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PORTAL HYPERTENSION

Definition:

Increase in portal vein pressure above the normal level of 5 to 10 mmHG.
When the resting portal venous pressure is above 10 mmHg.
Most commonly due to obstruction:
- Somewhere in the portal vein or its tributaries (Prehepatic).
- In the portal venules and sinusoides in the liver (Hepatic).
- In the Hepatic veins draining into the inferior vena cava (Post Hepatic).
Increased blood pressure in portal veins cause oesophageal varices.
Commonly Liver diseases and thrombosis in the vein causes portal hypertension and due to it occurs massive recurrent hematemesis and melaena.

Causes:

Commonest Causes: who puts COMMONEST? Most common

Prehepatic:

Congenital absence or abnormality of the portal vein.

Thrombosis of the portal vein.

Obstruction of the Portal vein.

IntraHepatic

Cirrhosis.
Schistosomiasis.

PostHepatic

Constrictive pericarditis.
Tricuspid valvular incompetence.

Other detail causes:

Extrahepatic obstruction of portal vein and its tributaries
- Congenital absence or abnormality of portal vein
- Portal vein thrombosis *
  - Idiopathic
  - Umbilical and portal sepsis
  - Malignancy
  - Pancreatitis
  - Hypercoagulable states
- Splenic vein thrombosis
Hepatic venous outflow obstruction (Postsinusoidal)
- Suprahepatic
  - Budd-Chiari syndrome *
  - Constrictive pericarditis
  - Right heart failure
  - Smaller hepatic veins and venules
- Veno-occlusive disease *
- Sclerosing hyaline necrosis
Hepatic causes
- Presinusoidal
  - Schistosomiasis *
  - Idiopathic portal hypertension
  - Primary biliray cirrhosis
  - Sarcoid
  - Myeloproliferative disease
  - Fibropolycystic disease
- Sinusoidal
  - Cirrhosis *
  - Chronic active hepatitis *
  - Alcoholic hepatitis and Fatty liver *
Increased hepatic blood flow (rare causes)
- Tropical splenomegaly syndrome
- Hematological and other conditions with massive splenomegaly
- Hepato-portal arteriovenous fistula

Pathogenesis:

The portal venous system lacks valves and hence resistance at any level between the right side of heart and splanchnic vessels results in retrograde transmission elevated pressure.
Increased resistance can occur at 3 levels

Presinusoidal

anatomically outside the liver but at a functional level proximal to the hepatic sinusoids

Sinusoidal

Occurring within the liver parenchyma, e.g. Cirrhosis

Postsinusoidal

Occurring outside the liver at the level of the hepatic veins

NB!
Cirrhosis is the most common cause of portal hypertension.
Portal vein obstruction the 2nd most common cause.
Presinusoidal portal obstruction accounts for nearly 20% of all cases and they are nearly always young and often a child.

Clinical features:

Some Commonest features:

ABCDE

A: Ascites.
B: Bleeding (hematemesis, piles).
C: Caput medusae.
D: Diminished liver.
E: Enlarged spleen.

Major clinical manifestations include

Bleeding from gastroesophageal varices
Splenomegaly with hypersplenism
Ascites
Acute and chronic hepatic encephalopathy

All these features are related, at least in part, to the development of portal-systemic collateral channels.

Investigations:

Blood examination:

Anemia.

Usually MicroCytic Hypochromic.
(Almost inevitable in Portal Hypertension)

Leukopenia and Thrombocytopenia:

Due to splenomegaly and hypersplenism of hypertension

Coagulation defect:

Due to thrombocytopenia and impaired synthesis of coagulation factors by damaged liver (Factor V, VII and X).

Liver function test:

LFT tests may be entirely normal in the presence of established cirrhosis.

Endoscopy:

Upper gastrointestinal endoscopy is the mostly reliable technique.
It shows the oesophageal varix and bleeding point.
- Oesophageal varix are seen as dilated longitudinal zigzag running.
Excludes peptic ulcer as a source of bleeding in a patient with documented varices

Radiology:

Upper gastrointestinal Barium:
- It can demonstrate oesophageal varices as filling defect in lower end of the oesophagus.
- Not very accurate in the diagnosis of gastric varices but can detect Peptic ulcers disease.
- Can be used when endoscopy is not available.

