12.2 Complications of fractures

Complications of fractures include fat embolism and fat embolism syndrome, reflex sympathetic dystrophy, avascular necrosis, vascular injuries, crush injuries, gas gangrene, and tetanus. Vascular injuries are dealt with in Chapter 12.9. Avacular necrosis is discussed in the chapters on hip fractures and scaphoid fractures (Chapters 12.29, 12.50, and 12.51).

Fat embolism syndrome is defined as the presence of globules of fat in the lungs and in other tissues. It occurs occasionally in long bone fractures (3.5%) and can rarely occur without trauma. It is commoner after multiple trauma (10%).

There is little correlation between the amount of fat in the lungs and the severity of the condition. Figure 12.2.1 summarizes the inflammatory cascade which occurs. Lipase is released by the lung which acts on the fat releasing free fatty acids and glycerol which are toxic to the lung.

The condition usually manifests itself 1–2 days after injury. Many features remain unexplained:

Table 12.2.1 summarizes the classical symptoms and signs (major and minor features). Tachypnoea, dyspnoea, and cyanosis are the earliest respiratory signs, but hypoxaemia may be detected earlier. Cerebral irritation can include headache and irritability to convulsions and coma. Embolization of fat into the dermis causes petechiae. They are transient but can be seen on the chest (Figure 12.2.2) neck, axillae, palate, eyelid (Figure 12.2.3), conjunctivae, and retina.

The diagnosis is based on clinical and laboratory tests. These include:

These should be combined with one major and four minor signs (see Table 12.2.1).

Pulmonary infiltrates on the chest radiograph, right heart strain, and ST segment changes on the electrocardiogram (ECG), together with anaemia, thrombocytopenia, and elevation of erythrocyte sedimentation rate, add support to the diagnosis but are not specific.

The incidence of fat embolism syndrome can be reduced by appropriate early management of the trauma victim. Adequate fluid resuscitation and oxygen therapy with fracture splintage and careful transport are important first aid measures. There is no evidence that intramedullary reaming increases the incidence. The mainstay of treatment in the established case is respiratory support. Specific therapies have been proposed, including heparin, alcohol, and aspirin, but the findings were equivocal. Steroids have been studied in both prophylaxis and treatment. They are reported as effective in maintaining arterial oxygen levels and reducing serum free fatty acids, but the dose required is high and complications can be severe. At the present time they are not in routine use.

The mortality rate approaches 15% mainly due to respiratory complications. Morbidity is mainly due to cerebral irritation.

A high index of suspicion and early treatment improves results.

Reflex sympathetic dystrophy is a syndrome characterized by intense or unduly prolonged pain, vasomotor disturbance, delayed functional recovery, and trophic changes. Many terms, including causalgia, Sudeck’s atrophy, and algodystrophy, have been used to describe the condition. It can occur as a response to trauma. Up to 30% of patients with tibial fractures and distal radial fractures may be affected. The cause is not known. Livingstone’s theory (Figure 12.2.4) is that there is a vicious circle initiated by capillary stasis, increased local pressure, and exudation, which is maintained by afferent fibre stimulation due to anoxia. The importance of inflammatory mediators and cytokines has been investigated but to date there is no reliable marker for reflex sympathetic dystrophy.

The severity of reflex sympathetic dystrophy is not related to the magnitude of the initial traumatic insult. The condition commonly affects the periphery, although it is being increasingly recognized in the knee and shoulder. The elbow and hip are rarely affected. It is more common in middle years but is recognized in children.

The clinical presentation is varied but three phases are commonly identified:

The acute phase may occur soon after injury but may be delayed for several weeks. Pain and tenderness are the first signs. Hyperpathia (increased sensitivity to a noxious stimulus) and allodynia (pain caused by stimuli not usually noted to be painful) are common. In the acute phase the limb is swollen, dry, hot, and pink (Figure 12.2.5), with increased hair growth. In the second phase the limb often remains swollen but becomes blue, cool, and damp with sweat. It may be several months before the third stage is entered. This is characterized by atrophy and joint contractures.

