AUTHORS
Lauren Titone, MD, Assistant Professor of Emergency Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, NY
Reena Sheth, MD, Resident Physician in Emergency Medicine, New York-Presbyterian Columbia & Cornell, New York, NY
PEER REVIEWER
Steven Winograd, MD, FACEP, Attending Emergency Physician, Trinity, Samaritan Hospital, Troy, NY
EXECUTIVE SUMMARY
- Perform neurovascular assessment before and after manipulation of the fracture.
- Immobilize open fractures, remove loose foreign bodies, and perform copious low-pressure irrigation with sterile saline followed by a saline-soaked gauze dressing.
- Administer parenteral antibiotics for open fractures based on the extent of the soft tissue injury and degree and source of contamination.
- Fractures that are associated with a higher risk of neurovascular injury include humeral shaft, supracondylar, radial, ulnar acetabulum, femur, tibia, and fibula.
- Primary repair of sharp nerve transections typically is performed three to seven days after the injury.
- Acute compartment syndrome is a clinical diagnosis suggested by the presence of pain out of proportion to the visible injury and supported by measurement of compartment pressure.
- The symptoms and signs of fat embolism typically manifest 24 to 72 hours after injury and most often affect the lungs, skin, and brain.
- There is mixed information regarding the management of fracture blisters, but most sources recommend leaving them intact to minimize the infection risk.
- Up to 25% of open fractures will develop post-traumatic osteomyelitis.
- Up to 10% of fractures will fail to heal appropriately.
- Chronic fracture-related pain is common in lower extremity injuries, seen in 55% to 60% of knee, tibia, and ankle fractures.
Fractures commonly are encountered in the emergency department (ED), with an annual incidence of nearly 200 million patients.1 As the average life expectancy continues to increase, there is a simultaneous increase in the prevalence of osteoporosis and, therefore, an increasing incidence of fractures.2
Management of long-bone fractures and their complications often is dependent on the fracture pattern. Fractures may be characterized by their location, orientation, displacement, angulation, and epiphyseal involvement (for pediatric patients).3 Following a fracture, the osseous healing process is broken down into formation of a hematoma, granulation tissue, and bony callus, ultimately followed by bony remodeling. This process is contingent upon the mechanical and biological environment of the fracture and, therefore, adequate blood supply, structural alignment, and stability must be maintained for appropriate healing to take place.4
Many fractures diagnosed in the ED can be managed with immobilization, reduction, and outpatient orthopedic care. However, there are a range of complications and sequelae that are important because they may result in recurrent ED visits, increased morbidity and mortality, and financial burden. The goal of this review is to familiarize emergency physicians with the initial assessment of fractures as well as the identification and management of immediate, early, and late-stage fracture complications. (See Table 1.)
Table 1. Timeline of Common Fracture-Related Complications |
||
Immediate (minutes to hours) |
Early (hours to days) |
Delayed (weeks to years) |
|
|
|
Initial Assessment
History and Physical Exam
Standard evaluation of all patients presenting with musculoskeletal injury or suspected fracture in the ED includes a thorough history and physical examination. The physical exam includes inspection, palpation, assessment of motor function, and a neurovascular assessment.3,5 First, inspect the affected extremity for signs of open wounds, skin breakdown, discoloration, and obvious deformity. Then, systematically palpate the injured area to identify areas of point tenderness, deformity, or tense compartments. Assess active range of motion to determine potential joint involvement but defer testing passive range of motion to avoid exacerbating potential fracture or neurovascular injury.5
Lastly, the neurovascular examination is critical because a missed injury could lead to loss of life or limb. Symptoms that are concerning for neurovascular injury can range from mild paresthesias or weakness to severe pain and complete loss of sensation or motor function. Mottling, pallor, edema, coolness to touch, weak or absent distal pulses, and slow capillary refill (> 2-3 sec) raises suspicion for vascular compromise. Diminished sensation, range of motion, and/or strength should prompt consideration of a nerve injury. Test sensorimotor function in the distribution of the associated peripheral nerves. Assess median, ulnar, and radial nerve function for upper extremity injuries, and saphenous, peroneal, and tibial nerve function for lower extremity injuries.3
Pain Control
Analgesia options include oral or intravenous (IV) nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, or opiates. Some orthopedic specialists may prefer to avoid NSAIDs since there may be an association with an increased risk of nonunion. However, evidence regarding the association between NSAID use and nonunion is conflicting, and their use for fracture-related pain should be determined based on local practice culture.6,7 Regional anesthesia is a useful adjunct for acute pain management or to facilitate interventions, and it may be of particular benefit in the elderly population or patients for whom the risk of opiates may not outweigh the benefits.8 (See Table 2.) For significant manipulation of fractures, procedural sedation may be required.
