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Objective: To study outcome from severe head injury (SHI: GCS < or = 8) and to investigate impact of prehospital factors and clinical intensive care parameters on outcome. To compare with former study results (1980-88) of our clinical setting., Methods: Retrospectively, the history of 228 patients with SHI treated between 1988 and 1995 was looked into. The outcome was measured with the Glasgow Outcome Scale (GOS) post intensive care (median 9, min-max 2-77 days) and 6 months after trauma by a questionnaire. The GOS was related to age, Glasgow Coma Scale (GCS on the scene), prehospital hypotension and hypoxia (HH), intracranial pressure (ICP), cerebral perfusion pressure (CPP), intensive therapy including Tromethamine and/or Thiopentone. The rate of infections was determined., Results: Increasing age influences outcome negatively. Prehospital GCS and HH were significantly correlated with outcome. GOS of 30 patients with HH: GOS 1: 53%, GOS 2 + 3: 27%, GOS 4 + 5: 20%. GOS of 40 patients without HH: GOS 1: 25%, GOS 2 + 3: 10%, GOS 4 + 5: 65%. During intensive care the level of CPP (not ICP) as well as tromethamine and/or thiopentone treatment for control of elevated ICP were significantly correlated with outcome. Mortality rate in 32 patients with CPP < 50 mmHq was 69%, in 29 patients with CPP > 50 mmHg only 20%. Patients treated additionally with Tromethamine and Thiopentone because of uncontrollable intracranial hypertension showed a significantly worse outcome: GOS 1: 66%, GOS 2 + 3: 6%, GOS 4 + 5: 28%, compared to those who needed neither Tromethamine nor Thiopentone: GOS 1: 27%, GOS 2 + 3: 18%, GOS 4 + 5: 55%. Thiopentone treatment was not associated with an increased rate of pulmonary and other infections. In comparison to our former outcome study, covering the years 1980-88, we have not seen any improvements in outcome, despite modifications in intensive care protocols., Conclusions: Prehospital hypotension and hypoxia have a significant negative impact on outcome by causing secondary brain damage. Despite various modifications in intensive care therapy an unchanged portion of secondary brain damage will not prove treatable. Therefore, prevention or early aggressive treatment of hypotension and hypoxia is the most promising way of improving outcome after severe head injury at the moment.

Introduction: The prehospitaly initiated endotracheal intubation and controlled ventilation, is especially in multi-system-trauma cases, recognized to be the "gold standard". Thus especially in view of the increasing demands being placed upon the quality of prehospital emergency treatment in general, the quality of such prehospital induced ventilation, is becoming of increasing importance. Thereby we must take into consideration the limited possabilities, which are afflicted with a high degree of uncertainess, which we have at our disposal to effectively evaluate the efficiency of emergency ventilation. The purpose of our study within a collective of severely traumatized patients, was to determine the quality of prehospitaly induced ventilation with regards to the adequacy of oxygenation and ventilation and as a result of our findings, to identify areas for procedural optimization., Results: The prospective study over an one year period involved n = 104 trauma cases (male: 79; female: 25/age: 39.8 +/- 20.8 years/ISS: 28.1 +/- 15.3) whose prehospital emergency treatment required and included endotracheal intubation and controlled ventilation. All patients were subject to a prehospital pulse oxymetric monitoring, whereas none were subject to an objectivating apparatus monitoring of ventilation: 94.2% of the patients were upon admission adequately oxygenated (paO2 > 80 mmHg); only one patient was hypoxemic (paO2 < 60 mmHg). 46.2% were adequately ventilated (paCO2: 35-45 mmHg), 43.2% however were hyperventilated (paCO2 < 35 mmHg), and 10.6% hypoventilated (paCO2 > 45 mmHg). A statistical significant relation between hyper-/hypoventilation and the degree of severity of trauma as well as to the individual injury pattern was not evident. However with reference to age: The group of > 60 years of age were significantly more frequently hyperventilated (paCO2 < 30 mmHg: 31.2%; p < 0.05). A noteworthy accumulation of hypoventilation was experienced amongst the group of patients, who during the prehospital treatment phase were hemodynamic instable (shock index > 1)., Conclusion: In summary it is evident, that as a rule, even very severe traumatized patients can prehospitaly be adequately oxygenated and that such oxygenation can with the assistance of pulse oxymetric monitoring be effectively controlled. Remaining problem is the emergency physicians ability to evaluate and control ventilation. The prehospital determination of minute volume (MV) in accordance with the presently valid recommendation: MV = 100-150 ml/kg body weight, in the majority of trauma cases results in inadequate ventilation. The introduction of an objectifying monitoring method is therefore urgently required.