Liver Angiography:

Two main advantages:

Measurement of Portal pressure.
Visualization of abnormal venous anatomy in case of portal hypertension.

NB! Anemia, Leukopenia and Thrombocytopenia may also occur due to bone marrow depression occurred in Alcoholic cirrhotic

Diagnosis:

H/o liver disease and other clinical features of portal hypertension – in maximum number of cases
Rarely – portal venous pressure is measured by
- Percutaneous transhepatic skinny needle catheterization
- Transjugular cannulation of hepatic vein
- Both free and wedged hepatic venous pressure should be measured
- WHVP will be raised in Sinusoidal and Postsinusoidal portal hypertension while it will be normal in Presinusoidal Postal hypertension
- Rarely – Mesenteric and hepatic angiography may be necessary

Management

Resuscitation.
Diagnosis.
Specific treatment.
Treatment of Complications.

Resuscitation of the patient.

Same as Upper G.I tract bleeding.

NB!
- In Coagulation abnormalities: Fresh frozen plasma and platelets.
  - Avoid Saline.
Regular Vitals recording with Input/Output charting.
Careful with giving sedation in hepatic cases:
- e.g. Valium I.V
- e.g.Librium in Alcohol withdrawals.
Purgatives and enema.
- Reducing Ammonia before Encephalopathy - good choice.
Gastric acid secretion should be decreased.
- e.g. Cimetidine.
If Ascites:
- Strict low-salt diet.
- Spirolactone.
- Paracentasis.

Diagnosis:

Endoscopy is the main diagnostic tool.
- Before endoscopy Lavage through Ewaled tube is good if too much bleeding.
- Peptic Ulcer bleeding should be excluded.
  - NB!
    - Bleeding due to gastritis in patients with portal hypertension should be managed as variceal bleeding.

Specific Treatment:

Vasopressin (Pitressin):

Controls variceal bleeding by splanchnic vasoconstriction.

In acute bleeding:
- 20 units in 100ml of 5% Dextrose I.V over 20 minutes.
- Followed by a continuous infusion of 0.4 unit/minute.

Side effects:

Cramping pain Abdomen.
Myocardial Ischemia.
Raynaud's syndrome.

Non-Selective Beta-Blockers:

e.g. Propranolol.
- Prevents recurrent bleeding.
NB!
- Non-Selective Beta-Blockers should not be used in decompensated liver disease, and if variceal bleeding occurs during treatment, the failure to mount a sympathetic nervous system response to blood volume loss may precipitate rapid circulatory collapse.

Endoscopic Variceal Sclerosis:

Revolution in variceal hemorrhage by decreasing mortality rate.

In acute bleeding:

- Intravariceal injection is preferred.
  - e.g. 2.5% sodium morrhuate followed by ethanolamine oleate.

NB>!

Complication:

Retrosternal Chest pain due to phlebitis.
Local microperforation. Major perforation is rare.
Pulmonary effusion with fever.

Balloon temponade:

Temporary method to control bleeding.

Should be used for Short time as possible.
NB!
Oesophageal balloon should be inflated to 45mmHG if the gastric balloon does not control bleeding.
In good risk patient: Avoiding it will be a good choice and urgent shunt operation will be a good choice.

Complications:

Aspiration is common.
Can produce more bleeding by sustained pressure on ulceration of gastric and oesophageal mucosa.
Oesophageal rupture is rare but if occurs it is FATAL.
Transhepatic Visceral Embolisation:
- It is a temporary step in poor risk patients who continues to bleed following Pitressin therapy, sclerotherapy and tamponade.
- It Occludes the feeding vessels.
- It Causes thrombosis within oesophageal varices.

Treatment of complication:

Shock:
- Barbiturates.
- Fresh blood transfusion.
Clotting problem:
- Vitamin K.
- Fresh blood transfusion.

Encephalopathy:

Continuous gastric lavage.
Magnesium sulphate and neomycin (500mg STAT then 2 hourly) through Sangstaken tube.
High bowel wash.

Liver failure:

Plenty of Carbohydrate Per OS.
Low Fat diet.

Ascites:

Strict Low salt diet
Diuretics.

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