01Approach to the Critical Patient/attcp53

Immediate stabilization

›Hemorrhagic shock recognition

›Shock index (HR/SBP) >=1 indicates hemodynamic instability

›Two large-bore IVs (16G or larger) immediately

›Activate massive transfusion protocol if ongoing hemorrhage

›Crystalloid resuscitation as bridge to blood products

›1 L isotonic crystalloid bolus

›Reassess after each bolus for response

›Packed red blood cells for Hgb <70 mmol/l (7 g/dL threshold)

›Restrictive transfusion strategy preferred (Class I, ACG 2023)

›Target Hgb 70–90 mmol/l in most patients

›Target Hgb 80–100 mmol/l in active cardiac ischemia

›Airway and oxygenation

›Supplemental oxygen for SpO2 <92%

›Anemia-related tissue hypoxia compounds hemodynamic instability

›Aspiration risk in actively vomiting or obtunded patients

›Suction at bedside

›Lateral decubitus positioning if unconscious

Monitoring and resuscitation targets

›Hemodynamic monitoring bundle

›Continuous cardiac monitoring and pulse oximetry

›Tachycardia as early hypovolemia marker

›Arrhythmia detection relevant for anticoagulation decisions

›Frequent blood pressure reassessment

›Orthostatic vitals if initial vitals stable

›MAP target >=65 mmHg

›Urine output monitoring

›Target >=0.5 mL/kg/hour

02History/hx68

Bleeding characterization

›Stool characteristics

›Hematochezia (bright red or maroon blood per rectum)

›Most common presentation of colonic angiodysplasia

›Painless nature distinguishes from ischemic colitis and IBD

›Melena suggests upper GI source or right-sided colonic source

›Up to 15% of apparent LGIB is actually UGIB

›Occult blood loss with iron deficiency anemia

›Chronic presentation common in angiodysplasia

›Volume and frequency of bleeding episodes

›Number of bloody bowel movements in 24 hours

›Passage of clots indicates significant hemorrhage

›Bleeding timeline

›Prior episodes of GI bleeding (recurrence rate ~34%)

›Frequency and severity of prior episodes

›Prior endoscopic treatments and response

›Duration of current episode

›Spontaneous cessation common but recurrence expected

›Transfusion history (prior requirements suggest severity)

Alarm features

›High-risk historical features

›Syncope or presyncope during bleeding episode

›Indicates significant hemodynamic compromise

›Hemoglobin drop >20 mmol/l from baseline

›Or hemoglobin <70 mmol/l on presentation

›Anticoagulated patient with uncontrolled bleeding

›Warfarin, DOAC, antiplatelet agents

›Ongoing transfusion requirement in prior admissions

Medication history

›Bleeding risk medications

›Anticoagulants

›Warfarin (supratherapeutic INR increases risk markedly)

›Direct oral anticoagulants (rivaroxaban, apixaban, dabigatran, edoxaban)

›Antiplatelet agents

›Aspirin — dose-dependent GI bleeding risk

›Clopidogrel, ticagrelor — dual antiplatelet therapy compounds risk

›NSAIDs — inhibit mucosal prostaglandins, increase bleeding risk

›Iron supplementation (prior or current — indicates known deficiency)

Risk factors

›Established risk factors for angiodysplasia

›Age >60 years — strongest risk factor; degenerative vessel changes

›Prevalence increases progressively with age

›Aortic stenosis (Heyde syndrome)

›Acquired von Willebrand factor deficiency due to shear stress

›Loss of high-molecular-weight vWF multimers promotes bleeding

›End-stage renal disease / chronic kidney disease

›Uremia impairs platelet function

›Dialysis patients have highest prevalence of GI angiodysplasia

›Von Willebrand disease (acquired or hereditary)

›Type 2 diabetes mellitus

›Prior pelvic radiation (radiation proctopathy differential)

›Liver disease / cirrhosis (coagulopathy, portal hypertension)

Review of systems

›GI symptoms

›Abdominal pain (absence favors angiodysplasia over ischemic colitis)

