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Diagnosis and Treatment of Complications
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Craig S. Roberts, M.D. Gregory E. Gleis, M.D. David Seligson, M.D.
A complication is a disease process that occurs in addition to a principal illness. In the lexicon of diagnosis-related groupings, complications are co-morbidities. However, a broken bone plate complicating the healing of a radius shaft fracture hardly seems to t either of these denitions. In orthopaedic trauma language, the term complication has come to mean an undesired turn of events specic to the care of a particular injury. Complications can be local or systemic and are caused by, among other things, physiologic processes, errors in judgment, or fate. A colleague once described a pin tract infection with external xation as a problem, not a complication. Preventing pin tract drainage is indeed a problem that needs a solution, but when it occurs in a patient, it becomes a complication. Additional terminology has been introduced by the Joint Commission on the Accreditation of Healthcare Organizations, such as the sentinel event, a type of major complication that involves unexpected occurrences such as limb loss, surgery on the wrong body part, and hemolytic transfusion reaction. This chapter presents current knowledge about three systemic complications (fat embolism syndrome, thromboembolic disorders, and multiple system organ failure), ve local complications of fractures (soft tissue damage, vascular problems, post-traumatic arthrosis, peripheral nerve injury, and reex sympathetic dystrophy [RSD]).
SYSTEMIC COMPLICATIONS Fat Embolism Syndrome
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Fat embolism syndrome (FES) is the occurrence of hypoxia, confusion, and petechiae a few days after long bone fractures. FES is distinct from post-traumatic pulmonary insufciency, shock lung, and adult respiratory distress syndrome (ARDS). When known etiologic factors
of post-traumatic pulmonary insufciency such as pulmonary contusion, inhalation pneumonitis, oxygen toxicity, and transfusion lung are excluded, there remains a group of patients who have FES with unanticipated respiratory compromise several days after long bone fractures. Fat embolism was rst described by Zenker in 1861 in a railroad worker who sustained a thoracoabdominal crush injury.76 It was initially hypothesized that the fat from the marrow space embolized to the lungs and caused the pulmonary damage.66 Fenger and Salisbury believed that fat embolized from fractures to the brain, resulting in death.21 Von Bergmann rst clinically diagnosed fat embolism in a patient with a fractured femur in 1873.73 The incidence of this now recognized complication of long bone fracture was extensively documented by Talucci and co-workers in 1913 and subsequently studied during World Wars I and II and the Korean conict.68 Mullins described the ndings in patients who died as lungs that looked like liver.43 Although the fat in the lungs comes from bone, careful investigation has shown that other processes are required to produce the physiologic damage to lung, brain, and other tissues. Although the term fat embolism syndrome does not describe the pathomechanics of this condition as neatly as was originally hypothesized, embolization of active substances and fat from the injured marrow space has traditionally been thought to be the source of embolic fat. However, recent studies suggest otherwise. Mudd and associates did not observe any myeloid tissue in any of the lung elds at autopsy in patients with fat embolism syndrome and suggested that the soft tissue injury, rather than fractures, was the primary cause of fat embolism syndrome.41 Ten Duis in a current review of the literature stated that future attempts to unravel this syndrome . . . should pay full attention to differences in the extent of accompanying soft-tissue injuries that surround a long-bone fracture.71 The index patient with FES is a young adult with an isolated tibia or femur fracture, transported from a
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Copyright 2003 Elsevier Science (USA). All rights reserved.
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SECTION I General Principles TABLE 181
distance with no oxygen therapy and inadequate splinting. Although denitive fracture stabilization is planned, the operative permit is hard to obtain because the patients behavior is inappropriate and the family notices a change in mood. The pulse rate is increased, the arterial oxygen concentration is decreased, and petechiae are present. Untreated, the patient will shortly be in an intensive care unit, if he or she survives. The chest radiograph shows bilateral uffy pulmonary inltrates, and concern shifts from when and how to nail the femur to when to begin life support.19 Although there are many unanswered questions about FES, several issues are apparent. It strikes the young and healthy, whereas older patients with signicant upper femoral fractures do not seem at risk. It usually occurs after lower, not upper, limb fractures, and is more frequent with closed fractures.16 Russell and associates reported a case of fat embolism in an isolated humerus fracture.61 In a prospective study, Chan and associates found an incidence of 8.75% of overt FES in all fracture patients, with a mortality rate of 2.5%.15 The incidence rose to 35% in patients with multiple fractures. Other investigators reported the incidence of FES between 0.9% and 3.5% in patients with long bone fractures.37, 57, 72 Early recognition of the syndrome is crucial to preventing a complex and potentially lethal course.2 Clinically, FES consists of a triad of hypoxia, confusion, and petechiae appearing in a patient with fractures.19 The disease characteristically begins 1 to 2 days after fracture, following what has been called the latent or lucid period.66 Sixty percent of all cases of FES are seen in the rst 24 hours after trauma, and 90% of all cases appear within 72 hours.7 Gurd and Wilsons criteria for fat embolism syndrome are commonly used, with the clinical manifestations grouped into either major or minor signs of FES.25 The major signs are respiratory insufciency, cerebral involvement, and petechial rash. The minor signs are fever, tachycardia, retinal changes, jaundice, and renal changes. Petechiae are caused by embolic fat. They are transient and are distributed on the cheek, neck axillae, palate, and conjunctivae. The fat itself can be visualized on the retina.1 A fall in hematocrit levels18 and alterations in blood clotting prole, including a prolongation of the prothrombin time, can be observed. The diagnosis of FES is made when one major and four minor signs are present (Table 181), along with the nding of macroglobulinemia.44 The most productive laboratory test is measurement of arterial oxygenation on room air. When the Po2 is less than 60 mm Hg, the patient is in the early stages of FES. Lindeque and colleagues35 believe that Gurd and Wilsons criteria are too restrictive and should also include the following: 1. A PCO2 of more than 55 mg Hg or a pH of less than 7.3, 2. A sustained respiratory rate of more than 35 breaths per minute, and 3. Dyspnea, tachycardia, and anxiety. If any one of these is present, then the diagnosis of FES is made. Other supportive ndings include ST segment
Major and Minor Criteria for the Diagnosis of Fat Embolism Syndrome*
Major Criteria Hypoxemia (PaO2 < 60 mm Hg) Central nervous system depression Petechial rash Pulmonary edema
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Minor Criteria Tachycardia >110 bpm Pyrexia >38.3C Retinal emboli on fundoscopy Fat in urine Fat in sputum Thrombocytopenia Decreased hematocrit
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*A positive diagnosis requires at least one major and four minor signs. Source: Gurd, A.R.; Wilson R.I. J Bone Joint Surg Br 56:408416, 1974.
changes on electrocardiography and pulmonary inltrates on chest radiography.20 It is important to assess the neurologic status of the patient to differentiate between fat embolization and intracranial mass lesions. Although hypoxia alone can cause confusion, in the FES, petechial hemorrhages, particularly in the reticular system, alter consciousness. These changes persist despite adequate oxygen therapy.7, 22, 24 Focal neurologic ndings should be investigated to rule out lesions caused by associated head trauma. Persistent alteration of consciousness or seizures are bad prognostic signs. Neurologic changes have been noted in up to 80% of patients.29 Fat globules are found in blood,33 sputum, urine, and cerebrospinal uid. The urine or sputum can be stained for fat using a saturated alcoholic solution of Sudan III. Sudan III stains neutral fat globules yellow or orange. The Gurd test, in which serum is treated with Sudan III and ltered, is also diagnostic. The specicity of these tests is in question. Fat droplets are normally found in sputum.46 In addition, Peltier believes that detection of fat droplets in circulating blood and urine is too sensitive a test for the clinical diagnosis of FES.52 Furthermore, because the embolic phenomena associated with FES are transient and may not be detected on spot testing, these laboratory investigations are of research interest only and are not part of the usual clinical workup. The experimental study of FES is linked historically to the study of the circulation of blood, the development of intravenous therapy, and transfusion. As early as 1866, Busch experimented with marrow injury in the rabbit tibia and showed that fat in the marrow cavity would embolize to the lungs.13 Pulmonary symptoms have been produced in the absence of fracture by the intravenous injection of fat from the tibia of one group of rabbits into another.9 Autopsy studies of accident victims with long bone fracture have identied fat within the pulmonary capillaries in up to 25% of the victims. Uncommonly, massive release of bone marrow fat actually plugs the pulmonary vessels and causes death. There are several reasons for uncertainty as to the role of bone fat in producing FES. First, researchers have failed
CHAPTER 18 Diagnosis and Treatment of Complications
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to develop an animal model that reproduces the human syndrome. Moreover, injection of human bone marrow fat into the veins of experimental animals has shown that neutral fat is a relatively benign substance, and it is not certain that the bones contain enough fat to cause FES. One hypothesis is that the fat that appears in the lungs originated in soft tissue stores and aggregated in the blood stream during post-traumatic shock.28 However, chromatographic analysis of pulmonary vasculature fat in dogs after femoral fracture has shown that the fat most closely resembles marrow fat.31 In contrast, Mudd and colleagues recently reported that there was no evidence of myeloid elements on post-mortem studies of lung tissue in patients with fat embolism syndrome.41 Furthermore, extraction of marrow fat from human long bones has shown that sufcient fat is present to account for the observed quantities in the lungs and other tissues.55 The relative lack of triolein in childrens bones may explain why they have a signicantly reduced incidence of FES compared with that in adults.24, 26, 32 ETIOLOGY Although the precise pathomechanics of FES are unclear, in a literature review, Levy found many nontraumatic and traumatic conditions associated with FES.34 The simplest hypothesis is that broken bones liberate marrow fat that embolizes to the lungs. These fat globules produce mechanical and metabolic effects culminating in FES. The mechanical theory postulates that fat droplets from the marrow enter the venous circulation via torn veins adjacent to the fracture site. Peltier56 coined the term intravasation to describe the process whereby fat gains access to the circulation. The conditions in the vascular bed that allow intravasation to take place also permit marrow embolization.40 Indeed, marrow particles are found when fat is found in the lungs (Fig. 181).70
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FIGURE 181. Histologic appearance of fat from a pulmonary fat embolism in a vessel of the pulmonary alveoli. Abbreviations: C, capillary; F fat globules (arrowheads). (From Teng, Q.S.; Li, G.; Zhang, B.X. , J Orthop Trauma 9[3]:183189, 1995.)
Mechanical obstruction of the pulmonary vasculature occurs because of the absolute size of the embolized particles. In a dog model, Teng and co-workers70 found 80% of fat droplets to be between 20 and 40 m. Consequently, vessels in the lung smaller than 20 m in diameter become obstructed. Fat globules of 10 to 40 m have been found after human trauma.34 Systemic embolization occurs either through precapillary shunts into pulmonary veins or through a patent foramen ovale.51 The biochemical theory suggests that mediators from the fracture site alter lipid solubility causing coalescence, because normal chylomicrons are less than 1 m in diameter. Many of the emboli have a histologic composition consisting of a fatty center with platelets and brin adhered.75 Large amounts of thromboplastin are liberated with the release of bone marrow, leading to activation of the coagulation cascade. Schlag demonstrated hypercoagulability following hip arthroplasty.63 Studies of the physiologic response to the circulatory injection of fats have shown that the unsaponied free fatty acids are much more toxic than the corresponding neutral fats. Peltier hypothesized that elevated serum lipase levels present after the embolization of neutral fat hydrolyzes this neutral fat to free fatty acids and causes local endothelial damage in the lungs and other tissues, resulting in FES.56 This chemical phase might in part explain the latency period seen between the arrival of embolic fat and more severe lung dysfunction. Elevated serum lipase levels have been reported in association with clinically fatal FES.59, 65 Alternative explanations are also possible for the toxic effect of fat on the pulmonary capillary bed. The combination of fat, brin, and (possibly) marrow may be sufcient to begin a biochemical cascade that damages the lungs without postulating enzymatic hydrolysis of neutral fat.24, 28, 64 Bleeding into the lungs is associated with a fall in the hematocrit level.17 The resulting hypoxemia from the mechanical and biochemical changes in the lungs can be severeeven to the point of death of the patient. Pape and associates50 demonstrated an increase in neutrophil proteases from central venous blood in a group of patients undergoing reamed femoral nailing. In another study, Pape and colleagues49 demonstrated the release of platelet-derived thromboxane (a potent vasoconstrictor of pulmonary microvasculature) from the marrow cavity. Peltier53 demonstrated the release of vasoactive platelet amines. These humoral factors can lead to pulmonary vasospasm and bronchospasm, resulting in vascular endothelial injury and increased pulmonary permeability. Indeed, thrombocytopenia is such a consistent nding that it is used as one of the diagnostic criteria of FES. Barie and co-workers6 associated pulmonary dysfunction with an alteration in the coagulation cascade and an increase in brinolytic activity. Autopsy ndings in patients dying of FES do not, however, show a consistent picture.66 This may not be caused solely by a lack of clear-cut criteria that dene patients included in a given series, but may also be because the manifestations of FES depend on a wide number of patient, accident, and treatment variables.56
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SECTION I General Principles
In light of the incidence of fat emboli and FES in trauma patients, it is likely that other precipitating or predisposing factors such as shock, sepsis, or disseminated intravascular coagulation are needed for the phenomenon of embolized fat to cause FES.23 Muller and associates42 summarized that fat embolism syndrome is likely the pathogenetic reaction of lung tissue to shock, hypercoagulability, and lipid mobilization. Two questions arise: (1) Is there an association between intramedullary nailing and other injuries? (2) Is there an effect from different nailing methods? Investigations by Pape and associates47, 48 provided insight into both of these questions. In a study group of patients with multiple trauma and thoracic injury, these researchers found that early operative fracture xation by nailing was associated with an increased risk of ARDS. These results are in contrast to those of the group without thoracic injury. Thoracic trauma is associated with direct pulmonary injury. The pathogenic mechanisms were examined by Lozman and colleagues.36 Thus, the timing as well as the associated injuries are crucial in deciding when and how to use a nail. In a prospective study, Pape and associates48 showed a signicant impairment of oxygenation in multiple trauma patients who underwent reamed nailing. A group of similar patients who had an unreamed nailing did not have the same signs of pulmonary dysfunction. These investigators reasoned that the most likely difference between the two groups was a lower degree of fat embolization in the unreamed group. In sheep, Pape and colleagues49 demonstrated intravasation of fat associated with reaming of the intramedullary (IM) canal. They concluded that the unreamed procedure caused substantially less severe lung damage than the reamed procedure. However, Heim and associates27 found that there was a signicant increase in IM pressure associated with unreamed nail insertion, and that both reamed and unreamed nailing leads to bone marrow intravasation (Fig. 182). Thus, the use of an unreamed nail does not solve the problem of bone marrow embolization and resultant pulmonary dysfunction. What inuences the degree of fat embolization? The answer to this question has not been fully elucidated. High IM pressures have been linked with fat embolization and FES.30 Wozasek and co-workers75 looked at the degree of fat intravasation during reaming and IM nailing and correlated this with IM pressure changes and echocardiographic ndings. They found peak IM pressures in both the tibial and the femoral nailings in the rst two reaming steps. Insertion of the nail caused only minimal pressure rises (but this was after reaming). Echocardiography, however, demonstrated that the maximal inltration of particles occurred when the nail was inserted. They concluded that the phenomenon of fat intravasation did not depend on the rise in IM pressure. Pinney and associates studied 274 patients with isolated femur fractures and found that waiting more than 10 hours after injury was associated with a 2.5-fold increase in fat embolism syndrome.58 Bulger and co-workers, in a 10-year review of the literature, state that early intramedullary xation did not seem to increase the incidence or severity of fat embolism syndrome.12
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FIGURE 182. Intramedullary pressure during reamed nailing of the femur. (From Heim, D.; Regazzori, P.; Tsakiris, D.A.; et al. Intramedullary nailing and pulmonary embolism: Does unreamed nailing prevent embolization? An in vivo study in rabbits. J Trauma 38[6]:899906, 1995.)
PREVENTION AND TREATMENT The risk of FES can be decreased by several measures. Proper fracture splinting and expeditious transport, use of oxygen therapy in the postinjury period, and early operative stabilization of long bone fractures of the lower extremities are three important measures that can be taken to reduce the incidence of this complication.3 Blood pressure, urinary output, blood gas values, andin the more critically injuredpulmonary wedge pressures should be monitored to evaluate uid status and tissue perfusion more precisely.34 Dramatic advances in emergency medical transport have resulted in increasing survival of patients with complex polytrauma and high injury severity scores. This, unfortunately, has led in some instances to a tendency to scoop and run without traction splinting. Unsplinted long bone fractures in patients transported over long distances provide the mechanical condition for intravenous fat intravasation. Oxygen therapy by mask or nasal prongs lessens the decrease in arterial oxygenation following fracture and appears to have value in the prevention of FES. In the hospital, if surgery is delayed, the patients arterial oxygen on room air is measured daily and supplemental oxygen therapy is continued until the post-traumatic fall in oxygen tension is complete and the PAO2 on room air returns toward normal. Alternatively, if inspired oxygen tension (Fio2) can be measured accurately, the shunt equation can be used to monitor pulmonary performance. Teng and co-workers70 completed preliminary development of a dog model of FES to establish
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diagnostic criteria sufciently sensitive and specic enough for diagnosis of FES in the early stages. They correlated blood gas analysis samples with computer image analysis of oil red Ostained pulmonary artery blood samples. Although fracture xation and particularly medullary nailing cause a transient decrease in oxygenation, the immediate stabilization of fractures before the development of low arterial saturation may prevent the occurrence of FES.60 In a prospective randomized study of 178 patients, Bone and associates10 conrmed that early fracture stabilization, within the initial 24 hours after injury, decreased the incidence of pulmonary complications. Likewise, Lozman and colleagues,36 in a prospective randomized study, concluded that patients receiving immediate xation had less pulmonary dysfunction following multiple trauma and long bone fractures than did those patients receiving conservative treatment. Although current data support primary fracture stabilization over delayed therapy, controversy still exists over the method of stabilization. Bostmann and co-workers found a higher incidence of local infections, delayed bone healing, and decreased stability with plate osteosynthesis compared with a lower incidence of these same complications with IM nailing.11 In general, IM nailing is the preferred method of stabilization. The timing of nailing, however, is a point of controversy.12 Among other reasons, this was due to the concern that immediate nailing of long bone fractures early in the post injury period would increase the incidence of pulmonary complications, including FES. The nonoperative method of treating major long bone fractures has been the use of balanced skeletal traction or delayed rigid xation, or both. External xation of long bone fractures is another option that can be used as a temporizing alternative to IM nailing. Earlier studies showed no evidence to support the view that the effect of reaming on intravascular fat is additive or that immediate reamed IM xation causes pulmonary compromise.5, 68 In fact, the opposite is true, probably because fracture stabilization removes the source of intravascular marrow fat and decreases shunting in the lung, because the patient can be mobilized to an upright position.38, 39, 72 In a retrospective study by Talucci and associates,69 in which 57 patients underwent immediate nailing, no cases of FES were seen. Similarly, Behrman and colleagues8 reported a lower incidence of pulmonary complications for patients undergoing early xation among 339 trauma patients who underwent either early or late xation of femoral fractures. In the study by Lozman and colleagues,36 patients who had delayed fracture xation had a higher intrapulmonary shunt fraction throughout the study period compared with that in the early xation group. However, early IM nailing of long bone fractures is not without complications. Pell and co-workers,51 using intraoperative transesophageal echocardiography, demonstrated varying degrees of embolic showers during reamed IM nailing. FES developed postoperatively in three patients, and one patient died. Other studies showed an increased number of pulmonary complications associated with reamed IM nailing of femoral shaft fractures.45, 50, 74 Specic therapy has been used to try to decrease the incidence of FES. Increased uid loading and the use of
hypertonic glucose, alcohol, heparin, low molecular weight dextran, and aspirin have no clinical effect on the rate of FES. Various studies have looked at the efcacy of steroids in reducing the clinical symptoms of FES. Large doses of steroids immediately after injury do have a benecial effect.4, 22, 35, 62, 67, 70 Corticosteroids most likely decrease the incidence of FES by limiting the endothelial damage caused by free fatty acids. Although this is encouraging, routine use of steroids is not without signicant risk. Complications, particularly infection and gastrointestinal bleeding, may outweigh the benets, because many of these patients have signicant multiple trauma. Clinical trials in which steroids were effective used a dose of 30 mg/kg body mass of methylprednisolone administered on admission and repeated once at 4 hours35 or 1 g on admission and two more doses at 8-hour intervals.67 However, FES is primarily a disease of the respiratory system, and current treatment is therefore mainly with oxygen and meticulous mechanical ventilation.54 The treatment of FES remains mainly supportive.12
Thromboembolic Disorders
PATHOGENESIS Deep venous thrombosis (DVT) and pulmonary embolism (PE) are the most common causes of morbidity and mortality in orthopaedic patients.100, 127, 236 In the trauma patient, the presence of DVT may complicate the patients treatment even more than in the case of elective surgery. If DVT or PE occurs before denitive management of the fracture, the method of treating the fracture may have to be modied because of the use of therapeutic anticoagulants. In contrast, the elective surgery patient can be treated perioperatively with selected prophylactic anticoagulants to reduce the incidence of DVT without altering the operative plan. This is practical for elective surgery patients, because the thrombi most commonly develop at surgery.107 However, for the trauma patient, it is not known when the patient is at greatest risk for the development of DVT.92 Certainly DVT can develop preoperatively, as was shown by Heatley and associates,156 who observed that when patients admitted for gastrointestinal evaluations were hospitalized preoperatively for 4 days or longer, there was a 62% incidence of DVT before operation. In 1846, Virchow proposed the triad of thrombogenesis: increased coagulability, stasis, and vessel wall damage (Fig. 183). These are all factors that are unfavorably affected by trauma. Virchow also linked the presence of DVT with PE and deduced that a clot in the large veins of the thigh embolized to the lungs.273 Laennec,191 in 1819, was the rst to describe the clinical presentation of an acute pulmonary embolus, and the pathosis of a proximal DVT was rst described by Cruveilhier114 in 1828. Venous thrombi have been shown to develop near the valve pockets on normal venous endothelium and are not necessarily related to inammation of the vessel wall.248 Trauma increases the propensity to develop a hypercoagulable state. Vessel wall injury with endothelial damage exposes blood to tissue factor, collagen, basement mem-
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Stasis Anesthesia Hospitalization Immobilization Congestive heart failure Myocardial infarction Cerebrovascular accident Shock Pregnancy Obesity Venous injury Surgery (orthopedic, gynecologic, cancer) Trauma Previous deep venous thrombosis Burn injury Fracture Hypercoagulability Inherited coagulopathy Acquired coagulopathy Pregnancy or parturition Hormonal therapy Malignancy
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FIGURE 183. Virchows triad.
Presentation
brane, and von Willebrand factor, which induce thrombosis through platelet attraction and the intrinsic and extrinsic coagulation pathway.184 Antithrombin (AT-III) activity, which decreases the activity of thrombin and factor Xa, was found to be below normal levels in 61% of critically injured trauma patients.222 Also, brinolysis is decreased and appears to be from increased levels of PAI-1, which inhibits tissue plasminogen activator and thus decreases the production of plasmin.146, 204 Although DVT is unusual in children, it has been observed in children with previously asymptomatic hypercoagulable disorders and following trauma. The increased risk with age appears to reach a plateau at age 30 years. Any additional increase in risk after age 30 is related to the presence of other risk factors (e.g., trauma, heart disease, infection, and cancer).107 The presence of heart disease alone increases the risk of pulmonary embolism by 3.5 times, and this is further increased if atrial brillation or congestive heart failure is present.107, 109 The risk of DVT is increased during pregnancy and is especially great in the postpartum period. Spinal cord injury is associated with a threefold increase in leg DVT and PE. Many other factors affect the risk of DVT. Obesity has been reported to have a twofold increase in the risk of DVT. Type O blood has a lower incidence of DVT, whereas type A has an increased frequency. The blood type association is related to high concentrations of clotting factor VIII, which is determined mostly by blood group and is related to increased risk of thrombosis.239 Gramnegative sepsis, myeloproliferative disorders, ulcerative colitis, Cushings disease, homocystinuria, and Behcets syndrome have all been reported to have an increased risk of DVT. Varicose veins are assumed to be an increased risk factor for the development of DVT. However, the presence of venous abnormalities as determined by preoperative plethysmography and Doppler studies alone do not correlate with increased risk.201 Barnes85 divided varicose vein patients into two groups: those with primary varicose veins that are usually associated with a strong family history and have no increased risk of DVT, and those with secondary varicose veins that usually occur following a history of DVT. Patients in the latter group do have an increased risk for recurrent thrombophlebitis.
A meta-analysis by Velmahos and co-workers338 looked at DVT and risk factors in trauma patients. Variables studied that did not have a statistically signicant effect for increasing the development of DVT were gender, head injury, long bone fracture, pelvic fracture, and units of blood transfused. The variables, which were statistically signicant, were spinal fractures and spinal cord injury, which increased the risk of DVT by twofold and threefold, respectively. The patients with DVT versus those without DVT were signicantly older by 8 years and had a signicantly higher injury severity score (ISS) by 1.430 0.747, although the ISS difference was of minimal clinical signicance. They could not conrm that the widely assumed risk factors of pelvic fractures, long bone fractures, and head injury affected the incidence of DVT but did note that the multiple trauma patients may have already been at the highest risk of DVT. The incidence of DVT and pulmonary embolism (PE) has always been difcult to establish. Less than 50% of actual DVT incidence can be diagnosed by clinical means. To determine the true incidence for study purposes, the most accurate techniques have been autopsy or venography. In autopsy studies, the incidence of pulmonary embolus as a signicant contributor to the cause of death was 7.9%. The incidence of DVT, when determined by complete leg dissections at autopsy, is three to ve times greater than that for pulmonary emboli.107 The risk of DVT is not just in the operated leg. Culver and colleagues115 found that for hip fractures, the incidence of DVT detected by venography in the fractured limb was 40%, whereas in the uninjured leg it was 50%. Autopsy studies conrm this; thrombosis is generally present bilaterally even when injury is limited to one extremity or when thrombosis is clinically present in just one leg.249 The nature of the injury has little effect on the incidence of DVT; rather, it is other factorsage, heart disease, and length of immobilizationthat determine the incidence.138, 156 In immobilized trauma patients with no prophylaxis, the incidence of venography-proven thigh and iliofemoral thrombosis was between 60% and 80%.135, 190 Even with full prophylaxis, the incidence of DVT is as high as 12%.187 Some investigators have concluded that there is no adequate prophylaxis against DVT in the trauma patient.260
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Trauma to the pelvis and lower extremities greatly increases the risk of DVT and PE.108, 159, 282 In an autopsy study of 486 trauma fatalities, Sevitt and Gallagher249 found 95 cases of PE for an incidence of 20%. At autopsy, the rate of PE following hip fracture was 52/114 (46%); for tibia fractures, 6/10 (60%); and for femoral fractures, 9/17 (53%). The rate of DVT for hip fractures increased to 39/47 (83%) and for femur fractures to 6/7 (86%) when supplemental special studies of the venous system were done at autopsy. PE is signicant as a cause of death following lower extremity injury. Two thirds of patients having a fatal pulmonary embolus die within 30 minutes of injury (Fig. 184).120 The incidence of fatal pulmonary embolus without prophylaxis after elective hip surgery is from 0.34% to 3.4%, whereas the incidence following emergency hip surgery is from 7.5% to 10%.126, 144, 207, 275, 283 Solheim258 reported an 0.5% incidence of fatal PE in a series of tibia and bula fractures. Similarly, Phillips and co-workers227 reported 1 of 138 patients (0.7%) with severe ankle fractures developed a nonfatal PE. In a study of 15 patients with tibia fractures, Nylander and Semb219 found that 70% had venographic changes compatible with DVT. The types of DVT that are at high risk for causing a PE are those that originate at the popliteal fossa or more proximally in the large veins of the thigh or pelvis. Moser and LeMoine215 found that the risk of pulmonary embolization from distal lower extremity DVT to be relatively low. Of DVTs that are rst limited to the calf, about 20% to 30% extend above the knee.90, 229 Those that extend above the knee carry the same risk as femoral and popliteal thrombi.243 Kakkar and colleagues182 speculated that thrombi in the calf are securely attached and resolve rapidly and spontaneously. However, embolization from calf only venous thrombi does occur. Calf vein thromboses are responsible for 5% to 35% of symptomatic pulmonary emboli,200, 226 15% to 25% of fatal PE,139, 208, 248 and 33% of silent PE.211, 212 In addition to PE, complications of DVT include recurrent thrombosis and post-thrombotic syndrome. Symptoms of post-thrombotic syndrome are edema,
induration, pain, pigmentation, ulceration, cellulitis, and stasis dermatitis.174, 176 Symptoms are present in 20% to 40% of those having DVT. Upper extremity DVT are much less common (2.5%) and can be divided into primary and secondary causes. The primary causes are idiopathic and effort thrombosis (Padget-Schroetter syndrome). Effort thrombosis is most common in athletes and laborers who do repetitive shoulder abduction and extension. Predisposing causes of thoracic outlet obstruction should be investigated. Secondary causes are venous catheters, venous trauma, extrinsic compression or malignancy, and hypercoagulable condition. DIAGNOSIS The clinical signs and symptoms of DVT are nonspecic. DVT was clinically silent in two thirds of cases in which thrombosis was found at autopsy or the ndings on leg venography were positive.129, 249 Patients usually present with swelling, calf tenderness, positive Homans sign, fever, and elevated white blood cell count. Changes in color and temperature, venous distention, edema, and calf tenderness are helpful diagnostic signs when present. Homans signpain in the calf on dorsiexion of the footis nonspecic. Clinically, the diagnosis of DVT and PE is frequently difcult. With PE, although some patients experience sudden death, many more present with gradual deterioration and symptoms similar to pneumonia, congestive heart failure, or hypotension. Because the clinical diagnosis is difcult, diagnostic studies are necessary so that early treatment can be instituted. Various test are described along with limitations and advantages. The venogram is the standard against which all other tests are measured. Venography is able to adequately demonstrate the calf veins in 70% of patients with DVT. Only the presence of an intraluminal defect is diagnostic of DVT; chronic venous disease can cause the other ndings. Criteria for a diagnosis of DVT should include well-dened defects on at least two radiographs, nonvisualization of the popliteal, supercial femoral, or common femoral veins with good visualization of the proximal and distal veins, and the presence of collateral channels.145 The major drawback of venography is that it is usually a one-time test that cannot be done on a serial basis. Venograms can be painful, can cause swelling of the leg, have been reported to cause phlebitis in about 4% to 24% of patients,91, 243 and may cause thrombosis.80 As with any contrast agent, anaphylactic reactions are a possibility, as are renal complications.145 Between 5% and 15% of venograms cannot be interpreted owing to technical considerations.281 In a study by Huisman and colleagues,162 20% of patients either could not undergo venography or had noninterpretable studies. Radioactive brinogen is effective in detecting thrombi in the calf but is less effective in the thigh.167 Fibrinogen I-125 is incorporated into a forming thrombus and can be detected. DVT in the thigh is poorly detected with this technique, and it is not used as a screening tool for trauma patients. Impedance plethysmography (IPG) detects the presence
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FIGURE 184. A large embolus in the pulmonary artery, which was the cause of death. (Courtesy of James E. Parker, M.D., University of Louisville, Louisville, KY.)
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of DVT by measuring the increased blood volume in the calf after temporary venous occlusion produced by a thigh tourniquet and the decrease in blood volume within 3 seconds after deation of the cuff.169, 278, 279 The IPG is very sensitive in diagnosing proximal DVT but is not sensitive for distal DVT.97, 155, 164, 280 It is a poor screening tool for the trauma patient. Continuous-wave Doppler (CWD) or Doppler ultrasound examination is easy to do and can be done at bedside, but it requires experience to reduce the falsepositive result rate.85 The principles of ultrasonic velocity detection have been outlined by Sigel and colleagues.254 Characteristics of a normal venous system are spontaneity (evidence of a ow signal), phasicity (respiratory variation), and augmentation (increased ow with distal compression of the leg). Venous thrombosis is characterized by the absence of venous ow at an expected site, loss of normal uctuation in ow associated with respiration, diminished augmentation of ow by distal limb compression, diminished augmentation of ow by release of proximal compression, and lack of change on Valsalva maneuver. Barnes and co-workers86 found that Doppler ultrasound was 94% accurate, and no errors were made in diagnosis above the level of the knee. However, for isolated calf vein thrombosis, CWD is insensitive. An additional disadvantage is that CWD may fail to detect nonobstructive thrombi even in proximal lesions.101 Compression ultrasound is the use of real-time B-mode ultrasonography, with the single criteria of compressibility of the common femoral and popliteal vein needed for the diagnosis of DVT. Normally the lumen of a vein collapses when enough pressure is applied to indent the skin; if a thrombus is present, the vein does not compress.112 Using this technique to monitor the veins of the thigh and calf and using venography as a control, Froehlich and associates130 found this test was 97% accurate, 100% sensitive, and 97% specic. Additionally, real-time B-scan ultrasound is able to visualize the clot and may be able to distinguish acute from chronic thrombus.265 In a prospective comparison study, Cogo and colleagues101 concluded that real-time B-mode ultrasonography using the sole criteria of common femoral and popliteal vein compressibility was superior to Doppler ultrasound in the detection of DVT. Likewise, in a prospective randomized trial, Heijboer and co-workers157 found real-time compression ultrasonography superior to IPG for the serial detection of venous thrombosis because the positive predictive value of an abnormal test was 94% for venous ultrasound versus 83% for IPG. One disadvantage is that B-scan ultrasound does not allow adequate visualization of the calf veins.97 A Duplex ultrasound is the combination of real-time ultrasound and pulse-gated Doppler ultrasound. The Doppler scan adds an audible or graphic representation of blood ow.192, 281 In an extensive literature review, White and associates282 reported a combined sensitivity of duplex ultrasound for proximal thrombi of 95% and specicity of 99%. An added advantage of duplex scanning is for the diagnosis of nonthrombotic causes of leg swelling such as Bakers cyst, hematoma, and lymphadenopathy.210 Color-ow duplex ultrasonography (CFDU) is the most recent advancement in ultrasound technology for the
diagnosis of lower extremity DVT. The real-time B-mode component displays stationary tissues in gray scale. The Doppler component is color-enhanced and detects blood ow by the shift in frequency from the backscatter of high-frequency sound. The frequency is shifted by an amount proportional to the ow velocity. Blood owing away from the transducer appears blue, whereas blood owing toward the transducer appears red. The newer technology can detect velocities as low as 0.3 cm/sec. The color saturation is proportional to the rate of ow. A black image indicates an absence of ow, ow velocities less than 0.3 cm/sec, or ow vectors at a right angle to the second beam.205 The addition of color allows for the easier and faster detection of vascular structures. This has provided improved imaging of the iliac region, the femoral vein in the adductor canal, and the calf veins.234 CFDU is superior to duplex scanning and B-mode imaging in detecting nonocclusive thrombi because the ow characteristics in the vessels are readily detected.205 Several studies have reported high sensitivity and specicity in symptomatic patients.89, 96, 206, 238 For screening of symptomatic trauma patients, ultrasound is an excellent study, but for asymptomatic patients it is less sensitive at detecting DVT, especially in the calf. Serial ultrasound has been used as surveillance screening to detect DVT in trauma patients, but it was thought not to be cost effective.147, 245 When DVT develops in the calf, about 25% extends to the thigh if left untreated. If the initial ultrasound missed the asymptomatic DVT and no treatment is given, approximately 2% will have an abnormal proximal scan on testing 1 week later.185 CONTEMPORARY TECHNIQUES FOR DETECTING DEEP VENOUS THROMBOSIS AND PULMONARY EMBOLISM Magnetic resonance imaging (MRI) has been recently applied to the detection of deep venous thrombosis. The gradient-recalled echo (GRE) images are obtained in shorter time and are intrinsically sensitive to ow. Flowing blood appears bright, and stationary soft tissues appear dark.99 MRI of the lower extremities has been compared with contrast venography for the detection of DVT. Sensitivities are reported to be 90% to 100% with specicities of 75% to 100%.99, 122, 261 Using the GRE technique, Spritzer and colleagues262 found that specicity was 100%. MRI is considered to have several advantages over venography and ultrasonography: c Noninvasive procedure c Relative lack of operator dependence c Improved evaluation of the pelvic and deep femoral veins c Simultaneous imaging of both legs c Imaging of adjacent soft tissue98, 128, 270 The primary disadvantage of MRI is cost, which is typically 2 to 2.5 times the cost of an ultrasound scan and 1.4 times the cost of venography.99, 193 MRI is rarely used to diagnose DVT. Multiple modalities exist for the diagnosis of PE. Of interest would be a highly sensitive blood test. Research in
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this area has been active for many years. A plasma marker for split products of cross-linked brin (D-dimer) has been evaluated for the diagnosis of PE and DVT.9395, 140, 246 D-dimers are formed when cross-linked brin polymers are produced in a stable brin clot. When the clot is degraded by plasmin, the D-dimers are released free in the plasma and can be measured by antibody assays.184 If the D-dimer level is low, the probability of DVT is low. This test has been used in trauma patients, but it has not been accepted as very useful.246 PE can be diagnosed with the gold standard pulmonary angiography or more commonly ventilation perfusion (VQ) scan. If the VQ scan results are abnormal but not diagnostic of a PE, then depending on the severity of symptoms, either pulmonary angiography or venous ultrasound can be done. Because PEs are rare in the absence of a DVT, if the venous ultrasound shows a DVT as a possible source of the PE, then anticoagulant therapy is indicated. Positive ndings on venous ultrasound are present in 5% to 10% of patients with nondiagnostic lung scans. Of patients who have a negative venous ultrasound result but suspected PE and a nondiagnostic VQ scan, 80% will not have had a PE. The remaining 20% will have had a PE, but the residual leg thrombus is too small or none is present. The risk of recurrent PE and recurrent DVT is highest within 2 weeks and can be monitored with serial venous ultrasounds to determine treatment. With this management approach, there is about 2% incidence of abnormal venous ultrasound on serial testing. The use of serial noninvasive ultrasound scanning has not been evaluated adequately. If there is a high suspicion of PE, then pulmonary angiography should be done.227 TREATMENT There are three major approaches to the treatment of DVT: prevent the thrombus, ignore it if it occurs, or treat the thrombus. Implicit in each of these approaches is a consideration of (1) the risk of the intervention and (2) the risk if no intervention is taken. For prophylaxis of thrombosis, what is the risk of the agent used versus the risk of DVT and its complications? Once DVT develops, if no treatment is undertaken, what is the risk of PE compared with the complications of therapy? PROPHYLAXIS Until recently, consideration for prophylaxis in trauma patients was largely based on nonsurgical patients or general surgical and orthopaedic elective surgical patients. DVT prophylaxis in trauma patients is an area of ongoing study. Various methods of DVT prophylaxis are reviewed. Physical Measures Prevention of thromboembolism depends on good preoperative conditioning, careful handling of the lower limbs during surgery, and early active postoperative mobilization. These approaches work by limiting venous stasis, one component of Virchows triad. Muscle tone increased with a preoperative exercise program sets the stage in elective surgery cases for resumption of activity immediately following surgery. The incidence of signicant venous
embolic events in the rst 3 days after surgery is very small and rises slowly until the fth postoperative day. Thus, if early mobilization and active use of the limbs can be achieved soon after surgery, many emboli may be prevented. Venous blood ow rate can be increased by muscular exercise and early ambulation.301, 302 This approach is widely used, and, as noted by Bolhofner and Spiegel,92 its value has not been proved. Wrapping the limbs with elastic bandages, avoidance of excessive tourniquet times, and good positioning are other factors that are thought to be important. Both the bent knee position and the semisitting position increase the incidence of postoperative thromboembolic complications. Physical measures can be used to decrease the risk of DVT. Venous stasis can be decreased by elevating the foot of the bed. This has been shown to increase the rate of blood ow and to decrease the incidence of DVT.154 Coutts111 reported in preliminary material that continuous passive motion causes venous blood ow rates to be increased and the incidence of DVT to be decreased. Contrary to Coutts ndings, Lynch and colleagues202 did not nd any signicant reduction in DVT among total knee arthroplasty patients using a continuous passive motion machine. External physical measures include graduated and uniform compression stockings, external pneumatic compression device (EPCD), sequential compression device (SCD), and arteriovenous foot pumps (AVFP). External compression decreases the cross-sectional area of the lower limb and increases the venous velocity. Compression improves the emptying of venous vascular cusp and decreases stasis, which can initiate venous thrombosis. Vasodilation can result in internal tears, which predispose to DVT by exposing blood to the thrombogenic subendothelial collagen. An external pressure of 15 mm Hg results in a 20% reduction in venous cross-sectional area.78 Graduated compression stockings help to increase venous blood ow velocity by 30% to 40% and therefore help to decrease the rate of DVT.242, 253 The optimal pressure gradient is 18 mm Hg at the ankle, decreasing to 8 mm Hg at midthigh.253 Evidence shows that knee-length stockings are as effective as thigh-length stockings and avoid the above-the-knee segment rolling down and acting as a garter-like constriction.78 Complications from compression stockings can occur by impairing subcutaneous tissue oxygenation, which can be critical if there is peripheral vascular disease. Skin ulcerations and amputations have been reported, so stockings are contraindicated in atrial compromise and peripheral neuropathy. Manufacturers recommend against the use of stockings when the ankle-to-brachial pressure index is less than 0.7. Stockings have been shown in randomized trials to decrease DVT by 57% after total hip replacement compared with that in control subjects.78 For total knee replacement, below-theknee stockings decreased DVT by 50% compared with that in control subjects, and above-the-knee stockings were less effective.161 For hip fractures, evaluations are still pending. No conclusions are available for the trauma patient, but tting the stockings to patients with lower extremity trauma is difcult. External pneumatic compression of the legs can decrease the incidence of DVT by 90% in major elective
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knee surgery.110, 163, 166, 267 Its benecial use in elective hip surgery is also established.220, 257 Fisher and coworkers126 demonstrated the effectiveness of an EPCD in reducing the incidence of isolated DVT in hip fracture patients. However, in patients with pelvic fracture, these investigators were unable to demonstrate a statistically signicant reduction in the incidence of thromboembolism. They postulated that EPCDs were less effective in preventing clots in the pelvic venous system. Cyclic compression prevents stasis, enhances brinolysis,266 and has no associated increased risk of bleeding. With sequential pneumatic compression, venous blood ow velocity can be more than doubled.110 This technique is more effective than nonsequential devices.218 Agu reports, Trauma guidelines currently recommend the use of SCD in high risk trauma patients, although, again, there is a paucity of a good data to support their use.78 Knudson found no benet with SCD in multiple trauma patients but did see a decrease in DVT in neurotrauma patients.188 Dennis also had isolated benet of DVT reduction in head injuries (16.7% decreased to 1.4%) and spinal cord injuries (27.3% to 10.3%).119 An alternative approach to external sequential pneumatic compression of the legs is external intermittent compression of the foot using AVFP. This technique arose out of work by Gardner and Fox,132 who investigated the physiology of venous return from the foot. Using video phlebography, they identied the presence of a venous pump in the foot. The venous foot pump is not a muscle pump and therefore is not affected by toe and ankle movement. However, it is immediately emptied by weight bearing due to attening of the plantar arch and the longitudinal stretching of the veins. The AVFP impulse device articially activates the venous foot pump to maintain pulsatile venous blood ow in patients after surgery or injury.133 The device consists of an ination pad that conforms to the plantar arch of the foot. It inates rapidly, holds a pressure of 50 to 200 mm Hg for 1 to 3 seconds, then deates for 20 seconds to allow relling of the venous plexus. Four studies have been done on high-risk trauma patients using AVFP and SCD. Spain and associates had 184 patients: 64% used SCD and 36% used AVFP with a DVT rate of 7% and 3%, respectively, which was not a signicant difference between the two methods.261 Anglen studied 124 randomized trauma patients with a DVT rate of SCD 0% and AVFP 4%.82 Purtill had 170 trauma patients: 81 with SCD and 89 with AVFP with a DVT rate of 8.6% and 8.9%, respectively.233 Knudson compared low molecular weight heparin (LMWH) with AVFP and SCD in trauma patients with a DVT incidence of AVFP 5.7%, SCD 2.5%, and LMWH 0.8%.187 Stranks and co-workers found, among patients undergoing surgery for hip fracture, a 23% incidence of proximal DVT in a control group (graduated compression stockings only) versus 0% in the group utilizing AVFP.265 Prophylactic Drugs When signicant risk factors are present, active prophylaxis by altering coagulabilitythe second component of Virchows triadbecomes increasingly justied. Prophylactic drugs include dextran, aspirin, mini heparin
(either with or without dihydroergotamine), warfarin, LMWH fractions, and potentially thrombin inhibitors. Dextran has been shown to be effective in elective and emergency hip procedures79, 124, 178, 216 and in femur fractures.83 It has not been studied adequately for knee procedures. It is not being used in the multiple-trauma victim. Dextran is a glucose polymer that is formulated with either a 40,000 or a 70,000 mean molecular weight. The 70,000 formula has a higher rate of allergic reactions associated with it. It is best started preoperatively and limited to less than 500 mL during operations because of increased bleeding associated with larger doses. Aspirin is an agent that decreases platelet adherence and thereby decreases coagulability. Initially, aspirin was believed to decrease the incidence of DVT. Harris and associates150152, 175 and DeLee and Rockwood118 all reported that aspirin decreased the incidence of DVT. Harris and colleagues148 in 1982 in a double-blind trial found that aspirin was effective for men but not for women. Evidence then showed that aspirin did not affect the incidence of DVT.100, 149, 171, 211, 214, 263 The most recent report is that aspirin does decrease the incidence of DVT and PE in hip fracture and arthroplasty patients but it should not be relied on for prophylaxis.232, 259 Warfarin has been shown to be effective in preventing DVT in orthopaedic patients.128, 166, 213, 225 Amstutz and associates81 reported no deaths from PE while using a prophylactic regimen with warfarin in 3000 total hip replacements. Postoperatively, the prothrombin time (PT) can be lengthened to an International Normalized Ratio (INR) of 2.0 to 3.0 (1.2 to 1.5 times controls).158, 172 This regimen is effective in decreasing the rate of DVT and has minimal bleeding complications. However, warfarin has a relatively narrow therapeutic window and thus necessitates accurate monitoring of patient response. Heparin has been tried as a prophylactic agent in an unfractionated (UFH) low dose of 5000 U subcutaneously 2 hours preoperatively and then every 8 hours. Although this is effective for decreasing the rate of DVT in general surgical patients undergoing abdominal procedures, it did not affect the rate of DVT in patients undergoing orthopaedic hip surgery.165, 211, 213, 243 Once an intravascular clot forms, low dose UFH has no effect on brinolysis. Adding low-dose unfractionated heparin to SCD does not provide any further protection over SCD alone.273 There is no role in trauma for the use of low-dose unfractionated heparin. In a study of adjusted-dose versus xed-dose heparin, the rate of DVT was 39% when given in a xed-dose compared with 13% when given in adjusted doses. Doses were adjusted to keep the activated partial thromboplastin time between 31.5 and 36 seconds.197 A meta-analysis of randomized trials of adjusteddosage UFH versus LMWH found that LMWH was more effective in preventing DVT and PE in total knee replacements.160 Heparin in low doses has also been combined with dihydroergotamine (DHE), an alpha-adrenergic receptor stimulant, and administered to patients undergoing elective hip surgery181, 183, 240 and to patients with hip fractures.239 The incidence of DVT was decreased in both groups. The role of this drug combination in trauma has not been studied. Complications include ergotism, which
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can result from DHE use and can lead to amputation or even death.134, 270 DHE use has also been associated with myocardial infarction.116 Heparin can also lead to multiple complications such as bleeding, allergic reaction, osteoporosis, and thrombocytopenia196; in fact, spontaneous venous and arterial thrombosis can occur from a severe form of heparininduced thrombocytopenia.84 One of the newer options for the prevention of DVT is the use of LMWH. Unfractionated heparin has a molecular weight of 6000 to 20,000 daltons, whereas the fractionated products are 4000 to 6000 daltons. Two LMWHs are currently being used; enoxaparin (Lovenox) and dalteparin (Fragmin), and reviparin is in trials. Like UFH, LMWH has antiFactor Xa activity, but unlike UFH, LMWH has much less effect on Factor IIa (thrombin).102 This should have the effect of decreasing thrombosis without inducing a hypocoagulable state. As a result, the rate of bleeding complications should be less with LMWH.236 LMWH has little effect on platelets and does not affect PT or activated partial thromboplastin time (aPTT) at dosages used. Additional benets are high bioavailability, longer half-life, and linear dose-dependent antiFactor Xa activity.131 Routine blood monitoring of aPTT or antiFactor Xa level is not recommended. However, in patients who are at risk for accumulating LMWH, such as those with renal insufciency (eliminated by renal excretion), or in those with active bleeding, then measuring antiFactor Xa may be a benet.121 If excess hemorrhage does occur with LMWH, protamine will partially reverse the effects of LMWH. Repeat protamines dosing is necessary because of its short half-life, compared with that of LMWH. In a study of 665 patients, Warkentin and coworkers275 found no cases of heparin-induced thrombocytopenia in 333 patients who received LMWH. Thrombocytopenia can still occur, and platelet counts should be checked at baseline and every 2 to 3 days with discontinuation of LMWH if the platelet count is below 100,000 or to less than half the original value. Several clinical studies demonstrated the effectiveness of LMWH in reducing the incidence of thromboembolism in elective hip surgery patients.103, 125, 168, 195 Likewise, LMWH prophylaxis has demonstrated a low incidence of DVT, PE, and bleeding complications in patients with spinal cord injury.142, 203 LMWH has also been used as a means of DVT prophylaxis following operative treatment in patients with hip fracture.87, 137, 180, 228 The incidence of DVT in the patients receiving LMWH was from 7% to 30%. The incidence of bleeding complications was equal to or less than the other treatment groups (placebo or warfarin). Knudson and associates187 studied enoxaparin (30 mg subcutaneously every 12 hours) in a controlled high-risk trauma setting. Enrollment required any injury with an abbreviated injury score of 3 or higher; major head injury (Glasgow Coma Scale [GCS] 8); spine, pelvic, or lower extremity fractures; acute venous injury; or older than 50 years. Exclusion for heparin use were severe neurologic injury, that is, GCS of 8 or lower, or spinal cord injury; lumbar or spleen injuries being treated nonoperatively; or continual bleeding after 24 hours. The no heparin group
all used either SCD or AVFP. In the group that was eligible for heparin, patients were randomized to receive LMWH or bilateral SCD or AVFP. Duplex scan monitoring was performed every 5 to 7 days. The predicted rate of DVT for trauma patients with one risk factor and no prophylaxis was 9.1%.188 The actual incidence was 0.8% in the LMWH group, 2.5% in the SCD group, and 5.7% in the AVFP group. Of 120 patients on LMWH, only one reoperation for major bleeding complication occurred that was potentially associated with LMWH. In the 199 patients with SCD, 4 had mild skin changes and continued to use SCD. In the 53 patients with AVFP, 8 had blistering and wound problems and 3 of these discontinued the use of AVFP. Only one clinical PE occurred and that was in an SCD patient. Knudson and associates concluded, the administration of LMWH is a safe and extremely effective method of preventing DVT in high-risk trauma patients. When heparin is contraindicated, aggressive attempts at mechanical compression are warranted. Kelsey and co-workers184 concur that the literature supports the use of LMWH in trauma for prophylaxis of DVT, but it still must be individualized because of bleeding risk. If there is an increased bleeding risk, then SCD is a good second-line prophylactic measure. A meta-analysis193 comparing LMWH and adjusted low-dose heparin statistically showed that LMWH had relative risk reductions of 53% for symptomatic thromboembolic complications, 68% for clinically signicant bleeding, and 47% for mortality. The investigators concluded that LMWH is more effective and safer than UFH for the treatment of venous thrombosis. Their conclusions were based primarily on trials using Fraxiparine (Sano, Paris, France) and Logiparin (Novo Nordisk Farmaka, Bagsvaerd, Denmark). The LMWHs each have distinct biologic activity proles, and each drug needs to be considered as an individual drug. Randomized trials using specic preparations need to be conducted. Nonetheless, LMWHs, because of their ease of administration, predictable response, and apparent effectiveness, are promising tools for the prevention and treatment of venous thromboembolism. The thrombin inhibitors, melagatran and hirudin, act on the enzymatic properties of thrombin and prevent the brin superstructures that support a blood clot. In melagatron clinical trials on total hip and knee replacement prophylaxis, the incidence of proximal DVT was 3% versus about 7% for LMWH. In hirudin (15 mg twice daily) clinical trials on hip replacements, the incidence of proximal DVT was 4.5% versus 7.5% for enoxaparin (40 mg once daily).123 The duration of prophylaxis for thromboembolism following orthopaedic procedures is a matter of debate. In a review by Johnson and colleagues,183 approximately 50% of fatal pulmonary emboli occurred between 7 and 14 days after surgery and 36% between 14 days and 3 months. The duration of prophylaxis should be individualized for a given patient, taking into account known risk factors such as age, type of injury or procedure, prolonged immobilization, estrogen use, and other known risk factors. Prophylaxis using warfarin following total hip arthroplasty can vary from 3 weeks81 to 12 weeks.223 Sharrock and co-workers252 used intravenous xed-dose
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TABLE 182
Recommendations for Anticoagulation

