Skin and Superficial Soft Tissue
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What kind of closure or coverage has been used?
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How much protection does it need?
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Is healing expected to be by primary or secondary intention?
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What kind of dressing is appropriate?
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Are there signs of any complications in wound healing (e.g., infection, contamination)?
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Can problems be expected with wound contraction and secondary joint contracture, or with adhesions?
Blood Vessels
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Which vessels were repaired?
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Does immobilization for other injuries adequately protect repaired blood vessels (2–4 weeks needed)?
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Is there a danger of arterial or venous insufficiency?
Nerves
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Which nerves were injured? Are there any nerve grafts?
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Were nerves repaired under tension?
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How much immobilization will be needed? (2–4 weeks of protection from excessive stress)?
Sensory Nerves
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Is there total loss of sensibility?
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What areas will need protection because of impaired sensibility?
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What will be the functional effects?
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Is there a need for desensitization and/or sensory reeducation?
Motor Nerves
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What muscle imbalance can be expected, and will orthotic repositioning be needed to improve function and prevent deformity?
Muscles and Tendons
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Which tendons were injured? What kind of repair was performed?
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Were both flexors and extensors injured? If so, how can each be protected and mobilized without endangering other injured structures?
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Is heavy scar formation expected (because of zone of injury, means of injury, or other factors)?
Bone and Articular Structures
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What structures were injured and need protection?
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What kind of fracture was sustained? How stable are the reduction and fixation? How will this affect the rate of healing, wound care, and mobilization programs?
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What is the optimum position of immobilization?
Inflammatory Phase
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Talk to the surgeon to find out what structures were injured and how they were repaired, and what future surgical plans are.
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Teach the patient about injuries and provide help with set goals.
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Encourage uncomplicated wound healing.
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Protect all repaired structures. Mobilize gently if indicated.
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Control edema and pain.
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Prevent future problems: mobilize uninvolved joints.
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Address difficulties with ADLs.
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Consider social services referrals.
Proliferative Phase
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Continue to do the following:
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Communicate with the surgeon.
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Educate the patient.
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Manage wound, edema, and pain.
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Mobilize uninvolved joints.
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Address ADL difficulties.
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Consider social services referrals.
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Introduce scar massage and retrograde massage if not contraindicated.
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Modify protection/mobilization as dictated by healing of involved structures. Identify potential joint contractures or other problems and modify splints and/or exercises as needed.
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Introduce light activities.
Scar Maturation–Remodeling Phase
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Continue to do the following:
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Communicate with the surgeon (focus on long-term goals and plans).
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Educate the patient (focus on return to previous activities/work and on any future surgery).
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Manage wound, scars, edema (more aggressively), and pain.
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Mobilize uninvolved joints.
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Address ADLs (address long-term needs).
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Consider social services referrals.
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Modify orthosis and exercise programs as dictated by frequent evaluation.
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Progress to more demanding activities.
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Begin strengthening, dexterity, and endurance training.
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Begin job simulation and make specific plans for return to work.
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Begin sensory reeducation.
ADLs, activities of daily living.
A complex injury encompasses multiple-system trauma: skeletal, neurovascular, and many soft tissue structures all may be involved. The injury may include amputation, crush, laceration, and avulsion in a single extremity, and thus presents a difficult problem in management. Close cooperation among patient, surgeon, and therapist is essential in this demanding course of treatment.
The goal of all hand rehabilitation is a hand that is functional and esthetically acceptable. All treatment efforts are in vain if, for any reason, the patient does not use his or her hand. From a psychological standpoint, the patient’s difficulties with confronting the injury and reintegrating the hand into normal use must be recognized and addressed. From a physical standpoint, functional motion, strength, and sensibility to the hand must be restored. In both cases, the formation and remodeling of scar tissue must be controlled; uncontrolled scar can render a hand both unattractive and useless ( Fig. 95-1 , online).
Normal hand function requires strong tissue repairs with free gliding between neighboring structures. Scar tissue may adhere tissues to one another and prevent normal gliding; inadequate scar formation at the repair site will not withstand the demands of normal hand use. Therefore, management of the complex hand injury necessitates selective control of healing, ensuring stable, durable scar where strength is needed and long, mobile, elastic scar where motion between adjacent tissues is crucial.
