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  2. 2. 1) INTRODUCTION:Acute gastroduodenal bleeding is a potentially life-threatening abdominal emergencythat remains a common cause of hospitalization. Upper gastrointestinal bleeding (UGIB)is defined as bleeding derived from a source proximal to the ligament of Treitz.The incidence of UGIB is approximately 100 cases per 100,000 population peryear.[1] Bleeding from the upper GI tract is approximately 4 times as common asbleeding from the lower GI tract and is a major cause of morbidity and mortality.Mortality rates from UGIB are 6-10% overall.[1] (See Epidemiology, below.)The diagnosis of and therapy for nonvariceal upper gastrointestinal bleeding (UGIB) hasevolved since the late 20th century from passive diagnosticIn patients with UGIB, comorbid illness, rather than actual bleeding, is the major causeof death. Comorbid illness has been noted in 50.9% of patients, with similaroccurrences in males (48.7%) and females (55.4%).One or more comorbid illnesses have been noted in 98.3% of mortalities in UGIB; in72.3% of patients, comorbid illnesses have been noted as the primary cause of death.[3,4] (See Epidemiology and Prognosis, below.)Significant comorbidities have become more prevalent as the patient population withUGIB has become progressively older. In a retrospective chart review by Yavorski et al,73.2% of deaths occurred in patients older than 60 years.[4] (See Epidemiology andPrognosis, below.)Rebleeding or continued bleeding is associated with increased mortality; therefore,differentiating the patient with a low probability of rebleeding and little comorbidity fromthe patient at high risk for rebleeding with serious comorbidities is imperative. (SeeClinical Presentation and Workup, below.)Annually, approximately 100,000 patients are admitted to US hospitals for therapy forUGIB.UGIB is a common occurrence throughout the world. In France, a report concludes thatthe mortality from UGIB has decreased from about 11% to 7%; however, a similar report
  3. 3. from Greece finds no decrease in mortality. In a nationwide study from Spain, UGIB was6 times more common than lower GI bleeding.[18]The incidence of UGIB is 2-fold greater in males than in females, in all age groups;however, the death rate is similar in both sexes.[4]The population with UGIB has become progressively older, with a concurrent increasein significant comorbidities that increase mortality. Mortality increases with older age(>60 y) in males and femalesAnatomy of the stomach
  4. 4. The stomach lies between the esophagus and the duodenum (the first part of the smallintestine). It is on the left upper part of the abdominal cavity. The top of the stomach liesagainst the diaphragm. Lying behind the stomach is the pancreas. The greateromentum hangs down from the greater curvatureThe stomach is surrounded by parasympathetic (stimulant) and orthosympathetic(inhibitor) plexuses (networks of blood vessels and nerves inthe anterior gastric, posterior, superior and inferior, celiac and myenteric), whichregulate both the secretions activity and the motor (motion) activity of its muscles.Inadult humans, the stomach has a relaxed, near empty volume of about 45 ml. Becauseit is a distensible organ, it normally expands to hold about one litre of food,[4] but canhold as much as two to three litres. The stomach of a newborn human baby will only beable to retain about 30 ml.Sections:The stomach is divided into four sections, each of which has different cellsand functions. The sections are:Cardia Where the contents of the oesophagus empty into the stomach.Fundus Formed by the upper curvature of the organ.Body or The main, central region.Corpus The lower section of the organ that facilitates emptying the contents intoPylorus the small intestine.Blood supply
  5. 5. Schematic image of the blood supply to the stomach: left and right gastricartery, left and right gastro-omental artery and short gastric artery.[5] Picture 1:A more realistic image, showing the celiac artery and its branches; the liver has beenraised, and the lesser omentum and anterior layer of the greater omentum removed.The lesser curvature of the stomach is supplied by the right gastric artery inferiorly, andthe left gastric artery superiorly, which also supplies the cardiac region. The greatercurvature is supplied by the right gastroepiploic artery inferiorly and the leftgastroepiploic artery superiorly. The fundus of the stomach, and also the upper portionof the greater curvature, is supplied by the short gastric artery which arises from splenicartery.Like the other parts of the gastrointestinal tract, the stomach walls are made of thefollowing layers, from inside to outside:
  6. 6. The first main layer. This consists of the epithelium and the lamina propria (composed of loose connective tissue), with a thin layermucosa ofsmooth muscle called the muscularis mucosae separating it from the submucosa beneath. This layer lies over the mucosa and consists of fibrous connectivesubmucosa tissue, separating the mucosa from the next layer. The Meissners plexus is in this layer (AKA submucosal plexus). Over the submucosa, the muscularisexterna in the stomach differs from that of other GI organs in that it has three layers of smooth muscle instead of two.  inner oblique layer: This layer is responsible for creating the motion that churns and physically breaks down the food. It is the only layer of the three which is not seen in other parts of the digestive system. The antrum has thicker skin cells in its walls and performs more forceful contractions than the fundus.  middle circular layer: At this layer, the pylorus is surrounded by amuscularisexterna thick circular muscular wall which is normally tonically constricted forming a functional (if not anatomically discrete) pyloric sphincter, which controls the movement of chyme into the duodenum. This layer is concentric to the longitudinal axis of the stomach.  Auerbachs plexus (AKA myenteric plexus) is found between the outer longitundinal and the middle circular layer and is responsible for the innervation of both (causing peristalsis and mixing)  outer longitudinal layer
  7. 7. This layer is over the muscularisexterna, consisting of layers ofserosa connective tissue continuous with the peritoneum.Ref :*^ Sherwood, Lauralee (1997). Human physiology: from cells to systems. Belmont, CA:worth Pub. Co. ISBN 0-314-09245-5. OCLC 35270048.*^ Anne M. R. Agur; Moore, Keith L. (2007). Essential Clinical Anatomy (Point(Lippincott Williams & Wilkins)). Hagerstown, MD: Lippincott Williams & Wilkins. ISBN 0-7817-6274-X.OCLC 172964542.; p. 150
  8. 8. Anatomy of duodenum :The duodenum is the first section of the small intestine.The duodenum precedes thejejunum and ileum and is the shortest part of the small intestine, where most chemicaldigestion takes place.the duodenum is a hollow jointed tube about 10–15 inches (25–38centimetres) long connecting the stomach to the jejunum. It begins with the duodenalbulb and ends at the ligament of Treitz.SectionsThe duodenum is divided into four sections for the purposes of description. The firstthree sections curve in a "C"-loop concavity in which the head of the pancreas lies. Onlythe first 2 cm of the superior part is mobile (covered by peritoneum) – the distal 3 cm ofthe first part along with the rest of the duodenum is retroperitoneal (immobile).First partThe first (superior) part begins as a continuation of the duodenal end of the pylorus.From here it passes laterally (right), superiorly and posteriorly, for approximately 5 cm,before making a sharp curve inferiorly into the superior duodenal flexure (the end of thesuperior part). It is the only intraperitoneal portion of the duodenum[8]. Relations: Anterior  Gallbladder  Quadrate lobe of liver Posterior  Bile duct  Gastroduodenal artery  Portal vein
  9. 9.  Inferior vena cava Superior  Neck of gallbladder  Hepatoduodenal ligament (lesser omentum) Inferior  Neck of pancreas  Greater omentumSecond partThe second (descending) part of the duodenum begins at the superior duodenal flexure.It passes inferiorly to the lower border of vertebral body L3, before making a sharp turnmedially into the inferior duodenal flexure (the end of the descending part).The pancreatic duct and common bile duct enter the descending duodenum, commonlyknown together as the hepatopancreatic duct (or pancreatic duct in the United States),through themajor duodenal papilla (known as Ampulla of Vater). This part of theduodenum also contains the minor duodenal papilla, the entrance for the accessorypancreatic duct(of Santorini). The junction between theembryological foregut and midgut lies just below the major duodenal papilla.Third partThe third (inferior/horizontal) part of the duodenum begins at the inferior duodenalflexure and passes transversely to the left, crossing the left ureter, left testicular/ovarianvessels, inferior vena cava, abdominal aorta, superior mesenteric artery andthe vertebral column.Fourth partThe fourth (ascending) part passes superiorly, either anterior to, or to the left of, theaorta, until it reaches the inferior border of the body of the pancreas. Then, it curvesanteriorly and terminates at the duodenojejunal flexure where it joins the jejunum. Theduodenojejunal flexure is surrounded by a peritoneal fold containing muscle fibres:the ligament of Treitz.Blood supply
  10. 10. The duodenum receives arterial blood from two different sources. The transitionbetween these sources is important as it demarcates the foregut from the midgut.Proximal to the 2nd part of the duodenum (approximately at the major duodenal papilla– where the bile duct enters) the arterial supply is from the gastroduodenal artery and itsbranch the superior pancreaticoduodenal artery. Distal to this point (the midgut) thearterial supply is from the superior mesenteric artery (SMA), and its branch the inferiorpancreaticoduodenal artery supplies the 3rd and 4th sections. The superior and inferiorpancreaticoduodenal arteries (from the gastroduodenal artery and SMA respectively)form an anastomotic loop between the celiac trunk and the SMA; so there is potentialfor collateral circulation here.The venous drainage of the duodenum follows the arteries. Ultimately these veins draininto the portal system, either directly or indirectly through the splenic or superiormesenteric vein.Ref :*http://bedahunmuh.wordpress.com/algoritma-bedah/*van Gijn J, Gijselhart JP (2011). "Treitz and his ligament.". NedTijdschrGeneeskd. 155 (8). PMID 21557825.