Thromboembolism Suspected Conrmed Recommendations
TREATMENT OF DEEP VENOUS THROMBOSIS AND PULMONARY EMBOLISM Once DVT or PE is suspected, the clinical impression should be conrmed with diagnostic testing. Heparin should be started unless contraindicated until diagnostic testing is done (Table 182). Contraindications include neurologic, spinal cord, or ocular injuries that could be worsened with bleeding. Heparin is started intravenously to reach therapeutic effect rapidly to prevent clot extension and decrease the risk of PE. Subcutaneous LMWH has also been proven to be effective in initial treatment of DVT. However, further documentation of its role in the trauma setting is needed because controlled trials excluded its use if there had been surgery in the prior 5 to 7 days.170, 255 Controlled trials of intravenous heparin versus LMWH in the presence of DVT have shown no difference in rates of symptomatic extension, recurrence, pulmonary embolism, or severe bleeding.170, 189, 194, 198, 231 LMWH has also been used in the treatment of pulmonary embolism.104, 255 If DVT is present, the patient is continued on heparin until converting to warfarin and continued for 3 to 6 months (Table 183). The dosage of warfarin is not standardized, and in younger patients the dosage is more difcult to predict. Two studies comparing an initial dose of 5 mg or 10 mg suggest that 5 mg is more appropriate.113, 153 Length of warfarin treatment for DVT and PE is from 3 months to 6 months98, 184 and depends on the risk of recurrence. The rate of recurrent DVT and PE is higher when the DVT occurred without an identiable risk factor
Give heparin 5000 U IV and order diagnostic study Rebolus heparin 500010,000 U IV and start maintenance infusion at 1300 U/hr (heparin 20,000 U in 500 ml D5W infused at 33 ml/hr) Check aPTT at 6 hr to keep aPTT between 1.5 and 2.5 times control Check platelet count daily Start warfarin therapy on day 1 at 10 mg daily for rst 2 days, then administer warfarin daily at estimated daily maintenance dose Stop heparin therapy after 57 days of joint therapy when INR is 2.03.0 off heparin; continue warfarin for 3 months at an INR of 2.03.0
Abbreviations: aPTT, activated partial thromboplastin time; D5W, 5% dextrose in water; INR, International Normalized Ratio; IV, intravenous. Source: Hyers, T.M.; Hull, R.D.; Weg, J.C. Chest 102:408S421S, 1992.
heparin only during the intraoperative period during total hip arthroplasty, whereas Fauno and associates125 used heparin for 8 days postoperatively in patients undergoing total knee arthroplasty. In trauma patients, the duration of prophylaxis is even less clear.
TABLE 183
Algorithm for Antithromboembolic Prophylaxis in Trauma Patients
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Patient Category
Low Risk* Extremity elevation Physical therapy Early mobilization If more aggressive prophylaxis is desired, such as patients with lower extremity cast, but without high-risk factors Add EPCD/SCD/AVFP and Aspirin or Minidose heparin SQ or Low-intensity warfarin (INR 1.52.0) Anticoagulation contraindicated EPCD/SCD/AVFP or Vena cava lter
High Risk* Anticoagulation not contraindicated LMWH or Adjusted-dose heparin or Moderate-intensity warfarin (INR 2.03.0) and EPCD/SCD/AVFP If complication due to anticoagulation or reembolization Vena cava lter and EPCD/SCD/AVFP
Abbreviations: AVFP, arteriovenous foot plexus; EPCD, external sequential pneumatic compression devices; SQ, subcutaneous; INR, International Normalized Ratio; LMWH, low-molecular-weight heparin; GCS, Glasgow Coma Scale; ISS, injury severity score; SCD, sequential compression device. *Risk factors: Age >40 years; history of venous thromboembolism; complex pelvic fracture; complex lower extremity fracture; greater than 3 days immobilization; coma (GCS <8); spinal cord injury, with or without paralysis; blunt trauma with ISS >15; penetrating injury with repair of major vein; presence of femoral venous catheters. A low-risk patient is one without any high-risk factors. A high-risk patient is one with one or more high-risk factors. Prospective randomized trials evaluating the safety and efcacy of LMWH in trauma patients are ongoing.
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than when there is an identiable transient risk factor.230, 235, 247 Longer treatment is indicated for trauma patients with major vein ligation or spinal cord injuries with paralysis. Evidence of reembolization is an indication for permanent anticoagulation and the placement of an inferior vena caval lter.264 Thrombolytic drugs are an alternative to heparin, but they are not suitable to the traumatized or postoperative patient for at least 2 weeks because of clot lysis at the surgical site. An advantage of thrombolytic drugs is that the venous system more closely returns to normal when the venous thrombosis is lysed rather than when propagation of the thrombus is arrested with heparin.105 The Urokinase Pulmonary Embolism Trial (UPET) found a statistically signicant lower mortality rate in the patients receiving thrombolytic therapy than in the group receiving heparin anticoagulation.269 In theory, there should be a lower incidence of post-thrombotic syndrome in patients receiving thrombolytic therapy than in those receiving heparin treatment, but randomized trials are lacking and the benecial effect of lysis is complicated by increased risk of bleeding.77, 244 Vena cava interruption is performed when heparinization is contraindicated, as in patients with a preexisting bleeding disorder; severe hypertension; neurologic injury; or bleeding problems of pulmonary, gastrointestinal, neurologic, or urologic etiology. If anticoagulation fails to stop pulmonary emboli, vena cava interruption is indicated.179 Also, if patients develop complications with anticoagulation, they can be switched to vena cava interruption. An additional approach is the preoperative use of vena cava interruption in patients who are at extremely high risk for PE. Vaughn and associates271 preoperatively inserted the Greeneld lter in 42 patients (scheduled for hip or knee arthroplasty) considered to be at extremely high risk for a fatal PE. The principal indication was a history of thromboembolism. None of the patients in this group experienced a PE immediately postoperatively. On follow-up, no lter-related complications were reported. The prophylactic use of vena cava interruption in trauma patients has also been examined. Rogers and colleagues237 identied four subsets of trauma patients who were at high risk for PE: (1) those with severe head injury and coma, (2) those with spinal cord injuries with neurologic decit, (3) those with multiple long bone fracture and pelvic fracture, and (4) elderly patients with isolated long bone fractures. In a prospective evaluation, these investigators prophylactically inserted vena cava lters in 34 patients identied as high risk for PE from among the general trauma population. PE was eliminated in this study group despite an expected incidence of DVT of 17.6%. Filter insertion was without complication. At 1-year follow-up, duplex scan revealed two caval thromboses. Vena cava lters have associated complications such as venous stasis leading to edema, pain, varicose veins, and skin ulcers in a condition known as the postphlebitic syndrome.277 Other complications include bleeding or thrombus formation at the site of insertion, migration of the lter, and perforation of the vena cava.141, 143 Martin and co-workers205 described a case report of phlegmasia
cerulea dolens as a complication of an inferior vena cava lter for prophylaxis against PE in a man with a fracture of the acetabulum. In addition, lters are not 100% effective.117 Surgical thrombectomy is only indicated for patients with massive thrombosis and those who have absolute contraindications for thrombolytic therapy or do not respond to treatment.88 Pulmonary embolectomy should be considered when thrombolysis is not effective or not feasible in patients with massive pulmonary embolism and hemodynamic instability.173 For elective and traumatic hip and knee surgery, the search for prophylactic measures indicates that modalities can be used to decrease the risk of DVT and PE. Hull and Raskob stated: The onus is now on the individual orthopedic surgeon to use prophylaxis, particularly in patients over the age of forty years and in the elderly, who are unquestionably at greatest risk.166 The trauma patient is in a different category from the elective arthroplasty patient. The incidence of thrombotic complications versus the risk of prophylaxis with anticoagulants is less clear. The rst step in solving this problem is identifying the relative degree of risk for the different types of injury or level of severity. The National Institutes of Health Consensus Conference held in 1986 estimated that the incidence of DVT in young multisystem trauma patients is 20%.106 Shackford and Moser251 found an average incidence of venous thromboembolism of 42%, with a range of 18% to 90%, in trauma patients during a literature review. In a study of major trauma patients, Shackford and associates250 found an incidence of 7% venous thromboembolism among trauma patients with at least one risk factor. Venous thromboembolism occurred within 1 week in 50% of these patients. Of 400 patients admitted into a DVT trauma study by Knudson and colleagues,188 251 patients completed the study and 15 (6%) developed lower extremity venous thrombosis. Dennis and co-workers119 evaluated 395 trauma patients with ISS greater than 9 who survived a minimum of 48 hours. These investigators found an overall incidence of 4.6% lower extremity DVT and 1.0% incidence of PE among patients with and without prophylaxis. Numerous studies have attempted to identify specic injuries and severity of injury that had a high incidence of DVT and PE. In a study by Myllynen and associates,217 a 100% incidence of DVT was seen within 25 days in patients with spinal cord injury. In another study, Dennis and co-workers119 identied the following risk factors for patients at high risk of venous thromboembolism: age older than 39 years; prolonged immobilization; blunt trauma with ISS greater than 9; spinal fractures or subluxations, with or without complete paralysis; severe acute head injuries; and penetrating injury requiring repair of a major vein. They found no basis for routine DVT prophylaxis in injured patients who did not have any recognized risk factors. Based on historical literature, Shackford and Moser,251 in a prospective study, placed trauma patients into lowand high-risk groups according to risk factors. They identied the following factors: (1) age older than 45 years and enforced bed rest for more than 3 days, (2) history of
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venous thromboembolism, (3) spine fracture without neurologic decit, (4) coma (GCS < 7), (5) quadriplegia or paraplegia, (6) pelvis fracture, (7) lower extremity fracture, (8) repair of a major lower extremity vein, and (9) complex wound of the lower extremity. If none of the factors were present, the patients were placed in the low-risk group. Patients with one or more risk factors were considered high risk for venous thromboembolism. The incidence of venous thromboembolism was 7% in the high-risk group and zero in the low-risk group. Spain and associates260 analyzed 2868 consecutive trauma admissions and identied 280 patients (10%) in a high-risk group who survived 48 hours or longer with these risk factors: (1) severe closed head injury with mechanical ventilation 72 hours or longer, (2) closed head injury with lower extremity fractures, (3) spinal column or cord injury, (4) combined pelvic and lower extremity fractures, and (5) major infrarenal venous injury. The remaining nonthermal injury patients were the low-risk group. Of the 280 high-risk patients, 241 patients received some form of prophylaxis, with 213 of these treated with SCD or AVFP. Thromboembolic events were investigated based on clinical suspicion, and routine screening with duplex scans was not done. In the high-risk group, there were 12 DVTs (5%) and 4 nonfatal PEs (1.4%); in the low-risk group, there were 3 DVTs (0.1%) and no PEs. Their conclusion was that aggressive screening and prophylactic IVC lters were not the standard of care. Only in the major venous injury group were they perhaps justied. They thought that compression devices were reasonably effective, low risk, and cost effective for prophylaxis. Knudson and colleagues188 also tried to identify which trauma patients were at risk for venous thromboembolism and consequently would benet from DVT prophylaxis or intense surveillance. Combining the results of their study with the work of other investigators, they developed the following list of risk factors: (1) age older than 30 years, (2) pelvic fractures, (3) spine fractures with paralysis, (4) coma (GCS < 8), (5) immobilization for more than 3 days, (6) lower extremity fractures, (7) direct venous injury, (8) ISS of 16 or greater, (9) large transfusion requirements, and (10) presence of femoral intravenous catheters. Likewise, Rogers and colleagues237 identied four groups of injury patterns associated with PE: (1) spinal cord injury with paraplegia or quadriplegia, (2) severe head injury with GCS less than 8, (3) age older than 55 years with isolated long bone fractures, and (4) complex pelvic fractures with associated long bone fractures. In contrast to other studies, two recent reports did not associate isolated long bone fractures with an increased risk for venous thromboembolism.209, 221 The current literature clearly indicates that certain subsets of trauma patients are at risk for venous thromboembolism and would benet from some type of prophylaxis or surveillance. Many experts think that prophylaxis for DVT is safer and more cost effective than surveillance tests.164, 209, 224, 241 In a study of surveillance venous scans for DVT in prophylactically evaluated multiple trauma patients, Meyer and co-workers209 performed 261 scans, 92% of which produced normal results. At their institu-
tion, the cost to identify each proximal DVT was $6688. The overall incidence of clinically signicant proximal DVT in their patients treated with DVT prophylaxis was 6%. They concluded that the routine use of venous surveillance scans should be limited to high-risk or symptomatic patients.
SUMMARY
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz The patient with multisystem trauma represents a challenge to provide DVT prophylaxis because of the nature and location of injuries; however, some type of prophylaxis, either pharmacologic or mechanical, is possible in almost every patient and should be instituted when signicant risk factors exist. Because orthopaedic injuries and other trauma are unforeseen, prophylaxis as stated by Rogers236 is in effect, ex post facto. Although current prophylactic regimens in trauma patients signicantly reduce the relative risk for DVT and PE, no method provides 100% protection. Further randomized controlled trials of DVT prophylaxis in trauma patients are needed. A suggested algorithm for the management of post-traumatic thromboembolic prophylaxis is given in Table 183.
Multiple Organ System Dysfunction and Failure

