the atlas; the most common form. The posterior ring of the atlas is wedged between occiput and C2, resulting in the fracture. Extension mechanism, usually stable. • Type III: Fracture of the ring involving both the anterior and posterior arches (Jefferson’s fracture; Fig. 2.47a). It occurs as a result of abnormal axial loading of the occipital condyles on the atlas with the head extended (compression fracture). This fracture is unstable if it is associated with a rupture of the transverse atlantal ligament. An indirect sign of ligament disruption on the odontoid view or on reformatted coronal CT images is bilateral displacement of the lateral articular masses of the atlas beyond the articular margins of the axis by more than 7 mm combined ( Fig. 2.47b). However, this sign may be masked in the presence of concomitant rotation, rendering a CT examination necessary for an exact assessment of the fracture. • Type IV: Unilateral or bilateral compression fracture of the lateral masses of the atlas; stable but unfavorable prognosis with regard to the development of posttraumatic osteoarthritis of the occipital-atlantal joints. • Type V: Fracture of a transverse process of the atlas (stable). Caution Traumatic dissection of the vertebral artery is a possible complication of a Type V Jefferson fracture. In addition there are a number of other nonclassified fracture types, such as a horizontal fracture of the anterior arch of the atlas due to traction of the anterior longitudinal ligament and the longus colli muscle, and the bilateral, vertical fracture of the posterior arch due to forced hyperextension of the head (which should be differentiated from a congenital unfused posterior arch of the atlas). Fig. 2.48 Asymmetry of the atlantodental intervals and the atlantoaxial joint spaces (known as the wink sign on the radiograph) as an indication of a rotational atlantoaxial injury. This traumatic dislocation occurs as a result of disruption of the transverse ligament of the atlas and/or the alar ligaments and is very rare. A distinction is made between anterior, posterior, and lateral dislocations of the atlas over the stable C2. The diagnosis is best made by CT or conventional radiography, which includes an open-mouth odontoid view. The atlantodental interval must not exceed 3 mm in adults and 5 mm in children (known as Spence’s rule). However, it should also be kept in mind that patients with congenital craniocervical junction abnormalities can develop atlantoaxial instability (e.g., unstable os odontoideum), while chronic inflammatory arthritides, such as rheumatoid arthritis, can also result in craniocervical and atlantoaxial ligamentous laxity. The assessment of traumatic rotational, atlantoaxial malalignment (subluxation or dislocation) and its differentiation from voluntary, postural rotation in the superior cranial joints are difficult. Clues for rotational injuries can include asymmetry on the AP odontoid view; in particular unilateral (rarely bilateral) loss of the atlantoaxial joint space on a correctly adjusted view (known as the wink sign; Fig. 2.48). The degree of rotation can be determined on axial CT sections (up to 45° is normal at maximum rotation), at which time pathologic anterior displacement of the atlas over the axis may also be detected. Fig. 2.47 Classic four-part burst fracture according to Jefferson (Type III). (a) Burst fracture of the atlas ring. Note the spatial proximity of the fracture of the atlas to the course of the vertebral arteries. (b) Indirect sign of a Type III fracture of the atlas: lateral displacement of the lateral masses of the atlas (x + y > 7 mm) relative to those of the axis. In addition, there is a bony avulsion of the transverse ligament of the atlas (arrow): unstable fracture. Classification System According to Fielding and Hawkins • Type I: Pure rotatory, unilateral atlantoaxial dislocation ( Fig. 2.49); without fracture, it is impossible to differentiate from a voluntary rotation of the head on a static CT image. Only after a dynamic examination is it possible to demonstrate a fixed rotational malalignment (when it is impossible to return the malalignment to the neutral position by turning the head to the opposite side). • Type II: Atlantoaxial rotatory abnormality with anterior dislocation and an atlantodental interval of less than 5 mm. The transverse ligament of the atlas may be ruptured. • Type III: Atlantoaxial rotatory abnormality with anterior dislocation and an atlantodental interval of less than 5 mm. Disruption of the transverse ligament of the atlas with instability. • Type IV: Atlantoaxial rotatory abnormality, with the atlas displaced unilaterally or bilaterally in a posterior direction in relation to the axis (posterior dislocation); usually in the presence of a Type II fracture of the dens or an unstable dens nonunion. Dens fractures are common and constitute approximately 20% of all cervical fractures. Hyperextension mechanisms are most commonly responsible for these fractures. Whereas more forceful accidents are mainly responsible in young adults, these fractures occur in the aged as a result of simple falls. Associated neurologic deficits are present in up to 30% of cases. A CT scan is best suited for assessing the fracture. Dens fractures are classified by Anderson and D’Alonzo into three types ( Fig. 2.50): • Type I: Obliquely through the tip of the dens; actually an avulsion fracture of the alar ligaments; an extremely rare fracture. • Type II: Transversely through the base (waist) of the dens, unstable, the most common fracture type ( Fig. 2.51). Nonunion develops in ~ 30% of cases. • Type III: Fracture of the body of C2, commonly with involvement of an atlantoaxial joint surface; anterior dislocation in 90% of cases. This fracture is also mechanically unstable, but does not tend to proceed to nonunion. Caution • A dens fracture is often simulated on conventional radiographs (AP targeted dens view) by what is known as the Mach effect ( Fig. 2.52). This is a linear lucency passing across the base of the dens that is an artifact (edge effect) occurring when two radiodense structures overlap (e.g., overlapping of the dens by the arch of the atlas). • The dens and body of the axis normally fuse between the ages of 3 and 7 years ( Fig. 2.53); however, fusion may be delayed or completely absent, thus creating the impression of a Type II fracture. Differential diagnostic aid: An os odontoideum develops when fusion is absent and, unlike a fracture, typically has a smooth margin, shows marginal sclerosis, and is usually rounded ( Fig. W2.5; see also Fig. 2.53). Often, the anterior arch of C1 is also hypertrophied in the presence of an os odontoideum, while the dens is hypoplastic. • Fusion of the ossiculum terminale of the dens, which is normally complete by the age of 12 years, may fail to occur. This simulates a Type I fracture (see Fig. 2.53). Also termed a “hangman’s fracture”, this injury occurs as a result of extension with simultaneous vertical compression, such as that which occurs in rear-end collisions. However, other mechanisms can also result in this injury, such as a pure flexion. The most commonly used classification system is that of Effendi: • Type I: Nondislocated fracture with intact intervertebral disk, stable. • Type II: Involvement of the C2–C3 intervertebral disk, sagittal displacement of the body of the axis by more than 3 mm, or angulation of the dens by more than 11°, unstable ( Figs. 2.54–2.56). • Type III: In addition to the findings with a Type II fracture, the facet joints at C2–C3 are dislocated and locked. Neurologic complications are less common than with other injuries due to the relatively large width of the spinal canal at this level. Fig. 2.49 Fielding and Hawkins Type I injury. (a) Unilateral atlantoaxial rotatory subluxation. (b) Locking of the atlantoaxial joint with a burst fracture of the lateral mass of C2. Fig. 2.51 Dislocated Anderson and D’Alonzo Type II dens fracture. (a) The anterior arch of the atlas rests upon the base of the dens. (b) The tip of the dens is clearly dislocated dorsally and may compress the adjacent cervical cord. Fig. 2.52 The Mach effect as an imaging pitfall. (a) Anderson and D’Alonzo Type III dens fracture. (b) No fracture! The radiolucent line is a Mach effect due to overlapping of the arch of the atlas. Fig. 2.54 Traumatic spondylolisthesis of C2 (hangman’s fracture). (a) Course of the fracture line through the body of the axis. (b) Involvement of the intervertebral disk (arrow): therefore an Effendi Type II injury. Fig. 2.56 Traumatic spondylolisthesis at C2. Spondylolysis of more than 3 mm: therefore an Effendi Type II injury. There are numerous definitions for the term “whiplash injury” including, in many cases, any form of acceleration/deceleration injury of the cervical spine. The Quebec Task Force defined symptoms following a whiplash injury as “whiplash-associated disorder.” It may occur with mechanisms other than rear-impact collisions, such as a side-impact collision. If injuries to the bony structures or the soft tissues are detected on diagnostic imaging, then this is referred to as a “whiplash injury.” Radiography. Radiographic examination is performed to exclude bony injury or segmental malalignment. MRI. Use of MRI is only indicated for cases with radicular symptoms or of unusually severe pain, in which case this should be done early to establish osseous and soft tissue edema or discoligamentous injuries. The value of MRI for evaluating the alar ligaments is a matter of great controversy and its routine use in this scenario is not recommended. Caution Loss of normal cervical lordosis does not necessarily indicate underlying pathology; it may merely be a positional abnormality of the cervical spine. When found in isolation it should not be regarded as pathologic. In children, skeletal structures still possess a high degree of elasticity. For this reason, bony injuries to the spine are relatively rare, even in the presence of accident-related neurologic deficits. This special feature is subsumed under the acronym “SCIWORA syndrome” (spinal cord injury without radiographic abnormality). Ligamentous laxity in childhood with associated discoligamentous flexibility results in significant degrees of movement, which can bruise, overstretch, and even disrupt the spinal cord. Intramedullary hemorrhage can also occur ( Fig. 2.57). The decisive point is that radiological signs (fractures, dislocations) are absent despite a severe neurologic deficit. This explains the central role of MRI in such cases. Children less than 10 years of age are mostly affected, especially those under the age of 3 years. The most common site of the spinal cord injury is at the level of C2. Another special feature of pediatric cervical injury is the vulnerability of the occipitoatlantal junction: The occipitoatlantal ligaments and membranes are unable to stabilize the still relatively large head of the child during severe deceleration events, resulting in disruption of the atlantoaxial complex and, in some cases, fatal occipitoatlantal dissociation. Incomplete ossification or fusion of the ossification centers must not be confused with a fracture. The following are important time points of ossification ( cf. also “Variants” in Chapter 2.2.1): • Atlas: ossification of the posterior arch at age 4 years, complete fusion during the 7th to 10th years. • Axis: fusion of the posterior arches between the ages of 2 and 3 years with fusion with the body of C2 by the age of 7 years. The ossiculum terminale of the dens fuses with the body of the dens around the age of 11 to 12 years. Subdental synchondrosis can persist until adolescence and may be confused with a Type II fracture of the dens. An MRI scan helps in equivocal cases since true injuries are typically associated with edema in the marrow and adjacent tissues. Anterior displacement of C2 on C3 or of C3 on C4 is a physiologic variant in ~ 20% of children up to the age of 5 years. However, alignment of the spinolaminar line is maintained in this “pseudo subluxation.” Inadequate distension of the pharynx can often produce a prevertebral soft tissue shadow on conventional radiographs that can be mistaken for a hematoma. MRI can help in equivocal cases. Both acquired and degenerative block vertebrae (synostoses) extending over several segments of the spine, e.g., in diffuse idiopathic skeletal hyperostosis (DISH) or ankylosing spondylitis) lead to long-segment loss of the normal excursion of the spine. This results in reduced flexibility during trauma, as well as a reduction in actual bone stability secondary to severe demineralization, particularly with ankylosing spondylitis. Because of absent segmental mobility, long rigid leverages, and vertebral osteoporosis, even apparently harmless falls can result in severe fractures with discoligamentous disruptions, subluxations, or dislocations ( Fig. 2.58). The fractures often course horizontally or obliquely through an entire vertebral body, adjacent disk space and into the posterior elements; consequently all three