Table 2. Regional Anesthesia for Long Bone Fractures |
||
Location |
Fracture Type |
Nerve Block |
Upper Extremity |
Proximal humerus |
Interscalene |
Humeral shaft |
Infraclavicular |
|
Distal humerus |
Supraclavicular Infraclavicular |
|
Forearm |
||
Lower Extremity |
Hip |
Fascia Iliaca Femoral nerve |
Femoral shaft or distal femur |
Femoral nerve |
|
Tibia or fibula |
Sciatic nerve Popliteal nerve |
|
Distal tibia or fibula, foot |
Sciatic nerve Popliteal nerve Saphenous nerve |
|
Adapted from Fisher ND, Bi AS, Umeh UO, et al. Regional anesthesia for acute and subacute orthopedic trauma: A review. Health Sciences Review 2022. |
||
Diagnosis
Diagnosis of fractures most commonly is made with multi-view plain radiography, but non-contrast computed tomography (CT), CT angiography, or magnetic resonance imaging (MRI) can be useful for better characterizing fractures and damage to surrounding structures. While imaging is useful for initial diagnosis of fractures, identification of fracture complications in the ED is largely reliant upon the physical exam.3
Serial Assessments
Document a baseline examination (including motor, sensory, and vascular components) so that any subsequent changes in clinical status can be identified. Perform and document serial exams if the patient remains in the ED setting for a prolonged period or before and after any interventions, such as reduction or splinting. While some fracture complications may be apparent immediately on initial ED evaluation, some complications are delayed or may be the result of manipulation of the extremity.3
Immediate Complications
Open Fractures
An open fracture is defined by a fracture that disrupts the overlying skin and soft tissue, thus creating a conduit between the environment and osseous structures.9 Such fractures are at high risk for infection, ranging from cellulitis to osteomyelitis. They typically are caused by high-velocity trauma and, therefore, often are associated with vascular, nerve, and soft tissue injury.
Open fractures may be categorized based on Gustilo-Anderson criteria. Gustilo-Anderson Type I involves a minimally contaminated, < 1 cm wound. Type II includes wounds > 1 cm, moderate contamination, or moderately comminuted fractures. Type III includes wounds with significant contamination, soft tissue loss, or damage to surrounding structures, and can be further categorized into three subgroups. Type IIIA fractures have extensive damage and contamination but adequate soft tissue coverage. Type IIIB fractures have extensive soft tissue damage with exposed bone and/or periosteal stripping. Type IIIC fractures have associated arterial injury, which requires operative repair.9-11
Initial management of open fractures is focused on resuscitation and standard Advanced Trauma Life Support (ATLS) protocols. Once the patient is stabilized, immobilize the fracture and carefully inspect the wound to evaluate for foreign bodies. Plain radiographs typically are sufficient for characterizing the fracture and may be able to identify any radio-opaque foreign bodies. For patients who are stable, CT and CT angiography can aid in better characterizing the injury.9 Non-contrast CT is useful for better visualization of the fracture and extent of soft tissue damage, while CT angiography helps identify vascular injury.
