Histology of the intestinal peritoneum in patients with cirrhosis of the liver and ascites

Portal hypertension and hypoalbuminemia are usually incriminated in the development of ascites in liver cirrhosis, and altered peritoneal permeability is considered only as a hypothetical possibility. Jejunal postmortem specimens were studied in 15 control patients and 16 patients dying with cirrhosis of the liver and ascites. In decompensated cirrhosis a fibrous thickening of the peritoneum was found, 159.0±96.4 m (mean±sd) compared to 24.5±10.6 m in controls (P<0.001). An increase in the size and number of blood vessels, lymphangiectasiae, and mononuclear cell infiltration were invariably present. These histological changes are consistent with a nonspecific chronic peritonitis. The findings indicate there is increased blood perfusion and lymph flow within the intestinal peritoneum in patients with decompensated cirrhosis of the liver and support the existence of an intestinal peritoneal factor in the pathogenesis of cirrhotic ascites.     

Laparoscopy in the diagnosis and differential diagnosis of ascites]

Out of 2,500 patients who underwent laparoscopy 772 (30.89%) had ascites; liver cirrhosis underlay it in 57.78%, peritoneal carcinosis in 26.29%, primary and metastatic carcinoma, respectively, in 12.95%, tuberculous peritonitis in 1.42%, more rarely other diseases. Liver cirrhosis, malignant tumours and the other hepatic affections with concomitant ascites in their course can certainly be diagnosed laparoscopically. Laparoscopy with oriented biopsy of peritoneum and liver is of decisive importance in differentiating peritoneal carcinosis from tuberculosis. In peritoneal carcinosis the diagnosis (as based in clinical and laboratory findings) coincided perfectly with the laparoscopic and histologic one in 24.5%, partially in 45.5%. In 30% there was no congruence at all. Laparoscopy and the test methods associated with it contributed to the accurate diagnosis of peritoneal carcinosis in 75.5% of the patients. Ovarian carcinoma (20.9%) and cancer of the stomach (16.3%) underlay peritoneal carcinosis most frequently, other diseases by far more seldom.     

Hepatic hydrothorax in the absence of ascites diagnosed by intraperitoneal spraying of indocyanine green

Hepatic hydrothorax in the absence of ascites is a rare complication of liver cirrhosis. A 56-year-old woman was referred to our hospital because of a massive pleural effusion on the right side, requiring continuous drainage. Although the patient was known to have chronic hepatitis C, she had no signs of hepatic failure including ascites. A laparoscopic examination revealed a nodular liver and a small volume of ascites in the peritoneal cavity. Indocyanine green sprayed into the intraperitoneal cavity was excreted from the pleural drain just after the spraying, indicating an intraperitoneal origin of the pleural fluid. Discontinuation of pleural drainage and an introduction of standard treatment for ascites due to liver cirrhosis (including restriction of salt intake and diuretic administration) resulted in a marked decrease of pleural effusion.     

56例结核性腹膜炎患者CT影像分析

目的 探讨结核性腹膜炎（TBP）特征性CT影像表现及治疗中影像动态变化的特点。方法 回顾性分析56例临床及病理确诊的TBP患者,观察分析CT影像特征,包括腹腔积液、腹膜（壁腹膜、肝包膜、大网膜及肠系膜）及腹腔淋巴结。56例均行CT平扫+增强扫描。治疗过程中收集动态复查CT影像。结果 腹腔积液45例,大量1例,中少量44例,限制性38例,CT值>20 HU者34例。壁腹膜增厚46例,肝脏边缘部腹膜均有受累,均匀增厚17例,扁丘状凸起或腹膜结核瘤29例,增强扫描结核瘤边缘强化,肝包膜或肝脏受累15例;网膜增厚35例,结节及斑片34例,网膜饼1例,增强扫描网膜饼呈轻度不均匀强化;肠系膜增厚41例,表现为斑片、结节及线状、星芒状条索状高密度影,与肠袢粘连,增强扫描肠系膜血管包埋其内,走形扭曲。腹腔及腹膜后淋巴结增大19例,伴钙化5例,簇集状排列,增强扫描环状或蜂窝状强化。17例完整的动态CT图像,腹腔积液吸收最快,网膜及肠系膜病变吸收稍慢,腹膜结核瘤缩小速度最慢。结论 TBP的CT诊断为多种征象的综合,中少量腹腔积液伴壁腹膜、网膜及肠系膜的增厚粘连是最为常见的影像表现;CT影像动态变化对临床评价疗效具有重要意义。     