columns of the axial skeleton are typically involved ( Fig. 2.59). Fractures are often encountered at multiple levels. Fig. 2.57 SCIWORA syndrome in a 6-year-old boy following a car accident. The radiograph was unremarkable. Fig. 2.58 Cervical extension fracture-dislocation of a stiff spine. Combined discovertebral injury with anterior malalignment and “pincerlike” compression of the spinal cord. These fractures are highly unstable because they result in disruption of all bony and often discoligamentous structures. Three factors make diagnosis of these fractures difficult: • Overlapping spondylophytes (e.g., DISH) and marked osteoporosis (e.g., ankylosing spondylitis) make it difficult to recognize the fractures on survey radiographs ( Fig. W2.6). • Fractures may occur at a distance from the site of impact or even at multiple sites (e.g., cervicothoracic and thoracolumbar in patients with ankylosing spondylitis). • Even traumatic events judged to be only mild (e.g., striking the head during a ground-level fall) can result in a significant vertebral injury. Conclusions. If the clinical history and clinical examination in a patient with a “stiff spine” suggest a spinal injury that is not evident on survey radiographs, a CT scan is indicated and should include long segments at potential risk of fracture. Given the above propensity for instability with these fractures and often coincidental spinal stenoses in elderly patients, an MRI should also be subsequently performed to better evaluate any spinal cord injury. Fig. 2.59 Extension injury following a fall from a ladder. Preexisting stiff vertebral column in ankylosing spondylitis. The fractures (arrows) traverse the anterior and posterior spinal segments. “Stability” with respect to spinal injuries means the spine’s capability for resistance to physiological loads without damage or progressive compromise to the spinal cord or nerve roots and without the development or progression of deformities or structural changes. Assessment of stability of the spinal column remains challenging in daily practice. The problem of assessing spinal stability using objective criteria has not been satisfactorily solved. Assessment of stability of fractures of atlas and odontoid has been discussed in the sections describing those injuries (Chapter 2.2.3). There are no universally recognized classification systems for assessing the stability of injuries involving the subaxial cervical spine, but the classification system according to Magerl is increasingly being applied to this portion of the spine. While there are no absolute criteria for diagnosing instability, the following criteria may serve as guidelines: • Horizontal translation of more than 3.5 mm between adjacent spinal segments (if the anterolisthesis or retrolisthesis is interpreted as being degenerative, then additional signs of degeneration should be clearly evident, e.g. disk space narrowing, osteophytes, etc.). • Angulation between two adjacent vertebrae of more than 11°. • Widening of a disk space. • Facet joint subluxation resulting in less than 50% overlap. • Increased interspinous distance. Caution If an unclear anterior wedge avulsion is evident in a cervical spine injury, it is extremely important to ascertain whether this is in fact a teardrop fracture. This injury is always unstable. A complete burst fracture (Type A3.3) is almost always associated with disruption of the posterior ligamentous structures and is considered to be an unstable Type B injury. There is currently broad agreement with regard to criteria for assessing the stability of thoracolumbar fractures, in particular with respect to osseous injury patterns, which can be assessed using the classification system according to Magerl (Chapter 2.2.2). Type A fractures are generally regarded as stable with the exception of Type A3, although this does not mean that they should necessarily be treated conservatively. There has been a tendency over recent years to regard Type A3 fractures as unstable (progressive collapse with malalignment of the axial skeleton and also, in the case of a large, avulsed posterior wall fragment, a possible neurologic deficit). The paradigm of the intact posterior wall as an exclusive discriminator of stability has been abandoned ( see “Anatomy” in Chapter 2.2.1). Type B fractures are unstable due to their potential for discoligamentous disruptions secondary to flexion or extension forces. However, these can be very difficult to identify using radiography or CT when bony injuries are either absent or extremely subtle in nature. This applies, for example, to small teardrop fragments, which are an indication of a severe flexion/extension injury. It may well be helpful to postulate instability using certain metric criteria (e.g., segment angulation by more than 11°, sagittal translation by more than 3.5 mm, subluxation of the facet joints by more than 50%), but it may not always apply in particular cases. Apart from confirming the integrity of sagittal alignment, it is also very important to confirm uniformity of disk heights and interspinous distances. Additionally, congruence of the facets on either side of the spine must be confirmed when using CT. Caution Any focal segmental change in the morphological criteria in a Type B injury described above demands a plausible explanation and—following significant trauma—must be regarded as a discoligamentous injury until proven otherwise, typically with MRI. Type C injuries pose a diagnostic challenge due to the subtle imaging findings in some of these cases. Type C injuries are rotational injuries and always result in significant instability; initially or over time, possibly resulting in a neurologic deficit. Any unilateral facet joint fracture or dislocation indicates a rotational injury. Fractures of proximal ribs and transverse processes may also reflect prior rotational trauma. The difficulty in identifying such rotational and shear injuries lies in the fact that they often reduce spontaneously during positioning and transport, thus masking the true nature of the injury. Determination of the age of a fracture appears simple but it can be problematic, or even impossible in some cases. First, there should be a clinical correlation between a vertebral deformity and pain at that site. If this is not the case, then the acuity of the fracture becomes doubtful. However, it must be remembered that osteoporotic fractures in particular can be clinically silent. Radiography. Differentiation using radiography is unreliable. The finding of vertebral deformity with sharp-edged fragments but without evidence of reactive osteophyte formation suggests an acute fracture. However, this is only valid for traumatic vertebral fractures; the age of an osteoporotic compression fracture, in particular, usually cannot be estimated with certainty unless there are recent radiographs available for comparison. CT. CT allows a better assessment of the integrity of the vertebral cortex in acute fractures ( Fig. 2.60). Evaluation of trabecular bone is problematic, however, because trabecular injuries are often not apparent until the development of microcallus that produces bandlike sclerotic patterns in later stages (see Fig. 2.60). The presence of thin linear cancellous densities parallel to the end plates is suggestive of an acute trabecular injury, whereas during subacute stages resorption bands may also become evident. MRI. MRI provides the most reliable way to differentiate between acute and older fractures, irrespective of their etiology. Fluid-sensitive sequences with fat suppression are well suited for detecting fracture-related edema in an acute injury. The hyperintense edema on these sequences is often bandlike, extending parallel to the superior or inferior end plates ( Fig. 2.61a). Similarly, T1W sequences will reveal corresponding hypointense fracture lines, but some normal, hyperintense fatty marrow should always be observed ( Fig. 2.61b). When the entire vertebral body is involved, the possibility of a pathologic fracture related to underlying neoplasm must be considered! IV contrast administration sometimes improves fracture line delineation. Fig. 2.60 Acute traumatic L2 fracture. (a) Equivocal features on the radiograph in the presence of severe osteoporosis. (b) The CT image confirms the acute fracture. Fig. 2.61 Acute osteoporotic fracture of the end plate. (a) Edema and contrast uptake are typically evident in a bandlike fashion along the involved end plate. (b) Multilevel end plate irregularities. Table 2.1 provides an overview of radiological decision aids and important radiological signs. Image examples with explanations of the radiological signs may be found in Figs. 2.62–2.65. Note Osteoporotic fractures are not classified as pathologic fractures. Pathologic fractures are usually related to malignant bone lesions; in rare cases, benign primary bone tumors within the spine will result in vertebral fractures (e.g., Langerhans’ cell histiocytosis, vertebral hemangioma, aneurysmal bone cyst). Stress reaction of the neural arches caused by repetitive trauma represents a chronic form of spinal injury. Physically active children and adolescents who participate in sports involving repetitive hyperlordosis (e.g., gymnastics, tennis, swimming) are at particular risk and are most commonly affected. Continued overloading may result in a true stress fracture of the interarticular portion of the neural arches (the pars intra-articularis), also known as spondylolysis. Note Persistent, low lumbar back pain is not physiologic in childhood and adolescence and should be investigated by MRI, which can detect a stress reaction or true spondylolysis of the affected pars intra-articularis ( Fig. 2.66). Caution A stress fracture of the vertebral arch is sometimes difficult to identify on MRI as the defect can be misinterpreted as a facet joint. Apart from the associated edemalike signal intensity, indirect signs may be helpful, such as widening of the spinal canal in the sagittal diameter and a horizontal or hourglass configuration of the neuroforamen. Insufficiency fractures, e.g., due to osteoporosis or associated with pregnancy, are common in the sacrum (see also Chapter 2.3.3). The diagnostic evaluation of the trauma patient is undergoing a paradigm shift due to the increasing availability, better accessibility, and hardware improvements of MRI scanners. Although MRI is still not the diagnostic modality of choice for the multiply injured patient, it is becoming increasingly important in the post-primary phase for assessing discoligamentous and spinal injuries. Fig. 2.63 Osteoporotic vertebral fracture with intravertebral cleft formation (cleft sign). (a) Vacuum phenomenon visible on the radiograph. (b) MRI demonstrates fluid in the intravertebral cleft (fluid sign), with an air–fluid level within the cleft related to the supine position of the patient. Fig. 2.65 Typical signs of a pathologic tumor-related fracture. (a) Convex eccentric dorsal displacement of the posterior margin. (b) The edema also involves the pedicles. (c) Bilateral indentation of the ventral thecal sac by tumor extending into the epidural space. Fig. 2.66 Incipient, stress-related spondylolysis in a competitive gymnast. (a) Bone marrow edema of the vertebral arch and articular processes. (b) The hypointense line (arrow) represents an incipient stress fracture. After interdisciplinary consultation (trauma surgeon, anesthetist, neurologist/neurosurgeon, and radiologist) it must be decided whether and when an MRI scan should be performed for a case of spinal injury. Essentially, we regard the following situations as indications for MRI scanning: • The patient presents an unclear, posttraumatic spinal neurologic deficit that is not sufficiently explained by CT. • CT shows a specific injury pattern that indicates a potentially unstable discoligamentous lesion (e.g., teardrop fractures, subluxations, or dislocations in hyperflexion injuries; widened disk spaces secondary to hyperextension mechanisms). • It is not possible to conduct a neurologic examination on a patient (obtunded, altered mental status) in whom there is a high suspicion of ligamentous or cord damage based on the mechanism of injury. • Spinal MRI should be more readily considered in children because, radiographs may appear normal despite severe trauma (SCIWORA), and CT of the entire axial skeleton should be avoided for reasons of radiation safety. • MRI may play an important role in the preoperative assessment and subsequent surgical planning by defining extent and site of spinal cord compression, presence of intraspinal hematomas, occult vertebral fractures, etc. However, MRI should not be undertaken if it will lead to a delay of essential therapeutic measures (e.g., emergent spinal decompression). Also, in cases where MRI is contraindicated, CT myelography may be considered as an alternative modality. In addition to assessment of the spinal cord, MRI is excellent for demonstrating discoligamentous injuries, which is critical given the potential for associated instability and poor