C. Arturo Solares

Tachycardia-induced cardiomyopathy

Systolic dysfunction associated with chronic tachyarrhythmias, known as tachycardia-induced cardiomyopathy, is a reversible form of heart failure characterized by left ventricular dilatation that is usually reversible once the tachyarrhythmia is controlled. Its development is related to both atrial and ventricular arrhythmias. The diagnosis is usually made following observation of a marked improvement in systolic function after normalization of heart rate. Clinicians should be aware that patients with unexplained systolic dysfunction may have tachycardia-induced cardiomyopathy, and that controlling the arrhythmia may result in improvement and even complete normalization of systolic function.

Intracapsular Partial Tonsillectomy for Tonsillar Hypertrophy in Children

Objective To review our experience with intracapsular tonsillectomy using powered instrumentation in the management of tonsillar hypertrophy causing obstructive sleep‐disordered breathing in children.

Transoral Robot-Assisted CO2 Laser Supraglottic Laryngectomy: Experimental and Clinical Data

Background: Transoral CO2 laser surgery for selected supraglottic tumors results in improved postoperative function and decreased morbidity, with comparable survival to open surgery. Recently, robot‐assisted techniques have been reported for the management of supraglottic lesions. There are no reports in the English literature of robotic technology coupled with CO2 laser technology. Our objective was to report the use of such technology.

Murine autoimmune hearing loss mediated by CD4+ T cells specific for inner ear peptides

Autoimmune sensorineural hearing loss (ASNHL) is characterized typically by bilateral, rapidly progressive hearing loss that responds therapeutically to corticosteroid treatment. Despite its name, data implicating autoimmunity in the etiopathogenesis of ASNHL have been limited, and targeted self-antigens have not been identified. In the current study we show that the inner ear-specific proteins cochlin and beta-tectorin are capable of targeting experimental autoimmune hearing loss (EAHL) in mice. Five weeks after immunization of SWXJ mice with either Coch 131-150 or beta-tectorin 71-90, auditory brainstem responses (ABR) showed significant hearing loss at all frequencies tested. Flow cytometry analysis showed that each peptide selectively activated CD4(+) T cells with a proinflammatory Th1-like phenotype. T cell mediation of EAHL was determined by showing significantly increased ABR thresholds 6 weeks after adoptive transfer of peptide-activated CD4(+) T cells into naive SWXJ recipients. Immunocytochemical analysis showed that leukocytic infiltration of inner ear tissues coincided with onset of hearing loss. Our study provides a contemporary mouse model for clarifying our understanding of ASNHL and facilitating the development of novel effective treatments for this clinical entity. Moreover, our data provide experimental confirmation that ASNHL may be a T cell-mediated organ-specific autoimmune disorder of the inner ear.

Increased Frequencies of Cochlin-Specific T Cells in Patients with Autoimmune Sensorineural Hearing Loss

Autoimmune sensorineural hearing loss (ASNHL) is the most common cause of sudden hearing loss in adults. Although autoimmune etiopathogenic events have long been suspected in ASNHL, inner ear-specific Ags capable of targeting T cell autoreactivity have not been identified in ASNHL. In this study, we show by ELISPOT analysis that compared with normal hearing age- and sex-matched control subjects, ASNHL patients have significantly higher frequencies of circulating T cells producing either IFN-γ (p = 0.0001) or IL-5 (p = 0.03) in response to recombinant human cochlin, the most abundant inner ear protein. In some patients, cochlin responsiveness involved both CD4+ and CD8+ T cells whereas other patients showed cochlin responsiveness confined to CD8+ T cells. ASNHL patients also showed significantly elevated cochlin-specific serum Ab titers compared with both normal hearing age- and sex-matched control subjects and patients with noise- and/or age-related hearing loss (p < 0.05 at all dilutions tested through 1/2048). Our study is the first to show T cell responsiveness to an inner ear-specific protein in ASNHL patients, and implicates cochlin as a prominent target Ag for mediating autoimmune inner ear inflammation and hearing loss.

Transnasal endoscopic resection of lesions of the clivus: a preliminary report.

Objective: To review our experience with transnasal endoscopic resection of clival lesions.

