The Study On Pathological Type And Molecular Cytology Of Pressure Sores

Pressure sores (also known as pressure sores, bed sores, pressure ulcers) is due toprolonged pressure on the local tissue and cause tissue ulceration necrosis, a disease sustainedischemia, hypoxia and malnutrition.It is more common in paraplegia, chronic wasting disease,a large area burns and deep coma bedridden patients. Simply because it is often easy to betreated as a special part of skin wounds in the clinical treatment of choice to consider pressuresores depth indexing, and we does not take into account in what pathological period thepressure sores are, so it often appear delayed healing in the clinical wound, expanding deepeninfections, skin graft or flap with the subject area difficult to heal, and even flap progressivenecrosis. Many pathogenic factors for pressure sores, usually are the result of the interactionof multiple factors, generally divided into exogenous factors and endogenous factors.Exogenous factors include the partial pressure, shear force, friction, local humidity,temperature and other endogenous factors including nutrition, sensory, age and gender,independent activities. Also found in our clinical work wound dehiscence incidence is high, inaddition to preoperative clinical assessment, to strengthen preventive measures, nutritionalsupport and improve the technical level, there are few reports of platelet-derived growthfactor (PDGF-BB) with in pressure sore wound treatment, but did not find the reportedpressure ulcers cytokines, to this end, we conducted the study to explore the reasons of wounddehiscence occurred cytokines.The present study, preoperative, postoperative and normal parts of specimens retainedcomplete wound healing, first of all, we are of different staging patients with pressure soreshistopathological examination, pathological features judgments wound clinicopathologicalstage.Ultimately determine16patients with degenerative phase,9patients with exudativephase and7patients with proliferative phase entering the study. Secondly, we tested EGF,TGF-β, β-FGF, PDGF-BB, VEGF and other cytokines in the samples. (1) We detected pathological changes of the16degenerative phase specimens in patients,and cytokine contents of IL-8, EGF, TGF-β, β-FGF, PDGF-BB, VEGF of patient’s samples.(2) We detected pathological changes of the9exudative phase specimens in patients, andcytokine contents of IL-8, EGF, TGF-β, β-FGF, PDGF-BB, VEGF of patient’s samples.(3) We detected pathological changes of the7proliferative phase specimens in patients,and cytokine contents of IL-8, EGF, TGF-β, β-FGF, PDGF-BB, VEGF of patient’s samples.Obtaining the following main results and conclusions by tests:(1)Through16cases of pathologically we confirmed deterioration of patients specimensof IL-8, β-FGF, PDGF-BB content was statistically significant, it need emergencydebridement surgery to control infection, and repair wound in limited operation.(2)Through nine cases of pathologically we confirmed patients with exudative phasesamples of β-FGF, PDGF-BB content statistically significant, we need debridement surgeryand repair wound in limited operation.(3) Hhyperplasia in patients with pathologically confirmed seven cases, specimenscontent of PDGF-BB statistically significant, we may elect surgery to do primary closure.Conclusion:Ⅲ and Ⅳ patients with pressure sores before surgery, we need to take tissue samplesfor histopathology in order to determine the clinical and pathological staging, then detect IL-8,β-FGF, PDGF-BB as a reference index when we operate, according to the different clinicalpathological staging, guide the clinical surgery treatment, improve the cure rate, reducewound dehiscence rate and recurrence rate and save medical costs.