  11. 11. * http://books.google.com.pe/books?id=ZR0RKtr7YBoC&pg=PA187&lpg=PA1 87&dq=duodenum+retroperitoneal+portions+anatomy&source=bl&ots=VkFzZ 4K6_G&sig=AlvypvJPNyT_DJHi6wccaYcro8c&hl=en&sa=X&ei=mWwDUIKK K- qm6gHWpd3_Bg&ved=0CEsQ6AEwBA#v=onepage&q=duodenum%20retrop eritoneal%20portions%20anatomy&f=falseEtiology of gastroduodenalbleding : 1) Ulcer-related UGIBPeptic ulcer is the most common cause of acute upper GI bleeding and accounts forapproximately 50% of all upper GI bleeding cases (69).There are approximately 150,000 hospitalizations per year in the United States for evaluationand treatment of bleeding ulcers. Although hospitalization and surgery for uncomplicatedulcers have decreased in the United States and Europe over the past three decades, thenumber of hospitalizations for hemorrhage associated with ulcers has remained unchanged
  12. 12. (70). Even though ulcer bleeding stops spontaneously in at least 80% of patients, the overallmortality is also unchanged over the last 30 years, ranging from 6 to 7% in the United States(70) and averaging14% in the United Kingdom (71).Without specific hemostatic intervention, peptic ulcer bleeding continues or recurs inapproximately20% of patients (72).Ulcer bleeding starts when the ulcer base erodes into a blood vessel. Spontaneous hemostasisoccurs when a sentinel clot (what is usually actually referred to as a “visible vessel”) plugs the“side hole” in the vessel.The clot may then enlarge, remain attached for some time as it organizes, and eventuallyslough off, leaving the underlying vessel covered with a flat pigmented spot that fades to leavea clean ulcer base (72). This process takes less than 72 hours, and rebleeding occurs if the clotundergoes lysis or falls off prematurely (72).The most common cause of peptic ulcer is H. pylori infection. Peptic ulcer can presentsilently with complications such as hemorrhage, particularly in patients on NSAIDs. PPIsare the mainstays of therapy and should be held prior to noninvasive diagnostic tests forH. pylori. Effective eradication of H. pylori involves regimens utilizing multiple antibiotics.COX-2 inhibitors have lower incidence of causing peptic ulcers. Upper endoscopyeffectively diagnoses peptic ulcers, reduces rebleeding, and allows for appropriatetriage of patients with upper GI bleeding complications.
  13. 13. 2) Tumors : A ) benign tumors: Most patients with benign stomach and duodenal tumors remain asymptomatic for long periods of time. When symptoms are present, these depend on the tumor size, location and complications arising from the tumor (eg: bleeding and ulceration). The most common presenting symptoms are bleeding (acute or chronic), abdominal pain and discomfort, nausea, weight loss, intestinal obstruction and as for periampullary tumors, such as adenomas in the papilla of Vater, recurrent pancreaticobiliary complications including jaundice, cholangitis, and pancreatitis may occur. Patients may be referred by another physician to the out-patient clinics with one of the above symptoms, or be admitted as an emergency due to massive upper gastrointestinal bleeding. Rarely, they may also present with intestinal obstruction Types:epithelial tumors of the stomachAccording to results published by Orlowska in 1995, the potential of these lesions becomingmalignant poses a much more worrying problem than the clinical symptomsthemselves. Orlowska found that 1.3% of Hyperplastic Polyps (HP) and 10% of Adenomas weremalignant. Her results support the belief that gastric HP, like adenomas, can become malignant,thus she concluded that it is sensible to differentiate a subgroup of Foveolar Hyperplasia (FH)from HP, since FH will not become malignant unless their histology changes to that of HP. Theview that FH and HP belong to the same category accounts mainly for the widespreadunderestimation of the malignant potential of HP. While it was believed that polyps that becomemalignant exceed 2 cm in diameter, Orlowska found cancer cells in very small polyps (diameter≈ 5 mm).Leiomyoma/Leiomyoblastoma
  14. 14. These tumors constitute 2% of all resected neoplasms of the stomach, and occur most frequentlyin males between fifty and seventy years old. 10–20% of leiomyomas of the small intestine arelocated in the duodenum. They are usually asymptomatic, but present with anemia in 50% ofcases as a result of mucosal ulceration. Leiomyomas are usually located in the corpus (40%) orin the antrum (25%). Even when histopathologic tests are conducted, it is difficult to distinguishbenign lesions from malignant ones, partly because leiomyomas are not encapsulated. Therelationship between Leiomyoma (LM), Leiomyoblastoma (LMB) and Leiomyosarcoma (LMS)is still unknown. The “enigma” of LMB is its unusual histology, coupled with a somewhatunpredictable clinical progression. Important in the assessment of the malignant potential ofLMB is the mitotic count, with counts over 5 for 50 high power fields, implying the possibilityof malignancy and subsequent metastasis. The accepted rate of malignant transformation isaround 12%.Duodenal adenomas in familial adenomatous polyposis (FAP)This association is being increasingly recognized. Early diagnosis and longterm surveillance ofasymptomatic patients with this disease allows the opportunity to diagnose and treat duodenaltumors at an early stage, thereby avoiding the dismal prognosis once invasive cancer hasdeveloped in patients who have survive for a mean period of 13 months.Duodenal (periampullary) tumorsThese tumors are rare. Villous and tubulovillous adenomas remain the most common of suchbenign tumors and many have probably undergone malignant change at the time of diagnosis.The presenting symptoms are uncharacteristic, and endoscopy and ERCP are the most sensitivetools for diagnosis. In the post-operative histology of one third of patients with adenoma, we canobserve severe third degree dysplasia (1).Neurogenic gastric and duodenal tumorsThese tumors constitute 4% of all benign neoplasms in stomach and 3% to 6% of all small boweltumors. The most common tumors are neurilemomas (schwanomas) and neurofibromas. About40% of tumors present with bleeding, and mechanical occlusion is not an unusual manifestationin the duodenum.Lipoma
  15. 15. Gastric lipoma is a benign tumor that occurs infrequently (1–3% of all benign gastric tumors),and it is usually located in the antrum. Most lipomas are found in the submucosa (95%), and theyusually occur singly. The most common clinical presentation (50– 60%) is gastrointestinalhemorrhage caused by ulceration of the tumor. Currently, CT scanning is the study of choicewhich identifies fatty tissue because of its low attenuation numbers, but the definitive diagnosisis reached with the excision of the lesion and its anatomopathologic study. In the duodenum wecan observe approximately 35% of small intestine lipomas.Brunner’s Gland AdenomaThis is the most common hamartoma, often found in the proximal duodenum. It is believed toindicate hyperplasia of Brunner’s glands, perhaps in response to excessive gastric acid secretion.Such hyperplasia has not been associated with malignant degeneration. These tumors are usuallysmaller than 1 cm, with multiple and polypoid incidence. As they are asymptomatic, Brunner’sgland adenomas are often incidental findings during endoscopy or radiographic examination.1)Alstrup N, Burcharth F, Hauge C, Horn T. Transduodenal excision of tumors of theampulla of Vater. Eur J Surg. (1996);162:961–967. [PubMed]2)Geis W, Baxt R, Kim H. Benign gastric tumors (Minimally invasiveapproach). SurgEndosc. (1996);10:407–410. [PubMed]
  16. 16. b)malignant tumors :The geographic incidence of gastric cancer has changed dramatically over the last fewdecades. Prior to 1950, it was the most common cause of cancer death in men, and thethird leading cause of cancer death in women in the U.S. Mortalityfrom gastric cancer inthe United States has declined, perhaps due to dietary changes. This cancer is twice ascommon in men than women, twice as common in blacks than whites, and morecommon with advancing age. Gastric cancer is also seen in higher rates in LatinAmerica, Northern Europe and the Far East. It remains the second leading causeof cancer death worldwide.Gastric cancer peaks in the seventh decade of life. Often, a delay in diagnosis mayaccount for the poor prognosis. Fortunately, dedicated research intoitspathogenesis and identification of new risk factors, treatment, and advancedendoscopic techniques have led to earlier detection of gastric cancer. Recognitionthat Helicobacter pylori infection causes most gastric ulcers has revolutionized theapproach to gastric cancer today. Gastric tumors include adenocarcinoma, non-Hodgkin’s lymphoma, and carcinoid tumors.AdenocarcinomaAdenocarcinomas arising from gastric epithelium are the most common malignancies ofthe stomach (90% of cases).LymphomaPrimary gastrointestinal lymphoma may be of B- or T-cell type, with primary Hodgkin’sdisease being extremely uncommon.
  17. 17. Hemorrhaging occurs in approximately 6%–10% of patients with advanced cancer [1]. Whenvisible, it can be particularly distressing to patients and their caregivers [2, 3]. In some patients, itmay be the immediate cause of death. This article focuses on hemorrhaging that is visible, asopposed to occult bleeding. It reviews treatment options in the context of advanced cancerBleeding may result from local vessel damage and invasion or from systemic processes such asdisseminated intravascular coagulopathy (DIC) or abnormalities in platelet functioning andnumber. The underlying causes of these abnormalities are varied and include liver failure,medications such as anticoagulants, chemotherapy, radiotherapy, surgery, and the cancer itself[4]. Occasionally, concurrent diseases, such as idiopathic thrombocytopenia, may be responsible.Hemorrhaging may manifest in a variety of ways, including hematemesis, hematochezia, melena,hemoptysis, hematuria, epistaxis, vaginal bleeding, or ulcerated skin lesions [4]. It may alsopresent as echymoses, petechiae, or bruising. Hemorrhage may occur as an acute catastrophicevent, episodic major bleeds, or ongoing low-volume oozing. These characteristics provide cluesas to the underlying cause and guide management.↵1 Pereira J, Mancini I, Bruera E. The management of bleeding in patients with advancedcancer. In: Portenoy RK, Bruera E, eds. Topics in Palliative Care, Volume 4. New York: OxfordUniversity Press, 2000:163–183.↵ Gagnon B, Mancini I, Pereira J et al. Palliative management of bleeding events in advancedcancer patients. J Palliat Care 1998;14:50–54.↵Hoskin P, Makin W. The role of surgical and radiological intervention in palliation. In:Oncology for Palliative Medicine. Oxford, UK: Oxford University Press, 1998:229–234.3)Acute stress gastritis in UGIBAcute stress gastritis results from predisposing clinical conditions that have the potentialto alter local mucosal protective barriers, such as mucus, bicarbonate, blood flow, and
  18. 18. prostaglandin synthesis. Any disease process that disrupts the balance of these factorsresults in diffuse gastric mucosal erosions.This is most commonly observed in patients who have undergone episodes of shock,multiple trauma, acute respiratory distress syndrome, systemic respiratory distresssyndrome, acute renal failure, and sepsis.The principal mechanisms involved are decreased splanchnic mucosal blood flow andaltered gastric luminal acidity.4)Mallory-Weiss tears in UGIBMallory-Weiss tears account for 15% of acute upper GI hemorrhage.[5] Kenneth Malloryand Soma Weiss first described the syndrome in 1929.[13] The massive UGIB resultsfrom a tear in the mucosa of the gastric cardia.This linear mucosal laceration is the result of forceful vomiting, retching, coughing, orstraining. These actions create a rapid increase in the gradient between intragastric andintrathoracic pressures, leading to a gastric mucosal tear from the forceful distention ofthe gastroesophageal junction.[14] In 80-90% of cases, this is a single, 1.75- to 2.5-cmmucosal tear along the lesser curve of the stomach just distal to the gastroesophagealjunction.[13]5) Dieulafoy lesions in UGIBThe Dieulafoy lesion, first described in 1896, is a vascular malformation of the proximalstomach, usually within 6 cm of the gastroesophageal junction along the lessercurvature of the stomach. However, it can occur anywhere along the GI tract. Thislesion accounts for 2-5% of acute UGIB episodes.[15]Endoscopically, the lesion appears as a large submucosal vessel that has becomeulcerated. Because of the large size of the vessel, bleeding can be massive and brisk.The vessel rupture usually occurs in the setting of chronic gastritis, which may induce
  19. 19. necrosis of the vessel wall. Alcohol consumption is reportedly associated with theDieulafoy lesion.In a review of 149 cases, the Dieulafoy lesion mostly occurred in men and mostly inthose in their third to tenth decade.[16]6) NSAIDs in UGIBNSAIDs cause gastric and duodenal ulcers by inhibiting cyclooxygenase, which causesdecreased mucosal prostaglandin synthesis and results in impaired mucosal defenses.Daily NSAID use causes an estimated 40-fold increase in gastric ulcer creation and an8-fold increase in duodenal ulcer creation.[11]Long-term NSAID use is associated with a 20% incidence in the development ofmucosal ulceration.[17] Medical therapy includes avoiding the ulcerogenic drug andbeginning a histamine-2 (H2)–receptor antagonist or a proton pump inhibitor thatprovides mucosal protection.7)Vomiting-related UGIBDuring vomiting, the lower esophagus and upper stomach are forcibly inverted.Vomiting attributable to any cause can lead to a mucosal tear of the lower esophagus orupper stomach. The depth of the tear determines the severity of the bleeding. Rarely,vomiting can result in esophageal rupture (Boerhaave syndrome), leading to bleeding,mediastinal air entry, left pleural effusion (salivary amylase can be present) or leftpulmonary infiltrate, and subcutaneous emphysema.
