Portal vein and portal hypertension
Portal Vein, Portal Hypertension and Portosystemic Anastomoses
Portal vein anatomy for FCPS Part 1: formation behind the pancreatic neck, tributaries, course in the lesser omentum and the portosystemic anastomoses. Explains varices, caput medusae, hypersplenism and why liver lesions favour the right lobe.
What a portal system is
- A portal system carries blood from one capillary bed to a second capillary bed before it returns to the heart. The hepatic portal system runs from gut capillaries to liver sinusoids; the hypophyseal portal system runs from the median eminence of the hypothalamus to the anterior pituitary (there is no portal link to the posterior pituitary).
- The portal vein has no valves, so pressure is transmitted freely backwards through all tributaries when flow through the liver is blocked.
Formation and course
- Formed behind the neck of the pancreas at about L1/L2 by the superior mesenteric vein and splenic vein. The inferior mesenteric vein usually joins the splenic vein (sometimes the SMV or the angle between them).
- Passes up behind the first part of the duodenum, then in the free edge of the lesser omentum, posterior to the bile duct (right) and hepatic artery (left), forming part of the anterior wall of the epiploic foramen.
- Divides at the porta hepatis into right and left branches, then into interlobular veins at the portal triads.
- Tributaries joining directly: left gastric (coronary) vein, right gastric, superior pancreaticoduodenal, cystic and paraumbilical veins.
- Liver blood flow: about 75% portal vein, 25% hepatic artery; each provides roughly half the oxygen.
Streaming within the portal vein
- Blood from the SMV and splenic vein mixes poorly. SMV blood streams mainly to the right lobe; splenic and IMV blood tends to reach the left lobe.
- The right lobe therefore receives most of the blood from the caecum and ascending colon, where *Entamoeba histolytica* invades. This, with its larger volume, is why amoebic liver abscess (and many colonic metastases) favour the right lobe. Most patients with amoebic abscess have no current dysentery.
Liver units around the portal triad
| Unit | Centre | Periphery | Emphasises |
|---|---|---|---|
| Classic hepatic lobule | Central vein | Portal triads at the corners of a hexagon | Blood flow towards the central vein |
| Portal lobule | Portal triad | Three central veins at the corners of a triangle | Bile flow (exocrine) |
| Hepatic acinus (Rappaport) | Line joining two triads | Two central veins at the ends of a diamond | Oxygen zones 1–3; zone 3 most vulnerable to hypoxia and paracetamol |
Portosystemic anastomoses
| Site | Portal side | Systemic side | Result in portal hypertension |
|---|---|---|---|
| Lower oesophagus | Left gastric vein | Oesophageal veins draining to azygos | Oesophageal varices: haematemesis, often fatal |
| Umbilicus | Paraumbilical veins (with ligamentum teres) | Superficial and inferior epigastric veins | Caput medusae |
| Anorectal junction | Superior rectal vein | Middle and inferior rectal veins | Anorectal varices |
| Retroperitoneum | Colic veins, splenic vein | Renal, lumbar, gonadal veins (veins of Retzius) | Bleeding at retroperitoneal surgery |
| Bare area of liver | Small portal radicles | Phrenic and intercostal veins | Minor collaterals |
- The vein that dilates in portal hypertension and feeds oesophageal varices is the left gastric vein; bleeding varices are veins, not the hepatic artery.
- In caput medusae, flow in the dilated veins radiates away from the umbilicus. In IVC obstruction, the dilated flank veins below the umbilicus carry blood upwards.
Haemorrhoids are not portal varices
- Internal haemorrhoids are enlarged anal cushions at 3, 7 and 11 o'clock. Their bright red blood comes from arteriovenous communications fed by the superior rectal artery.
- They are not more common in portal hypertension; true anorectal varices are a separate, less common finding.
Causes of portal hypertension
| Level | Examples |
|---|---|
| Prehepatic | Portal vein thrombosis (neonatal umbilical sepsis, pancreatitis, thrombophilia); splenic vein thrombosis gives left-sided portal hypertension with isolated gastric varices |
| Hepatic, presinusoidal | Schistosomiasis (eggs in portal venules), non-cirrhotic portal fibrosis |
| Hepatic, sinusoidal | Cirrhosis: commonest cause of oesophageal varices (in Pakistan largely from hepatitis B and C) |
| Posthepatic | Budd–Chiari (hepatic vein thrombosis), constrictive pericarditis, right heart failure |
- Pressure: normal hepatic venous pressure gradient is 1–5 mmHg; above 5 mmHg is portal hypertension; 10 mmHg or more is clinically significant (varices form); varices bleed when it exceeds about 12 mmHg.
