细支气管肺泡癌高分辨率CT征象的探讨

目的　探讨细支气管肺泡癌 (BAC)的高分辨率CT征象。方法　对 2 9例BAC进行回顾性分析。分别记录结节型、多发结节型和实变型BAC的HRCT征象 ,分析有助于诊断的征象及病理基础。结果　 14例结节型病灶中 86%位于肺野外周或胸膜下 ,43 %呈不规则形 ,空泡征出现率 5 1% ,磨玻璃密度 3 6% ,胸膜尾征 71% ;多发结节型的单个病灶与前者相同 ;11例实变型中磨玻璃密度、多发结节和段叶实变混合存在的 6例 ,肺段实变周围或其他肺野分布的磨玻璃密度影内伴随网格影 ,其中 1例呈“碎石路样”。结论　①周围性结节以及伴空泡征、磨玻璃密度、胸膜尾征 4项中有 3项者高度提示结节型BAC的诊断 ;②肺段叶“蜂房样”实变并其他肺野的“碎石路样”影对弥漫性细支气管肺泡癌 (DBAC)的诊断具有特征性。③HRCT是BAC早期诊断的重要手段之一。     

青年细支气管肺泡癌CT表现与临床病理比较分析

目的探讨青年细支气管肺泡癌(BAC)的CT表现与临床病理检查的差异,提高BAC诊断率。方法回顾性分析38例BAC患者临床资料,根据CT表现分为孤立结节组(17例)、多发结节组(11例)和肺叶实变组(10例),研究比较各型肺泡癌的影像特点与临床病理。结果孤立结节组CT表现特异型征象:分叶征、支气管充气征、胸膜凹陷征等;多发结节组CT表现为两肺弥漫多发结节状,碎路石征象,常伴有胸膜牵拉等征象;肺叶实变组CT表现为肺密度低、蜂窝肺征、血管造影征及枯树枝征等。结论熟悉BAC各型的CT表现与临床病理,利于提高本病的诊断符合率。     

细支气管肺泡癌的CT诊断

目的:探讨细支气管肺泡癌的CT表现。方法:回顾性分析经病理证实的BAC48例,进一步了解其CT表现特征。结果:BAC按影像表现分为三种类型:孤立结节型、肺炎型、弥漫型。本组分别有30例、12例、6例。孤立结节型病灶多位于外周(96·7%),同时具有分叶、毛刺、空泡征、胸膜凹陷的22例(73·3%);肺炎型中,均匀实变的7例(58·3%),蜂窝状实变2例(16·7%);磨玻璃样改变3例(25%)。支气管气相5例(71·4%),枯枝征4例(57·1%),CT血管造影征3例(42·9%);弥漫型6例均表现为双肺弥漫性分布的腺泡结节影。HRCT有助于病灶的显示。结论:熟悉BAC的CT征象,可以提高诊断正确率,减少误诊。     

CT对肺磨玻璃结节的早期诊断价值探讨

目的:探讨CT对肺磨玻璃结节的早期诊断价值。方法:针对我院收治的疑似肺磨玻璃结节患者71例进行临床观察,针对71例疑似肺磨玻璃结节患者实施CT诊断,将CT诊断的结果与病理学诊断结果进行对比分析,分析CT诊断对于肺磨玻璃结节的早期诊断价值。结果:经CT诊断后,71例疑似肺磨玻璃结节患者的诊断准确性为98.46%、灵敏度为83.33%、特异性为95.77%,诊断结果与病理学诊断结果进行对比后发现两者之间(P>0.05),无统计学意义;且不同病理类型的肺磨玻璃结节的CT诊断征象存在较为显著的差异。结论:针对肺磨玻璃结节患者实施CT诊断能获取较高的诊断价值,为临床中不同病理类型的诊断鉴别提供参考。     

