Peptic ulcer

1. Peptic Ulcer Peptic Ulcer
DiseaseDisease

2. DefinitionDefinition

An An ulcerulcer is defined as disruption of the mucosal is defined as disruption of the mucosal
integrity of the stomach and/or duodenum integrity of the stomach and/or duodenum
leading to a local defect or excavation due to leading to a local defect or excavation due to
imbalance between mucosal defensive imbalance between mucosal defensive
mechanism and aggressive luminal factors (acid, mechanism and aggressive luminal factors (acid,
pepsin); ulcers penetrate the muscularis pepsin); ulcers penetrate the muscularis
mucosae.mucosae.

Ulcers occur within the stomach and/or Ulcers 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 gastroenteric in the small bowel adjacent to gastroenteric
anastomoses, and within a Meckel's anastomoses, and within a Meckel's
diverticulum. diverticulum.

3. EpidemiologyEpidemiology

Although the prevalence of peptic ulcer is Although the prevalence of peptic ulcer is
decreasing in many Western communities, it still decreasing in many Western communities, it still
affects approximately 10% of all adults at some affects approximately 10% of all adults at some
time in their lives. time in their lives.

The male to female ratio for duodenal ulcer The male to female ratio for duodenal ulcer
varies from 5:1 to 2:1, whilst that for gastric ulcer varies from 5:1 to 2:1, whilst that for gastric ulcer
is 2:1 or less. is 2:1 or less.

The incidence of The incidence of duodenal ulcerduodenal ulcers declineds declined and and
physician visits have decreased by >50% over physician visits have decreased by >50% over
the past 30 years. The reason for the reduction the past 30 years. The reason for the reduction
in the frequency of DUs is likely related to the in the frequency of DUs is likely related to the
decreasing frequency of decreasing frequency of Helicobacter pyloriHelicobacter pylori. .

4. AetiologyAetiology
1. Helicobacter pylori1. Helicobacter pylori

The vast majority of colonised people The vast majority of colonised people
remain healthy and asymptomatic and remain healthy and asymptomatic and
only a minority develop clinical disease. only a minority develop clinical disease.

Around 90% of duodenal ulcer patients Around 90% of duodenal ulcer patients
and 70% of gastric ulcer patients are and 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 mucosal NSAIDs and aspirin can result in mucosal
damage anywhere in the GI tract and are damage anywhere in the GI tract and are
responsible for most peptic ulcers not due responsible 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 or concomitant corticosteroid or
anticoagulant therapy, high-dose or anticoagulant therapy, high-dose or
multiple NSAID therapy, and presence of multiple NSAID therapy, and presence of
serious comorbid medical illnesses all serious comorbid medical illnesses all
increase risk for PUD.increase risk for PUD.

7. 3. 3. A gastrin-secreting tumor or A gastrin-secreting tumor or
gastrinomagastrinoma can result in uncontrolled can result in uncontrolled
acid secretion, and accounts for <1% of all acid secretion, and accounts for <1% of all
peptic ulcers.peptic ulcers.
4.4. When none of the above etiologies is When none of the above etiologies is
evident, the ulcer is designated evident, the ulcer is designated
idiopathicidiopathic..
5. 5. Cigarette smokingCigarette smoking doubles the risk doubles the risk
for peptic ulcers.for peptic ulcers.

8. PathophysiologyPathophysiology

In most people H. pylori causes antral gastritis In most people H. pylori causes antral gastritis
associated with depletion of somatostatin (from D associated with depletion of somatostatin (from D
cells) and gastrin release from G cells. cells) and gastrin release from G cells.

The subsequent hypergastrinaemia stimulates The subsequent hypergastrinaemia stimulates
acid production by parietal cells, but in the acid production by parietal cells, but in the
majority of cases this has no clinical majority of cases this has no clinical
consequences. consequences.

In a minority of patients (perhaps those who In a minority of patients (perhaps those who
inherit a large parietal cell mass) this effect is inherit a large parietal cell mass) this effect is
exaggerated, leading to duodenal ulceration. exaggerated, leading to duodenal ulceration.

9. Sequence of events in the Sequence of events in the
pathophysiology of duodenal ulcerationpathophysiology of duodenal ulceration..

10. 
The role of H. pylori in the pathogenesis of The role of H. pylori in the pathogenesis of
gastric ulcer is less clear but H. pylori probably gastric ulcer is less clear but H. pylori probably
acts by reducing gastric mucosal resistance to acts by reducing gastric mucosal resistance to
attack from acid and pepsin. attack from acid and pepsin.