  20. 20. CLASSIFICATION:The gastrointestinal bleeding can be classified in acute or chronic; A) ACUTE GI BLEEDING The cardinal features are haematemesis and melaena. Following a bleed from the upper GI tract, unaltered blood can appear per rectum, but the bleeding must be massive and is almost always accompanied byshock. Peptic ulceration is the commonest cause of serious and life-threatening G.I bleeding. Drugs. Aspirin and NSAIDs can produce ulcers and erosions. These agents are alsoresponsible for GI haemorrhage from both duodenal and gastric ulcers, particularly inthe elderly. Corticosteroidsin the usual therapeutic doses probably have no influenceon GI haemorrhage. Anticoagulantsdo not cause acute GI haemorrhage per se but bleeding from any cause is greater if the patient is anticoagulated. All cases with a recent (i.e. within 48 hours) significant GI bleed should be seen in hospital. B) CHRONIC GI BLEEDING Usually present with iron-deficiency anaemia (IDA).Chronic blood loss producing IDA in all men and all women after the menopause is always due to bleeding from the GI tract. The primary concern is to exclude cancer, articularly of the stomach or right colon,and coeliac disease. Occult blood tests areunhelpful. Chronic blood loss can occur with any lesion of the GI tract that produces acute bleeding.FORMS OF PRESSENTING:1)HEMORAGic SHOKThe goal of the patients physical examination is to evaluate for shock and bloodloss.
  21. 21. Assessing the patient for hemodynamic instability and clinical signs of poorperfusion is important early in the initial evaluation to properly triage patients withmassive hemorrhage to ICU settings.Worrisome clinical signs and symptoms of hemodynamic compromise includetachycardia of more than 100 beats per minute (bpm),systolic blood pressure of less than 90 mm Hg, cool extremities,syncope, and other obvious signs of shock, such as ongoing brisk hematemesis or theoccurrence of maroon or bright-red stools, which requires rapid bloodtransfusion.[24]Pulse and blood pressure should be checked with the patient in supine and uprightpositions to note the effect of blood loss. Significant changes in vital signs withpostural changes indicate an acute blood loss of approximately 20% or more.Assessment of hemorrhagic shockAs previously mentioned, patients who present in hemorrhagic shock have a mortality rate ofup to 30%. Hemorrhage may be classified based on the amount of blood loss, as noted in thefollowing table.[25Table Estimated Fluid and Blood Losses in Shock Class 1 Class 2 Class 3 Class 4 Blood Loss, mL Up to 750 750-1500 1500-2000 >2000 Blood Loss,% blood volume Up to 15% 15-30% 30-40% >40% Pulse Rate, bpm < 100 >100 >120 >140 Blood Pressure Normal Normal Decreased Decreased Respiratory Rate Normal or Increased Decreased Decreased Decreased Urine Output, mL/h >35 30-40 20-30 14-20 CNS/Mental Status Slightly Mildly Anxious, Confused, anxious anxious confused lethargic
  22. 22. Fluid Replacement, 3-for-1 rule Crystalloid Crystalloid Crystalloid and blood Crystalloid and bloodThis classification scheme aids in understanding the clinical manifestations of hemorrhagicshock. In early class 1 shock, the patient may have normal vital signs, even with a 15% loss oftotal blood volume. As the percentage of blood volume loss increases, pertinent clinical signs,symptoms, and findings become more apparent.Although early cardiovascular changes occur as blood loss continues, urine output, as a sign ofend organ renal perfusion, is only mildly affected until class 3 hemorrhage has occurred.Bornman et al correlated the presence of shock (defined as a pulse rate >100 bpm or SBP < 100mm Hg) with the incidence of rebleeding rates after initial nonsurgical intervention.[25] Theyfound that rebleeding (a marker for increased mortality and need for surgery) occurred in 2% ofpatients without shock, in 18% with isolated tachycardia, and in 48% with shock.Schiller et al determined that SBP is a sensitive clinical marker for helping to predict mortality.They correlated mortality rates based on the patients SBP at the time of bleeding and foundmortality rates of 8% for patients with SBP more than 100 mm Hg, rates of 17% for SBP of 80-90mm Hg, and rates of more than 30% for SBP less than 80 mm Hg.Unless the patient has evidence of shock, orthostatic testing should be performed to assess anddocument a hypovolemic state. A positive tilt test finding is defined as an SBP decrease of 10mm Hg and a pulse rate increase of 20 bpm with standing compared to the supine position. TheASGE survey was able to correlate orthostatic changes with the incidence of mortality.[26] Themortality rate when orthostatic changes are present is 13.6%, compared to 8.7% when they areabsent.
  23. 23. Knopp et al studied the use of the tilt test in phlebotomized healthy volunteers and found thata positive tilt test result consistently correlated with a blood loss of 1000 mL. This becomesextremely useful when evaluating patients with class 1 hemorrhagic shock.2)iron deficiency anemiaAnemia is a condition in which the body does not have enough healthy red blood cells. Iron isan important building block for red blood cells.iron deficiency anemia related with chronic gastroduodenal bleeding is appearing when thebody is losing more blood cells and iron than the body can replace.Most of the time, symptoms are mild at first and develop slowly. Symptoms may include:Feeling grumpyFeeling weak or tired more often than usual, or with exerciseHeadachesProblems concentrating or thinkingAs the anemia gets worse, symptoms may include: Blue color to the whites of the eyes Brittle nails Light-headedness when you stand up Pale skin color Shortness of breath Sore tongueSymptoms of the conditions that cause iron deficiency anemia include: Pain in the upper belly (from ulcers) Weight loss (in people with cancer) Dark, tar-colored stools or bloodRef: Mabry-Hernandez IR. Screening for iron deficiency anemia--including iron supplementation forchildren and pregnant women. Am Fam Physician. 2009 May 15;79(10):897-8.
  24. 24. Alleyne M, Horne MK, Miller JL. Individualized treatment for iron-deficiency anemia in adults. Am J Med.2008;121:943-948..DIAGNOSIS:A)CLINICAL DIAGNOSIS:The history and physical examination of the patient provide crucial information for theinitial evaluation of persons presenting with a GI tract hemorrhage.[5]History findings include weakness, dizziness, syncope associated with hematemesis(coffee ground vomitus), and melena (black stools with a rotten odor).Occasionally, a brisk UGIB manifests as hematochezia (red or maroon stools); theredder the stool, the more rapid the transit, which suggests a large upper tracthemorrhage. Laine and Shah found that 15% of patients presenting with hematocheziahad an upper gastrointestinal source of bleeding identified at urgentesophagogastroduodenoscopy.[21]Patients may have a history of dyspepsia (especially nocturnal symptoms), ulcerdisease, early satiety, and NSAID or aspirin use. A history of recent aspirin ingestionsuggests that the patient may have NSAID gastropathy with an enhanced bleedingdiathesis from poor platelet adhesiveness.[5]Many patients with UGIB who are taking NSAIDs present without dyspepsia but withhematemesis or melena as their first symptom, owing to the analgesic effect of theNSAID. Low-dose aspirin (81 mg) has been associated with UGIB with or without theaddition of NSAID therapy. Using the lowest effective dose for both short-term and long-term users is recommended.[22]Patients with a history of ulcers are at an especially increased risk for UGIB whenplaced on aspirin or NSAID therapy and should receive continuous acid suppressionwith a proton pump inhibitor (PPI). The patient’s ulcer history is also important because
  25. 25. recurrence of ulcer disease is common, especially if he or she has not been treatedfor H pylori gastritis or antibiotic therapy has failed.Patients may present in a more subacute phase, with a history of dyspepsia and occultintestinal bleeding manifesting as a positive fecal occult blood test result or as irondeficiency anemia.A history of chronic alcohol use of more than 50 g/d or chronic hepatitis (B or C)increases the risk of variceal hemorrhage, gastric antral vascular ectasia (GAVE), orportal gastropathy.The finding of subcutaneous emphysema with a history of vomiting is suggestive ofBoerhaave syndrome (esophageal perforation) and requires prompt consideration ofsurgical therapy.The presence of postural hypotension indicates more rapid and severe blood loss.A meta-analysis documented the incidence of acute UGIB symptoms as follows (seealso Physical Examination, below)[23] : Hematemesis - 40-50% Melena - 70-80% Hematochezia - 15-20% Either hematochezia or melena - 90-98% Syncope - 14.4% Presyncope - 43.2% Symptoms 30 days prior to admission - No percentage available Dyspepsia - 18% Epigastric pain - 41% Heartburn - 21% Diffuse abdominal pain - 10% Dysphagia - 5% Weight loss - 12% Jaundice - 5.2%
  26. 26. b)Lab tests : CBC With Platelet CountA complete blood count (CBC) is necessary to assess the level of blood loss in a patientwith upper gastrointestinal bleeding. Where possible, having the patients previousresults is useful to gauge this loss. CBC should be checked frequently (q4-6h) duringthe first day. Hemoglobin Value and Type and Crossmatch BloodBased on the patients initial hemoglobin level and clinical assessment of shock, a typeand screen or type and crossmatch should be ordered. The patient should becrossmatched for 2-6 units, based on the rate of active bleeding. The hemoglobin levelshould be monitored serially in order to follow the trend. An unstable hemoglobin levelmay signify ongoing hemorrhage requiring further intervention.Patients generally require blood transfusions because of hypoperfusion andhypovolemia. Patients with significant comorbid conditions (eg, advancedcardiovascular disease) should receive blood transfusions to maintain myocardialoxygen delivery to avoid myocardial ischemia. BMP, BUN, and CoagulationThe basic metabolic profile (BMP) is useful in evaluating for renal comorbidity; however,blood in the upper intestine can elevate the BUN (blood urea nitrogen) level as well.Measurement of coagulation parameters is necessary to assess for continued bleeding.Abnormalities should be corrected rapidly.The BUN-to-creatinine ratio increases with upper gastrointestinal bleeding (UGIB). Aratio of greater than 36 in a patient without renal insufficiency is suggestive of UGIB.Coagulation Profile
