Gastrointestinal (GI) BleedingRalph Lee, MMEd(Dist), MD, FRCPC
Gastroenterologist and Assistant ProfessorUniversity of Ottawa, September 18, 2015
Objectives
Define upper and lower gastrointestinal (GI) bleeding.
Outline the etiologies and clinical features of upper and lower GI bleeding
Apply a systematic clinical approach to GI bleeding.
Outline the investigation and management of GI bleeding
Recognize clinical indicators suggesting urgent versus non‐urgent assessment.
What is Gastrointestinal Bleeding? (1)
Bleeding from anywhere in the GI tractEsophagus to rectum
Traditionally, classified into two groups, based on presumed location of bleeding:UpperLower
3rd category, ‘Mid- GI’ bleeding, is present, but infrequently used
What is Gastrointestinal Bleeding? (2)
Upper GI (UGI) Bleeding Traditional: Proximal to
the Ligament of Treitz New: Proximal to the
Ampulla of Vater Lower GI (LGI) Bleeding
Traditional: Distal to Ligament of Treitz
New: Distal to terminal ileum
Mid GI bleeding New: Ampulla of Vater to
terminal ileum
UPPER GI BLEEDING
UGI Bleeding
75 – 80% of GI bleedingannual hospitalization rate = 160/100,000
(US)Mortality rate = 3.5 – 10%Sex – M:F – 2:1 incidence with ageMore likely to present with hemodynamic
instability due to rich blood supply of UGI tract
UGI BleedingCauses (Common)
Peptic Ulcer disease (20 - 50%)
Varices (5 - 20%) Mallory-Weiss tears (8
- 15%) Erosions (8 - 15%) AV Malformations (5%) Tumours (5%) Dieulafoy’s lesions
(1%)
UGI BleedingCauses (Other)
Other (11%) Gastric Antral Vascular
Ectasia (GAVE) AKA ‘Watermelon’
stomach Portal hypertensive
gastropathy Hemobilia Hemosuccus pancreatitis Aortoenteric fistulas Cameron’s lesions/ulcers
UGI BleedingHow Do They Present? (1)
Hematemesis Vomiting blood Bright red blood, clots, ‘coffee ground’
emesis Melena
Passage of black, tarry, foul-smelling stools Digested blood Appears with ≥ 50cc of bleeding from UGI
tract Things that mimick melena:
Iron pills - greenish Bismuth subsalicylate (Peptol Bismol™) - non-
foul smelling
UGI BleedingHow Do They Present? (2)
Bowel movement frequencyBlood is cathartic and a great laxativeRough indicator of rapidity of bleeding
Hemodynamic symptomsPre/SyncopeOrthostatic dizziness/lightheadednessChest pain, dyspnea
UGI BleedingHow Do They Present? (3)
(Hematochezia - red blood per rectum)Usually sign of LGI Bleeding, but can occur with
rapid UGI bleeding (i.e. ≥ 1000cc)patient usually hemodynamically unstable
Other symptomsDependent on cause
Abdominal pain, heartburn, dysphagia, nausea, vomiting
LOWER GI BLEEDING
LGI Bleeding
20 – 30% of gastrointestinal bleedingUsually less hemodynamically significant,
higher Hb level, less blood transfusion requirements than UGI bleeds
Increased incidence with ageMean age at presentation: 63 – 77
Mortality rate among hospitalized acute lower GI bleeds – 2 - 4%
LGI BleedingCauses
Diverticulosis (25 - 65%) Cancers/polyps (17%) Colitis/ulcers (18%)
IBD, ischemic, vasculitis, infectious, radiation-induced, NSAID-induced
Unknown (16%) Angiodysplasia (3 - 15%) Other (8%)
Post-polypectomy, stercoral ulcers, aorto-colonic fistulas
Anorectal (24 - 64%) Fissures, hemorrhoids
LGI BleedingHow Do They Present? (1)
Red Blood per Rectum Bright Red Blood Per Rectum (BRBPR) – left colonic? Dark/maroon – right colonic/lower small bowel?
Stool frequency – blood is cathartic form – diarrhea Location of blood
Surface/side of stool/dripping – perianal source? Mixed in stool – R colonic?
(Melena)* Usually sign of UGI bleeding, but can occur with distal small
bowel, cecum or R-sided colonic bleeding source Typically, hemodynamically stable with less rapid bleeding
LGI BleedingHow Do They Present? (2)
Other SymptomsDependent on causeFecal urgency, tenesmus, incontinenceAbdominal pain/crampsFevers/chillsWeight loss
GI BLEEDING
GI BleedingOther important historical items
Past medical history: GI
Previous PUD/H. Pylori infection? GI Malignancy?
Previous endoscopies Previous polypectomy
Diverticulosis IBD Cirrhosis?
Varices?
