Esophageal varices (sometimes spelled oesophageal varices) are extremely dilated sub-mucosal veins in the lower third of the esophagus. They are most often a consequence of portal hypertension, commonly due to cirrhosis; patients with esophageal varices have a strong tendency to develop bleeding. Esophageal varices are typically diagnosed through an esophagogastroduodenoscopy.

Gastric varices can present in two major ways. First, patients with cirrhosis may be enrolled in screening gastroscopy programs to detect esophageal varices. These evaluations may detect gastric varices that are asymptomatic. When gastric varices are symptomatic, however, they usually present acutely and dramatically with upper gastrointestinal bleeding. The symptoms can include vomiting blood, melena (passing black, tarry stools); or passing maroon stools or frank blood in the stools. Many people with bleeding gastric varices present in shock due to the profound loss of blood.

Secondly, patients with acute pancreatitis may present with gastric varices as a complication of a blood clot in the splenic vein. The splenic vein sits over the pancreas anatomically and inflammation or cancers of the pancreas may result in a blot clot forming in the splenic vein. As the short gastric veins of the fundus of the stomach drain into the splenic vein, thrombosis of the splenic vein will result in increased pressure and engorgement of the short veins, leading to varices in the fundus of the stomach.

Laboratory testing usually shows low red blood cell count and often a low platelet count. If cirrhosis is present, there may be coagulopathy manifested by a prolonged INR; both of these may worsen the bleeding from gastric varices.

In very rare cases, gastric varices are caused by splenic vein occlusion as a result of the mass effect of slow-growing pancreatic neuroendocrine tumors.

Most patients with portal hypertensive gastropathy have either a stable or improving course in the appearance of the gastropathy on endoscopy. However, according to retrospective data, roughly one in seven patients with portal hypertensive gastropathy will develop bleeding (either acute or chronic) attributable to the gastropathy. Patients with chronic bleeding will usually come to the attention of the medical system because of anemia.

The diagnosis of portal hypertensive gastropathy is usually made on endoscopy. The usual appearance of portal hypertensive gastropathy on endoscopy is a mosaic-like or reticular pattern in the mucosa. Red spots may or may not be present. The pattern is usually seen throughout the stomach. A similar pattern can be seen with a related condition called gastric antral vascular ectasia (GAVE), or watermelon stomach. However, in GAVE, the ectatic blood vessels are more commonly found in the antrum or lower part of the stomach.

Gastric varices are dilated submucosal veins in the stomach, which can be a life-threatening cause of bleeding in the upper gastrointestinal tract. They are most commonly found in patients with portal hypertension, or elevated pressure in the portal vein system, which may be a complication of cirrhosis. Gastric varices may also be found in patients with thrombosis of the splenic vein, into which the short gastric veins which drain the fundus of the stomach flow. The latter may be a complication of acute pancreatitis, pancreatic cancer, or other abdominal tumours, as well as hepatitis C. Gastric varices and associated bleeding are a potential complication of schistosomiasis resulting from portal hypertension.

Patients with bleeding gastric varices can present with bloody vomiting (hematemesis), dark, tarry stools (melena), or rectal bleeding. The bleeding may be brisk, and patients may soon develop shock. Treatment of gastric varices can include injection of the varices with cyanoacrylate glue, or a radiological procedure to decrease the pressure in the portal vein, termed transjugular intrahepatic portosystemic shunt or TIPS. Treatment with intravenous octreotide is also useful to shunt blood flow away from the stomach's circulation. More aggressive treatment including splenectomy (or surgical removal of the spleen) or liver transplantation may be required in some cases.

Several studies have found that patients with portal hypertension develop increased blood flow to the stomach. The physiological findings that correlate with worsening portal hypertensive gastropathy include an increased portal venous pressure gradient and decreased hepatic blood flow. Biopsies of the stomach in patients with portal hypertensive gastropathy show ectatic (or dilated) blood vessels, evidence of bleeding by means of red blood cells in the lamina propria, and edema in the stomach wall.

Dilated submucosal veins are the most prominent histologic feature of esophageal varices. The expansion of the submucosa leads to elevation of the mucosa above the surrounding tissue, which is apparent during endoscopy and is a key diagnostic feature. Evidence of recent variceal hemorrhage includes necrosis and ulceration of the mucosa. Evidence of past variceal hemorrhage includes inflammation and venous thrombosis.