  27. 27. The patients prothrombin time (PT), activated partial thromboplastin time, andInternational Normalized Ratio (INR) should be checked to document the presence of acoagulopathy. The coagulopathy may be consumptive and associated with athrombocytopenia.A platelet count of less than 50 with active acute hemorrhage requires a platelettransfusion and fresh frozen plasma in an attempt to replete lost clotting factors.The coagulopathy could be a marker for advanced liver disease.The PT is used in calculating the Child-Pugh score.[11] Elevated aminotransferase levelsare a result of hepatocellular injury. Increased levels of alkaline phosphatase andgamma–glutamyltranspeptidase are indicative of cholestatic liver disease.Prolongation of the PT based on an INR of more than 1.5 may indicate moderate liverimpairment.A fibrinogen level of less than 100 mg/dL also indicates advanced liver disease withextremely poor synthetic function. Calcium LevelAssessing patients’ calcium levels is useful in identifying individuals withhyperparathyroidism as well as in monitoring calcium in patients receiving multipletransfusions of citrated blood. Hypercalcemia increases acid secretion. Gastrin levelA gastrin level can identify the rare patient with gastrinoma as the cause of uppergastrointestinal bleeding and multiple ulcers.c)imagestic studies :Radiography
  28. 28. Plain radiographs of the abdomen are not usually helpful in the diagnosis of acute uppergastrointestinal bleeding (UGIB). The pathophysiology of acute UGIB is often mucosalerosion with subsequent hemorrhage, which is not detected with plain radiographs.Occasionally, free air under the diaphragm is seen in cases of perforated viscous, andthis may be accompanied by UGIB. Other etiologies, such as upper GI masses (whichusually result in chronic, not acute, UGIB), aneurysms with calcifications, and ascitessuggestive of portal hypertension, may be seen on radiographs.[12]The radiographic findings, as outlined above, are usually nonspecific. Calcificationsassociated with aneurysms, in the aorta or branch vessels, are reliable but rare findingsregarding a source of upper gastrointestinal bleeding.Chest radiographs should be ordered to exclude aspiration pneumonia, effusion, andesophageal perforation.Barium Contrast StudiesBarium contrast studies are not usually helpful and can make endoscopic proceduresmore difficult (ie, white barium obscuring the view) and dangerous (ie, risk of aspiration)CT ScanningComputed tomography (CT) scanning and ultrasonography may be indicated for theevaluation of liver disease with cirrhosis, cholecystitis with hemorrhage, pancreatitis withpseudocyst and hemorrhage, aortoenteric fistula, and other unusual causes of upper GIhemorrhage.[29] The 2010 ACR criteria state that CT is particularly useful for localizingobscure UGIB and for evaluating a patient with UGIB and a history of aorticreconstruction or pancreaticobiliary procedure.[28]CT scanning is useful in the diagnosis of aortoenteric fistula because images mayreveal thickened bowel, perigraft fluid collection, extraluminal gas, or inflammatorychanges in the area of the duodenum and aortic graft.Nuclear Medicine ScanningNuclear medicine scans may be useful in determining the area of active hemorrhage.However, the 2010 ACR criteria state that Tc-99m-labeled erythrocyte scans are of
  29. 29. limited value in diagnosing UGIB, but continue to be useful in certain cases of obscureUGIB.[28]D)interventional procedures :Nasogastric LavageThis procedure may confirm recent bleeding (coffee ground appearance), possibleactive bleeding (red blood in the aspirate that does not clear), or a lack of blood in thestomach (active bleeding less likely but does not exclude an upper GI lesion).A nasogastric tube is an important diagnostic tool, and tube placement can reduce thepatients need to vomit. Placement for diagnostic purposes is not contraindicated inpatients with possible esophageal varices.The characteristics of the nasogastric lavage fluid (eg, red, coffee grounds, clear) andthe stool (eg, red, black, brown) can indicate the severity of the hemorrhage. Red bloodwith red stool is associated with an increased mortality rate from more active bleedingcompared with negative aspirate findings with brown stool.EndoscopyThe development of endoscopy has provided clinicians with the ability for diagnosticand therapeutic approaches to bleeding from the GI tract. Endoscopic examination ofthe upper GI tract provides useful information regarding the source and site ofbleeding.[26]After a positive NG lavage, and even with a negative one if there is high enoughsuspicion, the next step should be performance of an esophagogastroduodenoscopy(EGD) for localization of the bleeding source. Upper endoscopy is the primarymethod of evaluating a patient with UGI bleeding as it has a 90–95% success rate[72].There is debate as to the timing of early upper endoscopy [74]. Most agree
  30. 30. that an endoscopy should be performed within 24 hours [73] to evaluate UGIBbut several studies are evaluating whether some patients benefit from even earlierendoscopy. Clearly, patients who have persistent or severe bleeding should undergovery early endoscopy to avail themselves of the potential of endoscopic therapy[74].During the procedure, the endoscopist is looking for any lesion that might havecaused the bleeding and for characteristics that suggest the likelihood of recurrence.Forrest [16] classified peptic ulcers according to features that were associated withrisk of rebleeding (see Table 1).Table 1 Forrest classification of peptic ulcersType DescriptionIa Active spurting bleedingIb Active oozing bleedingIIa Non-bleeding but visible vesselIIb Non-bleeding with adherent clotIIc Non-bleeding with pigmented ulcer baseIII Clean base, no sign of bleedingmost ulcerswith a clean base, are associated with a 5%risk of rebleed and 2% mortality. Patientswith ulcers that have a flat, pigmented spot on endoscopy have a 10% risk of furtherbleeding and 3% mortality. The presence of adherent clots on top of an ulceris associated with a 22% risk of further bleeding and 7% mortality. A visible, nonbleedingvessel is correlated with a 43% risk of rebleed and 11% mortality, whileactively bleeding vessels have the highest risk of recurrence at about 55% and amortality of 11% [1]. Other lesions such as Mallory–Weiss tears are associated witha low risk (2%) of further bleeding [75]. These associations suggest that proper evaluationvia endoscopy is crucial, as endoscopic findings are directly associated with
  31. 31. patients’ prognosis and therefore will aid in decisions concerning therapy.Endoscopic findings and their incidence rate in patients with UGIB include the following: Duodenal ulcer - 24.3% Gastric erosion - 23.4% Gastric ulcer - 21.3% Esophageal varices - 10.3% Mallory-Weiss tear - 7.2% Esophagitis - 6.3% Duodenitis - 5.8% Neoplasm - 2.9% Stomal (marginal) ulcer - 1.8% Esophageal ulcer - 1.7% Other/miscellaneous - 6.8%Endoscopy should be performed immediately after endotracheal intubation (if indicated),hemodynamic stabilization, and adequate monitoring in an ICU setting have beenachieved. The 2010 American College of Radiology (ACR) appropriateness criteria forupper gastrointestinal bleeding recommend upper endoscopy as the initial diagnosticexamination for all patients presumed to have UGIB.[28]In spite of the excellent results with EGD, the procedure is not without complications.It can cause gastrointestinal perforations, precipitation of gastrointestinalbleeding, aspiration pneumonia, respiratory arrest, and cardiovascular complications[11]. The incidence of complications is low, but it is important to be certainthat in each patient the benefit of the procedure outweighs the riskAngiography
  32. 32. Angiography may be useful if bleeding persists and endoscopy fails to identify ableeding site. According to the 2010 ACR guidelines, angiography along withtranscatheter arterial embolization (TAE) should be considered for all patients with aknown source of arterial UGIB that does not respond to endoscopic management, withactive bleeding and a negative endoscopy.[28]In cases of aortoenteric fistula, angiography requires active bleeding (1 mL/min) to bediagnostic.Differential Diagnoses Abdominal Aortic Aneurysm Barrett Esophagus and Barrett UlcerEsophageal Cancer Esophageal Varices EsophagitisPancreatic pseudoaneurysm Cardiac cirrhosis Celiac sprue Cholecystitis Cirrhosis Disseminated intravascular coagulation Strongyloidiasis Syncope von Willebrand disease Zollinger-Ellison syndrome Dengue fever
  33. 33. Emergency treatment in GD bleeding :The goal of medical therapy in upper gastrointestinal bleeding (UGIB) is to correctshock and coagulation abnormalities and to stabilize the patient so that furtherevaluation and treatment can proceedResuscitation of a hemodynamically unstable patient begins with assessing andaddressing the ABCs (ie, airway, breathing, circulation) of initial management.(Baradarian et al demonstrated that early, aggressive resuscitation can reduce mortalityin acute UGIB.[30] )Patients presenting with severe blood loss and hemorrhagic shock present with mentalstatus changes and confusion. In such circumstances, patients cannot protect theirairway, especially when hematemesis is present. In these cases, patients are atincreased risk for aspiration, which is a potentially avoidable complication that cansignificantly affect morbidity and mortality. This situation must be recognized early, andpatients should be electively intubated in a controlled setting.Intravenous access must be obtained. Bilateral, 16-gauge (minimum), upper extremity,peripheral intravenous lines are adequate for volume resuscitative efforts. Poiseuille’slaw states that the rate of flow through a tube is proportional to the fourth power of theradius of the cannula and is inversely related to its length.[17] Thus, short, large-bore,peripheral intravenous lines are adequate for rapid fluid infusion.
