In the broadest sense of its meaning, traumatology can be described as the medical specialty that studies damage to the human body, especially to the cell. The traumatic agent can be physical (e.g., mechanical trauma, temperature changes, radiation), chemical, or biologic (e.g., bacteria, viruses, etc.). Regardless of the etiology, the body can be expected to exhibit two effects: a local effect at the site of the trauma, and a systemic effect on the body (e.g., shock, fever, and others).

In a narrower sense, traumatology deals with mechanically induced injuries of the musculoskeletal tissue. For practical reasons, other physical etiologies, such as thermal injuries, are included in this chapter.

A fracture is a break in the continuity of bone. Where the bone is not completely separated, a break is called a fissure.

Joint injury refers to any damage to the capsuloligamentous system, cartilaginous structures, and osseous articular surfaces following contusions, subluxations, and dislocations.

Since the ligaments that connect the joints are more or less incorporated in the joint capsule, the term ‘capsuloligamentous injury’ is frequently used. Such an injury can be an elastic strain, a plastic sprain, or a complete rupture.

Direct mechanical trauma (e.g., lacerations) and indirect trauma that triggers maximum muscular contraction can tear a tendon. The tear frequently occurs where the tendon shows signs of degeneration.

Roentgen’s discovery of X-rays at the end of the 19th century not only revolutionized the diagnostic evaluation of trauma, but also transformed the treatment of injuries to the skeleton, joints, and soft tissues. The dominant role of conventional radiology now must be reassessed at increasingly shorter intervals in view of the continuing emergence of new imaging modalities. Some of the recently introduced techniques use X-rays, such as digital radiography or CT, while others are based on completely different physical principles, such as sonography or MRI.

Fig. 1.2 Joint injury. Osteochondral fracture of the lateral talus.

Fig. 1.3 Tendon injury. Acute hematoma at the transition of the quadriceps femoris muscle with the quadriceps tendon on sagittal T1-weighted spin echo image.

Fig. 1.4 Tendon injury. Large subacute hematoma in the femoris muscle on enhanced T1-weighted spin echo image.

Fig. 1.5 Sonographic visualization of a muscle injury. Large hematoma in the gastrocnemius muscle secondary to torn muscle fibers. The tear itself is not discernible.

Diagnostic imaging and image-guided therapy are inconceivable today without digital manipulation. Computed tomography (CT), digital subtraction angiography (DSA), and magnetic resonance imaging (MRI) rely on digital image acquisition and processing.

Two digital methods are used for projection radiography today: digital image enhancement and digital luminescence radiography. Both methods store the intensity distribution of the transmitted X-rays as a set of binary data, instead of analog data as with the film-screen system.

Digital enhancement radiography is a fluoroscopic method that can be implemented as digital cardiography, digital subtraction angiography, and digital spot films. Their numerous advantages have led to the acceptance of digital methods in diagnostic and therapeutic cardiology and angiography. Because of digital enhancement radiography’s limited spatial resolution, it is rarely used as a substitute for X-rays, except for intra- and postoperative assessment of the position of fracture fragments.

CT generates images without superimposed structures, usually along the axial plane. While the patient is in a resting supine position, even anatomically difficult body regions can readily be evaluated noninvasively. A single section can be imaged in seconds and, with the addition of spiral technique (see below), an entire body region obtained during a single breath-hold. CT provides information about the bones and soft tissues and, while the resolution is slightly inferior compared to conventional radiography, is fully adequate to evaluate skeletal trauma.

Fig. 1.7 Different displays of a digital radiograph with:

a contrast scaling adjusted to that of a normal radiograph,

b frequency processing with edge enhancement.

Fig. 1.8 Further examples of various displays of digital images:

a contrast scaling adjusted to that of a normal radiograph,

b edge enhancement.

Fig. 1.14 Contusion of the spinal cord and posterior subluxation of C3 on C4 in a trauma patient with neurologic findings (T2-weighted SE images).

Fig. 1.15 Full-thickness tear of the supraspinatus tendon on T2-weighted SE image.

Fig. 1.16 Occult calcaneal fracture with associated bone marrow edema following minor trauma 6 weeks previously and with persistent pain. The radiograph was normal. a T1-weighted SE sequence showing the fracture line as low signal intensity, b STIR sequence showing the fracture line as high signal intensity surrounded by bone marrow edema.

