GASTROESOPHAGEAL

VARICES

13/5/2020
SYIKIN
◦Esophageal varices

◦Esophageal varices are enlarged veins in

the esophagus. They're often due to
obstructed blood flow through the portal
vein, which carries blood from the
intestine, pancreas and spleen to the liver.

◦MAYOCLINIC
WHY?

FORCES

 blood flows into
normal blood flow to The vessels can leak
INCREASE smaller blood vessels
the liver is blocked by blood or even
PRESSURE IN THE that aren't designed to VARICES
a clot or scar tissue in rupture, causing life-
PORTAL VEIN  carry large volumes of
the liver threatening bleeding.
blood

CIRRHOSIS
BLOOD CLOT
PARASITIC INFECTION
RISK FACTORS
◦ MOST WON'T HAVE BLEEDING.
◦ BLEED IF:
◦ High portal vein pressure (portal HPT)
◦ Large varices
◦ Red marks on the varices (OGDS) - long, red streaks/ red spots  
◦ Severe cirrhosis or liver failure
◦ Continued alcohol used
◦ Previous variceal bleed
SYMPTOMS, SIGNS
◦ Vomiting large amount of blood (hemetemesis)
◦ Black, tarry or bloody stool
◦ Lightheadedness
◦ LOC in severe cases
◦ Sign of liver dz: jaundice, easy bleeding r bruising, ascites
COMPLICATION

◦BLEEDING >>> RISK OF

ANOTHER EPISODE
INCREASES >>> SHOCK
>>> DEATH
PREVENTION
◦ NO TX CAN PREVENT DEVELOPMENT OF
VARICES IN CIRRHOSIS LIVER
◦ BETA BLOCKER???????  ONLY PREVENT
BLEEDING IN ESOPHAGEAL VARICES

◦ SO? WHAT TO DO?

KEEP LIVER HEALTHY
/ AVOID LIVER DZ CX
◦ No ALCOHOL
◦ HEALTHY DIET
◦ MAINTAIN HEALTHY WEIGHT –obesity/ excess amount of fat can damage liver, increase risk oof liver cirrhosis
◦ Use chemicals sparingly and carefully – when handling chemicals, follow instruction and safety precautions
◦ Reduce risk of hepatitis
◦ sharing needles
◦ Unprotected sex (multiple partner) *condom
◦ Vaccination? Hep a,b
DIAGNOSIS
◦ OGDS – dilated veins, measure, check for red streak, red spots
◦ Tx can be performed
◦ Imaging : CTA, Doppler US of splenic vein and portal veins
◦ Capsule endoscopy: diagnostic only – for unable or unwilling to have ogds
 MANAGEMENT?
1. ACTIVE VARICEAL BLEED 2. PROPHYLAXIS 3. CHRONIC MANAGEMENT
 1. ACTIVE VARICEAL BLEED
◦ Hemodynamically unstable patient
1. resuscitation 
- maintain airway – KIV intubation if ptn has encephalopathy or copious hemetemesis
- Supplemental high flow O2 (SpO2 > 94%)
- Insert 2 large bore
- Monitor vitals, ECG, pulse oximeter, urine output
- Labs: GXM (4U), FBC, BUSE, coagulation profile, +/- LFT,Cardiac enzyme
- Fluid- 1 L NS
- ICU bed
* NGT worsen variceal bleed
* blood volume expansion increases portal vein pressure in cirrhotic ptn causing active bleed or precipitate further bleeding
* Blood transfusion if hb <7g/dL, unstable CAD < 9g/dL 
2. pharmacological Mx
◦ IV broad spectrum Abx x 1/52   (ciprofloxacin 500mg bd / ceftriaxone 1g/ day )  --> reduce SBP, re-
bleeding, mortality
◦ IV Somatostatin 250ug bolus --> 250ug/h for 3-5/7
OR
◦ IV Octreotid 50mcg bolus --> 50mcg/h for 3-5/7
◦ IV Omeprazole 80mg bolus
◦ IV Vit K (10mg) - routinely given in cirrhotic with coagulopathy
◦ +/- IV Telipressin (2mg Q6H) - synthethic vasopressin is a vasoactive drug with 34% reduction in
mortality risk (IHD CI)
◦ +/- recombinant activated factor VII for correcting PT in cirrhotic 
3. management in severe variceal bleeding
(balloon tamponade)

