A. Hoxha

Incidence of early postoperative arterial hypoxemia after craniotomy for brain tumor surgery: 7AP6–1

Background and Goal of Study: In early postoperative phase patients are vulnerable to a variety of factors, especially to hypoxemia(1). Hypoxic insult may develop during early postoperative period especially in the presence of the hypoxemia. Materials and Methods: 321 adult patients without serious co-morbidities (age 47.82±9.64, Karnofsky ≥60%, ASA 1.56±0.35) scheduled for elective brain tumor surgery were included. They received sevofluran based anesthesia for 2.25-4.5 hours with fentanyl, and 8-12 mg pancuronium. After surgery patients were extubated in the operative room at EtMAC 0.2-0.3 and FiO2=0.5 maintaining spontaneous respiration (EtCO2≤45mmHg, SpO2≥98%) and hemodynamic stability. After extubation they breathed at 40%O2. SpO2, ABG and Tcore were recorded prior extubation and for 30min after. Fisher and Chi-tests were used and p≤0.05 is considered significant. Results and Discussion: Peroperative hypoxemic events were reverted prior to extubation. Data showed significant decrease of PaO2 in first 20 min after extubation corresponding to movement of the patients to PACU (SpO2≤91% in 54pts breathing 40%O2). ABG obtained at arrival in PACU (10min after extubation) showed PaO2≤90 in 58 patients (18.1%). 11 patients were reintubated and mechanically ventilated. Hypothermia strongly parallels PaO2≤90 in first 10 minutes. It was mostly present in long-lasting interventions (68 lasting over 3.5 hours) and after extubation for more than 10 min despite heating (p<0.05). 7.1% of patients developed insults after surgery. There was no correlation (p=0.245) between ASA and hypoxemia in our patients.

Respiratory complications in patients after surgery for aneurismal subarachnoid bleeding: A-313

using modified TEG. In each group, TEG parameters (R, K time and MA) were analyzed using paired t-test and one way ANOVA was used to determine the difference between groups. Results and Discussions: In group 1 (OPCAB patients) and group 2 (healthy subjects, before aspirin), the R and K time were increased significantly with the addition of heparin and then decreased subsequently with the platelet agonists (ADP or collagen) in the presence of anticoagulation (heparin). MA showed a decrease in both groups. This compares with no significant difference in all parameters in group 3 (healthy subjects, after aspirin) with the addition of heparin, ADP and collagen. There were no significant differences in each TEG parameter between groups. Conclusions: This study suggested that aspirin medication obliterated the effect of anticoagulation and platelet agonists in modified TEG. However modified TEG does not provide a comprehensive and sensitive reflection of platelet inhibition by aspirin. TEG should be supplemented by other methods of platelet function assessment. References: 1 Shore-Lesserson L. J Cardiothor Vasc Anesth 2001; 16: 99–106. 2 Kawasaki J, Tanaka KA, Okada K, et al. Anesthesiology: 2003; 99: A162. 84 Neurosciences