Upper Gastrointestinal Bleeding

Clinically reviewed Aug 13, 2026 Updated Aug 30, 2026

Clinical Snapshot

Upper gastrointestinal bleeding (UGIB) is bleeding arising proximal to the ligament of Treitz — most often from a peptic ulcer, gastric or esophageal erosions, a Mallory-Weiss tear, a Dieulafoy lesion, or a malignancy (nonvariceal causes), or from ruptured esophageal or gastric varices in a patient with portal hypertension and cirrhosis (variceal causes).[1] Initial management is identical regardless of cause — resuscitation, risk stratification, and prompt endoscopy — but the two pathways diverge sharply once the source is identified: variceal bleeding needs vasoactive drug therapy, prophylactic antibiotics, and band ligation that a nonvariceal ulcer does not, and a nonvariceal ulcer needs high-dose acid suppression that variceal bleeding does not depend on.[2] Recognizing which pathway a patient is on — often before endoscopy confirms it — is the pharmacist's first decision point in this condition.

Recognize the Condition

Typical presentation

Presentation depends on the site, rate, and volume of bleeding. Hematemesis may be fresh red blood or coffee-ground material; melena (black, tarry, foul-smelling stool) reflects blood altered by transit through the gut; brisk bleeding can produce hematochezia (red or maroon stool) that mimics a lower GI source. Associated symptoms from volume loss include dizziness, syncope, dyspnea, chest pain, altered mental status, tachycardia, and hypotension. Retching or vomiting immediately before the onset of hematemesis suggests a Mallory-Weiss tear.

Nonvariceal vs. variceal upper GI bleeding

Nonvariceal UGIB

The more common presentation. Suggested by a history of peptic ulcer disease, H. pylori infection, or use of ASA, an NSAID, clopidogrel, ticagrelor, or prasugrel. Causes include duodenal ulcer, gastric ulcer, gastric or esophageal erosions, a Dieulafoy lesion (an eroded, abnormally large submucosal artery), a Mallory-Weiss tear at the gastroesophageal junction, or a malignancy.

Variceal UGIB

Suggested by stigmata of chronic liver disease — jaundice, ascites, hepatosplenomegaly, hepatic encephalopathy, spider angiomata, or palmar erythema — or risk factors for cirrhosis such as heavy alcohol use, chronic hepatitis B or C infection, or long-standing nonalcoholic fatty liver disease. Portal hypertension from hepatic scarring redirects splanchnic blood flow through portosystemic shunts, raising pressure in submucosal esophageal and gastric veins until they rupture.

Risk Factors

  • Current or recent use of ASA, a nonsteroidal anti-inflammatory drug (NSAID), or a P2Y12 inhibitor (clopidogrel, ticagrelor, prasugrel).
  • Anticoagulant therapy (warfarin or a direct oral anticoagulant), especially combined with an antiplatelet agent.
  • Known or untreated Helicobacter pylori infection.
  • A personal history of peptic ulcer disease or a prior episode of UGIB.
  • Critical illness, mechanical ventilation, or major trauma/burns (stress-related mucosal disease).
  • Retching or forceful vomiting (Mallory-Weiss tear risk).
  • Chronic liver disease or cirrhosis from any cause, and its risk factors — heavy alcohol use, chronic viral hepatitis B or C, and long-standing nonalcoholic fatty liver disease (variceal bleeding risk).
  • Advanced age and significant comorbidity (renal disease, hepatic disease, malignancy), which worsen prognosis once bleeding occurs.
  • Tobacco use, which impairs mucosal healing.

Red Flags & Refer

Any suspected UGIB warrants urgent assessment; the following findings mean the patient needs immediate escalation rather than a routine work-up.

  • Hemodynamic instability — systolic blood pressure under 90 mmHg, a sustained heart rate over 100 bpm, or overt shock.
  • Ongoing hematemesis of fresh (not coffee-ground) blood.
  • Altered mental status, syncope, or signs of inadequate cerebral perfusion.
  • Massive or rapidly progressive bleeding, which needs a protocol-driven, massive-transfusion approach rather than standard resuscitation.
  • Suspected or known cirrhosis with hematemesis — treat as variceal bleeding until proven otherwise and escalate for urgent (not routine) endoscopy plus immediate empiric vasoactive drug and antibiotic therapy.
  • Signs of impending airway compromise from large-volume hematemesis — consider intubation before sedation for endoscopy.
  • Rebleeding after apparently successful endoscopic hemostasis.

Assessment & Diagnosis

Distinguishing an upper from a lower GI source

ClueWhat it suggests
Hematemesis (fresh red or coffee-ground)Confirms an upper source by definition
MelenaUsually an upper GI source (can occur with a slow right-colon source)
Nasogastric aspirateFresh blood strongly suggests an upper source; a clear, bile-stained aspirate makes an upper source less likely but does not exclude it
Blood urea nitrogen : creatinine ratioA disproportionately elevated ratio favors an upper source (digested blood protein absorbed in the small bowel raises urea more than creatinine)
HematocheziaUsually a lower GI source, but can indicate a brisk upper GI bleed with rapid transit

History

  • Characterize the bleeding — hematemesis (fresh vs. coffee-ground), melena, or hematochezia — and how long it has been occurring.
  • Ask specifically about ASA, NSAID, anticoagulant, and antiplatelet use, prior ulcer disease or UGIB, and alcohol intake.
  • Ask about symptoms of chronic liver disease and known risk factors for cirrhosis.
  • Ask whether retching or vomiting preceded the bleeding (Mallory-Weiss tear).
  • Assess for comorbidities that worsen prognosis — malignancy, renal disease, hepatic disease, and cardiovascular disease.

