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Lower Gastrointestinal Bleeding Treatment & Management

  • Author: Burt Cagir, MD, FACS; Chief Editor: BS Anand, MD  more...
 
Updated: Mar 29, 2016
 

Approach Considerations

The management of LGIB has 3 components, as follows:

  • Resuscitation and initial assessment
  • Localization of the bleeding site
  • Therapeutic intervention to stop bleeding at the site

With advances in diagnostic and therapeutic endoscopy and angiography, the ability to localize and subsequently treat lower gastrointestinal bleeding (LGIB) has resulted in improved patient outcomes and reduced healthcare costs.[19] The need for surgery also has been significantly reduced.

The sequence of using these modalities depends on the patient's clinical status, the rate of bleeding, and local expertise in specific surgical and nonsurgical procedures. Using any one modality should not preclude the subsequent use of another modality if required. In case of surgery, preoperative localization of bleeding is essential, because segmental colectomies performed after bleeding is localized are associated with the lowest morbidity and mortality.

According to the 2008 SIGN guideline, early endoscopy should be used within 24 hours of initial presentation of acute LGIB, where possible.[17]

Massive LGIB is a life-threatening condition; although this condition manifests as maroon stools or bright red blood from the rectum, patients with massive upper gastrointestinal bleeding (UGIB) may also present with similar findings. Regardless of the level of the bleeding, one of the most important elements in the management of patients with massive UGIB or LGIB is the initial resuscitation. These patients should receive 2 large-bore intravenous (IV) catheters and isotonic crystalloid infusions. Meanwhile, rapid assessment of vital signs, including heart rate, systolic blood pressure, pulse pressure, and urine output, should be performed. Orthostatic hypotension (ie, a blood pressure fall of >10 mm Hg) is usually indicative of blood loss of more than 1000 mL.

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Resuscitation and Initial Assessment

Initial resuscitation involves establishing large-bore IV access and administration of normal saline. Besides ordering routine laboratory studies (eg, complete blood cell (CBC) count, electrolyte levels, and coagulation studies), blood should be typed and cross-matched. The patient's blood loss and hemodynamic status should be ascertained, and in cases of severe bleeding, the patient may require invasive hemodynamic monitoring to direct therapy.

The 2008 SIGN guideline states that patients in shock should receive fluid volume replacement without delay. Colloid or crystalloid solutions may be used to achieve volume restoration before administering blood products. Red cell transfusion should be considered after loss of 30% of the circulating volume.[17]

Signs of hemodynamic compromise include postural changes with dyspnea, tachypnea, and tachycardia. An orthostatic drop in systolic blood pressure of more than 10 mm Hg or an increase in heart rate of more than 10 beats per minute is indicative of at least 15% of blood volume loss. The 2009 AAFP recommendations state that severe postural dizziness with a postural pulse increase of at least 30 beats per minute is a sensitive and specific indicator of acute blood loss of more than 630 mL.[22]

A hematocrit level of less than 18% or a decrease of about 6% is indicative of significant blood loss that requires blood transfusions; the goal is to achieve a target hematocrit level of approximately 20-25% in young patients and a target hematocrit level of around 30% in high-risk, older patients. A coagulopathy, such as an international normalized ratio (INR) of greater than 1.5, may require correction with fresh frozen plasma; thrombocytopenia can be corrected with platelet transfusions.

Transfer to ICU

Patients who require admission to the intensive care unit and early involvement of both a gastroenterologist and a surgeon include the following:

  • Patients in shock
  • Patients with continuous active bleeding
  • Patients at high risk, such as patients with serious comorbidities, those needing multiple blood transfusions, or those with an acute abdomen
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Localization of the Bleeding Site

In about 10% of patients presenting with LGIB, the source of bleeding is from the upper gastrointestinal (GI) tract. Some patients with LGIB should have a nasogastric (NG) tube placed, and if the aspirate or lavage does not show any blood or coffee ground–appearing material but does show bile, bleeding originating from the upper GI tract is unlikely. In case of high suspicion, obtain an esophagogastroduodenoscopy (EGD) evaluation (see Esophagogastroduodenoscopy).

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Initial Approach to Hemostasis

In patients who are hemodynamically stable with mild to moderate bleeding or in patients who have had a massive bleed that has stabilized, colonoscopy should be performed initially.[28] Once the bleeding site is localized, therapeutic options include coagulation and injection with vasoconstrictors or sclerosing agents.

In cases of diverticular bleeding, bipolar probe coagulation, epinephrine injection, and metallic clips may be used. If recurrent bleeding is present, the affected bowel segment can be resected. In cases of angiodysplasia, thermal therapy, such as electrocoagulation or argon plasma coagulation, is generally successful. Angiodysplastic lesions may be missed at colonoscopy if the lesions are small or covered with blood clots.

The 2008 SIGN guideline states that colonoscopic hemostasis is an effective way to control hemorrhage from active diverticular or post-polypectomy bleeding in patients with massive LGIB.[17]

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Therapeutic Colonoscopy

Colonoscopy is useful in radiation therapy–induced gastrointestinal (GI) bleeding and in the treatment of colonic polyp lesions. Endoscopic treatment of radiation-induced bleeding includes topical application of formalin, Nd:YAG laser therapy, and argon plasma coagulation. Neoplastic bleeding due to polyps requires polypectomy. Patients diagnosed with colonic tumors may require surgical resection.

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Vasoconstrictive Therapy

In patients in whom the bleeding site cannot be determined based on colonoscopy and in patients with active, brisk LGIB, angiography with or without a preceding radionuclide scan should be performed to locate the bleeding site as well as to intervene therapeutically.

