Effects of inspired oxygen fraction in discriminating venous from arterial blood in percutaneous central venous catheterization under general anesthesia / 대한마취과학회지

BACKGROUND: A low fraction of inspired oxygen (FiO2) increases venous deoxygenated hemoglobin concentrations, making the color of the blood darker. The present study was aimed to determine the effects of FiO2 on the ability to discriminate venous from arterial blood. METHODS: One-hundred and sixty surgical patients undergoing percutaneous central venous access of the internal jugular vein were randomly assigned to receive an FiO2 of 0.2, 0.4, 0.6, or 1.0 (n = 40 each) for at least 20 min prior to central line placement under general anesthesia. Vascular access was achieved with a 22-gauge needle; 2 ml of blood was withdrawn and shown to three physicians including the operator. Each of them was asked to identify the blood as 'arterial', 'venous' or 'not sure'. Simultaneous blood gas analysis of the samples was performed on blood taken from the puncture site and the artery after visual comparison to confirm blood's origin and hemodynamic measurements. RESULTS: Lowering FiO2 progressively increased venous deoxygenated hemoglobin concentrations (2.24 +/- 1.12, 3.30 +/- 1.08, 3.66 +/- 1.15, and 3.71 +/- 1.33 g/dl) in groups having an FiO2 of 1.0, 0.6, 0.4 and 0.2, respectively (P < 0.001), thereby facilitating the 'venous' blood identification (P < 0.001). Neither heart rate nor mean arterial pressure differed among the groups. None developed hypoxemia (percutaneous hemoglobin oxygen saturation < 90%) in any group during the study period. CONCLUSIONS: A low FiO2 increases venous deoxygenated hemoglobin levels, thereby facilitating the recognition by clinicians of its venous origin in percutaneous central venous catheterization under general anesthesia.

A Case of Thrombotic Thrombocytopenic Purpura Associated with Ticlopidine

Ticlopidine, a widely used antiplatelet agent, has been rarely reported to cause thrombotic thrombocytopenic purpura (TTP). To the best of our knowledge, its occurrence has never before been reported in Korea. A 69 years old female patient suffered from an acute ischemic stroke. Ticlopidine 250mg bid was started and she followed an uneventful clin-ical course. The platelet count was normal on the 1st and the 12th day of ticlopidine administration. Around the 31st day, at home, she developed purpura, dyspnea and a stuporous mental status. Under the diagnosis of TTP, a plasma exchange was performed and her condition eventually returned to the baseline status. Ticlopidine induced TTP can developed abruptly despite close monitoring of platelet count, as illustrated by this case. Physicians prescribing ticlopi-dine should be aware of this potentially dangerous complication.