Postsurgical Alar Retraction: Etiology and Treatment.

The cephalic trim technique is a popular maneuver that often leads to tip deformities, most notably postsurgical alar retraction (PSAR). We advocate using the external rhinoplasty approach to correct PSAR by (1) releasing and repositioning the retracted alar margin, (2) strengthening and immobilizing the central tip complex using a septal extension graft, (3) suspending and longitudinally tightening the mobilized lateral crural remnant by adjusting crural length to match the sidewall span, and (4) providing direct skeletal support to the repositioned alar margin using articulated alar rim grafts. Using this structural treatment paradigm, we have corrected severe PSAR in the preponderance of secondary rhinoplasty cases.

D-amino acids do not inhibit Pseudomonas aeruginosa biofilm formation.

OBJECTIVE: Pseudomonas aeruginosa, a known biofilm-forming organism, is an opportunistic pathogen that plays an important role in chronic otitis media, tracheitis, cholesteatoma, chronic wounds, and implant infections. Eradication of biofilm infections has been a challenge because the biofilm phenotype provides bacteria with a protective environment from the immune system and antibiotics; thus, there has been great interest in adjunctive molecules that may inhibit biofilm formation or cause biofilm dispersal. There are reports that D-amino acids may inhibit biofilms. In this study, we test the ability of various D-amino acids to inhibit P. aeruginosa biofilm formation in vitro. STUDY DESIGN: We evaluated the effect of D-alanine (10 mM), D-leucine (10 mM), D-methionine (10 mM), D-tryptophan (10 mM), and D-tyrosine (10 uM and 1 mM) on biofilm formation in two commonly studied laboratory strains of P. aeruginosa: PAO1 and PA14. METHODS: Biofilms were grown in 24-well and 96-well tissue culture plates, documented photographically and stained with 0.1% crystal violet and solubilized in 33% glacial acetic acid for quantification. RESULTS: In strains PAO1 and PA14, the addition of D-amino acids did not result in an inhibitory effect on biofilm growth in 24-well plates. Repeating the study in 96-well plates confirmed our findings that D-amino acids do not inhibit biofilm formation of P. aeruginosa. CONCLUSION: We conclude that D-amino acids only slow the production of biofilms rather than completely prevent biofilm formation; therefore, D-amino acids represent a poor option for potential clinically therapeutic interventions. LEVEL OF EVIDENCE: N/A.

Otoconia and otolithic membrane fragments within the posterior semicircular canal in benign paroxysmal positional vertigo.

OBJECTIVES/HYPOTHESIS: Benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder with an incidence between 10.7 and 17.3 per 100,000 persons per year. The mechanism for BPPV has been postulated to involve displaced otoconia resulting in canalithiasis. Although particulate matter has been observed in the endolymph of affected patients undergoing posterior canal occlusion surgery, an otoconial origin for the disease is still questioned. STUDY DESIGN: In this study, particulate matter was extracted from the posterior semicircular canal of two patients and examined with scanning electron microscopy. METHODS: The samples were obtained from two patients intraoperatively during posterior semicircular canal occlusion. The particles were fixed, stored in ethanol, and chemically dehydrated. The samples were sputter coated and viewed under a scanning electron microscope. Digital images were obtained. RESULTS: Intact and degenerating otoconia with and without linking filaments were found attached to amorphous particulate matter. Many otoconia appeared to be partially embedded in a gel matrix, presumably that which encases and anchors the otoconia within the otolith membrane, whereas others stood alone with no attached filaments and matrix. The otoconia measured roughly 2 to 8 µm in length and displayed a uniform outer shape with a cylindrical bulbous body and a 3 + 3 rhombohedral plane at each end. CONCLUSIONS: These findings suggest that the source of the particulate matter in the semicircular canals of patients with BPPV is broken off fragments of the utricular otolithic membrane with attached and detached otoconia. LEVEL OF EVIDENCE: NA Laryngoscope, 127:709-714, 2017.

FleQ, a Transcriptional Activator, Is Required for Biofilm Formation In Vitro But Does Not Alter Virulence in a Cholesteatomas Model.

HYPOTHESIS: Bacterial biofilm formation within cholesteatomas is responsible for increased persistence and tissue destruction and Pseudomonas aeruginosa deficient in biofilm formation (PAO1 ΔfleQ) are less virulent than the parent bacteria. BACKGROUND: Infected aural cholesteatomas have been demonstrated to be more destructive than uninfected cholesteatomas and infections are more persistent. The chronicity and persistence of infections within cholesteatomas may be because of the presence of biofilm formation. METHODS: Twenty-seven mutant strains of PAO1 were screened for surface adherence. These strains were also screened for static biofilm formation. The biofilms were quantified by staining with crystal violet. Aural cholesteatomas were then induced in Mongolian gerbils by ligation of the ear canal. At the time of ligation, the ear canals were inoculated with wild-type PAO1 and a biofilm deficient PAO1 ΔfleQ strain of P. aeruginosa. A 7 weeks course of ciprofloxacin (20 mg/kg/day) was started on postoperative day 7. Eight weeks after induction of cholesteatomas, the cholesteatoma size, levels of bone destruction, and levels of bone remodeling were evaluated using microCT imaging. RESULTS: PAO1 ΔfleQ was identified as a poorly adherent and deficient biofilm forming mutant strain of P. aeruginosa. Infected cholesteatomas had more growth, bone destruction and bone remodeling than uninfected cholesteatomas. However, there was no difference observed between cholesteatomas infected with PAO1 (biofilm competent strain) and PAO1 ΔfleQ (biofilm deficient strain). CONCLUSION: We demonstrate that the biofilm phenotype is not an important virulence factor in cholesteatomas infected with P. aeruginosa.