Practical Plastic Surgery

topical analgesics and dressings. Pharmacologic treatment is brought into play for the above-mentioned absolute and relative indications. Small lesions can be treated with direct intralesional infiltration of a corticosteroid. Multiple injections (4-7) are typically needed. For more extensive hemangiomas, prednisone given at 2-3 mg/kg daily is initiated; for life-threatening lesions, intravenous steroids are given, as stated above. Eighty percent of hemangiomas of infancy will respond to corticosteroid therapy. Responses should be seen within 2 weeks, and the steroids should then be tapered gradually over a period of several months. The clinician should be on guard for nonresponsiveness or rebound growth.

Laser therapy can occasionally prove useful for superficial hemangiomas and is perhaps most useful for telangiectasias remaining in the residual tissue following involution of the hemangioma. Mixed and deep lesions will have a greater tendency to result in distorting fibro-fatty sequelae, which may require excision or reconstruction. Surgery, as mentioned above, is definitively indicated for removal of a symptomatic hemangioma, as in the nasal tip. Uncomplicated hemangiomas are rarely resected; involuting hemangiomas may be resected for psychosocial reasons before the child reaches school age or, if in the opinion of the surgeon, the remaining scar would be persistent and would eventually require surgical removal anyway.

The other vascular tumors are treated differently. Pyogenic granulomas will typically require curettage and cauterization to stop bleeding. A NICH will require surgical excision, as it will not involute. Kasabach-Merrit syndrome is a consumptive coagulopathy in the setting of an enlarging soft tissue mass, usually a kaposiform hemangioendothelioma (KHE); the patient will display a thrombocytopenia and bleeding diathesis that may be unresponsive to platelet transfusions. These patients require admittance to a hospital, steroid infusions and antiplatelet/antifibrinolytic medications, with or without embolization of the lesion. Interferon-α is not as effective as other antineoplastics such as vincristine and cyclophosphamide in the treatment of a KHE involved in the Kasabach-Merritt syndrome. The KHE lesion should be surgically resected when possible; otherwise, these lesions are difficult to manage medically. As mentioned above, this syndrome does not occur in hemangioma of infancy; it is found only in tufted hemangiomas or kaposiform hemangioendotheliomas.

Vascular Malformations

The classification of the various types of vascular malformations was described

26above. These lesions are brought to the attention of the plastic surgeon for several reasons. The mainstay of treatment, except for small ones in the extremities, is a combined approach with radiologic-guided superselective embolization, and surgical debulking when necessary. Properly done, risks are minimized, although these can include ulceration, infection and occasionally catastrophic complications such as limb loss.

Unfortunately, due to their extensive intercalation and incorporation within tissues, dissection planes are nearly impossible to reliably discern. These tend to be space-occupying lesions, and recidivism is common. Like endothelial cells elsewhere in the body, the endothelial cells in these lesions are quiescent until stimulated to proliferate by injury, distressingly often by a surgical insult. This accounts for their recalcitrance following monotherapy such as surgery. Therefore, the treatment goals need to be clearly explained to the patient. They rarely include cure and instead are mostly palliative to control the complications of ulceration, bleeding, and for improved hygiene. Reoperation is unfortunately often the rule, rather than the exception.

Vascular malformations can be categorized as arteriovenous (AVM), venous, capillary, or lymphatic malformations. Unlike hemangiomas of infancy, these lesions do not display a proclivity for either sex.

Diagnosis

The history and physical can guide the diagnosis. Capillary malformations are typically noted at birth; they include the well-known port wine stain. Eighty percent of lymphatic lesions will become apparent either at birth or during the first year of life. Venous malformations will be noted at any time from birth to adulthood, a fact which is important when evaluating the young adult with prominent leg veins who presents for sclerotherapy. They are typically darker lesions seen on the skin or mucosal surfaces. Arteriovenous malformations can become evident during periods of hormonal fluctuations, such as puberty or pregnancy. Lymphatic malformations are composed of dilated lymphatic channels and vesicles; these lesions will typically swell with an infectious episode. They may be either macrocystic or microcystic.

