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Biomedical subjects

C A Gaillard

Publications and source records attributed to C A Gaillard.

At least 37 records · Page 2Linked to original sources

Intermittent enteral feeding: the influence on respiratory and digestive tract colonization in mechanically ventilated intensive-care-unit patients.

Continuous enteral feeding (CEF) has been associated with decreased gastric acidity, thereby stimulating gastric colonization and ventilator-associated pneumonia (VAP). Intermittent enteral feeding (IEF) could induce a temporary increase in gastric acidity and decrease the risk of VAP. We studied the influence of IEF (18 h/d) and CEF (24 h/d) on gastric and oropharyngeal colonization. Sixty patients were randomized to receive either IEF or CEF, and continuous intragastric pH monitoring was performed in 50 patients. Median intragastric pH levels were similar before enteral feeding was instituted (pH 2.5 for CEF and pH 2.4 for IEF), and median pH values increased slightly after institution of nutrition (NS). In patients receiving IEF, median pH decreased from 3.5 to 2.2 (p = 0.0002) when enteral feeding was discontinued. However, despite this, 80% of the patients in both study groups were colonized in the stomach after 7 d in study. In addition, colonization rates of the oropharynx and trachea, the incidence of VAP, and mortality were similar in both study groups. IEF was less well tolerated than CEF. We conclude that almost all patients receiving enteral feeding are colonized in the stomach with gram-negative bacteria. IEF resulted in a slight decrease in intragastric pH without influencing rates of colonization and infection of the respiratory tract.

Aged↗

Risk factors for pneumonia, and colonization of respiratory tract and stomach in mechanically ventilated ICU patients.

Risk factors for the development of ventilator-associated pneumonia (VAP) and colonization of the respiratory tract and stomach with enteric gram-negative bacteria (EGB) and Pseudomonadaceae were determined in 141 ventilated patients using univariate analysis and the Cox proportional hazards model. VAP was caused by EGB in 14 patients (10%), and by Pseudomonadaceae in 19 patients (13%). The duration of ventilation was a significant risk factor for VAP caused by EGB and Pseudomonadaceae, and for acquired colonization in oropharynx, stomach, and trachea with these species. Of 20 other variables, oropharyngeal colonization with EGB on admission (hazard ratio [HR] = 4.5) and an infection on admission (HR = 2.7) were selected as risk factors for VAP caused by EGB. Acquired colonization with Pseudomonadaceae in oropharynx (HR = 5.0) was the most important risk factor for VAP caused by these species. Gastric colonization with EGB or Pseudomonadaceae were no risk factors for VAP. For acquired oropharyngeal colonization with EGB only the duration of ventilation was a risk factor, whereas preceding colonization of the trachea with Pseudomonodaceae and duration of ventilation were risk factors for acquired oropharyngeal colonization with these species. In the Cox model, only the duration of ventilation was significantly related to acquired gastric colonization with EGB. Preceding colonization of the orophayrnx and of the trachea with Pseudomonadaceae were risk factors for acquired colonization with these species in the stomach. Twelve patients with VAP (46%) and 38 without VAP (33%) died (p = 0.21). In conclusion, duration of ventilation and colonization of the upper respiratory tract are the most important risk factors for VAP caused by EGB or Pseudomonadaceae.

Adult↗

A typical case of cross-acquisition? The importance of genotypic characterization of bacterial strains.

A 33-year-old trauma patient died of Serratia marcescens pneumonia and septic shock. Isolates from this patient were phenotypically identical to strains isolated from the only other intensive care unit patient colonized with S marcescens. Although cross-acquisition was suspected strongly, serotyping and plasmid analysis demonstrated that the isolates were genotypically different, underscoring the importance of genotypic characterization.

Adult↗

Colonization and infection with Enterococcus faecalis in intensive care units: the role of antimicrobial agents.

We studied the influences of antimicrobial agents on the colonization of the respiratory tract and infection with Enterococcus faecalis in intensive care unit (ICU) patients receiving mechanical respiration for at least 3 days. In a matched-cohort analysis, patients receiving topical antimicrobial prophylaxis (TAP) of the oropharynx and stomach with antimicrobial agents not treating E. faecalis were compared with patients not receiving TAP. Patients were matched with controls on the basis of their duration in the ICU, their use of systemic antibiotics treating and not treating E. faecalis, the administration of TAP, their APACHE II score, and surgical procedures they had undergone. In all, 276 patients were analyzed. The colonization of the oropharynx and/or trachea by E. faecalis at admission was demonstrated for 43 patients (16%). Twenty patients (9%) acquired tracheal colonization and 91 patients (40%) acquired oropharyngeal colonization with E. faecalis. In the matched-cohort analysis, 43 patients receiving TAP were matched in two controls each. TAP patients more frequently acquired tracheal colonization (15 of 43 versus 2 of 86 patients, P < 0.00001) and infections with E. faecalis (6 of 43 versus 1 of 86 patients, P < 0.01). The use of topical antibiotics and treating E. faecalis increased the risk for colonization and infection with E. faecalis.

