Der Anaesthesist
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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)
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A new closed tracheo-bronchial suction system was evaluated. With this device the patient need not be disconnected from the ventilator during suctioning, and can thus have a continuous supply of oxygen. The closed suction system is attached to the patient's endotracheal tube and ventilator Y-piece. The catheter, which is enveloped by a plastic sheet, can remain connected to the patient for as long as 24 h (Fig. 1). MATERIALS AND METHODS. In the medical and surgical intensive care unit of Alt/Neuötting General District Hospital, 39 trials on 16 mechanically ventilated patients receiving more than 8 cm H2O positive end-expiratory pressure (PEEP) and/or more than 60% FiO2 were performed. Each subject was suctioned using the open and closed methods. Arterial blood gases were obtained through an indwelling catheter before suctioning and then 1, 5, and 15 min after suctioning. Open suctioning: After 2 min preoxygenation with 100% oxygen the patient was disconnected from the ventilator, the suction catheter was inserted and the subject suctioned for a maximum of 15 s, then manually ventilated four times and reconnected. Closed suctioning: After preoxygenation the patient was suctioned without disconnection by means of the closed suction system. Statistical analysis was done by the two-tailed t-test on individual paired differences or by Student's t-test. P values of less than 0.05 were accepted as significant. ⋯ Patients were subdivided according to the PEEP level used (less or more than 8 cm H2O) and analysed separately. One minute after suctioning (T1) arterial pO2 was found to increase significantly for the open-system method when PEEP ventilation was < or = 8 cm H2O (Table 1) and for the closed system method when PEEP ventilation was both < or = 8 cm H2O (Table 1) and > 8 cm H2O (Table 2). Five (T5) and 15 (T15) min after suctioning, pO2 dropped significantly compared to baseline values in the open-system method when PEEP was > 8 cm H2O (Table 2). PO2 values 15 min after closed suctioning with PEEP > 8 cm H2O were significantly higher than those after open suctioning (Table 2). After the pO2 differences were formed between baseline and values 1, 5, and 15 min after suctioning, significant differences between open- and closed-system suctioning were found for PEEP > 8 cm H2O at T1, T5, and T15 (Table 2, Fig. 3). DISCUSSION. The increase in pO2 as a positive effect of preoxygenation with 100% oxygen before suctioning was less marked for open-system suctioning with PEEP > 8 cm H2O because FiO2, measured at the ventilator Y-piece, was abruptly reduced after disconnection and simultaneously PEEP was lost. As a consequence, pO2 values fell significantly 5 and 15 min after suctioning in this situation, whereas for all the other conditions pO2 reached baseline as well as slightly higher values. Patients with severe respiratory insufficiency need continuous positive airway pressure to keep unstable alveoli patent. Every maneuver that reduces intra-alveolar pressure may precipitate alveolar collapse. However, in the diseased lung closed alveoli may not re-expand at once when pressure is re-established. Therefore, closed-system suctioning may help to prevent prolonged deterioration of oxygenation in patients with severe respiratory failure.
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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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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.