Plain radiographs are only utilized when there exists a potential for bone or joint involvement. MRI and ultrasound can often play a complementary role in the treatment of these lesions. Ultrasound can be a confirmatory screening test to demonstrate the vascular nature of a soft tissue mass, and MRI will show the lesion’s relationship to adjacent structures as well as feeding and draining vessels. Because of these benefits, MRI is clearly the first-line diagnostic tool. However, angiography plays a larger role in the diagnosis and treatment of vascular malformations than in hemangiomas. The differential diagnosis of an AVM includes malignant vascular tumors such as angiosarcoma and rhabdomyosarcoma. When the benign nature of these lesions cannot be definitively ascertained through an imaging approach, a biopsy of the lesion is warranted.

Treatment

The optimal treatment should be tailored to the type of lesion and its location. Because of the wide variety of presenting symptoms and multitude of lesions, this is a discipline that is continuing to evolve. There are some lesions that require immediate treatment. Although the plastic surgeon may not be directly involved in the treatment phase of these lesions, he should be aware of what constitutes a life-threatening lesion so that the patient can be promptly referred if necessary.

Venous malformations are treated mainly by sclerotherapy (occasionally by an 26 interventional radiologist), typically when the lesion becomes symptomatic. Debulking surgery, when indicated, is performed 6-8 weeks following sclerotherapy. Occasionally, lesions in or near vital structures (such as the hand/digits) are treated

by surgical excision alone.

Lymphatic malformations are notoriously difficult to treat. Most patients present for treatment of cellulitis and will benefit initially from elevation of the affected body part and intravenous antibiotics. Macrocystic lymphatic malformations are best treated with sclerotherapy. Most lesions will require surgical resections, a procedure which is tedious, bloody and fraught with recidivism. Because of the often bloody procedures, they are best staged.

Capillary malformations can often be treated with laser therapy. Up to 75% of patients will benefit from this therapy. As these lesions can be accompanied by underlying soft tissue and bony hypertrophy, surgical resections of the involved tissues may be indicated.

AVMs are the most treacherous of vascular malformations to treat. They are treated when they become symptomatic; unfortunately, the herald symptoms may include life-threatening bleeding or heart failure. There are some guidelines to treatment of the AVM which all members of a multidisciplinary vascular anomalies team should be aware of. In terms of embolization of these lesions, proximal feeder vessels should never be embolized, as the lesion will only become more vascular via reactive neovascularization. In addition, as these lesions may require multiple interventions, a poorly planned embolization will make it difficult or impossible to perform future embolizations. These lesions will require wide, deep, extensive resections, often necessitating a microvascular free flap to achieve wound closure.

Pearls and Pitfalls

The most important point in treating vascular anomalies is establishing the correct diagnosis. Incorrect treatment for a lesion can have dire, even life-threatening, consequences. Radiologic imaging by a specialist radiologist is essential to preventing the above. Furthermore, there exist a set of vascular malignancies which demand treatment and not a “watchful waiting” approach. Even within the more benign subset of patients with hemangiomas, a sizable proportion will require some surgical treatment even if the lesions involute, particularly on the face. This is generally not appreciated by the referring physicians. In addition, these lesions often take years to involute, and the parents need to be so informed.

The use of novel markers, with GLUT-1 being a paradigm for this, will in the future enable more precise identification of the type and life-stage of these lesions. Novel approaches using anti-angiogenic factors may ease the effects of steroids or other anti-neoplastic regimens currently used to treat these lesions, and may be particularly beneficial for patients with vascular malformations, many of which end up as medical and surgical orphans. Finally, it may be possible to block vascular stem cell incorporation within these lesions, or conversely, exploit the proclivity of these lesions to attract vascular progenitors by genetically modifying vascular stem cells to impair the growth of hemangiomas or accelerate their involution.

