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to maintain or reestablish sinus function, or to eliminate sinus by obliteration or cranialization, as well as to reestablish facial contours to achieve optimal functional and aesthetic result in a single act. Liquor leakage and nasofrontal duct condition are the 2 most important elements that determine treatment approach. Dislocated fragment at the posterior frontal sinus wall is also an important factor that determines the type of surgical treatment.1,2,4,7,9 Active approach as sense of surgical intervention is mandatory for the management of complications after trauma and surgery of frontobasal injuries. Nonobliterative surgical procedures including endoscopy do not warrant permanent drainage and definite resolution of complications. The majority of authors believe that sinus obliteration is a criterion standard for the management of complications and impaired drainage system after frontal sinus trauma, nevertheless.2Y5,7,10 If obliteration failed, it would be necessary to explore the causes of that failure. Sinus infection requires complete revision, as we performed in our case. Nasofrontal duct orifice and ethmoidal cells must be isolated, and then the sinus is obliterated. It could be also carried out by cannulation of the nasofrontal duct if there was no comminuted posterior wall fracture. It is considered that adequate exploration and cleaning, as well as reposition, have to be performed before reconstruction.1,2,4,6 Reconstruction of frontal bone contours may be accomplished with autologous bone or alloplastic material. The perfect material for cranioplasty has to be biocompatible, biomechanically stable, easy to use, flexible, light, nonmagnetic, and permanently stable. When deciding on the type of reconstruction, the surgeon has to take into consideration the clinical findings, extent of a defect, and probability of complications.10,11 Carbonate and calcium phosphate (hydroxyapatite) cement and methyl methacrylate are often used for reconstruction of defects of the frontal region bones. Titanium mesh is widely used, and it provides excellent threedimensional stability. It is suitable for major defects; it may be easily adjusted to a defect and most precisely reestablishes natural contours in the area of defect. It is hard enough for major defects not allowing the loosening; complications are uncommon, and it gives artifacts on CT images.10,11 Combination of titanium mesh impregnated with hydroxyapatite cement has advantages of being suitable for major defects, absence of donor-site morbidity, and convenience of use and of not being time-consuming.11,12 Medpor (porous polyethylene implant) may be used for medium-size defects; it is a biocompatible and durable material, but expensive.10,11
CONCLUSIONS The complications resulting from treatment of frontobasal region fractures vary from aesthetics, such as forehead and orbit asymmetry, to local infections and life-threatening intracranial infections. Potentially severe complications that occur many years after treatment emphasize the need for elaboration of a definite, initial, primary treatment plan. Management of these complications requires an active surgical approach. Development of surgical techniques improved safety with minimal complications associated with surgical treatment. Creation of so-called safe sinus has primary significance, and to achieve it, it is often necessary to perform sinus obliteration. Minimally invasive techniques may also contribute to the management of complications. Timing of definite reconstruction must be carefully considered from case to case. Planning of reconstruction and reestablishing aesthetic frontal bone defect with autologous bone or alloplastic material must be made with regard to relationship with sinus and nasal cavities, local finding, and infection. Among biocompatible materials used for reconstruction, tita-
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nium mesh impregnated with hydroxyapatite provides excellent stability and reconstructs natural contours in the affected area.
REFERENCES 1. Bell RB, Dierks EJ, Brar P, et al. A protocol for the management of frontal sinus fractures emphasizing sinus preservation. J Oral Maxillofac Surg 2007;65:825Y839 2. Manolidis S, Hollier LH Jr. Management of frontal sinus fractures. PRS J 2007;120:32SY48S 3. Rontal ML. State of the art in craniomaxillofacial trauma: frontal sinus. Curr Opin Otolaryngol Head Neck Surg 2008;16:381Y386 4. Gabrielli MFR, Gabrielli MAC, Hochuli-Vieira E, et al. Immediate reconstruction of frontal sinus fractures: review of 26 cases. J Oral Maxillofac Surg 2004;62:582Y586 5. Grossman DG, Archer SM, Arosarena O. Management of frontal sinus fractures: a review of 96 cases. Laryngoscope 2006;116:1357Y1362 6. Stanley RB. Management of complications of frontal sinus and frontal bone fractures. Oper Tech Plast Reconstr Surg 1998;5:296Y301 7. Wynn R, Vaughan WC. Treatment of failed frontal sinus obliteration. Oper Tech Otolaryngol 2006;17:13Y18 8. Mourouzis C, Evans BT, Shenouda E. Late presentation of a mucocele of the frontal sinus: 50 years postinjury. J Oral Maxillofac Surg 2008;66:1510Y1513 9. Strong EB. Frontal sinus fractures. Oper Tech Otolaryngol 2008;19:151Y160 10. Marao HF, Gulinelli JL, Pereira CCS, et al. Use of titanium mesh for reconstruction of extensive defects in fronto-orbito-ethmoidal fracture. J Craniofac Surg 2010;21:748Y750 11. Brevi BC, Magri AS, Toma L, et al. Cranioplasty for repair of a large bone defect with autologous and homologous bone in children. J Pediatr Surg 2010;45:E17YE20 12. Ducic Y. Titanium mesh and hydroxyapatite cement cranioplasty: a report of 20 cases. J Oral Maxillofac Surg 2002;60:272Y276
Reconstruction of Soft Plate Necrosis After Endotracheal Intubation Hyuck Jae Lee, MD, So Young Lim, MD, PhD, Jai-Kyong Pyon, MD, PhD, Goo Hyun Mun, MD, PhD, Sa Ik Bang, MD, PhD, Kap Sung Oh, MD, PhD Abstract: Uvular necrosis after long-term endotracheal intubation has been previously reported, but there have been no reports regarding soft palate necrosis after endotracheal intubation. Recently, From the Department of Plastic Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. Received October 17, 2013. Accepted for publication November 11, 2013. Address correspondence and reprint requests to Dr. So Young Lim, Department of Plastic Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-dong, Gangnam-gu, Seoul, 135-710, Republic of Korea; E-mail: [email protected] Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal_s Web site (www.jcraniofacialsurgery.com). The authors report no conflicts of interest. Copyright * 2014 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000000530
* 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
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we encountered 2 patients who had a high degree of soft palate necrosis following endotracheal intubation during long-term care in the intensive care unit. This study reports noncongenital soft palate cleft caused by endotracheal intubation. Two patients, aged 30 and 38 years, with noncongenital cleft palate were treated with pharyngeal flap and/or palatoplasty at our institution from March 2011 to May 2013. Initially, the patients complained of acquired speech disorder and severe oronasal regurgitation caused by a palatal defect. Speech ability was evaluated preoperatively and postoperatively by a perceptual language test and nasopharyngoscopy. The cleft soft palates of both patients were completely repaired, and the aforementioned symptoms improved after surgery. Postoperative courses were uneventful in both of the cases, and neither patient experienced a recurrence. Although rare, long-term intensive care unit care with endotracheal intubation can cause noncongenital soft palate cleft. In cases with iatrogenic cleft palate that does not heal with conservative treatment, surgical procedures such as pharyngeal flap and palatoplasty can be helpful. Key Words: Cleft palate, endotracheal intubation, soft palate, necrosis
A
cquired soft palate necrosis is very rare. However, noncongenital soft palate necrosis can be caused by narcotics or cocaine inhalation,1,2 maxillary artery embolization,3 tumor,4 infection, endoscopy complication,5 and granulomatous disease.6 Various forms of oral trauma can also cause soft palate perforation.7 Several reports have identified uvula necrosis after endotracheal intubation,7Y11 but soft palate necrosis related to endotracheal intubation has never been reported. Uvular necrosis that occurs after endotracheal intubation can be treated conservatively.7Y11 However, soft palate necrosis cannot heal conservatively, and it can significantly affect the patient’s quality of life with symptoms such as speech disorder and oronasal regurgitation. Therefore, surgery should be performed to repair soft palate necrosis. Various palatoplasty techniques have been used to treat congenital cleft palate, and pharyngeal flap has been used for velopharyngeal inadequacy.12Y16 These methods can also be applied as treatment options for noncongenital soft palate necrosis or cleft. We encountered 2 patients who had soft palate necrosis after longterm endotracheal intubation during intensive care unit (ICU) care. This study reports the experience of patients with noncongenital soft palate necrosis and discusses the treatment plan with a literature review.
