乳糜性腹水
乳糜性腹水为乳状腹腔积液,富含甘油三酯。其是由胸部或肠道淋巴液进入腹腔所致[1]。
乳糜性腹水是一种少见的情况;据报道,其在一家大型教学医院中,20年间的发病率约为1/20,000例入院[2]。虽然近期没有大规模流行病学研究,但一般认为由于癌症患者生存时间延长以及侵袭性腹部及心胸介入操作的增多,其发病率已上升。
病理生理学 — 在创伤或梗阻(良性或恶性原因)引起淋巴系统破坏时,可出现乳糜性腹水。现已提出3种潜在机制[3]:
恶性肿瘤导致淋巴回流受阻,引起浆膜下淋巴管扩张,淋巴液渗漏至腹膜腔。肠道淋巴系统压力持续增加可导致胶原在淋巴管基底膜沉积,进一步影响肠黏膜的吸收能力。这可以最终导致发生蛋白丢失性肠病,出现慢性腹泻(脂肪泻)、吸收不良和营养不良。(参见“蛋白丢失性胃肠病”)
淋巴液通过扩张的无瓣膜腹膜后淋巴管的管壁渗出,这种淋巴管通过瘘管将淋巴液漏入腹膜腔(即先天性淋巴管扩张)。
创伤或手术引起的获得性胸导管阻断,使得乳糜液经淋巴管腹膜瘘直接漏入腹膜腔。(参见“乳糜胸的病因、临床表现和诊断”)
病因 — 乳糜性腹水有多种病因(表 1)。西方国家最常见的病因为腹部恶性肿瘤、淋巴管畸形和肝硬化,占所有病例的2/3以上。相比之下,发展中国家的大多数病例源自感染性病因,即结核和丝虫病。其他病因包括先天性、炎症性、术后性、创伤性及其他疾病。
一项系统评价纳入131项研究、共190例非创伤性乳糜性腹水患者,发现成人最常见的病因为:淋巴管畸形(32%)、恶性肿瘤(17%)、肝硬化(11%)、分枝杆菌(Mycobacterium)感染(15%)以及多种罕见原因(21%)[4]。淋巴管畸形和分枝杆菌感染的比例较高反映了所纳入的研究来自发展中国家和发达国家。儿童最常见的病因是淋巴管畸形(84%),其次为多种罕见病因(15%)。
各种情况导致乳糜性腹水形成的机制不同。例如:
心血管疾病(主要为缩窄性心包炎、右心衰竭和扩张型心肌病)可通过增高淋巴管压力而导致乳糜性腹水[5,6]。
腔静脉和肝静脉压升高(血管阻塞)导致肝脏淋巴液的生成大幅增加。
肝硬化引起肝脏淋巴液的生成增加。对门静脉高压患者行门静脉减压可减轻淋巴管高压[7-10]。
恶性肿瘤 — 恶性肿瘤是成人乳糜性腹水的常见原因。一项大型病例系列研究纳入了20年间识别出的患者,发现淋巴瘤至少占所有病例的1/3-1/2[2]。淋巴管阻塞及受侵犯会导致正常淋巴回流被中断[11]。其他肿瘤性原因包括乳腺癌、食管癌、胰腺癌、结肠癌、肾癌、睾丸癌、子宫内膜癌、宫颈癌、卵巢癌和前列腺癌,Kaposi肉瘤,类癌,以及淋巴管性肌瘤病[2,12-14]。存在乳糜性腹水和分泌性腹泻的患者需排除类癌。(参见“源自胃肠道和泌尿生殖道的高分化神经内分泌瘤(类癌)的临床特征”)
肝硬化 — 存在腹水的肝硬化患者中有0.5%-1%为乳糜性腹水[7,8,15,16]。其病理生理基础是淋巴回流过多(可高达20L/d)使浆膜层淋巴管扩张破裂。尚不清楚为何仅有一部分肝硬化患者发生乳糜性腹水。乳糜性腹水可为主诉症状(出现早);或在疾病较后期出现,由下列原因导致:肝细胞癌、分流术后或硬化治疗导致胸导管损伤[16-18]。肝硬化伴乳糜性腹水的患者通常没有必要采取积极措施来排除恶性肿瘤,除非高度怀疑。门静脉高压的其他原因(如门静脉血栓形成)也可造成乳糜性腹水[19,20]。