Signs and symptoms of portal hypertension include:

In addition, a widened portal vein as seen on a CT scan or MRI may raise the suspicion about portal hypertension. A cutoff of 13 mm is widely used in this regard, but the diameter is often larger than this is in normal individuals as well.

Portal hypertension is hypertension (high blood pressure) in the hepatic portal system – made up of the portal vein and its branches, that drain from most of the intestines to the liver. Portal hypertension is defined as a hepatic venous pressure gradient. Cirrhosis (a form of chronic liver failure) is the most common cause of portal hypertension; other, less frequent causes are therefore grouped as non-cirrhotic portal hypertension. When it becomes severe enough to cause symptoms or complications, treatment may be given to decrease portal hypertension itself or to manage its complications.

Hemosuccus pancreaticus is a rare entity, and estimates of its rate are based on small case series. It is the least frequent cause of upper gastrointestinal bleeding (1/1500) and is most often caused by chronic pancreatitis, pancreatic pseudocysts, or pancreatic tumors. As a result, the diagnosis may easily be overlooked. The usual presentation of hemosuccus is the development of symptoms of upper or lower gastrointestinal bleeding, such as melena (or dark, black tarry stools), maroon stools, or hematochezia, which is frank rectal bleeding. The source of hemorrhage is usually not determined by standard endoscopic techniques, and the symptoms of the condition are usually grouped as a cause of obscure overt gastrointestinal hemorrhage. Over one-half of patients with hemosuccus also develop abdominal pain, usually located in the epigastrium, or uppermost part of the abdomen. The pain is described as being "crescendo-decrescendo" in nature, meaning that it increases and decreases in intensity slowly with time. This is thought to be due to transient blockage of the pancreatic duct from the source of bleeding, or from clots. If the source of the bleeding also involves obstruction of the common bile duct (such as with some tumours of the head of the pancreas), the patient may develop jaundice, or "silver stools", an uncommon finding of acholic stools mixed with blood.

Cameron lesions are usually found in older adults with anemia symptoms such as fatigue, shortness of breath, and appearing pale. Blood tests in iron deficiency show low hemoglobin, microcytic hypochromic red cells, and low iron-binding saturation and ferritin levels. The lesions are visualized by esophagogastroduodenoscopy. Sometimes the lesions are found when endoscopy is done for other hernia symptoms than anemia such as heartburn, regurgitation, swallowing difficulty, pain or distention. When a person with iron deficiency anemia is found to have a large hernia and Cameron lesions on endoscopy, this usually explains the blood loss. A lower gastrointestinal bleeding site such as colon cancer may be excluded by colonscopy. and other tests as clinically indicated.

Radiation proctitis can occur at two times after treatment:

- "Acute radiation proctitis" — symptoms occur in the first few weeks after therapy. These symptoms include diarrhea and the urgent need to defecate, often with pain while doing so (tenesmus). Acute radiation proctitis usually resolves without treatment after several months, but symptoms may improve with butyrate enemas. This acute phase is due to direct damage of the lining (epithelium) of the colon.

- "Chronic radiation proctitis" — is a widely used term, but is not correct as in long term after radiotherapy, inflammation in the bowel is minimal and instead the term chronic radiation proctopathy — or better, Pelvic Radiation Disease — should be used. In the chronic setting the pathological changes are characterised by ischaemia and fibrosis. Symptoms may begin as early as several months after therapy but occasionally not until several years later. These symptoms include diarrhea, rectal bleeding, painful defecation, incontinence, excess flatulence and intestinal blockage. Intestinal blockage is a result of narrowing of the bowel which blocks the flow of feces. Connections (fistulae) may also develop between the colon and other parts of the body such as the skin or urinary system. Chronic radiation proctopathy occurs in part because of damage to the blood vessels which supply the colon. The colon is therefore deprived of oxygen and necessary nutrients.

The ulcerations may be superficial and confined to the mucosa, in which case they are more appropriately called erosions, or they may penetrate deeper into the submucosa. The former may cause diffuse mucosal oozing of blood, whereas the latter may erode into a submucosal vessel and produce frank hemorrhage.

