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Objectives: Accidental hypothermia increases mortality and morbidity after hemorrhage, but controversial data are available on the effects of therapeutic hypothermia. Therefore, we tested the hypothesis whether moderate pretreatment hypothermia would beneficially influence organ dysfunction during long-term, porcine hemorrhage and resuscitation., Design: Prospective, controlled, randomized study., Setting: University animal research laboratory., Subjects: Twenty domestic pigs of either gender., Interventions: Using an extracorporeal heat exchanger, anesthetized and instrumented animals were maintained at 38°C, 35°C, or 32°C core temperature and underwent 4 hours of hemorrhage (removal of 40% of the blood volume and subsequent blood removal/retransfusion to maintain mean arterial pressure at 30 mm Hg). Resuscitation comprised of hydroxyethyl starch and norepinephrine infusion titrated to maintain mean arterial pressure at preshock values., Measurements and Main Results: Before, immediately at the end of, and 12 and 22 hours after hemorrhage, we measured systemic and regional hemodynamics (portal vein, hepatic and right kidney artery ultrasound flow probes) and oxygen transport, and nitric oxide and cytokine production. Hemostasis was assessed by rotation thromboelastometry. Postmortem biopsies were analyzed for histomorphology (hematoxylin and eosin staining) and markers of apoptosis (kidney Bcl-xL and caspase-3 expression). Hypothermia at 32°C attenuated the shock-related lactic acidosis but caused metabolic acidosis, most likely resulting from reduced carbohydrate oxidation. Although hypothermia did not further aggravate shock-related coagulopathy, it caused a transitory attenuation of kidney and liver dysfunction, which was ultimately associated with reduced histological damage and more pronounced apoptosis., Conclusions: During long-term porcine hemorrhage and resuscitation, moderate pretreatment hypothermia was associated with a transitory attenuation of organ dysfunction and less severe histological tissue damage despite more pronounced metabolic acidosis. This effect is possibly due to a switch from necrotic to apoptotic cell death, ultimately resulting from reduced tissue energy deprivation during the shock phase.

We analyzed the results of open treatment in 30 patients with abdominal sepsis (11 patients after trauma [group 1], five patients with pancreatic abscess [group 2], and 14 patients with acute GI pathology [group 3]) uncontrolled by conventional methods as evidenced by continuing fever with leukocytosis and worsening organ functions. APACHE scores at the time of initial laparotomy and at the time of open management, respectively, were: group 1, 19.8 and 16.6; group 2, 8.4 and 12.4; and group 3, 14.2 and 15.0. Twenty-seven patients had multiple system failure. Sixteen (53%) of the 30 patients survived, 73% in group 1, 60% in group 2, and 36% in group 3. Survival correlated well with age less than 50 yr and the absence of multiple organ failure. The technique was easily performed and many of the pitfalls previously reported were not observed. In patients requiring fascial prosthesis, the absorbable polyglycol acid (Dexon) mesh was found to be superior to the nonabsorbable polypropylene. We conclude that the open technique is feasible, effective, and worthy of consideration in patients with extensive wound necrosis and uncontrolled abdominal sepsis.

Recent reports suggest that cimetidine acutely reduces liver blood flow in normal healthy subjects. To determine whether this finding is applicable to critically ill patients, we studied nine polytrauma patients admitted to a surgical ICU. All patients were being monitored with pulmonary artery catheters; all were stable with normal liver function. Liver blood flow was estimated by indocyanine green clearance, before and after administration of a single dose of 600 mg cimetidine. Hemodynamic variables were measured at the same times. Cimetidine did not significantly alter either hepatic blood flow or cardiovascular status in these critically ill patients.

Adequate opsonic capability is vital for normal host defense against infection. The presence of complement fraction 3 (C3) indicates both classical and alternative pathways of complement activation, while complement fraction 4 (C4) indicates only classical pathway activation. C-reactive protein (CRP) functions as an opsonic substance. We measured serum levels of C3, C4, and CRP in 32 trauma patients. Six suffered minor injuries and 26 suffered major injuries. Nineteen of the major-injury patients developed post-trauma sepsis. Complement levels fell immediately after injury and remained low for approximately 8 days in all patients. CRP levels rose by 12 h, peaked at 48 h, and correlated with the severity of injury and the presence of sepsis. Elevated CRP levels after 4 days postinjury indicated the presence of sepsis in all cases. CRP elevations preceded clinical diagnosis by an average of 2.4 days. Serial measurements of CRP are valuable in monitoring the course of trauma patients and may indicate the presence of septic complications before clinical detection.

Macrophages activated at sites of tissue injury produce interleukin-1, which induces hepatocytes to synthesize acute phase proteins (APP). Daily serum levels of C-reactive protein (CRP), haptoglobin (HPT), transferrin (TRF), alpha-1 antitrypsin, and ceruloplasmin (CER) were measured in 60 patients, 30 having inguinal herniorrhaphy (H), 18 cholecystectomy (C), and 12 major abdominal trauma (MAT). APP response was proportional to the level of tissue injury. CRP rose in all groups, MAT greater than C, which was greater than H. HPT levels were depressed in MAT, presumably due to removal of hemoglobin-HPT complexes from the serum. TRF was severely depressed in MAT and may be implicated in the higher infection susceptibility in this group. CER was elevated in C, suggesting a stimulating mechanism in this group as opposed to H and MAT. Explanation for this is unknown. APP changes, especially CRP, may be useful as markers of the amount of tissue damage.