Complications of Local Flaps

Bleeding

The most common causes of bleeding from facial reconstruction using local flaps are drug-associated coagulopathy and inadequate hemostasis. Patients are questioned preoperatively concerning use of all prescription and over-the-counter medications that may contribute to peri-operative bleeding. All aspirin containing products, nonsteroidal anti-inflammatory medicines, vitamin E, and most herbal remedies are discontinued one or more weeks before surgery. The exception to this policy is patients with cardiac stents. These patients remain on aspirin if 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 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 inserted into the wound and a compression dressing 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. Nevertheless, an appropriate size 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 is 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. Furthermore, iron compounds in a hematoma may promote free-radical production, leading to flap necrosis. ^, Hematoma formation also predisposes to infection, which may compromise flap vascularity secondary to inflammatory edema. ^,

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 (5cc to 10cc) hematomas may sometimes be aspirated through the suture line using 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 evacuated, and bleeding vessels 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 fresh clot of gel or liquid consistency. As the clot matures over the next several days, it becomes firmer and more 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, a repeat 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 will be reviewed.

Perhaps one of the most devastating complications associated with facial surgery is injury to the facial nerve or one of its branches. Although 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 can lead 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 or supratrochlear nerves leading to dysthesias in their sensory distributions. Similarly, the deep branch of the supraorbital nerve runs within the galea aponeurotica and may be injured when undermining the frontalis muscle in the subgaleal plane while closing defects of the lateral forehead skin. 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 peri-auricular area. This nerve is identified and preserved when dissecting skin away from its attachment to the superior aspect of the sternocleidomastoid muscle.

Avoiding injury to the nasal cartilaginous framework is important for maintaining nasal symmetry and function. Inadvertent injury to these structures may lead to obvious nasal deformities including alar retraction, nasal valve collapse, saddle nose deformity, and tip asymmetries. Occasionally, pre-existing 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 improvements 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. Nevertheless, infection rates associated with facial flaps are 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. Ischemia of flaps likely increases the risk for infection because tissue oxygenation is extremely important in prevention of wound bacterial colonization. ^{, ,}

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.

Although peri-operative antibiotic prophylaxis is controversial in clean wounds, it has been shown to be effective in decreasing wound infection rates when used for clean-contaminated wounds. ^{, ,} Antiseptic solutions for skin preparation, sterile technique, proper scrubbing, and surgical attire are key elements in helping prevent infection. Avoiding crushed, charred, or excessively thinned tissue is also important. 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. 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 greater than 3 days old, a 5-day course of oral cephalosporin is recommended before the surgical repair. This will decrease the bacterial colonization of the granulation tissue, which 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 to eighth days after wound closure. It is important to remember that topical allergies to antibiotic ointments and creams applied to the wound may be confused with wound infection. Topical allergic reactions manifest as erythema often with vesicle formation and exudates forming on all areas treated with the topical medication ( Fig. 26.4 ). Treatment consists of discontinuing the offending agent and cleaning the wound with soap and water to remove all residual topical medication.

If a wound infection does develop, gram stain and cultures of any drainage from the wound are obtained. 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 debridement to reduce the bacterial load. Topical antibiotic preparations may also be employed, and superficial sutures are removed to eliminate foreign bodies in the wound. 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 for 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. Intralesional triamcinolone acetonide (10mg/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, lower raised keloids, and 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. Repeat 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 that tan easily, particularly if the patient is exposed to 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. At this point, however, the wound is usually able to withstand the forces of normal physical activity. Over 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 longer than 24 hours are best left to heal by secondary intention with scar revision reserved for the future if necessary. ^,