healing if they are left untreated. Critical ligamentous structures include: • Anterior and posterior longitudinal ligaments. • Ligamenta flava. • Interspinous ligaments. The critical ligamentous structures of the upper cervical spine and the craniocervical junction worthy of particular mention are the transverse atlantal ligament, the tectorial membrane, and the posterior atlanto-occipital membrane. Evaluation of the alar ligaments requires great care due to their variability of morphology and signal intensity. Ligament disruptions are best recognized on fat-suppressed T2W or STIR sequences (STIR = short-tau inversion recovery). Hyperflexion injuries are often associated with disruptions of the posterior ligamentous complex and can be well identified by extensive edema within the interspinous tissues ( Figs. 2.31 and 2.33). It is often possible to identify directly discontinuity and tears of the longitudinal ligaments and the ligamenta flava (see Figs. 2.33 and 2.34). Hemorrhage and dislocations of vertebral fragments can elevate, or even obscure, the longitudinal ligaments. The effects of disk injury remain uncertain, despite various staging proposals. Traumatic disk prolapse. The occurrence of traumatic disk herniation is the focus of intense discussion—especially in the insurance law literature. Given adequate trauma, it can occur, albeit rarely ( Figs. 2.67 and 2.68). Associated findings suggesting an acute injury (soft tissue edema, ligament tears, hematomas, bone bruises) should be observed in these cases. Traumatic disk prolapse, along with the hyperflexion injury itself, may result in spinal cord injury (cord contusion or even intramedullary hemorrhage), especially in the cervical region. Trauma-related spinal hemorrhage predominantly involves the epidural space; subdural subarachnoid hemorrhages are extremely rare. Epidural hematomas are found between the periosteum of the vertebrae or vertebral arches and the dura mater of the thecal sac and extend a significant craniocaudal distance—usually over several segments. They are most commonly encountered in the ventral epidural space. In addition to uncomplicated epidural hemorrhages associated with traumatic vertebral fractures, hemorrhages associated with the epidural venous plexus will often form space-occupying hematomas that may result in compression of the cord or, less frequently the cauda equina. Rapidly progressive paraplegia makes an epidural hemorrhage an emergency situation demanding immediate intervention. In addition to traumatic epidural hematomas, spinal hemorrhages may develop during anticoagulant therapy either spontaneously ( Fig. 2.69) or after minimal trauma. Other possible causes of epidural hematomas include spinal interventional procedures or surgery. MRI. The MRI appearance of hemorrhage varies depending on its age. Fresh hematomas are often isointense to, and difficult to differentiate from, cerebrospinal fluid on T1W sequences, while on T2W sequences they can still appear hypointense in the acute phase but change rapidly to an intermediate or even hyperintense appearance. Typical methemoglobin formation occurs after a few days (the subacute phase) and is characterized by hyperintensity on T1W images. GRE (gradient echo) sequences can be helpful in identifying hemorrhage giving rise to typical susceptibility artifacts related to the iron content of the blood. Contrast administration can be dispensed with in the acute stage. Chronic epidural hematomas display marginal contrast enhancement. Epidural hemorrhages related to intermittent bleeding are characterized by marked signal heterogeneity. Fig. 2.69 Spontaneous epidural hematoma in a patient on anticoagulants. (a) Only increased intraspinal density, which can be easily overlooked, is evident on the plain CT image. (b) Active hemorrhage in the region of the thoracic spine is evident after contrast administration. (c) MRI demonstrates the space-occupying, epidural hematoma. Despite a suspicious clinical picture, epidural hematomas can be difficult to identify. Clues such as subtle disturbances of the epidural fat or mass effect upon the thecal sac must be searched for since even long-segment epidural hematomas can readily escape the cursory glance! In addition to the discoligamentous injuries already discussed, spinal cord lesions play an important prognostic role in patients with spine injuries. A distinction must be made between hemorrhagic and nonhemorrhagic spinal cord contusions. This differentiation is important because hemorrhagic contusions are typically associated with a poor neurologic outcome. MRI. Spinal cord contusions are evident on T2W sequences as hyperintense intramedullary lesions ( Fig. 2.67). The spinal cord signal abnormality can be either subtle and situated very distinctly at the level of the vertebral injury or occupy extensive cross-sectional areas of the cord and extend over several segmental levels. Attention should be paid to features of preexisting degenerative spinal canal stenosis (osteophytes, etc.) as these can result in cord contusion even after minor injuries. The degree of spinal cord signal abnormality (swelling, edema) correlates significantly with the ultimate prognosis. Intramedullary hemorrhage is evident as focal, sometimes only punctate alterations. Susceptibility-weighted sequences (DWI [diffusion weighted imaging], gradient echo [T2*W], or even FLAIR [fluid attenuated inversion recovery]) are therefore best suited to demonstrate intramedullary hemorrhage. Extensive intramedullary hemorrhage tends to be rare after trauma and raises the possibility of other conditions such as a cord tumor or vascular malformation but is associated with a severe neurologic deficit (symptoms of complete spinal cord injury), which aids in the diagnosis. The most severe form of traumatic cord damage is spinal cord disruption, which—provided the patient survives—is associated with spastic paraplegia or tetraplegia and the entire spectrum of autonomic dysfunction in addition to pain. Sequelae resulting from traumatic spinal cord injuries include myelomalacia, syringohydromyelia, medullary cyst formation, tethered cord syndrome of varying degrees (posttraumatic synechiae of the thecal sac), and spinal cord atrophy. Radiography. Survey radiography in standard projections is the primary modality for evaluating the postoperative spine. Improper placement of implants may thus be assessed before more sophisticated imaging procedures are undertaken. Additional functional studies of the spine can detect postoperative or adjacent degenerative instability, e.g., in adjacent segments after long-segment fusions. Provided the examination has been correctly performed, displacement in the sagittal plane by more than 3.5 mm or angulation of the adjacent level by more than 11° are considered signs of segmental instability. Myelography. With the ever improving availability of MRI, myelography in the postoperative patient increasingly serves as a back-up modality, especially in patients who are unable to undergo an MRI examination. In the late postoperative phase it may be a supportive diagnostic tool for identifying scar formation, e.g., in what is known as postnucleotomy syndrome. With the option of performing dynamic, “functional,” examinations, myelography is also well suited for demonstrating postoperative instability and secondary segmental hypermobility and their effect on cerebrospinal spaces and neural structures. CT. CT provides high-resolution depiction of bony structures and assessment of the location of implants. Secondary reconstructions with bone and soft tissue technique should be generated in all cases. Evaluation of the soft tissues, especially in the spinal canal, is limited in the postoperative setting. This can be improved by combining it with myelography (CT myelography). CT angiography is indicated for vascular issues (e.g., injury to the vertebral artery during surgery of the cervical spine). All paravertebral structures included on the images (e.g., pneumothorax secondary to lung injuries) must also be assessed. MRI. MRI is the best method for evaluating soft tissue structures of the spine. This applies to the spinal canal when looking for hemorrhage, recurrent disk extrusion, spinal canal injuries, myelopathy, or inflammatory conditions, as well as in assessing paravertebral soft tissues for hematoma, inflammatory changes, musculoligamentous injuries, or vascular issues (often with the aid of MR angiography). The ability to assess bone marrow is especially useful for demonstrating postoperative vertebral body edema or in cases of secondary fractures. The MRI protocol includes at least sagittal T1W and T2W sequences, axial T2W, and fat-suppressed coronal and/or sagittal T2W sequences. Obtaining additional heavily T2-weighted 3D sequences with MIP (maximum intensity projection) reconstructions can be helpful (“MR myelography”). Within the first 2 to 4 weeks postoperatively, intravenous contrast administration often leads to difficulties in interpretation due to postoperative changes and should therefore only be administered in specific situations, e.g., for suspected infection or abscess formation. Fat-suppressed sequences are often limited due to field heterogeneity caused by metallic implants, so other techniques such as inversion recovery (STIR) or subtraction imaging may be helpful. Susceptibility-weighted sequences are useful for suspected hemorrhage, and DWI sequences for suspected ischemia. Direct sequelae. This refers to postoperative complications involving the structures surrounding the spine, such as adjacent neurovascular structures ( Fig. 2.70). In the cervicothoracic region, the trachea, the esophagus ( Fig. 2.71), or the pleural cavity may be affected by direct trauma or indirectly as a result of swelling or space-occupying hematomas. Indirect sequelae. These include malpositioning or loosening of surgical implants and their effect on bony structures, iatrogenic instability caused by extensive resection of the posterior elements, and cement leakage during cement augmentations. In the late postoperative stage, infection of the vertebrae, disks, paravertebral space, and especially within the spinal canal poses a challenge for diagnostic examinations. After fusion of vertebral segments, accelerated degeneration develops in adjacent motion segments due to mechanical overuse and altered biomechanics (“junctional disease”). Adjacent segment instability in its proper sense refers to the detection of pathologic hypermobility of motion segments above and below a fusion. It does not develop immediately after surgery but usually appears years later and is more commonly situated above the fused segments. The diagnostic value of lateral flexion/extension studies is controversial because hypermobility is underestimated if movement is limited by pain and, conversely, translational movements of 4 mm are found in up to one-third of asymptomatic persons. See the specialized literature for the complex topic of postoperative symptoms secondary to scarring (postnucleotomy syndrome). Fig. 2.70 Postoperative epidural hematoma in a patient after laminectomy of the T10 vertebra. (a) Compression and edema of the spinal cord. (b) Completely absent fluid signal from CSF on the axial image. Fig. 2.71 Extensive subcutaneous emphysema involving the spinal canal and soft tissues of the neck after esophageal injury during anterior fusion. Posterior approach to the spinal canal. The classic approaches for disk surgery are access via interlaminar windowing (ILW) without the need to resect bony structures and, alternatively, extended interlaminar window (eILW). The term refers to extension of bony access to the spinal canal in addition to resection of the ligamentum flavum, sometimes extended even further for a medial facetotomy. Hemilaminectomy—the unilateral resection of the lamina of the vertebral arch—may be necessary in cases of more extensive disk sequestration or bony stenosis of the spinal canal; the spinous process remains untouched. A laminectomy involves the complete resection of the posterior vertebral elements together with removal of the spinous process. Fusion procedures. Procedures which are intended to create a permanent bony union of two vertebrae are included in the term “fusion.” Established procedures here are anterior lumbar interbody fusion (ALIF), posterior lumbar interbody fusion (PLIF), transforaminal interbody lumbar fusion (TLIF), and extreme lateral interbody fusion (XLIF), which differ in their respective approaches (see specialist literature). Posterior instrumentation. This term describes posterior stabilization with the aid of an internal fixator. Disk implants. The majority of implants have radiopaque markers that allow assessment of their position relative to the adjacent vertebrae, especially relative to the anterior and posterior margins, on survey radiographs. For evaluation of individual implants, consider consulting a surgeon or obtaining information from the manufacturer. Cages and vertebral body replacement. Tilting or even penetration