Open fractures require early irrigation and debridement to reduce the incidence of infection.12,13 Since debridement often occurs in the operating room, involve the orthopedic specialist early to facilitate surgical planning. In the ED, perform a thorough, low-pressure irrigation with sterile saline early in the clinical course. Sterile saline is the most commonly cited solution for irrigation and has demonstrated improved outcomes when compared to antiseptic or soap-based solutions, but there remains some debate regarding the ideal irrigation solution, volume, and pressure.12-14 Dress the wound in saline-soaked gauze to prevent further contamination.9
In addition to standard immobilization, administer tetanus prophylaxis and antibiotics to all patients with open fractures early in their clinical course. (See Table 3.) Standard antibiotic coverage for open fractures should cover gram-positive organisms, and early generation cephalosporins such as cefazolin are typical first-line agents. More extensive soft tissue injury (Gustilo-Anderson Type III) may prompt additional antibiotics for gram-negative coverage, with some guidelines recommending administration of gentamicin in addition to a first-generation cephalosporin, such as cefazolin.9,12,14 The presence of fecal or soil contamination requires anaerobic coverage of Clostridium sp. with metronidazole, high-dose penicillin, or clindamycin. Water contamination is treated with piperacillin-tazobactam for Pseudomonas coverage, with the addition of doxycycline for saltwater contamination to cover Vibrio sp.9,14
Table 3. Antimicrobial Coverage for Open Fractures Based on Gustilo-Anderson Type |
|||
Type |
Description |
Associated Microorganisms |
First-Line Antibiotic |
I |
|
Gram-positive (Staphylococcus and Streptococcus sp.) |
Cefazolin |
II |
|
Gram-positive (Staphylococcus and Streptococcus sp.) |
Cefazolin |
IIIA |
|
Gram-positive + gram-negative |
Cefazolin + gentamicin OR ceftriaxone (monotherapy) |
IIIB |
|
||
IIIC |
|
||
Soil contamination |
Anaerobes (i.e., Clostridium sp.) |
Cefazolin + gentamicin + metronidazole OR ceftriaxone + metronidazole |
|
Fresh water contamination |
Gram-negative (including Pseudomonas, Aeromonas) |
Piperacillin-tazobactam |
|
Saltwater contamination |
Gram-negative (including Vibrio sp.) |
Piperacillin-tazobactam + doxycycline |
|
Vascular Injury
Fracture-related vascular injuries can lead to life-threatening hemorrhage, significant morbidity, and/or loss of limb.15 Penetrating injuries, open fractures, or significant osseous displacement can cause laceration or traction of arteries, thus prohibiting adequate perfusion to the distal extremity. This can lead to limb ischemia, reperfusion syndrome, poor bone healing, or pseudo-aneurysm formation.
Depending on the location of a fracture, blood loss from associated vascular injury can range from 150 mL to
3,000 mL.16,17 Femur and pelvis fractures most commonly are associated with hemodynamically significant bleeding. For fractures with vascular injury and active extravasation, immediate management requires hemorrhage control, resuscitation, and correction of any possible bleeding diathesis. For open fractures with extravasation, direct pressure or tourniquets may be used.18 In the prehospital or acute resuscitation setting, traction splinting devices may be used to help tamponade bleeding associated with femoral shaft fractures, although there is some evidence that suggests traction devices are of limited benefit.17,19,20
Immediately reduce and immobilize any obvious deformity if there is concern for a perfusion deficit secondary to fracture displacement, even if imaging has not yet been performed.18 In these cases, emergent orthopedic and/or vascular surgery evaluation is necessary, even if clinical status improves after reduction.3
It is important to note that absence of circulatory deficits on physical examination does not rule out vascular injury. Open fractures or fractures involving the elbow, knee, and tibia are at higher risk of causing vascular compromise.15,21 Consider CT angiography of the affected limb in patients with an intact neurovascular physical exam but a high-risk fracture or mechanism of injury.18 Have a low threshold to discuss the case with an orthopedist if vascular injury is suspected. If left untreated, arterial injury can lead to tissue ischemia and limb loss.21
Nerve Injury
Peripheral nerve injury (PNI) associated with fractures may occur as an acute complication caused by direct injury or as an iatrogenic complication caused by immobilization or reduction. Penetrating or open injuries and displaced fractures are at higher risk for nerve damage.22 Direct injury ranges in severity from contusion or compression (neurapraxia) to transection (neurotmesis). In neurapraxia, the nerve structure remains intact, but there is focal demyelination causing local disruption of nerve impulses. Axonotmesis is more severe than neurapraxia, often caused by crush or traction injuries, and causes variable degrees of disruption of the axon and myelin sheath, but the epineurium remains intact. Neurotmesis is the most severe type of PNI and causes complete transection of the endoneurium, perineurium, and epineurium. The prognosis for neurotmesis is poor without surgical intervention, so close outpatient follow-up with orthopedics is required.23,24
Certain fractures are at higher likelihood of causing neurovascular compromise. For example, there is an association between humeral shaft fractures and radial nerve injury.25,26 Supracondylar, radial, and ulnar fractures are associated with median nerve injury. For the lower extremities, acetabulum, femur, tibial, and fibular fractures are associated with sciatic, femoral, tibial, and peroneal nerve injury, respectively. (See Table 4.)
