Treatment of the injured upper extremity and the appreciation of the severe disability that could result from poor management was the major driving force in the evolution of upper extremity and hand surgery as independent and distinct specialties.1
A primary theme was the recognition that many injuries to the upper extremity are combined injuries and that appropriate treatment could best be delivered by someone trained in management of both bone and soft tissue injuries. Today, the successful approach to the treatment of many upper extremity injuries requires microsurgical skills to deal with soft tissue coverage, nerve repair, and revascularization, in addition to fracture care.
HIGH-ENERGY VERSUS LOW-ENERGY TRAUMA
One useful way to classify injuries to the upper extremity relates to the amount of energy involved in their generation. Low-energy forces typically cause simple injuries, while high-energy forces lead to complex injuries involving soft tissue and bones that are often associated with joint, neurologic, or vascular involvement. A classic example is a distal radius fracture that typically occurs in two age groups with different mechanisms related to the transfer of energy. A low-energy distal radius fracture typically occurs in an elderly osteopenic woman where the mechanism was a simple fall on an outstretched hand. This usually results in a simple fracture pattern that may best be treated via closed reduction and splinting. A high-energy distal radius fracture, on the other hand, typically occurs in a young healthy and fit patient resulting from a high-speed motor vehicle crash or fall from a significant height. These injuries are associated with swelling of soft tissue, severely comminuted intra-articular shear-type fractures, and several associated potential complications. At first glimpse both scenarios share the diagnosis of “distal radius fracture” and may even seem similar, but it is extremely important to recognize that these are two very different entities. While the low-energy distal radius fracture is simply treated as noted above, the high-energy counterpart should be closely monitored for swelling that may lead to an “acute carpal tunnel syndrome” with subsequent injury to the median nerve, breakdown of soft tissue, and vascular insufficiency. Furthermore, high-energy distal radius fractures will often require surgical treatment including open reduction and internal fixation to restore articular congruency.
Similarly, soft tissue lacerations can be classified as high or low energy depending on the causative agent. A laceration from a sharp kitchen knife to the forearm is to be distinguished from a laceration to the same region caused by a high-speed electrical saw. While they may initially appear similar on presentation in the emergency department (ED), they are quite different. The former may be irrigated and sutured primarily, while the latter requires careful observation due to the late effects of thermal and kinetic energy causing burns of the skin and soft tissue. Skin breakdown with necrosis of the wound edges is typically seen with high-energy lacerations, and recurrent debridements in the operating room may be needed with more complex plastic reconstruction.
INJURY-SPECIFIC HISTORY AND PHYSICAL EXAMINATION
It is useful to gather information regarding the mechanism of injury in the initial evaluation and to classify injuries based on whether they were caused by high or low energy. The exact type of mechanism such as blunt, penetrating, lacerating, shear, or degloving and crushing injuries should be elicited, as each of these will deserve specific attention related to the mechanism. Other important components of the history include time of injury, whether the environment was clean or contaminated, whether the injury was work related, the patient’s occupation, hand dominance, and important activities. Finally, a previous history of an injury to an upper extremity should be elicited and any prior functional limitations should be described. Once the airway, breathing, and circulation are stabilized, the physical examination of the upper extremity should focus primarily on the soft tissue components of artery, nerve, and tendon, before focusing on bony injuries.
Circulation can be assessed by observation of the color of the skin and nail bed, skin temperature, and rate of capillary refill after blanching the skin with light pressure. One useful maneuver is to interpret findings by comparison with an uninjured extremity. This approach is useful in the evaluation of unclear x-ray findings, especially in the growing child, also. Arterial insufficiency produces a pale, cool limb with prolonged (>2 seconds) or absent capillary refill and loss of turgor. Venous insufficiency will result in a purple, congested extremity with faster than normal capillary refill. Evaluation of arterial pulses begins proximally with palpation of the brachial artery followed by the radial and ulnar arteries. A manual Allen’s test should be performed when the injury allows. When clinically indicated, confirmation of a positive manual Allen’s test can be obtained using Doppler ultrasound, pulse oximetry, or angiography.2,3
Sensation and motor function should be tested if there is any question of injury to a peripheral nerve. There are three autonomous zones in the hand. The median nerve zone is the index fingertip, the ulnar nerve zone is the small fingertip, and the radial nerve zone is the dorsal side of the first web space over the first dorsal interosseous muscle. More proximally, standard dermatome maps can be utilized. For sensibility, the most useful screening test is light touch perception that can be elicited by gently scratching or tapping the area of interest with a broken applicator stick. A more precise evaluation of distal innervation density can be accomplished by determining static and moving two-point discrimination at the fingertip. At the pulp, normal static two-point discrimination should be <6 mm and moving two-point discrimination <3 mm. Occasionally, threshold testing with a Semmes-Weinstein monofilament or vibration sensibility evaluation may be indicated.
Motor testing should begin distal to the level of suspected injury. A systematic evaluation of each muscle based on innervation is the ideal (Tables 39-1 and 39-2). In the trauma setting, recreating the maneuvers of rock, paper, and scissors from the childhood game of “roshambo” demonstrates function of the median, radial, and ulnar nerves, respectively. Integrity of the musculocutaneous, axillary, and suprascapular nerves can be grossly evaluated by asking the patient to grasp a cup and simulate drinking. The examination must be interpreted in light of any other soft tissue or bony injuries that might bias the examination.
The minimal x-ray examination includes the anterior–posterior (AP) or posterior–anterior (PA) and lateral views. When dealing with a long-bone fracture, an important rule is to image the entire bone from the joint above to the joint below the injury. Complete evaluation at any articular level, or within the hand itself, usually requires additional views designed to better visualize specific injuries. These may include fluoroscopic motion views and stress views to help diagnose ligamentous instability. More sophisticated x-ray studies such as arthrography, ultrasound, computed tomography (CT), and magnetic resonance imaging (MRI) may be important in future surgical planning, but are rarely indicated in the initial management of injury to an upper extremity. A practical guide to some commonly used x-ray views is suggested in Tables 39-3 to 39-6.
INJURIES NOT TO BE MISSED
When assessing injuries in the upper extremity, it is important to avoid missing secondary problems as described in Table 39-7.