感染性 — 腹膜结核和丝虫病是乳糜性腹水常见的感染性病因。
腹膜结核在世界各地均有发病,尤见于社会经济水平低下、营养不良高发和医疗保健条件差的地区[21]。(参见“腹腔结核”)
淋巴丝虫病由寄生虫班氏丝虫(Wuchereria bancrofti)导致,可引起乳糜性腹水。这种寄生虫可引起淋巴管严重炎症反应,导致淋巴水肿和乳糜性腹水[22]。(参见“淋巴丝虫病的流行病学、发病机制及临床表现”)
报道显示,鸟-胞内分枝杆菌(Mycobacterium avium-intracellulare)感染是AIDS患者出现乳糜性腹水的一个原因[23-25]。
先天性 — 先天性淋巴管畸形在儿科患者中较为常见,故对于乳糜性腹水患儿应寻找该病因。
原发性淋巴管发育不全是一种以淋巴水肿、乳糜胸和/或乳糜性腹水为特征的疾病[26]。乳糜性腹水也可见于原发性淋巴管增生[27],包括两类:“双侧增生”,淋巴管有瓣膜且扩张不严重;淋巴管扩张症(巨淋巴管),淋巴管缺少瓣膜且极度扩张。(参见“外周淋巴水肿的临床特征及诊断”)
静脉畸形骨肥大综合征是一种常染色体显性遗传病,其静脉和淋巴管发育不全性畸形可导致受累肢体组织肥大,且常伴有乳糜性腹水[28]。
黄甲综合征见于儿童,病因不明。患者淋巴管发育不全,导致乳糜性积液。其特征性三联征包括淋巴水肿、胸腔积液和/或乳糜性腹水,以及指(趾)甲变黄且营养不良[29]。(参见“蛋白丢失性胃肠病”)
炎症性 — 多种炎症性疾病可导致乳糜性腹水,包括:
腹部放疗,可导致小肠和肠系膜的淋巴管发生纤维化和阻塞[30]。
急、慢性胰腺炎,可导致邻近的淋巴管受压,从而造成乳糜性腹水和胸腔积液[31]。
缩窄性心包炎(如上所述),可造成肝静脉压增高,使淋巴液生成增加,进而导致乳糜性腹水[6],这是一种可逆且可治疗的腹水病因。
其他罕见的炎症性疾病,如特发性腹膜后纤维化(或称Ormond病)、结节病、回缩性肠系膜炎和Whipple病[32-36]。
术后性和创伤性 — 乳糜性腹水可在腹部手术后早期(1周左右)因淋巴管破裂而发生,也可在晚期(数周至数月)因淋巴管粘连或外源性压迫而发生[37]。可引起乳糜性腹水的手术操作包括:腹主动脉瘤修复术、腹膜后淋巴结清扫、胰十二指肠切除术、下腔静脉切除术、腹膜透析导管置入术、腹腔镜Nissen胃底折叠术、远端脾肾分流术、腹腔镜供体肾切除术、小肠和肝脏移植术,以及腹腔镜Roux-en-Y胃旁路术[38-51]。
造成肠和/或肠系膜损伤的腹部钝挫伤也可引起乳糜性腹水[52]。在儿童中,应排除受虐儿童综合征,其约占儿童乳糜性腹水病例的10%[53]。
其他原因
右心衰竭和扩张型心肌病可使淋巴液引流受损,淋巴管压力升高,从而造成淋巴液淤滞、淋巴管扩张和乳糜性腹水[5]。乳糜性腹水也可来源于甲状腺毒性心肌病或心脏淀粉样变导致的心力衰竭[54,55]。尽早治疗心力衰竭和甲亢状态可消除腹水[54]。
据报道,肾病综合征和局灶节段性肾小球硬化可引起乳糜性腹水和乳糜胸[56-58]。其潜在发病机制不明。一项阐述性报道纳入了140例肾病综合征患者,其中90例腹水患者中有35例进行了腹腔穿刺[59],以腹水呈乳白色作为界定标准,发现有16例患者(52%)为乳糜性腹水。该研究的局限在于未测定甘油三酯浓度,因此一些患者可能仅仅是积液呈乳白色。
