2. DefinitionDefinition
AnAn ulcerulcer is defined as disruption of the mucosalis defined as disruption of the mucosal
integrity of the stomach and/or duodenumintegrity of the stomach and/or duodenum
leading to a local defect or excavation due toleading to a local defect or excavation due to
imbalance between mucosal defensiveimbalance between mucosal defensive
mechanism and aggressive luminal factors (acid,mechanism and aggressive luminal factors (acid,
pepsin); ulcers penetrate the muscularispepsin); ulcers penetrate the muscularis
mucosae.mucosae.
Ulcers occur within the stomach and/orUlcers occur within the stomach and/or
duodenum and are often chronic in nature.duodenum and are often chronic in nature.
Peptic ulcers can also occur in the esophagus,Peptic ulcers can also occur in the esophagus,
in the small bowel adjacent to gastroentericin the small bowel adjacent to gastroenteric
anastomoses, and within a Meckel'sanastomoses, and within a Meckel's
diverticulum.diverticulum.
3. EpidemiologyEpidemiology
Although the prevalence of peptic ulcer isAlthough the prevalence of peptic ulcer is
decreasing in many Western communities, it stilldecreasing in many Western communities, it still
affects approximately 10% of all adults at someaffects approximately 10% of all adults at some
time in their lives.time in their lives.
The male to female ratio for duodenal ulcerThe male to female ratio for duodenal ulcer
varies from 5:1 to 2:1, whilst that for gastric ulcervaries from 5:1 to 2:1, whilst that for gastric ulcer
is 2:1 or less.is 2:1 or less.
The incidence ofThe incidence of duodenal ulcerduodenal ulcers declineds declined andand
physician visits have decreased by >50% overphysician visits have decreased by >50% over
the past 30 years. The reason for the reductionthe past 30 years. The reason for the reduction
in the frequency of DUs is likely related to thein the frequency of DUs is likely related to the
decreasing frequency ofdecreasing frequency of Helicobacter pyloriHelicobacter pylori..
4. AetiologyAetiology
1. Helicobacter pylori1. Helicobacter pylori
The vast majority of colonised peopleThe vast majority of colonised people
remain healthy and asymptomatic andremain healthy and asymptomatic and
only a minority develop clinical disease.only a minority develop clinical disease.
Around 90% of duodenal ulcer patientsAround 90% of duodenal ulcer patients
and 70% of gastric ulcer patients areand 70% of gastric ulcer patients are
infected with H. pylori.infected with H. pylori.
5. Natural history of H. pylori infectionNatural history of H. pylori infection
6. 2. NSAIDs2. NSAIDs
NSAIDs and aspirin can result in mucosalNSAIDs and aspirin can result in mucosal
damage anywhere in the GI tract and aredamage anywhere in the GI tract and are
responsible for most peptic ulcers not dueresponsible for most peptic ulcers not due
to H. pylori.to H. pylori.
Past history of PUD, age >Past history of PUD, age > 60 years,60 years,
concomitant corticosteroid orconcomitant corticosteroid or
anticoagulant therapy, high-dose oranticoagulant therapy, high-dose or
multiple NSAID therapy, and presence ofmultiple NSAID therapy, and presence of
serious comorbid medical illnesses allserious comorbid medical illnesses all
increase risk for PUD.increase risk for PUD.
7. 3.3. A gastrin-secreting tumor orA gastrin-secreting tumor or
gastrinomagastrinoma can result in uncontrolledcan result in uncontrolled
acid secretion, and accounts for <1% of allacid secretion, and accounts for <1% of all
peptic ulcers.peptic ulcers.
4.4. When none of the above etiologies isWhen none of the above etiologies is
evident, the ulcer is designatedevident, the ulcer is designated
idiopathicidiopathic..
5.5. Cigarette smokingCigarette smoking doubles the riskdoubles the risk
for peptic ulcers.for peptic ulcers.
8. PathophysiologyPathophysiology
In most people H. pylori causes antral gastritisIn most people H. pylori causes antral gastritis
associated with depletion of somatostatin (from Dassociated with depletion of somatostatin (from D
cells) and gastrin release from G cells.cells) and gastrin release from G cells.
