CT扫描在胸部创伤诊断中的应用体会

目的探讨胸部创伤中应用CT扫描的诊断要点。方法 26例胸部创伤中,20例有肺挫伤,6例单纯肋骨骨折。3例合并有胸骨骨折,6例合并有气胸及胸腔积液。全部患者均在伤后8 h内进行CT扫描,5例是伤后24 h后复查出现湿肺。结果 CT平扫能够及时准确地发现胸部损伤的程度及合并症。结论 CT扫描对胸部创伤的诊断具有很高的敏感性和特异性,并能发现平片不能检出的阳性征象。     

胸腔积液的治疗方法和效果

目的：探讨胸腔积液的治疗方法和效果。方法回顾大量胸腔积液患者305例,包括结核性胸膜炎引起胸腔积液75例,心功能不全引起胸腔积液15例,乳糜胸3例,脓胸28例,恶性肿瘤引起胸腔积液117例,外伤引起血胸67例。治疗方法分：单纯置管引流;置管引流＋胸腔内化疗胸膜粘连;引流后开胸。结果全组患者无严重并发症及死亡,大部分患者胸腔积液消失;少部分胸腔积液明显减少;咳嗽、胸闷症状消失。结论胸腔积液应以通。引流为主,彻底引流积液;药物治疗为辅;少部分患者手术。     

胸外伤后胸腔积液56例治疗体会

目的：总结胸部外伤后胸腔积液的诊治经验。方法：回顾分析2004年6月～2009年6月本院收治的56例胸部外伤患者的临床资料。结果：全组患者治愈54例,死亡2例,死亡患者均合并颅脑损伤,早期行胸膜腔闭式引流术。后期经反复胸腔穿刺抽液并注入药物。结论：及时排出胸腔积液,减轻壁层胸膜渗出,胸腔内注入粘连剂促进胸膜腔粘连,促进肺复张是治疗反复胸腔积液的重要因素。     

重度烧伤并发胸腔积液一例

[病例] 男,61岁.主因全身多处被开水烫伤4 h入院.无高血压、冠心病等病史.入院诊断:重度烧伤(TBSA:40%,深Ⅱ度32%,Ⅲ度8%).入院后即予吸氧,心电监护,深静脉补液并监测中心静脉压,抗感染,留置导尿,记录每小时尿量,暴露烧伤创面.补液总量以国内通用公式计算量为参考,烧伤后第1个24 h补液量7200 ml,晶体2800 ml,胶体2400 ml,水分2000 ml;第2个24 h补液量5100 ml,晶体1600 ml,胶体1200 ml,水分2300 ml;第3个24 h补液量5000 ml,晶体1600 ml,胶体1200 ml,水分2200 ml.伤后1、2、3 d尿量分别为1280、1600、1500 ml,白蛋白分别为42.2、25.8、28.7 g/L.伤后5 d出现胸闷、气促,无少尿及咳粉红色泡沫痰.查体:体温37.3℃,脉搏110/min,呼吸30/min,血压110/80 mmHg.无颈静脉怒张,肺部听诊可闻及少量湿啰音,无哮鸣音,双下肺呼吸音弱,无腹胀.血气分析结果:pH 7.5,氧分压65 mmHg,二氧化碳分压28 mmHg.给予高浓度吸氧后症状无明显好转.行胸部CT检查示双侧胸腔积液.遂行双侧胸腔穿刺分别引流出淡黄色液体310、280 ml,症状好转.随后限制液体量,加大白蛋白补充,予利尿脱水等治疗.于伤后7、15 d行手术治疗封闭创面,住院26 d痊愈,出院时胸腔积液已完全吸收.     