Compartment syndrome is mentioned due to the importance of early recognition and the devastating consequences of a missed or delayed diagnosis (Fig. 39-1). While compartment syndrome has been described in the arm, it is much more common in the forearm and hand.4 The forearm is composed of three distinct compartments including the volar, dorsal, and the mobile wad, while the hand has four dorsal and three volar interosseous compartments. After trauma, if acute swelling of the forearm or hand occurs, then one should be suspicious that a compartment syndrome is present (Fig. 39-2). Clinically, pain out of proportion to the clinical findings and pain on passive tendon stretching are probably the most reliable indication to pursue further diagnostic testing or operative treatment. Prompt diagnosis and treatment must be initiated before irreversible ischemic necrosis and tissue damage ensues. Therefore, late findings such as pallor, pulselessness, paresthesia, or paralysis should not be awaited for since their appearance is associated with irreversible damage. If a compartment syndrome is suspected after application of a cast or splint, it should be immediately split to the underlying skin.
FIGURE 39-1 End stage of compartment syndrome. This patient had multiple secondary infections and finally required an above-elbow amputation for this nonfunctional limb.
FIGURE 39-2 Forearm compartment syndrome after formal volar fasciotomy. Pressures measured in this patient exceeded 100 mm. Note the extent of muscle expansion as it escapes the boundaries of the volar compartment following release via fasciotomy.
At any time, measurement of a compartment pressure is a particularly valuable aid in diagnosis and may be the most useful tool in the unconscious or noncommunicative patient. Controversy still exists over the compartment pressure at which fasciotomy is deemed necessary. Whitesides et al.5 recommended fasciotomy when the pressure was measured at 10–30 mm Hg below the diastolic blood pressure. Others in the general trauma and vascular community have recommended that the compartment pressure alone be used as a guide for fasciotomy, but this recommendation has varied from 30 to 50 mm Hg in normotensive individuals. Another practical and safe indication to help guide decision making is when the intracompartmental pressure of the affected limb is higher than in the contralateral normal limb and progressively rises above 30 mm Hg. Regardless of which of the above methods is used, once a clinical suspicion arises, it is better to err on the side of early release to avoid devastating sequelae. Muscle damage begins within 4 hours of ischemia and is irreversible by 6 hours. In addition, nerve damage can put distal intrinsic function at risk and further limit reconstructive options.
“Fight Bite” Injuries of the Head of the Metacarpal Bone
It is important to recognize these injuries as they may lead to an intra-articular infection/septic arthritis of the metacarpophalangeal (MCP) joint. Clenched fist or “fight bite” injuries occur when the patient strikes the mouth of another person.6 This most commonly involves the metacarpal head of the long finger because of its prominence in the clenched position. The initial injury may appear quite innocuous; however, all injuries should be assumed to have penetrated deeper structures and to have entered the underlying joint. X-rays are mandatory for these injuries, not only to look for a fracture but to rule out the presence of a retained tooth fragment also. Even when seen acutely, these injuries should be explored by a formal arthrotomy in the operating room where cultures are obtained and the joint irrigated. It is preferable to enter the joint by taking down the ulnar sagittal band to decrease the possibility of ulnar luxation or subluxation of the extensor hood. Operative intervention should be followed by intravenous antibiotics targeting Staphylococcus sp. for 24–48 hours (see Chapter 18).
Appropriate wound debridement must first be done before adequate soft tissue coverage can be safely provided.7 Irrigation with a pressure of at least 7 psi is mandatory. Earlier studies of complex wounds in the lower extremity have shown a clear advantage for wound closure after debridement within 5 days of the injury with regard to flap survival, most rapid time to bone healing, reduced infection, and lowest number of hospital days.8,9 So-called emergency free flaps have been shown to have a high degree of success for complex upper extremity wounds.10 While early wound closure is desirable, it depends on the energy of the initial injury, degree of contamination involved, vital structures exposed, and the general health of the patient, as well as the availability of a surgical team. Excessive delay of wound closure results in prolongation of the inflammatory response to wounding, increases the formation of edema, allows joints to become stiff, increases fibrosis around moving structures, and delays hand therapy. Early wound coverage with a flap aborts the extended inflammatory phase of healing that is encountered in chronic wounds and inhibits contraction of the wound. Well-vascularized axial pattern muscle flaps seem to help combat infection, also.11,12 If wound closure is done late, after granulation has developed, then the inhibitory effect on wound contraction is lost.13
Once the wound satisfies the requirements for closure, the reconstructive ladder is borne in mind, and the simplest option that is best suited to both the general condition of the patient and the local requirements of the wound is then selected.
The reconstructive requirements for the upper extremity are listed as follows:
1. Replace missing tissue type with a similar type, for example, thin and pliable soft tissue coverage is required in the hand and fingers.
2. There may be a subsequent or simultaneous need for secondary reconstruction of bone, tendon, or nerve.
3. Flap reconstruction may need to be sensate.
4. The size of the defect must be considered three-dimensionally to provide deep volume fill as well as coverage of surface area.
5. Flap reconstruction may be functional and provide motion.
Skin grafts may be suitable for wounds of large surface area that do not expose important structures. In the hand, a more durable wound coverage such as a full-thickness skin graft or flap may be required to cover exposed important structures and to meet the frequent secondary need for later tenolysis and tendon transfers. Full-thickness skin grafts or flaps result in less wound contraction, probably by their effect on attenuating the life cycle of myofibroblasts.14 Axial and random pattern flaps may be helpful in covering large wounds, as well.15 The former is a single pedicled flap with an anatomically recognized arterial and venous system running along its axis. The groin flap was one of the first such axial pattern flaps that was used for resurfacing of the upper extremity, but suffers from the disadvantage of having to keep the arm dependent until it is cut free from the groin pedicle at a later date. Microvascular free flap reconstruction may be more elegant than a groin flap since the upper extremity can remain elevated and therapy might be initiated sooner. Axial flaps, either free or pedicle flaps, may consist of skin only, fascia and fasciocutaneous tissue (such as radial forearm, lateral arm, temporoparietal), or muscle and musculocutaneous tissue (such as latissimus dorsi, rectus abdominis, and gracilis muscles). The radial forearm flap and posterior interosseous flap may be pedicled on the distal blood supply so that venous flow is actually retrograde. Flaps have many advantages over skin grafts15 in that they avoid wound contraction, fill dead space, cover important structures (such as exposed vessels, bone, tendons, and nerves), help “clean up” infection, enhance vascularity, and provide specific functions (such as a latissimus muscle transfer to restore biceps function).
