Published online Jan 27, 2020. doi: 10.4240/wjgs.v12.i1.1
Peer-review started: August 5, 2019
First decision: August 31, 2019
Revised: September 25, 2019
Accepted: November 7, 2019
Article in press: November 7, 2019
Published online: January 27, 2020
Processing time: 143 Days and 14.4 Hours
Portal hypertension (PH) is known to be associated with changes in vascular structure and function of the portosplenomesenteric system (PSMS, portal hypertensive vasculopathy). Pathological abnormalities of PSMS has been described in the literature only for cirrhotic patients. This vasculopathy is believed to be related to raised portal pressure and hyperdynamic circulation (HC).
In view of similar circulatory changes in PSMS, it is anticipated that pathological changes in the splenic and portal veins, which are similar to those reported in cirrhotic patients with PH, may also be present in patients with non-cirrhotic PH (NCPH). Venous thrombosis is the terminal event of this vasculopathy. Early shunt surgery in NCPH may prevent the development of mesenteric venous thrombosis and its sequelae.
In this study, we aimed to study the possible association of long-term exposure of PSMS to raised pressure and HC, portal hypertensive vasculopathy (PHV) and resultant mesenteric venous thrombosis and its sequelae.
A prospective observational study was performed on 116 patients with NCPH (extrahepatic portal vein obstruction: 53 and non-cirrhotic portal fibrosis: 63) who underwent proximal splenorenal shunt, interposition shunt or splenectomy with devascularization in JIPMER, Pondicherry, India, a tertiary level referral center, between 2011-2016. All patients were evaluated by Doppler study of PSMS, computed tomography porto-venogram and upper gastrointestinal endoscopy. Acoustic resonance forced impulse scans and abdomen ultrasounds were done for all cases to exclude cirrhosis. Intraoperative and histopathological assessment of the harvested splenic vein was performed in all. The study group was divided into delayed and early presentation based on the median duration of symptoms (i.e. 108 mo).
Upon histopathological examination of veins, splenic veins in all patients with NCPH were found to be abnormal (based on the presence of one or more pathological characteristics studied).
There is no report in the literature on PHV in NCPH. PHV involving the splenic vein is similar in cirrhotic as well as non-cirrhotic portal hypertensive patients. They reflect the effect of HC and increased pressure in the PSMS. We show that these pathological venous changes in NCPH are observed in a greater proportion of patients in the delayed presentation group (P < 0.003). It would therefore be interesting to explore the utility of early aggressive intervention to reduce portal pressure and hemodynamic stress to avoid potential lethal effects of mesenteric venous thrombosis and its sequelae on the intestine, liver and pancreas.
It would be significant to investigate the role of early shunt surgery in NCPH to prevent the worsening of PHV and the development of mesenteric venous thrombosis and its sequelae in these patients.