重度烧伤并发胸腔积液一例

[病例] 男,61岁.主因全身多处被开水烫伤4 h入院.无高血压、冠心病等病史.入院诊断:重度烧伤(TBSA:40%,深Ⅱ度32%,Ⅲ度8%).入院后即予吸氧,心电监护,深静脉补液并监测中心静脉压,抗感染,留置导尿,记录每小时尿量,暴露烧伤创面.补液总量以国内通用公式计算量为参考,烧伤后第1个24 h补液量7200 ml,晶体2800 ml,胶体2400 ml,水分2000 ml;第2个24 h补液量5100 ml,晶体1600 ml,胶体1200 ml,水分2300 ml;第3个24 h补液量5000 ml,晶体1600 ml,胶体1200 ml,水分2200 ml.伤后1、2、3 d尿量分别为1280、1600、1500 ml,白蛋白分别为42.2、25.8、28.7 g/L.伤后5 d出现胸闷、气促,无少尿及咳粉红色泡沫痰.查体:体温37.3℃,脉搏110/min,呼吸30/min,血压110/80 mmHg.无颈静脉怒张,肺部听诊可闻及少量湿啰音,无哮鸣音,双下肺呼吸音弱,无腹胀.血气分析结果:pH 7.5,氧分压65 mmHg,二氧化碳分压28 mmHg.给予高浓度吸氧后症状无明显好转.行胸部CT检查示双侧胸腔积液.遂行双侧胸腔穿刺分别引流出淡黄色液体310、280 ml,症状好转.随后限制液体量,加大白蛋白补充,予利尿脱水等治疗.于伤后7、15 d行手术治疗封闭创面,住院26 d痊愈,出院时胸腔积液已完全吸收.     

胸腔置管引流并注入尿激酶治疗结核性胸腔积液疗效观察

目的：探讨胸膜腔置管引流并于胸膜腔内注入尿激酶治疗结核性包裹性胸腔积液的效果。方法将48例结核性包裹性胸腔积液患者随机分为2组,在常规抗结核药物的基础上,治疗组予以中心静脉导管留置胸膜腔并注入尿激酶20万 U ＋生理盐水20 ml,夹管24 h 后放液,每周2～3次;对照组胸腔穿刺抽液每周3次。结果治疗组胸腔积液吸收、胸膜肥厚粘连、肺功能改善方面明显优于对照组。结论胸膜腔内留置静脉导管并胸膜腔内注入尿激酶治疗结核性包裹性胸腔积液,能使胸腔积液引流更彻底,可有效降低胸膜肥厚、粘连的程度,减少肺穿刺次数及肺膨胀不全、脓胸等并发症的发生,改善肺功能,缩短了病程,减轻患者痛苦是治疗结核性包裹性胸腔积液的有效方法。     

沙培林胸腔内注射治疗术后胸腔积液疗效分析

目的：观察沙培林对胸腔恶性肿瘤术后胸腔积液的疗效，了解其毒副作用并探讨其作用机制。方法：选择1998－2001年胸腔恶性肿瘤术后胸腔积液28例，术后第二天开始平均胸引量大于300ml的病例，自胸管内注入沙培林5KE闭管，8小时后开放，观察24小时并记录引流量，若引流量大于100ml，再注入3KE后拔管，治疗前后摄胸片对照，治疗前胸引量按每日胸引量及3天胸水量之和评估，治疗后以胸片或B超定位胸穿抽液为准。结果：28例中完全缓解21例（75％），部分缓解6例（21．4％），总有效率96．4％。结论：沙培林胸腔内注射治疗胸腔恶性肿瘤术后胸腔积液疗效肯定，不良反应主要是发热，胸痛，无肝肾等不良反应。     

体腔热灌注治疗在胸外科恶性胸腔积液治疗中的临床应用

目的探讨外科胸腔镜胸腔探查加术后体腔热灌注治疗系统热灌注治疗恶性胸腔积液的临床效果。方法30例恶性胸腔积液的患者全麻胸腔镜下行胸膜腔探查及胸腔内清理术，术中胸腔内置28F胸管两根，术后24h、48h、72h利用体腔热灌注治疗机行循环热灌注治疗3次，灌注液为生理盐水，胸腔内温度控制在43℃左右，单次灌注时间为90rnin。结果除1例患者因不良反应停止治疗外，其余29例患者均顺利完成治疗，无治疗相关性死亡，恶性胸腔积液治疗总有效率为90％。结论胸腔镜探查加术后体腔热灌注治疗机循环热灌注治疗肺癌恶性胸腔积液，是一种安全、有效的方法。     

