Upper GI Bleed - Symposium

7/28/2019 Upper GI Bleed - Symposium

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UPPERGASTROINTESTINAL

BLEEDING


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ANATOMY OF

UPPER GASTROINTESTINALTRACT


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The gastrointestinal tract extends from mouth

to anus

On embryologic grounds, the GI tract should

be divided into

upper (mouth to major papilla in the duodenum),

middle (papilla to mid-transverse colon), and

lower (mid-transverse colon to anus)

Derivation of these 3 areas from the foregut,

midgut, and hindgut, respectively.


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From the point of view of GI bleeding,

however, the demarcation between the upperand lower GI tract is the duodenojejunal (DJ)

junction/ligamentum treitz

Bleeding above the DJ junction is called upper

GI bleeding, and that below the DJ junction is

called lower GI bleeding.


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Consist ofskeletal muscle from the diaphragm

and a fibromuscular band of smooth muscle

which inserts into the 3rd and 4th part ofduodenum and frequently the DJ junction

Contraction widens the angle of theduodenojejunal flexure, allowing movement

of the intestinal contents.


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Causes and pathophysiology of

Upper GI Bleeding


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Causes


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Peptic Ulcer


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gastric erosion

refers to endoscopically visualized

subepithelial hemorrhages and erosions

due to NSAID,stress and alcohol.

not much bleeding.

causes ulceration.


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Due to longitudinal mucosal lacerations (known asMallory-Weiss tears) at the gastroesophagealjunction or gastric cardia.

The original description by Mallory and Weiss in1929 involved patients with persistent retching andvomiting following an alcoholic binge.

However, Mallory-Weiss syndrome may occur afterany event that provokes a sudden rise in intragastricpressure or gastric prolapse into the esophagus.

May also occur in epileptic convulsions.

Mallory-Weiss Tear


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Bleeding esophageal varices are enlarged veins inthe walls of the lower part of the esophagus.

Scarring ( cirrhosis) of the liver is the most commoncause of esophageal varices. This scarring reducesblood flowing through the liver. As a result, moreblood is shunted to the veins of the esophagus.

This extra blood flow causes the veins in theesophagus to balloon outward. If these veins breakopen, they can bleed severely.

Any type of chronic liver disease can causeesophageal varices.

Varices can also occur in the upper part of thestomach.

Varices


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Clinical Features of upper

gastrointestinal bleeding


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Patients with upper GI hemorrhage often

present with:

A. hematemesis (vomiting of blood),

B. coffee ground vomiting,

C. melena (dark tarry stools),

D. hematochezia (blood in the feces) if thehemorrhage is severe.

E. dyspepsia (especially nocturnal symptoms)


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Patients may also present with complications

of anemia, including:

a. chest pain,

b. syncope (loss of consciousness resulting from

insufficient blood flow to the brain),

c. fatigue

d. shortness of breath.


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The finding of subcutaneous emphysema with

a history of vomiting is suggestive of

Boerhaave syndrome (esophageal perforation)

The presence of postural hypotension

indicates more rapid and severe blood loss.


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Probable Source of GI Bleeding Within

the Gut

Clinical IndicatorProbability of Upper GI

Source

Probability of Lower GI

Source

Hematemesis Almost certain Rare

Melena Probable Possible

Hematochezia Possible Probable

Blood-streaked stool Rare Almost certain

Occult blood in stool Possible Possible


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Investigations of uppergastrointestinal bleeding


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Investigations in Upper GI Bleeding

1. Urgent endoscopy (


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1. Plain radiographs of abdomen - free air under the

diaphragm is seen in cases of perforated viscous,

and this may be accompanied by UGIB. Other

etiologies, such as upper GI masses (which usually

result in chronic, not acute, UGIB), aneurysms

with calcifications, and ascites suggestive of

portal hypertension, may be seen on radiographs.2. Blood alcohol concentration

3. Blood glucose concentration

4. CVP monitoring, blood replacement and bladdercatheterisation (for those with severe bleeding)

5. Coagulation screen


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Thyroid chemistries, cortisol, and calcium levels

are obtained to exclude endocrinologic causes of

GI symptoms. Pregnancy testing is considered for

young women with unexplained nausea.

Serologies tests are available to screen for celiac

disease, IBD, and rheumatologic diseases such as

lupus or scleroderma.

Hormone levels are obtained for suspected

endocrine neoplasia.

Intraabdominal malignancies produce tumormarkers including the carcinoembryonic antigen

CA 19-9 and -fetoprotein


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MANAGEMENT


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Resuscitation and initial management Shocked patients should receive prompt volume replacement. It has been

demonstrated that early and aggressive resuscitation reduces mortality in UGIB.

Correct fluid losses. Either colloid or crystalloid solutions may be used to achievevolume restoration prior to administering blood products; red cell transfusion

should be considered after loss of 30% of the circulating volume.