Initially, vasoconstrictive agents, such as vasopressin (Pitressin), can be used. An experimental study of treatment of LGIB by selective arterial infusion of vasoconstrictors, such as epinephrine with propranolol and vasopressin, was reported. Although epinephrine and propranolol drastically reduced mesenteric blood flow, they also caused a rebound increase in blood flow and recurrent bleeding.

Vasopressin is a pituitary hormone that causes severe vasoconstriction in the splanchnic bed. Vasoconstriction reduces the blood flow and facilitates hemostatic plug formation in the bleeding vessel. Vasopressin infusions are more effective in diverticular bleeding, which is arterial, as opposed to angiodysplastic bleeding, which is of the venocapillary type. The results are less than satisfactory in patients with severe atherosclerosis and coagulopathy.

Intra-arterial vasopressin infusions begin at a rate of 0.2 U/min, with repeat angiography performed after 20 minutes. The bleeding stops in about 91% of patients receiving intra-arterial vasopressin but recurs in up to 50% of patients when the infusion is stopped.[42] If bleeding persists, the rate of the infusion is increased to 0.4-0.6 U/min. Once the bleeding is controlled, the infusion is continued in an intensive care setting for 12-48 hours and then tapered over the next 24 hours. In patients with rebleeding, surgery should be considered.

Complications

During vasopressin infusion, monitor patients for recurrent hemorrhage, myocardial ischemia, arrhythmias, hypertension, and volume overload with hyponatremia. Nitroglycerine paste or drip can be used to overcome cardiac complications. Selective mesenteric infusion induces bowel wall contraction and spasms, which should not be confused with bowel wall ischemia. Do not administer vasopressin into the systemic circulation intravenously, because this causes coronary vasoconstriction, diminished cardiac output, and tachyphylaxis. Vasopressin infusions are contraindicated in patients with severe coronary artery disease and peripheral artery disease.

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Superselective Embolization

An alternative to vasopressin infusion is embolization with agents such as gelatin sponge, coil springs, polyvinyl alcohol, and oxidized cellulose. Embolization involves superselective catheterization of the bleeding vessel to minimize necrosis, the most feared complication of ischemic colitis. This therapeutic modality is useful in patients in whom vasopressin is unsuccessful or contraindicated.

Initial experience with embolization suggested that complications of intestinal infarction were as high as 20%. With the advent of superselective catheterization and embolization of the vasa recta, successful embolization has been performed without intestinal infarction.[46, 47] Embolization is performed using a 3 French (F) microcatheter placed coaxially through the diagnostic 5F catheter. The therapeutic catheter is advanced as far as the vasa recta over a 0.018-inch guidewire so as to decrease the risk of infarction.

Once the bleeding vessel is identified, microcoils are used to occlude the bleeding vessel and to achieve hemostasis. Although microcoils are most commonly used, polyvinyl alcohol and Gelfoam are also used alone or in conjunction with microcoils.[6, 48, 49] However, if terminal mural branches of the bleeding vessel cannot be catheterized, abort the procedure and immediately perform surgery.

Kuo et al concluded superselective microcoil embolization for the treatment of LGIB is safe and effective.[50] They reported complete clinical success in 86% of patients with a rebleeding rate of 14%. Minor ischemic complication rates were noted as 4.5%, and major ischemic complication rates were reported as 0%. The investigators also reviewed the data from 122 cases of lower GI superselective microcoil embolization in the literature, with meta-analysis performed in 144 patients. The combined analysis revealed a minor ischemic complication rate of 9% and a major ischemic complication rate of 0%.[50]

Rossetti at al reviewed 11 years of experience in transarterial embolization of acute colonic bleeding in Switzerland.[51] Twenty-four patients underwent colonic embolization for diverticular, postpolypectomy, bleeding, as well as bleeding from cancer, angiodysplasia, and hemorrhoids. All the different types of bleeding stopped except hemorrhoidal bleeding, requiring hemorrhoidal ligature. The risk of bowel ischemia was 21%. In another study, 44 patients underwent microcoil embolizations for arterial gastrointestinal bleeding.[52] The technical success rate was 88%, with a clinical success rate of 57%. Intestinal ischemia occurred in 5% of patients. The mortality rate was 18%. It was concluded that microcoil embolization had a high success rate and the number of preprocedural and postprocedural transfusions did not affect the technical success.[52]

In another study by Yap et al, 95 patients underwent embolization for acute GI hemorrhage[53] ; 80% of the patients had upper GI hemorrhage and the rest had lower GI hemorrhage. Vessels embolized included gastroduodenal (39%), pancreatoduodenal (20%), gastric (19%), superior mesenteric (11%), inferior mesenteric (11%), and splenic artery (4%). Immediate hemostasis was obtained in 98% of patients. Complications included bowel ischemia in 4% and coil migration in 3% of patients. The overall 30-day mortality rate was 18%.

In Japan, therapeutic upper (n=16) and lower GI (n=23) embolization was performed on 39 occasions in 37 patients.[54]  N -butyl-2-cyanoacrylate was used in 1:1 and in 1:5 mixtures. Recurrent bleeding occurred in 2 patients, hepatic abscess in 2 cases, and lower limb ischemia in 1 patient. No intestinal necrosis occurred. It was concluded that transcatheter arterial embolizations using N -butyl-2-cyanoacrylate was safe and effective with a high rate of complete hemostasis.

Complications

Rosenkrantz et al reported 3 cases of colonic infarction.[55] One patient died following segmental colectomy, and the other patients revealed full-thickness bowel wall injury in the resected specimen. Intestinal ischemia and infarction have also been reported. To prevent this complication, perform embolization beyond the marginal artery as close as possible to the bleeding point in the terminal mural arteries. At least 139 cases have been collected from the medical literature since 1972.