of cages or vertebral replacements into the adjacent vertebral end plates must be noted ( Fig. 2.72). This is particularly relevant in spines weakened by osteoporosis and not stabilized by other means, where progressive penetration by implants can ensue. Implants that are not flush with the adjacent end plates can result in progressive malalignment and should be documented. Screws. “Suboptimal” screw positioning—such as penetration of the anterior vertebral cortex by a few millimeters; a lateral rather than concentrically medial course of the screw in the vertebral body; or injury to the medial or lateral pedicle wall—is generally of no clinical relevance. On the other hand, extrapedicular malposition of the screws through the spinal canal should be reported as it will usually require revision. Screws that impinge on the course of vessels must be mentioned and may need to be examined further by supplementary CT angiography ( Fig. 2.73). A lucent rim of more than 2 mm with sclerotic margins and/or a change of direction or penetration into the end plate over time suggest screw loosening ( Fig. 2.74). Cement. Cement leakage into intervertebral spaces becomes possible as soon as the cement abuts the end plates of the vertebra (see Fig. 2.74c). Mild cement leakage into the paravertebral space, paravertebral veins, or the epidural venous plexus is usually asymptomatic, whereas leakage into the spinal canal with a space-occupying effect or leakage into the venous system as far as the vena cava or the azygos/hemiazygos venous system, with the associated risk of pulmonary embolism, is to be regarded as a complication ( Figs. 2.75 and W2.7). Fig. 2.72 Implant migration following vertebral replacement and posterior instrumentation. (a) The superior margin of the vertebral replacement device does not run parallel to the inferior base plate and is impacted into the plate. (b) Follow-up after 5 months: despite the use of cement, migration of the vertebral replacement has occurred with subsequent destruction of the overlying vertebra. Fig. 2.73 Pedicle screw. The course of the right pedicle screw puts the vertebral artery at risk. CT angiography. Fig. 2.74 Complications after posterior lumbar interbody fusion and dorsal instrumentation at L2–3 and L3–4. (a) Unremarkable postoperative CT. (b) Follow-up 2 weeks later: superior end plate insufficiency fracture at L2 with breakthrough of a pedicle screw. (c) After vertebroplasty: cement leakage into the disk space as far as the inferior end plate of L1. Fig. 2.75 Cement leakage as a complication after posterior instrumentation with cement-augmented pedicular screws. Fig. W2.7 shows the chest radiograph of a patient with multiple pulmonary artery cement emboli. (a) Considerable leakage of cement into paravertebral and prevertebral vessels. (b) CT scan confirms cement in the inferior vena cava. Anatomy. See Chapter 2.3.1 including Fig. W2.8. Pathology. Injuries to the pelvic ring usually result from falls or direct impact injury. Whereas minor injuries predominate at an older age, pelvic ring fractures in younger patients are usually the result of high-energy trauma. Consequently, a host of associated injuries should be expected and are often the reason for the high mortality associated with complex pelvic fractures. Typical associated injuries include injuries to the genitourinary tract with bladder rupture and urethral avulsion, and vascular damage. The most established classification system for pelvic ring fractures, the AO classification, is based on the classification by Tile, who subdivides the fractures into three groups: • Stable fractures. • Rotationally unstable fractures. • Rotationally and vertically unstable fractures. The history of the injury with regard to energy and force vector are important features in addition to the imaging findings (see Radiography and CT). Type A: stable fractures of the pelvic ring ( Fig. 2.76). • A1: Fractures of this type result from spontaneous violent muscle contractions and are most commonly found in adolescent athletes ( Fig. 2.77). • A2: These are fractures of the iliac wing or fractures of the anterior pelvic ring and are usually due to a lateral compression injury. The CT scan often reveals associated compression fractures of the anterior sacrum. These A2 fractures typically do not become unstable ( Fig. 2.78). • A3: These are transverse fractures of the inferior end of the sacrum, including the coccyx. Type B: Fractures with rotational instability but preserved vertical stability ( Fig. 2.79). • B1: Unilateral external rotation injury with disruption of the symphysis pubis. The trauma impact mostly comes from anterior impact, so that the hemipelvises are forced apart (referred to as an open-book injury). A classic example of this injury is that of a motorcyclist involved in a head-on collision that results in the two halves of the pelvis being separated by the bike’s tank at the time of impact ( Figs. 2.80 and 2.81). • B2: Unilateral internal rotation injury with disruption of the symphysis pubis and overriding of the anterior pelvic ring. The impact comes from the side, causing the struck side of the pelvic to rotate inward. This results in a fracture of the anterior pelvic ring with internal rotation of the involved half of the pelvis. Here too, the opposing hemipelvises are forced apart, potentially resulting in disruption of the sacroiliac joints anteriorly due to rupture of the anterior sacroiliac ligaments. A typical example is a side-impact collision into the driver-side door of a car. • B3: Bilateral rotational instability due to bilateral B1 or B2 injuries. Fig. 2.77 Avulsion fracture at the anterior inferior iliac spine (Type A1) due to traction of the rectus femoris. Fig. 2.78 Type A2 fracture. Fracture of the anterior pelvic ring with associated anterior compression fracture of the sacrum; no instability. Oblique-axial reconstruction CT; for slice level see the small inset image. Fig. 2.79 Type B injuries. (a) Type B1 injury (open book) due to impact force in a sagittal plane; rotational instability. (b) Type B2 injury due to lateral compression; rotational instability. • C1: This injury is associated with a complete disruption of one hemipelvis, with a stable contralateral side ( Figs. 2.82 and 2.83). • C2: This is a Type C1 injury of one hemipelvis combined with a Type B injury of the contralateral side. • C3: This is a bilateral Type C1 injury ( Fig 2.84). One fracture type not included in the AO classification system is the suicidal jumper’s fracture, in which an axial compression injury results in separation of the spinal column from the pelvis ( Fig. 2.85). Radiography. If the apophysis is already mineralized and sufficiently retracted then it can be readily seen on the radiograph. US. Separation of the apophyses can be easily evaluated by US in the majority of cases. MRI. An MRI scan will demonstrate edema of the apophyseal growth plate and the adjacent soft tissues. Apophyseal avulsions may result from a single injury or from chronic repetitive microtrauma in athletes. This affects primarily the ischial tuberosity (origin of the hamstrings), the anterior inferior iliac spine (rectus femoris; see Fig. 2.77), anterior superior iliac spine (sartorius and tensor fasciae latae), and less frequently also the pubic bone (adductors). An avulsion fracture of the lesser trochanter (iliopsoas) is also possible, especially in the younger patient. Untreated apophyseal injuries can result in exuberant ossification that may resemble that of a cartilaginous exostosis (osteochondroma) or other bone-forming tumor. Radiography. Despite the current widespread availability of CT imaging, AP views of the pelvis are still the first study obtained not only for acute assessment but also because they can be used for comparison with postoperative radiographs. Inlet views of the pelvis allow for assessment of AP and rotational malalignment of the pelvic ring, while the outlet view demonstrates any vertical malalignment of the pelvic ring ( Fig. 2.86). CT. Apart from nondisplaced fractures of the anterior pelvic ring following minimal trauma and typical apophyseal avulsion fractures, CT is typically indicated for all pelvic fractures and multiplanar reconstructions should always be generated. When evaluating the CT, attention should be paid to the course of the fractures as well as to indirect signs of instability such as widening of one or both sacroiliac joints. Small bony avulsions from the caudal sacrum correspond in the majority of cases to avulsion fractures of the sacrotuberous or sacrospinous ligaments and indicate vertical instability. MRI. MRI has no role in the diagnostic work-up of acute trauma to the bony pelvis but plays an important role in the detection of fatigue fractures (Chapter 2.3.3). Acetabular fractures are almost invariably the result of high energy trauma. The position of the femur in the hip joint at the time of the accident and the vector of the transmitted force determine the type of fracture. Anatomy. The acetabulum arises from the innominate bone (os coxa), which forms from three ossification centers: the ilium, ischium, and pubis. These three segments join at the tri-radiate cartilage, a Y-shaped synchondrosis centered on the acetabulum. Complete fusion of the innominate bone occurs in the late teens. Seen from outside, the acetabulum is divided by a longer limb, forming the anterior column and a shorter one, the posterior column. These two columns serve as struts, mechanically representing the coalescence of bony trabeculae along lines of stress. The anterior column is composed of both pubic rami and a large portion of the ilium, extending from the iliac crest down the iliac wing and through the superior pubic ramus towards the pubic symphysis. The posterior column is composed mainly of the ischium and a small part of the ilium. Fig. 2.82 Type C1 injury. Combined rotational and vertical instability; complete dissociation of the left hemipelvis. Fig. 2.83 Type C1 injury with vertically displaced separation of the sacroiliac joint plus symphysis disruption. In addition, there is an anterior pelvic ring fracture on the left side. Fig. 2.84 Type C3 fracture with bilateral complete disruption of the posterior pelvic ring and symphysis diastasis. There is additional posterior dislocation of the left femoral head. For slice level see the small inset image. SIJ, sacroiliac joint. Fig. 2.85 Suicidal jumper’s fracture. Axial compression forces the spine out of the sacrum. (a) Bilateral longitudinal fracture of the sacrum. (b) Combined with a transverse fracture of the sacrum. Fig. 2.86 Inlet and outlet views of the pelvis. (a) Schematic diagram. (b) Outlet view. (c) Inlet view. The anterior and posterior acetabular walls are outward projections of their respective columns. The AO classification of acetabulum fractures ( Fig. 2.87) is closely based on the classification proposed by Judet and Letournel ( Fig. W2.9), which takes into account the embryonic development of the acetabulum and distinguishes between anterior and posterior columns (see Anatomy above). • Type A fracture: Only one column is involved; the main part of the joint is intact. • Type B fracture: Involvement of both columns; one part of the acetabular roof remains attached to the ilium. • Type C fracture: Complete detachment of the acetabulum from the ilium; both columns are involved. Radiography. Conventional radiographs are still used to evaluate acetabular fractures despite the availability of CT. In addition to the AP radiograph, iliac and obturator oblique (Judet) views are obtained. Classification is best done using these projections ( Figs. 2.88 and W2.10). Caution The term “both-column fracture” often leads to a misunderstanding. This is a clearly defined entity and does not mean that the fracture involves both columns. Instead, the classic both-column fracture involves a separation of both columns and discontinuity of all weight-bearing parts of the acetabulum from the posterior pelvic ring ( Fig. 2.89). The classic cause of a both-column fracture is a lateral collision trauma. The femoral head takes virtually all parts of the acetabulum medially with it, resulting in a central dislocation of the head of the femur; all articular fragments remain more or less congruent with the femoral head (see Fig. 2.89). The phenomenon is known as “secondary congruence.” The medial dislocation of the acetabulum brings the ilium into profile on the obturator view, giving rise to the spur sign, which is pathognomonic for a both-column fracture ( Figs. 2.90 and W2.11). CT. Currently, CT is an integral part of the diagnostic investigation of acetabular fractures. Although fracture classification is more difficult using CT, it provides for detailed assessment of fracture morphology. Small fragments that become entrapped in the joint space are readily evident ( Fig. 2.91). CT is also of crucial importance for optimal pre-operative planning. Fatigue fractures of the pelvis occur predominantly at the pubic rami and the parasymphyseal region. Stress fractures of the sacrum are also found in children, athletes, and pregnant women ( Fig. 2.92); osteoporosis-related insufficiency fractures also occur frequently at this location. Other common sites for an insufficiency fracture include the supra-acetabular region, the ilium, the pubic rami, and the parasymphyseal bone. Changes due to insufficiency fractures are often very subtle on conventional radiographs and are easily overlooked. CT and especially MRI are very well suited for detecting these fractures. Sacral insufficiency fractures (unilateral or bilateral) typically display vertical fracture lines near to the sacroiliac joint. Horizontal fracture lines are also found in the midsacrum (known as the H-pattern or Honda sign; Fig. 2.93). Fig. 2.88 Reference lines of the acetabulum on the AP projection. 