The diagnosis of hemosuccus pancreaticus can be difficult to make. Most patients who develop bleeding in the gastrointestinal tract have endoscopic procedures done to visualize the bowel in order to find and treat the source of the bleeding. With hemosuccus, the bleeding is coming from the pancreatic duct which enters into the first part of the small intestine, termed the duodenum. Typical gastroscopes used to visualize the esophagus, stomach and duodenum are designed with fiber-optic illumination that is directed in the same direction as the endoscope, meaning that visualization is in the forward direction. However, the pancreatic duct orifice is located on the side of the duodenum, meaning that it can be missed on forward-viewing endoscopy. A side-viewing endoscope (known as a "duodenoscope", or "side-viewer") used for endoscopic retrograde cholangiopancreatography (ERCP), a procedure to visualize the bile ducts and pancreatic duct on fluoroscopy, can be used to localize the bleeding to the pancreatic duct. It can be confused with bleeding from the common bile duct on endoscopy, leading to the term "pseudohematobilia".

Liver function test is normal apart from an increased serum bilirubin in the event of pancreaticobiliary reflux. Serum amylase is normal outside episodes of acute pancreatitis. It is difficult to diagnose HP because the bleeding is usually intermittent. Endoscopy is essential in ruling out other causes of upper gastrointestinal bleeding and in rare cases; active bleeding can be seen from the duodenal ampulla. Even though endoscopy may be normal, it helps to rule out other causes of upper digestive bleeding (erosive gastritis, peptic ulcers, and oesophageal and gastric fundus varices, etc.). Ultrasonography can be used to visualize pancreatic pseudocysts or aneurysm of the peripancreatic arteries. Doppler ultrasound or dynamic ultrasound has been reported to be diagnostic. Contrast-enhanced CT is an excellent modality for demonstrating the pancreatic pathology and can also demonstrate features of chronic pancreatitis, pseudocysts, and pseudoaneurysms. On precontrast CT, the characteristic finding of clotted blood in the pancreatic duct, known as the sentinel clot, is seldom seen. Computed tomography may show simultaneous opacification of an aneurysmal artery and pseudocyst or persistence of contrast within a pseudocyst after the arterial phase. Again, these findings are only suggestive of the diagnosis. Ultimately, angiography is the diagnostic reference standard. Angiography identifies the causative artery and allows for delineation of the arterial anatomy and therapeutic intervention.

It is characterized by 'obliterative portovenopathy', which leads to various problems such as portal hypertension, massive splenomegaly, and variceal bleeding. It is estimated that about 85% of people with NCPF have repeated episodes of variceal bleeding.

A stress ulcer is a single or multiple mucosal defect which can become complicated by upper gastrointestinal bleeding during the physiologic stress of serious illness. Ordinary peptic ulcers are found commonly in the gastric antrum and the duodenum whereas stress ulcers are found commonly in fundic mucosa and can be located anywhere within the stomach and proximal duodenum.

Coagulopathy may cause uncontrolled internal or external bleeding. Left untreated, uncontrolled bleeding may cause damage to joints, muscles, or internal organs and may be life-threatening. People should seek immediate medical care for serious symptoms, including heavy external bleeding, blood in the urine or stool, double vision, severe head or neck pain, repeated vomiting, difficulty walking, convulsions, or seizures. They should seek prompt medical care if they experience mild but unstoppable external bleeding or joint swelling and stiffness.

Hallmark of the disease is thrombosis/sclerosis of branches of portal vein. Vessels formed are often termed as mesangiosinusoids or periportal cavernoma.

AEN has never been recorded as a one symptom disorder, but instead present by multiple symptoms. The symptoms vary from the severity of the disorder. The most classic sign of AEN is the dark pigmentation of esophageal mucosa in an upper endoscopy, usually viewed as an ulcer or as an infectious disease. Necrosis can be found mostly between the three distals of the esophagus, but stops abruptly at the gastroesophageal junction. The basic and most common symptoms reported are blood in stool and blood in vomiting. Upper gastrointestinal bleeding then is reported, and is very commonly represented in elderly patients. Black or bloody stools and hematemesis account for over three quarters of the case presentations. Abdominal pain, nausea, vomiting, and unstable vital signs are common. A cardiovascular event (such as a heart attack) was reported in ten percent of the total known cases.

Radiation proctitis (and the related radiation colitis) is inflammation and damage to the lower parts of the colon after exposure to x-rays or other ionizing radiation as a part of radiation therapy. Radiation proctitis most commonly occurs after treatment for cancers such as cervical cancer, prostate cancer, and colon cancer. Radiation proctitis involves the lower intestine, primarily the sigmoid colon and the rectum and is part of the conditions known as pelvic radiation disease and radiation enteropathy.

