Upper Gastrointestinal Bleeding: Anthony Alexander University of The West Indies at Mona

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Upper gastrointestinal bleeding (UGIB) is bleeding from a source located in the upper GI tract above the ligament of Treitz. The most common causes are peptic ulcers, gastritis, and esophageal varices. Signs and symptoms include vomiting blood ('coffee grounds' vomit), black tarry stools, and circulatory instability. Treatment involves fluid resuscitation, medications to stop bleeding, and endoscopic procedures to identify and treat the source of bleeding.

The most common causes of upper gastrointestinal bleeding are peptic ulcers (35-50%), gastritis and gastric erosions (10-20%), and esophageal varices (2-9%). Less common causes include Mallory-Weiss tears, vascular malformations, cancers, and aortoenteric fistulas.

Signs and symptoms of upper gastrointestinal bleeding include vomiting blood ('coffee grounds' vomit), black tarry stools, abdominal pain, and signs of circulatory compromise such as tachycardia, hypotension, and decreased level of consciousness.

Upper Gastrointestinal

Bleeding
Anthony Alexander
University of the West Indies at Mona
Overview
Loss of blood from the upper gastrointestinal tract
Clinical spectrum ranging from haematemesis to
circulatory collapse
Occurs at any age
Particularly between the ages of 40-79
Mortality greatest in patients above 60
50-150/100,000 adults/year (US), 50-120/100,000 (UK)
Relevant Anatomy Ligament of
Treitz
•Runs from crus of
diaphragm to DJ
flexure
•Bleeds originating
above this point are
classified as UGIB
Aetiology
Common
Peptic ulcer (35-50%)
Gastritis & gastric erosions (10-20%)
Oesophagitis (10%)
Bleeding varices (2-9%)
Drugs: NSAID, aspirin, steroids, thrombolytics,
anticoagulants
No obvious cause
Aetiology
Less common
Mallory-Weiss tear (5%) & Boorhaave’s
Vascular malformations (5%)
Cancer of oesophagus/duodenum (2%)
Aortoenteric fistula (0.2%)
Pathophysiology
Depends on the aetiology, but…
Most commonly:
Mucosal erosion into blood vessels  haemorrhage
Strong association with:
 H. pylori: inflammatory effect on gastric mucosa
 NSAIDS: ↓COX activity thus impaired mucosal protection

against acid
 Alcohol consumption
Pathophysiology
Oesophageal varices
Portal hypertension leads to dilated submucosal
veins in lower oesophagus
 Blood that would flow through the portal circulation
is redirected to areas of lower venous pressure
 These dilated vessels are susceptible to bleeding
Pathophysiology
Mallory-Weiss tear
Retching against closed LES increased intragastric
pressure
There is now a gradient between intragastric and
intrathoracic pressures
If a shearing force is generated  longitudinal
laceration
Presentation
History
Haematemesis
Red with clots with severe bleeding
‘Coffee grounds’ when less
Melaena/Haematochezia
Dark, tarry foul smelling stool
Estimated blood loss and symptoms of hypovolaemia
Pain
Duration
Vomiting/retching
Past Mx Hx: Previous GI bleed, coagulopathy, known liver disease/varices
Comorbidities: cardiovascular, respiratory, hepatic/renal
Past Sx: AAA
Drugs
Social: alcohol consumption
Examination
General
Mucous membranes
Cool, clammy, pale skin
Decreased conscious level
Respiratory distress
Examination
Signs of circulatory compromise
Altered consciousness hepatic encephalopathy
Reduced urine output
Tachycardia
Hypotension (SBP <100 mmHg)
Postural drop in BP (>20 mmHg, systolic)
Examination
Signs of chronic liver disease
Leukonychia
Clubbing
Palmar
Asterixis
Jaundice
Gynaecomastia
Ascites
Spider Naevii
Distended veins
Signs of hepatic encephalopathy
Examination
Abdomen
Distension
Tender epigastrium, tender/enlarged liver, AA
Abdominal scars: aneurysm repair?
Caput medusae, distended veins
Ascites
Rectal
Melaena
Haemathochezia
Management
Secure airway
Sever haematemesis from bleeding varix/ulcer
↓conscious level due to extensive blood loss loss of
airway protective reflexes
May need to intubate
Management:
Secure breathing
Supplemental oxygen
Management
• Secure circulation
 2 large bore IV cannulae

