Bleeding

The most common causes of bleeding from facial reconstruction with local flaps are drug-associated coagulopathy and inadequate hemostasis.⁷ Patients are questioned preoperatively concerning use of all prescription and over-the-counter medications that may contribute to perioperative bleeding. All aspirin-containing products, nonsteroidal anti-inflammatory medicines, vitamin E, and most herbal remedies are discontinued 1 week or more before surgery. The exception to this policy is patients with cardiac stents. These patients continue to take aspirin if it is prescribed by their cardiologist. Cold and sinus medications are avoided because many contain substances that may affect clotting or cause adverse elevation in blood pressure. Discontinuation of any medications prescribed by a physician to reduce blood clotting is coordinated with the patient’s primary physician or cardiovascular specialist. Bleeding may also be associated with hypertensive events, hepatic or renal failure, vomiting, straining, or alterations in the hematopoietic system.

Hemostasis is essential. Larger (1 mm) arterial vessels are securely ligated when they are interrupted, and unipolar or bipolar electrocoagulation is used to control bleeding from smaller vessels. The wound is rinsed with sterile water, and gauze moistened with saline may be used to gently dab the wound bed to facilitate visualization of bleeding vessels. If bleeding persists despite electrocoagulation, the patient is placed in reverse Trendelenburg position and cotton pledgets soaked in a local anesthetic containing a vasoconstrictor are applied to the bleeding area with light compression. Electrocautery is then used, perhaps more successfully, once bleeding vessels are more easily visualized. If bleeding continues and is excessive, a coagulopathy should be suspected. In these cases, the procedure is discontinued, a drain is inserted into the wound, and a compression dressing is applied to the area. In addition, before any future surgery, a hematologist is consulted to evaluate the possibility of a hematologic disorder.

Drains are rarely used with local cutaneous flaps, with the exception of ear reconstruction. However, an appropriately sized drain is employed when a significant “dead space” is present or drainage is expected that cannot be controlled with a compression dressing. The author’s preference is to use a compression dressing that conforms to the anatomic contour of the surgical site to facilitate adherence of the facial flap to the recipient site. This is typically left in place for 24 to 48 hours. The dressing consists of nonadherent gauze, cotton balls, and elastic mesh tape. Patients are instructed to keep their head elevated, especially at night, for the first 36 to 48 hours after surgery, and antiemetics are prescribed to prevent nausea and vomiting. Coughing and straining are to be avoided whenever possible.

Hematomas may cause compromise of local flap vascularity by inducing vasospasm, stretching the subdermal plexus, or separating the flap from the surface of the recipient site.8–10 Furthermore, iron compounds in a hematoma may promote free radical production, leading to flap necrosis.^11,12 Hematoma formation also predisposes to infection, which may compromise flap vascularity secondary to inflammatory edema.^13,14

If a hematoma occurs, patients usually complain of significant pain. The wound may appear mottled, pale, or bluish, and palpation of the skin in the area of the hematoma usually reveals a tight, tense flap with oozing of blood from the suture lines. Small (5-10 mL) hematomas may sometimes be aspirated through the suture line by use of a 25-mL syringe attached to an 18-gauge needle. A compression dressing is then applied and the patient is re-examined in 24 to 48 hours. If the hematoma recurs, it may be necessary to return the patient to the operating room to properly drain it. There, the wound is opened at a dependent portion, the hematoma is evacuated, and bleeding vessels are controlled. A compression dressing is reapplied. The patient is examined within 24 hours. Expediency in treatment of large hematomas is essential to avoid compromise of flap vascularity and skin slough. Typically, within the first 48 hours after surgery, hematomas consist of a fresh clot of gel or liquid consistency. As the clot matures during the next several days, it becomes firmer and adherent to the underlying wound bed and cannot be easily aspirated. After approximately 2 weeks, fibrinolysis begins, and the hematoma liquefies (Fig. 26-1). At this point, repeated aspiration or drainage may be necessary to facilitate adherence of the flap to the wound bed (Fig. 26-2).

Injury of Adjacent Anatomic Structures

A thorough understanding and appreciation of facial anatomy is a crucial prerequisite for performing facial reconstructive procedures. It is beyond the scope of this chapter to detail all of the potential injuries to anatomic structures, and the reader is encouraged to review specifics in the preceding chapters. General considerations related to protecting adjacent anatomic structures are reviewed.

