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Nosocomial infections (NI) are one of the most frequent complications during inpatient stays in hospitals. They cause an increase in morbidity and mortality, although they could be largely prevented by observing a few basic hygiene rules. However, the practice of implementing lower hygiene standards results in financial, staff and process-related benefits for the clinical institution. Organizational structures that increase the prevalence of NI are deliberately planned by the hospitals with the aim of economic efficiency. Patients have the right to gain insight into their own records for treatment documentation but not into the hygiene protocols of a clinic. In the case of a damages claim due to NI, the burden of proof initially lies with the complainant who does not, however, have the possibility of obtaining information on the hygiene situation of a hospital as a whole. Within the scope of forensic expertise in cases of suspected NI-related death in hospitals, initial indications of insufficient diagnostic and surveillance measures in a clinic can, when appropriate, be obtained from the treatment documentation records, which then permits further investigations to be initiated by the public prosecution service. This gives the patient or relatives the possibility to assert claims under civil and criminal law.

Gewinnoptimierung versus Patientensicherheit – Immer wieder kommt es in Arztpraxen und Krankenhausern zur „voraussehbaren“ Schadigung von Patienten. Ihre Sicherheit fallt dem Sparzwang zum Opfer. Ermoglicht wird das auch durch die Justiz. Denn obwohl die Einflussmoglichkeiten eines Klinikgeschaftsfuhrers auf die Kostengestaltung und Behandlungsqualitat sehr hoch sind, ist sein Risiko, sich dabei strafbar zu machen, verhaltnismasig gering.

Behandlungssicherheit ist das entscheidende medizinische Qualitätsmerkmal bei der Arztwahl. Sie lässt sich jedoch gegenwärtig von Patienten nur schwer antizipieren. Diese Informationsasymmetrie zwischen Anbietern und Nachfragern medizinischer Leistungen führt wirtschaftstheoretisch zur wettbewerblichen Verdrängung von Leistungserbringern mit hohen Sicherheitsstandards. Zur praktischen Anschauung dient beispielhaft die Geburtshilfe. Gesetzgeber und Rechtsprechung könnten das Marktversagen verhindern durch Präzisierung statt Bürokratisierung von Informationspflichten im geplanten Patientenrechtegesetz1 sowie Anpassung der rechtlichen an die wirtschaftlichen Verantwortungsstrukturen in Gesundheitseinrichtungen.

Anesthesia mortality is remarkably low [1], and thus mass disasters can be discounted. Therefore, it is our task today to analyze rare adverse outcomes [2] so that we can identify some basic, still existing causes for morbidity and mortality and thus be able to overcome thses dangers and approach the infinitely distant goal of zero mortality in our speciality. Regarding safety in anesthesia, the words of an American anesthetist should be quoted [3]: We don’t need more powerful narcotics! We don’t need more sophisticated formulas for the kinetic modeling! We don’t need more studies to substantiate the studies that verified the studies that supported the studies that proved something in 1969! What we desperately need is information about how to better use the data and devices we already have!

A case of malignant hyperthermia (MH) in a three-year eight-month-old girl is presented. Definite symptoms of MH developed in the awake patient 30 min after termination of anaesthesia which had lasted five hours. This postoperative MH-episode resolved promptly following intravenous administration of dantrolene (2.5 mg X kg-1 initially, followed by 5 mg X kg-1 over 12 hours). Results of serial serum samples revealed a steady increase in creatine kinase (CK) concentration with the highest value being observed at the second day, despite dantrolene therapy. The unusual occurrence of MH in the postoperative period, when the major effects of anaesthesia were no longer an important consideration, is discussed with regard to the "human stress syndrome." The necessity to give this information to people usually not familiar in diagnosing MH (e.g., medical personnel in surgical wards) is stressed.

The effects of short-term infusion (10 min) of nifedipine (7.5 micrograms . kg-1) or verapamil (0.15 mg . kg-1) on left ventricular (LV) contractility and on systemic hemodynamics in patients with coronary artery disease, chronically treated with low-dose beta-adrenergic blocking drugs, exhibiting a normal LV function at rest, are presented. In order to analyze the interaction between calcium entry blocking drugs and halothane, the results are discussed in light of data, obtained in similar patients during halothane anesthesia, using identical experimental conditions, which have already been reported. LV dP/dtmax and LV end-diastolic pressure (LVEDP) remained unaffected when nifedipine was infused in the awake patients. Verapamil significantly decreased LV dP/dtmax in patients while awake, but LVEDP did not change. Both calcium entry blocking drugs caused decreases in blood pressure and systemic vascular resistance, accompanied by increases in heart rate. The only significant differences between the awake and the anesthetized patients were the absence of changes in heart rate and the greater reduction in LV dP/dtmax following administration of the calcium entry blocking drugs during anesthesia. Possible explanations for this may include the drugs' combined interference with calcium ion fluxes within the myocardial and smooth muscle fibers, the ability of halothane to modify the response of the autonomic nervous system to the calcium entry blocking drugs and altered kinetics of the calcium entry blocking drugs induced by the volatile anesthetic. It is impossible to determine from the present investigation which of these mechanisms is predominant.