Interferon-γ production to inner ear antigens by T cells from patients with autoimmune sensorineural hearing loss

Autoimmune sensorineural hearing loss (ASNHL) typically produces bilateral rapidly progressive loss of hearing over a few days or weeks, but may also produce sudden loss over a few hours. The diagnosis is made by excluding ototoxicity, systemic disease, and other factors that mimic ASNHL and by showing a therapeutic response to corticosteroid treatment. Antibody production and T-cell proliferative responses to inner ear antigens have been implicated in the etiopathogenesis of ASNHL. In the current study, we have extended these autoimmune investigations by determining the frequencies of inner ear specific IFN-γ producing T cells in peripheral blood mononuclear cells (PBMC) from ASNHL patients and from age- and sex-matched control subjects. ELISPOT analysis showed that 25% of ASNHL patients have significant increased frequencies of inner ear specific IFN-γ producing T cells in their PBMC. All control subjects were relatively unresponsive. Our results implicate inner ear specific IFN-γ producing proinflammatory T cells in the pathogenesis of ASNHL.

Autoimmune sensorineural hearing loss: an immunologic perspective

Autoimmune sensorineural hearing loss (ASNHL) typically produces a bilateral rapidly progressive loss of hearing that may occur suddenly. The diagnosis is made by excluding ototoxicity, systemic disease, and other factors that mimic ASNHL and by showing a therapeutic response to corticosteroid treatment. Although autoantibodies and autoreactive T cells have been implicated in the etiopathogenesis of ASNHL, several central issues remain unresolved, including the relative prominence of B cell or T cell autoimmunity in the initiation and progression of ASNHL, the identity of the putative inner ear self-antigen(s) that target ASNHL, and the development and application of immunosuppressive therapies for preventing the progressive hearing loss which may be profound and require cochlear implantation. In this review, we will examine the seminal human and animal studies that have led to our current views regarding the autoimmune etiopathogenesis of ASNHL. In addition, we will address the need for developing an inner ear-specific mouse model for ASNHL that may define the stages leading to the development of ASNHL and may also provide new diagnostic markers and help develop novel and effective treatments for preventing progressive hearing loss in ASNHL.

Starplasty: revisiting a pediatric tracheostomy technique.

OBJECTIVE: To determine the efficacy the “starplasty” pediatric tracheostomy technique in reducing the incidence of major complications and tracheotomy-related death. METHODS: Retrospective chart analysis of all the cases of starplasty performed at 2 tertiary care centers between 1990 and 2002. RESULTS: There were 94 children in our cohort ranging in age from 2 days to 14 years. Of the patients, 47 (50%) were females and 47 (50%) were males and 60 of the children (64%) were younger than 1 year of age. Forty-one patients (44%) had neurologically related airway problems as their primary indication for tracheostomy, 34 (36%) had upper airway obstruction, and the remainder had pulmonary diseases, prolonged intubation, or metabolic-related airway problems. There were 41 short-term complications including 5 cases of tracheal tube dislodgement. There were no instances of pneumothorax or tracheostomy-related death. There were 26 long-term complications. There were no cases of clinically relevant suprastomal collapse that compromised decannulation and no instances of tracheal stenosis. Twenty-six patients underwent decannulation, all of whom developed a tracheocutaneous fistula (TCF). Two patients had spontaneous closure of the TCF; 9 patients underwent surgical repair of their fistulas, 53 patients remain tracheostomy-dependent, and 8 patients died of their primary disease. CONCLUSION: The need for pediatric tracheotomy has increased as a consequence of our success in treating chronically ill children. Starplasty reduces the incidence of major complications, including pneumothorax and death from accidental decannulation. Its major drawback is the need for secondary reconstruction of a tracheocutaneous fistula. EBM rating: C.

Lateral Lamella of the Cribriform Plate: Software-Enabled Computed Tomographic Analysis and Its Clinical Relevance in Skull Base Surgery

OBJECTIVEnTo describe a quantitative analysis of the lateral lamella of the cribriform plate (LLCP) height in computed tomographic (CT) images. The LLCP is the thinnest anatomic structure in the skull base.nnnDESIGNnSoftware-enabled CT scan measurements.nnnSETTINGnAcademic center.nnnRESULTSnThe CT scans from 50 patients were analyzed. The median height of the LLCP in 100 sides was 2.4 mm. The LLCP height was 0 to 3.9 mm in 83 sides, 4.0 to 7.0 mm in 15 sides, and greater than 7.0 mm in 2 sides. When analyzing differences among sides, the LLCP height was greater on the right side in 28 patients and greater on the left side in 22. The differences between sides was 0 to 1.9 mm in 39 patients, 2.0 to 3.9 mm in 9 patients, and greater than 4.0 mm in 2 patients.nnnCONCLUSIONSnComputer-aided CT scan analysis allows for a quantitative analysis of the paranasal sinus skull base anatomy. Knowledge of these dimensions is invaluable during surgical planning and navigation. Asymmetry of the relative ethmoid roof position is common. Thus, the rhinologic surgeon must exercise caution to prevent unintentional skull base injury and cerebrospinal fluid leak.