急性呼吸窘迫综合征的影像学表现

急性呼吸窘迫综合征(acute respiratory distress,ARDS)是指由心源性以外的各种肺内、外致病因素所导致的急性、进行性缺氧性呼吸衰竭,肺内、外致病因素分别引起肺源性和肺外源性ARDS,其特征性病理表现为肺泡内液体渗出和透明膜形成,导致广泛肺泡实变。本病初期的胸片检查可见边界模糊的磨玻璃影,随病情进展则出现弥漫性、密度均匀的大片实变影;CT扫描可显示病变从头向足以及从腹向背两个方向上形成的密度递增征象,仰卧位时,腹侧肺野透亮度接近正常,而实变影位于背侧脊柱两旁,中间区域则呈现磨玻璃样改变。     

周围性腺型小肺癌的CT表现

目的 分析<2cm周围型肺腺癌的CT征象。 方法 收集经手术和病理证实的<2cm的周围型肺腺癌35例,男性20例,女性15例,年龄49-83岁,平均70岁。全部采用螺旋CT动态增强扫描,CT图像上观察病灶的部位、大小、密度、内部结构和边缘特点,以及动态增强表现。 结果 按照CT图像上的密度分布分为3种类型,Ⅰ型为不伴磨玻璃征的软组织密度结节17例(48.5％),Ⅱ型部分实性伴磨玻璃征12例(34.2％);Ⅲ型磨玻璃样结节6例(17.1％);CT征象有分叶征27／35、毛刺征27/35、支气管气相和空泡征25／35、磨玻璃征18／35、血管聚集征或血管穿过征29／35,及胸膜凹陷征25／35,其中磨玻璃或部分磨玻璃结节的、血管聚集及穿过征象和空泡征以及支气管气相征出现率高。结论 肺小腺癌的CT表现的各种征象与肺癌的大小以及病理类型有关。     

CT对肺淋巴瘤的诊断价值

目的总结肺淋巴瘤CT表现特征及分型,探讨CT诊断肺淋巴瘤的价值。方法回顾性分析经临床及组织病理证实的31例肺淋巴瘤患者的胸部CT影像资料。结果 CT诊断肺淋巴瘤18例,其中肿块结节型7例,肺炎实变型6例,混合型5例,诊断准确率58.06%;含气支气管征、正常血管穿越征、多种类型病灶并存征及跨叶分布征和磨玻璃征为肺淋巴瘤CT典型征象。结论 CT检查有助于肺淋巴瘤的诊断及鉴别诊断。     

百草枯中毒肺损伤CT征象及临床意义

目的:探讨CT对百草枯中毒肺损伤在治疗过程中影像学特征及在疗效评估中的价值。材料与方法:回顾性分析59例口服百草枯中毒患者影像资料。按病程分为早期(1周以内)、中期(1-2周)及后期(2周);按中毒剂量分为少量组(10~20ml)、中量组(21~30ml)和大量组(30ml),均采取规范的治疗措施后观察百草枯中毒肺损伤治疗过程中肺部CT征象的演变,比较三组病例在不同时期的影像学差异。结果:本组病例治愈45例,死亡14例,2例全部病程中表现阴性,余57例在第1周内肺部CT表现以渗出为主,第1~2周以肺实变及不张为主,2周后主要表现为肺纤维化;少量组主要表现为肺纹理增多和磨玻璃样变,中量组主要表现肺实变,大量组除肺实变及纤维化外,还合并肺外病变。结论:百草枯中毒性肺损伤在治疗过程中CT征象演变有一定的特征性,可有效评估预后。     

肺泡蛋白沉积症影像学分析

目的探讨肺泡蛋白沉积症(pulmonary alveolar proteinosis,PAP)的X线、CT影像学特征.方法回顾性分析6例经病理证实的PAP患者的胸部X线和CT表现.结果PAP X线表现为两肺对称或不对称分布磨玻璃样影和实变影,自肺门向外放射,可形成"蝶翼征".胸部CT呈多样化改变:①从弥散分布的模糊结节影到弥漫性斑片状磨玻璃影与气腔实变影(6例),呈地图样分布(5例);②蝶翼征(2例);③支气管充气征(3例);④铺路石征(5例).结论肺泡蛋白沉积症CT表现有一定特征性;纤支镜肺活检是本病确诊的主要依据.     

