Observation study of water outlet design from a cross-infection/user perspective: time for a radical re-think?

BACKGROUND: Handwashing is a key barrier to cross-infection performed at a handwash station (HWS). Elbow-operated outlets, if used incorrectly (with hands), become highly touched objects, potentially providing a route for cross-infection. AIM: To study how elbow-operated outlets were used by staff in this hospital, whether the correct type of HWS had been installed in the various ward areas according to the Health Building Note (HBN) 00-10 Part C: Sanitary Assemblies (hands-free outlets in clinical, food preparation and laboratory areas), and factors impinging on design/setup which may affect compliance with correct use. METHODS: Observation of outlet use was performed by mounting a video camera above four HWSs. Review of suitability of outlet was conducted by two of the authors by visiting ward areas and assessing compliance against HBN recommendations. Angle of elbow-operated lever setup was measured using a protractor and water temperature in relation to angle of movement of elbow lever was measured using a calibrated thermocouple. FINDINGS: Ninety-two percent of staff used hands to turn on the outlet and 68% used hands to turn the outlet off, potentially re-contaminating their hands. More than 70% of users moved the lever ≤45°. Almost half of elbow levers were set up incorrectly, being flush or within 3.5 cm of the rear panel, making elbow operation extremely difficult. Selection of outlet type according to HBN was most incorrect in the intensive treatment unit but also occurred in the newly built parts of the hospital. CONCLUSIONS: Although handwashing is a key barrier to cross-infection, poor selection and incorrect use of outlet undermines its effectiveness. Design and incorrect instalment further compromise the intended means of operation of elbow levers. Of equal concern is that this risk mostly goes unrecognized. There is an opportunity to improve handwashing safety, but it requires engagement across a broad stratum from Government Departments of Health and manufacturers down to the user.

Effect of prostaglandin F2 alpha and prostacyclin on asphyxic anoxia in cats.

The effects of exogenously applied prostaglandin F2 alpha (PGF2 alpha) and prostacyclin (PGI2) on asphyxic anoxia was studied in curarized and artificially ventilated cats. Anoxia was induced by stopping the ventilation and checking the changes in the EcoG. Cortical resistance (CRs) was evaluated as time between stopping the ventilation and the extinction of ECoG. Cortical recovery (CRc) was expressed as time between restitution of ventilation and reappearance of brain activity. Anoxia resistance index (ARI) was defined as the ratio between these two parameters (CRs/CRc). PGF2 alpha was applied by 5 minute i.v. and intracarotid (i.c.) infusion in a dose of 10 micrograms/kg/min, and PGI2 in a dose of 250 ng/kg/min for 15 minutes intracarotidly. The results show that both the i.c. and i.v. infusion with PGF2 alpha led to a significant decrease of CRs and prolongation of CRc resulting in decrease of ARI. The changes are more expressed at i.v. infusion, PGI2 does not improve the ECoG changes evoked by hypoxia. Suggestions for the possible mechanism of PGF2 alpha action and for the failure of PGI2 to protect the brain are made.

Anti-hypoxic effect of indomethacin and its interaction with prostacyclin.

The anti-hypoxic effect of indomethacin (1-10 mg/kg) was studied using the following experimental methods: asphyxic anoxia in cats, hypobaric and anoxic hypoxia in mice, incomplete ischemia by bilateral carotid occlusion and hemic hypoxia in rats. In hypobaric and anoxic hypoxia the interaction of indomethacin with the effect of prostacyclin (PCl2) was investigated. Indomethacin showed an anti-hypoxic effect in all the methods used: it enhanced anoxia resistance index in asphyxic anoxia and significantly increased survival of rats and mice subjected to experimental hypoxia. Indomethacin potentiated the effect of PGl2, shifting the anti-hypoxic dose-response curve of PGl2 to the left. The possible mechanism of action of indomethacin in relation to cyclo-oxygenase inhibition is discussed.

Study on the anti-hypoxic effect of some drugs used in the pharmacotherapy of cerebrovascular disease.