›Left-sided pain suggests ischemic colitis

›Crampy pain with bloody diarrhea suggests IBD

›Weight loss or change in bowel habits (raises malignancy concern)

›Nausea, vomiting, hematemesis (suggests upper GI source)

›Systemic symptoms

›Fatigue and exertional dyspnea (chronic anemia)

›Chest pain (demand ischemia from severe anemia)

›Lightheadedness or presyncope (hemodynamic compromise)

›Cardiovascular and hematologic

›Known aortic stenosis or cardiac murmur (Heyde syndrome)

›Easy bruising or bleeding diathesis (coagulation disorder)

›Dialysis status or known CKD

Family history

›Hereditary conditions

›Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)

›Autosomal dominant

›Mucocutaneous and visceral telangiectasias

›Von Willebrand disease (familial)

›Colorectal cancer family history (raises malignancy differential)

03Physical Exam/exam43

Hemodynamic assessment

›Vital sign evaluation

›Shock index (HR/SBP)

›>=1 indicates hemodynamic instability requiring urgent intervention

›>1.5 indicates severe hemorrhagic shock

›Orthostatic blood pressure and heart rate

›Drop in SBP >20 mmHg or rise in HR >20 bpm on standing

›Suggests intravascular volume depletion >15%

›Respiratory rate and oxygen saturation

›Tachypnea may reflect anemia-driven compensation or aspiration

General appearance

›Signs of hemodynamic compromise

›Pallor, diaphoresis, peripheral vasoconstriction

›Pallor of conjunctivae and nail beds indicates significant anemia

›Altered mental status (end-organ hypoperfusion)

›Skin turgor and mucous membrane moisture (volume status)

Cardiovascular exam

›Cardiac auscultation

›Systolic crescendo-decrescendo murmur at right upper sternal border

›Aortic stenosis — Heyde syndrome evaluation

›Radiation to carotids

›Signs of heart failure (S3, elevated JVP, peripheral edema)

›May complicate fluid resuscitation strategy

Abdominal exam

›Abdominal findings

›Tenderness assessment

›Non-tender abdomen typical of angiodysplasia

›Left-sided tenderness suggests ischemic colitis

04Differential Diagnosis/ddx44

Vascular causes

›Angiodysplasia (angioectasia)

›ICD-10: K31.819 (angiodysplasia of stomach and duodenum) / K55.20 (angiodysplasia of colon)

›Painless, episodic, often self-limiting

›Cecum and ascending colon most common sites (~54–77%)

›Dieulafoy lesion

›ICD-10: K31.82

›Rare; massive intermittent bleeding from aberrant submucosal vessel

›Diagnosed endoscopically

Diverticular disease

›Diverticular bleeding

›ICD-10: K57.31

›Most common cause of LGIB (~40%)

›Painless, large-volume, often self-limited

›Diverticula on colonoscopy with stigmata of recent hemorrhage

Neoplastic causes

›Colorectal malignancy

›ICD-10: C18.9 (colon), C20 (rectum)

›Weight loss, change in bowel habits, mass on colonoscopy

›Iron deficiency anemia as occult presentation

›Older patients, family history of CRC

Inflammatory and ischemic causes

›Ischemic colitis

›ICD-10: K55.039

›Abdominal pain (often left-sided) with bloody diarrhea

›Watershed distribution (splenic flexure, sigmoid)

›Associated with cardiovascular disease and hypotension

›Inflammatory bowel disease

05Laboratory Tests/lt49

Hematologic studies

›Complete blood count

›Hemoglobin and hematocrit (baseline and serial every 4–6 hours)

›Microcytic anemia (low MCV) suggests chronic blood loss

›Normocytic anemia may reflect acute hemorrhage before equilibration

›Platelet count

›Thrombocytopenia (<50 x10^9/L) increases hemorrhage severity

›White blood cell count

›Leukocytosis may suggest inflammatory or infectious etiology

Metabolic and renal studies

›Basic metabolic panel

›BUN and creatinine

›BUN:creatinine ratio >36 suggests upper GI source (protein digestion)

