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.     

心包穿刺置管引流治疗心包积液的护理

目的探讨心包经皮穿刺置管引流治疗心包积液的护理。方法对10例心包积液患者应用中心静脉导管进行心包穿刺并置管引流,加强术前护理,术中配合,置管后做好体位、留置导管、心理及生活方面的护理指导并密切观察病情。结果10例心包积液患者经皮穿刺置管术均穿刺成功,导管留置时间5～20d,中位时间12d。置管后2例出现穿刺处渗液,1例出现导管松脱,2例发生导管堵塞。结论心包经皮穿刺置管引流是治疗心包积液的安全、有效的方法,做好术前、术中、术后观察和护理,使患者积极配合,可减少并发症的发生,提高患者的生存质量。     

经皮心包穿刺置管持续引流治疗心包积液30例

目的 探讨经皮心包穿刺置管持续引流心包积液的疗效观察及安全性。方 法30例中等量到大量心包积液的病人在超声引导下穿刺置管行心包持续引流（采用中心静脉导管）。结果 30例病人均置管成功，留置时间平均10d（5d-26d），均无组织脏器损伤及感染。2例发生导管堵塞，经肝素生理盐水冲洗后再通，置管1～2周复查B超若心包积液消失则拔出导管。结论 经皮心包穿刺置管持续引流是一种创伤小、操作简便、安全、有效治疗心包积液的方法。     

Seldinger导管法心包穿刺引流心包积液38例

目的：评价Seldinger导管法心包穿刺置管引流治疗心包积液的临床疗效及安全性。方法：38例心包积液患在心尖部、左侧第5-6肋间隙心浊音界内1.5-2cm处穿刺心包，置入单腔中心静脉导管，观察患的心包积液引流及临床情况。结果：全部病例均完全置管引流，临床症状明显改善。所有患术中、术后未发生严重并发症，无1例并发感染。结论：Seldinger技术穿刺心包，置入单腔中静导管引流是安全、简便、实用的治疗方法。     

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。     

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     

Seldinger技术置管引流恶性心包积液35例分析

目的 评价中心静脉导管置管引流恶性心包积液的效果.方法 采用Seldinger技术将中心静脉导管置人心包腔引流恶性心包积液.结果 35例患者均一次穿刺成功,并发症少,置管引流心包积液后患者自觉症状很快缓解,引流效果好.结论 Seldinger技术置管引流心包腔积液是一项集诊断、急救、治疗为一体的综合性治疗方法,具有方便、快捷、安全、有效、痛苦小、并发症少,医疗费用较少的优点,特别适用于恶性心包积液引流.     

心包穿刺置管引流治疗心包积液的护理

目的探讨心包经皮穿刺置管引流治疗心包积液患者的护理。方法对4例心包积液患者应用中心静脉导管进行心包穿刺并置管引流,加强术前护理,术中配合,置管后做好体位、留置导管、心理及生活方面的护理指导并密切观察病情。结果 4例心包积液患者经皮穿刺置管术均穿刺成功,导管留置时间5～20 d,平均10d。置管后2例出现穿刺处渗液,1例出现导管松脱。结论心包经皮穿刺置管引流是治疗心包积液的安全有效的方法,做好术前、术中、术后观察护理,使患者积极配合,可减少并发症的发生,提高患者的生存质量。     

心电图监测下心包腔内贸置导管的临床应用

目的：本文对12例心包积液合并心包填塞者，施行床边非X线透视指导下经皮心包穿刺置管引流，以缓解心包填塞症状，方法：心电图监测指导操作过程。结果：12例留置导管均获成功。平均操作时间（9．6&;#177;3．5）min，导管留置心包腔内深度为（5．6&;#177;1.5)cm，导管保留时间为（8．7&;#177;2．4）d。对提高操作成功率，防止并发症及操作适应症，进行了讨论。     