The subsequent hypergastrinaemia stimulatesThe subsequent hypergastrinaemia stimulates
acid production by parietal cells, but in theacid production by parietal cells, but in the
majority of cases this has no clinicalmajority of cases this has no clinical
consequences.consequences.
In a minority of patients (perhaps those whoIn a minority of patients (perhaps those who
inherit a large parietal cell mass) this effect isinherit a large parietal cell mass) this effect is
exaggerated, leading to duodenal ulceration.exaggerated, leading to duodenal ulceration.
9. Sequence of events in theSequence of events in the
pathophysiology of duodenal ulcerationpathophysiology of duodenal ulceration..
10. The role of H. pylori in the pathogenesis ofThe role of H. pylori in the pathogenesis of
gastric ulcer is less clear but H. pylori probablygastric ulcer is less clear but H. pylori probably
acts by reducing gastric mucosal resistance toacts by reducing gastric mucosal resistance to
attack from acid and pepsin.attack from acid and pepsin.
In approximately 1% of infected people, H. pyloriIn approximately 1% of infected people, H. pylori
causes a pangastritis leading to gastric atrophycauses a pangastritis leading to gastric atrophy
and hypochlorhydria.and hypochlorhydria.
This allows bacteria to proliferate within theThis allows bacteria to proliferate within the
stomach; these may produce mutagenic nitritesstomach; these may produce mutagenic nitrites
from dietary nitrates, predisposing to thefrom dietary nitrates, predisposing to the
development of gastric cancer.development of gastric cancer.
The reasons for different outcomes are unclearThe reasons for different outcomes are unclear
but bacterial strain differences and host geneticbut bacterial strain differences and host genetic
factors are both likely.factors are both likely.
12. Mechanisms by which NSAIDsMechanisms by which NSAIDs
may induce mucosal injurymay induce mucosal injury
13. Clinical featuresClinical features
Peptic ulcer disease is a chronic condition with aPeptic ulcer disease is a chronic condition with a
natural history of spontaneous relapse andnatural history of spontaneous relapse and
remission lasting for decades, if not for liferemission lasting for decades, if not for life
((periodicityperiodicity).).
Although they are different diseases, duodenalAlthough they are different diseases, duodenal
and gastric ulcers share common symptomsand gastric ulcers share common symptoms
which will be considered together.which will be considered together.
The most common presentation is that ofThe most common presentation is that of
recurrent abdominal painrecurrent abdominal pain which has threewhich has three
notable characteristics: localisation to thenotable characteristics: localisation to the
epigastrium, relationship to food and episodicepigastrium, relationship to food and episodic
occurrence (occurrence (rhythmicityrhythmicity).).
14. OccasionalOccasional vomitingvomiting occurs in aboutoccurs in about
40% of ulcer subjects; persistent vomiting40% of ulcer subjects; persistent vomiting
occurring daily suggests gastric outletoccurring daily suggests gastric outlet
obstruction.obstruction.
In one-third of patients the history is lessIn one-third of patients the history is less
characteristic.characteristic.
This is especially true in elderly subjectsThis is especially true in elderly subjects
under treatment with NSAIDs.under treatment with NSAIDs.
In these patients pain may be absent or soIn these patients pain may be absent or so
slight that it is experienced only as aslight that it is experienced only as a
vague sense of epigastric unease.vague sense of epigastric unease.
15. Occasionally, the only symptoms areOccasionally, the only symptoms are anorexiaanorexia
andand nauseanausea, or a sense, or a sense of undue repletionof undue repletion
after mealsafter meals..
In some patients the ulcer is completelyIn some patients the ulcer is completely 'silent'silent',',
presenting for the first time withpresenting for the first time with anaemiaanaemia fromfrom
chronic undetected blood loss, as an abruptchronic undetected blood loss, as an abrupt
haematemesishaematemesis or asor as acute perforationacute perforation ; in; in
others there isothers there is recurrent acute bleedingrecurrent acute bleeding
without ulcer pain between the attacks.without ulcer pain between the attacks.
It should be noted that the diagnostic value ofIt should be noted that the diagnostic value of
individual symptoms for peptic ulcer disease isindividual symptoms for peptic ulcer disease is
poor, and the history is often a poor predictor ofpoor, and the history is often a poor predictor of
the presence of an ulcer.the presence of an ulcer.
