Gastrointestinal, UGI bleeding, Medicine, Surgery

1. Upper Gastrointestinal Bleeding

2. Objective
•Oesophageal varices
•Peptic ulcers disease
•Approach to UGIB

3. Upper gastrointestinal bleeding (UGIB) refers to GI blood loss proximal to the ligament of Treitz
at the duodenojejunal junction.
Acute UGIB can manifest in a variety of ways, with or without haemodynamic compromise,
including haematemesis, coffee-ground emesis, the return of bright red blood through a
nasogastric tube, and melaena.
UGIB results in more than 250,000 hospital admissions annually in the US.
In the UK, UGIB accounts for 70,000 hospital admissions annually.
Ordinarily, mortality is secondary to hypovolemic shock.

4. Aetiology
Patients with UGIB can typically be separated into two groups:
1. With variceal lesions (either oesophageal or gastric).
2. Those with non-variceal lesions (most commonly peptic ulcers).

5. The most frequently encountered aetiologies of UGIB are:
• Peptic ulcer disease (26%)
• Gastritis/erosions (16%)
• Oesophagitis (17%)
• No cause found (12%)
• Erosive duodenitis (9%)
• Varices (8%)
• Portal hypertensive gastropathy (4%)
• Mallory-Weiss tears (3%)
• Malignancy (3%)
• Vascular ectasia (2%).

6. Oesophageal varices

7. Definition
Oesophageal varices are dilated collateral blood vessels that develop as a complication of portal
HTN, usually in the setting of cirrhosis.
They can be seen on endoscopy.
In the US and Europe the major cause is alcoholic liver disease. Worldwide, hepatitis B virus
infection and hepatitis C virus infection are the major causes of cirrhosis.

8. Once cirrhosis has developed, increasing hepatic vein pressure gradient and deteriorating liver
function may result in the formation of oesophageal varices, which may grow up to a critical
point, when they rupture and cause life-threatening bleeding.
The most important predictor of variceal haemorrhage is the size of varices, with the highest risk
of first haemorrhage occurring in patients with large varices (15% per year). Other important
predictors of haemorrhage are decompensated cirrhosis (Child- Pugh B/C) and the endoscopic
finding of red wale marks.

9. diagnostic approach
ASYMPTOMATIC
evaluation for signs and symptoms of liver
disease.
Liver and spleen stiffness, spleen diameter,
and platelet count.
ACTIVE BLEEDING
presents with haematemesis and/or melaena.
other causes should be considered:
peptic ulceration, gastric erosions, and adverse
drug effects.

10. Medical history
• Alcohol abuse.
• Possible viral hepatitis should be made.
• Hiv infection may accelerate liver disease in patients with chronic viral hepatitis.
• Autoimmune liver disease,
• Haemochromatosis,
• Wilson's disease,
• Causes of portal HTN, such as budd-chiari syndrome, myeloproliferative disorders, and
sarcoidosis.

11. Clinical assessment
 signs of chronic liver disease such as ascites, jaundice, and splenomegaly.
 Other signs include spider angioma, bruising, petechiae, caput medusa, and tremor flapping.
 evidence of encephalopathy.
 Active variceal bleeding typically presents with haematemesis and/or melaena.

12. Laboratory investigations
FBC
metabolic panel
LFTs
C-profile
Hepatitis B and C serology
Blood typing and cross-matching.

13. Imaging
OGD
VCE

14. DDX
Condition Differentiating signs /
symptoms
Differentiating tests
Hiatal hernia heartburn and GERD OGD: absence of varices
Gastric varices • evidence of chronic liver
disease but may or may not
have cirrhosis: eg, splenic vein thrombosis
leads to isolated gastric varices.
• Pt who have
oesophageal varices may
also have gastric varices.
OGD: gastric varices but none in
Oesophagus.
Often gastric varices are an extension of
oesophageal varices, but isolated gastric
varices can
also be found.
Mallory-Weiss tear Haematemesis is preceded
by vomiting. Mallory-Weiss
tear is more frequent in
patients with history of
alcohol abuse and therefore
may be associated with
chronic liver disease.
OGD: lacerations of oesophageal
mucosa.
Peptic ulcer disease • Most commonly presents as
heartburn. In active bleeding
from an ulcer it may be
difficult to distinguish from
variceal bleeding.
OGD: PUD with ulcers
in the stomach and/or
duodenum.
Gastric antral vascular
ectasia
• Absence of signs of liver
disease.
OGD: multiple
erythematous mucosal linear
streaks in the antrum.