经皮心包穿刺置入中心静脉导管引流心包积液的体会

目的探讨应用Seldinger导管法置入中心静脉导管引流心包积液的疗效及安全性。方法20例中-大量心包积液患者在超声心动图的定位下应用Seldinger穿刺法,分别从心尖部及刽突下经皮置入中心静脉导管间断或持续引流心包积液。结果20例心包积液均一次成功置入中心静脉导管,未出现与导管穿刺相关并发症,引流时间：3—17d,平均5d。引流量305—3000ml,平均908．3ml。结论Seldinger穿刺法置入中心静脉导管引流中-大量心包积液安全有效,由于该操作简单,取材方便,成功率高,明显减少不良反应,可替代传统穿刺方法,便于推广。     

心包积液100例临床分析

目的探讨心包积液病因之间所占比重变化。方法从症状、体征、实验室检查、心脏超声、心包穿刺抽液及手术病理活检等来确立其病因，其后分析各类病因所占比重。结果100例心包积液病因前四位是心衰、心包切开综合征、肿瘤与结核。结论心衰是引起心包积液最常见原因。     

Primary pericardial synovial sarcoma

A 57-year-old man was admitted to our hospital with cardiomegaly on a chest roentgenogram. A mediastinal tumor was observed during a chest computed tomographic scan and the patient was diagnosed with pericardial synovial sarcoma as a result of a tumor biopsy. Surgery, radiotherapy and chemotherapy were carried out, and although the tumor temporarily decreased in size, it subsequently increased and the patient died approximately 3 years following the initial medical examination. Most synovial sarcomas commonly occur in the vicinity of the joints of the extremities. Therefore, we herein report a rare case of synovial sarcoma which occurred in the pericardium.     

甲状腺功能减退症合并心包积液的临床分析

目的 对甲状腺功能减退症（甲减）合并心包积液进行临床分析加以探讨,以使治疗工作中减少误诊、漏诊、提高治愈率。方法 诊断明确基础上用甲状腺素片治疗,初始用小剂量,每日15～30mg,逐增每日40～120mg,维持量40～80mg。结果 4～8周治疗,甲状症状明显改善,ECG恢复正常,X线及心动超声亦恢复正常,T3、T4、TSH恢复正常或明显好转。结论 遇到原因不明心包积液而心包填塞症状不明显,同时伴有或不伴有心动过缓均应想到甲减的可能,甲减性心包液不应行常规心包穿刺抽液,应早期强心利尿,使用尿状腺素片治疗,心包积液即可消失。     

Unusual presentation of a pericardial cyst

Pericardial cysts are rare abnormalities and usually do not cause any symptoms. Rarely, pericardial cysts cause symptoms and may lead to complications. There have been multiple case reports of rare complications of pericardial cysts including right ventricular outflow obstruction, pulmonary stenosis, pericardial tamponade, and partial erosion into the superior vena cava. We report a case of delayed presentation of a pericardial cyst following trauma causing a syndrome resembling congestive heart failure. To our knowledge there has been only one report of this complication.     

The anteroposterior pericardial sac diameter measured by echocardiography correlates with the volume of pericardial effusion and with effort dyspnea.

AIMS: To examine the value of the anteroposterior pericardial sac diameter (APD) for prediction of the volume of pericardial effusion. METHODS AND RESULTS: We measured the APD by echocardiography before 52 pericardiocentesis procedures and correlated it with the aspirate volume, etiology, symptoms, and clinical outcome. The volume of the aspirate ranged from 60 to 2300 ml (median 650 ml). The APD (range 8.0 cm-15.9 cm, median 12 cm) correlated well with the cubic root of the volume of the effusion [volume=(0.8APD-0.6)3, r2=0.533, p<0.01]. An APD>or=12 cm had a positive predictive value of 88% and a negative predictive value of 83% for effusion volume above the sample median (>or=650 ml) and a positive predictive value of 100% for effusion in the middle or upper aspirate volume tertiles. Effort dyspnea was more common among patients with APD>or=12.0 cm (n=13) than in those with APD<12.0 cm (n=11) (p=0.007). One-year survival after pericardiocentesis was closely related to the severity of the underlying etiology and was not influenced by the volume of the effusion before aspiration. CONCLUSIONS: The APD is a simple, valuable method for non-invasive prediction of pericardial fluid volume. A greater APD is associated with, and may explain, effort dyspnea.     