以烧伤为主诊的肺爆震伤临床分析

目的探讨以烧伤为主诊的肺爆震伤(BLI)的临床特征和救治方法。方法回顾性分析以烧伤为主诊的肺爆震伤39例患者资料,并用BLI评分方法评估其严重程度。结果 39例烧伤面积平均46.5%,其中Ⅲ°烧伤者Ⅲ°面积平均50.9%。按爆震伤评分,重度8例,中度14例,轻度17例。入院时均有程度不等的呼吸困难,13例严重者在12h内建立呼吸道和呼吸支持。入院时仅个别伤员X线胸片有改变,但24h内所有患者胸片均有阳性发现。中度以上的22例均行机械通气支持呼吸,呼吸支持平均4周。烧伤创面愈合时间平均27.8d。发生成人呼吸窘迫综合征(ARDS)6例,2例重度患者在48h内死亡。结论早期认识肺爆震伤,强化以呼吸支持为主的脏器支持和保护等综合性措施。     

65例仰卧位胸腔积液的X线表现

目的：探讨危重不能站立病人仰卧位胸片胸腔积液的X线表现。方法：选用65例经CT检查为游离胸腔积液病例。分析定位胸片上胸腔积液的各种征象，统计肺野均匀性密度增高、膈肌轮廓征、新月征以及肺尖帽征在各类型积液中的出现率。结果：肺野均匀性密度增高在小量、中等量、大量积液中的出现率分别为63．6％、100％、100％，肺尖帽征在中等量和大量积液中的出现率分别为4．3％、65．7％。结论：仰卧位胸腔积液的主要X线表现是肺野均匀性密度增高，肺尖帽征是大量胸腔积液的典型X线征象。     

Early indications of monocrotaline pyrrole-induced lung injury in rats

Monocrotaline pyrrole (MCTP), a putative metabolite of the naturally occurring plant toxin, monocrotaline (MCT), causes lung injury, pulmonary hypertension, and right cardioventricular hypertrophy when administered intravenously to rats. The lesions caused by MCTP administration are similar to those caused by MCT but appear to occur on a slightly accelerated time course. To explore the onset and development of lung lesions, male Sprague-Dawley rats were treated with a single, intravenous injection of MCTP, and several markers of lung injury were evaluated at early times after administration. Rats received 3.5 mg MCTP/kg or an equal volume of the vehicle, N,N-dimethylformamide (DMF), via the tail vein at time 0 and were killed at 4, 12, 24, 48, 72, or 120 hr after treatment. Beginning at 4 hr, MCTP-treated rats had increased wet lung-to-body-weight ratios (LW/BW). The LW/BW remained elevated at 12 hr, returned to baseline at 24 hr, then increased steadily over the next few days. At 24 hr, the protein concentration of cell-free bronchoalveolar lavage fluid (BALF) was slightly elevated. Lactate dehydrogenase activity in cell-free BALF samples was moderately increased 48 hr after MCTP. Changes in these markers were modest initially but became much more pronounced by 120 hr. Total nucleated cell counts in BALF were variable but were moderately elevated at 120 hr. Cytologic examination of the BALF samples revealed small but significant infiltrates of segmented neutrophils at 4 hr and relatively large infiltrates of segmented neutrophils and small lymphocytes at 120 hr post-treatment. Mature neutrophils had degenerate cytomorphologic characteristics at both 4 and 120 hr. These results confirm that pronounced lung injury is delayed for several days after a single, intravenous administration of MCTP, but they also indicate that subtle lung injury can be detected using quantitative markers quite early after MCTP administration.     

复方丹参注射液对大鼠体外循环后肺损伤的影响

目的:研究大鼠体外循环(CPB)后肺组织损伤以及复方丹参注射液对肺损伤的影响。方法:24只SD大鼠随机分为3组,对照组、CPB组和丹参组,每组8只。CPB组和丹参组建立体外循环,丹参组为停循环前5 min经体外循环的储血器给入复方丹参注射液1 ml.kg-1体重。对照组为假手术对照。CPB后60 min取部分肺组织,测定并计算丙二醛(MDA)、髓过氧化物酶(MPO)和组织含水量。取部分肺组织用多聚甲醛固定,制作石蜡切片,HE染色后观察形态学改变。结果:光学显微镜下观察可见,CPB组肺组织间质增厚、细胞浸润,丹参组的程度较CPB组有所减轻。CPB组和丹参组肺组织中MDA含量、MPO含量和含水量均明显高于对照组(P<0.05),丹参组升高程度小于CPB组(P<0.05)。结论:体外循环过程中应用复方丹参注射液能有效减轻肺损伤程度,可能与其清除氧自由基、减轻中性粒细胞浸润等作用有关。     