Complete tears of the anterior cruciate ligament (ACL) are detected with an average accuracy of 90%. Partial tears or distortions of the anterior cruciate ligament, which are characterized by partially intact fibers and severe intra- and periligamentous edema, are not always distinguishable from complete tears. Injuries of the posterior cruciate ligament are less common than ACL tears but are easily detected by MRI.

Even after numerous technical refinements, evaluation of the hyaline cartilage by MRI remains inferior to direct visualization by arthroscopy. This superiority of arthroscopy applies only to chondromalacia and superficial lesions of questionable therapeutic relevance. However, in many instances, osteochondral injuries are easily identified by MRI as the cause of hemarthrosis.

Bone scans are performed with Tc 99 m–labeled diphosphonate and can be obtained as a static study or a dynamic study using the three-phase technique. Other scintigraphic techniques, such as minor Tc 99 m–labeled white blood cell scans, or Tc 99 m–labeled monoclonal antibody scans do not play a significant role in the evaluation of trauma.

Bone scans are established for the detection of radiologically occult fractures, but MRI has replaced this technique in most centers.

The bone scan is well suited for surveying the patient with multiple trauma for the extent of skeletal involvement. It should be kept in mind that reparative changes in juxta-articular appendicular bone might be visible only after the third day. In the diaphyses of the long bones and in the central skeleton, the bone scan might even become positive as late as one week after the trauma. Because of the known low specificity of increased bone activity on bone scan, a positive finding should be correlated with the radiographs.

1. Any traumatized bone must be visualized in at least two projections. It is difficult to meet this requirement for certain anatomic locations, such as the hip or shoulder. Special projections have been proposed for these anatomic regions. (Refer to other texts dedicated to radiographic positioning.)
   
2. For any fracture visualized next to a joint, any articular extension must be searched for. Special views must often be added to the two standard views. If conventional imaging is inconclusive, MRI should be considered.
   
3. If one of two parallel long bones (such as the ulna and radius or the tibia and fibula) is fractured, a fracture of the companion bone must be excluded.
   
4. Any long bone must be visualized in its entire length. In other words, the proximal and distal joint bearing ends have to be included.
   
5. In patients with multiple fractures, subtle findings may be missed if other major injuries are present. A second look at a less busy time or a second reading can be beneficial in detecting findings which might be overlooked. This is particularly applicable to films of patients with multiple trauma.
   
6. Whenever possible, the referring physician should state the traumatic forces and the expected pattern of the traumatic changes. This allows a focused search with the expected injuries kept in mind.
   Example: The supination-adduction trauma to the ankle causes a transverse fracture of the lateral malleolus below the syndesmosis, or a rupture of the lateral collateral ligament. Furthermore, this can lead to a vertical osteochondral fracture of the medial talar articulating surface. An awareness of the mechanism of injury will help direct the search pattern. This follows the adage ‘you will find what you look for’.
   
7. It is mandatory to correlate clinical and radiological findings. If no exact or reliable clinical information is supplied, the radiologist or technologist must obtain it directly from the patient.
   
8. While many direct signs of fracture are easily appreciated, indirect signs such as soft-tissue changes are often overlooked. It is important for all images to include indirect signs in the diagnostic process (refer to special traumatology).
   
9. Equivocal radiographic findings should be further evaluated by additional views in other projections, such as oblique views. Other imaging modalities, such as sonography and CT, should be incorporated early in the diagnostic process.
   
10. Fracture lines are not invariably radiolucent. They can be radiodense if fracture fragments
    
    

    a) overlap,

    
    

    b) are impacted,

    
    

    c) are rotated relative to each other, with the radiodense line often sharply delineated, in contrast to a) and b).

Classification of fractures by their causative mechanisms:

1. Traumatic Fractures
   These fractures are caused by excessive mechanical loading, which can be sustained by deforming forces that act directly on bone such as tapping, crushing, or penetration, or indirectly from a distance, as occurs with traction, angulation, shearing, or compression. If the loading of bone exceeds a certain point, the bone will fail and fracture.
   
2. Stress and Insufficiency Fractures
   Stress fractures are caused by fatigue failure of otherwise normal bone induced by repeated or cyclical stresses. Insufficiency fractures are caused by normal forces or microtrauma and occur in bones of reduced internal strength, such those bones weakened by osteoporosis.
   
