209 Pelvic and Major Long Bone Fractures
Pelvic Fracture
Pelvic fractures are present in about 10% of patients presenting to a level I trauma center after blunt trauma.1 Pelvic fractures represent approximately 3% of skeletal injuries evaluated in major trauma centers.2 The incidence of pelvic fracture is highest after motorcycle crash, pedestrian trauma caused by a motor vehicle, falls from heights greater than 15 feet, and motor vehicle crash, in that order.1 Overall mortality due to pelvic fractures ranges from 10% to 16%; the highest mortality—around 45%—is attributed to open pelvic fractures.2,3 However, very few patients die as a direct result of hemorrhage from the pelvic fracture itself. Most deaths in patients with pelvic fracture are from head injury, nonpelvic hemorrhage, pulmonary injury, thromboembolic complications, or multiple organ system failure. The incidence of solid and hollow organ injury and other skeletal trauma is high in patients with pelvic fracture, owing to the powerful forces involved.1,4,5 More than 90% of these individuals have associated gastrointestinal (5%) and abdominal injuries (16.5%).1,4 Risk factors for associated abdominal injury include motor vehicle crash, fall greater than 15 feet, and pelvis Abbreviated Injury Severity Score (AISS) greater than 3.1,5 Overall Injury Severity Score (ISS) and mortality correlate with the severity of the pelvic fracture, although death is usually the result of associated injuries rather than the fracture itself.6
Complications occur in roughly a third of patients and can involve devitalized tissues, hematoma formation, and those related to internal or external fixation. Infections are the most common complication (15.7%), followed by respiratory (9.3%), hematologic (5.5%), and thromboembolic complications (3.4%).7 Cardiac complications occur in about 2.5% of patients.7 Patients with unstable pelvic fractures are at significantly greater risk of complications than those with stable fractures.7–9 Infections involving external devices usually occur at the level of the pin tracts.9 If cellulitis or excessive drainage develops, broad-spectrum antibiotic coverage is needed. If the infection persists despite treatment, pin loosening may require replacement of new pin sites. Internal fixation infections are usually due to significantly devitalized tissues that have become secondarily infected or inadequately débrided. These infections are more commonly found with posterior approaches.9 Open drainage must be considered as well as alternative fixation techniques.
The transfusion requirement for patients with pelvic fracture with a mean ISS of 21.3 is 8 units of packed red blood cells but can be much greater.7 The degree of hemorrhage is highly dependent on the type of fracture. Complete dissociation of the posterior pelvis has the highest degree of hemorrhage and connected mortality.10,12 Significant hemorrhage often occurs from other sites such as the abdomen or thorax as well. Less than 1% of all patients with pelvic fractures have hypotension secondary to blood loss due to the fracture itself.7,11 Nevertheless, 12% of patients with open pelvic fractures die as direct result of hemorrhage.8
Hemorrhage from unstable pelvic fractures can be minimized by early reapproximation and stabilization of the pelvic ring. Stabilization can be accomplished with external fixation devices such as the Browner clamp or expediently with as simple an appliance as a bed sheet wrapped tightly around the pelvis. If external pelvic fixation is unsuccessful at restoring hemodynamic stability after initial resuscitation and other sources of ongoing hemorrhage have been ruled out, angiography to evaluate and treat pelvic arterial bleeding is indicated. Pelvic arterial disruption is responsible for hemorrhage in less than 5% of all cases of pelvic fracture.11–13 A blush of contrast identified on pelvic computed tomography (CT) scan is evidence for arterial bleeding and is an indication for angiography.11 Predictors of positive angiography have been postulated to be the presence of sacroiliac joint (SIJ) disruption, female gender, and the duration of hypotension.13 Early and aggressive angioembolization have been shown to improve outcomes in properly selected patients. However, some European trauma groups have proposed pelvic packing as an early operative maneuver in order to provide stabilization prior to angioembolization. Others, such as Cothren et al., have suggested a modified technique of early direct preperitoneal pelvic packing, thereby reducing blood transfusion requirements and the need for angiography, with a subsequently lower mortality.14 Evidence for this is based on several small case series. Early angioembolization based on radiologic diagnostics and external fixation within 3 hours of injury has also been shown to be effective, reducing the need for transfusion by using an algorithmic approach.15
Long Bone Fracture
The most studied and serious long bone fracture is fracture of the femur. Approximately 15% of seriously injured motor vehicle passengers presenting to a level I trauma center have femur fractures.14 Some 8% to 10% of these patients have bilateral fractures.16,17 The mortality rate for unilateral fracture is 10% to 12%.16,17 Mortality increases to 26% to 33% with bilateral fractures and is 20% in patients older than age 65.16 The highest incidence of femur fractures in the trauma population occurs in young men, with midshaft fractures being the most common as a result of high-energy impacts.13 As in pelvic fractures, death is more closely connected with the severity of associated injuries rather than the fracture itself.16,17 As noted, mortality is very significant in complicated femur fracture patients with multiple injuries. Therefore, careful assessment following the guidelines of Advanced Trauma Life Support (ATLS) is mandatory.
