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11/2/2009 1 Khalid Khan MBChB University of Arizona Disclosures None Objectives Triage, resuscitation and initial management of gastrointestinal bleeding Medical therapy for nonvariceal gastrointestinal Medical therapy for nonvariceal gastrointestinal bleeding Medical therapy for variceal hemorrhage

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Page 1: GI Hemorrhage kkk (2).ppt - NASPGHAN Homepage

11/2/2009

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Khalid Khan MBChBUniversity of Arizona

Disclosures 

None

Objectives

Triage, resuscitation and initial management of gastrointestinal bleeding Medical therapy for non‐variceal gastrointestinal Medical therapy for non‐variceal gastrointestinal bleedingMedical therapy for variceal hemorrhage

Page 2: GI Hemorrhage kkk (2).ppt - NASPGHAN Homepage

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Incidence of GI HemorrhageAdult Pediatric

1‐2% hospital admits common ICU admissions

GI hemorrhage uncommon 

h h10% mortalityGreater ‐ recurrent bleeders

Majority stop sponateously

PICU inpatients  rather than admits

0.4% life threatening

Data on Pediatric GI Hemorrhage

PrevalencePICU data

Crit Care Med 1992; 20:35

Community/ ER: developing nations Indian J Pediatr 1994; 61:651

ManagementCases reports and seriesKhan K, et al. Gastrointest Endosc 2003;57:110‐12

Pediatric GI hemorrhage

Children and adultsCommunity/ 

ER 

ICU/ inpatient

Newborn and infants

ER 

Nursery

NICU

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Management of Pediatric GI Hemorrhage

None necessaryMedical managementEndoscopic therapyEndoscopic therapyInterventional radiologySurgery

Methods to Stop GI Hemorrhage

None necessary e.g., Mallory‐Weiss Tear (>90% stop)Medical managementEndoscopic therapyEndoscopic therapyInterventional radiologySurgery

Methods to Stop GI Hemorrhage

None necessary e.g., Nose bleedMedical managementEndoscopic therapyEndoscopic therapyInterventional radiologySurgery

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Methods to Stop GI Hemorrhage

None necessary e.g., maternal blood, food coloringMedical managementEndoscopic therapyEndoscopic therapyInterventional radiologySurgery

Methods to Stop GI Hemorrhage

None necessaryMedical managementEndoscopic therapy: next presentationEndoscopic therapy: next presentationInterventional radiology: e.g., coiling, TIPSSurgery: e.g., gastrectomy, Meckels, intussuception

Site of GI hemorrhageUpper (proximal to the ligament of Treitz)

Esophageal

LowerSmall bowelColon

StomachDoudenumPancreatobiliary

Anus

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Upper GI Upper GI 

Gastritis

Varices Ulcer

GastritisMallory‐Weiss  tear

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Upper GI hemorrhageIs it upper?

Majority of all GI hemorrhage is upperHematemesis diagnosticMelenaMelena

Acid‐hemoglobin to hematinIntestinal bacteria, digestive enzymes

Nasogastric tubeHematochezia

Patients with very rapid UGI source

GI Bleed‐ from the ER

Endotracheal intubation?Intravenous access and fluid resuscitationStat labs: Hct/CBC, coags, type/cross match

History: age, liver disease, bleeding disorder, risk of peptic ulcer, NSAIDSExam: morphology, bruising, jaundice, splenomegaly

Hematemesis/ melena/ NGT blood hematochezia

Upper  vs. Lower GI bleed

Acute upper GI hemorrhage‐ from the ER

Secure airwayResuscitation

Uncontrolled massive 

hemorrhage

Medical management

History suggestive of 

portal hypertension

EndoscopyHemorrhage controlled 

Negative:  consider  lower  GI bleed

Positive:disease specific 

treatment

Medicalmanagement

Melena , consider meckels

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Acute upper GI hemorrhage‐ inpatient/ICU

Endotracheal intubation?Hematemesis/ melena/ hematocheziaNGT blood

Risk factors: coagulation, effective anti‐acid prophylaxis, risk for gastric ulceration, underlying lying disease e.g., GVHD

Endoscopy/ 

Uncontrolled massive 

hemorrhage

Endoscopy/ colonoscopy/ 

flexible sigmoidoscopy Hemorrhage 

controlled 

Negative Consider  lower GI bleed

PositiveDisease specific treatment

Medical management of UGI bleeding

Acid suppression (Peptic ulcer):No good data on benefit in childrenIV Omeprazole prior to EGD reduced signs of active bleeding  need for therapy: N Engl J Med 2007  356 1631bleeding, need for therapy: N Engl J Med 2007; 356:1631

High dose IV PPI (Not H2 RA) reduce rate of rebleeding with/without endoscopic therapy: BMJ 2005; 330:568

Oral BID high dose equivalent to IV PPI (pH >6)Untreated visible vessel or clot

Peptic ulcerAdherent clot Visible vessel

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Medical management of UGI bleeding

Somatostatin and Octreotide (peptic ulcer bleeding):reduce splanchnic blood flowinhibit gastric acid

i   i   ffgastric cytoprotective effectsReduced risk of rebleeding: Ann Intern Med 1997; 127:1062

Adjunctive therapy before endoscopyUnsuccessful endoscopy, contraindicated, or unavailable 

Medical management of peptic ulcer

D/C NSAIDsAnti‐ulcer medication

d f lEradication of H. pyloriFollow up EGD for gastric ulcer in 6 weeks: adults

Other sources of UGI hemorrhage

Mucosal lesions (specific medical treatment)Gastritis, ischemia, stress ulcerationEosinophilic esophagitisPTLD, GVHD,

