Biomedical subjects

P Boiteau

Publications and source records attributed to P Boiteau.

15 recordsLinked to original sources

PubMed2000

Prospective randomized trial of 10% povidone-iodine versus 0.5% tincture of chlorhexidine as cutaneous antisepsis for prevention of central venous catheter infection.

A multicenter prospective, randomized, controlled trial, with 0.5% tincture of chlorhexidene versus 10% povidone-iodine as cutaneous antisepsis for central venous catheter (CVC) insertion, was conducted for patients in intensive care units. Of 374 patients, 242 had a CVC inserted for >3 days and were used for the primary analysis. Outcomes included catheter-related bacteremia, significant catheter colonization (> or = 15 colony-forming units [cfu]), exit-site infection, serial quantitative exit-site culture (every 72 h), and molecular subtyping of all isolates. Patients in both study groups were comparable with respect to age, sex, underlying disease, length of hospitalization, reason for line insertion, and baseline APACHE II score. Documented catheter-related bacteremia rates were 4.6 cases per 1000 catheter-days in the chlorhexidine group (n=125) and 4.1 cases per 1000 catheter-days in the povidone-iodine group (n=117; not significant [NS]). Significant catheter-tip colonization occurred in 24 (27%) of 88 patients in the povidone-iodine group and in 31 (34%) of 92 patients in the chlorhexidine group (NS). A mean exit-site colony count of 5.9 x 10(5) cfu/mL per 25 cm(2) of the surface area of skin in the povidone-iodine group versus 3.1 x 10(5) cfu/mL per 25 cm(2) in the chlorhexidine group (NS) was found. There was a trend toward fewer exit-site infections in the chlorhexidine group (0 of 125 patients) versus those in the povidone-iodine group (4 of 117 patients; P=.053). Results of an intention-to-treat analysis were unchanged from the primary analysis. No difference was demonstrable between 0.5% tincture of chlorhexidine and 10% povidone-iodine when used for cutaneous antisepsis for CVC insertion in patients in the intensive care unit.

Adult↗

PubMed1999

Safety and efficacy of a sustained inflation for alveolar recruitment in adults with respiratory failure.

OBJECTIVE: To assess the safety and efficacy of a sustained inflation, used as a lung volume recruitment maneuver in ventilated patients with hypoxemic respiratory failure. DESIGN: Prospective data collection as part of a quality assurance program following introduction of a lung volume recruitment guideline in the intensive care unit. SETTING: Academic medical-surgical critical care unit. PATIENTS: Hypoxemic patients with bilateral pulmonary infiltrates. Patients with chronic obstructive pulmonary disease, pulmonary barotrauma and hemodynamic instability were excluded. INTERVENTIONS: A sustained inflation using a pressure of 30 to 45 cmH2O was applied for 20 s. The pressure was determined as the lesser of 45 cmH2O or the peak pressure while ventilated at a tidal volume of 12 ml/kg. Intra-arterial blood pressure and pulse oximetry were monitored continuously. MEASUREMENTS AND RESULTS: Significant improvement in oxygenation occurred in the majority of patients within 10 min. The mean oxygen saturation improved from 86.9 +/- 5.5 to 94.3 +/- 2.3% (p < 0.01). No significant adverse effects were noted: hypotension and mild oxygen desaturation occurred in some patients during the 20-s inflation, reversing rapidly after inflation was terminated. No barotrauma occurred. CONCLUSIONS: A sustained inflation is a safe, clinically applicable method of lung volume recruitment which improves oxygenation in selected patients and may have a role in ventilatory management.

Critical Care↗

PubMed1995

Pulmonary edema during IL-2 therapy: combined effect of increased permeability and hydrostatic pressure.