Perhaps one of the most devastating complications associated with facial surgery is injury to the facial nerve or one of its branches. Although it is rare, extensive dissection in the preauricular area could lead to injury to the main branch of the facial nerve. More commonly, the marginal mandibular or temporal branches of the facial nerve are injured. Familiarity with cross-sectional anatomy of the temple and mandibular regions is essential before surgical dissection in these areas. Unfortunately, if more proximal branches of the facial nerve are cut, it leads to permanent impairment of facial movement because effective treatment is lacking.

Sensory nerves are also susceptible to injury during facial reconstructive procedures. Extensive undermining along the superior bony orbital rim may injure the supraorbital and supratrochlear nerves, leading to dysesthesias in their sensory distributions.¹⁵ Similarly, the deep branch of the supraorbital nerve runs within the galea aponeurotica and may be injured when the frontalis muscle is undermined in the subgaleal plane while defects of the lateral forehead skin are being closed. The infraorbital and mental nerves are less susceptible to injury but may be compromised during dissection in their respective areas. The great auricular nerve may be injured during subcutaneous dissection in the periauricular area. This nerve is identified and preserved when skin is dissected away from its attachment to the superior aspect of the sternocleidomastoid muscle.

Avoidance of injury to the nasal cartilaginous framework is important for nasal symmetry and function to be maintained. Inadvertent injury to these structures may lead to obvious nasal deformities, including alar retraction, nasal valve collapse, saddle nose deformity, and tip asymmetries. On occasion, preexisting structural abnormalities of the nose are corrected during reconstructive surgery of the nose, when the exposure of the nasal framework is sufficient to allow alterations that could provide potential improvement in aesthetic and functional outcomes.

Injury to eyelid structures may lead to devastating consequences, including lagophthalmos, lacrimal duct obstruction, visual field obstruction, and vision loss. Facial surgeons should be familiar with the cross-sectional anatomy of the upper and lower eyelids, especially the connective tissue support apparatus and the position and location of the levator muscle. Injury to these structures is best avoided because treatment is extremely difficult if scarring has occurred.

Infection

Fortunately, infection during facial surgery is reported to be as low at 2.8%, perhaps secondary to the rich vascularity of facial tissues.16–20 However, the infection rate associated with facial flaps is increased in certain circumstances. Higher infection rates are associated with wounds that are repaired in a delayed fashion, as is often the case with facial flaps used to repair wounds created by micrographic surgery.²¹ Ischemia of flaps is likely to increase the risk for infection because tissue oxygenation is extremely important in prevention of wound bacterial colonization.^16,22,23

Wound infection is associated with poor outcomes. Infection of a cutaneous flap is usually associated with distortion from inflammatory edema. Release of toxic substances and free radicals from inflammatory mediators leads to decreased collagen production and early degradation of suture materials with potential wound dehiscence. Necrosis of all or part of the flap may develop, with the final scar being widened or thickened. Systemic dissemination of bacteria may occur if wound infections are not treated promptly.²⁴

Although perioperative antibiotic prophylaxis is controversial in clean wounds, it has been shown to be effective in decreasing wound infection rates when it is used for clean-contaminated wounds.16,21,22 Antiseptic solutions for skin preparation, sterile technique, proper scrubbing, and surgical attire are key elements in helping prevent infection. It is also important to avoid crushed, charred, or excessively thinned tissue. Staphylococcus aureus is the most common single pathogen causing wound infections, but streptococci, gram-negative bacteria, and oral anaerobes may also be isolated from infected wounds.²¹ The author uses parenteral antibiotics when mucosal surfaces are incised, when cartilage grafting is performed, and during ear reconstruction to help prevent perichondritis. They are also employed in patients with underlying medical conditions that may predispose to infection, such as diabetes and immunosuppression. In these cases, a preoperative dose of intravenous cephalosporin is administered, followed by 5 days of an oral cephalosporin. In penicillin-allergic patients, clindamycin is used. In patients with open wounds older than 3 days, a 5-day course of oral cephalosporin is recommended before the surgical repair. This will decrease the bacterial colonization of the granulation tissue that has developed in the depths of the wound.

Excessive pain or erythema at the wound site may herald an infection (Fig. 26-3). These clinical signs usually appear between the fourth and eighth days after wound closure. Topical allergies to antibiotic ointments and creams applied to the wound may be confused with wound infection. Topical allergic reactions are manifested as erythema, often with vesicle formation and exudates forming on all areas treated with the topical medication (Fig. 26-4). Treatment consists of discontinuation of the offending agent and cleaning of the wound with soap and water to remove all residual topical medication.