Mallory‐WeissNo role for medical treatment

Dieulafoy’s No role for medical treatment

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Lower GI

LGI hemorrhageEvaluation

As for UGI hemorrhageIf unstable with hematochezia need EGD first

After stablized After stablized Rectal and anal examColonoscopy

Acute lower GI hemorrhageResuscitation

Rectal exam/ flexible sigmoidoscopy/ colonosocpy

Nasogastric tube/ EGD to r/o UGIH

Massive unexplained  lower GI hemorrhage, consider EGD

Slow or intermittent blood loss

Angiography/ radionucleide study/ VCE/ enteroscopy/

Surgery Disease specific treatment

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Portal hypertensionyp

Variceal hemorrhageCirrhosis

25% mortality for each bleeding episode (less in children)

Over 2/3 will rebleed in 1 yearOver 2/3 will rebleed in 1 year

Acute upper GI hemorrhage due to portal hypertension

Admit to ICU, gastric lavage

Bl di   h l  i

Endoscopy

Bl di   t i   i   t l  t th

Medical management

Tamponade

Bleeding esophageal varicesBleeding gastric varices or portal gastropathy

Medical prophylaxis

Therapy endoscopic/radiological/ surgical 

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Medical management of acute variceal hemorrhage

Transfusion of blood (avoid over transfusion)Correction of coagulopathyAntibiotics; Quinolones  CeftrioxoneAntibiotics; Quinolones, Ceftrioxone

Improve survival: Hepatology 2004;39:746–753

Reduction of portal pressureNo role for factor VIIa, beta blockersAcid reduction: adjunct

Acute variceal hemorrhage: portal pressure

Vasopressin: most potent splanchnic vasoconstrictor, related multiple side effects; max 24 hours

Nitrates: improves side effects of vasopressin; Hepatology 1982;2:757–762

Terlipressin: fewer side effects, improved survival; Sem Liv Dis 1999;19:475–505

Somatostatin/ Octreotide: initial control of bleeding,  5‐day hemostasis, no differences in mortality or severe adverse events; Hepatology 2002;305:609–615

Prophylaxis: variceal rebleedingNo comparative pediatric dataGood Adult data

Medical prophylaxisSurgeryg yTIPSCombination treatment

Less dataPVT vs. cirrhosisSurgery

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Prophylaxis for  Variceal hemorrhage

Primary prophylaxis

Normal esophagus

Varices, no hemorrhage

Recurrent varicealhemorrhage

Variceal hemorrhageSecondary prophylaxis

Gastric varices, portal gastropathy, gastric antral vascular ectasia

Prophylaxis for  Variceal hemorrhage

Endoscopic

Medication

CirrhosisEnd stage liver disease

Surgery

Non‐cirrhotic  portal hypertension

Portal vein thrombosis

TIPS

Prophylaxis:variceal rebleedingMedical

Non‐selective Beta Blockers: long acting Cirrhosis: Meta‐analysis. Lancet 1990;336:153 Non‐cirrhotic PH: BMJ 1989; 298:1363Portal gastropathy: Lancet 1991; 337:1431

Beta blocker + nitrates: Hepatology 1997; 26:34Negative: nitrates, spironolactone

EndoscopicCombination

Endoscopic + beta blocker: Ann Intern Med 2008; 149:109Endoscopic vs. combined medical: N Engl J Med 2001; 345:647

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Medical prophylaxis: pathophysiology

Variceal bleed recurs in over 2/3rd within a year (cirrhotics) and is associated with death if untreatredHighest risk first 6 weeksHVPGHVPG

Normal 6 mmhgVarices at 10 mmhgGI bleeding >12 mmhgNon‐selective Beta Blockers: increase mesenteric arteriolar tone, decrease cardiac outputNitrates: further reduce portal pressure

Medical prophylaxisClinical effect adults: 

Aim for heart rate 55‐65 bpmReduce heart rate by 25%Reduce HVPG by 20%Reduce HVPG to < 12 mmhgReduce HVPG to < 12 mmhg

Considerations in children (infants)Most experience with propranolol?Portal pressure change rarely measuredHeart rate reduction: 25%Effectiveness?

Secondary prophylaxisAGA guidelines: Hepatology 2007; 46:922

Cirrhotics surviving a variceal hemorrhage should receive secondary prophylaxis with non‐selective beta‐blockers plus EVLEVL

Beta‐blocker should be adjusted to the maximal tolerated dose. EVL repeated 1–2 weeks until obliteration, surveillance EGD 1–3 months, then 6–12 monthly

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Summary Cascade for medical management

1. Assess ABC‐need for airway management2. Estimate severity of blood loss3. Establish IV access and resuscitate4. Identify source (upper versus lower, NGT, EGD)5. Consider: 

1. Blood products and correct coagulopathyFor UGI hemorrhage1. IV vs. oral PPI2. IV Octreotide

Summary Medical cascade for portal hypertensive bleeding

1. Control airway, admit to PICU2. Resuscitate and tamponade if necessary3. Continue: 

1. Blood products and correct coagulopathy2. IV vs. oral PPI3. IV Octreotide4. Antibiotics

Summary Secondary prophylaxis after variceal hemorrhage

1. Initiate non‐selective beta‐blocker2. Increase dose to reduce heart rate by 25%3. Monitor‐what?4. Combine with endoscopic therapy5. Add nitrate to beta‐blocker?6. Gastric acid reduction?

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