TREATMENT OF INJURIES TO TENDONS IN THE DISTAL EXTREMITY
The extensor tendon is the end organ of a complex mechanism, which involves input from both the extrinsic and intrinsic muscles of the hand to maintain the balanced finger function that is expected by most individuals. Disruption of any component of this balance such as bone, skin, the musculotendinous system, or neurovascular structures can lead to stiffness and a poor functional outcome.
In the evaluation of injury to an extensor tendon, the hand and distal forearm are divided into eight zones that aid in communication and, to a degree, guide treatment. Zone I injuries involve disruption of the extensor mechanism over the distal interphalangeal (DIP) joint resulting in the classic mallet finger deformity. Closed injury results from forced flexion while the finger is in rigid extension. Rupture of the terminal tendon itself or avulsion of its insertion with a variable sized bony fragment results in an inability to extend the distal phalanx. Lacerations or other open injuries, with combined skin and tendon loss, can result in a similar deformity. A closed acute mallet finger should be treated initially by continuous splinting in extension for 6 weeks.16 The splint should not incorporate the other joints of the finger or hand, and active motion of the proximal interphalangeal (PIP) joint should be encouraged. If resisted extension is present at the end of 6 weeks, the splint can be limited to nighttime use for an additional 6 weeks with close follow-up. Any relapse should be treated with 3 weeks of additional continuous splinting. Care must be taken during this prolonged period of splint use that skin maceration and necrosis do not occur. Occasionally, operative fixation by a variety of pinning methods is required for complete healing or to more appropriately manage subluxation of the DIP joint.
Open mallet fingers can present a treatment challenge. Simple transverse lacerations are best treated by mass suturing with incorporation of the terminal tendon and skin with a series of interrupted, nonabsorbable sutures. Fingers with skin and tendon loss require soft tissue coverage and primary tendon grafting or late reconstruction. Emergency treatment consists of irrigation of the open wound/joint, dressing of the wound, antibiotic coverage, splinting in extension, and arranging urgent follow-up in the next 24 hours for surgical evaluation and treatment.
Zone II injuries occur over the shaft of the middle phalanx and are usually associated with a laceration or open fracture. Lacerations involving less than 50% of the tendon width, and with no extensor lag, can be treated by wound care and splinting in extension for 7–10 days, followed by active range of motion. If more than 50% of the tendon is lacerated, or an extensor lag at the DIP joint exists, then the tendon should be repaired followed by splinting or pinning the DIP in extension for 6–8 weeks in a mallet finger protocol. Open fractures with tendon involvement require fracture and tendon repair and extensive therapy to regain range of motion.
Zone III injuries involve the central slip of the extensor tendon over the PIP joint and initially result in loss of extensor power at this joint. Untreated, this injury results in palmar subluxation of the lateral bands and, within 1–2 weeks, development of the classic boutonniere (or buttonhole) deformity. With this deformity, the finger rests in a position of flexion at the PIP joint and hyperextension at the DIP joint. Physical examination will show weak or absent extension of the PIP joint with this injury. With a closed rupture of the central slip, initial evaluation may be difficult due to pain and swelling at the PIP joint. Extension splinting of the PIP joint with follow-up and reexamination at 7 days is a reasonable course of action in this situation. Splinting must not incorporate either the MCP joint or DIP joint. If, at 1 week, findings support the diagnosis of closed rupture of the central slip, then splinting should continue for 4–6 additional weeks with weekly follow-up. Formal therapy is usually required at the completion of splinting to successfully regain full range of motion. Open injury in Zone III requires wound management in the form of irrigation and debridement, formal arthrotomy if indicated, and soft tissue coverage if local tissue has been lost. Tendon repair may be primary or may be managed by transarticular pinning for 4–6 weeks to allow the tendon to heal on its own. Second intention healing of the tendon in this area is possible because of the design of the extensor apparatus that prevents retraction if the PIP joint is held in extension.
Zone IV lies over the proximal phalanx, and injury at this level is often associated with a proximal phalangeal fracture. Many tendon injuries at this level are incomplete, due to the broad nature of the extensor hood. Like Zone III injuries, even a complete laceration will not result in proximal migration of the tendon due to the constraints of the sagittal bands that tether the severed end.
Lacerations in Zone IV will need to be extended to allow complete exploration and primary repair. Early motion in this zone by an active flexion, passive extension protocol is recommended. When Zone IV injuries are associated with proximal phalangeal fractures, a stable repair of the fracture will greatly facilitate initiation of early tendon motion.
Open Zone V injuries are commonly associated with the “fight bite” wound, and treatment is addressed in Section “Infections in the Hand.” Closed tendon injuries in this zone are less common and usually involve the radial sagittal band, which results in subluxation or luxation of the extensor digitorum communis (EDC) tendon into the ulnar gutter. Splinting may be with the wrist neutral, the MCP joints in extension and the PIP and DIP joints free,17 or a recently described finger-based sagittal band bridge splint.18 If splinting for 6–8 weeks fails, or the injury is seen late, then operative recentralization should be performed.
Zone VI injuries can occur distal or proximal to the juncturae tendini, the tendinous connections between the EDC tendons. Diagnosis and treatment of these injuries are difficult and beyond the spectrum of this chapter, since the finger will still extend at the MP joints via the transmission of the adjacent tendon action through the juncturae. In these situations, exploration may be the only means of diagnosis, short of imaging techniques such as ultrasound or MRI. Proximal retraction of the lacerated tendon will occur. In these instances, exploration in the operating room is probably preferable to exploration in the ED.
Open injuries in Zone VI can be associated with extensive loss of soft tissue. Repair of such injuries often requires complex soft tissue coverage with immediate or delayed tendon reconstruction or transfer.
Zone VII injuries to the extensor tendons occur at the level of the wrist retinaculum where the tendons are divided into six compartments. In this zone, retraction of the tendon ends always occurs, making formal operative exploration imperative. Repair needs to be meticulous to avoid adhesions to the overlying retinaculum that often needs to be expanded by z-plasty during closure. Failure to appropriately repair the retinaculum will result in bowstringing of the extensor tendons at the level of the wrist. An associated injury to the dorsal sensory branches of the radial and ulnar nerves can occur with these injuries and requires a high level of suspicion to prompt exploration and microneural repair. Ignoring these associated nerve injuries can lead to loss of sensation over a portion of the dorsum of the hand and chronic neuropathic pain.