PATIENTS AND METHODS Patients Two male patients, aged 30 and 38 years, with soft palate necrosis caused by endotracheal intubation, were treated with pharyngeal flap
Brief Clinical Studies
and/or palatoplasty at the Samsung Medical Center from March 2011 to May 2013. One patient was treated with palatoplasty and pharyngeal flap, and the other patient was treated with pharyngeal flap (Table 1).
Patient 1 In April 2011, a 38-year-old man sustained multiple facial bone fractures caused by a traffic accident. Ten days after the accident, he received a facial bone fracture operation by open reduction and internal fixation. After the operation, he received care in the ICU and had an endotracheal intubation for 1 month. After extubation, the patient complained about vocal resonance change, oronasal regurgitation, and dysphagia. He was diagnosed with soft palate necrosis, which included the whole uvula, and he was seen in our outpatient clinic where he expressed concern about his dysphonia. The patient had severe nasality when he tried to speak that made his speech unintelligible. He also had dysphagia and uncontrollable oronasal food regurgitation, which made swallowing difficult. The patient was an hepatitis B virus carrier and a 10-pack-year smoker. His medical history was otherwise unremarkable, and the patient took no other medications. There was no personal or family history of inflammatory or autoimmune disease. A perceptual speech evaluation was performed by a certified speech-language pathologist and indicated that the patient had severe hypernasality and audible nasal emission. He consistently nasalized all fricative and plosive sounds, which require oral airflow or oral air trapping to produce. His speech intelligibility at the conversational level was significantly reduced. The physical examination and nasopharyngoscopy revealed that the center of the soft palate was notably absent; however, the hard palate was intact (Fig. 1).The patient also had an alveolar fracture with a gingival defect. The soft palate revealed a large gap during articulation, which required a surgical procedure to repair. We evaluated the appearance of the defect by the palate movement (Fig. 2). In addition, we observed hypertrophy of the Passavant ridge, which was caused by velopharyngeal insufficiency compensation. In the video, we observed overactive Passavant movement when the patient phonated (Supplementary video, http://links.lww.com/SCS/A81 Patient 1 nasopharyngoscopy video: velopharyngeal inadequacy is demonstrated with articulation. The soft palate revealed a large gap. The video also shows the horizontal mucosal folds [Passavant ridge] on the posterior pharyngeal wall upon velopharyngeal closure initiation). The remaining oropharynx appeared normal. Intranasal examination was also normal with no septal perforation. The preoperative computed tomography (CT) scan indicated that there was a alveolar bone defect caused by the previous traffic accident; however, the hard palate was intact (Fig. 3). Surgical repair of the soft palate defect was undertaken. There were some bilateral remnant tissues of the soft palate; therefore, a modified von Langenbeck palatoplasty was performed. To address the alveolar defect, a distractor was applied for alveolar bone osteogenesis. The postoperative recovery was uneventful. The patient’s oronasal regurgitation improved but was not completely recovered
TABLE 1. Patients Summary
Sex/Age, y
Cause of ICU Care (Duration of ICU Care)
Male/38
Multiple facial bone fractures (1 mo)
Male/30
Epidural hematoma (1 mo)
Symptom
Surgical Procedure
Ventriculoperitoneal Rating
Complication After Surgery
Speech disorder. Oronasal regurgitation Dysphasia Speech disorder Oronasal regurgitation Dysphasia
Palatoplasty and Pharyngeal flap
Severe
No
Pharyngeal flap
Severe
No
* 2014 Mutaz B. Habal, MD
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FIGURE 1. Patient 1 intraoral examination. Upper left, The preoperative soft palate defect. The center of the soft palate was notably absent; however, the hart palate was intact. Upper right, Preoperative alveolar defect. Lower left, The postoperative 3-month view of the soft palate repaired with palatoplasty and pharyngeal flap. Lower right, The postoperative 3-month view of the distracted alveolar defect.
because his soft palate was repaired transversely in the midline and remained deficient in the anteroposterior dimension. He was discharged on the fifth postoperative day. After 6 months, we performed a secondary operation with superior-based pharyngeal flap to improve the patient’s speech disorder. The alveolar distractor was removed simultaneously. The postoperative course was uneventful, and the patient was discharged on the eighth postoperative day.
Patient 2
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FIGURE 3. Patient 1 facial bone CT scan: Left, Preoperative view: the CT scan shows the alveolar bone defect with teeth loss. Right, Three-month postoperative view: the alveolar defect was repaired with bone distraction.
healing and reported satisfaction with their speech improvement. The follow-up perceptual speech evaluation indicated that hypernasality had been significantly decreased with greatly improved speech intelligibility. Both patient evaluations revealed that plosive sounds were primarily oral with little nasal air emission. The patients did not experience oronasal regurgitation and swallowing difficulties. The follow-up nasopharyngoscopy showed complete healing of the intraoral incisions and an intact pharyngeal flap (Fig. 2).
DISCUSSION
Follow-up was conducted with each patient at 3 months, 6 months, and 1 year after surgery. Both patients achieved primary wound
The cause of the soft palate defect was not definitely determined when the patients first visited our hospital. Possible causes of secondary midline palatal necrosis include trauma,7 narcotics or cocaine inhalation,1,2 maxillary artery embolization,3 tumor,4 infection, endoscopy complication,5 and granulomatous disease.6 Nasal cocaine inhalation is well documented for causing the destruction of midfacial structures, most commonly nasal septal perforations. Palatal defects from intranasal cocaine use, first described 17 years ago, are much less common.17 Fewer than 15 cases of cocaine-induced palatal defects, mostly involving the hard palate, have been reported in the literature to date, and only 3 cases of isolated soft palate defects were reported.1 The most current mechanism of tissue necrosis caused by inhaled cocaine is thought to be secondary to prolonged vasospasm and subsequent ischemia, chronic irritation and caustic effects, and superimposed infections.17 In addition, recent reports have documented several complications from the nasal inhalation of prescription narcotics. Soft palate involvement is more common with narcotics than with cocaine use, and 3 cases have been described since 2002.18 However, the mechanism by which crushed and inhaled prescription narcotics cause tissue necrosis is not known. The most likely cause of damage is chronic irritation and the inflammatory response that results from inhalation. The patients in this study did not experience tissue damage resulting from cocaine or other narcotic inhalation. The patients did not present with nasal septal perforation that often accompanies palate necrosis caused by inhalation of cocaine or narcotics; therefore, cocaine or narcotic inhalation was not the cause of the soft palate necrosis in these 2 patients. Two patients of internal maxillary artery embolization complications that caused palate necrosis have been reported.3,19 One of the patients was hard palate necrosis, and the other patient was soft palate fistula, both of which were accompanied by nasal necrosis.
FIGURE 2. Patient 1 nasopharyngoscopy. Left, Preoperative nasopharyngoscopy view, incomplete pharyngeal wall closure. Right, Nasopharyngoscopy view after pharyngeal flap operation (5 months postoperative). The intact pharyngeal flap and a narrowed pharyngeal wall can be observed.