15. Diagnostic criteria
Child-Pugh classification
North Italian endoscopic club classification

16. Child-Pugh classification of the severity of
cirrhosis
Encephalopathy • None: 1 point
• Grade 1 to 2: 2 points
• Grade 3 to 4: 3 points
Ascites • None: 1 point
• Mild/moderate: 2 points
• Tense: 3 points
Bilirubin (mg/dL) • <2 : 1 point
• 2 to 3 : 2 points
• >3 : 3 points
Albumin (g/dL) • >3.5 : 1 point
• 2.8 to 3.5 : 2 points
• <2.8 : 3 points
INR • <1.7: 1 point
• 1.7 to 2.3: 2 points
• >2.3: 3 points.

17. Treatment:
Risk of death in these patients is 10% to 20%.
Resuscitation
Assessment of the airway
Obtaining peripheral venous access
Blood transfusions
Possibly transfusion of fresh frozen plasma and platelets
Pharmacological therapy: (with terlipressin, somatostatin, or with a somatostatin analogue).

18.  Endoscopy should be performed within 12 hours to make the diagnosis and to treat variceal
hemorrhage, either with EVL or with sclerotherapy.
 Combined vasoactive and endoscopic therapy is currently considered as the first-choice
therapy.
 When reatment fails to control bleeding, trans-jugular intrahepatic porto-systemic shunt (tips)
is indicated.
 Uncontrollable bleeding should be treated by balloon tamponade (for up to 24 hours) as a
bridge to more definitive treatments.

19. Take Home Message…
A direct consequence of portal HTN as a progressive complication of cirrhosis.
The development of bleeding carries significant morbidity and mortality.
Non-selective beta-blockers and/or endoscopic ligation can prevent the development of variceal
bleeding.
Acute haemorrhage can be managed with resuscitation, terlipressin or somatostatin or somatostatin
analogues, and endoscopic ligation.
Additional management may include trans-jugular intrahepatic shunt therapy and prophylactic
antibiotics.
Diagnosis and surveillance by endoscopy is an important aspect of management.

20. THANK YOU

21. PUD
Abdullah Ahmad H. Saihb

22. Definition
■ A break in the mucosal lining of the stomach or duodenum more than 5 mm in
diameter, with depth to the submucosa. Ulcers smaller than this or without obvious
depth are called erosions.

23. Epidemiology
■ Accurate estimates require endoscopic studies because symptoms are insensitive and
non-specific
■ One systematic review of the literature reported an annual incidence of 0.1% .
■ gastric ulcers peak in the fifth to seventh decades
■ Duodenal ulcers tend to occur 2 decades earlier than gastric ulcers, but the incidence
of both increases with aging.
■ Duodenal ulcer more common than gastric ulcer
■ Both sexes are similarly affected.

24. Pathophysiology
■ Peptic ulcers result from an imbalance between factors promoting mucosal damage
(gastric acid, pepsin, Helicobacter pylori infection, non-steroidal anti-inflammatory
drug use) and
■ those mechanisms promoting gastroduodenal defense (prostaglandins, mucus,
bicarbonate, mucosal blood flow).

25. Risk factors
■ Helicobacter pylori infection
about 90% of patients with duodenal ulcers and more than 70% with gastric ulcers have H
pylori infection compared with 30% to 50% in the general population.
Infection increases the lifetime risk of peptic ulcers.
■ non-steroidal anti-inflammatory drug (NSAID) use
The incidence of ulcers in chronic NSAID users is about 20% compared with about 5% in
nonusers and concurrent use of corticosteroids.
■ NSAIDs more commonly cause gastric ulcers than duodenal ulcers and do so by
impairing mucosal defenses,