The most difficult aspect of management in complex injuries is the coordination of treatment of the various systems and tissues injured. In addition to basic knowledge of hand anatomy, physiology, and kinesiology, and a wide repertoire of therapeutic skills, the therapist must possess a thorough comprehension of the phases of normal and pathologic healing of each type of tissue injured, and an understanding of the relationships between the various systems. When the complex injury is being treated, the key is careful examination of the individual systems and a treatment plan based on logical analysis of the problems identified.
Toward that end, this chapter first presents a review of wound healing and how healing can be influenced. The various tissues and special considerations for their treatment as dictated by anatomy, surgical/medical management, and mechanism of healing are then considered. This discussion is followed by a review of treatment modalities, giving more emphasis to those techniques not covered in other chapters of this book. Guidelines for evaluation and treatment at each phase of healing are explored last.
Wound Healing
For full coverage of wound healing, the reader is referred to Chapter 18 , “Wound Classification and Management.” The following description is very simplified and general.
All wounds, in any type of tissue, heal in a similar manner. The time frame given here applies to uncomplicated soft tissue healing. Times vary from one tissue to another and are never absolutely exact, because healing is a continuum and the phases overlap. In addition, complex injuries are characterized by untidy and extensive wounds, often contaminated or subject to other influences that considerably alter the timing of wound healing. The various tissues involved will heal at different rates, which adds to the difficulty of evaluation and treatment planning.
The inflammatory phase of healing begins within hours of trauma and continues for at least 3 days, although it may persist for days or weeks, especially in complex injuries, and can be renewed in response to even a relatively minor trauma such as overuse of a newly healed structure. Hemostasis is established through initial vasoconstriction and coagulation, allowing formation of a fibrin clot that both limits loss of blood and provides a scaffold for further cell invasion. Local vasodilation permits the leakage of blood and plasma into the injured area, creating increased edema, heat, redness, and pain—the classic signs of inflammation. Inflammatory cells invade the wound. Macrophages remove bacteria and apoptotic cells from the area. Fibroblasts stimulate macrophage attraction. , Macrophages stimulate fibroblasts to begin epithelialization from the margins inward, usually completely covering small, clean wounds within 3 days. Early intercellular attachments are weak and easily disrupted.
The proliferative or fibroplasia phase begins at 3 to 4 days and lasts through 14 days. The wound matrix is formed through macrophage and fibroblast activity. Angiogenesis brings blood supply and nutrition to the area. Wound contraction is caused by fibroblast differentiation into myofibroblasts, which stimulate wound contraction. , Fibroblasts synthesize collagen at a rapid rate, but the tensile strength of the wound is still low, and excessive tension can rupture the fragile intercellular bonds.
The scar maturation and remodeling phase begins at day 8 and continues for at least 1 year, when the dynamic turnover of collagen provides for differentiation of scar to accommodate the tissue type and the stresses under which it is placed. Excessive mechanical loading early in this phase may prolong fibroblast synthesis of collagen, which could lead to hypertrophic scarring. Decreased mechanical loading slows collagen synthesis and stimulates apoptosis, thus controlling the rate of scar formation. , Mechanical loading can be exerted by excessive edema as well as compression or traction by external forces. Initially, all tissues involved in a wound develop a single, massive scar, with randomly oriented collagen fibers. In the remodeling phase, fibers reorient and scars assume some of the characteristics of the tissues being healed.
As noted above, controlled stress (compression or tension) and motion have been shown to influence collagen formation and organization, increasing strength of healing tissues and decreasing adherence between adjacent tissues. However, it is not yet known how much stress is necessary and at exactly what time and manner it must be applied to any given type of scar tissue to produce a desired change. It is known that low levels of stress encourage cell migration and the orientation of new collagen fibers to allow tissue extensibility and gliding between adjacent tissues, whereas greater stress may cause tissue trauma or uncontrolled scar formation, leading to scar hypertrophy and adhesions. It also is known that in connective tissue, stress deprivation (such as occurs with immobilization following injury) predictably causes degenerative changes that lead to stiffness and deformity.
