Upper Gastrointestinal Bleeding: Assessment and Management

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Upper Gastrointestinal BleedingAssessment and
Management

• ThomasGenuit, MD, MBA, FACS
• Sinai Hospital of Baltimore

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• Occult Bld. Stool Fe def. anemia
• Hematemesis BRB / coffee grd.
• Melena Hematochezia

• NSAIDS, anticoagulants coagulopathy
• ETOH, hepatitis
• Wt. loss/gain
• Hx cancer, trauma pancreatitis

Sx
Hx

• /- Abd. Pain
• /- Fever
• /- wt. gain/loss

• Cardio-pulm status
• Hx surgeries

UGIB

• Hemodyn. (in)stability

• Vitals
• Overall status
• Abd. Exam pain, guarding BS, masses hernias

Exam
Mgmt.

• Monitoring, FiO2, EKG - large bore IV, Foley, NGT
• TC, O-neg - CBC, Coags, CMP,
• ? airway protection - Specialists
• ? appropriate unit

• Definitive Care

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Upper GI Bleed Symptoms

• Differential diagnoses for UGIB
• Gastric ulcer
• Duodenal ulcer
• Esophageal varices
• Gastric varices
• Mallory-Weiss tear
• Esophagitis
• Neoplasm
• Hemorrhagic gastritis
• Dieulafoy lesion
• Angiodysplasia
• Hemobilia
• Pancreatic pseudocyst
• Pancreatic pseudoaneurysm
• Aortoenteric fistula

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Upper GI Bleed Symptoms

• Acute Sx
• Hematemesis - 40-50
• Hematochezia - 15-20
• Melena - 70-80
• Syncope - 14.4, Presyncope - 43.2
• Sx 30 days prior
• Dyspepsia - 18
• Epigastric pain - 41
• Heartburn - 21
• Diffuse abd. pain - 10
• Dysphagia - 5
• Weight loss - 12
• Jaundice - 5.2

Either / or - 90-98
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Assessment / Tests

• NGT
• Clears particulate matter, clots facilitates EGD
• Assessment volume of bleeding
• Increases/decreases risk of aspiration
• Blood/Coffee-grounds clear indication for EGD
• Clear aspirate no gastric sourceBilious
  aspirate no source proximal to lig. of Treiz
  OR bleeding has stopped

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Endoscopy

• For hematemesis lt 1st hour Consider intubation
• Other bleeding Urgent elective
• Diagnostic and therapeutic to 2nd portion of
  duodenum
• Consider Erythromycin
• 2 randomized controlled studies (146 pts) single
  dose (3 mg/kg IV over 20-30 min give 30-90 min
  prior to EGD) improves visibility, decreases EGD
  time, decreases need for second look
• Consider airway protection

EGD findings w. UGIB Duodenal ulcer -
24.3 Gastric erosion - 23.4 Gastric ulcer -
21.3 Esophageal varices - 10.3 Mallory-Weiss
tear - 7.2 Esophagitis - 6.3 Duodenitis -
5.8 Neoplasm - 2.9 Stomal (margin.) ulcer -
1.8 Esophageal ulcer - 1.7 Other/miscellaneous
- 6.8
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Capsule Endoscopy

• For bleeding beyond lig. Treitz
• Diagnostic only, time requirement up to 24 hours
• Decreased yield w. large vol. bleed and/or
  intermittend bleed
• Angiodysplasia and SB tumors most common

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RBC scan / Angiography

• 0.5 1 ml/min bleeding requirement,set up req.
  1-2 hours, test time 1-2 hours
• RBC scan may not accurately locate
  bleed,screening test
• Therapeutic (embolization) potential

Cave initial Hct lt 24, hemodyn unstable patient,
immediate gt 4-6 U PRBC req., ongoing gt 100-200
cc/h bleed
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Peptic Ulcer Disease

• History
• Pain / dyspepsia
• BRB (hematemesis) or Coffe-grounds
• NSAIDS, ETOH, Type A personalitypersonal Hx
  (antacids )
• First Line Therapy
• Hemodynamic Support, correction of coagulation /
  PLT. abnormalities (FFP, Cryo, PLT, F Via)
• PPI IV gtt vs. BID IV
• Endoscopy

