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UPPER GASTROINTESTINAL BLEEDING

ANATOMY OF UPPER GASTROINTESTINAL TRACT

The gastrointestinal tract extends from mouth to anus


On embryologic grounds, the GI tract should be divided into
upper (mouth to major papilla in the duodenum), middle (papilla to mid-transverse colon), and lower (mid-transverse colon to anus)

Derivation of these 3 areas from the foregut, midgut, and hindgut, respectively.

From the point of view of GI bleeding, however, the demarcation between the upper and lower GI tract is the duodenojejunal (DJ) junction/ligamentum treitz
Bleeding above the DJ junction is called upper GI bleeding, and that below the DJ junction is called lower GI bleeding.

Consist ofskeletal muscle from the diaphragm and a fibromuscular band of smooth muscle which inserts into the 3rd and 4th part of duodenum and frequently the DJ junction
Contraction widens the angle of the duodenojejunal flexure, allowing movement of the intestinal contents.

Causes and pathophysiology of Upper GI Bleeding

Peptic ulcer ( due to NSAIDs, H.Pylori) Gastric erosions ( due to NSAIDs, alcohol) Oesophagitis ( usually with hiatus hernia) Vascular malformations Mallory-Weiss tear Varices (Eg. Liver disease, portal vein thrombosis) Cancer of stomach or esophagus Aorto-duodenal fistula (after an aortic graft)

Causes

Peptic Ulcer

gastric erosion
refers to endoscopically visualized subepithelial hemorrhages and erosions due to NSAID,stress and alcohol. not much bleeding. causes ulceration.

Mallory-Weiss Tear
Due to longitudinal mucosal lacerations (known as Mallory-Weiss tears) at the gastroesophageal junction or gastric cardia. The original description by Mallory and Weiss in 1929 involved patients with persistent retching and vomiting following an alcoholic binge. However, Mallory-Weiss syndrome may occur after any event that provokes a sudden rise in intragastric pressure or gastric prolapse into the esophagus. May also occur in epileptic convulsions.

Varices
Bleeding esophageal varices are enlarged veins in the walls of the lower part of the esophagus. Scarring ( cirrhosis) of the liver is the most common cause of esophageal varices. This scarring reduces blood flowing through the liver. As a result, more blood is shunted to the veins of the esophagus. This extra blood flow causes the veins in the esophagus to balloon outward. If these veins break open, they can bleed severely. Any type of chronic liver disease can cause esophageal varices. Varices can also occur in the upper part of the stomach.

Clinical Features of upper gastrointestinal bleeding

Patients with upper GI hemorrhage often present with: A. hematemesis (vomiting of blood), B. coffee ground vomiting, C. melena (dark tarry stools), D. hematochezia (blood in the feces) if the hemorrhage is severe. E. dyspepsia (especially nocturnal symptoms)

Patients may also present with complications of anemia, including: a. chest pain, b. syncope (loss of consciousness resulting from insufficient blood flow to the brain), c. fatigue d. shortness of breath.

The finding of subcutaneous emphysema with a history of vomiting is suggestive of Boerhaave syndrome (esophageal perforation) The presence of postural hypotension indicates more rapid and severe blood loss.

Probable Source of GI Bleeding Within the Gut


Clinical Indicator Hematemesis Melena Hematochezia Blood-streaked stool Occult blood in stool

Probability of Upper GI Source


Almost certain Probable Possible Rare Possible

Probability of Lower GI Source


Rare Possible Probable Almost certain Possible

Investigations of upper gastrointestinal bleeding

Investigations in Upper GI Bleeding 1. Urgent endoscopy (<12 h) for all patients requiring ICU admission for GI bleeds) and diagnostic biopsy. 2. Complete blood count useful for comparison of serial values. Initial Haemoglobin concentration maybe normal if taken early, before heamodilution has taken place. 3. Liver function test may show evidence fo chronic liver failure 4. Renal function test urea maybe raised out of proportion to creatinine (indicates severe bleeding) 5. Serial ECGs and cardiac enzymes to exclude myocardial infarction (cmplicates 10% of severe GI bleeds) 6. Nasogastric tube insertion localize bleeding to upper GI tract, quantify ongoing blood loss , clearing blood from stomach to facilitate endoscopy.

1. Plain radiographs of abdomen - free air under the diaphragm is seen in cases of perforated viscous, and this may be accompanied by UGIB. Other etiologies, such as upper GI masses (which usually result in chronic, not acute, UGIB), aneurysms with calcifications, and ascites suggestive of portal hypertension, may be seen on radiographs. 2. Blood alcohol concentration 3. Blood glucose concentration 4. CVP monitoring, blood replacement and bladder catheterisation (for those with severe bleeding) 5. Coagulation screen

Other laboratory tests facilitate the diagnosis of GI disease.


Iron-deficiency anemia suggests mucosal blood loss. Change in lab values in iron deficiency anemia Decrease : ferritin, hemoglobin, MCV Increase : TIBC, transferrin, RDW Leukocytosis (wcc increase) and increased sedimentation rates are found in inflammatory , leukopenia ( wcc decrease) is seen in viremic illness. Pancreaticobiliary or liver disease is suggested by elevated pancreatic or liver chemistries.