Physical examination and bedside assessment

Resuscitate while taking a focused history and examining the patient, with particular attention to signs of chronic liver disease. At the bedside, suspect clinically significant intravascular volume loss when systolic blood pressure is under 100 mmHg, heart rate is over 100 bpm, or hemoglobin is under 100 g/L.

Investigations

  • Type and crossmatch (typically at least 4 units of packed red blood cells, more with severe bleeding), hemoglobin/hematocrit, electrolytes, creatinine and blood urea nitrogen, and coagulation studies (platelet count, INR, PTT).
  • A 12-lead ECG in older patients or those with suspected ischemic heart disease, and before giving erythromycin, to exclude a prolonged QTc interval.
  • Formal risk stratification with the Glasgow-Blatchford score before endoscopy, and the Rockall score after endoscopy (see below).

The nasogastric tube and upper GI series

A nasogastric tube is not needed if the patient has current or previously witnessed hematemesis, or if gastroscopy will be performed imminently. When placed, fresh blood in the aspirate indicates more severe bleeding and localizes the source to the upper GI tract; a clear or bile-stained aspirate does not reliably exclude an upper source, since the tube tip may not reach a pool of blood or the bleeding site may be beyond a closed pylorus. Nasogastric lavage is no longer routinely performed; a prokinetic (erythromycin) to clear retained blood before endoscopy has replaced it.[3] An upper GI series (e.g., barium swallow) must not be performed — its diagnostic accuracy is poor in active bleeding, and residual barium obscures the field for a subsequent endoscopy.

Endoscopy timing

Refer every patient with UGIB for endoscopy once resuscitation is underway. For nonvariceal bleeding, perform endoscopy within 24 hours of presentation — earlier, urgent endoscopy (within 6-12 hours) has not been shown to improve outcomes and may be harmful if performed before adequate resuscitation. For suspected variceal bleeding, endoscopy is performed earlier, generally within 12 hours, once the patient is hemodynamically stabilized.[3]

Pre-endoscopic risk stratification: Glasgow-Blatchford score

The Glasgow-Blatchford score (GBS) is calculated from history, vital signs, and a basic metabolic panel — entirely before endoscopy — and identifies patients at very low risk who may be safe for outpatient management without hospital admission.[4]

CriterionPoints
Blood urea nitrogen 6.5-7.9 mmol/L2
Blood urea nitrogen 8.0-9.9 mmol/L3
Blood urea nitrogen 10.0-24.9 mmol/L4
Blood urea nitrogen 25.0 mmol/L or higher6
Hemoglobin, male: 120-129 g/L1
Hemoglobin, male: 100-119 g/L3
Hemoglobin, male: under 100 g/L6
Hemoglobin, female: 100-119 g/L1
Hemoglobin, female: under 100 g/L6
Systolic blood pressure 100-109 mmHg1
Systolic blood pressure 90-99 mmHg2
Systolic blood pressure under 90 mmHg3
Pulse 100/min or higher1
Melena present1
Syncope2
Hepatic disease (known history or clinical/biochemical evidence)2
Cardiac failure (known history or clinical evidence)2

Add the points for every criterion the patient meets; the maximum possible score is 23. A GBS of 0 or 1 identifies a patient at very low risk of needing transfusion, endoscopic therapy, or surgery — outpatient management with prompt endoscopy and reliable follow-up can be considered in a stable, reliable patient with adequate support and transportation. A GBS of 12 or higher identifies a high-risk patient who needs urgent inpatient management.[1]

Post-endoscopic risk stratification: Rockall score

The complete Rockall score is calculated after endoscopy and adds the endoscopic diagnosis and stigmata of recent hemorrhage to the pre-endoscopic clinical variables (age, shock, comorbidity); it predicts rebleeding and mortality.[5]

VariablePoints
Age under 60 years0
Age 60-79 years1
Age 80 years or older2
No shock: systolic BP 100 mmHg or higher, pulse under 100/min0
Tachycardia: pulse 100/min or higher, systolic BP 100 mmHg or higher1
Hypotension: systolic BP under 100 mmHg2
No major comorbidity0
Congestive heart failure, ischemic heart disease, or other major comorbidity2
Renal failure, liver failure, or disseminated malignancy3
Endoscopic diagnosis: no lesion identified, or a Mallory-Weiss tear with no stigmata of recent hemorrhage0
Endoscopic diagnosis: all other diagnoses1
Endoscopic diagnosis: upper GI malignancy2
Stigmata: none, or a dark spot only0
Stigmata: blood in the upper GI tract, active bleeding, a visible vessel, or an adherent clot2

The pre-endoscopic (clinical) Rockall score uses only age, shock, and comorbidity (maximum 7); the complete score adds the endoscopic diagnosis and stigmata after EGD (maximum 11). A complete score of 2 or less identifies a low-risk patient. A complete score above 6 identifies a high-risk patient in whom an extended 10-day course of twice-daily oral PPI, after the initial high-dose IV course, reduces recurrent bleeding compared with the standard once-daily step-down regimen (see Drug Tables).[5][1]

Helicobacter pylori testing

Test every patient with a bleeding ulcer for H. pylori. Testing performed during the acute bleeding episode has a meaningfully higher false-negative rate than testing performed later, so a negative result obtained during active bleeding should not be treated as definitive — retest once the acute episode has resolved if the initial result is negative and clinical suspicion remains.[6]

Treatment Targets

  • Restore and maintain hemodynamic stability and adequate tissue oxygen delivery.
  • Achieve endoscopic hemostasis of the bleeding lesion within the appropriate time window for its cause.
  • Heal the underlying lesion (ulcer, erosion, or esophagitis) with an adequate course of acid suppression.
  • Prevent early rebleeding in the first 72 hours after endoscopic hemostasis, when the risk is highest.
  • Eradicate H. pylori when present, to prevent recurrent bleeding.
  • For variceal bleeding: control the acute hemorrhage, prevent bacterial infection, and establish secondary prophylaxis against future variceal bleeding.
  • Establish a safe long-term antithrombotic and NSAID strategy that minimizes recurrent-bleeding risk without leaving the patient unprotected from thrombosis.