Table 4. Common Fractures and Associated Nerve Injury |
|||
Fracture Type |
Associated Nerve Injury |
Motor Deficit |
Sensory Deficit |
Proximal humerus |
Axillary |
Deltoid abduction |
Deltoid, proximal arm |
Humeral shaft |
Radial |
Wrist dorsiflexion (wrist drop) |
Posterior arm, forearm, and dorsal aspect of first 3.5 digits |
Supracondylar humerus |
Anterior interosseous |
Paralysis or paresis of index finger flexor digitorum profundus, flexor pollicis longus, and/or pronator quadratus (inability to make “OK” sign) |
N/A |
Distal radius |
Median |
Contraction of lumbrical muscles and flexor digitorum superficialis (digit flexion and opposition) |
Palmar aspect of first 3.5 digits |
Femur |
Femoral |
Hip flexion, abduction, and adduction; knee extension |
Anteromedial thigh, medial leg, and foot |
Proximal fibula |
Peroneal |
Ankle dorsiflexion (foot drop) |
Anterolateral leg, dorsum of foot |
Identification of possible nerve injury in the ED is accomplished most commonly via the physical exam. Electromyography (EMG) or nerve conduction studies are the most accurate means of characterizing nerve injury, but they typically are not available in the ED.26 There is some evidence that ultrasound may be useful in the acute setting for characterizing PNI.26-28
For closed fractures with localized PNI, conservative management with splinting and physical therapy is appropriate.24 Perform a motor and sensory examination after splinting and immobilization and document any persistent deficits. If there are persistent neurologic deficits despite appropriate repositioning and splinting, orthopedic consultation in the ED is warranted. New deficits noted after immobilization may be due to iatrogenic traction or compression caused by the splint or positioning.3
The prognosis is favorable for neurapraxia, and normal function typically will return in weeks to months. However, if there is no recovery three to six months after the initial injury, surgical exploration with intraoperative measurement of nerve action potentials may be indicated.26,29 Neurotmesis will not improve without surgical intervention.30
Primary surgical nerve repair for sharp transections typically occurs within three to seven days of the injury, whereas delayed repair may be appropriate for blunt transections. Sharp transections have a better prognosis compared to those from blunt trauma.24 Because there is considerable variation in the preferred timing of operative intervention for PNI between orthopedic specialists, orthopedic consultation is useful for patients who present to the ED with fractures and associated motor or sensory changes that do not resolve with splinting.3
Even with appropriate surgical correction, neurotmesis can lead to neuroma formation and/or chronic pain syndromes, which are discussed later.30 In such cases, referral to a pain management specialist and neuropathic pain medications (such as gabapentin) may be helpful.
Early Complications
Compartment Syndrome
Hours to days after a fracture, soft tissue swelling and extravasation of blood into surrounding tissue may cause increased pressure within fascial compartments, resulting in progressive compression of neurovascular structures. As swelling increases, there is progressive collapse of vasculature, which subsequently worsens edema and further increases intracompartmental pressures. The presence of splinting material may iatrogenically cause increased compartment pressures if there is insufficient space to accommodate soft tissue swelling. Over time, this process can lead to ischemia, necrosis, and peripheral nerve damage, collectively referred to as acute compartment syndrome (ACS).31,32 ACS is a surgical emergency, and early diagnosis is paramount to salvaging the limb.