腹腔内镜检查对不明原因腹水的诊断价值

目的 探讨腹腔内镜检查及直视下腹膜活检对不明原因腹水的诊断价值,评价超细胃镜代替硬式腹腔镜检查的可行性。方法对35例不明原因腹水的患者进行腹腔内镜探查手术,并取可疑组织送病理检查。结果35例腹腔内镜探查确诊33例,确诊率94．3％,其中确诊结核性腹膜炎10例,转移性腹膜癌7例,肝癌5例,肝硬化3例,原发性腹膜癌3例,卵巢癌2例,肝血管肉瘤1例,脾淋巴瘤1例,嗜酸性肠炎1例,所有患者术后恢复顺利,无并发症。结论腹腔内镜检查安全,靶向性腹膜活检确诊率高,对不明原因腹水的诊断有重要价值。     

Ascites as the major manifestation of systemic lupus erythematosus

It is uncommon for ascites secondary to severe peritoneal inflammation to be the major manifestation of systemic lupus erythematosus. Chronic nonspecific inflammation with a granular type immunofluorescent staining along the mesothelial layer of the peritoneum and peritoneal blood vessels was demonstrated in peritoneal tissue obtained at laparotomy. Paramyxovirus-like structures were seen within vascular endothelium. The ascites diminished with high-dose prednisone and cyclophosphamide therapy.     

Lymphatic and nonlymphatic pathways of peritoneal absorption in mice: physiology versus pathology.

In conjunction with our studies of the pathogenesis of malignant ascites formation, we have analyzed the transperitoneal transport of macromolecules in mice. In this review, I summarize our experimental results concerning the influx (transport from the blood to the peritoneal cavity) and efflux (transport from the peritoneal cavity to the blood) of a number of different tracers [fluorescein-labeled dextrans (FITC-D), 51Cr-RBC, 125I-HSA, and 125I-fibrinogen]. We examined tracer transport in ascites tumor-bearing animals as a function of tumor growth and compared our results with transport properties obtained in normal awake mice and in mice that had received an intraperitoneal injection of a solution of 5% bovine serum albumin to simulate the protein-rich fluid accumulation associated with ascites tumor growth in the peritoneum. Our results indicate that both increased influx as well as impaired efflux are required to initiate and maintain tumor ascites fluid accumulation. To test the hypothesis that increased influx reflected increased vascular permeability, we monitored transport of intravenously injected FITC-D tracers (FITC-D) into the peritoneal cavity by fluorescence microscopy. To investigate the mechanisms involved in the decreased efflux, we determined tracer efflux rates both as the rate of appearance in the blood and as the rate of disappearance from the peritoneal cavity. We compared these transport properties for both soluble as well as particulate tracers. Our results indicate that there are additional routes of egress available to soluble macromolecules not available to particulate tracers such as 51Cr-RBC, and that in ascites tumor-bearing animals, the lymphatic pathway is shut off rather rapidly as judged by the decreased rate of 51Cr-RBC removal. By fluorescence microscopy we observed the interstitial tissue uptake of intraperitoneally injected soluble macromolecules (FITC-D) in the parietal peritoneal wall, particularly in animals with an increased intraperitoneal pressure, thereby confirming additional nonlymphatic pathways of peritoneal absorption in mice. Finally, we used the particulate tracer 51Cr-RBC to estimate the peritoneal lymphatic drainage rate, yielding a value of 1.6 microliters/min in normal awake mice based on the rate of tracer disappearance from the peritoneum.     

