Efficacy of an extracorporeal endotoxin adsorber system during hyperdynamic porcine endotoxemia.

BACKGROUND: Endotoxemia is a crucial factor in the pathogenesis of sepsis. Elimination of endotoxin is aimed at the reduction of sepsis-related morbidity and lethality. The objective of this study was to examine the impact of an endotoxin adsorber on hemodynamics, O(2) exchange and metabolism during resuscitated porcine endotoxemia. METHODS: Twenty pigs were randomized into 2 intervention groups (n = 7 each) and 1 control group (n = 6). Endotoxemia was induced by continuous intravenous application of lipopolysaccharide for 8 h. Adsorber therapy was started at the same time as the induction of endotoxemia or 2 h later. An extracorporeal hemoperfusion device using immobilized human serum albumin for endotoxin adsorption was used. RESULTS: Hemodynamic, metabolic and acid-base parameters, as well as the kinetics of interleukin (IL)-6, IL-8, IL-10 and tumor necrosis factor-alpha, were characteristic for endotoxic shock. Endotoxin plasma levels were low (arterial, hepatic and portal vein). None of the parameters were significantly influenced by the adsorber system. CONCLUSION: Despite typical clinical signs of endotoxemia, the adsorber system had no significant effect on hemodynamic, metabolic and acid-base parameters during endotoxic shock. The reasons for the absence of an effect are elusive; however, failure of the method per se or exceeded capacity of the adsorber cannot be excluded.

Is the activity of soluble CD14 enhanced following major trauma?

BACKGROUND: The molecule CD14 acts as a receptor for the protein-bound endotoxin (lipopolysaccharide [LPS]) complex and mediates the cellular effects of LPS. The soluble formation, sCD14, is supposed to neutralize circulating LPS (i.e., LPS antagonist) or transfer LPS effects to endothelial cells (i.e., LPS agonist). OBJECTIVE: To elucidate the release of sCD14 per se in patients with major trauma in the early posttrauma period. Our a priori hypothesis was that sCD14 release depends on the plasma LPS concentration simultaneously measured. PATIENTS: In a prospective study, 65 patients with multiple injuries (Injury Severity Score, 9-75) were enrolled. The patients were rescued by the medical helicopter service and directly admitted to our clinics. The plasma concentrations of sCD14 (enzyme immunoassay) and LPS (chromogenic limulus amebocyte lysate test) were analyzed. The first blood sample was collected immediately at the accident site. The following samples were drawn at intervals from 2 hours to daily for 2 weeks. RESULTS: Sixty-one patients survived the observation time. Immediately after trauma, their mean sCD14 level was not different from that of healthy individuals. Two hours later, a pronounced increase of sCD14 was observed and sustained throughout the observation period. Even nonsurvivors showed an increased sCD14 release, but less pronounced. In all patients, plasma LPS levels were elevated during the first 12 hours. CONCLUSIONS: Major trauma caused an increased release of sCD14. This elevation, however, was not correlated to LPS levels or to the severity of trauma (estimated by trauma scores). We found no evidence that sCD14 levels are of prognostic value regarding survival. Furthermore, the release of sCD14 did not occur in an LPS-neutralizing manner, but rendered possible an LPS-independent mechanism.

Bacterial colonization and endotoxin contamination of intravenous infusion fluids.

Bacterial colonization and endotoxin contamination of intravenous infusion fluids and catheter systems were examined in a surgical intensive care unit. Nineteen consecutive patients were randomly assigned to 48 h (N = 8) or 96 h (N = 11) change of infusion systems. Fluid from infusion bottles (51), infusion bottles plus burettes (102) and catheter systems (104) was cultured quantitatively for aerobic and anaerobic bacteria. Swabs (362) were taken from three-way stopcocks before and after the in-line infusion filters. Total and free endotoxin levels in infusion fluids were measured by quantitative chromogenic Limulus assay. The overall rate of bacterial colonization of bottles/burettes was 7.8% at 48 h and 15.7% at 96 h, while colonization rates of catheter fluid were 34.0% and 24.1%, respectively (n.s.). These high rates of colonization, despite regularly reinforced hand disinfection practices, may be explained by the high frequency of manipulations of the catheter systems, during acute interventions in emergency situations. Cell-bound endotoxin was found in 8.8% of the samples, but only 2.5% of the samples contained free endotoxin. The data support the use of in-line infusion filters, with bacterial-retaining property; however, these filters need not have endotoxin-retaining properties.