Transfuse patients with massive bleeding with blood, platelets and clottingfactors in line with local protocols for managing massive bleeding.

Platelet transfusions should not be offered to patients who are not activelybleeding and are haemodynamically stable.

Platelet transfusions should be offered to patients who are actively bleeding andhave a platelet count of less than 50 x 109/litre.

Fresh frozen plasma should be used for patients who have either a fibrinogenlevel of less than 1 g/litre, or a prothrombin time (INR) or activated partialthromboplastin time greater than 1.5 times normal.

Prothrombin complex concentrate should be used for patients who are takingwarfarin and actively bleeding.

Proton pump inhibitors (PPIs) should not be used prior to diagnosis by endoscopyin patients presenting with acute UGIB.


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Management of non-variceal bleeding

Endoscopy is now the method of choice for controlling active peptic-ulcer related UGIB.

Endoscopic therapy should only be delivered to actively bleeding lesions, non-bleeding visible

vessels and, when technically possible, to ulcers with an adherent blood clot. Clean ulcer

base with oozing do not merit endoscopic intervention since these lesions have an excellent

prognosis without intervention.

Adrenaline (epinephrine) should not be used as monotherapy for the endoscopic treatment

of non-variceal UGIB. For the endoscopic treatment of non-variceal UGIB, one of thefollowing should be used:

A mechanical method (eg clips) with or without adrenaline (epinephrine).

Thermal coagulation with adrenaline (epinephrine).

Fibrin or thrombin with adrenaline (epinephrine).

Interventional radiology should be offered to unstable patients who re-bleed after

endoscopic treatment. Refer urgently for surgery if interventional radiology is not

immediately available.

Acid-suppression drugs (PPIs or H2-receptor antagonists) should not be offered before

endoscopy to patients with suspected non-variceal UGIB. PPIs should be offered to patients

with non-variceal UGIB and stigmata of recent haemorrhage shown at endoscopy.


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Treatment after first or failed endoscopic treatment

Repeat endoscopy, with treatment as appropriate, should be

considered for all patients at high risk of re-bleeding, particularly ifthere is doubt about adequate haemostasis at the first endoscopy.

A repeat endoscopy should be offered to patients who re-bleedwith a view to further endoscopic treatment or emergency surgery.

Interventional radiology should be used for unstable patients who

re-bleed after endoscopic treatment. Percutaneous angiographymay be used to localise the bleeding point and embolisation of theartery using foam and coils to stop bleeding. The benefits ofembolisation have to be balanced against the risk of causingischaemic necrosis of the gastrointestinal tract.

Refer urgently for surgery if interventional radiology is not

immediately available.


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Management of variceal bleeding

Terlipressin should be offered to patients with suspected variceal bleedingat presentation. Treatment should be stopped after definitive haemostasis

has been achieved, or after five days, unless there is another indication forits use.

Prophylactic antibiotic therapy should be offered at presentation topatients with suspected or confirmed variceal bleeding.

Balloon tamponade should be considered as a temporary salvagetreatment for uncontrolled variceal haemorrhage.

Oesophageal varices: Band ligation should be used for patients with UGIB from oesophageal varices.

there is sufficient evidence to show that stent insertion is effective forselected patients with oesophageal varices in whom other methods oftreatment have failed to control bleeding.

Transjugular intrahepatic portosystemic shunts (TIPS) should be considered ifbleeding from oesophageal varices is not controlled by band ligation.

Gastric varices: Endoscopic injection of N-butyl-2-cyanoacrylate should be offered to patients

with UGIB from gastric varices.

TIPS should be offered if bleeding from gastric varices is not controlled byendoscopic injection of N-butyl-2-cyanoacrylate.


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Surgical intervention

Surgical intervention is required when endoscopic

techniques fail or are contra-indicated. Clinical judgementis required and consideration given to local expertise.

In general, it is recommended: To inform surgeons early of the possibility of surgery.

To use the most experienced personnel available.

To avoid operations in the middle of the night.

The particular procedure required depends on a number offactors, not least the site of bleeding. Gastric ulcers areprobably best excised. There are few studies comparing thedifferent techniques.


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Medical management post-endoscopy

Helicobacter pylorieradication All patients with a bleeding peptic ulcer should be tested for H. pylori, eg urea

breath test or biopsy specimen.

Patients who test positive should receive a one-week course of eradication

therapy. This should be followed by three further weeks with ulcer healing treatment.

All therapy can be discontinued after successful healing of peptic ulcers providedpatients are not taking NSAIDs.

A negative urea breath test should be confirmed on the initial biopsy specimentaken prior to diagnosis and before any PPI therapy was given.

Two weeks after successful therapy and stopping of all medication, a repeat ureabreath test should be performed to confirm successful eradication.

Unsuccessful eradication should be treated with second-line therapy.

Upper GI Bleed - Symposium

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