OBJECTIVEThis study observed the curative effect of sustained negative pressure drainage application on treatment of severe maxillofacial and neck space infection.

METHODSIncision and drainage were performed to treat 18 patients with severe maxillofacial and neck space infection. A small incision was made on the site of the most obvious swelling or fluctuations, and localized negative pressure was applied with a drainage device on the wound during suturing.

RESULTSAmong the 18 patients, 14 were healed, whereas 4 underwent dehiscence of the wound after the operation. Negative pressure was lost as the drainage tubes were removed, and non-negative pressure drainage method was used instead. During the negative pressure treatment, swelling and pain did not increase after the operation. Other complications, such as asphyxia, septic shock, or mediastinal abscess, did not occur. All the patients were healed and eventually discharged from the hospital.

CONCLUSIONSustained negative pressure drainage, which is a modified version of the traditional method of incision and drainage, is an alternative treatment for severe maxillofacial and neck space infection. Such treatment reduces patient pain and eases doctor exertion. Thus, this method provides a new therapeutic strategy for severe maxillofacial and neck space infection.

Objective To investigate whether lipopolysaccharide (LPS) can induce vascular endothelial cell growth factor (VEGF) expression in microglia regulated by hypoxia inducible factor-1α(HIF-1α). Methods The cultured BV2 cells were divided into four groups:control group, LPS (100 μg/L) simulated group, LPS (100 μg/L)+LPS antagonist (LRS, 200 μg/L) intervened group and LPS (100 μg/L)+HIF-1αinhibitors FM19G11 (10 mmol/L) intervened group. Immunofluorescence staining, Western blotting and ELISA were used to detect the expressions of VEGF and HIF-1α. Results Compared with the control group, the VEGF expression level was obvious high in LPS simulated group (P<0.05). LRS inhibited this effect of LPS (P<0.05). The HIF-1αlevel was increased in LPS simulated group at 8 h post-injury (P<0.05). FM19G11, the inhibitor of HIF-1αreduced the expression of VEGF induced by LPS (P<0.05). Conclusion LPS can up-regulate the expression of VEGF by HIF-1α.

Objective To investigate the clinical efficacy of biological dressing A covering bandage of Ⅲ° burn wounds given comprehensive treatment including dermabrasion.Methods For patients of non Ⅲ° ° burn wounds (deep Ⅱ ° and partial superficial Ⅲ ° wounds),28 cases in the treatment group,were given improved dermabrasion with tangential excision plus thin layer of skin graft from the body,the wounds were covered with biological dressing A bandage.21 patients in the control group were treated by traditional tangential excision,escharectomy and self-skin grafting.The clinical treatment effect was observed and compared between the two groups.Results The wounds were healed 2 ～ 3 weeks after surgery in treatment group,the cure rate of burns in patients with a total area of 40％ ～ 50％ TBSA was 99％,and after treatment the scar formation significantly reduced,self-donated skin significantly reduced,the hospital stay and postoperative recovery time of the patients were significantly shorter,patients were easier to accept.In the control group,the operation time was longer,the blood loss was more,the wounds had more scar healing wounds.The wound healing time of the treatment group was (14.8 ± 1.8) d,which was significantly shorter than (19.4 ± 3.0) d of the control group (P ＜ 0.05).Conclusion The improved grinding A scab plus biological dressings covering bandage has the advantages of simple operation,light damage,less complications,need less skin,to maximize retention of healthy tissue,wound healing speed up,healing scar lessened.