  34. 34. According to the 2008 SIGN guideline, either colloid or crystalloid solutions may beused to attain volume restoration prior to administering blood products.[27] A roughguideline for the total amount of crystalloid fluid volume needed to correct thehypovolemia is the 3-for-1 rule. Replace each milliliter of blood loss with 3 mL ofcrystalloid fluid. This restores the lost plasma volume. Patients with severe coexistingmedical illnesses, such as cardiovascular and pulmonary diseases, may requirepulmonary artery catheter insertion to closely monitor hemodynamic cardiacperformance profiles during the early resuscitative phase.Once the ABCs have been addressed, assess the patients response to resuscitation,based on evidence of end organ perfusion and oxygen delivery.Pulmonary artery catheters may be helpful to guide therapy.Foley catheter placement is mandatory to allow a continuous evaluation of the urinaryoutput as a guide to renal perfusion. This labor-intensive management should beperformed only in an ICU setting.Once the maneuvers to resuscitate are underway, insert a nasogastric tube and performan aspirate and lavage procedure. This should be the first procedure performed todetermine whether the GI bleeding is emanating from above or below the ligament ofTreitz. If the stomach contains bile but no blood, UGIB is less likely. If the aspiratereveals clear gastric fluid, a duodenal site of bleeding may still be possible.In a retrospective review of 1190 patients, Luk et al found that positive nasogastric-tubeaspirate findings were 93% predictive of an upper GI source of bleeding.[32]According to a study performed by the ASGE, however, a nasogastric-tube aspiratefinding can be negative even in the setting of a large duodenal bleeding ulcer. The studycompared nasogastric-tube aspirate findings with endoscopic findings of the bleedingsource.[20] The investigation revealed that 15.9% of patients with a clear nasogastric-tube aspirate, 29.9% of patients with coffee-ground aspirate, and 48.2% of patients withred blood aspirate had an active upper GI source of bleeding at the time of endoscopy.
  35. 35. A study correlated mortality with the color of the fluid from the nasogastric-tube aspirateand the color of the stool.[29] As shown in the following table, the color of thenasogastric-tube aspirate can be a prognostic indicator.Table 4. Effect of the Color of the Nasogastric Aspirate and of the Stool on UGIBMortality Rate)Nasogastric Aspirate Color Stool Color Mortality Rate, %Clear Brown or red 6Coffee-ground Brown or black 8.2 Red 19.1Red blood Black 12.3 Brown 19.4 Red 28.7SurgeryPrimary surgical intervention should be considered in patients with a perforated viscus(eg, from perforated duodenal ulcer, perforated gastric ulcer, or Boerhaave syndrome).In patients who are poor operative candidates, conservative treatment with nasogastricsuction and broad-spectrum antibiotics can be instituted. Endoscopic clipping or sewingtechniques have also been used in such patients.Emergency surgery in UBIG typically entails oversewing the bleeding vessel in thestomach or duodenum (usually preoperatively identified by endoscopy), vagotomy withpyloroplasty, or partial gastrectomy. Angiographic obliteration of the bleeding vessel isconsidered in patients with poor prognoses.Treatment-related contraindications :
  36. 36. Contraindications to upper endoscopy include an uncooperative or obtunded patient,severe cardiac decompensation, acute myocardial infarction (unless active, life-threatening hemorrhage is present), and perforated viscus (eg, esophagus, stomach,intestine).Contraindications to emergency surgery include impaired cardiopulmonary status andbleeding diathesis.Esophagogastroduodenoscopy may be more difficult or impossible if the patient hashad previous oropharyngeal surgery or radiation therapy to the oropharynx.The presence of a Zenker diverticulum can make intubation of the esophagus moredifficult.Patients with Down syndrome are more sensitive to conscious sedation and shouldreceive much less sedation, or they should be monitored by an anesthesiologist and/orintubated prophylactically prior to the procedure.Hypotension may be exacerbated by sedation; therefore, patients who are unstableshould be given less sedation.Patients with massive bleeding should be considered for intubation to reduce theincreased risk of aspiration. Such patients should be treated in an intensive care setting.Ideally, the patient should be stabilized prior to endoscopy and abnormalities incoagulation should be corrected. When this is not possible, the judgment of anexperienced endoscopist is vital.Endoscopy
  37. 37. Since the late 1980s, endoscopic techniques to achieve hemostasis for bleeding ulcersand varices have continued to evolve. Endoscopy is now the method of choice forcontrolling active ulcer hemorrhage.Several randomized clinical trials and meta-analyses have demonstrated and supportedthe idea that early endoscopic hemostatic therapy significantly reduces rates ofrecurrent bleeding, the need for emergent surgery, and mortality in patients with acutenonvariceal upper gastrointestinal bleeding (UGIB).In the early history of endoscopy for UGIB, multiple published studies questioned thecost-effectiveness of endoscopy in this setting, because it was unclear whether theoutcome was changed. In a setting in which 80% of patients respond to conservativemedical management, studies were hampered by type 2 errors because of the largenumber of patients needed to demonstrate statistical significance.In 1989, a National Institutes of Health (NIH) consensus conference on UGIB concludedthat effective therapy was needed in the presence of active bleeding or a visible vessel.The conference affirmed that the treatment, when performed by an experiencedendoscopist using 1 of 4 techniques (ie, injection of epinephrine or sclerosants, heater-probe coagulation, bipolar electrode coagulation, laser coagulation), was proveneffective by the published evidence.Three other techniques have since been developed: (1) endoscopic application of clips,(2) use of banding devices, and (3) argon plasma coagulation. Aside from ulcerhemorrhaging, other causes of gastrointestinal bleeding, including mucosal tears in theesophagus or upper stomach due to vomiting (Mallory-Weiss tears), venous blebs, andvascular ectasias, can also be treated with endoscopic coagulation.Patients should be considered for upper endoscopy if blood loss from the uppergastrointestinal tract is suspected.The patient should undergo upper endoscopy prior to any operative intervention in orderto diagnose and localize the bleeding site. Most patients (85-90%) respond toendoscopic therapy.
  38. 38. The bleeding from gastric cancers and ulcers in leiomyomas does not usually respondto endoscopic therapy; surgical or radiologic intervention is needed.Much debate has focused on the significance of the nonbleeding visible vessel (ie,color, size, diagnostic characteristics, risk of rebleeding) in ulcer hemorrhage. Thesematters became clarified after the characteristics and significance of the visible vessel inthe ulcer crater were defined and the evidence for endoscopic therapy was established,demonstrating that patients requiring therapy to control bleeding or rebleeding could bediagnosed and treated at the time of the upper endoscopy.During the endoscopy, the patient is monitored according to analgesia and sedationguidelines formulated by the American Society of Anesthesiology. The characteristics ofthe bleeding lesion are noted, and appropriate therapy is applied when necessary forhigh-risk lesions or active bleeding.Urgent endoscopyUrgent endoscopy is indicated when patients present with hematemesis, melena, orpostural changes in blood pressure. Cooper et al have demonstrated a lower rate of
  39. 39. rebleeding and shorter length of stay when endoscopy is performed within 24 hours ofadmission.[39, 32]Early endoscopyCooper et al studied the effectiveness of performing an early endoscopy within the first24 hours of an acute UGIB episode and found it to be associated with reductions in thelength of hospital stay, rate of recurrent bleeding, and need for emergent surgicalintervention.[39]According to the 2010 international consensus on nonvariceal upper gastrointestinalbleeding, early endoscopy (within 24 hours of presentation) is appropriate for mostpatients with UGIB.[40] In a retrospective review involving more than 30,000 cases,Yavorski et al showed that the mortality rates were more than twice as high for patientswho did not undergo an early endoscopic procedure than for those who did undergo theprocedure early on (11.1% vs 5.2%, respectively).Endoscopic techniquesThe following endoscopic techniques have been developed for achieving hemostasis[5] : Injection of epinephrine or sclerosants Bipolar electrocoagulation Band ligation[41] Heater probe coagulation Constant probe pressure tamponade Argon plasma coagulator Laser photocoagulation Rubber band ligation Application of hemostatic materials, including biologic glue Application of hemoclips or endoclips Application of nanopowder (experimental)[42]Treatment using a combination of endoscopic therapies has become more common.For example, injection therapy can be applied first to better clarify the bleeding site,especially in the actively bleeding patient, followed by the application of heater probe or
  40. 40. bipolar (gold) probe coagulation. Injection therapy can also be performed prior toendoscopic placement of hemoclips.According to the 2008 SIGN guideline, combinations of endoscopy with an injection ofat least 13 mL of 1:10,000 adrenaline, coupled with either a thermal or mechanicaltreatment, are more effective than single modalities.[27]The 2010 international consensus guidelines on UGIB recommend the use ofendoscopic clips or thermal therapy for high-risk lesions.[40] As another example,injection therapy is useful prior to laser therapy to reduce the heat sink effect of rapidlyflowing blood prior to laser coagulation.Heater probe coagulationThe heater probe consists of a resistor electrode enveloped by a titanium capsule andcovered by Teflon (to reduce sticking to the mucosa by the probe). The probetemperature rises to 250°C (482°F).Bipolar electrocoagulationThe bipolar probe consists of alternating bands of electrodes producing an electricalfield that heats the mucosa and the vessel. The electrodes are coated with gold toreduce adhesiveness. The probes are stiff in order to allow adequate pressure to thevessel to appose the walls and thus produce coaptive coagulation when the electrical-field energy is transmitted. Careful technique is required to heat-seal the perforatedvessel.Injection therapyInjection therapy involves the use of several different solutions injected into and aroundthe bleeding lesion. The different solutions available for injection are epinephrine,sclerosants, and clot-producing materials, such as fibrin glue.Laser therapyLaser phototherapy uses an Nd:YAG laser to create hemostasis by generating heat anddirect vessel coagulation. This is a noncontact thermal method. It is not as effective as
  41. 41. coaptive coagulation, because it lacks the use of compression to create a tamponadeeffect.[1] An additional deterrent to its use is expense.To perform laser coagulation, the area near the vessel is first injected with epinephrineto reduce blood flow (reducing the heat-sink effect); then, the laser is applied around thevessel, producing a wall of edema. Caution must be observed to avoid drilling into thevessel with the laser, causing increased bleeding.Hemostatic clips and endoclipsModification of the delivery system has made clip placement much easier than it was inthe original model. With careful placement of the clip, closing the defect in the vessel ispossible. Usually, multiple clips are applied. They vary in the size and the strength ofthe clip. Four models of hemoclips are available: QuickClip2, which is rotatable;Resolution Clip, which can be reopened after closure; TriClip, which has 3 prongs; andIn Scope, which is a multiclip applier with 4 endoclips. The Resolution Clip seems to bethe current clip of choice by experienced endoscopists.There are some clinical settings in which endoclips may be preferred over otherhemostatic methods. These include the treatment of ulcers in patients who arecoagulopathic or who require ongoing anticoagulation; in such patients,electrocoagulation will increase the size, depth, and healing time of treated lesions.Endoclips may also be preferable in the retreatment of lesions that rebleed after initialthermal hemostasis.Ulcers on the lesser curvature, the posterior duodenum, or the cardia increase thedifficulty of clip deployment and clip failure rates.Larger endoclips have advantages over smaller hemoclips for the hemostasis of chroniculcers and the closure of larger lesions.Argon plasma coagulationArgon plasma coagulation is a technique in which a stream of electrons flows along astream of argon gas. The coagulation is similar to monopolar cautery, with the currentflow going from a point of high current density (the point of contact of the gas with the
  42. 42. mucosa) to an area of low current density (the conductive pad on the patients body).The current flows through the body in an erratic path to the pad.NanopowderNanopowder has been found to be effective in a small study using a porcine model ofarterial bleeding.[42] Further trails are awaited.Endoscopic treatment decisionsThe choice of treatment modality is influenced by the size of the vessel. Animal studieshave demonstrated that the heater probe and bipolar probe are effective for vessels aslarge as 2 mm in diameter.Other techniques (eg, clips, band ligation) or a combination of techniques are neededfor larger vessels or vessels that are not approachable by the heater probe or bipolarprobe. (Surgical intervention should be considered when dealing with vessels largerthan 2 mm in diameter, discounting an enlargement due to the development ofpseudoaneurysm.)