FIGURE 4. Patient 2. Left, The preoperative soft palate defect; the soft palate center was notably absent, but the hart palate was intact. Right, Preoperative nasopharyngoscopy: velopharyngeal incompetence is demonstrated with articulation. The soft palate revealed a large gap.
In August 2010, a 30-year-old man experienced a left epidural hematoma caused by a traffic accident, and he received a frontotemporoparietal craniectomy with hematoma removal. In October 2010, he received a revisional craniotomy and fluid removal, and 1 week later, he received a ventriculoperitoneal shunt. After the operation, he received care in the ICU with endotracheal intubation for approximately 1 month. Following the ICU care, it was noted that soft palate necrosis had developed with speech disorder and oronasal regurgitation. He visited our treatment center and also complained of left eyeball enophthalmos and left frontotemporal-area skull deformity. He had no other medical problems. The patient took no other medications, and there was no personal or family history of inflammatory or autoimmune disease. The perceptual speech evaluation indicated that the patient had severe hypernasality and audible nasal emission. The physical examination and nasopharyngoscopy revealed that there was a large soft palate defect (Fig. 4).The posterior pharyngeal wall and lateral pharyngeal wall were intact, and the remaining oropharynx appeared normal. Intranasal examination was also normal with no septal perforation. His daily conversational speech intelligibility was generally adequate but was sometimes insufficient. In June 2011, the enophthalmos and skull deformity corrections were completed. In addition, we performed a pharyngeal flap for the velopharyngeal insufficiency. The postoperative course was uneventful, and the patient was discharged on the fourth postoperative day.
RESULTS
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The 2 patients in this study did not experience necrosis of the nose, and the internal maxillary arteries were intact. Other causes of soft palate necrosis include tumors, such as pleomorphic adenoma,5 and granulomatous disorders, such as sarcoidosis, tuberculosis, syphilis, and midline granuloma.6 These possibilities were ruled out in our patients based on pathology and serology results. The patients did not have histories of autoimmune disease or other notable conditions. Finally, an active infectious etiology was ruled out based on culture test results. Both of our patients acquired a soft palate defect after long-term endotracheal intubation during ICU care. However, there are no previous reports of soft palate necrosis after endotracheal intubation. A common complaint after intubation is a sore throat, which has been reported to be as high as 40%.20 Uvular necrosis is a rare endotracheal intubation complication,7 and there have been only 4 reports of uvular necrosis after endotracheal intubation.11 However, the soft palate was not involved in these cases, and the necrosis was attributed to mechanical disruption of the blood supply to the uvula. This usually resulted from the uvula being compressed either between the hard palate and a midline endotracheal tube or by vigorous suctioning of the oropharynx.7 Two cases of uvular necrosis after upper endoscopy have also been reported.11 In addition, a case of soft palate necrosis following a series of upper gastrointestinal procedures including multiple esophagogastroduodenoscopies, endotracheal intubation, Sengstaken-Blakemore and nasogastric intubation, and endoscopic sclerotherapy was reported in a patient with massive variceal hemorrhage.5 The mechanism of injury was similar to intubation and endoscopy; therefore, we proposed that the soft palate defect in our patients also occurred because of long-term intubation. Uvular necrosis treatments reported in the literature include observation, intravenous steroids, antihistamines, and topical epinephrine administration.8 Conservative management is frequently advised based on the patient’s symptoms, and regardless of the course of treatment, a full recovery should be expected within 2 weeks.7 However, soft palate necrosis cannot heal with conservative treatment, and the condition is much more problematic than uvular necrosis. The patients who experienced soft palate necrosis also had complaints of speech disorder and oronasal regurgitation. Speech disorder is caused by velopharyngeal insufficiency because the velar musculature cannot contract appropriately and causes the patient’s speech to be virtually unintelligible. In addition, uncontrollable oronasal reflux caused water and food regurgitation when the patients attempted to drink and eat. These symptoms significantly reduced the patients’ quality of life, and because conservative treatment could not improve these conditions, a surgical procedure was performed to repair the soft palate necrosis. There are several technical options for surgical reconstruction of velopharyngeal insufficiency and oronasal fistula. The pharyngeal flap operation, which was first performed by Schoenborn and popularized by Rosenthal, has widely been used to eliminate velopharyngeal incompetence. This study applied the pharyngeal flap technique, modified by Hogan,21 for both patient patients. In the less severe patient 1, we performed palatoplasty as the first stage operation; because the defect was linearly shaped in the center of the soft palate, there was some bilateral soft tissue that could be used to repair the soft palate defect. Next, we attached the pharyngeal flap to the repaired soft palate to repair the anteroposterior deficiency in the secondary operation. In patient 2, initially, the soft tissue remnants in the lateral area of the soft palate were limited; therefore, the pharyngeal flap operation was performed as the first treatment of choice. Buccal mucosal flap is another treatment option for palatal defect reconstruction. Jackson22 utilized local random buccal flaps to close secondary palatal fistulas and concluded that the buccal mucosal flap is valuable and can fit into various palatal defects. Tezel et al23
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summarized the utility and application of the buccal mucosal flap and reviewed its use for palatal reconstruction. Modification of this technique could use the buccal mucosal flap as a good treatment option for palatal reconstruction. A microvascular-free flap can be used to repair extensive palatal destruction because it is a more versatile approach.24 Oropharyngeal cancer resections often result in large soft palate defects, and these defects are usually reconstructed with the radial forearm free flap.25 However, velopharyngeal function is often compromised by oropharyngeal and palatal tumor reconstruction, although free tissue transfer has improved head and neck reconstruction outcomes.26 Recently, many technique modifications have been reported to overcome functional deficiencies after microvascular reconstruction.27Y29 Despite these technique modifications, additional techniques, such as pharyngeal flap, are required for palatal functional improvement.29 In addition, bone transfer is not recommended in cases with soft palate defect because bone tissue is not well attached to the soft tissue and can cause airway obstruction. In the 2 patients presented here, microvascular-free flap reconstruction could have been reserved as a secondary treatment option with or without the pharyngeal flap operation. Obturator appliance application is another option with palate loss.30 However, the application of the appliance can be problematic because of improper fit and hygienic concerns, the need for dental anchoring, and chronic irritation of the local oropharynx mucosa caused by the appliance. For these reasons, local tissue flaps should be used as the first treatment choice and external appliances should be reserved until necessary. In both of our cases, the patients were followed up for an average of 1 year and improved their velopharyngeal function.
CONCLUSIONS We encountered 2 patients who had soft palate necrosis following endotracheal intubation during ICU care. Although it is rare, longterm ICU care with endotracheal intubation can cause noncongenital soft palate cleft. Because iatrogenic cleft palate does not heal with conservative treatment, a surgical procedure, such as a pharyngeal flap or palatoplasty, can be applied to patients with these conditions.