Diverticular disease can present with painless rectal bleeding as bright red blood per rectum. Diverticular bleeding is the most common cause of acute lower gastrointestinal bleeding. However, it is estimated that 80% of these cases are self-limiting and require no specific therapy.

Based on their surgical observations, Windsor and Collis in 1967 proposed that blood loss was due to local trauma to the stomach where it rides to and fro in the hiatus on respiration. Boutelier et al. noted on gastroscopy ulcers and erosions at the level of the neck of the hernia in individuals with acute and chronic bleeding, but no detailed description was given. Cameron and Higgins in 1986 described linear gastric erosions, later called "Cameron lesions", in people with x-rays showing one-third or more of the stomach above the diaphragm. (figure 1). Over 6 years, Cameron and Higgins studied 109 persons with large hiatal hernias, 55 with anemia and 54 without anemia, at esophagogastroduodenoscopy. Cameron lesions, often multiple, were found at or near the level where the herniated stomach was constricted by the diaphragm. The lesions were typically white, superficial, linear, and oriented along the crests of inflamed appearing mucosal folds (figure 2). Small amounts of blood were often seen on the lesions (Fig 3). Mucosal folds at the diaphragm level were often seen rubbing against each other on respiration (Fig 4). It was proposed that the lesions were caused by mechanical trauma at the level of constriction by the diaphragm Cameron lesions were found in 42% of persons with anemia compared to 24% in those without anemia, a statistically significant difference, p<0.05. Spots of fresh or clotted blood were seen on the lesions in 25% of persons with anemia compared to 7% without anemia, also a significant difference, p<0.05. In the 109 persons in this study, 15 had reflux esophagitis, 11 had peptic ulcers, and 7 had Barrett's esophagus, but none of these findings correlated with anemia. Thus, in people with large hernias, Cameron lesions with evidence of slow bleeding were associated with iron deficiency anemia.

Acute bleeding from Cameron lesions, vomiting blood, or passing black bowel movements, is rare; in one report Cameron lesions were found in 3.8% of people presenting with anemia, but in only 0.2% of those with acute bleeding. Small hernias with 2–5 cm of stomach above the diaphragm are commoner than large hernias but Cameron lesions are usually found with large hernias.

Anemia in patients with large hernias was corrected by surgical repair in the majority of instances, but Cameron lesions were found in only about half of these individuals. One explanation is that endoscopists unfamiliar with their appearance can miss the lesions However, in the original description of Cameron lesions they were found in less than half the patients despite careful search, and no other causes of gastrointestinal bleeding. were seen. It is probable that these superficial lesions can heal and recur, with the bleeding stopping temporarily

About 20% of patients with acute ischemic colitis may develop a long-term complication known as "chronic ischemic colitis". Symptoms can include recurrent infections, bloody diarrhea, weight loss, and chronic abdominal pain. Chronic ischemic colitis is often treated with surgical removal of the chronically diseased portion of the bowel.

A "colonic stricture" is a band of scar tissue which forms as a result of the ischemic injury and narrows the lumen of the colon. Strictures are often treated observantly; they may heal spontaneously over 12–24 months. If a bowel obstruction develops as a result of the stricture, surgical resection is the usual treatment, although endoscopic dilatation and stenting have also been employed.

Some people with diverticulosis complain of symptoms such as cramping, bloating, flatulence, and irregular defecation. However, it is unclear if these symptoms are attributable to the underlying diverticulosis or to coexistent irritable bowel syndrome.

Diverticular disease was found associated with a higher risk of left sided colon cancer.

Acute esophageal necrosis can only be diagnosed by an upper gastrointestinal endoscopy.

Most patients with ischemic colitis recover fully, although the prognosis depends on the severity of the ischemia. Patients with pre-existing peripheral vascular disease or ischemia of the ascending (right) colon may be at increased risk for complications or death.

Non-gangrenous ischemic colitis, which comprises the vast majority of cases, is associated with a mortality rate of approximately 6%. However, the minority of patients who develop gangrene as a result of colonic ischemia have a mortality rate of 50-75% with surgical treatment; the mortality rate is almost 100% without surgical intervention.