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Beschreibung / Inhaltsverzeichnis: Abstract Continuous epidural infusion of bupivacaine with the opioid fentanyl represents an effective analgesic method in the therapy of strong postoperative pain after major surgery. Preparation of the required infusion solution in syringes with a volume of 50 ml immediately prior to administration is routinely performed by nursing staff in Germany. The effort required for the preparation is associated with logistical and pharmaceutical difficulties. The preparation of a mixture of bupivacaine hydrochloride 0.06% and fentanyl 0.0002% in 250 ml infusion bags at the pharmacy of the University Hospital Mainz is described. To determine the physicochemical stability, the concentration of bupivacaine-HCl and fentanyl was assessed using HPLC over a period of 32 days; in addition the pH values were determined. After 32 days 95% of the bupivacaine hydrochloride and fentanyl baseline values were recorded. The pH baseline value had decreased from 5.48–5.52 to 0.5–0.7 units. The measured values confirm the physicochemical stability of the mixture of bupivacaine hydrochloride 0.06% and fentanyl 0.0002% over a period of 32 days. The infusion bag can be stored for 4 weeks at room temperature.

Beschreibung / Inhaltsverzeichnis: Abstract Selecting a route for drug administration during CPR requires consideration of the speed with which access can be obtained, the technical difficulties involved in performing the procedure, the associated risk of complications, delays in drug delivery to the central circulation, and the duration of effective drug levels following injection. The peripheral venous route is the safest method, and drug delivery can be enhanced by a fluid bolus after injection of the medication. The circulation time is shortest after central venous injection, but there is some risk of complications. The femoral route is associated with a high incidence of unsuccessful catherization. The endotracheal tube provides an accessible route for administration of most drugs, but peak concentrations are lower than those obtained by other routes. While the results are almost the same as an intravenous injection, the intraosseous route is currently underrepresented in clinical practice. This method must not only be considered in pediatric patients, but in adult patients as well.

Beschreibung / Inhaltsverzeichnis: Abstract A paper published in various US journals on Emergency Medicine in 1997 [9], has raised considerable concerns. The authors [9] question if it is justified to continue to recommend initial ventilation as part of basic CPR when performed by lay-bystanders. A few aspects need to be discussed and some questions have to be answered before any changes in the current recommendations may even be considered: e.g. 1. How convincing does the available evidence support the following hypotheses: 1.1. Lay CPR without mouth-to-mouth-ventilation provides better outcome after cardiac arrest than lay CPR with mouth-to-mouth-ventilation. 1.2. Endotracheal intubation may be detrimental in patients suffering from hemodynamic compromises, particularly from VF [46]. 2. Is it scientifically and ethically acceptable to design and perform prospective randomized controlled trials(RCTs) to evaluate the efficacy of those components of BCLS and ACLS which have in accordance with AHA-, ERC Guidlines and ILCOR Statements in the past been applied in millions of cardiac arrest victims and have obviously enabled the patients to lead a meaningsful life after survival; under conditions of the proposed study design patients of the study group would be left without the treatment option ventilation, thus diminishing their chances of survival. Ad 1: The arguments presented by the authors are hardly convincing. The authors themselves state elsewhere that reluctance to perform mouth-to-mouth-ventilation should not represent a major problem because most cardiac arrests of cardiac etiology occur at home and in the presence of a relative or friend. Moreover, unreliable recommendations for mouth-to-mouth-ventilation(AHA) [4], lack of training, retention of skills and knowledge, and a deficit in motivation include the main causes of the disappointingly low figures of bystander CPR worldwide. This situation cannot be improved simply by eliminating a lifesaving component of CPR-ventilation. Instead, the proposal to abandon the administration of unreasonably high ventilation volumens (800–1200 ml/breath) from the present guidlines and to recommend volumes ranging from 400–500 ml/breath recently made by the ERC should be given serious consideration. Furthermore, equipment and training manikins need to be adapted to these more reasonable volumes. Independently of the mechanisms of slow decreases in SaO2 after cardiac arrest (provided no compressions are performed) independently of gasping,ventilatory effects of standard compression or ACD-HCPR in the absence of mouth-to-mouth-ventilation, it is essential to realise that the patient’s airways need to be maintained open at all times (this is unlike animal experiments where the airways are primarily kept open by the respective tissue structures): The minimum requirement of First Responder CPR is the guarantee that open airways are maintained. It may possibly be discussed if the present sequence of ABC might be changed to CAB, a practice adopted in the Netherlands many years ago, however, outcome trials an CAB have not been published to date. In addition, greater demands should be made of training requirements in BLS, attendance of refresher courses should be required, and other groups of the population should be included into these programmes than only relatives or friends of patients at risk of a cardiac arrest. The programmes need to be made mandatory for greater variety of groups and individuals to increase the efficacy and efficiency of bystander resuscitation. The hypotheses made by the above-mentioned authors are neither scientifically nor ethically acceptable. Ad 2: Pepe’s argument [46] regarding the efficacy of endotracheal intubation (ETI)in VF-patients has not been scientifically proven and lacks conclusive evidence. ETI serves to protect the airways and lungs against aspiration of regurgitated material and to facilitate artificial ventilation including PEEP, both under anaesthesia and resuscitation. The efficacy of ETI in the OR has long been proven in RCTs. There is therefore no reason to believe that the protective capabilities of ETI are in any way different for anaesthesia or CPR. There is thus no need to require RCTs which would place one group of patients at a gtreater risk of mortality from aspiration (under conditions which do not permit intubation) than any other group just because somebody is interested in finding out if there is a higher mortality rate in one group of VF patients which is due to a greater percentage of patients dying from aspiration than from VF. Based on these considerations it follows that the RCTs postulated by Becker e.a. are neither scientifically nor economically or ethically justified apart from the fact that in the German speaking countries not a single ethics committee would agree to a study design similar to that described by Becker e.a.

