ABSTRACT
OBJECTIVE@#To investigate the clinical significance of different plastic surgeries in the treatment of poor healing wound after posterior spinal internal fixation.@*METHODS@#In this study, 16 patients with poor incision healing after posterior spinal internal fixation were retrospectively included, and dif-ferent plastic surgery treatment plans were determined according to the wound characteristics and defect condition. The measures included debridement, vacuum sealing drainage (VSD), and different tissue flaps according to the location and extent of the defect.@*RESULTS@#A total of 16 patients meeting the criteria were included, of whom 3 were treated with debridement combined with VSD and wound suture directly, 6 were treated with debridement combined with Z-flap for wound repair, 1 was treated with bilateral sacrospinous muscle flap for dural defect repair combined with Z-flap for skin wound repair, 1 was treated with lectus dorsi flap for wound repair, 3 were treated with the fourth lumbar artery perforator flap for wound repair. The wound was repaired with local rotating flap in 1 case and gluteus maximus musculocutaneous flap in 1 case. Among the 16 patients, 7 cases were positive for wound culture, including 3 cases of Staphylococcus aureus, 1 case of Pseudomonas aeruginosa, 1 case of Staphylococcus epidermidis, 1 case of Escherichia coli, 1 case of Klebsiella pneumoniae, and the other 9 cases were negative. After surgery, there were 7 patients with different degrees of poor wound healing, including 3 patients undergoing dressing change, 2 patients undergoing secondary debridement and suture, 1 patient undergoing free scalp skin graft, and 1 patient undergoing local effusion suction treatment. All the above 7 patients were discharged from hospital after improvement, and the remaining 9 patients had good first-stage wound hea-ling after surgery. None of the 16 patients underwent internal fixation.@*CONCLUSION@#Multiple factors could lead to poor wound healing after posterior spinal internal fixation. Early intervention, thorough debridement, removal of necrotic/infected tissue, and selection of suitable skin flap for effective wound fil-ling and covering were important means to ensure wound healing after spinal surgery and reduce removal of internal fixation.
Subject(s)
Humans , Retrospective Studies , Wound Healing , Debridement , Plastic Surgery Procedures , Surgical Flaps/blood supply , Skin Transplantation , Treatment OutcomeABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of transforming growth factor beta(1) (TGF-beta(1)) in the pathogenesis of bronchial asthma in children and assess the effect of montelukast sodium (leukotriene receptor antagonist) on TGF-beta(1) levels.</p><p><b>METHOD</b>A 12 weeks single-blind, placebo-controlled trail was conducted in 60 children with mild persistent asthma [aged 5 - 14 years, mean (7.10 ± 0.27) years]. Patients were randomly assigned to receive 5 mg montelukast sodium or placebo for 12 weeks. And 30 healthy control children [aged 5 - 14 years, mean (7.60 ± 0.25) years] were also recruited in this study from Sep. 2009 to Sep. 2010. Clinical effects and pulmonary function were evaluated before and 12 weeks after treatment. The mRNA expression of TGF-beta(1) in the peripheral blood mononuclear cells was detected by using RT-PCR with beta-actin as internal control. The percentage of the different subpopulations of Foxp(3)(+)CD4(+) T cells was assayed by 4-color flow cytometric analysis system and the levels of TGF-beta(1) in plasma by ELISA.</p><p><b>RESULT</b>(1) The basic characteristics between asthma group and healthy group had no significant difference. (2) Following treatment, there was significant increase in pulmonary function in asthmatic children. The effect in the group of montelukast sodium was superior to that of placebo group (P < 0.05). (3) The serum expression of TGF-beta(1) in asthmatic children was lower than that in control group (q = 20.01, P < 0.01); after 12 weeks of treatment, the mean expression of TGF-beta(1) was (20.03 ± 1.14) ng/L for montelukast sodium group and (12.10 ± 3.91) ng/L for placebo group (P < 0.05). (4) The mRNA expression of TGF-beta(1) in asthma children was lower than that in control group (0.31 ± 0.07 vs 0.61 ± 0.2, q = 8.97, P < 0.05); after 12 weeks of treatment, the mean expression of TGF-beta(1) was (0.46 ± 0.13) for montelukast sodium group and (0.32 ± 0.04) for placebo group (q = 8.25, P < 0.05). (5) It was shown that the total Foxp(3)(+)CD(4)(+) cell percentage was higher in asthmatic children than those of control group (8.30% ± 1.30% vs 6.05% ± 1.80%); the proportion of the three subpopulation was different between groups: CD(45) RA(+)Foxp(3)(lo) was higher in asthmatic group (4.60% ± 1.04% vs 3.27% ± 1.03%) and CD(45) RA(-)Foxp(3)(hi) was lower (0.75% ± 0.13% vs 0.93% ± 0.26%); while CD(45) RA(-)Foxp(3)(lo) had no significant difference among groups (2.40% ± 0.83%, 1.61% ± 1.10%). After 12 weeks of treatment, the percentage of CD(45) RA(-)Foxp(3)(hi) was increased in montelukast sodium group compared with placebo group (1.16% ± 0.24% vs 0.89% ± 0.22%). (6) Spearman correlation analysis revealed that TGF-beta(1) levels had no correlation with the levels of pulmonary function.</p><p><b>CONCLUSION</b>The protein and mRNA expression level of TGF-beta(1) was low in those asthmatic children. Insufficient secretion of TGF-beta(1) and the defective ability of activated regulatory T cells (CD(45) RA(-)Foxp(3)(hi)) in Foxp(3)(+)CD(4)(+) Treg cells might play an important role in pathogenesis of asthma. Up-regulation of the expression of TGF-beta(1) and induction of the expression of CD(45) RA(-)Foxp(3)(hi) in Foxp(3)(+)CD(4)(+)Treg cells by montelukast sodium may be one of the immunomodulatory mechanisms in asthma.</p>