Approximately 6 million fractures and 7.5 million open wounds occur annually in the United States. Extrapolating from European studies, about 4% of all fractures are open, or about 250,000 open fractures occur annually in the United States. Other studies note that open fractures occur at a rate of 11.5 per 100,000 persons per year. Open fractures are unique, complex, and emergently presenting injuries that expose sterile bone to the contaminated environment. Because a fracture disrupts the intramedullary blood supply, the additionally stripped soft tissue envelope further devitalizes the bone. The more severe the soft tissue injury or open wound, the more severe the osseous injury. Historically, open fractures were associated with infection, delayed union, nonunion, amputation, or death. Because of these complications, infections have an associated health care burden with a reported lifetime cost of a severe open fracture being as high as $680,000. Many techniques have been established to lessen or eradicate these complications. The goals of treatment are patient assessment, injury classification, wound management, fracture stabilization, and osseous regeneration when needed. With time, though, an increase in motorized vehicle collisions, especially in developing countries, and types of war injuries have increased open fractures. Motor vehicles have become safer, but collisions have produced more survivable injuries. With war and improved body armor, new ways to treat open injuries have developed. This chapter reviews the current state-of-the-art evaluation, treatment, and outcomes for open fractures.
Open fractures can occur because of an extreme amount of force imparted to the bone via an axial load or bending moment. This type of fracture could be considered an “in-to-out” fracture. A crush injury or an explosion can create enough external force to cause a direct integument injury and an associated fracture. This type of fracture is termed an “out-to-in” fracture. Because the bone ends protrude through the skin from the inner sterile to the outer unsterile environment, the “in-to-out” fracture is theoretically “cleaner” than the “out-to-in” fracture.
A direct blow causes a local area of injury with limited extension. The open wound can be from the direct blow site causing an “out-to-in” mechanism or the potentially contracoup injury opposite from the direct blow site with an “in-to-out” injury ( Fig. 17-1 ). Both injuries are serious, but the direct site may be more contaminated and have a more serious associated soft tissue injury.
Crush injuries create immediate and sometimes irreversible associated soft tissue injury. If prolonged or severe enough, the injury will be similar to an internal amputation with an associated open fracture of varying severity. The fracture can be a simple pattern. The circumferential crush injury creates problematic limb salvage options. Complete musculotendinous, venous, and cutaneous disruption can be present, requiring assessment, and may worsen with time ( Fig. 17-2 ).
Explosion and Blast Injury
The pathophysiology of explosion or blast injuries depends on the force and location to the source and evolves with time. It starts with the detonation followed by the blast wave, blast wind, and anatomic stress wave. The detonation is from a high-speed chemical decomposition of an explosive gas. Space occupied by the explosive is now occupied by gas under high pressure and temperature. The blast wave is a pressure pulse a few millimeters thick that travels at supersonic speed radially from the center of the blast. The leading edge rapidly decreases in pressure and becomes an acoustic wave. The local effect is a positive destructive shock wave followed by a negative pressure wave. The pressure drops below ambient pressure, and a vacuum effect takes place. The mass movement of air causes a blast wind that can propel objects and people considerable distances. Anatomic stress wave caused by blast wave interaction with the person with local overpressure has increasing pressure up to eight times normal. The stress wave causes rapid acceleration of body surface and a stress wave. The positive pressure shock wave creates immediate muscle damage while the negative pressure shock wave takes time to allow the full destructive pattern to evolve and determine.
Three types of blast injuries are noted: primary, secondary, and tertiary. The primary blast wave is caused by the direct effect of the blast wave on the body. The effect depends on distance. The lethal radius is three times in water. It is increased at the reflecting surface. The injury is seen almost exclusively in air-filled structures. The ear is the most sensitive, but injuries to the respiratory system are the most common causes of morbidity and mortality. Injuries to gastrointestinal tract are the most common causes of delayed morbidity and mortality. Major limb amputation occurs as a result of the blast wave–induced fracture followed by the blast wind avulsing the fractured limb. The secondary blast injury occurs from the casualty of being struck by fragments from the explosive device or by secondary missiles being energized by the blast. This has the same principles of diagnosis and care as for bullets or open wounds. Flying casing fragments and debris are irregularly shaped and less aerodynamically stable. The drag slows the fragments’ speed; therefore, they travel shorter distances. The fragments can tumble upon contact with tissue, so they are associated with potentially greater tissue damage than a bullet. A higher risk of environmental debris being dragged into the wound, causing higher contamination, is present. A large, slow-moving projectile may crush a larger amount of tissue. Missile fragmentation can increase temporary cavitation effects. The tertiary blast injury occurs when the victim is thrown against the ground or solid objects. The injuries are similar to blunt trauma or falls. Care follows blunt trauma guidelines. The tertiary blast wave causes fractures, crush injuries, amputations, and associated lacerations as people tumble and impact stationary objects ( Fig. 17-3 ). Therefore, a patient with a blast injury can present with a spectrum of acuity (blast injury with all three components in varying degrees) and injuries (thermal, chemical, biologic, and multisystem). Patients require a multidisciplinary team secondary to the obvious and subtle injury patterns. Even though this injury is mainly associated with war injuries, terrorist (e.g., Boston City Marathon Bombing, 2013) or industrial explosions can generate forces similar to war casualties.
