Septal cartilage defined: implications for nasal dynamics and rhinoplasty.

BACKGROUND: Although the septal cartilage is integral to structural nasal stability, it is routinely violated during septorhinoplasty. This occurs during dorsal hump reduction, caudal septal reduction, submucoperichondrial resection of a deviated septum, or harvesting of cartilage graft material. Despite such routine alteration and/or use, the characteristics of septal cartilage have not been adequately defined. METHODS: By measuring septal length, height, and cartilage thickness mapped out at 5-mm intervals over the entire nasal septum in 11 fresh cadaver specimens, the characteristics of septal cartilage were determined. RESULTS: Septal thickness measurements demonstrated significant differences along the nasal septum, with the greatest thickness along the septal base (2.7 +/- 0.1 mm), followed by intermediate thickness along the septal dorsum (2.0 +/- 0.2 mm) and the least thickness along the central portion (1.3 +/- 0.2 mm) and at the anterior septal angle (1.2 +/- 0.1 mm) (p < 0.001). CONCLUSIONS: These observations clarify several nuances regarding septal structural stability, septal deformities, and the effects of septal alteration during rhinoplasty. The findings of this study reinforce several principles, including recognition of factors contributing to the high propensity of acquired central septal perforations; preservation of a generous L-strut width, especially at the anterior septal angle, or if planning dorsal hump reduction, prudent allocation of harvested septal cartilage; and clarifying the proclivity for supratip deformity following rhinoplasty.

Surgical design and algorithm for correction of earlobe ptosis and pseudoptosis deformity.

A previously described classification system for earlobe ptosis and criterion for earlobe pseudoptosis deformity was based on height measurements of the two earlobe components: the free caudal segment and the attached cephalic segment. The "ideal" ear lobule free caudal segment was found to be between 1 and 5 mm (grade I ptosis), and the "ideal" attached cephalic segment was 15 mm or less. Earlobe pseudoptosis was defined by an attached cephalic segment measuring greater than 15 mm. Previous studies revealed an association between the elongated free caudal segment and increasing patient age and between the elongated attached cephalic segment and rhytidectomy. Sixteen fresh cadaver earlobes were used to design surgical patterns that would differentially reduce the free caudal segment, the attached cephalic segment, or both. A horizontal, medially based triangular excision pattern was designed. Triangular excisions limited to the attached cephalic segment resulted in 98 +/- 5 percent reduction of excision height from the attached cephalic segment but also resulted in an unexpected 32 +/- 2 percent augmentation of the excision height in the free caudal segment. Triangular excisions limited to the free caudal segment resulted in 88 +/- 4 percent reduction of the excision height from the free caudal segment and negligible reduction of 4 +/- 4 percent of excision height in the cephalic attached segment. An algorithm for correction of earlobe ptosis and pseudoptosis was subsequently derived and implemented in a clinical case. The authors propose that surgical treatment of patients with pseudoptosis be dependent on the ptosis grade. If the ptosis is grade I (1 to 5 mm), then excision of only the attached cephalic segment is recommended. If the ptosis is grade II or higher (more than 5 mm), then a combined attached cephalic and free caudal segment excision is recommended. In cases of isolated ptosis grade II or higher without pseudoptosis, then excision location of only the free caudal segment is recommended. The above simple algorithm and surgical designs will enable plastic surgeons to differentially correct earlobe ptosis and pseudoptosis.

Vitamin E reduces cisplatin ototoxicity.

