Diverticular bleeding

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

A stretched penetrating artery at a diverticular neck or dome can rupture directly into the lumen, causing sudden painless fresh or maroon bleeding. Many episodes stop spontaneously, but the same vessel or another diverticulum may bleed again. Because diverticula are prevalent, the diagnosis remains provisional until endoscopic or radiological evidence supports the bleeding site.

Management follows acute lower gastrointestinal haemorrhage severity. Resuscitate first, calculate shock index and choose localisation that fits active bleeding. CT angiography provides the rapid bridge to embolisation in instability; prepared colonoscopy is used for stable major bleeding. A negative lower study in a shocked patient must renew concern for an upper source. Haemostasis is incomplete until antithrombotic restart and rebleeding follow-up are planned. In clinically stable patients requiring red-cell transfusion, BSG recommends a restrictive trigger of 70 g/L with a 70–90 g/L post-transfusion target, or trigger 80 g/L and target 100 g/L with cardiovascular disease; these stable thresholds do not replace physiology-led major-haemorrhage resuscitation.

Key points

Diverticular bleeding is classically abrupt, painless haematochezia from a vasa recta, but incidental diverticulosis does not prove the source.
Calculate shock index as heart rate divided by systolic blood pressure; a value above 1 indicates instability in the BSG lower-GI bleeding pathway.
After initial resuscitation, use CT angiography for suspected active bleeding or instability because it rapidly localises extravasation.
A positive CT angiogram should lead promptly to catheter angiography and embolisation when available; surgery requires localisation whenever possible.
Stable major bleeding warrants admission and colonoscopy on the next available list, while selected minor self-terminating bleeds with Oakland score 8 or lower may undergo urgent outpatient investigation.
Antithrombotic interruption, reversal and restart depend on bleed severity and thrombotic indication; do not leave an indefinite undocumented stop.
For clinically stable patients who need red cells, BSG uses a restrictive haemoglobin trigger of 70 g/L and target 70–90 g/L; with cardiovascular disease use trigger 80 g/L and target 100 g/L, while active major haemorrhage follows physiology and a major-haemorrhage protocol.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Vasa recta erosion

An artery crossing the neck or dome of a diverticulum becomes stretched and vulnerable to rupture directly into the lumen.

Haemostatic modifiers

Anticoagulants, antiplatelets and NSAIDs can increase bleeding or impair clot stability, while frailty reduces tolerance of the same blood loss.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Abrupt arterial loss
Direct vessel rupture can produce large-volume painless haematochezia before haemodilution makes the circulating haemoglobin concentration fall.
2
Intermittent haemostasis
Vasoconstriction and local thrombus may stop bleeding temporarily, but clot disruption permits recurrence from the same vessel.
3
Systemic hypoperfusion
Reduced circulating volume lowers cardiac preload and organ blood flow, causing tachycardia, oliguria, confusion, myocardial ischaemia and shock.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Bleeding pattern

Arterial rupture produces abrupt painless haematochezia that may stop spontaneously yet recur from the same or another diverticulum.

Perfusion assessment

Tachycardia, postural change, confusion, cool peripheries and oliguria can reveal significant loss before hypotension.

Medication effect

Anticoagulants, antiplatelets and NSAIDs can increase severity, but stopping them requires thrombosis-risk assessment.

Source uncertainty

Diverticula are common incidental findings, so the source should be assigned only when imaging or endoscopy supports it.

Red flags requiring action

Heart rate divided by systolic blood pressure above 1 after initial resuscitation identifies haemodynamic instability and supports urgent CT angiography.
Haematochezia with shock can arise from a brisk upper gastrointestinal bleed, especially when CT angiography does not show a lower source.
New abdominal pain, fever or peritonism after arterial embolisation suggests colonic ischaemia and requires urgent reassessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
ABCDE observations and blood bank samplesFirst step
Why
identify shock and prepare blood support.
Interpretation and limitations
Serial physiology and haemoglobin trend are more reliable than one early concentration.
02
CT angiography
Why
localise active haemorrhage in unstable or ongoing significant bleeding.
Interpretation and limitations
A positive arterial blush can direct rapid angiographic embolisation.
03
Colonoscopy
Why
identify mucosal stigmata and provide endoscopic haemostasis.
Interpretation and limitations
Preparation and haemodynamic stability affect timing, completion and safety.
04
Upper endoscopy when indicated
Why
exclude brisk upper-GI bleeding presenting as haematochezia.
Interpretation and limitations
Shock, melaena or upper-GI clues raise the value of this assessment.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Brisk upper gastrointestinal bleeding

Rapid proximal blood loss may pass as maroon stool or haematochezia, particularly when circulatory shock accompanies the presentation.

Colorectal neoplasia

Cancers and polyps may bleed intermittently and can coexist with incidental diverticulosis, requiring definitive colonic assessment.

Colitis or angioectasia

Inflammatory, ischaemic and vascular mucosal lesions require imaging or endoscopic discrimination because their treatment and recurrence patterns differ.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Worked case: unstable arterial diverticular bleedUse shock index to localise and treat active lossFirst stepA 74-year-old passes repeated maroon stools while taking apixaban for atrial fibrillation. Pulse is 128/min and systolic blood pressure is 92 mmHg after initial fluid, giving a shock index of 1.39; admission haemoglobin is 98 g/L.

