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of stasis converts to coagulated tissue. This underscores the importance of early debridement and wound care.
•The treatment of blisters in partial-thickness burns is controversial. Some advocate keeping the blisters intact since the fluid contained within is sterile and will aid in healing. Others prefer to debride the blisters and remove the separated skin layers since they can rapidly become colonized and act as a nidus for infection. Either approach is appropriate, as long the burns are cleaned and dressed daily and all non-viable tissue is debrided.
•The need for aggressive fluid resuscitation in extensive burns cannot be overemphasized. It is better to overthan under-resuscitate a burn patient. Following urine output is the most accurate means of tracking fluid status.
•Numerous burn dressing regimens exist. None of these are a replacement for adequate debridement and daily cleansing of the burn. Despite the many products that are commercially available, simple silver-containing gauze dressings have withstood the test of time.
Suggested Reading
1.Press B. Thermal, electrical, and chemical injuries. Grabb and Smith’s Plastic Surgery. 5th ed. Philadelphia: Lippincott-Raven, 1997.
2.Heimbach DM, Engrav L. Surgical management of the burn wound. New York: Raven Press, 1985.
3.Hunt JL, Purdue GF, Zbar RIS. Burns: Acute burns, burn surgery and post-burn reconstruction. Selected readings in plastic surgery, Vol. 9. 2000; (No. 12).
4.Moylan Jr JA, Inge Jr WW, Pruitt Jr BA. Circulatory changes following circumferential extremity burns evaluated by the ultrasonic flowmeter. An analysis of 60 thermally injured limbs. J Trauma 1971; 11:763.
5.Carvajal HF, Parks DH. Burns in children: Pediatric burn management. Chicago: Year Book Medical Publishers, 1988.
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Chapter 29
Head and Neck Cancer
Zol B. Kryger
Introduction
This chapter covers primary head and neck cancer, excluding neoplasms of the skin. Ninety percent of these tumors are squamous cell in origin and tend to affect elderly men. Most have a history of alcoholism and tobacco abuse. Tumors of the salivary, thyroid and parathyroid glands are not of the squamous cell type and can be found in a wider age distribution. Thyroid and parathyroid tumors are not usually treated by the plastic surgeon.
Anatomical Definitions
•The oral cavity extends from the vermilion border of the lip to the junction of the hard and soft palates.
•The pharynx is divided into three cavities:
1.The oropharynx extends from the hard and soft palate junction anteriorly to the posterior pharyngeal wall. The lateral borders are the tonsils and tonsilar pillars. The ceiling is the soft palate, and the floor is the soft tissue between the base of the tongue and the epiglottis.
2.The nasopharynx extends from the nasal septum to the posterior pharyngeal wall. Its ceiling is the skull base, and its floor is the soft and hard palate.
3.The hypopharynx spans from the vallecula and aryepiglottic folds to the inferior aspect of the cricoid cartilage.
•The larynx is divided into the supraglottis, glottis and infraglottis, with the true vocal cords defining the glottic region. The anterior and posterior commissure are also considered part of the glottis. The epiglottis, ventricles, erytenoids, and false vocal cords are all supraglottic structures.
Intraoral Tumors
Etiologic Factors
A history of tobacco use is the number one risk factor for head and neck cancer in the United States. As the duration and quantity of tobacco use increases, so does the risk of developing intraoral cancer.
Alcohol is another major risk factor. Heavy consumption increases the risk of developing aerodigestive cancer by sixfold. Furthermore, the risk from concomitant tobacco and alcohol use is synergistic compared to either one alone. Other risk factors include dentures and poor oral hygiene. In countries with poor dental care, these factors may play a greater etiologic role.