3. Pathologic Fractures
   These fractures occur in bone weakened by a preexisting condition and are caused by a force that would not break normal bone. They can be considered a local manifestation of an insufficiency fracture. The most common preexisting conditions are bone cysts, osteolytic metastases, and plasmocytoma.

Fig. 1.23 Creenstick fracture in a 7-year-old girl. Only one side of the cortex is fractured.

Fig. 1.24 Unusual fracture in the pediatric age group. Fracture across the metaphysis (corresponds to the Salter-Harris type II fracture), together with a subchondral fracture of the epiphysis (cartilage intact). a Unremarkable radiograph, b sagittal T1-weighted SE sequence, c axial T2-weighted sequence at the level of the femoral metaphyses.

The most important biomechanical properties of hyaline cartilage are protection against excessive strain and providing a smooth surface for the joint. These properties are determined by the chemical composition and the complex spatial interaction of the extracellular matrix of the cartilage. The matrix is primarily composed of water and macromolecules (collagen, proteoglycan, and other proteins). Hyaline cartilage consists of several layers, and the deep calcified zone and the subchondral bone are closely intertwined. An avulsion of the cartilage (traumatic separation) occurs primarily between the deep calcified and the juxta-articular noncalcified cartilage.

It is known from experimental studies that compression and trabecular fractures of the subchondral bone can occur without injury to the cartilage. This can be attributed to the greater elasticity of the cartilage in comparison to the subchondral trabecular osseous structure.

Fractures of the joints can be divided into typical skeletal fractures with articular involvement and specific fractures confined to the cartilage and subchondral bone. The latter fractures are caused primarily by pressure directly transmitted onto the cartilage by a vertical load. Concurrent shearing and rotatory load can not only increase the pressure on the articular surface but can also avulse cartilaginous fragments (with or without attached bone) from the articular surface.

Frequent causes of articular surface fractures are torsion or supination/pronation injuries and these are often associated with ligamentous injuries.

The clinical findings are nonspecific, but a hemorrhagic joint effusion is invariably present. This finding can also be associated with any trauma involving the intra-articular structures.

Dislodged chondral or osteochondral fragments must be surgically reattached, but shallow articular compression deformities can be treated conservatively.

Location: The principal sites of involvement are the ankle and knee, including the patella. Other less common locations are the femoral head and humeral head.

Technical considerations: If an osteo chrondral fracture of the ankle is suspected, a radiographic examination in three projections is indicated: AP, lateral, and AP oblique in slight internal rotation. The oblique view projects the articular surface of the talar trochlea without superimposition.

Fig. 1.26 Osteochondral fracture with loose fragment.

Fig. 1.27 Osteochondral fracture of the retropatellar articular surface.

Fig. 1.28 Osteochondral fracture of the lateral aspect of the talar trochlea.

Fig. 1.29 Osteochondral fracture of the lateral femoral condyle. Shell-like osseous fragment and irregular condylar contour.

Fig. 1.30 Large osseous fragment of osteochondral fracture of the femoral condyle.

Stress can be defined as the load sustained by bone. Bone is a dynamic tissue and needs stress for its normal development. The mechanical response to stress determines the osseous texture. Absence of normal stress induces rapid osteoclastic resorption of cancellous and cortical bone as well as cessation of the osteoblastic activity, leading to disuse osteoporosis.

Stress is also placed on bone from muscular activity and body weight.

It is not entirely understood how stress shapes the mechanical function of bone, but evidence suggests that the adaptive process is mediated by microfractures. Bone subjected to more than normal stress responds with osteoclastic resorption. The osteoclastic cavities are subsequently filled with lamented bone. The formation of new bone is a slow process (weeks to months), and stress in excess of the normal levels results in an imbalance between bone resorption and bone formation for the first few weeks. Therefore, new periosteal and endosteal bone formation represents a passing reparative mechanism needed to support the transiently weakened bone, especially the critical cortex. This process is basically the same in cortical and cancellous bone.

a T1-weighted CRE sequence after intravenous injection of contrast medium (indirect arthrography),

b T1-weighted SE sequence with frequency selective fat suppression following administration of contrast medium.

Fig. 1.33 Acute osteochondral fracture with surrounding edema laterally.

a Coronal T2-weighted CRE sequence with fat suppression,

b sagittal STIR sequence.

