[Hb 1.1 g/dl: successful treatment of a polytraumatized patient in hemorrhagic shock]. / Hb=1,1 g/dl: erfolgreiche Behandlung nach Polytrauma mit schwerem hämorrhagischen Schock. Effektives Zusammenspiel von präklinischer Versorgung, Schockraummanagement und Intensivtherapie.

We report on the successful treatment of a seriously traumatized patient (injury severity score=59) who presented with exsanguinating hemorrhage in the emergency room. Preclinical and emergency room management included "small volume" hypertonic resuscitation as well as massive transfusion, C-clamp stabilization of a pelvic ring instability, and attachment of external fixators to multiple bone fractures. During the intensive care period,we started enteral immunonutrition immediately after an abdominal compartment syndrome was removed by laparotomy and a jejunal catheter had been inserted. Multiple fractures were stabilized rapidly and the soft tissue wounds were covered by split skin grafts. Additionally, we provided sufficient analgesia with few side effects using an epidural catheter for continuous application of local anesthetics. In summary, an effective synthesis of up-to-date strategies for preclinical, emergency room, and intensive care management prevented multiple organ failure and achieved survival with good quality of life after a "fatal" multiple trauma.

[ARDS and severe brain injury. Therapeutic strategies in conflict]. / ARDS und schweres Schädelhirntrauma. Therapiestrategien im Konflikt.

The development of adult respiratory distress syndrome (ARDS) complicates the treatment of patients with severe head injury, since special therapeutic strategies for both conditions might lead to a "conflict of interest". We report on the intensive care treatment of a young man who suffered severe brain injury (Glasgow Coma Scale = 3) due to a traffic accident and simultaneously developed ARDS from the aspiration of gastric content. We performed extensive monitoring of cerebral hemodynamics and metabolism (intracranial pressure measurement, jugular bulb oxymetry, estimation of arterial-jugular bulb lactate concentration difference) to prevent cerebral hypoxia and to control cerebral hyperemia. The application of a "lung protective strategy" with "permissive hypercapnia" led to a conflict, since the development of cranial hyperemia combined with cranial hypertension a few days after trauma, warranted the concept of controlled, temporary hyperventilation. Therefore, we applied a pumpless extracorporeal lung assist to improve carbon dioxide elimination. Furthermore, we started the ventilation in the prone position, since arterial oxygenation continued to deteriorate, although there is a lack of data describing the effect of a prone position on acute cerebral injury. Positioning the patient prone, we observed a prompt increase in intracranial pressure, which resulted in pharmacological intervention (mannitol). Treating the patient by intermittent prone position, by continuous extracorporeal lung assist and aerosolized prostacyclin administration in the following period, lung function improved and ARDS was treated successfully. After withdrawing the analgo-sedation the patient's vigilance rose continuously. The patient was transferred to a rehabilitation ward 33 days after admission to the intensive care unit. The combination of ARDS and severe brain injury needs special treatment, which includes extensive monitoring techniques to find a solution for therapeutic conflicts.

Lung recruitment maneuver in patients with cerebral injury: effects on intracranial pressure and cerebral metabolism.

OBJECTIVE: To investigate the effects of a lung recruitment maneuver on intracranial pressure (ICP) and cerebral metabolism in patients with acute cerebral injury and respiratory failure. DESIGN: Prospective investigation. SETTING: Ten-bed intensive care unit of a university hospital. PATIENTS: Eleven patients with acute traumatic or non-traumatic cerebral lesions, who were on mechanical ventilation with acute lung injury. INTERVENTIONS: Hemodynamics, ICP, cerebral perfusion pressure (CPP), jugular venous oxygen saturation (SJO(2)), and arterial minus jugular venous lactate content difference (AJDL) were measured before, during and after a volume recruitment maneuver (VRM), which included a 30-s progressive increase in peak pressure up to 60 cmH(2)O and a sustained pressure at the same level for the next 30 s. RESULTS: At the end of VRM, ICP was elevated (16+/-5 mmHg vs 13+/-5 mmHg before VRM, P<0.05) and mean arterial pressure was reduced (75+/-10 vs 86+/-9 mmHg, P<0.01), which resulted in a decrease of CPP (60+/-10 vs 72+/-8 mmHg, P<0.01). SJO(2) deteriorated at the end of the procedure (59+/-7 vs 69+/-6%, P<0.05), AJDL was not altered. In the following period all parameters returned to normal values. An improvement in arterial oxygenation was observed at the end, but not in the period after the maneuver. CONCLUSIONS: Our VRM reduced cerebral hemodynamics and metabolism. We conclude that our VRM with high peak pressure effects only a marginal improvement in oxygenation but causes deterioration of cerebral hemodynamics. We therefore cannot recommend this technique for the ventilatory management of brain-injured patients.

Evaluation of a rapid, quantitative cardiac troponin I immunoassay.

We evaluated a rapid, quantitative immunoassay for the detection of cardiac troponin I. Coefficient of variation is between 1.29 and 13.63% for intra-assay and between 3.88 and 10.15% for inter-assay imprecision. Linearity is given up to 35 micrograms/l. Possible interfering substances (haemoglobin, bilirubin, triacylglycerol and rheuma factors) do not disturb the assay. The analyte is stable under normal storage conditions (+20 degrees C/48 h and +4 degrees C/l week) with decrease up to 30% after 3 months at -20 degrees C. Reference value for apparently healthy individuals is < 0.1 microgram/l. In plasma cardiac troponin I is measured up to 30% depressed compared to serum. Comparison with another cardiac troponin I assay (y = 0.92x + 2.42, r = 0.940) and cardiac troponin T is good with y = 6.61x - 1.94, r = 0.91 for the first generation cardiac troponin T assay and y = 5.59x - 0.68, r = 0.87 for the second generation cardiac troponin T assay. In summary, the evaluated assay is fast, easy to perform, and can be used not only in a specialized laboratory, but is also suitable for emergency laboratory or smaller laboratory units.