Presentation on theme: "The Approach to Upper GI Bleeding"— Presentation transcript:
1 The Approach to Upper GI Bleeding Group D – Analyst GrpVigilia, PatriceVillaflor, IreneVillafuerte, MarcVillar, CherryVillasis, RamonVistal, KristineYap, Margaux
2 Presentation Objectives Review of the anatomy and physiology of the digestive tract.Presentations of GI bleeding, its classifications, and its sources.Approach to a patient with Upper GI bleeding.Enumerate the different tools used in the evaluation and diagnosis of patients presenting with GI bleeding.
3 The Anatomy GI Tractextends from the mouth to the anus, and comprises several organs with distinct functionsseparating the organs are specialized independently controlled thickened sphincters that assist in the gut compartmentalizationgut wall: is organized into well-defined layers that contribute to the functional activities in each regionHarrison’s Principle of Internal Medicine, 17th ed.
4 Important Point:The anatomic cut-off for upper GI is the Ligament of TreitzIt is located in the fourth portion of the duodenum (the last 2 inches).It connects the fourth portion of the duodenum to the diaphragm near the splenic flexure of the colon.Snell’s Clinical Anatomy, 7th ed.
5 Functions of the GI Tract Two main functions:Assimilation of nutrientsElimination of wastesORGANSFUNCTIONEsophagusPropels the bolus of food to the stomachStomachFurthers food preparation by triturating and mixing the bolus with pepsin and acid.Small IntestinesSite of major nutrient absorption.Large IntestinesPrepares the waste materials for controlled evacuation.Harrison’s Principle of Internal Medicine, 17th ed.
6 GI Bleeding Presentation Hematemesis - vomitus of red blood or coffee-grounds materialMelena – black, tarry, foul-smelling stoolHematochezia – passage of bright red or maroon blood from the rectumOccult GI Bleeding – identified through fecal occult blood test or the presence of iron deficiencySystemic signs of Blood Loss or Anemia – lightheadedness, syncope, angina, dyspneaHarrison’s Principle of Internal Medicine, 17th ed.
7 GI Bleeding Classification Acute vs ChronicUGI Bleeding vs LGI Bleeding
8 Acute vs ChronicAcute - typically presents with overt blood loss that can be readily recognized by the patient or treating physicianChronic - long-term GI bleeding may go unnoticed or may cause fatigue, anemia, black stools, or a positive test for microscopic bloodWashington manual of medical therapeutics, 32nd editionemedicinehealth.com
9 UGI Bleeding vs LGI Bleeding Source of bleeding is ABOVE the ligament of TreitzUsually presented as:HEMATEMESISMELENA, indicates that blood has been present in the GI tract for at least 14 hrsMay also present as HEMATOCHEZIA if an upper lesion bleeds briskly that blood does not remain in the bowel long enough for melena to develop.May be occultLGISource of bleeding is BELOW the LIGAMENT of TREITZUsually presented asHEMATOCHEZIA – passage of bright red or maroon blood from the rectum.May be occultHarrison’s Principle of Internal Medicine, 17th ed.
10 The remaining portion of the Small Intestines Sources of GI BleedingUpper GIEsophagusStomachDuodenumLower GIThe remaining portion of the Small IntestinesColonic SourceHarrison’s Principle of Internal Medicine, 17th ed.
11 Approach to the patient Measurement of the heart rate and blood pressure is the best way to assess the patient.Clinically significant bleeding leads to postural changes in HR or BP, tachycardia and recumbent hypotension.
12 Approach to the patient Hemoglobin DeterminationDoes not fall immediately with acute GIB: this is due to the proportionate reduction in plasma and red cell volumes.As extravascular fluid enters the vascular space to restore volume, the hemoglobin falls.
13 UPPER GI BLEEDING History and PE in not usually diagnostic. Upper endoscopy is the test of choice and should be performed urgently in patients with hemodynamic instability.Harrison’s Principle of Internal Medicine, 17th ed.