细支气管肺泡癌的高分辨CT表现

目的：探讨细支气管肺泡癌的高分辨CT（HRCT）征象。方法：回顾分析经病理证实的41例细支气管肺泡癌的HRCT表现，分析有助诊断的HRCT征象及病理基础。结果：孤立结节型18例，其中15例位于肺外周或胸膜下，磨玻璃密度影10例，形态不规则或斑片状影8例，空泡征和/或空气支气管征14例，胸膜凹陷征12例；弥漫型14例，其中均匀实变7例，蜂房征4例，磨玻璃密度8例,支气管气像6例,腺泡样结节6例。结论：HRCT是细支气管肺泡癌的诊断及鉴别诊断的重要手段之一。     

窒息法和室颤法致猪心脏骤停后肺损伤的研究

目的 通过窒息和室颤的心脏骤停动物模型,对心肺复苏后肺损伤进行对照研究.方法 将近交系五指山小型猪随机(随机数字法)分为窒息组(AS)和室颤组(VF),每组各24只,分别采用阻塞气管插管和程控电刺激诱导方法制模,制模成功后给予标准的心肺复苏至ROSC,分别测量基础状态、ROSC即刻、15 min、30 min、1h、2h、4h和6h的氧合指数(OI)、呼吸指数(RI)、氧输送(DO2)、血乳酸,并监测同一时刻动物的肺顺应性(Cdyn)、气道阻力(Raw)、血管外肺水指数(EVLWI)和肺血管通透性指数(PVPI);于基础状态时和ROSC 4 h时进行肺核素灌注扫描和PET-CT扫描;ROSC后6h将动物处死后取肺组织进行病理及电镜检查,检测组织中Na+-K+-ATP酶、Ca2-ATP酶、SOD、MDA、Bcl-2、Bax及Caspase3蛋白水平及凋亡指数(AI％)等.结果 窒息组的ROSC率和6h生存率均显著低于室颤组(P＜0.01);在肺组织有关酶学及蛋白(Na+-K+-ATPase、Ca2-ATPase、SOD、MDA、AI％、Bax、Bcl-2和Caspase3)检测方面,窒息组重于室颤组,且凋亡现象更严重(P＜0.01);在呼吸力学各个时间点相关指标(OI、RI、DO2、血乳酸、Cdyn、Raw、EVLWI、PVPI)的监测中,窒息组的各项指标的变化较室颤组更明显,在6h后仍未能恢复至基础状态.窒息组和室颤组在肺灌注核素扫描上,无明显的充盈缺损;而在PET-CT扫描上则可见较明显的充盈缺损区.结论 心脏骤停后肺损伤的发生与导致心脏骤停的病因密切相关,窒息明显重于室颤,而心外按压不是导致此类肺损伤的主要原因.     

Contributions of vascular flow and pulmonary capillary pressure to ventilator-induced lung injury

OBJECTIVE: To evaluate the influence of vascular flow on ventilator-induced lung injury independent of vascular pressures. DESIGN: Laboratory study. SETTING: Hospital laboratory. SUBJECTS: Thirty-two New Zealand White rabbits. INTERVENTIONS: Thirty-two isolated perfused rabbit lungs were allocated into four groups: low flow/low pulmonary capillary pressure; high flow/high pulmonary capillary pressure; low flow/high pulmonary capillary pressure, and high flow/low pulmonary capillary pressure. All lungs were ventilated with peak airway pressure 30 cm H2O and positive end-expiratory pressure 5 cm H2O for 30 mins. MEASUREMENTS AND MAIN RESULTS: Outcome measures included frequency of gross structural failure (pulmonary rupture), pulmonary hemorrhage, edema formation, changes in lung compliance, pulmonary vascular resistance, and pulmonary ultrafiltration coefficient. Lungs exposed to high pulmonary vascular flow ruptured more frequently, displayed more hemorrhage, developed more edema, suffered larger decreases in compliance, and had larger increases in vascular resistance than lungs exposed to low vascular flows (p < .05 for each pairwise comparison between groups). CONCLUSIONS: These findings suggest that high pulmonary vascular flows might exacerbate ventilator-induced lung injury independent of their effects on pulmonary vascular pressures.     

