Extremity trauma is very common, occurring in up to 75% of patients with multisystem and pelvic ring injuries.1 Established patterns of injury are seen with common mechanisms, such as head-on and side-impact motor vehicle collisions, a pedestrian struck by a vehicle, and falls from a height. The extremity injuries include injuries to the bones, joints, soft tissues, vascular system, and peripheral nerves.
Head-on motor vehicle collisions often result in a closed head injury, flexion-distraction injuries of the spine, intraabdominal injuries, posterior element acetabular fractures, hip fracture dislocations, bilateral femur and tibia fractures, and posterior knee dislocation with associated popliteal artery injury. Lateral-impact collisions and pedestrian injuries also have their own distinct patterns. Falls from a height frequently result in head injury; thoracic vascular shear injuries; abdominal visceral lacerations; spinal burst fractures; vertical shear injuries of the pelvis; and lower extremity fractures, including femoral neck and shaft fractures; tibial plateau, shaft, and pilon fractures; and calcaneal fractures. Although every patient should be examined thoroughly for all injuries, these patterns help to direct the focus of assessment to the most likely areas of injury.
In general, all fractures need to be assessed for specific findings aside from the underlying fracture or dislocation. Excessive bleeding from fractures or vascular, neurologic, and soft tissue envelope injuries should be assessed, as well as the presence of compartment syndrome and open fractures.
Subtle injuries require palpation of each bone and motion of each joint. Even then, serial examinations several days after the initial injury may be required to detect all injuries. Any suspected areas should be imaged with radiographs in orthogonal planes.
Open fractures are graded by the system of Gustilo and Anderson24,25 (Table 96-2).
Table 96–2. Gustilo-Anderson Open Fracture Classification ||Download (.pdf)
Table 96–2. Gustilo-Anderson Open Fracture Classification
- Type I: Low-velocity injuries less than 1 cm long, usually compound from within, with minimal soft-tissue injury or comminution of the fracture.
- Type II: Lacerations more than 1 cm long, with minimal to moderate soft-tissue crushing.
- Type III: High-velocity injuries with severe crushing and the presence of skin flaps.
- IIIA: No soft tissue loss
- IIIB: Soft-tissue loss with periosteal stripping
- IIIC: Associated vascular injury requiring repair
Although the initial fracture care usually is done in the emergency department, occasionally patients will be admitted to the ICU before any treatment can be initiated. After the initial assessment, any wounds should be flushed with saline and covered with a sterile dressing. Gross limb deformity and joint dislocations should be reduced and splinted and the neurovascular examination repeated. All musculoskeletal injuries should be imaged, and repeat fracture reductions or reductions of dislocations may be performed at this time as necessary. The patient should be prepared for operative intervention if a vascular injury, open fracture, irreducible dislocation, or compartment syndrome is detected.
In the case of open fractures, intravenous antibiotics should be administered, with gram-positive coverage for all compound fractures and with the addition of gram-negative and anaerobic coverage for contaminated wounds. The patient's tetanus status should be determined, and tetanus toxoid and immunoglobulin should be administered as required (Table 96-3).
Table 96–3. Tetanus Immunization Schedule ||Download (.pdf)
Table 96–3. Tetanus Immunization Schedule
|Non-Tetanus-Prone Wounds||Tetanus-Prone Wounds|
|History of Absorbed Tetanus Toxoid, Number of Doses||Tda||TIGb||Td||TIG|
|Unknown or less than three||Yes||No||Yes||No|
|Three or morec||Nod||No||Noe||No|
All compound fractures should be treated with urgent irrigation and débridement within 8 hours, followed by provisional or definitive fixation, depending on the condition of the soft tissue envelope and the amount of wound contamination. Gustilo-Anderson type I, II, and IIIA fractures can be treated with irrigation and débridement and immediate definitive fixation, followed by serial débridements every 48 hours until the wound is clean. Type IIIB injuries usually require provisional external fixation and serial débridements until the wound is clean enough for definitive fixation and soft tissue coverage. For type IIIC injuries, the most pressing concern initially is reestablishment of perfusion to the extremity. After provisional fixation and vascular repair, serial débridements again may be required before definitive fixation can be performed, with soft tissue coverage as necessary. Prophylactic fasciotomies are frequently required to prevent reperfusion compartment syndrome. There is an increased risk of infection and nonunion with increasing grade of injury.