In approximately 1% of infected people, H. pylori In approximately 1% of infected people, H. pylori
causes a pangastritis leading to gastric atrophy causes a pangastritis leading to gastric atrophy
and hypochlorhydria. and hypochlorhydria.

This allows bacteria to proliferate within the This allows bacteria to proliferate within the
stomach; these may produce mutagenic nitrites stomach; these may produce mutagenic nitrites
from dietary nitrates, predisposing to the from dietary nitrates, predisposing to the
development of gastric cancer. development of gastric cancer.

The reasons for different outcomes are unclear The reasons for different outcomes are unclear
but bacterial strain differences and host genetic but bacterial strain differences and host genetic
factors are both likely. factors are both likely.

11. Consequences of H. pylori Consequences of H. pylori
infection.infection.

12. Mechanisms by which NSAIDs Mechanisms by which NSAIDs
may induce mucosal injurymay induce mucosal injury

13. Clinical featuresClinical features

Peptic ulcer disease is a chronic condition with a Peptic ulcer disease is a chronic condition with a
natural history of spontaneous relapse and natural history of spontaneous relapse and
remission lasting for decades, if not for life remission lasting for decades, if not for life
((periodicityperiodicity). ).

Although they are different diseases, duodenal Although they are different diseases, duodenal
and gastric ulcers share common symptoms and gastric ulcers share common symptoms
which will be considered together. which will be considered together.

The most common presentation is that of The most common presentation is that of
recurrent abdominal painrecurrent abdominal pain which has three which has three
notable characteristics: localisation to the notable characteristics: localisation to the
epigastrium, relationship to food and episodic epigastrium, relationship to food and episodic
occurrence (occurrence (rhythmicityrhythmicity). ).

14. 
Occasional Occasional vomitingvomiting occurs in about occurs in about
40% of ulcer subjects; persistent vomiting 40% of ulcer subjects; persistent vomiting
occurring daily suggests gastric outlet occurring daily suggests gastric outlet
obstruction. obstruction.

In one-third of patients the history is less In one-third of patients the history is less
characteristic. characteristic.

This is especially true in elderly subjects This is especially true in elderly subjects
under treatment with NSAIDs. under treatment with NSAIDs.

In these patients pain may be absent or so In these patients pain may be absent or so
slight that it is experienced only as a slight that it is experienced only as a
vague sense of epigastric unease. vague sense of epigastric unease.

15. 
Occasionally, the only symptoms are Occasionally, the only symptoms are anorexiaanorexia
and and nauseanausea, or a sense , or a sense of undue repletion of undue repletion
after mealsafter meals. .

In some patients the ulcer is completely In some patients the ulcer is completely 'silent'silent', ',
presenting for the first time with presenting for the first time with anaemiaanaemia from from
chronic undetected blood loss, as an abrupt chronic undetected blood loss, as an abrupt
haematemesishaematemesis or as or as acute perforationacute perforation; in ; in
others there is others 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 of It should be noted that the diagnostic value of
individual symptoms for peptic ulcer disease is individual symptoms for peptic ulcer disease is
poor, and the history is often a poor predictor of poor, 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 diagnosis is the gold standard for diagnosis
of peptic ulcers.of peptic ulcers.

Barium studiesBarium studies also have good sensitivity for also have good sensitivity for
diagnosis of ulcers, but smaller ulcers and diagnosis of ulcers, but smaller ulcers and
erosions may be missed; further, biopsies erosions may be missed; further, biopsies
cannot be taken.cannot be taken.

Rapid urease assayRapid urease assay (Campylobacter-like (Campylobacter-like
organism [CLO] test) and organism [CLO] test) and histopathologichistopathologic
examination of endoscopic biopsy specimens examination of endoscopic biopsy specimens
are commonly used for diagnosis in patients are commonly used for diagnosis in patients
undergoing endoscopy; these tests may be undergoing 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 be Very occasionally, a gastric ulcer may be
malignant (3 % of cases); therefore malignant (3 % of cases); therefore
endoscopy and biopsy are mandatory endoscopy and biopsy are mandatory
when a gastric ulcer is detected on barium when a gastric ulcer is detected on barium
examination.examination.

Moreover, in gastric ulcer disease Moreover, in gastric ulcer disease
endoscopy must be repeated after suitable endoscopy must be repeated after suitable
treatment to confirm that the ulcer has treatment to confirm that the ulcer has
healed and to obtain further biopsies if it healed and to obtain further biopsies if it
has not. has not.