实验性特发性肺纤维化早期的HRCT—病理对照

目的通过对不同药物作用时间段的兔肺HRCT图像与病理结果的对照,分析IPF在兔中的影像特征及其病理基础.方法20只新西兰白兔被随机地分为4组.每组内任选3只作为实验对象(处理组),将盐酸平阳霉素灌注于支气管内.在预设的时间点取一组动物进行HRCT扫描、肺Heitzman法固定及HE染色和胶原纤维Van Gieson染色.结果对处理组动物的HRCT连续观察发现肺内病变呈明显的进行性发展,此与病理切片的表现相一致.在7天时,肺内主要以弥漫性的密度增高为主.14天后病灶明显局限化,出现特征性的磨玻璃样影和类纤维灶,后者病理证实主要为水肿、组织细胞浸润引起的小叶间隔增厚.21天纤维增生逐渐明显,28天时可见纤维增生所形成的杂乱线状影,小叶间隔、胸膜、支气管血管束增厚,CT图像中显示严重的牵拉性支气管扩张,扩张的支气管直达胸膜面,VG染色示显著增生、分布散乱的纤维组织.小叶间隔定量测量四组间对比有显著性差异(p＜0.05).结论平阳霉素处理后的2周内,兔肺内的渗出达到最明显的程度,故可以考虑从影像学角度将2周作为IPF病程的早期阶段.HRCT可以清楚地显示兔肺间质的增厚.     

油酸型家兔肺损伤亚急性期的超声表现

目的通过建立家兔油酸型动物模型,研究肺损伤亚急性期的声像图表现及病理基础,探讨亚急性期声像图表现的临床应用价值。 方法将实验兔分为实验组与对照组,制模前留取全部实验兔的肺声像图,随即处死对照组实验兔。实验组制备油酸型急性肺损伤动物模型,制模成功的标准为至少一个肺区出现弥漫性"彗星尾"征。制模成功后,在不做任何干预条件下,普通级饲养,每周观察一次,留取肺声像图。于第2周末处死。解剖所有实验兔,取出肺脏,制备组织切片。观察、记录实验兔肺脏的大体观及镜下组织学改变。 结果对照组肺脏声像图主要表现为A线;肺脏大体病理表现为：肺组织形态大小正常、呈粉红色且表面光滑。实验组制模的成功率为100%;在制模成功2周后即亚急性期,肺声像图的主要表现为：A线与B线同时存在,"彗星尾"征特点为短而宽,仅局限于近场,未达远场;实验组肺大体病理表现为：双肺表面呈暗红色兼有灰色区,双肺边缘呈灰白色;主要镜下病理表现为肺实变（8/12,66.7%）、肺纤维化（6/12,50.0%）及胸膜增厚（4/12,33.3%）,实验组未见肺水肿及肺淤血性出血。 结论A线与B线同时存在及短而宽的"彗星尾"征是提示肺损伤进入亚急性期的主要声像图指征。     

Rapid change in pulmonary vascular hemodynamics with pulmonary edema during cardiopulmonary resuscitation

Previous studies have shown that pulmonary edema occurs in half of all pre-hospital cardiac arrest victims who cannot be successfully resuscitated and is a major cause of hypoxemia and poor lung compliance during resuscitation. Pulmonary vascular hypertension and elevation of pulmonary capillary wedge pressure have been observed during cardiac resuscitation in humans. To further define the time course of the pulmonary hemodynamic changes, pulmonary artery diastolic pressure (PAd) was measured on a computerized trend recorder prior to, during, and immediately after arrest in three adult patients. Prior to arrest, PADP was 20.9 +/- 3.1 mm Hg. The PADP rose in all three patients by an average of 30.6% after 5-10 minutes and 71.3% after 10-15 minutes of CPR. Peak PADP reached 35.8 +/- 5.1 mm Hg (difference from pre-arrest level significant, P less than 0.001). In both patients who were resuscitated successfully, the PADP returned to baseline within 5 minutes of effective spontaneous circulation. The finding that such hemodynamic changes occur rapidly during resuscitation and can reverse quickly with resumption of effective spontaneous circulation is consistent with the time course for the early development of pulmonary edema. Development of pulmonary edema many hours following successful resuscitation likely involves other mechanisms.     