›Elevated creatinine identifies CKD (angiodysplasia risk factor)

›Electrolytes

›Hypokalemia and hypochloremia from large-volume blood loss

›Glucose

›Diabetes mellitus as associated risk factor

›Lactate

›Elevated lactate (>2 mmol/l) indicates tissue hypoperfusion

›Serial lactate for resuscitation monitoring

›Lactate clearance target >=10% per 2 hours

Coagulation studies

›Coagulation panel

›PT/INR and aPTT

›Supratherapeutic INR in anticoagulated patients

›Guides reversal decisions

›Fibrinogen

06Diagnostic Tests/dt75

Scoring Systems

›Oakland Score (LGIB risk stratification)

›Score <=8 associated with safe outpatient management

›Variables: age, sex, prior LGIB admission, DRE findings, heart rate, SBP, hemoglobin

›Score >8 indicates admission required

›Validated for prediction of adverse outcomes in LGIB

›ACG 2023 guideline recommends Oakland Score for disposition decisions

›Level B recommendation

›NOBLADS Score

›Predicts severe LGIB (AUROC 0.77)

›Variables: NSAIDs, no diarrhea, no abdominal tenderness, blood on DRE, antiplatelet use, disease activity score, sex

›Higher score predicts need for intervention

›Useful for triage and resource allocation

›Shock Index (HR/SBP)

›Hemodynamic instability threshold

›>=1 indicates need for urgent intervention

›>1.5 indicates severe hemodynamic compromise

›Simple, rapid, bedside calculation

MRI

›MRI enterography

›Role in small bowel angiodysplasia evaluation

›Indicated when upper and lower endoscopy non-diagnostic

›Superior soft tissue contrast for mucosal vascular lesions

›No ionizing radiation — preferred in younger patients

›Limitations in acute GI bleeding

›Cannot detect active extravasation in real-time

›Requires patient cooperation and breath-holding

›Not first-line in acute hemorrhage

CT

›CT angiography (CTA) of abdomen and pelvis

›First-line imaging in hemodynamically unstable patients

›Sensitivity ~90% for active bleeding source identification

›Multiphase technique: non-contrast, arterial, and venous phases

›Look for contrast extravasation (blush) in arterial phase

›Positive CTA guides catheter angiography and embolization

›~80% of patients with negative CTA will not rebleed

›ACR Appropriateness Criteria: usually appropriate for acute LGIB with hemodynamic instability

›Limitations

›Cannot identify bleeding <0.3–0.5 mL/min

›Intermittent bleeding may be missed

›Not first-line in hemodynamically stable patients where colonoscopy preferred

›CT colonography

›Role limited in acute active bleeding

›May detect mucosal lesions in non-bleeding interval

›Not suitable for therapeutic intervention

Ultrasound

›Bedside ultrasonography

›FAST exam role

›Limited utility for GI bleeding diagnosis

›May identify free fluid if perforation complicates presentation

›Abdominal ultrasound

›Hepatic assessment in liver disease patients

›Portal hypertension screening

›Echocardiography

›Indicated if aortic stenosis suspected (Heyde syndrome)

›Aortic valve replacement resolves Heyde-syndrome-related bleeding

›Assess valve gradient and area for surgical planning

Endoscopy

›Colonoscopy

›Preferred diagnostic and therapeutic modality in hemodynamically stable patients

›Requires adequate bowel preparation (4–6 L PEG solution)

›ACG 2023: perform within 24 hours of hospitalization

›Lesion appearance: flat, red ectatic vessels <10 mm, radiating from central feeder

›Diagnostic yield 48–90% when adequate preparation achieved

›40–60% of patients have multiple lesions

›~20% have synchronous lesions in other GI segments

›Capsule endoscopy

›Indicated for suspected small bowel angiodysplasia when upper and lower endoscopy non-diagnostic

›Sensitivity 62–80% for small bowel vascular lesions

›Non-invasive; requires no sedation

›Cannot provide therapeutic intervention

›Device-assisted enteroscopy (push or balloon)