  43. 43. Ulcers with an overlying clotIn the patient who has an ulcer with an overlying clot, attempting to remove the clot bytarget washing is critical. Endoscopic removal of the clot by washing or cold snare hasbeen demonstrated to be effective in reducing the recurrence of bleeding.[47] (Cuttingaway the adherent clot is somewhat controversial but is recommended based on studyresults from experienced centers.)The findings under the clot (eg, bleeding vessel, visible vessel, flat spot, clean base,examples of which are seen in the images below) help to determine the therapy neededand improve efficacy by allowing treatment to be applied directly to the vessel. (See thetable below.)
  44. 44. Ulcer with active bleeding. Ulcerwith a clean base. Diagram of an ulcer with a clean base. Ulcer with a flat spot. Ulcer with
  45. 45. an overlying clot. Ulcer with a visible vessel. Diagram of an ulcer with a visible vessel.Table 5. Ulcer Characteristics and Correlations (Open Table in a new window)If the clot cannot be removed by washing, then cutting away the clot using a cold snarecan be considered by experienced endoscopists.Vigorous washing of the clot formed after therapy is useful in determining the adequacyof coagulation. A combination of injection with heater probe or bipolar coaptivecoagulation is often used and has been shown to be more effective in patients withactive bleeding.Active bleeding and rebleedingThe endoscopy should not be started unless the endoscopist is equipped for anypotential lesions (eg, ulcer, varix, angioectasia, tear, tumor). The patient should bemonitored for recurrent bleeding and treated a second time if appropriate. A surgicalconsultation should be considered for all patients with gastrointestinal hemorrhage.
  46. 46. Rebleeding occurs in 10-30% of endoscopically treated patients. A second attempt atendoscopic control is warranted. Some authorities have concerns about the perils of asecond esophagogastroduodenoscopy, which may result in delayed surgery,perforation, and increased morbidity and mortality rates. However, this approach hasbeen validated in a large, randomized, controlled trial that showed decreased morbidityand mortality rates.[48]Specific characteristics at endoscopy can predict rebleeding. Rebleeding occurs in 55%of patients who have active bleeding (pulsatile, oozing), in 43% who have a nonbleedingvisible vessel, in 22% who have an ulcer with an adherent clot, and in 0-5% who havean ulcer with a clean base.At endoscopy, the prevalence rate for a clean base is 42%, for a flat spot is 20%, for anadherent clot is 17%, for a visible vessel is 17%, and for active bleeding is 18%. (Seethe images below.)Freeman et al have described a pale, visible vessel that appears to have a very highrisk for rebleeding.[49] This must be differentiated from the presence of a clean ulcerbase.Good visualization is important. The uncleared fundal pool may obscure an ulcer,mucosal tear, gastric varices, portal gastropathy, or tumor (eg, leiomyoma,adenocarcinoma, lymphoma). Endoscopic therapy is recommended for ulcers atincreased risk for rebleeding.According to the 2008 SIGN guidelines, TIPS should be considered to prevent gastricvaricealrebleeding.[27]Using a combination of techniques is prudent when re-treating the ulcer site becausethe first therapy produced necrosis and weakening of the intestinal wall. Ulcers on theanterior surface of the stomach and duodenum are at increased risk for perforation.Using injection as the first step increases the thickness of the submucosal layer, thusproviding an extra margin of safety.
  47. 47. Even operative techniques can have a significant rebleeding rate with significantmortality, as noted in the study of Poxon et al. In this investigation, the rebleeding ratewas 10% (80% mortality for rebleeders) in patients who underwent a conservativesurgical technique in which the ulcer base was undersewn.[50] This more conservativeapproach was compared with the standard surgical technique (ie, vagotomy andpyloroplasty or partial gastrectomy). The comparison of the conservative approach witha standard gastrectomy resulted in similar mortality rates, ie, 26% versus 19%,respectively, with no rebleeding after partial gastrectomy.Postendoscopic monitoringPostoperatively, the patient is monitored for recovery from conscious sedation afterendoscopy and from general anesthesia after abdominal surgery. Monitor the patientsmental status, vital signs, chest, cardiac, and abdominal findings to ascertain that thepatients clinical status has stabilized and that no complications (eg, aspiration,perforation, recurrent bleeding, myocardial infarction due to hypotension) haveoccurred. Monitor the hemoglobin level.TREATMENT OF MAJOR CAUSES OF GASTRODUODENAL DISEASES :1)Bleeding Peptic Ulcer TreatmentUpper GI endoscopy is the most effective diagnostic tool for PUD and has become themethod of choice for controlling active ulcer hemorrhage. Failure of endoscopy tomaintain hemostasis is one of the indications to initiate surgical intervention, especiallyin high-risk patients.Regardless of the endoscopic therapy, however, 10-12% of patients with acute ulceroushemorrhage require an operation as the definitive procedure to control the bleedingulcer. In most circumstances, the operation is performed emergently, and theassociated mortality rate is as high as 15-25%.Medical therapy used in conjunction with endoscopy involves PPI administration. PPIsdecrease rebleeding rates in patients with bleeding ulcers associated with an overlyingclot or visible, nonbleeding vessel in the base of the ulcer.[52, 53] Consider
  48. 48. transcatheterangiographic embolization in patients who are poor surgical candidates.Because of the extensive collateral circulation of the upper GI tract, ischemiccomplications are rare.Surgical treatmentIf 2 attempts at endoscopic control of the bleeding vessel are unsuccessful, avoidfurther attempts (ie, because of increased rebleeding and mortality rates) and pursuesurgical intervention. The indications for surgery in patients with bleeding peptic ulcersare as follows: Severe, life-threatening hemorrhage not responsive to resuscitative efforts Failure of medical therapy and endoscopic hemostasis with persistent recurrent bleeding A coexisting reason for surgery, such as perforation, obstruction, or malignancy Prolonged bleeding, with loss of 50% or more of the patients blood volume A second hospitalization for peptic ulcer hemorrhageThe operative treatment options for a bleeding duodenal ulcer historically includevagotomy, gastric resection, and drainage procedures. Each specific operative option isassociated with its own incidence of ulcer recurrence, postgastrectomy syndrome, andmortality (as seen in the table below). When making an intraoperative judgment on howto best manage the bleeding ulcer, it is extremely important for the surgeon to be awareof these differences.[11]Table 6. Recurrent Ulcer and Postgastrectomy Syndromes After Operations forDuodenal Ulcer Recurrence Postgastrectomy Syndrome MortalityOriginal Operation Rate, % Rate, % Rate, %Proximal gastric vagotomy 10 5 0.1Truncalvagotomy and 7 20-30 <1
  49. 49. drainageTruncalvagotomy and 1 30-50 0-5antrectomyBillroth I or Billroth IITruncalvagotomy and 5-10 50-60 0-5antrectomyRoux-en-YThe 3 most common operations performed for a bleeding duodenal ulcer are asfollows[5] : Truncalvagotomy and pyloroplasty with suture ligation of the bleeding ulcer Truncalvagotomy and antrectomy with resection or suture ligation of the bleeding ulcer Proximal (highly selective) gastric vagotomy with duodenostomy and suture ligation of the bleeding ulcerThe purpose of the vagotomy is to divide the nerves to the acid-producing body andfundus of the stomach. This inhibits the acid production that occurs during the cephalicphase of gastric secretion. Although acid secretion is controlled, gastric motility andgastric emptying is affected, as indicated in the following table.[11]Proximal vagotomy abolishes gastric receptive relaxation and impairs storage in theproximal stomach. As a result, a more rapid gastric emptying of liquids occurs. A
  50. 50. drainage procedure is not required, because the innervation of the antrum and pylorusis still intact. Because of this, the gastric emptying of solid food is not altered. Theantropyloric mechanism still functions normally and continues to prevent duodenogastricreflux.In addition to having the same effects as a highly selective vagotomy in the proximalstomach, a truncalvagotomy also has marked effects on distal gastric motor function. Itweakens distal gastric peristalsis, thus requiring the creation of a pyloroplasty todecrease the resistance to outflow from the stomach.Truncalvagotomy and suture ligation of a bleeding ulcer is a frequently used operationfor treating upper gastrointestinal bleeding (UGIB) in elderly patients with life-threatening hemorrhage and shock. The procedure can be performed rapidly,minimizing the time spent in the operating room under general anesthesia.The principles of suture ligation of a duodenal bleeding ulcer that involves thegastroduodenal artery require use of the 3-point ligation technique.The gastroduodenal artery is ligated proximally and distally to the arterial bleeding site.The third suture is a horizontal mattress placed to control hemorrhage from thetransverse pancreatic branch of the gastroduodenal artery. Failure to place this thirdstitch may result in recurrent bleeding that requires another emergent laparotomy of theabdomen. Vagotomy with antrectomy is reserved for patients whose conditions havefailed to respond to more conservative attempts at surgical intervention and for thosewith aggressive and recurrent duodenal ulcer diathesis, such as gastric outletobstruction.When performing a highly selective vagotomy, the duodenostomy or thepyloroduodenostomy is closed anatomically, preserving the normal pyloric sphinctermuscle. Most commonly, this operation is reserved for young, stable, low-risk patients.Although long-term follow-up care is still necessary, the recurrent ulcer rate is less than10% at a mean follow-up of 3.5 years.[5]Much of what is now known about the operations performed for bleeding duodenalulcers came from the era before the etiologic role for H pylori and NSAIDs in the
  51. 51. development of peptic ulcers was understood. Reducing gastric acidity has been provento be beneficial, with lower rebleeding rates when using high-doseomeprazole.[1] Although PPIs seem to have an advantage, they have no affect onmortality.The diagnosis of H pylori infection is important in the management of patients with acomplicated bleeding peptic ulcer. If a patient with a bleeding ulcer requires surgery,then knowledge of the patients H pylori status becomes pertinent, because it may helpto guide the decision to choose a particular surgical procedure, eg, simply oversewingthe ulcer as opposed to performing an antiulcer operation. Many studies support thedecision to manage the bleeding ulcer in conjunction with eradication of H pylori.Bleeding Gastric Ulcer TreatmentThe surgical management of bleeding gastric ulcers is slightly different from that of duodenalulcers, but the concepts are identical. The 3 most common complications of a gastric ulcer thatmandate emergent surgical intervention are hemorrhage, perforation, and obstruction. The goalsof surgery are to correct the underlying emergent problem, prevent recurrent bleeding orulceration, and exclude malignancy.A bleeding gastric ulcer is most commonly managed by a distal gastrectomy that includes theulcer, with a gastroduodenostomy or a gastrojejunostomy reconstruction.The common operations for the management of a bleeding gastric ulcer include (1)truncalvagotomy and pyloroplasty with a wedge resection of the ulcer, (2) antrectomy withwedge excision of the proximal ulcer, (3) distal gastrectomy to include the ulcer, with or withouttruncalvagotomy, and (4) wedge resection of the ulcer only.Types of gastric ulcersThe choice of operation for a bleeding gastric ulcer depends on the location of the ulcer and thehemodynamic stability of the patient to withstand an operation. Five types of gastric ulcersoccur, based on their location and acid-secretory status.