淋巴管平滑肌瘤病是一种罕见疾病,其病因不明,特点为肺、淋巴管以及纵隔、腹部和颈部下段淋巴结的平滑肌增生。该病几乎仅见于育龄期女性,可有多种临床表现,包括乳糜性胸腔积液和腹水。(参见“散发性淋巴管平滑肌瘤病的流行病学和发病机制”)
钙通道阻滞剂也可导致腹膜透析患者出现乳糜性腹水[60-63]。
临床表现 — 乳糜性腹水常常表现为进行性无痛性腹部膨隆,病程为数周至数月,取决于基础病因。一项系统评价纳入了131项研究、共190例非创伤性乳糜性腹水患者[4],发现最常见的主诉症状是腹部膨隆(81%)。接受过胸腹部手术的患者可能表现为急性发病。
患者可能诉体重增加和/或腹压增加导致的呼吸困难。其他特征包括非特异性腹痛、体重减轻、腹泻和脂肪泻、营养不良、水肿、恶心、淋巴结肿大、早饱、发热和盗汗[2,3,12]。然而,大部分病例在行诊断性腹腔穿刺之前并未怀疑该诊断。
评估 — 对每位腹水患者都应详细询问病史并进行细致的体格检查。应向患者询问体重的增减、恶性肿瘤相关症状、家族史、近期腹部手术、旅行情况、腹部创伤以及肝肾基础疾病。全身症状(如厌食、无力和不适)很常见,但不具特异性。(参见“成人腹水的评估”)
体格检查时可能存在的表现包括液波、移动性浊音、胸腔积液、下肢水肿、淋巴结肿大、恶病质、颞部消瘦、腹部肿块和疝。肝硬化患者可能存在慢性肝病的特征,如黄疸、肝掌、胸部蜘蛛痣以及脑病。
穿刺术及实验室数据 — 腹腔穿刺是评估和治疗腹水患者最重要的诊断性手段(表 2)。与肝硬化和门静脉高压所致的腹水呈黄色透明外观不同,乳糜液通常呈云雾混浊状。在一些肝硬化患者中,腹水的外观可能因感染或恶性肿瘤而呈乳白色,实际并不含高水平的甘油三酯[64]。(参见“成人腹水的评估”)
腹水中的甘油三酯水平对于界定乳糜性腹水十分关键。甘油三酯值通常高于200mg/dL,但一些作者以110mg/dL为临界值[1,2,65,66]。总蛋白含量因基础病因而异,在2.5-7.0g/dL之间(表 2)[65]。血清-腹水白蛋白梯度(serum to ascites albumin gradient, SAAG)应该用血清白蛋白值减去腹水白蛋白值来计算,以判断腹水与门静脉高压有关还是由其他原因造成[15,67]。
除甘油三酯水平外,还应取腹水送检细胞计数、培养、革兰染色、总蛋白浓度、白蛋白、葡萄糖、乳酸脱氢酶、淀粉酶和细胞学[67,68]。当怀疑为结核病时,应对这类病例行结核涂片、培养和腺苷脱氨酶(adenosine deaminase, ADA)检查。ADA是一种参与腺苷向肌苷转化过程的酶,在细胞免疫应答中由巨噬细胞和淋巴细胞释放。腹水中的ADA值可在结核性腹水的诊断中用作间接指标。美国之外的研究报道:在结核患病率高的地区,ADA诊断结核性腹膜炎的敏感性和特异性均较高。相比之下,ADA测定在肝硬化患病率较高人群(例如美国)中的效用有限[69]。结核性腹膜炎的诊断通常需要腹膜活检。(参见“腹腔结核”)
应行标准血液检测,包括全血细胞计数、电解质、肝功能、总蛋白、白蛋白、乳酸脱氢酶、甘油三酯、胆固醇、淀粉酶和脂肪酶[67,68]。其他检查应根据临床情况而定。