Zone VIII represents the musculotendinous junctions of the extensors. Injury at this level is always associated with penetrating trauma or massive injury to soft tissue, often with an associated open forearm fracture. Initial evaluation of penetrating trauma, usually by glass or knives, may show a relatively small wound that belies the damage that has been caused internally. Even with what appears to be normal extension on examination, significant damage can be found with surgical exploration.19 Repair of the musculotendinous junction itself is difficult because muscle does not hold sutures well. Large figure of eight sutures are required to restore continuity, and repair should be followed by 4–6 weeks of splinting with the wrist in 20° of extension and the MCP joints in 20° of flexion. If the injury is distal to the posterior interosseous nerve, good restoration of function is possible. Injury to the posterior interosseous nerve requires a thorough exploration and repair by an experienced microneural surgeon to maximize functional recovery. Even with meticulous repair of the nerve, a tendon transfer may be required at a later date. In order to salvage a functionally threatened extremity, a massive combined injury in Zone VIII requires application of the principles discussed in Section “Compound, Complex, and Mangled Upper Extremities.”
The thumb represents a unique structure in many contexts including its extensor anatomy. Because the thumb has only two phalanges, the zones are slightly different and often referred to as T I–V. T I and T II are over the only interphalangeal joint of the thumb and the proximal phalanx, respectively. Injuries in these areas can result in a mallet deformity similar to Zone I injuries in the fingers. Treatment principles in these thumb zones remain the same as previously described for Zone I of the fingers.
T III is over the MCP joint of the thumb and, unlike the fingers, two tendons are vulnerable to injury at this level. The extensor pollicis brevis (EPB) inserts here in the radial aspect of the base of the proximal phalanx, while the extensor pollicis longus (EPL) passes ulnarly and inserts on the distal phalanx. Injury to the EPB at this level can be isolated or associated with injury to the dorsal capsule and radial collateral ligament. Examination of patients with injury at this level should include a thorough evaluation of the stability of the MCP joint and, at surgical exploration, all potentially injured structures should be evaluated and repaired. After surgical repair, both the thumb and wrist should be immobilized.
In T IV, the EPL and EPB tend to become more oval, making them amenable to both core and epitendinous sutures. These two tendons remain closely associated at this level, and, with isolated injury of one tendon, retraction may be prevented by the remaining intact tendon; however, one should be prepared for more proximal exploration, particularly with injury to the EPL.
T V injuries may involve the EPL, EPB, and/or abductor pollicis longus. In addition, injury to branches of the superficial radial nerve is often present at this level. Failure to repair the superficial radial nerve branches can result in not only sensory loss in its distribution but also a syndrome of chronic neuropathic pain.
Flexor Tendons and “Spaghetti Wrist”
Because of its complexity, the treatment of an injury to a flexor tendon is a major component of the history of the development of hand surgery.20 Today, despite many advances in the surgical treatment of an injury to a flexor tendon and rehabilitation, the care of these injuries remains a significant challenge. Because of the proximity of neurovascular structures at all levels along the course of the flexor tendons in the forearm, wrist, and hand, combined injury of these soft tissue structures is common and adds to the complexity of care.
Examination of the flexor tendons of the fingers and thumb is based on the anatomical relationship of the flexors to specific joint function. In the fingers, both the DIP and PIP joints can be flexed by the flexor digitorum profundus (FDP), a muscle that has its radial component (index and long fingers) innervated by the anterior interosseous (median) nerve and its ulnar component (ring and small fingers) innervated by the ulnar nerve. In contrast, the flexor digitorum superficialis (FDS), which flexes the PIP joint alone, is innervated only by the anterior interosseous (median) nerve. Specific simple maneuvers, however, can be performed to separate FDP and FDS function during examination of the hand. The thumb is flexed predominantly by the flexor pollicis longus, which is innervated by the anterior interosseous nerve and is solely responsible for flexion of the IP joint.
Flexor tendon repair, in general, consists of both core and epitendinous sutures. A number of core stitches have been described, and while all have been shown to be effective when applied correctly, the recent addition of preformed loop sutures offers several advantages in repair and should be considered for use.21 These sutures allow easier placement of an increased number of strands, which proportionally increases the strength of the repair allowing earlier and more aggressive therapy.22
As with injuries to extensor tendons, various zones (I–V) have been defined for injuries to flexor tendons. This classification helps in communication when describing an injury and in determining appropriate treatment and rehabilitation. Zone I injuries involve the insertion of the FDP or FPL into the distal phalanx of the finger or thumb. If the distal stump is less than 1 cm, then suture repair will not be sufficient and the FDP should be advanced and reinserted into the bone. FDP avulsions at this level, often called “jersey fingers,” occur as three patterns of decreasing severity.23 Type I avulsions are the most severe and the most easily missed because of lack of x-ray evidence of injury. In this instance, the tendon pulls off the bone and ruptures the vincula within the finger. This allows complete retraction of the proximal tendon into the palm. Early recognition and treatment of this injury is necessary to avoid the need for two-stage tendon reconstruction. Repair can be accomplished early by a pullout button or suture anchor with equal outcome.24 In Type II avulsions, the tendon is held at the level of the vincula, which does not rupture. With a Type III avulsion, a large bony fragment is associated with the distal FDP, which causes the tendon to be retained at the level of the distal A-4 pulley. Repair in this instance is often possible by reinsertion using a pullout stitch or fixation of the bony fragment with a Kirschner wire or screw.
Zone II has historically been referred to as “no-man’s land” because of the difficulty of rehabilitation with this level of injury.20 This zone is defined by the presence of the adjacent FDS and FDP within the flexor sheath. Skillful repair with preservation of the pulley system during this repair may require passage of the proximally retrieved end with a small catheter that has been passed from the distal site of the injury. Even when all principles are adhered to, secondary tenolysis may be required due to the development of peritendinous adhesions. Early motion protocols are needed for functional restoration.
Zone III injuries are in the palm between the distal extent of the carpal tunnel and the proximal border of the A-1 pulley. Because this zone is not constrained by the fibro-osseous canal, the prognosis for recovery is markedly improved over an injury in Zone II.