If the patient has not been optimized or there is some other delay postponing definitive treatment, provisional treatment of the fractures by splints, traction, or external fixation may be necessary. In addition, prophylaxis for DVT should be initiated, as discussed earlier. Attention to the skin, especially in dependent areas such as the sacrum, heels, and posterior scalp, should be maintained, with frequent log-rolling and skin care to avoid the development of decubitus ulcers.
Definitive fixation of most fractures allows greater ease of mobilization for general care and pulmonary toilet. Early mobilization and physical therapy also prevent the development of joint contractures and muscle atrophy, resulting in a faster recovery and reduced morbidity. DVT prophylaxis should be maintained during the postoperative period until the patient is mobilizing well independently.
Blood loss from fractures alone can be enough to cause hemodynamic instability. Even without a significant arterial laceration, femur fractures can result in blood loss of up to 2 units, tibia fractures 1 unit, and pelvic and acetabular fractures 4 units or more. Aggressive fluid resuscitation must be maintained while reassessing for other causes of hemodynamic instability. With increasing swelling of the extremities from fracture bleeding, there must be a high index of suspicion for compartment syndrome.
The vascular status of each limb must be assessed by checking for the presence and quality of peripheral pulses, as well as the perfusion of the tissues distal to the zone of injury. Blunt or nonpenetrating vascular injuries often are associated with traction or avulsion injuries, fractures, and dislocations. It is important to assess the entire peripheral vasculature if there are multiple ipsilateral injuries, such as concomitant femur and tibia fractures. Knee dislocations and tibia fractures have the highest incidence of arterial injury, followed by femur fractures and traction injuries to the shoulder girdle. An abnormal vascular examination may be due to vascular spasm, external compression, intimal tear, or disruption of the artery itself. If the vascular examination is abnormal before or after gross realignment of fractures and reduction of dislocations, further investigation with an ankle-brachial index, angiogram, or magnetic resonance angiography is indicated to determine the nature of the injury. External compression of the artery usually can be relieved by reduction of the fracture or dislocation, and vascular spasm usually resolves after reduction as well.
Penetrating injuries such as gunshot and knife wounds also have a high incidence of vascular injury. All structures in the path of the projectile should be assessed from entry to exit wounds, including a generous surrounding area of collateral damage.
If the limb remains dysvascular, urgent operative intervention is required because muscle necrosis begins after 6 hours of warm ischemic time.26 The sequence of events for vascular repair usually begins with provisional fracture stabilization with an external fixator or rapid internal fixation followed by the establishment of a provisional shunt to restore perfusion.27 Definitive vascular repair, ideally with an end-to-end anastamosis or saphenous vein graft, if necessary, then can be performed, followed by definitive fracture fixation.26 Reperfusion edema and compartment syndrome are common; thus a prophylactic fasciotomy usually is indicated. Wound coverage by skin graft or free flap can be achieved after the wound has undergone serial débridements to minimize the risk of wound infection and sloughing of the graft28 (Fig. 96-4).