放射影像学检查 — 腹部CT有助于发现病理性腹腔内淋巴结和肿块。在术后性或创伤性乳糜性腹水的情况下,该检查还有助于确定积液的位置和范围,特别是怀疑胸导管损伤时。其他检查,如淋巴管造影(lymphangiography, LAG)和淋巴显像,可以帮助检测异常的腹膜后淋巴结、扩张淋巴管的渗漏、瘘管形成以及胸导管的通畅性[19,70]。LAG是确诊淋巴管阻塞的金标准,但可能带来一些并发症,如组织坏死、脂肪栓塞以及超敏反应(与所用造影剂的类型和剂量有关)[70]。在一项研究中,16例患者共有17处乳糜漏,这些患者均接受了LAG,所有病例的渗漏均被检出。在4例患者中,只有LAG诊断了乳糜漏并确定其位置,而在6例患者中,只有LAG后的CT扫描诊断了乳糜漏并确定其位置。在其余6例患者中,两种检查方法均确定了渗漏的位置。没有报道严重副作用[71]。除了对淋巴管进行显像和识别渗漏的部位,LAG可能还具有治疗作用。数项报告显示,采用微弹簧圈或胶可成功栓塞乳糜胸或乳糜性腹水患者的渗漏部位[72]。
治疗 — 只要条件允许,应解决基础病因。对于大多数病例,纠正基础病变可消除症状和腹水。对于存在感染性、炎症性或血流动力学病因的患者尤其如此。
只有少数研究阐述了旨在减少腹水形成的具体治疗[37,73,74]。根据有限的资料,对于病因不明或对基础疾病治疗无反应的患者,一种合理的初始治疗方法是推荐高蛋白、补充中链甘油三酯(medium-chain triglyceride, MCT)的低脂饮食。限制饮食中的长链甘油三酯(long-chain triglyceride, LCT)可避免其转化成甘油单酯和游离脂肪酸(free fatty acid, FFA),这两者会作为乳糜微粒转运到肠淋巴管。相比之下,MCT可以直接吸收进入肠细胞并以FFA和甘油的形式通过门静脉被直接转运到肝脏。因此,补充MCT的低脂饮食可减少乳糜的生成和乳糜流[75,76]。
市售的MCT为MCT油。MCT油作为营养补充剂的成人初始口服剂量通常为1汤匙,一日3-4次。常见的不良反应有恶心、偶见呕吐、腹痛和腹泻。MCT油应该与果汁混合,或用于沙拉和蔬菜,或混入酱汁用于鱼肉、鸡肉或瘦肉,或可用于烹饪或烘焙。MCT油不应该用于晚期肝硬化患者,因为可能出现嗜睡和昏迷。这类患者应采用低钠饮食以及利尿剂(如螺内酯)[68]。(参见“成人肝硬化腹水的初始治疗”)
病例报告或小型观察性研究还报道了一些其他措施。
奥利司他,一种胃脂肪酶和胰脂肪酶的可逆性抑制剂,据报道可以最大程度减少肝硬化所致乳糜性腹水患者的腹水量和腹水中的甘油三酯水平[77]。
生长抑素和奥曲肽已被成功用于治疗黄甲综合征患者和胸腹部手术所致淋巴管渗漏患者的乳糜性积液[20,78-82]。有病例报告提示:生长抑素及皮下给予奥曲肽治疗乳糜性腹水也均有效[20,80,81,83]。其作用机制可能涉及通过肠壁正常淋巴管中的特定受体来抑制淋巴液排泄[84,85]。
手术治疗可能对术后性、肿瘤性和先天性因素所致的乳糜性腹水患者有益[12]。然而,一项纳入36项研究的系统评价显示,保守治疗几乎对所有术后乳糜性腹水患者均有效[73]。术前LAG或淋巴显像有助于确定渗漏的解剖位置以及有无瘘管。