›Diagnostic and therapeutic for small bowel lesions identified on capsule endoscopy

›Single or double balloon enteroscopy

›Allows argon plasma coagulation of small bowel angiodysplasia

Nuclear medicine

›Tc-99m red blood cell scintigraphy

›Detects active bleeding at lower rates than CTA

›Detects bleeding as low as 0.1 mL/min

›Not routinely recommended by ACG 2023

›May localize intermittent bleeding not detected by CTA

07Disposition/dispo39

ICU admission criteria

›ICU-level care indications

›Hemodynamic instability (shock index >=1) despite initial resuscitation

›Vasopressor requirement

›Massive transfusion protocol activation

›Active hemorrhage requiring emergent intervention

›Ongoing hematochezia with hemodynamic deterioration

›End-organ compromise

›Acute kidney injury, altered mental status, demand ischemia

General ward admission criteria

›Inpatient admission indications

›Oakland Score >8

›Hemoglobin <70 mmol/l

›Ongoing or recent active bleeding

›Significant comorbidities requiring monitoring

›Anticoagulated patients with significant bleeding

›CKD, liver disease, cardiovascular disease

›Transfusion requirement

›Any patient requiring blood products warrants admission

›Planned inpatient colonoscopy within 24 hours

Observation criteria

›Observation unit indications

›Borderline hemoglobin (70–90 mmol/l) with cessation of bleeding

›Serial hemoglobin monitoring every 4–6 hours

›Ongoing concern for rebleeding in higher-risk patients

›Outpatient colonoscopy scheduling within 14 days

Discharge criteria

›Safe discharge requirements

08Treatment/t108

Resuscitation

›Initial resuscitation protocol

›Two large-bore peripheral IVs (16G or larger)

›Intraosseous access if IV access not obtainable

›Crystalloid resuscitation

›Normal saline or lactated Ringer's 500 mL bolus

›Reassess after each bolus; avoid over-resuscitation

›Blood product transfusion

›Packed red blood cells: transfuse for Hgb <70 mmol/l (Class I, ACG 2023)

›Threshold 80 mmol/l if active myocardial ischemia or cardiovascular disease

›Restrictive strategy: transfuse 1 unit then reassess

›Massive transfusion protocol (MTP) if ongoing hemorrhage

›1:1:1 ratio PRBC:FFP:platelets

›Cryoprecipitate for fibrinogen <1.5 g/L

Anticoagulation reversal

›Reversal strategy by agent

›Warfarin reversal

›Vitamin K 10 mg IV (slow infusion over 30 minutes)

›4-factor prothrombin complex concentrate (4F-PCC) 25–50 units/kg IV

›Target INR <1.5 before endoscopic intervention

›Dabigatran reversal

›Idarucizumab (Praxbind) 5 g IV (two 2.5 g vials administered consecutively)

›Immediate and complete reversal

›Factor Xa inhibitor reversal (rivaroxaban, apixaban, edoxaban)

›Andexanet alfa: low dose 400 mg IV bolus over 30 min then 480 mg over 2 hours

›High dose 800 mg IV bolus then 960 mg over 2 hours (if last dose >8 hours or rivaroxaban >10 mg)

Endoscopic therapy

›Argon plasma coagulation (APC) — first-line endoscopic therapy

›Technique and parameters

›Flow rate 0.8–1.0 L/min

›Power 20–40 W

›Excellent safety profile for superficial vascular lesions

›For large right-sided lesions

›Submucosal saline injection before APC to reduce perforation risk

›Post-treatment

›Tattoo or clip adjacent to treated lesion for relocalization if rebleeding

›Rebleeding rate after APC approximately 20–40% at 1 year

›Multiple sessions often required for complete treatment

›Hemostatic clipping

›Indications

›Refractory bleeding after APC

›Active spurting vessel

›Through-the-scope clips for accessible lesions

›May close defect after thermal therapy

›Bipolar electrocoagulation

›Alternative to APC for discrete vascular lesions

›Lower risk of transmural injury compared to monopolar

›Less effective for diffuse lesions

Interventional radiology

›Transcatheter arterial embolization (TAE)

