Quality Assessment of Blood Transfusion in Operating Room / 대한구급학회지

BACKGOUND: Transfusion of red blood cells is a life saving measure in the management of a variety of surgical conditions. A guideline for blood transfusion during elective surgical procedure is necessary to reduce the risks of transfusion-associated complications, excessive blood bank workload, excessive blood request and overtransfusion, and the cost. From this, a program of quality assessment was adopted to improve blood transfusion practice and to establish the guideline for blood transfusion in elective surgery at Pusan National University Hospital. METHODS: Fifty-six patients undergoing elective surgery was divided 2 groups. Transfusion (T) group was 18 persons. Non-transfusion (NT) group was 38 persons. The preoperative, pre-transfusion, postoperative, and post-transfusion hemoglobin (Hb), hematocrit, mean arterial blood pressure (MAP), heart rate (HR), average amount of transfused red blood cell units, allowable blood loss, and the amount of infused crystalloids and colloids was estimated for 9 months in Pusan National University Hospital. RESULTS: There were no significant differences in Hb between T & NT group. Hb decreased significantly until postoperative 3rd day in NT group. Platelet count decreased in NT group on postop. 3rd day. There were no significant differences in MAP & HR. One-ninth of T group was overestimated blood loss & 18.4% of NT group was underestimated blood loss. One-third of transfusion patient were overtransfused & 36.2% of transfused RBC was unnecessary. Nearly 90% of patient was transfused packed RBC with FFP concurrently. CONCLUSIONS: To minimize overtransfusion, transfusion based on intraoperative hematocrit is necessary. If possible, single use of packed RBC is recommended when the blood loss is below allowable blood loss. In massive bleeding above allowable blood loss, combined administration of FFP and packed RBC or transfusion of whole blood will be better.

The Effect of Nitric Oxide on Edema Formation in Cryogenic Brain Injury Model of the Rat / 대한마취과학회지

BACKGROUND: Nitric oxide (NO) is a simple molecule with a complex involvement in a wide variety of biologic functions. However, whether NO protects or aggravates brain injury is still controversial. This study was conducted to determine the effect of nitric oxide on the formation of brain edema resulting from a focal cryogenic injury in rats. METHODS: Thirty nine Sprague-Dawley rats (200~250 gm) were allowed food and water ad libitum. Anesthesia was induced in a specially designed plastic box with 5% halothane in oxygen. In experiment I (24 rats), animals were divided randomly into eight group (3 rats in each group) according to the decapitation time in control, 15, 30, 45, 60, 90, 120, and 180 min. Cryogenic injury was made by pouring liquid nitrogen to exposed temporo-parietal area through metal funnel for 60 seconds. After cryogenic injury, brain was quickly removed and cerebral hemispheres were seperated. Separated cerebral hemispheres were dried in a drying oven for 7 days at 60 degrees C. Cerebral water content was assessed by dry-weight method. In experiment II (15 rats), one subgroup (n=8) was control group, normal saline 0.5 ml was injected intraperitoneally 30 minutes before injury. the other (n=7) was experimental group, and a competitive nitiric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), was given intraperitoneally 30 minutes before injury in a dose of 20 mg/kg. Body temperature was monitored during whole experiment. Ninety minutes after injury, brain was quickly removed and cerebral hemispheres were seperated. The cerebral water content of separated cerebral hemisphere was assessed by dry-weight method. RESULTS: In time courses of cryogenic brain edema of experiment I, the amount of brain edema was increased till 90 minutes after cryogenic brain injury and then decreased. In L-NAME group of ex-periment II, the amount of cerebral edema was not changed significantly (p<0.05). But, there was a tendency of decrease in brain edema formation in L-NAME group than control group. CONCLUSION: It was not proved that nitric oxide had a major role in the edema formation aftercryogenic brain injury, but it still seems that nitric oxide has at least partly involved in the pathogenesis of cerebral edema resulting from traumatic brain injury.