Charles T. Cloutier

Incidence and timing of hypothermia in trauma patients undergoing operations.

Hypothermia is a major problem in patients who have sustained trauma. We reviewed the cases of 100 consecutive trauma patients transferred directly to the operating room (OR) from the Emergency Department (ED) in a Level I trauma center; 26 cases could not be evaluated. Forty-two patients (57%) became hypothermic at some time between injury and leaving the OR. Fifty-five patients (74%) had a temperature (T) recorded on arrival to the ED; but only 7 (12%) were hypothermic (34.7 degrees +/- 1.5 degrees C). In contrast, 34 patients (46%) arrived in the OR hypothermic (34.8 degrees +/- 0.9 degrees C) and 26 (76%) of these left the OR hypothermic (34.8 degrees +/- 0.9 degrees C). Eight additional patients (20%) arriving in the OR with a T greater than 35.9 degrees C left the OR hypothermic (35.1 degrees +/- 0.4 degrees C). The mean T loss in the ED was significantly greater than that lost in the OR (-0.8 degrees +/- 0.7 degrees C vs. 0.0 degrees +/- 0.6 degrees C; p less than 0.0001, ANOVA). Ninety-two percent of the patients lost temperature in the ED, while 43% of the patients gained temperature in the OR. Hypothermia was associated with lower Trauma Scores, and those patients who were severely hypothermic received more intravenous fluids. However, the impact of fluid infusion was not independent from Trauma Score and did not fully explain the magnitude of the heat loss. These data suggest that hypothermia in trauma patients has a multifactoral etiology related to the magnitude of injury and that the major T loss occurs in the ED rather than in the OR.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnostic laparoscopy as an adjunct to selective conservative management of solid organ injuries after blunt abdominal trauma.

To investigate the efficacy of diagnostic laparoscopy (DL) as an adjunct in patient selection for conservative management of solid organ injuries (SOI) following blunt abdominal trauma, 15 patients with injuries documented by computed tomographic (CT) scanning were prospectively evaluated. Diagnostic laparoscopy was performed in an attempt to characterize SOI, to evaluate the abdomen for associated occult injuries, and to select patients for conservative management or laparotomy. The 15 patients had CT evidence of 17 SOIs (nine spleen, eight liver), and DL allowed adequate visualization of 15 of the 17 injuries. Occult hollow viscus injury was discovered in 2 of 15 patients (one colon, one small bowel) and required laparotomy. In the remaining 13 patients, DL revealed ongoing hemorrhage in four patients and poor visualization in one patient that prompted laparotomy (four splenorrhaphy, one hepatorrhaphy). Conservative management was employed in the treatment of eight patients with findings of minor injury or adequate hemostasis on DL. The average transfusion requirement in this group was 1.8 U. No patient failed conservative management. There were no complications attributable to DL. These data demonstrate that DL may become an effective adjunct in patient selection for conservative management of SOI following blunt abdominal trauma.

Comparison of live bacteria infusions in a porcine model of acute respiratory failure

Acute respiratory failure (ARF) related to sepsis continues to have a high mortality and uncertain pathogenesis. With a reproducible live Pseudomonas aeruginosa infusion pig model, the gas exchange, hemodynamics, and pulmonary clearance of this organism were compared with live Staphylococcus aureus and Escherichia coli. Lightly anesthetized, male, mixed-breed pigs, 15-30 kg, were intubated, allowed to breathe spontaneously, and had femoral artery, central venous, and Swan-Ganz catheterization through cutdowns. After baseline data were collected, approximately 1 X 10(9) organisms/20 kg/min were infused into a central vein for 4 hr with frequent monitoring of the variables. Immediate autopsies were done for related quantitative tissue culture studies. S. aureus pigs maintained a high rate of lung bacterial clearance with pulmonary hypertension, a nonsignificant decrease in PaO2, and relatively normal lungs at autopsy. Ps. aeruginosa and E. coli animals developed systemic hypotension, pulmonary hypertension, increased pulmonary vascular resistance, hypoxemia, and decreased pulmonary clearance. Their lungs had gross congestion and edema. These studies confirm the suitability of E. coli and Ps. aeruginosa infusion into pigs as a model of sepsis-induced ARF in man. The findings also indicate that neither pulmonary hypertension nor bacterial clearance by the lungs is sufficient to cause ARF.