[Change in the surgical strategy in acute and complicated colonic diverticulitis]. / Chirurgischer Strategiewandel bei akuter und komplizierter Colondivertikelerkrankung.

The records of 312 patients with acute colonic diverticulitis were reviewed. 129 patients required an operation. The operative management is presented and compared to the international literature. One-stage resection was performed in 79% of all patients. In 84% of patients with a localized inflammation a one-stage resection was possible. Fifty-seven percent of patients with peritonitis due to colonic perforation required a multiple stage procedure. In 70% the preferred surgical procedure of multiple stage treatment was Hartmann's operation. These therapeutical regimens are current standard. Lethality was 1.6% for all 129 patients and the postoperative morbidity was 22%.

A case of sporadic Echinococcus granulosus infection originating from Southern Germany.

A 67-year-old woman with cystic echinococcosis (CE) is presented. She had complained of upper abdominal discomfort due to large hepatic cysts. These cysts showed no typical infrastructure characteristic for CE and she had never left the rural areas of southern Germany. Most remarkably, this area is highly endemic for alveolar echinococcosis, caused by Echinococcus multilocularis, but only sporadic cases of CE have been described. Due to the discrepancy between positive Echinococcus serology, atypical morphology and residency in an area non-endemic for Echinococcus granulosus, diagnostic puncture was performed with albendazole coverage. Puncture was complicated by anaphylaxis, from which the patient recovered without sequelae. The diagnosis of CE was highly likely due to the combination of positive serology with post puncture anaphylaxis, increasing antibody titers and eosinophilia. Retrospectively, the cysts had initially corresponded to the WHO stage CE 1. The patient was treated with albendazole for 15 weeks. Under treatment, the parasitic membrane detached from the cyst wall, revealing characteristic morphology for CE, now corresponding to the WHO stage CE 3. The patient remained asymptomatic during follow-up visits.

[Is there a drug treatment approach for prevention and therapy of fat embolism syndrome?]. / Gibt es einen medikamentösen Ansatz zur Prophylaxe und Therapie des Fettemboliesyndroms?

The pathogenesis of fat embolism has been subject to considerable debate ever since it was first described by Zenker in 1864. The clinical course, management and pathophysiology of a typical case are described. As no single causative factor has been implied in the development of fat embolism, its therapy and prevention primarily involves the adequate treatment of shock and of the underlying traumatic lesions.

Endotoxin-induced release of interleukin 6 and interleukin 1 beta in human blood is independent of tumor necrosis factor alpha.

It has been suggested that tumor necrosis factor alpha (TNF alpha) acts not only by direct toxicity, but also as a proximal mediator which is able to induce the production of other cytokines, especially interleukin 6 (IL-6) and interleukin 1 beta (IL-1 beta). In order to test the dependence of the release of these two cytokines from leukocytes upon induction by TNF alpha, we stimulated whole blood in vitro with TNF alpha and compared the cytokine levels with those induced by endotoxin. The cytokine release was also determined after stimulation by endotoxin with added TNF alpha and by endotoxin with monoclonal antibodies against TNF alpha (anti-TNF alpha) added in order to reduce TNF alpha. Unstimulated blood samples were used as controls. The plasma levels of both IL-6 and IL-1 beta were significantly higher after stimulation with endotoxin than after stimulation with TNF alpha. TNF alpha did not induce cytokine levels significantly higher than controls. The cytokine levels were the same whether or not anti-TNF alpha was included together with the endotoxin. Plasma from samples with added anti-TNF alpha had no detectable TNF alpha. Our results indicate that the leukocyte-derived production of IL-6 and IL-1 beta in whole blood is stimulated directly by endotoxin and is not mediated by TNF alpha.