16. InvestigationsInvestigations
EndoscopyEndoscopy is the gold standard for diagnosisis the gold standard for diagnosis
of peptic ulcers.of peptic ulcers.
Barium studiesBarium studies also have good sensitivity foralso have good sensitivity for
diagnosis of ulcers, but smaller ulcers anddiagnosis of ulcers, but smaller ulcers and
erosions may be missed; further, biopsieserosions may be missed; further, biopsies
cannot be taken.cannot be taken.
Rapid urease assayRapid urease assay (Campylobacter-like(Campylobacter-like
organism [CLO] test) andorganism [CLO] test) and histopathologichistopathologic
examination of endoscopic biopsy specimensexamination of endoscopic biopsy specimens
are commonly used for diagnosis in patientsare commonly used for diagnosis in patients
undergoing endoscopy; these tests may beundergoing endoscopy; these tests may be
falsely negative in patients on PPI therapy.falsely negative in patients on PPI therapy.
17. Very occasionally, a gastric ulcer may beVery occasionally, a gastric ulcer may be
malignant (3 % of cases); thereforemalignant (3 % of cases); therefore
endoscopy and biopsy are mandatoryendoscopy and biopsy are mandatory
when a gastric ulcer is detected on bariumwhen a gastric ulcer is detected on barium
examination.examination.
Moreover, in gastric ulcer diseaseMoreover, in gastric ulcer disease
endoscopy must be repeated after suitableendoscopy must be repeated after suitable
treatment to confirm that the ulcer hastreatment to confirm that the ulcer has
healed and to obtain further biopsies if ithealed and to obtain further biopsies if it
has not.has not.
In contrast, it is not necessary to repeatIn contrast, it is not necessary to repeat
endoscopy after treating duodenal ulcers.endoscopy after treating duodenal ulcers.
18. Serum H. pylori antibody testingSerum H. pylori antibody testing is theis the
cheapest noninvasive test for diagnosing H.cheapest noninvasive test for diagnosing H.
pylori infection; the antibody remains detectablepylori infection; the antibody remains detectable
as long as 18 months after successfulas long as 18 months after successful
eradication, and therefore this test cannot beeradication, and therefore this test cannot be
used to document successful eradication of theused to document successful eradication of the
organism.organism.
Stool H. pylori antigen testingStool H. pylori antigen testing also hasalso has
high sensitivity and specificity for the diagnosishigh sensitivity and specificity for the diagnosis
of H. pylori infection.of H. pylori infection.
Carbon-labeled urea breath testingCarbon-labeled urea breath testing is theis the
most accurate noninvasive test for diagnosis.most accurate noninvasive test for diagnosis.
This test is often used to document successfulThis test is often used to document successful
eradication after therapy in patients with ongoingeradication after therapy in patients with ongoing
dyspeptic symptoms or complicated ulcerdyspeptic symptoms or complicated ulcer
disease.disease.
20. Duodenal ulcerDuodenal ulcer:: Ulcer with a visible vessel (Ulcer with a visible vessel (arrowarrow))
in a patient with recent hemorrhagein a patient with recent hemorrhage
22. Malignant gastric ulcer involvingMalignant gastric ulcer involving
greater curvature of stomach.greater curvature of stomach.
23. Stigmata of hemorrhage in peptic ulcersStigmata of hemorrhage in peptic ulcers::
Gastric antral ulcer with a clean base.Gastric antral ulcer with a clean base.
24. Stigmata of hemorrhage in peptic ulcersStigmata of hemorrhage in peptic ulcers::
Duodenal ulcer with flat pigmented spots.Duodenal ulcer with flat pigmented spots.
25. Stigmata of hemorrhage in peptic ulcersStigmata of hemorrhage in peptic ulcers::
Duodenal ulcer with a dense adherent clot.Duodenal ulcer with a dense adherent clot.
26. Stigmata of hemorrhage in peptic ulcersStigmata of hemorrhage in peptic ulcers:: Gastric ulcer withGastric ulcer with
a pigmented protuberance/visible vessel.a pigmented protuberance/visible vessel.
