水囊填塞术治疗宫缩乏力性产后出血30例疗效观察

子宫收缩（宫缩）乏力造成胎盘剥离面出血，是产后出血的主要原因。临床上控制产后出血的方法很多。2004～2005年，我们应用水囊填塞术治疗宫缩乏力性产后出血30例，效果满意。现报告如下。     

子宫收缩乏力性产后出血的病因及治疗进展

产后出血居我国孕产妇死亡原因的首位,其中宫缩乏力占70%～80%。一旦发现子宫收缩乏力导致产后出血,应尽早使用宫缩剂,采取宫腔填塞、子宫加压缝合,动脉结扎术以及选择性动脉栓塞等作为控制出血的手段,经以上治疗无效应及时行子宫切除术。     

云南白药纱袋配合水囊填塞宫腔治疗产后出血临床观察

产后出血是分挽期严重并发症,是产妇死亡的首要原因,及时采取恰当的止血措施是治疗产后出血的关键。我们采用云南白药纱袋配合水囊填塞宫腔处理产后出血30例,取得了良好的临床效果。现报告如下。     

卡孕栓联合自制纱条宫腔填塞在产后出血中的应用

目的 探讨卡孕栓联合宫腔填塞纱条控制产后出血（PPH）的临床效果.方法 将172例PPH患者随机分为对照组131例和治疗组41例.两组均予子宫按摩、催产素及米索前列醇等常规止血方法,在此基础上,治疗组予卡孕栓联合宫腔填塞止血.结果 治疗组产后2 h及24 h出血量均少于对照组（P＜0.05）;无继发自制纱条PPH或严重感染,均避免了子宫切除.结论 卡孕栓联合宫腔填塞纱条治疗简单、安全、快速、有效,是治疗PPH、保留子宫的有效方法之一,值得推广.     

护理干预在宫缩乏力性产后出血的临床应用研究

目的 探讨护理干预对宫缩乏力性产后出血的临床应用价值.方法 选取我院2009年8月-2011年9月收治的宫缩乏力性产后出血患者42例,分为治疗组(22例)和对照组(20例).治疗组患者采用无创性护理干预,对照组患者采用常规有创护理,比较两组患者的止血效果及护理满意度.结果 治疗组患者止血效果与对照组患者比较,差异无统计学意义(P＞0.05);治疗组患者护理满意度明显高于对照组,差异有统计学意义(P＜O.05).结论 对宫缩乏力性产后出血产妇进行无创护理,止血效果好.护理满意度高,值得在临床推广.     

严重产后出血32例手术治疗效果分析

目的探讨严重产后出血的手术治疗方法及治疗效果。方法随机选取2012年1月~2015年1月期间我院收治的分娩后严重出血产妇32例作为研究对象,分别给予盆腔血管结扎、子宫压迫法、盆腔动脉栓塞及子宫切除术,统计手术治疗的效果。结果 32例患者中,给予单用宫缩剂止血2例,宫腔填塞术治疗23例,6例子宫动脉栓塞术及1例子宫切除术,均成功止血。结论严重产后出血患者的治疗应根据其个体差异选择治疗方法,综合患者生育要求等因素,合理确定治疗方案。     

优质护理干预在宫缩乏力性产后出血患者中的应用价值研究

目的探讨优质护理干预在宫缩乏力性产后出血患者中的应用价值。方法选择2015年4月-2018年5月我院宫缩乏力性产后出血产妇60例,将60例患者进行随机分组(观察组30例、对照组30例),对照组按照常规护理流程进行干预,观察组在常规护理干预的同时,加入优质护理干预。收集研究对象产后2 h的出血量、住院时间、止血效果。结果(1)观察组止血效果明显优于对照组,差异有统计学意义(P<0.05)。(2)观察组与对照组产后2 h的出血量、住院时间差异有统计学意义(P<0.05),观察组产后2 h的出血量、住院时间明显更少(P<0.05)。结论优质护理干预在宫缩乏力性产后出血患者中的应用价值高,效果满意,可减少产妇产后出血量,缩短治疗时间,优势明显,值得推广。     