Administration, Topical↗

The role of intragastric acidity and stress ulcus prophylaxis on colonization and infection in mechanically ventilated ICU patients. A stratified, randomized, double-blind study of sucralfate versus antacids.

UNLABELLED: This study evaluates the effects of sucralfate and antacids on intragastric acidity, colonization of stomach, oropharynx and trachea, and the incidence of ventilator-associated pneumonia (VAP) in mechanically ventilated patients in intensive care units. We conducted a prospective randomized double-blind trial in which patients were stratified on initial gastric pH. Intragastric acidity was measured with computerized, continuous intragastric monitoring. The diagnosis of VAP was established with protected specimen brush and/or bronchoalveolar lavage. The study included consecutive eligible patients with mechanical ventilation and nasogastric tube. INTERVENTIONS: After stratification on initial intragastric pH into two groups, patients from both groups were randomly assigned to receive either antacids (a suspension of aluminum hydroxide and magnesium hydroxide), 30 mL every 4 h, or sucralfate, 1 g every 4 h. Continuous intragastric pH monitoring was performed in 112 patients (58 antacids, 54 sucralfate). Using predetermined criteria, colonization of stomach, oropharynx, and trachea, and the incidence of VAP were assessed. Altogether, 141 patients were included (74 receiving antacids, 67 sucralfate) and continuous intragastric pH monitoring was performed in 112 patients, with a mean of 75 h per patient. The median pH and the percentage of time with a pH < 4.0 were calculated from each measurement. No significant differences in median pH values (4.7 +/- 2.2 and 4.5 +/- 2.0 for antacids and sucralfate, respectively) were observed. Median pH values were higher in patients with gastric bacterial colonization than in noncolonized patients (5.5 +/- 2.1 and 3.3 +/- 2.0, p < 0.01), but colonization of oropharynx and trachea was not related to intragastric acidity. Thirty-one patients (22%) developed VAP, with a similar incidence in both treatment groups. In addition, antibiotic use, duration of hospitalization, and mortality rates were similar in both groups. Enteral feeding did not change intragastric acidity significantly but increased gastric colonization with Enterobacteriaceae, without influencing oropharyngeal and tracheal colonization. Antacids and sucralfate had a similar effect on intragastric acidity, colonization rates, and incidence of VAP. Intragastric acidity influenced gastric colonization but not colonization of the upper respiratory tract or the incidence of VAP. Therefore, it is unlikely that the gastropulmonary route is important for the development of VAP.

Antacids↗

Continuous enteral feeding counteracts preventive measures for gastric colonization in intensive care unit patients.

OBJECTIVE: To test the influence of continuously administered enteral feeding on gastric pH and gastric colonization in patients receiving or not receiving topical antimicrobial prophylaxis of the oropharynx and stomach, including sucralfate as stress ulcer prophylaxis. DESIGN: Prospective, open trial. SETTING: Two university hospital general intensive care units (ICUs). PATIENTS: Patients (n = 95) with an ICU stay for at least 5 days. INTERVENTIONS: Thirty-one patients received antimicrobial agents into the stomach and oropharynx in combination with sucralfate (1 g/6 hrs) as stress ulcer prophylaxis. Sixty-four other patients did not receive antimicrobial prophylaxis or sucralfate, but instead received gastric pH-increasing stress ulcer prophylactic agents, if indicated. Gastric colonization and gastric pH were measured on admission and subsequently at least two times a week. Forty-eight patients (14 receiving and 34 not receiving antimicrobial prophylaxis) received enteral feeding. MEASUREMENTS AND MAIN RESULTS: Both enteral feeding and gastric pH-increasing stress ulcer prophylaxis independently increased gastric pH: the risks for a gastric pH of > 3.5 were, respectively, 4.54 and 2.04 (odds ratios). Enteral feeding also increased the risk for gastric colonization by potentially pathogenic microorganisms (odds ratio = 4.52). Patients receiving both topical antimicrobial prophylaxis and sucralfate remained free of gastric colonization for a longer period than those patients receiving gastric pH-increasing stress ulcer prophylaxis. In these two groups, patients without enteral feeding remained free of gastric colonization for a longer period than those patients receiving enteral feeding. CONCLUSIONS: Topical antimicrobial prophylaxis, including sucralfate, successfully prevented gastric colonization with potentially pathogenic microorganisms and was correlated with lower gastric pH values. However, the efficacy was markedly decreased when continuous enteral feeding was administered simultaneously.

Adolescent↗

Colonization in patients receiving and not receiving topical antimicrobial prophylaxis.

