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Purpose: There is increasing evidence for gender differences in the pharmacokinetics and pharmacodynamics of anaesthetic drugs and neuromuscular blocking agents, e.g. rocuronium (Roc). Females require 30% less Roc than males to achieve the same degree of neuromuscular block and onset times are shorter. However, whether this leads to an improvement of the intubation conditions in females is unclear.Methods: After approval of the ethics committee 60 female and 60 male patients were each randomised into 2 groups to receive 0.6 mg/kg body weight Roc or 1.0 mg/kg succinylcholine (Sux; control group). Induction: thiopentone (5 mg/kg), fentanyl (3 microg/kg) then Roc (Roc groups) or Sux (Sux groups) and tracheal intubation after 60 s. Time to intubation, glottic exposure and intubating conditions were assessed.Results: Men were significantly larger and heavier (p<0.001) than women, but the body mass index was comparable (ns). Number of attempts, time to intubation, and Cormack grades were comparable (ns). However, the rate of clinically acceptable intubation conditions was significantly higher in the female compared to the male Roc group: 80% vs 47%, p<0.05. The incidence of clinically acceptable intubation conditions in the female Roc and Sux groups were similar (80%).Conclusion: The intubation conditions after Roc were significantly better in women than in men. The differences were Roc-related and did not occur in the control groups. [ABSTRACT FROM AUTHOR]

We report the case of a penetrating injury of the abdomen by an iron bar of a side impact protection after a traffic accident. The iron bar of the side impact protection entered the lateral thigh, penetrated the pelvis and retroperitoneum and left the body lateral of the spine at the L4 level. The patient was fixed by the iron bar to the car seat. The mechanism of the accident, the patient's symptoms and the initial treatment of the patient are described and discussed. [ABSTRACT FROM AUTHOR]

Multiple organ failure (MOV) still represents the leading medical and economical problem in the care of the critically ill surgical patient. Although the incidence of MOF has tended to decrease over the last several years reflecting improved surgical and supportive therapy in the ICU, prognosis still remains serious when MOF develops. MOF seems to reflect a dysregulation of host-defence systems, such as innate immune, coagulation and complement systems, which are likely to reflect a more general dysregulation of cellular and subcellular functions, such as signal transduction and stress gene expression. Besides complexity and redundancy of the mediator systems involved, their beneficial local reparative as opposed to detrimental systemic effects may have contributed to the disappointing results of anti-mediator strategies in the treatment of MOF and sepsis. Although treatment of the underlying disease remains the cornerstone of the care of the critically ill patient to prevent MOF, recent results indicating a decreased mortality in severely septic patients receiving activated protein C as a supportive treatment suggest that modulation of the mediator cascades of sepsis and MOF remains a generally promising therapeutic strategy. [ABSTRACT FROM AUTHOR]

Copyright of Anaesthesist is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Anaesthesist is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Innate and acquired immunity plays a pivotal role in the host defense response. Pain, stress, necrotic tissue and invading microorganisms are known modulators of the complex immune response of patients undergoing major surgery. Anaesthesia itself or perioperative interventions of the anaesthesiologist may substantially alter the immune function with potential impact on the postoperative course. For instance, transfusion of allogenic blood and administration of dopamine or metoclopramide may interfere with immunity. Stress and pain are associated with immune tolerance, increased susceptibility to infection and tumor spreading in animal models. Thus, anaesthesia may--through modulation of the neurohumoral stress response--indirectly affect immunity of the surgical patient. In particular epidural anaesthesia and/or administration of epidural or spinal opioids seem to attenuate the stress response with beneficial effects on cellular and humoral immunity. In addition, anaesthetics, such as etomidate, propofol, or thiopentone and opioid analgesics may directly affect function of immune competent cells. However, these actions may only be apparent with high or supraclinical concentrations and/or long-term exposure. Regarding the latter, evidence suggests that long-term sedation using thiopentone in neurosurgical patients is paralleled by infectious complications in a dose-dependent manner. At present, no data are available regarding the significance of the observed alterations associated with various anaesthetic procedures of the incidence of postoperative complications associated with impaired immunity, such as infection or metastatic spreading in oncological surgery. [ABSTRACT FROM AUTHOR]

Copyright of Anaesthesist is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: Recent evidence suggests a possible role for Haeme oxygenase (HO)-derived carbon monoxide (CO) in the regulation of vascular tone through elevation of cyclic 3'-5' guanosine monophosphate (cGMP). Previous work from our laboratory has shown that blockade of the HO pathway by tin-protoporphyrin-IX (SnPP) after resuscitation from hemorrhage leads to a specific and profound increase in portal resistance while neither systemic nor hepatic arterial resistance are affected. We therefore investigated the organ-specific expression pattern of the stress-inducible protein haeme oxygenase-1/heat shock protein 32 after haemorrhage and resuscitation.Materials and Methods: After approval of the protocol by the local review board, male Sprague-Dawley rats (n = 6/group) were anaesthetised with pentobarbitone, instrumented for assessment of central haemodynamics and subjected to haemorrhagic hypotension (40 mm Hg for 1 h) followed by resuscitation with 60% shed blood and Ringer's solution or a time-matched sham protocol. Samples of liver, spleen, kidney intestine, aorta, and lungs were harvested 5 h after the onset of resuscitation and subjected to Western-blot analysis using a specific anti-rat HO-1/hsp 32 antibody (StressGen, Sidney, Canada).Results: Resuscitation with shed blood/Ringer's solution restored central haemodynamics and acid-base status while significant haemodilution was observed. Haemorrhage and resuscitation led to strong induction of HO-1 in the liver and slight induction in aortic tissue, while no increase in steady-state protein levels was observed in the other organs studied.Conclusion: These results suggest a specific contribution of the HO/CO pathway to maintenance of low hepatic portal resistance in vivo in a clinically relevant model of haemorrhagic shock and adequate resuscitation. [ABSTRACT FROM AUTHOR]