Multiple organ failure (MOF) can be dened as the sequential failure of two or more organ systems remote from the site of the original insult following injury, operation, or sepsis. The organ failure can be pulmonary, renal, hepatic, gastrointestinal, central nervous system, or hematologic.306, 329 These systems can be monitored for objective criteria for failure, but criteria vary from series to series (Tables 184 and 185).307, 329 The risk of developing MOF and the severity of the MOF can also be graded by measuring the effects on specic organ systems.312 MOF is the end result of a transition from the normal metabolic response to injury to persistent hypermetabolism and eventual failure of organs to maintain their physiologic function. A 1991 consensus conference used the term multiple organ dysfunction syndrome (MODS) to describe this spectrum of changes.294 Organ dysfunction is the result of either a direct insult or a systemic inammatory response, known clinically as the systemic inammatory response syndrome (SIRS),293 which can be reversible or progress to MODS or MOF SIRS can be caused by a . variety of infectious and noninfectious stimuli294 (Fig. 185). Treatment of the offending source must be undertaken early, because once organ failure has begun, treatment modalities become progressively ineffective.299 Fry identied the mortality rate for failure of two or more organ systems as about 75%. If two organ systems fail and renal failure occurs, then the mortality is 98%.307 Today, MOF is the number one cause of death in surgical intensive care units.303 The basic theory behind the development of MOF and the closely related ARDS has undergone modication since
CHAPTER 18 Diagnosis and Treatment of Complications TABLE 184
451
Criteria for Organ Dysfunction and Failure

