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References from Sabiston, UptoDate
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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