Variceal management

Question 1

Small varices and child’s C or red whale marks and primary prophylaxis

Answer 1

NSBB eg propanolol- aiming to reduce resting HR by 25% or to 55-60 beats per min.
If on beta blocker, eliminates need to keep doing endoscopies.

Question 2

Small varices without Childs C or red whale marks and primary prophylaxis

Answer 2

May consider NSBB but more studies needed to confirm benefit

No clear mortality benefit

Question 3

Large varices and primary prophylaxis

Answer 3

NSBB or varicael band ligation
This decreases risk of bleeding by 40% either way
But no mortality effect with EVL proven

Question 4

Hepatic vein portal gradient- how do you use to distinguish cirrhosis from extrahepatic portal vein obstruction?

Answer 4

Gradient is increased in sinusoidal portal hypertension
If thrombus in the portal vein, normal gradient across the liver but HIGH in the portal vein (still)

Remember varices do not form unless pressures over 10mmHg

Question 5

In secondary prophylaxis, how is the HPVG useful?

Answer 5

Fall in 10% from baseline of HPVG in response to medical therapy predicts lower rebleeding risk.

If you are a “haemodynamic non responder” - can add ISMN.

Question 6

How long after the bleed would you start secondary prophylaxis?

Answer 6

6 days

Question 7

What is the preferred approach to secondary prophylaxis in patients with cirrhosis?

Answer 7

Combination of beta blockers and band ligation compared with either alone
If refuse EBL then give beta blockers and ISMN
Keep going 1-2 weekly until obliterated

If fail endoscopic and pharmacological treatment–>TIPS or transplant

Question 8

What are the 4Hs of acute liver failure?

Answer 8

Hypocapnoea (actually aim 30-45)
Hypothermia
Hypernatraemia
Haemofiltration

Question 9

What is the effect of rifamixin in HE prophylaxis?

Answer 9

Add on to lactulose for prevention of recurrent episodes of HE

Reduces risk of hospitalisation

Question 10

What is the mortality with a bleeding varix?

Answer 10

15-20%

Question 11

Cirrhosis and no varices on initial screen?

Answer 11

surveillance every 2-3 years (immediate if decompensation though)

Question 12

What about gastric varices?

Answer 12

NSBB and VBL are not as effective with large gastric varices and no history of bleed.

If they bleed, endoscopic variceal obliteration FIRST and band ligation SECOND but risk rebleeding his high

Secondary prophylaxis with TIPs if eligible

Question 13

What are the three main risk factors for varices being present in cirrhotics?

Answer 13

Thrombocytopaenia
Portal vein over 13mm
INR over 1.5

If all 3 then 90% chance of varices

Question 14

In Africa/Egypt, what is the most common cause of varices?

Answer 14

Schistosomiasis

Liver function well maintained and rarely decompensate, but may die from bleeding

Question 15

Remember, peptic ulcers also more common in cirrhotics!!

Answer 15

Free mark!

Question 16

Which measure has an effect on mortality in bleeding varices?

Answer 16

Endoscopic therapy

Question 17

Which therapies reduce bleeding but not mortality in bleeding varices?

Answer 17

Vasopressin and somatostatin analogues (somatostatin may be superior to octreotide)
Non cardioselective beta blockers (30% people are non responders in terms of their HVPG but invasive to testP)
ISMN drops BP and cause AKI

Question 18

Acute variceal haemorrhage; management steps.

Answer 18

ABCs- non aggressive volume but maintain urine output

Abx up to seven days prophylaxis- ceftriaxone followed by norflox reduce all infection and SBP, improve survival by 9%, reduce rebleeding rate

Continue terlipressin or somatostatin or octreotide or vapreotide 2-5 days after confirm dx
Terlipressin is first choice: reduces failure to control bleeding and mortality
Somatostatin analogue reduces need for blood transfusion but not death

Question 19

Terlipressin MOA

Answer 19

Terlipressin is a long-acting analogue of vasopressin, acts mainly on splenic circulation

Question 20

What is the mechanism of NSBB in primary prophylaxis?

Answer 20

Non-selective beta-blocker therapy (Propranolol) block adrenergic dilatory tone in mesenteric arterioles –>unopposed alpha adrenergic mediated vasoconstriction –>decreases portal infow

Question 21

What is happening pathophysiologically in portal hypertension?

Answer 21

Increased flow and increased resistance

Question 22

What is the hepatic venous portal gradient?

Answer 22

HVPG = WHVP - FHVP (free)

portal hypertension if HVPG over 5
Clinically significant if over 10 and predicts likelihood of varices, clinical decompensation, HCC

Question 23

How many cirrhotics get varices each year?

Answer 23

7%

Question 24

Per year bleeding risk varices?

Answer 24

5% small

15% large

Question 25

Transfuse at what level in variceal haemorrhage?

Answer 25

under 70, aim for 70-90 (superior to aiming 90-110), especially beneficial in childs A and B- no difference childs C
- superior survival, reduced rebleeding rates, fewer AE
Also if ongoing massive haemorrhage consider factor seven replacement

Question 26

Evidence for PPI in bleeding ULCERs?

• before?
• after?

Answer 26

ONLY difference was improved endoscopic stigmata in patients given PPI before endoscopy, and reduced need for endoscopic therapy

After endoscopy, high dose IV reduces rebleeding, blood transfusion requirement, duration of hospital stay (not mortality)

Question 27

What is worse for an ulcer? Visible vessel or adherent clot?

Answer 27

visible vessel- 50% rebleeding rate

Clot removal prior to clip reduces rebleeding rates

Actively bleeding is the worse (100%)

Question 28

What does blood in the stomach do for your rapid ureas?

Answer 28

false positives

Question 29

What is better in bleeding varices? Terlipressin or abx?

Answer 29

Abx- reduce mortality

Terlipressin possible mortality benefit but not clear.

Question 30

See gastric varices- what could be happening?

Answer 30

Splenic vein thrombosis –>sinistral portal hypertension

Cannot band or use sclerotherapy as makes worse! Inject with superglue.