Skin Grafting of the Dorsum of the Hand

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A 35-year-old male was 1 of 6 men injured when a grain silo exploded. The patient was taken to the operating room on the day of admission and the deep burns on the dorsum of the hands were tangentially excised, under tourniquet control, to viable dermis and fat. Care was taken to preserve the dorsal veins and the paratenon over the extensor tendons. A split-thickness skin graft (STSG) was harvested at a depth of 14/1000 of an inch from the patient's left thigh, applied to the wound as sheets, and sutured in place (Figure 1). The hands were dressed with a petrolatum-based fine mesh gauze impregnated with 3% bismuth tribromophenate (Xeroform), and the fingers were individually wrapped with the fingertips exposed. A bulky dressing was applied, and a volar plaster splint was fashioned to the wrist and forearm to maintain the hands in a protective position. Range of motion exercises were begun after the first dressing change on postoperative day 5, and the patient was fitted with compression gloves. There was a 100% skin graft "take," and the patient ultimately demonstrated full flexion and extension of the fingers and wrists, with follow-up over 1 year.

Figure 1. The appearance of the left hand (A) on admission, (B) following excision of burn eschar to viable yellow fat and white reticular dermis. (C) The hand is resurfaced with sheet split-thickness skin grafts. (D) Appearance at 3 months, with full extension of the digits, and (E) with full flexion of the digits.

The term skin graft "take" is the incorporation of the graft into the recipient wound bed and relies on a dynamic and intricate array of coordinated physiological events. The process can be divided into 3 overlapping stages: plasma imbibition, revascularization, and maturation (Figure 2).

Figure 2. Stages of skin graft healing. (A) Harvested skin graft with no circulation. (B) Plasmatic imbibition (0-48 hours). (C) Revascularization (days 2-21). Blood vessels from the wound bed invade the graft as the native graft vessels regress and reconnection (inosculation) occurs. (D) Maturation (1 year). Fibroblasts produce collagen to strengthen the extracellular matrix. Myofibroblasts induce wound contraction.

Plasma Imbibition occurs during the first 24 to 48 hours when the skin graft is bound to the wound bed by fibrin and nourished by osmotic diffusion.¹ The graft becomes edematous, gaining 40% weight,² and respires anaerobically, as evidenced by reduced levels of adenosine triphosphate and glucose.³ A thin STSG may tolerate ischemia for up to 5 days compared with 3 days for a thick STSG or a full-thickness skin graft.

Revascularization involves the maturation of vascular connections, establishing a unidirectional flow through afferent and efferent vessels. Simultaneously, the restoration of lymphatic circulation drains the edema. Studies indicate 3 critical steps of revascularization: vascular ingrowth (neovascularization), regression, and reconnection (inosculation).⁴ Hypoxia-induced angiogenesis triggers the ingrowth of new vessels from the wound bed into the graft. Approximately 20% of these vessels are derived from endothelial progenitor cells that originate in the bone marrow. The tips of the outgrowing microvessels express matrix metalloproteinase MT1-MMP, which prunes the preexisting graft capillaries.⁵ Although the vasculature regresses, the basal lamina of these graft capillaries persists, providing a conduit for vascular ingrowth and connection.

Maturation continues for over a year. The wound becomes populated with fibroblasts as collagen is deposited and becomes cross-linked to reinforce the strength of the extracellular matrix. The differentiation of fibroblasts into myofibroblasts induces wound contraction.

Hand function relies on sensory perception. Excision of full-thickness burns severs receptors and nerve endings in the skin. Restoration of sensation depends on the connection between nerves in the host bed and the sensory receptors in the skin graft. Free nerve endings, unmyelinated terminal branches of neurons, ramify in the superficial layers of the skin and respond to pain and thermal sensation. They also terminate in Merkel-cell neurite complexes (Merkel's disks) that convey discriminative touch. Encapsulated mechanoreceptors, however, (Meissner, Ruffini, and Pacinian corpuscles) are primarily confined to glabrous skin, which accounts for the reduced 2-point discrimination on the dorsal surface of the hand (Table 1).

Table 1. Skin mechanoreceptors. Slowly adapting mechanoreceptors continue responding as long as the stimulus is present, whereas rapidly adapting receptors respond quickly but briefly to the stimulation.

