脾外伤致门静脉海绵样变性1例

1临床资料患者,男,52岁,汉族,吉林省扶余县人,因间断性左上腹部隐痛1年,加重伴乏力3个月来我院就诊。该患者1年前因左上腹部撞击伤后开始出现上腹部疼痛,疼痛性质为隐痛,无恶心、呕吐,无腹胀,无反酸、胃内烧灼感,无厌油腻,无呕血、黑便,自行服用"消炎药"后症状略缓解,因不影响日常生活,未系统     

亲体肝移植治疗小儿门静脉海绵样变1例

门静脉海绵样变（PVCT）是由于门静脉主干及其肝内分支完全或部分阻塞后引起门静脉高压症,肝门区及其周围侧支循环形成并扩张迂曲呈静脉血管瘤样改变是其特征性的病理改变。它属于肝前性门静脉高压症的一种,临床少见。目前治疗该病的方法较多,但疗效均欠理想。我们对1例小儿PVCT用亲体肝移植加脾切除和门奇断流术治疗，效果良好。[第一段]     

门静脉海绵样变22例临床分析

目的 探讨门静脉海绵样变的临床特点、诊断方法及治疗.方法 对22例门静脉海绵样变患者的临床资料进行回顾性分析.结果 22例患者多以反复呕血便血、脾肿大、脾功能亢进为主要症状;肝功能检查多正常或仅表现为白蛋白的轻度降低.21例经超声检查确诊,1例经门静脉造影确诊.4例患者进行手术治疗,大多行脾切除,分流术加断流术.结论 门静脉海绵样变的临床表现以继发性门静脉高压为主,超声检查多能确诊.内科保守治疗效果不佳,手术以分流加断流术为主.     

门静脉海绵样变伴肺栓塞一例

正病例资料患者男,29岁,因左侧胸痛,咯血5 d于2014年9月13日转入我院呼吸科ICU。患者9月8日无明显诱因出现左侧胸痛,咳嗽,痰中带血,无发热,无畏寒,气促不明显,就诊于当地医院,胸片检查未见明显异常,肺部CT平扫检查显示左舌叶支扩支扩并感染,予抗感染,止咳化痰等对症处理     

先天性门静脉海绵样变致上消化道出血1例报道

本文报道1例先天性门静脉海绵样变致上消化道出血患者的临床诊疗过程,以提高我们对致上消化道出血罕见病因的认识,避免误诊。     

成人门静脉海绵样变性1例

门静脉海绵样变性（cavemous transformation of poemvein，cTPv）为肝前性门静脉高压症，主要表现为脾功能亢进症、食管、胃底静脉曲张及反复上消化道出血，临床上极为少见，易误诊为肝硬化。我院收治1例CTPV患者，现将临床资料分析报告如下。     

骨髓增生性疾病所致门静脉海绵样变性1例报告

<正>1 病例资料患者男性,64岁,因“乏力1周,黑便3天”于2021年11月22日收入本院。患者于1周前无明显诱因下出现乏力,未重视未就诊,3天前进食辛辣食物后出现中上腹不适,后解黑色糊状便,每天2次,每次约200 mL,头晕乏力较前加重,无畏寒发热,无恶心呕吐,无呕血,无腹痛。患者20年前有胃溃疡伴出血病史,曾行胃镜检查明确,保守治疗后好转,曾因胃溃疡穿孔行修补手术治疗。既往否认慢性病史,否认肝炎、结核、吸烟嗜酒以及特殊服药史。     

门静脉海绵样变的诊治进展

门静脉海绵样变(CTPV)是由于各种原因造成门静脉主干或分支、完全或部分阻塞,导致血管内血流受阻,门静脉压力增高,机体为缓解门静脉高压而形成大量的门静脉周围侧支血管而引起的疾病。因此,CTPV是一种代偿性病变,其代偿能力不够,无法阻止门静脉压力的上升,是导致肝前型门静脉高压的原因之一,约占门静脉高压症各病因的3.5%。因其在大体标本上表现为海绵样外观而被命名为CTPV。     