Zone IV (within the carpal tunnel) and Zone V injuries (distal to the musculotendinous junction) have a high probability of associated injuries to a major vessel and/or nerve. Preoperative examination should include a thorough evaluation of the motor and sensory status of the patient with appropriate documentation. Hemorrhage in these situations can be quite dramatic, but can usually be controlled by direct pressure. Blind clamping or use of a tourniquet is discouraged and is usually unnecessary. Only rarely, with laceration of both the ulnar and radial arteries is the hand truly threatened by ischemia. Collateral circulation through the interosseous arteries will maintain adequate distal perfusion if not obstructed by application of a proximal tourniquet.
On the volar side of the wrist there are 16 structures, including 12 tendons, 2 nerves, and 2 arteries in close proximity to the skin. This leaves these structures vulnerable to trauma when the integument is violated. Because of the appearance when the wrist at this level is lacerated resulting in exposure of numerous white string appearing structures, the term “spaghetti wrist” has frequently been applied. Other colloquialisms include “full house wrist” and “suicide wrist.”
Even when this injury is complete, with involvement of both the radial and ulnar arteries, only rarely is circulation to the hand compromised because of the abundant collateral circulation via the anterior and posterior interosseous arteries and dorsal branches from the ulnar and radial arteries. While blood loss may be dramatic, initial hemostasis can often be achieved by direct pressure or brief use of a tourniquet and closure of the skin. These maneuvers should be followed by application of a splint and compressive dressing. Once this is accomplished, if this was a self-inflicted injury, the patient’s inciting cause can be addressed and at least initial postoperative cooperation assured.
Repair of the “spaghetti wrist” is performed in a sequential manner from deep to superficial. This is undertaken in the operating room with tourniquet control. Following a thorough exploration and cataloging of injured structures, tendon repair is usually followed by microscopic nerve repair, and, finally, repair of the ulnar and radial arteries. At this point the tourniquet is decompressed and final hemostasis is assured prior to closure of the skin. An initial dorsal blocking splint with the wrist neutral and the fingers in the intrinsic plus position is applied. A controlled tendon rehabilitation program is initiated as soon as the patient’s cooperation can be assured.
As with most injuries of the upper extremity, the final determining factor in degree of disability in this injury is successful recovery of the injured nerve.25,26 Both sensory and motor recoveries are required for an optimal result. Factors that affect outcome even with application of modern microsurgical nerve repair are age (<16 years with a better prognosis than >40 years), nerve repair before 3 months, and whether the ulnar nerve is involved. Sensory recovery is usually equal for both ulnar and median nerve injury and repair; however, the failure to recover critical intrinsic muscle function innervated by the ulnar nerve invariably leads to an unbalanced weak hand with significant long-term disability.
TREATMENT OF INJURIES TO THE FINGERTIP AND NAIL BED
All patients who have injuries to the nail bed must have x-rays, and any underlying distal phalangeal fracture is appropriately reduced to improve alignment and splinted for protection. Internal fixation may occasionally be needed. This is generally performed by placing a longitudinal 0.028-in Kirschner wire. These fractures are technically open, and appropriate antibiotics must be administered.
Dorsal Fingertip Injuries
The least severe of these injuries is the nail bed hematoma. If it is seen early, the hematoma can be decompressed by perforating the nail plate after administration of a digital local anesthetic block.27 If the nail plate is split, then the nail should be gently removed to examine the underlying nail bed. Many injuries to a fingertip and/or nail bed can be evaluated and treated in the emergency room by simple placement of digital block anesthesia and use of a Penrose drain at the base of the finger to act as a tourniquet. Suture repair of the nail bed after irrigation and cleansing is performed by using loupe magnification and 6-0 catgut suture. Even in a crushing injury, a stellate injury of the nail bed can often be meticulously repaired.
Once the nail bed has been repaired, the thoroughly cleaned nail can be placed back under the nail fold where it serves as a rigid splint for any underlying distal phalangeal fracture and prevents adhesions from forming between the germinal matrix and the nail fold. These synechiae would lead to a future unsightly “split” nail deformity and pterygium formation. If a portion of the nail bed is missing, the undersurface of the nail plate should be examined as the missing nail bed may often still be adherent to the nail. It can then be gently removed from the nail and replaced as a nail bed graft. If a substantial portion of the sterile nail bed matrix is missing, it cannot be replaced by a split-thickness skin graft since the outgrowing nail would not adhere to the surface provided. Such a missing piece of nail bed is best treated by obtaining a split nail bed graft from the adjacent nail or from a toenail bed. For more severe dorsal fingertip injuries, a reverse cross-finger subcutaneous fascial flap as described by Atasoy28 may provide an excellent bed on which to place either a split-thickness skin graft or a nail bed graft. When the dorsal fingertip injury is more extensive, and there is no hope of reconstructing the nail bed, preservation of digit length can still be achieved by use of the more recently described homodigital retrograde-flow intrinsic finger flap.29 This retrograde vascular flap is based on the extensive “stepladder”-type collateral arterial circulation between adjacent radial and ulnar digital vascular structures. Some fingertip injuries may be so severe that amputation revision is the most sensible functional solution.
Volar Fingertip Injures
Smaller volar pulp injuries without exposure of bone and of a diameter less than 1 cm in an adult are best treated open with soaks and dressings and will heal with excellent cosmetic and functional results.27 Larger soft tissue wounds, but still without exposure of bone, may be more appropriately treated with a split-thickness skin graft. If bone is exposed, either flap coverage is required to maintain the length of the digit or the amputation is revised by trimming back exposed bone to accomplish coverage with soft tissue. Once again, a reverse-flow homodigital island vascular flap may provide good soft tissue coverage or a cross-finger flap should be considered.27 The cross-finger flap suffers from the disadvantage of a two-stage procedure and unnecessary flexion of the finger that may potentially lead to a flexion contracture of the PIP joint.30,31 A large V-Y neurovascular homodigital island flap may be considered, especially when the distal amputation of soft tissue is angulated more dorsally.29 This technique requires capabilities.