During the inflammatory phase, efforts are directed toward controlling pain and edema and promoting uncomplicated wound healing. The patient is taught that orthoses, dressings, and gentle motion help prevent further damage by avoiding excessive physical stress to the injured tissues. Pain, exposure to cold, and even emotional stress all can impair oxygen perfusion of the wound microenvironment, thus lowering resistance to infection and slowing healing. The resultant prolonged inflammatory response may lead to excessive fibrosis. During the proliferative and early remodeling phases, control of edema continues and undue stress to the injured area is avoided. Depending on the nature of the injury and the tissues injured, some form of controlled stress may be started to further decrease edema and increase or maintain joint and soft tissue mobility. During the remodeling phase, the focus on mobility is increased gradually, and as healing allows, strengthening, dexterity training, and other intervention aimed toward return to former activity should begin.
Although the phases are described here in simple terms and as discrete entities, in reality they overlap considerably and involve simultaneous complex processes; treatment should always take this into account. For example, although as fibroplasia begins gentle controlled stress may be initiated, some inflammatory activity remains. Careful evaluation will reveal the signs of continued inflammation, and treatment is modified accordingly.
Healing of Specific Tissues
Skin and Superficial Soft Tissue
Skin wounds heal relatively quickly, with a simple sutured wound tolerating mobilization within a few days. Sutures can be removed in 10 to 21 days, depending on the wound and the stresses to which it is subject. Grafts need more protection, the timing of which depends on the type of coverage. Areas left open and allowed to heal by secondary intention may take several weeks, depending on the size of the wound. See Chapter 18 and the references for further detail. Wound healing may be delayed by systemic disease such as diabetes or hypothyroidism, or by other factors such as smoking, age, tight bandages causing ischemia, excessive edema, or infection.
Superficial scar management begins with early wound care, avoiding trauma that could prolong or exacerbate the inflammatory response and stimulate excessive scar formation. Treatment is aimed toward prevention of restrictive scar adhesions between superficial and deep soft tissues. If the skin is not allowed to glide normally over underlying tissues, motion may be severely limited. This is especially true of the dorsum of the hand, where the normal skin redundancy allows digit and wrist mobility.
Blood Vessels
Blood vessels require 1 to 2 weeks of protection. This generally is provided by the immobilization necessary for protection of other tissues. Bandages should be nonconstrictive. Close attention should be paid to signs of vascular insufficiency during this phase. Signs of arterial insufficiency include skin pallor, decreased temperature (measured with digit temperature probes or by touch), increased pain, sluggish capillary refill, and loss of pulse. Venous insufficiency is indicated by cyanosis and abnormally rapid capillary refill; with persistent venous insufficiency, temperature also may be reduced. Venous return can be assisted by elevation of the hand above heart level, which also assists lymphatic drainage and thus minimizes the compression placed on vessels by excessive edema. However, if arteries have been repaired, they should not be required to work too hard against gravity. If signs of arterial insufficiency are noted, elevation should be modified accordingly, as discussed subsequently in this chapter.
Nerves
Although healing at the site of nerve repair is similar to the healing of other tissues, the functional recovery of a repaired peripheral nerve involves the very different process of axonal regeneration, which is described in Chapter 43 . Therefore, the suture site is protected according to the usual phases of soft tissue healing, but the return of sensory or motor function is expected to vary depending on the location of the injury.
The suture site of a completely transected and well-repaired nerve must be protected from excessive stress for 3 weeks. In general, orthoses should immobilize the joints distal and proximal to the repair without placing it under tension or direct compression, or placing it at risk of adherence to adjacent tissues that will later restrict nerve gliding. An adherent nerve is subject to alternating compression and stretch, which may produce internal scar and impede transmission of nerve impulses. An example is the hyperflexed wrist after repair of median and ulnar nerves. The nerves may become adherent and compressed beneath the flexor retinaculum, and later attempts to regain wrist extension will subject the nerve to potentially harmful traction.
If the nerve is incompletely transected, is repaired under no tension, or is only contused, little or no immobilization may be needed. In fact, protected early mobilization of an intact but contused nerve may help restore gliding and prevent constriction and traction by scar adhesions. In the case of a digital nerve repaired along with flexor tendon repairs in zone II, early mobilization of the tendon will significantly improve the ultimate result, and clinically this has not proven to compromise the sensory recovery. If the nerve was repaired under tension, limiting metacarpophalangeal (MCP) or proximal interphalangeal (PIP) joint extension may provide adequate protection while still allowing active or passive flexion. Bear in mind, however, that there is some early evidence in the literature that early mobilization of repaired nerves may impair healing, so caution is necessary. Decisions to mobilize repaired nerves early should be made by therapist and surgeon together.