门静脉海绵样变的MRI表现

<正>门静脉海绵样变性(cavernous transformation of portal vein,CTPV)是指由于不同病因导致门静脉主干和(或)分支完全或部分闭塞后,其周围形成海绵样扭曲的代偿静脉。CTPV构成的侧支静脉或旁路是机体保证肝脏血流量及肝脏营养的一种代偿改变,它是门静脉阻塞后病理改变的最终结果,在缓解门静脉高压过程中起重要作用。CTPV的诊断以往主要依靠彩色多普勒超声、数字减影血管造影     

Cavernous transformation of the portal vein: etiology determines the outcome

BACKGROUND/AIMS: Cavernous transformation of the portal vein is a rare condition with various etiologies and diverse clinical presentations. We aim to assess the disease outcome of different etiologic groups. METHODOLOGY: We retrospectively scrutinized the clinicopathologic characteristics of 35 patients with cavernous transformation of the portal vein, placing special emphasis on the disease extent, progression, and outcome after stratification into different etiologic groups. RESULTS: There were 20 males and 15 females with a mean age of 40.4 years. The etiologies of these patients could be classified into four groups including hematologic disease (n=12, 34.2%), malignant disease (n=8, 22.9%), non-malignant disease (n=6, 17.2%), and idiopathic (n=9, 25.7%). The hematologic disease group had 9 patients with myeloproliferative disease and 3 patients with protein C or protein S deficiency. The hematologic disease group survived well after medication or surgical management. Hepatocellular carcinoma (n=6) was the leading cause in the malignant diseases group, which had a significantly poorer survival rate than the rest (p<0.05). CONCLUSIONS: Cavernous transformation of the portal vein is a long-term sequele of portal vein thrombosis in which the etiology determines the outcome. More aggressive management including long-term anticoagulation in patients with myeloproliferative disorder or underlying prothrombotic states and endoscopic therapy in controlling variceal bleeding may be a more effective treatment for these patients.     

Cavernous transformation of the portal vein in nephrotic syndrome

We report a 19-year-old man with thrombosis of the portal vein associated with a nephrotic syndrome. A computed tomography showed obstruction of the portal vein with prominent collaterals and cavernous transformation. This case is noteworthy as a report of nephrotic syndrome accompanied by extensive abdominal venous thrombosis and was cured successfully.     

Laparoscopic splenectomy for variceal bleeding with non-cirrhotic portal vein thrombosis: a case report

A 57-year-old man was referred to our hospital for treatment of refractory gastric bleeding from gastric varices secondary to portal vein thrombosis. The patient's liver function tests and coagulation profile were normal. The venous phase of the superior mesenteric arteriogram, on the other hand, showed superior mesenteric vein-portal vein occlusion with surrounding hepatopetal variceal collaterals. The venous phase of the splenic arteriogram additionally showed splenic vein occlusion and collateral vessels from the gastric and retroperitoneal regions flowing into a portal cavernous transformation. Gastroscopy confirmed that the patient had gastric varices in the cardia. We performed laparoscopic splenectomy to treat refractory gastric bleeding from varices and symptomatic hypersplenism. The postoperative course was uneventful; the patient's gastric varices were less prominent on follow-up gastroscopy and the hematologic profile returned to normal. Extrahepatic portal vein thrombosis is the leading cause of variceal hemorrhage in patients with healthy livers. There is a consensus in the literature that splenectomy alone is of minimal value in preventing variceal bleeding in portal vein thrombosis. Splenectomy is, however, indicated in cases in which the patient has hepatopetal collaterals from the mesenteric vein system and whose hemorrhagic gastric varices are related to splenic vein thrombosis as in our case.     

脾切除术后胃底副脾一例

胃部副脾临床少见,本文报道了1例45岁女性患者,因间断上腹胀7个月余就诊,10年前因外伤曾行脾脏切除术。术前胃镜、超声内镜和腹部CT均提示胃底占位,行内镜黏膜下剥离术切除,术后病理提示为副脾组织。     

Cavernous transformation of the portal vein associated to multiorgan developmental abnormalities.