Choose Initial Treatment

Direct treatment rule

Resuscitation and transfusion

Secure two large-bore (18-gauge or larger) IV lines, start crystalloid resuscitation titrated to hemodynamic status, and provide supplemental oxygen; protect the airway and consider intubation before endoscopy if hematemesis is severe or ongoing, or mental status is impaired.

Use a restrictive transfusion strategy: transfuse packed red blood cells at a hemoglobin threshold of 70 g/L in most patients, using a higher threshold of 80 g/L in patients with significant coronary artery disease or massive ongoing hemorrhage.[1][7]

Pre-endoscopic pharmacotherapy

Start immediately, before endoscopy high-dose IV pantoprazole in every patient with suspected UGIB — it may downstage a high-risk lesion by the time of endoscopy and is supported by cost-effectiveness evidence where early endoscopy is not immediately available, even though it has not been shown to change hard outcomes on its own.[3]

If variceal bleeding is suspected start empiric octreotide and a prophylactic antibiotic at presentation, before endoscopy confirms the diagnosis, because both improve outcomes and delaying them until confirmation forfeits their benefit.[2]

Do not use an oral or IV H2-receptor antagonist for acute UGIB — PPIs are superior and H2RAs have no role here.

Do not use tranexamic acid routinely for nonvariceal or variceal UGIB — a large randomized trial found no mortality benefit and an increased risk of venous thromboembolic and other thrombotic events; reserve it only for massive hemorrhage under a specialized protocol.[8]

Endoscopy timing

Perform endoscopy within 24 hours of presentation for nonvariceal UGIB, and within 12 hours for suspected variceal bleeding, in both cases once resuscitation is underway.[3]

Endoscopic hemostasis and lesion-specific technique

Use endoscopic hemostatic therapy for any high-risk nonvariceal stigmata (active bleeding or a nonbleeding visible vessel) — a single thermal or mechanical modality, or a combination, but never epinephrine injection alone, which is inferior.[1]

For esophageal varices, use endoscopic band ligation, preferred over sclerotherapy given fewer complications; for gastric varices, use tissue adhesive (cyanoacrylate) injection, with or without endoscopic ultrasound guidance.[2]

For a Dieulafoy lesion, a Mallory-Weiss tear with active bleeding, gastric antral vascular ectasia, or a bleeding malignant tumor, use the lesion-specific technique detailed in Non-Pharmacologic Treatment — these are not managed the same way as a bleeding peptic ulcer.[9]

Post-endoscopic acid suppression

High-risk nonvariceal stigmata (active bleeding, visible vessel, or adherent clot) after successful endoscopic hemostasis — high-dose IV pantoprazole for 72 hours, given as either a continuous infusion or intermittent high-dose bolus dosing; the two approaches are equally effective.[10]

Low-risk stigmata (clean-based ulcer or a flat pigmented spot) — standard-dose oral PPI is sufficient; high-dose IV therapy is not required.

Non-Pharmacologic Treatment

  • Two large-bore IV lines, crystalloid resuscitation, supplemental oxygen, and airway protection or elective intubation before endoscopy when hematemesis is active or mental status is impaired.
  • A nasogastric tube is not routinely required; do not perform an upper GI series (barium study).
  • Angiographic embolization for nonvariceal bleeding refractory to a second attempt at endoscopic hemostasis; surgery is reserved for refractory or special cases.
  • A transjugular intrahepatic portosystemic shunt (TIPS), placed within 72 hours and ideally within 24 hours, for variceal bleeding at high risk of treatment failure or after early rebleeding or failed endoscopic hemostasis.
  • Balloon tamponade or a dedicated esophageal self-expandable stent as a bridge to more definitive therapy in refractory variceal bleeding.
  • Counsel every patient to avoid alcohol and NSAIDs going forward, and support smoking cessation, since tobacco use impairs mucosal healing.

Endoscopic hemostatic technique by lesion type

Peptic ulcer, high-risk stigmata

Thermal coagulation, mechanical clipping, and/or injection of dilute epinephrine — never epinephrine injection alone. Hemostatic powder or spray can be used as an initial or rescue modality; over-the-scope clips are useful in refractory cases.

Esophageal varices

Endoscopic band ligation, preferred over sclerotherapy given fewer complications.

Gastric varices

Tissue adhesive (cyanoacrylate) injection, with or without endoscopic ultrasound guidance.

