12.24 Soft tissue hand injuries

Normal hand function is determined by a complex, delicate interaction of soft tissue and skeletal elements. Key soft tissue structures include musculotendinous units, neurovascular bundles, and skin. When the soft tissues are damaged by trauma, infection, or burns, function is compromised. Surgical and non-surgical management of soft tissue hand injuries is therefore aimed at limiting initial soft tissue damage, reconstructing key soft tissue elements, and functional rehabilitation of the hand and patient. Complex open hand injuries present a challenging problem to all reconstructive hand surgeons.

The pattern of swelling after trauma and burns, the spread of infection and injected substances, and the susceptibility of tissues to raised intracompartmental pressure, are all influenced by anatomy. The complex arrangement of fascia and synovium in the hand forms a number of compartments and spaces, whose walls may contain the spread of infection, channel the spread of substances injected at high pressure, and prevent the dissipation of rising intracompartmental pressure. If neglected, infections may breach these anatomical boundaries and enter adjacent spaces and compartments.

A compartment is a volume of tissue partially or completely enclosed by anatomical structures. A space lies between anatomical structures, normally occupies a minimal volume, and contains only loose connective tissue and interstitial fluid or a small volume of synovial or other physiological fluid.

Subcutaneous compartments contain fat, a variable amount of fibrous tissue, and nerves, blood vessels, and lymphatics. On the dorsum of the hand and fingers, the skin is not bound down, allowing massive swelling after injury, and the subcutaneous fat is a single compartment within which infection spreads easily. Along the sides of the digits, in the fingertip pulp, at the flexion creases, and in the palm, the skin is bound to the skeleton, via septa, cutaneous ligaments, and other fibrous structures which limit both distension and the spread of infection.

There are ten muscle compartments in the hand containing intrinsic muscles (Figure 12.24.1).

They comprise the thenar and hypothenar eminences, adductor pollicis, four dorsal interossei, and three palmar interossei. Their fascial envelopes allow very little distension and therefore their response to injury or inflammation is predominantly a rise in pressure.

In the hand the main tunnels are the carpal tunnel and Guyon’s canal. Although the proximal and distal ends of these are not closed off by rigid structures, the structures within them are not capable of longitudinal displacement and so inflammation and oedema manifest themselves as raised intracompartmental pressure.

In the digits are the fibrous flexor sheaths (see Chapter 12.22). Within the fibrous sheaths are synovial spaces around the flexor tendons (a space within a compartment), where increased compartmental pressure may contribute to the damage caused by infection.

In the distal palm are the web spaces—strictly these are compartments—which contain fat, digital neurovascular bundles, and the tendons of the lumbricals and interossei. Their proximal limit is where these structures enter the fibrous tunnels between the palmar fascia and deep transverse metacarpal ligament. They are bounded medially and laterally by the fibrous flexor sheaths, and dorsally and palmarly by the skin of the web, with the natatory ligament on the palmar aspect.

Deep to the most superficial, longitudinally orientated layer of the palmar aponeurosis and the transverse palmar ligament a series of vertical fibres form septa on either side of each pair of flexor tendons, and attached to the metacarpals. The best developed of these pass from the radial and ulnar borders of the palmar aponeurosis to the third and fifth metacarpals respectively. Between these, the potential space deep to the long flexor tendons and superficial to the interossei is known as the palmar or midpalmar space (Figure 12.24.2). Radial to the third metacarpal, the potential space deep to the flexor pollicis longus tendon and superficial to the adductor pollicis muscle is the thenar space (Figure 12.24.2).

High pressure injection injuries (HPII) are caused by devices used for injecting or spraying liquids or gases, and by leaks in pressurized pipes. They are uncommon, frequently underestimated, and even with the best treatment, both short- and long-term morbidity is often severe.

The exact incidence of HPII of the upper limb is unknown. Around two patients per year present to large hand surgery units in the United Kingdom and China.

Most HPII occur in young male manual workers, and the commonest injection sites are the index or middle fingers or the palm of the non-dominant hand. The commonest devices responsible are grease guns, spray guns, diesel fuel injectors, and leaking hydraulic pipes; the commonest substances injected are grease, paint or paint solvent, diesel oil, and hydraulic fluid, though other substances including water, oil, dry cleaning solvents, and gases have been reported. The most common mechanism identified is a break in a high pressure hose, followed by cleaning or adjusting the equipment, inadvertent triggering, and gun malfunction.

Fluid materials at a pressure of 7 × 10⁵ Nm² (100PSI) or more penetrate the skin and spread within the tissues; contact between ejection point and skin is not necessary. Many devices operate at much higher pressures.