Blunt trauma patients who present with femur fracture have a higher incidence of abdominal, thoracic, and skeletal injuries compared with patients without femur fracture.16,17 Those with bilateral fractures have an increased incidence of head injury, requirement for laparotomy, and pelvic fracture compared to those with a unilateral femur fracture.16,17
The risk of complications, including acute respiratory distress syndrome (ARDS), pneumonia, and fat embolism syndrome, in the multiply injured patient with femur fracture can be markedly decreased by early operative fixation within 24 hours.18,19 Early operative repair also results in decreased ICU length of stay, hospital stay, cost, and risk of mortality.19,20
The American College of Surgery’s Committee on Trauma has recommended that femur fractures in polytrauma patients be repaired with 12 hours, provided the patient is hemodynamically stable.21 For trauma patients with multiple severe injuries, however, earlier repair can sometimes lead to higher morbidity secondary to the patient’s inability to tolerate excessive physiologic stress. The currently evolving damage control surgery concept is playing a more definitive role in managing long bone fractures; delaying definitive surgery may be the best approach and ultimately prove to be life saving.22 Damage control with external fixation of femur fractures in polytrauma patients is becoming the standard of treatment in many trauma centers.23
Although hemorrhage is a feared complication of femur fracture, a study of isolated femur fracture found that blood loss from the fracture itself is insufficient to cause hypotension.24 Of 100 patients with isolated femur fractures, only 24% were in class I or II shock. None were in class III or IV shock. Nevertheless, hemorrhage is the cause of death in a significant proportion of polytrauma patients with femur fracture, an indication of the importance of other sites of hemorrhage in these patients.20 Despite central nervous system injury being the predominant cause of death in polytrauma patients, mortality secondary to exsanguinations has been reported to be 12% to 26%.25 In addition, special attention must be paid to avoiding occult hypoperfusion (nonhypotensive shock), which is associated with an increased incidence of complications, especially infections, in patients with femur fracture.26 Hemorrhage from long bone fractures is best managed by early stabilization. Stabilization can be initiated with traction splints such as a Hare traction splint for femur fractures or closed reduction and splinting for other fracture sites. Neurologic injury due to femur fracture is a rare event.27
Local Complications
Infection
Infection can manifest as an acute complication in the setting of both long bone and pelvic fractures. Osteomyelitis can be the result of a grossly contaminated open fracture as well as a surgically repaired closed fracture. Acute infection of a fracture hematoma or fracture repair can manifest with cutaneous signs such as erythema, warmth, and induration. However, if the infected site is deep to the fascia, infection may manifest with systemic signs such as leukocytosis and fever without cutaneous signs.28 Diagnosis can be achieved using CT, magnetic resonance imaging (MRI), three-phase bone scan, or radiolabeled white blood cell scans. Plain radiographs are unlikely to aid in the early diagnosis of osteomyelitis, as findings are often delayed up to 21 days. The most common causative organism is Staphylococcus aureus, but infection may be due to many other organisms, including Pseudomonas aeruginosa and Enterobacteriaceae.9,28 Generally these infections take a week or more to manifest.