Consequences
- Varices: oesophageal, gastric, anorectal, umbilical.
- Congestive splenomegaly with hypersplenism: the large spleen pools platelets (normally about one-third of the platelet mass; much more when enlarged). Thrombocytopenia with normal marrow and normal platelet lifespan is due to pooling, not destruction.
- Ascites: raised sinusoidal pressure, hypoalbuminaemia and secondary hyperaldosteronism; high serum-ascites albumin gradient (≥ 11 g/L).
- Hepatic encephalopathy: ammonia and other gut toxins bypass hepatic clearance.
- Portal hypertensive gastropathy.
Management of variceal bleeding
- Resuscitate; terlipressin (or octreotide) to constrict splanchnic vessels; prophylactic antibiotics; urgent endoscopy with band ligation (cyanoacrylate glue for gastric varices).
- Balloon tamponade (Sengstaken–Blakemore) as a bridge; TIPS (transjugular intrahepatic portosystemic shunt, from a hepatic vein to a portal branch) for refractory bleeding.
- Prevention: non-selective beta-blocker (propranolol, carvedilol) or banding. Surgical portocaval shunts lower pressure but worsen encephalopathy.
Remember Left gastric to azygos at the oesophagus, paraumbilical to epigastric at the umbilicus, superior rectal to middle and inferior rectal at the anus.
Exam trap The portal vein lies behind the bile duct and hepatic artery in the lesser omentum, not in front.
Exam trap Isolated gastric varices with a normal liver suggest splenic vein thrombosis.
How FCPS asks about this
- Formation of the portal vein: SMV plus splenic vein behind the neck of the pancreas; IMV joins the splenic vein.
- Vein feeding bleeding oesophageal varices: left gastric vein draining against azygos tributaries.
- Portocaval pair at the umbilicus: paraumbilical veins with superficial epigastric veins (caput medusae).
- Amoebic abscess in the right lobe: streaming of SMV blood to the right lobe.
- Low platelets with splenomegaly: splenic pooling (hypersplenism).
- Commonest cause of varices: cirrhosis; schistosomiasis is the classic presinusoidal cause.
- Hepatic lobule versus portal acinus: central vein at the centre of the classic lobule; triad at the centre of the portal lobule.
Test yourself on this topic
5 of the 23 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A 52-year-old man with hepatitis C cirrhosis has a transjugular measurement of the hepatic venous pressure gradient. Which of the following values defines clinically significant portal hypertension, at which varices can form?
Answer: 10 mmHg or more
The hepatic venous pressure gradient (wedged minus free hepatic venous pressure) estimates sinusoidal portal pressure. Normal is about 1–5 mmHg; above 5 mmHg is portal hypertension. At 10 mmHg or more it is clinically significant: varices and ascites can develop. Variceal bleeding usually needs about 12 mmHg or more, and values of 20 mmHg or more during a bleed predict a poor outcome.
HVPG thresholds
- Normal: 1–5 mmHg
- > 5: portal hypertension
- ≥ 10: clinically significant, varices
- ≥ 12: bleeding; ≥ 20: poor outcome
Remember Five is abnormal, ten makes varices, twelve makes them bleed.
Exam trap Portal hypertension begins above 5 mmHg, but varices need 10 or more.
Why the other options are wrong
- 5 mmHg or more Upper limit of normal; above this is portal hypertension.
- 3 mmHg or more Within the normal range.
- 20 mmHg or more Predicts failure to control bleeding.
- 30 mmHg or more Not a defining threshold.
A man with cirrhosis keeps rebleeding from oesophageal varices despite banding and terlipressin. A radiologist creates a channel through the liver. Which two vessels does this connect?
Answer: Hepatic vein and portal vein
A transjugular intrahepatic portosystemic shunt (TIPS) is placed through the internal jugular vein into a hepatic vein, then through liver tissue into a branch of the portal vein, and held open with a stent. Portal blood bypasses the high-resistance cirrhotic liver into the systemic circulation, lowering portal pressure and variceal bleeding. Hepatic encephalopathy can worsen because ammonia bypasses the liver.
TIPS
- Via internal jugular
- Hepatic vein to portal vein
- Lowers portal pressure
- Risk: encephalopathy
Remember TIPS goes through the liver, not around it.
Exam trap Hepatic encephalopathy after TIPS reflects blood bypassing the liver.
