Gastrointestinal bleeding definitions (I) -...

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2010.10.14. 1 Gastrointestinal bleeding 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 Gastrointestinal bleeding 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

Transcript of Gastrointestinal bleeding definitions (I) -...

2010.10.14.

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Gastrointestinal bleedingdefinitions (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

Gastrointestinal bleedingdefinitions (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

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Gastrointestinal bleedingdefinitions (III)

• ESTIMATED CONSEQUENCES OF ACUTE BLOOD VOLUME LOST10% (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

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Gastrointestinal bleedingsymptoms

• 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

Gastrointestinal bleedingmanagement 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

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Gastrointestinal bleedingmanagement 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

Gastrointestinal bleedingmanagement 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)

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Gastrointestinal bleedingmain 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 herniatumoursperforation or rupture (traumatic,

iatrogenic..)

Development of esophageal varicosity

Hepatic resistency Portal inflow

Portal hypertension

Appearance of varices

Dilatation of varices

Varix rupture

HPVG > 10 Hgmm

HPVG > 12 Hgmm

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Gastrointestinal bleedingmain 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

angiodysplasiaforeign bodies in the stomachcancer of the head of the pancreas

Classification of peptic ulcer bleeding according to Forrest

• Forrest I.: active bleeding seenI/A: spurting arterial bleedingI/B: oozing venous bleeding

• Forrest II.: stigmata of recent hemorrhageII/A: visible vessel, protuberance II/B: adherent clotII/C: ulcer base with digested Hb

• Forrest III: clean base, no stigmata of bleeding

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Visible vessel, infiltration with diluted epinephrine

Forrest II.B, clot, infiltration

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Gastrointestinal bleedingmain sources (III)

• SMALL BOWEL (3-10 % of all cases) teleangiectasiae (Osler)tumours (mainly lymphomas are bleeding) Crohn´s enteritis

enteritis necrotisans, tuberculosisacut mesenterial ischemia

Meckel´s diverticulum volvulus or intussusception of the intestine

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Gastrointestinal bleedingmain sources (IV)

• COLON AND RECTUM (~15-20 % of all) diverticulosis hemorrhoids, rectal fissures, ulcers and varicesneoplasms (cancer and polyps) arteriovenous malformations (right colon!) IBD (ulcerative colitis, Crohn´s colitis) Infectious colitis (Shigella, Salmonella, ameba) Ischemic colitis, radiation colitis

Gastrointestinal bleedingstrategy 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

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Gastrointestinal bleedingstrategy of treatment (II)

• ENDOSCOPIC HEMOSTATIC METHODSinjection therapy: tonogen 1:10 000 dilution, saline, etanolamin-oleat, sodium-tetradecyl-sulphate, 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

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Haemostatic clips

Clipping device

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Gastrointestinal bleedingstrategy 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 48-96 h. 2. terlipressin (triglycil-lysin vasopressin) - lactulose, 3 x 20-40 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.1.

8-12,2004)Suspection of variceal bleeding

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)

Early starting of vasoactiv drug administration: 1. Terlipressin 2. Somatostatin or octreotid

Antibiotics, volume replacement

Repeated endoscopic treatment trial

Rescue TIPS / Surgery

rFVIIa?

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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)

Gastrointestinal bleedingstrategy 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

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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 rebleedingElective surgery: giant ulcer in elderly, malignancy

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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: 15-20 % lower GI tract: < 10 %

• SURGICAL INTERVENTION : along with modern, GI intensive care unit 3-10 %

• OVERALL MORTALITY : 8-30 %