Abstract
Objective: to evaluate the efficiency of intravenous and inhaled antibiotic therapy for nosocomial pneumonia caused by gram-negative bacteria by quantifying lipopolysaccharide (LPS). Subjects and methods. Examinations were made in 54 patients with mechanical ventilation-associated nosocomial pneumonia. Conventional de-escalating intravenous antibiotic therapy (with carbapenems) was used in Group 1 (n=26). Inhaled antibiotic monotherapy with TOBI (tobramycin) in a dose of 300 mg every 12 hours for 10—12 days was performed in Group 2 (n=28). The use of inhaled tobramycin as a monodrug was due to the absence of other infection foci. LPS was quantified using a diagnostic activated particle-method-endotox spp. kit (A. N. Bakulev Research Center of Cardiovascular Surgery, Russian Academy of Medical Sciences, OOO ROKHAT Research-and-Production Firm, Russia). Results. The first administration of the antibiotic is accompanied by a higher arteriovenous difference in the content of gram-negative bacterial LPS due to increased arterial endotoxemia. Conclusion. Elevated arterial blood LPS levels after initiation of systemic or inhaled antibiotic therapy for nosocomial pneumonia may be employed as an early criterion for its efficiency. Tobramycin inhalations give rise to a significant increase in arterial lipopolysaccharidemia as compared to de-escalation therapy with carbapenems with low rates of adverse reactions and undesirable events. Key words: nosocomial pneumonia, lipopolysaccharide, arteriovenous difference, inhaled tobramycin.
Highlights
One percent of hospital patients suffer from the noso comial pneumonia (NP) that is developed in 20% of mechan ically ventilated patients
LPS level in arterial blood was higher than in venous blood that can be explained by the high concentration of gram neg ative bacteria and bacterial decay products in the lung tissue (Table 2)
After the beginning of the systemic or inhalation antibacterial therapy in patients with NP LPS level is increased in arterial blood
Summary
One percent of hospital patients suffer from the noso comial pneumonia (NP) that is developed in 20% of mechan ically ventilated patients. The diversity of «problem» bacteria causing nosocomial infections and high lethality are due to inade quacy of ABD use or delay in ABD administration These obstacles are usually circumventing by the use of evidence based regimens of treatment with those ABD that are active against most actual germs and capable to overcome resis tance mechanisms of hospital flora [6]. This is considered as a reason for a deescalation therapy [7,8,9]
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