26. ■ smoking
Smoking is a risk factor for peptic ulcers. One population-based study found that the
prevalence of ulcer disease in current and former smokers (11.4% and 11.5%) is nearly
double that of people who have never smoked (6.0%).
■ increasing age
The incidence of peptic ulcers and associated complications increase with age.
■ personal history of peptic ulcer disease
■ family history of peptic ulcer disease

27. History & examination factors
■ abdominal pain (common)
■ Dyspepsia, a chronic or recurrent abdominal pain or discomfort centred in the upper
abdomen, is a common clinical feature.
■ Commonly related to eating.
■ In patients with duodenal ulcers, pain may be severe and radiate through to back as a
result of penetration of the ulcer posteriorly into the pancreas.
■ 'pointing sign' (uncommon).
■ epigastric tenderness (common)

28. Diagnostic tests
1st test to order

29. OTHERTESTSTO CONSIDER

30. active bleeding ulcer
■ (NSAIDs), including aspirin, should be discontinued. »
■ Blood transfusion (transfusion only for haemoglobin < [7 g/dL]) has been shown to
significantly improve patient outcomes»
■ Endoscopy aids in confirming the diagnosis and identifying the cause of bleeding, as
well as stopping the bleeding. Adrenaline is injected into the bleeding site, together
with cautery and/or clip application. »
■ After intervention, the presence of Helicobacter pylori should be assessed, and the
patient treated according to the guidelines for patients with no active bleeding. plus
proton-pump inhibitor (PPI) Treatment recommended for ALL patients.

31. Treatment

33. therapy for H pylori infection remains
■ an option for first-line therapy in areas of low (< 15%) clarithromycin resistance and
consists of the following:
■ Proton pump inhibitor (PPI) (eg, omeprazole 20 mg BID, lansoprazole 30 mg BID,
esomeprazole 40 mg QD, pantoprazole 40 mg QD, rabeprazole 20 mg BID) plus
Clarithromycin 500 mg BID (first-line and continues to be recommended in areas
where H pylori clarithromycin resistance is less than 15% and in patients without
previous macrolide exposure or metronidazole 500 mg BID (when clarithromycin
resistance is increasing) plus Amoxicillin 1000 mg BID or metronidazole 500 mg BID (if
not already selected)
■ 55 studies concluded that 14 days is the optimal duration of triple therapy

34. Complications
■ Penetration
■ gastric outlet obstruction
■ upper gastrointestinal (GI) bleeding
Peptic ulcer disease is the cause of over 20% of all acute upper GI bleeding.
Bleeding is an infrequent complication of peptic ulcers but the most common cause of
hospitalisation and mortality. It occurs when an ulcer erodes into the wall of a
gastroduodenal blood vessel. Despite the decrease in Helicobacter pylori incidence, peptic
ulcer disease remains a major issue, largely due to the use of non-steroidal anti-
inflammatory drugs (NSAIDs) in older patients. NSAIDs a the major risk factor for peptic
ulcer bleeding and promote bleeding partly through their anti-platelet effects.

35. Quick recap
■ Peptic ulcers usually present as chronic, upper abdominal pain related to eating a meal
(dyspepsia).
■ ◊ Use of (NSAIDs) and Helicobacter pylori infection are the most common causes.
■ ◊There may be some epigastric tenderness only on physical examination.
■ ◊ Endoscopy is diagnostic and may show an ulcer in the stomach or proximal
duodenum. H pylori infection should be sought.
■ ◊ In the absence of 'alarm' (red flag) symptoms or signs, testing for and treating H
pylori and/or
empirical acid inhibition therapy is appropriate.
■ ◊The most common complication is gastroduodenal bleeding. Perforation is a less
frequent but potentially life-threatening complication. Either of these may be the
presenting symptom, particularly in patients taking NSAIDs..

37. APPROACHTO UGIB
Presented by Ahmed Almakrami

38. Step-by-step diagnostic approach
■ History
■ Physical examination
■ Laboratory tests and imaging
■ Endoscopy

39. History
■ Nausea and Hematemesis
■ Melaena
■ Haematochezia
■ Diet
■ Constitutional symptoms
■ Medications
■ History of alcoholism or chronic liver disease
■ Other relevant medical history
■ Social history

40. Nausea and Hematemesis
■ Bleeding with Nausea and Hematemesis is suggestion of moderate to large volume.
■ The absence of nausea and vomiting in the setting of melaena suggests a bleeding
source distal to the pylorus.