The relevance of surgery after embolization of gastrointestinal and abdominal surgery was also examined.[56] In a retrospective study, a total of 54 patients with 55 bleeding events were identified; only 25 patients (45%) had LGIB. Of those, 9 patients had bleeding in the small intestine, 14 in the colon, and 2 in the rectum. The rebleeding rate was 24% (n=6), and 50% of those with recurrent LGIB required surgery.[56]

The study revealed a primary clinical embolization success rate of 82%, the rate of early recurrent bleeding (< 30 d) was 18%, and the rate of delayed bleeding (>30 days) was 3.6%.[56] Surgery after embolization was required in 20% of patients (n=11). The investigators concluded that surgery has an important role after successful embolization.[56]

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Endoscopic Therapies

One of the advantages of upper or lower endoscopic evaluation is that it provides access to therapy in patients with gastrointestinal (GI) bleeding. Endoscopic control of bleeding can be achieved using thermal modalities or sclerosing agents. Absolute alcohol, morrhuate sodium, and sodium tetradecyl sulfate can be used for sclerotherapy of upper and lower GI lesions.

Endoscopic epinephrine injection is used commonly because of its low cost, easy accessibility, and low risk of complications. In a recent study, 175 patients underwent endoscopic epinephrine injection. Univariate analysis of 31 patients with rebleeding indicated that factors predictive of a high rebleeding rate included older age (≥60 y), American Society of Anesthesiology category III, IV, and V; severe anemia of greater than 8 g/dL; shock; epinephrine injection dose greater than or equal to 12 mL; and severe bleeding signs (hematemesis or hematochezia).[57] An additional hemostatic method such as clips or thermoregulation is needed to prevent subsequent bleeding.[57]

Endoscopic thermal modalities (eg, laser photocoagulation, electrocoagulation, heater probe) can also be used to arrest hemorrhage. Endoscopic control of hemorrhage is suitable for GI polyps and cancers, arteriovenous malformations, mucosal lesions, postpolypectomy hemorrhage, endometriosis, and colonic and rectal varices. Postpolypectomy hemorrhage can be managed by electrocoagulation of the polypectomy site bleeding with either snare or hot biopsy forceps or by epinephrine injection.

The medical literature has also been reviewed for endoscopic treatment of significant lower GI bleeding (total of 286 patients in 8 publications). Hemorrhage was successfully arrested in 70% of patients, with a rebleeding rate of 15%. Endoscopic therapy for LGIB is a minimally invasive and viable option in carefully selected patients.[58]

Hunter et al evaluated 222 GI endoscopic laser procedures in 122 patients and reported hemorrhage was arrested in 84% of the patients with GI bleeding.[59] No perforations were reported in this series, but 1 death occurred and was attributed to laser therapy in a patient with duodenal ulcer and gastroduodenal artery bleeding.

Forty patients with GI arteriovenous malformations (AVMs) underwent 72 photocoagulation sessions with mostly argon laser; 15 of the 40 patients had significant hemorrhage from colonic AVMs; of those 15, there were no deaths following ablation.

Although the treatment options for angiodysplasias are numerous, including segmental bowel resection and selective mesenteric embolization, endoscopic coagulation of angiodysplasias is becoming a treatment of choice using either heated probe or lasers, such as Nd:YAG and argon. Argon laser treatment is recommended for mucosal or superficial lesions, because the energy penetrates only 1 mm. Nd:YAG lasers are more useful for deeper lesions, because they penetrate 3-4 mm.

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Emergent Surgery

Emergency surgery is required in about 10-25% of patients with lower gastrointestinal bleeding (LGIB) in whom nonoperative management was unsuccessful or unavailable.[15]  Failure of embolization warrants surgical intervention.[28]

Surgical indications

The indications for surgery include the following[21, 11] :

  • Persistent hemodynamic instability with active bleeding
  • Persistent, recurrent bleeding
  • Transfusion of more than 4 units packed red bloods cells in a 24-hour period, with active or recurrent bleeding

In addition, factors such as comorbid disease and individual surgical practices play a role in deciding which patient requires surgery. No contraindications exist with regard to surgery in hemodynamically unstable patients with active bleeding. In fact, if the patient is hemodynamically unstable because of ongoing hemorrhage, perform an emergency operation before any diagnostic study.

Segmental bowel resection and subtotal colectomy

Segmental bowel resection following precise localization of the bleeding point is a well-accepted surgical practice in hemodynamically stable patients. Subtotal colectomy is the procedure of choice in patients who are actively bleeding from an unknown source. According to the 2008 SIGN guideline, subtotal colectomy is recommended for the management of colonic hemorrhage that is uncontrolled by other procedures.[17]

Intraoperative esophagogastroduodenoscopy (EGD), surgeon-guided enteroscopy, and colonoscopy may be helpful in diagnosing undiagnosed massive GI bleeding. Depending on the availability of local resources and the patient's condition, it may sometimes be better to perform subtotal colectomy with distal ileal inspection than to try to jperform these tests, particularly if the surgeon is not privileged or comfortable with endoscopy.

Patients who are hemodynamically stable should have preoperative localization of the bleeding site; patients who are hemodynamically unstable with active bleeding may undergo emergency exploratory laparotomy with intraoperative endoscopy. In patients who are hemodynamically stable, once the bleeding site is preoperatively localized, intra-arterial vasopressin is used as a temporizing measure to reduce the bleeding before patients undergo segmental colectomy. Using this approach the operative morbidity rate is approximately 8.6%, the mortality rate is around 10%, and the rate of rebleed ranges from 0-14%.[42]

In patients undergoing emergency laparotomy, every attempt should be made to localize the bleeding intraoperatively, because segmental colectomy is the preferred procedure. If the bleeding site is not localized, a subtotal colectomy is performed with an inherent morbidity rate of around 37% and a mortality rate of about 11%-33%. In unstable patients, a two-stage procedure is preferred: temporary end ileostomy and delayed ileoproctostomy. In a small group of hemodynamically stable patients with minimal medical morbidity, this procedure can be performed as a one-stage procedure with ileoproctostomy. In addition, postoperative diarrhea can be a significant problem in elderly patients who undergo subtotal colectomy and ileoproctostomy.