Fig. 1.34 a Stress reaction with periosteal and endosteal adaptation. The patient played volleyball for 30 years but was asymptomatic. The radiographic examination was obtained because of acute trauma. b Normal radiograph for comparison.

Fig. 1.35 Elderly female patient with pain for two years. a Remote insufficiency fracture of the right sacral ala. b The diagnosis of an insufficiency fracture is supported by a remote insufficiency fracture in the left superior ischial ramus (axial CT).

Stress fractures: The density and structure of bone are normal. Only the stressed portion of the bone is (reversibly) weakened according to the mechanism described above.

Fig. 1.38 Remote stress fracture in a marathon runner, seen as a subtle band of increased density.

Fig. 1.39 Bilateral insufficiency fractures of the sacrum. Enhanced T1-weighted MR sequence with fat suppression showing the ‘H’ configuration (‘Honda sign’).

Fig. 1.40 Insufficiency fracture of the tibial plateau in an overweight osteoporotic woman with pain for three weeks.

Fig. 1.41 Insufficiency fracture of the calcaneus, T1-weighted spin echo sequence before (a) and after (b) administration of contrast medium. After enhancement, the fracture line is seen as a band of decreased signal intensity.

Fig. 1.44 Pain for three months, no discernible fracture line: Stress fracture with periosteal new bone formation.

Fig. 1.45 Insufficiency fracture in osteogenesis imperfecta.

Below:
Fig. 1.46 Pathologic fracture in fibrous dysplasia (a). The patient suffered minor trauma. b Control radiography after internal fixation. The fibrous dysplasia was initially overlooked and only recognized after removal of the internal fixation device. c Conventional tomography.

Definition: Primary healing is characterized by the absence of callus formation and requires:

• Contact between fragments with a maximum fracture gap of 0.5 mm. Internal compression fixation of the fragments increases the chance of a primary fracture healing.
  
• Immobilization of the fracture fragments (e.g., internal fixation).
  
• Adequate blood supply and viability of the fragments.

The fracture fragments unite by direct extension of the Haversian canals from one fragment to the other (‘contact healing’), or by the formation of lamellar bone, which is later replaced by longitudinally oriented osteons (‘gap healing’). The periosteal or endosteal mesenchymal cells are not activated in this setting.

Indistinct cortical structures, invisible or faint fracture line.

Visualized interosseous or periosteal callous formation indicates the formation of ‘restless’ callus, followed by fixation callus. Furthermore, widening of the fracture line or the appearance of a ‘new’ fracture line reflects osseous resorption of the fracture fragments and indicates an impaired primary fracture healing.

A widened fracture line or inadequate mechanical fixation of the fracture fragments results in secondary fracture healing, consisting of the formation of a ‘periosteal cuff’ around the fracture gap. This cuff arises from connective tissue and represents mesenchymal new bone formation. In addition to connective tissue proliferation, cartilage is usually formed by metaplasia and ultimately transformed into osseous tissue. Thus, the original structure is restored via a detour (lamellar osseous tissue, osteons).

• The osseous bridging of the fracture is solid.
  
• The fracture callus is of homogeneous density.
  
• The density of the fracture callus equals the density of the cortex.
  
• These findings must be seen in at least two projections.

Caution: Underexposed films overestimate the degree of osseous bridging.

The conservative (closed) treatment follows three approaches:

1. Primary functional treatment (without cast). This requires adequate axial relationships and exercise stability; for example, a subcapital fracture of the humerus in an elderly person.
   
2. Repositioning and immobilization by casting, for instance, a distal radial fracture.
   
3. Repositioning and immobilization by means of traction; for instance, a femur fracture.

The goals of operative (open) therapy are to restore the normal anatomic relationship of the axial planes and articular surfaces and to stabilize fracture fragments. Several approaches are available and can be combined.

• Internal fixation by screws; for example, avulsion of juxta-articular or joint-bearing fragments,
  
• Internal fixation by compression plates and screws,
  
• Internal fixation by wire fixation (cerclage); for example, the olecranon and patella,
  
• Intramedullary fixation; for example, by rod and pins,
  
• External fixation; for example, the compound fracture of the lower leg.

Fig. 1.47 Callus formation following internal fixation of a femoral fracture. Indistinct fracture line.