Why the other options are wrong
- Splenic vein and left renal vein That is a surgical distal splenorenal shunt.
- Portal vein and inferior vena cava outside the liver That is a surgical portacaval shunt.
- Hepatic artery and portal vein Would increase portal pressure.
- Left gastric vein and azygos vein These already connect as a natural varix route.
A 40-year-old man has painless bright red blood on the toilet paper after defecation. Proctoscopy shows enlarged anal cushions at 3, 7 and 11 o'clock. He has no liver disease. What best explains why the blood is bright red?
Answer: Arteriovenous communications in the cushions
Haemorrhoids are enlarged, displaced anal vascular cushions, not varicose veins. The cushions contain a submucosal plexus with direct arteriovenous communications from the terminal branches of the superior rectal artery. Bleeding from this plexus is therefore oxygenated, bright red and is seen on the paper or in the pan. Anorectal varices in portal hypertension are a separate condition and do not cause haemorrhoids more often.
Internal haemorrhoids
- Enlarged anal cushions
- At 3, 7, 11 o'clock (lithotomy)
- Arteriovenous communications: bright red blood
- Not varices; not caused by portal hypertension
Remember Cushions bleed arterial-looking blood.
Exam trap Haemorrhoids are not more common in portal hypertension.
Why the other options are wrong
- Rupture of portosystemic varices Anorectal varices are separate and he has no liver disease.
- Bleeding from the inferior rectal veins External plexus; internal haemorrhoids are above the line.
- Ulceration of anal canal squamous skin Fissure or ulcer pain would be present.
- Mixing with acidic rectal mucus Mucus does not change the colour of blood.
A 64-year-old man has an adenocarcinoma of the upper anal canal, 1 cm above the pectinate line. Staging CT shows several liver metastases but no lung lesions. Through which venous route did the tumour most likely reach the liver?
Answer: Superior rectal vein to the portal system
The pectinate line separates the endoderm-derived upper anal canal from the ectoderm-derived lower canal, and venous, lymphatic and nerve supply all change across it. Above the line, veins drain mainly through the superior rectal vein to the inferior mesenteric vein and then the portal vein, so tumour cells reach the liver first. Below the line, the inferior rectal veins drain to the internal pudendal and internal iliac veins (systemic), so spread goes to the lungs. Lymph above the line goes to the internal iliac nodes, and below it to the superficial inguinal nodes.
Pectinate line
- Above: superior rectal vein to portal (liver)
- Below: inferior rectal vein to systemic (lungs)
- Lymph above: internal iliac; below: superficial inguinal
- Above: painless; below: painful
Remember Above the line, blood goes to the liver.
Exam trap Tumour site relative to the pectinate line predicts liver versus lung spread.
Why the other options are wrong
- Inferior rectal vein to the internal iliac Systemic drainage from below the line; spreads to the lungs.
- Middle rectal vein to the internal iliac Systemic; would favour lung spread.
- Vertebral venous plexus of Batson Carries prostatic and pelvic tumours to the spine.
- Paraumbilical veins to the portal vein Drain the anterior abdominal wall, not the anal canal.
A 40-year-old man with cirrhosis and portal hypertension has a spleen palpable 8 cm below the costal margin. His platelets are 55 × 10⁹/L with normal marrow and a normal platelet lifespan. Which of the following is the main cause of the low platelets?
Answer: Pooling of platelets in the spleen
Normally about one-third of the circulating platelet mass is held in the spleen and exchanges freely with blood. In an enlarged, congested spleen this pool rises greatly, so fewer platelets circulate even though production and survival are normal. In cirrhosis, reduced hepatic thrombopoietin production adds to this. Splenectomy or reducing portal pressure raises the count. Immune destruction would shorten platelet lifespan.
Hypersplenism
- Normal spleen holds one-third of platelets
- Big spleen pools much more
- Normal marrow and lifespan
- Cirrhosis also lowers thrombopoietin
Remember Big spleen hides the platelets.
Exam trap Thrombocytopenia from pooling does not mean platelets are being destroyed.
Why the other options are wrong
- Marrow failure from alcohol The marrow is normal.
- Immune destruction of platelets Lifespan is normal, so destruction is not the main cause.
- Consumption in DIC Would also cause clotting abnormalities and fragments.
- Loss of thrombopoietin receptors Not a recognised cause.
Where this sits in the CPSP syllabus
- Paper 1: Abdomen, Portal vein and portosystemic anastomoses
- Surgery & Allied, Paper 2: Abdomen, Portal vein and portosystemic anastomoses
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