Office-based esophagoscopy: a preliminary report.

OBJECTIVE: Preliminary study that describes unsedated, transnasal esophagoscopy (TNE) in an office setting. STUDY DESIGN AND SETTING: TNE was prospectively performed on 14 consecutive out-patients with dysphagia whose initial oropharyngeal dysphagia evaluation was insufficient to reveal the cause of their swallowing problem. TNE was carried out without conscious sedation while the patients were sitting in an examining chair. Ease of endoscope insertion, optical quality of images, and examination findings were assessed. Heart rate before and after the procedure and incidence of epistaxis and airway compromise was also determined. Patients were asked to rate the level of discomfort of TNE on a validated 10-point scale (1 representing none/well tolerated and 10 severe/poorly tolerated). RESULTS: All patients completed TNE with the esophagus readily intubated and esophageal mucosa clearly visualized. Findings included esophageal stricture, patulous upper esophageal sphincter, and Zenker's diverticulum. There were no incidences of epistaxis or airway compromise and no significant changes in heart rate. Overall tolerance of TNE was rated by the patients as 2.0 (SD, 1.2). CONCLUSIONS: TNE is well tolerated and can be safely performed in patients with dysphagia in an office setting. TNE may have a role in the comprehensive evaluation of the dysphagic patient in the office.

Free radical production by antibiotic-killed bacteria in the guinea pig middle ear.

OBJECTIVES: Oxygen free radicals are implicated in the pathogenesis of otitis media Recent investigations with animal models have demonstrated that free radical-mediated damage of the middle ear mucosa, measured as lipid hydroperoxide, occurs when the middle ear cavity is inoculated with Streptococcus pneumoniae. The present study was conducted to examine the effect of antibiotics on free radical-mediated damage in pneumococcal acute otitis media. STUDY DESIGN: Animal model of acute otitis media. METHODS: Seventy-eight guinea pigs underwent bilateral middle ear inoculation with 100 microl of 1) sterile saline as a control, 2) 50 microg/mL amoxicillin, 3) 10(7) colony forming units (CFU)/mL Streptococcus pneumoniae killed with 50 microg/mL amoxicillin, or 4) 10(7) CFU/mL S. pneumoniae. Animals were killed on postoperative day 1 or 5, and the middle ear mucosa was examined for lipid peroxidation as evidence of free radical damage. RESULTS: Mucosal lipid hydroperoxide was significantly elevated compared with control subjects on day 1 in both the antibiotic-killed S. pneumoniae group and the S. pneumoniae-infected group. On day 5, the S. pneumoniae-infected mucosa had significantly higher lipid hydroperoxide levels compared with the antibiotic-killed group and the control subjects. Histological studies confirmed mucosal edema and the presence of inflammatory cells in the infected groups. CONCLUSIONS: Antibiotic-killed bacteria seem to produce free radical-mediated damage to the middle ear mucosa in the early phase of acute otitis media. The clinical implication of this study is that free radical damage to the middle ear mucosa may occur in otitis media despite appropriate antibiotic therapy.

Nonsusceptible Streptococcus pneumoniae in children with chronic otitis media with effusion and recurrent otitis media undergoing ventilating tube placement.

CONTEXT: Children with chronic otitis media are at risk for nonsusceptible Streptococcus pneumoniae (NSP) infection. If these children undergo ventilating tube placement, there is an opportunity to culture middle ear fluid and the nasopharynx to determine carriage of NSP. OBJECTIVE: To determine the incidence of NSP carriage, NSP antibiotic susceptibility and risk factors for NSP carriage in children with chronic otitis media undergoing tube placement. DESIGN AND SETTING: Prospective cohort study in an academic medical center with recruitment of patients from an otolaryngology private practice and clinic. PATIENTS: Children < 18 years of age undergoing tube placement for chronic otitis media. INTERVENTIONS: Myringotomy and tube placement, with culture of middle ear fluid and nasopharynx. MAIN OUTCOME MEASURES: The incidence of NSP cultured from the middle ears and nasopharynx of recruited subjects with the use of the minimum inhibitory concentration break points for penicillin susceptibility recommended by the National Committee for Clinical Laboratory Standards. RESULTS: S. pneumoniae was identified in at least 1 site from 23 of 300 study subjects (7.6%); of these 23, 12 case subjects (52.2%) harbored NSP. Of the risk factors assessed by preoperative questionnaire, only younger age was associated with NSP colonization (P < 0.0001). Of the six oral cephalosporins studied, cefpodoxime and cefuroxime showed good in vitro activity against S. pneumoniae isolates with intermediate penicillin resistance. CONCLUSIONS: Children with chronic otitis media undergoing tube placement may carry NSP and provide a means of monitoring the incidence of NSP and antibiotic susceptibilities for children with ear infections in their communities. Younger age is a risk factor for NSP carriage in this population.

Lipid peroxides in middle ear fluid after acute otitis media in guinea pigs.

Oxygen free radical damage has been demonstrated in the middle ear mucosa of a guinea pig model of acute otitis media (AOM). Potential sources of free radicals include both neutrophils responding to infection and Streptococcus pneumoniae, a common AOM pathogen. This project was conducted to examine the middle ear fluid in a guinea pig model of AOM for evidence of elevated lipid peroxide (LPO) as a marker of free radical damage. Twenty-one guinea pigs were injected transtympanically with bacteria into the left (infected) middle ear cavity and sterile saline into the right (control) middle ear. Middle ear fluid was recovered on postoperative day 5. The fluid was weighed and analyzed for quantity of LPO. Results indicated an increased absolute level of LPO, as well as an increased level of LPO divided by the weight of the fluid recovered. Histologic examination confirmed leukocyte infiltration and mucosal edema that were consistent with mucosal damage. While free radical damage to the middle ear mucosa in a guinea pig model of AOM is well documented, this is the first study to demonstrate evidence of free radical damage in middle ear fluid. These results are relevant because they correlate mucosal damage with lipoperoxidation in fluid. Additionally, this serves as an important precursor to human studies, since middle ear fluid is readily available in patients with otitis media.