The diagnosis is primarily clinical. Several investigations are useful in assessing the severity and stage of the disease. Tenderness can be assessed using dolorimetry, joint stiffness can be recorded, and thermography can be used to assess vasomotor function. Bone scans are positive in the early stages, and when they return to normal there is visible demineralization on plain radiography.

Early diagnosis is the key to successful management as the first two phases are reversible. The primary treatment of reflex sympathetic dystrophy involves reassurance, analgesia, and physiotherapy to maintain joint movement. In severe cases, treatment involves sympathetic interruption, for example, with intravenous guanethidine. Surgical sympathectomy is rarely indicated. A multidisciplinary team approach, including physiotherapists, pain specialists, and, in certain cases, psychologists, is helpful.

Even in a mild form reflex sympathetic dystrophy gives rise to severe and permanent morbidity. There is little evidence in the literature for efficacy of the various treatments. It is essential to maintain movement to avoid long-term contractures after recovery.

This typically affects intra-articular bone after fracture (talus, hip, scaphoid, humeral head). In displaced talar neck fractures it may occur in up to 70% of cases.

Post-traumatic avascular necrosis may be due to any of these mechanisms. Avascular necrosis of the femoral head may occur as a result of tamponade due to intracapsular haemarthrosis or by vessel kinking or rupture. The degree of displacement and the interval between injury and reduction are important predictors of the likelihood of the occurrence of avascular necrosis.

The progression of the condition is independent of the initial mechanism. Within 2 weeks of injury, there may be histological signs of marrow necrosis with osteocyte death. Cell death leads to liposome release and tissue acidification. Saponification occurs in the presence of free fatty acids and calcium. Marrow oedema and tissue necrosis lead to the earliest detectable signs on magnetic resonance imaging (MRI). This may be associated with a quantifiable increase in intraosseous pressure. Commonly these changes are confined to the medullary bone of the metaphysis and do not involve the subchondral plate.

Repair occurs by creeping substitution and may take 2 years.

Without a viable cell population the normal process of remodelling does not occur and microfractures cannot be repaired. This can result in collapse of the subchondral bone and chondral flaps, both of which then lead to joint incongruity and arthritis.

Table 12.2.2 summarizes the classification.

Early diagnosis is important to limit transarticular load.

Management is directed at preventing the complications of avascular necrosis, such as segmental collapse and osteoarthritis.

Clinical studies have shown clear evidence that the incidence of avascular necrosis in many injuries can be correlated with the severity of the initial injury and the delay to reduction. Therefore prompt accurate reduction with secure fixation can lessen the incidence of avascular necrosis, particularly in weight-bearing joints. This must be accompanied by evacuation of the associated haemarthrosis to reduce the effect of tamponade.

Early diagnosis allows preventive measures such as limiting weight bearing to be instituted to prevent propagation and segmental collapse.

Procedures to enhance revascularity have been advocated. Most commonly, these have been for the management of femoral head avascularity after intracapsular fractures of the proximal femur. Posterior muscle pedicle grafting has been used as an acute procedure and to enhance vascularity in established avascular necrosis. These techniques are infrequently used in modern practice, particularly with the increasing acceptance of hip arthroplasty.

Once segmental collapse has become established and symptomatic, reconstructive procedures such as arthroplasty and arthrodesis are indicated.

See Chapter 12.9.

Major crush injuries of the limbs are mercifully rare. All structures can be injured by crush. Fractures may occur and prolonged crush can cause ischaemia. Muscle repair may be accompanied by fibrous tissue, and myositis ossificans can occur (20% of those with quadriceps haematoma).

In response to trauma, there is a tendency to hypovolaemia with expansion of the extracellular space. This results in an active antidiuresis with rapid renal tubular resorption. Excreted myoglobin and haemoglobin become concentrated in the renal tubules, causing tubular blockage, and may lead to acute renal failure. Sudden release and reperfusion of the affected limb may lead to metabolic acidosis and rapid rises in plasma potassium levels sufficient to cause cardiac arrest.

