Clinical analysis of a patient with severe hypoproteinemia and ascites: the logic of searching and combining puzzles

Abstract

Clinical analysis of patient B., 38 years old, who complained of abdominal enlargement, spastic abdominal pain without clear localization, feeling of incomplete bowel movements and discharge of clear, almost colourless fluid from the rectum, progressive weight loss.

Preliminary studies provided data in favour of portal hypertension (PH), hepatomegaly, ascites, esophageal varices and hypoproteinemia, which could be interpreted as cirrhosis. At the same time, severe trophological insufficiency was combined with the complete absence of any signs of liver failure and “small” hepatic signs. Capsule endoscopy confirmed our assumption of intestinal lymphangiectasia (IL). After that, we began to search for possible causes of secondary IL. The results of the previous upper endoscopy, colonoscopy and capsule endoscopy allowed us to exclude Crohn's disease and Whipple's disease; we excluded also viral hepatitis, cirrhosis, HIV infection, autoimmune liver diseases, systemic vasculitis, antiphospholipid syndrome, tuberculosis, lung and heart disease.

We assumed that the recurrent acute pancreatic inflammation and the last episode of acute pancreatitis, which was complicated by ascites and pseudocyst formation, were also accompanied by the appearance of a relatively rare complication — splenic vein (SV) thrombosis and superior mesenteric vein occlusion. SV thrombosis, in turn, contributed to the development of left-sided PH, which is characterised by an increase in venous pressure in the SV without obstruction of the portal vein, damage to the liver parenchyma and the formation of collateral blood flow. Already against the background of left-sided PH, congestive enteropathy occurred, which was exacerbated by small intestinal lymphangiectasia, which led to protein loss, a drop in oncological pressure and the development of ascites. We do not exclude that IL is not only the result of stagnation in the lymphatic capillaries of the small intestine, but also the result of stagnation in larger lymphatic vessels (trunks, cisterns (?)), but their rupture.

The seemingly typical clinical case turned out to be quite complicated. Evaluation of laboratory and instrumental data in the appropriate clinical context led to the suspicion of a pathology other than liver cirrhosis. A thorough diagnostic search required not only the analysis of modern literature, but also the coordinated work of a multidisciplinary team.