消胀贴膏外敷对小鼠肝硬化腹水的消退作用及对腹腔血管通透性的影响

目的评价消胀贴膏外敷对实验性肝硬化腹水的药效作用,探讨其影响腹腔血管通透性的作用机制。方法以二甲基亚硝胺(DMN)腹腔注射,药效评价实验模型动物随机分为模型对照组、安慰剂对照组、消胀贴膏低、中、高剂量组共5组,机制实验分为模型对照组、消胀贴膏中剂量组共2组,均设正常对照组。消胀贴膏组脐部外敷消胀贴膏,安慰剂对照组脐部外敷空白贴膏,每日1贴,共7d,模型对照组不敷贴任何药物。称量或测量模型动物的腹水量、腹围、体重,HE与天狼星红染色观察肝组织炎症与纤维化,生化检测血清ALT活性和Alb、TBil与一氧化氮(NO)含量,蛋白质印迹法分析肝组织血管内皮生长因子(VEGF)表达水平,通过测定小鼠腹腔积液及肝组织中渗漏伊文氏蓝(EB)含量的方法检测动物腹腔血管通透性。结果敷药前,各组模型动物的腹围、体重等基线资料一致。给药结束,与正常组比较,模型对照组小鼠的体重、腹围、腹水、腹水体重比等明显增加,腹腔积液及肝组织中渗漏EB含量明显增多,血清NO浓度及肝组织中VEGF蛋白表达明显增加。与模型对照组比较,安慰剂对照组的腹水量、腹围与体重等无明显改变。与安慰剂对照组比较,消胀贴膏中、高剂量组的腹水量、腹水体重比值明显下降,高剂量组的腹围、体重也明显下降;高剂量组与低剂量组比较,腹围、体重明显下降。各剂量消胀贴膏对肝功能及肝组织病理均无明显影响。与模型对照组比较,中剂量消胀贴膏组小鼠腹腔积液中渗漏EB含量降低,血清NO浓度及肝组织中VEGF蛋白表达明显减少。结论消胀贴膏明显减少肝硬化腹水模型动物的腹水量,中剂量(0.25 cm2消胀贴膏,652.9 mg生药/kg小鼠)开始发挥药效,其部分机制在于下调肝硬化腹水模型动物的肝组织VEGF表达、降低血清NO含量,从而抑制其异常增强的腹腔血管通透性。     

Chronic lupus peritonitis with massive ascites at elderly onset: case report and review of the literature

A 77-year-old Japanese woman with massive painless ascites caused by chronic lupus peritonitis is reported. Peritoneal effusion had been resistant to the administration of steroids during the whole treatment period. It was characteristic that the titers of anti-DNA antibodies and the level of immune complex were elevated in the peritoneal fluid with suppressed levels of complements in ascites, although serum immunological markers reflecting the activity of SLE presented improvement after initiation of the treatment. Fifteen patients with chronic lupus peritonitis were reported previously. We reviewed the literature and suggest that chronic lupus peritonitis at elderly onset may demonstrate a poor response to the glucocorticoid therapy because of persistent inflammation in the peritoneum and the presence of impaired vascular circulation in addition to immunological mechanisms.     