对于有大量腹水的患者,应行单次全量穿刺放液以缓解腹部不适及呼吸困难,并可按需重复穿刺。除非是肝硬化患者,否则无需用白蛋白来补充血管内容量以预防穿刺后发生循环功能障碍。对于内科治疗和手术治疗无效的终末期疾病患者,多次大量穿刺放液是一个合理的选择。
对于保留有肝功能的内科难治性肝硬化合并乳糜性腹水患者,经颈静脉肝内门体静脉分流术(transjugular intrahepatic portosystemic shunt, TIPS)是一项有效的措施,可通过降低门静脉压力而显著减少腹水[9,10]。一项纳入4例肝硬化患者的病例系列研究表明,TIPS治疗肝硬化相关的乳糜性积液安全有效[86]。由于实施TIPS之后可能出现一些重大问题,故对肝硬化患者行该手术之前必须仔细评估。
过去认为,对非手术治疗方式效果差的患者可选择腹腔静脉分流术。但是,分流术的并发症(包括脓毒症、弥散性血管内凝血、电解质紊乱、小肠梗阻和空气栓塞)发生率较高,故很少使用。另外,乳糜液黏度高,使得分流管道堵塞的发生率较高[87,88]。(参见“肝肾综合征”,关于‘腹腔静脉分流术’一节)
血性腹水
血性腹水定义为腹膜腔内腹水的红细胞计数大于50,000/mm3。腹水的红细胞计数通常低于1000/mm3。红细胞计数约为10,000/mm3时腹水将呈粉红色。
病因 — 血性腹水有多种原因。血性腹水在肝硬化患者中的发生率可高达19%[89]。这些患者的腹腔积血可自发发生或在创伤性穿刺术之后发生。血性腹水最常见于后者,这种情况下血液通常会凝固;而非创伤性血性腹水中的血液溶解,并不凝固[90]。存在非创伤性血性腹水的肝硬化患者的并发症发病率和死亡率增加,因为此类患者常常存在基础恶性肿瘤,如肝细胞癌[89,91,92]。恶性腹水患者的腹水标本约20%为血性[65],大部分(50%)这类病例为肝细胞癌[65]。腹膜转移癌患者的腹水标本只有约10%为血性。(参见“恶性肿瘤相关性腹水”)
分类 — 血性腹水可根据造成血液渗漏的基础病因进行分类。大多数病例的基础病理生理与侵入小血管的占位效应或施加于小血管和淋巴管的高剪切应力相关。相关病变部位可分类如下:
肝实质–肝细胞癌[91]、肝硬化伴静脉曲张破裂[90,92]、特发性非肝硬化性门静脉高压[90]、淋巴瘤[93]、肝血管瘤破裂[94]及转移性肝肿瘤[90]。
腹膜受累–平滑肌母细胞瘤[95]、结核,以及腹膜透析伴硬化性包裹性腹膜炎[96]。
邻近器官–卵巢癌[90]、子宫内膜异位症[97,98]、淋巴瘤[93]、前列腺癌[99]、胰腺炎[90]、脾淋巴瘤[100]、膀胱破裂[101]及卵巢囊肿破裂[102]。
全身性疾病–结节病[103]、系统性红斑狼疮、IgA血管炎(过敏性紫癜)[104]和寄生虫感染[肝片吸虫(Fasciola hepatica)][105]。
心血管疾病–心力衰竭[106]。
肝硬化患者遭受创伤–操作(如肝活检、TIPS、腹腔镜或腹腔穿刺术)后发生肝、脾创伤。
治疗 — 对于肉眼血性腹水患者,应尝试在另一不同部位进行穿刺以排除血管局部损伤。若证实为非创伤性血性腹水,则应行腹部超声检查或CT。
治疗应着眼于纠正基础病因。对穿刺损伤的患者,应予密切观察,需严密监测生命体征、全血细胞计数和凝血功能。