Beschreibung / Inhaltsverzeichnis: Abstract Objectives: The cardiotoxic properties of bupivacain have been well documented under in-vitro, as well as under in-vivio conditions. A further mechanism of cardiovascular impairment by bupivacaine via the central nervous system gained investigational interest in animal studies. The aim of our study was to demonstrate the effect of a ventriculocisternal perfusion of bupivacain on systemic hemodynamic variabels and their reversability by wash-out with mock-CSF. Methods: After obtaining animal investional commitee consent, nine anaesthetized and relaxated pigs were prepared for a ventriculocisternal perfusion (VCP). Hemodynamic data were obtained by invasive blood pressure measurements in the high and low pressure system as well as cardiac output (thermodilution technique), intracranial pressure and electrocardiogram. Systemic vascular resistance and stroke volume were calculated using standard formulas. A second group of three animals were exposed to an intravenous infusion of the same dose of bupivacain over the same period of time to rule out direct cardiac effects. After instrumentation baseline data were obtained (KO 1) under VCP with mock-CSF for 30 minutes. The mock-CSF was replaced by 0,05% bupivacaine in mock-CSF and VCP was continued with 3 ml · h–1 for 20 minutes. After adminstration of 500 µg bupivacaine data were collected (BU). The bupivacaine solution was replaced by mock-CSF and after twenty minutes hemodynamic measurement were repeated (KO2). Results: The intravenous adminstration of 500µg bupivacaine had no effect on all measured variables. VCP of the same dose resulted in significant increase in heart rate, systolic, diastolic and mean arterial blood pressures. Left and right heart filling pressures as well as systemic vascular resistance were not affected while the stroke volume decreased. After continuation of VCP with mock-CSF hemodynamic changes were reversed. Discussion: Our results demonstrate that bupivacaine initiates an indirect cardiovascular stimulating effect of a VCP with 500 µg of bupivacaine via the central nervous system. The intravenous administration of the same dose had no effect. The centrally mediated cardiovascular effect of bupivacaine was reversed by wash-out with mock-CSF. The cardiovascular stimulation observed in this animal experiment may be of clinical relevance as a potential sign of toxic effects of bupivacaine on the CNS.