If a wound infection does develop, Gram stain and culture of any drainage from the wound are performed. The patient is treated with an appropriate broad-spectrum antibiotic until culture results and sensitivities are available. Any wound fluctuance is drained and the wound irrigated. Significant fluid collections beneath a cutaneous flap usually require the placement of a drain or wick to facilitate further drainage and adherence of the flap to the underlying wound bed. The presence of excessive granulation tissue may require débridement to reduce the bacterial load. Topical antibiotic preparations may also be employed, and superficial sutures are removed to eliminate foreign bodies in the wound.²⁵ Open wounds are allowed to heal by secondary intention. The resulting scar is addressed at a later time once the infection has been adequately treated and scarring has matured.

Viral and fungal infections of facial wounds are rare and almost always are associated with skin resurfacing procedures, such as dermabrasion and laser peels. Although these infections may occur anywhere on the face where resurfacing has been performed, they occur predominantly in the area of the lips when this facial region is treated (Fig. 26-5). Patients undergoing dermabrasion or laser treatment to scars of the lip should receive antiviral therapy before treatment and postoperatively until the treated area has completely re-epithelialized.

Abnormal Scarring

Patients with darker skin and those with a family history of excessive scarring are prone to the development of hypertrophic scars and keloids after surgery. Although numerous treatment modalities have been proposed, there is no definitive method of managing or preventing these problems.²⁶ Intralesional triamcinolone acetonide (10 mg/mL) is often helpful in reducing the volume of scar tissue within a hypertrophic or keloid scar. If the scar is responsive to the injections, surgical excision may be performed after a preoperative injection 1 week before surgery. Several injections are usually required postoperatively every 2 months after excision of the scar for an indeterminate time interval (Fig. 26-6). Rarely, irradiation is considered for extremely problematic keloids.

Glucocorticoids have a profound anti-inflammatory effect. The most common form used is triamcinolone acetonide suspension, which is injected into the depths of the scar. Injections are used to soften firm scars, to lower raised keloids, and to prevent their recurrence. Steroids decrease fibroblast proliferation, reduce blood vessel formation, and interfere with fibrosis by inhibiting extracellular matrix protein gene expression. When steroid injection is used at the time of keloid excision, it is injected at the wound margins immediately after excision. Repeated injection is performed at 3- to 6-week intervals. Multiple injections are usually necessary. Excessive steroid injection of scars may lead to skin atrophy, hypopigmentation, and telangiectasia (Fig. 26-7).

Scar hyperpigmentation may be seen in patients who tan easily, particularly if the patient has excessive sun exposure during the immediate postoperative period. Hyperpigmentation improves over time and with sun avoidance. Use of topical hydroquinone gel with or without the administration of an anti-inflammatory drug may be helpful in preventing permanent discoloration of the scar (Fig. 26-8).

Wound Dehiscence

Wound dehiscence may develop secondary to infection, hematoma, or skin necrosis (Fig. 26-9). In addition, dynamic motion or trauma to wounds may also lead to wound separation. Typically, wounds have 3% to 5% of normal skin tensile strength at 2 weeks after surgery, emphasizing the need for subcutaneous sutures. At 1 month, only 35% of the maximum wound tensile strength has been gained. However, at this point, the wound is usually able to withstand the forces of normal physical activity. During the succeeding months, wound tensile strength increases to 80% of the strength of normal tissue. Wound separations in uncomplicated, clean wounds may be repaired with sutures if this is performed within 24 hours of wound dehiscence. Wound separations that have been present for more than 24 hours are best left to heal by secondary intention, with scar revision reserved for the future if necessary.24,27

Ischemia

Appropriate flap design is essential to ensure sufficient perfusion pressure of the entire flap.³⁴ According to their vascularity, local and regional flaps may be classified as random pattern or axial pattern flaps. Flap dissection should proceed at the appropriate tissue depth to preserve the blood supply to the skin (Fig. 26-10). Random pattern flaps require an intact subdermal plexus, and dissection is performed in the subcutaneous tissue plane. Too superficial dissection or improper flap design may lead to compromise of the flap’s vascularity. Random patterned flaps have a critical length beyond which the perfusion of the distal flap does not occur. Although increasing the width of a flap’s pedicle potentially increases the number of vessels contained in the subdermal plexus of the flap, it does not increase the perfusion pressure to the distal portion of the flap. Therefore, within certain limits, widening the pedicle does not increase the survival of the distal flap. Axial pattern flaps are nourished by a named artery that is located within the tissues of the flap and is parallel to the linear axis of the flap.