1Continue ABCDE resuscitation, obtain two large-bore cannulas and crossmatch samples, assess organ perfusion and activate major-haemorrhage support according to ongoing loss rather than the first haemoglobin alone.
2Interrupt apixaban, establish the last dose and renal function, and make any reversal decision with senior haematology guidance from bleeding severity and stroke risk.
3Urgent CT angiography shows active extravasation from an ascending-colon diverticulum; transfer promptly for selective catheter angiography.
4Interventional radiology embolises the responsible branch, after which blood pressure rises to 116/68 mmHg and no further haematochezia occurs.
5Haemoglobin stabilises at 88 g/L without further transfusion, abdominal examination remains painless and apixaban is restarted on day five after documented haemostasis and individual thrombotic review.

02Minor self-terminating bleedingDischarge only after structured risk assessmentA 48-year-old reports one small painless episode of fresh rectal bleeding. Observations are normal, haemoglobin is 151 g/L, rectal examination shows no mass, the calculated Oakland score is 6 and there is no other reason for admission.

1Confirm bleeding has stopped, take a full history and examination including the anus and rectum, and check that the haemoglobin and physiology remain stable.
2Use the Oakland score as an aid rather than a substitute for judgement; a score of 6 is within the BSG example threshold of 8 or lower for minor bleeding.
3Discharge with urgent outpatient colonic investigation and specific instructions to return for recurrent volume, dizziness, syncope, melaena or abdominal pain.
4Colonoscopy twelve days later identifies a diverticulum with a non-bleeding visible vessel, treats it with a clip and excludes colorectal cancer.
5At four-week review there has been no recurrence and haemoglobin remains 150 g/L; record the supported diverticular source and future bleeding advice.

03Shock with negative lower CT angiographySearch promptly for an upper gastrointestinal sourceA 67-year-old has maroon haematochezia, pulse 118/min and systolic pressure 86 mmHg. CT angiography performed after initial resuscitation shows no lower gastrointestinal extravasation.

1Continue resuscitation and reassess the history for melaena, haematemesis, peptic ulcer risk, liver disease and medication exposure.
2Do not attribute the event to diverticula merely because they are visible on CT; instability makes a brisk upper source plausible.
3Arrange immediate upper endoscopy as recommended when an unstable lower-GI presentation has no source on initial CT angiography.
4Endoscopy finds a spurting duodenal ulcer, which is injected and clipped, replacing the provisional diverticular diagnosis.
5Verify haemostasis through stable physiology, stool colour and haemoglobin trend, and institute ulcer-specific treatment and secondary prevention.

Key medicines and prescribing safety1 treatment · regimens, roles and cautions

Corrects clinically important anaemia while avoiding unnecessary transfusion after haemostasis in stable lower-gastrointestinal bleeding.

Red blood cell transfusion in stable lower-GI bleeding

In a clinically stable patient who needs transfusion, use haemoglobin 70 g/L as the trigger and target 70–90 g/L; for a patient with cardiovascular disease use an 80 g/L trigger and 100 g/L target.

Do not apply stable restrictive thresholds mechanically during active major haemorrhage or shock, when blood loss, perfusion, myocardial ischaemia, coagulopathy and the major-haemorrhage protocol determine replacement; reassess after each unit when feasible.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Haemorrhagic shock

Continued arterial loss can cause acute kidney injury, myocardial ischaemia, altered consciousness and death without effective resuscitation and haemostasis.

Rebleeding

Spontaneous or procedural haemostasis does not remove all vulnerable diverticular vessels, so recurrent haemorrhage remains possible.

Embolisation-related ischaemia

Arterial occlusion can compromise colonic perfusion and present with new pain, fever, raised lactate or peritonism after treatment.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Chart stool frequency and volume, heart rate, blood pressure, urine output and mental state; acute haemoglobin concentration may lag behind blood loss.
After embolisation, examine repeatedly for new abdominal pain, tenderness, fever or lactate rise that could signal segmental colonic ischaemia.
Document the indication, timing and responsible clinician for antiplatelet or anticoagulant restart after haemostasis, balancing rebleeding against thrombosis.
Ensure definitive colonic or upper gastrointestinal investigation explains the episode; diverticulosis alone should remain a possible rather than confirmed source.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Haematochezia can be upper GI

Fast proximal bleeding may transit before melaena forms, particularly when shock is present.

CTA is a localisation test

It can connect active bleeding to a vessel and intervention more directly than an unprepared urgent colonoscopy.

A diverticulum is not proof

Common incidental diverticula should not be named the source unless clinical or procedural evidence supports it.

Restart planning prevents harm

Indefinite anticoagulant cessation after haemostasis can expose the patient to preventable thromboembolism.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for a low haemoglobin before treating shock ignores the early physiology of acute blood loss.
02
Giving tranexamic acid routinely for GI bleeding conflicts with the February 2026 BSG/ACPGBI position after HALT-IT; any truly exceptional consultant-led use needs a documented rationale, and research use belongs in an approved study.
03
Calling the source diverticular from CT diverticulosis alone can misdirect embolisation or surgery.
04
Stopping apixaban without a documented restart decision trades bleeding risk for unmonitored stroke risk.

Find your next topic