预防宫缩乏力致产后出血的临床护理分析

目的 探讨预防宫缩乏力导致产后出血的临床护理措施.方法 回顾性分析并总结我院2009年3月-2011年9月收治的73例因宫缩乏力导致产后出血患者临床护理方法,主要是及时对出现宫缩乏力的产妇进行子宫按摩并应用促进宫缩药物,加强产后出血护理.结果 73例产妇产后出血经快速有效止血和加强产后出血护理后,抢救成功.73例产妇中无一例进行子宫切除止血,无一例因产后大出血死亡.结论 进行有效的护理措施,能有效降低出血后子宫切除率,提高产妇的生存质量.     

宫缩乏力性产后出血的护理干预对促进产妇产后康复的作用

目的:探究对宫缩乏力性产后出血患者予以护理干预,其产后康复效果发生的变化.方法:80例宫缩乏力性产后出血患者(2020.1～2021.1),随机分成2组,40例/组.开展一般护理的作为参照组,开展针对性护理的作为研究组.比对各症状改善时间以及护理满意情况.结果:研究组各症状改善时间比参照组短,有差异性(p<0.05);...     

子宫背带式缝合术在剖宫产产后出血中的应用价值

目的探讨背带式缝合术在治疗剖宫产产后出血中的应用价值。方法对15例剖宫产产后因宫缩乏力出血的患者采用背带式缝合术治疗,观察其止血效果。结果 15例产后出血患者经背带式缝合13例有效,出血减少,无继发产后出血,成功地保留了子宫,术后无任何并发症发生,2例无效,有效率为86.76%。结论子宫背带式缝合术具有操作简单,止血迅速可靠,且能保留子宫等优点,是治疗剖宫产产后出血行之有效的止血方法,值得临床推广应用。     

超选择经导管子宫动脉分支栓塞治疗子宫肌瘤

目的 探讨超选择经导管子宫动脉分支栓塞治疗子宫肌瘤的临床价值。方法 将65例子宫肌瘤患者分为观察组及对照组。对照组52例插管至子宫动脉主干栓塞,观察组13例使用微导管栓塞子宫动脉肌瘤供血分支。结果 两组临床症状改善情况、性激素水平及子宫、肌瘤的平均体积、缩小率均无显著差异（P均〈0．05）;观察组不良反应发生率为0、平均住院时间6d,对照组为13．5％、11d,P均〈0．05。结论 超选择经导管子宫动脉分支栓塞治疗子宫肌瘤效果确切,术后并发症发生率较低。     

Implementation of uterine artery embolisation for symptomatic uterine fibroids: an inventory

The validity of uterine artery embolisation (UAE ) as an alternative treatment for hysterectomy to treat symptomatic uterine fibroids has been well established. Despite its favourable outcomes, UAE is still only marginally applied in the Netherlands. The aim of this inventory is to identify factors which either restrict or facilitate the implementation of UAE. Gynaecologists and interventional-radiologists in three hospitals in Amsterdam were interviewed by means of questionnaires. One of these hospitals had ample experience in UAE for uterine fibroids, one hospital had just started providing this treatment, and one hospital did not perform UAE. Also patients with symptomatic fibroids who were scheduled for either UAE or hysterectomy were interviewed about the counselling for UAE. The following obstacles in the implementation of UAE were found: lack of knowledge about UAE , absence of a multidisciplinary protocol, and above all, the absence of UAE as one of the treatment options in the Dutch national guideline on the management of menorrhagia. 75% of all patients claimed to be well informed about UAE by their gynaecologist. Our recommendations for the implementation of UAE are: 1) adding UAE to the Dutch guideline for the management of menorrhagia with clearly defined indications and contraindications; 2) educating gynaecologists about UAE; 3) composing a patient information leaflet and a website, and 4) arranging a protocol in a multidisciplinary team.     