Design of axial pattern flaps requires a thorough knowledge of the location and orientation of the arterial vessels supplying the skin of the donor area to properly align the flap with the axis of the artery and to avoid inadvertent injury to the flap’s blood supply. Careful dissection is performed around the flap’s pedicle. Increasing the width of the pedicle of axial flaps does not necessarily improve perfusion.35,36 In fact, it is more prudent to raise a thicker flap that contains deeper subcutaneous vessels than to design the flap with a wider base (Fig. 26-11). An excessively wide pedicle may also complicate the use of the donor site for repair of future defects (Fig. 26-12).

Ischemia is defined as vascular perfusion insufficient to provide the required oxygenation of tissue.²⁵ Cutaneous flaps are more vulnerable to tissue ischemia than are wounds closed primarily, given that the vascularity is isolated to the pedicle of the flap used for repair of the wound.³⁷ This is especially true in the distal portion of the flap.^38,39 Dissection of flaps causes release of catecholamines from severed sympathetic nerves, thromboxane A from platelet microthrombi, and oxygen free radicals. All of these substances cause vasoconstriction, which can enhance tissue ischemia.^40,41 The type of flap also is a factor influencing the degree of tissue ischemia. Transposition flaps generate less distal wound tension than rotation or advancement flaps do. This is because the greatest wound closure tension is at the donor site when transposition flaps are used, whereas wound tension is greatest at the distal borders of advancement and rotation flaps⁴² (Fig. 26-13). Because rotation and advancement flaps have innate wound closure tension at the distal closure site, they likely benefit from multiple, precisely placed subcutaneous “tacking” sutures to evenly distribute wound tension along the distal suture line (see Chapter 6).

With proper technique, cutaneous flap necrosis is uncommon because most tissue can survive on a fraction of its average blood flow,³⁷ and eventual neovascularization reduces flap dependency on the pedicle’s blood supply.^10,36,42,43 However, reversible ischemia may become irreversible if improper surgical technique or postoperative wound care causes additional vascular compromise. Excessive flap thinning, aggressive electrocautery, crush injury with surgical instruments, and excessive wound closure tension may worsen flap ischemia^44,45 (Fig. 26-14). Injection of local anesthetic containing vasoconstrictor agents is used judiciously and avoided in wounds in which vascular perfusion is a concern.^46,47 Infection is treated expeditiously because edema from inflammation may decrease tissue perfusion. The effects of excessive wound closure tension, tight compression dressings, bacterial contamination, and blood beneath the flap may all cause irreversible ischemia of the flap.²⁴ When flap ischemia is evident, local wound factors and factors related to the patient are assessed and medical conditions are optimized as discussed previously. In such situations, use of nicotine by the patient must be avoided.

Ischemia of a skin flap is signaled by color changes of the flap. Pale flaps and slow capillary refill when the skin of the flap is compressed are signs of impending ischemia. A reduced flap temperature below ambience and the absence of bleeding after pinprick of the flap suggest arterial insufficiency. Flaps with edema, purple-blue color, and brisk bleeding of dark blood after pinprick suggest venous congestion. Flaps may survive arterial insufficiency for up to 13 hours, but venous congestion can cause necrosis in as quickly as 3 hours.²⁵ No widely accepted methods of monitoring flap vascularity have been established, and most surgeons rely on careful and frequent examinations of the flap when ischemia is a concern. Repeated pinpricks of the flap or a trial of medicinal leeches may be helpful in treating flaps with venous insufficiency.^48,49 Aeromonas infection secondary to treatment with leeches may occur and should be treated promptly with appropriate antibiotic coverage.^50,51

Arterial insufficiency of a flap may be caused by kinking of the flap’s pedicle, an excessively tight compression dressing, or excessive wound closure tension. If these causative factors are corrected early in the postoperative period, the ischemia is usually reversible. Correction of these conditions should improve the vascularity of the flap. In the case of excessive wound closure tension, the flap may be returned to its donor site and allowed to remain in situ for a few days. This has the effect of delaying the flap, which will cause an enhanced blood supply to the flap. The flap is then usually transferred to the recipient site without ischemia.²⁴ There are numerous reported experimental treatments for flap ischemia with pharmacologic agents, such as vasodilators, sympatholytics, and free radical scavengers; however, there is no widely accepted agent for treatment of arterial insufficiency.^52–55 Skin blanching may become progressively prolonged with digital compression until capillary refill cannot be elicited, signaling flap failure.^34,55 When ischemia causes epidermolysis or skin necrosis, the tissue is allowed to demarcate because the more proximal portion of the flap is usually viable (Fig. 26-15). Devitalized tissue that is easily removed from the wound bed is débrided. Tissue adherence signifies some underlying viable tissue and is left as a biologic wound dressing. Patients are instructed to keep the wound moist with petroleum or water-based antibiotic ointment, and the wound is allowed to heal by secondary intention. Frequent follow-up examination is essential for maintaining appropriate wound care and providing reassurance to the patient.