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Peptic Ulcer Disease

• Endoscopic therapy
• Injection of vasoactive / sclerosing agents
• Bipolar electro- / thermal probe coagulation
• Band ligation / constant probe pressure tamponade
• Argon plasma / laser photocoagulation
• Hemostatic materials, including biologic glue
• Predictors of re-bleeding
• Active bleeding during EGD- 90 recurrence
• Visible vessel- 50 recurrence
• Adherent clot- 25-30 recurrence

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Peptic Ulcer Disease

• Failure No hemostasis /
• re-bleed after 2 attempts

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Peptic Ulcer Disease

• If bleeding controlled
• pantoprazole, 80 mg bolus then 8 mg/hr infusion
  x 24 hrs. then 40 mg IV qd-BIDthen transition
  to oral PPIs for 6-8 wks or lifelong
• Helicobacter pylori treatment, if presenttriple
  or quadruple drug regimen x 2-3 wksrecurrent
  colonization 70-90 within few month to yr.
• Eliminate/reduce NSAIDs, add misoprostol (PGE2)
• Repeat endoscopy lt 6-8 wks

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Peptic Ulcer Disease

• Indications for Surgery
• Severe life-threatening hemorrhage not responsive
  to resuscitative efforts
• Failure of medical therapy and endoscopic
  hemostasis with persistent / recurrent bleeding
• A coexisting reason for surgery such as
  perforation, obstruction, or malignancy
• Prolonged bleeding with loss of 50 or more of
  the patient's blood volume
• A second hospitalization for peptic ulcer
  hemorrhage

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Peptic Ulcer Disease

• If bleeding not controlled
• Angiography / embolization
• Emergent operation
• Duodenal ulcer most common posterior
  bleedlongitudinal anterior duodenotomy,
  quadrant over-sewprotection of bile duct !!!

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Peptic Ulcer Disease

• If bleeding not controlled
• Emergent operation
• Gastric ulcer wedge excision gastric ulcer
  always send for frozen to r/o cancergastric
  devascularization anti-ulcer operation ???
  TVA, SVP (PV), HSV
• For both post-OP PPI, H.P. therapy, follow-up
  endoscopy

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Peptic Ulcer Disease
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Peptic Ulcer Disease

• Treatment regimens for H pylori infection
  (Corson, 2001)
• Omeprazole 40 mg/d plus clarithromycin 500 mg q8h
  for 2 weeks. Then omeprazole at 20 mg/d for 2
  weeks.
• Ranitidine bismuth citrate 400 mg q12h plus
  clarithromycin 500 mg q8h for 2 weeks. Then
  ranitidine bismuth citrate at 400 mg q12h for 2
  weeks.
• Bismuth subsalicylate 525 mg q6h plus
  metronidazole at 250 mg q6h plus tetracycline at
  500 mg q6h for 2 weeks plus an H2-receptor
  antagonist for 4 weeks.
• Lansoprazole 30 mg plus amoxicillin at 1 g plus
  clarithromycin at 500 mg q12h for 2 weeks.

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Acute Hemorrhagic Gastritis

• Usually in severely ill pts
• Mild 10-20 req transfusion 1-2
• Predisposing shock (pressors), multi-trauma,
  ARDS, SIRS/Sepsis, renal hepatic failure
• 7-10 day delay
• Prophlaxis / medical managementessentialAntacid
  s lt Carafate lt H2 blockers lt PPIs effective H.
  pylori therapy is adjunct

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Acute Hemorrhagic Gastritis

• Surgical management
• Rarely necessary goal control bleeding, reduce
  recurrence mortality. (pts. are at extremely
  high risk)
• Simple oversewing of actively bleeding erosion
  sometimes effective
• W. life-threatening hemorrhage gastric
  resection with or without vagotomy with
  reconstruction may.Type of gastric resection
  depends on the location of the gastric
  erosionsantrectomy and subtotal, near total, or
  total gastrectomy. Operative mortality - 30-100