REFERENCES 1. Birchenough SA, Borowitz K, Lin KY. Complete soft palate necrosis and velopharyngeal insufficiency resulting from intranasal inhalation of prescription narcotics and cocaine. J Craniofac Surg 2007;18:1482Y1485 2. Goodger NM, Wang J, Pogrel MA. Palatal and nasal necrosis resulting from cocaine misuse. Br Dent J 2005;198:333Y334 3. Ntomouchtsis A, Venetis G, Zouloumis L, et al. Ischemic necrosis of nose and palate after embolization for epistaxis. A case report. Oral Maxillofac Surg 2010;14:123Y127 4. Kurokawa H, Yoshida M, Igawa K, et al. Extensive necrosis of pleomorphic adenoma in the soft palate: a case report and review of the literature. J Oral Maxillofac Surg 2008;66:797Y800 5. Pastrich HJ, Brandt LJ, St Onge G. Necrosis of the soft palate secondary to upper gastrointestinal tract intubation. Gastrointest Endosc 1988;34:363Y364 6. Villa PD. Midfacial complications of prolonged cocaine snorting. J Can Dent Assoc 1999;65:218Y223 7. Evans DP, Lo BM. Uvular necrosis after orotracheal intubation. Am J Emerg Med 2009;27:631, e633Ye634 8. Krantz MA, Solomon DL, Poulos JG. Uvular necrosis following endotracheal intubation. J Clin Anesth 1994;6:139Y141
* 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
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9. Salengros JC, El Founas W, Velghe-Lenelle CE, et al. Uvular and tonsillar pillar mucosal necrosis as a cause of severe sore throat after orotracheal intubation. Anaesth Intensive Care 2011;39:772Y773 10. Calikapan GT, Karakus F. Uvula necrosis after endotracheal intubation for rhinoplasty. Aesthetic Plast Surg 2008;32:710Y711 11. Tang SJ, Kanwal F, Gralnek IM. Uvular necrosis after upper endoscopy: a case report and review of the literature. Endoscopy 2002;34:585Y587 12. Seyfer AE, Prohazka D, Leahy E. The effectiveness of the superiorly based pharyngeal flap in relation to the type of palatal defect and timing of the operation. Plast Reconstr Surg 1988;82:760Y764 13. Schmelzeisen R, Hausamen JE, Loebell E, et al. Long-term results following velopharyngoplasty with a cranially based pharyngeal flap. Plast Reconstr Surg 1992;90:774Y778 14. Sloan GM. Posterior pharyngeal flap and sphincter pharyngoplasty: the state of the art. Cleft Palate Craniofac J 2000; 37:112Y122 15. Meek MF, Coert JH, Hofer SO, et al. Short-term and long-term results of speech improvement after surgery for velopharyngeal insufficiency with pharyngeal flaps in patients younger and older than 6 years old: 10-year experience. Ann Plast Surg 2003;50:13Y17 16. Dailey SA, Karnell MP, Karnell LH, et al. Comparison of resonance outcomes after pharyngeal flap and Furlow double-opposing z-plasty for surgical management of velopharyngeal incompetence. Cleft Palate Craniofac J 2006;43:38Y43 17. Deutsch HL, Millard DR Jr. A new cocaine abuse complex. Involvement of nose, septum, palate, and pharynx. Arch Otolaryngol Head Neck Surg 1989;115:235Y237 18. Greene D. Total necrosis of the intranasal structures and soft palate as a result of nasal inhalation of crushed OxyContin. Ear Nose Throat J 2005;84:512, 514, 516 19. Guss J, Cohen MA, Mirza N. Hard palate necrosis after bilateral internal maxillary artery embolization for epistaxis. Laryngoscope 2007;117:1683Y1684 20. Biro P, Seifert B, Pasch T. Complaints of sore throat after tracheal intubation: a prospective evaluation. Eur J Anaesthesiol 2005;22:307Y311 21. Hogan VM. A clarification of the surgical goals in cleft palate speech and the introduction of the lateral port control (l.p.c.) pharyngeal flap. Cleft Palate J 1973;10:331Y345 22. Jackson IT. Closure of secondary palatal fistulae with intra-oral tissue and bone grafting. Br J Plast Surg 1972;25:93Y105 23. Tezel E. Buccal mucosal flaps: a review. Plast Reconstr Surg 2002;109:735Y741 24. Turk AE, Chang J, Soroudi AE, et al. Free flap closure in complex congenital and acquired defects of the palate. Ann Plast Surg 2000;45:274Y279 25. Sinha UK, Young P, Hurvitz K, et al. Functional outcomes following palatal reconstruction with a folded radial forearm free flap. Ear Nose Throat J 2004;83:45Y48 26. McCombe D, Lyons B, Winkler R, et al. Speech and swallowing following radial forearm flap reconstruction of major soft palate defects. Br J Plast Surg 2005;58:306Y311 27. Roh TS, Lee WJ, Choi EC, et al. Radial forearm-palmaris longus tenocutaneous free flap; implication in the repair of the moderate-sized postoncologic soft palate defect. Head Neck 2009;31:1220Y1227 28. Kim JH, Chu HR, Kang JM, et al. Functional benefit after modification of radial forearm free flap for soft palate reconstruction. Clin Exp Otorhinolaryngol 2008;1:161Y165 29. Brown JS, Zuydam AC, Jones DC, et al. Functional outcome in soft palate reconstruction using a radial forearm free flap in conjunction with a superiorly based pharyngeal flap. Head Neck 1997;19:524Y534 30. Mari A, Arranz C, Gimeno X, et al. Nasal cocaine abuse and centrofacial destructive process: report of three cases including treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;93:435Y439
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Unusual Complication After Genioplasty Rafael Linard Avelar, MSc,*Þ Carlos Diego Lopes Sa´, DDS,þ Diego Felipe Silveira Esses, DDS,þ Ota´vio Emmel Becker, MSc,* Eduardo Costa Studart Soares, PhD,þ Rogerio Belle de Oliveira, PhD* Abstract: Facial beauty depends on shape, proportion, and harmony between the facial thirds. The chin is one of the most important components of the inferior third and has an important role on the definition of facial aesthetic and harmony in both frontal and lateral views. There are 2 principal therapeutic approaches that one can choose to treat mental deformities, alloplastic implants, and mental basilar ostectomy, also known as genioplasty. The latest is more commonly used because of great versatility in the correction of three-dimensional deformities of the chin and smaller taxes of postoperative complications. Possible transoperative and postoperative complications of genioplasty include mental nerve lesion, bleeding, damage to tooth roots, bone resorption of the mobilized segment, mandibular fracture, ptosis of the lower lip, and failure to stabilize the ostectomized segment. The study presents 2 cases of displacement of the osteotomized segment after genioplasty associated with facial trauma during postoperative orthognathic surgery followed by rare complications with no reports in the literature. Key Words: Genioplasty, chin, esthetics
F
acial beauty depends on the shape, proportion, position, and harmony of the facial thirds. The chin is one of the main anatomical structures of the lower third occupying a prominent position and influencing the definition of facial aesthetics and harmony, both in front and profile views.1 Chin surgery can be performed to refine orthognathic surgery, to provide an aesthetic gain of the technique or as an isolated aesthetic procedure in patients with satisfactory maxillomandibular relationship but who have a protruding or retropositioned chin.2 In mild to moderate cases of obstructive sleep apnea syndrome, chin advancement surgery is part of the treatment protocol, contributing to the high level of success.3 Aesthetic modifications to reposition the chin involve the lower lip, mentolabial sulcus, soft pogonion, and mentocervical distance.