›Indications

›Active extravasation on CTA with failed or unavailable endoscopy

›Hemodynamic instability precluding colonoscopy

›Technique

›Superselective catheterization of vasa recta

›Microcoil or n-butyl cyanoacrylate (glue) embolization

›Technical success rate 80–100%

›Rebleeding rate 10–20% at 30 days

›Complications

›Bowel ischemia (1–4%)

›Post-embolization syndrome

›Catheter-directed vasopressin

›Historical use; largely replaced by embolization

›Reserved for patients who are not embolization candidates

›Vasopressin 0.2 units/min infusion; titrate to 0.4 units/min if no response

Pharmacologic therapy for recurrent/refractory bleeding

›Octreotide LAR (somatostatin analogue) — first-line pharmacologic adjunct

›Dosing

›Octreotide LAR 10–30 mg IM every 28 days

›Evaluate response at 6 months

›Continue long-term if effective; can be maintained for years

›Efficacy data

›82% reduction in transfusion requirements (systematic review, Lancet GH 2021)

›83% of patients achieve >=50% reduction in bleeding episodes

›Indicated for transfusion-dependent recurrent angiodysplasia bleeding refractory to endoscopic therapy

›Thalidomide (antiangiogenic) — reserved for refractory cases

›Dosing

›50–100 mg/day orally

›Dose-dependent reduction in rebleeding at 1 year (NEJM 2023 trial)

›Adverse effects requiring counseling

›Peripheral neuropathy (dose-limiting)

›Constipation

›Teratogenicity (absolute contraindication in pregnancy; REMS program required)

›Thromboembolism risk

›Reserve for failure of endoscopic, angiographic, and octreotide therapy

›Hormonal therapy (estrogen-progesterone)

›Not recommended

›Multiple randomized trials demonstrate lack of efficacy (ACEP Level A evidence against use)

›Adverse effects include thromboembolism and cardiovascular risk

Iron replacement therapy

›Iron supplementation

›Oral iron

›Ferrous sulfate 325 mg (65 mg elemental iron) orally two to three times daily

›Ferrous gluconate 300 mg orally twice daily as alternative

›Take on empty stomach for absorption; GI side effects limit adherence

›Intravenous iron

›Preferred for severe iron deficiency, intolerance to oral iron, or malabsorption

›Ferric carboxymaltose 750 mg IV over 15 minutes (up to 1500 mg per course)

›Low molecular weight iron dextran 1000 mg IV over 1 hour

›Continue until ferritin >100 mcg/L and transferrin saturation >20%

Surgical management

›Surgical resection

›Indications

›Last resort for uncontrolled hemorrhage after failed endoscopic and angiographic interventions

›Rarely required (<5% of angiodysplasia cases)

›Segmental resection guided by CTA localization

›Right hemicolectomy most common (cecum/ascending colon predominance)

›Blind resection without localization has poor outcomes

›High rebleeding rate

Heyde syndrome specific management

›Aortic valve replacement

›Consider when aortic stenosis identified with recurrent angiodysplasia bleeding

›Valve replacement restores vWF multimers and resolves bleeding

›Cardiology and cardiac surgery referral required

›TAVR (transcatheter aortic valve replacement) as alternative if high surgical risk

›May also reduce GI bleeding from angiodysplasia in Heyde syndrome

09Special Populations/sp54

Pregnancy

›Angiodysplasia in pregnancy

›Incidence

›Extremely rare; angiodysplasia is primarily a disease of the elderly

›Case reports document presentation in pregnancy with hereditary conditions

›Diagnostic considerations

›Avoid CTA if possible due to fetal radiation exposure

›MRI enterography preferred for small bowel evaluation

›Colonoscopy generally safe in all trimesters with appropriate precautions

›Treatment modifications

›Octreotide: limited safety data; use only if benefit outweighs risk

›Thalidomide: absolutely contraindicated (Category X)