1, iliopectineal line (anterior column); 2, ilioischial line (posterior column); 3, acetabular roof; 4, anterior acetabular rim; 5, posterior acetabular rim; 6, Koehler’s teardrop. Fig. 2.89 Both-column fracture. All weight-bearing parts are dissociated from the posterior pelvic ring. Fig. 2.92 Sacral fracture in a pregnant patient. MRI. This is most likely a combination of insufficiency and fatigue fractures. Fig. 2.93 Osteoporotic insufficiency fractures of the sacrum. Also termed “H fracture” because of the course of the fractures (arrows). Oblique coronal MPR (multiplanar reformatting) from one CT dataset. Dislocation of the hip joint is usually due to high-energy axial compression. Hip dislocations also occur from extreme muscle convulsions, such as during an epileptic seizure or an electrical accident. We differentiate between various types of dislocation (posterior: iliac and ischiadic; anterior: pubic and obturator). In rare cases fracture of the femoral head may occur during dislocation of the hip joint, either in the form of an avulsion fracture of the ligamentum teres or in the form of a shearing fracture related to the posterior acetabular rim. Such fractures of the femoral head are classified according to Pipkin ( Fig. 2.94). CT is essential for assessing Pipkin fractures and provides the only method for correctly assessing the size of the sheared fragment and of the defect within the femoral head ( Fig. W2.12). Anatomy. See Chapter 2.3.5 including Fig. W2.13. Pathology. Osteitis (symphysitis) pubis is a chronic overuse injury of the symphysis and the adjacent pubic rami. This stress reaction may also be associated with adductor pathology. It is often the cause of groin pain in athletes and affects football players in particular. Caution The majority of patients (athletes) with osteitis pubis present with the clinical diagnosis “inguinal hernia.” Radiography/CT. The appearance depends on the chronicity of the stress reaction. Initially, resorptive changes may predominate, in which case the joint space is widened ( Figs. 2.95a and 2.96). In more chronic cases, subchondral sclerosis and osteophytes predominate, often with joint space narrowing ( Fig. 2.95b). MRI. MRI allows differentiation of osteitis pubis from adductor injuries and other causes of groin pain. Findings in osteitis pubis: • Increased signal intensity on water-sensitive sequences or enhancement (after IV administration of gadolinium) in the bones adjacent to the symphysis and in the symphyseal joint space ( Fig. 2.97). • Concomitant involvement of the adjacent adductor entheses (in ~ 60% of cases; see Fig. 2.97). • Osteophytes. • Cysts or geodes (in ~ 80% of cases; Fig. 2.98) • Erosions at the insertions of the pubic ligament. • So-called secondary cleft sign (a bright line between bone and the joint space; Fig. 2.99). US. Ultrasound is helpful for injuries of the nearby tendon insertions of the rectus abdominis and the adductors but is unable to demonstrate stress changes within the bones. DD. Infections. In cases of infection, MRI should be used to detect intra-articular or para-articular abscesses ( Fig. 2.100). Laboratory results should also be examined. Rheumatic disorders. Seronegative spondylarthropathies can also affect the symphysis. The underlying condition is almost always known, so there are rarely any differential diagnostic difficulties. Inguinal hernia. A sound physical examination and, in some cases, the use of ultrasound should allow for accurate diagnosis. Tendinopathy of the adductors or rectus abdominis. The use of ultrasound or MRI will provide an accurate diagnosis ( Fig. 2.101). Fig. 2.95 Clinical forms of osteitis pubis. (a) Predominantly erosive changes with bone resorption, often in the early phase. (b) Increased sclerosis and osteophyte formations, commonly in the late phase. Fig. 2.99 Osteitis pubis. Hyperintense line (arrows) between bone and cartilage (secondary cleft sign). Osteophyte at the upper and lower margins of the left pubis. Anatomy. See Chapter 2.4.1 including Figs. W2.13– W2.19. The shape of the acromion demonstrates considerable variation. The variants reported by Bigliani and Gagey ( Fig. 2.102) refer to the differences in morphology of the acromion in the sagittal plane, but this provides an incomplete definition of the geometry of the subacromial space because of additional variation in acromial morphology in the coronal plane. Os acromiale ( Fig. 2.103) refers to a persistent ossification center of the anterior acromion. The finding occurs bilaterally in about 60% of cases and must not be mistaken for a fracture of the acromion. It should be kept in mind that fusion of the acromial ossification center is not complete until relatively late (between 21 and 25 years of age). Anatomically, the glenoid labrum is a highly variable structure. Its cross-sectional shape ranges from triangular to round and is of variable size. A sublabral foramen ( Figs. 2.104 and 2.105) is a relatively common normal variant (incidence: 7–12% of individuals). This refers to a lack of attachment of the labrum to the anterosuperior part at the glenoid (at the 1 to 3 o’clock position). A “Buford complex” refers to absence of the labrum in this region associated with a thickened, cordlike middle glenohumeral ligament, which may rarely insert on the long biceps tendon. This anomaly is less common, with an incidence of 1.5 to 2% (see Fig. 2.104). The anteroinferior labrum is normal in both of these variants. The anatomy of the biceps tendon anchor varies considerably. A firm attachment of the superior labrum to the glenoid margin is evident in only 30% of individuals ( Fig. 2.106a). A sublabral cleft of variable depth (2–10 mm), lined with a synovial membrane, is commonly found and known as a sublabral recess ( Fig. 2.106b). In the presence of a deep recess, the superior labrum may be meniscoid and hypermobile. A sublabral recess may extend anteriorly into a sublabral foramen. The following rules should be observed for MRI of the shoulder: • The examination should include three planes: transverse, oblique coronal (parallel to the supraspinatus tendon), and oblique sagittal (parallel to the surface of the glenoid surface). • Routine sequences include a PDW sequence with fat saturation (oblique coronal, transverse), as well as a T1W (oblique coronal) and a T2W (oblique sagittal) FSE sequence (fast spin echo sequence). GRE sequences are reserved for special cases. The slice thickness should not exceed 3 mm. • The arm should be placed in the neutral position. • An advantage of an additional sequence in abduction and external rotation (ABER position) with MR arthrography is the better assessment of the anteroinferior labrum and anterior labroligamentous complex. For this position, the hand is placed behind the head or neck of the patient. Oblique sagittal slices parallel to the proximal humerus are then obtained. Primary indications for MR arthrography (following the intra-articular injection of a gadolinium-containing solution) • All forms of shoulder instability. • Suspected SLAP lesion (superior labral anterior-to-posterior lesion; see relevant part of Chapter 2.4.6). • Diagnostic work-up for shoulder pain in competitive athletes. Fig. 2.104 Variants of the anterior glenoid labrum. Sagittal schematic diagrams. IGHL, inferior glenohumeral ligament; LBT, long biceps tendon; MGHL, middle glenohumeral ligament; SGHL, superior glenohumeral ligament. Fig. 2.106 Superior labrum and biceps anchor. MR arthrography. (a) Firm attachment. (b) Sublabral recess and meniscoid labrum. Impingement syndromes are among the most common types of pathology of the shoulder joint. A distinction is made between primary and secondary extrinsic, and secondary intrinsic impingement syndromes ( Table 2.2). Pathology. Primary extrinsic impingement (i.e., outlet impingement) is due to narrowing of the subacromial space. Impingement of the supraspinatus tendon and the subacromial bursa between the anterior acromion and the head of the humerus causes chronic bursitis and tendinopathy of the supraspinatus. A tendon tear may develop over time. Affected patients are typically older than 40 years of age and do not present with shoulder instability. Predisposing factors for subacromial impingement include a Bigliani Type 3 acromion (see Fig. 2.102), subacromial osteophytes, a laterally downsloping acromion, a thickened coracoacromial ligament, and an (unstable) os acromiale. Osteoarthritis of the acromioclavicular joint with marked osteophytes and hypertrophy of the rotator cuff are rare causes. Clinical presentation. Classic symptoms are nocturnal pain, pain on elevation of the arm between 60 and 120° (“painful arc”), shoulder stiffness, and weakness. Radiography. Assessment of acromial morphology is best accomplished on an outlet view (SST [supraspinatus tendon] view, Neer view). Subacromial osteophytes are found at the anterior margin of the acromion in the region of the insertion of the coracoacromial ligament; strictly speaking, therefore, they are enthesophytes. Narrowing of the acromiohumeral interval to less than 7 mm is considered pathologic and is suggestive of a rotator cuff tear ( Fig. 2.107). Tendon calcification is not part of the subacromial impingement syndrome, but instead indicates calcific tendinitis secondary to calcium hydroxyapatite deposition disease (Chapter 10.9.3). MRI. Subacromial impingement is a clinical diagnosis. MRI ( Figs. 2.108 and 2.109) may demonstrate a typical constellation of findings but is unable to establish the diagnosis. The task of MRI is to define the stage of disease, especially with regard to rotator cuff integrity. Fluid-sensitive images may demonstrate increased fluid content and/or thickening of the wall of the subacromial bursa, which is often the only finding in early stages of the disorder. Over time, tendinopathy of the supraspinatus develops (Chapter 2.4.3). Thickening of the tendon will further narrow the subacromial space. Rotator cuff tears typically involve the anterior fibers of the supraspinatus tendon from where they can progress further. The morphology of the acromion can be well appreciated on oblique sagittal and oblique coronal views, while an os acromiale is best seen on transverse slices. Commonly reported, but less meaningful, findings include thickening or a convex course of the coracoacromial ligament and the absence of the subacromial fat pad. US. Ultrasound demonstrates thickening of the wall of the subacromial/subdeltoid bursa, which may be partially fluid-filled. A recognizable sign of subacromial impingement during abduction of the arm is a “ballooning” of the lateral part of the subdeltoid bursa, which results from fluid being pressed out of the medial part of the bursa as the bursa glides beneath the acromion. Signs of tendinopathy are thickening of the tendon, decreased and somewhat heterogeneous echogenicity, and loss of the normal fibrillar structure of the tendon; comparison with the contralateral side is sometimes helpful. Identification of tendinopathy, however, does not prove the presence of a subacromial impingement syndrome. Table 2.2 Classification of impingement at the shoulder
2.1 Cranial Vault, Facial Bones, and Skull Base
2.1.1 Fractures of the Cranial Vault
2.1.2 Basilar Skull Fractures
2.1.3 Fractures of the Petrous Bone
2.1.4 Facial Bone Fractures
Isolated Facial Bone Fractures
Midfacial Fractures
Mandibular Fractures
2.2 Spine
2.2.1 Anatomy, Variants, Technique, and Indications
Technique and Indications
2.2.2 Mechanisms of Injury and Classifications
Compression Injuries
Extension Injuries
Flexion Injuries
Rotational Injuries
Translational Injuries (Shearing Injuries)
Special Fracture Types That Do Not Threaten Spinal Stability
Sequelae of Trauma to the Sacral and Coccygeal Bones
2.2.3 Special Traumatology of the Cervical Spine and the Craniocervical Junction
Fractures of the Occipital Condyles
Craniocervical Dissociation
Fractures of the Atlas
Atlantoaxial Dislocation and Atlantoaxial Rotational Dissociation
Fractures of the Axis and Dens
Traumatic Spondylolisthesis of the Axis
Whiplash Injury of the Cervical Spine
Special Features of Pediatric Cervical Spine Injuries
2.2.4 Injury Patterns of the “Stiff” Spine
2.2.5 Stable or Unstable Fracture?
What is Meant by “Stable”?