因肝硬化而出现自发性血性腹水的患者,若无肝细胞癌,通常无需特殊治疗[92]。由穿刺放液本身引起出血的患者通常也有肾衰竭(基于一项纳入近5000例穿刺的研究),接受去氨加压素治疗可能获益[107]。
对于因肝细胞癌而出现血性腹水的患者,栓塞出血的肿瘤血管可能获益。若患者继续表现出持续失血的征象(血红蛋白水平下降、心动过速、低血压),则应行血管造影并请外科会诊。
胰性腹水
胰性腹水定义为胰液在腹膜腔内大量聚积[108]。腹水中淀粉酶水平通常高于1000U/L,腹水淀粉酶/血清淀粉酶的比值约6.0[109]。在一项纳入8例患者的报道中,腹水淀粉酶浓度为280-5730U/L,为血浆淀粉酶浓度的3倍以上[110]。
胰性腹水最常见的基础病因为酗酒引起的慢性胰腺炎[111]。据报道,约4%的慢性胰腺炎患者和6%-14%的胰腺假性囊肿患者有胰性腹水[112,113]。其也可在急性胰腺炎发作后或胰腺创伤后发生[111]。据报道,胰性腹水也可在治疗性超声内镜下胰腺细针抽吸活检后发生[114,115]。但是,多达2/3的患者并无近期胰腺炎发作史[116]。
临床表现 — 患者可能有慢性胰腺炎病史,也可能近期在腹部创伤后不久发生急性胰腺炎,或为新发腹水。患者可能没有疼痛或胰腺疾病的症状,酗酒者尤其如此;因此,诊断可能会与肝硬化和门静脉高压症引起的腹水相混淆。
也可能存在胸腔积液。例如,在一项病例系列研究中,28例患者中有15例(54%)除了胰性腹水外还存在胸腔积液[108,111]。
评估 — 如上所述,每一位腹水患者都应行诊断性腹腔穿刺术。部分情况下,腹水可能呈血清血液性或乳白色。若疑为胰性腹水,应对腹水进行常规检查,例如细胞计数、培养、革兰染色以及淀粉酶、白蛋白和总蛋白测定。若同时出现SAAG低于1.1g/dL、总蛋白高于3g/dL以及腹水中淀粉酶升高,则可诊断胰性腹水。在某些情况下,由于合并腹水感染,白细胞计数可能升高。(参见“成人腹水的评估”)
一旦确立诊断,应行腹部CT扫描来评估假性囊肿。许多专家认为,应行内镜下逆行胰胆管造影术(endoscopic retrograde cholangiopancreatography, ERCP)以明确渗漏的部位,可能的话并行内镜下治疗(胰管支架术)[117-120]。虽然尚无资料关于磁共振胰胆管成像(magnetic resonance cholangiopancreatography, MRCP)在该病诊断中的作用,但该检查可准确地显示正常胰管并发现其任何异常[121]。因此,对于不适合行ERCP的患者应考虑MRCP。
治疗 — 在所有患者的治疗中,第一步均应是内科保守治疗。禁止经口进食并开始全胃肠外营养可将胰腺外分泌降至最低[122]。1/3的患者经保守治疗可改善,不需要进一步干预[123]。生长抑素或奥曲肽联合利尿剂以及多次穿刺放液可能对部分患者有益[124,125]。
ERCP显示胰管破坏的胰性腹水患者可尝试经十二指肠乳头置入胰管支架[110,117-119]。置入的支架可通过部分闭塞渗漏的胰管或绕过胰腺括约肌而降低胰管内压力,从而促进胰管破损的愈合。(参见“胰管支架置入术及其并发症概述”)