In a subset of patients, surgery is still required, but with the use of nonsurgical diagnosis and intervention, the morbidity rate has been substantially reduced from around 37% to 8.6% in patients undergoing segmental colectomy. With advances in endoscopy and angiography, the rate of preoperative bleeding localization has steadily improved, impacting surgical outcomes in a positive way.

Contraindicated: Blind segmental resection

Practitioners must understand that blind segmental resection should not be performed because of a prohibitively high rebleeding rate of up to 75%, a morbidity rate up to 83%, and a mortality rate up to 60%. Once the bleeding point is identified, a limited segmental resection should be performed.

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Preoperative Details

Acute LGIB is a common clinical entity and is associated with significant morbidity and mortality (10-20%). The high-risk factors are the patient's age (>60 y), the presence of multiorgan system disease, transfusion requirements (>4 units), need for operation, and recent stress (eg, surgery, trauma, sepsis).

As discussed earlier, 3 major aspects are involved in managing LGIB. The initial priority is to treat the shock. Second, localization of the source of bleeding is required to perform the third task—formulating an interventional plan.

Insert a nasogastric (NG) tube in all patients. A clear bile-stained aspirate generally excludes bleeding proximal to the Treitz ligamentum. After initial resuscitation, undertake a search for the cause of the bleeding to precisely locate the bleeding point.

Following accurate localization by an angiogram, bleeding can be temporarily controlled with either angiographic embolization or vasopressin infusion to stabilize the patient in anticipation of semiurgent segmental bowel resection. Segmental bowel resection is performed in the next 24-48 hours following correction of the patient's physiologic parameters, which include hypotension, hypothermia, acute hemorrhagic anemia, and deficient coagulation factors.

Use selective mesenteric embolization in high-risk patients for whom the operative management is associated with prohibitive risk of morbidity and mortality. If mesenteric embolization is used, these patients must be carefully monitored for bowel ischemia and perforation. Any evidence of ongoing bowel ischemia and/or unexplained sepsis following mesenteric embolization requires exploratory laparotomy to resect the affected bowel segment. Perform subtotal colectomy with ileoproctostomy in patients with nonlocalized LGIB or bilateral sources of colonic hemorrhage.

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Intraoperative Details

Surgical intervention is required in only a small percentage of patients with LGIB. The surgical option depends on whether the bleeding source has been accurately identified preoperatively; if so, it is then possible to perform segmental intestinal resection.

If the bleeding source is unknown, an upper gastrointestinal endoscopy should be performed before any surgical exploration. At celiotomy, identifying the bleeding point is often impossible, as blood refluxes into the proximal and distal bowel.

The abdominal cavity is explored through a midline vertical incision. The assistance of a gastroenterologist or another surgical endoscopist or surgeon is required for intraoperative endoscopic evaluation. The colonoscope is introduced, and the surgeon assists its passage. On-table colonic lavage and colonoscopy may identify the colonic source of bleeding. Surgeon-guided intraoperative small bowel enteroscopy is also performed when no colonic source of bleeding is identified. Again, the colonoscope can be used for this procedure.

Unlike colonoscopy, enteroscopy is performed during the advancement of the scope. Colonoscopic manipulation of the small bowel may cause iatrogenic mucosal tears and hematomas, which may be mistakenly identified as a source of bleeding. Another intraoperative strategy is to clamp segments of the bowel with noncrushing intestinal clamps to identify the segment that fills with blood. If the bleeding point cannot be diagnosed through intraoperative pan-intestinal endoscopy and examination, and if evidence points to a colonic bleeding, perform a subtotal colectomy with end ileostomy.

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Postoperative Details

Hypotension and shock are the eventual consequences of blood loss, but this depends on the rate of bleeding and the patient's response. Clinical development of shock may precipitate myocardial infarction, cerebrovascular accident, and renal or hepatic failure. Azotemia occurs in patients with gastrointestinal blood loss.

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Complications of LGIB

Complications of blood transfusions can be summarized as acute and delayed hemolytic reactions, nonhemolytic reactions, and infectious diseases transmission. Complications related to massive blood transfusions are hypothermia, hypocalcemia, hyperkalemia, dilutional thrombocytopenia, and coagulation factor deficiencies.

Patients who have had surgery of the lower gastrointestinal (GI) tract are prone to the development of complications. The most common early postoperative complications are intra-abdominal or anastomotic bleeding, ileus, mechanical small bowel obstruction (SBO), intra-abdominal sepsis, localized or generalized peritonitis, wound infection and/or dehiscence, Clostridium difficile colitis, pneumonia, urinary retention, urinary tract infection (UTI), deep venous thrombosis (DVT), and pulmonary embolus (PE).

Intra-abdominal sepsis following colorectal surgery is a life-threatening complication and requires aggressive resuscitation. Systemic conditions (eg, severe blood loss and shock, poor bowel preparation, irradiation, diabetes, malnutrition, hypoalbuminemia) may adversely affect anastomotic healing. Changes in the anatomy and physiology of the large bowel, high bacterial content, improper operative technique, tension at the anastomosis, and ischemia can cause anastomotic leak associated with abscess and intra-abdominal sepsis. This condition requires either laparotomy (if the sepsis is generalized) or percutaneous drainage (if the sepsis is localized).