The extent of spread depends on site of entry, anatomical barriers, and the volume and pressure of the substance injected. Material penetrates tissue in its line of fire until it reaches a resistant structure, such as bone, tendon, or fibrous flexor sheath, and is deflected. In the finger, injection over the main annular pulleys prevents penetration of the sheath and material spreads proximally and distally, particularly along the neurovascular bundles. The thinner parts of the sheath are less resistant, and material enters and spreads throughout the synovial space. Joints are usually not penetrated. In the palm the palmar fascia and all deeper layers are penetrated through to the dorsum, with spread of material at all levels. Spread may be very extensive, and substances injected into the finger can reach the proximal forearm.

Early tissue damage is due both to direct physical and chemical effects, and to secondary ischaemia. Injections of paint rapidly dissolve in fat lobules, causing tissue necrosis and an intense necrotizing acute inflammatory reaction. This leads to fibrinoid degeneration of blood vessel walls and vascular thrombosis. The immediate toxicity of grease is less severe, but it may lead to more chronic fibrosis and other problems, particularly discharging granulomas.

Regional and systemic effects can occur, and lymphangitis, lymphadenitis, tachycardia, hypotension, pyrexia, confusion, leucocytosis, anaemia, and impaired renal function, have been reported after injection of paint, solvents, and diesel fuel. The pathophysiology of these effects is not understood, but both direct toxicity and the embolic effects of fatty materials have been suggested.

Plain radiographs in two planes help delineate the extent of involvement, particularly if the injected material is radio-opaque; however, radiological and clinical findings must be correlated. Haematological and biochemical parameters should be monitored if systemic effects are noted.

The authors propose a modified classification of HPII (see Table 12.24.1), based on our review of the literature.

For all injuries, analgesia should be administered. Intravenous opiates should be given but may be inadequate and a brachial (not digital) nerve block may be necessary. If systemic effects are present, monitoring of vital signs and urine output should be started. Antibiotic prophylaxis against secondary infection and both steroidal and non-steroidal anti-inflammatory drugs have all been recommended, but none are of proven value. Mild injuries may be treated initially with elevation and observation, however, the threshold for surgical exploration should be low, and the patient prepared for surgery.

Moderate and severe injuries, as well as patients with mild injuries who complain of increasing pain, require urgent exploration, decompression, and removal of as much of the injected material as possible. This is performed under tourniquet without forced exsanguination. Starting at the entrance wound the incision is extended proximally and distally until the full extent of spread is revealed—the smell of solvents can be a useful sign. Removal of all foreign material may be facilitated by use of the operating microscope and helps preserve vital structures. The skin should be left open, or at most partially and loosely closed. Inevitably some material is left, and repeat debridement at 48h should be performed.

After operation the hand is elevated and splinted in the position of safe immobilization, and aggressive active and passive mobilization begun within a few days. Delayed primary amputation is necessary if the digit becomes clearly non-viable. Late reconstruction may include tenolysis, tendon grafting, neurolysis, nerve grafting, scar contracture release, and skin replacement.

Two factors have been shown to predict amputation in HPII: site of injection in the finger compared to the thumb or palm; and injection of an organic solvent (paint, paint thinner, diesel, or oil) compared to other substances. In addition, a delay to debridement of more than 6h lead to significantly more amputations when organic solvent injections were considered alone, but not when all HPIIs were analysed. Furthermore, there was a trend towards higher amputation rates with higher pressures of injection. The presence of infection and the use of steroids have not been shown to affect amputation rate significantly. In one series, all fingers which were noted to be poorly perfused at presentation were subsequently amputated.

Functional outcome of the hand is also poor. At an average 8.5 year follow-up a significantly decreased range of motion has been demonstrated at affected metacarpophalangeal (MCP), proximal interphalangeal (PIP), and distal interphalangeal (DIP) joints compared to the unaffected side. In addition, decreased grip and pinch strength, and increased two-point discrimination threshold has been recognized. Furthermore, 78% of patients complained of continuing cold intolerance, 61% of hypersensitivity, and 22% of constant pain in the affected digit. The average time to return to work was 7.5 months, and over half of patients had changed jobs or remained unemployed after the injury.

Compartment syndrome exists when the pressure within an anatomical compartment is increased to a level where the viability of the tissues within the compartment is compromised. The increase in pressure causes tissue ischaemia, especially of muscles and nerves within the compartment, and may lead to permanent loss of function. The fascial compartments of the hand are illustrated in Figure 12.24.1.

