Stroke volume variation as a predictor of fluid responsiveness in patients undergoing airway pressure release ventilation.

We investigated the effectiveness of stroke volume variation (SVV) shown by the Vigileo-FloTrac™ system (Edwards Lifesciences, Irvine, CA) to predict fluid responsiveness in patients undergoing airway pressure release ventilation (APRV). All 80 patients mechanically ventilated in the intensive care unit of our hospital from April to November 2010 were included in this study. After starting APRV, Ringer's lactate solution was administered for 30 minutes. Haemodynamic variables including heart rate, mean arterial pressure, cardiac index (CI), stroke volume index (SVI) and SVV were measured before and after volume loading. SVV before volume loading was significantly correlated with absolute change in SVV (ΔSVV) and percentage change in stroke volume index (ΔSVI) after volume loading (ΔSVV: P<0.05, r2=0.534; ΔSVI: P<0.05, r2=0.217). Of the 80 patients, 38 (47.5%) were responders to intravascular volume expansion (increase in CI≥15%) and 42 (52.5%) were non-responders (increase in CI<15%). Receiver operating characteristic (ROC) curves were generated for SVV and central venous pressure by varying the discriminating threshold of the variable and areas under the ROC curves were calculated. The areas under the ROC curves were 0.793 for SVV (95% confidence interval: 0.709-0.877) and 0.442 for central venous pressure (95% confidence interval: 0.336-0.549), which were significantly different (P<0.05). The optimal threshold value of SVV to discriminate between responders and nonresponders was 14% (sensitivity: 78.9%; specificity: 64.3%). We found that SVV was able to predict fluid responsiveness in patients undergoing APRV with acceptable levels of sensitivity and specificity.

[A case of Salmonella subdural empyema developed in chronic subdural hematoma].

A case of Salmonella subdural empyema developed in chronic subdural hematoma (Infected Subdural Hematoma; ISH) was reported. A 64-year-old man had been in a nearby hospital due to myelodysplastic syndrome with cerebral infarction for two months. His condition there had been almost uneventful. But spike fever occurred and the patient became drowsy two days before his transfer to our medical center. His consciousness level deteriorated progressively and CT scan showed a right chronic subdural hematoma. He had had no history of head trauma in the previous two months. On admission to our center, his consciousness level was semicoma with anisocoria. An emergency operation was performed via a single burr hole initially. From the burr hole, old bloody fluid accompanied by yellowish pus was obtained. Thus so-called ISH was diagnosed and the craniotomy was carried out. Gram stain of the specimen revealed gram negative rods. Although an epileptic state developed after the operation, it was controlled by barbiturate coma therapy for 3 days, followed by phenytoin administration. Fever subsided gradually with antibiotics sensitive to the bacteria and his anisocoria disappeared on the 4th postoperative day. In this case, Salmonella enteritidis was detected from bacterial culture both of the specimen and of the arterial blood. Salmonella enteritidis might have been implanted on the capsule of the chronic subdural hematoma by bacteremia derived from immunological dysfunction due to myelodysplastic syndrome. In conclusion, the possibility of ISH should be considered in chronic subdural hematoma patients with immunological dysfunction.