UPPER GIT BLEEDINGDr Paing P MyintDHSH Surgery

DEFINITION OF UGIB

Any bleeding that arises from proximal to Ligament of Treitz

UGIB is an emergency!

Quick initial assessment and resuscitation is key

Ligament of Treitz at the duodenojejunal flexure

EPIDEMIOLOGY OF UGIB

PATIENT PRESENTS WITH

Haematemesis

Melena

Haematochezia - if bleeding is rapid enough

Occult bleeding

PAST MEDICAL HISTORY

Liver disease or alcohol abuse - Variceal bleeding

Previous Helicobacter pylori, NSAID use, smoking - PUD

Immunodeficiency - Oesophageal Candidiasis

Smoking, alcohol abuse, H. Pylori, constitutional symptoms - Malignancy

Previous gastroenteric anastomosis - Marginal ulcers

Abdominal aortic aneurysm or an aortic graft - Aorto-enteric fistula

Renal disease, aortic stenosis, or hereditary hemorrhagic telangiectasia - Angiodysplasia

MEDICATION

NSAIDs - PUD

Anticoagulants/Antiplatelet therapy - increased bleeding tendency

Certain Antibiotics (clindamycin, doxycycline) + Bisphosphonates - Medication-induced oesophagitis

Anaemic patients on Iron Sulphate

ASSESSMENT OF SIGNS AND SYMPTOMS

More severe if:

1. orthostatic dizziness

2. confusion

3. angina

4. palpitations

5. cold/clammy extremities

SPECIFIC CAUSES CAN BE SUGGESTED BY SYMPTOMS

Peptic ulcer: Epigastric or right upper quadrant pain

Oesophageal ulcer: Odynophagia, gastroesophageal reflux, dysphagia

Mallory-Weiss tear: Emesis, retching, or coughing prior to haematemesis

Variceal haemorrhage/portal hypertensive gastropathy: Jaundice, weakness, fatigue, anorexia, abdominal distention

Malignancy: Dysphagia, early satiety, involuntary weight loss, cachexia

EXAMINATION

2 questions to ask yourself:

1. What is the degree of anaemia/hypovolaemia?

2. Are there signs of chronic liver disease that might suggest bleeding varices?

1. WHAT IS THE DEGREE OF HYPOVOLAEMIA/ANAEMIA?

Mild to moderate hypovolaemia: Resting tachycardia.

Blood volume ±15 percent: Orthostatic hypotension (a decrease in the systolic blood pressure > 20 mmHg and/or an increase in heart rate of 20 beats per minute when moving from supine to standing).

Blood volume loss ± 40 percent: Supine hypotension.

2. ARE THERE SIGNS OF CHRONIC LIVER DISEASE: BLEEDING VARICES?

Encephalopathy with or without asterixis

Scleral icterus

Spider telangiectasia on the face, chest, or abdomen

Gynaecomastia

Hepatomegaly or splenomegaly

Ascites

Caput medusae with or without Cruveilhier-Baumgarten's bruit

Hypogonadism

Terry's nails (white nails)

Palmar erythema.

RISK STRATIFICATION

All UGIB must be assessed promptly BUT not all need admission

Risk factors

Non-specific scoring systems e.g. APACHE II can be applied to predict risk of mortality

BLEED CLASSIFICATION

If any one of these criteria present, patient is in high-risk group for poor outcome

CAUSES OF UGIBVariceal vs Non-variceal

PORTAL HYPERTENSION

Portal pressure increases due to:

1. Increased resistance to flow in fibrous nodular liver

2. active intra-hepatic vasoconstriction

3. splanchnic vasodilatation

VARICEAL BLEEDING

Portal hypertension leads to:

1. Gastroesophageal varices

2. Isolated Gastric varices

3. Hypertensive Portal Gastropathy

OESOPHAGEAL VARICES

Dilated submucosal veins develop in response to the portal hypertension

Provide a collateral pathway for decompression of the portal system into the systemic venous circulation

Usually distal oesophagus and 1 to 2 cm in size

As they enlarge, the overlying mucosa becomes increasingly weak, easily damaged with minimal trauma

ISOLATED GASTRIC VARICES

Similar pathogenesis as Oesophageal varices

Localised to Gastric veins

HYPERTENSIVE PORTAL GASTROPATHY

Incompletely understood

Diffuse dilation of the mucosal and submucosal venous plexus of the stomach

Overlying gastritis

Snake-skin appearance with cherry-red spots

MAIN POINTS IN VARICEAL BLEEDING

1. Increased risk of rebleeding

2. Increased need for transfusions

3. Longer hospital stay

4. Increased mortality (20% 6-week mortality)

5. Haemorrhage is often massive and patients are haemodynamically unstable

ALGORITHM FOR VARICEAL BLEEDING

ABCS

Fluid resuscitation - delicate balance

Liver cirrhosis = hyperaldosteronism = fluid retention + ascites

Correcting too quickly = ↑ risk of bleeding

Correcting too slowly = Hypovolaemic shock

CVP, U-catheter, close intake and output monitoring

ICU may be warranted

VASOPRESSIN VS OCTREOTIDE

Vasopressin = splanchnic vasoconstriction = ↓ bleeding = cardiac vasoconstriction = myocardial ischaemia thus combined with nitroglycerin if used

Octreotide (somatostatin analogue) = ↓ risk of myocardial ischaemia

Allow temporary relief of bleeding to resuscitate and to perform diagnostic + therapeutic procedures

ENDOSCOPYEarly endoscopy improves outcome

Bleeding varices => banding (less complications, needs expertise) => sclerotherapy (more complications: strictures perforation, mediastinitis) => up to 3 treatments may be required in 24hrs and repeat therapy in 10-14 days => 90% success rate