Incidence varies with aetiology and severity of the primary injury; in severe upper limb burns for example it is up to 70%.

The commonest causes are crush injuries and burns, but there are a large variety of potential causes, many of which can occur in patients who are unconscious and therefore do not display classical symptoms and signs (Box 12.24.1). Compartment syndrome is an important cause of iatrogenic morbidity as a complication of tight casts or dressings, intravenous drug administration, and arterial lines.

The diagnosis of compartment syndrome is clinical, and once made mandates immediate surgical intervention. Direct measurement of intracompartmental pressures can be achieved by a variety of methods, all of which involve the principle of placing a column of fluid between the compartment and a measuring device. Normal compartment pressure in an uninjured extremity is 0–8mmHg, and normal capillary perfusion pressure is 20–25mmHg. No consensus exists as to a threshold for compartment decompression, and indeed the threshold may vary depending on patient factors such as blood pressure, which affects capillary perfusion pressure. Furthermore, the multiple compartments in the hand make measurement a complex process even with the simplest techniques. We therefore recommend the measurement of intracompartmental pressures only where there is strong doubt about the presence of a compartment syndrome and a strong contraindication to surgical treatment, which is a rare situation.

The treatment of a suspected compartment syndrome is surgical decompression without delay. In the meantime, any external pressure, such as tight bandages or casts, should be removed. The hand should be placed level with the heart to maximize perfusion pressure whilst minimizing swelling and hypovolaemia should be corrected.

The exact site of incisions is not critical, and all compartments can be reached through two dorsal incisions (see Figure 12.24.1). Should any doubt remain as to whether a particular compartment has been decompressed, a further incision over the compartment should be made. The carpal tunnel should also be released. Decompression of digits is not necessary unless the digit itself has been injured; the commonest indication is after burns (see later). The wounds should be left open and dressed.

In circumstances where the probability of a compartment syndrome is very high, such as after revascularization after a long ischaemia time, or following a severe crush injury, fasciotomies of the intrinsic muscles and carpal tunnel decompression should be performed prophylactically.

After decompression, the hand should be elevated and splinted in the position of safe immobilization. After 3–5 days the patient should be returned to theatre and the skin closed if this can be done easily. If not, dorsal wounds should be covered with thin partial thickness skin grafts and the hand mobilized soon afterwards.

In a retrospective study of nineteen patients who had undergone hand and/or forearm fasciotomy for raised intracompartmental pressure, a good outcome in 13 patients and a poor result was recorded in four. In those four patients, the time from diagnosis to decompression was over 6h, and all four were obtunded or under general anaesthesia when the compartment syndrome developed. However, good results were achieved in three patients decompressed over 12h after diagnosis, so fasciotomy should still be performed when there is a late presentation.

Intrinsic tightness leading to intrinsic contracture is the characteristic complication of unrecognized or under treated compartment syndrome of the hand. This is caused by fibrosis of the affected lumbricals and interossei. Intrinsic tightness can be diagnosed clinically by increased resistance to flexion of the IP joints when the MCP joint is held extended compared to when the MCP joint is flexed. Symptomatically, patients with mild intrinsic contractures complain of persistent limited interphalangeal (IP) joint flexion months after injury. In more severe cases, flexion contractures of the MCP joints and extension contractures of the IP joints may develop. Severe complications of untreated compartment syndrome include digital necrosis, and persistent nerve dysfunction.

Burns of the hands require specialist assessment and treatment. The British Burn Association recognizes that burns to the hands involving dermal or full thickness skin loss are more likely to follow a complex clinical course and therefore should be referred to a specialist burn care facility. Furthermore, the need for skin grafting of hand burns is independently correlated with reduced quality of life in burn survivors.

Hand burns are common, and occur out of proportion to their percentage body surface area. Many small injuries are treated as outpatients and the total incidence is unknown but high. In diverse countries such as the United Kingdom, United States of America, and Iran, two to three patients per 10 000 population per year are admitted to hospital with burns, and ten times this number may be treated without hospital admission; the arms and hands are involved in around 45% of cases. Both incidence and cause vary markedly with age, geography, and sex.

The causes of burns are thermal, chemical, and electrical. The majority are thermal, caused by hot liquids, fire, and contact with hot objects. Chemical and electrical burns have their own special effects, and are not discussed further. The amount of damage in a thermal burn depends on the temperature and duration of burning.