27. Stigmata of hemorrhage in peptic ulcersStigmata of hemorrhage in peptic ulcers::
Duodenal ulcer with active spurting (Duodenal ulcer with active spurting (arrowarrow).).
30. ManagementManagement
The aims of management are:The aims of management are:
to relieve symptoms,to relieve symptoms,
induce ulcer healing in the short term, andinduce ulcer healing in the short term, and
cure the ulcer in the long term.cure the ulcer in the long term.
H. pylori eradication is the cornerstone ofH. pylori eradication is the cornerstone of
therapy for peptic ulcers, as this willtherapy for peptic ulcers, as this will
successfully prevent relapse and eliminatesuccessfully prevent relapse and eliminate
the need for long-term therapy in thethe need for long-term therapy in the
majority of patients.majority of patients.
31. H. pylori eradicationH. pylori eradication
All patients with proven duodenal ulcer diseaseAll patients with proven duodenal ulcer disease
and those with gastric ulcers who are H. pylori-and those with gastric ulcers who are H. pylori-
positive should be offered eradication therapy aspositive should be offered eradication therapy as
primary therapy.primary therapy.
Treatment is based upon a proton pump inhibitorTreatment is based upon a proton pump inhibitor
taken simultaneously with two antibiotics (fromtaken simultaneously with two antibiotics (from
amoxicillin, clarithromycin and metronidazole) foramoxicillin, clarithromycin and metronidazole) for
7 days.7 days.
Compliance, side-effects and metronidazoleCompliance, side-effects and metronidazole
resistance influence the success of therapy.resistance influence the success of therapy.
For those who are still colonised after twoFor those who are still colonised after two
treatments, the choice lies between a thirdtreatments, the choice lies between a third
attempt with quadruple therapy (bismuth, protonattempt with quadruple therapy (bismuth, proton
pump inhibitor and two antibiotics) or long-termpump inhibitor and two antibiotics) or long-term
maintenance therapy with acid suppression.maintenance therapy with acid suppression.
32. Common side-effects of H. pyloriCommon side-effects of H. pylori
eradication therapyeradication therapy
33. Indications for H. pylori eradicationIndications for H. pylori eradication
35. Antacids.Antacids.
These are widely available for self-medicationThese are widely available for self-medication
and are used for relief of minor dyspepticand are used for relief of minor dyspeptic
symptoms.symptoms.
The majority are based on combinations ofThe majority are based on combinations of
calcium, aluminium and magnesium salts, all ofcalcium, aluminium and magnesium salts, all of
which have individual side-effects.which have individual side-effects.
Calcium compounds cause constipation, whileCalcium compounds cause constipation, while
magnesium-containing agents cause diarrhoea.magnesium-containing agents cause diarrhoea.
Aluminium compounds block absorption ofAluminium compounds block absorption of
digoxin, tetracycline and dietary phosphates.digoxin, tetracycline and dietary phosphates.
Most have a high sodium content and canMost have a high sodium content and can
exacerbate congestive heart failure.exacerbate congestive heart failure.
36. Histamine H2-receptorHistamine H2-receptor
antagonist drugs.antagonist drugs.
These are competitive inhibitors of histamine atThese are competitive inhibitors of histamine at
the H2-receptor on the parietal cell.the H2-receptor on the parietal cell.
Dyspeptic symptoms remit promptly, usuallyDyspeptic symptoms remit promptly, usually
within days of starting treatment, and 80% ofwithin days of starting treatment, and 80% of
duodenal ulcers will heal after 4 weeks.duodenal ulcers will heal after 4 weeks.
These drugs do not inhibit acid secretion to theThese drugs do not inhibit acid secretion to the
same degree as the proton pump inhibitors butsame degree as the proton pump inhibitors but
are useful for the short-term management ofare useful for the short-term management of
acid dyspeptic symptoms prior to investigation.acid dyspeptic symptoms prior to investigation.
37. H+/K+ ATPase ('proton pump')H+/K+ ATPase ('proton pump')
inhibitors.inhibitors.
