Measurements of peak inspiratory flow obtained through the tracheostomy cannula (MIFT) during tidal breathing were compared to peak inspiratory flow measurements obtained through the mouth (MIFM) in 40 children to assess physiologic readiness to decannulate the tracheostomized pediatric patient. Ratio of peak flow MIFM/MIFT was 1.40 for 34 successfully decannulated children compared to 0.83 for 22 unsuccessful attempts (p less than 0.01). Tidal flow measurements are highly predictive (84%) in identifying children who are unlikely to be ready for decannulation. A schema is proposed to utilize tidal flow measurements as the first step in the decannulation process.

Quinolinic acid (QUIN) is an endogenous metabolite that exerts a neurotoxic effect by binding to specific neuronal receptors. Studies involving a broad spectrum of infectious and inflammatory central nervous system diseases have suggested a role for QUIN in causing neuronal injury. Since there is evidence for presence of the QUIN receptor in mammalian cochleas, QUIN was measured in middle ear effusions (MEEs). Gas chromatography/mass spectrometry detected QUIN in each of 65 diluted human MEEs, with a mean of 482 +/- 75 (SEM) nmol/L and a range from 15 to 2667 nmol/L. QUIN was also detected in each of 197 chinchilla MEEs from five different models of otitis media, with a mean of 10.6 +/- 1.3 (SEM) mumol/L and a range from 0.23 to 146.0 mumol/L (corrected for dilution). To determine whether QUIN causes sensorineural hearing loss (SNHL), QUIN solutions were placed on round window membranes (RWM) for 20 to 240 minutes, in 20 chinchillas. SNHL was detected by electrocochleography in QUIN-exposed animals, but not in saline controls. We conclude that QUIN is present in MEEs and that QUIN in the middle ear has the potential to cross the RWM and cause sensorineural hearing loss, possibly by binding to specific neuronal receptors in mammalian cochleas.

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