Frequency, causes, and outcome of home ventilator failure

STUDY OBJECTIVES: The safety of home ventilators has been questioned. We collected data to study the following: frequency of home ventilator failure, apparent causes for the failure or malfunction, and adverse consequences following the failure. STUDY DESIGN: Information on all requests to correct home ventilator failures reported to a home respiratory equipment vendor was collected prospectively between November 1991, and November 1992. PATIENTS: There were 150 ventilator-assisted patients aged 2 to 77 years; 44 were < or = 18 years. They received 841,234 h of home mechanical ventilation (average, 15.4 h/d per ventilator-assisted patient). RESULTS: There were 189 reports of home ventilator failure. Defective equipment or mechanical failure was found in only 39% (73 reports), equivalent to one home ventilator failure for every 1.25 years of continuous use. Other causes of ventilator failure included the following: improper care, damage, or tampering with the ventilator by caregivers (13%), functional equipment improperly used by caregivers (30%), and equipment functional but the patient's condition changed, mimicking ventilator failure (3%). No problem could be identified in 16%. The following actions were required: ventilator replacement (44%), repair of a defective part (6%), replacement of a functioning ventilator for psychological comfort (14%), ventilator adjustments made (21%), caregiver reeducation (7%), caregiver anxiety or distress reduced (3%), and no action required (4%). Hospitalization was required only in two cases (1%). No adverse outcomes, deaths, or serious injuries were associated with home ventilator failure. CONCLUSIONS: We conclude that in 150 patients requiring home mechanical ventilation, ventilator failure occurred relatively infrequently, and there were no adverse outcomes as a result of equipment failure at home. We speculate that equipment failure is not a frequent or serious problem for ventilator-assisted patients treated at home.     

Physical interpretation of information entropy: Numerical evidence of the Collins conjecture

The effect of altering the dietary Ca:P ratio during critical points of growth (based on reproductive and skeletal age) on kidney calcification in female rats was investigated. Groups of weanling animals were fed one of three nutritionally complete but calcium-altered diets (0.25, 0.5 or 1.0 g Ca/100 g diet) from 4 to 12 wk of age (Phase 1). Phosphorus concentration remained constant at 0.4 g/100 g diet resulting in Ca:P molar ratios of 0.48, 0.96 and 1.92, respectively. During Phase 2, the same animals within each diet group were then rerandomized into one of the above diets and fed for an additional 25 wk. Each group contained five rats. The data from the nine treatment groups were analyzed statistically using a two-way ANOVA (Phase 1 dietary Ca level by Phase 2 dietary Ca level). The level of dietary Ca during Phase 1 only exerted a significant influence on kidney Ca accumulation. Rats fed the two lower dietary Ca levels, and hence lower dietary Ca:P molar ratios, during Phase 1 had two- to threefold greater kidney Ca concentration and kidney ash Ca concentration than rats fed the diet with the highest dietary Ca level (1.92 Ca:P molar ratio) during Phase 1, regardless of the Ca intake during Phase 2. In contrast, the dietary Ca:P molar ratio during Phase 2 had little effect either positively or negatively on the kidney Ca concentration that had been established during Phase 1. The results indicate that dietary-induced nephrocalcinosis in female rats is irreversible and is induced primarily before the completion of adolescence (approximately 12 wk of age) in Sprague-Dawley female rats.     

Identification and localization of type IV collagen chains in the inner ear cochlea

The expressions of cysteine dioxygenase (CDO) gene in the liver, lung, skeletal muscle, and kidney were studied by in situ hybridization with a cDNA probe from rat liver CDO under normal conditions. Significant expression of the CDO gene was detected in the liver, lung, and kidney, but not skeletal muscle. In the liver, the signal was confined to the cytoplasm of the hepatocytes. Furthermore, the signal was stronger in the periportal than that in the perivenous areas. In the lung, an intensive signal was found in the bronchiolar epithelium. As to the kidney, an intensive signal was observed in the distal convoluted tubules, while no signal was found in the proximal convultions.     

Assessing the role of the biomaterial Aquavene in patient reactions to Landmark midline catheters

Generators of early cortical somatosensory evoked potentials (SEPs) still remain to be precisely localised. This gap in knowledge has often resulted in unclear and contrasting SEPs localisation in patients with focal hemispheric lesions. We recorded SEPs to median nerve stimulation in a patient with right frontal astrocytoma, using a 19-channel recording technique. After stimulation of the left median nerve, N20 amplitude was normal when recorded by the parietal electrode contralateral to the stimulation, while it was abnormally enhanced in traces obtained by the contralateral central electrode. The amplitude of the frontal P20 response was within normal limits. This finding suggests that two dipolar sources, tangential and radial to the scalp surface, respectively, contribute concomitantly to N20 generation. The possible location of the N20 radial source in area 3a is discussed. The P22 potential was also recorded with increased amplitude by the central electrode contralateral to the stimulation, while N30 amplitude was normal in frontal and central traces. We propose that the radial dipolar source of P22 response is independent from both N20 and N30 generators and can be located either in 3a or in area 4. This report illustrates the usefulness of multichannel recordings in diagnosing dysfunction of the sensorimotor cortex in focal cortical lesions.