Initial diagnosis of cavernous transformation of the portal vein (portal cavernoma) is rarely made in adults. Its main clinical manifestation is upper gastrointestinal hemorrhage due to variceal bleeding. More rarely, diagnosis is made from obstructive jaundice. In children, this condition is frequently associated to prehepatic portal hypertension and congenital anomalies, the most frequent of which are atrial septal defects or malformations of the biliary tract or of the inferior vena cava. We describe here a case of a 23-year-old female presenting with massive hematemesis due to the presence of esophageal and small intestinal varices. She had a cavernous transformation of the portal vein with prehepatic portal hypertension associated with heretofore unreported malformations such as right pulmonary hypoplasia, cardiac dextroposition, and right renal ectopia. A unifying hypothesis (e.g. an intrauterine vascular insult) to explain the pathogenesis of these defects seems unlikely. Appropriate tests failed to identify specific functional abnormalities in these organs. Although she bled more than once, the combination of sclerotherapy and beta-blockers has been, thus far, able to control the major clinical consequences of this disease.     

胰腺脓肿压迫脾静脉致区域性门静脉高压1例报告

1 病例资料
　　患者男性,43岁,主因“腹痛、气紧、乏力2个月余”入院。病史：患者缘于20余天前无明显诱因出现中上腹隐痛于外院住院治疗,诊断为“急性胰腺炎、高血压、糖尿病”,给予相应治疗（具体不详）,之后出现间断发热,经抗生素及对症治疗后好转,12 d 后患者出现高热,最高达39．7℃,自觉气促、心跳加快,磁共振胰胆管造影提示胆囊增大,遂转入本院治疗。入院后给予泰能抗感染、胆囊穿刺引流、胸腹腔穿刺引流,对症及支持治疗后上述症状有所好转,后自行要求出院。出院后,仍间断发热、腹痛,遂再次入院。查体：神清,精神差,腹部膨隆,中上腹、左上腹及中下腹可见3条引流管,腹软,全腹无压痛、反跳痛及肌紧张,肝脾肋下未及,肝脾肾区无叩痛,肠鸣音约3次／min,移动性浊音阴性,双下肢无水肿。查血常规示：白细胞计数8．44×109／L,红细胞计数2．98×1012／L↓,血红蛋白浓度84 g／L↓,中性粒细胞比率81．51％↑;血生化：肌酐41．30μmol／L↓,葡萄糖7．21 mmol／L↑,GGT 126．00 U ／L↑,ALP 197．10 U ／L↑,降钙素原＜0．05 ng／ml;尿常规：隐血（＋）↑。余肝肾功能、电解质未见异常。查腹部 CT 示：急性坏死性胰腺炎治疗后改变,腹腔积液引流术后,胰腺体见一5．7 cm ×2．7 cm 大小脓肿,邻近脾静脉、门静脉主干,肠系膜上静脉上段稍显狭窄,周围结构显示不清,侧枝血管形成,食管胃底静脉曲张（图1）。胃镜检查示：胃底见团块状静脉曲张,无红色征;胃底、胃体广泛黏膜肿胀,诊断为：（1）胃底重度静脉曲张（无红色征）;（2）门静脉高压性胃病（图2）。     

华法林抗凝治疗乙型肝炎肝硬化继发血栓性门静脉海绵样变性1例报告

正1病例资料患者男性,36岁,因"反复黑便、呕血2年余,上腹部不适2周"于2011年2月4日首次来上海市公共卫生临床中心治疗。患者于2009年9月起开始出现反复呕血、黑便,曾多次就诊于当地医院,诊断为"失代偿期乙型肝炎肝硬化,食管胃底静脉曲张破裂出血",并于2009年11月因"巨脾,脾功能亢进"行脾切除术。术后1周因继发性PLT增多,予以口服拜阿司匹