Acute Gastrointestinal Bleeding

7/17/2019 Acute Gastrointestinal Bleeding

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Acute gastrointestinal bleeding Joseph JY Sung

Acute gastrointestinal (GI) bleeding is a common admis-sion to the intensive care unit (ICU) and a major causeof morbidity and mortality. Peptic ulcer disease accountsfor 75% of upper GI bleeding.1,2 Bleeding from varices,oesophagitis, duodenitis and Mallory–Weiss syndromeeach account for between 5% and 15% of cases. About20% of GI bleeding arises from the lower GI tract.Common aetiological causes for GI bleeding are listed

in Box 42.1. Mortality from upper GI bleeding hasremained at approximately 10% for decades, but recentreports suggest that mortality from ulcers bleeding hasfallen substantially, to about 5%.3 Furthermore, themajority of cases died of causes unrelated to bleeding,but rather to cardiopulmonary or multi-organ failure.4 This observation emphasises the benet of good sup-portive care in the intensive care unit for patients pre-senting with gastrointestinal bleeding. Variceal bleedinghas a much higher mortality of about 30%. Risk factorsfor mortality include old age, associated medical prob-lems, coagulopathy and the magnitude of bleeding.

UPPER GASTROINTESTINAL BLEEDING

CLINICAL PRESENTATION

The patient may or may not present with a history ofupper GI problems. There may be pain but bleedingulcers can be painless, especially in elderly patients andusers of non-steroidal anti-inammatory drugs. Fre-quently, the common symptoms of hypovolaemia suchas tachycardia, pallor, sweating, cyanosis, mental con-fusion and oliguria are present, especially in massiveGI bleeding. A history of vomiting and retching preced-ing haematemesis suggests Mallory–Weiss syndrome.

Haematemesis and melaena are the most commonpresentations of acute upper GI bleeding. Haematocheziais the passage of bright red or maroon blood from therectum, in the form of pure blood or admixed with stool.It usually represents a lower intestinal source of bleeding,but can also be a feature of massive upper GI bleeding.

INVESTIGATION

ENDOSCOPY OR BARIUM STUDY As history and physical examination are seldomuseful in identifying the specic site of bleeding,

investigations are necessary in most cases of GI bleed-ing. Endoscopy has replaced barium studies as theinvestigation of choice and recent studies show thatendoscopy should be offered within 24 hours of pres-entation to hospital to provide optimal clinical outcome.5

Endoscopy is preferred to barium X-rays for the fol-lowing reasons:

• Endoscopy allows more precise identication of thesite and nature of bleeding.

• Endoscopic appearance often predicts the risk ofrecurrent bleeding from ulcer and varices (see below).

• Lesions such as gastritis, portal hypertensive gas-tropathy and duodenitis are difcult to diagnose bybarium X-ray.

• Treatments such as injecting ulcers may be insti-gated during endoscopy (see below).

• Barium X-ray is notoriously unreliable in patientswith previous gastric surgery.

However, endoscopy is not without potential problemsand in particular can induce serious hypoxia in patients

with cardiorespiratory diseases. Careful supervisionwith continuous monitoring of blood pressure, pulseand oxygen saturation with a pulse oximeter is manda-tory. Oxygen should be administered by nasal cannulawhen necessary.

ANGIOGRAPHY Angiography is seldom used for the diagnosis of upperGI bleeding. Theoretically, when the bleeding is verybrisk (greater than 0.5 mL/minute), and obscures theendoscopic view, angiography may help to identify thesources of bleeding and may sometimes be used toembolise the bleeding point. In practice, however, most

patients with this degree of haemorrhage should beconsidered for emergency laparotomy.

MANAGEMENT OF NON-VARICEAL UPPERGI BLEEDING

The goals of managing a patient with acute GI bleedingare, rst, to resuscitate, second, to control active bleed-ing and, third, to prevent recurrence of haemorrhage.