›Iron supplementation: oral or IV iron safe in pregnancy for iron deficiency anemia

›Transfusion thresholds: Hgb <70 mmol/l with same approach as non-pregnant

›Multidisciplinary care

›Maternal-fetal medicine consultation for all cases

›GI and surgery consultations as appropriate

Geriatric

›Older adults (age >65 years)

›Epidemiology

›Angiodysplasia is predominantly a disease of the elderly (>60 years)

›Prevalence increases with age; most common vascular lesion of GI tract in elderly

›Physiologic considerations

›Reduced cardiac reserve limits tolerance of hemorrhage

›Higher baseline comorbidity burden (cardiac, renal, hepatic)

›Higher prevalence of anticoagulant and antiplatelet use

›Resuscitation modifications

›Lower threshold for transfusion (Hgb 80 mmol/l threshold if cardiac disease)

10Background/b66

Epidemiology

›Prevalence and incidence

›Most common vascular lesion of the GI tract

›Accounts for 3–40% of all lower GI bleeding episodes

›Accounts for 35–50% of small bowel bleeding

›Age distribution

›Predominantly affects patients >60 years

›Prevalence 1–2% in general population; higher in elderly

›Recurrence

›Pooled rebleeding risk approximately 34% at 1–2 years

›Chronic recurrent course expected in most patients

›Anatomic distribution

›Cecum and ascending colon: 54–77% of cases

›Multiple lesions in 40–60% of patients

›Synchronous small bowel lesions in ~20%

Pathophysiology

›Vascular degeneration mechanism

›Acquired degenerative process

›Age-related degeneration of mucosal and submucosal vessels

›Repeated intermittent obstruction of submucosal veins where they penetrate muscularis propria

›Resultant vessel changes

›Dilation and tortuosity of mucosal and submucosal arterioles, capillaries, and venules

›Formation of arteriovenous communications

›Loss of precapillary sphincter control

›Macroscopic appearance

›Flat, red ectatic vessels <10 mm diameter

›Radiating from central feeding vessel (stellate or fern-like pattern)

›Heyde syndrome mechanism

›Aortic stenosis and acquired vWD

›High shear stress across stenotic aortic valve cleaves vWF multimers

›Selective loss of high-molecular-weight vWF multimers (most hemostatically active)

›Impaired primary hemostasis at angiodysplasia sites

›Resolution after aortic valve replacement

›Restoration of vWF multimers within weeks

›Reduction in GI bleeding frequency

›ESRD and CKD mechanism

›Uremia-related platelet dysfunction

›Impaired platelet adhesion and aggregation

›Guanidinosuccinic acid and phenolic acids inhibit platelet function

›Increased vascular shear stress in dialysis patients

Therapeutic Considerations

›Endoscopic therapy evidence

›Argon plasma coagulation

›Treatment of choice for accessible colonic and gastric angiodysplasia

›Multiple sessions often required

›Cochrane systematic review (2024): APC superior to no treatment but long-term rebleeding common

›Long-term recurrence after endoscopic therapy

›Rebleeding rate 20–40% at 1 year despite treatment

›Surveillance colonoscopy recommended

›Pharmacologic therapy evidence base

›Octreotide LAR: strongest pharmacologic evidence

›Somatostatin analogues reduce splanchnic blood flow and inhibit angiogenesis

›Systematic review (Lancet GH 2021): 82% reduction in transfusion requirements

›Predictors of response: fewer prior transfusions, higher baseline hemoglobin

›Thalidomide: emerging evidence

›Antiangiogenic mechanism via inhibition of VEGF and TNF-alpha

›NEJM 2023 RCT: significant reduction in rebleeding at 1 year vs. placebo for small bowel angiodysplasia