  52. 52. Type 1 gastric ulcers are located on the lesser curvature of the stomach, at or near theincisuraangularis. These ulcers are not associated with a hypersecretory acid state.Type 2 ulcers represent a combination of 2 ulcers that are associated with a hypersecretory acidstate. The ulcer locations occur in the body of the stomach in the region of the incisura. Thesecond ulcer occurs in the duodenum.Type 3 ulcers are prepyloric ulcers. They are associated with high acid output and are usuallywithin 3 cm of the pylorus.Type 4 ulcers are located high on the lesser curvature of the stomach and (as with type 1 ulcers)are not associated with high acid output.Type 5 ulcers are related to the ingestion of NSAIDs or aspirin. These ulcers can occur anywherein the stomach.Surgical management according to ulcer typeA vagotomy is added to manage type 2 or type 3 gastric ulcers.Patients who are hemodynamically stable but have intermittent bleeding requiring bloodtransfusions should undergo a truncalvagotomy and distal gastric resection to include the ulcerfor type 1, 2, and 3 ulcers.In patients who present with life-threatening hemorrhage and a type 1, 2, or 3 ulcer, biopsy andoversew or excision of the ulcer in combination with a truncalvagotomy and a drainageprocedure should be considered.Patients with type 4 ulcers usually present with hemorrhage. The left gastric artery should beligated, and a biopsy should be performed on the ulcer. Then, the ulcer should be oversewnthrough a high gastrotomy.Rebleeding rates for the procedures that keep the ulcer in situ range from 20-40%.[11]Gastric bleeding in the immediate postoperative period from recurrent PUD is initially bestmanaged by endoscopic or angiographic means. If reoperation is required, gastric resection is
  53. 53. usually indicated, because a repeat vagotomy is not reliable. A more definitive solution iswarranted.According to the 2008 SIGN guidelines, patients with confirmed gastric variceal hemorrhagerequire endoscopic therapy, preferably with cyanoacrylate injection.[27]Stress Gastritis TreatmentKnowledge of the predisposing conditions for stress ulceration allows the clinician toidentify patients at risk for developing gastritis and GI bleeding. Treatment in this groupof high-risk patients should focus on prevention. This is best accomplished by treatingthe underlying causes of ulceration.Aggressive support of hemodynamic parameters ensures adequate mucosal blood flow.In addition, several strategies have evolved to treat gastric luminal acidity. Histaminereceptor antagonists (HRAs) have proven to be the most effective at controllingstomach pH. Proton pump inhibitors (PPIs) are superior to the HRAs at suppressingacid; however, their role in stress ulceration prophylaxis is still being studied.[12]Stress-related bleeding usually occurs 7-10 days after the initial insult but may manifestsooner. Initially, endoscopy is the most important diagnostic tool. The acute superficialerosions are multiple, begin in the fundus, and progress toward the antrum. Ninetypercent of patients stop bleeding with conservative medical therapy that includes NGTlavage and gastric acid–controlling medications to maintain the gastric luminal pHabove 5.0.[13]Endoscopic hemostasis is attempted using electrocoagulation, laser, or injectiontherapy. Selective angiographic catheterization of the left gastric artery may beattempted with selective infusion of vasopressin (48-72 h) or embolization usingGelfoam, coils, or autologous clot to embolize the left gastric artery. Regardless of theangiographic technique used, it is often unsuccessful because of the rich and extensivesubmucosal plexus and collateral circulation within the stomach.Surgical treatment
  54. 54. Surgical intervention becomes necessary if nonoperative therapy fails and blood losscontinues. The goals of operative treatment are to control bleeding and to reducerecurrent bleeding and mortality. These patients are at extremely high risk, and the mostexpeditious procedure is the best option.Simply oversewingan actively bleeding erosion is sometimes effective enough to controlthe bleeding. In the setting of life-threatening hemorrhage not amenable to endoscopiccontrol, gastric resection with or without vagotomy with reconstruction may benecessary.The type of gastric resection depends on the location of the gastric erosions, ie, whetherthey are proximal or distal. The options are antrectomy and subtotal, near total, or totalgastrectomy. Operative mortality rates range from 4-17%.[54] The choice of the initialoperation must be made with an understanding of the patients condition, the amountand location of gastric disease, and an accurate assessment of ones technical ability torapidly and safely perform a gastric resection. The trend has been to perform lesssurgery in general and to minialize the type of surgical procedure performed. [55]Managing the underlying insult causing the gastric stress ulcerations is also important.This involves supportive measures to maintain acceptable hemodynamic parameters, toprovide adequate nutritional support in the critically ill patient, and to treat sepsis (ifpresent).Mallory-Weiss Syndrome TreatmentDistinguishing Mallory-Weiss syndrome from Boerhaave syndrome is critical. Althoughboth entities share a common pathogenesis, their management is completely different.Boerhaave syndrome represents a full-thickness transmural laceration with perforationof the esophagus. A Gastrografin swallow helps to confirm the presence of theperforation in most cases, and prompt surgical intervention is necessary to preventmediastinitis and sepsis.
  55. 55. On the other hand, surgical intervention in Mallory-Weiss syndrome is required toachieve hemostasis in only 10% of cases.[13] The bleeding from a Mallory-Weiss tearspontaneously ceases in 50-80% of patients by the time endoscopy is performed.[13]For patients in whom bleeding is visualized at endoscopy, the endoscopic treatmentoptions are electrocoagulation, heater-probe application, hemoclips, epinephrineinjection, or sclerotherapy.In a series published by Bataller et al, hemostasis was achieved in 100% of patientswith Mallory-Weiss tears by using endoscopic sclerotherapy with epinephrine (1:10,000)and 1% polidocanol. Other nonoperative therapies are reserved for cases in whichendoscopic attempts at creating hemostasis have failed.Other available options are angiographic intra-arterial infusion of vasopressin andtranscatheter embolization of branches of the left gastric artery using Gelfoam. Avoidthe balloon tamponade technique using the Sengstaken-Blakemore tube in thisparticular circumstance, because this apparatus may extend the mucosal laceration intoa transmural laceration with perforation.[13]Surgical intervention is indicated in patients with continued bleeding after failed attemptsat nonoperative therapies.Bleeding from the gastroesophageal junction is visualized through an anteriorgastrotomy. Once the tear is localized, the bleeding is controlled by oversewing thelesion.The overall mortality rates for patients who require emergent surgery is 15-25%, incontrast to a mortality rate of 3% or less for patients whose bleeding stops by the timeof the initial endoscopy.[13]Dieulafoy Lesion TreatmentThe initial endoscopic management of this lesion can be highly successful. In a reportby Norton et al describing their experience with 90 Dieulafoy lesions, endoscopicmanagement achieved primary hemostasis in 96% of cases.
  56. 56. Contact thermal ablation with a heater probe is the most effective technique, with orwithout the combined use of epinephrine to slow or stop the bleeding prior to applyingthe heater probe. No studies have been performed that compare surgical andendoscopic therapy for Dieulafoy lesions.Although surgical intervention may be required after failed endoscopic therapy,endoscopy is still an important adjunct for management, because anonbleedingDieulafoy lesion may be undetectable through a gastrotomy.Because of this potential problem, a combined endoscopic and surgical approach hasbeen adopted. The vascular malformation can be marked with India ink through theendoscope.Rebleeding after endoscopic therapy occurs in 11-15% of cases, with most cases ofrebleeding controlled at repeat endoscopy.[16] (Repeat endoscopy for patients who haverebleeding has been validated in controlled studies of endoscopy and surgery.)The 30-day mortality rate from the study by Norton et al was 42%, which is a reflectionof the severe comorbid conditions associated with patients who have bleeding from aDieulafoy lesion.Angiodysplasia TreatmentBleeding from angiodysplasias can range from occult blood loss to life-threateninghemorrhage. Because the lesions are small and superficial, endoscopic therapy ishighly successful. Endoscopic treatments and devices used for hemostasis includelasers, contact heat probes, electrocoagulation, and injection therapy.The contact probe coagulators have been the most common form of endoscopictreatment because of their proven success and ability to target a bleeding lesiontangentially.Recurrent bleeding can occur from the mucosal injury caused by the coagulation. Toovercome the possibility of a delayed hemorrhage, endoscopic band ligation has beenapplied for hemostasis in nonvariceal GI bleeding, including angiodysplasias. [56]
  57. 57. When endoscopic techniques fail, surgical resection becomes necessary. Whenpangastric involvement is the source of bleeding, a total gastrectomy may be required;however, this is extremely rare. Available nonsurgical options include angiography withcatheter-directed vasopressin. Combined hormonal therapy with estrogen andprogesterone for patients in whom the diagnosis is unknown and vascular lesions aresuggested has not been demonstrated to be effective.Aortoenteric FistulaPatients with an aortoenteric fistula most often present with a self-limiting sentinelhemorrhage that is then followed by an exsanguinating, massive GI bleed. For thewarning lesser sentinel bleed in a patient with a history of an abdominal aortic aneurysmrepair or a known aortic aneurysm, the diagnosis of a graft-enteric fistula should beconsidered.An upper endoscopy is the procedure of choice to help diagnose the fistula. It should beperformed to the ligament of Treitz. Upper endoscopy findings also help to excludeother sources of UGIB.Once the diagnosis of aortoenteric fistula is confirmed or seriously considered,emergency surgical intervention is required. In most instances, the aortic graft isremoved after debridement and closure of the duodenum, followed by an extra-anatomic vascular bypass in order to bypass the ligated aorta and revascularize thelower extremities.The perioperative mortality rate is 22-75%,[57] and major complications are common.Published opinions state that graft excision is not necessary as long as no grosscontamination and purulence are present at the time of laparotomy.[58]Under thesecircumstances, antibiotics are administered long-term.Another option emerging in the surgical literature is the use of endovascular stents torepair the fistula.[59, 60] Endovascular stent management is technically feasible and maybe used as a bridge to more definitive treatment after hemodynamic stabilization inhigh-risk surgical patients.