RESUSCITATION Blood and plasma expanders should be given throughlarge-bore intravenous cannulae. Vital signs should be



488 Acute gastrointestinal bleeding

impairs platelet function and haemostasis. Therefore,reducing the secretion of gastric acid should reducebleeding and encourage ulcer healing. A recent studyhas shown that potent acid suppression using intrave-nous proton pump inhibitors reduces recurrent bleed-ing after endoscopic therapy.6 Proton pump inhibitors

should be recommended in high-risk peptic ulcerbleeding patients as an adjuvant to endoscopic therapy.In contrast, antibrinolytic agents such as tranexamicacid have not been effective in reducing the operativerate and mortality of acute GI haemorrhage. Recentstudies show that, in patients at high risk of recurrentbleeding, pharmacological control without endoscopichaemostasis is inadequate.7 Thus a combination ofendoscopic and pharmacological therapy offers the besttherapy for ulcer-bleeding patients.8,9

Endoscopic therapy Most patients with acute upper GI haemorrhage stopbleeding spontaneously and have an uneventful recov-ery. No specic intervention is required in thesepatients. Endoscopic haemostasis should be used inpatients with a high risk of persistent or recurrentbleeding. In the last two decades, endoscopic haemos-tasis, with its high efcacy and low morbidity, hasresulted in a dramatic decrease in emergency surgery,and has reduced the mortality of ulcer bleeding. Thethree most popular methods of haemostasis are asfollows.

Epinephrine (adrenaline) injection

Endoscopic injection of epinephrine (1 : 10 000 dilution)at 0.5–1.0 mL aliquots (up to 10–15 mL) into and aroundthe ulcer bleeding point has achieved successful hae-mostasis in over 90% of cases.8 Debate exists as towhether the haemostatic effect is a result of local tam-ponade by the volume injected or vasoconstriction byepinephrine. Absorption of epinephrine into the sys-temic circulation has been documented, but withoutany signicant effect on the haemodynamic status ofthe patient.10 Epinephrine injection is an effective,cheap, portable and easy-to-learn method of haemosta-sis, and has acquired worldwide popularity.

closely monitored. In patients with hypovolaemicshock, central venous pressure and hourly urine output

should also be observed (see Ch. 15). Following ade-quate resuscitation, management is directed at identify-ing the lesion and distinguishing the high-risk patient,who is likely to require early endoscopic or surgicaltreatment.

THE HIGH-RISK PATIENT Signicant GI bleeding is indicated by syncope, hae-matemesis, systolic blood pressure below 100 mmHg(13.3 kPa), postural hypotension and a blood transfu-sion requirement of more than 4 units of blood in 12hours, to maintain blood pressure. Patients over 60years old and with multiple co-morbidities are at even

higher risk.3

Those admitted for other medical prob-lems (e.g. heart or respiratory failure, or cerebrovascu-lar bleed) and who have GI bleeding duringhospitalisation also have a higher mortality.

THE HIGH-RISK ULCER Peptic ulcers that are actively bleeding or have bledrecently may show stigmata of haemorrhage on endos-copy. These include localised active bleeding (i.e. pul-satile, arterial spurting or simple oozing), an adherentblood clot, a protuberant vessel or a at, pigmentedspot on the ulcer base. Stigmata of haemorrhage areimportant predictors of recurrent bleeding (Table 42.1).

The proximal postero-inferior wall of the duodenalbulb and the high lesser curve of the stomach arecommon sites for severe recurrent bleeding, probablyowing to their respective large arteries (gastroduodenaland left gastric arteries).

TREATMENT

Pharmacological control Acid-suppressing drugs such as H2-receptor antago-nists and proton pump inhibitors are very effectivedrugs to promote ulcer healing. An acidic environment

Table 42.1 Stigmata of haemorrhage and risk ofrecurrent bleeding in peptic ulcers

STIGMATA OFHAEMORRHAGE % RECURRENT BLEEDING

Spurter or oozer 85–90

Protuberant vessel 35–55

Adherent clot 30–40

Flat spot 5–10

None 5

Box 42.1 Common causes of acute gastrointestinalbleeding

Upper gastrointestinal bleedingPeptic ulcers (DU : GU 3 : 1)Varices (oesophageal varices : gastric varices 9 : 1)Portal hypertensive gastropathyMallory–Weiss syndromeGastritis, duodenitis and oesophagitisLower gastrointestinal bleedingDiverticular bleedingAngiodysplasia and arteriovenous malformationColonic polyps or tumoursMeckel’s diverticulumInflammatory bowel diseases

DU=duodenal ulcer; GU=gastrointestinal ulcer.