Ascites in patients undergoing maintenance hemodialysis: Report of six cases and physiopathologic approach

Six patients with chronic uremia in whom ascites developed during maintenance hemodialysis are described. Their clinical and biochemical findings are reviewed and compared with data of 10 hemodialyzed patients without ascites. Liver cirrhosis was the origin of ascites in only one case. Hypoalbuminemia, liver cirrhosis, congestive heart failure, peritonitis, peritoneal tuberculosis and carcinomatosis were uniformly absent in the other patients. Long-term and marked overhydration seems to be at the origin of ascites. Lack of peripheral edema, probably due to ascites compartmentalization, was a constant finding in every noncirrhotic patient with ascites. When long-term overhydration was stopped after successful kidney transplantation or by means of diminished water and salt ingestion, reversal of the syndrome was attained. Nevertheless, ascites because of liver cirrhosis was not influenced by means of kidney transplantation. In three patients with ascites who did not receive a transplant, a significant reduction in water and salt ingestion was reached after intensive psychotherapy which led to reversal of the ascitic syndrome. In one anephric patient ascites did not develop despite water overloading. Survival has not been influenced by the formation of ascites.Further research is needed to determine the mechanism of sodium transfer across the peritoneal membrane. Influence of humoral factors can be considered, if an active transport mechanism could be demonstrated.     

Genesis of fibronectin in ascites--detection of cellular and plasma fibronectin in portal and malignant ascites

Measurement of fibronectin in ascites has been proposed for the differentiation of ascites either due to malignant growth in the peritoneal cavity or liver cirrhosis with portal hypertension. The high ascitic fibronectin concentration in patients with peritoneal carcinomatosis was thought to be due to the synthesis of this protein by neoplastic cells. Therefore in ascites of malignant origin cellular fibronectin should be present as it is synthesized by neoplastic cells. On the other side the transsudative ascites due to liver cirrhosis with portal hypertension should mainly contain plasma-fibronectin, which is secreted by hepatocytes into the bloodstream. With the aid of two different monoclonal antibodies and immunoblotting of partially digested or intact ascitic fibronectin, cellular fibronectin could be demonstrated in ascitic fluid of 10 patients with peritoneal carcinomatosis, 13 patients with liver cirrhosis, one patient with right-sided heart failure and one patient with Budd-Chiari-Syndrome. As determined by a specific ELISA 8 out of 10 samples of malignant ascites contained more than 30 mg/l of cellular fibronectin, whereas 10 out of 13 samples of ascites due to liver cirrhosis contained less than 10 mg/l. Whereas in ascites of malignant origin cellular fibronectin represented about 20% of total fibronectin, in portal ascites fibronectin represented sometimes more than 50% of total fibronectin. Cellular fibronectin of non-malignant origin is probably produced by mesothelial cells or peritoneal macrophages. Therefore, fibronectin accumulating in peritoneal carcinomatosis is only to some extent locally produced, but mainly caused by an unhindered exsudation of plasma-fibronectin.     

Liver cirrhosis with encapsulating peritoneal sclerosis after 4 years of peritoneal dialysis: A case report

Rationale:Encapsulating peritoneal sclerosis (EPS), or abdominal cocoon, is a rare but fatal syndrome characterized by intestinal obstruction owing to adhesions in a diffusely thickened peritoneum. Long-term peritoneal dialysis (PD) for more than 5 years is commonly associated with EPS, while liver cirrhosis also carries a risk of EPS. However, there have been only a few reports that describe a case of EPS complicated with both cirrhosis and PD. We herein describe a case of advanced liver cirrhosis with end-stage renal disease (ESRD) who developed EPS after 4 years of PD and who was successfully recovered by surgery.Patient concerns:A 58-year-old man with alcoholic liver cirrhosis suffered abdominal pain. The patient had a 4-year history of continuous cycling PD to manage ESRD as well as cirrhotic complications of refractory ascites and hypotension. Laboratory test results showed increased levels of inflammation, and contrast-enhanced computed tomography scan showed dilated loops of small bowel proximal to the site of intestinal obstruction. The patient was suspected to have developed intestinal obstruction owing to EPS. The patient discontinued continuous cycling peritoneal dialysis and switched to hemodiafiltration.Diagnoses:Laparoscopy revealed a whitish membranous material wrapped around the bowel, especially at the terminal ileum with a narrowed portion, consistent with EPS.Interventions:Repeated decortication of fibrous peritoneal membranes successfully released the intestinal obstruction.Outcomes:The postoperative course went well and abdominal pain remained in remission. Because abdominal distension owing to ascites got intolerable in a few days after surgery, a PD catheter was re-inserted and ascitic fluid drainage was resumed with peritoneal lavage. The patient continued hemodiafiltration using vasopressor agents.Lessons:The Cirrhotic patient with ESRD undergoing PD could develop EPS after a short duration of PD.     

