Key Points
- Stabilize ABCs; begin targeted evaluation without delaying life-saving therapy.
- Use system-specific risk tools to guide testing and disposition.
- Order high-yield tests first; escalate imaging when indicated.
- Start evidence-based initial therapy and reassess frequently.
Algorithm
- Primary survey and vitals; IV access and monitors.
- Focused history/physical; identify red flags and likely etiologies.
- Order system-appropriate labs and imaging (see Investigations).
- Initiate guideline-based empiric therapy (see Pharmacology).
- Reassess response; arrange consultation and definitive management.
Clinical Synopsis & Reasoning
UGIB commonly arises from peptic ulcer disease, portal hypertension, or mucosal injury. Stabilize hemodynamics, obtain type and crossmatch, and risk‑stratify (Glasgow‑Blatchford, Rockall). Identify liver disease stigmata and encephalopathy when variceal sources are possible. Early endoscopy within 24 h is diagnostic and therapeutic; correct coagulopathy guided by clinical context rather than INR alone.
Treatment Strategy & Disposition
Administer IV PPI for suspected nonvariceal bleed; give vasoactive therapy and prophylactic antibiotics if variceal hemorrhage is likely. Perform endoscopic hemostasis for high‑risk stigmata, then transition to oral PPI and H. pylori eradication if indicated. Manage anticoagulants/antiplatelets based on thrombotic risk; resume when hemostasis secured. Admit based on risk scores and comorbidities; ICU for ongoing transfusion needs or instability.
Epidemiology / Risk Factors
- NSAIDs/alcohol; biliary disease
Investigations
| Test | Role / Rationale | Typical Findings | Notes |
|---|---|---|---|
| CBC | Bleeding/anemia | Low Hgb | |
| CMP | LFTs/electrolytes | Abnormal LFTs | |
| Lipase (if pancreatitis) | Pancreatic enzyme | Elevated | |
| CT Abd/Pelvis (selected) | Complications | Findings vary |
Endoscopic Stigmata and Therapy
| Finding | Therapy |
|---|---|
| Active bleeding or visible vessel | Dual modality (epinephrine plus thermal or mechanical) |
| Adherent clot | Irrigation and therapy if high risk; PPI thereafter |
| Clean-based ulcer | No endoscopic therapy; PPI and discharge when stable |
Pharmacology
| Medication | Mechanism | Onset | Role in Therapy | Limitations |
|---|---|---|---|---|
| Ceftriaxone (cirrhosis) | Cephalosporin | Hours | SBP prophylaxis in variceal bleed | Allergy; ED use |
| Packed RBC | O₂-carrying capacity | Immediate | Transfuse to Hgb threshold | Transfusion reactions; ED use |
| Octreotide (variceal) | Splanchnic vasoconstriction | Minutes | Acute variceal bleed | Abdominal cramps; ED use |
| PPI (IV) | H+/K+ ATPase inhibition | Hours | Non-variceal UGIB | Infection risk long-term; ED use |
| Balanced crystalloids | Plasma volume expansion | Immediate | Resuscitation | Fluid overload; ED use |
Prognosis / Complications
- Varies by etiology and bleeding severity; rebleeding/perforation
Patient Education / Counseling
- Explain red flags and when to seek emergent care.
- Reinforce medication adherence and follow-up plan.
Notes
Prefer balanced resuscitation; avoid over-transfusion. Restart anticoagulation after hemostasis based on thrombotic risk and rebleeding risk.