中心静脉导管留置治疗结核性心包积液的临床评价

目的探讨中心静脉导管留置引流在治疗结核性心包炎伴有大量心包积液的应用价值。方法将76例结核性渗出性心包炎患者随机分为A组和B组,均予以全身规则抗结核治疗。A组留置中心静脉导管引流及心包腔内注药,B组常规心包穿刺抽液及心包腔内注药。结果A组与B组相比,两组间在消除心包填塞症状时间,退热时间,心包积液消失时间等方面有显著性差异(P＜ 0．01)。结论心包穿刺留置导管引流心包积液安全可行,操作简便,可迅速消除心包填塞症状,能及时彻底引流心包积液,疗效明显,降低了缩窄性心包炎的发生率。     

2例结核性心包炎行中心静脉导管引流护理

结核性心包炎是重症结核病,常产生大量的渗出液,短期内心包的大量积液可造成急性心包填塞而严重危及患者生命。其治疗除全身应用抗结核药物外应及时消除心包填塞症状和尽量减少缩窄性心包炎的发生。采用心包腔穿刺留置中心静脉导管引流治疗结核性心包炎效果满意。现将护理体会介绍如下。     

留置中心静脉导管治疗结核性心包积液30例的临床分析

我国结核性心包炎在心包疾病中占有重要的位置,占心包疾病的21.3%～35.8%,高于国外.结核性心包积液患者若积液量较多或增长较快引起心包填塞症状时,需行心包穿刺抽液治疗,常规心包穿刺抽液容易损伤血管、心脏,风险较大.我院2000年以来收治的30例中等量以上结核性心包积液患者行中心静脉导管（Central Venous Catheter，CVC）留置引流心包积液，效果满意，现报告如下。[第一段]     

B超引导下中心静脉导管留置引流心包积液的临床探讨

目的 探讨床旁B超引导下中心静脉导管留置引流术在心包积液诊治中的临床应用.方法 采用Seldinger法,在床旁B超定位下,于心尖部或剑下穿刺留置中心静脉导管引流心包积液.结果 穿刺及急救心包填塞成功率高.导管留置 3 d～23 d不等,无严重并发症.结论 B超引导下,中心静脉导管留置引流心包积液,具有安全、方便,有效等优点.     

心包穿刺留置中心静脉导管引流心包积液

目的　探讨采用心包穿刺留置中心静脉导管引流心包积液的方法、引流液量控制和引流的体位。方法　患者半坐位或平卧位 ,根据超声心动图定位的穿刺点、穿刺深度及方向 ,1 6例采用剑突下进针 ,36例采取左侧胸壁进针 ,将中心静脉导管置入心包腔内 ,连接无菌引流袋引流心包积液。结果　 52例心包积液患者心包穿刺均获得成功 ,无明显并发症 ,52例患者引流管平均留置时间 1 4 .68± 4.66(8～ 48) d,平均引流量为 790±2 78(32 0～ 2 90 0 ) ml,心包穿刺引流后 ,心包填塞症状缓解或消失 ,心率显著减慢、收缩压和平均压明显升高 (P<0 .0 5)。结论　采用超声心动图定位 ,床边行心包穿刺 ,置入中心静脉导管引流中等量和大量心包积液安全可靠 ,引流彻底 ,疗效可靠 ,无明显并发症。     

Seldinger导管法心包穿刺置管引流治疗心包积液25例

心包穿刺是治疗心包积液的重要方法之一 ,传统的心包穿刺有一定的危险性 ,1 997年 2月～2 0 0 0年 7月来 ,我们采用 Seldinger导管法 [1]进行心包穿刺抽液 ,为 2 5例心包积液患者安全地施行了心包穿刺留置单腔中心静脉导管引流治疗 ,取得了较好的效果 ,现报道如下 :1　资料与方法1 .1　临床资料 :1 .1 .1　本组全部为住院患者 ,并经 X线检查心影扩大 ,术前均以二维超声确认有心包积液 ,2 5例中男 1 8例 ,女 7例 ,年龄 1 7～ 73岁。心包积液量中等以上并伴有心包填塞症状 1 5例。1 .1 .2　病因 :癌性心包炎 8例 (均示大量心包积液 ) ,结核性…     

超声下心包腔内置管间断抽吸治疗心包积液11例临床分析

大量心包积液的治疗常需反复心包穿刺放液 ,操作烦琐 ,并发症多。我院自 1999年起采用超声导引下 ,经皮肤心包腔内置入中心静脉导管 ,间断抽吸积液 ,并根据病情需要经导管注入治疗药物至心包腔 ,取得满意的临床疗效 ,现总结报道如下。11例均为住院患者 ,男 6例、女 5例 ,年龄 14～ 6 6岁 ,均有不同程度的心包填塞症状 ,全部病例经Ｘ线胸片和Ｂ型超声证实为中至大量心包积液。其中结核性心包炎 6例、系统性红斑狼疮 1例、恶性肿瘤心包转移 4例。所用穿刺器械为广东省佛山特种医用导管有限责任公司生产的中心静脉穿刺套管针盒 :由中心静脉导管…     