14 Endoscopy procedure is the best method for examining upper GI mucosa minimally invasive diagnostic medical procedureused to assess interior surfaces of organs by inserting a tube into the bodyinstrument may have a rigid or flexible tube & not only provide an image for visual inspection and photography, but also enable taking biopsies & retrieval of foreign objectssedatives may be given so as to relieve discomfortHarrison’s Principle of Internal Medicine, 17th ed.
15 EndoscopyUsed to determine the cause of bleeding, pain, nausea and vomiting, weight loss, altered bowel function and feverUpper endoscopyevaluates the esophagus, stomach and duodenuminitial test performed in patients with suspected ulcer disease, esophagitis, neoplasm, malabsorption and Barrett's metaplasia because it directly visualizes abnormalityHarrison’s Principle of Internal Medicine, 17th ed.
16 Endoscopy Risks of procedure: risk of bleeding gastrointestinal perforationHarrison’s Principle of Internal Medicine, 17th ed.
17 Algorithm for patients with acute upper gastrointestinal bleeding IV PPI therapy + endoscopic therapyICU for 1-2 days; ward for 2-3 daysEndoscopic therapyNo endoscopic therapyWard for 1-2 daysDischarg eICU for 1 day; ward for 2 daysIV PPI therapy +/- endoscopic therapyNo IV PPI or endoscopic therapyWard for 3 daysDischargeActive bleeding or visible vesselLigation (preferred) or sclerotherapy + IV octreotideClean baseAdherent ClotFlat, pigmented spotActive bleedingNo active bleedingAcute Upper GI BleedingUlcerEsophageal VaricesMallory-Weiss TearHarrison’s Principle of Internal Medicine, 17th ed.
18 Other tests that may be performed: Laboratory Tests (CBC, Serum Electrolyte, Fecal Occult Blood, BUN/Crea Ratio)Radiography (Barium Swallow, CT Scan)Harrison’s Principle of Internal Medicine, 17th ed.
19 Summary Assess the patient by doing History and PE Heart Rate and Blood PressureDo an Endoscopic ExamPerform other laboratory and radiographic exams if necessary
20 Salient Features 55 y/o female History of vague epigastric discomfort hematochezia [2 episodes of melena (2 cupfuls/episode)]hematemesis [1 episode of coffee ground vomiting]cold clammy sweats and dizzinessintake of Diclofenac Na intermittentlyregular medications: clopidogrel (anticoagulant)(+) DMoverweight [BMI = 26.5]
21 10 kg weight loss for the past 6 months orthostatic hypotension (BP 120/80 when supine, 100/60 at sitting)PR 105/min RR 22/minPale palpebral conjuctiva and anicteric sclerano cervical lymphadenopathylung and heart sounds are normalapex beat at 6th LICSAbdomen with hyperactive bowel sounds, soft non tender, without palpable mass or organomegalyDRE maroon colored stools
22 Clinical Impression:Acute Upper GI bleeding secondary to PUD (to rule out Gastric CA)
23 Hemorrhagic or Erosive gastropathy Peptic UlcerCauses of Upper GIBleedingEsophageal VaricesMallory Weiss TearsHemorrhagic or Erosive gastropathyGastric CADifferential Diagnosis
26 Incidence and Epidemiology Acid peptic disorders - 4 million individuals (new cases and recurrences) affected per yearLifetime prevalence of PUD in the United States~12% in men and 10% in womenan estimated 15,000 deaths per year - as a consequence of complicated PUDestimated burden on direct and indirect health care costs of ~$10 billion per year in the United StatesHarrisons principles of internal madicine 17th ed p1838
27 Incidence and Epidemiology Duodenal Ulcersoccur in 6–15% of the Western populationincidence of DUs declined steadily from 1960 to 1980 and has remained stable since then.death rates, need for surgery, and physician visits have decreased by >50% over the past 30 yearsEradication of H. pylori has greatly reduced recurrence rates.The reason for the reduction in the frequency of DUs is likely related to the decreasing frequency of Helicobacter pylori. Before the discovery of H. pylori, the natural history of DUs was typified by frequent recurrences after initial therapy. Eradication of H. pylori has greatly reduced these recurrence rates.Harrisons principles of internal madicine 17th ed p1838