Treatment depends on the organism or organisms present. The best option in high-risk open fractures remains prophylactic antibiotics administered parentally within 6 hours, tailored to provide coverage against both gram-positive and gram-negative organisms. One common regimen consists of a first-generation cephalosporin (e.g., cefazolin, 1 g intravenously [IV] immediately, then every 8 hours) and an aminoglycoside (e.g., tobramycin, 7 g/kg body weight IV immediately, then every 24 hours) administered for 72 hours starting prior to surgery. For established infections, the mainstay of treatment is débridement of devitalized and infected bone and soft tissue followed by antibiotic therapy tailored to operative culture results. Hyperbaric oxygen has been used as an adjunct to therapy for osteomyelitis, but convincing data showing efficacy are lacking.28,29
Gas gangrene or necrotizing fasciitis can appear within the first 24 hours after fracture or operative repair. These fulminant, necrotizing infections usually occur in the setting of open fracture with extensive soft-tissue injury requiring débridement and are especially likely if there is a delay in treatment. The causative organism is Clostridium perfringens in 10% of cases, with synergistic multiple organisms including Streptococcus, anaerobes, and coliform bacteria causing the remainder.9,28 Findings can include skin changes, purulent or “dishwater” wound drainage, and profound shock due to vasodilatation. Treatment is aggressive surgical débridement of necrotic tissue, which may require amputation, and broad-spectrum antibiotics or high-dose penicillin. Hyperbaric oxygen also can be used in conjunction with surgical and pharmacologic treatment. Prophylaxis consists of early treatment of open fractures with thorough débridement of all devitalized tissue. Despite treatment, gas gangrene often results in fatality due to the severe septic manifestations of this infection.9,28 This is not to be confused with the diagnosis of a fracture blister (blood filled or clear filled) in the zone of injury, associated with closed fractures of the lower extremity. These are typically avoided surgically and left intact thus allowing spontaneous rupture. When spontaneous rupture occurs, they are deroofed and covered with a sterile nonadherent dressing.30 Some orthopedic surgeons advocate unroofing the fracture blister(s) in diabetic patients and treatment with silver sulfadiazine (Silvadene).31
Tetanus can result from any open fracture, but patients with fractures caused by farming accidents are at particularly high risk. Symptoms, caused by Clostridium tetani toxin, occur 1 to 2 weeks after injury and are often fatal. The case fatality rate is about 60%.7 Presenting symptoms include trismus, difficulty swallowing, restlessness, and headache. The syndrome progresses to convulsions and asphyxia. Muscle spasm and convulsions are due to excitation of spinal motor neurons. Diagnosis relies on clinical recognition, as cultures are positive in only a third of cases.9,28
Prophylaxis consists of 0.5 mL adsorbed tetanus toxoid administered promptly intramuscularly (IM) on presentation for all patients with traumatic wounds, including open fractures, who have not received a booster within the last 5 years. High-risk patients, such as those involved in farming accidents or with neglected wounds, are candidates for tetanus immunoglobulin (250 units administered by deep IM injection). Antibiotics are inadequate prophylaxis. Treatment of diagnosed tetanus infection consists of sedation, supportive care including airway management with intubation or a surgical airway, surgical débridement of the infected wound, passive immunization with tetanus immunoglobulin (recommended doses vary from 500 International Units to 10,000 International Units administered IM), and antibiotics (metronidazole, 500 mg IV every 8 hours).9,28
Compartment Syndrome
Compartment syndrome (CS) is a potentially devastating complication that arises in the setting of either open or closed fracture. Tissue edema and bleeding raise the pressure in the fixed volume of a fascial compartment, which impedes blood flow, especially in arterioles and capillaries, resulting in tissue ischemia. The degree of tissue necrosis depends on the pressure within the compartment, the duration of time during which compartment pressure is elevated, and the sensitivity of specific tissues to ischemia. Nervous tissue demonstrates functional abnormalities after 30 minutes of ischemia, with irreversible loss of function occurring after 12 to 24 hours. Muscle, on the other hand, does not exhibit functional effects for 2 to 4 hours, and irreversible loss of function occurs after 4 to 12 hours. Capillary permeability also increases, resulting in further tissue edema.9,32
The most common location for compartment syndrome after lower-extremity fracture is the anterior compartment of the leg. This complication usually results from closed tibia fracture. As many as 17% of patients with a tibia fracture secondary to a motor vehicle crash develop a compartment syndrome.27 Compartment syndrome of the thigh can develop after open or closed fracture and may develop after operative treatment of the fracture. Compartment syndrome of the arm, buttock, and foot are also possible after fracture. Risk factors associated with developing compartment syndrome include the severity of the fracture and associated soft-tissue injury, the use of compressive devises such as military antishock trousers or tourniquets, and systemic hypotension.9,32,33