Evidence of oxygen free radical damage in human otitis media.

Recent work with a guinea pig model of otitis media has demonstrated evidence of oxygen free radical damage to the middle ear mucosa. However, the relevance of an animal model to human disease is uncertain. Accordingly, the following pilot study was conducted to examine human middle ear fluid for lipid hydroperoxides as evidence of free radical damage. Thirty-five specimens of middle ear fluid from children with chronic otitis media were collected and described as mucoid (n = 19), purulent (n = 10), or serous (n = 6); specimens were weighed and analyzed for lipid hydroperoxide content. The results demonstrated the presence of lipid hydroperoxide in all 3 types of middle ear fluid. Additionally, there was a statistically significant elevation of total lipid hydroperoxide content in mucoid effusions compared with serous effusions, as well as a significant elevation of lipid hydroperoxide divided by weight of purulent effusions compared with serous effusions. This is the first study to document free radical damage in human otitis media.

Retropharyngeal abscess and Epstein-Barr virus infection in children.

A 6-year retrospective chart review was conducted of all pediatric patients with the diagnosis of retropharyngeal abscess (RPA) at the Columbia-Presbyterian Medical Center. The charts were examined for signs, symptoms, and serologic findings consistent with recent acute Epstein-Barr virus (EBV) infection. Of the 7 patients we studied, 4 had elevated immunoglobulin G antibodies that were consistent with recent acute EBV infection, and 3 patients were not tested. The 4 patients with positive titers also presented with signs typical for acute EBV infection, including fever (3/4), lymphadenopathy (4/4), and pharyngitis (4/4). Of note, the 2 patients who were older than expected for RPA (ages 18 and 11) had the most severe infections. We submit that there may be a role for EBV infection in the pathogenesis of RPA formation in children. Increasing age may correlate with a more severe infection in this setting.

Effects of 21-aminosteroid U-74389G on acute otitis media in a guinea pig model.

Free radicals participate in the development of disease under inflammatory conditions. Lipid peroxides such as malondialdehyde are regarded as markers of cell membrane damage by oxidative stresses. Previous work from our laboratory has demonstrated that lipidperoxidation is increased in acute otitis media in guinea pigs, implicating a role for free radicals as contributors to inflammation. In this study we examined the effect of lazaroid U-74389G, a 21-aminosteroid, on acute otitis media in guinea pigs. Streptococcus pneumoniae organisms were inoculated into the right tympanic cavity; sterilized phosphate-buffered saline solution was injected into the left ear to serve as a control. The guinea pigs were given intraperitoneal injections of 40 mg/kg of a lazaroid compound or its vehicle every 12 hours. Middle ear mucosa was collected and used for assay. We quantified lipid peroxide by means of the methylene blue-hemoglobin method and by means of measurement of thiobarbituric acid reactive substance. Lazaroid significantly (p < 0.05) suppressed production of lipid hyproperoxide of the middle ear mucosa of the guinea pigs with acute otitis media for up to 24 hours. These results suggest that lazaroid may reduce lipoperoxidation in the middle ear at an early stage of acute otitis media.

Hydrogen peroxide in acute otitis media in guinea pigs.

Evidence has emerged that oxygen free radicals contribute to middle-ear mucosa damage in acute otitis media (AOM). Streptococcus pneumoniae is the most common pathogen in AOM and produces hydrogen peroxide, a free radical intermediate, as it grows. To better characterize the mechanism of free radical damage in AOM, an experiment was conducted to examine the production of hydrogen peroxide. Thirty-two guinea pigs were injected transtympanically with bacteria in the left (infected) middle ear and sterile saline into the right (control) middle ear. Middle-ear fluid was removed and analyzed for quantity of hydrogen peroxide. Results indicated significantly greater hydrogen peroxide levels in infected versus control middle-ear fluid at 6, 12, and 24 h. Likely sources of hydrogen peroxide include both the neutrophil response to infection and pneumococcal growth and death.

Time course of perfusion-induced myocardial edema resolution in rats.

Previous studies have demonstrated that crystalloid coronary perfusion can cause myocardial edema, but the time required for resolution of this edema has not been defined. Accordingly, studies were conducted in 30 rats. Myocardial edema was induced by coronary perfusion with 20 cc/kg of Plegisol (294 mOsm/liter) during aortic occlusion, which produced diastolic arrest. This was followed by whole blood reperfusion, which restored normal contractile function. Duration of reperfusion in minutes was zero (group 0, n = 6), one (group 1, n = 6), five (group 5, n = 6), or fifteen (group 15, n = 6). A control group (n = 6) was studied without edema or reperfusion. Data included heart weight and myocardial water content. Left ventricular pressure-volume curves were measured in groups 1, 5, and 15. Myocardial water content increased significantly from 75.7 +/- 0.5% (SD) in the control group to 79.7 +/- 1.1% (P < 0.05) in group 0 and then decreased significantly to 77.3 +/- 0.7, 75.2 +/- 1.4, and 75.3 +/- 1.6% in groups 1, 5, and 15, respectively. Water content in group 1 was also significantly greater than in groups 5 and 15. Heart weight changes were not statistically significant. Normalized pressure-volume relationships shifted rightward with increasing reperfusion time, but changes were not statistically significant. We conclude that edema induced by crystalloid coronary perfusion of the arrested heart resolves in the beating heart after less than 5 min of blood reperfusion.