By Jeyashree Sundaram (MBA)
Portal hypertensive gastropathy (PHG) is a topic of intense interest to clinicians and endoscopists. PHG refers to a wide range of distinct gastric lesions that appear in the gastric mucous membrane. These lesions may arise as a result of endoscopic variceal blockages, portal hypertension in the lower abdomen, or in patients with gastric cirrhosis.
There is no clear documented evidence about its pathology, natural history, and advanced treatment methods. It is referred to by some as a “clinically significant puzzle.”
VIDEO Primary Symptoms
Although generally asymptomatic, the only clinical manifestation of PHG is chronic or overt bleeding in the upper gastrointestinal tract. Research indicates that around one in seven PHG-affected patients have severe or long-term bleeding.
Chronic gastrointestinal loss of blood owing to ferropenic anemia is often an indication of PHG. The bleeding in portal hypertension patients is identified and confirmed by examination of the entire gastrointestinal region using colonoscopy, endoscopy, and small intestine evaluation.
More than 90% of severe bleeding occurs due to acute portal hypertensive gastropathy, whereas only 10% of severe bleeding is due to mild portal hypertensive gastropathy.
The rate of occurrence of chronic bleeding ranges from 3% to 26%.
If only decreased hemoglobin is used as a factor for diagnosis, then the chronic gastrointestinal bleeding may be overestimated. Generally, chronic patients of liver disease may have anemia and gastrointestinal bleeding formed due to chronic renal disease, alcoholism, and bone marrow extension or hypersplenism.
The above symptoms may occur as a result of many other related diseases; hence, consultation with the physician regarding the symptoms is essential, in order to identify the disease correctly and take steps to obtain a cure.
Stomach in watermelon shape — this is termed as gastric antral vascular ectasia or GAVE. This is a rare but important cause for severe or long-term gastrointestinal blood loss. Other Common Symptoms
Anemia: People with PHG, due to chronic blood loss, get anemia.
Ascites: The greater pressure in the portal vessels may result in serous fluid (pale yellow liquid) to leak from the liver and the intestine and collect in the region of the stomach, leading to ascites.
Blood vomiting: Vomiting of blood occurs due to sudden hemorrhage through varices.
Flatulence: The alimentary canal accumulates gas, leading to flatulence.
Upper abdomen pain: The pain can be for long or short periods.
Presence of blood in stools
Vomiting and nausea
Constipation Endoscopic Signs of PHG
The endoscopic appearance of PHG manifests as pink lesions, bleeding papules, fine speckling, multiple bleeding spots, reddened areas, cherry red spots, snakelike skin, and scarlet fever-like rashes. These signs appear in different forms in mild, moderate, and severe PHG. The severe stage presents with widely spread hemorrhagic spots. PHG is considered to be severe when there is a mosaic pattern in the mucosa background, with red spots on it. Lesions having a snake-skin pattern range from 93–100 of the symptoms of PHG.
Although the natural evolution of PHG is still not very clear, it is commonly discerned that these lesions may be progressive or regressive, i.e., they vary over time from increasing or decreasing, or sometimes even disappearing altogether.
Dilatation of capillaries
A specific marker and histology of PHG is a distinct expansion of the capillaries and venules that collect blood in the gastric mucosal region. The veins in the submucosa become thickened and appear dilated and irregular. In studies of morphology, patients of PHG have shown a greater average area of capillary cross section than those without PHG. These alterations may be present without any visible inflammation or erosion of the gastric mucosa.
Microvascular studies on animals as well as humans have found the presence of a great many arteriovenous shunts in the gastric mucosa of cirrhotics.
Increase in mucosal vessels
Investigations have revealed that patients of portal hypertension have an increased number and size of mucosal blood vessels. Studies also show that disorder in the shear rate mechanism for microcirculation is a sign of severe PHG.
Elevated portal vein pressure found in cirrhotic patients has a major role to play in the development of PHG. The severity of liver dysfunction is strongly correlated to the severity of PHG. Other humoral signs of a possibility of PHG include increased levels of the vasodilators norepinephrine, glucogen, gastrin, and vasoactive intestinal peptide.
The gastric blood flow is found to be increased in patients of PHG; conversely, there are other studies that affirm that the mucosal perfusion is decreased. This discrepancy of facts may be due to the specific endoscopic tool used and the accurate analysis of the signals emitted.
Bleeding in PHG patients is not the only risk factor for survival; other causes like cirrhosis also play an important part. However, severe recurring bleeding episodes may lead to serious liver damage.