On admission, a detailed assessment should include an ECG, relevant radiographs, measurement of electrolytes, arterial blood gases, and measurement of urinary output. Estimation of urinary myoglobin and haemoglobin are indicated if compromise of renal function is thought likely. Special investigations may include angiography if an associated vascular injury is suspected.

General resuscitative measures should be instigated with administration of analgesia, intravenous fluids, and insertion of a urinary catheter. Electrolyte and acid–base derangement should be corrected. In the case of an open wound, precautions against infection should be taken with administration of broad-spectrum antibiotics and antitetanus prophylaxis.

Specific management of the injuries will be required. This will include fracture reduction and fixation, arterial exploration and reconstruction if indicated, and the limb deemed viable. The fracture pattern may demonstrate extreme comminution.

Decompressive fasciotomy of myofascial compartments surrounding and distal to the crush injury will be required. All non-viable tissue including muscle and bone should be excised. Wounds should be dressed without skin closure.

Complications can be local or general. General complications may include cardiac arrhythmias and acute renal failure. Cardiac manifestations of hyperkalaemia are reduction in P-wave amplitude and widening of the QRS interval into the ST segment. Sudden rises in serum potassium may result in cardiac arrest. Renal failure may occur as a result of myoglobinuria in the presence of hypovolaemia.

The incidence of deep venous thrombosis (DVT) in trauma patients is high. A number of demographic studies have demonstrated an incidence approaching 60% after trauma. This may reach 80% in patients with femoral and tibial shaft fractures and in those with spinal cord injuries.

The lower limb veins are most commonly affected due to local endothelial damage, venous stasis, and post-traumatic hypercoagulability and age. Direct trauma to the venous endothelium releases thromboplastic substances and exposes the basement membrane, initiating local thrombosis by the extrinsic coagulation mechanism. Trauma remote from the venous lining may also initiate these changes, explaining the widespread distribution of thrombi. Stasis, in association with immobilization and bed rest, may cause accumulation of platelets around valve cusps which promote the thrombotic process by the release of procoagulants. The frequency of deep venous thrombosis has been shown to rise with increasing periods of immobilization.

Pulmonary embolism may occur in up to 5% of patients.

The clinical symptoms and signs of DVT are pain, tender swelling of the limb distal to the thrombus, and peripheral oedema. It is frequently associated with a low-grade pyrexia of less than 38°C. However, these signs are difficult to interpret, and clinical diagnosis may be difficult and will underestimate the number of cases seen.

Impedance plethysmography and contrast venography are widely available to confirm the diagnosis of DVT. Contrast venography is the most specific test, but is invasive and requires transfer to the radiology department. Impedance plethysmography may be performed at the bedside, but is less specific for smaller distal DVT where proximal veins are patent.

Prevention is best. Early mobilization and prophylaxis with low-molecular-weight heparin is widely used. The National Health Service in the United Kingdom has published NICE (National Institute for Health and Clinical Excellence) guidelines for prophylaxis. They recommend graduated DVT stockings for all adults, and 4 weeks of low-molecular-weight heparin for patients undergoing surgery for hip fracture. They also support the use of intermittent pneumatic compression where possible, and emphasize the importance of risk assessment for DVT.

Useful pharmacological agents include aspirin, heparin, fractionated heparin, and oral anticoagulants. The use of these agents in prophylaxis has to be balanced against the risk of haemorrhagic complication. For this reason, use of heparin in patients with acetabular, pelvic, or spinal fractures is not indicated in the first 48h after injury. Studies in patients with below-knee casts indicate that the incidence of DVT can be reduced by the use of fractionated heparin.

Treatment of DVT depends on the anatomical site of the thrombus; asymptomatic below-knee thrombus may not require specific therapy. The standard treatment of symptomatic DVT is anticoagulation, initially with heparin, and commencement of warfarin therapy. Oral anticoagulants should be continued for 6–12 weeks, and clotting should be monitored to ensure that the dosage is within the therapeutic range.