From the *Oral and Maxillofacial Surgery Department, Pontifı´cia, Universidade Cato´lica do Rio Grande do Sul, Porto Alegre; †Department Faculdade Cato´lica Rainha do Serta˜o, Quixada´; and ‡Department Oral and Maxillofacial Surgery Service, Walter Cantı´dio University Hospital, Federal University of Ceara´, Fortaleza, Brazil. Received August 28, 2013. Accepted for publication November 26, 2013. Address correspondence and reprint requests to Rafael Linard Avelar, MSc, Pontifı´cia Universidade Cato´lica do Rio Grande do Sul, Av. Ipiranga, 6681, Porto Alegre/RS, Brazil CEP 90619-900; E-mail: [email protected] The authors report no conflicts of interest. Copyright * 2014 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000000618
* 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
Brief Clinical Studies
to maintain or reestablish sinus function, or to eliminate sinus by obliteration or cranialization, as well as to reestablish facial contours to achieve optimal functional and aesthetic result in a single act. Liquor leakage and nasofrontal duct condition are the 2 most important elements that determine treatment approach. Dislocated fragment at the posterior frontal sinus wall is also an important factor that determines the type of surgical treatment.1,2,4,7,9 Active approach as sense of surgical intervention is mandatory for the management of complications after trauma and surgery of frontobasal injuries. Nonobliterative surgical procedures including endoscopy do not warrant permanent drainage and definite resolution of complications. The majority of authors believe that sinus obliteration is a criterion standard for the management of complications and impaired drainage system after frontal sinus trauma, nevertheless.2Y5,7,10 If obliteration failed, it would be necessary to explore the causes of that failure. Sinus infection requires complete revision, as we performed in our case. Nasofrontal duct orifice and ethmoidal cells must be isolated, and then the sinus is obliterated. It could be also carried out by cannulation of the nasofrontal duct if there was no comminuted posterior wall fracture. It is considered that adequate exploration and cleaning, as well as reposition, have to be performed before reconstruction.1,2,4,6 Reconstruction of frontal bone contours may be accomplished with autologous bone or alloplastic material. The perfect material for cranioplasty has to be biocompatible, biomechanically stable, easy to use, flexible, light, nonmagnetic, and permanently stable. When deciding on the type of reconstruction, the surgeon has to take into consideration the clinical findings, extent of a defect, and probability of complications.10,11 Carbonate and calcium phosphate (hydroxyapatite) cement and methyl methacrylate are often used for reconstruction of defects of the frontal region bones. Titanium mesh is widely used, and it provides excellent threedimensional stability. It is suitable for major defects; it may be easily adjusted to a defect and most precisely reestablishes natural contours in the area of defect. It is hard enough for major defects not allowing the loosening; complications are uncommon, and it gives artifacts on CT images.10,11 Combination of titanium mesh impregnated with hydroxyapatite cement has advantages of being suitable for major defects, absence of donor-site morbidity, and convenience of use and of not being time-consuming.11,12 Medpor (porous polyethylene implant) may be used for medium-size defects; it is a biocompatible and durable material, but expensive.10,11
CONCLUSIONS The complications resulting from treatment of frontobasal region fractures vary from aesthetics, such as forehead and orbit asymmetry, to local infections and life-threatening intracranial infections. Potentially severe complications that occur many years after treatment emphasize the need for elaboration of a definite, initial, primary treatment plan. Management of these complications requires an active surgical approach. Development of surgical techniques improved safety with minimal complications associated with surgical treatment. Creation of so-called safe sinus has primary significance, and to achieve it, it is often necessary to perform sinus obliteration. Minimally invasive techniques may also contribute to the management of complications. Timing of definite reconstruction must be carefully considered from case to case. Planning of reconstruction and reestablishing aesthetic frontal bone defect with autologous bone or alloplastic material must be made with regard to relationship with sinus and nasal cavities, local finding, and infection. Among biocompatible materials used for reconstruction, tita-
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nium mesh impregnated with hydroxyapatite provides excellent stability and reconstructs natural contours in the affected area.
REFERENCES 1. Bell RB, Dierks EJ, Brar P, et al. A protocol for the management of frontal sinus fractures emphasizing sinus preservation. J Oral Maxillofac Surg 2007;65:825Y839 2. Manolidis S, Hollier LH Jr. Management of frontal sinus fractures. PRS J 2007;120:32SY48S 3. Rontal ML. State of the art in craniomaxillofacial trauma: frontal sinus. Curr Opin Otolaryngol Head Neck Surg 2008;16:381Y386 4. Gabrielli MFR, Gabrielli MAC, Hochuli-Vieira E, et al. Immediate reconstruction of frontal sinus fractures: review of 26 cases. J Oral Maxillofac Surg 2004;62:582Y586 5. Grossman DG, Archer SM, Arosarena O. Management of frontal sinus fractures: a review of 96 cases. Laryngoscope 2006;116:1357Y1362 6. Stanley RB. Management of complications of frontal sinus and frontal bone fractures. Oper Tech Plast Reconstr Surg 1998;5:296Y301 7. Wynn R, Vaughan WC. Treatment of failed frontal sinus obliteration. Oper Tech Otolaryngol 2006;17:13Y18 8. Mourouzis C, Evans BT, Shenouda E. Late presentation of a mucocele of the frontal sinus: 50 years postinjury. J Oral Maxillofac Surg 2008;66:1510Y1513 9. Strong EB. Frontal sinus fractures. Oper Tech Otolaryngol 2008;19:151Y160 10. Marao HF, Gulinelli JL, Pereira CCS, et al. Use of titanium mesh for reconstruction of extensive defects in fronto-orbito-ethmoidal fracture. J Craniofac Surg 2010;21:748Y750 11. Brevi BC, Magri AS, Toma L, et al. Cranioplasty for repair of a large bone defect with autologous and homologous bone in children. J Pediatr Surg 2010;45:E17YE20 12. Ducic Y. Titanium mesh and hydroxyapatite cement cranioplasty: a report of 20 cases. J Oral Maxillofac Surg 2002;60:272Y276
Reconstruction of Soft Plate Necrosis After Endotracheal Intubation Hyuck Jae Lee, MD, So Young Lim, MD, PhD, Jai-Kyong Pyon, MD, PhD, Goo Hyun Mun, MD, PhD, Sa Ik Bang, MD, PhD, Kap Sung Oh, MD, PhD Abstract: Uvular necrosis after long-term endotracheal intubation has been previously reported, but there have been no reports regarding soft palate necrosis after endotracheal intubation. Recently, From the Department of Plastic Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. Received October 17, 2013. Accepted for publication November 11, 2013. Address correspondence and reprint requests to Dr. So Young Lim, Department of Plastic Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-dong, Gangnam-gu, Seoul, 135-710, Republic of Korea; E-mail: [email protected] Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal_s Web site (www.jcraniofacialsurgery.com). The authors report no conflicts of interest. Copyright * 2014 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000000530
* 2014 Mutaz B. Habal, MD
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we encountered 2 patients who had a high degree of soft palate necrosis following endotracheal intubation during long-term care in the intensive care unit. This study reports noncongenital soft palate cleft caused by endotracheal intubation. Two patients, aged 30 and 38 years, with noncongenital cleft palate were treated with pharyngeal flap and/or palatoplasty at our institution from March 2011 to May 2013. Initially, the patients complained of acquired speech disorder and severe oronasal regurgitation caused by a palatal defect. Speech ability was evaluated preoperatively and postoperatively by a perceptual language test and nasopharyngoscopy. The cleft soft palates of both patients were completely repaired, and the aforementioned symptoms improved after surgery. Postoperative courses were uneventful in both of the cases, and neither patient experienced a recurrence. Although rare, long-term intensive care unit care with endotracheal intubation can cause noncongenital soft palate cleft. In cases with iatrogenic cleft palate that does not heal with conservative treatment, surgical procedures such as pharyngeal flap and palatoplasty can be helpful. Key Words: Cleft palate, endotracheal intubation, soft palate, necrosis
A
cquired soft palate necrosis is very rare. However, noncongenital soft palate necrosis can be caused by narcotics or cocaine inhalation,1,2 maxillary artery embolization,3 tumor,4 infection, endoscopy complication,5 and granulomatous disease.6 Various forms of oral trauma can also cause soft palate perforation.7 Several reports have identified uvula necrosis after endotracheal intubation,7Y11 but soft palate necrosis related to endotracheal intubation has never been reported. Uvular necrosis that occurs after endotracheal intubation can be treated conservatively.7Y11 However, soft palate necrosis cannot heal conservatively, and it can significantly affect the patient’s quality of life with symptoms such as speech disorder and oronasal regurgitation. Therefore, surgery should be performed to repair soft palate necrosis. Various palatoplasty techniques have been used to treat congenital cleft palate, and pharyngeal flap has been used for velopharyngeal inadequacy.12Y16 These methods can also be applied as treatment options for noncongenital soft palate necrosis or cleft. We encountered 2 patients who had soft palate necrosis after longterm endotracheal intubation during intensive care unit (ICU) care. This study reports the experience of patients with noncongenital soft palate necrosis and discusses the treatment plan with a literature review.