Dieulafoy lesion

A mechanical modality — endoscopic band ligation or a through-the-scope clip — contact thermocoagulation, or sclerosant injection; avoid epinephrine injection alone.[9]

Mallory-Weiss tear, active bleeding

Endoscopic band ligation or a through-the-scope clip; endoscopic therapy is not needed for a nonbleeding visible vessel, adherent clot, flat pigmented spot, or clean-based ulcer at this site.[9]

Gastric antral vascular ectasia (GAVE)

Endoscopic band ligation, preferred over argon plasma coagulation.[9]

Malignant tumor bleeding

A topical hemostatic agent, preferred over conventional endoscopic hemostatic therapy, followed by definitive oncologic treatment.[9]

Pharmacologic Treatment Options

Drug / interventionRoleDose / useImportant adverse effectsTeaching points
Pantoprazole IV
Preferred
Pre-endoscopic and post-endoscopic acid suppression, nonvariceal UGIB80 mg IV bolus, then 8 mg/h continuous infusion x 72 hours (or 40 mg IV Q8-12H intermittent dosing, equally effective)Headache, abdominal pain, injection-site reactionStart as soon as UGIB is suspected — do not wait for endoscopy to confirm the diagnosis.
Octreotide
Preferred
Suspected or confirmed variceal bleeding, adjunct to band ligation50-100 mcg IV bolus, then 25-50 mcg/h IV infusion for up to 5 days after bleeding stopsHyperglycemia, abdominal pain, nausea, headache, flushingStart empirically as soon as variceal bleeding is suspected. May blunt opioid analgesia.
Ceftriaxone
Preferred
Prophylactic antibiotic, variceal bleeding in cirrhosis1 g IV once daily for 5-7 daysHypersensitivity, GI upsetPreferred over norfloxacin in advanced cirrhosis, in centres with high fluoroquinolone resistance, or if the patient is already on quinolone prophylaxis.
Norfloxacin
Alternative
Prophylactic antibiotic, variceal bleeding in cirrhosis, oral option400 mg PO BID for 5-7 daysGI upset, rare tendinopathyDefault oral choice for most patients able to tolerate oral therapy; start at admission, before endoscopy.
Erythromycin IV
Special situation
Pre-endoscopic prokinetic, active hematemesis or suspected large gastric blood volume250 mg IV single dose, 30-90 minutes before endoscopyQT prolongation, GI crampingObtain a baseline ECG to exclude a prolonged QTc before giving it.
ASA (cardioprotective dose)
Special situation
Continue or resume in a patient on ASA for secondary cardiovascular preventionContinue at presentation; if held, resume on the day endoscopic hemostasis is confirmedGI upset, bleedingDo not hold routinely — interrupting it barely changes the acute bleeding course but delays cardioprotection.
Omeprazole, oral
Alternative
Oral acid suppression when IV PPI is not available40 mg PO BIDHeadache, GI upset, hypomagnesemia with long-term useWeaker evidence base than IV therapy; use only when IV access or formulation is unavailable.
Tranexamic acid
Avoid
Not routinely indicated for nonvariceal or variceal UGIBNot applicable — do not use routinelyVenous thromboembolism, other thrombotic eventsReserve only for massive hemorrhage under a specialized protocol; a large RCT showed no mortality benefit for routine use.

Special Populations

Pregnancy: endoscopic hemostatic therapy can be performed in pregnancy; avoid thermal unipolar electrocoagulation modalities where an alternative exists, ensure fetal monitoring, and have obstetric support immediately available. PPIs are considered safe in pregnancy and may be used based on the endoscopic findings. Octreotide has limited pregnancy safety data — reserve it for life-threatening variceal bleeding where the benefit clearly outweighs the uncertainty.

Breastfeeding: PPIs (omeprazole, pantoprazole) are considered compatible with breastfeeding, based on low milk concentrations and destruction of ingested drug in the infant's acidic stomach. Data on octreotide in breastfeeding are limited; weigh the benefit of controlling active variceal hemorrhage against the uncertainty in consultation with the care team.

Older adults

Older patients carry a higher risk of rebleeding and death from UGIB, and more often have the comorbidities that raise the Glasgow-Blatchford and Rockall scores. Apply the same resuscitation, PPI, and endoscopy protocols, with a lower threshold for admission and close monitoring given the reduced physiologic reserve to tolerate ongoing blood loss.

Renal and hepatic impairment

PPI dosing does not require adjustment for renal or hepatic impairment. In cirrhosis, classify severity by Child-Pugh class — it directly changes variceal-bleeding management, since a high-risk-of-failure profile (Child-Pugh class C above 14 points, or class B with active bleeding) is itself the trigger for early TIPS. Prophylactic antibiotics are mandatory in cirrhotic patients with UGIB regardless of renal function. Gastrointestinal bleeding is a recognized precipitant of hepatic encephalopathy in cirrhosis, from the protein/blood load delivered to the gut — monitor mental status closely and manage encephalopathy per standard protocol if it develops.

Restarting antithrombotic and NSAID therapy after bleeding resolves

Cardiac ASA or single antiplatelet monotherapy

Do not hold cardiac-dose ASA for secondary cardiovascular prevention. If it was held at presentation, resume it on the day endoscopic hemostasis is confirmed — waiting longer trades a real cardiovascular risk for little additional bleeding protection, since ASA's antiplatelet effect is already present well before the bleed.[11][12]

Dual antiplatelet therapy with a recent coronary stent

Continue ASA throughout; involve cardiology before interrupting the P2Y12 inhibitor, since stent thrombosis is a real, potentially fatal risk in the months after stent placement. Once hemostasis is secured, resume the P2Y12 inhibitor as soon as the bleeding risk allows — individualize the exact timing jointly with cardiology.