Effects of ibuprofen on a porcine model of acute respiratory failure.

Blockade of the arachidonic acid cascade has been shown to improve survival and hemodynamic alterations in animal models of sepsis and acute respiratory failure (ARF). The effects of intravenous ibuprofen, a cyclooxygenase inhibitor, were observed in 20-30 kg pigs with ARF induced by a continuous LD100 infusion of live Pseudomonas aeruginosa (2 X 10(8)/20 kg/min). Cardiopulmonary parameters were monitored in animals intubated, paralyzed, and ventilated at a 250-ml tidal volume and 0.5 FiO2. Pigs were randomly assigned to three groups: Group I received 2 bolus infusions of ibuprofen (12.5 mg/kg) at 20 and 210 min after baseline; Group II had Ps. aeruginosa (2 X 10(8) CFU/20 kg/min) only; Group III received Ps. aeruginosa and 12.5 mg/kg of ibuprofen at 20 and 210 min of ARF. Ibuprofen alone caused no significant changes in cardiorespiratory parameters. With Ps. aeruginosa infusion, significant pulmonary hypertension, hypoxemia, increased intrapulmonary shunt fraction, and systemic hypotension occurred. In the septic animals treated with ibuprofen, oxygenation was improved by a significant decrease in shunt, pulmonary edema, and pulmonary hypertension.

Complement depletion in a porcine model of septic acute respiratory disease.

In a porcine model of severe septic acute respiratory failure produced by continuous infusion of live Pseudomonas aeruginosa, the role of the complement system was studied by pretreating animals with cobra venom factor (CVF) to deplete C3. Three groups of spontaneously breathing animals were monitored with Swan-Ganz and arterial thermodilution catheters. Group I was pretreated with 80 U/kg of CVF iv 16-18 hours before testing. Group II received Ps. aeruginosa iv (2 X 10(8)/20 kg/minute). Group III was pretreated with CVF and later given the Pseudomonas infusion. The CH50 as a measure of complement activity was less than 7% of normal level in Groups I and III. No changes in respiratory variables occurred in Group I. In Group II, the mean pulmonary artery pressure doubled, intrapulmonary shunt fraction (Qs/Qt) increased, PaO2 decreased, and extravascular lung water doubled in 4 hours. In Group III, the pulmonary hypertension, hypoxemia, increase in Qs/Qt, and increase in EVLW were all significantly less than in Group II. Neutropenia occurred with the Pseudomonas infusion in Groups II and III.

Effect of positive end-expiratory pressure on extravascular lung water in porcine acute respiratory failure.

Recent studies of acute respiratory failure suggest that PEEP causes increased pulmonary interstitial fluid collection and therefore increased extravascular lung water (EVLW). We examined the effect of increasing levels of PEEP on EVLW in 20 to 25-kg pigs with acute respiratory failure induced by continuous infusion of live Pseudomonas aeruginosa (2 X 10(8) organisms/20 kg.min). Animals were intubated, paralyzed, and ventilated at 15 ml/kg tidal volume and an FIO2 of 0.4. Pigs in group 1 were given 4 ml/kg.h of iv fluid (lactated Ringers solution) with no PEEP administered. Animals in groups 2 through 5 were given 0, 4, 17, and 44 ml/kg.h of lactated Ringers solution, respectively, and PEEP was added at 5-cm H2O increments per half-hour, starting one hour after beginning P. aeruginosa infusion. EVLW in PEEP animals was less than or equal to that in controls despite variation in the administration of lactated Ringers solution. This suggests that PEEP may slow EVLW accumulation over time and provide a protective effect that allows increased amounts of crystalloid fluids to be administered.

Prostacyclin in experimental septic acute respiratory failure.

