ABSTRACT
Objective To construct a three-dimensional finite element model to investigate the biomechanical mechanism of carotid blast injuries.Methods Based on the head and neck CT angiography data of a healthy male volunteer,the 3D geometric model was extracted by Mimics software.The 3D solid model was obtained by fitting the geometric model to the non-uniform rational B-splines (NURBS) by Geomagic Studio software.The mesh of blood vessels,blood and soft tissue was divided by HyperMesh software to obtain the three-dimensional finite element model of the carotid artery.The material parameters and boundary conditions were set,and the vessel wall rupture damage threshold was 1 MPa.The dynamic process of carotid injury caused by MK3A2 grenade explosion shock wave at the distance of 60,70 and 80 cm to the neck was simulated using the LS-DYNA,generating the shock waveform and peak overpressure.The stress cloud map was used to analyze the stress distribution and damage morphology,and the stress curve was used to analyze the mechanical changes.Results The peak values of shock wave overpressure were 0.45,0.63 and 0.96 MPa at the distance of 80,70 and 60 cm away from the explosion center,respectively.At 80 cm,the peak stress of vessel wall was 0.43 MPa,and the vessel wall was not ruptured;at 70 cm,the peak stress of anonyma was greater than 1 MPa,which resulted in small rupture;at 60 cm,the peak stress of both anonyma the ascending aorta were greater than 1 MPa,leading to obvious rupture.The root part of the common carotid artery,anonyma and the arch of the aorta were high stress concentration areas,manifested as high-prevalence areas of damage and rupture.Conclusions The finite element model of explosive carotid artery injury is successfully constructed,which can be used to analyze the mechanical response and damage mechanism of carotid blast injuries.The main cause of injury and rupture is that the sudden change of stress in the process of explosion shock reaches or exceeds the threshold of vascular wall injury.Carotid artery rupture will occur when the vessel wall stress peak is greater than 1 MPa at 60 and 70 cm away from the explosion center,providing references for the clinical treatment and injury prevention.
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Objective To discuss the correlation between dynamic changes in pulmonary function and chronic cough in 5-to-14-year-old children with Mycoplasma pneumoniae pneumonia(MPP)after acute period(about 2 weeks after admission). Methods One hundred and fifty - six hospitalized children diagnosed with MPP from Lianyungang Maternal and Child Health Care Hospital Affiliated to Yangzhou University from February 2014 to May 2017 were selected. According to the results of routine ventilatory pulmonary function before discharge(10-14 days in hospital;acute phase group),there were 50 patients with normal pulmonary function and 106 patients with abnormal pulmonary function. All patients continued to take oral azithromycin for 2 to 3 courses after discharge,and the indexes of lung function were dynamically tracked in 1 month(1-month group)and 2 months(2-month group)in the group of abnormal lung function after leaving the hospital,and the incidences and causes of chronic cough were followed up. Results (1)There were 106 cases with abnormal pulmonary function in 156 cases with MPP in acute phase group,and the rate of incidence was 67. 95%. Twenty-seven(29. 35%)out of 97 children were still abnormal in pulmonary functional testing 1 month after leaving hospital( 1-month group). Among the 27 cases,about 18. 52%(5/27 cases) of them still did not return to normal 2 months after discharge( 2-month group ). There were significant differences in the occurrence of abnormal pulmonary function among 3 groups mentioned above(χ2 ＝162. 64,P<0. 001).(2)Ratios of measured values and predicted ones of forced vital capacity( FVC ),forced expiratory volume in one second (FEV1 ),peak expiratory flow(PEF)and maximum mid-expiratory flow(MMEF 25% -75%)in the lung function of 2-month group after the acute phase of MPP were significantly higher than those of 1-month group and acute phase group,and the values of 1 -month group were better than those in acute phase one,which were statistically different among 3 groups(P<0. 01).(3)The rate of occurrence of chronic cough in normal lung function group was about 18. 00%(9/50 cases),and in abnormal pulmonary function group,it was about 70. 75%(75/106 cases). There was a significant difference between them(χ2 ＝35. 96,P<0. 05). Abnormal pulmonary functions were the influencing factors of chronic cough(r＝0. 55,P<0. 01).(4)There were 5 cases with upper airway cough syndrome(UACS)and 4 cases with post-infection cough(PIC)found in the normal lung function group. By contrast,75 cases suffered from chronic cough in abnormal pulmonary functions group,of which 36 cases with cough variant asthma( CVA),24 cases with UACS,8 cases with comorbidity of CVA and UACS and 7 cases with PIC. Conclusions Abnormal lung function after acute period of MPP may last 4 to 8 weeks,or probably even longer. In normal lung function group,UACS is the most common cause,then followed by PIC. On the contrary,the main cause of chronic cough in abnormal pulmonary function group is CVA,followed by UACS. Chronic cough is related to abnormal lung function after acute phase of MPP.
ABSTRACT
Objective To investigate the roles of fiberoptic bronchoscopy in diagnosis and treatment for infants with refractory and persistent wheezing. Methods From Jun. 2012 to Dec. 2013, 52 hospitalized children with age between four 4 months and 1 year old were recruited for ifberoptic bronchoscopy, who had been wheezing for at least four weeks and treated ineffectively with conventional anti-inlfammatory agents:budesonide and compound ipratropium bromide solution. Then, the pathogenesis of refractory and persistent wheezing was summarized based on clinical features, detection of CT imaging of three-dimensional airway reconstruction and cardiac CT, results of bronchoscopy inspection, and bronchoalveolar lavage lfuid culture. Results Among the 52 cases, 40 were with ground glass-like changes (76.92%) in pulmonary spiral CT testing, 4 with mosaic perfusion syndrome (7.69%), 8 with segmental pulmonary consolidation (15.38%), 8 with obstructive pulmonary emphysema (15.38%), and 1 with left primary bronchial foreign body. In addition, through bronchofibroscopy, there were 52 cases with imlfammation (100%),3 with tracheal stenosis (5.77%), 3 with left and/or right main bronchus stenosis of the external pressure, 18 with bronchomalacia(34.62%), 2 cases with foreign body (3.84%), one in trachea (1.92%), the other in left main bronchus (1.92%), 10 with bronchial mucus plug (19.23%), and 8 (15.38%) with congenital airway malformations (including 3 at tracheal bronchus, 1 at left upper lobe bronchial stenosis and 1 at bronchial Bridge). The culture of bronchoalveolar lavage lfuid were conducted for all patients. The positive rate of bronchoalveolar lavage lfuid was 9.62%(5/52 cases), including 2 cases with tip Escherichia coli, 2 with Haemophilus inlfuenzae, and 1 with Acinetobacter baumannii. Conclusions First, infection is the primary cause of refractory and persistent wheezing, which is persistent in airway resulted from multi-drug resistant bacteriua. Second, refractory and persistent wheezing is often caused by multi-factors including infection, congenital airway malformations, the endogenous and exogenous foreign body, cardiovascular malformation, etc. These factors often lead to dififcult wheezing control. The last, the diagnosis rate of the refractory and persistent wheezing can be improved by combination of ifberoptic bronchoscopy and lung spiral CT.