Diagnosis of compartment syndrome can be made on clinical grounds and is established when the compartment is tense on physical examination, severe pain is present with passive motion, the compartment is tender throughout, and sensory nervous function is impaired. Loss of distal pulses is often the last manifestation of compartment syndrome. By the time pulses and distal perfusion are diminished, extensive necrosis of tissues within the compartment already may be present. It is important to be aware that compartment syndrome can occur both acutely and after operative fixation of a fracture. The diagnosis must be made early before permanent tissue damage has occurred. Serial examinations are critical to monitor for compartment syndrome in patients at risk.9,32
Measurement of compartment pressure is an additional way to confirm the diagnosis; however, measurements are unnecessary when the diagnosis is evident on clinical grounds. Measurement of compartment pressure is useful when the physical examination is limited because the patient is unresponsive due to head injury or sedation. Compartment pressure values ranging from 30 to 45 mm Hg have been recommended as the threshold for triggering surgical intervention.27 Compartment pressures are measured by placement of a sterile needle connected to a pressure transducer into each compartment. Alternatively, commercial devices such as the Stryker compartment monitor (Stryker, Kalamazoo, Michigan) are available that accomplish the same task.
Treatment is by urgent, complete surgical fasciotomy to open all affected compartments. Care must be taken to adequately open the skin because it may constrict the compartment, even if the fascia has been opened. Fasciotomy can be performed in the ICU if the patient is too unstable to be transported to the operating room. Complete fasciotomy within 12 hours of onset results in a normal functional outcome in 68% of cases, whereas delay decreases the likelihood of successful outcome to 8%.29
In light of the fact that compartment syndrome can lead to irreversible neurologic and muscular damage, early diagnosis cannot rely solely on clinical findings, so prophylactic fasciotomy has been advocated. Subsequently, a trend toward liberal use of “prophylactic fasciotomy” was noted. According to Abouezzi et al., the most important factor influencing the need for fasciotomy was location of the vascular injury. Popliteal vessel injuries are often associated with warm ischemia and prolonged repair time in the operating room.34 The overall incidence of neurologic damage due to a delayed or lack of fasciotomy is difficult to determine.34
Once the compartment has been opened, wash-out of the metabolic products of the ischemic compartment occurs. It is critical to closely monitor acid-base status, serum potassium and phosphate concentration, serum and urine myoglobin concentrations, fluid status, and renal function. Adequate hydration and monitoring of urine output are critical to successful postoperative care of these patients. The clinician must also be aware of the high incidence of infection at the fasciotomy site.33,35
Rhabdomyolysis
Rhabdomyolysis can occur for several reasons after skeletal trauma. The disease and its pathophysiology were first described in 1941 during the “Blitz” of London. The severity of the muscle necrosis depends on multiple factors including loss of arterial supply, increased compartment pressure secondary to prolonged or severe compression/injury, length of time without effective blood flow, and delayed resuscitation leading to hypovolemic shock.74 A high index of suspicion must be maintained to facilitate early diagnosis. There are over 40 compartments in the body. Approximately 70% of compartment syndrome occurrences are associated with fractures leading to rhabdomyolysis. The most obvious reason is direct injury to muscles surrounding the fracture site. Direct injury to skeletal muscle tissue is especially likely when the mechanism of injury resulted in transfer of a great deal of energy; an example is a motor vehicle crash. Second, rhabdomyolysis can occur secondary to compression of tissues for a prolonged period after the injury. The compression causes an ischemic injury to the involved muscle. Lastly, rhabdomyolysis can result from compartment syndrome due to a fracture. Again, the mechanism involves compression of circulation resulting in an ischemic injury. All three mechanisms of rhabdomyolysis can be exacerbated by hemorrhagic shock.36,37 Since myoglobinuria does not occur in the absence of rhabdomyolysis, serum myoglobin is the best diagnostic marker.38 The serum elevation of myoglobin occurs before the rise in serum creatine phosphokinase (CPK). With adequate resuscitation, the serum myoglobin will decrease with an inverse rise in the urine myoglobin.
