Gastrointestinal bleeding definitions (I)

Transcription

1 definitions (I) Acute bleeding: vomiting blood or profuse rectal bleeding within 3 days, leading to hemodynamically unstable condition of the patient. Problems arising from blood loss must be treated often before proceeding to diagnosis Chronic bleeding: repeated episodes of presence of occult blood in stool definitions (II) Hematemesis: - fresh, red vomitus, containing hemoglobin (above lig. Treitz) suggesting acute bleeding - brown, containing digested blood (previous bleeding) Melena: (min. 100 ml) digested blood in faeces Hematochesia: fresh blood in the stool 1

2 definitions (III) ESTIMATED CONSEQUENCES OF ACUTE BLOOD VOLUME LOST 10% (500 ml) occasional vasovagal syncope 20% (1000 ml) exercise-induced tachycardia 30% (1500 ml) postural hypotension, pulse 40% (2000 ml) resting supine hypotension and severe tachycardia 50% (2500 ml) severe shock and death Main pathogenetic causes of gastrointestinal bleedings I. Damage (disruption) of the continuity of vessel wall: - ulcer bleeding, tumorous erosion, trauma II. Alteration of circulation: - portal hypertension, thrombosis etc. III. Changes of haemostasis: - thrombocytopenia - pathia, inferited of acquired factor deficiency 2

3 symptoms MILD BLEEDING: ortostatic changes of pulse and RR CONTINUOUS BLEEDING: weakness, fatigue, dizziness, pallor, thrist, air hunger, cold extremities, diminished urinary output SEVERE BLOOD LOSS: signs of perturbed organ perfusion, hepatic encephalopathy, altered mental status, hepatorenal/ or renal insufficiency, metabolic acidosis, ischemic heart attack management of diagnosis (I) HISTORY - previous GI bleeding episodes, abdominal surgery, known bleeding tendency, hematologic disorders, known severe liver, kidney or heart diseases - current medication - aspirin, NSAIDs coumarol, habits of alcohol consumption - onset, duration of present complains - form os bleeding, characteristics of stool 3

4 management of diagnosis (II) Physical examination: pulse and RR in both supine and upright position, signs of hypovolemia, anemia and coagulopathy, abdominal status, ascites, bowel sounds, tongue, rectal digital examination etc. Initial laboratory studies: Hb, htc, WBC, platelet count, PT (INR), PTT, serum BUN and creatinine, liver function management of diagnosis (III) Stabilization of the patient s condition: monitoring of ECG, RR, oxygen saturation, volume replacement (~300 ml/h saline), nasal oxygen, if necessary blood transfusion, FFP Insertion of nasogastric tube: (?) Endoscopy: emergency (<2 h) - urgent (within 12 h) - routine (next day) - diagnostic; therapeutic Angiography, Radionuclid scintigraphy (Tc99) 4

5 main sources (I) OESOPHAGUS (~ 1/3 of all GI bleeding cases ) variceal bleeding (portal hypertension) Mallory-Weiss tears Reflux oesophagitis stage III-IV. Corrosive oesophagitis hiatal hernia tumours perforation or rupture (traumatic, iatrogenic..) Development of esophageal varicosity Hepatic resistency Portal inflow Portal hypertension Appearance of varices HPVG > 10 Hgmm Dilatation of varices HPVG > 12 Hgmm Varix rupture 5

6 main sources (II) STOMACH AND DUODENUM (~ 1/2 of all) gastric and duodenal erosions (~ 30%) gastric ulcer and Dielaufoy lesion (~ 20%) duodenal ulcer (~ 30%) tumours (also benign!) anastomositis, jejunal ulcer angiodysplasia foreign bodies in the stomach cancer of the head of the pancreas Classification of peptic ulcer bleeding according to Forrest Forrest I.: active bleeding seen I/A: spurting arterial bleeding I/B: oozing venous bleeding Forrest II.: stigmata of recent hemorrhage II/A: visible vessel, protuberance II/B: adherent clot II/C: ulcer base with digested Hb Forrest III: clean base, no stigmata of bleeding 6