In the event of a pulmonary embolus occurring during treatment of DVT, consideration can be given to insertion of inferior vena caval filters to prevent the formation of further emboli.

The complications of DVT include pulmonary embolism and postphlebitic limb.

Gas gangrene is a rapidly developing, spreading infection of devitalized tissue by toxin-producing clostridial species, especially Clostridium perfringens (formerly known as Clostridium welchii). It is a Gram- positive, anaerobic, capsulate, and non-motile bacillus. The most characteristic feature is the spore, which is produced whenever the organism faces adverse conditions. It is accompanied by profound toxaemia, massive tissue necrosis, and gas production, and is invariably fatal unless treated. Clostridial contamination is reported in up to 39% of wounds. The incidence is related to the interval between injury and treatment, as well as to the site and severity of injury.

Clostridial infection can be classified into three types.

The exact processes by which clostridial contamination and cellulitis lead to gas gangrene are not clear, but a reduction in local oxygen potential is an important factor. The inoculum of C. perfringens required to produce fatal gas gangrene is reduced by a factor of 10³ if the tissue is devitalized or contaminated with sterile dirt. The most important exotoxins are the α-toxins (lecithinase), although several others are well recognized (e.g. collagenase, hyaluronidase, and protease).

Muscle carbohydrate is fermented to lactic acid and ‘gas’ (mainly hydrogen and carbon dioxide). Putrefaction follows extensive necrosis. At this stage the characteristic smell is produced and the evolution of ‘gas gangrene’ is complete.

The original insult often involves a penetrating injury to muscle. The buttock and thigh are common sites. The incubation period can be as long as 4 days or as short as 6h. The progression of the disease can be rapid and devastating. Sudden onset of pain is the first symptom, followed by oedema and a thin serous ooze. The pain increases in severity and the skin becomes stretched, developing a ‘bronzed’ discoloration. Haemorrhagic vesicles may appear before areas of frank necrosis. Tachycardia out of proportion to temperature elevation and mental awareness marked by a ‘terror of death’ are characteristic. Profound shock follows in the untreated case, and death occurs within 48h. The mortality rate is about 30%.

Emergency surgical debridement is required to save the patient’s life, and compartment decompression. X-rays may show gas in the soft tissues, but its absence does not exclude the diagnosis.

A patient with suspected gas gangrene should receive intravenous penicillin. Consideration should be given to adding broad-spectrum antibiotics to cover other organisms. Hyperbaric oxygen is recognized to be of benefit in reducing toxin production and improving oxygen delivery to devitalized tissues.

Tetanus is a rare but often fatal disease caused by Clostridium tetani. All the clinical effects are caused by the effects of an exotoxin (tetanospasmin) on various receptor sites.

The incidence of tetanus is now rare in Western countries. In developing countries, where standards of hygiene and primary wound care are poor and the majority of the population are not immunized, it remains an important cause of mortality.

C. tetani is a Gram-positive, anaerobic, motile, and non-capsulate bacillus which forms a characteristic terminal ‘drumstick’ spore. The spore is very resistant and may remain dormant in wounds for long periods.

C. tetani is found in soil and faeces, but frequently contaminates the skin. A wound is identified as the portal of entry in only 60% of cases. Two factors favour progression of the infection: wounds with low oxygen potential or ischaemic tissue and wounds infected with other organisms. The initial traumatic lesion may appear innocuous compared with the outcome as clinically ‘tetanus’ is a disease of the central nervous system.

The incubation period varies from 3–21 days and is generally shorter in more severe cases. The period of onset is the time from first symptom to first spasm. This can vary from less than 24h to over 10 days; the shorter the period the more severe is the tetanus.

C. tetani produces two exotoxins. Tetanospasmin is a powerful neurotoxin which is carried slowly by peripheral nerves to the central nervous system, where it is avidly taken up by gangliosides. It is responsible for the characteristic clinical features of the disease. The toxin does not affect sensory nerves, the cerebral cortex, or the cerebellum. Tetanolysin is haemolytic and may contribute to the overall clinical picture.