Cardiac CAD, angina, MI, CHF
Previous aortic
aneurysms/grafts/vascular
surgery? Previous radiation therapy? Bleeding episodes
Medications Anti-platelet agents (i.e.
ASA, Plavix),
anticoagulants (i.e.
warfarin, pradaxa) NSAIDs
Habits – EtOH Family history:
PUD, gastric cancer Colonic polyps, cancer IBD
GI BleedingPhysical Exam (1)
Look for: Hemodynamic instability Intravascular depletion Potential etiologies of bleeding
General: Altered mentation, jaundice
Vitals Hypotension Tachycardia Orthostatic changes
in BP and/or HR with position change from supine to standing
Suggests intravascular volume depletion of ≥ 2L
Head and Neck: Conjunctival pallor Scleral icterus Dry mucous membranes,
furrowed tongue, ↓ JVP Chest:
↓skin turgor at sternal angle Axilla: dry or moist
Abdomen: Tenderness, masses,
hepatosplenomegaly, stigmata of chronic liver disease
Digital rectal exam: Red blood? Melena? Hemorrhoids, fissures Masses
GI BleedingShock
SHOCK Class I Class II Class III Class IV
Blood Loss (mL) Up to 750 750-1500 1500-2000 >2000
Blood Loss (%) Up to 15 15-30 30-40 >40
HR (bpm) <100 >100 >120 >140
BP (mmHg) Normal Normal ↓ ↓
RR (breaths/min) 14-20 20-30 30-40 >35
Urine Output (cc/h) >30 20-30 5-15 Insig.
CNS Slightly anxious Mild anxious Anxious, confused Confused/ lethargic
GI BleedingManagement (Overview)
ABC’sResuscitationFocused History and Physical Exam
Upper vs. lower GI bleed InvestigationsTreatment
GI BleedingInitial Management
ABC’s Resuscitation
Intravenous (IV) accessMonitoring
Need for monitored area ? (i.e. ICU)Cardiac, respiratory (i.e pulse oximetry)
Volume re-expansionIV fluids
Keep patient NPO (nil per os) Focused history and physical exam
Upper vs. lower GI Bleed
GI BleedingInvestigations (1)
BloodworkType and crossmatch - PRBC’s, blood productsComplete Blood Cell Count
Hemoglobin MCV – mean corpuscular volume
MCV Fe deficiency chronic blood loss?Platelets
Clotting abilityElectrolytes
GI BleedingInvestigations (2)
Blood Urea Nitrogen (BUN), CreatinineIntravascular dehydration renal perfusion BUN, Cr
UGI bleed blood digestion in stomach/duodenum protein absorption urea nitrogen
[BUN x 10]: Cr > 1.5:1 May suggest UGI bleed
Liver enzymes and liver function testsINR - Coagulation status (i.e. INR)Liver disease (i.e. cirrhosis)
Albumin INR AST > ALT Platelets, MCV
(Nasogastric aspirate)
GI BleedingInitial Treatment (1)
Fluid ManagementIV crystalloids (i.e. normal saline); colloids (i.e.
volume expanders)Transfusion - Packed red blood cells
Reverse anti-coagulation INR - Vitamin K, fresh frozen plasma,
prothrombin complex concentrate (i.e. Octaplex) Platelets – Platelets transfusion
GI BleedingInitial Treatment (2)
Pharmacotherapy UGI Bleeds:
IV Proton Pump Inhibitor Mechanism: ↑ pH > 6 Promotes clot stability
↓ acid/pepsin on lesion ↑ platelet aggregation + fibrin formation
Empirically started to treat possible PUD until EGD performed IV PPI before endoscopy:
Lau et al. (2007): ↓ need for endoscopic therapy + accelerated
healing of ulcers Cochrane Meta-analysis (Sreedharan et al., 2010):
DOESN’T: mortality, rebleeding or progression to surgery DOES: high risk stigmata, need for endoscopic therapy
IV PPI after endoscopic therapy: rebleeding, mortality Dose: Pantoprazole 80mg IV bolus, then 8mg/h x 72 hours
GI BleedingInitial Treatment (3)
IV Somatostatin (i.e. octreotide) For possible variceal bleeds (i.e. patients with cirrhosis) –
started empirically Mechanism: splanchnic vasoconstriction portal
hypertension bleedingProkinetics (20 – 120 minutes before)
i.e. metoclopramide (Maxeran) or IV erythromycin To clear UGI tract of blood for better visualization Meta-analysis (Barkun et al., 2010): need for repeat
endoscopyLGI Bleeds: No specific medications
Urgent vs. Non-urgent Management
Urgent Hematemesis Serious co-morbid illness
Malignancy, cirrhosis Hemodynamic instability
Shock SBP < 100mmHg HR > 100bpm (Orthostatic hypotension)
Hb < 80 Transfusion requirement
> 2u PRBC’s Severe, ongoing bleeding
Non-urgent Young, healthy, minimal
bleeding
GI BleedingEndoscopy
UGI Bleed – EGD Timing: Within 24 hours of presentation To:
Diagnose cause of bleeding (high sensitivity/specificity)Stratify risk of rebleeding/adverse eventsPotentially treat underlying pathology
LGI Bleed – Colonoscopy Timing: Controversial
Severe bleeds: Within 8 – 24 hours Generally, LGI bleeds less severe than UGI bleeds Often, more difficult to identify source; therefore, mostly
diagnostic rather than therapeutic Unclear: EGD Colonoscopy
Upper vs. Lower EndoscopyPresumed Upper GI Bleed
Hematemesis
EGD
Upper vs. Lower EndoscopyPresumed Lower GI Bleed
Upper vs. Lower EndoscopyMassive Rectal Bleeding
Upper vs. Lower EndoscopyOccult Bleeding
Occult bleeding Stool testing positive for
occult blood Unexplained Fe
deficiency anemia
GI BleedingEndoscopic Hemostasis (1)
Injection i.e. Vasoconstrictors (i.e.