All open fractures are contaminated. The number of bacteria initially present, the virulence of the bacteria, the severity of the wound, and the immune status of the host are important variables that contribute to the risk of infection that surgeons cannot change. Bacteria replicate quickly and can form a biofilm within 5 hours. The biofilm phenotype is sessile and has a lower metabolic rate and higher resistance to antibiotics and mechanical removal from irrigation. To add to the difficulty of managing open wounds, bacteria that are in the biofilm phenotype do not replicate on culture plates; this may help explain why culturing of wounds has little value. Colonization of bacteria or infection interferes with normal healing by heightened or prolonged inflammation or direct interference with host cells.
Gustilo and Anderson
Veliskakis proposed the initial open fracture classification based on three types and worsening severity. Gustilo and Anderson formulated and confirmed the classification in the 1960s and 1970s. Gustilo modified the classification further. The classification was based on open tibial fractures and the size of the wound. They determined a relationship between an increasing wound size and the risk of infection or osteomyelitis. The classification did not determine outcome or treatment.
Type I fractures have a skin laceration of less than 1 cm. This is usually a poke hole through the skin from the bone poking out or a direct blow from out to in. Type II fractures have a laceration greater than 1 cm and less than 10 cm. Type III fractures fall into a large and varied category, including extensive skin damage with muscle involvement, high-energy injury, crush injury, segmental or highly comminuted fracture, segmental diaphyseal osseous defect, high-velocity weapon, extensive contamination of the wound, or farm yard injury. Type IIIA fractures have lacerations greater than 10 cm, but the integument can be closed or reapproximated. Type IIIA also includes any wound size with heavy contamination with or without segmental or comminuted fracture patterns. Type IIIB fractures have lacerations greater than 10 cm, but the wound cannot be reapproximated and requires a rotational or free tissue transfer for closure. Skin grafting closure does not make the wound a type IIIB. Modifications of this classification can be considered if using a circular frame for treatment. If the fracture is treated with an external fixator that allows for bending or shortening, the wound can then be closed. This is then considered a type IIIB converted to a type IIIA wound. The amount of bending and shortening is restricted before secondary consequences such as vascular kinking and congestion can result in a limb at risk. Type IIIC fractures are open wounds with an associated vascular injury requiring repair for limb salvage ( Table 17-1 ). Gustilo also classified an open fracture that presents longer than 8 hours after injury as a special type III open fracture.
|1||Open clean wound <1 cm length|
|2||Open wound >1 cm and <10 cm without extensive soft tissue damage|
|3A||Open wound >10 cm that is able to be reapproximated with extensive soft tissue damage, special circumstance for gun shot wounds and farm/contaminated wounds|
|3B||Open wound that requires rotational or free tissue transfer for osseous coverage|
|3C||Associated vascular injury that requires repair for viability of limb|
The Gustilo-Anderson classification has been able to recommend antibiotic usage based on the type of fracture. The more severe wound requires broader spectrum antibiotic coverage. Type I and II wounds with mainly gram-positive bacteria require only a cephalosporin. Type III wounds require gram-negative coverage in addition. Contaminated wounds require penicillin for Clostridium and group A streptococcus coverage. Increasing wound size and classification severity was correlated with wound infection and amputation rates. Therefore, the classification was subdivided later (1970–1980s) into three types (A, B, C) of type III injuries. The risk of wound infection was type IIIA, 4%; type IIIB, 53%; and type IIIC, 42%. The risk of amputation was type IIIA, 0%; type IIIB, 16%; and type IIIC, 42%. Despite the correlative increasing severity, the classification has a poor interobserver reliability at only 60%. Even though this problem exists, the classification has generated worldwide acceptability. It is simple and logically stratifies open fractures. Despite originally determined to describe open tibial fracture patterns only, it has, rightly or wrongly, expanded to classify other fractures of the body. The system does recommend methods for closure (primary, delayed, free tissue transfer) but does not recommend overall treatment methods. Treatments do change over time and can change the classification type today. For example, vacuum-assisted closure (VAC) allows us to close many wounds today (type IIIA) that would have required free tissue transfer (type IIIB) without this method. In addition, circular external fixator frames with or without proximal corticotomy facilitate fracture manipulation to close the wound and accelerate local blood flow.
Other Open Fracture Classifications
Tscherne and colleagues developed an open and closed fracture classification. The types were type I, puncture hole; type II, moderate contamination; type III, heavy contamination, soft tissue problems; and type IV, incomplete or complete amputation. This was combined with a closed fracture, soft tissue injury classification. The types were type 0, minimal soft tissue damage with indirect violence, simple fracture pattern (e.g., torsion fracture of the tibia in skiers); type I, superficial abrasion or contusion caused by pressure from within, mild to moderate severe fracture pattern (e.g., ankle pronation fracture-dislocation with soft tissue over medial malleolus); type II, deep contaminated abrasion associated with localized skin or muscle contusion, impending compartment syndrome (e.g., segmental “bumper” tibial fracture); and type III, extensive skin contusion or crush, underlying muscle damage may be severe, subcutaneous avulsion or degloving, associated major vascular injury, severe or comminuted fracture pattern. The injury systems are complete, but the categories contain too much variability and subjective discrimination.
