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Title: Chlorhexidine Oral Wash Fails to Inhibit VAP But Shows Secondary Benefits: Presented at CHEST
URL: http://www.pslgroup.com/dg/21643A.htm
Doctor's Guide
October 25, 2007


By John Gever

CHICAGO, IL -- October 25, 2007 -- Although ventilator-associated pneumonia (VAP) is thought to originate most often from oropharyngeal bacteria colonisation, oral washes with chlorhexidine failed to reduce VAP incidence in a prospective study reported here at CHEST 2007, the annual meeting of the American College of Chest Physicians.

The treatment was associated with some benefits, however, including reduced time on ventilation and substantial oral decolonisation.

VAP is an airways infection that must be proven to have developed more than 48 hours after the patient is intubated.

According to the Institute for Healthcare Improvement, VAP is the leading cause of death amongst hospital-acquired infections, with an even higher rate of deaths than occur with central line infections, severe sepsis, and respiratory tract infections in the non-intubated patient.

Darlene Tad-Y, MD, Internal Medicine Resident, Lutheran Medical Center, Brooklyn, New York, United States, reported the findings in an oral presentation on October 24.

The randomised, controlled, partially-blinded trial included 82 patients undergoing mechanical ventilation at a single clinical centre. Patients' oral cavities were swabbed twice daily during ventilation with 2 mL of a 0.12% chlorhexidine solution or a non-antiseptic enzymatic liquid used to prevent dry mouth in ventilated patients.

All patients also received standard procedures to prevent VAP (the "VAP bundle"), which includes elevation of the head of the bed, daily sedation vacations and assessment of readiness to extubate, and prophylaxis for peptic ulcer disease and deep venous thrombosis.

Caregivers administering the washes knew which treatment was being used, but patients and physician evaluators did not.

Oropharyngeal swab samples were collected and cultured, and patients were assessed clinically for potential VAP beginning 48 hours after intubation.

Eight cases of VAP were seen in each treatment group, meaning there was no significant difference in VAP incidence rates with the chlorhexidine wash compared with control. Dr. Tad-Y said the study "may have been underpowered" to find VAP incidence reduction, the primary endpoint.

However, the mean duration of ventilation was significantly reduced in the chlorhexidine group (5.1 days vs 9.5 days, P =.011).

The culture studies indicated that bacterial growth was markedly reduced with chlorhexidine on day 3 of ventilation, as measured by the mean percentage of oral cultures showing no growth with chlorhexidine treatment versus control (day 3, 43.4% vs 17.9%).

On the other hand, no notable difference was found on day 1 or on day 9, Dr. Tad-Y said.

She said it was possible that the study, by not looking for VAP until 48 hours after intubation, failed to identify potential differences in early-onset VAP. Also, she said, the chlorhexidine solution may have been too weak to be maximally effective.

Based on the findings of reduced duration of ventilation and medium-term reductions in oral bacterial loads, Dr. Tad-Y said that chlorhexidine oral washes could be part of an effective anti-VAP strategy for ventilator patients.


[Presentation title: Efficacy of Chlorhexidine Oral Decontamination in the Prevention of Ventilator-Associated Pneumonia. Session 897]

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