Objective To investigate the spiral CT findings in hemopathic patients with druginduced pulmonary injury.Methods CT images obtained in 11patients with drug-induced pulmonary injury were retrospectively analyzed.Six patients had antineoplastic agent-induced pulmonary injury and 5 patients had non-neoplastic agent-induced pulmonary injury (immunosuppressor in 2 patients,antifungal in 2 patients,antineoplastic immunomodulators in 1 patient).CT findings were reviewed by a chest radiologist.Results All 11patients had parenchymal abnormalities on MSCT scans,including ground-glass opacities( n =8 ),consolidation( n =5 ),interlobular septal thickening( n =3 ) and focal fibrosis ( n =2 ).The abnormalities were bilateral and asymmetric in all patients.They were mainly in the peripheral lung regions in 6 patients,in the central lung regions in four,and irregularly located in one.The abnormalities involved mainly the lower lung zones in six patients,the upper lung zones in two,and all lung zones homogeneously in three.One patient had fluid in bilateral pleural cavities.Three patients were given the same agent once more after the imaging turned to normal,and they presented with same clinical symptoms and similar but more serious imaging findings.Conclusions Drug-induced pulmonary injury usually manifests as areas of ground-glass opacity and consolidation,which most commonly involves the peripheral lungs and lower lung zones.Drug-induced pulmonary injury shows reproducible but more serious lesions when the patient is given the same agent once more.

Objective To study the imaging features and possible aetiology of osteonecrosis in adults with acute leukemia.Methods Ten adult patients with acute leukemia for osteonecrosis were reviewed retrospectively.All the lesions were confirmed with MRI.Results Four patients with ALL had accepted chemotherapy contained corticosteroids,two of them were performed HSCT,and one patient suffered GVHD.Six patients with AML had accepted chemotherapy without steroids,five of them were performed HSCT,and four patients suffered GVHD.One patient with AML-M3 had accepted chemotherapy including four courses of ATRA.The mean time between diagnosis of osteonecrosis and leukemia was 25.1 months.Nine cases had multiple lesions,one case had single lesion.The lesions involved femurs,tibias,patellas,iliums,and lumbars.Plain radiographs in six patients can not detect any lesion.Circinal reaction ossification could be detected in CT images of four cases.All the cases had typical feature in MRI.Conclusions In adult leukemia patients,osteonecrosis is a complication after chemotherapy or HSCT.Steroids in chemotherapy protocols or treatment for GVHD,ATRA for APML,chemotherapy-induced direct cytotoxic effect or leukemia itself can be the possible risk factor.For the diagnosis,MRI is the most effective way,and CT features of osteonecrosis in leukemia patients are different from those in non-leukemia patients.

Objective To observe the effects of atorvastatin on the microglia activation after traumatic brain injury (TBI). Methods Sixty adult male C57/BL6 mice were randomly divided into sham group, atorvastatin group and saline group, 20 mice for each group. The atorvastatin group and saline group were given hydraulic combat to establish TBI mouse model. The shame group underwent the same surgical procedure without being exposed to percussion injury. The atorvastatin group was treated with atorvastatin (orally, 1 mg/kg)1 h after TBI and for 7 consecutive days. The saline group was given sa?line orally. The expression of microglia (Iba-1+) at the 1st, 3rd, and 7th day after TBI and matrix metalloproteinase-9 (MMP-9) around the lesion at the 3rd day after TBI were detected by immunohistochemical staining. Tumor necrosis factor (TNF)-αwas detected by Western blot assay at the 3rd day after TBI. Results The positive expression of Iba-1+microglia was signifi?cantly decreased in atorvastatin group than that of saline group at the 1st, 3rd, and 7th day after TBI (80.00±7.44 vs. 118.40± 6.65,85.60±10.87 vs. 189.00±7.51,69.40±5.54 vs. 102.40±10.89, P<0.05). The positive expression of MMP-9 was signifi?cantly decreased in atorvastatin group compared with that of saline group at the 3rd day after TBI (86.80 ± 8.40 vs. 133.80 ± 8.46, P<0.05). Results of Western blot assay showed that the positive expression of TNF-αwas significantly decreased in astorvastatin group than that of saline group at the 3rd day after TBI (0.64±0.01 vs. 0.97±0.02,P<0.05). Conclusion Ator?vastatin can reduce inflammation factor by influencing the microglia activation after TBI in mice.