If the patient is awake and cooperative, a detailed neurologic examination of each extremity should be done, with particular attention distal to the zone of injury. If the patient cannot participate in the examination, general observations of gross limb movements and reaction to pain stimulus help to establish baseline function. Most peripheral nerve injuries are neuropraxias, which begin to recover spontaneously over 6 to 12 weeks. The progress of recovery can be monitored with serial nerve conduction studies. In the situation of penetrating injuries or dissection for open reduction and internal fixation of fractures, the nerve may be explored to assess for injury. If it is found to be lacerated, direct primary repair is indicated once the wound is clean.29
With or without nerve repair, it is important to splint the extremity in a functional position of rest, with occupational and physical therapy involvement to maintain motion of the affected joints. Muscle stimulators also may be beneficial to decrease the rate of atrophy of the affected muscles. If acute repair or grafting has been performed, the extremity should be splinted in a resting position temporarily (1 to 2 weeks) to allow the repair to begin to heal and then gradually mobilized to prevent arthrofibrosis and contractures.
Increased compartment pressures result from intercompartmental edema and bleeding associated with fractures or vascular injury. The increase in pressure causes a compressive occlusion of capillary venules, stopping capillary flow and perfusion of tissues, the most sensitive of which are the muscles and nerves. Because the compressive phenomenon affects the microvasculature, distal pulses usually are maintained during this process.30
Clinically, compartment syndrome is manifested by the “five P's”. In order of clinical relevance, these are pain out of proportion to the injury,31 pain with passive stretching of the affected muscles, paresthesia (numbness) involving the nerves within and distal to the compartment, powerlessness (weakness) of the muscles within the compartment, and a pulseless extremity (which may not necessarily ever happen). If left untreated, the muscles and nerves undergo necrosis, resulting in ischemic contractures and loss of sensation or painful paresthesias, leaving the limb with very poor function.
The most common sites affected are the lower leg, in association with tibia fractures, and the forearm, in association with radius and ulna fractures. Compartment syndrome also can occur in the thigh, buttock, upper arm, hand, and foot.32,33
Early recognition is mandatory either clinically, as described earlier, or by compartment pressure monitoring. A compartment pressure greater than 30 mm Hg or within 30 mm Hg of the diastolic pressure is diagnostic for compartment syndrome. It may be necessary to rely on pressure monitoring if the patient is obtunded, there are significant distracting injuries, or the clinical examination is unreliable (psychiatric conditions, intoxication, etc).
The initial treatment includes elevation of the limb to the level of the heart and release of all circumferential or compressive dressings. If there has been no improvement within 1 hour, a fasciotomy is required. If in doubt, it is far better to perform a fasciotomy because the consequences of untreated compartment syndrome are extremely debilitating and usually permanent. Owing to the typical amount of swelling with these injuries, the wound usually cannot be closed and requires coverage with a skin graft several days after release.34
Fat embolism syndrome (FES) encompasses the respiratory, neurologic, and other systemic sequelae of the embolism of fat from the marrow space of long bones. It occurs in up to 2% of isolated long bone fractures and up to 10% of multiply injured patients. The most significant feature of FES is the potentially severe respiratory effects, which may result in adult respiratory distress syndrome (see Chap. 27). It usually occurs within 1 to 3 days following injury, and the clinical presentation includes the following: lethargy, disorientation, and irritability with the appearance of petechiae on the trunk and in the axillary folds, conjunctiva, and fundi in 50% of cases. Blood tests may demonstrate anemia and thrombocytopenia, and examination of the urine may show lipiduria.
The diagnosis of FES can be made on major and minor criteria. The major criteria include respiratory insufficiency, central neurologic impairment, and petechial rash. The minor criteria include tachycardia, fever, retinal fat emboli, lipiduria, anemia, and thrombocytopenia.35
Once the patient becomes hypoxemic, supportive measures are all that can be done, including positive end-expiratory pressure (PEEP) and lung-protective ventilation. The most significant treatment aspect of FES is prevention. Early long bone fracture fixation has been shown to be a key factor,36 particularly with tibia and femur fractures. Aggressively fluid resuscitation and maintaining an adequate circulatory volume also have been shown to be protective. Despite aggressive management, the mortality rate of full-blown FES is up to 15%; thus the importance of early fracture fixation is critical.