Burns are classified clinically according to depth of skin necrosis (Table 12.24.2). Four grades of burn are clinically recognisable: epidermal, superficial partial thickness (SPT), deep partial thickness (DPT), and full thickness (FT) (Figure 12.24.3). Full thickness burns may also involve deeper tissues.

Burn depth forms the basis for decisions about management as it indicates whether the skin will heal and the likely degree of scarring. Epidermal burns, for example sunburn, heal spontaneously within 2–3 days and require treatment with moisturizer and mobilization. SPT burns heal in 7–14 days without scarring. DPT burns may heal in 14–21 days or more but often produce hypertrophic scars that contract and may interfere with function. FT burns heal by secondary intention, which is only acceptable if they are small. In the hand a distinction should also be made between palmar skin, which is thick, specialized, and more likely to heal well after apparently deeper burns, and dorsal skin, which is thinner, non-specialized, and less likely to heal well after anything more than SPT injury.

For all burns deeper than epidermal, oedema occurs in nearby tissues, and swelling reaches its maximum at 24–36h. A swollen, unsplinted hand takes up a position of wrist flexion, MCP joint extension, IP joint flexion, and thumb adduction, exactly the opposite of the position of safe immobilization, and if this is allowed to persist then secondary joint changes make mobilization difficult and can result in permanent joint contractures.

Coagulated protein contracts, and FT burns have lost their ability to stretch because of destruction of elastin within the dermis. Therefore, circumferential FT burns of the hand or digits, together with increased interstitial pressure due to oedema, may cut off the distal circulation and necessitate emergency release by escharotomy. With extensive FT burns a muscle compartment syndrome can also develop, especially if escharotomy is delayed.

No special investigations are needed for hand burns. Various imaging techniques have been tried for measuring burn depth, but none has proved to be of practical clinical use.

Hand burns may occur as part of a larger burn, the systemic effects of which dominate the clinical picture at first, although the hands must be considered in the overall management plan from the start. The initial management of major burns follows ATLS^® principles. Analgesia is important, and thermally burned hands should be protected from desiccation and contamination. Clingfilm is useful for temporary cover.

Once the patient is stable a decision about wound protection must be made. For the hand, either dressings or plastic bags can be used. It is important at this stage not to apply creams, ointments, or liquids, for example silver sulphadiazine cream that will make depth assessment by the burn surgeon difficult.

Elevation to reduce swelling is important, except when escharotomy and/or fasciotomy is planned, when the hand should be kept at heart level. Active mobilization should be pursued if the burn is treated in a plastic bag or glove, combined with resting night-splints. If the burn is treated with dressings, the hand should be splinted in the position of safe immobilization.

Most chemical burns should be treated by immediate and copious lavage with water, although there are exceptions. Emergency workplace showers are available in many factories, along with specific antidotes for particular chemicals.

Domestic electrical injuries can cause cardiac arrhythmias and myocardial damage, and if evidence of either is found the patient should be monitored for at least 24h. High voltage electrical injury, often from industrial source, is a major emergency requiring immediate resuscitation and surgical exploration, fasciotomy, debridement, and vascular reconstruction, with amputation if the limb is irretrievably damaged.

Escharotomy and fasciotomy, if indicated, are emergencies. Distal circulation in the burned hand may be difficult to assess, and the indication for escharotomy is a full thickness or possibly full-thickness burn that is circumferential or almost circumferential and might cause ischaemia. Both escharotomy and fasciotomy should be performed under general or regional anaesthesia, and if anything more than one hand requires escharotomy blood should be available for transfusion.

Apart from escharotomy and fasciotomy, the decision about operative or non-operative treatment and timing of surgery should be taken by a specialist burn surgeon. Decision making depends on the depth and distribution of the burn and on other injuries. SPT burns do not need surgery, but should be re-examined after 48h to make sure they are truly SPT and have not become deeper. Definite FT burns, dorsal or palmar, should be excised and grafted in a specialist unit. In large burns the hands are second only to the face and neck in order of priority for grafting.

The management of DPT burns is less clear cut. On the dorsum, the results of early tangential excision and skin grafting are so good that there is an argument for early surgery in all but definite SPT wounds, but this is controversial and good results can also be obtained by grafting only wounds that have not healed by 2–3 weeks. Grafts to the dorsum should be applied with the wrist and finger joints fully flexed in order to maximize the amount of skin applied and therefore prevent subsequent dorsal contracture. On the palmar surface depth is more difficult to assess and, because of the thickness of the skin, healing frequently occurs after burns that appear at first to be deeper than SPT. This is specialized skin and if it is capable of healing in 2–3 weeks or even longer without grafting, then this is likely to produce the best result.