The systemic effects of rhabdomyolysis are the result of anaerobic metabolism and cell lysis. Lactic acid release can lead to systemic acidosis, especially if volume replacement is inadequate. Potassium and myoglobin are released by the lysed myocytes. Hyperkalemia can lead to life-threatening cardiac arrhythmias. Intravenous calcium should be used with caution in this setting because it can rapidly combine with phosphate anions, leading to precipitation of calcium salts if hyperphosphatemia from muscle necrosis is present. Elevated serum myoglobin levels can cause direct renal tubular damage, leading to acute renal failure. CPK had been used traditionally to diagnose and trend compartment syndrome. However, it should not be used for early detection but can be used for monitoring after compartment decompression.39
Successful treatment of rhabdomyolysis involves aggressive IV fluid therapy to maximize tubular flow rate, avoiding the accumulation of myoglobin in the renal tubules and aiding the clearance of hyperkalemia. Administration of iron-chelating agents such as desferrioxamine (standard dosage for rhabdomyolysis not established) and alkalinization of urine using sodium bicarbonate as 50% of the resuscitation fluid (150 mEq dissolved in 1 L of 5% dextrose solution) or a carbonic anhydrase inhibitor such as acetazolamide is recommended by some experts. Ultimately, acute renal failure may necessitate hemofiltration or hemodialysis.36,40,41 In our institution, we aim to maintain a urine output greater than 1 to 2 mL/kg/h using IV fluids, and we follow serial serum and urine myoglobin levels. We have had good success in avoiding acute renal failure without the use of urine alkalinization or iron-chelating agents.
Fat Embolism Syndrome
Pathophysiology
In experimental models of fat embolism syndrome and autopsy series of blunt trauma patients, the degree of fat embolization, the severity of pulmonary compromise, and deaths attributable to fat embolism syndrome correlate with the severity and number of fractures.42,43 Other causes of systemic embolization include intrapulmonary shunts and patent foramen ovale.44
Beyond simple occlusion of capillaries, liberation of free fatty acids is thought to be pathophysiologically significant through the activation of inflammatory processes and/or direct toxicity to lung capillaries and pneumocytes. Histamine and serotonin are also released, exacerbating pulmonary dysfunction and causing bronchospasm and vasospasm.28,45,46
Epidemiology
Estimates of the number of patients with fractures who develop the pulmonary, skin, and neurologic manifestations of fat embolism syndrome vary between 0.5% and 20%.9,28,46 The incidence of fat embolism syndrome increases to 5% to 35% after multiple fractures.9,28 The mortality rate is about 10%, and death is usually due to severe pulmonary dysfunction and multiple organ system failure and severe neurologic dysfunction.9,28,46,47 It is estimated that 5000 deaths due to fat embolism syndrome occur annually after pathologic fractures, traumatic fractures, and orthopedic surgery.45
Clinical Manifestations
Clinical diagnosis of fat embolism syndrome is based on the presence of the classic triad of respiratory compromise, mental status changes, and petechial rash in the setting of long bone fractures or orthopedic surgery involving long bone manipulation.52 In patients with long bone fractures, 60% manifest symptoms within 24 hours of injury and 85% within 48 hours.9,28 Therefore, in the appropriate setting, the rash is pathognomonic and present in only 20% to 50% of cases.48
Severity can vary from subclinical to subacute clinically apparent symptoms to fulminant acute symptoms.49 Subclinical emboli probably occur in nearly all patients with long bone fractures or intramedullary manipulation.9,50 The subacute course is associated with mild respiratory dysfunction and mild neurologic manifestations or cardiovascular compromise. Supportive care is usually adequate in these cases. The fulminant variety can involve any of the following: rapidly progressive ARDS, complete cardiovascular collapse, or deep coma, possibly resulting in death.51
Some degree of respiratory compromise is always present and is often the most severe and life-threatening of the manifestations of fat embolism syndrome.44 In trauma patients, it may be difficult to distinguish fat embolism syndrome from other causes of compromised pulmonary function. Indeed, the cause of respiratory compromise in multitrauma patients with significant long bone fractures can be multifactorial, including fat embolism syndrome, direct pulmonary/thoracic cavity trauma, and ischemia reperfusion injury and systemic activation of the inflammatory response. However, an isolated long bone fracture can produce cardiac as well as respiratory symptoms.