Trap-Door Deformity

Trap-door deformity may result from persistent edema and poor lymphatic drainage of flaps with incisions on three borders (Fig. 26-16). Flaps with curvilinear borders are particularly prone to development of trap-door deformity. The scar around the border of the flap contracts in a concentric fashion. This concentric contraction combines with contraction of the scar sheet beneath the flap to push the skin upward in a mushroom effect.56–58 Bilobe flaps of the nasal skin are particularly susceptible to development of trap-door deformity because of the two circular lobes used for construction of the flap. The deformity is even more likely to occur when a bilobe flap is used to repair a nasal cutaneous defect in which the nasal skin is thick and has sebaceous gland hypertrophy (Fig. 26-17). Proper flap design and adequate tissue undermining reduce the incidence of trap-door deformity. Wide skin undermining around the border of the recipient site of the flap is thought to limit trap-door deformity. Wide undermining presumably reduces scar contractile vectors toward the center of the flap by enlarging the area of the underlying sheet of scar.^56,57,59,60 Flaps that are superiorly based are more prone to development of trap-door deformity than inferiorly based flaps because lymphatic channels of the face drain in an inferior direction.

Trap-door deformity usually improves with time. Steroid injections into the subcutaneous tissue plane beneath the flap may be performed with triamcinolone acetonide (10 mg/mL). If time and steroid injections are not successful, contouring of the flap with or without scar revision is necessary. This involves incising the flap along one of its borders, removing subcutaneous fat and scar tissue beneath the flap, and redraping the skin. Excess skin is trimmed as indicated. Z-plasties performed along the incision are helpful in preventing recurrence of the trap-door deformity by preventing a concentric scar from redeveloping.

Unsightly Scars

Scars continue to change and to improve during the remodeling phase of wound healing. This includes collagen remodeling and collagen fiber reorientation for up to 18 months. This process may be longer in children. Young patients may have an exaggerated healing reaction with increased scar erythema and hypertrophy, so scar revisions in children should be delayed as long as feasible. Immature scars tend to be erythematous, which will usually fade over time. The scar’s appearance will also improve as it matures. There are a number of factors during wound healing that influence the ultimate appearance of a scar. Wounds subjected to excessive wound closure tension typically result in scars that are hypopigmented and often hypertrophied. Incisions made in thick skin, especially if there is sebaceous gland hypertrophy, often heal with depressed or widened scars (Fig. 26-18). Patients who can bend their thumb back to the volar surface of their forearm or touch their tongues to their noses (Gorlin’s sign) are more flexible than the average person. These individuals possess more elastin within the dermis and are more likely to spread their scars (Fig. 26-19).

Distortion of Facial Features

Scar contracture may lead to poor aesthetic and functional outcomes, especially in regions of the face with mobile facial structures, such as the eyelids, lips, and nasal alae. This is especially a problem in the periocular and oral area, where inadequate lip or eyelid closure leads to problems with eating, phonation, excessive tearing, and dry eye symptoms. Excessive wound closure tension may also lead to flap compromise and distortion of adjacent facial structures. Cervical facial flaps used to repair cutaneous defects near the lower eyelids should be secured to the periosteum of the maxilla or nasal bones with a tacking suture to reduce wound closure tension on the lower eyelid. This in turn reduces the risk for development of lower eyelid retraction. A temporary Frost suture may also be used to limit the downward pull of the flap on the eyelid skin. In spite of these precautionary measures, reconstruction of large cutaneous defects adjacent to the lower eyelid is often associated with lower eyelid retraction or ectropion. This is especially true in elderly patients because they have less muscle tone of the orbicularis oculi and less overall connective tissue to support the eyelid (Fig. 26-20). In the case of nasal reconstruction, flaps used for repair of the nose are designed sufficiently large to avoid alar retraction. For defects adjacent to the alar rim, cartilage grafting is routinely employed to provide a strut against the contractive forces of wound healing.