PATIENTS AND METHODS Patients Two male patients, aged 30 and 38 years, with soft palate necrosis caused by endotracheal intubation, were treated with pharyngeal flap
Brief Clinical Studies
and/or palatoplasty at the Samsung Medical Center from March 2011 to May 2013. One patient was treated with palatoplasty and pharyngeal flap, and the other patient was treated with pharyngeal flap (Table 1).
Patient 1 In April 2011, a 38-year-old man sustained multiple facial bone fractures caused by a traffic accident. Ten days after the accident, he received a facial bone fracture operation by open reduction and internal fixation. After the operation, he received care in the ICU and had an endotracheal intubation for 1 month. After extubation, the patient complained about vocal resonance change, oronasal regurgitation, and dysphagia. He was diagnosed with soft palate necrosis, which included the whole uvula, and he was seen in our outpatient clinic where he expressed concern about his dysphonia. The patient had severe nasality when he tried to speak that made his speech unintelligible. He also had dysphagia and uncontrollable oronasal food regurgitation, which made swallowing difficult. The patient was an hepatitis B virus carrier and a 10-pack-year smoker. His medical history was otherwise unremarkable, and the patient took no other medications. There was no personal or family history of inflammatory or autoimmune disease. A perceptual speech evaluation was performed by a certified speech-language pathologist and indicated that the patient had severe hypernasality and audible nasal emission. He consistently nasalized all fricative and plosive sounds, which require oral airflow or oral air trapping to produce. His speech intelligibility at the conversational level was significantly reduced. The physical examination and nasopharyngoscopy revealed that the center of the soft palate was notably absent; however, the hard palate was intact (Fig. 1).The patient also had an alveolar fracture with a gingival defect. The soft palate revealed a large gap during articulation, which required a surgical procedure to repair. We evaluated the appearance of the defect by the palate movement (Fig. 2). In addition, we observed hypertrophy of the Passavant ridge, which was caused by velopharyngeal insufficiency compensation. In the video, we observed overactive Passavant movement when the patient phonated (Supplementary video, http://links.lww.com/SCS/A81 Patient 1 nasopharyngoscopy video: velopharyngeal inadequacy is demonstrated with articulation. The soft palate revealed a large gap. The video also shows the horizontal mucosal folds [Passavant ridge] on the posterior pharyngeal wall upon velopharyngeal closure initiation). The remaining oropharynx appeared normal. Intranasal examination was also normal with no septal perforation. The preoperative computed tomography (CT) scan indicated that there was a alveolar bone defect caused by the previous traffic accident; however, the hard palate was intact (Fig. 3). Surgical repair of the soft palate defect was undertaken. There were some bilateral remnant tissues of the soft palate; therefore, a modified von Langenbeck palatoplasty was performed. To address the alveolar defect, a distractor was applied for alveolar bone osteogenesis. The postoperative recovery was uneventful. The patient’s oronasal regurgitation improved but was not completely recovered
TABLE 1. Patients Summary
Sex/Age, y
Cause of ICU Care (Duration of ICU Care)
Male/38
Multiple facial bone fractures (1 mo)
Male/30
Epidural hematoma (1 mo)
Symptom
Surgical Procedure
Ventriculoperitoneal Rating
Complication After Surgery
Speech disorder. Oronasal regurgitation Dysphasia Speech disorder Oronasal regurgitation Dysphasia
Palatoplasty and Pharyngeal flap
Severe
No
Pharyngeal flap
Severe
No
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FIGURE 1. Patient 1 intraoral examination. Upper left, The preoperative soft palate defect. The center of the soft palate was notably absent; however, the hart palate was intact. Upper right, Preoperative alveolar defect. Lower left, The postoperative 3-month view of the soft palate repaired with palatoplasty and pharyngeal flap. Lower right, The postoperative 3-month view of the distracted alveolar defect.
because his soft palate was repaired transversely in the midline and remained deficient in the anteroposterior dimension. He was discharged on the fifth postoperative day. After 6 months, we performed a secondary operation with superior-based pharyngeal flap to improve the patient’s speech disorder. The alveolar distractor was removed simultaneously. The postoperative course was uneventful, and the patient was discharged on the eighth postoperative day.
Patient 2
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FIGURE 3. Patient 1 facial bone CT scan: Left, Preoperative view: the CT scan shows the alveolar bone defect with teeth loss. Right, Three-month postoperative view: the alveolar defect was repaired with bone distraction.
healing and reported satisfaction with their speech improvement. The follow-up perceptual speech evaluation indicated that hypernasality had been significantly decreased with greatly improved speech intelligibility. Both patient evaluations revealed that plosive sounds were primarily oral with little nasal air emission. The patients did not experience oronasal regurgitation and swallowing difficulties. The follow-up nasopharyngoscopy showed complete healing of the intraoral incisions and an intact pharyngeal flap (Fig. 2).
DISCUSSION
Follow-up was conducted with each patient at 3 months, 6 months, and 1 year after surgery. Both patients achieved primary wound
The cause of the soft palate defect was not definitely determined when the patients first visited our hospital. Possible causes of secondary midline palatal necrosis include trauma,7 narcotics or cocaine inhalation,1,2 maxillary artery embolization,3 tumor,4 infection, endoscopy complication,5 and granulomatous disease.6 Nasal cocaine inhalation is well documented for causing the destruction of midfacial structures, most commonly nasal septal perforations. Palatal defects from intranasal cocaine use, first described 17 years ago, are much less common.17 Fewer than 15 cases of cocaine-induced palatal defects, mostly involving the hard palate, have been reported in the literature to date, and only 3 cases of isolated soft palate defects were reported.1 The most current mechanism of tissue necrosis caused by inhaled cocaine is thought to be secondary to prolonged vasospasm and subsequent ischemia, chronic irritation and caustic effects, and superimposed infections.17 In addition, recent reports have documented several complications from the nasal inhalation of prescription narcotics. Soft palate involvement is more common with narcotics than with cocaine use, and 3 cases have been described since 2002.18 However, the mechanism by which crushed and inhaled prescription narcotics cause tissue necrosis is not known. The most likely cause of damage is chronic irritation and the inflammatory response that results from inhalation. The patients in this study did not experience tissue damage resulting from cocaine or other narcotic inhalation. The patients did not present with nasal septal perforation that often accompanies palate necrosis caused by inhalation of cocaine or narcotics; therefore, cocaine or narcotic inhalation was not the cause of the soft palate necrosis in these 2 patients. Two patients of internal maxillary artery embolization complications that caused palate necrosis have been reported.3,19 One of the patients was hard palate necrosis, and the other patient was soft palate fistula, both of which were accompanied by nasal necrosis.
FIGURE 2. Patient 1 nasopharyngoscopy. Left, Preoperative nasopharyngoscopy view, incomplete pharyngeal wall closure. Right, Nasopharyngoscopy view after pharyngeal flap operation (5 months postoperative). The intact pharyngeal flap and a narrowed pharyngeal wall can be observed.