Induction of microsomal epoxide hydrolase by nitrosamines in rat liver. Effect on messenger ribonucleic acids

Nitrosomethylethylamine and nitrosomethylpropylamine were found to be more potent inducers of rat liver microsomal epoxide hydrolase (styrene oxide hydrolase) than nitrosodiethylamine or nitrosodimethylamine. The time course of induction following a single administration of nitrosodimethylethylamine, nitrosomethylpropylamine or nitrosodiethylamine each showed a delay of 24 hr during which enzyme activity was unaltered. After that time activity increased and reached a maximum at between 72 and 120 hr. Increased enzyme activity following NDEA was paralleled by changes in the content of epoxide hydrolase in microsomes as measured by Western blots. Nitrosamines caused an increase of mRNA for epoxide hydrolase which was detected by probing Northern blots with a [32]-P labelled epoxide hydrolase cDNA and by in vitro translation of polyadenylated mRNA. Both methods showed a maximal increase at 72 hr after nitrosodiethylamine treatment but a significant increase was also observed at 24 hr although at this time no increase in enzyme activity was apparent.     

Diurnal fluctuation and pharmacological alteration of mouse organ glutathione content

Mouse liver glutathione content showed a diurnal variation with a maximum GSH + 2 GSSG content at 6 to 10 a.m. of 62 +/- 8 nmole per mg protein and a minimum of 42 +/- 7 at 6 p.m. Starvation for more than 24 hr decreased the hepatic glutathione content to 22 +/- 3 nmole/mg protein and abolished the diurnal rhythm. Artificial reversal of the feeding habit of the animals reversed the diurnal rhythm. Kidney, spleen and lung glutathione contents showed no such rhythm. The organ glutathione content decreased by 50% or more upon starvation. The increase of the liver glutathione content by injection of either free or liposomally entrapped GSH to starved animals was not dependent on the time of administration. The physiological maximum level could not be exceeded by this treatment. It was not possible to influence the glutathione content of kidney, lung or intestine by glutathione injections in either form. Intravenous injections of equimolar doses of 2,3-dimercaptopropanol, 2-mercaptoethanesulfonic acid, N-2-mercaptopropionylglycine, D-penicillamine, or cysteamine did not lead to any significant change in liver, kidney, spleen or lung glutathione contents 2 hr after administration. Intravenously given N-acetylcysteine, methionine, GSH or GSSG restored liver glutathione levels of starved animals to the contents observed in the fed state. The diurnal hepatic variation of GSH caused by the food intake habit of the animals may limit the capacity of the intracellular detoxication system.     

Vehicle alteration of paraquat lethality in mice.

The lethal toxicity to mice of paraquat dissolved in saline was lower than when it was dissolved in distilled water. This was true whether paraquat was administered ip or sc. This apparent protective effect of saline was not observed when paraquat was given iv, or when saline was given by a different route concomitant with paraquat dissolved in water. The absorption of ip paraquat was apparently more rapid when water was the vehicle and significantly higher paraquat concentrations were observed in plasma, lung, and kidney 24 hr after injection. In untreated mice and those pretreated ip with paraquat in saline 24 hr earlier the decay of iv-administered paraquat from blood was slower when dissolved in water compared with saline. However, the disappearance of iv paraquat dissolved in saline or water was the same in mice that had been pretreated 24 hr earlier with ip paraquat dissolved in water. It is concluded that paraquat is more toxic dissolved in water because of a combination of increased absorption from the peritoneal cavity and decreased excretion at the later times after administration, thereby allowing higher concentrations of the herbicide to be accumulated in the lung.     