Effect of hypertransfusion on the gastrointestinal tract after cardiac arrest in a porcine model

BACKGROUND:

This study aimed to determine the potential protective effect of inducing hypertransfusion to the gastrointestinal tract following a porcine model of cardiac arrest and cardiopulmonary resuscitation (CPR) by evaluating the influence of gastrointestinal ultrastructure, ATPase and serum diamine oxidase.

METHODS:

Ventricular fibrillation was induced by programmed electrical stimulation in 16 male domestic pigs (n=8/group). Four minutes after ventricular fibrillation, CPR was performed. The pigs that successfully restored spontaneous circulation received intravenous infusion of either norepinephrine to maintain the mean arterial pressure at 130% of the baseline before ventricular fibrillation or normal saline. Serum diamine oxidase and gastrointestinal ATPase activity were determined, and histopathological examination of the gastrointestinal tract was performed by light and electron microscopy.

RESULTS:

CPR caused significant injury to the gastrointestinal tract, elevating serum diamine oxidase and causing destruction of intestinal microvillus in control animals. Na⁺-K⁺ ATPase and Ca²⁺ ATPase activity in gastric tissue were significantly elevated in animals receiving hypertransfusion treatment compared with the control animals. Hypertransfusion also significantly reduced serum diamine oxidase to below control levels after CPR. Moreover, severe injury sustained by the gastrointestinal tissue was markedly ameliorated under hypertransfusion conditions compared with the control animals.

CONCLUSIONS:

Gastrointestinal injury and abnormal energy metabolism were strikingly evident following CPR. Hypertransfusion inducing hypertension can improve energy metabolism and ameliorate gastrointestinal mucosal injury, indicating that hypothermia significantly ameliorates gastrointestinal injury sustained following cardiac arrest.KEY WORDS: Cardiopulmonary resuscitation, Cardiac arrest, Gastrointestinal tract, Diamine oxidase, Ultra structure     

有机氟中毒性肺水肿的CT诊断价值(附3例报告)

目的探讨有机氟中毒性肺水肿的CT诊断价值。方法回顾性分析本院收治的有机氟中毒3例,分析其临床和CT表现。结果中毒性肺水肿是有机氟中毒的主要损伤,CT主要表现为肺内团絮状影伴磨玻璃影,病变愈重密度愈高;胸腔积液;纵隔、皮下气肿。肺内病变吸收时先是密度降低,逐渐呈磨玻璃影,最后才范围缩小,直至完全吸收。经正确积极治疗肺内病变和胸腔积液可在60-72h吸收;纵隔、皮下气肿需6d以后吸收。结论CT对有机氟中毒性肺水肿早期诊断和恢复期评价、并发症的发现具有重要意义,同时也对职业性损伤的鉴别诊断具有重要价值。     

Effects of naloxone on the adrenomedullary response during and after cardiopulmonary resuscitation in dogs

To determine the effects of naloxone, an opiate antagonist, on the adrenomedullary response to cardiac arrest, plasma epinephrine and norepinephrine levels were measured before, during, and after cardiac arrest in dogs. Ventricular fibrillation was induced in 12 dogs anesthetized with pentobarital sodium (30 mg/kg) and standard American Heart Association cardiopulmonary resuscitation (CPR) was begun using a mechanical device. At 6.5 minutes of CPR, naloxone (10 mg/kg) or 0.9% saline (10 ml) was given intravenously. At 12 minutes of CPR, the cardiac ventricles were electrically defibrillated. Plasma epinephrine and norepinephrine levels were measured before ventricular fibrillation; at 2.5, 4.5, 9.5, and 11.5, minutes of CPR; and at 5, 10, 15, and 20 minutes after resuscitation. Epinephrine and norepinephrine increased from prearrest levels of 3.66 +/- 0.67 (+/- SE) and 24.02 +/- 3.67 ng/ml to 66.67 +/- 9.65 and 74.00 +/- 9.91 ng/ml, respectively, at 4.5 minutes of CPR. After resuscitation, norepinephrine levels remained slightly elevated, while epinephrine fell to prearrest levels. Naloxone did not cause a significant change in either epinephrine or norepinephrine from 6.5 minutes of CPR (time of treatment) through 20 minutes postresuscitation. In addition, naloxone had no effect on either the end-diastolic pressure difference during CPR or resuscitation outcome. We conclude that cardiac arrest causes significant increases in plasma epinephrine and norepinephrine levels, which remain elevated for the duration of the arrest, and that naloxone has no effect on these levels.     