Retained Amputated Fingertip
If the amputated fingertip is retained and is not too severely crushed, reimplantation may be considered. Reimplantation of avulsed tissue containing a large proportion of thumb pulp should always be considered in view of the functional importance. If the amputated part from the thumb has been too severely crushed, then thumb pulp may be reconstructed with a neurovascular island sensate “kite flap” that is based on the vascular branches of the first dorsal metacarpal artery.29 Another consideration for reconstruction of the volar pulp of the thumb is a microvascular medial toe pulp transfer.32
For fingertip amputations, a simple revision of the amputation may be an option in spite of the patient bringing in the amputated tip or replantation may be considered. Replacement of the fingertip simply as a composite graft after removing distal bone may at least suffice as a biologic dressing for the healing fingertip even if it were to fail. As there is a high incidence of tissue necrosis with fingertip composite grafts, an alternate solution is to retain the perionychial tissues as a full-thickness graft and to reconstruct the volar pulp support with alternative measures such as one of the local flaps already described.33
TREATMENT OF HIGH-PRESSURE INJECTION INJURIES
These injuries to the hand are relatively uncommon, but the consequences of a misdiagnosis are very serious.34,35 High-pressure injection guns are found in industrial settings and are used for painting, cleaning, and lubricating. Potential injected materials include paint, paint thinner, oil, grease, water, and plastics. The injection is most frequently at the level of the DIP joint of the nondominant index finger that is directly opposite to the nozzle of the injection gun. High-pressure injection guns generate pressures ranging between 3,000 and 12,000 psi. A pressure of 100 psi is sufficient to penetrate the skin. In addition to injection guns, these injuries may result from other sources such as pneumatic hoses and hydraulic lines.
The type of material injected is the most important prognostic factor. Oil-based paints and paint thinners can generate significant inflammation and fibrosis. The injectate will generally enter the tendon sheath and flow down its path into the hand. X-rays are often helpful in determining the extent of dispersion of the injected material. Non-lead-based paints may appear as subcutaneous emphysema, grease may be lucent, and lead-based paints may be seen as radiopaque densities in soft tissue. Antibiotic prophylaxis is started, and incisions are made to decompress the affected part and to enable extensive exploration and debridement of injected material. Wounds are either closed loosely over Penrose drains or left open to be closed in a delayed manner. Despite recognition and treatment, many of these injuries can still ultimately result in surgical amputation of the affected digits.
TREATMENT OF FROSTBITE, CHEMICAL BURNS, ELECTRICAL INJURIES, AND THERMAL INJURIES
The management of frostbite consists of restoring core body temperature by rapid rewarming of the frozen extremity in a 44°C water bath. Active hand therapy must be instituted, also. Ibuprofen may be helpful and has been recommended for potential prevention of frostbite injuries prior to cold exposure such as on mountaineering expeditions. Thrombolytic therapy using tissue plasminogen activator (tPA) early in treatment has recently emerged as a modality to save digits and limit the extent of subsequent amputation.36 It is important to avoid premature amputation, as demarcation and mummification of digits may take as long as 2–3 months. If a disabling vasospastic syndrome persists as a chronic problem following an occult cold injury, digital sympathectomy may be helpful.37
Many follow the therapy protocol described by McCauley et al.38 On completion of rewarming, the protocol is as follows:
1. White blisters are debrided, and topical aloe vera is applied every 6 hours in order to prevent the synthesis of thromboxane.
2. Hemorrhagic blisters are drained but left intact to prevent desiccation of the underlying dermis, and topical aloe vera is applied every 6 hours.
3. The injured part is splinted and elevated in order to minimize edema.
4. Tetanus prophylaxis is given as appropriate.
5. Intravenous narcotics may be utilized.
6. Oral ibuprofen is given in a dose of 400 mg every 12 hours to inhibit the eicosanoid cascade.
7. Penicillin G is administered intravenously in a dose of 500,000 U every 6 hours for 48 hours to potentially decrease streptococcal infection during the edema phase.
8. Daily hand therapy is instituted to provide both active and passive range of joint motion.
(This protocol was suggested prior to recent research on tPA, and the surgeon may consider adding tPA to this regimen.)
The long interval from initial injury to definitive debridement and reconstruction may subject patients to increased risk of local infection and may cause great psychological stress and inconvenience for the patient. The initial use of radioisotope scans has been helpful in predicting the need for future amputation.39 A triple-phase technetium (Tc-99) bone scan is performed within 48 hours of rewarming for all but the most superficial frostbite injuries. Patients with an absent early blood pool phase on scanning as well as no bone uptake are restudied 72 hours later. If the second scan does not demonstrate significant blood flow, then mummification and amputation are highly likely. Based on these findings the following protocol for deep frostbite injuries using technetium bone scans has been recommended. A triple-phase bone scan is performed at 48 hours and then at 5 days. If there are normal blood and bone pool images, then one proceeds with expectant observation. If there are diminished but visible blood pool images, then continued observation is undertaken with delayed debridement if necessary. If there is little or no flow in either blood or bone pool images, early debridement or amputation is recommended with potential salvage with vascularized tissue.40
Chemical burns may affect hands and upper extremities in the industrial environment. The most important part of treatment is water lavage that must be started at the scene of the accident and is continued for 1–2 hours for acid burns and even longer for alkali burns. General principles of chemical burns follow those of thermal burns, but there are some specific therapeutic antidotes for chemicals.41
If massive water lavage is not immediately available, then reducing agents such as hydrochloric acid will only be diluted if small amounts of water are available. Under such circumstances the agent must be neutralized with soap or soda lime. Hydrofluoric acid is a common ingredient in rust removers and degreasers and causes hypocalcemia and hypomagnesemia with a burn greater than 5% of body surface area. Immediate water lavage is required followed by subdermal injection of 10% calcium and gluconate. This can be painful if it is not combined with local or regional anesthesia. More recently, calcium carbonate gel has been used for topical application instead of the injection therapy. In contrast, phenol is not water soluble and requires specific treatment with topical polyethylene glycol (PEG 400) followed by water lavage. Treatment of white phosphorous burns chiefly involves water lavage followed by identification and excision of any remaining phosphorus particles. A 1% copper sulfate irrigation solution helps identify these particles, and this is followed immediately by water lavage to avoid the toxic effects of the copper sulfate. Sterile debridement then follows.
When contact with high voltage occurs, it is usually established by an arc that is a hot, electrically conducting gas. Ten to 20 kV is required to establish an arc of a distance of 1 cm. Arcing also occurs across joint flexion creases such as the elbow. Current flow begins when a complete circuit is made. The hand and upper extremity are the most common body parts affected by electrical injuries since this is often the contact area for electrocution. The arc is intensely hot, usually in the range of 5,000–20,000°C.