Organ or System Pulmonary Hepatic Renal Gastrointestinal Hematologic Central nervous system Cardiovascular Dysfunction
Advanced Failure ARDS requiring PEEP >10 cm H2O and FiO2 >0.5 Clinical jaundice with total bilirubin 810 mg/dl Dialysis Stress ulcers, acalculous cholecystitis DIC Progressive coma Refractory cardiogenic shock
Hypoxia requiring intubation for 35 d Serum total bilirubin 23 mg/dl or liver function tests twice normal Oliguria 479 ml/d or creatinine 23 mg/dl Ileus with intolerance of enteral feeds >5 d PT/PTT >125% normal, platelets <50,00080,000 Confusion, mild disorientation Decreased ejection fraction or capillary leak syndrome
Abbreviations: ARDS, adult respiratory distress syndrome; PEEP, positive end-expiratory pressure; FiO2, fraction of inspired air in oxygen; PT, prothrombin time; PTT, partial thromboplastin time; DIC, disseminated intravascular coagulation. Source: Dietch, E.A.; Goodman, E.R. Surg Clin North Am 79(6), 1999; which was adapted from Deitch, E.A. Ann Surg 216:117134, 1992, with permission.
the 1970s and mid-1980s. Moore and Moore326 provided an excellent and concise overview of the evolving concepts of postinjury multiple organ failure. In brief, the earlier models promoted an infectious basis for ARDS/MOF with , two possible scenarios: (1) insult ARDS pulmonary sepsis MOF or (2) insult sepsis ARDS/MOF The , . current thinking promotes an inammatory model of MOF As previously mentioned, this inammatory re. sponse can arise from a number of infectious and noninfectious stimuli. Again, two patterns exist: the one-hit model (massive insult severe SIRS early MOF) and the more common two-hit model (moderate insult moderate SIRS second insult late MOF). In recent years, research into the pathogenesis of MOF has focused on how the inammatory response is propagated, independent of infection. Moore and Moore have the global hypothesis that postinjury MOF occurs as the result of a dysfunctional inammatory response.326 Deitch created an integrated paradigm of the mechanisms of MOF 303 In general, three broad overlapping hypothe. ses have been proposed in the pathogenesis of MOF: (1) macrophage cytokine hypothesis, (2) microcirculatory hypothesis, and (3) gut hypothesis. Attempts to understand this highly complex syndrome must extend to the cellular and molecular levels.
TABLE 185
Denition of Organ Failure Based on Fry Criteria

Pulmonary Hepatic Gastrointestinal
Need of ventilator support at an FiO2 of 0.4 or greater for 5 consecutive days Hyperbilirubinemia greater than 2.0 g/dl and an increase of serum glutamicoxaloacetic transaminase Hemorrhage from documented or presumed stress-induced acute gastric ulceration. This can be documented by endoscopy; if endoscopy is not performed, then the hemorrhage must be sufcient to require two units of blood transfusion. Serum creatinine level greater than 2.0 mg/dl. If a patient has preexisting renal disease with elevated serum creatinine level, then doubling of the admission level is dened as failure.
Renal
Research indicates that organ injury in MOF is largely the result of the hosts own endogenously produced mediators and less due to exogenous factors like bacteria or endotoxins (Table 186).303 There is increasing evidence that there are biologic markers for the risk of development of MOF that may be more useful than anatomic descriptions of injuries. Nast-Kolb and associates45 measured various inammatory markers in a prospective study of 66 patients with multiple injuries (ISS > 18) and found that the degree of inammatory response corresponded with the development of posttraumatic organ failure.45 Specically, lactate, neutrophil elastase, interleukin-6, and interleukin-8 were found to correlate with organ dysfunction. Strecker and coworkers335 studied 107 patients prospectively and found that the amount of fracture and soft tissue damage can be estimated early by analysis of serum interleukin-6 and creatine kinase and is of great importance with regard to long-term outcome after trauma. Specically, these investigators found signicant correlations between fracture and soft tissue trauma and intensive care unit stay, hospital stay, infections, systemic inammatory response syndrome, multiple organ failure score, and serum concentrations or activities of serum interleukin-6, interleukin-8, and creatine kinase during the rst 24 hours after trauma. Blood transfusions are a frequent part of polytrauma treatment and an independent risk factor for MOF Zallen . and associates have identied the age of packed red blood cells (PRBCs) to be a risk factor, with the number of units over 14 days and 21 days as independent risk factors for MOF 339 Old but not outdated PRBCs prime the neutro. phils for superoxide production and activate the endothelial cells, which are pathogenic mediators for MOF . Nonetheless, our knowledge of the pathogenesis of MOF is constantly increasing; the reader is referred to Beal and Cerra,293 Deitch and Goodman,304 Baue and associates,292 Livingston and Deitch,321 and Moore and Moore.326 The complexities for evaluating the pathogenesis and treatment of MOF should evolve further because the treatments in the aforementioned articles have continued to fail with therapies aimed at antimediator therapies. This has led to a hypothesis considering complex nonlinear systems, which Seely has described.333 Although treatment and recognition of MOF has improved, there has been little impact on the mortality rate in the past
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Print Graphic
Presentation
FIGURE 185. The interrelationship among systemic inammatory response syndrome (SIRS), sepsis, and infection. (From Bone, R.C.; Balk, R.A.; Cerra, F et al. Denitions for .C.; sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Chest 101:16441655, 1992.)
20 years.304 It has been suggested that future treatment strategies must address multimodality combination therapy aimed at suppressing the inammatory response while preserving immune competence and antimicrobial defenses.304 MOF is a syndrome distinct from respiratory failure, which can complicate airway injury, resuscitation, or anesthesia following an accident. With the development of improved patient categorization, transport, and emergency care, it has become recognized that there is a threshold beyond which the survival from injury is problematic. With simple injuries (e.g., an ankle fracture and laceration from a fall), the physiologic effects are not additive. However, in high-energy blunt trauma, the effectsfor example, of a pulmonary contusion, ruptured spleen, and fractured pelvisbecome more than additive. The ISS is one of several scales currently available to quantify the extent of trauma.288 The ISS was derived from the Abbreviated Injury Score (AIS) of the American Medical Association Committee on Medical Aspects of Automotive Safety,302 updated in 1985 as AIS-85. Injuries to six body regions (head and neck, face, chest, abdomen and pelvic viscera, extremities and bony pelvis, and integument) are graded as (1) mild, (2) moderate, (3) severe, (4) criticaloutcome usually favorable, and (5) criticaloutcome usually lethal. The ISS equals the sum of the squares of the three highest AIS grades. The ISS score has a maximal value of 75. When the ISS is 25 or greater, a patient who is considered polytraumatized and is at risk for MOF will benet from specialized trauma center care. The median lethal ISS scores have been determined by age group (in years): ages 15 to 44, an ISS of 40; ages 45 to 64, and ISS
TABLE 186
Potential Mediators Involved in the Pathogenesis of Multiple Organ Failure

HUMORAL MEDIATORS Complement Products of arachidonic acid metabolism Lipoxygenase products Cyclooxygenase products Tumor necrosis factor Interleukins (113) Growth factors Adhesion molecules Platelet activating factor Procalcitonin Procoagulants Fibronectin and opsonins Toxic oxygen-free radicals Endogenous opioids-endorphins Vasoactive polypeptides and amines Bradykinin and other kinins Neuroendocrine factors Myocardial depressant factor Coagulation factors and their degradation products CELLULAR INFLAMMATORY MEDIATORS Polymorphonuclear leukocytes Monocytes/macrophages Platelets Endothelial cells EXOGENOUS MEDIATORS Endotoxin Exotoxin and other toxins
Source: Adapted with permission from Balk, R.A. Crit Care Clin 16(2):113, 2000.
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Risk Stratication for Postinjury Multiple System Organ Failure