Upper gastrointestinal bleeding 489

vessels. A protocol to manage bleeding peptic ulcer isshown in Figure 42.1.15

ACUTE STRESS ULCERATION

Acute stress ulceration is associated with shock, sepsis,burns, multiple trauma, head injuries, spinal injuriesand respiratory, renal and hepatic failure. Bleeding maybe occult or overt, from ‘coffee-grounds’ aspirates tofrank haemorrhage. Lesions are most commonly seen

in the gastric fundus, and range from mild erosions toacute ulcerations. The exact mechanism leading toacute mucosal erosion/ulceration in critically ill patientsis still unclear. Hypoxia and hypoperfusion of the gas-troduodenal mucosa are probably the most importantfactors, but haemodynamic instability, respiratoryfailure and coagulopathy are also strong independentfactors in critically ill patients. The reported incidenceof stress-related mucosal bleeding in ICU patientsranges from 8 to 45%.16 It has been declining in the lastdecade as a result of highly effective management ofhypotension and hypoxaemia.

Coaptive coagulationThis method uses direct pressure and heat energy(heater probe) or electrocoagulation (bipolar coagula-tion probe (BICAP)) to control ulcer bleeding. Thedepth of tissue injury induced by these devices isminimal, as the bleeding vessel is tamponaded prior tocoagulation. The overall efcacy of the epinephrine

injection, heater probe and BICAP probe methods arecomparable.11 Occasionally, it is not possible to obtaina view en face of the bleeding ulcers, particularly thoseon the lesser curve or on the posterior wall of the duo-denal bulb. In these situations, direct pressure cannotbe applied, and the failure rate of coaptive coagulationtends to be higher.

HaemoclipsEndoscopic clipping of a bleeding vessel is an appeal-ing alternative treatment that has gained popularity inrecent years. The advantage of haemoclips over ther-mocoagulation is that there is no tissue injury inducedand hence the risk of perforation is reduced. Studiescomparing haemoclips with injection and thermoco-agulation have shown favourable results.12,13 However,the application of haemoclips in certain sites, forexample lesser curve, gastric fundus and posterior wallof the duodenum, is technically difcult. Loading ofclips on to the application device is cumbersome andtime-consuming and transfer of torque from the handleto the tip of the device is limited.

SURGERY Surgery remains the denitive method of stoppinghaemorrhage, but there is little agreement on the exactindications and best timing for surgical intervention.These issues are even less clear now that endoscopictreatment is so effective. Accordingly, good coopera-tion among intensivists, gastroenterologists and sur-geons is essential. Indications for surgery can be:

• arterial bleeding that cannot be controlled by endo-scopic haemostasis

• massive transfusion (i.e. total of 6–8 units of blood)required to maintain blood pressure

• recurrent clinical bleeding after initial success inendoscopic haemostasis

• evidence suggestive of GI perforation.

Surgical procedures include underrunning of the ulcer,underrunning plus vagotomy and drainage, andvarious types of gastrectomy. The overall mortality ofemergency surgery for GI bleeding is about 15–20%. Ina study investigating the best salvage treatment forpatients with recurrent bleeding after endoscopictherapy, surgery was found to be comparable to repeat-ing endoscopic treatment in securing haemostasis.14 However, morbidity is signicantly higher in surgicalpatients than in endoscopic patients. Early surgeryshould be considered in patients with hypovolaemicshock and/or large peptic ulcer with protuberant

Figure 42.1 Management of peptic ulcer bleeding.

Suspected ulcer bleeding

Resuscitation

Endoscopy to confirm source and site

of bleeding

Ulcer with active bleeding,

blood clot or protuberant

vessel

Endoscopic haemostasis and

i.v. proton pump inhibitor

Clean base non-bleeding

ulcer

No bleeding Rebleeding

Repeat

endoscopic Rx

Rebleeding

Surgery




parietal cell, namely the proton pump. All proton pumpinhibitors (omeprazole, lansoprazole, pantoprazole andrabeprazole) can be given as oral medications. Omepra-zole and pantoprazole are also available in intravenousform for those who cannot be fed orally. In twonon-randomised studies, intravenous omeprazole wasshown to protect critically ill patients requiring ventila-

tion from the development of stress-related mucosalbleeding from the upper GI tract.20 As yet, there are noprospective data indicating which are the high-riskpatients who might benet from this treatment.

VARICEAL BLEEDING

Acute variceal bleeding is a serious complication ofportal hypertension, with a high mortality. About 50%of patients with bleeding varices have had an earlierbleed during hospitalisation. The degree of liver failure,using Child–Pugh’s classication (see Ch. 44), is themost important prognostic factor for early rebleeding

and survival.