Unlabelled: There is compelling data from several clinical studies on the impact of various anti- and proinflammatory mediators on traumatized patients. Immediate trauma-related results, however, are only available from animal experiments so far. Therefore, in this prospective clinical study the following questions were addressed: (I) Is there any marker in the preclinical phase that give information independent of and better than conventional studies conducted so far, (II) does this possible factor prove to be a (significant) predictor of late complications and/or poor overall outcome, and (III) does this mediator provide information that can alter treatment decisions?, Methods: Upon approval of the local IRB/IEC, 85 patients (pts) were enrolled who suffered from multiple injuries. The pts were rescued by the helicopter-based service of the German Army Hospital in Ulm. The first blood samples were drawn at the site of accident and at admission, then in hourly to daily intervals. The plasma concentrations of following mediators were analyzed: Prostanoids, products of O2-radicals, soluble adhesion molecules, various cytokines, C-reactive protein, creatinine kinase, and neopterin. All values were calculated in relation to the actual plasma protein content to eliminate fluid-induced dilution effects. Subsets of patients were performed according to the severity of trauma (ISS < 9; 9-17; 18-31; > 32), based on the different injury pattern, and survivors versus nonsurvivors as well., Results: As early as at the scene of accident, all patients revealed a severity-dependent increase in most mediators' plasma levels. There was, however, also a pattern-related inflammatory response that was most pronounced in pts who had suffered from thoracic trauma irrespective of whether it was associated with multiple trauma. In a total, 15 pts died within 72 h after the accident. In those casualties, the plasma concentrations of prostaglandin E2 (P < 0.03), glutathione (P < 0.01) as well as creatinine kinase (P < 0.05) were more markedly elevated when compared with survivors., Conclusion: Although there were severity-dependent as well as pattern-related releases of various mediators, which in part were more apparent in nonsurviving patients, we failed in proving any predictive marker to specifically discriminate outcome.

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.

Membrane-fixed CD14 acts as a receptor for the protein-bound endotoxin (LPS) complex and mediates the cellular effects of endotoxin. Soluble CD14 (sCD14) is suggested to neutralize circulating LPS, i.e., acting as an endotoxin antagonist. The aim of this study was to elucidate the release of both sCD14 and endotoxin in traumatized patients, starting from the earliest phase after trauma. A total of 15 patients (O ISS = 19, 9-75) suffering major trauma were enrolled in this prospective study. Blood samples were collected as early as immediately at the site of accident, on hospital admission, and thereafter hourly, then daily. For patients (O ISS = 47) died within 24 h because of their severe injuries. Immediately after the accident as well as during the first 2 h after hospital admission, the mean sCD14 levels of surviving patients did not differ from those of healthy volunteers (n = 53). Thereafter, however, sCD14 increased continuously in the trauma group. The concentrations remained elevated throughout the entire observation period. There was, however, no relation between the sCD14 release and the pattern or the severity of injury. In contrast, endotoxin levels revealed a pattern-specific release. The highest plasma concentrations of LPS were observed in patients suffering from (additional) thoracic injury. On the basis of these results we conclude that the release of sCD14 after trauma does not reflect a strict principle such as action/reaction caused by the appearance of endotoxin immediately after the injury. Soluble CD14 is more likely release by an endotoxin-independent mechanism.