Category I II III IV Risk Factors ISS 1524 ISS 25 ISS 25 plus >6 U RBCs/rst 12 hr ISS 25 plus >6 U RBCs/rst 12 hr plus lactate 2.5 mmol at 1224 hr
MSOF Probability (%) 4 14 54 75
Abbreviations: ISS, injury severity score; MSOF, multiple system organ failure; RBCs, red blood cells. Source: Moore, F.A.; Moore, E.E. Surg Clin North Am 75:257277, 1995.
of 29; and ages 65 and older, an ISS of 20.313 Moore and Moore326 identied the following variables to be predictive of MOF: age older than 55 years, ISS 25 or greater, more than 6 units of blood in the rst 24 hours after admission, high base decit, and high lactate level. These investigators stratied patients at risk for MOF (Table 187). One of the consequences of MOF is the depletion of body protein reserves. Amino acids are essential components of the energy systems that maintain the bodys homeostasis; this decit cannot be replenished by intravenous glucose or lipids.295 As the MOF progresses, the peripheral metabolic energy source switches from the conventional energy fuels of glucose, fatty acids, and triglycerides to the catabolism of essential branched-chain amino acids. The multiple-injury patient is like a diesel submarine on the bottom of the ocean with a limited air supply. Once the air supply is exhausted, damage control systems can no longer be maintained. Amino acids are lost as muscles are oxidized for energy, and the supply is not replenished.315, 322 Tscherne emphasized the role of necrotic tissue in the pathogenesis of MOF 337 It is well known that a gangre. nous limb, for example, can provoke a systemic catabolic response. Those with military experience have observed the dramatic reversal of alarming symptoms that occurs when an urgent amputation is undertaken for gangrene. Dead tissue (e.g., muscle, bone, marrow, and skin) provokes an inammatory autophagocytic response.310, 328 In this setting, consumption of complement and plasma opsonins has been measured.287, 316, 327 The complement system is activated in this setting with depletion of factors C3 and C5 with elevated levels of C3a and increased metabolism of C5a. C3a and C5a are anaphylotoxins and may cause the pulmonary edema in ARDS by affecting the smooth muscle contraction and vascular permeability.316 Plasma opsonin activity is decreased with the consumption of the complement system. The opsonins are critical for antibacterial defense, and their consumption may lead to an increased susceptibility to infection.287 Several investigators identied serum factors that stimulate muscle destruction.289, 301 Multiple mediators and effectors have been implicated in the pathogenesis of MOF but exactly , which mediator or combination of mediators is responsible for the hypermetabolic response is not known.314 This response consumes the individuals energy reserve and
leads to MOF Once MOF is established, the sequence . of organ failure apparently follows a consistent pattern, with involvement rst of the lung, then the liver, gastric mucosa, and kidney.308 Positive blood culture results have been documented in 75% of patients with MOF but it is not clear whether , infection is the cause or simply accompanies MOF 308, 323 . Most probably, it is a contributing factor. Goris and associates310 were able to induce MOF in rats by injecting a material that causes an inammatory response. Sepsis causes tissue destruction and, therefore, like broken bones, releases activators of autophagic systems into the blood stream. The immune systems response in polytrauma can be measured. Polk and colleagues329 dened a scoring system for predicting outcome by combining points for ISS and contamination with a measurement of monocyte function (the surface expression of D-related antigen). This method appears promising in predicting survival.317 A combined service approach to the multiple-injury patient has proved valuable in preventing the development of MOF (Table 188). Avoidance of pulmonary failure, prevention of sepsis, and nutritional support are the keys.291 Mechanical ventilation is regulated in a special care unit under the supervision of anesthesiologists or traumatologists with experience and training in this area of intensive care. Immediate wound debridement and con stant attention to the details of wound management, pulmonary toilet, cleanliness of access lines, and urinary tract sterility are required to prevent sepsis. With open fractures, parenteral or local wound antibiotics are therapeutic. An assessment of nutritional reserve, including measurement of triceps skin fold, a total lymphocyte count, and measurement of serum transferrin, is helpful in determining the need for nutritional support. If possible, the gastrointestinal tract should be used, but in patients with extensive intra-abdominal injury and poor nutritional reserves, early total parenteral nutrition with amino acid supplementation is essential. Nutrition has an important role in preventing the translocation of bacteria and toxins
TABLE 188
Prevention of Multiple Organ Failure
RESUSCITATIVE PHASE Aggressive volume resuscitation in early stages of treatment Appropriate monitoring of volume resuscitation with measurement of arterial base decit and serum lactate level, use of pulmonary artery catheters, calculation of oxygen delivery and consumption, use of gastric tonometry OPERATIVE PHASE Timely operative management of soft tissue injuries with debridement of nonviable and infected tissue Early xation of all possible long bone and pelvic fractures Vigilance in preventing the missed injury ICU PHASE Early nutritional support Appropriate use of antibiotics Specic organ support Timely reoperative surgery for missed injuries and complications of trauma
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GUT HYPOTHESIS
Liver injury
Hepatocellular Macrophage-mediated
Absorption Toxins Organisms Print Graphic Translocation Toxins Organisms Presentation Systemic injury
FIGURE 186. Diagrammatic representation of the interrelationship of the gut and liver. Shock, malnutrition, and bacterial overgrowth are hypothesized to potentiate gut absorption and translocation of bacteria or toxins, or both, that can either directly alter liver cell function or indirectly inuence it through the Kupffer cell. (Redrawn from Cerra, F .B.; West, M.; Keller, G.; et al. Prog Clin Biol Res 264:2742, Copyright 1988. Reprinted by permission of Wiley-Liss, a division of John Wiley and Sons, Inc.)
Malnutrition Altered microflora Gut Disuse Ischemic injury
from the gut into the splanchnic circulation; once bacteria and toxins are in the circulation, they are transported to the liver, altering liver (Kupffer) cell function and causing progressive hepatocyte hypermetabolism and organ failure (Fig. 186).298, 325 ORTHOPAEDIC MANAGEMENT Early stabilization of signicant pelvic, spinal, and femoral fractures is emerging as a powerful tool in avoiding the cascade of events leading to pulmonary failure, sepsis, and death.320, 321, 331 Increased understanding of the metabolic consequences of the various techniques of skeletal stabilization, including external xation, plate osteosynthesis, closed IM nailing, and traction-casting methods in patients with varying injury patterns and metabolic tness, will be an area of exciting research in the future. Demling305 stressed control of the inammatory process to prevent further stimulus to MOF He recommended early . rapid removal of injured tissue and prevention of further tissue damage by early fracture xation. Necrotic and injured soft tissue in experimental fractures results in a reduction of hepatic blood ow similar to that seen in sepsis.332 Consequently, early stabilization of fractures may prevent organ dysfunction by improving splanchnic perfusion. The optimal timing and type of fracture xation is controversial and unknown. Timing of fracture xation balances the need to rapidly mobilize the patient versus the deleterious by-products of fracture xation that can contribute to the inammatory response. Type of fracture xation may determine the amount of inammatory tissue released into the circulation.
Overall, early xation has been shown to decrease rates of respiratory, renal, and liver failure.297 Seibel and associates showed that in the blunt multiple-trauma patient with an ISS ranging from 22 to 57, immediate internal xation followed by ventilatory respiratory support greatly reduces the incidence of respiratory failure, positive blood culture results, complications of fracture treatment, and MOF 334 When patients were treated with . the same ventilatory support but with 10 days of traction before fracture xation, pulmonary failure lasted twice as long, positive blood culture results increased 10-fold, and fracture complications increased by a factor of 3.5. If no ventilatory support was used and traction was used for 30 days, pulmonary failure lasted three to ve times as long, positive blood culture results increased by a factor of 74, and fracture complications increased by a factor of 17. Carlson and co-workers demonstrated that xation in less than 24 hours after injury versus nonoperative fracture management decreased the late septic mortality from 13.5% to less then 1%.297 In a series of 56 multiple-injury patients, Goris and colleagues311 showed that the advantage of controlled ventilation combined with early fracture xation was greater than that of either ventilation or fracture xation alone. The greatest advantage was observed in patients with an ISS of more than 50.311 Meek and co-workers324 retrospectively studied 71 multipletrauma patients with similar age and ISS with respect to timing of fracture stabilization. The group with long bone fractures rigidly stabilized within 24 hours had a markedly lower mortality than the group treated with traction and cast methods. In a prospective study, Bone and associates294 compared the incidence of pulmonary dysfunction in 178 patients with acute femoral fractures who underwent either early (the rst 24 hours after injury) or late (more than 48 hours after injury) stabilization. The patients were further divided into those who had multiple injuries and those with isolated fracture of the femur. In none of the patients with isolated femoral fractures, whether treated with early or late stabilization, did respiratory insufciency, required intubation, or needed placement in the intensive care unit occur. In the patients with multiple injuries, those who had delayed stabilization of fractures had a signicantly higher incidence of pulmonary dysfunction. However, in the aggressively managed surgical intensive care unit, early femoral xation may not play as critical a role in the outcome. Reynolds and associates studied 424 consecutive patients with femur fractures treated with IM rods and half of these were done in the rst 24 hours.330 Of these 424 patients, 105 had an ISS of 18 or greater; these patients were studied for the relationship of fracture, xation, timing, and outcomes. IM xation was done in the rst 24 hours in 35 of 105, between 24 and 48 hours in 12 of 105, and more than 48 hours in 58 of 105. Modest delays in fracture xation did not adversely affect the outcomes, and pulmonary complications were related to the severity of injury rather than to timing of fracture xation. The type of xation may play a role in risk consideration. With IM nailing, there is the risk of additional bone marrow emboli and potential associated lung dysfunction. Pape and associates found ARDS in a higher percentage of
455
patients treated with a reamed IM femoral nail acutely performed (8/24, 33%) versus delayed nailing (2/26, 8%) in patients with femur fractures and severe thoracic injuries.50 Charash and co-workers repeated the Pape study design and reported contradictory ndings with favorable results in acute reamed IM nailing versus delayed nailing; pneumonia (14% vs. 48%), pulmonary complications (16% vs. 56%).300 Bosse and co-workers studied severe chest injured patients with femur fracture treated within 24 hours with reamed IM nail or plating.296 The retrospective study was controlled for Group A, femur fracture with thoracic injury; Group B, femur fracture with no thoracic injury; and Group C, thoracic injury with no femur fracture. The overall ARDS rate in patients with femur fracture was 10 of 453 (2%). There was no significant difference in ARDS or pulmonary complications/ MOF whether the femur fracture was treated with rodding or plating. Bosse and associates found no contraindication for reamed femoral nailing in the rst 24 hours even if a thoracic injury were present. Pape and associates assessed lung function in two groups of patients undergoing early (24 hours) IM femoral nailing.47 One group had femoral nailing after reaming of the medullary canal (RFN) and the other group had a small-diameter solid nail inserted without reaming (UFN). These investigators found that lung function was stable in UFN patients but deteriorated in RFN patients. They concluded that IM nailing after reaming might potentiate lung dysfunction, particularly in patients with preexisting pulmonary damage such as lung contusion. In contrast, Heim and associates, in a rabbit model, compared reamed versus unreamed nailing of femoral shaft fractures and the effect on pulmonary dysfunction.27 Their research showed that both techniques resulted in bone marrow intravasation and resulting pulmonary dysfunction. They concluded that the unreamed nailing technique with a solid nail would not prevent pulmonary embolization. These are examples of the controversiesto ream versus not to ream, rod versus plate, early versus latein which incisive investigation is needed to guide decision making for a complex patient problem. The preponderance of evidence points to the value of the upright chest position in the prevention of MOF . Immediate fracture xation in polytrauma, although allowing the patient to sit up, may decrease patient exposure to long periods of stressful nonoperative intervention. Tscherne337 also drew thoughtful attention to the role of pain in the activation of potentially destructive organism defense responses. Because many of these patients present with a lifethreatening condition, the initial evaluations may overlook minor injuries. These early missed injuries are frequent even in trauma centers and often include small bone fractures and soft tissue injuries. In a series of 206 patients, Janjua and co-workers reported a 39% incidence of missed injuries, which included 12 missed thoracoabdominal injuries, 7 missed hemopneumothoraces, and 2 deaths from missed injury complications.319 A secondary evaluation of the patient at 24 hours and serial examinations are needed to nd these injuries. In treatment of the patient with overt MOF the team , must recognize that a potentially lethal condition is
present and that the usual methods to control specic complications (e.g., pneumonia, renal failure, gastrointestinal bleeding) will be ineffective. The patient must be assessed as a whole, and dramatic intervention is required to turn the situation around. In such conditions, delay in performing operative procedures is deadly. In particular, signicant unstable long bone, pelvic, and spinal fractures must be stabilized; any uid collection should be drained; and all necrotic tissue must be excised. The patient needs blood, calories (preferably enteral when feasible), and effective antibiotics. Controlled ventilation and dialysis is probably necessary. All of these must be continuously monitored in an intensive care setting. In the future, progress will likely be made in the control of mediators of the inammatory response.293 The orthopaedists role is to assess those fractures that are causing continued recumbency and to locate sources of devitalized tissue and sepsis in the musculoskeletal system. Sacrice of a crushed but viable limb, loss of fracture reduction, or performance of a quick but not optimal limb stabilization are examples of the difcult choices or procedures that have to be made to save a life. The lower limb fracture in traction has a dual deleterious effect on physiology: the supine position causes shunting with ventilation-perfusion mismatch in the lungs, and continued interfragmental motion of the fractured bone releases necrotic tissue debris into the circulation. Special mechanical beds that allow some tilting of the thorax and prevent pressure sores by alternating contact with the skin are not effective substitutes for skeletal stabilization. External xation (traveling traction),318 although not the method of choice for denitive fracture care, is a good option because of its minimal additional tissue trauma. In summary, in the presence of major thoracic and head injuries, there are potential risks of worsening a brain injury or precipitating ARDS. Carlson297 and Velmahos and associates338 have shown no added morbidity of early xation when chest or head injuries are present. However, Townsend336 and Pape report increased risk for secondary brain and ARDS associated with early xation.47 Reynolds and associates showed modest delay did not affect the outcome.330 Deitch and Goodman prefer to delay operative fracture xation for 24 to 48 hours in patients with severe head or thoracic injuries.304 Deitch and Goodman noted that the best way to treat multiple organ failure is the prevention of MOF in the rst place.304
LOCAL COMPLICATIONS OF FRACTURES
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz Local complications, meaning unwanted therapeutic outcomes, are part of the care of broken bones. Local failures of fracture treatment can manifest as immediate, delayed, or long-term adverse outcomes. Delayed complications include complex pain syndromes and disuse atrophythe fracture disease. Arthrosis and malunion are examples of the long-term adverse results with permanent impairment and economic importance. Any treatment program, no matter how thoughtfully conceived and carefully per-
456
formed, has a failure rate that cannot be entirely eliminated. The patient, physician, and system variables inherent in each given clinical situation mean that, in practice, complication rates are usually in excess of those rates published in the literature. With multiple injuries, the rates become more than additive. This is expressed in the ISS by adding the squares of injury components.342 The purpose of this section is to provide a framework for understanding local complications of fractures.
Soft Tissue and Vascular Problems

An accident, unlike an elective operation, causes the transmission of force of an undetermined magnitude to human tissue. However, through accident reconstruction it is possible to estimate the magnitude of energy transfer. For example, a fall from 30 feet is equivalent to being struck by a car going 30 miles per hour. In the immediate hours, days, and fortnight after injury, it should not be surprising that areas of skin demarcation, skin slough, bruising, or thrombosed vessels appear. These areas, if operative interventions are appropriate, are the consequences of injury and not of its treatment. In addition, after an osteosynthesis, there is additional opportunity for the slow accumulation of hematoma from bleeding from bone surfaces. Todays shortened hospitalization with early mobilization has increased the incidence of postoperative hematoma. Postoperative hematoma manifests as swelling, pain, loss of function, and, not infrequently, serous drainage either from a wound or from the drain tract. Signicant hematomas do not resorb but instead continue to increase in size and cause wound separation, skin sloughs, and infection. Collections of blood or uid can be detected with ultrasonography. It is best to re-explore the wound under an adequate anesthesia, evacuate the hematoma, irrigate the fracture site, and drain the eld. Vascular injuries may manifest acutely with signs of hemorrhage and ischemia, or the presentation may be delayed, as in an arteriovenous stula or a pseudoaneurysm. In civilian injuries with associated fractures or dislocations, the arterial injury rate is from 2% to 6%. For isolated fractures or dislocations, the arterial injury rate is less than 1%. War-related extremity injuries, a high proportion of which result from high-velocity gunshot wounds, consist of a long bone fracture with associated vascular injury in about one third of cases.354 Even if a pulse is present, a vascular injury may still have occurred. The most accurate means of diagnosis is an angiogram, which should be performed if there is evidence of an ischemic extremity, a weak or absent pulse, or a bruit, or if the trajectory of the bullet passes in the vicinity of a major artery. Certain injury patterns such as a knee dislocation, especially a posterior one, have a 30% incidence of associated popliteal artery damage. Therefore, with these injuries, an arteriogram is indicated as soon as practical. When femur fractures are associated with femoral artery injury, the results of vascular repair and limb function are characteristically good, although delayed diagnosis of pseudoaneurysm and claudication can be a problem.366 Cases requiring amputation because of a delay
in diagnosis can occur. Popliteal artery injury, when diagnosed early, is amenable to vascular reconstruction. However, vascular injuries distal to the popliteal trifurcation carry a much worse prognosis. Revascularization is usually not needed if one vessel is patent on angiogram and the distal pressure is 50% of the brachial artery pressure. When revascularization is required, a good functional result can be expected in only about 25% of cases. In Flint and Richardsons experience, 6 of 16 patients undergoing revascularization required early amputation, and 6 more required late amputation (total, 12/16) for osteomyelitis, nonunion, and persistent neuropathy and its associated complications.366 Early amputation without revascularization is often appropriate in the patient with loss of vascular inow, long bone fracture, and extensive soft tissue damage. The high rate of infection and complications can result in a delayed amputation when revascularization is done.452
Post-traumatic Arthrosis
Post-traumatic arthrosis is commonly noted to be a complication of fractures (Fig. 187). However, there is limited insightful research on the actual pathomechanics of post-traumatic arthrosis. Wright, a retired judge, used a questionnaire to determine a consensus view of the factors
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FIGURE 187. Radiograph of a hip 18 years after limited internal xation, an older technique, of a posterior wall acetabular fracture, which demonstrates post-traumatic arthrosis likely secondary to articular cartilage impact and degeneration, and joint incongruity. Total hip replacement is currently being considered.
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related to the development of post-traumatic arthrosis after fracture.475 He found the following: that lower limb joints are more likely to develop arthritis than upper extremity joints, that older patients are at higher risk for the development of post-traumatic arthrosis (although younger patients have a longer time frame to develop post-traumatic arthrosis), and that occupation is a risk factor. Kern and associates also reported the association of osteoarthritis and certain occupations.389 The potential causes of post-traumatic arthrosis include the following: (1) incongruity of the articular surface, (2) cartilage damage from the load transfer, (3) malalignment, (4) malorientation of the joint, and (5) repetitive loading injury. JOINT INCONGRUITY The emphasis on anatomic reduction in fracture surgery focuses on the reestablishment of joint congruity usually at the expense of the soft tissue attachments. Extensive bony comminution of the articular surface, particularly of the knee and the distal tibia, can make a repair of joint congruity a formidable or even an impossible task. Acetabular fractures are a good example of articular fractures that are associated with the development of post-traumatic arthrosis411 largely because of failure to reestablish joint congruity and the articular cartilage injury itself.410 ARTICULAR CARTILAGE DAMAGE The impact to the articular cartilage at the time of injury in high-energy trauma is a likely contributor to the articular cartilage damage and the subsequent development of post-traumatic arthrosis (Figs. 188 and 189). However, the clinical data are not clear-cut. Volpin and co-workers reported at an average follow-up of 14 years of intraarticular fractures of the knee joint that there were 77% good-to-excellent results.467 Repo and associates stated that the impact loads sufcient to fracture a femoral shaft of an automobile occupant are nearly sufcient to cause signicant articular cartilage (chondrocyte death and ssuring).442 There is an increasing appreciation of cartilage injury from impact. The advent of MRI of knee injuries has enhanced our appreciation of damage to the articular surfaces (bone bruising) (Fig. 1810). Spindler and associates studied 54 patients with anterior cruciate ligament tears and found a bone bruise present in 80% of cases, of which 68% were in the lateral femoral condyle.456 Miller and co-workers studied 65 patients who had MRI-detected trabecular microfractures associated with isolated medial collateral ligament injuries.417 Although these bone bruises were approximately half as common as bone bruises associated with anterior cruciate ligament tears, these investigators stated that medial collateral ligamentassociated trabecular microfractures may be a better natural history model.417 Bone bruises in combination with anterior cruciate ligament tears may be harbingers of future arthritis. Wright and associates noted that isolated bone bruises not associated with ligamentous or
FIGURE 188. Anteroposterior radiograph of a knee with post-traumatic arthrosis secondary to joint incongruity and articular cartilage degeneration 5 years after a high-energy tibial plateau fracture.
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meniscal injury may have a better prognosis than bone bruises noted in conjunction with ligamentous and meniscal injury.474 The biologic basis for the cartilage degradation is being studied: the pathologic process involves degradation of articular cartilage.417a It has been theorized that the impact at the time of injury damages the articular
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FIGURE 189. Correlative arthroscopic view of the lateral compartment of the knee in Figure 188, which demonstrates post-traumatic arthrosis secondary to joint incongruity, articular cartilage degradation, and meniscal degeneration 5 years after a high-energy tibial plateau fracture.
458
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joint. However, the knee is most vulnerable to changes in the normal coronal plane relationship of the lower extremity.464 Axial malalignment of the knee, which changes the mechanical axis creates a moment arm, which increases force transmission across either the medial or lateral compartments of the knee joint.429, 430 This moment arm, termed the mechanical axis deviation, is represented by drawing a line from the center of the knee and reects the magnitude of alteration in stress distribution across the knee.464 The effect of the deformity on the mechanical axis increases as the apex of the deformity approaches the knee. Nonetheless, there is conicting clinical data regarding whether these factors lead to post-traumatic arthrosis. Kettlekamp and associates stated that there are no data to support the position that malalignment always leads to degenerative arthritis.390 Kristensen and co-workers reported no arthrosis of the ankle 20 years after malaligned tibial fractures.398 In contrast, Puno and co-workers studied 27 patients with 28 tibial fractures and found that greater degrees of ankle malalignment produced poorer clinical results.436 Merchant and Dietz stated that they did not nd any support in their study for the hypotheses that angulation results in shear rather than compressive forces on articular cartilage and that these forces lead to early arthrosis.414 MALORIENTATION
FIGURE 1810. Sagittal MR image of the lateral compartment of a knee that demonstrates a bone contusion involving the lateral femoral condyle and the lateral tibial plateau in association with a recent anterior cruciate ligament tear. (Courtesy of Theresa M. Corrigan, M.D.)
cartilage or its blood supply irreversibly and initiates a cascade of post-traumatic arthritis.442 This etiology of impact arthritis has not been well-studied.442, 465, 468 Attempts to develop a model have been made. Vrahas and co-workers developed a method of impacting quantifying blows to articular cartilage in a rabbit model.468 Nonetheless, cartilage damage, particularly when it is unassociated with bone changes, may not necessarily progress to arthritis.438 Radin noted that full-thickness cartilage lesions that are less than 1 cm usually will not progress to arthritis.438 MALALIGNMENT Tetsworth and Paley have focused on the relationship between malalignment and degenerative arthropathy.464 These investigators focused on degenerative arthritis and changes in the weight-bearing line or mechanical axis (malalignment), changes in the position of each articular surface relative to the axis of the individual segments (malorientation), and changes in joint incongruity. They noted that the joints of the lower extremity are nearly collinear and that any disturbance in this relationship (malalignment) affects the transmission of load across the joint surfaces.464 The hip and shoulder joints, because of their sphericity, tolerate malalignment. The ankle joint is also fairly tolerant of deformity because of compensation through the subtalar
Another postfracture residual deformity that can contribute to post-traumatic arthrosis is malorientation (a change in the orientation of a joint to the mechanical axis). The association of malorientation of the knee and osteoarthritis has been demonstrated.357, 358 Malorientation can result from translation or rotation. When the orientation of the joint is substantially changed in relation to the mechanical axis, the theory is that abnormal loading of the articular cartilage and subchondral plate will occur, which will accelerate joint deterioration and ultimately lead to osteoarthritis. Malorientation is probably more of a problem with weight-bearing joints such as the knee, which are subject to higher and more frequent loading. REPETITIVE LOADING INJURY Articular cartilage damage can occur either by sudden impact loading or by repetitive impulsive loading.361, 362, 407, 437 As a result, portions of the matrix can be fractured, cause cartilage necrosis, and produce subclinical microfractures in the calcied cartilage layer.372 The effect on cartilage homeostasis appears to lead to changes that are seen in association with osteoarthritis.361, 437, 469 Radiographic evidence of knee arthritis after meniscectomy, called Fairbanks changes,365 most likely result from repetitive loading to the articular after changes in load distribution of the knee joint. Deterioration of damaged articular cartilage by repetitive loading may be asymptomatic because cartilage is relatively aneural.372 Adult canine articular cartilage after indirect blunt trauma demonstrates signicant alterations in its histologic, biomechanical, and ultrastructural characteristics
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without disruption of the articular surface.362 Thompson and associates found arthritic-like degeneration of the articular cartilage in an animal model within 6 months after transarticular loads.365 These investigators also noted that degenerative changes that occur in patients who sustained traumatic insult to the joint may represent a phenomenon similar to their animal model.365 Damage to articular cartilage often can occur without perceptible alteration in the macroscopic appearance of the tissue.372 There is limited potential for cartilage self-repair. Yet there is some evidence that some cartilage repair is possible, which has led to the proliferation of procedures such as autologous cartilage transplantation350 and microfracture.460
TABLE 189
SUMMARY
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz We have tabulated the incidence of post-traumatic arthrosis associated with some common fractures and dislocations (Table 189). In addition, post-traumatic arthrosis is discussed elsewhere in the text. Post-traumatic arthrosis may be an inevitable consequence of musculoskeletal injury. It appears to be related to the magnitude of the original injury. Fracture surgery techniques cannot fully reverse the articular cartilage injury. Gelber and associates reported that an injury to the knee joint in young adulthood was related to a substantial increased risk for future knee osteoarthritis.370
Incidence of Post-traumatic Arthritis
Upper Extremity
Shoulder Acromioclavicular joint dislocations Scapula fractures Anterior shoulder dislocation Elbow Elbow dislocationssimple Elbow dislocations with a radial head fracture Wrist Colles fractures Colles fractures Scapholunate dislocations Trans-scaphoid perilunate dislocations; fracture Lower Extremity Acetabular Fractures Hip Dislocations Anterior Posterior Posterior <6 hr time to reduction >6 hr time to reduction 6.5%56% 17% 30% 76% 22% (patellofemoral joint) 5% (tibiofemoral joint) 18% Fracture patterns Bicondylar fractures Medial plateau fractures Lateral plateau fractures valgus Normal 42% 21% 16% 31% 13% 2040% Ankle Joint 15% 36% 69% Subtalar Joint 24% 66% 63% 56% 78% (15-yr follow-up) Young adults 4.3-yr follow-up 3%18% 57%65% 58% 50% 24-yr follow-up 38% 63% Superior lateral angle 25%43% 61% 7%
Supracondylar/Intercondylar Femur Fractures Patella Fractures Tibial Plateau Fractures
Association with alignment after plateau fractures Ankle Fractures Talar Neck Fractures Hawkins I Hawkins II Hawkins III Subtalar Joint Dislocations Tarsometatarsal Fracture-Dislocation (Lisfranc Joint Injuries)
Source: Data from Fagg, P.S.; Foy, M.A. Philadelphia, Churchill-Livingstone, 1995.
460
SECTION I General Principles TABLE 1810
Other confounding factors in determining the relationship between fractures and the development of posttraumatic arthrosis are normal age-related changes noted on radiographs. Bonsell and associates reported that age was a signicant predictor for degenerative changes observed on radiographs of the shoulder in asymptomatic individuals.348 Specic components of the pathomechanics of posttraumatic arthrosis include malalignment, malorientation, joint incongruity, articular cartilage destruction, ligamentous or brocartilaginous injury, and repetitive loading injury. Salvage procedures such as joint replacement or osteotomy are less successful for post-traumatic arthrosis than for osteoarthritis.401 Postinjury counseling and patient education is necessary to convey realistic expectations after fracture surgery. Prospective, long-term studies are needed to better understand the natural history of posttraumatic arthrosis and to be able to decipher it from normal age-related osteoarthrosis.
Types of Peripheral Nerve Injuries