RESUSCITATION Immediate resuscitation with whole blood and uidis mandatory. Overtransfusion may cause a reboundincrease in portal pressure (with a consequent increasedrisk of rebleeding) and must be avoided. Fresh frozenplasma and platelet concentrates transfusion may beindicated. A nasogastric cannula is often inserted forthe removal of blood (and also drug administration).Forceful aspiration through the nasogastric tube shouldbe discouraged as bleeding may be induced. Lactulose(15–30 mL every 4–6 hours) should be given to prevent

or correct hepatic encephalopathy. A colonic wash-outcan be used, but a magnesium-containing enema shouldbe avoided in the presence of renal failure. Close atten-tion must be given to haemodynamic monitoring.

When the patient is haemodynamically stable, upperGI endoscopy should be performed to identify thesource of bleeding. Patients with portal hypertensioncould bleed from oesophageal or gastric varices, pepticulcers or portal hypertensive gastropathy or combina-tions of these.

PHARMACOLOGICAL CONTROL

Vasopressin (0.2–0.4 U/min) used to be the most widelyused agent to reduce portal blood pressure and controlvariceal bleeding. Adverse effects of vasopressin suchas cardiac ischaemia (in about 10% of patients) andworsening coagulopathy (by release of plasminogenactivator) have discouraged the use of this drug inrecent years. Terlipressin, a triglycyl synthetic analogueof vasopressin, has a longer half-life and fewer cardiacside-effects and appears more effective and safe whenused in combination with glyceryl trinitrate.22 Infusionof somatostatin and its analogue (octreotide, vapre-otide) reduces portal blood pressure and azygous bloodow. They are safe and effective vasoactive agents to

PROPHYLAXIS AND TREATMENT Signicant ulcerations are managed as above. Minorbleeding and prophylactic treatment are consideredtogether. Prophylactic treatment aims for gastric alka-linisation (gastric pH > 3.5), with the rationale thatgastric acidity is the main cause of stress ulceration. 16 The incidence of stress ulceration appears to be lower

with prophylactic gastric alkalinisation than with pla-cebos, although an improvement in survival has notbeen shown.17,18 Concerns have included gastric bacte-rial overgrowth and associated nosocomial pneumonia,but these have not been substantiated by existing data.On balance, prophylactic treatment should probably bereserved only for at-risk patients. The mainstay ofprophylaxis and treatment for minor bleeding remainssupportive – optimise oxygenation and tissue perfusionand control of infection. There is little consensus amongcritical care experts in the choice of prophylactic treat-ment used.19,20 Drugs given include the following:

AntacidsAntacids given hourly via a nasogastric tube can main-tain gastric alkalinisation. Gastric pH monitoring is nec-essary. Antacids contain magnesium, aluminium, calciumor sodium, and complications may arise from excessiveintake of these minerals. Bowel stasis and diarrhoea canalso be problems. They are used less commonly now.

Sucralfate This is a basic aluminium salt of sucrose octasulphate.It is effective in healing ulcers by increasing mucussecretion, mucosal blood ow and local prostaglandinproduction. These effects promote mucosal resistance

against acid and pepsin (i.e. they are cytoprotective). Asit does not alter gastric pH, Gram-negative bacterialcolonisation of gastric juice is less likely. The incidenceof nosocomial pneumonia may be less with sucralfatethan with antacids or H2-receptor antagonists, but thisis debatable and is offset by the potential risk of aspira-tion.17 Sucralfate is given via a nasogastric tube as 1.0 gevery 4–6 hours. Constipation is a side-effect, and alu-minium toxicity may arise from renal dysfunction.

H 2 -receptor antagonistsThese drugs suppress acid secretion by competing forthe histamine receptor on the parietal cell. Cimetidine

is less potent and has interactions with anticonvulsants,theophyllines and warfarin. Famotidine and nizatidineare newer agents but have no particular advantage overranitidine. The problem of H2-receptor antagonists isthe development of tachyphylaxis after the rst day ofadministration, leading to reduction of effectiveness inacid suppression. At least one meta-analysis suggestedthat ranitidine did not confer any protection againststress ulcer in intensive care patients.21

Proton pump inhibitorsThese are potent acid-suppressing agents as they blockthe nal common pathway of acid secretion by the



Upper gastrointestinal bleeding 491

together in an attempt to improve the outcome. Existingdata so far do not suggest this combined therapy is anybetter, however, hence combined endoscopic therapycannot be recommended.