Diagnostic value of fibrolaparoscopy and direct-vision peritoneal biopsy in atypical tuberculous peritonitis]

Fifty-three cases of atypical tuberculous peritonitis were diagnosed by Machida FLA-8 fibrolaparoscope and direct-vision peritoneal biopsy in our hospital during the last few years. The misdiagnosis rate of this disease is very high. The rate of accurate clinical diagnosis was only 39.6% in patients of this study, while 60.4% was misdiagnosed as other diseases, such as cirrhosis, chronic hepatitis, hepatic carcinoma ovarian cyst etc. In addition, many patients with other diseases were misdiagnosed as tuberculous peritonitis by clinical consideration, for instance, 56 cases who were diagnosed or doubted as tuberculous peritonitis by clinical consideration were diagnosed as other diseases by laparoscopy and liver and peritoneal biopsy under direct-vision. Among them chronic hepatitis accounted for 32 cases, peritoneal carcinoma 11 cases, cirrhosis 7 cases, normal peritoneum, liver, gall bladder and spleen 6 cases. Therefore, the patient who is presumptively diagnosed as tuberculous peritonitis by clinical consideration should have laparoscopy and direct-vision peritoneal biopsy performed.     

Ascitic fluid concentrations of fibronectin and cholesterol: comparison of differential diagnostic value with the conventional protein determination

Ascitic fluid concentrations of fibronectin, cholesterol and protein were determined in 95 patients: 38 with cirrhosis of the liver, 10 with miscellaneous nonmalignant diseases, 43 with peritoneal carcinomatosis and 4 with liver metastases or hepatocellular carcinoma. Fibronectin, cholesterol and protein at discrimination values of 7.5 mg/100 ml, 45 mg/100 ml and 3.0 g/100 ml, respectively, separated patients with peritoneal carcinomatosis from patients with cirrhosis with an efficiency of 94%, 90% and 85%, respectively. Thus, ascitic fluid determinations of fibronectin and cholesterol offer good discrimination of cirrhotic ascites from ascites related to peritoneal carcinomatosis, superior to the conventional protein determination. However, the failure of all parameters to distinguish ascites caused by miscellaneous nonmalignant diseases from malignancy-related ascites underscores the importance of highly specific methods to confirm a suspected diagnosis of malignancy-related ascites.     

Management of ascites in children

Ascites is the pathologic accumulation of fluid within the peritoneal cavity. There are many causes of fetal, neonatal and pediatric ascites; however, chronic liver disease and subsequent cirrhosis remain the most common. The medical and surgical management of ascites in children is dependent on targeting the underlying etiology. Broad categories of management strategies include: sodium restriction, diuresis, paracentesis, intravenous albumin, prevention and treatment of infection, surgical and endovascular shunts and liver transplantation. This review updates and expands the discussion of the unique considerations regarding the management of cirrhotic and non-cirrhotic ascites in the pediatric patient.     

MRI manifestations of peritoneal carcinomatosis.

Three cases of proved peritoneal carcinomatosis were examined by magnetic resonance imaging (MRI). Air was used to distend the entire gastrointestinal tract via an antegrade method. The findings included seedings along the small intestine, transverse and sigmoid colon, stellate pattern in the mesentery, plaque-like and bulky tumor masses in the mesentery and greater omentum, and focal thickenings along the right subdiaphragmatic parietal peritoneum. Stenosis caused by tumor encasement at the duodenojejunal junction and ileocolic anastomosis were first detected by MRI and later confirmed by barium studies. Ascites was present in all cases. One case showed ascites located only along the left paracolic gutter. This report shows that MRI is also able to demonstrate peritoneal carcinomatosis by using air as a gastrointestinal contrast medium.     