The Arbeitsgemeinschaft für Osteosynthesefragen (AO) classification system is a modification of the Tscherne classification and uses a grading system based on skin (I), muscles and tendons (MT), and neurovascular (NV). Each grade is further divided into five degrees of severity. This is the first system to grade wounds more on severity than just size. In addition, it indirectly attempts to measure the amount of function based on the soft tissue injury to the muscle and nerves. The problem with this classification is the complexity of the multiple choices for different categories and therefore the inability to deploy or use it for daily practices or consumption.
Arbeitsgemeinschaft für Osteosynthesefragen/Orthopaedic Trauma Association Open Fracture Classification
Despite the widespread use of the Gustilo-Anderson classification, a better way to quantify the severity of open fractures is needed. For example, a Gustilo open IIIB tibial fracture with a small-sized anterior pretibial defect, no bone loss, and minimal contamination but requiring a soleus muscle rotational flap is typed the same as a Gustilo open IIIB tibial fracture with extensive degloving and contamination, more than 4 cm of segmental bone loss, and loss of the entire anterior compartment and requiring bone transport or massive autografting, free tissue transfer, and extensive split-thickness skin grafts (STSGs). To address these limitations and better define these injuries, the Orthopaedic Trauma Association (OTA), in collaboration with the AO group, created the OTA Open Fracture Study Group. With the use of the three electronic databases (PubMed, EMBASE, and Web of Science), factors used to evaluate open fractures of the upper extremity, pelvis, and lower extremity were compiled. Based on their clinical experience and the existing literature, seven fellow-trained orthopaedic trauma surgeons independently examined and prioritized factors for inclusion or exclusion for this new open fracture classification ( Table 17-2 ). A rank-order mean for each factor was calculated and measured as to its relative importance ( Table 17-3 ). The other factors were simplicity, pathoanatomy, the exclusion of systemic issues, and anatomic characteristics of the injury. This group recently finalized a new open fracture classification system to facilitate consistent application and communication in assessment, treatment, and research. The new OTA/AO Open Fracture Classification (OFC) includes five assessment categories: (1) skin defect, (2) muscle injury, (3) arterial injury, (4) bone loss, and an additional (5) contamination with each category subdivided into three descriptors (mild, moderate, and severe) of increasing severity ( Table 17-4 ). The classification was successfully tested for feasibility and ease of clinical data collection. The advantage of this classification is better classifying the injury severity, which is a continuous variable, into different groupings of severity instead of just three categories.
|Reference||AAAM||Bosse, et al.||Bosse, et al.||Byrd, et al.||Castillo, et al.||Collins, et al.||Gregory, et al.||Gustilo, et al.||Hamson, et al.||Howe, et al.||Johansen, et al.||Johansen, et al.||Lange, et al.||McNamara, et al.||Muller, et al.||Russell, et al.||Slauterbeck, et al.||Suedkamp, et al.||Swiontkowski, et al.||Togawa, et al.||Tscherne, et al.||Tally|
|Mechanism of soft-tissue/muscle injury||X||X||X||X||X||X||X||X||X||X||X||11|
|Warm ischemic time||X||X||X||X||X||5|
|Seventy and duration of shock||X||X||X||X||4|
|Injury Seventy Score (ISS)||X||X||X||3|
|Energy of injury||X||X||2|
|Injury status of ipsilateral foot||X||X||2|
|Wounding mechanism (blunt vs. penetrating)||X||1|
|Loss of soft tissues of foot||X||1|
|Muscle viability at operation||X||1|
|Intercaiary ischemic zone after revascularization||X||1|
|Delay of revascularization||X||1|
|Trauma center vs. community hospital||X||1|
|AIS seventy category||X||1|
|Open joint injury/fx||X||1|
|Item||Variable||Rank Order Mean (ROM)||7/7 in Top 10||6/7 in Top 10||5/7 in Top 10||4/7 in Top 10||3/7 in Top 10||2/7 in Top 10||1/7 in Top 10||0/7 in Top 10|
|1||Muscle viability at operation||5.571||X|
|2||Mechanism/soft-tissue injury kinetics/muscle injury||3.286||X|
|3||Energy of injury||6.571||X|
|5||Severity and duration of shock||8.571||X|
|6||Delay of revascularization||12.143||X|
|7||Loss of soft tissues of distal part||15.571||X|
|8||Injury status of ipsilateral part||17.429||X|
|9||Intercalary ischemic zone after revascularization||16.000||X|
|10||Warm ischemic time||10.571||X|
|13||Open joint injury/fx||16.429||X|
|25||AIS severity category||20.571||X|
|31||Trauma center vs. community hospital||27.571||X|
|32||Wounding mechanism (blunt vs. penetrating)||18.000||X|