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164 Practical Plastic Surgery
Table 29.1. TNM classification
T = extent of the primary tumor
Tis |
In-situ tumor |
T1 |
≤ 2 cm |
T2 |
2-4 cm |
T3 |
> 4 cm |
T4 |
Invades adjacent structures (varies by site of tumor) |
N = regional lymph node status
N0 No nodal involvement
N1 Movable, ipsilateral nodes
N2 Movable, contralateral or bilateral nodes
N3 Fixed nodes
M = distant metastases
M0 No mets
M1 Distant mets present
Stage I |
T1N0M0 |
Stage II |
T2N0M0 |
Stage III |
T3N0MO or T1-3N1M0 |
Sage IV |
One or more of the following: T4, N2, N3 or M1 |
Pathology
Squamous cell carcinomas can present as white patches, termed leukoplakia, or as an erythematous patch, known as erythroplakia. As a general rule, erythematous lesions have a higher risk of malignancy than leukoplakic lesions. The need to biopsy every leukoplakic area is controversial. Most advanced squamous cell carcinomas are endophytic (ulcerated, deeply infiltrating). They may also be exophytic (projecting outward).
Staging and Treatment
Staging is based primarily on the TNM classification shown in Table 29.1. The treatment of intraoral cancers is summarized in Table 29.2.
Tongue
The tongue is the most common site of intraoral malignancy. In addition to alcohol and tobacco, Plummer Vinson syndrome is a risk factor. Most lesions are on the anterolateral two thirds of the tongue. These tumors are usually painless and thus are often neglected. The average stage at presentation is T2 (2-4 cm). T1 tumors are treated
29with either wedge resection or radiation. T2 lesions require partial glossectomy and T3 tumors require total or subtotal glossectomy. T2 and T3 lesions are resected in combination with an elective neck dissection even if there are no palpable neck nodes (N0) due to the high risk of occult nodal metastasis.
Table 29.2. Summary of the treatment of intraoral cancers
Stage |
Treatment |
Adjuvant Therapy |
Stage I |
Excision or radiation |
None |
Stage II and III |
Surgical resection (see below) |
Preor postop radiation |
Stage IV |
Chemo± palliative resection |
Radiation |
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Floor of Mouth |
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The floor of the mouth is the second most common site of intraoral cancer. |
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Lesions are usually anterior and often present with a palpable submandibular node. |
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Fifty percent of patients present with stage III or IV disease due to the paucity of |
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symptoms. The survival rate for stage I and II lesions is high (80-90%); advanced |
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disease has a poorer prognosis (30-60%). An important consideration in any form of |
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treatment is the risk of submandibular duct stenosis with subsequent enlargement of |
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the gland. If this occurs, referral to a specialist in this condition is warranted. |
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Alveolar Gingiva and Buccal Mucosa |
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The third most common site of intraoral tumors is the lower alveolar gingiva. |
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Eighty percent of these tumors occur on the lower alveolus. Lesions begin on the |
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alveolar ridge and spread laterally. Nodal metastasis at time of presentation is com- |
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mon. Cancer of the buccal mucosa is found primarily in tobacco chewers in the |
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U.S. There is a higher incidence in India due to the custom of betel leaf chewing. |
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Tonsil |
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The tonsil is the most frequent site of squamous carcinoma in the oropharynx. |
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Most tumors present late, as stage III or IV lesions. Hence, the prognosis is poor. |
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Hypopharynx |
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As with cancer of the tongue, Plummer Vinson syndrome is a risk factor. Pa- |
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tients often present with advanced disease with dysphagia and clinically positive |
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neck nodes. Extensive resections with free flap reconstruction are usually required. |
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Larynx |
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In cancer of the larynx, the vocal cords are involved in about 50% of the cases. |
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This allows for relatively early detection due to hoarseness and respiratory symp- |
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toms. If the glottis is involved, radiotherapy is more successful at preserving speech |
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than surgery. Advanced disease occurs more frequently with subglottic tumors and |
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requires total laryngectomy with neck dissection. |
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Nasopharynx |
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Cancer of the nasopharynx is unique among head and neck tumors in its etiol- |
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ogy. Chronic inflammation of the mucosa is the main risk factor; chronic sinusitis, |
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human papilloma virus and Epstein-Barr virus infections have all been implicated. |
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There is also in increased incidence among individuals from mainland China for |
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unknown reasons. Tumors of the nasopharynx often present as locally advanced |
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neck masses. The primary mode of treatment is radiation rather than surgery. Since |
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most tumors present with nodal metastases, the neck should also be irradiated. In |
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certain cases, chemotherapy is indicated. |
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Salivary Gland Tumors |
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Parotid Gland |
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The parotid glands are the largest of the salivary glands. They are located in the |
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infra-auricular region. The parotid has a deep and a superficial lobe. The facial nerve |
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traverses the deep lobe. The parotid has a fascial covering which is continuous with |
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the SMAS. The parotid duct (Stenson’s duct) passes superficial to the masseter muscle |
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and pierces the buccinator muscle. It enters the oral cavity at the level of the upper |
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second molar. All parotid masses should undergo fine needle aspiration for diagnosis. Imaging is usually not necessary, although an MRI may be useful if the tumor is large (over 3 cm).