41. Melaena
■ Melaena is predominantly associated with UGIB.
■ The duration of melaena can be helpful in determining whether the UGIB is acute or
chronic
■ Medication that affect stool color like Bismuth-containing products, iron supplements
can give false Melaena.
■ A digital rectal examination, including a faecal occult blood test, must be conducted.

42. Haematochezia
■ Haematochezia is more often seen in LGIB than in UGIB
■ However, can be seen in a large UGIB where the rapidity of the transit time precludes
any digestion.
■ Gastric varices and Aortoenteric fistulae are strongly associated with massive bleeding
and rapid haemodynamic compromise.

43. ■ In order of severity of the bleed:
Hematochezia (brisk upper GI bleed) > Hematemesis > Coffee ground emesis > Melena >
Occult blood in stool

44. Diet
■ Red gelatine or red coloured
beverages can interpret red coloured
vomitus as haematemesis.
Constitutional symptoms
■ Upper GI tumours can be associated
with involuntary weight loss or night
sweats.

45. Medications
■ Non-steroidal anti-inflammatory drugs
■ Corticosteroids
■ Antiplatelet
■ Anticoagulant agents.

46. History of alcoholism or chronic liver
disease
■ History of chronic and excessive alcohol use,
■ Intravenous drug use (or other behaviour that places people at risk of contracting
hepatitis),
■ Underlying liver disease
■ Of note, compromised liver function leads to coagulopathy; this can be severe and can
complicate endoscopic therapy.

47. Other relevant medical history
■ Oesophagitis is often seen in the context of long-standing heartburn, complained
from globus sensation, hoarseness, melaena.
■ Any prior history of PUD makes a recurrence more likely.
■ A history of a vascular graft or aortic aneurysm should markedly heighten clinical
suspicion for aortoenteric fistulae.

48. Social history
■ Low socioeconomic status and travelled to underdeveloped countries or endemic with
Helicobacter pylori.
■ Travelled to endemic area with schistosomiasis.

49. Physical examination
■ In general, the physical examination should be directed at answering two primary
questions:
1. What is the degree of anaemia/hypovolaemia?
2. Are there signs of chronic liver disease that might suggest bleeding varices?

50. What is the degree of
anaemia/hypovolaemia
■ Vital signs: tachycardia with hypotension
■ orthostatic blood pressures
■ Capillary refill
■ Mucous membranes moisture
■ Pallor

51. Are there signs of chronic liver disease
that might suggest bleeding varices?
■ Encephalopathy with or without asterixis
■ Scleral icterus
■ spider angioma, on the face, chest, or abdomen
■ Gynaecomastia
■ Hepatomegaly or splenomegaly
■ Ascites
■ Caput medusae
■ Hypogonadism
■ Terry's nails (white nails)
■ Palmar erythema.

52. Physical examination cont.
■ Nose and Oral cavity can sometimes identify a source of bleeding, as epistaxis or
gingival bleeding.
■ Digital rectal examination is mandatory.
■ The degree, location, and character of pain and discomfort can be helpful

53. Laboratory tests and imaging
■ CBC and coagulation profile.
■ Typing and cross-matching
■ Blood transfusion may be initiated when haemoglobin level reaches 7 g/dL, with a
target of approximately 8 g/dL.
■ Gastric lavage by saline infused and aspirated.
■ Abdominal CT scan with oral and intravenous contrast

54. Endoscopy
■ Early endoscopy (within 24 hours of hospital admission) has a greater impact than
later endoscopy on length of hospital stay and requirements for blood transfusion.