Following transplantation, nerve fibers within the skin graft degenerate. New fibers invade the graft from the wound margins and bed, following the evacuated neurilemmal sheaths.⁶ Only fibers that follow degenerated former pathways can reach nerve endings. Thick skin grafts offer better sensory recovery than STSGs due to increased accessibility. Studies on the reinnervation of STSGs have conflicting results, with some suggesting that the neural network of grafts assumes the sensory pattern of the donor skin,⁷ whereas others propose the grafts adopt the pattern of the host tissue.⁸ In either case, sensation usually returns at 4 to 5 weeks post grafting but may be delayed for up to 5 months, with maximal recovery observed between 12 and 24 months. Pain sensation returns first, and the graft may be hyperalgesic for up to a year. Two-point discrimination approximates normal skin, although the return of touch, temperature, and tactile discrimination is less predictable.⁶

Autologous skin grafts will fail if there is any interference with serum imbibition or vascularization. They will not "take" on avascular structures, such as bare tendon, bone, or cartilage, where there is a barrier between the graft and the recipient bed; following infection, where there is shearing of the graft; or when systemic conditions are unfavorable. Skin grafts take less readily to fat, which is more susceptible to desiccation and infection and less vascular.

Hematoma formation is the most common cause of graft failure, as the clot separates the graft from new vessel ingrowth. Similar effects will occur with the accumulation of seroma or pus. Should excess intraoperative bleeding occur, it may be prudent to delay the procedure by 24 hours. Evacuation of hematoma can sometimes salvage the graft during the early postoperative period. Bacterial counts greater than 10⁵ organisms per gram of tissue,⁹ the presence of plasmin, proteolytic enzymes, and bacterial streptokinase in contaminated wounds result in the dissolution of the fibrin bond.¹⁰

Shearing forces, caused by premature movement or inadequate graft fixation, can tear inosculated vessels. For this reason, the author prefers to avoid disturbing the dressings for 5 days. Negative pressure dressings have demonstrated benefits in immobilizing the graft and enhancing adherence and survival, particularly in complex anatomical regions such as the axilla.¹¹ Graft failure is also associated with systemic conditions that impair wound healing, including malnutrition, vasculitis, chemotherapeutic agents, radiation injury, use of corticosteroids, and hyperglycemia.¹²

Autologous STSGs grafts may fail to capture necessary skin appendages,¹³ resulting in dry and brittle grafts without sebaceous glands. Maturation can cause significant contraction, distorting surrounding tissue and resulting in joint contractures. With burn edema, the hand can assume a position of wrist flexion, metacarpophalangeal (MP) joint hyperextension, proximal interphalangeal (PIP) joint flexion, and thumb adduction. Various protocols prevent detrimental joint positions. The hand should be immobilized in the intrinsic plus position with the thumb rotated into abduction-opposition, with moderate dorsiflexion of the wrist (20-30 degrees), flexion of the MP joints (70 degrees), and extension of the PIP joints to tighten collateral ligaments. Some surgeons stabilize PIP joints in extension with 0.028 Kirschner wire for 3 to 6 weeks,¹⁴ while others advocate early gentle active range of motion postoperatively.

The unsatisfactory appearance of STSGs can cause body image dissatisfaction. Meshed grafts are best relegated to patients with extensive burns and limited donor sites, as secondary healing and scarring of the interstices produce an unattractive cobblestone appearance. Contraction of the wound bed creates unsightly ridging where the graft abuts against the unburned skin and between adjacent grafts. The deformity can be minimized by providing a 2-mm gap between seams. A pilot survey found interesting gender-based preferences regarding the placement of dorsal seams; male raters preferred the ulnar side seam, being less noticeable during handshakes, while most female raters preferred the seam closer to the radius, away from the ring finger.¹⁵

In cases where the paratenon of the extensor mechanism is compromised, options include allowing granulation tissue to form on the tendons before skin grafting, application of a regeneration dermal template, or flap coverage. Donor site morbidity is also a notable limitation, resulting in a painful large trans/exudative wound in the short term and a hyper/hypopigmented, scarred, dysesthetic region in the long term.