28 Incidence and Epidemiology Gastric Ulcersoccur later in life than duodenal lesions (peak incidence reported in the sixth decade)More than half occur in malesless common than Duodenal UlcersAutopsy studies suggest a similar incidence of DUs and GUs.Harrisons principles of internal madicine 17th ed p1838
29 Incidence and Epidemiology Helicobacter pyloriPrevalence : developing parts of the world (80% of the population by age of 20)industrialized countries (20 – 50 %)United States (~30%)About 10% of Americans <30 are colonized with the bacteriaIn contrast, in the United States this organism is rare in childhood. The overall prevalence of H. pylori in the United States is ~30%, with individuals born before 1950 having a higher rate of infection than those born later. About 10% of Americans <30 are colonized with the bacteria. The rate of infection with H. pylori in industrialized countries has decreased substantially in recent decades. The steady increase in the prevalence of H. pylori noted with increasing age is due primarily to a cohort effect, reflecting higher transmission during a period in which the earlier cohorts were children. It has been calculated through mathematical models that improved sanitation during the latter half of the nineteenth century dramatically decreased transmission of H. pylori. Moreover, with the present rate of intervention, the organism will be ultimately eliminated from the United States.The risk of H. pylori infection is declining in developing countries.Harrisons principles of internal madicine 17th ed p1838
30 Incidence and Epidemiology Helicobacter pyloriThe rate of infection in the United States has fallen by >50% when compared to 30 years ago.Transmission of H. pylori occurs from person to person, following an oral-oral or fecal-oral routeHarrisons principles of internal madicine 17th ed p1838
31 Incidence and Epidemiology Helicobacter pyloriRisk Factors :(1) birth or residence in a developing country(2) domestic crowding(3) unsanitary living conditions(4) unclean food or water(5) exposure to gastric contents of an infected individual.Two factors that predispose to higher colonization rates include poor socioeconomic status and less education. These factors, not race, are responsible for the rate of H. pylori infection in blacks and Hispanic Americans being double the rate seen in whites of comparable age. Other risk factors for H. pylori infection are (1) birth or residence in a developing country, (2) domestic crowding, (3) unsanitary living conditions, (4) unclean food or water, and (5) exposure to gastric contents of an infected individual.Harrisons principles of internal madicine 17th ed p1838
32 Clinical Presentation of Upper GI Bleeding due to PUD HistoryPE
33 History Abdominal or Epigastric pain Duodenal Ulcer Described as burning, gnawing, aching sensation or hunger painImportant to know the temporal patternDuodenal UlcerOccurs 90 mins to 3 h after a mealRelieved by antacids or foodPain that awakes the patient fr sleeping (bet. midnight & 3 am)Gastric UlcerDiscomfort precipitated by foodNausea & weight loss occur here more commonlyNSAID induced mucosal diseaseCan present with complications like bleeding, perforation, and obstruction without antecedent symptom
34 History Penetrating ulcer (pancreas) Constant dyspepsia , no longer relieved by food or antacids, radiates to the backPerforationSudden onset of severe, generalized abdominal painGastric outlet obstructionPain worsening with meals, nausea & vomiting of undigested foodBleedingTarry stools or coffee ground emesis
35 Physical ExaminationEpigastric tenderness is the most frequent finding in patients with GU or PUPain may be found at the right side of the midline.Tachycardia and orthostasis may be suggestive of dehydration secondary to vomiting or active gastrointestinal blood loss.
36 Physical ExaminationPerforation is possible if patients manifest severely tender broad like abdomenPresence of succussion splash indicated retain fluid in the stomach suggestive of intestinal obstruction.
