11.1.1 Introduction

The surgeon should be vigilant for complications related to the injury. In many cases, the force that caused the orthopaedic injury also caused damage to vital organs. For instance, a fracture of the scapula should alert the surgeon to the possibility of a lung contusion or rupture of the thoracic aorta. Pelvic fractures are often associated with significant vascular lesions within the pelvis, ureteral tears, and ruptures to hollow and/or solid organs. Furthermore, soft-tissue injuries such as crush, burns, or electrical injuries may have a profound systemic effect.

11.1.2 Compartment syndrome

Compartment syndrome occurs when the pressure within a muscle compartment exceeds the end arteriolar pressure ( Animation 11.1-1 ). While sustained pressures above capillary pressure may lead to chronic problems, pressures above ~ 30 mmHg (end arteriolar pressure) may lead to the death of muscle, nerve and other soft tissues. Permanent damage may occur in as short a time as 6 hours after onset, thus, early diagnosis and emergent treatment is essential.

The most common location for compartment syndrome to occur is the lower leg, specifically in the anterior and deep posterior compartments. It is also commonly seen in the forearm. Less common and therefore frequently overlooked locations include the foot, hand, thigh, and buttocks. Compartment syndrome may occur after blunt trauma or crush injury with or without a fracture. When associated with fractures, the presence of an open wound does not exclude compartment syndrome.

The five “P”s remain the cornerstone of diagnosis:

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  pain out of proportion to the injury or with passive stretching

  
  
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  pallor

  
  
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  pulselessness

  
  
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  paresthesia

  
  
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  paralysis.

Of these signs, the cardinal sign is pain in excess of what one would expect due to the injury, or severe pain with passive stretching. Furthermore, pain that is not responding adequately to pain medication (ie, opiates) may also indicate compartment syndrome. Often, there are no other signs until much later in the course of the injury. These symptoms may be difficult to elicit in an unconscious patient, therefore, invasive monitoring with a pressure transducer may be required.

Several techniques for the measurement of compartment pressures are available. They should not substitute a clinical exam (pain out of proportion to the injury, nonresponse to pain medication) if possible. Standard fracture textbooks describe these techniques well and, therefore, they are not presented here. When compartment measurements are taken [1] as an adjunct to clinical examination and in order to decide whether the muscle compartment should be released ot not, the surgeon may use either an absolute value of > 30 mmHg or a δ P value of < 30 mmHg, which represents the difference between the diastolic blood pressure and the measured compartment pressure. Surgeons should note that pressures within a compartment may vary inversely to distance from the fracture, and, therefore, should attempt to measure at the area associated with peak pressures, ie, near the fracture site.

The treatment for compartment syndrome consists in an emergent and generous fasciotomy. The key to successful treatment of compartment syndrome after diagnosis is adequate release of the constricting muscle fascia. In most cases, this involves a long incision over the affected compartment and a release of the fascia. Once the skin and muscle fascia are incised, immediate release of pressure is noted as the muscle forcefully bulges through the fascia.

The surgical approach for the lower leg involves long incisions on the medial and lateral sides of the leg ( Fig 11.1-1a–c ). Care should be taken in order to avoid injury, on the lateral side to the superficial fibular nerve, and on the medial side to the posterior tibial artery respectively tibial nerve. In every case, all four compartments should be fully released. Two or 3 days later, the medial wound may often be closed (chapter 10.1), but the lateral wound often requires a split-thickness skin graft (chapter 10.2), as swelling will not have subsided fully yet. Do not attempt to close the muscle fascia, as recurrence of the compartment syndrome may occur. Moreover, long-term bulging of the muscles through the longitudinally incised muscle fascia will usually not affect the function of the patient′s muscle compartment.

Forearm compartment syndrome often involves the anterior compartment but not the posterior one. In selected cases, it is permissible to release only the anterior compartment, if the patient can be assessed clinically after surgery. However, in unconscious patients or in patients who will not undergo subsequent surgery, both compartments should be released at once. The approach utilizes an extensile anterior approach, which may be extended across the wrist in order to decompress the carpal tunnel ( Fig 11.1-2a–b ). Dorsally, a mid-line approach may be chosen.