Warfarin

Guideline evidence is currently insufficient to mandate an exact resumption day. Do not use fresh frozen plasma or vitamin K to reverse warfarin for GI bleeding; if reversal is genuinely needed, prothrombin complex concentrate is preferred over fresh frozen plasma. Once hemostasis is secured, individualize the resumption timeline against the patient's specific thromboembolic risk (a mechanical heart valve or a high CHADS2/CHA2DS2-VASc score favors earlier resumption) versus rebleeding risk (high-risk endoscopic stigmata favor waiting longer) — most patients who resume do so within about a week of confirmed hemostasis.[11]

Direct oral anticoagulants (DOACs)

Do not routinely use prothrombin complex concentrate, idarucizumab (dabigatran), or andexanet alfa (rivaroxaban/apixaban) for acute GI bleeding on a DOAC — evidence does not support their routine use in this setting. As with warfarin, individualize the resumption timeline against thromboembolic versus rebleeding risk once hemostasis is secured.[11]

NSAIDs

Avoid a nonselective NSAID after any UGIB when possible. If ongoing NSAID therapy is genuinely unavoidable, use the lowest effective dose for the shortest duration, prefer a COX-2-selective agent over a nonselective NSAID, and co-prescribe a PPI. Test for and treat H. pylori before starting long-term NSAID therapy in any patient with a prior ulcer history.

Monitoring & Follow-Up

During the acute admission, monitor vital signs, urine output, and serial hemoglobin, with the frequency guided by bleeding severity and ongoing losses, and watch for signs of rebleeding — recurrent hematemesis or melena, new hemodynamic instability, or a falling hemoglobin. Most rebleeding occurs within the first 72 hours after endoscopic hemostasis, exactly the window the high-dose IV PPI course is timed to cover. In variceal bleeding, monitor for hepatic encephalopathy, and continue endoscopic band-ligation surveillance on a defined schedule until varices are eradicated, then periodically thereafter. Confirm H. pylori eradication with a urea breath test, stool antigen test, or biopsy at least 4 weeks after antibiotic therapy ends and at least 1-2 weeks after stopping the PPI, since ongoing acid suppression can produce a false-negative result; if eradication fails, retreat with an appropriate second-line or salvage regimen (see Drug Tables) and retest again after that course.[6] At every follow-up, confirm the patient's antithrombotic and NSAID plan matches what was intended at discharge — long-term PPI co-therapy should be documented on the chart and on any ongoing ASA, NSAID, or anticoagulant prescription. Community pharmacists are well placed to catch a patient who has silently stopped a necessary long-term PPI, or who has resumed a held anticoagulant without the intended follow-up plan.

Treatment Failure / Next Step

  1. Confirm true rebleeding — recurrent hematemesis or melena, new hemodynamic instability, or a significant hemoglobin drop — rather than the expected tail of the initial bleed.
  2. Repeat endoscopy for a second attempt at hemostasis; most rebleeding after initially successful endoscopic therapy can still be controlled endoscopically.
  3. If a second endoscopic attempt fails or is not feasible, escalate to angiographic embolization for nonvariceal bleeding, or early TIPS for variceal bleeding, especially in a patient with a high-risk Child-Pugh profile.[13]
  4. Obtain surgical consultation for refractory nonvariceal bleeding once endoscopic and angiographic options are exhausted.
  5. For refractory variceal bleeding, bridge to definitive therapy with balloon tamponade or a dedicated esophageal self-expandable stent.
  6. If bleeding recurs weeks to months after apparent healing, reassess for the most common preventable causes first — unconfirmed or untreated H. pylori, and resumed ASA, NSAID, or antithrombotic therapy without PPI co-therapy — before assuming a new or missed lesion.

Common Errors to Avoid

  • Placing a nasogastric tube or ordering a barium upper GI series when neither is needed — this delays endoscopy and can obscure the endoscopic field.
  • Using an oral or IV H2-receptor antagonist instead of a PPI for acute UGIB.
  • Waiting for endoscopy or GI consultation before starting IV PPI therapy — start it empirically as soon as UGIB is suspected.
  • Managing a patient with cirrhosis and hematemesis on the nonvariceal pathway — missing empiric octreotide and prophylactic antibiotics delays interventions that measurably improve outcomes in variceal bleeding.
  • Treating prophylactic antibiotics in cirrhotic UGIB as optional — they are a mandatory, independent intervention, not an afterthought to endoscopy.
  • Continuing high-dose IV PPI infusion beyond 72 hours, or beyond the need for it once endoscopy shows a low-risk lesion (clean-based ulcer).
  • Holding cardiac-dose ASA for a prolonged period after hemostasis instead of resuming it on the day hemostasis is confirmed.
  • Accepting a negative H. pylori test obtained during active bleeding as definitive, given its high false-negative rate in that setting, and failing to retest later.
  • Discharging a patient who must continue an NSAID or ASA without co-prescribing a PPI.
  • Transfusing to a liberal hemoglobin target instead of the evidence-based restrictive threshold.
  • Missing that octreotide can blunt opioid analgesia, or that clarithromycin in an H. pylori regimen is a meaningful CYP3A4 interaction risk.

