Selective Decontamination of the Digestive Tract as a Method of Infection Prevention in Granulocytopenic Patients; A Follow-Up Study in 102 Patients
Several years ago selected decontamination of the digestive tract (SDD) (1) was proposed for prevention of infection in the neutropenic patient. This method aims at elimination of potentially pathogenic bacteria from the gut without affecting the anaerobic microflora. From the infection preventing point of view this is acceptable because anaerobic bacteria seldomly cause infections in the granulocytopenic patient (2). On the other hand anaerobes have been shown to play a key role in the normal interbacterial balance. The presence of an intact anaerobic flora in the gut hinders colonization by potentially pathogenic bacteria such as aerobic Gram-negative bacilli, yeasts and staphylococci. The mechanism which prevents colonization by potentially pathogenic microorganisms (ppmo) in the gut has been first described by Van der Waaij who introduced the term colonization resistance (CR) (3). The above mentioned ppmo are also the most frequently involved ppmo in infections in the neutropenic patient (2). The majority of these infections find their porte of entry in the digestive tract (4). In order to prevent infection it is therefore attempted to clear the digestive tract from these potentially pathogenic microorganisms. Moreover it was attempted to preserve an intact CR, so that the natural barrier against colonization is at least maintained. It may even be artificially increased by oral administration of antimicrobial agents which are able to eliminate selectively certain ppmo. In a prospective controlled clinical trial SDD appeared to be effective in reducing the infection frequency (1). The difference however was only significant at granulocyte levels below 0.5x109/l.
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- 7.De Vries EGE, Mulder NH, Houwen BH, De Vries-Hospers HG. Enteral nutrition by nasogastric tube in adult patients treated with intensive chemotherapy for acute leukemia. Am J Clin Nutrition 1982; 35: 1490–6.Google Scholar