These are substituted benzimidazole compounds thatThese are substituted benzimidazole compounds that
specifically and irreversibly inhibit the proton pumpspecifically and irreversibly inhibit the proton pump
hydrogen/potassium ATPase in the parietal cellhydrogen/potassium ATPase in the parietal cell
membrane.membrane.
They are the most powerful inhibitors of gastric secretionThey are the most powerful inhibitors of gastric secretion
yet discovered, with maximal inhibition occurring 3-6yet discovered, with maximal inhibition occurring 3-6
hours after an oral dose.hours after an oral dose.
They have an excellent safety profile.They have an excellent safety profile.
After a few days of treatment virtual achlorhydria isAfter a few days of treatment virtual achlorhydria is
achieved and rapid healing of both gastric and duodenalachieved and rapid healing of both gastric and duodenal
ulcers follows.ulcers follows.
Omeprazole and lansoprazole are important componentsOmeprazole and lansoprazole are important components
of H. pylori eradication regimens.of H. pylori eradication regimens.
38. Colloidal bismuth compounds.Colloidal bismuth compounds.
Colloidal bismuth subcitrate (CBS) is anColloidal bismuth subcitrate (CBS) is an
ammoniacal suspension of a complexammoniacal suspension of a complex
colloidal bismuth salt.colloidal bismuth salt.
It has little, if any, effect on gastric acidIt has little, if any, effect on gastric acid
secretion and its ulcer-healing effect issecretion and its ulcer-healing effect is
probably due to a combination of activityprobably due to a combination of activity
against H. pylori and enhancement ofagainst H. pylori and enhancement of
mucosal defence mechanisms.mucosal defence mechanisms.
39. Sucralfate.Sucralfate.
This is a basic aluminium salt of sucroseThis is a basic aluminium salt of sucrose
octasulphate.octasulphate.
It has little effect on acid secretion but probablyIt has little effect on acid secretion but probably
acts to protect the ulcer base from peptic activityacts to protect the ulcer base from peptic activity
in a number of ways.in a number of ways.
It binds to fibroblast growth factor and to theIt binds to fibroblast growth factor and to the
ulcer base, reducing the access of pepsin andulcer base, reducing the access of pepsin and
acid.acid.
It may also enhance epithelial cell turnover.It may also enhance epithelial cell turnover.
It should be taken 30-60 minutes before meals.It should be taken 30-60 minutes before meals.
40. Synthetic prostaglandinSynthetic prostaglandin
analogues (misoprostol).analogues (misoprostol).
Prostaglandins exert complex effects on theProstaglandins exert complex effects on the
gastroduodenal mucosa.gastroduodenal mucosa.
In low doses they protect against injury inducedIn low doses they protect against injury induced
by aspirin and NSAIDs by enhancing mucosalby aspirin and NSAIDs by enhancing mucosal
blood flow, and by stimulating mucus andblood flow, and by stimulating mucus and
bicarbonate secretion and epithelial cellbicarbonate secretion and epithelial cell
proliferation.proliferation.
At high doses acid secretion is inhibited.At high doses acid secretion is inhibited.
Misoprostol is effective for the prevention andMisoprostol is effective for the prevention and
treatment of NSAID-induced ulcers, but intreatment of NSAID-induced ulcers, but in
clinical practice proton pump inhibitors areclinical practice proton pump inhibitors are
preferred, since they are at least as effective andpreferred, since they are at least as effective and
have fewer side-effects.have fewer side-effects.
43. Gastric outlet obstructionGastric outlet obstruction
Gastric outlet obstruction is more likely to occurGastric outlet obstruction is more likely to occur
with ulcers that are close to the pyloric channel.with ulcers that are close to the pyloric channel.
Nausea and vomiting, sometimes several hoursNausea and vomiting, sometimes several hours
after meals, may occur.after meals, may occur.
Plain abdominal radiographs often show aPlain abdominal radiographs often show a
dilated stomach with an airdilated stomach with an air--fluid level.fluid level.
NNasogastricasogastric suction should be maintained for 2suction should be maintained for 2--
3 days to decompress the stomach while3 days to decompress the stomach while
repleting fluids and electrolytes intravenously.repleting fluids and electrolytes intravenously.