Clinical Decision Algorithm

Initial resuscitation and triage
Suspected acute UGIB: hematemesis, melena, or hematochezia with a likely upper source
Resuscitate: 2 large-bore IV lines, crystalloid, oxygen, airway protection if needed; send type and crossmatch, CBC, electrolytes, creatinine, coagulation studies
Start high-dose IV pantoprazole immediately, before endoscopy
History or exam suggests cirrhosis/portal hypertension
Treat as suspected variceal bleeding: start octreotide and a prophylactic antibiotic now, proceed to the variceal pathway
No suggestion of chronic liver disease
Calculate the Glasgow-Blatchford score, proceed to the nonvariceal pathway
Nonvariceal upper GI bleeding
Nonvariceal pathway
Glasgow-Blatchford score 0-1, stable, reliable, good follow-up access
May be suitable for outpatient management once endoscopy confirms a low-risk lesion
Glasgow-Blatchford score 2 or higher, or other high-risk features
Admit; endoscopy within 24 hours once resuscitation is underway
Endoscopy: identify the lesion and assess stigmata of recent hemorrhage
High risk: active bleeding or a nonbleeding visible vessel
Endoscopic hemostatic therapy, then high-dose IV pantoprazole (80 mg bolus + 8 mg/h infusion, or intermittent high-dose bolus) x 72 hours
Adherent clot
Endoscopic hemostatic therapy after clot removal, per endoscopist judgment; high-dose IV pantoprazole x 72 hours
Low risk: clean base or flat pigmented spot
No endoscopic therapy needed; standard-dose oral PPI is sufficient
Transition to oral PPI after the high-dose IV course (or immediately for a low-risk lesion); test for H. pylori[3]
H. pylori positive
Quadruple eradication therapy x 10-14 days, then continue PPI to complete the ulcer-healing course (4 weeks duodenal, 8 weeks gastric/esophagitis); confirm eradication at least 4 weeks after antibiotics end
H. pylori negative, or ASA/NSAID/antithrombotic therapy must continue
Indefinite long-term secondary-prophylaxis PPI is indicated
Variceal upper GI bleeding
Suspected or confirmed variceal UGIB in a patient with cirrhosis/portal hypertension
Start octreotide 50-100 mcg IV bolus then 25-50 mcg/h infusion, and a prophylactic antibiotic (norfloxacin PO or ceftriaxone IV) at admission[2]
Endoscopy within 12 hours once resuscitated
Esophageal varices
Endoscopic band ligation, preferred over sclerotherapy
Gastric varices
Tissue adhesive (cyanoacrylate) injection, with or without EUS guidance
Continue octreotide up to 5 days after bleeding stops; complete 5-7 days of antibiotic prophylaxis
High risk of treatment failure (Child-Pugh C above 14 points, or Child-Pugh B with active bleeding), or early rebleeding/failed hemostasis
Early TIPS within 72 hours, ideally within 24 hours
Lower risk, hemostasis achieved
Start a nonselective beta-blocker (propranolol, nadolol, or carvedilol) and continue a band-ligation program for secondary prophylaxis
Bleeding continues despite endoscopic and TIPS options: bridge with balloon tamponade or an esophageal self-expandable stent to definitive therapy

Drug Tables

How to use this table: Doses are adult doses and require patient-specific confirmation, including renal/hepatic adjustment. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.

Proton pump inhibitors, parenteral

Pantoprazole IV is the standard parenteral PPI used for UGIB in Canada.

DrugDosageAdverse effectsComments
Pantoprazole
Adults — continuous infusion: 80 mg IV bolus over 2 minutes, then 8 mg/h continuous IV infusion x 72 hours
Adults — intermittent bolus (non-inferior alternative): 40 mg IV Q8-12H x 72 hours
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Headache, abdominal pain, rash, injection-site reactionPreferred pre- and post-endoscopic high-dose regimen for nonvariceal bleeding with high-risk stigmata; switch to an oral PPI after 3 days.

Proton pump inhibitors, oral

Used as the step-down after IV therapy, or as initial therapy where IV PPI is unavailable. All share the adverse-effect profile noted below. The initial 10-day course matches the high-dose IV induction phase; continue twice daily for esophagitis, or step down to once daily for a duodenal or gastric ulcer.

DrugDosageAdverse effectsComments
Omeprazole
Adults — initial (10 days): 20 mg PO BID
Adults — duodenal ulcer maintenance: 20 mg PO once daily
Adults — gastric ulcer/esophagitis maintenance: 20 mg PO once daily (gastric ulcer) or 20 mg PO BID (esophagitis)
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Abdominal pain, diarrhea, flatulence, nausea, headache, constipation, hypomagnesemia and decreased vitamin B12 with long-term useContinue BID for esophagitis (8 weeks total); step down to once daily for duodenal ulcer (4 weeks total) or gastric ulcer (8 weeks total).
Esomeprazole
Adults — initial (10 days): 40 mg PO BID
Adults — duodenal ulcer maintenance: 40 mg PO once daily
Adults — gastric ulcer/esophagitis maintenance: 40 mg PO once daily (gastric ulcer) or 40 mg PO BID (esophagitis)
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Abdominal pain, diarrhea, flatulence, nausea, headache, constipation, hypomagnesemia and decreased vitamin B12 with long-term useThe S-isomer of omeprazole. Same step-down structure as omeprazole.
Lansoprazole
Adults — initial (10 days): 30 mg PO BID
Adults — duodenal ulcer maintenance: 30 mg PO once daily
Adults — gastric ulcer/esophagitis maintenance: 30 mg PO once daily (gastric ulcer) or 30 mg PO BID (esophagitis)
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Abdominal pain, diarrhea, flatulence, nausea, headache, constipation, hypomagnesemia and decreased vitamin B12 with long-term useSame step-down structure.
Dexlansoprazole
Adults — initial (10 days): 60 mg PO BID
Adults — duodenal ulcer maintenance: 60 mg PO once daily
Adults — gastric ulcer/esophagitis maintenance: 60 mg PO once daily (gastric ulcer) or 60 mg PO BID (esophagitis)
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Abdominal pain, diarrhea, flatulence, nausea, headache, constipation, hypomagnesemia and decreased vitamin B12 with long-term useDual delayed-release formulation. Same step-down structure.
Pantoprazole, oral
Adults — initial (10 days): 40 mg PO BID
Adults — duodenal ulcer maintenance: 40 mg PO once daily
Adults — gastric ulcer/esophagitis maintenance: 40 mg PO once daily (gastric ulcer) or 40 mg PO BID (esophagitis)
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Abdominal pain, diarrhea, flatulence, nausea, headache, constipation, hypomagnesemia and decreased vitamin B12 with long-term useSame step-down structure as the other agents in this class.
Rabeprazole
Adults — initial (10 days): 20 mg PO BID
Adults — duodenal ulcer maintenance: 20 mg PO once daily
Adults — gastric ulcer/esophagitis maintenance: 20 mg PO once daily (gastric ulcer) or 20 mg PO BID (esophagitis)
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Abdominal pain, diarrhea, flatulence, nausea, headache, constipation, hypomagnesemia and decreased vitamin B12 with long-term useSame step-down structure.