56. Differential diagnosis overview
Common
■ Peptic ulcer disease (PUD)
■ Oesophageal varices
■ Oesophagitis
■ Mallory-Weiss tear
Uncommon
■ Boerhaave syndrome (spontaneous
oesophageal perforation)
■ Gastric varices
■ Arteriovenous malformations (AVMs)
■ Dieulafoy's lesions
■ Upper GI tumours
■ Aortoenteric fistulae (AEF)
■ Coagulopathy

57. Oesophagitis
■ Hx of GERD
■ Dysphagia, odynophagia.
■ Globus sensation; hoarseness
■ Melaena
■ Pain induce by swallowing.
■ Esophagogastroduodenoscopy.
Mallory-Weiss tear
■ Classically, patients retching
or vomiting then haematemesis
■ Intra-esophageal pressure (e.g.,
from seizures, hiccups, or straining)
■ Some tears develop spontaneously;
alcohol use, advanced age, and
presence of hiatal hernias are
common underlying features

58. Urgent considerations
■ All patients experiencing an acute UGIB should be admitted to hospital and placed on
observation for adequate monitoring.
■ Specially in first time and/or in moderate and large volume bleeding.

59. Scoring systems
■ Glasgow-Blatchford bleeding score (GBS)
■ Rockall score.
■ In the UK, the National Institute for Health and Care Excellence recommends that all
patients with acute upper gastrointestinal bleeding should be risk-assessed using
the GBS at first assessment and the full Rockall score after endoscopy.

60. Glasgow-Blatchford bleeding score
(GBS)
■ Urea
■ Hb
■ Systolic blood pressure
■ Heart rate
■ Melaena at presentation
■ Syncope at presentation
■ Presence of liver disease
■ Cardiac failure
A score of '0' indicates low risk and potential suitability for outpatient management or deferment of
endoscopic treatment. A score of '6 or more' is associated with >50% risk of needing an intervention.

62. ■ Two large- bore intravenous lines should be placed immediately for adequate venous
access.
■ Crystalloid fluids should be infused to maintain adequate blood pressure.
■ Packed RBCs should be transfused in patients with evidence of ongoing active blood
loss or in patients who have experienced significant blood loss or cardiac ischaemia.
■ Fresh frozen plasma should be used to correct coagulopathy (as is commonly seen in
patients with underlying liver disease).

63. Non-variceal bleeding
■ In extreme cases where adequate perfusion cannot be maintained by other means,
vasopressors can be used.
■ Antisecretory therapy with a proton-pump inhibitor (PPI) oral or IV.
■ Once haemodynamically stabilised, patients can proceed to endoscopy
■ Intravenous infusion of erythromycin before endoscopy should be considered to
improve diagnostic yield and decrease the need for repeat endoscopy.
■ Patients with ongoing, significant haematemesis or those who may not be able to
protect their airway for any reason (active haematemesis, altered mental status,
etc.) and are at risk for aspiration should be considered for endotracheal intubation
before undergoing endoscopy.

64. Variceal UGIB
■ Terlipressin, a vasopressin analogue, given intravenously until bleeding has stopped or
for a maximum of 5, Alternatively, octreotide.
■ Transjugular intrahepatic portosystemic shunting is the treatment of last resort for
patients with variceal UGIB irremediable to endoscopy.
■ A balloon tamponade device can be used to quell the bleeding until the shunt is placed
(Sengstaken-Blakemore for oesophageal varices; Linton- Nachlas for gastric varices).

66. VIGNETTES: MOST
LIKELY DIAGNOSIS

67. ■ A 27-year-old man is brought by his concerned friends in the middle of the night after
his bachelor party because he was seen to be vomiting blood...
■ Dx is Mallory-Weiss tear

68. ■ A 57-year-old woman presents to the ED after having vomited blood this morning, she
has a long-standing hx of GERD which has been refractory to therapy. She is also a 40-
pack-year smoker and an alcoholic..
■ Dx is Esophageal cancer

69. ■ A 63-year-old man is brought by EMS after an episode of vomiting blood. He has had
another episode since arriving at the hospital. He has a history of alcoholism. His BP is
90/55...
■ Dx is Ruptured esophageal varices vs. Mallory-Weiss tear

70. ■ A 59-year-old woman presents to the ED having had an episode of bright red blood in
the stool this morning. She also complains of abdominal pain, primarily lower and left
sided. She has no other contributory history...
■ Dx is Diverticulitis