Delayed facial nerve weakness after intact canal wall tympanomastoidectomy.

OBJECTIVE: To find the etiology, frequency, and prognosis of delayed facial nerve weakness (DFW) in our department after intact canal wall tympanomastoidectomy for a tubotympanic (TT) type of chronic suppurative otitis media (CSOM) without cholesteatoma. STUDY DESIGN: Retrospective case review. SETTING: Tertiary care center. SUBJECTS AND METHODS: A total of 315 patients who underwent intact canal wall tympanomastoidectomy for TT type of CSOM without cholesteatoma in our department for the past 3 years were selected. Patients with facial nerve weakness after 72 hours of surgery were noted and assessed for a history of herpes zoster virus infection. There were 6 patients who developed DFW; of these, blood samples of 4 patients for serum antibody titers to varicella zoster virus and herpes simplex type 1 were sent on the 3rd day of developing DFW. Blood samples of each of the remaining 2 patients were sent on the 13th day and 1st day of developing DFW. All 6 patients were treated with prednisolone and acyclovir, and their prognosis was assessed. MAIN OUTCOME MEASURE: House-Brackmann facial nerve grading system and serum antibody titers for varicella zoster virus and herpes simplex type 1. RESULTS: Six patients (1.9%) developed DFW in this study. All patients had a history of herpes zoster virus infection. Serology results of 4 patients showed positive immunoglobulins M and G for varicella zoster virus and had significantly elevated titers of serum immunoglobulin G for varicella zoster virus, thus confirming the etiology. CONCLUSION: The incidence of DFW after tympanomastoidectomy is low and is due to viral reactivation, that is, varicella zoster. The overall prognosis seems impressive because all of the patients' facial nerve function improved by the end of 6 weeks. This study also illustrates the medicolegal importance of informing the patients with a history of herpes zoster virus infection the chance of developing DFW after undergoing tympanomastoidectomy.

[Microbial biocenoss in chronic purulent otitis media].

The objective of the present work was to study microflora in the middle ear of 100 patients aged from 30 to 70 years presenting with chronic purulent otitis media (CPOM) by microbiological and genetic (PCR) methods. An important role of persistence factors, pathogenicity, and microbial antibiotic resistance in the development of CPOM was demonstrated. The frequency of occurrence of herpes and papilloma viruses was estimated. The most common form of the mixed infection was two-component virobacterial associations (46.2%). Three-component associations of viruses with bacteria (Chlamydiae or Mycoplasmas) formed less frequently (34.6%). In 19.2% of the cases, yeast-like fungi of the genus Candida were identified in these associations.

Inner ear and facial nerve complications of acute otitis media with focus on bacteriology and virology.

CONCLUSION: Among 20 patients with inner ear complications and/or peripheral facial palsy secondary to acute otitis media (AOM) a proven or probable bacteriological cause was found in 13 (65%). In seven patients (35%), a proven or probable viral cause was found. Only two of the patients (10%), with a proven bacterial AOM and a clinical picture of a purulent labyrinthitis in both, together with a facial palsy in one, had a substantial degree of dysfunction. Although the number of patients in this study is relatively low our findings show that inner ear complications and facial palsy due to AOM can be of both bacterial and viral origin. Severe sequelae were found only where a bacterial origin was proven. OBJECTIVES: Inner ear complications and/or peripheral facial palsy secondary to AOM are rare. The general understanding is that they are due to bacterial infections. However, in some of these patients there are no clinical or laboratory signs of bacterial infections and they have negative bacterial cultures. During recent years different viruses have been isolated from the middle ear or serologically proven in AOM patients and are thought to play a pathogenetic role. We suggest that in some cases of AOM complications from the inner ear and the facial nerve can be caused by viruses. The purpose of our study was to analyze infectious agents present in patients with inner ear complications and/or facial palsy arising from AOM. PATIENTS AND METHODS: The medical records of 20 patients who had inner ear complications and/or facial palsy following AOM ( unilateral in 18, bilateral in 2) between January 1989 and March 2003 were evaluated. Bacterial cultures were carried out for all patients. Sera from 12 of the patients were stored and tested for a battery of specific viral antibodies. In three patients, investigated between November 2002 and March 2003, viral cultures were also performed on samples from the middle ear and nasopharynx. RESULTS: Nineteen patients had inner ear symptoms. Eight of them had a unilateral sensorineural hearing loss and vertigo, three had vertigo as an isolated symptom and one, with bilateral AOM, had bilateral sensorineural hearing loss. Seven patients had a combination of facial palsy and inner ear symptoms (unilateral sensorineural hearing loss in three, unilateral sensorineural hearing loss and vertigo in two, bilateral sensorineural hearing loss and vertigo in one, with bilateral AOM, and vertigo alone in one). One patient had an isolated facial palsy. Healing was complete in 11 of the 20 patients. In seven patients a minor defect remained at follow-up (a sensorineural hearing loss at higher frequencies in all). Only two patients had obvious defects (a pronounced hearing loss in combination with a moderate to severe facial palsy (House-Brackman grade 4) in one, distinct vestibular symptoms and a total caloric loss in combination with a high-frequency loss in the other. Eight patients had positive bacteriological cultures from middle ear contents: Streptococcus pneumoniae in two, beta-hemolytic Streptococcus group A in two, beta-hemolytic Streptococcus group A together with Staphylococcus aureus in one, Staph. aureus alone in one and coagulase-negative staphylococci (interpreted as pathogens) in two. In the 12 patients with negative cultures, there was a probable bacteriological cause due to the outcome in SR/CRP and leukocyte count in five. In four patients serological testing showed a concomitant viral infection that was interpreted to be the cause (varicella zoster virus in two, herpes simplex virus in one and adenovirus in one.) In three there was a probable viral cause despite negative viral antibody test due to normal outcome in SR/CRP, normal leukocyte count, serous fluid at myringotomy and a relatively short pre-complication antibiotic treatment period.