Foot fasciotomies ( Fig 11.1-3a–d ) [2] are performed less commonly than those of the leg or forearm, possibly because this condition may not have been recognized, but also in part, because the sequelae of an untreated foot compartment syndrome are far less debilitating than those of the forearm or leg. There are nine compartments of the foot which are commonly recognized: the medial, lateral and superficial compartments run the length of the mid foot/forefoot. There are four interosseous and one central compartment within the forefoot ( Fig 11.1-3d ) as well as the calcaneal compartment in the hindfoot ( Fig 11.1-3c ). All of these compartments may be accessed by two dorsal and a medial approach.

Unfortunately, fasciotomies are associated with complications. Multiple surgical procedures may be required in order to close the wound (eg, delayed wound closure with elastic vessel loops, split-thickness skin graft, and secondary skin graft) (chapter 10.1, 10.2). Infection rates are high and damage to neurovascular structures may occur if care is not taken in order to avoid them during the fasciotomy. In the presence of a fracture, the bone must be stabilized just as in an open fracture.

11.1.3 Rhabdomyolysis

Rhabdomyolysis is the rapid breakdown (lysis) of skeletal muscle. Most often it is the result of long periods of recumbency while unconscious, but may also occur following blunt or penetrating trauma, or in extreme cases, exercise. Failure to adequately debride all necrotic tissue may also lead to rhabdomyolysis. Recently, rhabdomyolysis has been described as a cause of death in earthquake survivors [3].

Clinical signs include nausea, vomiting, mental status changes from confusion to coma, and dark, tea-colored urine. The latter is caused by the release of the breakdown products of damaged muscle cells such as myoglobin, which are harmful to the kidneys. A dramatic decrease of urine output may follow as a sign of acute kidney failure. Laboratory abnormalities include extremely high concentrations of creatine kinase and transaminases as well as hyperkalemia. A standard urine dipstick may test false positive for blood because the reaction of myoglobin is the same as that for hemoglobin.

If untreated, myoglobin casts accumulate in the nephrons and cause acute tubular necrosis and finally obstructive renal failure.

Treatment involves fluid therapy, combined with diuretics in order to promote high renal flow. Alkalinization of the urine in order to reduce the formation of casts may be beneficial and, in severe cases, hemodialysis may be required. Correction of electrolyte abnormalities and treatment of the underlying cause are important as well. In selected cases, dialysis is mandatory in order for patients to recover from acute renal failure.

11.1.4 Nerve injury

Nerves may be injured in any kind of soft-tissue trauma. Nerve tissue tolerates stretching far better than bone, but, depending on the extent of damage to the different structures and nerve components, several degrees of injury are observed. A nerve consists of axons surrounded by a myelin sheath. Individual nerve fibers are surrounded by a thin connective tissue called endoneurium. Many individual nerves are grouped into a fascicle ( Fig 11.1-4 ). Each fascicle is encapsulated by a connective-tissue layer called perineurium. Blood vessels travel between fascicles and supply the nerve fibers. Several fascicles are grouped together and surrounded by epineurium to form a peripheral nerve.

Sunderland classified nerve injuries according to the individual components that are disrupted ( Table 11.1-1 ) [4]:

Grade I injuries, also called neurapraxia, involve injury to the myelin sheath. Neurapraxia presents clinically as a reversible paresthesia. Motor loss may be more severe than sensory damage in these injuries, although incomplete loss of sensation is common. Most neurapraxia injuries occur as a result of local stretching or crushing mechanisms. These injuries are treated expectantly, with a prognosis to full recovery in most cases within 3 months.

Grade II injuries, called axonotmesis, involve disruption of the axon body in addition to that of the myelin sheath. The endoneurium and surrounding structures, however, remain intact. Although the nerve undergoes Wallerian degeneration, nerve recovery is expected to occur in time because the perineurium as a tube is not damaged. Peripheral nerves regenerate at a rate of 1mm per day. In most cases, these injuries are also treated conservatively.