After grafting the hand is elevated and splinted until the graft is stable enough to tolerate mobilization, usually 4–7 days. Mobilization should be started as soon as possible. If the patient is unable to mobilize themselves, passive mobilization by the therapist should be continued until they are.

Wounds that have taken more than 14 days to heal, and grafted areas once they are healed and stable, benefit from compression gloves, which help to minimize scar hypertrophy and accelerate scar maturation.

The outcome of a SPT burn should be a normal hand, although stiffness can occur if it has not been exercised or splinted. The outcome of deeper burns depends on the severity of injury and the timing and adequacy of surgical treatment, splintage, mobilization and post-burn therapy. When burns are very deep, and involve the extensor mechanism, the results are poor, with loss of motion and difficulty performing activities of daily living.

Complications of hand burns are often a consequence of delayed healing with subsequent adverse scarring and contracture, or poor cooperation with therapy and splintage resulting in stiffness. Even with the best management, complications occur. Frequently seen problems include: first webspace adduction contracture, other webspace contractures, dorsal skin contractures, little finger abduction deformity, MCP joint hyperextension, PIP joint flexion contracture, extensor tendon adhesion, Boutonnière deformity, median and ulnar nerve compression neuropathy, amputation secondary to gangrene. Secondary surgery to release scars and reconstruct skin and soft tissues may be required. The growing hand is especially vulnerable and likely to need multiple secondary procedures.

Hand infections are common, and the consequences of poor or delayed treatment can be severe. Infections may be acute or chronic, bacterial, viral, fungal, or protozoal. Most are acute, and most of these are bacterial. The following discussion applies to acute bacterial infections. The majority are due to trauma, including animal and human bites (usually the patient has punched someone in the mouth), but a few are haematogenous.

The total incidence is not known because many minor infections are treated by primary care physicians and accident departments, but large hand surgery units in the developed world may admit 40–100 patients per year with more serious infections. Accurate worldwide figures are not available.

A large variety of bacteria have been cultured from hand infections. The most common organisms are flora of the mouth or skin, especially the gram-positive aerobes streptococci and staphylococci. However mixed infections are common and anaerobes are present not infrequently, particularly after human bites and in paronychia. Human bites have a high incidence of Eikenella corrodens and dog and cat bites of Pasteurella multocida. The majority of acute hand infections occur in immunocompetent hosts. However, a significant minority occur in patients with predisposing immunocompromise, caused by diabetes mellitus, HIV infection, or steroid treatment, for example. Immunocompromise may not be diagnosed prior to the onset of infection, and can predispose to infection with unusual organisms, including Gram-negative and mixed organisms, and mycobacteria. Clinicians must also be aware of the possibility of hand infection caused by community acquired meticillin resistant Staphylococcus aureus (MRSA). This may be particularly important as the delay before receiving appropriate antibiotics for patients with MRSA hand infections has been shown to be increased compared to those with non-MRSA hand infection.

Most infections are confined, at least initially, to a particular anatomical site, space, or compartment, and are classified accordingly. The classification and relative incidence of those infections requiring operative treatment are listed in Table 12.24.3. This is necessarily a biased estimate of the true frequency of different types of hand infection, as already it has been noted that many infections are treated successfully in a primary care or emergency department setting.

Most patients give a history of trauma, with a penetrating injury that may have been trivial, or a more severe injury that has been neglected. The history may suggest likely pathogens, but sometimes the history is unreliable, such as after a human ‘bite’. A full general history should be taken, particularly regarding predisposing conditions and tetanus immunity. The duration of symptoms and severity of pain, particularly pain that has prevented sleep, indicate whether the infection is early or whether a localized collection of pus is likely.

Cellulitis alone occurs most commonly on the dorsum of the fingers or hand, often following a minor wound, and is usually due to beta-haemolytic streptococcus. Erythema and swelling may spread rapidly, sometimes with associated lymphangitis and systemic illness, and there may be skin damage ranging from blistering to frank necrosis. Necrotizing fasciitis is uncommon but can affect the hand and upper limb as elsewhere.

Mixed infections, particularly with S. aureus and anaerobes, are common. It starts with swelling, erythema, and tenderness around the nail-fold, usually on one side (paronychia), or at the base of the nail (eponychia). After 24h pus may be detectable, in the nail-fold and sometimes under the nail. In late cases the whole of the nail-fold, both sides and the base, may be involved.