The influence of topical antimicrobial prophylaxis (TAP) on colonization of oropharynx and trachea was studied in patients receiving and not receiving prophylaxis. Twenty-two patients in Intensive Care Unit (ICU) I (Group 1) received TAP (tobramycin, colistin, and amphotericine B in oropharynx and stomach). Simultaneous to Group 1, 21 patients (Group 2) not receiving TAP were studied in ICU I. A control group of patients admitted to another, identical, ICU (ICU II), where no TAP was administered, were studied simultaneously (Group 3a, n = 23). A second control group (Group 3b, n = 31), was formed by collecting data from patients admitted to ICU I in Period II. Patients receiving TAP were less frequently colonized than patients not receiving prophylaxis. Moreover, of the patients not receiving TAP, those staying in the ICU where TAP was administered (Group 2) were less frequently colonized than patients in another ICU (Group 3). Of the patients not colonized on admission, those staying in the ICU where TAP was administered remained free of colonization for a longer time. In the ICU where no TAP was administered, more patients were colonized simultaneously and cross-acquisition occurred more frequently. TAP significantly influenced colonization of oropharynx and trachea in patients receiving and not receiving prophylaxis within the same ICU as compared with patients not receiving prophylaxis in another identical ICU.

Administration, Topical↗

The stomach is not a source for colonization of the upper respiratory tract and pneumonia in ICU patients.

STUDY OBJECTIVE: To study sequences of colonization of different species of microorganisms and to determine the importance of gastric colonization for the development of nosocomial pneumonia. DESIGN: A prospective study. SETTING: Two identical ICUs of a university hospital. PATIENTS: Sixty-four patients admitted to ICU for at least 5 days; 59 were intubated. INTERVENTIONS: Microbiologic cultures of serially taken samples of gastric aspirates, oropharyngeal swabs, and tracheal aspirates were performed at the time of ICU admission and subsequently twice a week. Diagnosis of pneumonia was based on quantitative cultures from bronchoalveolar lavage (BAL) and protected specimen brush (PSB). Sequences of colonization were examined by comparing isolates of the same species, with concordance of minimum inhibitory concentration values to six antibiotics. MEASUREMENTS AND RESULTS: Eleven patients developed 14 episodes of nosocomial pneumonia, yielding 20 species of microorganisms. Seventeen of 20 species (85 percent), associated with pneumonia, were cultured, previous to or on the day of diagnosis, from tracheal aspirates, and 6 of 20 (30 percent) species were cultured from gastric samples. A sequence of colonization from the stomach to the upper respiratory tract eventually leading to pneumonia was not observed in any of the six species. Initial colonization with Pseudomonas aeruginosa and Enterobacter species was more often demonstrated in the trachea (16/24 and 13/25 cases) as compared with the stomach (1/24 and 6/25 cases; p < 0.0001 and p = 0.02 respectively). In contrast, initial colonization with Klebsiella species and Enterococcus faecalis was more frequently demonstrated in the stomach (13/28 and 8/15 cases) as compared with the trachea (6/28 and 0/15 cases; p = 0.02 and p < 0.0001, respectively). CONCLUSIONS: Based on studying sequences of colonization in ICU patients, we concluded that the stomach is unlikely to be an important source of pathogens leading to nosocomial pneumonia as diagnosed by BAL/PSB. Furthermore, the initial site and route of colonization might not be the same for all microorganisms.

Bacterial Infections↗

Problems in diagnosing nosocomial pneumonia in mechanically ventilated patients: a review.

OBJECTIVE: To review the available information about diagnosing nosocomial pneumonia in mechanically ventilated intensive care unit patients. DATA SOURCES: The National Library of Medicine MEDLINE database and bibliographies of the reviewed articles. STUDY SELECTION AND DATA EXTRACTION: Studies were selected from the English literature, with an emphasis on recent studies. Studies were selected on the basis of their historical value and originality. A total of 82 articles was considered relevant. DATA SYNTHESIS: Many efforts have been made to diagnose nosocomial pneumonia with more accuracy. Two promising new diagnostic modalities are the protected specimen brush and bronchoalveolar lavage, both performed via flexible bronchoscopy. Depending on the study design and patient selection, sensitivity and specificity of bronchoalveolar lavage and protected specimen brush differ widely, ranging from 50% to 100%. However, interpretation of study results is seriously hampered because a standardized diagnostic threshold is not available, the influence of previous antimicrobial therapy on culture results remains unclear, and, most importantly, a well-defined gold standard to study the value of both methods is lacking. CONCLUSIONS: Because studies of bronchoalveolar lavage and protected specimen brush are seriously hampered by several pitfalls, these studies as well as clinical results must be interpreted with caution.

Bronchoalveolar Lavage Fluid↗

Clinical experiences with trandolapril.

In this article the clinical experiences with the new non-sulfhydryl angiotensin-converting enzyme inhibitor trandolapril are reviewed. The drug lowers blood pressure effectively in patients with mild-to-severe hypertension including elderly and obese patients. Distinguishing features of the compound are its long plasma half-life and high degree of lipophilicity.

Angiotensin-Converting Enzyme Inhibitors↗