38 Radiographic Procedure (Barium Study) Commonly used as a first test for documenting an ulcerSensitivity: 80% (single contrast barium meals); 90% (double contrast)Sensitivity is decreased in small ulcers (<0.5cm), presence of previous scarring, postoperative patients
39 Film reveals a small duodenal ulcer crater on the inferior aspect of the bulb with a moderately severe cloverleaf deformity of the bulb.Benign duodenal ulcer appears as a well demarcated crater, seen at the bulb
40 Benign gastric ulcerUlcer crater-collection of barium on dependent surface which usually projects beyond anticipated wall of stomach in profile (penetration)Hampton’s line-1 mm thin straight line at neck of ulcer in profile view which represents the thin rim of undermined gastric mucosaUlcer collar-smooth, thick, lucent band at neck of ulcer in profile view representing thicker rim of edematous gastric wallUlcer mound-smooth, sharply delineated tissue mass surrounding a benign ulcerRing shadow-thin rim of contrast which represents an ulcer on the non-dependent surface of an air-contrast studyThickened folds radiating directly to the base of the ulcer en faceBenign. lesser curvature gastric ulcer. Red arrows point to Hampton's Line, a thin, straight line at neck of ulcer in profile view which represents the thin rim of undermined gastric mucosa. The blue arrows point to the ulcer mound, a smooth, sharply delineated soft-tissue mass surrounding a benign ulcer. Note how the ulcer projects beyond the confines of the expected wall of the stomach.
41 EndoscopyProvides the most sensitive and the most specific approach for examining the upper GIPermits direct visualization of the mucosaFacilitates photographic documentation of mucosal defect and tissue biopsy to rule out malignancy or H. pyloriHelpful in identifying lesions too small to detect by radiographic examination, for evaluation of atypical radiographic abnormalities, determine if ulcer is source of loss of blood
44 GOALS in treating PUD Provide relief of symptoms (pain or dyspepsia) Promote ulcer healingPrevent ulcer recurrence and complications
45 Drugs used in the Treatment of PUD Drug TypeExamplesDoseAcid-suppressing (Antacids)Mylanta, Maalox, Tums, Gavisconmeq/L 1-3 h after meals and hsH2 receptor antagonistsCimetidine400 mg bidRanitidine300 mg hsFamotidine40 mg hsNizatidineProton Pump inhibitorsOmeprazole20 mg/dLansoprazole30 mg/dRabeprazolePantoprazole40 mg/dEsomeprazoleHarrison’s Principle of Internal Medicine 17th edition
46 Mucosal Protective Agents Drugs used in the Treatment of PUDDrug TypeExamplesDoseMucosal Protective AgentsSucralfate1 g qidProstaglandin analogueMisoprostol200 ug qidBismuth-containing compoundsBismuth subsalicylate (BSS)See anti-H. pylori regimenHarrison’s Principle of Internal Medicine 17th edition
47 Drugs used in the Treatment of PUD Acid neutralizing/inhibitory drugs (Antacids)MOA: neutralize secreted acidsOften used by patients for symptomatic relief of dyspepsiaAntacidsSide effectsMaaloxMagnesium OHDiarrhea and hypermagnesemiaAluminum OHConstipation and phospahte depletionCalcium carbonateMilk alkali syndrome – hypercalcemia, hyperphosphatemia, renal calcinosis renal insufficiency (long term use)Sodium bicarbonateSystemic alkalosisCombination of Mg and Al OH avoid the side effects.Maalox contraindicated in chronic renal failure patients because of possible hyperphosphatemia (Mg) and neurotoxicity (Al)
48 Drugs used in the Treatment of PUD H2 receptor antagonistsMOA: Competitive inhibitors of the action of histamine at H2 receptorsHealing in 80-90% of cases after 4-8 weeks of therapyCimetidine has an anti-androgenic effect due to cytochrome p450 enzyme inhibition reversible gynecomastia and impotenceHarrison’s Principle of Internal Medicine 17th edition
49 Drugs used in the Treatment of PUD Proton Pump (H+,K+ ATPase) inhibitorsMOA: Covalently bind and irreversibly inhibit H+K+ ATPaseGiven before meal, activation in acidic environmentExamples of drugsOmeprazoleAdministered as enteric-coated grabules in a sustained-release capsule that dissolves in SI at pH 6, Lanoprazole can be taken in an orally disintegrating tablet (with or w/out water)LanoprazolePantoprazoleEnteric-coated tablet, ParenteralRabeprazoleEnteric-coated tablet