Injury Neurapraxia Pathophysiology
Prognosis Good
Axonotmesis Neurotmesis
Reversible conduction block characterized by local ischemia and selective demyelination of the axon sheath More severe injury with disruption of the axon and myelin sheath but with an intact epineurium Complete nerve division with disruption of the endoneurium
Fair Poor
Source: Brinker, M.R.; Lou, E.C. General principles of trauma. In: Brinker, M.R., ed. Review of Orthopaedic Trauma. Philadelphia, W.B. Saunders, 2001, p. 8, with permission.
Peripheral Nerve Injuries

Few entities can overshadow the outcome of the treatment of a fracture as much as a peripheral nerve injury. Whether the nerve palsy is diagnosed before or after surgery, it is certain that the patient and other health care providers will be inordinately focused on the nerve palsy itself. Peripheral nerve injuries in orthopaedic trauma are probably underreported because clinical assessment of peripheral lesions is often impossible or impractical. Electrodiagnostic testing is more sensitive than clinical examination alone and can facilitate the diagnosis of traumatic peripheral nerve injuries. A scientic understanding and approach to peripheral nerve injury is imperative. HISTORY OF THE TREATMENT OF NERVE INJURY George Omer traces the history of the treatment of peripheral nerve injuries to William A. Hammond, Surgeon General of the U.S. Army during the American Civil War.425 Drawing largely on the United States military experience, Omer traces the evolution of understanding and treatment of peripheral nerve injuries from the Civil War through the two World Wars, the Vietnam and Korean conicts, and the development of The Sunderland Society.425 The greatest advances have come from the intraoperative microscope and the ingenuity of the surgeon.457 CLASSIFICATION OF NERVE INJURY Historically, Seddon is credited with the scientic classication of peripheral nerve injury into three categories: neurotmesis, axonotmesis, and neurapraxia (Table 1810).451 Seddon, however, noted that these three terms were not his originally and were coined by Professor Henry Cohen in 1941.451 Understanding peripheral nerve injury is predicated on understanding the anatomy of myelinated nerves (Fig. 1811). Neurotmesis implies a cutting or separation of related parts in which all essential structures have been sun-
dered.451 He noted that although there is not necessarily an obvious anatomic gap in the nerve and the epineural sheath may appear to be in continuity, the effect is as if anatomic continuity has been lost.451 Axonotmesis involves a lesion to the peripheral nerve of such severity that wallerian degeneration occurs but the epineurium and supporting structures of the nerve have been so little disturbed that the internal architecture is fairly well-preserved.451 Neurapraxia is described as a lesion in which paralysis occurs in the absence of peripheral degeneration. Seddon noted that neurapraxia is preferred to transient block because the recovery time can be lengthy and is invariably complete.451 Seddon notes that of the three terms neurotmesis is probably the best understood and that in clinical practice the existence of axonotmesis or neurapraxia could only be surmised.451 The advent of electrodiagnostic testing however has made the distinction between an axonotmesis and a neurotmesis much easier. Seddon noted that the most common variety of neurotmesis was from anatomic division. Wallerian nerve degeneration occurs peripherally, and the clinical picture is that of complete interruption of the nerve. Axonotmesis is characterized by complete interruption of axons but with preservation of the supporting structures of the nerve (Schwann tubes, endoneurium, and perineurium). On a histologic level, there is complete interruption of the axons, preservation of the Schwann tubes and endoneurium, and wallerian degeneration peripherally. Seddon noted that clinically axonotmesis was indistinguishable from neurotmesis until recovery occurs, which in axonotmesis was spontaneous.451 When exploration is performed, the nding of an intact nerve suggests that the lesion is an axonotmesis.451 A fusiform neuroma nding suggests that the injury was a mixed lesion of an axonotmesis and a neurotmesis with the rst predominating.451 A nding of intraneural brosis is evidence that the lesion was a neurotmesis. Seddon noted that with a neurapraxia, there is no axonal degeneration. There is localized degeneration of the myelin sheaths. Blunt injuries and compression were the most common cause of neurapraxias.451 He noted that
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FIGURE 1811. Cross-sectional anatomy of peripheral nerve. Inset at left shows an unmyelinated ber. Inset at bottom shows a myelinated ber. (From Lee, S.K.; Wolfe, S.W. Peripheral nerve injury and repair. J Am Acad Orthop Surg 8:243252, 2000.)
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the clinical picture is one of complete motor paralysis and incomplete sensory paralysis.451 Also, he noted that there was no anatomic march to recovery as seen after nerve suture or axonotmesis.451 Finally, Seddon noted that there were in fact many nerve injuries that were in fact combinations of the three different nerve injuries he described.451 Of a series of 537 nerve injuries, he noted that there were 96 cases in which a neurotmesis and an axonotmesis were combined.451 Sunderland added to the work of Seddon by subdividing peripheral nerve injury into ve degrees by basically subdividing the neurotmesis into three types (third, fourth, and fth degree injuries) while maintaining the concepts of neurapraxia (rst-degree injury) and axonotmesis (second-degree injury).461 He dened ve degrees of nerve injury based on changes induced in the normal nerve. Seddon described these injuries in ascending order which affected successively: (1) conduction in the axon; (2) continuity of the axon; (3) the endoneurial tube and its axon; (4) the funiculus and its contents; (5) the entire nerve trunk.461 The most important part of Sunderlands work is his clarication that injuries previously classied by Seddon as a neurotmesis were not all equal. Sunderland also added to the knowledge of partial and mixed nerve injuries. He noted that some bers in a nerve may escape injury while others sustain a variable degree of damage.461 He noted that in partial severance injuries and fourth-degree injuries, it was unlikely that the remaining bers would escape some injury. This type of injury should be described as a mixed lesion.461 However, fourth- and fth-degree lesions could not coexist together or in combination with any of the minor types of injuries.461 There are problems with the classication of peripheral nerve injury. Many nerve injuries are mixed injuries in which all nerve bers are affected to varying degrees.402 In addition, the subtypes of Seddons classication are usually discernible only on histologic examination of the nerve
and are seldom possible on the basis of clinical or electromyographic data. INCIDENCE OF NERVE INJURIES ASSOCIATED WITH FRACTURES There is a fairly high incidence of nerve injury with some common orthopaedic entities (Table 1811). Conway and Hubbell reported electromyographic abnormalities associated with pelvic fracture and noted that patients with double vertical pelvic fractures (combined injury to the anterior third of the pelvic ring and the sacroiliac area) were most at risk, with a 46% incidence of neurologic injury.356 Goodall noted that 95% of fractures with an associated nerve injury occur in the upper extremity.374 Of all fracture types, a humerus fracture is the most likely fracture to have an associated nerve injury.343 Omer reported, based on a collected series,424
TABLE 1811
Common Orthopaedic Entities Associated with Peripheral Nerve Injuries

Anatomic Location Humerus Pelvis Tibia Type of Injury Midshaft fractures Double vertical pelvic fractures Tibia fractures
Incidence Nerve Injury 12%19% incidence radial nerve palsy391, 433, 453, 455 46% incidence neurologic injury356 19%30% incidence neurologic ndings after intramedullary nailing396, 472 86% incidence of neurologic ndings419
Ankle
Ankle eversion injuries
462
the following distribution of nerve injuries associated with fractures and fracture-dislocations: radial nerve (60%), ulnar nerve (18%), common peroneal nerve (15%), and median nerve (6%).374, 377, 403 EVALUATION OF PERIPHERAL NERVE INJURIES In the polytrauma patient, the neurologic assessment is incorporated in the initial assessment, which uses the alphabetABCDin which D is for disability and neurologic assessment.463 The GCS, developed by Teasdale and Jennet, specically assesses eye opening, motor response, and verbal response in a maximum 15-point rating scale. The assessment of peripheral nerve injury during orthopaedic surgery rounds and emergency department assessments oftentimes is reduced to the terms neurovascularly intact or N/V intact. In our opinion, such terms, although convenient, should never be used unless a complete neurologic examination (cutaneous sensation including light touch, pain, and temperature; vibratory sensation; motor strength in all muscles with grading; deep tendon reexes; and special tests for clonus, etc.) and a complete vascular examination (pulses, capillary rell, venous examination, tests for thrombosis, auscultation for bruits, etc.) are performed. Formal assessment of peripheral nerve injury is usually performed using electromyography (EMG). Electromyography and Electrodiagnostics In a broad sense, EMG refers to a set of diagnostic tests using neurophysiologic techniques that are performed on muscles and nerves.462 Strictly speaking, EMG refers to one of these tests, in which a small needle is used to probe selected muscles, recording electrical potentials from the muscle bers.462 Although electrodiagnostic testing has historically been of little interest to the orthopaedic surgeon, there is heightened interest in electrodiagnostics as a result of intraoperative use of sensory-evoked potentials and motorevoked potentials in spine surgery, brachial plexus surgery, and acetabular surgery. It has been said that the best times for electrodiagnostic studies are the day before injury and then about 10 to 14 days after injury. The former is, of course, generally impossible but nonetheless underscores the importance of baseline studies and changes over time, particularly when one is looking for evidence of reinnervation (which would
TABLE 1812
be consistent with an axonotmesis) or denervation (which would be consistent with a neurotmesis). The latter highlights the fact that reinnervation following wallerian degeneration takes at least 10 to 14 days to be able to detect on electrodiagnostic testing. Basic Science of Electrodiagnostics. To understand EMG, it is necessary to review some basics of nerve structure and function. A motor neuron has a cell body in the spinal cord and extends into the nerve root, an axon that exits the spine, traverses the plexus, travels within a nerve, and then forms many distinct branches.462 A motor unit consists of one such cell and the several muscle bers that it innervates.462 Muscles contain many motor units that are analogous to colored pencils in a bundle.462 Muscle forces are created by activation of an increasing number of motor units under the command of the brain.462 When a motor unit res, a small electrical signal is generated and can be recorded by placing a small needle through the skin and into the muscle near the motor unit bers acting electronically like an antennae.462 This signal is amplied, ltered, digitized, and displaced on a computer screen.462 Single motor unit potentials are sampled rst on the oscilloscope. As greater force is generated, there is recruitment of more motor units and an increase in the ring rate.462 When full muscle force is generated, the oscilloscope screen lls with signals, which has an appearance called the full interference pattern.462 Another important component of EMG interpretation is the sound of the motor potentials, which are amplied and broadcast through a speaker.462 The experienced electromyographer can recognize characteristic sounds and audible patterns.462 The usefulness of EMG for the trauma patient is the ability to localize neurologic lesions anatomically based on a pattern of denervated muscle. EMG is also useful for following nerve recovery over time. Characteristic Electromyography Patterns. If there is an injury to the axon, as with an axonotmesis or neurotmesis, distal degeneration of the nerve (wallerian degeneration) causes it to be electrically irritable.462 Needle movement generates denervation potentials called brillations and positive waves, which have both characteristic appearances on the oscilloscope and sounds on the loudspeaker.462 These ndings are delayed, occurring at least 10 days even after complete transection.462 Sprouting and reinnervation that would occur with a recovering axonotmesis creates a high amplitude polyphasic motor unit potential (Table 1812).462
Electromyographic Findings Related to Trauma

Condition Normal study Neurapraxia Axonotmesis (after 2 wks) Neurotmesis (after 2 wks)
Insertional Activity Normal Normal Increased Increased Activity at Rest Silence Silence Fibrillations and positive sharp waves Fibrillations and positive sharp waves Minimal Contraction Biphasic and triphasic potential Reduced number of potentials None None Interference Complete Reduced None None
Source: Adapted with permission from Brinker, M.R.; Lou, E.C. General Principles of Trauma. In Brinker, M.R., ed. Review of Orthopaedic Trauma. Philadelphia, WB Saunders, 2001, p. 9, of which the data was adapted with modications from Jahss, M.H. Disorders of the foot. In Miller, M.D., ed. Review of Orthopaedics, 3rd ed. Philadelphia, WB Saunders, 2000.
463
Nerve Conduction Study Results Related to Trauma

Condition Normal study Neurapraxia Proximal to lesion Distal to lesion Axonotmesis Proximal to lesion Distal to lesion (immediate) Distal to lesion (>7 d) Neurotmesis Proximal to lesion Distal to lesion (immediate) Distal to lesion (>7 d) Latency Normal
Conduction Velocity Upper extremities: >48 m/sec Lower extremities: >40 m/sec Absent or low voltage (if partial) Normal Absent Normal Absent Absent Normal Absent Evoked Response Biphasic Absent Normal Absent Normal Absent Absent Normal Absent
Absent or low voltage (if partial) Normal Absent Normal Absent Absent Normal Absent
Source: Adapted with permission from Brinker, M.R.; Lou, E.C. General Principles of Trauma. In: Review of Orthopaedic Trauma. Philadelphia, W.B. Saunders, 2001, p. 8, of which the data was from Jahss, M.S. Disorders of the foot. In: Miller, M.D.; Brinker, M.R., eds. Review of Orthopaedics, 3rd ed. Philadelphia, W.B. Saunders, 1982.
Nerve Conduction Studies Distinct from EMG are nerve conduction studies. Nerve conduction studies can be used to test both sensory and motor nerves and skeletal muscle. These studies test only large myelinated nerve ber function. Nerve bers commonly evaluated include the ulnar, medial, radial, and tibial nerves (motor and sensory bers); the sciatic, femoral, and peroneal bers (motor bers only); and the musculocutaneous, supercial peroneal, sural, and saphenous nerves (sensory only). The procedure of nerve conduction testing uses surface electrodes, often silver discs or ring electrodes, to record extracellular electrical activity from muscle or nerve. EMG machines have a nerve stimulator that can apply an electrical shock to the skin surface at accessible points on the nerve.462 This stimulus depolarizes a segment of the nerve and generates an action potential, which travels in both direction from the point that it was stimulated.461 When a sensory nerve is tested, the action potential can be recorded from a distal point (surface electrodes or nger electrodes).462 By measuring the distance from the stimulus point to the recording site and using the oscilloscope values of the time of slight (latency) and action potential amplitude, the examiner can determine the sensory conduction velocity.462 Motor nerve conduction velocities (motor NCVs) are recorded from surface electrodes taped over muscles distally in the limb.461 Normative control values for motor nerve conduction velocities at different ages are used for comparison. This difference is attributable to the degree of myelination, which increases with age over the early developmental years. Although nerve conduction velocities are fairly uniform from age 3 years through adulthood,462 nerve conduction velocities can vary based on several conditions. Nerve conduction values at birth are about 50% of adult values. As surface temperature decreases below 34 C, there is a progressive increase in latency and a decrease in conduction velocity.345 Upper extremity conduction velocities are generally about 10% to 15% faster than those of the lower extremity. Conduction velocity in the proximal segments is usually 5% to 10%
faster than in the distal segments,345 which is a function of nerve root diameter. To study motor conduction, the nerve is supramaximally stimulated at two or more points along its course where it is most supercial. At a distal muscle that is innervated by the nerve, a motor response is recorded.345 Various parameters measured include latency, conduction velocity, amplitude, and duration. Characteristic nerve conduction study ndings for various nerve injuries are shown in Table 1813. Sensory nerve conductions are generally unaffected by lesions proximal to the dorsal root ganglion even though there is sensory loss.345 Sensory testing is good for localizing a lesion either proximal (root or spinal cord) or distal (plexus or nerve) to the dorsal root ganglia. In addition, sensory nerve potential is lower in amplitude than compound motor action potentials and can be obscured by electrical activity or artifacts. Sensory axons are evaluated in four ways: (1) stimulating and recording from a cutaneous nerve, (2) recording from a cutaneous nerve while stimulating a mixed nerve, (3) recording from a mixed nerve while stimulating a cutaneous nerve, and (4) recording from the spinal column while a cutaneous nerve or mixed nerve is stimulated.345 Variables measured include onset latency, peak latency, and peak-to-peak amplitude. Two other parameters, which are measured, are the F-wave and the H-reex. The F-wave is a late motor response attributed a small percentage of bers ring after the original stimulus impulse reaches the cell body. These F-waves are particularly useful for the evaluation of the proximal segments of peripheral nerves.345 However, the F-wave is only useful in the assessment of proximal lesions only in the absence of more distal pathology. There is also variability in the F-wave response because different bers re each time, making it less quantitative. The H-reex is an electrically evoked spinal monosynaptic reex that activates the Ia afferent bers (large myelinated bers with the lowest threshold for activation). The Achilles tendon reex (S1) is the easiest to record and can differentiate between an S-1 and an L-5 radiculopathy.345 Again, distal
464
pathology must be ruled out if the latency is prolonged and being used to assess for proximal pathosis. Somatosensory-Evoked Potentials Although the use of somatosensory-evoked potentials (SSEPs) was popular380 for acetabular surgery, SSEPs have been supplanted by spontaneous EMG379 when monitoring is desired. However, the general use of SSEPs or electromyographic modalities does not seem to be justied.416 The method of performing SSEPs involves an afferent pulse of large nerve ber sensory activity travels proximally and enters the spinal cord and then ascends to the brain via the posterior columns in the brain stem after the nerve is stimulated.462 This postsynaptic activity ultimately reaches the thalamus and the parietal cortex of the brain.462 A small brain wave occurs following nerve stimulation at a xed time following nerve stimulation and is recordable from surface electrodes in the scalp.462 These SSEPs can be recorded simultaneously from various points such as Erbs point, which overlies the brachial plexus, over the cervical spine, and from the scalp overlying the cortex.462 SSEPs are useful for monitoring the lower extremity in spinal surgery. Upper extremity SSEPs are useful in brachial plexus surgery. ASSOCIATION OF PERIPHERAL NERVE INJURY AND CAUSALGIA There is a potential overlap between peripheral nerve injury and causalgia (type II complex regional pain syndrome). According to Bonica, the incidence of causalgia is 1% to 5% of peripheral nerve injuries.346 Data from the Vietnam War indicate a lower incidence of causalgia than the data from World War II (1.5% versus 1.8%13.8%). Rothberg and associates and Bonica346 suggest that this lower incidence was due to the more rapid transport of the wounded (usually within 12 hours and by helicopter) and the high quality of care by an ample number of neurosurgeons in Army hospitals. PROGNOSIS Nerve Injuries Associated with Open and Closed Fractures and Dislocations Omer noted a spontaneous return of nerve function in 83% of nerve injuries associated with fractures.427 Radial nerve palsy associated with humerus fractures is perhaps a good example in which nerve recovery can be expected in roughly 90% of cases.391, 433, 453, 455 There are further distinctions in prognosis including lower recovery rates of nerve function with open fractures than with closed fractures (17% vs. 83.5% in one series).450 Omer also reported that nerve injuries associated with a dislocation were less likely to show spontaneous recovery than nerve injuries associated with a fracture.426 Omer noted that peripheral neuropathy associated with closed fractures is usually neurapraxia lesions, which have an excellent prognosis for recovery.426 Peripheral neuropathy associated with open fractures had a prognosis related to the etiology: lacerations are usually neurotmesis
lesions and should be closely examined, explored, and sutured.426 Nerve Injuries Associated with Projectile Injuries Data from Vietnam on 595 gunshot wounds studied by Omer had a 69% spontaneous recovery rate for lowvelocity gunshot wounds and a 69% spontaneous recovery rate for high-velocity gunshot wounds.423 Proximal nerve injuries in extremities take longer to show clinical recovery than more distal extremity injuries.423 Civilian peripheral nerve injuries from projectiles with associated vascular injury have a poor prognosis. In one series, only 10% of these nerve injuries resolved.378 Shotgun injuries have a higher incidence of nerve injuries than other types of gunshot injuries, have a worse prognosis (spontaneous recovery rate of about 45%),405 and have a higher percentage of complete nerve transaction (neurotmesis) than even high-velocity missile wounds. High-velocity missiles often create axonotmesis lesions and have a better prognosis for recovery than low-velocity missile wounds.423
SUMMARY
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz Peripheral nerve injuries associated with fractures and dislocations are probably underappreciated in the acute trauma setting. The orthopaedic surgeon ought to refrain from using the term neurovascularly intact unless a complete neurologic and vascular examination has been performed. Instead, documentation should be limited to what was observed and performed (e.g., toes up and down, 1+ dorsalis pedis pulse). Heightened surveillance for neurologic injury is protective for the clinician because failure to diagnose nerve injuries may result in patient dissatisfaction, disability, and litigation. The orthopaedic surgeon needs to be facile with the lexicon of nerve injury (neurapraxia, axonotmesis, and neurotmesis) to communicate with neurologic colleagues. From a practical standpoint, evaluation of recovery after a peripheral nerve injury is best performed by serial physical examinations. However, there is a role for electrodiagnostic testing, particularly when there is no sign of recovery of nerve function. Electrodiagnostic studies should be delayed for at least 3 weeks and often need to be repeated serially. Research in nerve regeneration techniques may also hold the key to the treatment of peripheral nerve injuries in the future.
Post-traumatic Reex Sympathetic Dystrophy

