No abstract available.
Acute Kidney Injury* ; Edema* ; Hemofiltration*

No abstract available.
Acute Kidney Injury* ; Edema* ; Hemofiltration*

BACKGROUND: To avoid the risks associated with transfusion of homologous blood products, artificial colloid solutions represent an alternative for intra-operative blood loss replacement. However, synthetic colloids have been implicated as a cause of coagulopathy when administered in large quantities. We investigated the effect of Hydroxyethyl starch (HES) on blood coagulation in vitro under thromboelastography (TEG). METHODS: Whole blood was withdrawn from fifteen volunteers undergoing peripheral surgery who had no history of coagulation defect. Whole blood was diluted with HES to 25, 50 and 75 vol% concentrations, and the changes in coagulation status were analysed using TEG and were compared with those of an undiluted control specimen obtained concurrently from the same patients. RESULTS: Hemodilution with HES solution at 50 vol% concentration decreased the MA and alpha angle values (P < 0.05), but the R and K values remained unchanged. In case of profound hemodilution at a 75 vol% concentration, the values of MA and alpha angle were severely decreased (P < 0.05) and the values of R and K were severely increased (P < 0.05). CONCLUSIONS:There were many reports that moderate hemodilution with crystalloids increased coagulability, but hemodilutions up to 50 vol% concentration with HES solution did not significantly change blood coagulability. Significant hypocoagulability occurred at a 75 vol% hemodilution with HES.
Blood Coagulation ; Colloids ; Hemodilution ; Humans ; Starch* ; Thrombelastography* ; Volunteers

BACKGROUND: Aprotinin is a potent, nonspecific broad serine protease inhibitor. It's inhibitory effects on intrinsic pathway of coagulation cascade can augment anticoagulation by heparin. This study designed to demonstrate augmented anticoagulation of aprotinin to heparin contaminated blood on thromboelastography(TEG). METHODS: This study designed into two phases for 21 healthy volunteers undergoing elective opeation. The first phase study, it was for looking at TEG differences between blood treated with aprotinin 200 KIU and blood treated with heparin 0.05 unit and 0.1 unit per blood 1 ml. The second phase study was for looking at anticoagulation of aprotinin added by heparin 0.05 unit and 0.1 unit per blood 1 ml and their reversal added by optimal dose of protamine sulfate. RESULTS: The aprotinin treated blood showed only a prolonged reaction time. Blood treated with incremental dose of heparin showed longer reaction time and smaller alpha angle than TEGs of native blood. Aprotinin added to the heparin contaminated blood showed much longer reaction time and much less alpha angle when compared with TEGs of aprotinin or heparin treated blood. Depressed TEG pattern by the heparin and aprotinin mixture reversed back to the TEGs of blood treated with aprotinin when optimal dose of protamine added. CONCLUSIONS: Those results suggest that aprotinin administered in open cardiac surgery can augment the remained anticoagulation effect due to heparin even after first dose fo protamine after weaning of cardiopulmonary bypass. This is of clinically improtance to distinguish heparin related coagulopathy from heparin non related coagulopathy by thromboelastography.
Aprotinin* ; Cardiopulmonary Bypass ; Healthy Volunteers ; Heparin* ; Protamines ; Reaction Time ; Serine Proteases ; Thoracic Surgery ; Thrombelastography* ; Weaning

Recently, the incidence of fungal infection increases because of immunosuppressive therapy and chemotherapy. In immunosuppressed transplant recipients, Aspergillus can be a dangerous pathogen, capable of inducing fulminant clinical disease. Invasive fungal infections are life-threatening complications in solid-organ transplantation. Although the rate of fungal infections in transplant recipients is lower than that of other infections, the mortality rate is higher. A 34 year-old male was admitted to our hospital with fever and gross hematuria. He had received renal transplantation 2 years ago and had been transferred the other hospital 1 month ago. Initial laboratory data evaluation showed a pancytopenia and azotemia. We thought that pancytopenia was caused by immunosuppressive agents and infection. The patient was treated with antibiotics but fever was not subsided. After 4 days, he complained of transplant site pain and tenderness to percussion. A percutaneous renal biopsy was performed. Microscopic examination showed invasive aspergillosis in transplanted kidney and perirenal area. We removed the transplanted kidney and perirenal tissue, and prescribed antifungal agents for 3 months.
Anti-Bacterial Agents ; Antifungal Agents ; Aspergillosis ; Aspergillus ; Azotemia ; Biopsy ; Fever ; Hematuria ; Humans ; Immunosuppressive Agents ; Incidence ; Kidney ; Kidney Transplantation ; Male ; Pancytopenia ; Percussion ; Transplants

