Conclusion: This form of treatment provides a less-invasive option with a more concrete evaluation of the venous abnormality and its drainage during venous aneurysm occlusion.
MATERIALS AND METHODS: A retrospective review of 22 TEPs was performed between January 1998 and December 2008. The timing of TEP, type of voice prosthesis, surgical and prosthesis-related complications, and TEP closure were noted.
RESULTS: Eighteen percent of the patients underwent primary and 82% secondary TEP. Our patients were predominantly males (95.4%) of Chinese descent with a mean age of 62.1 years. The types of voice prostheses used were ProvoxTM (n = 15), Voicemasters (n = 6), and Blom-Singer (n = 1). Prosthesis- related complications occurred in 77.3%. Notable complications were leakage (82.5%), prosthesis displacement (41.2%), intractable aspiration (29.4%), and aspiration of prosthesis (23.5%). The most common surgical-related complication was tracheostomal stenosis. An array of interventions comprising resizing or changing prosthesis type, nasogastric catheter insertion, stomaplasty, purse string suturing, and bronchoscopic removal of bronchial aspirated prosthesis were implemented to address encountered complications. In a mean follow-up of 34.8 months, 68.2% of patients achieved functional tracheoesophageal speech (75% of primary TEP and 67% of secondary TEP). There were 7 TEP closures indicated by persistent leakage, recurrent dislodgement, phonatory failure and, in 1 patient, persistent pain.
CONCLUSIONS: TEP has become an integral part in the rehabilitation of a laryngectomee. However, management of the frequent complications related to TEP requires specific efforts and specialistic commitments in order to treat them.
METHODS: Mice were dosed intraperitoneally with mefenamic acid either as a single dose (100 or 200 mg/kg in 10% Dimethyl sulfoxide/Palm oil) or as single daily doses for 14 days (50 or 100 mg/kg in 10% Dimethyl sulfoxide/Palm oil per day). Venous blood samples from mice during the dosing period were taken prior to and 14 days post-dosing from cardiac puncture into heparinized vials. Plasma blood urea nitrogen (BUN) and creatinine activities were measured.
RESULTS: Single dose of mefenamic acid induced mild alteration of kidney histology mainly mild glomerular necrosis and tubular atrophy. Interestingly, chronic doses induced a dose dependent glomerular necrosis, massive degeneration, inflammation and tubular atrophy. Plasma blood urea nitrogen was statistically elevated in mice treated with mefenamic acid for 14 days similar to plasma creatinine.
CONCLUSION: RESULTS from this study suggest that mefenamic acid as with other NSAIDs capable of producing nephrotoxicity. Therefore, the study of the exact mechanism of mefenamic acid induced severe nephrotoxicity can be done in this animal model.