OBJECTIVES/HYPOTHESIS: Cisplatin ototoxicity is a major dose-limiting factor in the treatment of several neoplasms. Vitamin E, a slow-acting free radical scavenger, has been shown to ameliorate nephrotoxicity and endothelial cell damage in animals receiving cisplatin. The purpose of the study was to determine the effectiveness of vitamin E as an otoprotectant. STUDY DESIGN: Prospective, randomized controlled trial in the rat model. METHODS: Wistar rats (weight, 261-386 g) were sedated using 172.4 mg/kg intramuscular ketamine and 3.4 mg/kg xylazine. Baseline auditory brainstem response (ABR) testing was performed in response to clicks and 8-, 16-, and 32-kHz tone bursts. After auditory thresholds were determined, the animals received intraperitoneal drug administration according to one of three group classifications. Group 1 received 4 g/kg vitamin E followed after 30 minutes by 16 mg/kg cisplatin. Group 2 received 6 mL/kg soybean oil followed after 30 minutes by cisplatin. Group 3 received soybean oil followed after 30 minutes by 16 mL/kg saline. After 3 days' follow-up, ABR testing was performed and threshold changes were recorded. Cochleae were removed and processed for scanning electron microscopy after follow-up auditory testing was carried out. RESULTS: Group 2 animals showed marked hearing loss with average threshold shifts of 28.75 +/- 2.3 dB for clicks, 30.0 +/- 1.9 dB at 8 kHz, 21.25 +/- 4.0 dB at 16 kHz, and 45.0 +/- 4.2 dB at 32 kHz. No significant loss was observed in group 3 with shifts of 2 +/- 1.3 dB, 3 +/-3.0 dB, -2.2 +/- 3.1 dB, and -1.1 +/- 4.0 dB for clicks and tone bursts at 8, 16, and 32 kHz, respectively. Significant protection was seen in group 1 animals compared with group 2 animals. In the former group, threshold shifts of 12.5 +/- 3.1 dB for clicks, 7.5 +/- 2.5 dB at 8 kHz, 5.0 +/- 3.3 dB at 16 kHz, and 24.4 +/- 5.6 dB at 32 kHz were observed. These findings were supported by the scanning electron microscope observations that severe outer hair cell destruction occurred in group 2 rats, whereas outer hair cells were preserved to a much greater extent in the cochleae of rats in group 1 that were pretreated with vitamin E. CONCLUSION: Vitamin E appears to have a protective effect against cisplatin ototoxicity.

Volume analysis of preadipocyte injection for vocal cord medialization.

OBJECTIVE: To compare the volume retention of injected preadipocytes with that of standard fat injection in a paralyzed rabbit true vocal cord. STUDY DESIGN: Prospective analysis with blinded data collection. METHODS: Thirteen New Zealand white rabbits were divided into two groups. Group 1 consisted of seven animals undergoing left-side vocal cord paralysis by resection of a 1-cm segment of the left-side recurrent laryngeal nerve and abdominal fat harvest for isolation of preadipocytes. Preadipocytes were cultured under sterile conditions in cell culture media. Animals in group 2 also underwent left-side vocal cord paralysis without fat harvest. After 10 to 14 days, in a second procedure, group 1 underwent injection of 0.1 mL cultured autologous preadipocytes, and group 2 underwent routine injection of 0.1 mL abdominal fat harvested during the same procedure. At 6 and 12 months, volumetric analysis was performed. RESULTS: Volume analysis at 6 months showed a mean volume of 0.029 mL retained fat in group 2 representing a retention of approximately 29% (SD = 0.023) of the original injected volume. Retention in group 1 animals approximated 0.002 mL (SD = 0.0024) or 2% of the injected volume. Analysis at 12 months showed a mean volume of 0.008 mL (SD = 0.0078) in group 2 and of 0.002 mL (SD = 0.0015) in group 1. Group 2 showed significantly higher volumes of the injected fat at 6 and 12 months (P <.033). CONCLUSION: Volumes obtained with standard fat injection were superior to those obtained with preadipocyte injection at both 6 and 12 months.

Self-inflicted vocal cord paralysis in patients with vagus nerve stimulators. Report of two cases.

Vagus nerve stimulation for treatment of epilepsy is considered safe; reports of severe complications are rare. The authors report on two developmentally disabled patients who experienced vocal cord paralysis weeks after placement of a vagus nerve stimulator. In both cases, traction injury to the vagus nerve resulting in vocal cord paralysis was caused by rotation of the pulse generator at the subclavicular pocket by the patient. Traumatic vagus nerve injury caused by patients tampering with their device has never been reported and may be analogous to a similar phenomenon reported for cardiac pacemakers in the literature. As the use of vagus nerve stimulation becomes widespread it is important to consider the potential for this adverse event.