Ocular disturbances related to cranial nerve lesion or increased intracranial pressure are well known in cryptococcal meningitis, but internuclear ophthaloplegia is very rare and only two cases have been reported to our knowledge. We report the third patient of internuclear ophthalmoplegia in cryptococal meningitis. The internuclear ophthalmoplegia in our case persisted for one year with a demonstrable lesion in brain MRI, in contrast to the other cases in which intranuclear ophthalmoplegia was transient and no responsible lesion was observed.
Brain ; Cranial Nerves ; Cryptococcosis* ; Humans ; Intracranial Pressure ; Magnetic Resonance Imaging ; Meningitis ; Meningitis, Cryptococcal ; Ocular Motility Disorders ; Ophthalmoplegia

Of the case of malignant astrocytoma, spontaneous transdural extension is very rare. Only several cases of transdural extension of primary intracranial tumor are reported. However, these cases are through the foramina of the skull base. We have experienced a case of malignant astrocytoma which directly extended out through the dura and calvarium near the pterion of the left side.
Astrocytoma* ; Skull ; Skull Base

We have experienced 3 cases of localized cervical adhesive arachnoiditis. 2 of them had history of operation under spinal anesthesia. Paresthetic pain and weakness are the commonest presenting symptoms and signs in our cases. Myelographically, findings are simulating the intramedullary lesion in 2 cases. With surgical intervention, 2 cases have good results.
Adhesives* ; Anesthesia, Spinal ; Arachnoid* ; Arachnoiditis*

A 30 years old female patient was diagnosed valvular heart disease and double valve replacement was ndertaken. After operation, mediastinitis developed and we had done continuous mediastinal irrigation and had used IV antibiotics for 3 weeks. During outpatient follow-up, infection signs developed, so she readmitted and was reoperated because CT revealed mediastinal abscess. No infected material was observed at the operation. Infection signs continued for 3 weeks. Chest CT revealed giant pseudoaneurysm of ascending aorta. We resected the pseudoaneurysm and performed an aortoplasty with bovine pericardium under deep hypothermia and total circulatroy arrest. She recovered well and was discharged without any complication.
Abscess ; Adult ; Aneurysm, False ; Anti-Bacterial Agents ; Aorta* ; Female ; Follow-Up Studies ; Heart Valve Diseases ; Humans ; Hypothermia ; Mediastinitis* ; Outpatients ; Pericardium ; Thoracic Surgery* ; Tomography, X-Ray Computed

OBJECTIVE: The authors present the effect of VEGF upon neuronal and glial response following transient global ischemia of the rat METHODS: We studied the effect of VEGF in 36 rats subjected to 15 minutes of transient global ischemia. Animals were devided into control group(transient global ischemia only: day-3, day-7, day-14, respectively n=6) and VEGF-treated group(transient global ischemia with intraventricular injection of 100 micro gram VEGF: day-3, day-7, day-14, respectively n=6). These animals were sacrificed at 3 days, 7 days and 14 days after induction of ischemia. Nissle stain and immunohistochemistry of GFAP(glial fibrillary acidic protein), OX-42, and ED1 were done for assessment of neuronal and glial responses. RESULTS: In the CA1 hippocampus, there was a significant reduction of pyramidal cell damage in VEGF-treated group as compared with control group in post-ischemia 3, 7, 14 days(p<0.05). In the CA3 hippocampus which is relatively resistant to ischemia, reduction of pyramidal cell damage was significant in post-ischemia 7 days(p<0.05), not significant in post-ischemia 3, 14 days(p>0.05). In the assessment of CA1 hippocampus with GFAP stained areas, there was significant reduction of reactivity in post-ischemia 3, 7 days(p<0.05), not significant in post-ischemia 14 days(p>0.05). In the CA3 hippocampus, reduction of GFAP reactivity was significant in post-ischemia 3, 7 days(p<0.05), not significant in post-ischemia 14 days(p>0.05). In the assessment of CA1 hippocampus with OX-42 stained areas, there was significant reduction of reactivity in post-ischemia 3, 7, 14 days(p<0.05). But in the CA3 hippocampus, the difference was not significant in post-ischemia 3, 7 days(p<0.05). In the assessment of of CA1 hippocampus with ED1 stained areas, there was significant reduction of reactivity in post-ischemia 3, 7, 14 days(p<0.05). But in the CA3 hippocampus, the difference was significant in post-ischemia 3 days only(p<0.05). CONCLUSION: These results suggest that VEGF can reduce neuronal damage in transient global ischemia, thus have protective effect on ischemic brain injury. In our experiment, the reduction of glial response with VEGF seems to be related to the secondary neuroprotective effect of VEGF. However, the proliferation of endothelial cells and new vessel formation take days to months, the thus neuroprotective effect of VEGF against ischemia seems to related to a certain mechanism rather than angiogenesis.
Animals ; Astrocytes ; Brain Injuries ; Endothelial Cells ; Hippocampus ; Immunohistochemistry ; Injections, Intraventricular ; Ischemia* ; Microglia ; Neurons* ; Neuroprotective Agents ; Pyramidal Cells ; Rats* ; Vascular Endothelial Growth Factor A*