FIGURE 4. Patient 2. Left, The preoperative soft palate defect; the soft palate center was notably absent, but the hart palate was intact. Right, Preoperative nasopharyngoscopy: velopharyngeal incompetence is demonstrated with articulation. The soft palate revealed a large gap.
In August 2010, a 30-year-old man experienced a left epidural hematoma caused by a traffic accident, and he received a frontotemporoparietal craniectomy with hematoma removal. In October 2010, he received a revisional craniotomy and fluid removal, and 1 week later, he received a ventriculoperitoneal shunt. After the operation, he received care in the ICU with endotracheal intubation for approximately 1 month. Following the ICU care, it was noted that soft palate necrosis had developed with speech disorder and oronasal regurgitation. He visited our treatment center and also complained of left eyeball enophthalmos and left frontotemporal-area skull deformity. He had no other medical problems. The patient took no other medications, and there was no personal or family history of inflammatory or autoimmune disease. The perceptual speech evaluation indicated that the patient had severe hypernasality and audible nasal emission. The physical examination and nasopharyngoscopy revealed that there was a large soft palate defect (Fig. 4).The posterior pharyngeal wall and lateral pharyngeal wall were intact, and the remaining oropharynx appeared normal. Intranasal examination was also normal with no septal perforation. His daily conversational speech intelligibility was generally adequate but was sometimes insufficient. In June 2011, the enophthalmos and skull deformity corrections were completed. In addition, we performed a pharyngeal flap for the velopharyngeal insufficiency. The postoperative course was uneventful, and the patient was discharged on the fourth postoperative day.
RESULTS
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The 2 patients in this study did not experience necrosis of the nose, and the internal maxillary arteries were intact. Other causes of soft palate necrosis include tumors, such as pleomorphic adenoma,5 and granulomatous disorders, such as sarcoidosis, tuberculosis, syphilis, and midline granuloma.6 These possibilities were ruled out in our patients based on pathology and serology results. The patients did not have histories of autoimmune disease or other notable conditions. Finally, an active infectious etiology was ruled out based on culture test results. Both of our patients acquired a soft palate defect after long-term endotracheal intubation during ICU care. However, there are no previous reports of soft palate necrosis after endotracheal intubation. A common complaint after intubation is a sore throat, which has been reported to be as high as 40%.20 Uvular necrosis is a rare endotracheal intubation complication,7 and there have been only 4 reports of uvular necrosis after endotracheal intubation.11 However, the soft palate was not involved in these cases, and the necrosis was attributed to mechanical disruption of the blood supply to the uvula. This usually resulted from the uvula being compressed either between the hard palate and a midline endotracheal tube or by vigorous suctioning of the oropharynx.7 Two cases of uvular necrosis after upper endoscopy have also been reported.11 In addition, a case of soft palate necrosis following a series of upper gastrointestinal procedures including multiple esophagogastroduodenoscopies, endotracheal intubation, Sengstaken-Blakemore and nasogastric intubation, and endoscopic sclerotherapy was reported in a patient with massive variceal hemorrhage.5 The mechanism of injury was similar to intubation and endoscopy; therefore, we proposed that the soft palate defect in our patients also occurred because of long-term intubation. Uvular necrosis treatments reported in the literature include observation, intravenous steroids, antihistamines, and topical epinephrine administration.8 Conservative management is frequently advised based on the patient’s symptoms, and regardless of the course of treatment, a full recovery should be expected within 2 weeks.7 However, soft palate necrosis cannot heal with conservative treatment, and the condition is much more problematic than uvular necrosis. The patients who experienced soft palate necrosis also had complaints of speech disorder and oronasal regurgitation. Speech disorder is caused by velopharyngeal insufficiency because the velar musculature cannot contract appropriately and causes the patient’s speech to be virtually unintelligible. In addition, uncontrollable oronasal reflux caused water and food regurgitation when the patients attempted to drink and eat. These symptoms significantly reduced the patients’ quality of life, and because conservative treatment could not improve these conditions, a surgical procedure was performed to repair the soft palate necrosis. There are several technical options for surgical reconstruction of velopharyngeal insufficiency and oronasal fistula. The pharyngeal flap operation, which was first performed by Schoenborn and popularized by Rosenthal, has widely been used to eliminate velopharyngeal incompetence. This study applied the pharyngeal flap technique, modified by Hogan,21 for both patient patients. In the less severe patient 1, we performed palatoplasty as the first stage operation; because the defect was linearly shaped in the center of the soft palate, there was some bilateral soft tissue that could be used to repair the soft palate defect. Next, we attached the pharyngeal flap to the repaired soft palate to repair the anteroposterior deficiency in the secondary operation. In patient 2, initially, the soft tissue remnants in the lateral area of the soft palate were limited; therefore, the pharyngeal flap operation was performed as the first treatment of choice. Buccal mucosal flap is another treatment option for palatal defect reconstruction. Jackson22 utilized local random buccal flaps to close secondary palatal fistulas and concluded that the buccal mucosal flap is valuable and can fit into various palatal defects. Tezel et al23
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summarized the utility and application of the buccal mucosal flap and reviewed its use for palatal reconstruction. Modification of this technique could use the buccal mucosal flap as a good treatment option for palatal reconstruction. A microvascular-free flap can be used to repair extensive palatal destruction because it is a more versatile approach.24 Oropharyngeal cancer resections often result in large soft palate defects, and these defects are usually reconstructed with the radial forearm free flap.25 However, velopharyngeal function is often compromised by oropharyngeal and palatal tumor reconstruction, although free tissue transfer has improved head and neck reconstruction outcomes.26 Recently, many technique modifications have been reported to overcome functional deficiencies after microvascular reconstruction.27Y29 Despite these technique modifications, additional techniques, such as pharyngeal flap, are required for palatal functional improvement.29 In addition, bone transfer is not recommended in cases with soft palate defect because bone tissue is not well attached to the soft tissue and can cause airway obstruction. In the 2 patients presented here, microvascular-free flap reconstruction could have been reserved as a secondary treatment option with or without the pharyngeal flap operation. Obturator appliance application is another option with palate loss.30 However, the application of the appliance can be problematic because of improper fit and hygienic concerns, the need for dental anchoring, and chronic irritation of the local oropharynx mucosa caused by the appliance. For these reasons, local tissue flaps should be used as the first treatment choice and external appliances should be reserved until necessary. In both of our cases, the patients were followed up for an average of 1 year and improved their velopharyngeal function.
CONCLUSIONS We encountered 2 patients who had soft palate necrosis following endotracheal intubation during ICU care. Although it is rare, longterm ICU care with endotracheal intubation can cause noncongenital soft palate cleft. Because iatrogenic cleft palate does not heal with conservative treatment, a surgical procedure, such as a pharyngeal flap or palatoplasty, can be applied to patients with these conditions.