In contrast, it is not necessary to repeat In 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 the is the
cheapest noninvasive test for diagnosing H. cheapest noninvasive test for diagnosing H.
pylori infection; the antibody remains detectable pylori infection; the antibody remains detectable
as long as 18 months after successful as long as 18 months after successful
eradication, and therefore this test cannot be eradication, and therefore this test cannot be
used to document successful eradication of the used to document successful eradication of the
organism.organism.

Stool H. pylori antigen testingStool H. pylori antigen testing also has also has
high sensitivity and specificity for the diagnosis high sensitivity and specificity for the diagnosis
of H. pylori infection. of H. pylori infection.

Carbon-labeled urea breath testingCarbon-labeled urea breath testing is the is the
most accurate noninvasive test for diagnosis. most accurate noninvasive test for diagnosis.
This test is often used to document successful This test is often used to document successful
eradication after therapy in patients with ongoing eradication after therapy in patients with ongoing
dyspeptic symptoms or complicated ulcer dyspeptic symptoms or complicated ulcer
disease.disease.

19. Duodenal ulcersDuodenal ulcers: : Ulcer with a Ulcer with a
clean base clean base

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

21. Gastric ulcersGastric ulcers: : Benign gastric ulcer.Benign gastric ulcer.

22. Malignant gastric ulcer involving Malignant 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 with Gastric 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).).

28. Barium study demonstrating:Barium study demonstrating:
a benign duodenal ulcer; a benign duodenal ulcer;

29. Barium study demonstrating:Barium study demonstrating:
a benign gastric ulcera benign gastric ulcer

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, and induce 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 of H. pylori eradication is the cornerstone of
therapy for peptic ulcers, as this will therapy for peptic ulcers, as this will
successfully prevent relapse and eliminate successfully prevent relapse and eliminate
the need for long-term therapy in the the 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 disease All 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 as positive should be offered eradication therapy as
primary therapy. primary therapy.

Treatment is based upon a proton pump inhibitor Treatment is based upon a proton pump inhibitor
taken simultaneously with two antibiotics (from taken simultaneously with two antibiotics (from
amoxicillin, clarithromycin and metronidazole) for amoxicillin, clarithromycin and metronidazole) for
7 days. 7 days.

Compliance, side-effects and metronidazole Compliance, side-effects and metronidazole
resistance influence the success of therapy.resistance influence the success of therapy.

For those who are still colonised after two For those who are still colonised after two
treatments, the choice lies between a third treatments, the choice lies between a third
attempt with quadruple therapy (bismuth, proton attempt with quadruple therapy (bismuth, proton
pump inhibitor and two antibiotics) or long-term pump inhibitor and two antibiotics) or long-term
maintenance therapy with acid suppression. maintenance therapy with acid suppression.

32. Common side-effects of H. pylori Common side-effects of H. pylori
eradication therapyeradication therapy

33. Indications for H. pylori eradication Indications for H. pylori eradication

34. Short-term managementShort-term management

35. Antacids.Antacids.

These are widely available for self-medication These are widely available for self-medication
and are used for relief of minor dyspeptic and are used for relief of minor dyspeptic
symptoms. symptoms.

The majority are based on combinations of The majority are based on combinations of
calcium, aluminium and magnesium salts, all of calcium, aluminium and magnesium salts, all of
which have individual side-effects. which have individual side-effects.

Calcium compounds cause constipation, while Calcium compounds cause constipation, while
magnesium-containing agents cause diarrhoea. magnesium-containing agents cause diarrhoea.

Aluminium compounds block absorption of Aluminium compounds block absorption of
digoxin, tetracycline and dietary phosphates. digoxin, tetracycline and dietary phosphates.

Most have a high sodium content and can Most have a high sodium content and can
exacerbate congestive heart failure. exacerbate congestive heart failure.

36. Histamine H2-receptor Histamine H2-receptor
antagonist drugs.antagonist drugs.

These are competitive inhibitors of histamine at These are competitive inhibitors of histamine at
the H2-receptor on the parietal cell. the H2-receptor on the parietal cell.

Dyspeptic symptoms remit promptly, usually Dyspeptic symptoms remit promptly, usually
within days of starting treatment, and 80% of within 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 the These drugs do not inhibit acid secretion to the
same degree as the proton pump inhibitors but same degree as the proton pump inhibitors but
are useful for the short-term management of are 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 that These are substituted benzimidazole compounds that
specifically and irreversibly inhibit the proton pump specifically and irreversibly inhibit the proton pump
hydrogen/potassium ATPase in the parietal cell hydrogen/potassium ATPase in the parietal cell
membrane. membrane.