Effect of ozone exposure on lung functions and plasma prostaglandin and thromboxane concentrations in guinea pigs

Male Hartley guinea pigs were exposed either to filtered air or to 1 ppm ozone (O3) for 1 hr. At 2, 8, 24, or 48 hr after exposure we measured ventilation, respiratory mechanics, lung volumes, diffusing capacity for carbon monoxide (DLCO), and alveolar volume (VA) in anesthetized, tracheotomized animals. Respiratory frequency and tidal volume were unchanged in all groups. Pulmonary resistance was increased 2 hr after O3 but returned to control at 8 hr and thereafter. Prolonged reductions in lung volumes (total lung capacity, vital capacity, functional residual capacity, and residual volume) as well as in DLCO and VA occurred after O3, with maximum decreases at 8 and 24 hr postexposure. Increased ratios of wet lung weight to body weight were seen at 2, 8, and 24 hr. In separate groups of animals, also exposed either to filtered air or to 1 ppm O3, plasma eicosanoid (EC) concentrations were measured at 2, 8, 24, 48, or 72 hr after exposure. Significant increases in thromboxane B2 concentrations were seen at 2, 24, and 48 hr after exposure. Plasma concentrations of 6-keto prostaglandin F1 alpha (PGF1 alpha) and prostaglandin E1 (PGE1) were increased at 24 hr and at 24, 48, and 72 hr, respectively. The nature of this long-term pulmonary response to a short-term exposure to O3 suggests alveolar involvement, including probable alveolar duct constriction and localized pulmonary edema. Although changes in plasma EC concentrations were observed concurrent with impaired lung functions, no simple causal relationship was apparent from these studies.     

Effect of nitrogen dioxide on surface membrane fluidity and insulin receptor binding of pulmonary endothelial cells

Nitrogen dioxide (NO2), an environmental oxidant pollutant, is known to peroxidize membrane lipids of lung cells. We evaluated the ability of NO2 to alter the surface membrane fluidity, lipid composition, and insulin receptor binding of porcine pulmonary artery endothelial cells in culture. After 3- to 24-hr exposure to 5 ppm NO2, cells were labeled with either 1-(4-trimethylaminophenyl)-6-phenyl-1,3,5-hexatriene (TMA-DPH), a cationic fluorescent aromatic hydrocarbon that anchors at the lipid-water interface, or fluorescamine, a fluorescent molecular probe that covalently binds with amino groups of surface phospholipids and proteins. Membrane fluidity was measured by monitoring changes in the steady-state fluorescence anisotropies (rs) for TMA-DPH and fluorescamine. Insulin specific receptor binding was monitored by measuring time-dependent binding of 125I-insulin. Following NO2 exposure, rs values for TMA-DPH and fluorescamine were increased significantly in a time-dependent fashion, with maximum increases at 24 hr (P less than 0.001). Similar increases in rs values were observed in isolated plasma membranes as well as in lipid vesicles prepared from total lipid extracts of endothelial cells or their plasma membranes. Phosphatidylethanolamine plus phosphatidylserine content in lipid extracts from 24-hr but not 3- to 12-hr NO2-exposed cells was increased significantly (P less than 0.01) compared to control cells. Specific binding of 125I-insulin to cells exposed to NO2 for 12 and 24 hr (but not 3 and 6 hr) was reduced significantly (P less than 0.05) compared to binding in control cells. Scatchard analysis of the binding data indicated that NO2 exposure caused a 5-fold reduction in insulin receptor binding sites in endothelial cells. Recovery was achieved 24 hr after NO2 exposure with, but not without, changing culture medium. These results indicate that NO2 exposure causes reversible changes in the physical state of lipids in the superficial lipid domains of the pulmonary endothelial cell plasma membrane, and these alterations may interfere with plasma membrane-dependent functions such as receptor-ligand interaction.     