部分患者内科治疗失败,最终需要手术[126]。手术适应证包括:持续性或反复性腹水聚积和/或患者临床状况突然恶化。外科干预方式取决于胰管的解剖、胰管或假性囊肿渗漏的部位以及术中所见。当胰管扩张时,理想术式是在破裂胰管和Roux-en-Y空肠袢之间进行吻合,保证吻合口足够宽。有假性囊肿且内衬层成熟的患者可行囊肿内引流至空肠袢内。若胰管口径正常或为胰尾部异常,则远端胰腺切除后行胰管结扎是一种可接受的替代选择[127]。
对于ERCP示胰管破坏的胰性腹水患者,一种替代治疗选择是经十二指肠乳头置入胰管支架[110,117-119]。该支架可通过部分闭塞渗漏的胰管或绕过胰腺括约肌来降低胰管内压力,从而促进胰管破损的愈合。(参见“胰管支架置入术及其并发症概述”)
学会指南链接
部分国家及地区的学会指南和政府指南的链接参见其他专题。(参见“Society guideline links: Portal hypertension and ascites”)
患者教育
UpToDate提供两种类型的患者教育资料:“基础篇”和“高级篇”。基础篇通俗易懂,相当于5-6年级阅读水平(美国),可以解答关于某种疾病患者可能想了解的4-5个关键问题;基础篇更适合想了解疾病概况且喜欢阅读简短易读资料的患者。高级篇篇幅较长,内容更深入详尽;相当于10-12年级阅读水平(美国),适合想深入了解并且能接受一些医学术语的患者。
以下是与此专题相关的患者教育资料。我们建议您以打印或电子邮件的方式给予患者。(您也可以通过检索“患者教育”和关键词找到更多相关专题内容。)
基础篇(参见“患者教育:腹腔积液(腹水)(基础篇)”)
总结与推荐
乳糜性腹水
乳糜性腹水为乳状腹腔积液,富含甘油三酯。在创伤或梗阻(良性或恶性原因)引起淋巴系统破坏时,可出现乳糜性腹水。
乳糜性腹水有多种病因(表 1)。西方国家最常见的病因为腹部恶性肿瘤和肝硬化,占所有病例的2/3以上。
腹腔穿刺是评估和治疗腹水患者最重要的诊断手段(表 2)。也可能需要放射影像学评估。
只要可行,应解决基础病因。
只有少数研究阐述了旨在减少腹水形成的具体治疗。对于病因不明或对基础疾病治疗无效的患者,我们建议给予高蛋白、补充中链甘油三酯(MCT)的低脂膳食(Grade 2C)。但是,MCT油不应用于晚期肝硬化患者,因其可能诱发嗜睡和昏迷。对上述措施无反应的患者常常需要持续的治疗性腹腔穿刺放液。对于代偿性肝硬化患者,可考虑行经颈静脉肝内门体静脉分流术(TIPS)。
血性腹水
血性腹水定义为腹膜腔内腹水中红细胞计数高于50,000/mm3。其有多种病因。
对于肉眼血性腹水的患者,应尝试在另一不同部位进行腹腔穿刺以排除血管局部创伤。若证实为非创伤性血性腹水,则应行腹部超声检查或CT。治疗应针对纠正基础病因。
胰性腹水
胰性腹水定义为胰液在腹膜腔内大量积聚。最常见的基础病因是酗酒引起的慢性胰腺炎。
我们建议所有患者治疗的第一步是内科保守治疗(Grade 2C)。患者应禁食并接受胃肠外营养。多达1/3的患者仅采取这一措施即可得到缓解。
保守治疗无效的患者,我们建议以奥曲肽(50μg皮下注射,一日3次,连用2周)治疗,并行内镜下逆行胰胆管造影(ERCP)置入胰管支架(Grade 2C)。对于上述治疗失败的患者,我们建议进行手术评估。
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