BALLOON TAMPONADE Variceal bleeding can be controlled by exerting pres-

sure directly on the bleeding point using a balloon. TheSengstaken–Blackmore tube has been replaced by thefour-lumen Minnesota tube, which allows aspiration ofgastric and oesophageal contents. Ination of the gastricballoon (by 250–350 mL of water) is often sufcient tostop the bleeding by occluding the feeding veins to theoesophageal varices. If bleeding continues, the oesopha-geal balloon can be inated by air and kept at a pressureof 50–60 mmHg (6.7–8.0 kPa). Duration of using balloontamponade should be limited to 24 hours to avoidtissue pressure necrosis. Because of available effectivepharmacological and endoscopic therapies, balloontamponade should be used only in the exceptional cases

when these therapies fail to effect control of bleeding.

TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMICSHUNT (TIPS)Using a transjugular approach, a catheter is insertedinto the hepatic vein, and advanced under uoroscopicguidance into a branch of the portal vein.27 By means ofa guidewire and dilators, a self-expandable metal stentis introduced to create an intrahepatic portosystemicshunt. In good hands, success can be achieved in over90% of cases. This procedure signicantly reducesportal blood pressure and thus bleeding from varices.Major complications include intra-abdominal haemor-

rhage and stent occlusion. Hepatic encephalopathy hasbeen reported in 25–60% of patients. Nevertheless,this is an effective salvage treatment for uncontrolledvariceal bleeding. Meta-analysis comparing TIPS withendoscopic therapy showed that the former has securehaemostasis but at the cost of increasing risk of hepaticencephalopathy.28

A number of markers of outcome after TIPS havebeen under investigation, including the Acute Physiol-ogy, Age and Chronic Health Evaluation (APACHE)score, presence of hyponatraemia and Child C liverdisease, hepatic encephalopathy before TIPS, presence

of ascites and serum albumin. Until a reliable markerof outcome can be identied, TIPS should be reservedfor the subset of patients who continue to bleed ordevelop recurrent bleeding after endoscopic therapy.Unlike shunt surgery, TIPS will not reduce the chanceof future liver transplantation.

SURGERY Surgical treatments for variceal bleeding include directdevascularisation of the lower oesophagus plus theproximal stomach and a variety of surgical shunts. Therole of surgery has diminished since the advent ofendoscopic treatment and TIPS.29 Surgery is now used

be used in acute variceal bleeding.23 The benet is morepronounced if these vasoactive agents are given early,even before endoscopy.22,24 Octreotide has also beenshown to be effective when used as an adjuvant therapyin combination with endoscopic therapy.25 Recurrentbleeding episodes and hence requirement of transfu-sion are signicantly reduced. Activated factor VII has

recently been tested for control of variceal bleeding.Despite its initial promise in correcting coagulopathy,this drug has not been found effective in controllingvariceal bleeding.26

ENDOSCOPIC SCLEROTHERAPY Endoscopic injection sclerotherapy is the mainstay oftreatment. At endoscopy, sclerosants can be injecteddirectly into the variceal columns (intravariceal injec-tion) or into the mucosa adjacent to the varices (para-variceal injection) to cause venous thrombosis andinammation, and tissue brosis. Commonly used scle-rosants are ethanolamine oleate, sodium tetradecyl sul-

phate (1–3%), polidocanol and ethyl alcohol. None hasappreciable advantage over the others and the choice isvery much a personal preference of the endoscopist,and depends also on availability. Endoscopic sclero-therapy controls 80–90% of acute variceal bleeding.Complications such as ulcer formation, fever, chest painand mediastinitis are common. Bleeding from gastricvarices is more difcult to control by injection sclero-therapy because of difcult access.

Butylcyanoacrylate (Histoacryl®) has recently beenused for gastric variceal injections, with a claimed supe-rior haemostatic effect. It is mixed with lipiodol to delaythe rate of polymerisation and allow radiological moni-toring of the injection.