Characterization of purified rabbit uterine renin: influence of pregnancy on uterine inactive renin

Using specific antibody raised against renal renin, we have documented that the majority of the uterine renin-like activity in gravid and nongravid uteri is immunoreactive renin. To characterize its physiochemical properties, we obtained highly purified uterine renin by two affinity chromatographic steps, pepstatin and antirenin. Uterine renin has a pH optimum of 6, an apparent mol wt of 38K, and a Km of 1.7 microM for homologous substrate. These properties are identical to those of renal renin and are not influenced by the pregnant state. In the basal state, an inactive form of the uterine enzyme constitute 55 +/- 10% of the total uterine renin. During pregnancy, active renin increased 40-fold as inactive renin fell to 4 +/- 3% of the total renin concentration. The renal renin concentration fell as plasma renin increased during pregnancy. These data suggest that the increased uterine renin concentrations during pregnancy are probably due to increased local production and conversion of renin precursor to the active enzyme. This stimulation of the uterine renin level appears to be independent of renal renin.     

Stimulation of glucose transport in cultured uterine cells by rat and rabbit uterine extracts

Estradiol-17 beta was previously shown to stimulate glucose transport (as measured by phosphorylation of 2-deoxyglucose) in rat uterine tissue in vivo (Meier, D.A. and Garner, C.W. (1987) Endocrinology 121, 1366-1374) but attempts to demonstrate this in uterine organ strips in vitro, in uterine tumor cell lines or in uterine cells in primary culture have been unsuccessful. However, aqueous uterine extracts and uterine luminal fluid did stimulate glucose transport in uterine tumor cells and uterine cells in primary culture. Estradiol in vivo and uterine extracts in vitro each increased the initial rate of glucose transport 1.5- to 3-fold. In each case, 2-3 h were required for the stimulation to be fully expressed. The stimulation was not inhibited by cycloheximide suggesting that protein synthesis was not required. Uteri from ovariectomized rats injected daily for 4 days with 10 micrograms estradiol contained 4-fold more activity than uteri from saline-injected control animals. The activity was acid- and heat-stable, inactivated by trypsin treatment but not removed by dextran-coated charcoal treatment, suggesting that the activity is (or is associated with) a protein. The activity eluted in the 6-12 kDa range upon chromatography on Sephadex G-50. Insulin (1-1000 ng/ml) and epidermal growth factor (1-100 ng/ml) stimulated glucose transport, but only less than 50% of the stimulation by extracts. The substance(s) present in the extracts, possibly a known growth factor, may be involved in the estradiol stimulation of glucose transport and other estradiol actions in vivo.     

Augmentation of the response of mouse uterine epithelial cells to estradiol by uterine stroma

The effect of estrogen on the in vitro growth of mouse uterine epithelial cells was assessed. Epithelial cells from the immature mouse uterus were successfully cultivated in a 1:1 mixture of Dulbecco's Modified Eagle's Medium and Ham's F-12 supplemented with insulin (5 micrograms/ml), transferrin (10 micrograms/ml), hydrocortisone (10(-7) M), BSA (2 mg/ml), and fetuin (1 mg/ml). Addition of 17 beta-estradiol in the range of 1-100 nM did not significantly change the total DNA content of the epithelial cells. A binding component of [3H]estradiol by cultured uterine cells was shown to be specific, saturable, and of high affinity. Kd values for specific binding by epithelial and stromal cells were 1.0-1.7 x 10(-10) M. Maximal specific binding was 0.74 and 2.3 fmol/micrograms DNA for epithelial and stromal cells, respectively. Treatment of epithelial and stromal cells for 4 days with 10 nM estradiol led to a 2- to 6-fold increase in progesterone receptor concentration. Treatment of epithelial and stromal cells in mixed culture for 4 days with 10 nM estradiol resulted in a significant increase in total DNA. That epithelial-stromal contact was critical for estradiol stimulation was shown by the fact that if the cell types were separated into two compartments which still allowed free media mixing, total DNA was not enhanced by estradiol. These observations are organized into a model for mitogenic action of estradiol that seems to reconcile observed disparities in the action of the hormone in vivo and in vitro.