Grade III injuries include disruption of the axon body, the myelin sheath and the endoneurium. These injuries have a poorer prognosis for recovery than less severe injuries of grade I or II. The axon undergoes Wallerain degeneration. Attempts of the nerve to regenerate are hindered by fibrosis and the lack of intact neural tubular structures to guide the regeneration processes.

Grade IV injuries involve injury to all structures except the perineurium. No functional recovery is expected without surgical repair or nerve grafting.

Grade V injuries, called neurotmesis, involve complete transection of the nerve. Nerve repair or grafting is required for the recovery of any function.

11.2.1 Introduction

“The operative technique is extremely important, for upon the success of the primary operation in removing the causes of infection depends the entire after course of the wound and perhaps the life of the patient.”

LTC Joseph A Blake, (US Army Medical Corps) 1919, World War I.

The importance of adequate debridement and its central role in the management of open fractures has been accepted since the early 1900s. However, the consequences of inadequate medical care can be seen even today, whenever prompt medical attention is delayed due to natural disasters, military conflict or lack of medical resources. Therefore, it is important for surgeons to understand the complications that may result from inadequate or delayed debridement.

11.2.2 Superficial infection

Superficial infection ( Fig 11.2-1 ) may occur after any surgical procedure, whether emergency or elective. In case of a fracture, there is often an implant beneath the infection and the surgeon must be very suspicious of colonization of this hardware. Therefore, the treatment of superficial infection must occur as early as possible, treatment has to be aggressive, usually with a proper surgical debridement (chapter 7.1) and involving irrigation (chapter 7.2) in the operating room.

Aseptic abscesses may mimic superficial infection. Both may present with pain and swelling, but in many cases, the degree of erythema and surrounding induration is less in the case of a sterile abscess. These will usually discharge a fragment of suture and then resolve. Local heat may be beneficial. Oral antibiotics are indicated.

11.2.3 Deep infection

A deep infection may occur following trauma or surgical procedures. It may be the result of hematogenous spread or direct inoculation after inadequate debridement. Direct inoculation, however, is the more common mechanism.

Clinically, postoperative patients typically show slightly elevated temperatures over several days and a high C-reactive protein (CRP) level without any local signs of inflammation. After hospital discharge, they return with pain and often with a draining wound that commenced suddenly and then persisted. Clear drainage is often a result of “subcutaneous” seroma, but is always a reason for concern and the suspicion of a deeper origin. Serous drainage may last longer than usual in patients on anticoagulation medication, but the surgeon should always be concerned about drainage that continues after 5 days after surgery or drainage, which does not show a clear trend toward decreasing. The discharge may present with purulence or may be a cloudy fluid. Both are most suspicious indicators for a possible deep infection. Alternatively, patients may present weeks or even months after surgical treatment with purulent drainage despite a normal early healing process. In these rare cases, deep infection is believed to have spread hematogenously. Persistent pain in the region of a wound should always raise the suspicion of a deep infection.

Deep infections involve the attachment of bacteria to a surface such as necrotic bone or implants, where the fight against infection is impeded, especially if the bacteria produce a protective biofilm [5]. At present, there are no treatment options for eliminating infection established on an implant except for the removal of the implant. The treatment algorithm for deep infections is shown in Fig 11.2-2 .

Infected fractures may heal in the presence of an implant, provided the hardware material is not loose and the fracture fixation is stable, but do not always do so. Any loose implant material or dead bone fragment must be removed and, if needed, the stability of fixation should be improved. Leaving the rigidly fixed implant in place and suppressing the infection until the fracture has healed is a valid option until the implant can be removed safely. Therapy with antibiotics is selected on the basis of cultures taken from tissue samples from the depth, not from superficial skin swabs or cultures from a sinus tract. Staphylococcus aureus is often responsive to sulfacycline and/or tetracycline and many infectious disease specialists, who should be consulted in every case, might consider adding rifampicin to the coverage. Intravenous antibiotics over a prolonged period of time are, however, only indicated if the patient has undergone a surgical debridement, but are not expected to cure the infection as long as the implants remain.

