Der Anaesthesist
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Raised intracranial pressure is the final common path to brain damage and brain death from a variety of intracranial conditions. Since the introduction of continuous monitoring of intracranial pressure into neurosurgical practice, much work has been undertaken which has advanced our knowledge of intracranial pressure and its management. The treatment of raised intracranial pressure should begin as soon as possible. ⋯ The serum sodium should be checked to ensure that hyponatraemia is not the cause of the intracranial hypertension. If intracranial hypertension persists despite the meticulous applications of these measures, then more specific therapy is required. This essentially reduces to a choice between osmotic agents, hypnotic drugs and drainage of cerebrospinal fluid.
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Massive intraoperative embolism is a life-threatening condition that may lead to immediate death. Important for the survival of the patient are rapid diagnosis and prompt surgical embolectomy. Case report. ⋯ During closure of the sternotomy, heart function was monitored by TEE and we again noted large emboli in the right atrium (Fig. 1 c). To remove these, we reinstated CPB and then placed an inferior vena cava filter. The final TEE control showed free heart chambers with good contractility (Fig. 1 d).(ABSTRACT TRUNCATED AT 250 WORDS)
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Conventional treatment of the adult respiratory distress syndrome (ARDS) includes pressure-limited ventilation, permissive hypercapnia, posture changes, aggressive dehydration, selective lung ventilation, and extracorporeal gas exchange. New strategies such as nitric oxide inhalation, the implantation of an intravenous membrane oxygenator (IVOX), and surfactant replacement are currently under evaluation. Nitric oxide (NO) is an important endothelium-derived relaxing factor that is rapidly inactivated by binding to haemoglobin. ⋯ Furthermore, the surfactant surface tension-lowering activity is abnormal. Thus, administration of exogenous surfactant may have therapeutic benefits. However, the optimal surfactant preparation, the optimal amount required to restore lung surfactant activity, and the optimal method to deliver it to patients with ARDS are unknown and currently under evaluation.
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Trauma scores in emergency medicine quantitatively characterise the severity of trauma victims' injuries and physiologic derangements. They are used to detect and assess patients and have applications in guiding patient care and early therapeutic decisions. In the pre-clinical setting, an effective trauma index meets the following criteria: It is highly reliable with regard to identifying high- and low-risk patients. ⋯ Mortality and patient outcome do not strictly correlate with injury severity scoring. In addition, intubated or paralysed patients were excluded from outcome studies since the scoring systems lacked options for evaluation of pathophysiological conditions after therapeutic interventions. Thus, therapeutic efficacy could hardly be assessed, and subsequent scoring during time periods was impossible.(ABSTRACT TRUNCATED AT 250 WORDS)
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Consumptive coagulation disorders are frequently observed in critically ill patients secondary to other underlying diseases. Initial hypercoagulability leads to subsequent hypocoagulability due to consumption of procoagulant proteins, inhibitors, and platelets. This process evolves in three distinct phases: an initial increase in coagulation activity is characterised by the activation of coagulation factors and platelets without any clinical symptoms of a haemorrhagic diathesis. ⋯ Hypocoagulability, reactive hyperfibrinolysis, and diffuse bleeding lead to an irreversible systemic breakdown of haemostatic mechanisms (disseminated intravascular coagulation, DIC). The laboratory diagnosis of accelerated consumption is based on the course of global coagulation tests (e.g., prothrombin time, activated partial thromboplastin time, platelet count) and more sensitive ("dynamic") activation parameters such as prothrombin fragment F1 + 2, thrombin-AT III complex, fibrin monomers, or d-dimer. Measurements of plasminogen, tissue plasminogen activator, plasminogen activator inhibitor 1, and alpha 2-antiplasmin-plasmin complex provide information on fibrinolytic turnover.(ABSTRACT TRUNCATED AT 250 WORDS)