The most common tumor of the parotid is the benign pleomorphic adenoma (benign mixed tumor). They are treated by superficial parotidectomy (unless the tumor is in the deep lobe which is rare). If incompletely resected, they can recur and become locally invasive. If left untreated, they can degenerate into a malignant mixed tumor that is prone to early metastasis.
Warthin’s tumor is a benign cystic tumor. Ten percent are bilateral, making it the most common bilateral parotid tumor. It occurs primarily in male smokers. Superficial parotidectomy is sufficient treatment.
The most common malignancy in the parotid is the mucoepidermoid carcinoma. Such malignant tumors require excision of both the superficial and deep lobes of the parotid. The facial nerve is spared unless the tumor directly invades the nerve. Nerve contaminated with tumor that is left behind should receive adjuvant radiation postoperatively. High-grade (anaplastic) mucoepidermoid carcinoma warrants a simultaneous neck dissection.
Complications from parotidectomy are uncommon. Facial nerve injury is the most devastating; any recognized facial nerve injury should be repaired at the time of injury. Hematoma can be avoided by meticulous hemostatic technique. Frey’s syndrome (auricular temporal syndrome) is gustatory sweating due to reinnervation of sweat fibers by severed salivomotor fibers. Botox injections have shown some promise in treating this condition. Development of a sialocele is treated by aspiration and compression.
Submandibular and Sublingual Glands
The paired submandibular and sublingual glands are located below the mandible and in the floor of the mouth, respectively. Wharton’s duct is the submandibular duct that enters the floor of the mouth. The most common malignancy in these glands is the mucoepidermoid carcinoma. Complete excision of the affected gland is required.
Minor Salivary Glands
Minor salivary glands are mucus-secreting glands located below the oral submucosa. Most minor salivary gland tumors are malignant. The most common variety of these glands is the adenoid cystic carcinoma. Treatment consists of wide local excision.
Neck Dissection
29Nodal metastases spread in a predictable fashion:
•Level I nodes are found in the submental/submandibular triangle
•Level II nodes are in the upper jugular region
•Level III nodes are in the middle jugular region
•Level IV nodes are in the lower jugular region
•Level V nodes are in the posterior triangle
Patients with a clinically positive node or a large primary lesion should undergo simultaneous neck dissection. Nodal metastasis is an indication for adjuvant radiation therapy. Bilateral neck dissections for midline lesions are staged. At least one of the two internal jugular veins should be preserved.