They are the most powerful inhibitors of gastric secretion They are the most powerful inhibitors of gastric secretion
yet discovered, with maximal inhibition occurring 3-6 yet 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 is After a few days of treatment virtual achlorhydria is
achieved and rapid healing of both gastric and duodenal achieved and rapid healing of both gastric and duodenal
ulcers follows. ulcers follows.

Omeprazole and lansoprazole are important components Omeprazole 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 an Colloidal bismuth subcitrate (CBS) is an
ammoniacal suspension of a complex ammoniacal suspension of a complex
colloidal bismuth salt. colloidal bismuth salt.

It has little, if any, effect on gastric acid It has little, if any, effect on gastric acid
secretion and its ulcer-healing effect is secretion and its ulcer-healing effect is
probably due to a combination of activity probably due to a combination of activity
against H. pylori and enhancement of against H. pylori and enhancement of
mucosal defence mechanisms. mucosal defence mechanisms.

39. Sucralfate.Sucralfate.

This is a basic aluminium salt of sucrose This is a basic aluminium salt of sucrose
octasulphate. octasulphate.

It has little effect on acid secretion but probably It has little effect on acid secretion but probably
acts to protect the ulcer base from peptic activity acts 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 the It binds to fibroblast growth factor and to the
ulcer base, reducing the access of pepsin and ulcer 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 prostaglandin Synthetic prostaglandin
analogues (misoprostol).analogues (misoprostol).

Prostaglandins exert complex effects on the Prostaglandins exert complex effects on the
gastroduodenal mucosa. gastroduodenal mucosa.

In low doses they protect against injury induced In low doses they protect against injury induced
by aspirin and NSAIDs by enhancing mucosal by aspirin and NSAIDs by enhancing mucosal
blood flow, and by stimulating mucus and blood flow, and by stimulating mucus and
bicarbonate secretion and epithelial cell bicarbonate 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 and Misoprostol is effective for the prevention and
treatment of NSAID-induced ulcers, but in treatment of NSAID-induced ulcers, but in
clinical practice proton pump inhibitors are clinical practice proton pump inhibitors are
preferred, since they are at least as effective and preferred, since they are at least as effective and
have fewer side-effects. have fewer side-effects.

41. Indications for surgery in peptic ulcerIndications for surgery in peptic ulcer

42. Complications of peptic Complications of peptic
ulcer diseaseulcer disease

Perforation;Perforation;

Penetration;Penetration;

Gastric outlet obstruction;Gastric outlet obstruction;

Bleeding;Bleeding;

Malignization.Malignization.

43. Gastric outlet obstructionGastric outlet obstruction

Gastric outlet obstruction is more likely to occur Gastric 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 hours Nausea and vomiting, sometimes several hours
after meals, may occur. after meals, may occur.

Plain abdominal radiographs often show a Plain abdominal radiographs often show a
dilated stomach with an airdilated stomach with an air--fluid level. fluid level.

NNasogastricasogastric suction should be maintained for 2 suction should be maintained for 2--
3 days to decompress the stomach while 3 days to decompress the stomach while
repleting fluids and electrolytes intravenously.repleting fluids and electrolytes intravenously.

Although medical management may be Although medical management may be
temporarily effective, recurrence is common, and temporarily effective, recurrence is common, and
endoscopic balloon dilation or surgery is often endoscopic balloon dilation or surgery is often
necessary for definitive correction.necessary for definitive correction.

44. PerforationPerforation

When free perforation occurs, the contents When free perforation occurs, the contents
of the stomach escape into the peritoneal of the stomach escape into the peritoneal
cavity, leading to peritonitis. cavity, leading to peritonitis.

Perforation occurs more commonly in Perforation occurs more commonly in
duodenal than in gastric ulcers, and duodenal 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 occur About one-quarter of all perforations occur
in acute ulcers and NSAIDs are often in acute ulcers and NSAIDs are often
incriminated. incriminated.

45. Clinical features.Clinical features.

Perforation is often the first sign of ulcer, and a Perforation 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, severe The most striking symptom is sudden, severe
pain; its distribution follows the spread of the pain; its distribution follows the spread of the
gastric contents over the peritoneum. gastric contents over the peritoneum.

Pain initially develops in the upper abdomen and Pain initially develops in the upper abdomen and
rapidly becomes generalised; shoulder tip pain is rapidly becomes generalised; shoulder tip pain is
due to irritation of the diaphragm. due to irritation of the diaphragm.

The pain is accompanied by shallow respiration The 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 is The abdomen is held immobile and there is
generalised 'board-like' rigidity. generalised 'board-like' rigidity.