Delayed complications usually occur more than 1 week after surgery, the most common of which are anastomotic stricture, incisional hernia, and incontinence.

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Transfusion-Free Management of LGIB

The management of lower GI bleeding (LGIB) can be challenging in patients who refuse transfusions of blood or blood products. However, transfusion-free management of GI bleeding is possiblewith an acceptable mortality rate.[60]

In a retrospective review of 96 patients with LGIB who did not accept transfusions of blood and blood products, 30 of 37 patients (81%) with hemoglobin levels less than 6 g/dL, and 4 of 7 patients (57%) with hemoglobin levels lower than 3 g/dL survived.[60] The inclusion criteria were frank LGIB, presenting hemoglobin levels lower than 12 g/dL or a decrease in hemoglobin of more than1.5 g/dL. Forty-one patients had upper GI bleeding and the remaining 48 had LGIB.[60]

The mean hemoglobin level was 8.8 g/dl. Surviving patients were treated with epoetin alfa (Procrit) once daily for 5 days, IV iron dextran infusion once daily for 10 days, IV folic acid daily, vitamin C twice daily, as well as IM vitamin B12 injection once. These patients also received beta-blockers (to reduce the cardiac workload) and supplemental oxygen (100%) with intubation (to improve the oxygen delivery as much as possible without blood transfusions). The overall mortality rate was 10%.

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Consultations

Patients who are hemodynamically unstable with active bleeding should be admitted to the medical intensive care unit (MICU). Early consultation with both a gastroenterologist and a surgeon is recommended.

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Long Term Monitoring

Postoperative office visits every 2 weeks are essential to ensure proper wound healing. Upon discharge, a general diet abundant in fruits and vegetables is recommended. Patients are instructed to drink 6-8 glasses of fluid per day. Psyllium seed preparations should also be started. The AAFP recommends 32 g of fiber supplementation per day.[22]

Increased levels of physical activity may prevent the progression of diverticular disease, according to the AAFP 2009 recommendations. The AAFP also notes that aspirin and NSAID use is associated with increased risk of diverticular bleeding.[22]

The need for a follow-up colonoscopy is determined by a recurrence of symptoms. Angiodysplasia is more likely to rebleed if untreated and may require follow-up intervention to localize and treat recurrent bleeding. Colonoscopic electrocoagulation is generally successful in such situations.

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Contributor Information and Disclosures
Author

Burt Cagir, MD, FACS Clinical Professor of Surgery, The Commonwealth Medical College; Attending Surgeon, Assistant Program Director, Robert Packer Hospital; Attending Surgeon, Corning Hospital

Burt Cagir, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, Society for Surgery of the Alimentary Tract

Disclosure: Nothing to disclose.

Coauthor(s)

Elizabeth Cirincione, MD Director of Colon and Rectal Surgery, Department of Surgery, Nassau University Medical Center

Elizabeth Cirincione, MD is a member of the following medical societies: American College of Surgeons, American Society of Colon and Rectal Surgeons

Disclosure: Nothing to disclose.

Gavin F Chico, MD Consulting Staff, CHRISTUS Coushatta Rural Health Clinic

Disclosure: Nothing to disclose.

Kenneth J Manas, MD Assistant Professor, Department of Medicine, Section of Gastroenterology and Hepatology, Louisiana State University Health Sciences Center

Kenneth J Manas, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Marc D Basson, MD, PhD, MBA, FACS Associate Dean for Medicine, Professor of Surgery and Basic Science, University of North Dakota School of Medicine and Health Sciences

Marc D Basson, MD, PhD, MBA, FACS is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Gastroenterological Association, Phi Beta Kappa, Sigma Xi

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

David Greenwald, MD Professor of Clinical Medicine, Fellowship Program Director, Department of Medicine, Division of Gastroenterology, Montefiore Medical Center, Albert Einstein College of Medicine

David Greenwald, MD is a member of the following medical societies: Alpha Omega Alpha, New York Society for Gastrointestinal Endoscopy, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.

References
  1. Ernst O, Bulois P, Saint-Drenant S, Leroy C, Paris JC, Sergent G. Helical CT in acute lower gastrointestinal bleeding. Eur Radiol. 2003 Jan. 13(1):114-7. [Medline].

  2. Yamaguchi T, Yoshikawa K. Enhanced CT for initial localization of active lower gastrointestinal bleeding. Abdom Imaging. 2003 Sep-Oct. 28(5):634-6. [Medline].

  3. Talley NJ, Jones M. Self-reported rectal bleeding in a United States community: prevalence, risk factors, and health care seeking. Am J Gastroenterol. 1998 Nov. 93(11):2179-83. [Medline].

  4. Qayed E, Dagar G, Nanchal RS. Lower gastrointestinal hemorrhage. Crit Care Clin. 2016 Apr. 32 (2):241-54. [Medline].

  5. Baum S, Nusbaum M, Blakemore WS, Finkelstein AK. The preoperative radiographic demonstration of intra-abdominal bleeding from undetermined sites by percutaneous selective celiac and superior mesenteric arteriography. Surgery. 1965 Nov. 58(5):797-805. [Medline].

  6. Rosch J, Gray RK, Grollman JH Jr, et al. Selective arterial drug infusions in the treatment of acute gastrointestinal bleeding. A preliminary report. Gastroenterology. 1971. 59(3):341-9.

  7. Rösch J, Dotter CT, Brown MJ. Selective arterial embolization. A new method for control of acute gastrointestinal bleeding. Radiology. 1972 Feb. 102(2):303-6. [Medline].

  8. Meyers MA, Alonso DR, Gray GF, Baer JW. Pathogenesis of bleeding colonic diverticulosis. Gastroenterology. 1976 Oct. 71(4):577-83. [Medline].