ENDOSCOPIC VARICEAL LIGATION Endoscopic variceal ligation was introduced in the late1980s as a mechanical method to control bleeding fromvarices. Rubber bands mounted on the banding deviceat the tip of the endoscope are released to strangulatethe bleeding varices. Numerous studies comparingendoscopic variceal ligation with endoscopic sclero-therapy showed that the technique is as effective asinjection sclerotherapy in acute bleeding. Procedure-related complications are signicantly fewer, as there is

no tissue chemical irritation. An overtube to facilitatebanding avoids aspiration during the procedure, butmay result in serious oesophageal injury if used improp-erly. The tunnel vision produced by the banding deviceas originally designed restricts visibility, and thusmakes the procedure technically difcult when bleed-ing is heavy. With the introduction of multiple bandingdevices that are loaded with 5–10 rubber bands, and theuse of transparent caps, the problems of overtube injuryand tunnel vision have been overcome. In many centres,endoscopic variceal ligation has replaced injection scle-rotherapy as the rst choice for variceal haemorrhage.Many have combined the two endoscopic treatments




occur on the right-sided colon), colonic polyps and car-cinoma, and inammatory bowel diseases.

CLINICAL PRESENTATION

Haematochezia (bright-red blood) is the most commonpresentation of lower GI bleeding. However, bleedingfrom small intestine and right colon may also presentas melaena. Abdominal pain preceding a massivebleeding episode suggests either ischaemia or inam-matory bowel disease. Painless massive bleeding is

common in diverticulosis, angiodysplasia or from aMeckel’s diverticulum. In a patient with portal hyper-tension, haemorrhoids may present with massivehaematochezia.

INVESTIGATIONS

Haemorrhoids and rectal tumour can easily be identi-ed by proctosigmoidoscopy, which should always beperformed. Since upper GI bleeding is about ve timesas common as lower GI bleeding, the former should beexcluded. When both proctosigmoidoscopy and gas-troscopy are negative, the lower GI tract should be

as a second-line treatment, when bleeding continues orrecurs after two sessions of injection sclerotherapy orbanding ligation. Both staple transection of the oeso-phagus and portocaval shunt surgery are highly effec-tive emergency measures. Despite successful controlof bleeding, long-term survival is not signicantlyimproved. Hepatic encephalopathy is one of the majorcomplications of shunting operations. Expectations thatthe Warren distal splenorenal shunt will preserve ante-grade portal ow and avoid accelerated deteriorationof liver function have not been realised. The Warren

shunt is technically more difcult, especially if per-formed as an emergency. Choice of surgery should becarefully made in those who are potential transplantcandidates, as it may complicate subsequent surgery. Aprotocol to manage variceal bleeding is shown inFigure 42.2.

LOWER GASTROINTESTINAL BLEEDING

Lower GI bleeding arises from a source distal to theligament of Treitz. It accounts for 10–20% of acute GIbleeding. Common causes of colonic bleeding includediverticular haemorrhage and angiodysplasia (both

Figure 42.2 Management of varicealhaemorrhage. TIPS= transjugular intrahepaticportosystemic shunt.

Suspected variceal bleeding

Resuscitation and i.v. vasoactive agent

Haemodynamically stable?

Bleeding stopped?

Endoscopy obliteration

programme

Repeat endoscopy

within 24 h plus

vasoactive agents

Maintenance

β-blocker therapy Bleeding stopped

TIPS TIPS not available/

feasible

Surgical shunt

Next available

elected endoscopy

Emergency

endoscopy

Yes

Yes

No

No

Yes No



Lower gastrointestinal bleeding 493

has been reported to detect the source of active bleedingin over 80% of cases.

Diagnostic angiography is helpful in two situations:(1) when the view of endoscopy is completely obscuredby active haemorrhage; (2) in dening abnormal vascu-latures, where angiography is more sensitive even ifextravasation of contrast material is not seen. These

lesions include angiodysplasia, arteriovenous malforma-tion and various inherited vascular anomalies (e.g.Rendu–Osler–Weber syndrome, pseudoxanthoma elas-ticum and Ehlers–Danlos syndrome). Angiography maylocalise the site of bleeding in 80–85% of patients whenthe bleeding rate is more than 0.5 mL/min. Both supe-rior and inferior mesenteric angiograms are often needed.

MANAGEMENT

ENDOSCOPY Bleeding from vascular anomalies can be treated byelectrocoagulation, heater probe and laser photocoagu-

lation, unless the anomalies are too large or too diffuse.Bleeding colonic polyps can be removed by polypec-tomy or coagulated by hot biopsy forceps. Bleeding

examined by colonoscopy, angiography or radionucle-otide scan. Barium enema plays no role in the manage-ment of acute rectal bleeding.