The modified radical neck dissection has become the procedure of choice for elective cases. It involves removal of all the nodes from level I-V as described above. The
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internal jugular vein, accessory nerve and sternoclidomastoid muscle are spared. This |
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results in decreased facial edema, shoulder dysfunction and a less cosmetic defect. If |
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possible, the neck dissection should be done in-continuity with the primary resection. |
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Reconstruction |
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The primary goals of reconstruction include the following: adequate degluti- |
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tion, preservation of speech, avoiding salivary fistulas and drooling and achieving an |
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acceptable cosmetic result. Small defects are often amenable to primary closure. |
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Moderate-sized defects may require tongue flaps and split-thickness skin grafts (if |
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no bone or buccal mucosa is exposed). |
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Large defects often necessitate pedicled skin and myocutaneous flaps including |
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the deltopectoral, pectoralis major, forehead, latissimus and trapezius flaps. Many |
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surgeons favor microvascular free flaps as a first choice. The radial forearm free flap |
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may be used for mucosal defects alone. For defects involving both bone and mu- |
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cosa, the fibula free flap is often used. For circumferential defects of the hypophar- |
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ynx or esophagus, the jejunal interposition free flap is the first choice; however, the |
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anterolateral thigh flap is rapidly becoming more popular than the jejunal flap for |
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esophageal reconstruction. These free flaps are described in detail in the flap harvest |
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section of this book. |
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Post maxillectomy—these defects can often be skin-grafted and a dental pros- |
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thesis placed once the tissue has healed. |
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Pearls and Pitfalls |
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In elderly patients, especially those with a history of tobacco or alcohol use, any |
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neck mass is cancer until proven otherwise. Patients with a neck mass should undergo |
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a thorough head and neck exam including examination of the auditory canal, na- |
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sopharynx, oral cavity and oropharynx. Furthermore, all suspicious palpable neck |
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masses should undergo fine needle aspiration, and most plastic surgeons have limited |
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experience in performing this procedure. Therefore, it would be prudent to refer pa- |
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tients suspected of having carcinoma of the head and neck to a specialist who routinely |
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treat such cancers. Treatment is often multimodal and requires the collaboration of |
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multiple disciplines. Experienced head and neck surgeons have an established network |
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of such experts and are better suited to coordinate the patient’s diagnosis and treat- |
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ment. The role of the plastic surgeon should focus on the post-resection reconstruc- |
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tion. |
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Suggested Reading |
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1. Ballantyne AJ. Modified neck dissection. Recent Adv Plast Surg 1985; 3:169. |
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2. Cooper JS et al. Postoperative concurrent radiotherapy and chemotherapy for high risk |
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sqaumous-cell carcinoma of the head and neck. New Eng J Med 2004; 350(19):1937. |
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3.Day TA et al. Salivary gland neoplasms. Curr Treat Options Onc 2004; 5(1):11.
4.In: Fleming ID et al, eds. AJCC Cancer Staging Manual. Philadelphia: Lippincott-Raven, 1997.
5.Hidalgo DA. Fibula free flap: A new method of mandible reconstruction. Plast Reconstr Surg 1989; 84:71.
6.Jackson IT. Intraoral tumors and cervical lymphadenectomy. Grabb and Smith’s Plastic Surgery. 5th ed. Philadelphia: Lippincott-Raven, 1997:439.
7.Robinson DW, MacLeod A. Microvascular free jejunum transfer. Br J Plast Surg 1982; 35:258.
8.Shaha AR et al. Squamous carcinoma of the floor of the mouth. Am J Surg 1984; 148:455.
9.Soutar DS et al. The radial forearm flap: A versatile method of intraoral reconstruction. Br J Plast Surg 1983; 36:1.
Chapter 30
Ear Reconstruction
Amir H. Taghinia, Theodore C. Marentis, Ankit I. Mehta, Paul Gigante and Bernard T. Lee
Introduction
Acquired ear deformities are usually the result of trauma, burns, or ablative skin cancer operations. Reconstruction of these deformities is primarily an aesthetic endeavor. Nevertheless, seemingly minor deformities can cause significant patient anxiety and concern. Auricular deformities can be divided into defects of the helical rim, upper third, middle third and lower third of the ear. Defects of the upper ear complicate the use of eyewear, but they are more easily camouflaged by hair. Defects of the lower ear are harder to hide and thus, more aesthetically important. Unfortunately, these defects are also the hardest to reconstruct well. Despite many variations in ear anatomy, there are several consistent landmarks shown in Figure 30.1.
Figure 30.1. Topographic anatomy of the ear.
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Acute Auricular Trauma
Otohematoma
An injury frequently associated with contact sports, otohematoma (‘cauliflower ear’) results from blunt trauma or excessive traction that causes hemorrhage between the perichondrium and the cartilage. Subperichondrial blood produces a clot that, if left untreated, leads to the formation of neocartilage and eventual deformity of the ear’s convolutions. Treatment should be administered soon after injury. Needle aspiration drains the fluid but rarely removes the clots. Preferred treatment is incision and drainage followed by the placement of sutured bolsters or a thermoplastic splint for 7-10 days to maintain a broad area of pressure.