Fig. 1.48 Status 4 years post-femoral fracture. Since the history of previous trauma was not known, the finding was initially diagnosed incorrectly as metastasis from the patient’s known breast carcinoma.

Fig. 1.49 Status 3 years post-green-stick fracture. Subtle post-traumatic cortical thickening.

Delayed fracture healing takes place in the following situations:

• extension of the fracture into the joint,
  
• elderly patients with slow osseous metabolism,
  
• poor alignment of the fracture fragments,
  
• inadequate immobilization of the fracture fragments,
  
• extensive soft-tissue injury (poor condition for perfusion!).

Fracture healing is categorized as delayed (impaired) if the time of healing exceeds twice the expected time period (about 4 to 6 months). The primary causes are:

• inadequate immobilization,
  
• impaired perfusion,
  
• infection.

A delay in fracture healing can result in a pseudarthrosis.

• inadequate immobilization,
  
• soft tissues interposed in the fracture gap,
  
• extensive loss of osseous substance,
  
• inadequate blood supply,
  
• infection (with/without sequestration).

Based on appearance (descriptive):

• hypertrophic form,
  
• atrophic form,
  
• defect with pseudarthrosis.

Based on viability (biologic):

• biologically reactive pseudarthroses.
  This type is caused by bridging of the fracture gap by fibrous tissue or inadequate callus formation, resulting in mobility of the fragments.
  
• biologically nonreactive pseudarthroses. This group represents nonviable pseudarthroses with severely impaired blood supplies directly beneath the ends of the fracture fragments. They are usually caused by large defects, necroses, and infections. The therapeutic goal is to restore stability with autologous cancellous bone grafts. Ultrasound may also be used for that purpose.

Hypertrophic type:

• The fracture fragments are smoothly outlined and sclerotic.
  
• The surrounding bone is eburnated.
  
• There is no evidence of osseous bridging.
  
• The fracture fragments are widened (‘elephant foot’).
  
• The fracture fragments can be rounded.

Atrophic type:

• There is only minimal evidence of sclerosis of the ends of the fracture fragments.

Avascular necrosis develops if a fracture or dislocation deprives the bone of an adequate blood supply.

Fig. 1.51 a Surgically treated talar fracture with development of a pseudarthrosis. Metallic fixation device removed. b T2-weighted CRE sequence, c T1-weighted SE sequence.

Fig. 1.52 Avascular necrosis of the left hip following medial subcapital fracture of the femoral neck. There is no perfusion of the femoral head on the T1-weighted sequence with fat suppression following enhancement.

Fig. 1.53 Avascular necrosis (osteonecrosis) of the lunate (Kienböck’s disease), T1-weighted SE image.

Disuse osteoporosis is an acute form of demineralization due to immobilization.

It can have the following radiographic manifestations:

• Decreased bone density confined to the cancellous bone without cortical involvement. The small trabeculae resolve, with thickening and indistinctness of the remaining trabeculae.
  
• Patchy decrease in bone density seen as ovoid and round, but also irregularly outlined, radiolucencies. These changes are frequently observed in older patients and in the hands and feet.
  
• Radiolucent lines. They are usually juxta-articular, and are most frequently seen along the old growth plates.
  
• Punctate and patchy radiolucencies with the cortex (enlarged Haversian canals).

Bone growth can be affected by many different situations. Any traumatic change involving a growth plate can potentially cause growth acceleration, generally explained by the hyperemia from trauma. This growth acceleration is transient and compensated by subsequent growth retardation.

Post-traumatic growth retardation has greater clinical implications. It is generally caused by an ossified growth plate. Partial involvement of the growth plate will induce asymmetric growth retardation while involvement of the entire growth plate will shorten the affected limb.

Partial fusion of the central region of the growth plate causes so-called ‘cupping’, which consists of cone-like widening of the epiphyses toward the metaphysis of the affected tubular bone.

Fig. 1.55 Residual defect following osteochondral fractures 2 years earlier. There is a predisposition to degenerative osteoarthritis in this setting.

Fig. 1.56 Osseous reaction to retained metallic foreign body.

Fig. 1.57 a Proximal humeral fracture in a 13-year-old girl. b 3 years later: large central radiolucency caused by a hematoma. Lamellated periosteal reaction as evidence of repair. c After a further 3 years: incomplete resolution of the osteolytic area.