中心静脉导管置管引流治疗心包积液38例

目的观察应用中心静脉导管置管引流治疗心包积液的安全性、可行性.方法 38例心包积液病人均应用Seldinger法从剑突下穿刺,将单腔中心静脉导管置入心包腔引流.结果 38例均穿刺成功,引流管留置时间3 d～21 d,平均5.7 d,引流积液量300 mL～3 200 mL,平均634 mL,无明显并发症.结论中心静脉导管经皮穿刺置管引流可用于治疗心包积液.     

心包腔深静脉留置管引流治疗心包积液

目的观察经皮心包穿刺置管引流及腔内注入药物治疗心包积液的疗效及安全性。方法 26例有大量心包积液伴心脏压塞症状者在B超引导下行心包穿刺并留置深静脉引流管引流、腔内注药。结果穿刺成功率100%。置管引流后心脏压塞症状迅速缓解,总有效率92.3%。结论心包积液量较大有心脏压塞症状时心包腔内置深静脉引流管引流、注药治疗,安全有效,可迅速缓解心脏压塞症状,适合基层医院临床应用。     

超声下Seldinger技术心包穿刺置管引流治疗急性心包填塞的临床观察

目的　评价超声下 Seldinger技术心包穿刺置管引流治疗急性心包填塞的疗效及安全性。方法　 16例中到大量心包积液发生急性心包填塞患者 ,在超声心动图引导下 ,采用 Seldinger技术 ,经皮穿刺心包腔内置中心静脉导管进行间断抽液。结果　 16例患者均一次穿刺成功 ,穿刺成功时间 2～ 5 min。无 1例出现心肌或其它脏器损伤 ,4例出现抽吸时导管堵塞 ,用生理盐水冲洗后通畅 ,1例出现局限性皮下渗液 ,1例穿刺处皮肤轻度红肿 ,经处理后消失。留置导管时间一般 2～ 14 d,最长 2月余。结论　超声下Seldinger技术心包穿刺置入中心静脉导管引流治疗急性心包填塞 ,方法简单 ,能安全有效缓解心包填塞症状 ,成功率高 ,可替代传统穿刺方法     

Cardiac tamponade due to low-volume effusive constrictive pericarditis in a patient with uncontrolled type II autoimmune polyglandular syndrome

Abstract

Type II autoimmune polyglandular syndrome (APS), a relatively common endocrine disorder, includes primary adrenal insufficiency coupled with type 1 diabetes mellitus and/or autoimmune primary hypothyroidism. Autoimmune serositis, an associated disease, may present as symptomatic pericardial effusion. We present a case of a 54-year old male with APS who developed pericarditis leading to cardiac tamponade with a subacute loculated effusion. After urgent pericardiocentesis intrapericardial pressure dropped to 0, while central venous pressures remain elevated, consistent with acute effusive constrictive pericarditis. Contrast computerized tomography confirmed increased pericardial contrast enhancement. The patient recovered after prolonged inotropic support and glucocorticoid administration. He re-accumulated the effusion 16 days later, requiring repeat pericardiocentesis. Effusive–constrictive pericarditis, an uncommon pericardial syndrome, is characterized by simultaneous pericardial inflammation and tamponade. Prior cases of APS associated with cardiac tamponade despite low volumes of effusion have been reported, albeit without good demonstration of hemodynamic findings. We report a case of APS with recurrent pericardial effusion due to pericarditis and marked hypotension with comprehensive clinical and hemodynamic assessment. These patients may require aggressive support with pericardiocentesis, inotropes, and hormone replacement therapy. They should be followed closely for recurrent tamponade.     

Neue Möglichkeiten der Diagnostik und Therapie der Perikarditis

Pericarditis is an inflammatory disorder of the pericardium with or without an associated pericardial effusion. The diagnosis is based on the clinical manifestations and typical ECG changes. Echocardiography is essential to reveal the size of the pericardial effusion and to determine its hemodynamic significance. The precise etiology of pericarditis may be established by pericardiocentesis, pericardioscopy and targeted biopsy and consecutive pericardial fluid and biopsy analysis by molecular biology, cytology, microbiology and immunological techniques. Non steroidal anti-inflammatory drugs and/or colchicine are the mainstay of anti-inflammatory treatment of pericarditis. Systemic corticoid treatment should be restricted to patients with associated autoimmune disorder, relapsing pericarditis and as a complementary therapy in tuberculous pericarditis. In autoreactive pericarditis intrapericardial instillation of triamcinolone is effective with few side effects. In malignant pericarditis the intrapericardial administration of cisplatin prevents early recurrences.     