  9. Vernava AM, Longo WE, Virgo KS. A nationwide study of the incidence and etiology of lower gastrointestinal bleeding. Surg Res Commun. 1996. 18:113-20.

  10. Gayer C, Chino A, Lucas C, Tokioka S, Yamasaki T, Edelman DA, et al. Acute lower gastrointestinal bleeding in 1,112 patients admitted to an urban emergency medical center. Surgery. 2009 Oct. 146(4):600-6; discussion 606-7. [Medline].

  11. Vernava AM 3rd, Moore BA, Longo WE, Johnson FE. Lower gastrointestinal bleeding. Dis Colon Rectum. 1997 Jul. 40(7):846-58. [Medline].

  12. Longstreth GF. Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal hemorrhage: a population-based study. Am J Gastroenterol. 1997 Mar. 92(3):419-24. [Medline].

  13. Gupta N, Longo WE, Vernava AM 3rd. Angiodysplasia of the lower gastrointestinal tract: an entity readily diagnosed by colonoscopy and primarily managed nonoperatively. Dis Colon Rectum. 1995 Sep. 38(9):979-82. [Medline].

  14. Saperas E, Videla S, Dot J, Bayarri C, Lobo B, Abu-Suboh M, et al. Risk factors for recurrence of acute gastrointestinal bleeding from angiodysplasia. Eur J Gastroenterol Hepatol. 2009 Dec. 21(12):1333-9. [Medline].

  15. Chalasani N, Wilcox CM. Etiology and outcome of lower gastrointestinal bleeding in patients with AIDS. Am J Gastroenterol. 1998 Feb. 93(2):175-8. [Medline].

  16. Huang ES, Strate LL, Ho WW, Lee SS, Chan AT. Long-term use of aspirin and the risk of gastrointestinal bleeding. Am J Med. 2011 May. 124(5):426-33. [Medline]. [Full Text].

  17. [Guideline] Scottish Intercollegiate Guidelines Network (SIGN). Management of acute upper and lower gastrointestinal bleeding. A national clinical guideline. Edinburgh (Scotland): Scottish Intercollegiate Guidelines Network (SIGN); 2008 Sep. SIGN publication; no. 105: [Full Text].

  18. Andrei GN, Popa B, Gulie L, et al. Highlighted steps of the management algorithm in acute lower gastrointestinal bleeding - case reports and literature review. Chirurgia (Bucur). 2016 Jan-Feb. 111 (1):74-9. [Medline].

  19. Cirocchi R, Grassi V, Cavaliere D, et al. New trends in acute management of colonic diverticular bleeding: a systematic review. Medicine (Baltimore). 2015 Nov. 94 (44):e1710. [Medline].

  20. Zuckerman GR, Prakash C. Acute lower intestinal bleeding. Part II: etiology, therapy, and outcomes. Gastrointest Endosc. 1999 Feb. 49(2):228-38. [Medline].

  21. McGuire HH Jr. Bleeding colonic diverticula. A reappraisal of natural history and management. Ann Surg. 1994 Nov. 220(5):653-6. [Medline]. [Full Text].

  22. [Guideline] Wilkins T, Baird C, Pearson AN, Schade RR. Diverticular bleeding. Am Fam Physician. 2009 Nov 1. 80(9):977-83. [Medline].

  23. Ryan MJ, Key SM, Dumbleton SA, MD, et al. Nonlocalized Lower Gastrointestinal Bleeding: Provocative Bleeding Studies with Intraarterial tPA, Heparin, and Tolazoline. J Vasc Interv Radiol. 2001. 12:1273-77.

  24. Macari M, Chandarana H, Balthazar E, Babb J. Intestinal ischemia versus intramural hemorrhage: CT evaluation. AJR Am J Roentgenol. 2003 Jan. 180(1):177-84. [Medline].

  25. Sabharwal R, Vladica P, Chou R, Law WP. Helical CT in the diagnosis of acute lower gastrointestinal haemorrhage. Eur J Radiol. 2006 May. 58(2):273-9. [Medline].

  26. Lee S, Welman CJ, Ramsay D. Investigation of acute lower gastrointestinal bleeding with 16- and 64-slice multidetector CT. J Med Imaging Radiat Oncol. 2009 Feb. 53(1):56-63. [Medline].

  27. Frattaroli FM, Casciani E, Spoletini D, Polettini E, Nunziale A, Bertini L, et al. Prospective study comparing multi-detector row CT and endoscopy in acute gastrointestinal bleeding. World J Surg. 2009 Oct. 33(10):2209-17. [Medline].

  28. Moss AJ, Tuffaha H, Malik A. Lower GI bleeding: a review of current management, controversies and advances. Int J Colorectal Dis. 2015 Oct 10. [Medline].

  29. Wong RC. Immediate unprepared hydroflush colonoscopy for management of severe lower gastrointestinal bleeding. Gastroenterol Hepatol (N Y). 2013 Jan. 9(1):31-4. [Medline]. [Full Text].

  30. Jensen DM, Machicado GA. Diagnosis and treatment of severe hematochezia. The role of urgent colonoscopy after purge. Gastroenterology. 1988 Dec. 95(6):1569-74. [Medline].

  31. Cohn SM, Moller BA, Zieg PM, Milner KA, Angood PB. Angiography for preoperative evaluation in patients with lower gastrointestinal bleeding: are the benefits worth the risks?. Arch Surg. 1998 Jan. 133(1):50-5. [Medline].

  32. Laine L, Shah A. Randomized trial of urgent vs. elective colonoscopy in patients hospitalized with lower GI bleeding. Am J Gastroenterol. 2010 Dec. 105(12):2636-41; quiz 2642. [Medline].

