Antiseptic impregnated endotracheal tubes for the prevention of bacterial colonization

https://doi.org/10.1016/j.jhin.2004.03.011Get rights and content

Abstract

The effect of endotracheal tubes (ETTs) impregnated with chlorhexidine (CHX) and silver carbonate (antiseptic ETTs) against Staphylococcus aureus, methicillin-resistant S. aureus (MRSA), Pseudomonas aeruginosa, Acinetobacter baumannii, and Enterobacter aerogenes [organisms associated with ventilator-associated pneumonia (VAP)], was evaluated in a laboratory airway model. Antiseptic ETTs and control ETTs (unimpregnated) were inserted in culture tubes half-filled with agar media (airway model) previously contaminated at the surface with 108 cfu/mL of the selected test organism. After five days of incubation, bacterial colony counts on all ETT segments were determined. Swabs of proximal and distal ends of the agar tract in antiseptic and control models were subcultured. The initial and residual CHX levels, (five days post-implantation in the model) were determined. Cultures of antiseptic ETTs revealed colonization by the tested pathogens ranging from 1–100 cfu/tube, compared with approximately 106 cfu/tube for the control ETTs (P<0.001). Subcultures from proximal and distal ends of the agar tract showed minimal or no growth in the antiseptic ETTs compared with the control ETTs (P<0.001). The amount of CHX retained in the antiseptic ETTs after five days of implantation was an average of 45% of the initial level. Antiseptic ETTs prevented bacterial colonization in the airway model and also retained significant amounts of the antiseptic. These results indicate that the effectiveness of antiseptic-impregnated ETTs in preventing the growth of bacterial pathogens associated with VAP may vary with different organisms.

Introduction

Ventilator-associated pneumonia (VAP) is one of the leading causes of mortality in intensive care units. The incidence of pneumonia in patients on these units ranges between 7% and 40%. Rates of pneumonia are increased six- to 21-fold for intubated patients and show a further rise with increased duration of mechanical ventilation.1., 2., 3., 4., 5., 6., 7., 8.

Conceptually, VAP can be divided into early-onset and late-onset disease. Early-onset VAP occurs during the first four days that the patient receives mechanical ventilation and is often caused by Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, or, uncommonly, by anaerobes. In comparison, late-onset VAP, occurring over four days after intubation, is more commonly caused by Pseudomonas aeruginosa, Acinetobacter or Enterobacter spp, or methicillin-resistant Staphylococcus aureus (MRSA).3., 4., 8., 9., 10., 11.

Two important processes are thought to be involved in the pathogenesis of VAP; bacterial colonization of the aero-digestive tract and the aspiration of contaminated secretions into the lower airway.12., 13. The endotracheal tube (ETT) is thought to play a prominent role in the development of these processes, not only by introducing oropharyngeal content into the airway at the time of ETT placement in the airway, but also by serving as a ‘bridge’ for bacteria to travel from the oropharynx to the lower airway. In addition, there is increasing evidence showing that the biofilm formed on the ETT surface may serve as a reservoir from which bacteria are continuously seeded into the lower respiratory tree, making the hypothesis of biofilm as potential contributing factor to the pathogenesis of VAP more plausible.12., 13., 14. Furthermore, the effectiveness of systemic antibiotics could be limited by their inability to penetrate such biofilms, and the small amount of antibiotic that actually penetrates the biofilm could increase the risk of emergence of resistant bacteria that can subsequently colonize the respiratory tract of the patient.12

One method of reducing device-related infections is by bonding antimicrobials to such devices. Several studies have documented the effectiveness of antimicrobial-coated medical devices in significantly reducing infection rates.15., 16., 17. In the past we have used a synergistic combination of a silver salt and chlorhexidine (CHX) to impregnate central venous catheters and soft-tissue patches, and these devices have been found to significantly reduce infection.15., 16., 17. Central venous catheters impregnated with CHX and silver sulfadiazine have also been reported to prevent biofilm formation in vivo.18

The objective of our study was to investigate, using a laboratory model, the potential effectiveness of impregnating ETTs with antiseptic to reduce colonization of bacterial flora known to be associated with VAP.

Section snippets

Airway model

Our airway model is based on the theory that bacterial contamination and subsequent colonization of the ETT during and after endotracheal intubation may play a significant role on the pathophysiology of VAP as pathogens proliferate, migrate within, and dislodge from the tube. This model does not attempt to reproduce the physiological conditions within the trachea. It merely tests the effectiveness of impregnated antiseptics in inhibiting or reducing bacterial colonization of an ETT segment

Evaluation of bacterial colonization of ETTs in the airway model

The colonization of antiseptic ETTs by MRSA, S. aureus, A. baumannii, E. aerogenes, and P. aeruginosa was 1–106 cfu/tube compared with approximately 106 cfu/tube of the respective control ETTs (P<0.001). Proximal and distal subcultures of the agar tract in the antiseptic ETTs groups showed counts of 0–285 cfu/plate for the relevant pathogens, except for those involving E. aerogenes. For E. aerogenes, subcultures from the insertion site and from the distal ends of the antiseptic ETTs were 103 and 10

Discussion

Several recent studies implicate ETTs, both directly and indirectly with the development of VAP.1., 2., 12., 13., 20., 21., 22. One study demonstrated less involvement of gastric flora than previously noted.20 Furthermore, the formation of biofilm on ETTs has been described as a possible causative factor for VAP due to pathogens seeding from it into the lower airway.12., 13. Systemic antibiotics can not reach inside biofilm-coated ETTs.13., 18. Such findings and considerations make it plausible

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