The cardiovascular effects of fat embolism syndrome are mainly attributable to partial occlusion of pulmonary arterial flow resulting in acute pulmonary hypertension and increased right ventricular afterload. The cardiovascular effects of fat embolism syndrome vary in severity from sinus tachycardia to reversible hypotension to irreversible profound shock due to right heart failure resulting in death.28,35,45 Changes on the electrocardiogram include sinus tachycardia, bradycardia, other arrhythmias, and ST-segment changes.28,35,49 Treatment is supportive, with inotropic agents to increase contractility of the right ventricle to overcome the adverse effect of increased afterload. Increasing preload with IV fluids is usually not helpful and can lead to overdistention of an already overloaded right ventricle. To make matters worse, increased right heart pressure resulting from pulmonary hypertension can cause a closed foramen ovale to open, contributing to systemic embolization.45
Central nervous system manifestations of varying degrees are present in 70% to 80% of patients with fat embolism syndrome.44 These findings can vary from mild confusion or restlessness to profound coma resulting in death.9,51 Most commonly, agitation, confusion, and lethargy not attributable to hypoxia are encountered.35,46,49 Patients can also develop focal changes such as hemiplegia due to cerebral ischemia.35 The more severe neurologic outcomes are often attributed to paradoxical emboli through a patent foramen ovale, although massive systemic embolization with profound coma and petechial hemorrhage of the brain in the absence of a patent foramen ovale can occur.43,44,53
Petechial rash is present in up to 50% of cases and is usually present on the chest, neck, and axilla, although less often the rash appears on mucous membranes or the conjunctiva.43,46,49 Retinal changes also can be observed and include microinfarcts, cotton-wool spots, and flame-like hemorrhages.9,44,49 Petechial rash is usually a late sign of fat embolism syndrome. The petechial rash is attributed to capillary occlusion or distention by fat globules.49 Although it appears late and is often not present, when it does appear it can greatly aid in the definitive diagnosis.
