Prevention of ventilator-associated pneumonia by oral decontamination: a prospective, randomized, double-blind, placebo-controlled study.

UNLABELLED: Colonization of the intestinal tract has been assumed to be important in the pathogenesis of ventilator-associated pneumonia (VAP), but relative impacts of oropharyngeal, gastric, or intestinal colonization have not been elucidated. Our aim was to prevent VAP by modulation of oropharyngeal colonization, without influencing gastric and intestinal colonization and without systemic prophylaxis. In a prospective, randomized, placebo-controlled, double-blind study, 87 patients received topical antimicrobial prophylaxis (gentamicin/ colistin/vancomycin 2% in Orabase, every 6 h) in the oropharynx and 139 patients, divided over two control groups, received placebo (78 patients were studied in the presence of patients receiving topical prophylaxis [control group A] and 61 patients were studied in an intensive care unit where no topical prophylaxis was used [control group B]). Baseline characteristics were comparable in all three groups. Topical prophylaxis eradicated colonization present on admission in oropharynx (75% in study group versus 0% in control group A [p < 0.00001] and 9% in control group B patients [p < 0.00001]) and in trachea (52% versus 22% in A [p = 0.03] and 7% in B [p = 0.004]). Moreover, topical prophylaxis prevented acquired oropharyngeal colonization (10% versus 59% in A [p < 0.00001] and 63% in B [p < 0.00001]). Colonization rates in stomach and intestine were not affected. Incidences of VAP were 10% in study patients, 31% in Group A, and 23% in Group B patients (p = 0.001 and p = 0.04, respectively). This was not associated with shorter durations of ventilation or ICU stay or better survival. Oropharyngeal colonization is of paramount importance in the pathogenesis of VAP, and a targeted approach to prevent colonization at this site is a very effective method of infection prevention. KEYWORDS: cross infection, prevention and control; respiration, artificial, adverse effects; antibiotics, administration and dosage infection control methods; pneumonia, etiology, prevention and control; intubation, intratracheal, adverse effects

The abdominal compartment syndrome: a complication with many faces.

BACKGROUND: Lately renewed attention has been given to the abdominal compartment syndrome. Despite of this there still remain a lot of controversies with regard to the pathophysiological mechanisms underlying this syndrome and the therapeutic options. METHODS: Two cases of patients with this syndrome are described and the data from animal and human trials concerning the abdominal compartment syndrome are presented and discussed. RESULTS: A variety of clinical disorders may lead to the abdominal compartment syndrome. It mainly affects the cardiovascular, pulmonary and renal organ systems. Although some clinical effects are clearly described, the exact mechanisms underlying these changes in humans are incompletely understood. It is still unclear why some patients develop abdominal compartment syndrome and others do not. The intra-abdominal pressure can easily be assessed by measuring the urine bladder pressure, which correlates well with the actual intra-abdominal pressure. All authors agree that a decompression of the abdomen by means of a laparotomy is the treatment of choice for the abdominal compartment syndrome. Which parameters should determine the indication however, remains controversial, since the correlation between clinical signs and pressure is not straightforward. CONCLUSIONS: The abdominal compartment syndrome is a well-recognised disease entity related to acutely increased abdominal pressure. Urgent laparotomy can be lifesaving in some cases. However no single threshold of abdominal pressure can be applied universally. Pending further clinical trials the best therapeutic option seems to be to decompress the abdomen surgically if the intravesical pressure is 25 mmHg or higher in patients with refractory hypotension, acute renal failure or respiratory failure due to abdominal distension.

Blunted rise in platelet count in critically ill patients is associated with worse outcome.

OBJECTIVE: To test the hypothesis that a low rate of change of platelet counts (PCs) after admission to the intensive care unit (ICU) is associated with mortality. Low PCs are known to be associated with disease severity in critically ill patients, but the relevance of time-dependent changes of PCs has not been investigated. DESIGN: Retrospective study. SETTING: A 12-bed surgical ICU of a university hospital. PATIENTS: All adult patients admitted to the ICU for at least 4 days during a 7-yr period. INTERVENTIONS: At admission, Acute Physiology and Chronic Health Evaluation scores were calculated. PCs and leukocyte counts were analyzed from admission to day 10. The daily rise of the PCs (deltaPC/deltat from day 2 to day 10 was calculated. Rates for 30-day mortality as well as hospital mortality were determined. MEASUREMENTS AND MAIN RESULTS: A total of 1,415 admissions were studied. Median PCs (interquartile range) initially decreased and subsequently increased, with a higher PC in 1,203 survivors than in 212 nonsurvivors from day 2 onward (302 [range,181-438] x 10(3)/mm3/day vs. 129 [range, 62-228] x 10(3)/mm3 at day 10; p < 0.001). After stratification of patients per type of surgery, within each group PC was also higher in survivors. Mean deltaPC/deltat was more than five times higher in survivors compared with nonsurvivors: 30 +/- 46 x 10(3)/mm3/day vs. 6 +/- 28 x 10(3)/mm3/day (p < 0.001). The area under the receiving operating characteristic curve of deltaPC/deltat for 30-day survival was 0.743 compared with 0.728 for the Acute Physiology and Chronic Health Evaluation. Leukocyte counts showed marginal differences between nonsurvivors and survivors. CONCLUSION: A blunted or absent rise in PCs in critically ill patients is associated with increased mortality. deltaPC/deltat is a readily available and simple parameter to improve assessment of critically ill patients.