This is commonly due to a puncture wound and a foreign body may be present. Diabetics can get pulp infections caused by pricking their fingers for blood glucose monitoring. S. aureus and anaerobes are the commonest pathogens. Early on there may be localized cellulitis or a small collection of pus, but soon the whole pulp becomes swollen, tense, and very tender.

Localized subcutaneous infection may occur anywhere in the hand. In the palm the infection may extend via a narrow channel through the palmar fascia to form a subfascial abscess, which together with the subcutaneous component is known as a collar-stud abscess.

Infective tenosynovitis affects almost exclusively the flexor tendons. Most cases are caused by penetrating trauma, but some are haematogenous, and in these gonococcus is a likely pathogen. Kanavel’s four cardinal signs are: digit held in slight flexion, fusiform swelling of whole digit, tenderness over the flexor sheath, and severe pain on passive extension. In early disease, the signs may be subtle. In tenosynovitis of the thumb and little fingers tenderness may extend proximally to the wrist and into the distal forearm via the radial and ulnar bursae.

The potential spaces in the hand (Figure 12.24.2) can become actual spaces, occupied by pus, most often following a penetrating injury or extension of infection from a tenosynovial sheath or an adjacent deep space.

The fingers on either side of the web are abducted away from the web, and there is swelling and tenderness on dorsal and palmar aspects.

The thumb is held abducted, with tenderness and swelling over the thenar eminence, first web (palmar and dorsal), and index metacarpal, and pain on thumb extension or attempted opposition.

The normal concavity of the palm is lost, there is dorsal swelling that may be more prominent than the palmar swelling, and finger movements, especially of the middle and ring fingers, are painful.

Septic arthritis may be caused by penetrating injury (when it may co-exist with tenosynovitis caused by the same injury), extension of another infection (most commonly tenosynovitis), or haematogenous spread from an infection elsewhere. In children Haemophillus influenzae is a likely pathogen, and in sexually active adults gonoccus should be considered. Bite wounds caused by punching someone in the teeth can result in septic arthritis of the MCP joints of the fingers if the joint is penetrated. An important anatomical point is that the wound occurs with the joints in maximum flexion, and if explored with the joints in extension the defects in the different layers (skin, extensor apparatus, joint capsule) will be out of line and the involvement of the joint missed if not looked for.

There is swelling and erythema around the joint, which is held in the position that maximizes its volume (MCP joint extension and IP joint partial flexion). The joint is tender, and any movement is painful.

Osteomyelitis of the hand is uncommon and affects almost exclusively the long bones. It may follow infections in adjacent tissues or compound fractures (including for example, a Seymour fracture) or may be due to haematogenous spread. S. aureus is the commonest pathogen, and Haemophillus influenzae is common in young children. There is local swelling, erythema, and tenderness over part of the affected bone.

In acute infections the decision to operate is a clinical one. Plain radiographs in two planes may show foreign bodies, including broken teeth, but apart from these and soft tissue swelling most radiographs of infected hands are normal at the time of presentation. Microbiological specimens usually have to await surgical exploration, though in septic arthritis joint aspiration may confirm the diagnosis. Microbiology for osteomyelitis is best by bone biopsy. Blood cultures should be done in the presence of systemic illness.

Relevant biochemical and haematological tests should be done if an underlying cause such as diabetes or immune compromise is suspected.

Many conditions can mimic acute hand infections, the more common differential diagnoses being acute arthritis, acute gout, herpetic whitlow, compartment syndrome, hand fracture, and rarely primary hand tumour.

The principles of treatment are the same for all acute bacterial infections: surgical drainage of localized infections, elevation, splintage, antibiotics, and mobilization as infection is controlled and swelling subsides.

Cellulitis and early osteomyelitis may be treated with elevation and intravenous antibiotics. Patients awaiting surgery for other acute hand infections are treated with elevation and analgesia. Antibiotic administration should be delayed until microbiological specimens have been obtained, unless there is a strong indication for starting them immediately, such as spreading infection or systemic illness.

The decision to operate depends on history, examination, and suspected site of infection. Visible pus or fluctuation in nail-fold infections and subcutaneous abscesses may be obvious, but at other sites severe pain and/or loss of sleep strongly indicate localization and the need for drainage. Suspected septic arthritis and tenosynovitis require urgent drainage. Necrotizing fasciitis is a life-threatening emergency requiring immediate resuscitation and radical excision. Cellulitis needs surgery if an abscess develops or there is skin necrosis requiring excision. Haematogenous osteomyelitis is treated by operation if there is no improvement in 24h, and osteomyelitis due to compound fractures or extension of soft tissue infections is drained and debrided along with the primary lesion.