Thyroid chemistries, cortisol, and calcium levels are obtained to exclude endocrinologic causes of GI symptoms. Pregnancy testing is considered for young women with unexplained nausea. Serologies tests are available to screen for celiac disease, IBD, and rheumatologic diseases such as lupus or scleroderma. Hormone levels are obtained for suspected endocrine neoplasia. Intraabdominal malignancies produce tumor markers including the carcinoembryonic antigen CA 19-9 and -fetoprotein

Endoscopy The gut is accessible with endoscopy which can provide the diagnosis of the causes of bleeding, pain, nausea and vomiting, weight loss, altered bowel function, and fever. Upper endoscopy evaluates the esophagus, stomach, and duodenum, Upper endoscopy is advocated as the initial structural test performed in patients with suspected ulcer disease, esophagitis, neoplasm, malabsorption, and Barrett's metaplasia because of its ability to directly visualize as well as biopsy the abnormality. In cases of UGIB, this should be carried out after adequate resuscitation, ideally within 24 hours, and will yield a diagnosis in 80% of cases.

MANAGEMENT

Resuscitation and initial management

Shocked patients should receive prompt volume replacement. It has been demonstrated that early and aggressive resuscitation reduces mortality in UGIB. Correct fluid losses. Either colloid or crystalloid solutions may be used to achieve volume restoration prior to administering blood products; red cell transfusion should be considered after loss of 30% of the circulating volume. Transfuse patients with massive bleeding with blood, platelets and clotting factors in line with local protocols for managing massive bleeding. Platelet transfusions should not be offered to patients who are not actively bleeding and are haemodynamically stable. Platelet transfusions should be offered to patients who are actively bleeding and have a platelet count of less than 50 x 109/litre. Fresh frozen plasma should be used for patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (INR) or activated partial thromboplastin time greater than 1.5 times normal. Prothrombin complex concentrate should be used for patients who are taking warfarin and actively bleeding. Proton pump inhibitors (PPIs) should not be used prior to diagnosis by endoscopy in patients presenting with acute UGIB.

Management of non-variceal bleeding


Endoscopy is now the method of choice for controlling active peptic-ulcer related UGIB. Endoscopic therapy should only be delivered to actively bleeding lesions, non-bleeding visible vessels and, when technically possible, to ulcers with an adherent blood clot. Clean ulcer base with oozing do not merit endoscopic intervention since these lesions have an excellent prognosis without intervention. Adrenaline (epinephrine) should not be used as monotherapy for the endoscopic treatment of non-variceal UGIB. For the endoscopic treatment of non-variceal UGIB, one of the following should be used: A mechanical method (eg clips) with or without adrenaline (epinephrine). Thermal coagulation with adrenaline (epinephrine). Fibrin or thrombin with adrenaline (epinephrine). Interventional radiology should be offered to unstable patients who re-bleed after endoscopic treatment. Refer urgently for surgery if interventional radiology is not immediately available. Acid-suppression drugs (PPIs or H2-receptor antagonists) should not be offered before endoscopy to patients with suspected non-variceal UGIB. PPIs should be offered to patients with non-variceal UGIB and stigmata of recent haemorrhage shown at endoscopy.

Treatment after first or failed endoscopic treatment

Repeat endoscopy, with treatment as appropriate, should be considered for all patients at high risk of re-bleeding, particularly if there is doubt about adequate haemostasis at the first endoscopy. A repeat endoscopy should be offered to patients who re-bleed with a view to further endoscopic treatment or emergency surgery. Interventional radiology should be used for unstable patients who re-bleed after endoscopic treatment. Percutaneous angiography may be used to localise the bleeding point and embolisation of the artery using foam and coils to stop bleeding. The benefits of embolisation have to be balanced against the risk of causing ischaemic necrosis of the gastrointestinal tract. Refer urgently for surgery if interventional radiology is not immediately available.

Management of variceal bleeding

Terlipressin should be offered to patients with suspected variceal bleeding at presentation. Treatment should be stopped after definitive haemostasis has been achieved, or after five days, unless there is another indication for its use. Prophylactic antibiotic therapy should be offered at presentation to patients with suspected or confirmed variceal bleeding. Balloon tamponade should be considered as a temporary salvage treatment for uncontrolled variceal haemorrhage. Oesophageal varices:
Band ligation should be used for patients with UGIB from oesophageal varices. there is sufficient evidence to show that stent insertion is effective for selected patients with oesophageal varices in whom other methods of treatment have failed to control bleeding. Transjugular intrahepatic portosystemic shunts (TIPS) should be considered if bleeding from oesophageal varices is not controlled by band ligation.

Gastric varices:
Endoscopic injection of N-butyl-2-cyanoacrylate should be offered to patients with UGIB from gastric varices. TIPS should be offered if bleeding from gastric varices is not controlled by endoscopic injection of N-butyl-2-cyanoacrylate.

Surgical intervention Surgical intervention is required when endoscopic techniques fail or are contra-indicated. Clinical judgement is required and consideration given to local expertise. In general, it is recommended:
To inform surgeons early of the possibility of surgery. To use the most experienced personnel available. To avoid operations in the middle of the night.

The particular procedure required depends on a number of factors, not least the site of bleeding. Gastric ulcers are probably best excised. There are few studies comparing the different techniques.

Medical management post-endoscopy Helicobacter pylori eradication


All patients with a bleeding peptic ulcer should be tested for H. pylori, eg urea breath test or biopsy specimen. Patients who test positive should receive a one-week course of eradication therapy. This should be followed by three further weeks with ulcer healing treatment. All therapy can be discontinued after successful healing of peptic ulcers provided patients are not taking NSAIDs. A negative urea breath test should be confirmed on the initial biopsy specimen taken prior to diagnosis and before any PPI therapy was given. Two weeks after successful therapy and stopping of all medication, a repeat urea breath test should be performed to confirm successful eradication. Unsuccessful eradication should be treated with second-line therapy.