If bleeding cannot be controlled => Sengstaken-Blakemore tube

SENGSTAKEN-BLAKEMORE TUBE

2 balloons

Gastric balloon inflated tension applied to GE-junction

If bleeding not controlled, inflate oesophageal balloon to compress the venous plexus

High complication rate: aspiration, incorrect placement, oesophageal perforation

PORTAL DECOMPRESSIONRequired in 10% of variceal bleeds

Equal success rates between surgical shunting and percutaneous TIPS (transjugular intrahepatic portosystemic shunt)

TIPS if better liver function + candidate for future transplant

TIPS complications: shunt thrombosis, hepatic encephalopathy 50% in 1yr

After bleeding controlled, must prevent rebleeding = β-blocker + PPI x 2-4/52

RECAP: UGIB CAUSES

PEPTIC ULCER DISEASE40% of UGIB

10-15% of patients with PUD develop UGIB at some point

Less common complications from bleeding PUD due to PPI and H.Pylori eradication

Less surgery for perforated PUD, but equivocal amount for bleeding PUD

PEPTIC ULCER DISEASE

Bleeding due to erosion of mucosa by peptic acid

Significant haemorrhage when erosion into an artery:

Posterior gastric ulcer => left gastric artery

Posterior duodenal ulcer => gastroduodenal artery

Gastric ulcers bleed more than duodenal

ALGORITHM: PUD BLEEDING

ABCs

Start PPI: Pantaloc 40mg 12hrly IV

OGD within 24hrs

Forrest classification based Rx

FORREST CLASSIFICATION

Predicts risk of rebleeding

I - IIa: endoscopic therapy

IIb: remove clot and evaluate underlying ulcer

IIc - III: medical therapy

GLASGOW-BLATCHFORD SCORE

> 6 points = > 50% chance of endoscopic therapy required

Pre-endoscopic scoring system

ROCKALL SCORE

< 3 = good prognosis

> 8 = high mortality

Need OGD to use

MEDICAL THERAPY

Lifestyle: diet, smoking, alcohol

PPI + H. Pylori eradication

Stop NSAIDs (replace with selective COX-2 inhibitor)

ENDOSCOPIC THERAPY

After identification of bleeding ulcer, use combo of:

1. Adrenaline injection (1:10000 in all 4 quadrants)

2. Heater probes (superficial or deep bleeding ulcers)

3. Haemoclips (better for spurting vessels)

4. Argon laser coagulation (superficial bleeding ulcers)

5. Electrocautery (deep bleeding ulcers)

25% first attempt failure rate => repeat attempt warranted before surgical therapy

SURGICAL THERAPY

10% of bleeding ulcers require surgery

Firstly: control haemorrhage

Secondly: definitive acid reducing procedure

Choice of procedure depends on whether duodenal or gastric ulcer

MALLORY-WEISS TEAR

Forceful contraction of abdominal wall against unrelaxed cardia due to increased intragastric pressure

Mucosal and submucosal tears near gastroesophageal junction

Alcohol history - retching and vomiting after binging

Endoscopy - NB to retroflex to see area just below GE junction

Supportive therapy usually adequate

Endoscopic therapy options

High gastrectomy + suturing tear

STRESS-GASTRITISMultiple superficial erosions, esp. in the body of stomach

Increased acid and pepsin exposure

NSAIDs

Different to solitary ulcers in ICU patients (Cushing’s ulcer) and burns (Curling’s ulcer)

Medical therapy usually enough

Endoscopic therapy options

OESOPHAGITISGORD => increased acid exposure to oesophagus

Slower rate of bleeding = anaemia

Increased in immunocompromised e.g. HSV, Candida

PPI ± target antibiotic/antifungal

Endoscopic cautery/heater probe

DIEULAFOY’S LESION

Vascular malformations

Rupture of unusually large vessels in submucosa

Usually along lesser curve within 6cm of GE-junction

Massive bleeding can occur

Endoscopic thermal/sclerotherapy

Gastrostomy with overlaying suture/ partial gastrectomy

GASTRIC ANTRAL VASCULAR ECTASIA (GAVE)

“Watermelon stomach”

Collection of dilated venules: linear streaks meeting at antrum

Occult blood loss and anaemia

Medical therapy

If persistent => APC laser => antrectomy

MALIGNANCY

Occult bleeding and anaemia

Some present with ulcerative lesions: GIST, lymphomas, leiomyomas

Endoscopic therapy to control bleeding

Curative: complete resection

Palliative: wedge resection

AORTA-ENTERIC FISTULA

Usually after previous AAA repair

Pseudoaneurysm formation at proximal anastomotic line, with concurrent infection => fistulises into overlying distal duodenum

Usually within 3 years of repair

Self-limited sentinel bleed at first then massive fatal haemorrhage

Ligate aorta proximal to graft => remove infected prosthesis => extra-anatomic bypass; primary repair duodenum

HAEMOBILIA

Trauma

Recent manipulation of biliary tree e.g. ERCP

Hepatic tumours

△ UGIB, RUQ pain, Jaundice

Endoscopy: blood at ampulla

Angiographic embolisation

HAEMOSUCCUS PANCREATICUS

Erosion of pancreatic pseudocyst into splenic artery => bleeding from duct of Wirsung

Abdominal pain, UGIB in a patient with previous pancreatitis

Angiographic embolisation to control bleeding

Distal Pancreatectomy: curative

CONCLUSION

UGIB common presentation with multiple pathologies

Stabilise then diagnose and treat

History will give 80% of the diagnosis

Differentiate variceal vs non-variceal bleeding

Risk Stratification

Medical, Endoscopic and Surgical therapies

Follow-up required

THANK YOU