Surgical drainage should be performed in an operating theatre, under tourniquet control but without forced exsanguination. Incisions for localized infections at different sites should conform to general principles of hand incisions. Wounds should be left open or drained, and a planned wound inspection at 48h is recommended. If infection is severe, or the symptoms do not improve after initial treatment, earlier wound inspection and further exploration is indicated.

Antibiotics should be started intravenously, the choice depending on likely pathogens, and local sensitivity patterns in consultation with microbiology colleagues. In most cases the choice should cover Staphylococcus aureus, beta haemolytic Streptococcus, and anaerobes. Eikenella corrodens and Pasteurella multocida are both usually sensitive to penicillins. Initial antibiotic treatment should be reviewed depending on clinical response and the results of microbiological investigation.

Hands should be splinted in the position of safe immobilization until acute inflammation is subsiding. Active mobilization should then be started, with resting splintage during the intervening periods and at night. As swelling diminishes, passive mobilization should be introduced with increasing active use and decreasing periods of splintage.

The outcome of a hand infection treated early and adequately should be a normal hand. Stiffness is the commonest complication (10–30%), and late or inadequate treatment can lead to irreversible damage to the tissues involved, spread to other tissues (including systemic and metastatic sepsis), and chronic infection both with the primarily infecting agent and other secondary organisms.

Cellulitis and pulp infections can cause skin and fat necrosis with exposure of deeper structures, especially extensor tendons, loss of pulp padding over distal phalanges, and osteomyelitis. Paronychia can lead to nail deformity, and sometimes chronic infection, often a secondary fungal infection. Tenosynovitis can cause scarring and adhesions between sheath and tendons, with loss of mobility, necrosis of the flexor tendons, extension into adjacent bone and joints, and more proximally into the deep spaces of the palm and wrist. Septic arthritis can result in secondary osteoarthritis or fusion. Septic PIP joint arthritis may lead to a septic boutonniere deformity caused by rupture of the dorsal capsule and destruction of the central extensor tendon slip. Osteomyelitis can lead to loss of bone and skeletal collapse.

Open hand injuries can present one of the most challenging problems to the reconstructive hand surgeon. Severe soft tissue injuries complicate the management of underlying fractures, and carry a worse functional prognosis. Adherence to the principles outlined in Box 12.24.3 will help to optimize long-term functional outcomes after these potentially devastating injuries.

Reconstructive techniques used for gaining soft tissue coverage have traditionally been conceptualized as a ‘reconstructive ladder’, whereby each rung of the ladder represents a more complex reconstruction, and the surgeon chooses the simplest possible reconstructive option. More recently, the concept of the ‘reconstructive toolbox’ has become more widely accepted, whereby not the simplest, but the most appropriate option from a toolbox of reconstructive techniques is applied to a particular clinical problem. This concept is particularly important in dealing with severe open hand injuries, where stable vascularized soft tissue coverage is vital to allow early mobilization and functional rehabilitation.

The incidence of all open hand, wrist and forearm injuries has been calculated as 966 per 100 000 person-years in a population-based study in Norway. Males were affected over twice as commonly as females, and this bias was more evident in more severe injuries. Furthermore, open fractures constituted 37.9% of hand fractures presenting to a hand surgery service in Hong Kong over a 10-year period.

The history indicates the type and degree of damage to both soft tissues and skeleton. Common injury mechanisms vary with geography, work and social factors. Industrial injuries commonly involve crushing and shearing forces, while domestic injuries are more frequently due to sharp cuts.

Plain radiographs in two planes, guided by the results of clinical examination, will demonstrate bony injuries. Occasionally, special views will be required in order to diagnose specific injuries. Laboratory studies as dictated by the clinical condition of the patient should be obtained.

We favour the classification described in Table 12.24.4, though other similar classifications have been described.

The ultimate goals of reconstruction in relation to the individual patient should be determined in order to formulate a reconstructive surgical plan. For some patients, early amputation is the most appropriate reconstruction, allowing early functional rehabilitation, and early return to work.

A rapid initial assessment and resuscitation following the principles of ATLS^® should be undertaken. Wounds should be irrigated, and dressed with a non-adherent layer and saline-soaked gauze in order to prevent desiccation of the wound. If there is no suspicion of a vascular injury or compartment syndrome, the limb should be elevated. The open hand injury should receive the same tetanus and antibiotic coverage that any open fracture would receive.