The Influence of Humic Substances on the Absorption and Distribution of Cadmium in Mice

Abstract: The complex binding of cadmium ions to humic and fulvic acids in water may influence the absorption and distribution of drinking-water Cd in humans. Thus, in the present study mice were given a single oral dose of Cd (¹⁰⁹CdCl₂, 25 μg/l) in 100 μl Millipore® water containing different concentrations of humic compounds (0, 1, 10 and 100 mg dissolved organic carbon/l). The complex binding of Cd was studied by dialysis. At neutral pH, 1 mg dissolved organic carbon/l caused complex binding of more than 50% of the Cd, whereas more than 90% of Cd was bound at 10 and 100 mg dissolved organic carbon/l. At pH 3 the complex binding of Cd decreased somewhat, but over 90%) of the Cd was bound at 100 mg dissolved organic carbon/l. Complex binding of Cd increased the lipid solubility of Cd, expressed as an octanol/water partition coefficient, Nevertheless, more than 99% of the bound Cd was present as hydrophilic binding forms. Irrespective of the bound of Cd, the intestinal uptake and intracellular distribution (gel filtration on Sephadex G-75 column) were not affected by the humic substances 6 hr after dosage. Moreover, complex binding did not influence the intestinal absorption of Cd 24 hr after exposure. The median Cd retention in the kidneys of the 100 mg dissolved organic carbon/1 group was 23%> and 46% lower than that of the control group 6 and 24 hr after administration, respectively, indicating alterations in the distribution of Cd after absorption. Thus humic substances may affect the metabolism of toxic heavy metals, such as Cd, in vivo in mice, indicating that the presence of humic and fulvic acids in drinking water should be considered in future risk assessments of metals in drinking water.     

Pulmonary toxicity of trichloroethylene in mice. Covalent binding and morphological manifestations

We examined the time course of trichloroethylene (TCE)-induced pulmonary injury and focused on morphological changes and covalent binding of [14C]TCE soon after administration of a single dose of TCE (2000 mg/kg) to CD-1 male mice. At 1 hr after chemical treatment, Clara cells of the bronchiolar epithelium exhibited necrotic changes involving the mitochondria and endoplasmic reticulum. Dilatation of the endoplasmic reticulum became more severe at 2 hr after TCE administration and, by 4 hr, distended cisternae coalesced to form small vacuoles within the cytoplasmic matrix of the Clara cell. The severity of cellular damage increased progressively between 8 and 12 hr and, by 24 hr, the majority of Clara cells within an airway were severely vacuolated. Covalent binding of [14C]TCE to lung macromolecules was evident at 1 hr, peaked at 4 hr, declined thereafter, and reached a plateau between 12 and 24 hr. Peak binding (142.6 +/- 31.8 nmol/g of wet weight) represented approximately 20% of [14C]TCE distributed to the lung. Although the levels of binding in the liver were at all times greater than those in the lung, liver injury was relatively insignificant. The results demonstrate a positive correlation between the onset of Clara cell injury and the formation of reactive metabolites, as assessed by covalent binding of [14C]TCE.     

The influence of humic substances on the absorption and distribution of cadmium in mice.

The complex binding of cadmium ions to humic and fulvic acids in water may influence the absorption and distribution of drinking-water Cd in humans. Thus, in the present study mice were given a single oral dose of Cd (109CdCl2, 25 microg/l) in 100 microl Millipore water containing different concentrations of humic compounds (0, 1, 10 and 100 mg dissolved organic carbon/l). The complex binding of Cd was studied by dialysis. At neutral pH, 1 mg dissolved organic carbon/l caused complex binding of more than 50% of the Cd, whereas more than 90% of Cd was bound at 10 and 100 mg dissolved organic carbon/l. At pH 3 the complex binding of Cd decreased somewhat, but over 90% of the Cd was bound at 100 mg dissolved organic carbon/l. Complex binding of Cd increased the lipid solubility of Cd, expressed as an octanol/ water partition coefficient, Nevertheless, more than 99% of the bound Cd was present as hydrophilic binding forms. Irrespective of the bound of Cd, the intestinal uptake and intracellular distribution (gel filtration on Sephadex G-75 column) were not affected by the humic substances 6 hr after dosage. Moreover, complex binding did not influence the intestinal absorption of Cd 24 hr after exposure. The median Cd retention in the kidneys of the 100 mg dissolved organic carbon/l group was 23% and 46% lower than that of the control group 6 and 24 hr after administration, respectively, indicating alterations in the distribution of Cd after absorption. Thus humic substances may affect the metabolism of toxic heavy metals, such as Cd, in vivo in mice, indicating that the presence of humic and fulvic acids in drinking water should be considered in future risk assessments of metals in drinking water.