50 Drugs used in the Treatment of PUD Cytoprotective agentsDrugsMOASucralfatePhysicochemical barrier, promote trophic action by binding to growth factors, enhance prostaglandin synthesis, stimulate mucous and HCO3 secretion, enhance mucosal defense and repairColloidal bismuth subcitrate and bismuth subsalicylatePrevention of further pepsin/HCl-induced damage, stimulation of prostaglandin, HCO3 and mucous secretionProstaglandin analogueMaintain mucosal integrity and repair, enhance mucous and HCO3 secretion, stimulate mucosal blood flow, decrease mucosal cell turnoverHarrison’s Principle of Internal Medicine 17th edition
51 Regimens recommended for eradication of H. pylori infection TRIPLE THERAPYDoseBismuth salicylateMetronidazoleTetracycline2 tablets qid250 mg qid500 mg qidRanitidine bismuth citrateAzithromycin or Metronidazole400 mg bid500 mg bidOmeprazole (lansoprazole)ClarithromycinMetronidazole or Amoxicillin20 mg (30 mg) bid250 or 500 mg bid500 mg bid or 1 g bidHarrison’s Principle of Internal Medicine 17th edition
52 Regimens recommended for eradication of H. pylori infection QUADRUPLE THERAPYDoseOmeprazole (Lansoprazole)Bismuth subsalicylateMetronidazoleTetracycline20 mg (30 mg) daily2 tablets bid250 mg bid500 mg bid** combination therapy for 14 days provides greatest efficacyHarrison’s Principle of Internal Medicine 17th edition
53 SURGICAL THERAPY Surgical intervention in PUD 1. elective for treatment of medically refractory disease2. urgent/emergent for the treatment of ulcer-related complications ( hemorrhage, perforation and obstruction)Pharmacologic and endoscopic approaches for treatment of PUD and its complications decreased number of operations
54 TAN, GENEVIEVE: PATHOPHYSIOLOGY TAN, KURT: CLINICAL FEATURES (SYMPTOMS, RISK FACTORS) TAN, MARIE: DIAGNOSIS AND TREATMENT TAN, SAMANTHA: COMPILER GROUP B BGD 1: UPPER GI BLEEDINGNSAID Gastropathy
55 Harrison’s Principles of Internal Medicine 17th edition PathophysiologyNSAIDs decrease mucosal defense and repair through prostaglandin depletionHCl secretionMucin secretionBicarbonate secretionSurface active phospholipid secretionEpithelial cell proliferationDirect toxicity “ion trapping”Endothelial effects causing stasisHarrison’s Principles of Internal Medicine 17th edition
57 PathophysiologySchematic 1. Possible Pathogenesis of NSAID Induced Small Bowel Damage.J Pharm Pharmaceut Sci (www.ualberta.ca/~csps) 3(1): , 2000
58 Harrison’s Principles of Internal Medicine 17th edition Symptoms:dyspepsianausea, vomitingdiarrheagastric and duodenal ulcerationupper GI bleedingHarrison’s Principles of Internal Medicine 17th edition
59 Harrison’s Principles of Internal Medicine 17th edition Risk Factors:advanced age (>60 y/o)History of ulcerConcomitant use of glucocorticoidsMultiple, high-dose NSAIDsCorticosteroidsConcomitant anticoagulation or coagulopathySerious or multisystem diseasePotential risk factors: smoking, alcohol, H. pylori infectionHarrison’s Principles of Internal Medicine 17th edition
61 Treatment of NSAID-related mucosal injury CLINICAL SETTINGRECOMMENDATIONActive UlcerNSAID discontinuedNSAID continuesH2 receptor antagonist / PPIPPIProphylactic TherapyMisoprostolSelective COX-2 InhibitorH. Pylori infectionEradication if active ulcer present or there is a past history or peptic ulcer diseaseHarrison’s Principles of Internal Medicine 17th edition
62 Guide to NSAID therapy NO or LOW NSAID GI Risk NSAID GI Risk NO Cardiovascular Risk(no Aspirin)Traditional NSAIDTraditional NSAID / Coxibplus PPIConsider non-NSAID therapyWITHCardiovascular Risk(consider Aspirin)Traditional NSAID plus PPI if GI risk warrants gastroprotectionA gastro-protective agent must be added if a traditional NSAID is prescribed.Harrison’s Principles of Internal Medicine 17th edition