Wound excision is initiated at the skin surface and carried towards the depths of the wound. Any non-viable or grossly contaminated tissues should be excised. Marginally vascularized tissue, especially muscle, should be excised. Particular attention should be paid to the intrinsic muscles of the hand, as necrosis and subsequent fibrosis can lead to significant functional impairment. Critical structures, such as vessels, nerves and tendons should be retained. Any bone fragments which are maintained on a soft-tissue pedicle should be retained if not grossly contaminated. Any extensive wound in the palm should be extended to decompress the carpal tunnel. This extension not only prevents the development of acute carpal tunnel syndrome, but allows a reference to the planes of the palm.

Primary excision is undertaken under loupe magnification with the limb exsanguinated and tourniquet inflated. Secondary excision is carried out immediately afterwards with the tourniquet deflated to further trim any remaining devitalized tissue. Special attention should be paid to the soft tissue envelope after release of the tourniquet. Any parts which are to be amputated during the initial excision should be assessed for use as ‘spare parts’ in primary reconstruction, for example, a fillet flap may provide vascularized soft tissue coverage; a digit may provide bone graft.

After excision, the wound should be thoroughly irrigated with normal saline. If soft tissue reconstruction cannot be immediately performed, or if doubts remain as to the viability of some tissues, a ‘second look’ procedure at 24–48h should be undertaken. Subsequent skeletal stabilization and soft tissue reconstruction should be undertaken at the time of definitive soft tissue coverage.

The initial reconstructive step is skeletal stabilization. The most important consideration for skeletal reconstruction in the hand is obtaining stability. A stable bone base allows early rehabilitation, and a lack of rigid fixation is associated with a worse outcome. Anatomical length maintains the extrinsic and intrinsic relationships necessary for function. The particular form of stabilization undertaken depends on the precise fracture pattern. Segmental bone gaps can be primarily reconstructed with corticocancellous bone grafts.

Next, tendons should be trimmed and repaired using standard core and epitendinous suture techniques (Chapters 12.22 and 12.23). The A2 and A4 pulleys should also be repaired or reconstructed. If primary repair is not possible, silicone rods can be placed and a second stage reconstruction subsequently performed. The next procedure is vascular reconstruction, which is discussed in Chapter 12.27. Nerve reconstruction is undertaken next. Crushed nerve should be excised back to healthy fascicles, and the nerve repaired using an epineural technique under the operating microscope. If there is a nerve gap, conduits (reversed vein, muscle) or nerve graft—often harvested from amputated parts—can be utilized.

Finally, vascularized soft tissue coverage should be obtained. The range of options available is large (Table 12.24.5), but some basic principles emerge:

The hand should be elevated and splinted in the position of safe immobilization. A well-planned therapy regimen should be instituted in order to achieve maximal functional rehabilitation. The use of custom made thermoplastic splints from a few days postoperatively facilitates wound care and therapy. Skin grafts require immobilization for 5 days to prevent shear and allow adequate take, but otherwise skeletal fixation and soft tissue repair should be stable enough to allow early active motion. Desensitization therapy should also be started early following nerve repair.

The final outcome after treatment of open hand injuries depends on the extent of the injury, the surgical management, and the postoperative rehabilitation. This rehabilitation includes psychological and social support. Open fractures of the fingers and thumb have a significantly worse outcome than closed fractures. In the fingers, 46.6% of open fractures and 80.7% closed fractures have been reported as having a good or excellent outcome. For the thumb, the equivalent figures were 78.8% and 97.8%.

The complications of open injuries depend on the tissues injured. Failure to recognize the true zone of injury and perform adequate wound excision can lead to infection, sepsis, and even death. Skeletal fixation can result in non-union, malunion, or osteomyelitis. Joint contractures and stiffness can occur. Tendon repairs may rupture, or become adherent to scar tissue. Vascular repairs may thrombose. Nerve injury often leads to cold intolerance, hypersensitivity, and painful neuromas may form, in addition to incomplete sensory and motor recovery. Scars may become hypertrophic, and soft tissue ulceration may be problematic. Secondary procedures to address these complications include osteotomies, joint replacement, nerve grafting, sensory reconstruction, tendon transfers, tenolysis, arthrolysis, and contracture release.

Soft tissue hand injuries comprise a wide variety of pathologies. All share a common theme, in that optimization of outcome depends on early diagnosis and timely, adequate treatment. Non-surgical management, especially splintage and therapy, is a crucial component of a successful outcome, and a team approach is necessary. Even with optimal treatment, long-term results following some injuries are suboptimal, and mechanisms to rehabilitate the patient into society, work and leisure are important.