Beschreibung / Inhaltsverzeichnis: Abstract We performed a prospective multi-center study in order to determine the causes of 30-day perioperative mortality. Methods: In accordance with the CEPOD-Study and with the kind permission of Dr. N. Lunn, we forwarded two different questionnaires to 135 hospitals. One questionnaire was to be answered by the anaesthetist and the other one by the surgeon involved in cases of perioperative death within the first 30 days after the operation. 12 out of 135 addressed hospitals agreed to participate in the study. These included four small hospitals, six medical centres of medium capacity (about 500 beds) and two University hospitals. In order to obtain an exact description of the events leading to perioperative death, the questionnaires consisted of approximately 60 questions for the collection of demographic data and the surgical as well as anaesthesiological perioperative management. Results: From 1989 to 1993 more than 300 cases of perioperative death were reported. Only 200 cases could be analyzed due to incompletely answered or unreturned questionnaires. The mean risk-classification (ASA) was 3.46, mean age 74.6 years. Approximately 40 percent of deaths occurred in patients older than 80 years. More than 80 percent of patients had at least one pre-existing cardiovascular disease with prevalence of 41% for pulmonary and gastrointestinal diseases. In the majority of cases abdominal operations were performed, followed by hip-surgery and surgery of the aorta. In 86% of the cases, the surgeon was experienced and had performed the respective operation more than 20 times. In 38.2% an anaesthetist intraining was responsible for anaesthesia, but only 11.6% were without supervision of a specialist anaesthetist. The majority of patients received general anaesthesia (78%) and 8.5% had a combination of EDA and general anaesthesia. Regional anaesthesia was performed in 12.5%, local anaesthesia in only 1%. The average blood loss was approximately 1.600 ml (with a very wide range) and 42.5% of the patients needed a transfusion of blood components, primarily in the form of packed red blood cells. Seventeen serious incidents occurred intraoperatively, including three „exitus in tabula”. Four patients died shortly after the operation in the ICU, the other ten incidents were managed in the operating room. In 11 of 17 incidents the patients suffered a cardiac arrest; nine patients were resuscitated. Two patients were not resuscitated in view of pre-existing diseases and inoperability. All of the hospitals had an ICU for postoperative care, but two of the smaller hospitals had no recovery rooms. In 22 cases of emergency operations, there was a delay due to a lack of personnel or to logistic problems. In five of these cases, the delay was described as a possible cofactor of perioperative mortality. The most frequent causes of perioperative death were myocardial failure (33.7%) and multi-organ-failure (19.2%), followed by respiratory insufficiency (13%) and septic shock in 9.3%. A necropsy was carried out in only 28 of 200 perioperative deaths (14%); 13% of the cases were discussed in a surgical and only 2.5% in an anaesthesiological mortality-conference. In 9 out of 12 hospitals no mortality-conferences were held. All surgeons and anaesthetists were asked for self-assessment on the basis of an analog scale ranging from 0 and 10 points. The average score was 8.52 points (surgical management) and 9.36 points (anaesthesiological management respectively), which is not always in correspondance with the information provided in the questionnaires. Conclusions: In order to further reduce perioperative mortality in critically ill patients, every hospital should aim to optimize the structure of the surgical and anaesthesiological departments. A delay due to logistical or personnel problems may be a co-factor in perioperative mortality. Recovery rooms with experienced personnel should be the standard in postoperative anaesthesiological care. All cases of perioperative death should be discussed in a mortality conference by anaesthetists and surgeons in order to determine possible medical or logistic problems and avoid them in future.

Beschreibung / Inhaltsverzeichnis: Abstract Neurogenic pulmonary edema (NPE) is a rare but always life-threatening complication in patients with central nervous system lesions. NPE is evident if patients shortly after cerebral lesions suddenly develop pulmonary edema and other causes of the symptoms, such as aspiration of gastric content, congestive heart failiure and direct toxic exposure, are ruled out. Methods: The current body of literature, partially obtained by computer-guided search (Winspirs) regarding epidemiology, pathophysiology and therapy of NPE was reviewed. Additionally, the case of a patient who developed a sudden pulmonary edema after an episode of tonic-clonic seizures is analyzed. We first provide information about history, definition, incidence and mortality of NPE. Second, a case report of a postictal NPE is presented to illustrate the clinical picture of NPE, and the applied therapeutic strategies are discussed. Third, recent pathophysiologic concepts about symptoms and possible therapeutic principles are reviewed. Fourth, a rational therapeutic plan for the prehospital emergency therapy of NPE is outlined. Results: The different ethiologies all have one characteristic feature: an acute emergency which causes increased intracerebral pressure (ICP). NPE is known in patients after cerebral trauma, intracranial hemorrhage, stroke, intracranial tumor or seizures. The incidence is estimated at around 1% after cerebral trauma, at 71% after cerebral hemorrhage and at 2% after seizures. Mortality is appraised to lie between 60 and 100%, independent of etiology. There is a definite pathophysiologic sequence leading to NPE: a central nervous system lesion causes a sudden increase in ICP which triggers an upregulation of sympathetic signal transduction to assure brain perfusion. Increased tonus of venous and arterial vessels and of myocardial function are the immediate consequences. However, if systemic vascular resistance (SVR) increases excessively, left ventricular failure and finally pulmonary edema (NPE) may result. Additionally, the protein-rich edema fluid points to an increased endothelial permeability within the pulmonary circuit. This is thought to be caused by the acute pressure increase and by neurohumoral mechanisms, possibly similar to those described for the systemic inflammatory response syndrome (SIRS). The most important central nervous system structures involved in NPE are the medulla oblongata and the hypothalamus. Conclusion: NPE is always a life-threatening symptom after increased ICP, where immediate therapeutic interventions are imperative. A rational therapeutic approach needs to be focused on decreasing ICP as primary goal. Additionally, attempts should be made to optimize body oxygenation, decrease pre- and afterload and increase myocardial contractility. Postictal patients suspicious for incipient ventilation problems must be admitted to hospital for further evaluation.