REFERENCES 1. Birchenough SA, Borowitz K, Lin KY. Complete soft palate necrosis and velopharyngeal insufficiency resulting from intranasal inhalation of prescription narcotics and cocaine. J Craniofac Surg 2007;18:1482Y1485 2. Goodger NM, Wang J, Pogrel MA. Palatal and nasal necrosis resulting from cocaine misuse. Br Dent J 2005;198:333Y334 3. Ntomouchtsis A, Venetis G, Zouloumis L, et al. Ischemic necrosis of nose and palate after embolization for epistaxis. A case report. Oral Maxillofac Surg 2010;14:123Y127 4. Kurokawa H, Yoshida M, Igawa K, et al. Extensive necrosis of pleomorphic adenoma in the soft palate: a case report and review of the literature. J Oral Maxillofac Surg 2008;66:797Y800 5. Pastrich HJ, Brandt LJ, St Onge G. Necrosis of the soft palate secondary to upper gastrointestinal tract intubation. Gastrointest Endosc 1988;34:363Y364 6. Villa PD. Midfacial complications of prolonged cocaine snorting. J Can Dent Assoc 1999;65:218Y223 7. Evans DP, Lo BM. Uvular necrosis after orotracheal intubation. Am J Emerg Med 2009;27:631, e633Ye634 8. Krantz MA, Solomon DL, Poulos JG. Uvular necrosis following endotracheal intubation. J Clin Anesth 1994;6:139Y141
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9. Salengros JC, El Founas W, Velghe-Lenelle CE, et al. Uvular and tonsillar pillar mucosal necrosis as a cause of severe sore throat after orotracheal intubation. Anaesth Intensive Care 2011;39:772Y773 10. Calikapan GT, Karakus F. Uvula necrosis after endotracheal intubation for rhinoplasty. Aesthetic Plast Surg 2008;32:710Y711 11. Tang SJ, Kanwal F, Gralnek IM. Uvular necrosis after upper endoscopy: a case report and review of the literature. Endoscopy 2002;34:585Y587 12. Seyfer AE, Prohazka D, Leahy E. The effectiveness of the superiorly based pharyngeal flap in relation to the type of palatal defect and timing of the operation. Plast Reconstr Surg 1988;82:760Y764 13. Schmelzeisen R, Hausamen JE, Loebell E, et al. Long-term results following velopharyngoplasty with a cranially based pharyngeal flap. Plast Reconstr Surg 1992;90:774Y778 14. Sloan GM. Posterior pharyngeal flap and sphincter pharyngoplasty: the state of the art. Cleft Palate Craniofac J 2000; 37:112Y122 15. Meek MF, Coert JH, Hofer SO, et al. Short-term and long-term results of speech improvement after surgery for velopharyngeal insufficiency with pharyngeal flaps in patients younger and older than 6 years old: 10-year experience. Ann Plast Surg 2003;50:13Y17 16. Dailey SA, Karnell MP, Karnell LH, et al. Comparison of resonance outcomes after pharyngeal flap and Furlow double-opposing z-plasty for surgical management of velopharyngeal incompetence. Cleft Palate Craniofac J 2006;43:38Y43 17. Deutsch HL, Millard DR Jr. A new cocaine abuse complex. Involvement of nose, septum, palate, and pharynx. Arch Otolaryngol Head Neck Surg 1989;115:235Y237 18. Greene D. Total necrosis of the intranasal structures and soft palate as a result of nasal inhalation of crushed OxyContin. Ear Nose Throat J 2005;84:512, 514, 516 19. Guss J, Cohen MA, Mirza N. Hard palate necrosis after bilateral internal maxillary artery embolization for epistaxis. Laryngoscope 2007;117:1683Y1684 20. Biro P, Seifert B, Pasch T. Complaints of sore throat after tracheal intubation: a prospective evaluation. Eur J Anaesthesiol 2005;22:307Y311 21. Hogan VM. A clarification of the surgical goals in cleft palate speech and the introduction of the lateral port control (l.p.c.) pharyngeal flap. Cleft Palate J 1973;10:331Y345 22. Jackson IT. Closure of secondary palatal fistulae with intra-oral tissue and bone grafting. Br J Plast Surg 1972;25:93Y105 23. Tezel E. Buccal mucosal flaps: a review. Plast Reconstr Surg 2002;109:735Y741 24. Turk AE, Chang J, Soroudi AE, et al. Free flap closure in complex congenital and acquired defects of the palate. Ann Plast Surg 2000;45:274Y279 25. Sinha UK, Young P, Hurvitz K, et al. Functional outcomes following palatal reconstruction with a folded radial forearm free flap. Ear Nose Throat J 2004;83:45Y48 26. McCombe D, Lyons B, Winkler R, et al. Speech and swallowing following radial forearm flap reconstruction of major soft palate defects. Br J Plast Surg 2005;58:306Y311 27. Roh TS, Lee WJ, Choi EC, et al. Radial forearm-palmaris longus tenocutaneous free flap; implication in the repair of the moderate-sized postoncologic soft palate defect. Head Neck 2009;31:1220Y1227 28. Kim JH, Chu HR, Kang JM, et al. Functional benefit after modification of radial forearm free flap for soft palate reconstruction. Clin Exp Otorhinolaryngol 2008;1:161Y165 29. Brown JS, Zuydam AC, Jones DC, et al. Functional outcome in soft palate reconstruction using a radial forearm free flap in conjunction with a superiorly based pharyngeal flap. Head Neck 1997;19:524Y534 30. Mari A, Arranz C, Gimeno X, et al. Nasal cocaine abuse and centrofacial destructive process: report of three cases including treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002;93:435Y439
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Unusual Complication After Genioplasty Rafael Linard Avelar, MSc,*Þ Carlos Diego Lopes Sa´, DDS,þ Diego Felipe Silveira Esses, DDS,þ Ota´vio Emmel Becker, MSc,* Eduardo Costa Studart Soares, PhD,þ Rogerio Belle de Oliveira, PhD* Abstract: Facial beauty depends on shape, proportion, and harmony between the facial thirds. The chin is one of the most important components of the inferior third and has an important role on the definition of facial aesthetic and harmony in both frontal and lateral views. There are 2 principal therapeutic approaches that one can choose to treat mental deformities, alloplastic implants, and mental basilar ostectomy, also known as genioplasty. The latest is more commonly used because of great versatility in the correction of three-dimensional deformities of the chin and smaller taxes of postoperative complications. Possible transoperative and postoperative complications of genioplasty include mental nerve lesion, bleeding, damage to tooth roots, bone resorption of the mobilized segment, mandibular fracture, ptosis of the lower lip, and failure to stabilize the ostectomized segment. The study presents 2 cases of displacement of the osteotomized segment after genioplasty associated with facial trauma during postoperative orthognathic surgery followed by rare complications with no reports in the literature. Key Words: Genioplasty, chin, esthetics
F
acial beauty depends on the shape, proportion, position, and harmony of the facial thirds. The chin is one of the main anatomical structures of the lower third occupying a prominent position and influencing the definition of facial aesthetics and harmony, both in front and profile views.1 Chin surgery can be performed to refine orthognathic surgery, to provide an aesthetic gain of the technique or as an isolated aesthetic procedure in patients with satisfactory maxillomandibular relationship but who have a protruding or retropositioned chin.2 In mild to moderate cases of obstructive sleep apnea syndrome, chin advancement surgery is part of the treatment protocol, contributing to the high level of success.3 Aesthetic modifications to reposition the chin involve the lower lip, mentolabial sulcus, soft pogonion, and mentocervical distance.
From the *Oral and Maxillofacial Surgery Department, Pontifı´cia, Universidade Cato´lica do Rio Grande do Sul, Porto Alegre; †Department Faculdade Cato´lica Rainha do Serta˜o, Quixada´; and ‡Department Oral and Maxillofacial Surgery Service, Walter Cantı´dio University Hospital, Federal University of Ceara´, Fortaleza, Brazil. Received August 28, 2013. Accepted for publication November 26, 2013. Address correspondence and reprint requests to Rafael Linard Avelar, MSc, Pontifı´cia Universidade Cato´lica do Rio Grande do Sul, Av. Ipiranga, 6681, Porto Alegre/RS, Brazil CEP 90619-900; E-mail: [email protected] The authors report no conflicts of interest. Copyright * 2014 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000000618
* 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