Suggested Reading

extirpations. Skin grafts and skin substitutes are commonly used to provide coverage over a broad spectrum of open soft tissue defects. Unlike surgical flaps, however, skin grafts and skin substitutes do not have their own blood supply and are limited by their thinness. Thus, the recipient bed must be well-vascularized in order to provide the transferred skin with nutrients to survive. Tendon may be grafted if the paratenon is intact; likewise, bone may be grafted if there is intact periosteum. On the other hand, irradiated tissue is not a good candidate for a skin graft, as radiation often leads to capillary depletion and inadequate nutrition to the transferred skin. Furthermore, open wounds with exposed bone often require more soft tissue padding than a skin graft is able to provide.

Types of Skin Grafts

Skin harvested from another species is called a xenograft. Skin harvested from another person from the same species is called an allograft. Skin that is harvested from one part of the body and used to cover another part of the same person’s body is called an autograft. While xenografts and allografts may be used to provide temporary coverage over open wound defects, their MHC class II mismatch will cause rejection over time. They are very useful as biological dressings, however, to allow a recipient bed to improve before it is ready for an autograft. In particular, allografts are useful to test a questionable recipient bed. Ultimately, however, an autograft is necessary for permanent coverage of the wound.

Split-Thickness vs. Full-Thickness

There are two primary types of skin autografts: split-thickness skin grafts (STSG) and full-thickness skin grafts (FTSG). A STSG includes the entire epidermis as well as varying portions of the underlying dermis. A FTSG includes both the epidermis and the entire dermis and thus retains more of the normal characteristics of skin including color, texture and thickness. Since the FTSG contains more dermis, it has greater primary contraction than a STSG; however, full-thickness dermis impairs secondary wound contraction to a greater degree than a split-thickness graft. Of course, thicker grafts demand greater vascularity in the recipient bed in order to maintain cellular respiration.

Whether to use a fullor a split-thickness skin graft depends upon the condition and location of the defect, its size, as well as aesthetic considerations. Areas of high cosmetic concern, such as visible parts of the face or the hands, may benefit from a FTSG. An example is using full-thickness postauricular skin to cover the thin skin

27of the eyelid. In addition, areas that tolerate little wound contraction, such as the interphalangeal joints or antecubital fossa, do better with a full-thickness skin graft.

STSG-Advantages

STSG are much more versatile. Since a skin graft does not have its own blood supply, any condition that impairs the means by which the graft is nourished and oxygenated (imbibition, inosculation and neovascularization-described below) may threaten graft take. Not only does this include infection and poor vascularity in the underlying recipient bed, but any condition that prevents firm adherence of the skin graft to the recipient bed. Such conditions include seroma, hematoma, foreign body, graft wrinkling or tenting, shear forces, necrotic material and bumpy irregularities in the underlying wound surface. STSG will do better than FTSG in these conditions. Furthermore, STSG can be used to cover a larger surface area. Donor

sites for STSG are able to heal spontaneously due to the epidermal appendages that remain in the unharvested dermis. Additionally, once the donor site has healed, it may be used again to harvest more skin.

STSG-Disadvantages

While the STSG has broader use, it also has its drawbacks. A healed STSG does not accurately resemble uninjured skin. The lack of epidermal appendages gives it an abnormally shiny and smooth appearance, and the color is often noticeably lighter or darker than that of the surrounding skin. In addition, while the thinner graft may take more easily, it also fails to prevent wound contraction, which can lead to functional and aesthetic problems. Thinner grafts are more fragile from lack of bulk and do not tolerate subsequent radiation therapy well. Despite its aesthetic deficiencies, STSG are used for many purposes including replacing lost skin in burn injuries, resurfacing large wounds and muscle flaps, lining cavities and covering mucosal deficits.