Pain typically is the first finding that manifests in ACS, and physical examination may reveal a tense or swollen compartment. However, these findings are unreliable, with poor sensitivity, and, therefore, cannot be used to exclude compartment syndrome. The presence of pain is 19% sensitive for detecting ACS, and clinicians’ ability to detect ACS via palpation of an affected compartment is only 25% sensitive.33,34 Classically taught findings, such as pallor, paresthesias, diminished or absent pulses, poikilothermia, and weakness, are late findings, and their presence suggests that irreversible damage already has occurred. Because history and physical exam cannot reliably confirm or exclude compartment syndrome, maintain a high index of suspicion when patients present with disproportionate pain, swelling, or higher-risk fractures.31 The anterior compartment of the distal lower extremity is the most commonly affected compartment and frequently is associated with tibial plateau fractures. In the upper extremity, the volar compartment of the forearm is most associated with ACS, often in the setting of distal radius fractures or diaphyseal forearm fractures.31,35-37
The diagnosis of ACS is supported by direct measurement of intra-compartmental pressures within 5 cm of the fracture site. This can be accomplished with a commercial device or arterial line setup.36 Commercial compartment manometers commonly consist of a needle connected to a diaphragm chamber and syringe. Once the device is calibrated per the manufacturer, insert the needle 1 cm to 3 cm into the compartment and slowly inject 3 mL of sterile saline. The device subsequently will produce a pressure reading. Continuous measurement of compartment pressure can be obtained by connecting a catheter to an arterial line transducer.33,37
Normal compartment pressure is less than 9 mmHg. A pressure measurement of greater than 30 mmHg can support a diagnosis of compartment syndrome, but ultimately the diagnosis is determined based on the delta pressure (also known as the compartment perfusion pressure).36 Delta pressure is the difference between diastolic arterial blood pressure measured by a sphygmomanometer and the compartment pressure. A delta pressure less than 30 mmHg is indicative of compartment syndrome and requires emergent evaluation for a surgical intervention.32,38 While the delta pressure is the current diagnostic standard, it is prone to false-positive readings, which may lead to unnecessary invasive treatments.39 Therefore, some guidelines recommend a delta pressure threshold of 20 mmHg, since this is associated with a lower false-positive rate.40
It is important to note that early during ACS, the compartment pressure may be elevated, or delta pressure may be reduced but not yet meet the criteria for diagnosis of compartment pressure. For patients who fall into this intermediate category, inpatient compartment pressure monitoring may be appropriate if there are high-risk features and concern for progression of the compartment swelling.41
Fasciotomy is the mainstay treatment of ACS. There is debate over optimal timing of fasciotomy, but for the purposes of emergency physicians, early consultation with the surgical service is critical. If required, initiate transfer to a center with adequate surgical capabilities early in the clinical course since delayed fasciotomy (> 6 hours after onset) is unlikely to be beneficial since irreversible tissue damage already has occurred. Delayed fasciotomy also is associated with a greater risk of subsequent infection.42-44
Fat Embolism Syndrome
Fat embolism syndrome is a rare but potentially life-threatening sequela of long bone fractures. Most patients with orthopedic trauma will have fat particles released into their circulation from the fracture site.45 These fat globules may embolize into the pulmonary circulation and cause transient hypoxemia. However, fat embolism syndrome (FES) is much less common and is defined by dissemination of fat globules in microcirculation, which then causes a systemic inflammatory response and subsequent multi-organ damage.45 The inflammatory response is thought to be mediated by endothelial damage caused by free fatty acids.46
The exact incidence of FES after long bone fracture is unknown but suspected to be less than 20% depending on the source.46,47 While any long bone fracture can cause FES, femur fractures are most commonly implicated. Pathological fractures have a higher incidence of FES when compared to traumatic fractures. Unsurprisingly, bilateral femur fractures have a higher incidence compared to unilateral fractures.46 Tibiofibular fractures are the second most common etiology of fracture-related FES.48
Symptoms of FES typically manifest between 24 and 72 hours after the initial injury.47 The lungs, skin, and brain are affected most commonly, thus resulting in the classic triad of respiratory distress, petechial rash, and neurologic dysfunction.49 Respiratory findings, such as shortness of breath or hypoxia, are likely to manifest early. Although the classic triad is common, any number of organ systems may be involved, including the heart, kidneys, eyes, and liver. Metabolic and hematologic dysfunction also may occur.47,49
There are several proposed diagnostic criteria for FES, including the Gurd and Wilson’s criteria, Schonfeld scoring system, and Lindeque criteria. However, none of these scoring systems have been prospectively validated, so FES remains primarily a clinical diagnosis.45 Of note, the respiratory dysfunction associated with FES is indistinguishable from acute respiratory distress syndrome (ARDS).