The transit of the toxin in the peripheral nerves is slow; the first effect is produced in muscle groups with short motor neurons, i.e. the head and neck muscles. Severe trismus and dysphagia due to masseteric spasm (‘lockjaw’) are seen, and facial muscle spasm produces the characteristic risus sardonicus. The muscular spasm spreads to affect the neck, back, abdomen, and limbs. Opisthotonos—severe spasm such that the whole body is arched off the bed—may be seen.

Muscle spasm of increasing severity and duration may lead to crush fractures of the vertebrae and death from respiratory failure and exhaustion.

The diagnosis is clinical. The organism is only cultured in one-third of cases, reflecting the specific anaerobic growth requirements of C. tetani.

The treatment incorporates specific measures including wound care, passive immunization, and antibiotics. When a wound is identified it should be excised along with all devitalized tissue. C. tetani remains sensitive to penicillin, which should be given. Human tetanus immunoglobulin should also be given.

Supportive therapy may be needed depending on the severity of the case and sedation is often helpful. The most important factor is the maintenance of respiratory function and mechanical ventilation via a tracheostomy is required in severe cases.

Active immunization with absorbed tetanus toxoid is extremely safe and effective. If the wound is severe, passive immunization with tetanus immunoglobulin should be given. The American College of Surgeons Committee on Trauma (1986) has published a guide to prophylaxis against tetanus in wound management.

Raised pressure within a closed compartment resulting in tissue ischaemia and if untreated, necrosis followed by fibrosis and muscle contracture.

The capillary bed pressure is usually 20–30mmHg, and this is sufficient to create an adequate tissue perfusion, with an interstitial pressure of about 5mmHg. Compartment syndrome occurs when tissue pressure rises and tissue perfusion decreases or ceases. An increase in interstitial tissue pressure is possible in closed compartments, either by intrinsic or extrinsic causes. An increase in the volume in a contained compartment, giving rise to an intrinsic compression, may be caused by blood or other fluid shifts. Extrinsic compression similarly affects an increase in pressure.

If the pressure in the veins does not rise above the compartment pressure, the veins will remain collapsed, venous pressure rises and perfusion ends. Capillary pressure will then rise towards arterial pressure and there will be rapid diffusion of fluid out of the vascular compartment into the extracellular compartment of the muscle. The pressure in the compartment will continue to rise and the muscle becomes ischaemic. This hypoxic cellular injury causes a release of vasoactive substances, such as serotonin and histamine, which further increase endothelial permeability and extracellular fluid accumulation. Muscle necrosis will occur and myoglobin will be released.

It is important to note that arteries passing through this compartment are not squeezed shut during this process. This is because their intraluminal pressure is high (arterial blood pressure) and their walls are thicker and therefore resist compression. Therefore the presence of distal pulses does not exclude a compartment syndrome.

The prognosis is dependant on the speed of diagnosis and treatment. Acute compartment syndrome is a true surgical emergency.

Once a compartment syndrome is established, some measurable changes in the affected muscle may occur within 2h. Within 4–6h these changes will have significant long-term effects. After 12h there is likely to be severe irreversible damage.

Acute traumatic compartment syndromes can be divided into primary intrinsic, where swelling within the compartment is primarily responsible for the rise in pressure, and primary extrinsic, where there is a constricting cast or bandage. Intrinsic are much more common.

Intrinsic compartment syndrome develops when the volume in an injured compartment rises following a traumatic injury. It is important to note that even open injuries may have intact fascial compartments. Bleeding or direct tissue injury may initiate the pressure increase. Manipulation and intramedullary nailing may precipitate compartment syndrome. This should not be used as a reason to delay these procedures but the surgeon must be aware of the possibility.

Pure extrinsic causes are much less common and are unlikely to produce a compartment syndrome unless there is damage to tissues within the compartment leading to swelling. However, it is important to consider this when planning treatment, as removal of a cast alone can reduce compartment pressure by as much as 30%.