Pericardial involvement in end-stage renal disease

Pericardial involvement in end-stage renal disease (ESRD) is manifested most commonly as acute uremic or dialysis pericarditis and infrequently as chronic constrictive pericarditis. The causes of uremic and dialysis pericarditis remain uncertain. The clinical and laboratory manifestations of acute pericarditis, pericardial effusion, cardiac tamponade, and constrictive pericarditis in patients with chronic renal failure are similar to those observed in nonuremic patients with similar pericardial involvement, except that chest pain occurs less frequently in those with ESRD. Therapeutic interventions for acute uremic or dialysis pericarditis with or without pericardial effusion include intensive hemodialysis, pericardiocentesis (infrequently used), pericardiostomy with or without instillation of intrapericardial glucocorticoids, pericardial window, and pericardiectomy. Chronic constrictive pericarditis is treated with pericardiectomy.     

Acute suppurative amebic pericarditis

A 33 year old mulatto man presented with acute pericarditis and severe cardiac tamponade. Trophozoites of Entamoeba histolytica were found in the “anchovy sauce” pus obtained by pericardiocentesis. A large abscess in the left lobe of the liver with extension into the pericardial cavity was revealed by X-ray study after the injection of 75 percent Hypaque into the pericardial cavity. Clinical improvement occurred after treatment with chloroquine, metronidazole and emetine hydrochloride. Forty-five days after discharge the patient was readmitted with signs of constrictive pericarditis, and this lesion was confirmed by cardiac catheterization studies.     

Effusive-constrictive pericarditis

Effusive-constrictive pericarditis (ECP) is an increasingly recognized clinical syndrome. It has been best characterized in patients with tamponade who continue to have elevated intracardiac pressure after the removal of pericardial fluid. The disorder is due to pericardial inflammation causing constriction in conjunction with the presence of pericardial fluid under pressure. The etiology is diverse with similar causes to constrictive pericarditis and the condition is more prevalent with certain etiologies such as tuberculous pericarditis. The diagnosis is most accurately made using simultaneous intrapericardial and right atrial pressure measurements with pericardiocentesis, although non-invasive Doppler hemodynamic assessment can assess residual hemodynamic findings of constriction following pericardiocentesis. The clinical presentation has considerable overlap with other pericardial syndromes and as yet there are no biomarkers or non-invasive findings that can accurately predict the condition. Identifying patients with ECP therefore requires a certain index of clinical suspicion at the outset, and in practice, a proportion of patients may be identified once there is objective evidence for persistent atrial pressure elevation after pericardiocentesis. Although a significant number of patients will require pericardiectomy, a proportion of patients have a predominantly inflammatory and reversible pericardial reaction and may improve with the treatment of the underlying cause and the use of anti-inflammatory medications. Patients should therefore be observed for the improvement on these treatments for a period, whenever possible, before advocating pericardiectomy. Imaging modalities identifying ongoing pericardial inflammation such as contrast-enhanced magnetic resonance imaging or nuclear imaging may identify those subsets more likely to respond to medical therapies. Pericardiectomy, if necessary, requires removal of the visceral pericardium.     

Cardiac constriction syndromes

This article focuses on syndromes associated with cardiac constriction (i.e., constrictive pericarditis). These include classic chronic constrictive pericarditis, subacute constriction including effusive-constrictive pericarditis, transient cardiac constriction, and occult constrictive pericarditis, all of which have their own clinical and developmental peculiarities. Establishing clinical suspicion is the basic first step in making a diagnosis, which can subsequently be confirmed by careful interpretation of imaging studies. With pericardial calcification, a simple chest radiograph may be sufficient; in other cases, Doppler echocardiography or chest computed tomography are necessary. The diagnosis of effusive-constrictive pericarditis requires cardiac catheterization combined with pericardiocentesis and the recording of intracavitary and intrapericardial pressures both before and after pericardiocentesis. It should be remembered that spontaneous regression is possible in some forms of constrictive pericarditis, particularly those that appear during the resolution of acute idiopathic pericarditis with effusion or that develop after cardiac surgery. Finally, there are only a few reports in the literature about occult constrictive pericarditis and its diagnosis is problematic.     