Preparing the Recipient Bed

The key factor in the successful take of skin grafts is a healthy well-vascularized recipient bed. Necrotic tissue must be completely debrided, as decaying tissue contains no blood supply and produces toxins that retard wound healing. Likewise, the wound must be free of infection, defined as bacterial counts less than 100,000/cm2, since bacterial overgrowth can infect and destroy the skin graft. Devascularized tissues, such as bone without periosteum, cartilage without perichondrium, tendon without paratenon, and nerve without perneurium, need an overlying layer of granulation tissue in order to be grafted. While skin grafts can survive on periosteum, perichondrium, peritenon, perineurium, dermis, fascia, muscle, fat and granulation tissue, irradiated wounds have a compromised blood supply and may not be able to nourish a skin graft. Finally, vasculopaths with arterial insufficiency or venous stasis ulcers need to correct underlying vascular problems to support a skin graft.

A contaminated or chronic wound often needs to undergo a prolonged course of wound care in preparation for skin grafting. Multiple surgical debridements may be required either at the bedside or in the operating suite. Enzymatic debriders may be used to dissolve necrotic tissue. Topical or systemic antibiotics may be necessary to reduce the bacterial count. Wet-to-dry dressing changes or vacuum-assisted closure therapy should be carried out until the underlying recipient bed appears clean, healthy and red with punctate bleeding. The importance of adequate recipient bed prepara-

tion cannot be overstated. Not only does graft failure prolong the time the primary 27 wound stays open, but it creates a secondary wound at the donor site that will also

need to heal. Indeed, the exposure of raw nerve endings in the donor site defect often makes it more painful to the patient than the original wound itself.

Operative Technique

Once a clean, well-vascularized recipient bed has been achieved, the patient may be taken to the operating room for skin grafting. The wound is prepped and draped in the usual sterile fashion. Any overlying layer of granulation tissue should be scraped off with a blunt instrument; the back end of a pair of forceps or the handle of a scalpel work nicely. The top layer of contaminated tissue should be eliminated and healthy bleeding tissue exposed. If the underlying tissue is covered with eschar or severely burned skin, then the overlying dead tissue needs to be excised sharply.

Pre-Grafting Excision

Surgical excision may be either fascial or tangential. Fascial excision removes both viable and nonviable tissue down to the muscle fascia and yields an easily defined plane that is well-vascularized. Blood loss is minimized with fascial excision because vessels are more easily identified, and the entire excision can be performed with electrocautery. The excision inevitably includes healthy, viable subcutaneous tissue, however, and a contour deformity often results. To address these issues, tangential excision is designed to limit excision only to nonviable tissue, leaving the healthy tissue intact, and it also minimizes the contour deformity. Instruments used for tangential excision include the Weck/Goulian blade and the Watson knife, which are handheld knives that tangentially excise slices of eschar until a layer of viable tissue is seen with diffuse punctate bleeding. Sharp excision of eschar makes it more difficult to control diffuse bleeding, however, and it can also be difficult to assess the suitability of the underlying fat for accepting a graft. Hemostasis can be obtained with epinephrine-soaked Telfa pads, topical pressure and, if necessary, electrocautery. Only after complete hemostasis has been obtained and the wound bed defined, can the skin be grafted.

FTSG Harvest

A full-thickness skin graft is harvested with a scalpel. The wound defect is measured and a pattern made, and then this is traced over the donor site. The FTSG is then harvested sharply by dissecting the dermis off of the underlying subcutaneous tissue. Any fat that remains on the graft must be removed sharply with scissors, as fat is poorly vascularized and will prevent firm adherence between the graft dermis and the recipient bed. All yellow fat must be trimmed until all that remains is the shiny white undersurface of the dermis. The donor site is usually closed primarily or, occasionally, with a STSG.

STSG Harvest

A split-thickness skin graft is most commonly harvested with a dermatome. Dermatomes may be air-powered, electric, or manually operated, and they facilitate skin harvest of uniform thickness. Frequently used dermatomes include the Padgett-Hood, Zimmer, Brown and Davol-Simon. Care must be taken to set the desired thickness of the skin graft prior to harvest, and then to double-check the setting again prior to operating the device. A 15-blade scalpel simulates a thickness of 0.015 inches and can

27be run along the blade to check a uniform depth setting. The blade must also be checked for proper orientation and the appropriate guard width chosen.