epinephrine), saline, sclerosants, tissue adhesives
Creates submucosal cushion of fluid which tamponades site +/- vasoconstriction
Thermal therapy i.e. Mono/bipolar
electrocoagulation, Argon Plasma Coagulation (APC), Laser Photocoagulation
Cauterizes vessel closed
GI BleedingEndoscopic Hemostasis (2)
Mechanical therapy i.e. Hemoclips, rubber
bands Closes and
tamponades vessel Animation
http://www.youtube.com/watch?v=59uO-8UVC2A
Hemospray New therapy Nano particle spray
UGI BleedingPeptic Ulcer Disease (1)
Most commonly due to NSAIDS, H.
Pylori 75 – 80% stop spontaneously Ulcer appearance indicates risk of
rebleeding and determines whether
therapy required Forrest Classification
UGI BleedingPeptic Ulcer Disease (2)
Endoscopic intervention: Risk of rebleeding Need for surgery Mortality
UGI BleedingVarices
Often unstable UGI bleeds Esophageal – Options:
Ligated with rubber bands (band ligation)
Injection with sclerosants Gastric – Options:
Injected with ‘glue’ (cyanoacrylate)
Band Ligation If endoscopy unsuccessful:
Transjugular intrahepatic portosystemic shunt (TIPS)
Liver transplant
LGI BleedingDiverticular Bleeding
Complicates 3 – 15% with colonic
diverticulae Pathophysiology:
Trauma of vasa recta at neck or
dome of diverticulum
Presentation: Painless hematochezia
Treatment: 75 - 80% resolve spontaneously
Recurrence within 4 years 25 – 40%
Endoscopic hemostasis If site can be identified < 30d rebleeding: Uncommon
Angiography (85% effective) < 30d rebleeding: 22%
Surgical resection
LGI BleedingAngiodysplasia
Increases with age Pathophysiology
Degenerative changes Chronic, intermittent obstruction
of submucosal vessels Presentation
Usually asymptomatic Overt or occult bleeding
Usually in right colon Treatment
Iron replacement Cauterization if bleeding or Fe
deficiency anemia (Estrogen/progesterone)
GI BleedingOther Options (1)
If endoscopy fails to identify source or fails to stop the bleeding
Mesenteric angiography Performed by interventional radiology Catheter introduced through femoral artery, passed to celiac
trunk, SMA, IMA + branches to: Diagnose bleeding site
Requires blood loss of ≥ 0.5-1mL/min Low sensitivity (47%) but high specificity (100%)
Perform therapy Feeding arteries can be embolized with microscopic gel foam, microcoils or
EtOH particles Success rate: 52 – 94% http://www.youtube.com/watch?v=jvi2WwvXIew
Complications (17%): Nephrotoxicity, bowel infarction, hematomas
GI BleedingOther Options (2)
RBC scan Patient infused with technetium
tagged RBC’s to locate site of
bleeding Disadvantages:
Not therapeutic Only localizes bleeding to
generalized area of abdomen
Requires blood loss ≥
0.1mL/min Higher sensitivity; lower
specificity Surgery
Intraoperative enteroscopy Oversew, resection
Summary (1)
Upper GI Bleed Hematemesis Melena Hemodynamic instability Elevated BUN x 10: Cr
Lower GI Bleed Dark/bright red blood per
rectum (hematochezia)
Longer course Tend to be more
hemodynamically stable
Summary (2)
PUD is most common cause of UGIB bleeding Diverticular disease is the most common cause of significant LGIB Approach includes
ABC’s Resuscitation History and Physical Exam Initial Investigations Initial Treatment Endoscopy Radiology Surgery
IV PPI’s are started empirically if UGIB is suspected Endoscopy is the primary diagnostic and therapeutic tool for GI
bleeds
Questions?
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