Stimulation of alveolar epithelial fluid clearance in human lungs by exogenous epinephrine

OBJECTIVES: Because several experimental studies have demonstrated that cyclic adenosine monophosphate generation following beta-adrenoceptor activation can markedly stimulate alveolar fluid clearance, we determined whether the endogenous levels of catecholamines that occur in the pulmonary edema fluid and plasma of patients with acute lung injury are high enough to stimulate alveolar fluid clearance in the human lung. DESIGN: Observational clinical study. SETTING: Academic university hospital and laboratory. PATIENTS: Twenty-one patients with acute pulmonary edema plus ex vivo human lungs. INTERVENTIONS: Measurements of catecholamine levels in patient samples and controlled laboratory studies of the effects of these catecholamine levels on the rates of alveolar fluid clearance in ex vivo human lungs. MEASUREMENTS AND MAIN RESULTS: The concentrations of both epinephrine and norepinephrine in the pulmonary edema fluid and plasma were approximately 10 M (range of 1-8x10 M) in hydrostatic pulmonary edema (n=6) and acute lung injury patients (n=15). We therefore tested whether 10 M epinephrine or norepinephrine stimulated alveolar fluid clearance in isolated human lungs and found that these epinephrine or norepinephrine concentrations did not stimulate alveolar fluid clearance. However, higher concentrations of epinephrine (10 M), but not norepinephrine (10 M), significantly stimulated alveolar fluid clearance by 84% above control. Glibenclamide (10 M) and CFTRinh-172 (10 M), cystic fibrosis transmembrane conductance regulator inhibitors, completely inhibited the epinephrine-induced stimulation of alveolar fluid clearance. CONCLUSIONS: These results indicate that endogenous catecholamine concentrations in pulmonary edema fluid are probably not sufficient to stimulate alveolar fluid clearance. In contrast, administration of exogenous catecholamines into the distal airspaces can stimulate alveolar fluid clearance in the human lung, an effect that is mediated in part by cystic fibrosis transmembrane conductance regulator. Therefore, exogenous cyclic adenosine monophosphate-dependent stimulation will probably be required to accelerate the resolution of alveolar edema in the lungs of patients with pulmonary edema.     

External cardiopulmonary resuscitation preserves brain viability after prolonged cardiac arrest in dogs.

Standard external cardiopulmonary resuscitation (CPR) steps A-B-C produce a low blood flow that may or may not preserve brain viability during prolonged cardiac arrest. A dog model was used with ventricular fibrillation (VF) of 20 minutes, reperfusion with brief cardiopulmonary bypass, controlled ventilation to 20 hours, and intensive care to 96 hours. A retrospective comparison was made of the results of one series, now called "group I" (n = 10)--which received CPR basic life support interposed from VF 10 to 15 minutes, and CPR advanced life support with epinephrine (without defibrillation) from VF 15 to 20 minutes--to the results of another series, now "control group II" (n = 10)--which received VF no flow (no CPR) for 20 minutes. All 20 dogs within protocol were resuscitated. All 10 of group I and 7 of 10 of group II survived to 96 hours. Pupillary light reflex returned after the start of cardiopulmonary bypass at 7.7 +/- 3.7 minutes in CPR group I, versus 16.3 +/- 7.4 minutes in control group II (P = .032). At 96 hours postarrest, final overall performance categories (1, normal; 5, brain death) were better in group I. Six of 10 dogs achieved normality (overall performance category 1) in group I, as compared with none of 10 in group II (P = .004). Final neurologic deficit score (0%, best; 100% worst) was lower (better) in group I (15% +/- 20%) than in group II (51% +/- 6%; P less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)