After the wound is measured, the surgeon calculates the area of coverage needed and marks the donor site. The most common donor site is the anterior or lateral thigh, as it is easily accessible and straightforward to camouflage, although any region with available skin may be harvested. The donor site is often lubricated with mineral oil or Hibiclens solution although other substances can be used according to surgeon preference. One or more assistants press along the edges of the donor site to create a firm, flat surface. The dermatome is then moved along the donor site at a 45-degree angle with equal pressure on all areas. An assistant picks up the harvested skin with forceps to prevent the graft from getting caught in the instrument. Multiple strips of skin graft should be harvested without any gaps between adjacent donor sites. When the skin has been harvested, epinephrine-soaked Telfa pads are placed on the donor site to obtain hemostasis.

connection between graft and host vessels develops further as the graft revascularizes and newly formed vascular connections differentiate into afferent and efferent vessels between days four and seven. Lymphatic drainage is present by the fifth or sixth postgraft day, and the graft begins to lose weight until it reaches its pregraft weight by the ninth day.

Graft Contracture

Once the skin graft is harvested, it also begins to shrink. Primary contraction is passive and occurs immediately after harvest. A FTSG loses about 40% of its original area; a medium-thickness skin graft about 20%; and a thin STSG about 10%. Secondary contraction occurs when the skin graft is transferred to the recipient bed, and it is only seen in STSG. The amount of wound contraction depends upon the amount of dermis in the skin graft. The more dermis there is in a skin graft, the less the wound bed will contract. Secondary contraction is minimal in a FTSG, which is actually able to grow after it heals. Wound contraction can be useful in reducing wound size, but a contracted wound can also be tight and immobile, leading to distortion of surrounding normal tissue.

Return of Function

As the skin graft heals, it reinnervates and undergoes color changes. Nerves grow into skin grafts from the wound margins and recipient bed, and skin grafts may begin to show sensory recovery anywhere from 4-5 weeks to 5 months postgraft. Full return of two-point sensation is usually complete by 12-24 months, but temperature and pain sensation may never return. With regard to color, grafts from the abdomen, buttocks and thigh tend to darken over time, whereas grafts from the palm tend to lighten. Thin grafts are also usually darker than thick ones.

Depending on thickness, skin grafts may also regain function of transferred epithelial appendages, such as sweat glands, sebaceous glands and hair follicles. Usually, only FTSG are reliably capable of sweat production, oil secretion and hair growth. Sweat production depends on the number of sweat glands transferred during grafting and the extent of sympathetic reinnervation. The graft will sweat according to incoming sympathetic nerve fibers so that a graft on the abdomen sweats in response to physical activity while the same graft on the palm will sweat in response to emotional stimuli. With regard to oil secretion, sebaceous gland activity can be seen in both fulland split-thickness grafts, but they are usually not functional in thin STSG. Similarly, FTSG produce hair, while STSG

27produce little or no hair. In addition, inadequate revascularization or disruptions in graft take will damage graft hair follicles and result in sparse, random and unpigmented hair growth.

Skin Substitutes

When the amount of skin loss has been too great to allow adequate replacement with skin autografts, it may be necessary to use tissue-engineered skin substitutes (Table 27.1). Skin substitutes are designed to be left in place for long periods of time, and may be autologous, allogeneic, xenogeneic, or recombinant. They can either be used for wound coverage or wound closure. Materials intended for wound coverage provide a barrier against infection, control water loss, and create an environment suitable for epidermal regeneration. Materials used for wound closure restore the epidermal barrier and become incorporated into the healing wound.

Wound Coverage

Skin substitutes used for wound coverage include Biobrane, TransCyte, cultured epidermal allogeneic keratinocytes, Dermagraft and Apligraf.