Synonyms: Sudeck disease, Sudeck’s atrophy, algodystrophy.

Causalgia: Manifestation of reflex sympathetic dystrophy with severe pain.

Shoulder-hand syndrome: Reflex sympathetic dystrophy of the hand secondary to humeroscapular periarthritis.

Because of its still unexplained pathogenesis and unspecific presentation, reflex sympathetic dystrophy is known under various names. According to the latest definition published by the American Association of Hand Surgery, reflex sympathetic dystrophy is a pain syndrome associated with functional loss and detectable autonomous dysfunction. The original description by Sudeck seems to express the relevant findings best:

Reflex sympathetic dystrophy is usually posttraumatic, typically following distal radial or tibial fractures, but it can be induced by a variety of other conditions including myocardial infarction and cerebrovascular accidents. In some cases, no predisposing condition can be found.

The pathophysiology of this condition is unclear but the most frequently postulated theory proposes that afferent pain stimulates a hyperactive sympathetic nerve system to induce a change in blood flow that increases bone resorption. Recent research supports Sudeck’s original hypothesis of excessive regional inflammatory reaction.

The diagnosis is made if four of these five clinical criteria are fulfilled:

• diffuse pain,
  
• change in skin color,
  
• diffuse soft-tissue edema,
  
• different skin temperature,
  
• limited range of active motion.

The complaints increase with weight bearing.

Clinical course: Three stages are observed:

1. Inflammatory stage: burning pain, soft tissue swelling, weakness and hyperesthesia.
   
2. Dystrophic stage: vasospasm or vasodilatation, skin changes (atrophy, pigmentation, hyperhidrosis, nail changes), contractures.
   
3. Atrophic stage: skin atrophy, resolution of other symptoms.

Therapy: Conservative therapy, initially with lymph drainage, cryotherapy, later with thermotherapy and active physical therapy.

Fig. 1.59 Reflex sympathetic dystrophy of the left leg with patchy and striate radiolucencies.

Fig. 1.60 Reflex sympathetic dystrophy following partial fasciectomy for Dupuytren contracture. The typical bone scan findings are diffuse hyperemia as well as lateralization of the early and late blood pool images, followed by increased uptake in the carpal and metacarpal bones in the bone phase.

Fig. 1.61 Reflex sympathetic dystrophy of the right hand three months following a distal radial fracture. Osteoporosis with indistinct trabecular lines and patchy radiolucencies. The STIR sequence (b) shows increased signal intensity of the soft-tissues and an absence of bone marrow edema.

Tendons attach muscles to bone, usually bridge a joint, and have a high tensile strength. To function normally, they need an intact gliding bed, usually formed by a coarsely textured layer of connective tissues. Where the gliding range is wide, the tendons are surrounded by a sheath (e.g., fingers).

Traumatic rupture of the tendon results in tendon and muscle retraction. Small gaps can be spontaneously bridged by the ingrowth of soft tissues.

Mechanism of trauma:

• separation,
  
• rupture,
  
• degeneration (age, sports-induced stress, inflammation, long-term corticosteroid therapy, hypercholesteremia, diabetes mellitus).

Acute injuries to the tendons are easily detected by MRI. Since these injuries are diagnosed clinically, MRI is rarely performed.

Direct visualization of ligamentous structures requires MRI or sonography. Functional radiographic views (e.g., ‘stress views’) only provide indirect evidence of ligamentous lesions.

Ligaments are of low signal intensity on both Tl-weighted and T2-weighted images. A complete tear, best appreciated on STIR or T2-weighted SE MR images, appears as a high signal area (edema, blood) within the substance of the ligament. The tear may also be seen on the short TE images (Tl-weighted or proton density). Images should be obtained in the plane that most optimally displays the ligamentous anatomy (see Special Traumatology: Knee, Ankle).

Sonography is well suited to diagnose ligamentous injuries. While normal ligaments are seen as echogenic structures, injuries at the ligamentous insertion and involving the ligament itself are not only seen as continuity breaks but also as diffuse thickening and decreased echogenicity.

Muscle fibers do not regenerate after injuries and muscular injuries result in a scar, which has less functional strength.

Types of injuries:

• Strain: Stretching of the muscle without exceeding its tensile strength. Hemorrhage occurs within the muscle.
  