Pain after musculoskeletal injury usually subsides. When patients have peculiar, disagreeable, and persistent painful symptoms several weeks after injury, they may have RSD. RSD, now referred to as type I complex regional pain syndrome (CRPS), is increasingly recognized as a cause of disability after injury.470 The index of suspicion in general is not high enough, and many patients are not diagnosed
465
until the later stages when the prognosis is less favorable.470 Advances have been made in the understanding and treatment of RSD. Nevertheless, many treatment methods are empirical, and there is a need for research in this area.470 MODERN TERMINOLOGY More than six dozen different terms have been used over the past two decades to describe RSD in the English, French, and German literature.470 A complicated lexicon of RSD has evolved from the more general category of pain dysfunction syndromes,341 to the terminology adopted in 1994 by the International Association for the Study of Pain into complex regional pain syndromes.459 CRPS is subdivided into type I CRPS (RSD) and type II CRPS (causalgia).459 The distinction is based on the absence of a documented nerve injury for RSD and a documented nerve injury for causalgia (Table 1814). The focus here is on RSD associated with traumatic orthopaedic injuries. Because the older terminology is still widely used, we will use the term RSD herein. ETIOLOGY AND EPIDEMIOLOGY Trauma secondary to accidental injury has been described as the most common cause of RSD.346 These injuries include sprains; dislocations; fractures, usually of the hands, feet, or wrists; traumatic nger amputations; crush injuries of the hands, ngers, or wrists; contusions; and lacerations or punctures of the ngers, hands, toes, or feet.346 It has been reported that RSD develops in 1% to
5% of patients with peripheral nerve injury, 28% of patients with Colles fracture,344 and 30% of patients with tibial fracture.447 In a recent series, the three most common inciting events were a sprain or strain in 29%, postsurgical in 24%, and a fracture in 16%.340 Interestingly, in this same series, 6% of patients could not remember an inciting event.340 Saphenous neuralgia has been called a forme fruste of sympathetically mediated pain.432 External xators appear to be associated with RSD in the upper extremity, although whether it is a result of the fracture immobilization, possible traction injury to the nerves, or direct neural trauma from the pins is unclear. RSD also seems to be associated commonly with arthroscopic surgical procedures360 and prolonged usage of extremity tourniquets. Allen and associates340 reported on the epidemiologic variables of patients with CRPS. They noted in a series of 134 patients evaluated at a tertiary chronic pain clinic that patients presented with a history of having seen on average 4.8 different physicians before referral.340 The average duration of symptoms of CRPS before presentation was 30 months.340 In addition 54% of patients had a workmens compensation claim and 17% of patients had a lawsuit related to the CRPS.340 Of the 51 of 135 patients who underwent a bone scan, only 53% of the studies were interpreted as consistent with the diagnosis of CRPS.340
PATHOPHYSIOLOGY Breivik noted that, as described by The International Association for the Study of Pain, CRPS is a complex neurologic disease involving the somatosensory, somatomotor, and autonomic nervous system in various combinations, with distorted information processing of afferent sensory signals to the spinal cord.349, 415 Autonomic nervous system dysregulation occurs only in 25% to 50% of patients with CRPS.347, 365, 415 The role of the sympathetic system was further claried by Ide and associates, who used a noninvasive laser Doppler to assess ngertip blood ow and vasoconstrictor response and found that skin blood ow and vasoconstrictor response returned to normal following successful treatment of the condition.384 These investigators suggested that the sympathetic nervous system function is altered and is different in the various stages of RSD. Many RSD patients have a combination of sympathetically maintained pain and sympathetically independent pain. Sympathetically maintained pain (SMP) is dened as pain that is maintained by sympathetic efferent nerve activity or by circulating catecholamines.347, 365, 415 SMP is relieved by sympatholytic procedures.349 Sympathetically maintained pain follows a nonanatomic distribution.404 Nonetheless, SMP is not essential in the development of CRPS.349 In some patients, sympatholytic procedures will not relieve their pain.349 Breivik notes that more than half of all patients with CRPS have sympathetically independent pain. In one series, symptoms of increased sympathetic activity occurred in 57% of patients, whereas signs of inammation and muscle dysfunction occurred in 90% of patients.466
TABLE 1814
International Association for the Study of Pain: Diagnostic Criteria for Complex Regional Pain Syndrome
COMPLEX REGIONAL PAIN SYNDROME TYPE I (REFLEX SYMPATHETIC DYSTROPHY) 1. The presence of an initiating noxious event or a cause of immobilization. 2. Continuing pain, allodynia or hyperalgesia with which the pain is disproportionate to the inciting event. 3. Evidence at some time of edema, changes in skin blood ow or abnormal sudomotor activity in the painful region. 4. The diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction. Note: Criteria 2, 3, and 4 are necessary for a diagnosis of complex regional pain syndrome. COMPLEX REGIONAL PAIN SYNDROME TYPE II (CAUSALGIA) 1. The presence of continuing pain, allodynia or hyperalgesia after a nerve injury, not necessarily limited to the distribution of the injured nerve. 2. Evidence at some time of edema, changes in skin blood ow or abnormal sudomotor activity in the region of the pain. 3. The diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction. Note: All three criteria must be satised.
Source: Adapted with permission from Pittman, D.M.; Belgrade, M.J. Am Fam Phys 56(9):22652270, 1997; which was adapted with permission from Merskey, H.; Bodguk, N., eds. Classication of Chronic Pain, Descriptions of Chronic Pain Syndromes and Denitions of Pain Terms, 2nd ed. Seattle, IASP Press, pp. 4043.
466
TABLE 1815
Selected Differential Diagnosis of Reex Sympathetic Dystrophy

MUSCULOSKELETAL Bursitis Myofascial pain syndrome Rotator cuff tear (Buergers disease) Undiagnosed local pathology (e.g., fracture or sprain) NEUROLOGIC Poststroke pain syndrome Peripheral neuropathy Postherpetic neuralgia Radiculopathy INFECTIOUS Cellulitis Infectious arthritis PAIN OF UNEXPLAINED ETIOLOGY
VASCULAR Raynauds disease Thromboangiitis obliterans Thrombosis Traumatic vasospasm RHEUMATIC Rheumatoid arthritis Systemic lupus erythematosus PSYCHIATRIC Factitious disorder Hysterical conversion reaction
that measures sympathetic nerve function.448 Sympathetic reactivity was obliterated or diminished in the affected hands of patients with CRPS type I in contrast to agematched controls and normal fracture patterns.448 STAGING OF REFLEX SYMPATHETIC DYSTROPHY RSD has been divided into three stages: acute, dystrophic (ischemic), and atrophic.400, 434, 449 These stages are generally based on chronology, with stage I lasting about 3 months, stage II from 3 to 6 months after the onset of symptoms, and stage III beginning 6 to 9 months after the injury.359 Stages are also determined based on their symptom complexes, with stage I characterized by swelling, edema, increased temperature in the extremity, and pain aggravated by movement. Stage I is associated with hyperpathia (delayed overreaction and aftersensation to a stimulus, particularly a repetitive one), exaggerated pain response, hyperhidrosis, and allodynia (pain elicited by a normally non-noxious stimuli, particularly if repetitive or prolonged).359, 440 Sympathetic blocks may be curative during this stage of RSD. After about 3 months, the initial edema becomes brawny, trophic changes of the skin appear, the joint may become cyanotic, and joint motion decreases in the second stage of RSD. In the third stage, the pain may begin to decrease, trophic changes are more pronounced, edema is less prominent, the skin becomes cooler and drier with a thinning and glossy appearance, and joint stiffness occurs.359 DIAGNOSTIC TESTING The diagnosis of RSD is usually based on clinical ndings. The new criteria for diagnosing RSD do not include the results of diagnostic testing, and the discerning clinician may disagree on the true presence of RSD. Therefore, diagnostic tests probably have less importance in RSD than they did previously. Selected diagnostic tests are discussed. Radiography The early ndings of RSD are patchy demineralization of the epiphyses and short bones of the hand and feet.440 Genant and associates371 dened ve types of bone resorption that may occur in RSD. These are irregular resorption of trabecular bone in the metaphysis, creating the patchy or spotty osteoporosis, subperiosteal bone resorption, intracortical bone resorption, endosteal bone resorption, and surface erosions of subchondral and juxtaarticular bone.371 Other radiographic ndings such as subperiosteal resorption, striation, and tunneling of the cortex may occur but are not diagnostic of RSD and may occur with any condition causing disuse.440 Once patchy osteopenia is present, the patient is usually already in stage II RSD.364, 473 Osteopenia of the patella is the most common nding of RSD of the knee.359 Bone Scanning Three-phase bone scanning with technetium has long been used as a diagnostic study for RSD, with the pervasive notion that scans will be hot in all three phases. Although this may often be the case in phase I or in acute RSD, the
Source: Adapted with permission from Pittman, D.M.; Belgrade, M.J. Am Fam Phys 56(9):22652270, 1997.
CLINICAL PRESENTATION Although the differential diagnosis of RSD is extensive (Table 1815), the diagnosis of orid RSD is not generally difcult.446 However, recognizing milder cases is challenging because of the changing clinical features of this syndrome over time (that is, vasodilatation rst, then vasoconstriction, and nally dystrophic changes), dynamic alterations including diurnal uctuations, and the subjectivity of some of the complaints.446 Nonetheless, the importance of early diagnosis is highlighted by the fact that results of treatment are better if treatment is initiated earlier. Some investigators have prospectively studied whether certain clinical characteristics and laboratory indices correlated with the diagnosis of CRPS type I.446 They found that both the clinically based CRPS I scoring system, which graded allodynia, vasomotor, and swelling, and the laboratory-based CRPS I grading system, which incorporated a sudomotor index, vasomotor index, and a resting sweat index, were sensitive and reliable tools and could be combined to provide an improved set of diagnostic criteria for CRPS I. Oerlemans and associates found that bedside evaluation of CRPS type I with Veldmans criteria was in good accord with psychometric or laboratory testing of these criteria.422 Veldmans criteria are dened as follows: (1) the presence of four or ve of the following signs and symptoms: unexplained diffuse pain, difference in skin color relative to the other limb, diffuse edema, difference in skin temperature relative to the other limb, or limited active range of motion; (2) the occurrence or increase of the above signs and symptoms after use; and (3) the presence of the above signs and symptoms in an area larger than the area of primary injury or operation and including the area distal to the primary injury.466 Schurmann and co-workers studied the incidence of specic clinical features in CRPS type I patients and normal post-traumatic patients and assessed the diagnostic value of a bedside test
467
bone scan ndings in stage II and stage III RSD are more subtle. There are many false-negative bone scan results in stages II and III RSD.439 Raj and associates noted that in stage II RSD the rst two phases of the bone scan are normal and the delayed images (static phase) of the bone scan demonstrate increased activity.439 Stage III RSD has decreased activity in phases one and two and normal activity in the third phase (delayed or static phase).439 Bone scans have been used to assess the response to treatment of RSD and have been found to have no value in monitoring treatment.476 However, these investigators found that the bone scan had prognostic value: marked hyperxation of the tracer indicates better nal outcome. In contrast, a study of quantitative analysis of three-phase scintigraphy concluded that scintigraphy should not be considered as the denitive technique for the diagnosis of RSD.477 Bone Densitometry Bone density measurements may provide a method of determining a quantitative baseline measurement and be able to assess changes over time in RSD.439 Otake and associates measured bone mass by microdensitometry in the follow-up of CRPS and for the evaluation of treatment.428 They found that repeated stellate ganglion blocks did not ameliorate bone atrophy, but the 5-HT2 antagonist sarpogrelate hydrochloride did. Thermography Thermography images temperature distribution of the body surface.440 Gulevich and associates reported on the use of stress infrared telethermography for the diagnosis of CRPS type I and reported that as a diagnostic technique it was both sensitive and specic.376 Further study of thermography is needed before global usage can be recommended.
CURRENT CONCEPTS IN TREATMENT Overview The rst line of treatment of RSD includes nonsteroidal anti-inammatory drugs (NSAIDs), topical capsaicin cream, a low-dose antidepressant, and physical therapy (contrast baths, TENS unit treatments, gentle range of motion to prevent joint contractures, and isometric strengthening exercises to prevent atrophy). Treatment at this time can usually be initiated by the orthopaedic surgeon. However, if the patient fails to respond, then referral to a pain specialist, generally an anesthesiologist with a special interest in pain management, should also be considered. The second line of treatment includes possible sympathetic blocks, anticonvulsants (Neurontin), calcium channel blockers (nifedipine), adrenergic blocking agents (phenoxybenzamine), and antidepressants in higher doses. The third line of treatment includes possible sympathectomy (surgical or chemical), implantable spinal cord stimulators, and corticosteroids. Table 1816 shows the medications commonly used for RSD. Nonsteroidal Anti-inammatory Drugs The possibility that the inammatory response is important in the pathophysiology of RSD466 highlights the role of NSAIDs in treatment. Veldman and associates466 suggested that the early symptoms of RSD are more suggestive of an exaggerated inammatory response to
TABLE 1816
Medications Commonly Used to Treat Reex Sympathetic Dystrophy