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Mallory-Weiss Tears

• Large, rapidly occurring, transient transmural
  pressure gradient across gastroesophageal
  junction typical Hx found only in 30-50
• 5-15 of UGIB, malefemale 31, ETOH in 45-70,
  NSAIDS in 30-40, hiatal hernia predisposes
  35-70
• no specific physical signs abd. Pain uncommon
• Bleeding stops spont. in 80-90, most heal lt
  48-72 hours can easily be missed if endoscopy is
  delayed
• transfusions req. in 40-70 hemodynamic
  instability and shock lt10 mortality -gt 8.6
  earlier series now lt 3
• Therapy supportive, surgery needed -gt 10 for
  perforation, uncontrolled bleeding mortality w.
  (emergent) surgery 15-25

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Dieulafoys Lesions

• Aka exulceratio simplex
• Dilated aberrant submucosal artery, lt 6 cm GE
  jct. 1-3 mm diameter, 2-5 of UGIB
• ETOH association, 30-50 yr old patients, mgtf
• Endoscopic therapy (coagulation/clipping) 95
  successful, re-bleeding 10-15 - most controlled
  endoscopically
• Surgical wedge resection if repeat endoscopic
  therapy fails mortality 25-40 reflection of
  co-morbid conditions

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Angiodysplasia

• Dilated, thin-walled vmucosal ascular channels
  appear macroscopically as a cluster of cherry
  spots, 2-4 of UGIB and 5-6 LGIB
• Most common stomach duodenum.
• Acquired or congenital Hereditary hemorrhagic
  telangiectasia Rendu-Osler-Weber syndrome von
  Willebrand disease Chronic renal failure req.
  hemodialysis Cirrhosis Aortic valvular disease
  (esp. aortic stenosis).

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Angiodysplasia

• Bleeding can be occult lifethreatening
• Endoscopic treatment gt 90 successful (contact
  probe coagulation, injection, band ligation)
• When surgery required (often multiple lesions)
  partial / total gastrectomy may be required

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Cameron Lesions

• Linear erosions/ulcers in hiatal hernia sac at
  the level of the diaphragm
• May be present in -gt 5 of pts with hiatal hernia
• Rare cause of acute or chronic UGIB, Fe-def.
  anemia
• Bleeding is treated endoscopically
• Stable pt surgical repair of hernia since this
  lesion is mechanically induced

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Neoplasms
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Portal HTN, Esophagogastric Varices

• Often life threatening bleeding, 50-60 bleed,
  30-40 bleed lt 2 y from Dx mortality 30-50
  (better w. nl. liver fct.)
• Segmental or systemic portal HTN (gt 10 mm Hg
  pressure), diversion of -gt 1l/min portal flow
• Presinusoidal, Sinusoidal, Post Sinusoidal

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Portal HTN, Esophagogastric Varices

MELD score (0.957 x log(e) (creatinine mg/dl)
0.378 x log(e) (bilirubin mg/dl) 1.120 x log(e)
(INR) 0.643)x10
PHVG gt12 -15mm Hg nearly all pts. bleed early
re-bleeding 20-50, 7-10 days. Risk for
re-bleeding lt 1yr 30
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Esophagogastric Varices

• Treatment strategies
• Resuscitation, supportive therapy, balloon
  tamponade
• Pharmacologic therapy
• Endoscopic therapy
• Decompressive therapy (radiologic and surgical)
• Liver transplantation

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Esophagogastric Varices

• Balloon tamponade
• Initially temporizing measure in all pts, now lt
  10temporary hemostasis in 85, neear 100
  re-bleed on removal
• 20 complication rateEsophageal rupture,
  Tracheal rupture, Duodenal rupture, Respiratory
  tract obstruction, Aspiration, Tracheoesophageal
  fistula, Esophageal necrosis / ulcer

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Esophagogastric Varices

• Pharmacologic treatment
• Vasopressin splanchnic vasoconstriction 0.2-0.4
  (0.7) U/min improved hemostasis, no survival
  benefit newst studies Tellipressin (pro-drug)
  w. benefits in hemostasis and survival
• Nitroglycerine gtt 40 mcg/min systemic
  hypotension and venous pooling, counteract
  cardiac effects of vasopressin titrate to SBP
  90-100
• Beta-Blockers Propranolol 40 mg BID maintenance
  therapy before incidence and after bleeding
  controlled

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Esophagogastric Varices

• Pharmacologic treatment
• Octreotide 250 mcg bolus, 250 mcg/hr infusion
  Decreases gastric acid, pepsin, gastric blood
  flow
• Endoscopy
• Cornerstone band ligation and sclerotherapy,
  glue
• Lower mortality, re-bleed, esoph perf and
  stricture w. banding can be done
  prophylactically
• Initial success rate -gt 90, re-bleed 30-50
• Endoscopic surveillance q3 mo x 1 y then q6 mo x
  1 y then annually