Diagnosis
Many laboratory abnormalities are encountered in cases of fat embolism syndrome, but none is specific. These laboratory findings include decreased PaO2 with decreased or increased PCO2, thrombocytopenia, slowly decreasing hematocrit, increased fibrin split products, and decreased fibrinogen.46,49
Bronchoalveolar lavage has been advocated as a more specific test to diagnose fat embolism syndrome. The percentage of alveolar macrophages laden with fat droplets in the bronchoalveolar lavage fluid as determined by fat stains is elevated in patients with fat embolism syndrome. This finding may be helpful in confirming suspected cases of fat embolism syndrome, although precise diagnostic criteria have not been established. False-positive results are seen in patients with long bone fractures and after orthopedic procedures without clinical evidence of fat embolism syndrome.50,54
Findings on chest CT scan include patchy ground-glass or nodular opacities and thickening of the interlobar septa. Differential diagnosis of these findings includes pulmonary contusion and aspiration. Because they most often occur 24 hours or more after injury, they can usually be differentiated from contusion, which should be evident earlier. CT findings in more severe cases of fat embolism syndrome include more extensive bilateral patchy airspace consolidation; similar abnormalities can also be seen on the chest radiograph.47,55 Occasionally, CT imaging also reveals large emboli lodged in the femoral veins, inferior vena cava, or the proximal pulmonary circulation.56
Treatment
The most important treatment of fat embolism syndrome is prevention. In the setting of traumatic fracture, prevention is achieved by providing early fixation. Multiple experimental and clinical studies clearly show that early fracture fixation (within 24 hours) decreases both the pulmonary and cardiac effects of fat embolism syndrome when compared with delayed (>24 hours) fixation and nonoperative treatment.28,35,49,57–59 Intraoperative use of transesophageal echocardiography (TEE) can be a very sensitive monitor to detect fat emboli. The emboli appear as showering white flakes flowing or tumbling through the right atrium.59
Thromboembolism
Pathophysiology
Venous injury, stasis, and hypercoagulability can all contribute to the risk of thromboembolism after pelvic or long bone fractures.9 Embolic thrombi to the pulmonary circulation or systemic circulation (paradoxical embolization) can originate in the deep veins of the thigh, pelvis, or upper extremity. Calf vein thrombosis, in general, does not embolize but extends to involve more proximal deep veins 20% to 25% of the time.9
Risk Factors
A number of risk factors for thromboembolic disease, including femur, tibia, and pelvic fractures, have been identified in trauma patients. Other identified risk factors include age older than 40 years, immobility, blood transfusion, multiple trauma, head injury, spinal fracture, spinal cord injury, and high ISS.28,49,60–66 However, a systematic review of the literature by the Eastern Association for the Surgery of Trauma (EAST) found that only spinal fractures and spinal cord injuries were consistently shown to be associated with a higher risk of deep vein thrombosis (DVT).67 Despite these data, most trauma and orthopedic surgeons regard the risk of thromboembolic disease in trauma patients with long bone or pelvic fractures as real.28
Prophylaxis
Elevation of the affected extremity and passive motion exercises increase lower-extremity venous flow rates and reduce DVT.28 Lower-extremity sequential compression devices decrease the incidence of DVT by up to 90% in orthopedic patients.28 Compression devices placed on the foot have also been shown to decrease the incidence of DVT in patients undergoing orthopedic surgery for elective indications or trauma.28 These devices are useful when the anatomy of injury and surgery precludes placement of sequential compression devices on the leg.28 Similar improvements in the thromboembolism rate have been seen in the surgical ICU population.68 In the multitrauma population, some studies have shown sequential compression device use to be equivalent to low-dose heparin, whereas other studies have shown no improvement in thromboembolic events when compared to no prophylaxis.66 Despite conflicting data in the literature, the use of sequential compression devices continues to be a mainstay of thromboembolism prophylaxis in the skeletal trauma population because of its low cost, ease of use, and inherent safety. The salutary effects of sequential compression devices are thought to include improved venous flow and activation of endogenous antithrombotic mechanisms. The anticoagulant effects of sequential compression devices decrease minutes after discontinuing the device, emphasizing the importance of continuous therapy.67,68 Because of its low cost, noninvasive nature, and high accuracy, color-flow duplex ultrasonography has become the test of choice for DVT.69 Aggressive screening and prophylaxis can reduce the incidence of asymptomatic venous thromboembolism (VTE) diagnosed by duplex ultrasonography.62
Low-dose unfractionated heparin (5000 units IV, 2-3 times daily) decreases the incidence of thromboembolic events when compared with placebo in various populations of acutely ill patients. These studies have included orthopedic and nonorthopedic critically ill and noncritically ill patients. Overall reduction in thromboembolic rates are on the order of two- to threefold.67,68 However, multiple studies of trauma and orthopedic patients, including two meta-analyses, have failed to show significant improvement in the rate of thromboembolic events when low-dose unfractionated heparin is compared to placebo.28,67
The literature on low-molecular-weight heparin (LMWH) is more convincing. Several studies have shown that treatment with LMWH decreases the incidence of thromboembolism and has an excellent safety profile in patients with hip fracture or multisystem trauma.28,60 Moreover, studies have also shown that LMWH (enoxaparin, 30 mg subcutaneously [SQ] every 12 hours) provides superior VTE prophylaxis when compared to low-dose unfractionated heparin (5000 units SQ every 12 hours) in the trauma population.67,70
Several studies have shown improved efficacy using combined sequential compression devices and low-dose unfractionated heparin or LMWH therapy when compared to either therapy alone in stroke, cardiac surgery, and neurosurgery populations.69 Other studies, however, have shown no difference between combined and single-modality therapy.68 Further study of the fracture population is needed.