Somatostatin analogue

Reduces portal pressure, splanchnic blood flow, and acid/pepsin secretion. Terlipressin, used for variceal bleeding in some countries, is not currently marketed in Canada — octreotide is the vasoactive agent of choice domestically.

DrugDosageAdverse effectsComments
Octreotide
Adults: 50-100 mcg IV bolus in 0.9% NaCl, then 25-50 mcg/h IV infusion for up to 5 days after bleeding stops
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Abdominal pain, nausea, diarrhea, hyperglycemia, headache, flushingStart empirically as soon as variceal bleeding is suspected, before endoscopic confirmation. May blunt opioid analgesia.

Prokinetic

DrugDosageAdverse effectsComments
Erythromycin
Adults: 250 mg IV single dose, given 30-90 minutes before endoscopy
Children: Not established for routine pre-endoscopic use in UGIB — specialist-directed only.
QT prolongation, GI cramping, injection-site phlebitisObtain a baseline ECG to exclude a prolonged QTc before administration. Clears retained blood/clot from the stomach, improving visualization and reducing the need for a repeat endoscopy.[14]

Prophylactic antibiotics, variceal bleeding in cirrhosis

Start at admission, before endoscopy, in every cirrhotic patient with UGIB — this reduces bacterial infection, rebleeding, and mortality.

DrugDosageAdverse effectsComments
Ceftriaxone
Adults: 1 g IV once daily for 5-7 days
Children: Not established for routine use in this specific indication — specialist-directed only.
Hypersensitivity, GI upset, rare biliary sludgingPreferred over norfloxacin in advanced cirrhosis (Child-Pugh B/C), in centres with high fluoroquinolone-resistance rates, or if the patient is already on quinolone prophylaxis.
Norfloxacin
Adults: 400 mg PO BID for 5-7 days
Children: Not established for routine use in this specific indication — specialist-directed only.
GI upset, rare tendinopathy or CNS effects (fluoroquinolone class)Default oral choice for most patients able to tolerate oral therapy.

Helicobacter pylori eradication regimens

Treat every H. pylori-positive patient with a bleeding ulcer; confirm eradication at least 4 weeks after therapy ends. Component doses use the ComboDose "+" notation for each multi-drug regimen.

DrugDosageAdverse effectsComments
Bismuth quadruple therapy (fixed-dose combination)
Adults — Combo, 10-14 days: Combo: bismuth subcitrate/metronidazole/tetracycline fixed-dose combination 3 capsules PO QID + PPI standard dose PO BID
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Dark stools/tongue, GI upset, metallic taste, photosensitivityPreferred first-line option, particularly after recent macrolide exposure or with penicillin allergy. Avoid alcohol during treatment.[6]
Concomitant quadruple therapy
Adults — Combo, 10-14 days: Combo: PPI standard dose PO BID + amoxicillin 1 g PO BID + clarithromycin 500 mg PO BID + metronidazole 500 mg PO BID
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
GI upset, metallic taste, rash, C. difficile riskFirst-line alternative to bismuth quadruple therapy. Clarithromycin is a CYP3A4 inhibitor — check for interactions. Avoid alcohol.[6]
Clarithromycin triple therapy
Adults — Combo, 14 days: Combo: PPI standard dose PO BID + amoxicillin 1 g PO BID + clarithromycin 500 mg PO BID
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
GI upset, metallic-type taste, rashReserve for patients with no prior macrolide exposure and low local clarithromycin resistance — no longer a default first-line choice given rising resistance rates.[6]
Levofloxacin salvage therapy
Adults — Combo, 14 days: Combo: PPI standard dose PO BID + amoxicillin 1 g PO BID + levofloxacin 500 mg PO once daily
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Tendinopathy, QT prolongation, GI upset (fluoroquinolone class)Second-line/salvage option after failure of bismuth or concomitant quadruple therapy. Confirm eradication after retreatment.[6]

NSAID-associated ulcer risk reduction

For a patient who requires ongoing NSAID therapy despite a prior UGIB — always co-prescribe gastroprotection.