Distorted anatomic structures may respond to massage but may also require surgical revision, sometimes with cartilaginous grafts for support (Fig. 26-21). Like the nose, the lip is vulnerable to distortion by scars because of the mobile nature of the lips and the discrete borderline between the skin and vermilion. During healing, vertically oriented scars of the upper lip require only minimal contraction to cause notching or distortion of the vermilion-cutaneous border. Such distortion is quite noticeable to the observer, particularly when the vermilion is well-developed (Fig. 26-22). As with all lip wound closures, tension should be minimized. Precise alignment of the opposing edges of the lip wound in the vicinity of the vermilion-cutaneous borders is extremely important in repair of lacerations or cutaneous defects of the lip.

Facial Aesthetic Regions and Units

It is important to respect the borders of facial aesthetic regions and units when designing cutaneous flaps to avoid unsightly scars. This is particularly true of the alar-facial sulcus, which is an important boundary between the aesthetic regions of the nose, cheek, and upper lip. Larger defects of the ala are best reconstructed with interpolated cheek flaps that cross over the alar-facial sulcus rather than with transposition or advancement cheek flaps because these flaps obliterate this aesthetic boundary line (Fig. 26-23).

Cutaneous defects that extend from the nose to the medial cheek or to the upper lip are best repaired with separate flaps for each aesthetic region. Individual flaps are designed to repair the nasal component of the defect and the cheek or lip component of the defect. This approach positions some of the borders of the flaps in aesthetic boundary lines that help camouflage scars. More important, the concave topography of the sulcus separating the nose from the cheek and the nose from the lip is not obliterated by advancing or transposing skin from the cheek to the nose (Fig. 26-24).

The principle of employing separate flaps is equally important in reconstructing skin defects that cross over the melolabial crease from the lip to the cheek. When a cheek advancement flap is used to repair both the lip and cheek component of the defect, the flap inevitably obscures the melolabial crease, which is the aesthetic boundary line between the lip and cheek aesthetic regions (Fig. 26-25).

Standing cutaneous deformities should be anticipated during facial reconstructive surgery and removed when possible along relaxed skin tension lines. Care is taken to avoid narrowing the pedicle of the flap during the process of removing the deformity. When this is not possible, it may be prudent to remove the deformity as a second-stage procedure, 2 to 3 weeks after the initial transfer of the flap.

Standing cutaneous deformities result from transfer of local flaps or from wound closures that result in unequal wound borders. In the majority of cases, these deformities may be safely excised at the time of wound repair. It is a common error to underestimate the size of standing cutaneous deformities and to excise too little skin. This is particularly true for wounds repaired on the cheek and lips (Fig. 26-26). This may in part be related to the swelling of the soft tissues in the vicinity of the flap donor site during dissection and transfer of the flap. This swelling may prevent an accurate estimate of the size of the deformity and thus leads to an error in the amount of skin excised (Fig. 26-27).

Excessive Wound Closure Tension

Improper Flap Design

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40. Angel, MR, Narayanan, K, Swartz, WM, et al. Deferoxamine increases skin flap survival: additional evidence of free radical involvement in ischemic flap surgery. Br J Plast Surg. 1986; 39:469.

41. Angel, MF, Ramasastry, SS, Swartz, WM, et al. The critical relationship between free radicals and degree of ischemia: evidence for tissue intolerance of marginal perfusion. Plast Reconstr Surg. 1988; 81:233.

42. Angel, MF, Kaufman, T, Swartz, WM, et al. Studies of the nature of flap/bed interactions in rodents: part I. Ann Plast Surg. 1986; 17:317.

43. Angel, MF, Ramasastry, SS, Narayanan, K, et al. Studies on the nature of flap/bed interactions in rodents: part II. Ann Plast Surg. 1986; 17:434.

44. Larrabee, WF, Jr., Holloway, GA, Jr., Trachy, RE, et al. Skin flap tension and wound slough: correlation with laser Doppler velocimetry. Otolaryngol Head Neck Surg. 1982; 90:185.

45. Larrabee, WF, Jr., Holloway, GA, Jr., Sutton, D. Wound tension and blood flow in skin flap. Ann Otol Rhinol Laryngol. 1984; 93:112.

46. Pang, CY, Neligan, PC, Forrest, CR, et al. Hemodynamics and vascular sensitivity to circulating norepinephrine in normal skin and delayed and acute random skin flaps in the pig. Plast Reconstr Surg. 1986; 78:75.

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