›Dose-dependent efficacy and toxicity

›Natural history and clinical course

›Majority of acute episodes self-limit without intervention

›80% of patients stop bleeding spontaneously

›Chronic recurrent course is the norm

›Iron deficiency anemia develops from cumulative blood loss

›Transfusion dependence develops in a minority

›ICD-10 coding

›K55.20: Angiodysplasia of colon without hemorrhage

›K55.21: Angiodysplasia of colon with hemorrhage

›K31.819: Angiodysplasia of stomach and duodenum without hemorrhage

›K31.811: Angiodysplasia of stomach and duodenum with bleeding

11Patient Discharge Instructions/pdi29

copy discharge instructions

›Discharge instructions for Lower GI Bleed (Angiodysplasia)

›Diagnosis and explanation

›Angiodysplasia is an abnormal blood vessel in the digestive tract that can bleed

›Bleeding episodes are often recurrent; this is expected and does not mean treatment failed

›About 1 in 3 patients will have a repeat bleeding episode within 1–2 years

›Medications

›Take all prescribed medications as directed

›If prescribed iron supplements: take on an empty stomach if tolerated; dark stools are expected and normal

›Do not stop aspirin, blood thinners, or heart medications without speaking to your doctor first

›Discuss any blood thinners (warfarin, apixaban, rivaroxaban, clopidogrel) with your prescribing doctor before resuming

›Diet and activity

›No specific dietary restrictions for angiodysplasia

›Eat iron-rich foods (red meat, beans, leafy greens, fortified cereals) to help rebuild iron stores

›Stay well hydrated

›Avoid excessive alcohol (can worsen bleeding risk)

›Light activity is acceptable; avoid strenuous exercise until follow-up

›Follow-up appointments

›GI (gastroenterology) appointment within 1–2 weeks

›Colonoscopy scheduled within 14 days if not completed in hospital

›Blood work to recheck hemoglobin in 1–2 weeks

›Family doctor or internist within 1 week

›Return to emergency department immediately if you develop

›Recurrent bright red blood or dark tarry stools

›Lightheadedness, dizziness, or fainting

›Chest pain or shortness of breath

›Rapid or irregular heartbeat

›Severe abdominal pain

12References/r41

Guidelines and key sources

›ACG Clinical Guideline: Management of Patients With Acute Lower Gastrointestinal Bleeding

›Sengupta N, Feuerstein JD, Jairath V, et al.

›American Journal of Gastroenterology. 2023

›Provides evidence-based recommendations for LGIB including angiodysplasia

›ACG 2023 key recommendations: restrictive transfusion, Oakland Score, early colonoscopy

›ACR Appropriateness Criteria: Radiologic Management of Lower GI Tract Bleeding (2021 Update)

›Karuppasamy K, Kapoor BS, Fidelman N, et al.

›Journal of the American College of Radiology. 2021

›CTA as appropriate first-line in hemodynamically unstable patients

›Endoscopic Therapy for Gastrointestinal Angiodysplasia (Cochrane Review)

›Alhamid A, Aljarad Z, Chaar A, Grimshaw A, Hanafi I.

›Cochrane Database of Systematic Reviews. 2024

›APC effectiveness; long-term rebleeding; risk stratification tools

›Effectiveness and Predictors of Response to Somatostatin Analogues in GI Angiodysplasias

›Goltstein LCMJ, Grooteman KV, Rocco A, et al.

›Lancet Gastroenterology and Hepatology. 2021

›Individual patient data meta-analysis supporting octreotide LAR; 82% transfusion reduction

›Thalidomide for Recurrent Bleeding Due to Small-Intestinal Angiodysplasia

›Chen H, Wu S, Tang M, et al.

›New England Journal of Medicine. 2023

›Landmark RCT demonstrating thalidomide efficacy vs. placebo for refractory small bowel angiodysplasia

›Advances in the Management of Lower Gastrointestinal Bleeding

›Alali AA, Almadi MA, Barkun AN.

›Alimentary Pharmacology and Therapeutics. 2024

›Comprehensive review including angiodysplasia management algorithms

›The Role of Imaging for Gastrointestinal Bleeding: Consensus Recommendations

›Sengupta N, Kastenberg DM, Bruining DH, et al.

Evidence & Review

Evidence & Review