 CBC
 U+E
 LFT
 Clotting studies
 Group and crossmatch
 Crystalloid bolus: 2L or 20ml/kg
 Blood: type O if necessary

before results of crossmatch


 U cath to monitor U/O
Monitor
Vitals
U/O
CVP indicated in severe bleed
Indications for Transfusion
Low blood pressure
Evidence of volume depletion after crystalloid bolus
Severe distress, cardiac ischaemia, massive blood loss
Platelets <50,000 platelet concentrates
Indications for FFP or Vit. K
GIB + elevated PT:
Liver disease
Warfarin therapy
Vit. K deficiency
Coagulopathy (DIC, haemophilia)
Vit K effects delayed
Investigations
NGT & gastric lavage
CXR
Perforated viscus
Ruptured oesophagus
ECG
Cardiac ischaemia
ABG
NG lavage
NG tube placed in all patients with UGIB
Gentle gastric lavage used to see if bleeding has
stopped. If yes then tube may be removed.
False negatives:
Intermittent bleeding
Bleeding below pylorus which is in spasm. If bile but no
blood, then true negative
False positive
Traumatic placement
Do not place in pt. with gastric bypass or fundoplication
Arrange urgent endoscopy
Both diagnostic and therapeutic
Visualises oesophagus, gastric mucosa and duodenum
If performed within 12-24hrs of bleeding, allows
identification of source of bleeding in 78%-95% of
cases
Allows for localisation of bleed as well as therapeutic
intervention
Treatment at endoscopy
Treatment methods
Sclerotherapy
Injection
Thermal
Clips
Banding (varices)
NOT usually used to stabilise the patient. In fact,
torrential bleeding may impair the endoscopic view
ENDOSCOPY
Contraindications:
Uncooperative or obtunded patient

Severe cardiac decompensation

Acute myocardial infarction (unless active, life-

threatening hemorrhage is present)


Perforated viscus (eg, esophagus, stomach, intestine).
Drugs
Histamine (H2) blockers and proton pump inhibitors
(PPIs)
decrease the acid secretion which contributes to gastric
or duodenal ulcer formation. These medications are
routinely given to patients with UGIB, not to stop the
bleeding, but to initiate ulcer or gastritis treatment. This
may reduce further bleeding in the future. E.g.
omeprazole 40 mg IV post endoscopy
Drugs
Vasopressors
vasoconstrictor which effects the entire circulatory
system, including the splanchnic bed. It is extremely
potent and should be used in an exsanguinating patient,
when endoscopy is unavailable or not possible.
Vasopressin requires cautious use, because end organ
damage may occur.
Terlipressin 2mg then mg/4h IV for <3d in variceal
bleeding
Drugs
Somatostatin and Octreotide
These are vasoactive proteins that cause selective
constriction of the splanchnic vascular bed and decrease
gastric acid secretion. The use of these medications
decreases blood flow to the esophagus, stomach, and
duodenum, usually decreasing blood loss from UGIB
This effect, however is limited
Drugs
Antacids not recommended
Do not decrease bleeding
Coat stomach and reduce visibility at endoscopy
Also consider
Oesophageal tamponade
Where endoscopy unavailable, and medications do not
control bleed
Can be used for 12-24 hours
Tamponade may be accomplished with a specialized
gastric tube that incorporates two expanding balloons.
Complications:
 Oesophageal rupture
 Airway compression
 Aspiration
For surgical consult
Continued bleeding despite medications, endoscopy
and tamponade
≥ 5 units of blood transfused in 6 hrs
Haematemesis & melaena
Rebleeding
Bleeding vessel on endoscopy or clot in base of ulcer
Hx of aortic graft placement
Special considerations: Kids
Common causes
Oesophagitis
Gastritis
Ulcer
Varices
M-W tears
Similar mxn, but bleeding more often benign
Less blood loss haemodynamic instability
Special considerations: Elderly
Beta blockers mask diagnosis of hypovolaemia
More non-specific complaints
Visually impaired, thus may not identify melaena or
blood
Less cardiovascular reserve
Thus need lower threshold for admission
For admission/consultation
In other centres:
Patients who are unstable or have an Hb less than 10 g/dL
GE service
Patients who continue to be unstable despite initial
managemet
Patients with UGIB and a history of AAA repair vascular
surgeons
Patients with comorbidities which cannot be managed on
an outpatient basis
However, at the UHWI
All patients referred to Gen Med & Sx
For ED observation
Patient whose bleeding has stopped, with Hb
>10mg/dl
Serial Hb looking for drop >2mg/dl admit
For discharge
Historically, all patients admitted
However, stable UGIB patients with a normal Hb, few
or no comorbidities, and a small amount of bleeding
that has resolved may be discharged if close follow-
up(1–2 days) is available.
Advised to return immediately if any symptoms return
COMPLICATIONS
Shock
DIC
Azotemia
COMPLICATIONS
 Endoscopy

 Aspiration pneumonia

 Perforation (1% for the first endoscopic therapy, 3% for the second)

 Bleeding can be caused by drilling into the vessel with the laser, by

perforating the vessel with an injection, or by removing the clot with a


failure to coagulate the vessel.
 Surgery

 Ileus

 Sepsis

 Poor wound healing

 Myocardial infarction
Prognosis
10 % die
Summary
UGIB is the most common GI emergency
PUD is the commonest cause
ABC’s, monitoring
PPI’s
Arrange for urgent endoscopy

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