• Crush: Blunt external force ruptures muscle fibers, possibly inducing areas of muscular necrosis.
  
• Rupture: This can occur after trauma to normal or degeneratively predamaged muscle. The muscle is partially or completely severed, but complete loss of function is rare.

Diffuse edema and hemorrhage are the characteristic findings of acute as well as repetitive trauma and are easily identified as diffusely increased signal intensity on STIR and T2-weighted images (most conspicuous on turbo-SE sequences with fat suppression). The differentiation between sprain and (partial) tear rests on detecting a break in the ligamentous continuity. Tears result in large localized (hemorrhagic) fluid accumulations. MR findings are rarely seen in sprain or crush injury.

With immobilization of the affected extremity, the signal changes of a tear generally resolve within 14 days.

Fig. 1.63 Sonographic visualization of an Achilles tendon tear.

Fig. 1.64 Small hematoma as manifestation of a partial tear of the quadriceps tendon.

Fig. 1.65 Subfascial hyperintense hematoma of the calf without known injury. Clinical and sonographic findings were suggestive of tumor (T1-weighted sequence).

The possible causes of loss of cellular integrity of muscle tissue are strain, trauma, burn, and exposure to toxins (drugs).

Soft-tissue injuries can lead to traumatic myositis ossificans (see pp. 286ff).

Burns: Burn-induced osseous and articular changes usually depend on the size of the burned area.

The radiographic findings reflect the effect of ischemia (endothelial capillary damage) and the concurrent hyperemia of the remaining vascularized tissue:

• Focal or regional osteoporosis (immobilization or vasomotor reflex as probable cause).
  
• Periosteal reaction, similar to that of hypertrophic osteoarthropathy.
  
• Periarticular calcifications and ossifications, especially around hip, elbow, and shoulder.
  
• Progressive joint destruction, probably due to subchondral osteonecrosis along the articular fossa.
  
• Acro-osteolysis

Caution: Extensive burns frequently lead to secondary infections. They cause a multifarious picture and complicate the above-mentioned radiographic findings.

Frostbites: Temperatures below 8–12°C damage soft tissues and nutrient vessels by causing decreased blood flow, erythema, and edema. The affected parts are usually the most distal ends of the extremities.

The most prominent radiographic sign of frostbitten bones is subchondral osteonecrosis, especially in the phalanges of the hands and feet, as well as in the metacarpal and metatarsal bones.

Fig. 1.67 Rhabdomyolysis in a drug addict (T2-weighted image).

Fig. 1.68 Muscle necrosis in compartment syndrome (T1-weighted sequence after frequency selected fat suppression and enhancement), a Coronal, b axial imaging plane.

Fig. 1.69 Soft-tissue calcifications following compartment syndrome 24 years previously.

Fig. 1.70 Severe osteolysis of the second to fifth ray after frostbite.

The radiologic report should address the following items:

Judgmental terms, such as ‘good’, ‘adequate’, ‘acceptable’, or similar expressions, should be avoided.

Likewise, statements describing the osseous bridging as ‘solid,’ ‘delayed,’ ‘partial,’ or ‘absent’ should not be used. These statements require an intimate familiarity with the clinical condition. Instead, the callus should be described by its appearance (how does the callus look?) and it should be stated whether its appearance indicates osseous bridging or not. Furthermore, it should be stated whether the fracture line is still visible.

It should be kept in mind that it is difficult to judge any possible rotation of the fragments on conventional radiographs. If a clinically relevant rotation is suspected, CT or MRI should be recommended.

Fig. 1.72 Typical findings: trauma films. Oblique fracture of the proximal ulna with articular involvement and anterior ulnar dislocation. There is no displacement of the olecranon fragment.

Fig. 1.73 Typical findings: trauma films. Trimalleolar fracture-dislocation of the ankle with posterolateral displacement and medial angulation of the talus. There is a fibular fracture at the level of the ruptured interosseous membrane with medial angulation (approximately 20 degrees). The fractured medial malleolus is displaced laterally by about 8 mm and the posterior cortical fragment of the tibia (Volkmann triangle) is displaced upward by 5 mm.

Fractures of the cranial vault are differentiated according to location, mechanism, and configuration. Depending on the severity and type of causative force, three fracture types can be distinguished:

These represent 80% of all fractures of the cranial vault and generally are temporoparietal, occipital, and frontal in location. Only the presence of intracranial complications (bleeding, edema, intracranial air, etc.) requires therapeutic intervention.