In the body, current is carried by electrolyte ions in solution. Current density is highest at the contact points and rapid conversion to heat occurs, leading to the deepest burns at the entrance and exit wounds. As the current enters the deeper tissues, it spreads out in proportion with the conductance of the tissues. Injuries result both from the heating and from the direct electric forces acting on larger cells. The latter results in excessive charging of the cell membrane, high transmembrane potentials, and subsequent membrane electroporation.42 Tissue adjacent to bone appears to be damaged more severely since cortical bone is denser than soft tissue and may thus store the heat generated from the adjacent soft tissue. The heat is returned to the surrounding tissue later. Due to electroporation and deep tissue heating, the damage caused is often nonuniform and difficult to interpret clinically. Electroporated muscle appears viable on gross inspection for hours and, coupled with subsequent damage from tissue reheating, initial diagnosis of the extent of the tissue undergoing necrosis remains problematic.
High-tension electrical injuries are devastating, and a compartment syndrome may result. Not only is there a conversion of electrical energy into heat that causes coagulation necrosis of tissues, but also thrombosis of blood vessels may lead to further occlusion of major blood vessels and subsequent necrosis of tissue.43 Rhabdomyolysis may lead to myoglobinemia and myoglobinuria and possible renal failure. There may be coexistent problems such as cardiac arrhythmias, spinal fractures due to tetanic muscular contractions, other skeletal injuries, serum electrolyte derangements, and blast trauma. Because peripheral nerves are very sensitive to electrical injury, even minor electrical trauma may cause a temporary dysfunction.
Once the patient has been stabilized, attention is directed toward debridement of clearly necrotic parts, preservation of residual function, and soft tissue coverage of open wounds (especially of exposed vital structures) to prevent infection. Also, forearm and hand fasciotomies may be required early in the treatment of electrical injuries to the upper extremity.44 One might use temporary soft tissue coverage with porcine or artificial skin substitutes, but, once the viability of the remaining tissue has been established, fasciocutaneous flaps or microvascular free flaps will close wounds and salvage the injured extremity.45,46 Occasionally, survival of the patient and the best functional outcome may mandate an early amputation of the proximal limb.
Postoperative care will include physical therapy and, possibly, fitting of a prosthesis. Successful rehabilitation may require tendon transfers, transferring of innervated muscle, or even toe transfer for missing digits. The upper extremity is involved in about 80% of all electrical injuries, amputation rates range between 40% and 70%, and mortality ranges from 8% to 14%.47
Treatment of major burns and resuscitation is outside of the scope of this chapter (see Chapter 48) that will focus only on the management of a burn in the upper extremity. Initial first aid for hand burns requires immediate cooling of the wound by rinsing in cold water for 5–10 minutes. This helps reduce subsequent edema formation, also.38 Capillary refill must be documented to decide upon the need for an escharotomy or fasciotomy. Full-thickness circumferential burns of an upper extremity frequently require an escharotomy.48 Fasciotomy of the hand for the interossei and the first web space should be performed in situations of severe edema of the hand.49
The hand often assumes the intrinsic minus posture because of swelling. The wrist is drawn into flexion with hyperextension at the MCP joints and flexion at the proximal and distal IP joints that results in a claw deformity. The thumb adducts toward the palm, and the interphalangeal joint is hyperextended.43 Appropriate early splinting is necessary to overcome this posture in the severely burned hand. Splinting in the intrinsic plus position places the ligaments of the digital joints in maximal stretch and minimizes their shortening. Customized thermoplastic splints are effective and can be adjusted easily.
Local wound care depends on the depth of the burn. Partial-thickness superficial second-degree burns are expected to heal within 7–14 days. Larger blisters may be aspirated or removed by incision and debridement. Moist wound healing is required for the wound to heal spontaneously. The burn wound is cleaned daily, followed by the application of an antibacterial cream. As epithelialization occurs, a bland ointment is helpful to prevent desiccation of the newly formed epithelium.
Deep dermal and full-thickness burns of the hand are best treated by early excision and grafting. A burn wound is uninfected initially and suitable for primary surgical treatment during the first 5 days. Tangential excision is performed down to punctate bleeding. Blood loss can be minimized by use of an upper arm tourniquet. Exsanguination of the arm by simple elevation rather than by wrapping with a rubber bandage will still enable the surgeon to determine the appropriate depth of tangential excision and visualization of punctate bleeding. Residual devitalized tissue must not be left behind as this could be a cause of failure of a skin graft. Resurfacing the wound with a split-thickness skin graft is then immediately performed.50,51 Skin grafting is rarely necessary for palmar burns due to its capacity for spontaneous healing from the skin appendages at this site. A full-thickness burn, however, may occasionally lead to exposure of tendons, bones, and joints. In this situation primary coverage of soft tissue by regional flaps or even free flaps may be required. It has been found that fascial flaps are very useful to provide coverage of dorsal hand wounds since cutaneous flaps may be too thick. Suitable fascial flaps include temporoparietal, serratus anterior, or anterolateral thigh.52
After a skin graft is placed, the hand is immobilized for 5 days until healing of the graft has occurred. Passive and active hand therapy is then initiated to reduce stiffness and contractures. Once again, the importance of appropriate postoperative splinting should be emphasized. In the first few months following the burn injury, there is a period of scar hypertrophy. This scar tightness is overcome with range of motion exercises of the joints. An important adjunct to management of the scar is having the patient use a custom-fitted elastic pressure garment that should be initiated as early as 2–3 weeks after skin grafting. Pressure garments may be required for as long as 6 months, while secondary surgical procedures for release of contractures may be required at a later date.
VASCULAR INJURIES IN THE UPPER EXTREMITY
A vascular injury can occur with either closed or open trauma (see Chapter 41). Closed injuries associated with arterial disruption include scapulothoracic dissociation, shoulder dislocation, and elbow fractures and dislocations. A scapulothoracic dissociation represents a complex injury with a high incidence of both vascular disruption and concurrent rupture or avulsion of the brachial plexus. Successful treatment requires prompt diagnosis, preoperative angiography, and reconstruction of the axillary or brachial artery with an interposition graft.
Despite the frequency of shoulder dislocations or fractures, an associated arterial injury remains a relatively rare complication. Anterior dislocation in the elderly patient is the most common scenario where vascular injury occurs with blunt shoulder trauma. Predisposing atherosclerotic disease with a more tortuous and noncompliant artery may play a role in this injury, and the injury is just as likely to occur during relocation for the same reasons. Because of this, the distal vascular status should be assessed prior to reduction of any anterior dislocation.