  58. 58. Stent grafting immediately controls hemorrhage; however, the device is placed in aninfected field. As a result, adjunctive measures, such as long-term antibiotic use,percutaneous drainage, and bowel diversion, may be required.[61]According to the 2010 ACR UGIB guidelines, variceal UGIB that does not respond toendoscopic management should be treated with a transjugular intrahepaticportosystemic stent shunt (TIPS).[28] The 2008 SIGN guidelines consider TIPS to be thetreatment of choice for uncontrolled variceal bleeding.[27] Primary and secondary TIPSpatency rates have greatly improved with the use of stent grafts in lieu of bare metalstents. Doppler ultrasonography of the liver is useful for TIPS monitoring, and bothDoppler ultrasonography and CT may be useful for planning TIPS insertion.[28] Althoughendovascular stents have been shown to be effective in treating aortoenteric fistulas,case reports are emerging describing aortoenteric fistulas in patients with abdominalaortic aneurysm treated initially with stent grafts as well.[62]Treatment ComplicationsComplications of endoscopic therapy include aspiration pneumonia and perforation (1%for the first endoscopic therapy, 3% for the second). Bleeding can be caused by drillinginto the vessel with the laser, by perforating the vessel with an injection, or by removingthe clot with failure to coagulate the vessel.Tseng et al investigated the cardiovascular effects of emergency endoscopy for UGIB inpatients with stable coronary artery disease (CAD)[63] and found that the patientscommonly experienced, primarily on a subclinical level, ventricular arrhythmias andmyocardial ischemia. The authors results were as follows: Incidence of ventricular arrhythmias during endoscopy - 42% (patients with CAD) versus 16% (controls) Frequency of ventricular arrhythmias during endoscopy - 1.19 events per minute (patients with CAD) versus 0.12 events per minute (controls) Number of patients with ischemic ST changes - 9 patients with CAD versus 1 controlComplications from emergency abdominal surgery include ileus, sepsis, poor woundhealing, and myocardial infarction.
  59. 59. Salvage surgery is associated with a high mortality rate, reflecting the comorbidities ofpatients who rebleed or continue to bleed.Post-treatment Monitoring and CareThe 2010 international consensus guidelines on UGIB state that selected low-riskpatients may be discharged immediately following endoscopy, but high-risk patientsshould remain hospitalized for at least 72 hours.[40]According to the 2008 SIGN guideline, patients with a post-endoscopic Rockall score ofless than 3 have a low risk of rebleeding or death and are candidates for earlydischarge and outpatient follow up.[27]The goal is to maintain the intragastric pH above 6 to maintain the clot. This is mosteasily achieved by intravenous proton pump inhibitor (PPI) therapy. After the acutephase, 72 hours, the coagulated vessel should be stable and the patient can beswitched to oral therapy. If the patient rebleeds or has ongoing bleeding, then repeat ofendoscopic therapy would be considered. If this is not successful, then interventionalradiology is performed to clot the bleeding vessel. If this fails, then surgery would beconsidered.In the subsequent 48-72 hours after endoscopic therapy, the patient should receiveacid-suppressive therapy to maintain a high gastric pH (above 6). A high gastric pH canbe achieved by a continuous infusion of high-dose intravenous PPI therapy.
  60. 60. Patients who do not require endoscopic therapy and do not have other comorbiditiesshould be considered for discharge.Patients who did not require endoscopic treatment should receive routine, oral dosing ofa PPI, ie, daily dosing prior to breakfast. Whether high-dose intravenous PPI therapy isadvantageous in this setting remains controversial.Oral PPI therapy can be achieved with any of the oral PPI preparations.Patients should be tested for H pylori either by histology of gastric biopsy specimenstaken on initial upper endoscopy or by serologic tests. If positive, H pylori therapyshould be instituted after the patient has been discharged and is in stable condition.Moreover, H pylori eradication should be confirmed 4-6 weeks later in patients withUGIB. This can be done by checking the stool for the H pyloriantigen.Tachyphylaxis may develop within 24 hours if H2-receptor antagonists areadministered.Data on acid suppression via oral PPI therapy in order to produce a reduction inrebleeding are limited. High-dose intravenous PPI therapy appears to reducerebleeding, but PPIs are not currently approved by the US Food and DrugAdministration (FDA) for such treatment. The patient may be fed after recovery fromlocal and intravenous anesthesia.Some patients may require further endoscopic therapy. If repeat endoscopic therapy isneeded, the stomach will empty liquids without residue within 3 hours. The 2008 SIGNguideline recommends repeat endoscopy and endotherapy within 24 hours when initialendoscopic treatment is deemed suboptimal or in patients in whom rebleeding will likelybe life threatening.[27]If the patient remains stable, the patient can then be started on therapy for ulcerhealing.The patient should continue oral therapy for ulcer disease noted on endoscopy or forulcers caused by cautery techniques during endoscopic therapy. The greatest risk forperforation is usually within the first 48 hours after endoscopic therapy. Long-term acid
  61. 61. suppression therapy should be offered with either full-dose H2-receptor antagonists orlow-dose PPIs to prevent ulcer recurrence or its complications.[64]Aspirin and NSAID therapies should be avoided in view of their adverse effect onplatelet aggregation and ulcer healing. However, according to the 2010 internationalconsensus guidelines, resumption of aspirin therapy in patients who require anticlottingprophylaxis should not be delayed as cardiovascular risks outweigh the risk ofrebleeding.[40]The 2008 SIGN guidelines state that patients with healed bleeding ulcers who arenegative for H pylori require concomitant PPI therapy at the usual daily dose if NSAIDs,aspirin, or COX-2 inhibitors are indicated.[27]If patients must remain on NSAIDs or low-dose aspirin, secondary prophylaxis againstNSAID-induced ulcers should be given. According to the 2010 international consensusguidelines on UGIB, postdischarge use of aspirin or NSAIDs requires cotherapy withPPI.[40]Only lansoprazole (15 mg or 30 mg daily),[65] esomeprazole (20-40 mg daily), andmisoprostol (200 µg 4 times daily)[66] are approved by the FDA for prophylaxis againstNSAID-induced ulcers.The patients hemoglobin value should be monitored to assess the efficacy of irontherapy as an outpatient; further improvement should be noted. Erythropoietinanalogues have been shown to be effective in increasing the rate of hemoglobinproduction after ulcer hemorrhage.Repeat endoscopy should be done in a few weeks in patients with gastric ulcers todocument ulcer healing and to exclude cancer.[67]
  62. 62. Deterrence and Prevention of UGIBAntibiotic therapy should be given if H pylori is present in the setting of any history ofulcer disease. Eradication of H pylori has been demonstrated to reduce the risk ofrecurrent ulcers and, therefore, recurrent ulcer hemorrhages.NSAIDs should be avoided. If not possible, they should be used at the lowest dose andduration.PPI or misoprostol cotherapy should be used along with NSAIDs.The use of cyclooxygenase-2 inhibitors has been shown to reduce the risk of ulcerhemorrhage, although only when not combined with aspirin therapy. Concerns havebeen raised about an increase in myocardial infarction and stroke in patients takingselective cyclooxygenase-2 inhibitors.As demonstrated in the study by al-Assi et al, the combination of H pylori infection andNSAID use may increase the risk of ulcer hemorrhage; however, the treatment of Hpylori in patients who are taking NSAIDs remains controversial.[23]Medication SummaryRebleeding is associated with increased morbidity and mortality; therefore, this is themajor goal of therapy.As advised in the 2008 SIGN guidelines, patients with chronic liver disease who presentwith acute UGIB should be started on antibiotic therapy.[27]The use of H2-receptor antagonists has not been shown to be effective in altering thecourse of UGIB. A meta-analysis concluded that there was a possible minor benefit withintravenous H2 antagonists in bleeding gastric ulcers but no benefit in duodenalulcers.[68]The use of cyclooxygenase-2 inhibitors has been shown to reduce the risk of ulcerhemorrhage, although only when not combined with aspirin therapy. Concerns havebeen raised about an increase in myocardial infarction and stroke in patients takingselective cyclooxygenase-2 inhibitors.
  63. 63. As demonstrated in the study by al-Assi et al, the combination of H pylori infection andNSAID use may increase the risk of ulcer hemorrhage; however, the treatment of Hpylori in patients who are taking NSAIDs remains controversial.[23]The 2008 SIGN guidelines clearly advocate the discontinuation of aspirin and NSAIDsin patients who present with peptic ulcer bleeding. When ulcer healing and eradicationof H pylori are confirmed, aspirin and NSAIDs should only be resumed if there is a clearindication for their use.[27]Eradication of H pylori can reduce the risk of rebleeding. Current anti-H pyloriregimensinclude a variety of drug combinations. Typically, an antimicrobial agent is combinedwith an H2-receptor antagonist or a PPI.The treatment regimens approved by FDA have eradication rates for H pylori of 70-90%.[11]Drugs used to treat H pylori infection include the following: Omeprazole Ranitidine bismuth citrate Bismuth subsalicylate LansoprazoleConsider for admission and early endoscopy (and calculation of full Rockall score) if: aged ≥60 years (all patients who are aged >70 years should be admitted); or witnessed haematemesis or haematochezia (suspected continued bleeding); or haemodynamic disturbance (systolic blood pressure <100 mm Hg, pulse ≥100 beats per minute); or liver disease or known varices.Other significant comorbidity (especially cardiac disease, malignancy) should also lower thethreshold for admission.RISK ASSESSMENT AND PROGNOSIS IN GASTRODUODENAL BLEEDING: