Postoperative Outcomes of Intracapsular Tonsillectomy With Coblation: A Systematic Review and Meta-Analysis.

OBJECTIVE: Following tonsillectomy, postoperative pain and hemorrhage from the tonsillar bed are causes of significant morbidity. Intracapsular tonsillectomy with Coblation is suggested to minimize such morbidity while remaining efficacious in long-term outcomes. This systematic review and meta-analysis assessed short-term morbidity and long-term outcomes from intracapsular tonsillectomy with Coblation, focusing primarily on posttonsillectomy hemorrhage. DATA SOURCES: Medline, Embase, and the Cochrane Library. REVIEW METHODS: Guided by PRISMA guidelines, studies on intracapsular tonsillectomy with Coblation published between December 2002 and July 2022 evaluating frequency of posttonsillectomy hemorrhage were screened. Studies without primary data were excluded. Meta-analysis was conducted using the random-effect model. The primary outcome was the proportion of patients who experienced posttonsillectomy hemorrhage. The secondary outcomes were posttonsillectomy pain, the proportion requiring revision tonsillectomy, and severity of sleep-disordered breathing measured by polysomnography outcomes. RESULTS: From 14 studies there were 9821 patients. The proportion of total posttonsillectomy hemorrhage was 1.0% (95% confidence interval [CI] 0.5%-1.6%, n = 9821). The proportion experiencing primary hemorrhage, secondary hemorrhage, and those requiring further tonsil surgery were 0.1% (95% CI 0.0%-0.1%; study n = 7), 0.8% (95% CI 0.2%-1.4%; study n = 7), and 1.4% (95% CI 0.6%-2.2%; study n = 6), respectively. Mean reduction in apnea-hypopnea index was -16.0 events per hour (95% CI -8.8 to -23.3, study n = 3) and mean increase in oxygen nadir was 5.9% (95% CI 2.6%-9.1%, study n = 3). CONCLUSION: Intracapsular tonsillectomy with Coblation has been demonstrated to have a low rate of posttonsillectomy hemorrhage. Data regarding long-term tonsil regrowth and need for reoperation were encouraging of the efficacy of this technique.

Bacterial microcolonies exist within the sphenoid bone in chronic rhinosinusitis and healthy controls.

BACKGROUND: Some patients with chronic rhinosinusitis (CRS) exhibit thickening of the sinus bones that has been termed osteitis. The histopathology and microbiology of these changes have not been fully described. The aim of this study was to look for the presence of bacteria and immune cells within samples of bone from patients with and without CRS and correlate these findings to radiological findings. METHODS: Bone on the anterior face of the sphenoid was examined radiologically and histologically in 8 patients with CRS with nasal polyposis, 8 patients with CRS without polyposis, and 6 control patients with pituitary adenomas and normal sinuses. Bone thickness and density were measured by computed tomography (CT) scanning. Bone samples were collected intraoperatively and 20 tissue sections were analyzed for each patient. Bacteria were identified by Giemsa and Gram stains. Immune cells were identified by conventional histology and immunohistochemistry. RESULTS: Small colonies of bacteria were identified within the bone in 3 of 16 CRS patients and 2 of 6 control subjects (p = 0.6). Isolated immune cells were identified within the bone in 3 of 16 CRS patients and 2 of 6 control subjects (p = 0.6) but both bacteria and immune cells occurred together in only 1 case. The presence of bacteria or immune cells within bone samples did not correlate with either bone thickness or bone density. CONCLUSION: This study describes the presence of bacteria and immune cells within a minority of CRS patients and normal controls. The bacterial microcolonies identified do not appear to be the cause of the bone changes seen in many CRS patients.

Is chronic rhinosinusitis caused by persistent respiratory virus infection?

BACKGROUND: Many chronic rhinosinusitis (CRS) patients recall an upper respiratory tract infection as the inciting event of their chronic illness. Viral infections have been shown to cause obstruction of the osteomeatal complex, which is likely to be a critical step in the development of CRS. There is clear overlap between the pathogenesis of CRS and asthma. Infections with respiratory viruses in childhood increase the risk of subsequently developing asthma. Viral infections in established asthmatics are associated with acute exacerbations. We sought to determine whether respiratory viruses could be detected within the sinonasal mucosa of CRS patients using polymerase chain reaction (PCR) techniques. METHODS: Sinus mucosa was sampled from 13 patients with CRS and 2 patients with normal sinuses. PCR was used to look for common respiratory viruses (parainfluenza 1, 2, and 3; respiratory syncytial virus [RSV]; human metapneumovirus [hMPV]; adenovirus [ADV]; rhinovirus; coronavirus; bocavirus [BoV]; cytomegalovirus [CMV]; and influenza A and B). RESULTS: No respiratory viruses were detected in any of the samples. CONCLUSION: Persistence of respiratory viruses within the sinonasal mucosa is unlikely to be a cause of ongoing inflammation in CRS. The possibility remains that a transient viral infection provides the initial inflammatory stimulus.

Are biofilms associated with an inflammatory response in chronic rhinosinusitis?

BACKGROUND: Bacterial biofilms have been identified on the sinonasal mucosa of patients with chronic rhinosinusitis (CRS) but also on control samples. Their role in the disease pathogenesis is unproven. The objective of this study was to further evaluate the role of biofilms in CRS by assessing whether they are associated with an inflammatory response. METHODS: Mucosal samples were collected from 18 patients with CRS and 7 normal subjects. Bacteria on the mucosal surface were identified by Gram stain. Immune cells were identified by Giemsa stain and immunohistochemistry (IHC). The number of local immune cells was recorded beneath areas of the mucosal surface both colonized with and free from bacteria. RESULTS: In CRS patients, biofilms that were directly opposed to a disrupted epithelial layer were associated with more T lymphocytes (p = 0.01), and more macrophages (p = 0.003) than areas of mucosa without bacteria present. Biofilms associated with but not directly opposed to the epithelium were not associated with raised numbers of immune cells. CONCLUSION: Not all surface bacterial colonies are associated with a particular inflammatory response in CRS. Biofilms adherent to a disrupted epithelial layer are associated with higher numbers of immune cells and therefore appear to have a role in the pathogenesis of CRS.