DrugDosageAdverse effectsComments
Misoprostol
Adults: 200 mcg PO QID (or 400 mcg PO BID as tolerated) with NSAID therapy
Children: Not established for this indication — specialist-directed only.
Diarrhea, abdominal cramping, uterine contractionsAbsolutely contraindicated in pregnancy given its abortifacient/uterotonic effect. PPI co-therapy is generally better tolerated and equally effective for ulcer-risk reduction.
Celecoxib
Adults: Lowest effective dose for the shortest duration necessary, per the approved indication
Children: Per product-specific pediatric indication only.
Cardiovascular risk (class effect), GI upset, renal effectsPreferred over a nonselective NSAID in a patient with a prior UGIB who requires ongoing NSAID therapy — lower ulcer risk than a nonselective NSAID, but not zero, so still co-prescribe a PPI in a high-risk patient. Weigh cardiovascular risk before selecting.

Secondary prophylaxis of variceal bleeding: nonselective beta-blockers

First-line secondary prophylaxis, combined with an endoscopic band-ligation program, for every patient after variceal bleeding. Reduce or discontinue if systolic BP falls below 90 mmHg, hyponatremia (under 130 mEq/L) develops, or acute kidney injury occurs.

DrugDosageAdverse effectsComments
Propranolol
Adults: Initial 20 mg PO BID; titrate every 2-3 days (commonly up to 160 mg/day in cirrhosis)
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Bradycardia, hypotension, fatigue, bronchospasmTitrate to a resting heart rate of approximately 55-60 bpm or the maximum tolerated dose.
Nadolol
Adults: Initial 20-40 mg PO once daily; titrate every few days
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Bradycardia, hypotension, fatigueOnce-daily alternative to propranolol; same heart-rate/blood-pressure targets.
Carvedilol
Adults: Initial 6.25 mg PO once daily; may increase to 6.25 mg PO BID after 1 week if tolerated (typical maximum 12.5 mg/day in cirrhosis)
Children: Not established for routine pediatric use in UGIB — specialist-directed only.
Bradycardia, hypotension, fatigue, bronchospasm (non-selective plus alpha blockade)May lower portal pressure more than propranolol or nadolol per unit dose, hence the lower maximum dose.

References

  1. ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding — American College of Gastroenterology (Laine L, Barkun AN, Saltzman JR, Martel M, Leontiadis GI). Am J Gastroenterol 2021;116(5):899-917
  2. Baveno VII - Renewing consensus in portal hypertension — Journal of Hepatology (de Franchis R, Bosch J, Garcia-Tsao G, et al.). J Hepatol 2022;76(4):959-974
  3. Management of Nonvariceal Upper Gastrointestinal Bleeding: Guideline Recommendations From the International Consensus Group — Annals of Internal Medicine (Barkun AN, Almadi M, Kuipers EJ, et al.). Ann Intern Med 2019;171(11):805-822
  4. A risk score to predict need for treatment for upper-gastrointestinal haemorrhage — The Lancet (Blatchford O, Murray WR, Blatchford M). Lancet 2000;356(9238):1318-1321
  5. Risk assessment after acute upper gastrointestinal haemorrhage — Gut (Rockall TA, Logan RF, Devlin HB, Northfield TC). Gut 1996;38(3):316-321
  6. The Toronto Consensus for the Treatment of Helicobacter pylori Infection in Adults — Gastroenterology (Fallone CA, Chiba N, van Zanten SV, et al.). Gastroenterology 2016;151(1):51-69
  7. Restrictive versus liberal blood transfusion for gastrointestinal bleeding: a systematic review and meta-analysis of randomised controlled trials — The Lancet Gastroenterology & Hepatology (Odutayo A, Desborough MJ, Trivella M, et al.). Lancet Gastroenterol Hepatol 2017;2(5):354-360
  8. Effects of a high-dose 24-h infusion of tranexamic acid on death and thromboembolic events in patients with acute gastrointestinal bleeding (HALT-IT): an international randomised, double-blind, placebo-controlled trial — The Lancet (HALT-IT Trial Collaborators). Lancet 2020;395(10241):1927-1936
  9. Canadian Association of Gastroenterology Clinical Practice Guideline for the Endoscopic Management of Nonvariceal Nonpeptic Ulcer Upper Gastrointestinal Bleeding — Gastroenterology, Canadian Association of Gastroenterology (Barkun AN, Laine L, Leontiadis GI, et al.). Gastroenterology 2025 (in press)
  10. Intermittent vs continuous proton pump inhibitor therapy for high-risk bleeding ulcers: a systematic review and meta-analysis — JAMA Internal Medicine (Sachar H, Vaidya K, Laine L). JAMA Intern Med 2014;174(11):1755-1762
  11. American College of Gastroenterology-Canadian Association of Gastroenterology Clinical Practice Guideline: Management of Anticoagulants and Antiplatelets During Acute Gastrointestinal Bleeding and the Periendoscopic Period — American Journal of Gastroenterology (Abraham NS, Barkun AN, Sauer BG, et al.). Am J Gastroenterol 2022;117(4):542-558
  12. Continuation of low-dose aspirin therapy in peptic ulcer bleeding: a randomized trial — Annals of Internal Medicine (Sung JJ, Lau JY, Ching JY, et al.). Ann Intern Med 2010;152(1):1-9
  13. AASLD Practice Guidance on the use of TIPS, variceal embolization, and retrograde transvenous obliteration in the management of variceal hemorrhage — Hepatology, American Association for the Study of Liver Diseases (Lee EW, Eghtesad B, Garcia-Tsao G, et al.). Hepatology 2024;79(1):224-250
  14. Pre-endoscopic erythromycin administration in upper gastrointestinal bleeding: an updated meta-analysis and systematic review — Annals of Gastroenterology (Rahman R, Nguyen DL, Sohail U, et al.). Ann Gastroenterol 2016;29(3):312-317

Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.

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