7 Visible vessel, infiltration with diluted epinephrine Forrest II.B, clot, infiltration 7

8 8

9 main sources (III) SMALL BOWEL (3-10 % of all cases) teleangiectasiae (Osler) tumours (mainly lymphomas are bleeding) Crohn s enteritis enteritis necrotisans, tuberculosis acut mesenterial ischemia Meckel s diverticulum volvulus or intussusception of the intestine Capsule ( Wireless ) endoscop miniature CCD camera, battery for 8 h, frames: 2-4/sec up to pictures Own energy supplementation and light source, optic Microwave radio-communication with the detector Indications: unclear bleedings in the small intestine, incipient Crohn s disease, tumours, coeliakia Self-digesting capsule Colon: delayed activation of the battery?, longer lasting battery? Therapeutic applications? 9

10 main sources (IV) COLON AND RECTUM (~15-20 % of all) diverticulosis hemorrhoids, rectal fissures, ulcers and varices neoplasms (cancer and polyps) arteriovenous malformations (right colon!) IBD (ulcerative colitis, Crohn s colitis) Infectious colitis (Shigella, Salmonella, ameba) Ischemic colitis, radiation colitis strategy of treatment (I) Administration to intensive care unit, with permanent endoscopic, surgical, radiological consultation, laboratory, availability of blood products Proper assessment of the hemodynamic status, evaluation of prognostic factors, immediate volume replacement, laboratory studies, blood group determination, necessary supplementation 10

11 strategy of treatment (II) ENDOSCOPIC HEMOSTATIC METHODS injection therapy: tonogen 1: dilution, saline, etanolamin-oleat, sodium-tetradecylsulphate, etc., sclerotherapy with polydocanol tissue glues: fibrin glue, Histoacryl mechanic hemostasis: metal clips, rubber band ligation, mini-loop ligation thermo-photocoagulation: HPU, Nd-YAG laser Argon plasma coagulation Varix ligation using rubber band 11

12 Haemostatic clips Clipping device 12

13 strategy of treatment (III) MEDICAL THERAPY - acid suppression (PPI or H2RA infusion i.v.) - vasoactive drugs for the reduction of portal pressure: 1. octreotid (somatostatin) infusion: 100 µg i.v. bolus, 25 µg/h infusion for h. 2. terlipressin (triglycil-lysin vasopressin) - lactulose, 3 x ml/day, sucralphate, - Helicobacter pylori eradication therapy - propranolol, neomycin, ISMN, DDAVP etc. Algorithm for treatment of acute variceal bleeding (J.Bosch, J.G. Abraldes, Semin.Hemat.41, Suppl ,2004) Suspection of variceal bleeding Early starting of vasoactiv drug administration: 1. Terlipressin 2. Somatostatin or octreotid Antibiotics, volume replacement Endoscopy: ligature, or sclerotherapy, in extreme: ballon tamponade, and continuation of drug therapy for about 5 days Further bleeding/early rebleeding Further bleeding(failure to control) Repeated endoscopic treatment trial rfviia? Rescue TIPS / Surgery 13

14 Further treatment options human albumin infusion, in case of severe haemostatic disturbance fresh frozen plasma, eventually platelet suspension, especially of hugh amount of transfusions was given, - consider dilution and Ca supplementation! Decomtamination of the intestine: lactulose, neomycin, rifaximin (Normix), SBP (spontaneous bacterial peritonitis) profilaxis: norfloxacin adequat diet (low in fat, rich in carbohydrate and vitamines, less protein) strategy of treatment (IV) OTHER THERAPEUTIC POSSIBILITIES - balloon tamponade (Sengstaken-Blakemore, Linton tube, Minnesotta tube) - TIPS (transjugular intrahep. portosyst. shunt) - arterial embolisation during angiography - surgical intervention (suture, resection etc.) - tradition surgical shunt (porto-caval, spleno-renal) - liver transplantation 14

15 Sengstaken-Blakemore tube Surgical treatment of acute gastrointestinal bleeding Primary acute operation: if acute bleeding could not been stopped (e.g. Forrest I/A ulcer) Early elective surgery: within 48 hours following successful primary hemostasis, because of high risk of rebleeding or other conditions (predominantly resection is carried out) Secondary acute operation: in case of rebleeding Elective surgery: giant ulcer in elderly, malignancy 15

16 Further perspectives in GI bleeding SPONTANEOUSLY STOPS up to 80 % of all cases, if varix rupture is excluded SEVERE REBLEEDING (within 48 hours) upper GI tract: % lower GI tract: < 10 % SURGICAL INTERVENTION: along with modern, GI intensive care unit 3-10 % OVERALL MORTALITY: 8-30 % 16