Although medical management may beAlthough medical management may be
temporarily effective, recurrence is common, andtemporarily effective, recurrence is common, and
endoscopic balloon dilation or surgery is oftenendoscopic balloon dilation or surgery is often
necessary for definitive correction.necessary for definitive correction.
44. PerforationPerforation
When free perforation occurs, the contentsWhen free perforation occurs, the contents
of the stomach escape into the peritonealof the stomach escape into the peritoneal
cavity, leading to peritonitis.cavity, leading to peritonitis.
Perforation occurs more commonly inPerforation occurs more commonly in
duodenal than in gastric ulcers, andduodenal than in gastric ulcers, and
usually in ulcers on the anterior wall.usually in ulcers on the anterior wall.
About one-quarter of all perforations occurAbout one-quarter of all perforations occur
in acute ulcers and NSAIDs are oftenin acute ulcers and NSAIDs are often
incriminated.incriminated.
45. Clinical features.Clinical features.
Perforation is often the first sign of ulcer, and aPerforation is often the first sign of ulcer, and a
history of recurrent epigastric pain is uncommon.history of recurrent epigastric pain is uncommon.
The most striking symptom is sudden, severeThe most striking symptom is sudden, severe
pain; its distribution follows the spread of thepain; its distribution follows the spread of the
gastric contents over the peritoneum.gastric contents over the peritoneum.
Pain initially develops in the upper abdomen andPain initially develops in the upper abdomen and
rapidly becomes generalised; shoulder tip pain israpidly becomes generalised; shoulder tip pain is
due to irritation of the diaphragm.due to irritation of the diaphragm.
The pain is accompanied by shallow respirationThe pain is accompanied by shallow respiration
due to limitation of diaphragmatic movements,due to limitation of diaphragmatic movements,
and by shock.and by shock.
46. The abdomen is held immobile and there isThe abdomen is held immobile and there is
generalised 'board-like' rigidity.generalised 'board-like' rigidity.
Intestinal sounds are absent and liver dullness toIntestinal sounds are absent and liver dullness to
percussion decreases due to the presence ofpercussion decreases due to the presence of
gas under the diaphragm.gas under the diaphragm.
After some hours symptoms may improve,After some hours symptoms may improve,
although abdominal rigidity remains.although abdominal rigidity remains.
Later the patient's condition deteriorates asLater the patient's condition deteriorates as
general peritonitis develops.general peritonitis develops.
In at least 50% of cases an erect chestIn at least 50% of cases an erect chest
radiograph shows free air beneath theradiograph shows free air beneath the
diaphragm. If not, a water-soluble contrastdiaphragm. If not, a water-soluble contrast
swallow will confirm leakage of gastroduodenalswallow will confirm leakage of gastroduodenal
contents.contents.
47. Management and prognosisManagement and prognosis
After resuscitation, the acute perforation isAfter resuscitation, the acute perforation is
treated surgically, either by simple closure, or bytreated surgically, either by simple closure, or by
converting the perforation into a pyloroplasty if itconverting the perforation into a pyloroplasty if it
is large.is large.
On rare occasions a partial gastrectomy isOn rare occasions a partial gastrectomy is
required.required.
Following surgery H. pylori is treated (if present)Following surgery H. pylori is treated (if present)
and NSAIDs are avoided.and NSAIDs are avoided.
Perforation carries a mortality of 25%.Perforation carries a mortality of 25%.
This high figure reflects the high age andThis high figure reflects the high age and
comorbidity of this population.comorbidity of this population.
48. PenetrationPenetration
Pancreatitis can result from penetrationPancreatitis can result from penetration
into the pancreas, most commonly seeninto the pancreas, most commonly seen
with ulcers in the posterior wall of thewith ulcers in the posterior wall of the
duodenal bulb.duodenal bulb.
The pain becomes severe and continuous,The pain becomes severe and continuous,
radiates to the back, and is no longerradiates to the back, and is no longer
relieved by antisecretory therapy.relieved by antisecretory therapy.
Serum amylase may be elevated.Serum amylase may be elevated.
Computed tomography scanning may beComputed tomography scanning may be
diagnostic.diagnostic.
These patients frequently require surgery.These patients frequently require surgery.