Systemic administration of recombinant interleukin-2 (rIL-2) has been shown to be promising against certain metastatic cancers. However, major side effects, such as pulmonary edema, have limited its widespread use. Although this pulmonary edema has been attributed to a vascular leak syndrome, this hypothesis has not been verified in humans. The purpose of our study was to determine both the severity and mechanism of pulmonary edema in seven patients treated with rIL-2. The severity of edema was assessed by daily evaluation of chest radiographs, using a semiquantitative scale, as well as by repeated measurements of the alveolar-to-arterial oxygen gradient (A-aDO2) in each patient. To determine the mechanism of pulmonary edema, we serially measured in each patient the lung clearance of technetium 99m-diethylenetriamine pentaacetic acid (DTPA) 99mTc-DTPA), the plasma levels of Von Willebrand factor antigen, and the pulmonary capillary wedge pressure (PCWP). Our results show that there was a gradual increase in the chest radiography edema score that was paralleled by a significant increase in A-aDO2 over its baseline value. During rIL-2 treatment, 99mTc-DTPA clearance was augmented, and the plasma concentration of Von Willebrand factor antigen was elevated. PCWP climbed from 7 to 14 mm Hg and serum total protein fell from 66.1 to 42.1 gm/L. The results obtained indicate that although pulmonary edema associated with rIL-2 treatment is partially dependent on increased permeability of the lung, changes in hydrostatic and oncotic forces may be the principal determinants of edema development.

Blood-Air Barrier↗

PubMed1989

Hydrochlorothiazide-associated pulmonary edema.

The findings in a patient who developed low-pressure pulmonary edema on two separate occasions immediately following the ingestion of a single triamterene-hydrochlorothiazide tablet (Dyazide) are presented. It is postulated that this was related to the hydrocholorothiazide component of the drug. Although 12 cases have been reported, the pathophysiology remains obscure. Mitogenic stimulation of the patient's lymphocytes to concanavalin A, phytohemagglutinin, and pokeweed mitogen was assessed. Blastogenic responses to Staphylococcus aureus antigen, triamterene, and hydrochlorothiazide were also assessed. No hypersensitivity response could be demonstrated to either triamterene or hydrochlorothiazide. The initially low white blood cell count, associated with hemoconcentration, increased in the first 24 h in the hospital. This observation is consistent with intrapulmonary sequestration of granulocytes causing pulmonary edema.

Antihypertensive Agents↗

PubMed1987

Treatment of canine pulmonary hypertension: effects of norepinephrine and isoproterenol on pulmonary vascular pressure-flow characteristics.

Pulmonary vascular flow resistive properties may be described by mean pulmonary arterial pressure (PAP)-cardiac output (CO) plots. The slope of the PAP-CO relationship defines the incremental resistance and the extrapolated pressure intercept defines the effective outflow pressure. We investigated effects of norepinephrine (11 dogs) and isoproterenol (seven dogs) on the pulmonary vascular PAP-CO relationship in a model of pulmonary hypertension produced by injection of autologous blood clots. Multiple PAP-CO coordinates were obtained with and without drug infusion. CO was varied by opening systemic arteriovenous fistulas. PAP-CO relationships were well described by a linear equation (mean r value .964 +/- .032). Isoproterenol increased mean CO by 61% (p less than .01), and calculated pulmonary vascular resistance (PVR) decreased by 31% (p less than .05), corresponding to a 35% decrease (5.1 +/- 2.0 to 3.3 +/- 0.9 mm Hg X liter X min-1; p less than .01) incremental resistance. In the first seven dogs to receive norepinephrine, despite a 25% increase in blood pressure (p less than .01) no significant effects on CO, PAP, PVR, or PAP-CO relationship were observed. In the next four dogs, norepinephrine was infused at a lower dose to increase blood pressure 50% and a higher dose to ensure an increase in CO. In both conditions, calculated PVR fell (p less than .05) compared with that before norepinephrine. However, measured incremental resistance and effective outflow pressure did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Pulmonary vascular pressure-flow relationship in canine oleic acid pulmonary edema.

We tested the hypothesis that the increased impedance to flow in canine oleic acid (OA) lung injury is predominantly due to an increase in effective downstream pressure (EDP), obtained by extrapolating to zero flow the linear portion of the pulmonary artery pressure (PAP)/flow (Q) relationship. PAP-Q coordinates were obtained in eight anesthetized, O2-ventilated dogs by varying Q through systemic arteriovenous fistulae. PAP-Q lines were obtained before and approximately 5 h after injection of OA. A second group of six dogs served as a time control (TC) group. There was a linear relationship between PAP and Q in both experimental and control groups (mean r value 0.948). The presence of pulmonary edema in the OA group caused the EDP to almost double, from 7 to 12 mmHg (P less than 0.01). In contrast, EDP remained constant in TCs. Incremental vascular conductance (IVC), slope of the PAP/Q line, decreased (P less than 0.05) a similar amount in both groups. The above findings are consistent with the modeling of the pulmonary circulation according to a Starling resistor in that large amounts of edema changed EDP but not incremental conductance.

Animals↗

PubMed1971