Supracondylar fractures in children infrequently involve the brachial artery; however, the extension-type fracture with posterolateral displacement of the distal fragment and wide separation can result in injury to this vessel. The ischemia present after this injury can be caused by direct impingement from the medial spike, secondary to vascular spasm and progressive soft tissue swelling, or thrombosis of the distal brachial artery. When vascular trauma is suspected, a gentle closed manipulation of the fracture and percutaneous pin fixation should be followed by a repeat clinical examination. If distal pulses do not return with reduction, then angiography should be obtained. A surgical release of the artery from entrapment in the fracture or a formal vascular repair may be needed.
An open injury with pulsatile hemorrhage in the upper extremity should be managed initially with pressure alone, whenever feasible. Blind clamping and ligation can lead to devastating injury of closely associated nerves that can result in a successfully revascularized, but worthless limb. With such injuries to nerves multiple procedures may be needed to restore less than satisfactory function. Similarly, use of the tourniquet should be limited to avoid contributing further to ischemic damage from occlusion of collateral flow. Once hemorrhage is controlled, few would argue that prompt surgical repair of a subclavian, axillary, or brachial artery injury is indicated. Less obvious is the treatment of a single-vessel injury in the forearm. Many have argued that, with documentation of adequate collateral flow from the remaining artery, it is more expeditious to ligate the injured vessel. With improvements in microvascular surgery, however, repair of arteries this size has become quite straightforward and the procedure itself adds little time to an exploration of the wrist or forearm where other associated injuries are being addressed.
NERVE INJURIES IN THE UPPER EXTREMITY
Treatment of injury to a peripheral nerve represents a major component of upper extremity surgery, and the end result of the care of this injury is often the major determinant of the degree of functional recovery. A nerve injury should be looked for with a high level of suspicion based on the anatomical location of injury to the extremity. Furthermore, serial examinations over the course of the patient’s recovery are warranted. Also, if surgery is planned to deal with other injuries, the opportunity for direct exploration of known at-risk nerves in the zone of injury being addressed should not be missed. This is particularly indicated in the presence of sharp penetrating trauma.
The terms neurapraxia, axonotmesis, and neurotmesis are commonly used to describe different degrees of the continuum of injury to a peripheral nerve, and each term correlates with the potential for recovery. Neurapraxia, the most minor form of injury, represents a conduction block with preservation of anatomical continuity. The neuropraxic injury may be complete or partial and, although recovery will be complete, it may take up to 3 months. Importantly, there is no nerve regeneration involved in this recovery and there is no advancing Tinel’s sign as there is no axonal involvement. It should be remembered that a neuropraxic injury can be associated with a concussive blow or a compressive injury such as a promptly released compartment syndrome or a tourniquet-type injury, as well.
In axonotmesis there is structural damage to the axon while the endoneurium and perineurium remain intact. A Tinel’s sign is present in this form of injury, and it can be followed during recovery as it progresses distally with axonal regrowth. In this injury, there is classic histological Wallerian degeneration distal to the site of axonal disruption. Because the axon sheaths remain essentially undisturbed, complete restoration of the original pattern of innervation is possible.
Neurotmesis represents complete severance of the nerve from traction, rupture, or penetrating trauma. Recovery in this situation is not possible without microsurgical repair.
In large nerves it is possible to have all forms of injury present within the same nerve. This situation can complicate both initial diagnosis and interpretation of recovery as well as delay and complicate surgical intervention.
Surgical interventions with injury to a peripheral nerve include decompression, neurolysis, direct repair, and nerve grafting.53 In complex injuries involving multiple nerves or nerve segments, all these techniques may be required. Direct nerve repair may be by epineural or fascicular suturing. While fascicular repair intuitively seems like it would give more precise anatomical alignment, this has never been substantiated and the principle of less is more seems to apply. Minimal foreign material in the form of suture, minimal or no tension, and minimal trauma are required for a successful repair. When a tension-free repair is not possible, a nerve conduit in the form of an autogenous nerve graft or a vein or artificial conduit for a short segment replacement must be utilized to fill the defect and serve as a guide for new axonal growth. A number of sensory nerves can be sacrificed with minimal deficit, but the most common is the sural nerve from the lower leg.
Timing of nerve repairs can be defined as primary when repaired within 1 week of injury, while nerve repairs after this time are considered secondary. Direct end-to-end tensionless suture neurorrhaphy may not always be possible in the case of secondary repair, and one should be prepared for interposition grafting or employment of other techniques to achieve successful reinnervation.
In general, nerve injuries associated with sharp penetrating trauma should be explored early. If the injury is a sharp laceration, immediate direct repair is usually the best option for optimal recovery. When the precise zone of injury to the nerve cannot be determined, as after a traction or crush injury, a delayed repair is indicated so that the zone of injury is more clearly defined. Simple tagging of injured nerves at the time of exploration in itself probably serves no useful purpose since the experienced peripheral nerve surgeon will readily locate the injured nerve proximal and distal to the injury at the time of reexploration. Suture tagging the nerve to a stable adjacent structure, however, may serve to prevent the inevitable retraction and minimize the distance that requires grafting at the time of definitive repair.
An exception to early exploration of penetrating injuries is the gunshot wound. In these injuries the mechanism of injury includes heat and shock wave effects, and expectant management is usually appropriate. A vascular injury where the vessel is enclosed with the nerve in a common sheath, however, may lead to similar injury to both the nerve and vessel. In these situations, it is imperative that continuity of the nerve is verified during repair of the vessel.
Nerve transfer represents another option for dealing with both motor and sensory losses in what potentially would be a nonreconstructable injury.53,54 The theory behind nerve transfer is to convert a high-level nerve injury into a low-level injury. This is accomplished by utilizing redundant or unimportant nerves or fascicles of the donor nerve to innervate critical motor or sensory targets. Initial experience with this concept was in brachial plexus surgery with the now classic intercostal to musculocutaneous nerve transfer to restore elbow flexion. This technique has now been expanded in brachial plexus neurotization to a number of nerve transfers with specific functional targets and more recently to reconstruct a number of other injuries to nerves.
An important example of a nerve transfer outside of the brachial plexus is the transfer of the distal anterior interosseous nerve to the motor branch of the ulnar nerve to restore intrinsic function. This gives a very simple functional alternative to complex tendon transfer and preserves muscle mass within the hand resulting in a more cosmetic outcome.