By Jeyashree Sundaram (MBA)
Portal hypertensive colopathy (PHC) is a condition in which changes occur in the mucosal membrane of colon in patients affected with portal hypertension and liver cirrhosis. PHC is the main cause of bleeding in lower gastro intestinal (GI) tract, erytherma in the mucosal membrane of colon, telangiectasias, vascular lesions, and angiodysplasia-like lesions.
Severity of PHC is dependent on the stage of the lesions. Early stage lesion is identified by slightly dilated, thin-walled, tortuous venules and veins lined by endothelial cells found in tela submucosa. Advance-stage lesions are more expanded submucosal veins, capillaries, and tortuous venules in the colonic mucous membrane or mucosa. Nevertheless, the occurrence of portal hypertensive colopathy and anorectal varices is very high in patients with portal hypertension.
The term portal hypertensive colopathy was first described in 1991. It is mainly caused due to portal hypertension and liver cirrhosis.
In the case of patients with portal hypertension, PHC is the result of the constant accumulation of blood within portal venous system that leads to ectasia and dilation on the layer of tissue vessels in in the colonic mucosa. Portal hypertension is a condition in which the blood pressure in the portal veins increase due to the disturbance in blood flow through the liver. It results in changes in the colonic mucosal area, which is indicated by friability in tissues.
PHC is significantly related to cirrhotic patients with Child-Pugh class B and C. Complications of Child-Pugh class such as decrease in platelet count may result in bleeding of the lower GI tract. This decrease in platelet count increases the prevalence of PHC in cirrhotic patients.
Symptoms and Signs
PHC is generally asymptomatic. First-line indication of PHC is chronic bleeding in lower GI tract, which may result in anemia. Hematochezia is the common symptom of PHC, which is indicated by bleeding from colon, GI tract, and rectum; stools may also appear in tarry black color.
Other signs observed through endoscopy are edematous mucosa and diffuse erythematous, colitis-like lesions, and anorectal varices. Fluid gets accumulated in abdomen. Drop in the count of white blood cells or platelets can also happen.
PHC can be diagnosed with the help of colonoscopy and endoscopy; where flat or red lesions setting of nearly ten millimeter in diameter is identified on a colonic mucosal membrane.
During the diagnosis of PHC through colonoscopy, penetration of rectal varices into the lumen of rectum can also be examined. Diameters of these penetrated veins are completely higher than the normal veins of rectum.
The patients in endoscopy will show lesions that appear to be vascular ectasia or distributed red spot, vasodilatation, vascular irregularity, and hemorrhoid.
Vascular ectasia is an unusual cause of the chronic GI bleeding or anemia, which is associated with the small blood vessel dilation in the inner part of the stomach. Three types of vascular ectasia are identified as follows:
a flat, spider-like vascular lesion
a flat or cherry-reddish lesion or slightly raised red lesion with a diameter of lesser than 10 mm
a slightly raised submucosal cancer like lesion appeared to be red in color.
Vasodilation is described as increase in the diameter (3 mm to 6 mm) of venous blood vessels. The appearance of the vessels is coil-like structure in the colonic submucosa, which is termed as vascular abnormality or irregularity.
There is no standard treatment available for PHC. The acquirable treatment is based on the case reports.
Treatment for portal hypertensive colopathy is suggested based on various factors such as symptoms, bleeding rate, and severity of the disease.
It had been observed that the β-blocker works well and provides effective results in patients with lower GI bleeding secondary to the PHC.
The effective treatment to reduce acute bleeding due to PHC is vasoactive medications that include terlipressin or octreotide. The stability of the blood flow is achieved through the suggested non-selective β-blockers.
A case report from the PHC patient with bleeding indicated that the octreotide extract reduces the pressure gradient of hepatic venous and blocks the bleeding.
If the patient with GI bleeding had not recovered even after the treatment with β-blocker or vasoactive medications, then the rescue therapy is transjugular intrahepatic portosystemic shunt (TIPS). Case studies prove that for patients with portal hypertension and cirrhosis in whom the bleeding was not stopped by propanol initially, TIPS therapy was effective.
TIPS procedure leads to the reduction of portosystemic gradient; through colonoscopy continuously done for nine days in patients who underwent this therapy, reduction in the number of lesions within the lining of the colon and their size was noticed. Recurrence of GI bleeding was not observed in the patients until one and half year.
Surgery may also be considered for treating this condition. Complete treatment for curing the PHC patient with GI bleeding is yet in research stage.
[Reference:Portal Hypertensive Colopathy]