Treatment
Treatment of DVT and pulmonary embolism in patients with orthopedic injuries or multiple trauma involves a balance between the risk of bleeding and thromboembolic disease. Although virtually all pulmonary emboli arise from DVT in the thigh, pelvis, or upper extremity, calf vein thrombosis tends to propagate into the proximal veins, meaning that treatment should be to avoid embolic phenomena.71,38 Treatment of DVT and pulmonary embolism usually starts with full anticoagulation using unfractionated heparin. Once therapeutic heparinization has been achieved for an average of 72 hours, treatment with sodium warfarin is begun. Patients are usually kept on bedrest for this period to prevent embolic events.71,72 Alternative therapy includes LMWH.
Inferior vena cava filters are generally reserved for patients who have failed anticoagulation, exhibit embolic phenomena or propagation of clot while on full anticoagulation, or are inappropriate candidates for systemic anticoagulation.68,73 Prophylactic use of inferior vena cava filters involves patients who have no documented pulmonary embolus or DVT but are thought to be high risk due to numerous factors. The literature varies attempting to ascertain what defines the “high-risk” patient. It is well recognized, however, that immobility, venous stasis/injury, inflammatory hypercoagulable states, and severely injured patients at risk for bleeding are contributory factors to the development of VTE and thromboprophylaxis failure.75–79 Therefore, prophylactic use of inferior vena cava filters should be limited to those patients deemed high risk despite standard preventive measures (compression devices, anticoagulation).
Prognosis
More than 50% of deaths caused by pulmonary embolism occur within the first hour. After the first hour, patients are at a 2.5% to 10% risk of dying when treated adequately. Inadequate treatment carries a 30% risk of death.49
Key Points
Bone LB, Johnson KD, Weigelt J, Scheinberg R. Early versus delayed stabilization of femoral fractures: a prospective randomized study. J Bone Joint Surg Am. 1989;71:336-340.
Scannell BP, Waldrop NE, Sasser HC, et al. Skeletal traction versus external fixation in the initial temporization of femoral shaft fractures in severely injured patients. J Trauma. 2010;68:633-640.
Crowl AC, Young JS, Kahler DM, et al. Occult hypoperfusion is associated with increased morbidity in patients undergoing early femur fracture fixation. J Trauma. 2000;48:260-267.
Demetriades D, Karaiskakis M, Toutouzas K, et al. Pelvic fractures: epidemiology and predictors of associated abdominal injuries and outcomes. J Am Coll Surg. 2002;195:1-10.
Akhtar S. Fat embolism. Anesthesiol Clin. 2009;27:533-550.
Fabian TC, Hoots AV, Stanford DS, et al. Fat embolism syndrome: prospective evaluation in 92 fracture patients. Crit Care Med. 1990;18:42-46.
Geerts WH, Jay RM, Code KI, et al. A comparison of low-dose heparin with low-molecular-weight heparin as prophylaxis against venous thromboembolism after major trauma. N Engl J Med. 1996;335:701-707.
Adams RC, Hamrick M, Berenguer C, et al. Four years of an aggressive prophylaxis and screening protocol for venous thromboembolism in a large trauma population. J Trauma. 2006;65:300-308.
Jeske HC, Larndorfer R, Krappinger D, et al. Management of hemorrhage in severe pelvic injuries. J Trauma. 2010;68:415-420.
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