Manipulation of prostaglandins (PG) in animal models of sepsis and acute respiratory failure (ARF) is promising. Prostacyclin (PGI2), a short-acting vasodilator, was evaluated in a porcine model of ARF produced by continuous infusion of live Pseudomonas aeruginosa (Ps.). Cardiopulmonary parameters were monitored in three groups of spontaneously breathing animals that received 0.1 micrograms PGI2/kg/min begun 20 min after baseline (Group I); 2 X 10(8) Ps./20 kg/min (Group II); identical Ps. infusion and then PGI2 begun at 20 min (Group III). The decrease in mean arterial blood pressure and cardiac index with Ps. infusion was improved by PGI2 treatment. In Groups II and III, mean pulmonary artery pressure (PAP) doubled (P less than 0.005) and pulmonary vascular resistance (PVR) tripled (P less than 0.01) by 15 min. Both PAP and PVR were decreased significantly with PGI2 treatment. In both Ps. groups, significant hypoxemia occurred. PGI2 improves cardiac output and acts as a pulmonary vasodilator, but does not improve oxygenation in this porcine model of severe ARF.

Amelioration of pulmonary pathophysiology of adult respiratory distress syndrome by sulindac, a cyclo-oxygenase inhibitor

The effects of sulindac, a cyclo-oxygenase inhibitor, were tested in a bacteremic porcine model of acute respiratory failure produced by a continuous infusion of live Pseudomonas aeruginosa. Control groups received either a single intravenous dose of sulindac (6 mg/kg) 20 minutes after baseline determinations or a continuous infusion of Ps. aeruginosa (10(7) CFU/kg/min) beginning at time 0. The experimental group received both. Sulindac alone had no effect on any hemodynamic or gas exchange parameter. Ps. aeruginosa infusion caused pulmonary hypertension, hypoxemia, increased intrapulmonary shunt fraction, systemic hypotension, and increased extravascular lung water. Sulindac treatment reversed the pulmonary hypertension, hypoxemia, and increased intrapulmonary shunting, prevented the systemic hypotension, but had no effect on the rising extravascular lung water.

Does compliance reflect oxygen delivery in porcine septic respiratory failure treated with positive end-expiratory pressure?

Oxygen delivery (Do2) in patients with acute respiratory failure has been correlated with total lung and chest wall compliance (CT), the optimal positive end- expiratory pressure (PEEP) level reportedly corresponds to maximal Do2. To test the validity of the relationship, we studied the correlation between CT and Do2 in 12 septic pigs with acute respiratory failure induced by continuous infusion of live Pseudomonas aeruginosa bacteria. Cardiac output, pulmonary and systemic arterial BP, blood gases, extravascular lung water, tidal volume, and airway pressure were measured serially in six control animals and six animals receiving increasing amounts of PEEP. There was no significant correlation between Do2 and CT in either group; however, animals receiving PEEP had less extravascular lung water.

DESPITE MAINTENANCE OF SYSTEMIC AND REGIONAL PERFUSION, ENDOTOXEMIA FOLLOWING COMPLEMENT DEPLETION PRODUCES HEPATOCELLULAR DYSFUNCTION

Experimental endotoxemia causes hypotension and a reduction in regional blood flow, including hepatic blood flow. Complement depletion prior to endotoxemia is known to attenuate these perfusion deficits. We depleted complement with cobra venom factor prior to the administration of Escherichia coli lipopolysaccharide in Sprague-Dawley rats and studied the effects of this treatment on systemic hemodynamics, regional hepatic perfusion, and hepatocellular integrity. Complement-depleted endotoxemic rats were compared with untreated rats, rats with complement depletion alone, and rats with endotoxemia alone. Systemic hemodynamics (cardiac index, mean arterial pressure), regional hepatic perfusion (effective hepatic blood flow), and hepatocellular integrity (adenosine triphosphate [ATP], lipid peroxidation) were determined 4-6 hr after the onset of endotoxemia. The endotoxemic animals exhibited a significant decrease in systemic hemodynamic performance and regional perfusion. Complement depletion prior to endotoxemia resulted in preservation of normal systemic and hepatic perfusion. ATP and lipid peroxide levels were significantly abnormal in both groups of endotoxemic animals. Complement depletion alone did not significantly affect any of the variables studied. The maintenance of systemic and regional perfusion during endotoxemia was not cytoprotective implicating direct cellular injury independent of perfusion deficits in the pathogenesis of hepatic failure during endotoxemia.