What is the role of diagnostic laparoscopy in a gastroenterology unit?

Background Diagnostic laparoscopy is known to be a relatively safe invasive procedure. However, its use has decreased owing to the development of imaging techniques, and fewer gastroenterologists now practice diagnostic laparoscopy. Our aim was to examine the role of diagnostic laparoscopy in a gastroenterology unit in the era of advanced imaging techniques. Methods We retrospectively reviewed 855 diagnostic laparoscopy cases. Its safety and efficacy were evaluated for various indications. Results No mortality was observed, and complications were noted in ten patients (1.2%). Among the indications were evaluation of chronic liver disease (n = 673), liver tumor (n = 15), ascites of unknown origin and peritoneal disease (n = 142), and staging of intra-abdominal malignancy (n = 25). In patients with chronic liver disease, 461 were diagnosed as having chronic viral hepatitis, based on clinical data including imaging studies, but the diagnosis was changed to cirrhosis after a laparoscopic exam in 69 patients (15.0%). In patients with ascites of unknown origin and peritoneal disease, the diagnostic yield was 87.2% (123/141). In 24 (19.5%) of the 123 patients, the diagnosis changed or the less probable diagnosis was confirmed after laparoscopic examination. The confirmed diagnoses were mainly primary peritoneal disease, including peritoneal tuberculosis, in 17 patients, peritoneal metastatic carcinoma in five, and mesothelioma in two. Conclusions Diagnostic laparoscopy in a gastroenterology unit is safe and useful, especially for confirmation of liver cirrhosis and primary peritoneal disease evaluation.     

Ultrasound documentation of diaphragmatic rent in hepatic hydrothorax

Two patients with alcoholic cirrhosis of the liver with ascites were evaluated for the pathogenesis of right sided massive pleural effusion. The clinical course of events suggested a large communication between the peritoneal space and right pleural cavity. Real time ultrasonography revealed evidence of a tear in the right hemidiaphragm. The role of ultrasound in the documentation of cause of hydrothorax in chronic liver disease is highlighted.     

Right diaphragmatic defect in hepatic hydrothorax exposed by contrast-enhanced ultrasonography after radiofrequency ablation

A 68-year-old male with liver cirrhosis and hepatocellular carcinoma treated by radiofrequency ablation was hospitalized for right hepatic hydrothorax and ascites. Perflubutane injected into the peritoneal cavity after an ultrasonography contrast agent revealed jet-like flow from the ascites to a pleural effusion, indicating a diaphragmatic defect. A hepatic hydrothorax was sutured under thoracoscopy and did not recur. An intraperitoneal injection of perflubutane enables a less-invasive diagnosis of a diaphragmatic defect.     

Immunological parameters in the differential diagnosis of ascites secondary to peritoneal carcinomatosis, hepatic cirrhosis, and congestive heart failure]

As a contribution to the study of ascites in patients with liver cirrhosis, congestive heart failure and peritoneal carcinomatosis evaluate in serum and ascites the concentrations of alphafetoprotein, carcinoembryonic antigen and fibronectin, they might suggest a diagnosis for the basic pathology. Forty-seven patients were studied, from whom 23 with cirrhosis, 17 peritoneal carcinomatosis and 7 with congestive heart failure. We conclude that: a) none of the tools usually employed in the analysis of ascitic fluid alone can make the base pathological process responsible for producing ascites; b) fibronectins were more useful for differential diagnosis between cirrhosis and carcinomatosis; c) alpha-fetoprotein and carcinoembryonic antigen were not useful for the definition for differential diagnosis.