COLONOSCOPY Patients with mild-to-moderate haematochezia can beexamined safely by colonoscopy. Colonoscopy is dif-

cult in an actively bleeding patient, and may carry anincreased risk of perforation. Visualisation is oftenunsatisfactory due to the dark discoloration of blood.Colonoscopy yields much better results with adequatebowel preparation once bleeding has stopped. Thereforeas a technique urgent/emergency colonoscopy does notseem to be necessary as it will not improve the outcomeof patients with lower gastrointestinal bleeding.30

ANGIOGRAPHY OR RADIONUCLIDE SCAN The diagnostic efcacy of radionuclide scan and angi-ography varies in different studies. 99mTc sulphurcolloid is quickly removed from the bloodstream after

injection. Its diagnostic yield is low because of its shortcirculatory half-life. 99mTc labelling of red cells prolongsthe duration of radioactivity in the body. Red cell scan

Figure 42.3 Management of lowergastrointestinal (GI) bleeding.

Suspected lower GI bleeding

Upper endoscopy to rule

out upper GI bleeding

Colonoscopy

Rapid bleeding (>0.5 ml/min) Slow bleeding (<0.5 ml/min)

–ve

Angiography 99mTc-rbc scanTreat

accordinglyTreat

accordingly

+ve

Massive bleeding

Laparotomy +

intraoperative99mTc-rbc scan

Small-bowel

enema

Observe and arrange

angiography if rebleed

Angiography

Mild bleedingSmall-bowel enema

Treat

accordingly

Treat

accordingly

Treat

accordingly

–ve –ve

–ve

–ve

+ve –ve




SURGERY Diverticular bleeding usually arises from a relativelylarge vessel, and may be difcult to control with endo-scopic or angiographic therapy. Partial resection of thecolon is warranted after localisation of the bleeding site.Surgery is also indicated in vascular anomalies whenendoscopic treatment fails. When an obvious and

refractory massive lower GI bleeding is not identiedby endoscopic or angiographic examinations, immedi-ate laparotomy with possible subtotal colectomy shouldbe offered. A protocol to manage lower GI bleeding isshown in Figure 42.3.

from colonic diverticula can also be controlled withthermocoagulation through colonoscopy.31

ANGIOGRAPHY Angiographic intra-arterial infusion of vasopressin orocclusion of the bleeding artery with embolic agentssuch as an absorbable gelatin sponge (Gelfoam®) may

be used in lower GI bleeding pathologies. Both diver-ticular bleeding and bleeding from angiodysplasia canbe stopped by vasopressin infusion during angiogra-phy, but recurrence of bleeding frequently occurs withdiverticular disease.

http://www.expertconsult.comAccess the complete references list online at

4. Sung JJY, Tsoi KKF, Ma T, et al. Causes of mortality in patients with peptic ulcer bleeding: a prospective cohort study of 10,428 cases. Am J Gastroenterol2010;105:84–9.

5. Tsoi KKF, Ma T, Sung JJY. Endoscopy for upper gas-trointestinal bleeding: how urgent is it? Nat Rev Gas-troenterol Hepatol 2009;6:463–9.

7. Lau JYW, Sung JJY, Lee KK, et al. Effect of intrave-nous omeprazole on recurrent bleeding after endo-scopic treatment of bleeding peptic ulcers [see comment]. N Engl J Med 2000;343:310–16.

16. Cook DJ, Fuller HD, Guyatt GH, et al. Risk factors for gastrointestinal bleeding in critically ill patients. Canadian Critical Care Trials Group. N Engl J Med1994;330:377–81.

22. Levacher S, Letoumelin P, Pateron D, et al. Early administration of terlipressin plus glyceryl trinitrate

to control active upper gastrointestinal bleeding in cirrhotic patients. Lancet 1995;346:865–8.

26. Bosch J, Thabut D, Albillos A, et al. Recombinant factor VIIa for variceal bleeding in patients with

advanced cirrhosis: a randomized controlled trial. Hepatology 2008;47:1604–14.28. Papatheodoridis GV, Goulis J, Leandro G, et al.

Transjugular intrahepatic portosystemic shunt com-pared with endoscopic treatment for prevention of variceal rebleeding: a meta-analysis. Hepatology1999;30:612–22.

30. Laine L, Shah A. Randomized trial of urgent vs elec-tive colonoscopy in patients hospitalized with lower GI bleeding. Am J Gastroenterol 2010;105:2636–41.

http://www.expertconsult.com/

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Acute Gastrointestinal Bleeding