Prevention of wound infections is a challenge in clinical practice. The aim of this study was to assess the efficacy of polyhexamethylene biguanide (PHMB, polihexanide) 0.04% on acute traumatic wounds. It was a randomized, double-blind, placebo-controlled prospective trial which included 61 patients. The polihexanide group showed a significant decrease in log10 colony-forming units (cfu) (P < 0.001) after 60 min treatment in comparison to baseline cfu, whereas the Ringer solution group did not show a significant change in cfu during 60 min treatment. Treatment of polihexanide 0.04% resulted in a significant reduction of bacterial load in acute traumatic wounds.

In a rat model of traumatic brain injury cell activation was characterized immunohistochemically from 2 h up to 2 weeks. Reactive astrocytosis became apparent perivascularly and in the grey matter within 4 h after trauma. Increased OX42 immunoreactivity indicated microglial activation in cortex and hippocampus as early as 4 h, whereas up-regulation of MHC class II (OX6) was evident in white matter tracts at 24 h. Although macrophage (ED1) numbers increased in the meninges and perivascularly, brain infiltration appeared marginal. Accumulation of lymphocytes and granulocytes was not observed. Our results show that traumatic axonal injury induces a rapid and sustained glial activation in the absence of leukocyte infiltration. Thus, cell activation following diffuse trauma strongly differs from that found after focal brain damage, awaiting further functional characterization.

Between April 1992 and March 1994 Duo-cup endoprosthesis was inserted in 90 patients (mean age 80 years, 49-99 years) with fractures of the femoral neck, admitted to the Division of Trauma Surgery. University Hospital of Zürich, Switzerland. The purpose of this study was the clinical and radiological evaluation during a follow-up period of 3 to 24 months. The mechanism of trauma, pre-existing morbidity of the patients, operative stress and postoperative complications were analyzed retrospectively. The functional outcome of 75% of the patients was assessed according to a standardized protocol. In the follow-up, 85% of the patients showed good to excellent results. Radiolucent zones around the cement-bone interface were detected by x-ray scan in 7 patients without loosening of the prosthesis. In half of the patient group heterotopic ossifications appeared, but without clinical relevance. Complications appeared as followed: 3.3% superficial infections, 3.3% deep wound infections followed by replacement of the prostheses, 8.8% hematomas, 2.2% extraprothetic luxations. The perioperative lethality was 0%, whereas the lethality during hospitalisation was 2.2% and the average lethality of the first postoperative year 13%. Overall, 93% of the patients returned to their pre-existing housing environment. These results show that good to excellent clinical and functional results can be achieved in the treatment of femoral neck fractures with duo-cup prosthesis in elderly patients which enables the patients to return in their known social environment.

Controlling the extent of inflammatory responses following brain injury may be beneficial since posttraumatic intracranial inflammation has been associated with adverse outcome. In order to elucidate the potential role of anti-inflammatory mediators, the production of interleukin-10 (IL-10) was monitored in paired cerebrospinal fluid (CSF) and serum of 28 patients with severe traumatic brain injury (TBI) and compared to control samples. The pattern of IL-10 was analyzed with respect to the patterns of IL-6, tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) in both fluids during a time period of up to 22 days. In parallel, the function/dysfunction of the blood-brain barrier (BBB) was monitored using the CSF-/serum-albumin quotient (Q(A)) and compared to intrathecal cytokine levels. Mean IL-10 concentration in CSF was elevated in 26 out of 28 TBI patients (range: 1.3-41.7 pg/ml) compared to controls (cut-off: 1.06 pg/ml), whereas only seven patients had elevated mean IL-10 concentration in serum (range: 5.4-23 pg/ml; cut-off: 5.14 pg/ml). The time course of IL-10 was similar in both fluids, showing a peak during the first days and a second, lower rise in the second week. Intrathecal IL-10 synthesis is hypothesized since CSF-IL-10 levels exceeded serum-IL-10 levels in most of the patients, IL-10-index (CSF/serum-IL-10/QA) was elevated in 23 individuals, and elevation of CSF-IL-10 showed to be independent from severe BBB dysfunction. Neither CSF nor serum IL-10 values correlated with the dysfunction of the BBB. IL-10, IL-6 and TGF-beta1 showed similar patterns in CSF over time, whereas rises of TNF-alpha corresponded to declines of IL-10 levels. Our results suggest that IL-10 is predominantly induced intrathecally after severe TBI where it may downregulate inflammatory events following traumatic brain damage.

Patients with severe head injury still carry a high risk of mortality and morbidity despite progress in clinical management (Frankowski et al. 1985; Alberico et al. 1987). Major causes of mortality in these patients are untreatable elevated intracranial pressure (ICP) in the early phase and septic-infectious complications during the later phase (Shackford et al. 1989). The importance of inflammatory events following head trauma even in the absence of systemic injuries has been recognized. Within a short period of time after hospitalization these patients show a depressed T-cell function, an anergy to delayed-type hypersensitivity skin testing, a decrease in the expression of interleukin-2 receptors on T-cells and, furthermore, a diminished in vitro interleukin-2 and γ-interferon production of T-cells as well as suppressed cell cytotoxicity (Quattrocchi et al. 1991; Hoyt et al. 1990). However, the depression of the peripheral immune system may be of a secondary nature and may be regulated by immunological events initiated as a result of the traumatic injury within the brain. In particular cytokines produced and released in the central nervous system (CNS) may play important roles in the pathophysiological events following brain trauma.

A profound inflammatory response is initiated immediately following traumatic brain injury (TBI) and is characterized by the release of several cytokines with pro- and anti-inflammatory functions. In order to elucidate which cytokines are released in the human brain in response to injury as well as in the peripheral compartment, IL-1, IL-6, IL-8, IL-10, TNF-α and TGF-β were monitored in CSF and serum of severely brain-injured patients. Furthermore, we investigated the possible modulation of systemic reactions by IL-6 and the ability of IL-6 and IL-8 to promote the synthesis of nerve growth factor.

Csuka, E.; Morganti-Kossmann, C. M.; Lenzlinger, P. M.; Trentz, O.; Ammann, E.; Kossmann, T. Author Information