There is no clear consensus on definitive management and prevention of FES. Regarding prevention, there is some evidence that corticosteroids have a role in reducing the incidence of FES, but this effect is not consistently replicated in studies and there is a dearth of methodologically sound data.50
For the purposes of the emergency physician, FES is less likely to be encountered in the ED setting compared to other fracture-related complications, given the typical time of onset. However, there are case reports of FES occurring as early as one hour after initial injury, so maintain a high index of suspicion if concerning symptoms arise.51 Similar to other systemic inflammatory syndromes, treatment primarily is supportive care, including resuscitation with fluids, blood products, vasoactive medications, and mechanical ventilation if needed.49 As fat globules embolize into the lungs, subsequent right ventricular failure may be precipitated, and inotropic support may be required.45
Fracture Blisters
When disrupted, skin and soft tissue overlying fracture sites can form blisters. Fracture blisters typically will form one to two days after the initial injury but may occur as early as six hours after sustaining a fracture.52 They are thought to be the result of a disrupted dermo-epidermal junction and in part mediated by edema and local tissue hypoxia. Blisters may be serous or hemorrhagic, with hemorrhagic blisters representing more significant soft tissue injury.52 The ankle, wrist, elbow, and distal tibia are at higher risk of developing fracture blisters since there is less underlying subcutaneous tissue.52,53
There is some mixed information regarding management of fracture blisters, but most sources recommend leaving blisters intact to minimize infection risk.52-54 Early surgical intervention has been shown to minimize blister formation. The use of antibiotics has not been shown to be beneficial and is not routinely recommended.55 If they are present prior to surgical management, blisters may further delay orthopedic intervention, since incising through the blister bed poses a risk of postoperative infection.52
When discharging a patient with fractures involving areas at higher risk of developing a fracture blister (ankle, wrist, elbow), patients should be instructed to return for evaluation if blistering develops. Ensure close follow-up for patients with comorbidities that predispose to poor wound healing, since they are at higher risk of blister formation.52
Venous Thromboembolism
Venous thromboembolism (VTE) confers significant morbidity and mortality for patients who have sustained orthopedic trauma. The inflammation, extremity immobilization, and weight-bearing limitations work synergistically to increase the risk of deep venous thrombosis (DVT) formation.56 VTE can develop days to months after an orthopedic injury.57
Hospitalized patients typically will receive VTE prophylaxis with low molecular weight heparin or sequential compression devices, but VTE still may occur despite adequate preventive measures.58,59 Some orthopedists may choose aspirin for VTE prophylaxis, and there are data that suggest that aspirin is noninferior to low molecular weight heparin.60 VTE prophylaxis is not typically administered for patients with minor fractures who are not hospitalized, but it is important to note that these patients still are at increased risk of VTE.54 Maintain a high index of suspicion for patients with recent orthopedic trauma who present with even subtle signs or symptoms of VTE. Doppler ultrasound, D-dimer, or CT angiography may be used to facilitate diagnosis.
Delayed Complications
Osteomyelitis
Post-traumatic osteomyelitis (PTO) may occur weeks to years after open fractures or surgical management of acute fractures.61 Up to 25% of open fractures subsequently will develop osteomyelitis, therefore PTO should remain high on the differential in any patient with concerning symptoms and a history of fracture-related soft tissue injury.62 Staphylococcus aureus species are identified most frequently as the causative pathogen, followed by anaerobes and gram-negative bacilli.62 Bacterial pathogens are able to penetrate bone and proliferate in the anaerobic environment for years, resulting in chronic or relapsing osteomyelitis.63
The diagnosis of PTO in the ED can be difficult since it often presents with gradual onset of nonspecific symptoms. Clinical features include pain, edema, erythema, and drainage at the site of prior fracture or surgery.63 MRI and CT may be considered to support a diagnosis of PTO, but they may have limited accuracy.61,64 Inflammatory markers, such as a white blood cell count (WBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP), have some diagnostic utility.