中心静脉导管留置在结核性胸膜炎中的应用评价

目的探讨中心静脉导管留置引流在治疗结核性胸膜炎的应用价值。方法将72例结核性胸膜炎患者随机分为A组和B组，均予以全身规则抗结核治疗。A组留置中心静脉导管引流，B组常规胸腔穿刺抽液。结果两组间在抽放胸液量、胸液消失时间等方面有显著差异性（P〈0．01）。结论胸腔穿刺留置导管引流胸腔积液安全可行，操作简便，降低胸膜肥厚的发生。     

A modern approach to tuberculous pericarditis

The human immunodeficiency virus (HIV) epidemic has been associated with an increase in all forms of extrapulmonary tuberculosis including tuberculous pericarditis. Tuberculosis is responsible for approximately 70% of cases of large pericardial effusion and most cases of constrictive pericarditis in developing countries, where most of the world's population live. However, in industrialized countries, tuberculosis accounts for only 4% of cases of pericardial effusion and an even smaller proportion of instances of constrictive pericarditis. Tuberculous pericarditis is a dangerous disease with a mortality of 17% to 40%; constriction occurs in a similar proportion of cases after tuberculous pericardial effusion. Early diagnosis and institution of appropriate therapy are critical to prevent mortality. A definite or proven diagnosis is based on demonstration of tubercle bacilli in pericardial fluid or on histologic section of the pericardium. A probable or presumed diagnosis is based on proof of tuberculosis elsewhere in a patient with otherwise unexplained pericarditis, a lymphocytic pericardial exudate with elevated biomarkers of tuberculous infection, and/or appropriate response to a trial of antituberculosis chemotherapy. Treatment consists of 4-drug therapy (isoniazid, rifampicin, pyrazinamide, and ethambutol) for 2 months followed by 2 drugs (isoniazid and rifampicin) for 4 months regardless of HIV status. It is uncertain whether adjunctive corticosteroids are effective in reducing mortality or pericardial constriction, and their safety in HIV-infected patients has not been established conclusively. Surgical resection of the pericardium is indicated for those with calcific constrictive pericarditis or with persistent signs of constriction after a 6 to 8 week trial of antituberculosis treatment in patients with noncalcific constrictive pericarditis.     

Diagnosis and management of pericardial effusion

Pericardial effusion is a common finding in everyday clinical practice.The first challenge to the clinician is to try to establish an etiologic diagnosis.Sometimes,the pericardial effusion can be easily related to a known underlying disease,such as acute myocardial infarction, cardiac surgery,end-stage renal disease or widespread metastatic neoplasm.When no obvious cause is apparent,some clinical findings can be useful to establish a diagnosis of probability.The presence of acute inflammatory signs(chest pain,fever,pericardial friction rub) is predictive for acute idiopathic pericarditis irrespective of the size of the effusion or the presence or absence of tamponade.Severe effusion with absence of inflammatory signs and absence of tamponade is predictive for chronic idiopathic pericardial effusion,and tamponade without inflammatory signs for neoplastic pericardial effusion.Epidemiologic considerations are very important,as in developed countries acute idiopathic pericarditis and idiopathic pericardial effusion are the most common etiologies,but in some underdeveloped geographic areas tuberculous pericarditis is the leading cause of pericardial effusion.The second point is the evaluation of the hemodynamic compromise caused by pericardial fluid.Cardiac tamponade is not an"all or none"phenomenon,but a syndrome with a continuum of severity ranging from an asymptomatic elevationof intrapericardial pressure detectable only through hemodynamic methods to a clinical tamponade recognized by the presence of dyspnea,tachycardia,jugular venous distension,pulsus paradoxus and in the more severe cases arterial hypotension and shock.In the middle,echocardiographic tamponade is recognized by the presence of cardiac chamber collapses and characteristic alterations in respiratory variations of mitral and tricuspid flow.Medical treatment of pericardial effusion is mainly dictated by the presence of inflammatory signs and by the underlying disease if present.Pericardial drainage is mandatory when clinical tamponade is present.In the absence of clinical tamponade,examination of the pericardial fluid is indicated when there is a clinical suspicion of purulent pericarditis and in patients with underlying neoplasia.Patients with chronic massive idiopathic pericardial effusion should also be submitted to pericardial drainage because of the risk of developing unexpected tamponade.The selection of the pericardial drainage procedure depends on the etiology of the effusion.Simple pericardiocentesis is usually sufficient in patients with acute idiopathic or viral pericarditis.Purulent pericarditis should be drained surgically,usually through subxiphoid pericardiotomy. Neoplastic pericardial effusion constitutes a more difficult challenge because reaccumulation of pericardial fluid is a concern.The therapeutic possibilities include extended indwelling pericardial catheter,percutaneous pericardiostomy and intrapericardial instillation of antineoplastic and sclerosing agents.Massive chronic idiopathic pericardial effusions do not respond to medical treatment and tend to recur after pericardiocentesis, so wide anterior pericardiectomy is finally necessary in many cases.