◦ Protect airway before inserting tube

◦ Sengstaken-Blakemore tube / Minnesota tube
◦ (maximum 24 hours – temporary deflate after 12 hours to
prevent pressure necrosis) in patients with uncontrollable
bleeding for whom a more definitive therapy is planned
(i.e. TIPS or endoscopic therapy) 
4. definitive mx (endoscopy, TIPSS)
Endoscopy - Confirms diagnosis and institute definitive management - 
(1) Sclerotherapy (into bleeding varies or overlying mucosa) 
Induce inflammation and fibrosis 
◦ Controls bleeding in 70% after 1st injection and 85%after a second 

(2) Variceal band ligation >>ligation is superior to sclerotherapy in initial control of bleeding and associated with fewer adverse effects
TIPSS (Transjugular Intrahepatic Porto-Systemic Shunt) 
◦ Involves radiologically guided intra-hepatic placement of a stent between branches of the hepatic and portal venous circulation >> acute decompression of portal
pressure thus controlling refractory variceal bleed 
◦ Considered in patients whose bleeding is refractory to pharmacological and endoscopic therapy 
◦ TIPSS is not a good long-term preventive strategy 

Emergency Shunt surgery 

◦ Risk of more frequent encephalopathy and higher mortality (can be extrapolated to TIPSS because its physiology is the same as that of surgical shunts (i.e. divert blood
away from liver) 
◦ Selective 
◦ Proximal splenorenal shunt (splenectomy with end-to-side anastomosis of portal side of splenic vein to left renal vein) 
◦ Distal splenorenal shunt (Warren-Zeppa shunt – splenic vein divided and splenic side anastomosed end-to-side to left renal vein) 

◦ Non-selective 
◦ Portacaval shunts (joining portal vein to IVC) – side-to-side, end-to-side 
◦ Mesocaval shunts (joining superior mesenteric vein to IVC)
THANK YOU
 MANAGEMENT?
1. ACTIVE VARICEAL BLEED 2. PROPHYLAXIS 3. CHRONIC MANAGEMENT
2. PROPHYLAXIS
1. Secondary prophylaxis of variceal bleeding
- Patients with cirrhosis who survive an episode of active variceal bleed should receive therapy to prevent recurrent of variceal
haemorrhage
- Best option is combination of:
◦ Band ligation (3 weekly ligation until completely obliterated) & 
◦ Non-selective beta-blockers (Propranolol unless CI) 
2. Primary prophylaxis of variceal bleeding 
- Prevention of variceal haemorrhage in patients who have never bled (reduce bleeding risk by 30-45%)
- Patients with large varices (grade 3) or medium varices (grade 2) with endoscopic red signs or Child’s C cirrhosis
should be treated 

- Best option is: Non-selective beta-blockers (Propranolol & Nadolol) --> reduce risk of bleeding and slow progression
of small varices into larger ones 
1. block ß1 receptor --> decrease cardiac output 
2. block ß2 receptor --> produce splanchnic vasoconstriction and reduce portal flow and portal pressure 
- If contraindicated to BB --> long acting nitrates (isosorbide mononitrate) 
- Insufficient evidence to support treatment of patients with small varices 
- No evidence for prophylaxis with BB in patients with cirrhosis without varices 
3. CHRONIC MX
- Start patient on an ablation regimen (endoscopy with initial ligation/sclerotherapy and
subsequent endoscopic monitoring and repeated ligation/sclerotherapy as required to completely
ablate varices) 
- If patient bleeds again --> failed ablation --> consider surgery (as above – shunts, or Sugiura) 
- LT propranolol + PPI --> Acid suppressive therapy is theorized to improve the stability of clot,
and infusion of omeprazole has been shown to reduce risk of recurrent bleeding and need for
emergent surgery in all cases of UBGIT
Predictors of variceal haemorrhage:
 1 Site: - Varices at the gastro-oesophageal junction have the thinnest coat of supporting tissue and are at highest risk of rupture and
bleeding 
2 Size: 
- Grade 1: Small straight varices not disappearing with insufflation
- Grade 2: Enlarged tortuous varices that occupy less than one-third of the lumen
- Grade 3: Large varices that occupy more than one-third of the lumen
3 Child’s score – patients with higher Child’s score have higher risk 
4 Red signs: Endoscopic Stigmata of Recent Haemorrhage (ESRH) 
- Red wale marks (longitudinal red streaks)
- Cherry red spots (flat discrete spots)
- Hematocystic spots (raised discrete spots – resemble “blood blisters”) 
- Diffuse erythema
5 Previous variceal haemorrhage: 
- 70% of patients will have further variceal bleeds after an index bleed (risk highest in first 48hours after first bleed)
- 30% re-bleed within 6 weeks, 30% re-bleed after 6 weeks
THANK YOU