  33. Emslie JT, Zarnegar K, Siegel ME, Beart RW Jr. Technetium-99m-labeled red blood cell scans in the investigation of gastrointestinal bleeding. Dis Colon Rectum. 1996 Jul. 39(7):750-4. [Medline].

  34. Ng DA, Opelka FG, Beck DE, Milburn JM, Witherspoon LR, Hicks TC, et al. Predictive value of technetium Tc 99m-labeled red blood cell scintigraphy for positive angiogram in massive lower gastrointestinal hemorrhage. Dis Colon Rectum. 1997 Apr. 40(4):471-7. [Medline].

  35. Ryan P, Styles CB, Chmiel R. Identification of the site of severe colon bleeding by technetium-labeled red-cell scan. Dis Colon Rectum. 1992 Mar. 35(3):219-22. [Medline].

  36. Kester RR, Welch JP, Sziklas JP. The 99mTc-labeled RBC scan. A diagnostic method for lower gastrointestinal bleeding. Dis Colon Rectum. 1984 Jan. 27(1):47-52. [Medline].

  37. Ferrant A, Dehasque N, Leners N, Meunier H. Scintigraphy with In-111-labeled red cells in intermittent gastrointestinal bleeding. J Nucl Med. 1980 Sep. 21(9):844-5. [Medline].

  38. Schmidt KG, Rasmussen JW, Grove O, Andersen D. The use of indium-111-labelled platelets for scintigraphic localization of gastrointestinal bleeding, with special reference to occult bleeding. Scand J Gastroenterol. 1986 May. 21(4):407-14. [Medline].

  39. Mole DJ, Hughes SJ, Khosraviani K. 111Indium-labelled red-cell scintigraphy to detect intermittent gastrointestinal bleeding from synchronous small- and large-bowel adenocarcinomas. Eur J Gastroenterol Hepatol. 2004 Aug. 16(8):795-9. [Medline].

  40. Bentley DE, Richardson JD. The role of tagged red blood cell imaging in the localization of gastrointestinal bleeding. Arch Surg. 1991 Jul. 126(7):821-4. [Medline].

  41. Hunter JM, Pezim ME. Limited value of technetium 99m-labeled red cell scintigraphy in localization of lower gastrointestinal bleeding. Am J Surg. 1990 May. 159(5):504-6. [Medline].

  42. Browder W, Cerise EJ, Litwin MS. Impact of emergency angiography in massive lower gastrointestinal bleeding. Ann Surg. 1986 Nov. 204(5):530-6. [Medline]. [Full Text].

  43. Widlus DM, Salis AI. Reteplase provocative visceral arteriography. J Clin Gastroenterol. 2007 Oct. 41(9):830-3. [Medline].

  44. Sahn B, Bitton S. Lower gastrointestinal bleeding in children. Gastrointest Endosc Clin N Am. 2016 Jan. 26 (1):75-98. [Medline].

  45. Ell C, Remke S, May A, Helou L, Henrich R, Mayer G. The first prospective controlled trial comparing wireless capsule endoscopy with push enteroscopy in chronic gastrointestinal bleeding. Endoscopy. 2002 Sep. 34(9):685-9. [Medline].

  46. Ledermann HP, Schoch E, Jost R, Decurtins M, Zollikofer CL. Superselective coil embolization in acute gastrointestinal hemorrhage: personal experience in 10 patients and review of the literature. J Vasc Interv Radiol. 1998 Sep-Oct. 9(5):753-60. [Medline].

  47. Gordon RL, Ahl KL, Kerlan RK, Wilson MW, LaBerge JM, Sandhu JS, et al. Selective arterial embolization for the control of lower gastrointestinal bleeding. Am J Surg. 1997 Jul. 174(1):24-8. [Medline].

  48. Frodsham A, Berkmen T, Ananian C, Fung A. Initial experience using N-butyl cyanoacrylate for embolization of lower gastrointestinal hemorrhage. J Vasc Interv Radiol. 2009 Oct. 20(10):1312-9. [Medline].

  49. Guy GE, Shetty PC, Sharma RP, Burke MW, Burke TH. Acute lower gastrointestinal hemorrhage: treatment by superselective embolization with polyvinyl alcohol particles. AJR Am J Roentgenol. 1992 Sep. 159(3):521-6. [Medline].

  50. Kuo WT, Lee DE, Saad WE, Patel N, Sahler LG, Waldman DL. Superselective microcoil embolization for the treatment of lower gastrointestinal hemorrhage. J Vasc Interv Radiol. 2003 Dec. 14(12):1503-9. [Medline].

  51. Rossetti A, Buchs NC, Breguet R, Bucher P, Terraz S, Morel P. Transarterial embolization in acute colonic bleeding: review of 11 years of experience and long-term results. Int J Colorectal Dis. 2012 Dec 4. [Medline].

  52. Mensel B, Kühn JP, Kraft M, et al. Selective microcoil embolization of arterial gastrointestinal bleeding in the acute situation: outcome, complications, and factors affecting treatment success. Eur J Gastroenterol Hepatol. 2012 Feb. 24(2):155-63. [Medline].

  53. Yap FY, Omene BO, Patel MN, et al. Transcatheter Embolotherapy for Gastrointestinal Bleeding: A Single Center Review of Safety, Efficacy, and Clinical Outcomes. Dig Dis Sci. 2013 Jan 30. [Medline].

  54. Yata S, Ihaya T, Kaminou T, et al. Transcatheter arterial embolization of acute arterial bleeding in the upper and lower gastrointestinal tract with N-butyl-2-cyanoacrylate. J Vasc Interv Radiol. 2013 Mar. 24(3):422-31. [Medline].

  55. Rosenkrantz H, Bookstein JJ, Rosen RJ, Goff WB 2nd, Healy JF. Postembolic colonic infarction. Radiology. 1982 Jan. 142(1):47-51. [Medline].