Upper Cervical Spine
Middle and Lower Cervical Spine
Thoracic and Lumbar Spine
2.2.6 Fresh or Old Fracture?
2.2.7 Differential Diagnosis “Osteoporotic Versus Pathologic Fracture”
2.2.8 Stress Phenomena in the Spine: Stress Reaction and Stress Fracture (Spondylolysis) of the Neural Arches
2.2.9 Value of MRI in Acute Trauma
Indication for MRI
Ligamentous Injuries
Disk Injury
Hematomas
Traumatic Spinal Cord Injuries
2.2.10 Radiological Assessment after Surgery of the Spine
Indication and Value of Imaging Modalities
Complications of Spinal Surgery
Expressions Used by Surgeons
Postoperative Assessment of the Position of Spinal Implants
2.3 Pelvis
2.3.1 Fractures of the Pelvic Ring
Classification
Imaging
Stress-Related Apophyseal Avulsion Fractures
2.3.2 Acetabular Fractures
2.3.3 Fatigue Fractures of the Pelvis
2.3.4 Hip Dislocation/Fracture Dislocations of the Hip
2.3.5 Pubalgia (Osteitis Pubis)
2.4 Shoulder Joint
2.4.1 Anatomy, Variants, and Technique
Variants
Technique
2.4.2 Impingement
Primary Extrinsic Impingement
Subacromial Impingement
Type | Etiology | Affected soft tissue structures |
Primary extrinsic impingement | ||
• Subacromial impingement | • Subacromial narrowing | • Subacromial bursa, supraspinatus tendon (anterior) |
• Subcoracoid impingement | • Subcoracoid narrowing | • Subscapularis tendon |
Secondary extrinsic impingement | Instability | Supraspinatus tendon |
Secondary intrinsic impingement | ||
• Posterosuperior impingement | • Microinstability | • Supraspinatus tendon (posterior), infraspinatus tendon, posterosuperior labrum |
• Anterosuperior impingement | • Microinstability | • Subscapularis tendon, pulley system |
Fig. 2.108 MRI findings in subacromial impingement. SSP, supraspinatus. (a) Heterogeneous increased signal intensity within the supraspinatus tendon. (b) Bone marrow edema and evidence of subacromial/subdeltoid bursitis (thickening of bursal wall and bursal fluid). (c) Enthesophyte at the insertion of the coracoacromial ligament.
Subcoracoid Impingement
Pathology. Subcoracoid impingement arises when the subscapularis tendon becomes impinged between the coracoid process and humeral head, resulting in tendon pathology. The syndrome is rare and occurs predominantly with acquired alterations of the coracoid (fracture, surgery) and sometimes as a result of a congenital deformity of the coracoid. Other cases may be related to unrecognized shoulder instability and are more appropriately placed into the group of secondary impingement syndromes.
Radiography/CT. Radiographs may demonstrate abnormal coracoid morphology, but equivocal cases will require CT.
MRI. MRI is useful for revealing lesions of the subscapularis tendon or to exclude other pathology. From measurement of the width of the coracohumeral interval various authors have reported that measurements of less than 6 to 11 mm are pathologic, but these measurements are not considered to be reliable.
US. Abnormalities of the subscapularis tendon are readily assessed by ultrasound and may be an indication of subcoracoid impingement.
Secondary Extrinsic Impingement
Pathology. Secondary extrinsic impingement is the result of shoulder instability. Impingement of the soft tissue structures between the acromion and head of the humerus is due to the abnormal mobility of the humeral head. Distinction of this from primary impingement cannot be made on the basis of imaging findings and requires correlation with the clinical examination.
MRI. MRI findings of instability impingement do not differ from those of primary subacromial impingement with respect to the changes of the subacromial space (see Subacromial Impingement at the beginning of Chapter 2.4.2).
Secondary Intrinsic Impingement
See also Chapter 2.4.5.
2.4.3 Rotator Cuff Pathology and Biceps Tendinopathy
Rotator Cuff Lesions
Pathology. The vast majority of lesions of the rotator cuff are caused by tendon failure secondary to chronic overuse. The actual tendon tear is the final event of this chronic process due to various intrinsic and extrinsic factors. Older individuals with a history of subacromial impingement syndrome are usually affected. Whereas younger patients are more likely to suffer a bony avulsion secondary to an acute injury rather than a tendon rupture, repetitive eccentric overuse associated with chronic microtrauma and intrinsic impingement can lead to tendon lesions in young athletes, especially those participating in overhead sports (pitchers, tennis players, etc.).
Classification of Rotator Cuff Lesions
A basic distinction is made between tendinopathy, partial-thickness and full-thickness tears. With tendinopathy only degenerative changes of the tendon are present, without macroscopically evident interruption of continuity. Partial-thickness tears involve only a portion of the tendon, whereas full-thickness tears extend across the entire thickness of the tendon, at least at one site ( Fig. 2.110). Full-thickness tears are therefore “transtendinous” and result in a communication between the joint cavity and the subacromial bursa.
Table 2.3 Variants of partial lesions of the rotator cuff
Term | Meaning of the acronym | Morphology |
PASTA lesion, also known as rim-rent tear | Partial articular-sided supraspinatus tendon avulsion | Articular-sided partial-thickness tear of the supraspinatus tendon with extension to the tendon insertion (footprint lesion), delamination of the tendon with variable retraction of the articular-sided layer (see Fig. 2.115a) |
CID lesion | Concealed intratendinous delamination | Concealed intratendinous partial-thickness tear (delamination) |
PAINT lesion, also known as a delamination tear | Partial articular-sided tear with intratendinous extension | Articular-sided partial tear with intratendinous component (see Fig. 2.115b) |
STAS lesion | Supraspinatus tendon articular-sided but not at footprint | Articular-sided lesion of the supraspinatus tendon outside the footprint region |
With regard to tendon tears, the terms “partial-thickness” (partial) and “full-thickness” (complete) do not state (as is often erroneously assumed) whether the rupture involves the entire tendon or only a part of the tendon.
Partial-thickness Tears
These are classified according to their location as articular-sided (most common type), bursal-sided, or intratendinous. In recent years, several variants of partial tears have been reported ( Table 2.3; see also Fig. 2.110). The depth of articular- or bursal-sided partial tears may be classified according to Ellman ( Table W2.1 in Chapter 2.4.3).
Full-thickness Tears
Full-thickness tears typically result from progression of a partial-thickness tear over time. A distinction is made between small (≤ 1 cm), intermediate (1–3 cm), large (3–5 cm), and massive tears (larger than 5 cm in the sagittal plane). Larger defects may be associated with retraction of the proximal tendon stump in a medial direction. The extent of the retraction may be classified according to Patte ( Fig. 2.111).
Tears of the Subscapularis Tendon
The subscapularis tendon is often involved in cases of extensive degenerative rotator cuff lesions. Isolated tears are less common and occur, for example, after traumatic anterior shoulder dislocation. Because defects of the subscapularis tendon typically progress in a cranial to caudal direction, Fox and Romeo have proposed a specific classification system ( Table 2.4).
Radiography. It is not possible to diagnose focal lesions of the rotator cuff on radiographs. Cranial migration of the humeral head with an acromiohumeral distance of less than 7 mm indicates a large defect of the supraspinatus and infraspinatus tendons. The term “defect arthropathy” ( Fig. 2.112) describes contact of the humeral head and acromion resulting in osseous remodeling and degenerative cyst formation as well as glenohumeral osteoarthritis in long-standing, extensive rotator cuff tears.
MRI. Tendinopathy displays increased signal intensity of the tendon on sequences with short echo times (T1W, PDW) and less-intense signal elevation on sequences with long echo times ( Fig. 2.113). The affected tendon can appear thickened but does not demonstrate any fiber discontinuity. Magic-angle artifacts may result in a similar appearance but are not usually a problem if intermediate-weighted pulse sequences (with echo times > 35 milliseconds) are used.
A tendon tear is diagnosed when fluidlike signal intensity is seen within the tendon on intermediate-weighted or T2W images. In a partial-thickness tear ( Fig. 2.114a), the alteration affects only a part of the tendon thickness, whereas the entire thickness of the tendon is involved in a full-thickness tear ( Fig. 2.114b). Apart from signal characteristics, attention should also be paid to tendon morphology, i.e., to evidence of interruption in the course of the tendon fibers. A limitation of conventional MRI lies in its difficulty in differentiating tendinopathy from a partial-thickness tear. While the sensitivity for detecting partial tears is therefore relatively low, the accuracy in diagnosing of full-thickness tears is high.
With the aid of MR arthrography the sensitivity increases to over 80% for articular-sided partial-thickness tears. An additional diagnostic criterion for diagnosing a partial-thickness tear rather than tendinopathy is the leakage of contrast into the substance of the tendon ( Figs. 2.115 and 2.116). With a full-thickness tear, contrast passes through the transtendinous defect into the subacromial bursa (see Fig. 2.114b).
Rotator cuff tears may result in atrophy and, over time, irreversible fatty degeneration of the affected muscles. Assessment of the rotator cuff muscles can be made using the semiquantitative Goutallier classification system ( Table 2.5). The most lateral image of an oblique sagittal T1W or T2W sequence (obtained without fat saturation!) where the scapula is seen to form a Y shape is used as a reference level ( Fig. 2.117).
Note
The amount of loss of functioning muscle in a patient with a rotator cuff tear is decisive for the prognosis of a cuff repair. Any description of a rotator cuff injury without mention of the state of the muscles is incomplete.
Table 2.4 Fox and Romeo classification of tears of the subscapularis tendon
Grade | Tear type |
1 | Partial-thickness tear |
2 | Full-thickness tear of the upper 25% of the tendon |
3 | Full-thickness tear of the upper 50% of the tendon |
4 | Full-thickness tear of all parts of the tendon |
Table 2.5 Semiquantitative classification of fatty degeneration of muscles according to Goutallier
Grade | Morphology |
0 | Normal muscle, no fat |
1 | Some streaks of fat |
2 | Pronounced fatty infiltration, but still more muscle than fat |
3 | Advanced fatty infiltration; as much fat as muscle |
4 | Advanced fatty infiltration; more fat than muscle |
Fig. 2.113 Tendinopathy of the supraspinatus tendon. MR arthrography. (a) Increased intratendinous signal intensity on the FS T1W image, in part due to the magic angle effect. (b) Less signal increase on intermediate-weighted sequence.
Fig. 2.114 Rotator cuff tears. Partial-thickness tear versus full-thickness tear. (a) Partial thickness undersurface tear of the supraspinatus tendon. (b) Full-thickness tear of the supraspinatus tendon.
Fig. 2.115 Rotator cuff tears. MR arthrography. (a) PASTA lesion. (b) PAINT lesion. SSP = supraspinatus muscle.
Fig. 2.116 Fox and Romeo Grade 2–3 tear of the subscapularis tendon. MR arthrography. (a) Leakage of contrast medium into the tendon at its insertion. (b) The classification according to Fox and Romeo is made using the sagittal plane. SSC, subscapularis muscle.
US. In experienced hands, ultrasound can provide results comparable with those of conventional MRI with regard to the recognition of tendon defects. Differentiation between tendinopathy and a partial-thickness tear remains difficult, however. Furthermore, it should be borne in mind that anisotropy of tendon fibers can create the impression of a defect. To avoid this, any suspicious finding should be examined from several aspects with different probe angles. Apart from direct signs of tear, such as interruption of tendon fibers and release of fluid into the tendon or bursa ( Fig. 2.118a), indirect signs should also be looked for. A focal impression (“dent”) in the convexity of the tendon surface or a circumscribed double contour over the surface area of the humeral head ( Fig. 2.118b), corresponding to hyaline articular cartilage, is encountered only with a tear, not with tendinopathy. Limitations of ultrasound include only moderate reliability in evaluating the state of muscles and its low sensitivity for concomitant pathologic states (e.g., labral pathology).
Caution
With massive full-thickness tears of the rotator cuff associated with a retracted tendon, the deltoid lies directly adjacent to the humeral head and can be confused with components of the rotator cuff.