49. BleedingBleeding
HematemesisHematemesis, coffee-ground emesis,, coffee-ground emesis,
and aspiration of blood or coffee groundsand aspiration of blood or coffee grounds
from a nasogastric (NG) tube suggest anfrom a nasogastric (NG) tube suggest an
upper GI source of blood loss.upper GI source of blood loss.
MelenaMelena, black sticky stool with a, black sticky stool with a
characteristic odor, indicates an upper GIcharacteristic odor, indicates an upper GI
source of blood losssource of blood loss..
Other symptoms may include fatigue,Other symptoms may include fatigue,
weakness, abdominal pain, pallor, orweakness, abdominal pain, pallor, or
dyspnea.dyspnea.
50. Laboratory StudiesLaboratory Studies
Complete blood countComplete blood count
Coagulation parameters (prothrombinCoagulation parameters (prothrombin
time, partial thromboplastin time, platelettime, partial thromboplastin time, platelet
count)count)
Blood group, cross matching of 2Blood group, cross matching of 2--4 units4 units
of bloodof blood
Comprehensive chemical profile (includingComprehensive chemical profile (including
liver function tests, serum creatinine)liver function tests, serum creatinine)
51. ManagementManagement
Restoration of intravascular volumeRestoration of intravascular volume
((Isotonic saline, lactated Ringer solutionIsotonic saline, lactated Ringer solution
can be initiatedcan be initiated).).
Packed red blood cell (RBC) transfusionPacked red blood cell (RBC) transfusion
should be used for volume replacementshould be used for volume replacement
whenever possiblewhenever possible..
Correction of coagulopathyCorrection of coagulopathy..
Airway protectionAirway protection..
52. Esophagogastroduodenoscopy (EGD) isEsophagogastroduodenoscopy (EGD) is
the preferred method of investigation andthe preferred method of investigation and
therapy of upper GI bleeding and istherapy of upper GI bleeding and is
associated with high diagnostic accuracy,associated with high diagnostic accuracy,
therapeutic capability, and low morbidity.therapeutic capability, and low morbidity.
Volume resuscitation or blood transfusionVolume resuscitation or blood transfusion
should precede endoscopy inshould precede endoscopy in
hemodynamically unstable patients.hemodynamically unstable patients.
Patients with ongoing bleeding benefitPatients with ongoing bleeding benefit
most from urgent EGD, while stablemost from urgent EGD, while stable
patients with minimal bleeding (e.g. coffeepatients with minimal bleeding (e.g. coffee
groundground emesis with stable hematocrit) canemesis with stable hematocrit) can
have the procedure performed electivelyhave the procedure performed electively
during the hospitalization.during the hospitalization.
53. MedicationsMedications
Intravenous proton pump inhibitors (PPIs)Intravenous proton pump inhibitors (PPIs)
or high-dose PPIs administered orallyor high-dose PPIs administered orally
(e.g., omeprazole, 40 mg PO bid) reduce(e.g., omeprazole, 40 mg PO bid) reduce
the rate of recurrent bleeding and thethe rate of recurrent bleeding and the
need for surgery in patients with upper GIneed for surgery in patients with upper GI
bleeding awaiting endoscopic treatment orbleeding awaiting endoscopic treatment or
if endoscopy is contraindicated orif endoscopy is contraindicated or
postponed;postponed;
54. Endoscopic TherapyEndoscopic Therapy
Therapeutic endoscopy offers the advantage ofTherapeutic endoscopy offers the advantage of
immediate treatment and should beimmediate treatment and should be
implemented in all patients early in the hospitalimplemented in all patients early in the hospital
course (within 24 hours).course (within 24 hours).
Fluid resuscitation and hemodynamic stabilityFluid resuscitation and hemodynamic stability
are essential before endoscopy.are essential before endoscopy.
Administration of promotility agents such asAdministration of promotility agents such as
metoclopramide or erythromycin may acceleratemetoclopramide or erythromycin may accelerate
gastric emptying, and thereby help clear thegastric emptying, and thereby help clear the
stomach of blood or clots prior to endoscopy instomach of blood or clots prior to endoscopy in
patients with significant or ongoing bleeding.patients with significant or ongoing bleeding.