The anti-hypoxic effect of some agents used in the pharmacotherapy of cerebrovascular disease was studied using the following methods: incomplete ischemia by bilateral carotid ligation in rats, anoxic hypoxia by inhalation of argon in mice, and hemic hypoxia induced by injection of sodium nitrite (120 mg/kg s.c.) in rats. The following drugs were studied: piracetam, orotic acid, centrophenoxine, pentobarbital, vincamine, vinpocetine, cinnarizine, aligeron, xanthinol nicotinate and papaverine. The most pronounced anti-hypoxic effect was shown primarily with the metabolic acting drugs, such as orotic acid, centrophenoxine, piracetam and pentobarbital, followed by the preparations with combined metabolic and vasoactive properties (vincamine and vinpocetine). The predominantly vasoactive drugs were less effective in anoxic hypoxia, but showed more pronounced effect in incomplete ischemia.

Anti-hypoxic effect of piracetam and its interaction with prostacyclin.

The anti-hypoxic effect of piracetam was studied using the following experimental methods: hypobaric and anoxic hypoxia in mice, complete ischemia by decapitation in mice, incomplete ischemia by bilateral carotid occlusion in rats and hemic hypoxia in rats. Cinnarizine and vinpocetine were used as reference drugs. In hypobaric hypoxia, anoxic hypoxia, and complete ischemia by decapitation the interaction of piracetam with the effect of prostacyclin (PGI2) was investigated. Piracetam showed anti-hypoxic effect in all the methods used. Its effect was greater than that of cinnarizine and similar to that of vinpocetine. Piracetam potentiated the effect of PGI2 shifting the anti-hypoxic dose-response curve of PGI2 to the left.

Study on the anti-hypoxic effect of cinnarizine and its interaction with prostacyclin.

The anti-hypoxic effect of cinnarizine was studied using the following experimental methods: hypobaric and anoxic hypoxia in mice, complete ischemia by decapitation in mice and hemic hypoxia in rats. Papaverine, xanthinol nicotinate and naftidrofuryl were used as reference drugs. In hypobaric and anoxic hypoxia the interaction of cinnarizine with the effect of prostacyclin (PGI2) was investigated. Cinnarizine showed an anti-hypoxic effect in all the methods used. It was more effective in hypobaric and anoxic hypoxia, in incomplete ischemia by decapitation, and less effective in hemic hypoxia. Cinnarizine potentiated the effect of PGI2 shifting the anti-hypoxic dose-response curve of PGI2 to the left. Suggestions as to the possible mechanism of anti-hypoxic action of cinnarizine are made.

Anti-hypoxic effect of prostacyclin.

The anti-hypoxic effect of prostacyclin (PGI2) was studied using the following methods: hypoventilation hypoxia and hypovolemic oligemia in cats and hypobaric hypoxia and complete ischemia by decapitation in mice. In experiments on cats PGI2 (250 ng/kg/min i.v.) led to an improvement of hypoxia-impaired EEG activity. In hypobaric hypoxia, PGI2 at all doses applied (50-500 micrograms/kg) led to a significant increase in the survival time (from 67.5% to 196%). In complete ischemia by decapitation, PGI2 at doses from 50 to 500 micrograms/kg significantly prolonged the gasping movements (from 7.8% to 20.6%). Different mechanisms of the anti-hypoxic effect of PGI2 are discussed. The effect observed would be potentially beneficial in hypoxic and ischemic states.

Anti-hypoxic effect of centrally and systemically administered prostacyclin (PGI2).

Prostacyclin (PGI2) induced a dose-dependent prolongation of survival time of mice subjected to hypoxic and anoxic hypoxia, when administered either intracerebroventricularly (i.c.v., 0.001-10 micrograms/mouse), intravenously (i.v., 0.5-500 micrograms/kg) or intraperitoneally (i.p., 50-500 micrograms/kg). The effects of a single dose of 50 micrograms/kg i.v. or i.p. and of 1 microgram/mouse i.c.v. persisted for about 30 min. The anti-hypoxic effect of PGI2 is most likely due to an action upon the CNS.