CT. CT arthrography using multidetector technology with image reconstructions in all three anatomical planes may be used as a “back-up procedure,” for example when there are contraindications against an MRI examination. Transtendinous defects and articular surface partial tears of the supraspinatus and infraspinatus tendons are detectable with high sensitivity and specificity ( Fig. 2.119). This technique is limited, however, by low sensitivity for intratendinous and bursal-sided lesions and for many lesions of the subscapularis tendon. The Goutallier classification system can be used because it was originally developed for CT scanning.
DD. There is a differential diagnosis for the clinical symptoms of a rotator cuff tear.
With the development of acute symptoms, a distinction must be made between isolated subacromial bursitis without rotator cuff defect, calcific tendinitis secondary to calcium hydroxyapatite deposition disease, and an avulsion fracture of the greater tuberosity. Suprascapular nerve palsy secondary to entrapment neuropathy or a postinfectious neuritis (Parsonage–Turner syndrome) is a relatively rare differential diagnosis. Other pathologies that can have a clinical presentation similar to that of a rotator cuff tear include SLAP lesions (Chapter 2.4.6) and traumatic osteolysis of the distal clavicle (Chapter 2.5.6).
Biceps Tendinopathy
Pathology. Tendinopathy of the long head of the biceps tendon is often an associated condition in patients with subacromial impingement and lesions of the rotator cuff as well as secondary to instability of the tendon (pulley lesion; Chapter 2.4.4). However, biceps tendinopathy can also develop as an isolated overuse injury in athletes involved in overhead and throwing activites. Anterior shoulder pain is the cardinal clinical symptom. Partial-thickness tendon tears and eventually full-thickness tears can develop from initial tendinopathy, which typically involves the horizontal (intra-articular) part of the tendon.
MRI. MRI signs of biceps tendinopathy are thickening and irregular contours of the tendon and increased signal intensity on sequences with short echo times. These alterations are best identified on oblique sagittal images ( Fig. 2.120). Partial tears can manifest as an increase in caliber and signal intensity of the tendon on T1W and T2W sequences or as attenuation of the tendon. Discontinuity or complete absence of the horizontal portion of the tendon are signs of a full-thickness tear ( Fig. 2.121).
US. It is not possible to demonstrate the proximal insertion of the biceps tendon at the glenoid by ultrasound, but its more lateral intra-articular segment can be well visualized. Difficulties can arise in obese patients. Tendinopathy of the biceps tendon with thickening, heterogeneous echogenicity and increased vascularization may be detected with ultrasound, as may partial or full-thickness tears. An “empty” intertubercular groove requires differentiation between a tear and a dislocation of the long biceps tendon out of its groove (cf. Fig. 2.125). This is possible by tracing the tendon from its myotendinous junction in a cranial direction.
2.4.4 Pathology of the Rotator Interval
Pathology. Various types of injury involving the anatomical structures of this region are subsumed under the term “rotator interval lesion.” Tears of the rotator interval capsule can be found in patients with anterior shoulder instability and usually show a horizontal orientation.
Injuries of the superior glenohumeral ligament, also termed pulley lesions, are of more clinical significance and can occur in isolation or in combination with tears of the supraspinatus tendon and/or subscapularis tendon, resulting in instability of the long biceps tendon. Habermeyer has described four types of pulley lesions ( Fig. 2.122 and Table W2.2); Type 1 (frequency: 29–74%) refers to an isolated tear of the superior glenohumeral ligament.
Fig. 2.117 Atrophy and fatty degeneration of the supraspinatus muscle Grade 2 to 3 according to Goutallier in a case of a full-thickness tear.
Fig. 2.118 Ultrasound of rotator cuff tears. (a) Partial articular-sided tear of the supraspinatus tendon (longitudinal section). (b) Full-thickness tear of the supraspinatus tendon (cross section).
Fig. 2.120 Isolated tendinopathy of the long head of the biceps tendon. MR arthrography. ISP, infraspinatus muscle; SGHL, superior glenohumeral ligament; SSC, subscapularis muscle; SSP = supraspinatus muscle.
MRI. Rotator interval lesions are well demonstrated only with the aid of MR arthrography. Pulley lesions can be diagnosed on oblique sagittal MR arthrographic images with a sensitivity and specificity of more than 80%. Reliable signs are inferior displacement of the long head of the biceps tendon onto the subscapularis tendon within the rotator interval (displacement sign) and discontinuity of the superior glenohumeral ligament ( Fig. 2.123). This is almost always associated with tendinosis of the biceps tendon. Medial displacement of the biceps tendon, recognizable on transverse sections, is usually only encountered in conjunction with a simultaneous lesion of the subscapularis tendon, but not with an isolated tear of the superior glenohumeral ligament. With a lesion of the superior glenohumeral ligament and a partial defect of the subscapularis tendon, the biceps tendon can dislocate into the defect, i.e., deep to the coracohumeral ligament. Intra-articular dislocation can occur with a full-thickness tear of the subscapularis tendon ( Fig. 2.124). Extracapsular dislocations of the biceps tendon (ventral to the subscapularis tendon) associated with a tear of the coracohumeral ligament are very rare. Capsular tears can occasionally be identified as contrast leakage in the region of the interval into the subacromial/subdeltoid bursa.
US. Instability of the long biceps tendon can be recognized using ultrasound when it is seen to subluxate or dislocate out of the intertubercular sulcus. This is best achieved with a dynamic examination during forced external rotation ( Fig. 2.125).
2.4.5 Shoulder Instability
Traumatic Anterior Instability
Pathology. Anterior (anteroinferior) glenohumeral instability is the most common form of traumatic (unidirectional) shoulder instability (more than 95% of cases). Pathoanatomically there is an interruption of continuity of the anteroinferior labroligamentous complex, which results in insufficiency of the inferior glenohumeral ligament and subsequently leads to recurrent anterior dislocation or subluxation. A traumatic injury (traumatic first-time acute dislocation) results in an acute anterior shoulder dislocation in which the humeral head impacts against the anteroinferior glenoid rim; this can result in a labroligamentous injury (see following text sections) and/or a posterolateral impaction fracture of the head of the humerus (Hill–Sachs fracture).
Bankart and Perthes Lesions
Bankart lesions and Perthes lesions represent approximately 90% of the injuries that occur secondarily to traumatic anterior first-time acute dislocation. In the classic Bankart lesion, the anteroinferior labrum, together with the inferior glenohumeral ligament, is completely detached from osseous glenoid ( Fig. 2.126). Because there is also an additional disruption of the scapular periosteum, the labrum is usually displaced from its normal anatomical position, and may be “floating” freely in the anterior joint space.
A Perthes lesion is distinguished from a Bankart lesion by the fact that although an avulsion of the labrum off the glenoid exists, it is still attached to the glenoid via scapular periosteum, which is stripped anteromedially but not disrupted. The unstable labrum often remains in a relatively normal position and the tear can be masked by scar tissue and re-synovialization. Fluid may be seen tracking between the labrum and glenoid or beneath the periosteum and is sometimes more readily apparent in the ABER position, i.e., with the inferior glenohumeral ligament under tension ( Fig. 2.127).
Fig. 2.122 Habermeyer classification of pulley lesions. Sagittal schematic diagrams. CHL, coracohumeral ligament; LBT, long head of the biceps tendon; SGHL, superior glenohumeral ligament; SSC, subscapularis muscle; SSP, supraspinatus muscle.
Fig. 2.123 Type 1 pulley lesion. MR arthrography. The long head of the biceps tendon shows increased signal intensity, compatible with tendinopathy, and is displaced caudally onto the subscapularis tendon (cf. Fig. 2.120). SGHL, superior glenohumeral ligament; SSC, subscapularis muscle.
Fig. 2.124 Intra-articular dislocation of the long head of the biceps tendon. SSC, subscapularis muscle.
Fig. 2.125 Dislocation of the long head of the biceps tendon. Ultrasonic cross section of the proximal upper arm.
Fig. 2.127 Perthes lesion. MR arthrography. (a) The anteroinferior labrum is undermined by contrast medium, but remains in a normal position. (b) The detachment of the labrum is more clearly depicted in the ABER position. IGHL, inferior glenohumeral ligament.
ALPSA Lesion
An ALPSA lesion (anterior labroligamentous periosteal sleeve avulsion) is found as a chronic variant of a Perthes lesion, usually after multiple anterior shoulder dislocations (chronic instability). With this type of lesion, the anteroinferior labroligamentous complex becomes detached from the glenoid rim and is displaced medially, where it scars over along with its periosteal attachment to the scapular neck. Although there is no actual ligament disruption, incompetence of the inferior glenohumeral ligament develops due to the abnormal labral position. The result is shoulder instability. Characteristic signs of an ALPSA lesion are medially and caudally displaced labral tissue ( Fig. 2.128) which appears larger due to a proliferation of associated scar tissue along the scapular neck, and a crease, or cleft, between the glenoid and the labrum (cleft sign; see Fig. 2.128b).
Bony Bankart Lesion
The bony Bankart lesion is an avulsion fracture in which the anteroinferior labroligamentous complex is detached from the glenoid together with a bony fragment of variable size ( Fig. 2.129). While small bony fragments may be regarded as therapeutically and prognostically irrelevant, larger fragments require refixation or reconstruction of the glenoid.
HAGL Lesion
In the very rare HAGL lesion (humeral avulsion of glenohumeral ligament), the anteroinferior labroligamentous complex is not disrupted at its glenoid attachment but is at the humerus ( Fig. 2.130). The inferior glenohumeral ligament may be avulsed directly or together with a bone fragment (~ 20% of cases) from its insertion on the humeral neck. The anterior capsule of the axillary recess no longer appears U-shaped on coronal images but rather is J-shaped due to the lateral discontinuity of the inferior glenohumeral ligament (“Jsign”). Acute HAGL lesions may be associated with fluid leakage and/or a hematoma at the insertion site of the inferior glenohumeral ligament.
Hill–Sachs Defect/Fracture
Hill–Sachs defects are detectable after traumatic first-time acute dislocations in 47 to 100% of cases. This lesion may or may not be present in patients who have sustained a significant anterior labroligamentous injury. Except for very large lesions, Hill–Sachs defects are of little clinical relevance, but detection of such a lesion indicates a previous anterior shoulder dislocation. On axial images, a Hill–Sachs defect is always located posterolaterally at or above the level of the coracoid. Acute lesions are usually surrounded by areas of bone contusion ( Fig. 2.131).
Radiography. It is hardly possible to miss an acute anteroinferior shoulder dislocation on conventional radiographs ( Fig. 2.132). Follow-up films after reduction serve to exclude any associated bony injuries (osseous Bankart lesion, fracture of the greater tuberosity). Smaller bony avulsions from the anteroinferior glenoid rim are usually not visible on standard projection views. If a conventional radiological depiction is requested, then an osseous Bankart lesion is best seen on a Westpoint or axillary view, whereas a Hill–Sachs defect is best displayed on an AP radiograph in internal rotation or on a Stryker view.
CT/CT arthrography. CT is the modality of choice for demonstrating the extent of an acute glenoid fracture or chronic glenoid defect resulting from progressive bone loss after multiple dislocations; quantification of the size of the bony abnormality is best accomplished on oblique sagittal image reconstructions. Hill–Sachs defects are also readily detected with CT. The results of CT arthrography are comparable to those of MR arthrography with respect to the assessment of labroligamentous injuries. The advantages of CT arthrography lie in the recognition of bony Bankart lesions and in diagnosing articular cartilage lesions. Its disadvantages include its limited ability to assess soft tissue structures and its use of ionizing radiation (especially important in young patients).