64 EpidemiologyIncidence and mortality decreased markedly for the past 75 years, worldwideRemains high in Japan, China, Chile & IrelandRisk is greater among lower socioeconomic classesEnvironmental exposure (begins in early life)Migrants (high low) maintain their susceptibility, while the risk of offspring approximate the homelandDietary carcinogens – most likely factors
65 Clinical Features of Gastric Carcinoma Superficial & surgically curable – no symptomsMore extensive – insidious upper abdominal discomfortAnorexia with slight nausea – very common but is not the usual presenting complaintWeight loss - observedNausea and vomiting – prominent with tumors of the pylorusDysphagia and early satiety – symptoms caused by diffuse lesions originating in the cardiaNo early physical signsPalpable abdominal mass – long standing growth and regional extension
66 Gastric CA spread by:Direct extension through the gastric wall to the perigastric tissues, adhering to adjacent organs (pancreas, colon, or liver). Liver is most common site for hematogenous spread.LymphaticsSeeding of peritoneal surfacesMetastases that occur frequently:intraabdominal and supraclavicular nodesKrukenberg’s tumor – metastatic nodules to the ovary“Sister Mary Joseph node” – periumbilical regionPeritoneal cul-de-sac (Blumer’s shelf palpable on rectal/vaginal exam)
67 Unusual clinical features: Presence of Iron deficiency anemia in men and occult blood in stool for both sexes mandates a search for occult GI tract lesionCareful assessment is of particular importance in patients with atrophic gastritis or pernicious anemiaUnusual clinical features:Migratory thrombophlebitisMicroangiopathic hemolytic anemiaAcanthosis nigricans
68 Risk Factors high concentration of nitrates smoked, dried, salted food Diethigh concentration of nitratessmoked, dried, salted foodEnvironmentlower socioeconomic classesbacterially-contaminated foodexogenous source of nitrate-converting bacteriaKasama pa ba age and gender dito? (m>f, elderly >65???) Or is it under epidemiology?
69 Risk FactorsMedical ConditionsMenetrier’s diseasepernicious anemiaatrophic gastritishx of gastric ulcerGeneticblood type Aadenomatous polypsmutation in E-cadherin geneMenetrier’s dse – extreme hypertrophy of gastric rugal foldsPernicious anemia – vitamin B12 deficiencyAtrophic gastritis – chronic inflammation of the stomach; intestinal metaplasia cellular atypia neoplasiaUnder medical conditions, not sure if included: hx of gastric ulcer (possible risk factor, cause-effect not yet established, more data needed)Pernicious anemia, atrophic gastritis seen in elderly accdg to Harrison?GeneticType A – may be related to differences in mucous secretion, leading to altered mucosal protection from carcinogensHNPCC – hereditary nonpolyposis colorectal cancerFAP – familial adenomatous polyposis
70 Risk Factors + Hypothesis Acquireddecreased gastric acidityH. pylori infectionprior gastric surgery (antrectomy)prolonged exposure to histamine H2-receptor antagonists↑ Nitrate-converting BacteriaConversion of dietary nitrates to carcinogenic nitritesHypothesis: nsa baba… should we include??
72 Diagnosis Simplest diagnostic procedure Double-Contrast Radiographic ExaminationSimplest diagnostic procedureEvaluates patient with epigastric complaintsHelps detect small lesions by improving mucosal detailStomach should be distended every radiographic examination, decrease distensibility is the only indication of a diffuse infiltrative carcinoma
73 Diagnosis Gastroscopy Diagnostic method of choice Involves insertion of a fibre optic camera into the stomach to visualize itNot a mandatory if the radiographic features are typically benign
74 Diagnosis Gastroscopic Biopsy and Brush Cytology Endoscopic Biopsy Recommended to all patient with gastric ulcer in order to exclude a malignancyEndoscopic Biopsydone with the help of a fiber-optic endoscope which is inserted into the gastrointestinal tractSince gastric carcinomas are difficult to distinguish clinically or radiographically from gastric lymphomas, endoscopic biopsy should be made as deeply as possible due to the submucosal location of lymphoid tumors.