The cardiovascular effects of equipotent doses (1,25 X ED95) of vecuronium (70 micrograms/kg iv) and pancuronium (80 micrograms/kg iv) were studied in 16 patients scheduled for elective coronary artery bypass surgery during steady-state conditions of isoflurane (0,4-0,5 vol% end-tidal)-nitrous oxide anaesthesia. All patients were chronically treated with oral beta receptor-blocking agents. Vecuronium did not cause any significant cardiovascular changes whereas pancuronium produced increases in heart rate (13%), cardiac index (15%) and mean arterial pressure (4%) while systemic vascular resistance decreased (8%). In a second part of this study we analysed whether the magnitude of the vagolytic effects of pancuronium is influenced by the anaesthetic procedure and/or by preoperative beta-blocker therapy. A group of 8 patients who were pretreated with beta-receptor blockers and received fentanyl (7 micrograms/kg) during the anaesthetic procedure showed low control values of heart rate (HR), cardiac index (CI), mean arterial pressure (MAP) and the rate-pressure product (RPP) which were due to both, the antisympathetic effects of beta-blocker therapy and the central vagomimetic properties of fentanyl. The administration of pancuronium (80 micrograms/kg) caused the greatest percentage increases in HR (20%), CI (22%), MAP (8%) and RPP (31%) in this group of patients. In contrast, patients (n = 8) anaesthetized with isoflurane-nitrous oxide who were not on preoperative beta-receptor blocker medication, demonstrated higher haemodynamic control values and less increases in HR (10%), CI (10%) and RPP (15%), MAP did not change. The clinical significance of these findings is discussed.

The pulmonary vascular responses to 50 per cent nitrous oxide were studied in 32 anesthetized patients ventilated to maintain normal PaCO2. One group consisted of sixteen patients with coronary artery disease (CAD) and normal pulmonary vascular resistance (PVR) about to undergo coronary artery bypass surgery. A second group consisted of 16 patients with markedly elevated PVR values due to chronic mitral valve stenosis (MVS). CAD patients showed a significant increase in PVR irrespective of whether halothane or fentanyl was used as background anesthetic. Individual changes, however, did not exceed the upper limit of normal and therefore are not considered to be of clinical importance in these patients. In patients with MVS subjected to fentanyl anesthesia, N2O caused a marked increase in PVR from 357 to 530 dyn . s. cm-5. Halothane anesthesia did not significantly attenuate the effect of nitrous oxide on the pulmonary vasculature as mean PVR increased from 351 to 451 dyn . s. cm-5. These results suggest that the preexisting PVR value is of more importance for the pulmonary vascular response to N2O than the influence of background anesthesia. We conclude that nitrous oxide should be used with caution in patients with elevated pulmonary vascular resistance, particularly in the presence of right ventricular dysfunction and/or right coronary artery disease.

The interaction of halothane anesthesia and intravenous verapamil (0.15 mg/kg over 10 min) was investigated in eight patients scheduled for coronary artery bypass surgery. All patients had a normal left ventricular (LV) function at rest and were on chronic beta-blocker therapy. Halothane produced a marked reduction in mean arterial pressure (MAP), cardiac index, and in LV contractility as documented by a decrease in LV peak positive dP/dt. Verapamil caused an additional depression (16%) of LV peak positive dP/dt accompanied by a small increase (3 mm Hg) in LV end-diastolic pressure. The combined negative inotropic propensities of halothane and verapamil did not produce any overt untoward effects even in the presence of chronic low dose beta-blocker therapy. The predominant hemodynamic effect of verapamil was a systemic vasodilation resulting in a further reduction in MAP (12%) while heart rate remained unaffected. Despite reducing myocardial oxygen demand, caution must be exercised in dose selection in each drug to avoid regional myocardial ischemia due to the combined hypotensive effects of halothane and verapamil.

A case of malignant hyperthermia (MH) in a three-year eight-month-old girl is presented. Definite symptoms of MH developed in the awake patient 30 min after termination of anaesthesia which had lasted five hours. This postoperative MH-episode resolved promptly following intravenous administration of dantrolene (2.5 mg X kg-1 initially, followed by 5 mg X kg-1 over 12 hours). Results of serial serum samples revealed a steady increase in creatine kinase (CK) concentration with the highest value being observed at the second day, despite dantrolene therapy. The unusual occurrence of MH in the postoperative period, when the major effects of anaesthesia were no longer an important consideration, is discussed with regard to the "human stress syndrome." The necessity to give this information to people usually not familiar in diagnosing MH (e.g., medical personnel in surgical wards) is stressed.