The treatment of PTO includes systemic and/or local antibiotics as well as surgical debridement.63-65 For patients with symptoms of chronic osteomyelitis, without systemic signs of infection or hemodynamic instability, close outpatient orthopedic follow-up typically is appropriate. Systemic signs of infection, osseous instability, or presence of hardware warrants immediate discussion with an orthopedist. Patients likely will require admission, initiation of IV antibiotics, and surgical management. When possible, the systemic antibiotic regimen should be delayed so that it may be tailored to cultures from bone debridement or biopsy.65 However, if the patient is unstable or demonstrating systemic signs of infection, antibiotics should not be delayed, and ED administration is indicated prior to obtaining cultures. Empiric therapy consists of vancomycin and a third- or fourth-generation cephalosporin.65
Nonunion
Up to 10% of fractures will fail to heal appropriately.66,67 The diagnosis of nonunion can be considered when an adequate time has passed for healing — nine months after traumatic injury — and there are absent signs of healing for three months.66 Bone healing relies on structural stability and adequate blood supply, both of which are influenced by biological risk factors and fracture features.68 Patient-specific factors that predispose to nonunion include tobacco use, diabetes, age, obesity, and metabolic dysfunction. Fracture location, degree of displacement, comminution, presence of infection, and type of surgical intervention also play a role.66,68,69 Many orthopedic surgeons advise against the use of NSAIDs, specifically COX-2 inhibitors, because of the possible association with impaired bone healing, although evidence for this is mixed.70
There is no universal standard for determining fracture union, and diagnosis of nonunion can be difficult. A mix of clinical features (such as persistent pain or inability to bear weight) and radiographic features are used to determine the extent of fracture healing.67 Nonunion caused by fracture instability causes production of a hypertrophic callus without appropriate bridging of bone fragments. Nonunion caused by inadequate vascular supply results in an atrophic, biologically inactive fracture site. Fractures with intermediate fragments, comminution, or significant defect between bone fragments also are prone to atrophic nonunion.66,71
In the ED, obtain X-ray or CT imaging to help characterize nonunion. It is important to evaluate for infection and/or metabolic disarray, since these can contribute to impaired bone healing.72 If nonunion is suspected, ensure that the fracture is appropriately immobilized. Outpatient orthopedic referral is appropriate to determine further management, such as internal fixation, bone grafting, biologic stimulation, debridement, or removal of existing hardware.66,71
Chronic Pain
Patients may present to the ED weeks to months after sustaining osseous injury with persistent pain in the absence of other fracture complications. Chronic fracture-related pain is common, with an incidence of 61.7% after ankle and knee fractures and 55.1% after tibial fractures.73 Some patients develop chronic regional pain syndrome (CRPS), which is a poorly understood condition that can cause allodynia, hyperalgesia, and autonomic disturbance after sustaining tissue injury.74
First-line therapy for chronic pain includes standard analgesics, such as acetaminophen and NSAIDs. Although helpful in the acute setting, the use of opioids is not shown to be beneficial for chronic musculoskeletal pain and may contribute to analgesic dependence and impaired functional status.75-77 Adjunctive medications include gabapentin (may be initiated at a starting dose of 100 mg three times daily) or topical analgesics (lidocaine, diclofenac, or capsaicin). Patients who remain refractory to first-line treatments should be referred to physical therapy, occupational therapy, and pain management specialists.
Conclusions
Fracture-related complications are likely to be encountered in the ED, and appropriate management by emergency physicians is critical to prevent further disability. Initial assessment of musculoskeletal injury is heavily reliant on the physical exam, and accurate diagnosis and management can prevent the development or progression of complications. Close collaboration with orthopedic specialists often is necessary to ensure favorable outcomes, so emergency physicians should be familiar with complications that require emergent or urgent evaluation by an orthopedic surgeon.
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The goal of this review is to familiarize emergency physicians with the initial assessment of fractures as well as the identification and management of immediate, early, and late-stage fracture complications.
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