If a nerve was avulsed or a portion of the nerve was destroyed, leaving a gap, the nerve may be left unrepaired or may be grafted primarily or secondarily. In the first case, any insensate areas must be carefully protected. In the second case, the two suture sites must be protected appropriately.
After motor nerve injury, treatment considers the functional imbalance produced by loss of specific muscle function. Such imbalance can lead to development of secondary deformity during the lag time required for nerve regeneration. After sensory nerve injury, patients must be taught to protect insensate areas from injury.
In any nerve repair, exact end-to-end approximation of each severed axon is impossible to achieve, and a certain percentage of nerve function is therefore destined to be lost. Even if a nerve were perfectly repaired, with the two halves of each axon approximated precisely, axonal regeneration would take a long time (1 to 3 mm per day, after a 3- to 4-week latent period ). Regeneration after crush injury is more rapid but may seem agonizingly slow to the patient. Sensory and motor function must be reevaluated frequently after peripheral nerve injury and the treatment plan adapted as needed. Because nerve regeneration is slow, this aspect of recovery can be neglected all too easily, to the great detriment of the patient.
After an amputation or other injury in which a nerve is transected and left unrepaired, neuroma formation is the inevitable result. Neuromas can be asymptomatic, but in many cases they are quite painful. If not addressed promptly, a painful neuroma may become an enormous obstacle to functional recovery. Therefore, in the presence of unrepaired transected nerves, early prophylactic desensitization and protection of hypersensitive areas are advisable.
Muscles and Tendons
Detailed discussions of tendon healing and management are available elsewhere in this book and in the literature. The following is a simplified overview of tendon healing.
In the inflammatory phase the repair site is weak, relying on the sutures to maintain continuity. In the proliferative phase, strength increases steadily as collagen is laid down. As noted previously, the quantity of collagen stabilizes by the end of fibroplasia. During the remodeling phase, destruction and replacement of collagen allows for stronger collagen cross-linking and differential reorientation of fibers. The parallel orientation of fibers within the tendon provides increased tensile strength, and the random orientation of peritendinous fibers allows tendon gliding.
The goal of tendon repair and rehabilitation is a strong repair that heals with a minimum of restrictive adhesion formation. As already noted, numerous studies have demonstrated that the strength of the repair increases in response to controlled stress. For example, the strength of an immobilized tendon repair has been noted to decrease temporarily at 10 to 14 days, but a tendon that is subject to some form of controlled mobilization develops an increased breaking strength, while developing more pliable, gliding adhesions to the surrounding tissues. Therefore, if an injured tendon is not mobilized until 2 weeks after repair to protect other healing structures, exercise should be very gentle because of the decreased strength of the juncture at this stage. If the tendon is first mobilized after 3 to 4 weeks, the repair will be somewhat stronger, but still not as strong as in a tendon that was first mobilized within a day or two of repair.
In general, immobilized repaired tendons have sufficient strength to withstand gentle active motion at 3 to 4 weeks, and they can tolerate light resistance after another 2 to 3 weeks. Tendons that have been mobilized passively will be stronger when active motion is started at 3 weeks. However, these are general guidelines; the specifics of each case should be considered carefully in the timing of the progression of treatment. For example, repaired extensor tendons in zones I and II require 6 to 8 weeks of immobilization, due to the unique anatomic features of that zone. Greater protection should be given if healing may be impaired by systemic conditions such as diabetes , or by habitual tobacco smoking, or if flexor tendon vinculae have been damaged. If both flexor and extensor tendons are repaired, the program must be modified to prevent excessive stress to either tendon.
An injury to the richly vascularized muscle belly or musculotendinous junction heals more quickly and easily. Adhesions at this level can be strong but pose fewer problems than do tendon adhesions, because in general, less gliding is demanded between muscle belly and surrounding tissues than between tendon and peritendinous tissues.
