RESUMEN
INTRODUCTION: To investigate the changes in coagulation function and component transfusion time in patients with massive hemorrhage. METHODS: Sixty-two patients with massive hemorrhage were enrolled in the study. Blood samples were collected from each patient when the blood loss reached 1000, 1500, 1700 and 2000 ml. The parameters FIB, PT, APTT, HGB, HCT, PLT and MAP were recorded for all patients. RESULTS: Sixty-two, 30, 20 and 8 patients showed blood loss exceeding 1000, 1500, 1700 and 2000 ml, respectively. Blood samples were successfully collected from all patients when the volume of blood lost reached 1000, 1500, 1700 and 2000 ml. However, at this time point, FIB, MAP, HGB, HCT and PLT were significantly lower than the baseline/preoperative values. These indices decreased progressively with increasing blood loss. PT and APTT were significantly higher than at baseline and increased progressively with increased blood loss. FIB, HCT and HGB were below the normal reference range when blood loss was 1500 ml. During surgery, FIB, MAP, HCT, HGB and PLT decreased substantially, whereas APTT and PT increased when blood loss exceeded 1500 ml. PT and MAP were beyond the normal range when blood loss reached 2000 ml. There was a correlation between FIB, HCT and HGB with intraoperative blood loss; the correlation coefficient was greatest between and FIB and blood loss. CONCLUSION: There were marked correlations between FIB, HCT and HGB with intraoperative blood loss, and the correlation was greatest with FIB.
Asunto(s)
Pruebas de Coagulación Sanguínea , Transfusión de Componentes Sanguíneos , Pérdida de Sangre Quirúrgica , Hipovolemia/sangre , Cuidados Intraoperatorios , Choque Hemorrágico/sangre , Biomarcadores , Neoplasias Encefálicas/sangre , Neoplasias Encefálicas/cirugía , Empiema Pleural/sangre , Empiema Pleural/cirugía , Femenino , Fibrinógeno/análisis , Glioma/sangre , Glioma/cirugía , Hemodinámica , Humanos , Hipovolemia/etiología , Hipovolemia/terapia , Masculino , Persona de Mediana Edad , Procedimientos Neuroquirúrgicos , Plasma , Estudios Prospectivos , Choque Hemorrágico/terapia , Procedimientos Quirúrgicos Torácicos , Factores de TiempoRESUMEN
BACKGROUND: Cyclooxygenase-2 (COX-2) contributes to ventilation induced lung injury (VILI) and acute respiratory distress syndrome (ARDS). The objective of present study was to observe the therapeutic effect of parecoxib on VILI in ARDS. METHODS: In this parallel controlled study performed at Harbin Medical University, China between January 2016 and March 2016, 24 rats were randomly allocated into sham group (S), volume ventilation group/ARDS (VA), parecoxib/volume ventilation group/ARDS (PVA). Rats in the S group only received anesthesia; rats in the VA and PVA group received intravenous injection of endotoxin to induce ARDS, and then received ventilation. Rats in the VA and PVA groups were treated with intravenous injection of saline or parecoxib. The ratio of arterial oxygen pressure to fractional inspired oxygen (PaO2/FiO2), the wet to dry weight ratio of lung tissue, inflammatory factors in serum and bronchoalveolar lavage fluid (BALF), and histopathologic analyses of lung tissue were examined. In addition, survival was calculated at 24 h after VILI. RESULTS: Compared to the VA group, in the PVA group, PaO2/FiO2 was significantly increased; lung tissue wet to dry weight ratio; macrophage and neutrophil counts, total protein and neutrophil elastase levels in BALF; tumor necrosis factor-α, interleukin-1ß, and prostaglandin E2 levels in BALF and serum; and myeloperoxidase (MPO) activity, malondialdehyde levels, and Bax and COX-2 protein levels in lung tissue were significantly decreased, while Bcl-2 protein levels were significantly increased. Lung histopathogical changes and apoptosis were reduced by parecpxib in the PVA group. Survival was increased in the PVA group. CONCLUSIONS: Parecoxib improves gas exchange and epithelial permeability, decreases edema, reduces local and systemic inflammation, ameliorates lung injury and apoptosis, and increases survival in a rat model of VILI.