There is a history of trauma, although this may have been quite minor, followed by a history of increasing pain over a period of hours. Pain as a clinical sign is unreliable if the patient’s level of consciousness is altered. Most specifically, the patient will be extremely unwilling to move any part of the limb, especially the extremities. The patient may also complain that the limb feels numb or cold.

The cardinal sign is pain, especially when increasing or out of proportion. The patient has immediate and severe pain on passive stretching of the muscles of the involved compartment. It may be useful to distract children to ensure that it is not their fear of the injured limb being touched which produces the response.

Examination should then include a full release of any bandages down to skin and opening of any casts. This may produce some relief. The limb may also feel cold, have reduced sensation, and be pulseless; these are late signs and suggest a poorer prognosis.

However, it must be emphasized that the presence of normal sensation and pulses distal to a possible compartment syndrome does not exclude the diagnosis.

The main diagnosis of compartment syndrome is based on clinical examination. A high index of suspicion is one key to making the diagnosis. Prompt decompression should not be delayed and if there is any doubt the surgeon should err on the side of caution and perform a fasciotomy. Intracompartmental pressure measurement can be performed and has a role in unconscious patients, and in those with unclear or unreliable clinical signs, such as children. Continuous monitoring may be needed in obtunded patients.

There are various methods available, most commonly a pressure transducer, is flushed, zeroed at the compartment level, and inserted into each compartment in turn to obtain a reading. Reproducibility and reliability of these measurements is poor. The pressure obtained can be used as an absolute value, or related to the diastolic or mean blood pressure.

Circumferential bandages and casts should be avoided if at all possible in the first 12h after trauma or surgery. If they are used they should be split, and then closed or replaced when the swelling is no longer increasing.

All patients sent home with bandages or casts should be warned of the possibility of the development of a compartment syndrome.

Casts, bandages, and padding need to be removed down to the skin. Soft cotton dressing soaked in blood can produce a tight constricting band. If removal of the cast compromises the reduction of the fracture, then this must be accepted. A compartment syndrome takes priority over fracture position. If there is not immediate and sustained improvement in pain and movement once the dressing has been released, an immediate surgical fasciotomy is required.

Fasciotomies should be performed open, as the skin itself can constrict compartments in severe swelling. Open fasciotomy allows the surgeon to avoid damaging nerves with a variable path through the fascia. The anatomy needs careful review before embarking on the fasciotomy. All compartments at risk need to be split along their whole length.

The fasciotomy should be left open, both to reduce pressure and to allow regular reinspection of the muscle. If any parts of the muscle fail to revascularize, they should be debrided. A second look should be performed at 48h and closure can be considered. Complete closure is often not possible and other methods of skin cover will be required. Mechanical closure devices are available but split-skin grafting, which can be later excised is the most commonly used technique. When compartment syndrome has occurred in the presence of an underlying fracture, the fasciotomy creates an open fracture, and should be managed with early coverage to avoid problems with hospital acquired infection.

Delayed fasciotomy following a crush injury or failed revascularization can potentially do more harm than good. If there has been a full compartment syndrome for more than 12h, the chances of the muscle recovery is remote. Fasciotomy will result in extensive debridement of the compartments and expose large volumes of devitalized tissue to hospital-acquired organisms. Late fasciotomies have been associated with a high frequency of morbidity and mortality related to sepsis. Non-operative treatment will be associated with dangerous levels of muscle breakdown products and the risk of renal failure. Temporary dialysis or amputation will need to be considered.

Compartment syndromes occur wherever muscles are bound within rigid fascia compartments. All muscles have an investing fascia, but some are more constrained than others, and it is these which seem to be most susceptible to compartment syndrome. Compartment syndromes of the hands and feet, and their treatments, are described in their relevant chapters.

The classic site is the flexor compartment of the forearm. In the lower leg it is the anterior tibial and the deep posterior compartments. However, compartment syndromes are well described in all of the five compartments of the lower leg (including the separate tibialis posterior compartment).