Bone and Articular Structures
As with other tissues, bone healing has three phases. During the inflammatory phase, a fracture hematoma forms and cellular debris is cleared away. The next phase can take considerably longer than the typical proliferative phase, depending on the location of the fracture. In this period, a soft tissue collar or soft callus develops and unites the fracture fragments, providing support for a fibrocartilaginous union. This callus, though joining fracture fragments, is not strong, forming what is known as a clinical union , not sufficiently solid to be visible on radiographs. Often, active and active-assisted motion of the joints adjacent to the healing bone is begun at this point because a clinically healed bone shows no motion at the site of fracture, and therefore controlled stress is safe. However, in many cases radiographic healing must be seen to ensure stability in difficult fractures. Radiographic healing occurs during the remodeling phase, when true cortical and cancellous bone is formed and gradually increases in strength in response to longitudinal and shearing stresses.
Remodeling may begin within a month and continue for several years. The healing rate of fractures varies widely depending on the bone and what part of the bone is affected. In the upper extremity a fracture may be considered clinically healed at as early as 2 to 5 weeks or may require several months of immobilization. The type of fracture and fracture fixation naturally also affect the course of treatment. In fact, with open reduction and internal fixation using compression plates, primary bone healing can occur, in effect skipping the stage of callus formation. This may speed healing, and a sufficiently rigid fixation also will allow earlier motion of the involved bone.
Injured articular cartilage generally heals poorly, without regeneration of true hyaline cartilage. The result is an irregular joint surface, which opens up the possibility of post-traumatic arthritis. Because cartilage is avascular, nutrition is supplied entirely through diffusion and the contribution from the highly vascular perichondrium. In the absence of blood vessels in the cartilage itself, there can be no inflammatory response but instead a limited and unpredictable healing via chondrocyte activity. If the injury extends to the vascular subchondral bone, healing is aided by the inflammatory response of the injured bone and may actually improve the recovery of functional joint surfaces.
Ligaments present a different set of problems. In injured ligaments, scar tissue contraction can limit considerably the available motion of a joint. In addition, even if there is no direct ligament injury, inflammation of adjacent tissues can lead to fibrosis in an immobilized or edematous joint, thus diminishing ligamentous elasticity. Therefore, if joints must be immobilized, ligaments should be kept at the greatest length possible so that they do not shorten and produce joint contractures.
Overview of Treatment Techniques
Patient Education
Many patients are overwhelmed by the gravity of a complex hand injury. Because the recovery of function depends on psychological and physical recuperation, patient education is crucial. From the first visit, patient education must be oriented toward both current status and future return to a normal way of life.
The complexity of the injury usually demands multifaceted and time-consuming therapy. The home program must be as clear and simple as possible, so that the patient can and will follow through on his or her own. This means tailoring the program not only to the patient’s physical needs but also to his or her psychosocial status. How extensive a program can the patient understand? How much time does the patient have during the day? What are the other demands on his or her time? Will the patient’s health insurance cover everything desirable for therapy, or will limited coverage restrict the options open to him or her? The program is adapted as needed, beginning with a simple set of instructions. New elements are added as the patient becomes ready, and elements are deleted when no longer necessary. The home program strikes a balance between physical and psychosocial well-being; exercises must be performed often enough to meet physical needs but should not dominate the patient’s life.
The home program is written out, demonstrated to the patient, and discussed thoroughly. The patient then reads the program and demonstrates to the therapist a full understanding of all instructions. This is repeated at each successive visit and with each addition or change to the program, until the therapist is satisfied that the patient is following through well at home.
The patient may require therapy for months or years, with a series of surgical reconstructions and postoperative rehabilitation. Over time, some patients become dependent on hand therapy as a way of life. This dependence can be kept to a minimum or prevented altogether by careful patient education and early enlistment of family support. Referral to a psychologist or social worker also may be indicated. Such a referral can contribute immeasurably to the patient’s successful recovery. Chapter 101 explores in greater depth the psychological effects of traumatic hand injuries.
Wound Care
Careful wound management can control scar formation and thus result in a more cosmetically acceptable hand with greater mobility and function. Detailed discussion of wound care can be found in Chapter 18 . Only a few key points are included here.
