Y2 W18 S1 - Portal Hypertension

Front 1

Portal HTN: Definition

Back 1

Increased resistance to portal blood flow

Front 2

Portal HTN: Causes

Tip: Think pre-, hepatic, and post-

Back 2

Pre-hepatic:
obstructive thrombosis,
narrowing of portal vein,
massive splenomegaly

Hepatic:
cirrhosis (most common cause),
schistosomiasis (parasite matures in liver - enlargement and damage),
massive fatty change,
sarcoidosis etc.

Post-hepatic:
severe right heart failure,
constrictive pericarditis,
hepatic vein outflow obstruction

Front 3

MECHANISM: Portal HTN

Back 3

Contraction of vascular smooth muscle
+ Disruption by scarring/nodules at sinusoid level.
-> Increased resistance to portal flow

Arterial vasodilation
(esp. splanchnic circulation)
-> Hyperdynamic circulation
-> Increase in portal blood flow

Front 4

Cirrhosis: 4 major consequences

Back 4

Ascities
Formation of portosystemic shunts
Splenomegaly (congestive, can reach 1000 grams)
Hepatic encephalopathy

Front 5

Cirrhosis: Ascities

Definition

Back 5

Accumulation of fluid in peritoneal cavity.

Front 6

Cirrhosis: Ascities

Clinical features (in relation of cirrhosis)

Back 6

85% of cases caused by cirrhosis.

Noticeable when >500mL.

Fluid is typically serous (low protein).

Front 7

Cirrhosis: Ascities

3 mechanisms

Tip: Think of why hepatic lymph or portal blood would get into abdomen

Back 7

1. Sinusoidal hypertension:
Fluid driven into space
of Disse,
-> Removed by hepatic lymphatics (promoted by hypoalbuminemia)

2. Very high hepatic lymph production
(cirrhosis can lead to up to 20L/day, normal ≤1L/day)

3. Splanchnic vasodilation/ hyperdynamic circulation

Front 8

MECHANISM

Cirrhosis: Formation of portosystemic shunts

Back 8

Rise in portal pressure
-> Dilation of collateral vessels
+
Development of new blood vessels where portal and system circulation share common capillary beds
-> Reversal of flow from portal to systemic circulation
(i.e. systemic blood flows into portal circulation)

New blood vessels lead to:
Hemorrhoids
Oesophago-gastric junction varices

Abdominal wall collaterals appear dilated:
Caput Medusae

Front 9

Cirrhosis: Formation of portosystemic shunts

Complications

Back 9

Rarely cause massive bleeding

Oesophagogastric varices appear in 40% of individuals with advanced cirrhosis

Causes massive hematemaesis in about half of these patients (each episode associated with 30% mortality)

Front 10

Ascites: Why is it important to establish cause?

Back 10

Ascites may be simply caused by cirrhosis, or via other causes MASKED by the cirrhosis.

e.g. A patient with cirrhosis may have ascites due to occult HCC, rather than via the cirrhosis.

Front 11

Ascites: Dx tests + what are they looking for?

Back 11

Diagnostic paracentesis (100mL-150mL):
Examination for
- gross appearance,
- protein content,
- albumin level,
- cell count,
- Gram’s, acid-fast stains and culture
-> Can probably confer Dx

Cytology & cell-block examination
-> May reveal occult carcinoma

Serum ascites-albumin gradient
SAAG = [serum albumin] - [ascites albumin]
-> Ascites = transudate or exudate (protein-rich)
- Gradient correlates with portal pressure
-> Assess portal HTN severity?
->

Front 12

Ascites: Serum ascites-albumin gradient (SAAG)

What does it mean if the gradient is more than 1.1g/dL? Or less than 1.1?

Back 12

More than 1.1g/dL = Ascites due to portal HTN
(probably regular cirrotic ascites)

Less than 1.1 = Not due to portal HTN

Differentiation accurate 97% of time.

Front 13

Cirrosis: Ascites

Tx?

Back 13

- Spironolactone
(Side-effects: anti-androgenic, hyperkalemia, azotaemia, renal tubular acidosis)

- Amiloride
(SEs: Hyperkalemia)

- Frusemide
(SEs: Hyponatremia, hypokalemia, azotamia)

- Therapeutic paracentesis (needle drainage of fluid):
Repeated large volume paracentesis and IV albumin is more effective than standard diuretics.
IV albumin is important in avoiding renal and electrolyte complications and activation of endogenous vasopressor systems.
Total paracentesis with IV albumin is effective w/o increasing risk of complications.