Medication ADRENERGIC AGENTS Beta blocker: propranolol (Inderal) Alpha blocker: Phenoxybenzamine (Dibenzyline) Alpha and beta blocker: guanethidine (Ismelin) Alpha agonist: clonidine (Catapres-TTS) CALCIUM CHANNEL BLOCKING AGENT Nifedipine (Adalat, Procardia) DRUGS FOR NEUROPATHIC PAIN Tricyclic antidepressants: Amitriptyline (Elavil) Doxepin (Sinequan) Serotonin reuptake inhibitors: Fluoxetine (Prozac) Anticonvulsant: gabapentin (Neurontin) Corticosteroid: prednisone
Initial Dosage*
40 mg bid 10 mg bid 10 mg/day One 0.1 mg patch/week
PSYCHOLOGIC OR PSYCHIATRIC ASSESSMENT Psychologic assessment of patients with CRPS have included structured clinical interviews and personality measures such as the Minnesota Multiphasic Personality Inventory (MMPI) and Hopelessness Index.440 The MMPI proles of patients with RSD resemble those of patients with chronic pain (increasing elevations on the hypochondriasis, depression, and hysteria scales).440 Patients in stage I RSD have more pessimism than patients in the second and third stages. More pessimism and depression is seen in younger patients with RSD than in older patients.439 Bruehl and Carlson examined the literature for evidence that psychologic factors predispose certain individuals to development of RSD.351 They found that 15 of 20 studies reported the presence of depression, anxiety, and/or life stress in patients with RSD351 and hypothesized a theoretical model in which these factors inuenced the development of RSD through their effects on alphaadrenergic activity. These investigators also noted that they could not determine whether depression, anxiety, and life stress preceded the RSD and were etiologically related to it.
30 mg/day
10 to 25 mg/d 25 mg/d 20 mg/day 300 mg on the rst day, 300 mg bid on the second day, and 300 mg tid thereafter 60 mg per day, then rapidly taper over 23 wk
*The initial dosage may need to be adjusted based on individual circumstances. Consult a drug therapy manual for further information about specic medications. Source: Adapted with modications with permission from Pittman, D.M.; Belgrade, M.J. Am Fam Phys 56(9):22652270, 1997.
468
injury or surgery than a disturbance of the sympathetic nervous system.466 Nonetheless, Sieweke and associates found no effect of an anti-inammatory agent and hypothesized a noninammatory pathogenesis in CRPS that is presumably central in origin.454 Antidepressants Antidepressants are useful in treating RSD primarily by causing sedation, analgesia, and mood elevation. Analgesic action has been attributed to inhibition of serotonin reuptake at nerve terminals of neurons that act to suppress pain transmission, with resulting prolongation of serotonin activity at the receptor.363 Narcotic Analgesics There is a potential for abuse of narcotics in RSD because of the associated chronic pain. These agents do little to relieve sympathetically mediated pain. However, when narcotics are given epidurally in combination with local anesthetic agents, they are very effective. Epidural administration of fentanyl (0.030.05 mg/hr) allows maximum effect on the dorsal horn with minimal plasma concentration and minimal side effects. Anticonvulsants Mellick reported their results of using gabapentin (Neurontin) in patients with severe and refractory RSD pain.412 He noted satisfactory pain relief, early evidence of disease reversal, and even one case of a successful treatment of RSD with gabapentin alone. The specic effects noted included reduced hyperpathia, allodynia, hyperalgesia, and early reversal of skin and soft tissue manifestations. Calcium Channel Blockers (Nifedipine) and Adrenergic Blocking Agents (Phenoxybenzamine) Nifedipine, a calcium channel blocker, has been used orally to treat RSD. At a dosage of 10 to 30 mg thrice daily, it induces peripheral vasodilatation. Initial treatment is usually at a dosage of 10 mg thrice daily for 1 week, which is increased if there is no effect to 20 mg thrice daily for 1 week, which is increased to 30 mg thrice daily the following week if there is no effect. If partial improvement or relief occurs at any of these doses, then the dosage is continued for 2 weeks and then tapered and discontinued over several days.435 The most common side effect of nifedipine is headache, which is most likely due to increased cerebral blood ow. Muizelaar and coworkers418 assessed treatment of both CRPS type I and type II with nifedipine or phenoxybenzamine, or both, in 59 patients. They found a higher success rate using phenoxybenzamine in 11 of 12 patients. A lower success rate was found in treating chronic CRP with a success rate of treatment of 40%. Although long-term oral use of phenoxybenzamine has been reported for the treatment of RSD, there has been a high incidence of orthostatic hypotension (43%).373 In an attempt to avoid these side effects, intravenous regional phenoxybenzamine has been used to treat RSD with good results in a small series of patients.406 Corticosteroids It has been reported that the patients who respond to corticosteroids had chronic pain of a mean duration of 25
weeks.397 Although the use of corticosteroids in the treatment of RSD is much less common, Raj and associates note that a trial of steroids might be a reasonable treatment for patients with long-standing pain who have failed to respond to blocks.440 Physical Therapy Physical therapy has long been an integral part of treatment of type I CRPS. Oerlemans and associates prospectively studied whether physical therapy or occupational therapy could reduce the ultimate impairment rating in patients with RSD and found that physical therapy and occupational therapy did not reduce impairment percentages in patients with RSD.421 Nonetheless, these same investigators have also reported that adjuvant physical therapy in patients with RSD results in a more rapid improvement in an impairment level sum score.420 Electroacupuncture Chan and Chow reported their results with acupuncture with electrical stimulation in 20 patients with features of RSD.353 They found that 70% had marked improvement in pain relief and an additional 20% had further improvement. In addition, at later follow-up reassessment of these patients showed maintenance or continued improvement of their pain relief 3 to 22 months after their course of electroacupuncture.353 There has been a resurgence of interest in electroacupuncture.382, 441 Regional Intravenous and Arterial Blockade The use of intravenous or intra-arterial infusions of ganglionic blocking agents is becoming increasingly popular in the treatment of RSD.440 Guanethidine, bretylium, and reserpine have been used with promising results.440 Guanethidine has been substituted for reserpine in the intravenous regional block format to lessen side effects.440 Sympathetic Blocks Sympathetic blockade has historically been useful both as a diagnostic test (when placebo injections are included and documented temperature elevation after blockade) and a basic treatment. Increasing recognition of the presence of non-sympathetically mediated pain in RSD has contributed to the decreased use of diagnostic sympathetic blockade. A series of injections are generally performed on an outpatient basis. Alternatively, continuous epidural infusions can also be performed on an inpatient basis if the patient is unable or unwilling to have a series of outpatient nerve blocks.360 For upper extremity RSD, the site of blockade is either the stellate ganglion or the brachial plexus. For lower extremity RSD, the lumbar sympathetic chain or epidural space is the preferred site for sympathetic blockade. Transcutaneous Electrical Stimulation Transcutaneous electrical nerve stimulation (TENS) has been useful in the treatment of RSD. It most likely works
469
via the gate theory of pain introduced by Melzack and Wall in 1965 in which stimulation of the larger nerve bers transcutaneously closes the gate and may inhibit the transmission of pain.413 Topical Capsaicin Topical capsaicin cream in concentrations of 0.025% to 0.075%, used previously for postherpetic neuralgia and painful diabetic neuropathy, has been noted to be worth considering for treating localized areas of hyperalgesia.355, 458 The effectiveness of topical capsaicin cream decreases after 3 weeks of daily usage. Chemical Sympathectomy Neurolytic sympathetic block is an alternative for the lower extremity but usually not the upper extremity. The proximity of the cervical sympathetic chain to the brachial plexus makes a cervical neurolytic sympathectomy too hazardous unless placed under uoroscopic or CT guidance. Neurolytic lumbar sympathetic blockade is considered to be a viable alternative to surgical sympathectomy for lower extremity RSD.440 However, there are potential complications in such procedures including dermatologic problems and sympathalgia in the second or third postoperative weeks, which is characterized by muscle fatigue, deep pain, and tenderness.381 Surgical Sympathectomy Surgical sympathetectomy has been advocated for patients who do not get permanent pain relief from blocks and is somewhat of a last resort or end-of-the-road treatment. Criteria have been suggested that should be met before selecting surgical sympathetectomy: patients should have had pain relief from sympathetic blocks on several occasions, pain relief should last as long as the vascular effects of the blocks, placebo injections should produce no pain relief, and secondary gain and psychopathology should be ruled out.440 Failure of surgical sympathectomy has been attributed to reinnervation from the contralateral sympathetic chain.392, 393 Surgical sympathectomy in our opinion is less effective than chemical sympathectomy. Electrical Spinal Cord Stimulation Electrical spinal cord stimulation is generally reserved for patients who have severe pain that is unresponsive to conventional treatments. Kemler and associates retrospectively studied the clinical efcacy and possible adverse effects of electrical spinal cord stimulation for the treatment of patients with RSD.388 About 78% of patients (18 of 23) reported subjective improvement during the test period, and 50% had complications related to the device. Prospective studies are needed to assess the efcacy of spinal cord stimulation. Nontraditional Therapies Certain patients are responsive to nontraditional treatment such as art and music therapy, herbal medicines, and massage therapy. These approaches should be viewed with an open mind because evidence-based therapies may not be successful in relieving pain associated with RSD.
PREVENTION OF REFLEX SYMPATHETIC DYSTROPHY It has been suggested that optimal pain relief after surgery can reduce the incidence of chronic postoperative pain syndromes, such as those that occur in almost 50% of thoracotomies.387 This hypothesis is based on the concept that an abnormally exaggerated and prolonged hyperalgesia reaction is involved in the development of complex post-traumatic syndromes.349 Although the potential for dose escalation and dependency has to be considered, perioperative management of pain with appropriate analgesics appears to help prevent RSD. PROGNOSIS The prognosis of RSD has historically been grim. The assumption has generally been that stage I RSD will progress in most cases to stage II and then to stage III. In addition, the prognosis has also been linked to the time of diagnosis, with early diagnosis having a better prognosis. Zyluk studied the natural history of post-traumatic RSD without treatment and found that the signs and symptoms of RSD were largely gone in 26 of 27 patients who completed the study at 13 months after diagnosis.478 Nonetheless, the hands were still functionally impaired, and three patients who withdrew from the study had worsening of the signs and symptoms of RSD.478 Geertzen and associates studied 65 patients with RSD to analyze the relationship between impairment and disability.369 They found that RSD patients had impairments and perceived disabilities after a mean interval of 5 years.369 Furthermore, these investigators found no differences in impairments in patients who were diagnosed within 2 months of the causative event and those diagnosed 2 to 5 months after it. Nonetheless, there is evidence that the effect of treatment for sympathetically mediated pain is better during the rst few months after onset.349 Cooper and DeLee noted that the most favorable prognostic indicator in the management of RSD of the knee was early diagnosis and early institution of treatment (before 6 months of onset).359
SUMMARY
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz Key for the orthopaedic surgeon is to recognize that the fracture patient may have RSD, distinct from either another undetected condition or inadequately treated pain. Tipoffs to the presence of RSD are inordinate requests for narcotic medicine, inappropriate emergency department visits, and aggressive contacts with the ofce staff. Although RSD takes time to evaluate, it is important to have heightened awareness of it to protect the practitioner if there really is an undetected additional injury (especially in polytrauma patients) and to make the diagnosis of RSD when appropriate to initiate timely treatment and possible referral to a caregiver interested in pain management. RSD should be considered any time that pain is out of proportion to what is expected. In addition, the new International Pain criteria for RSD (type I CRPS) make the diagnosis of RSD easier but less specic. The new terminology appears
470
to make RSD into a constellation of symptoms rather than a distinct disease. New developments in pain management such as the use of intrathecal methylprednisolone for postherpetic neuralgia395 may expand the armamentarium of treatments for post-traumatic RSD in the future.
MANAGEMENT OF COMPLICATIONS
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz In this chapter, a complication of fracture treatment has been dened as an undesired turn of events in the treatment of a fracture. But because patient, doctor, and insurer each bring a different set of values into the assessment of medical outcomes, the question might be asked, Undesired by whom? Patient and doctor, for example, may agree to attempt to salvage a difcult compound tibial fracture with contamination and arterial injury. The insurer, facing charges in excess of a quarter of a million dollars for vascular repair, free ap coverage, fracture xation, bone grafting, and multiple reoperations if infection develops, combined with a prolonged time of total disability before the patient is able to return to work, may regard the outcome as an undesired event when compared with below-the-knee amputation, prosthesis tting, and early return to work. An explicit understanding of the desired course of events is therefore crucial to recognizing complications. In this respect, fracture treatment is different from many other areas of orthopaedics and, indeed, medicine in general for two reasons. First, the goal of treatment, although often unstated, is generally obvious: secure complete functional healing of a broken bone with return to full activity. Second, the patient did not anticipate the injury; therefore, patient education begins at the perioperative visit, and the choice of physician is largely determined by institutional lines of case referral. Also, the patient must adjust to pain, inconvenience, and an unexpected loss of productivity. To make matters more difcult, some accident victims have associated psychopathology that makes communication difcult.486 These patients may be stigmatized as mentally ill, thereby setting the stage for withholding appropriate care. Many fractures with good results of treatment yield permanent disability. A difcult supracondylar fracture of the humerus repaired with an open reduction may have a residual loss of 15 of elbow extension. The result is excellent in terms of present state-of-the-art treatment despite the presence of measurable permanent impairment. The chain of causation that led to this impairment began when the patient fell and landed on the elbow. It is crucial to maintain this link. When the physician does not acknowledge the presence of impairment and, even worse, fails to recognize that the patient is bothered, for example, by a prominent screw that has backed out of an olecranon osteotomy, there is a risk that the patient, or the patients lawyer, will attempt to shorten the chain of causation to the operative event. For many patients, an understanding of the loss sustained in injury and the recognition of the complication by the physician are crucial steps that diffuse a potentially explosive situation and allow the process of
controlling and treating complications to put the matter right. Local complications occurring late in the course of treatment are most often related to disturbances in fracture healing. These may develop insidiously over weeks or months. Often in such cases, the patient is anticipating recovery, and the orthopaedist overlooks a trend toward deformity that, on retrospective viewing of radiographs arranged in sequence, is all too evident. Each fracture has two complementary problems that must be solved: a biologic and a mechanical one. The biologic problem consists of providing the setting for fracture healing. In most simple closed fractures, adequate biologic factors are present so that healing will occur. In high-grade compound fractures, the biologic issue is an important one. Only a few strategies are available to improve biology; these include autogenous bone grafting, electrical stimulation, and free tissue transfer. New techniques harnessing the power of gene therapy to ensure and accelerate future healing will soon be available. Their safety and cost-effectiveness require incisive evidencebased research. The mechanical problem includes the selection of an operative or nonoperative treatment strategy that anticipates the mechanical behavior of a fractured bone and provides an environment that allows biologic processes to heal the fracture. Work by Goodship and associates484 and by Rubin and Lanyon489 have begun to dene the mechanical circumstances favorable to fracture healing. Closed reamed IM nailing works well. Although it destroys marrow content, the enveloping soft tissues are not disturbed, and the biomechanics of fracture site loading are favorable. When the vitality of the tissues surrounding a fracture is compromised, the margin of safety is smaller, and adverse outcomes become more prevalent. In this situation, modication of the method (e.g., by eliminating reaming and using a mechanically stronger but thinner improved implant) may reduce the incidence of complications to an acceptable level. New therapies such as absorbable antibiotic implants, biologic bone glues, implantable proteins that stimulate fracture healing, absorbable fracture xation devices, and gene therapy hold promise for improved results. Database management is at the heart of analyzing complications. Todays information technology explosion provides a tremendous opportunity to improve fracture care information. The data collected must, however, be meaningful. What is put into a database determines what comes out. The standard fracture nomenclature adopted by the Orthopaedic Trauma Association is an attempt to create groupings of similar cases for long-term study. Because the risk-to-benet ratio is at the heart of decision making in fracture treatment and in an era of results analysis, new factors will emerge that will have a powerful inuence on the expenditure of health care resources for fracture care. The categorization of complications will assume great importance.492 A model for fracture treatment must be shaped to ensure that equal weight is given to the long-term outcome of a particular treatment pattern and that the focus is shifted from short-term economic monitors (e.g., days in the hospital,
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readmission within 2 weeks, implant costs), because these factors do not disclose the true socioeconomic morbidity of this disease and the potential lasting impact of local complications of fracture treatment. The insurance industry has a desire to set practice pattern algorithms to predict and control costs. The problem in trying to standardize treatment routines is that algorithms for care of human conditions are based on faulty assumptions.490 Despite the appearance of systematization in todays microprocessorproduced output, practice patterns are dependent on human variables, and the treatment of broken limbs remains an art as well as a science.
MISSED INJURIES Missed injuries are reported in 2% to 9% of patients with multiple injuries.480, 482, 483, 487, 491 The majority of these injuries are musculoskeletal injuries. In one series, Buduhan and McRitchie reported that 54% of the injuries were musculoskeletal and 14.3% affected the peripheral nerves (14.3%) (Fig. 1812).482 They noted that patients with missed injuries tend to be more severely injured and to have initial neurologic compromise. Buduhan and McRitchie reported that in 46 of 567 (8.1%) injuries, 43.8% were unavoidable.482 Born and associates in 1989 reported a delay in diagnosis of musculoskeletal injuries in 26 of 1006 consecutive blunt trauma patients and a total of 39 fractures with a delay in diagnosis.480 The most common reason for the delay in diagnosis was a lack of radiographs at admission. Enderson and associates in 1990483 reported that a tertiary survey was able to nd additional injuries in patients who had already undergone primary and secondary trauma surveys and that the use of the tertiary survey found a higher percentage of injuries (9%) then the 2% incidence in their trauma registry. These investigators noted that the most common reason that injuries were missed was altered level of consciousness due to head injury or alcohol. Ward and Nunley in 1991 reported that 6% (24 of 111) of orthopaedic injuries were not initially diagnosed in 111 multitrauma patients.491 Seventy percent of occult bony injuries were ultimately diagnosed by physical examination and plain radiographs alone. Risk factors for occult orthopaedic injuries were (1) signicant multisystem trauma with another more apparent orthopaedic injury within the same extremity, (2) trauma victim too unstable for full initial orthopaedic evaluation, (3) altered sensorium, (4) hastily applied splint obscuring a less apparent injury, (5) poor quality or inadequate initial radiographs, and (6) inadequate significance assigned to minor sign or symptoms in a major trauma victim. These investigators noted that all orthopaedic injuries cannot be diagnosed on initial patient evaluation. Spine injuries are a subgroup of injuries that are frequently diagnosed late. In 1996 Anderson and coworkers noted that in 43 of 181 patients with major thoracolumbar spine fractures, there was a delay in diagnosis.479 This delay in diagnosis was associated with an unstable patient condition that necessitates higherpriority procedures than emergency department thoracolumbar spine radiographs. Lumbar transverse process fractures have also been reported to be associated with
Risk Management
No discussion about complications would be complete without reviewing the risks and medicolegal implications of complications. Many complications result in a degree of permanence, whether it is pain, decreased range of motion, or muscle weakness. The mere existence of a complication potentially fullls the criterion that there were damages, one of the triad of criteria for medical malpractice. Malpractice is simply dened as an event in violation of the standard of care that causes damages. Rogal noted that a theory of fault can be created for any adverse outcome that occurs while a person is under a physicians care.488 A bad outcome after surgery itself is associated with the risk of a lawsuit.481 There are several reasons why orthopaedic surgeons are near the top of the list in the number of malpractice claims.488 The work of the orthopaedist is often visible on a radiograph.488 Because of the emphasis on radiographic cosmesis, fracture surgery is particularly susceptible to scrutiny by anyone. These factors, coupled with the fact that fracture surgery can rarely be performed perfectly, makes fracture surgery a target for malpractice allegations. Rogal also notes that many orthopaedic injuries are irreconcilable and cites the example of a decimated articular surface, which is coupled with the public perception that modern technology can return any injury back to normal.488 He also noted that in many situations time is of the essence (e.g., neurovascular compromise, compartment syndrome), and he states that lawsuits are often spawned when care is delayed even if the outcome is minimally adverse. Related to this last scenario, is the unique entity in orthopaedic traumatology of the missed injury.
FIGURE 1812. Pie diagram of the types of missed injuries in patients with multiple trauma, which demonstrates that the majority of missed injuries are musculoskeletal. (From Buduhan, G.; McRitchie, D.I. Missed injuries in patients with multiple trauma. J Trauma 49:600605, 2000 with permission.)
Print Graphic
Presentation
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signicant lumbar spine fractures in 11% of cases and can be easily missed if CT scanning is not used in addition to plain radiographs.485 DOCUMENTATION OF COMPLICATIONS Several factors should be considered in documentation. One key point is documenting the precise date that the complication was discussed with the patient. Common sense and tact are critical in these discussions. It may be more difcult to have these discussions in major teaching hospitals, in which the patient and family are seeing the resident physicians daily and the attending physician less frequently. Axiomatic in discussing complications with patients and their families is avoidance of self-blame. In a legal context, statements such as I wish we had done it differently have the force of a confession and are known as admissions. The complication needs to be disclosed but not adopted. The mere presence of a complication may place the physician at risk for litigation, because the more disabling the outcome of injury, the higher the chance of an accusation of medical malpractice.481 When multiple services are caring for a trauma patient, delineation of responsibility in the medical record is important. It may not be clear to the patient or to the family which service is responsible for what aspect of the patients care. For example, the patient might assume that the orthopaedic trauma service is responsible for metacarpal fractures when in fact there is a separate hand surgery service. Nevertheless, a team approach that presents a united front is important, because there are often multiple services taking care of these patients. Another signicant development is the need to satisfy Health Care Financing Administration compliance issues for billing in the medical record by documenting that the attending physician was present at surgery for the key and critical parts of the operation. The patient, who subsequently acquires a copy of the medical record, will then know for which part of the surgery the attending physician was present. If any complications arose intraoperatively, particularly if the attending physician was not present for that part of the operation, the situation may become a medicolegal nightmare. A clarifying discussion with the patient and family should include the fact that many hands are needed to treat broken bones. Documenting systems problems is another potential challenge for the orthopaedic traumatologist. Dening such issues in the medical record, for example that the surgery was delayed an additional 2 days because no operating room time was available, can be risky for the physician. Often, from the patients and the patients attorneys perspective, the physician and the institution are inextricably linked, even when the physician is an independent contractor. Furthermore, there is tremendous pressure for physicians to support and not to criticize the institution in which they work. The survival of orthopaedic trauma as a eld depends on our skill in negotiating outside of the patient record a good environment for musculoskeletal care.
SUMMARY
zzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzzz This chapter has dened complications of fracture treatment and presented specic information about three important systemic disturbancesfat embolism syndrome, thromboembolic disorders, and multiple system organ dysfunction and failurethat can result from broken bones. In addition, a framework for approaching fracture-specic complicationssoft tissue and vascular problems, post-traumatic arthrosis, peripheral nerve injury, and RSDwas presented. Lastly, strategies for realistically managing complications were suggested. Complications, such as missed injuries, are intrinsic to fracture care and are a part of the natural history of fractures rather than markers that something went wrong. In the nal analysis, the management of complications begins with understanding the scientic basis for the treatment of injury, listening to what the patient is telling us, and accepting the fact that we as fracture surgeons cannot avoid adverse circumstances.
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457.
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482
SECTION I General Principles 488. Rogal, M.J. Comment: Orthopaedic malpracticeIdentifying and managing the high risk of orthopaedic surgery. Pitt Orthop J 11:242243, 2000. 489. Rubin, C.T.; Lanyon, L.E. Regulation of bone formation by applied dynamic loads. J Bone Joint Surg Am 66:397402, 1984. 490. Sadler, C. Pitfalls in the use of clinical algorithms. Orthop Clin North Am 17:545547, 1986. 491. Ward, W.G.; Nunley, J.A. Occult orthopaedic trauma in the multiply injured patient. J Orthop Trauma 5:308312, 1991. 492. Wiesel, S.W.; Michelson, L.D. Monitoring orthopedic patients using computerized algorithms. Orthop Clin North Am 17:541544, 1986.
484. Goodship, A.E.; Lanyon, L.E.; McFie, H. Functional adaptation of bone to increased stress. J Bone Joint Surg Am 61:539546, 1979. 485. Krueger, M.A.; Green, D.A.; Hoyt, D.; Garn, S.R. Overlooked spine injuries associated with lumbar transverse process fractures. Clin Orthop Rel Res 327:191195, 1996. 486. Kuhn, W.F Laceeld, P.K. Patient, surgeon, nurse: The psycholog.; ical impact of fracture treatment. In: Seligson, D., ed. Concepts in Intramedullary Nailing. New York, Grune & Stratton, 1985, pp. 187197. 487. Laaasonen, E.M.; Kivioj, A. Delayed diagnosis of extremity injuries in patients with multiple injuries. J Trauma 31:257260, 1991.

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SYSTEMIC COMPLICATIONS Fat Embolism Syndrome

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SECTION I General Principles TABLE 181

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CHAPTER 18 Diagnosis and Treatment of Complications

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SECTION I General Principles

Copyright 2003 Elsevier Science (USA). All rights reserved.

CHAPTER 18 Diagnosis and Treatment of Complications

Copyright 2003 Elsevier Science (USA). All rights reserved.

SECTION I General Principles

Copyright 2003 Elsevier Science (USA). All rights reserved.

CHAPTER 18 Diagnosis and Treatment of Complications

Copyright 2003 Elsevier Science (USA). All rights reserved.

SECTION I General Principles

Copyright 2003 Elsevier Science (USA). All rights reserved.

CHAPTER 18 Diagnosis and Treatment of Complications

Copyright 2003 Elsevier Science (USA). All rights reserved.

SECTION I General Principles

Copyright 2003 Elsevier Science (USA). All rights reserved.

CHAPTER 18 Diagnosis and Treatment of Complications

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SECTION I General Principles

Recommendations for Anticoagulation

Algorithm for Antithromboembolic Prophylaxis in Trauma Patients

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CHAPTER 18 Diagnosis and Treatment of Complications

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SECTION I General Principles

Multiple Organ System Dysfunction and Failure

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CHAPTER 18 Diagnosis and Treatment of Complications TABLE 184

Criteria for Organ Dysfunction and Failure

Denition of Organ Failure Based on Fry Criteria

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SECTION I General Principles

Potential Mediators Involved in the Pathogenesis of Multiple Organ Failure

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CHAPTER 18 Diagnosis and Treatment of Complications TABLE 187

Risk Stratication for Postinjury Multiple System Organ Failure

Prevention of Multiple Organ Failure

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SECTION I General Principles

Malnutrition Altered microflora Gut Disuse Ischemic injury

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CHAPTER 18 Diagnosis and Treatment of Complications

LOCAL COMPLICATIONS OF FRACTURES

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SECTION I General Principles

Soft Tissue and Vascular Problems

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CHAPTER 18 Diagnosis and Treatment of Complications

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SECTION I General Principles

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CHAPTER 18 Diagnosis and Treatment of Complications

Incidence of Post-traumatic Arthritis

Supracondylar/Intercondylar Femur Fractures Patella Fractures Tibial Plateau Fractures

SECTION I General Principles TABLE 1810

Types of Peripheral Nerve Injuries

Peripheral Nerve Injuries