Step 1: what comes next?
IV access, blood count, type and screen, resuscitation
GI
A painless bleed can come from a fragile vascular circuit.
Perfusion territories
The figure links arterial supply to vulnerable tissue and the expected ischemic findings.
Quick check
A 79-year-old with CKD has recurrent painless maroon stools and iron deficiency. Colonoscopy shows a flat red fernlike lesion in the cecum.
Reason it through
Location helps, but the entire gut can harbor lesions.
Cecal and ascending-colon walls have high wall tension and are common sites for degenerative vascular ectasia.
Endoscopy shows a flat or slightly elevated bright-red lesion with fernlike or radiating vessels.
Small-bowel angioectasias should be considered when upper endoscopy and colonoscopy do not explain recurrent iron deficiency or overt bleeding.
Match each lesion to its clinical implication.
Classic colonic distribution
Ectatic fragile channels lie near the luminal surface
Consider capsule or enteroscopy after negative bidirectional endoscopy
High shear can produce acquired von Willebrand dysfunction
A vasa recta source favors diverticular hemorrhage
Hemodynamics come before lesion branding.
Resuscitate significant bleeding, review antithrombotic drugs, and determine whether bleeding is active.
Colonoscopy after appropriate preparation is the main diagnostic and therapeutic test in a stable patient; CTA can localize brisk ongoing bleeding.
Treat culprit lesions endoscopically, commonly with argon plasma coagulation; recurrent refractory bleeding may require medical, angiographic, valve-directed, or surgical strategies.
Order the workflow.
Step 1: what comes next?
IV access, blood count, type and screen, resuscitation
Step 2: what comes next?
Colonoscopy when stable; CTA for brisk active hemorrhage
Step 3: what comes next?
Flat or slightly raised red ectatic vessels with radiating branches
Step 4: what comes next?
Endoscopic thermal therapy such as argon plasma coagulation
Step 5: what comes next?
Look for multiple lesions, CKD, acquired von Willebrand dysfunction, or severe aortic stenosis
The lesion matters less than what it is doing to the patient.
Occult iron deficiency is lower acuity but still requires evaluation for alternative lesions.
Recurrent overt bleeding, transfusion dependence, hemodynamic instability, and failure of endoscopic therapy progressively raise urgency.
A single normal colonoscopy does not end the workup when bleeding is intermittent and small-bowel disease remains plausible.
Place the presentations by urgency.
Bleeding pattern and substrate narrow the source.
Angiodysplasias are thin-walled ectatic mucosal and submucosal vessels, commonly in the cecum and ascending colon of older adults.
Bleeding is painless, intermittent, and can be occult or overt; lesions may be multiple.
Diverticular hemorrhage is also painless and brisk, but arises from an injured vasa recta at a diverticulum rather than a flat vascular tuft.
Separate common painless lower-GI sources.
Older adult, recurrent or occult bleeding, right-colon vascular ectasias
Often abrupt, larger-volume painless hematochezia from a diverticulum
Crampy pain precedes hematochezia
Chronic occult loss, altered bowel habits, or focal mass
A valve can create a bleeding disorder downstream.
Severe aortic stenosis can produce high shear, loss of high-molecular-weight von Willebrand multimers, and bleeding from angiodysplasias: Heyde syndrome.
CKD is associated with angiodysplasia and adds platelet dysfunction and recurrent bleeding risk.
Association does not prove that every incidental lesion caused the hemorrhage; correlate with active bleeding and exclude other sources.
Select the accurate statement.
Treat the culprit and the recurrence driver.
Endoscopic argon plasma coagulation is a common first-line therapy for accessible bleeding lesions.
Active bleeding not controlled or reached endoscopically can be localized and embolized angiographically; surgery is reserved for selected localized refractory disease.
For recurrent transfusion-dependent bleeding from diffuse lesions, somatostatin analog therapy has evidence; severe aortic stenosis with Heyde syndrome warrants valve-team assessment because valve replacement can reduce bleeding.
Reveal the clinical implication of each finding.
Stage 1 of 3: Overview
Overview
Hemodynamics come before lesion branding.
Flow check
Choose the perfusion clue that localizes the injured tissue.
Which diagnosis is most likely?
The challenge is proving that a vascular ectasia is the culprit rather than an incidental passenger.
Cross out the wrong vascular territory and highlight the threatened tissue. Each case links vessel, bed, and consequence.
A 76-year-old with severe calcific aortic stenosis has recurrent painless hematochezia. Colonoscopy shows clusters of dilated tortuous vessels in the ascending colon.
Reason it through
An older adult has recurrent GI bleeding, severe calcific aortic stenosis, and reduced high-molecular-weight von Willebrand multimers.
Reason it through
A stable patient has a cecal angiodysplasia actively oozing during colonoscopy.
Reason it through
A patient develops sudden large-volume painless hematochezia. Colonoscopy identifies an exposed vessel at a sigmoid diverticulum and no vascular tufts.
Reason it through
A patient with diffuse small-bowel angioectasias remains transfusion dependent despite repeated endoscopic therapy.
Reason it through
Rapid review
Colonic angiodysplasia. The age, right-colon location, recurrent painless bleeding, and ectatic appearance are characteristic.
Painless intermittent bleeding favors a vascular lesion.
Angiodysplasia often involves the cecum or ascending colon.

PGY-1 Resident Physician in Psychiatry
University Hospitals, Columbia
DO from Kansas City University
Resident physician and founding medical reviewer at Bone Wizardry, focused on clinical accuracy, clear diagnostic reasoning, and practical board-oriented teaching across the curriculum.
Languages: English, Urdu
Medically reviewed
Bone Wizardry is a study resource for medical students. It is not medical advice.