Early wound care may include conservative debridement, removing only dead tissues that come away easily and avoiding trauma to the involved tissues. If the whirlpool is used for gentle debridement and cleansing, treatment time is short (from 5 to 20 minutes) to limit the time spent with the hand in a dependent position, because this could increase edema. Careful thought is given to the water temperature, the level of agitation, and any additives to be used for their cleansing or antibacterial effects. Neither elevation nor active motion appears to affect post-whirlpool edema, but whirlpool temperatures have a significant effect. A temperature of 32° to 35° C is recommended. In recent years, pulsed lavage has come into use. This modality offers not only debridement but facilitation of wound granulation.
Whirlpools generally are contraindicated in the early care of grafts and flaps, when, in fact, it is often better to leave dressings undisturbed if possible, to ensure that the graft or flap takes. When whirlpools are used, they should be of short duration (5 minutes), agitation should be kept low, and the water should not be too cold, because this could produce vasoconstriction and ischemia.
Wounds with delayed healing may be treated with vacuum-assisted closure using VAC. therapy (KCI, San Antonio, TX), also known as negative-pressure wound therapy or simply the wound vac. This device, developed at Wake Forest University, applies negative pressure to the wound, draining excess fluids and exerting mechanical force on soft tissues. The mechanisms involved are not completely understood, but results have been good.
Many more options for wound dressings are available now than in the past. Although the simple sutured wound is clean and often kept dry, many open wounds may be best treated with moist, occlusive dressings. The practice varies from center to center. It is best to follow the practice of the referring surgeon. See also Chapter 18 .
Whether the wound is kept moist or dry, the goals are protection from undue stress and provision of the appropriate microenvironment for healing. Forceful removal of an adherent dressing can inflict trauma to the tissues and prolong the inflammatory response. This is especially important with grafts. Graft “take” involves the establishment of new vascular supply to the graft, and this tenuous developing circulation is easily disrupted. In addition, even after vascularity is established, the scar interface between graft and bed is weak in early stages. Therefore shearing force and pressure must be avoided until at least 2 weeks after grafting. Several types of nonstick dressings on the market can prevent adherence to grafts or open areas and provide antibiotic protection as well ( Fig. 95-2 online).
All gauze bandages should be nonconstrictive and wrapped in a figure-of-eight from distal to proximal to avoid creating a tourniquet with a circular wrap. Revascularizations, flaps awaiting division, free flaps and composite tissue transfers, and replanted parts present a more difficult problem in dressing application, but in these cases it is doubly important to avoid all constriction during the early stages when vascularity is being established. Skin color and temperature are monitored carefully for signs of ischemia or venous congestion after all microsurgical vascular procedures, and any problems are immediately reported to the attending surgeon.
Many patients with more simple wound care needs can perform dressing changes at home. External fixators are cleaned daily at the skin entrance sites by the patient, using clean cotton swabs and hydrogen peroxide or a hydrogen peroxide solution. Some surgeons prefer to follow cleaning with application of antibiotic ointment and/or a light dressing.
Patients should be instructed to monitor pin sites and all wounds for signs of infection: increased local redness or warmth, pain, or exudate. A fever also may be present. If the patient has any doubts, he or she should contact the therapist or doctor at once, and if the therapist identifies a possible infection, it should be reported immediately to the attending physician. A culture may be necessary to determine the appropriate antibiotic treatment.
Superficial Scar Management
Although the exact mechanism is still under investigation, continuous pressure over a bulky superficial scar flattens it and may make it softer, more elastic, and more cosmetically acceptable to the patient. In the hand, continuous pressure can be provided with elasticized gloves such as Jobst gloves (Jobst Co., Toledo, OH), with Coban elasticized paper bandage (3M Coban Self-Adherent Wraps; 3M Co., St. Paul, MN), or for firmer and more localized pressure, with elastomer or gel sheets (mineral oil-based or silicone gel).
There are two types of elastomer, both of which are applied quickly to allow time to set through a catalytic reaction. For the first type, the catalyst is added to a sticky liquid and thoroughly mixed before applying. For the second type, equal parts of two different putties are mixed in the therapist’s hands. One of the two putties is the catalyst. As the elastomer sets, it forms an exact mold of the scar and all the skin creases ( Fig. 95-3 online). For the best results the pad is worn constantly if possible, and is held in place by a closely fitting orthosis or Coban wrapping. As the scar compresses over time, new molds must be made to accommodate changes.