Depending on its angle and velocity, the penetrating force can result in a depressed, punched-out, or burst fracture.

These fractures primarily involve the orbital roof, petrous pyramid, and occipital bone. The central areas of the cranial base are less often involved. Since the neurovascular structures pass through an aperture in the mechanically weak sites of the central cranial base, these fractures can be associated with considerable clinical findings (brain stem paralysis, paresthesia, vision loss, CSF fistula).

Historically, these fractures have been categorized relative to the longitudinal axis of the temporal bone as longitudinal, transverse, and mixed fractures. This categorization is arbitrary, however, since many fractures follow a winding course through the temporal bone.

Fig. 1.75 Linear fracture in a child.

Fig. 1.76 Depressed fracture of the calvaria. Caution! This case illustrates that searching for radiolucent fracture lines is not adequate. A CTscan is necessary to determine the extent of the impression and to exclude intracranial injuries.

Fig. 1.77 Fracture of the sphenoid sinus as seen on conventional radiographs (a) and on axial CT (b bone window, c soft-tissue window). The conventional radiograph only provides indirect evidence of a fracture of the cranial base.

This is the imaging method of choice for the evaluation of the traumatized temporal bone. The fracture signs are the same as those for conventional radiography. Furthermore, a change of the chain of the auditory ossicles (subluxation, dislocation, fracture) might be detected. Traumatic lesions of the stapes, however, are rarely adequately visualized.

MRI is only indicated when injuries of intracranial structures or cranial nerves dominate the clinical findings or are otherwise suspected together with fractures of the temporal bone.

Because of their pathogenesis, fractures of the facial bone are frequently multiple and complex.

Fig. 1.79 Transverse fracture of the temporal bone on axial CT.

Fig. 1.80 Schematic diagram of the zygoma and the four typical fracture sites.

Fracture of the Nasal Bones

This is the commonest localized facial fracture and the extent of injury depends on the direction and severity of the traumatic blow. The spectrum ranges from a widened nasofrontal suture and a simple nasal fracture to a comminuted fracture with involvement of the orbit and base of the frontal bone.

Fracture of the Zygoma

This is the second commonest facial fracture. The mechanically weakest point is the zygomatic arch. The most frequent manifestation is a depressed fracture with medial displacement of the fragments.

Clinically, the lateral facial structures are asymmetric, and involvement of the temporomandibular joint causes impaired movement of the mandible.

Fracture of the Zygomaticomaxillary Complex (ZMC)

Fig. 1.84 Blow-out fracture of the orbit as seen on coronal CT. The herniation of intraorbital fat and inferior rectus muscle is clearly displayed.

Fig. 1.85 Schematic diagram of the fracture lines of Le Fort fractures.

Fig. 1.86 Le Fort fractures I–III. coronal CT. These fractures are invariably associated with other facial bone injuries. A combination of the different Le Fort fracture types is common. The involvement of the left medial orbital wall of the Le Fort III fracture is best seen on more anterior sections.

Fractures, dislocations and soft-tissue injuries can affect the spine at any level. In the majority of cases, clinical and radiologic findings can readily establish the correct diagnosis. Insufficient experience, as well as inadequate image quality (mobile units, poor positioning of immobile patients), is responsible for the relatively high rate of missed vertebral injuries (approximately 25–50%). Improvement in detection can be expected from a better understanding of the different trauma patterns and pathogenic mechanisms and from familiarity with the radiographic approach.

Spinal injuries can be categorized according to the traumatic forces that cause them:

• Compression,
  
• Flexion,
  
• Extension,
  
• Rotation,
  
• Translation.

Since the severity of the traumatic force determines the extent of the damage, the spectrum of damage varies from trivial soft-tissue lesions to severe osseous and ligamentous injury.

Distinguishing between stable and unstable injuries will be discussed at the end of the chapter.

• Interrupted posterior cervical line: displacement, rotation, angulation, absence, and doubling are abnormal,
  
• Increased interpedicular width on the AP view (secondary to fracture of the lamina),
  
• Forward displacement,
  
• Segmental hypermobility,
  
• Subluxation or dislocation of the facet joints,
  
• Narrowed intervertebral disk space – usually above the fractured vertebra.