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Esophagogastric Varices

• TIPS
• Goal reduction of PHVP lt 12 mm Hg
• Primary bleeding control gt 90 Re-bleeding rate
  16-30 at 1-year Shunt dysfunction 50-60 at 6
  months W. re-dilation of the stent 1-year
  patency 83-85 Risk of hepatic encephalopathy
  25-35 can usually be managed medically30-day
  mortality 14-16, most deaths in patients with
  Child C cirrhosis as a result of multisystem
  organ failure

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Esophagogastric Varices

• Surgical Shunts
• Goal decompression of the high-pressure portal
  venous system into a low-pressure systemic venous
  system and devascularization of the distal
  esophagus and proximal stomach

• Portacaval shunt (end-to-side, side to side,
  interposition graft)
• Mesocaval shunt (Large- or small diameter
  interposition graft)
• Distal splenorenal (Warren) shunt
• Esophagogastric devascularization,
• Esophageal transsection, reanastomosis
• Orthotopic liver transplantation
• Splenectomy (for splenic vein thrombosis)

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Esophagogastric Varices

• Surgical Shunts
• bleeding control rate gt90
• Different incidence of encephalopathy and risk
  of worsening ascites w. nonselective, selective,
  or partial.
• Encephalopathy 10-15 after selective shunt
  (distal splenorenal), 10-20 after a partial
  shunt, and in 30-40 after a total shunt.
• No differences in survival rates 5.

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Hemobilia

• Rare
• Parasitic, tumors, traumatic, iatrogenic
• Diagnosis with endoscopy , ERCP, angiography
• Therapy
• Embolization then treatment of cause
• Surgery for failed embolization
• Selective hepatic artery ligation
• Hepatic resection if necessary

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Hemosuccus Pancreaticus

• Rare
• Direct communication present from
  retro-/peripancreatic vessel (usually splenic
  artery)
• Tumor or pancratitis, pseudocyst erosion, trauma,
  iatrogenic after ERCP
• Presentation Upper abdominal pain followed by
  hematochezia or hemeatemesis
• Diagnosis CT /- angiography
• Treatment angiography/surgery

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Aortoenteric Fistula

• Rare
• Aortic graft erosion, usually 3rd 4th portion of
  duodenum,
• Graft infection, peptic ulcer, tumor, trauma
• High mortality delayed diagnosis -gt
  100 operative 25-90
• Presentation
• History of AAA repair!
• Herald bleed
• May be followed by massive hemorrhage

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Aortoenteric Fistula

• Diagnosis
• CT thickened bowel, periaortic inflammation,
  pseudoaneurysm, extraluminal gas or fluid
  collection
• Angio req active bleed
• Ultrasound
• Therapy
• Endoluminal stent graft
• Graft repair/replacement, long-term Abx, bowel
  diversion,

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A 55-year-old man presents with hematemesis that
began 2 hours ago. He is hypotensive and has
altered mental status. No medical history is
available. How would you initiate management?

• ABCs, Oxygen, 2 large bore IVs, IVF, labs, TC
  for blood, FFP, foley, r/o MI, transfer to ICU
• NGT placement

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Patient receives 2 units of PRBCs. NGT is
placed. What would you conclude from the
following

• Clear, non-bilious aspirate
• Clear, bilious aspirate
• Bloody aspirate

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Blood is aspirated from NGT. How would you
proceed?

• Intubate
• EGD

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Diagnosis?

• Esophageal varices
• Management?
• Banding or sclerotherapy
• Administer concurrent somatostatin bolus/infusion
• After bleeding stops, start propranolol

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Pts bleeding stops initially and he stabilizes.
However, he intermittently requires 1-2 units of
PRBC over the next 48 hrs. totaling an additional
5 unit transfusion. No further hematemesis. How
would you proceed?

• CT/USG to rule out splenic vein thrombosis
• TIPS
• Who does TIPS in your hospital?
• Lets say all the radiologists in the state are
  at a conference and are unavailable
• Mesocaval shunt with interposition PTFE graft