Osteomyelitis occurs when bacteria adhere to bone—usually nonviable or necrotic bone—and begin to multiply. Osteomyelitis may develop in a trauma setting either from direct inoculation from the open wound or by spreading from adjacent infected implants. In the case of sequestered necrotic bone, surgical removal must be performed and the dead space managed. When osteomyelitis involves adjacent implants, medical suppression may be carried out as long as the fracture fixation remains stable. However, if fracture fixation is lost, the infected implants must be removed and stabilization must be achieved by other means.

After the fracture has healed and the implants have been removed, the patient′s osteomyelitis may still persist. Cierny and Mader described a classification system for osteomyelitis based on four anatomical stages and three host types ( Table 11.2-1a–b ) [6]. This classification is associated with a treatment protocol shown in Fig 11.2-3a–b . In general, the surgeon should endeavor to optimize host factors—eg, smoking, control of diabetes, complete or transient cessation of intake of medication interfering with immunosuppression and/or coagulation—prior to undertaking surgical treatment of chronic osteomyelitis (chapter 4.1, 4.3, 4.4). The next step is to adequately debride the bone, including the intramedullary canal and to stabilize the fracture. Finally, after the wound bed is sterile, bone reconstruction may begin. Complete coverage of the treatment of osteomyelitis as well as delayed union and nonunion, however, is beyond the scope of this book.

While treatment of osteomyelitis may be technically possible in most cases, it may turn out to be very time consuming and require major reconstructive efforts. In some very rare cases, patients may prefer amputation in order to avoid a protracted reconstruction. Moreover, some patients may not be healthy enough to undergo complicated reconstruction while others may not have sufficient vascular supply to support free bone transfers.

11.2.4 Gas gangrene

Debridement is the cornerstone of treatment for severe open or closed soft-tissue injuries (chapter 7.1). When debridement has either been delayed for too long or inadequately performed, significant complications may result, such as infection or even gas gangrene. Gas gangrene is a potentially life-threatening necrotizing soft-tissue infection often occurring as a complication of wound treatment, typically such, with exposure to soil and no or delayed debridement.

In diabetic patients, it may occur without such exposure. It is caused by Clostridium perfringens, a gram-positive anaerobic rod bacterium. Clostridium perfringens produces a number of exotoxins causing widespread systemic damage including hemolysis or vascular injury as well as destruction of collagen and fascial planes. The time of incubation may be rapid, ie, within hours, or delayed and depends on a low local tissue oxygen tension. Clostridium perfringens is sensitive to high-dose penicillin.

The clinical symptoms usually include local crepitation within the soft tissues. Wound exploration may reveal gas, watery discharge, and necrotic muscle. Muscle tissue may be pale, edematous, and may not bleed when cut nor contract when stimulated with electricity. Often, crepitation is associated with free air in the muscles visible on x-rays of the affected extremity. In addition, tachycardia, hypotension, hemodynamic shock, and renal failure may be present. A rapidly progressive course is often seen, and patients may succumb to sepsis within 12 hours [7].

Patients with suspected gas gangrene should be considered critically ill and only immediate and aggressive treatment will save the patient′s life. Supportive treatment includes administration of supplemental oxygen and resuscitation with fluids that must be started without delay. Adequate tetanus immunity must be ensured. In spite of the patient′s critical situation, surgical debridement must be performed as an emergency. Wide debridement of all involved tissue is required, no dead spaces may remain unexposed and the wounds must remain open. Extensive extremity involvement may even require amputation that may be the lifesaving measure in some cases. Since the disease process may continue to involve additional tissue, frequent subsequent debridements are necessary in order to ensure that all necrotic tissues are removed and recesses, which still may harbor Clostridium perfringens, are cleansed. Finally, hyperbaric oxygen therapy should be taken into consideration. Clostridia lack superoxide dismutase, making them incapable of surviving in the oxygen-rich environment created within a hyperbaric chamber. This inhibits clostridial growth, exotoxin production as well as the binding of exotoxins to host tissues. Yet, the mortality rate is universal in untreated cases and is 20% even with prompt treatment [8]. In surviving patients, the wound may either be closed at a later date or allowed to heal secondarily by wound contraction and spontaneous reepithelialization.