  56. Köhler G, Koch OO, Antoniou SA, et al. Relevance of surgery after embolization of gastrointestinal and abdominal hemorrhage. World J Surg. 2014 Sep. 38(9):2258-66. [Medline].

  57. Hu ML, Wu KL, Chiu KW, et al. Predictors of rebleeding after initial hemostasis with epinephrine injection in high-risk ulcers. World J Gastroenterol. 2010 Nov 21. 16(43):5490-5. [Medline]. [Full Text].

  58. Fusaroli P, Grillo A, Zanarini S, Caletti G. Usefulness of a second endoscopic arm to improve therapeutic endoscopy in the lower gastrointestinal tract. Preliminary experience - a case series. Endoscopy. 2009 Nov. 41(11):997-1000. [Medline].

  59. Hunter JG, Bowers JH, Burt RW, Sullivan JJ, Stevens SL, Dixon JA. Lasers in endoscopic gastrointestinal surgery. Am J Surg. 1984 Dec. 148(6):736-41. [Medline].

  60. Sharma P, Barajas FJ, Krishnamoorthy P, Campo LM, Blumenthal E, Spinnell M. Transfusion-free Management of Gastrointestinal Bleeding: The Experience of a Bloodless Institute. J Clin Gastroenterol. 2014 Aug 20. [Medline].

  61. Barnert J, Messmann H. Management of lower gastrointestinal tract bleeding. Best Pract Res Clin Gastroenterol. 2008. 22(2):295-312. [Medline].

  62. Cryer B, Li C, Simon LS, Singh G, Stillman MJ, Berger MF. GI-REASONS: a novel 6-month, prospective, randomized, open-label, blinded endpoint (PROBE) trial. Am J Gastroenterol. 2013 Mar. 108(3):392-400. [Medline]. [Full Text].

  63. Hammond KL, Beck DE, Hicks TC, Timmcke AE, Whitlow CW, Margolin DA. Implications of negative technetium 99m-labeled red blood cell scintigraphy in patients presenting with lower gastrointestinal bleeding. Am J Surg. 2007 Mar. 193(3):404-7; discussion 407-8. [Medline].

  64. Miller FH, Hwang CM. An initial experience: using helical CT imaging to detect obscure gastrointestinal bleeding. Clin Imaging. 2004 Jul-Aug. 28(4):245-51. [Medline].

  65. Moukarbel GV, Signorovitch JE, Pfeffer MA, McMurray JJ, White HD, Maggioni AP, et al. Gastrointestinal bleeding in high risk survivors of myocardial infarction: the VALIANT Trial. Eur Heart J. 2009 Sep. 30(18):2226-32. [Medline].

  66. Mönkemüller K, Neumann H, Meyer F, Kuhn R, Malfertheiner P, Fry LC. A retrospective analysis of emergency double-balloon enteroscopy for small-bowel bleeding. Endoscopy. 2009 Aug. 41(8):715-7. [Medline].

  67. Wong Kee Song LM, Baron TH. Endoscopic management of acute lower gastrointestinal bleeding. Am J Gastroenterol. 2008 Aug. 103(8):1881-7. [Medline].

  68. Zuccaro G. Epidemiology of lower gastrointestinal bleeding. Best Pract Res Clin Gastroenterol. 2008. 22(2):225-32. [Medline].

  69. Thomson M, Belsha D. Endoscopic management of acute gastrointestinal bleeding in children: Time for a radical rethink. J Pediatr Surg. 2015 Dec 1. [Medline].

  70. Nagata N, Niikura R, Yamada A, et al. Acute middle gastrointestinal bleeding risk associated with NSAIDs, antithrombotic drugs, and PPIs: a multicenter case-control study. PLoS One. 2016. 11 (3):e0151332. [Medline].

 
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Types of lower gastrointestinal bleeding (LGIB).
Methods used to treat lower gastrointestinal bleeding (LGIB).
Types of lower gastrointestinal (GI) bleeding. HR = heart rate; SBP = systolic blood pressure.
Algorithm for massive lower gastrointestinal (GI) bleeding, surgical perspective. EGD = esophagogastroduodenoscopy; NG = nasogastric; 99mTc RBC = technetium-99m pertechnetate–labeled autologous RBC.
Table 1. Common Causes of Lower Gastrointestinal Bleeding in Adults
Lower Gastrointestinal Bleeding in Adults Percentage of Patients
Diverticular disease
  • Diverticulosis/diverticulitis of small intestine
  • Diverticulosis/diverticulitis of colon
60%
Inflammatory bowel disease
  • Crohn disease of small bowel, colon, or both
  • Ulcerative colitis
  • Noninfectious gastroenteritis and colitis
13%
Benign anorectal diseases
  • Hemorrhoids
  • Anal fissure
  • Fistula-in-ano
11%
Neoplasia
  • Malignant neoplasia of small intestine
  • Malignant neoplasia of colon, rectum, and anus
9%
Coagulopathy 4%
Arteriovenous malformations (AVMs) 3%
TOTAL 100%
Source: Vernava AM, Longo WE, Virgo KS. A nationwide study of the incidence and etiology of lower gastrointestinal bleeding. Surg Res Commun. 1996;18:113-20.[9]
Table 2. Common Causes of Lower Gastrointestinal Bleeding in Children and Adolescents
Lower Gastrointestinal Bleeding in Children and Adolescents
Intussusception
Polyps and polyposis syndromes
  • Juvenile polyps and polyposis
  • Peutz-Jeghers syndrome
  • Familial adenomatous polyposis (FAP)
Inflammatory
  • Crohn disease
  • Ulcerative colitis
  • Indeterminate colitis
Meckel diverticulum
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