75 Staging system for gastric ca StageTNMFeaturesNo. of Cases %5 year survival, %TisN0M0Node negative;Limited to mucosa190IAT1N0M0Invasion of lamina propria or submucosa759IBT2N0M0Invasion of muscularis propria1044IIT1N2M0T2N1M0Node positive; invasion beyond mucosa but within wall1729T3N0M0Node negative, extension through wallIIIAT2N2M0T3N1-2M0Node positive; invasion of muscularis propria or through wall2115IIIBT4N0-1M0Node negative; adherence to surrounding tissue149IVT4N2M0Node positive; adherence to surrounding tissue303T1-4N0-2M1Distant metastases
76 TREATMENTComplete surgical removal of the tumor + resection of adjacent lymph nodes-only chance for cureSubtotal gastrectomyTreatment of choice for distal tumorsTotal / Near-Total gastrectomyTreatment for proximal tumorsExtended lymph node dissectionAdded risk of complications w/o enhancement of survivalReduction of tumor bulk is the best form of palliationMay enhance benefit from subsequent therapy
77 TREATMENT PROGNOSIS depends on 5 year survival probability Degree of tumor penetration into gastric wallRegional lymph node involvementVascular invasionAbnormal DNA content (aneuploidy)5 year survival probability~20% for distal tumors<10% for proximal tumorsRecurrences for ≥ 8 years post surgery
78 TREATMENT Radiotherapy Chemo + Radio therapy Palliation of pain Radiotherapy alone after complete resection does not prolong survivalChemo + Radio therapy5FU combined with radiation therapy slightly improved survival5FU may function as a radiosensitizerGASTRIC ADENOCARCINOMA – relatively radioresistant tumor; adequate tumor control requires doses of irradiation exceeding the tolerance of surrounding structures (ie bowel mucosa and spinal cord) therefore, radiotherapy is mainly for PALLIATION
79 TREATMENT Cytotoxic Drugs Cisplatin + epirubicin or 5FU (infusional) or irinotecanAssociated with partial responses in 30-50% of casesMinimal improvement of survival with adjuvant chemotherapy alone ff. complete resectionPerioperative treatment and post-op chemotherapy + radiotherapy reduces recurrence rate and prolongs survivalPerioperative treatmetn
82 Gastrointestinal Bleeding Upper- Refers to bleeding from esophagus, stomach, duodenum (above the Ligament of Treitz)Lower- Refers to bleeding from distal small bowel, colon, rectum, and anal canal (below the Ligament of Treitz)Fauci et al Harrison’s Principles of Internal Medicine (17th ed)
83 Clinical Presentation Upper GI BleedingHematemesisMelenaHematochezia (associated with hemodynamic instability and dropping hemoglobin)Hyperactive bowel soundsElevated BUNLower GI BleedingHematocheziaFauci et al Harrison’s Principles of Internal Medicine (17th ed)
84 Mallory Weiss TearsHx: vomiting, retching, coughing preceding hematemesis especially in alcoholicsStops spontaneously (80-90%)Fauci et al Harrison’s Principles of Internal Medicine (17th ed)
85 Esophageal Varices 4-31% of causes Most often it is a consequence of portal hypertensionFauci et al Harrison’s Principles of Internal Medicine (17th ed)
86 Hemorrhagic or Erosive gastropathy 3-11% (less common)mucosal lesions and thus do not cause major bleeding.Risk factors for NSAID-induced gastroduodenal ulceration: old age,high dose/multiple NSAID use, concomitant use of anticoagulant (clopidogrel), serious or multisystem disease (DM, HPN)Fauci et al Harrison’s Principles of Internal Medicine (17th ed)
87 Gastric CA 1-4% of causes (rare) risk factors present in our patient: old age and overweightPresents with significant weight loss, progressive epigastric pain and GI bleedingFauci et al Harrison’s Principles of Internal Medicine (17th ed)
88 Peptic Ulcer 35-62% (most common),1/3 of patients w/ active bleeding abdominal or epigastric pain is described as burning, gnawing, aching sensation or hunger painRisk Factors present in our patient: age, NSAID use , anticoagulant use (clopidogrel)Fauci et al Harrison’s Principles of Internal Medicine (17th ed)