Intestinal sounds are absent and liver dullness to Intestinal sounds are absent and liver dullness to
percussion decreases due to the presence of percussion 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 as Later the patient's condition deteriorates as
general peritonitis develops. general peritonitis develops.

In at least 50% of cases an erect chest In at least 50% of cases an erect chest
radiograph shows free air beneath the radiograph shows free air beneath the
diaphragm. If not, a water-soluble contrast diaphragm. If not, a water-soluble contrast
swallow will confirm leakage of gastroduodenal swallow will confirm leakage of gastroduodenal
contents. contents.

47. Management and prognosisManagement and prognosis

After resuscitation, the acute perforation is After resuscitation, the acute perforation is
treated surgically, either by simple closure, or by treated surgically, either by simple closure, or by
converting the perforation into a pyloroplasty if it converting the perforation into a pyloroplasty if it
is large. is large.

On rare occasions a partial gastrectomy is On 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 and This high figure reflects the high age and
comorbidity of this population. comorbidity of this population.

48. PenetrationPenetration

Pancreatitis can result from penetration Pancreatitis can result from penetration
into the pancreas, most commonly seen into the pancreas, most commonly seen
with ulcers in the posterior wall of the with 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 longer radiates 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 be Computed 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 grounds and aspiration of blood or coffee grounds
from a nasogastric (NG) tube suggest an from 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 GI characteristic 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, or weakness, abdominal pain, pallor, or
dyspnea.dyspnea.

50. Laboratory StudiesLaboratory Studies

Complete blood countComplete blood count

Coagulation parameters (prothrombin Coagulation parameters (prothrombin
time, partial thromboplastin time, platelet time, partial thromboplastin time, platelet
count)count)

Blood group, cross matching of 2Blood group, cross matching of 2--4 units 4 units
of bloodof blood

Comprehensive chemical profile (including Comprehensive chemical profile (including
liver function tests, serum creatinine)liver function tests, serum creatinine)

51. Management Management

Restoration of intravascular volumeRestoration of intravascular volume
((Isotonic saline, lactated Ringer solution Isotonic saline, lactated Ringer solution
can be initiatedcan be initiated).).

Packed red blood cell (RBC) transfusion Packed red blood cell (RBC) transfusion
should be used for volume replacement should be used for volume replacement
whenever possiblewhenever possible..

Correction of coagulopathyCorrection of coagulopathy..

Airway protectionAirway protection..

52. 
Esophagogastroduodenoscopy (EGD) is Esophagogastroduodenoscopy (EGD) is
the preferred method of investigation and the preferred method of investigation and
therapy of upper GI bleeding and is therapy 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 transfusion Volume resuscitation or blood transfusion
should precede endoscopy in should precede endoscopy in
hemodynamically unstable patients. hemodynamically unstable patients.

Patients with ongoing bleeding benefit Patients with ongoing bleeding benefit
most from urgent EGD, while stable most from urgent EGD, while stable
patients with minimal bleeding (e.g. coffee patients with minimal bleeding (e.g. coffee
groundground emesis with stable hematocrit) can emesis with stable hematocrit) can
have the procedure performed electively have the procedure performed electively
during the hospitalization.during the hospitalization.

53. Medications Medications

Intravenous proton pump inhibitors (PPIs) Intravenous proton pump inhibitors (PPIs)
or high-dose PPIs administered orally or 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 the the rate of recurrent bleeding and the
need for surgery in patients with upper GI need for surgery in patients with upper GI
bleeding awaiting endoscopic treatment or bleeding awaiting endoscopic treatment or
if endoscopy is contraindicated or if endoscopy is contraindicated or
postponed; postponed;

54. Endoscopic Therapy Endoscopic Therapy

Therapeutic endoscopy offers the advantage of Therapeutic endoscopy offers the advantage of
immediate treatment and should be immediate treatment and should be
implemented in all patients early in the hospital implemented in all patients early in the hospital
course (within 24 hours). course (within 24 hours).

Fluid resuscitation and hemodynamic stability Fluid resuscitation and hemodynamic stability
are essential before endoscopy. are essential before endoscopy.

Administration of promotility agents such as Administration of promotility agents such as
metoclopramide or erythromycin may accelerate metoclopramide or erythromycin may accelerate
gastric emptying, and thereby help clear the gastric emptying, and thereby help clear the
stomach of blood or clots prior to endoscopy in stomach of blood or clots prior to endoscopy in
patients with significant or ongoing bleeding. patients with significant or ongoing bleeding.