MRI/MR arthrography. Conventional MRI is most suitable for demonstrating injuries immediately after the event, i.e., within a few days after the acute dislocation, since an associated joint effusion or hemarthrosis will act as a natural contrast medium and allow for more accurate assessment of the labrocapsular structures. Direct MR arthrography is the modality of choice, with a sensitivity of more than 88% and a specificity of more than 90% for the detection of labroligamentous lesions. Its accuracy in characterizing the type of injury as compared with arthroscopic findings is 84%. This technique also allows for reliable detection of associated injuries, such as SLAP lesions (Chapter 2.4.6).
DD. Differentiation of a labroligamentous injury from an anatomical variant of the glenoid labrum is relatively easy. An abnormality seen exclusively within the anterosuperior quadrant of the labrum (a sublabral foramen or a Buford complex) (Chapter 2.4.1) it is always located in the anterosuperior quadrant, whereas most true labroligamentous lesions typically involve the anteroinferior quadrant, or at least begin there.
Fig. 2.128 ALPSA lesion. MR arthrography. (a) The labroligamentous complex is displaced medially and inferiorly. (b) Typical cleft sign (arrow). IGHL, inferior glenohumeral ligament; LLC, labroligamentous complex.
Fig. 2.129 Bony Bankart lesion. (a) MR arthrography. The inferior glenohumeral ligament itself is intact. (b) Anteroinferior bony avulsion (arrow) from the glenoid. IGHL, inferior glenohumeral ligament.
Traumatic Posterior Instability
Pathology. Traumatic posterior shoulder instability is comparatively rare (2–4 % of cases). In most cases, a posterior dislocation is the result of considerable muscular contraction during an epileptic seizure or an electrical accident (occasionally resulting in bilateral posterior dislocations) or during abnormal axial loading of the upper arm while it is abducted and internally rotated. The lesion pattern is a mirror image of those seen with anterior instability, including a posterior labroligamentous injury and an anteromedial “reverse” Hill–Sachs lesion of the humeral head. Classification of posterior labroligamentous lesions analogous to injuries of the anterior structures (“reverse” [bony] Bankart lesion; POLPSA [posterior labrocapsular periosteal sleeve avulsion] lesion; posterior HAGL lesion, etc.), has not become generally accepted. It is possible to miss an unreduced (“locked”) posterior dislocation clinically and on standard frontal radiographs. One clue to its presence is an inability to externally rotate the arm, which is fixed in adduction and internal rotation.
Radiography. Radiographs are diagnostic for acute or locked posterior shoulder dislocation. In a “true” AP projection, overlapping of the contours of the internally rotated head of the humerus and the joint socket is evident ( Fig. 2.133). There is often a line of density running parallel to the medial contour of the humeral head (trough line; see Fig. 2.133), corresponding to the lateral margin of the “reverse” Hill–Sachs defect (trough sign). In questionable cases, a radiograph in a second projection (axillary, transscapular or transthoracic) confirms the posterior dislocation of the humeral head.
CT. CT accurately shows the size and orientation of “reverse” Hill–Sachs defects as well as additional bony injuries of the posterior glenoid rim and whether the dislocated humeral head is “locked” along the posterior glenoid rim ( Fig. 2.134).
MRI. As with anterior instability, a conventional MRI examination is most useful immediately after the dislocation, whereas in the more chronic setting, MR arthrography should be considered ( Fig. 2.135). In addition to damage to the posterior labroligamentous complex, patients with posterior shoulder instability are not uncommonly found to have concomitant lesions of the rotator cuff.
Atraumatic Instability
Pathology. Atraumatic shoulder instability is typically multidirectional, occurs bilaterally, and often affects patients with generalized hyperlaxity of the joints (congenital hypermobility syndrome). Multiple subluxations or dislocations are typical, and can also occasionally be produced voluntarily. Apart from a capacious joint capsule, intra-articular findings are commonly absent. However, in athletes with multidirectional shoulder instability, labral and rotator cuff lesions are not uncommonly present.
MRI. With multidirectional shoulder instability, the primary role of MR arthrography is to exclude the presence of associated intra-articular pathology. Frequently a stretching and redundancy of the capsule can be readily recognized, especially in the region of the rotator interval. A glenohumeral ligament that does not appear to be stretched on images in the ABER position is also suggestive of capsular redundancy.
Microinstability
Pathology. Microinstability (also known as “functional instability” or “microtraumatic instability”) represents a subclinical form of shoulder instability that develops mainly in athletes secondarily to chronic overuse with repetitive injury to the capsular structures. These forms of instability are most commonly found in sports that involve abduction and external rotation of the shoulder (overhead sports). These patients typically present with pain and reduced motion of the shoulder rather than overt subluxation or dislocation events. Secondary damage to articular structures may develop, especially to the glenoid labrum and rotator cuff.
Posterosuperior glenoid impingement is a typical intrinsic form of impingement that occurs in the overhead athlete due to microinstability with abnormal anterior translation of the humeral head during the cocking phase. It most commonly manifests clinically as acute or chronic posterior shoulder pain. With posterosuperior glenoid impingement, there is repetitive pathologic contact between the joint surface of the rotator cuff (especially the posterior fibers of the supraspinatus and anterior fibers of the infraspinatus tendons) and the posterior superior glenoid rim during external rotation and abduction. These tendons may also become entrapped between the glenoid and greater tubercle, resulting in injuries to the posterior cuff and posterosuperior glenoid labrum.
Anterosuperior impingement is much less common and involves the subscapularis tendon and pulley system when the arm is brought into internal rotation and adduction (followthrough phase of throwing or striking movements) during which these structures become entrapped between the anterior superior glenoid rim and the humeral head. The most common clinical symptom is anterior shoulder pain.
MRI. MR arthrography is the most useful imaging technique for evaluating athletes presenting with shoulder problems. A variety of often subtle articular lesions can result from microinstability: Stretching of the joint capsule, an array of labral pathology (degeneration, tear, avulsion, SLAP lesion), or rotator cuff lesions may occur in isolation or in combination ( Fig. 2.136).
Fig. 2.136 Microinstability: posterosuperior glenoid impingement. MR arthrography. Combination of the findings from a, b, and c may be related to microinstability. The ABER position demonstrates the corresponding lesions of labrum and supraspinatus tendon. (a) Rotator cuff lesion. (b) Degenerative fraying of the posterosuperior labrum. (c) Degeneration of the inferior glenohumeral ligament. IGHL, inferior glenohumeral ligament; SSP, supraspinatus muscle.
A characteristic pattern of “kissing lesions” is found in patients with posterosuperior glenoid impingement (see Fig. 2.136c). MR arthrography typically demonstrates an articular-sided partial-thickness tear of the posterior fibers of the supraspinatus tendon and/or anterior fibers of the infraspinatus tendon, combined with a lesion of the posterosuperior glenoid labrum. With excessive contact, bony alterations such as bone marrow edema, cyst formation, and sclerotic changes in the greater tubercle and superior glenoid may also be seen. Lesions of the anterior joint capsule are evident on axial views and may be accentuated on views obtained in the ABER position and vary from degenerative changes to elongation and tear of the inferior glenohumeral ligament.
In cases of anterosuperior glenoid impingement, MR arthrography can demonstrate the pulley lesion with discontinuity of the superior glenohumeral ligament and the sequelae of the associated instability of the biceps tendon. Lesions of the subscapularis tendon typically start along the articular surface of the superior part of the tendon.
2.4.6 Other Labral Pathology
SLAP Lesions
Pathology. SLAP lesions are injuries to the superior glenoid labrum and the biceps/labral anchor, extending in an anteroposterior direction. They have a frequency of 4 to 10% in arthroscopic series. Common mechanisms of injury include a fall on an outstretched hand or flexed elbow, an anterior shoulder dislocation, and chronic overuse injuries due to repetitive torsion of the biceps anchor in overhead sports (pitching and striking sports, swimming). Following a shoulder dislocation, the SLAP lesion ultimately often represents the superior extension of an anteroinferior labral lesion (e.g., Bankart lesion).
The classification system of Snyder distinguishes four different types of SLAP lesions ( Table 2.6 and Fig. 2.137). Whereas the Type 1 SLAP lesion, as a purely degenerative alteration, is of hardly any clinical relevance, Type 2 (the most common type) and Type 4 lesions often cause instability of the biceps anchor and are an indication for superior labral repair or biceps tenodesis. The biceps tendon is stable in the Type 3 SLAP lesion; treatment therefore involves only resection of the bucket-handle tear. Various other reported lesions mostly represent combination injuries of a Type 2 SLAP lesion plus damage to the labrum, the middle glenohumeral ligament or the rotator cuff. This extended classification is not typically used, however.
MRI. Conventional MRI has only a low sensitivity for the detection of SLAP lesions and, as a result, MR arthrography is the method of choice; it exhibits high sensitivity (82–92%) and specificity (80–99%) in this regard ( Fig. 2.138).
Type 1 SLAP lesions manifest as contour irregularities of the superior labrum, but are only rarely detectable. With a Type 2 lesion, leakage of contrast medium into the superior labrum and the biceps/labral anchor is observed. A cleft of contrast extending laterally into the substance of the labrum is a very predictive sign of a true SLAP tear since a Type 2 SLAP tear can be very difficult to differentiate from a sublabral recess. However, the normal recess is typically oriented in a medial direction (Chapter 2.4.1). Other findings suggesting a true Type 2 SLAP lesion are irregular labral margins and a wide separation between the labrum and glenoid. Types 3 and 4 are bucket-handle tears, in which the torn fragment may be displaced caudally into the joint to a greater or lesser degree. In Type 3, the fragment typically appears triangular on coronal views and separated from the intact biceps tendon. In Type 4 the bucket-handle fragment includes both the superior labrum and parts of the biceps tendon.
CT/Arthrography. CT arthrography is considered equivalent to MR arthrography in diagnosing SLAP lesions.
DD. Differentiation between a Type 2 SLAP lesion and a sublabral recess (Chapter 2.4.1 and Fig. 2.137) may be difficult, if not impossible, but the orientation of the “cleft” and its morphology should provide helpful clues for accurate diagnosis.
GLAD Lesion
Pathology. The GLAD lesion (glenolabral articular disruption) involves a combination of a focal articular cartilage defect along the anteroinferior glenoid, typically with a subtle tear of the adjacent labrum. It is not typically associated with glenohumeral instability. The cause is presumed to be an eccentric impaction of the head of the humerus against the glenoid during a fall on the outstretched arm or on the shoulder. A posterior variant of the GLAD lesion has also been reported.
MRI. MR arthrography demonstrates a tear near the base of the nondisplaced labrum and a cartilaginous lesion involving the adjacent anteroinferior or posteroinferior quadrant of the glenoid ( Fig. 2.139). There is no injury to the inferior glenohumeral ligament. The extent of glenoid cartilage damage varies.
Table 2.6 Snyder classification of SLAP lesions
Type | Lesion |
1 | Degenerative fraying of the superior labrum |
2 | Avulsion of the superior labrum and detachment of the biceps anchor from the glenoid. |
3 | Bucket-handle tear of the superior labrum with intact biceps anchor |
4 | Bucket-handle tear of the superior labrum with involvement of the biceps anchor |