Burns
The ear is uniquely susceptible to thermal injury because of its exposed, unprotected position. Deep ear burns destabilize the skin and are likely to involve the cartilage. Chondritis is a serious infectious complication that occurs most commonly between the third and fifth weeks post-burn. General burn management should include liberal use of mafenide, frequent soap and water cleansing, and avoidance of pressure on the affected ear. Adequate healing time should be allowed, and a maximal amount of viable cartilage should be salvaged prior to reconstruction. Should chondritis occur, systemic antibiotics must be administered. Severe infections may require incision, drainage and debridement of skin and cartilage.
Lacerations
The ear is protected from traumatic forces by its resilient, pliable cartilaginous framework. Nevertheless, lacerations are the commonest form of auricular trauma. Preservation of tissue is critical to ensuring optimal aesthetic outcome in these injuries. The ear’s rich blood supply allows for excellent tissue recovery in most cases. Compromised flaps of skin (with or without cartilage) usually survive, even if based on a thin pedicle. At the initial time of treatment, one should debride grossly necrotic tissues only. Animal or human bites require thorough irrigation and systemic antibiotics. In laceration repair, discernable landmarks must be approximated meticulously to avoid poor aesthetic outcome or exposed cartilage. As with auricular burns, major reconstructive intervention is usually delayed until adequate healing is complete.
Acquired Auricular Deformities
Traditionally, deformities of the ear have been classified based on the location, and methods have been developed to address each anatomic site (e.g., helix or lobule). However, many of these methods can be applied in multiple locations, thus
confusing the novice. In this chapter, methods for reconstruction will be presented 30 based on defect size and the affected part of the ear.
Wedge and Star-Wedge Excisions and Primary Closure
Application: Defects anywhere on the ear Defect size: Small
Illustration: Figure 30.2.
Small defects of the ear can usually be repaired using wedge excision and primary closure. If the angle of the wedge is too obtuse, apposition of the edges creates a standing cone that makes the ear bulge outward. This problem is alleviated by additional triangular excisions at the wedge borders yielding a star-shaped
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Figure 30.2. Wedge excision and star-wedge excision. Small defects of the ear can usually be closed primarily after wedge excision. Additional triangular excisions creating a star-shaped wedge facilitate closure of larger wounds.
excision. Closure of wedge-shaped earlobe defects requires an offset flap or Z-plasty to prevent a notch in the inferior contour (see earlobe reconstruction).
Chondrocutaneous Helical Advancement (Antia-Buch Procedure)
Application: Helical defects of the upperand middle-third of the ear Defect size: Small, moderate, or large
Illustration: Figure 30.3.
This method is commonly used because most ear lesions occur on the periphery. Advancing the helical stumps from both directions can repair helical defects up to 3 cm. To achieve adequate mobility, the entire helix must be freed from the scapha using an incision in the helical sulcus that extends through the anterior skin and cartilage but not through the posterior skin. The posterior skin is then undermined (above the perichondrium) until the entire superior and inferior helical remnants are hanging as composite flaps. The flaps are then brought together and sutured. Additional length can be gained by a V-Y advancement of the helical root.
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Figure 30.3. Antia-Buch helical advancement. A V-Y advancement closure at the root of the helix can be used for additional flap mobility.
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Figure 30.4. Tube skin flap. A tube skin flap can be fashioned in the retroauricular sulcus and transferred in stages to reconstruct the helical rim. The donor site can be closed primarily or with a skin graft if a large tube is made.
Tubed Skin Flaps
Application: Helical rim defects Defect size: Moderate or large Illustration: Figure 30.4.
Minor burns frequently destroy the helical rim but leave the posterior ear intact. Thin, tubed skin flaps can then be fashioned from skin in the auriculocephalic sulcus. These flaps require multiple delay and inset procedures to achieve a final result. Furthermore, it is technically difficult to obtain the required length and width using this technique; often the flaps are too bulky or too thin. If performed well, however, these flaps can give a pleasing aesthetic outcome.
Banner Flap (Crikelair)
Application: Upper-third defects of the ear
Defect size: Moderate
Illustration: Figure 30.5.
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Figure 30.5. Banner flap (Crikelair flap). The ear is retracted anteriorly and a superiorly-based flap is designed in the retroauricular sulcus. The flap is raised and placed on an anchored cartilage graft in the defect (not shown).