Value of two-dimensional echocardiography in the diagnosis of pericardial cysts

Four adult patients with pericardial cysts were studied by two-dimensionalechocardiography. In all cases echocardiography demonstrateda round echo-free structure, of varying size, related to oneof the cardiac chambers, from which it was separated by a definitewall of echoes. M-mode echocardiography in the three cases inwhich it was performed, failed to yield the diagnosis. This report assesses the importance of two-dimensional echocardiographyand its greater reliability and sensitivity compared with: (1) M-mode echo in identifying pericardial tumors and establishingtheir relationships to nearby cardiac structures, and (2) standard chest X-ray in differentiating solid masses fromcysts and in defining the characteristics of cysts walls. Particular stress is laid on the role of two-dimensional echocardiography leading directly to surgery in patient number 4,who had a teratoma and in whom early surgery was essential. The high sensitivity and the ability of the technique to differentiatesolid from cystic masses and to define their relationships withcardiac chambers make it a reliable method for assessing pericardialcysts.     

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.     

Percutaneous balloon pericardiotomy for the treatment of recurrent malignant pericardial effusion

Malignant disease with pericardial metastasis is one of the most common causes of recurrent pericardial effusion (PE) with tamponade. While surgical pericardiotomy in these patients is very morbid and may not be a viable option, a palliative treatment percutaneously with percutaneous balloon pericardiotomy (PBP) can be a preferred treatment. We report herewith a case of PBP technique done using our day-to-day catheterisation laboratory equipment.     

Diagnostic features of localised pericardial constriction

We report a case of localised pericardial constriction leading to right ventricular outflow tract obstruction. Localised pericardial constriction is rare, but the diagnosis should be considered in patients who present with recurrent pericardial constriction following previous partial pericardiectomy. Close attention to physical findings may enable the diagnosis to be made prior to cardiac catheterisation.     

The composition of normal pericardial fluid and its implications for diagnosing pericardial effusions

BACKGROUND: Pericardial fluid obtained at pericardiocentesis is often subjected to biochemical and hematological analysis, and interpreted using criteria borrowed from pleural effusions. However, the validity and diagnostic yield of this approach is uncertain. Moreover, there is little data regarding the normal composition of the physiological pericardial fluid, which could serve as a reference for pathological effusions. METHODS: Pericardial fluid from 30 patients undergoing elective open heart surgery was collected. Patients were excluded if they had known pericardial disease, had systemic disorders known to be associated with pericardial disease, or if the fluid samples were hemolytic. The biochemical and hematological parameters of the fluid were determined using standard laboratory techniques, and compared with the results obtained for concurrently drawn venous blood. RESULTS: The median age of the study population was 64.5 +/- 10.6 years. Chemistry results of soluble molecules were consistent with the plasma ultrafiltrate nature of the fluid. However, fluid lactate dehydrogenase (LDH) level was unexpectedly high, averaging 2.4 times the serum level, and the mean protein level was 0.6 of the serum level. No correlation was found between comorbidities of patients and fluid characteristics. Fluids contained an average of 1430 leukocytes/muL, with a differential count that was predominated by lymphocytes (53.2 +/- 14%) and monocytes (11.6 +/- 6%). CONCLUSIONS: The composition of the physiologic pericardial fluid is remarkable for high LDH and protein content, and for predominance of lymphocytes. Thus, the biochemical criteria useful for diagnosing pleural effusions are probably not applicable for differentiating transudative from exudative pericardial effusions, and lymphocytosis should be interpreted cautiously.