Systemic-portal anastomoses are venous communications between tributaries of the hepatic portal venous system and veins of the systemic circulation. Major sites occur around the lower esophagus, rectum and anal canal, umbilicus, and retroperitoneal gastrointestinal organs. These communications become clinically important when portal venous pressure rises.
Systemic-portal anastomoses, also called portosystemic anastomoses or portocaval anastomoses, are venous communications between tributaries of the hepatic portal venous system and tributaries of the systemic venous circulation. These connections provide potential alternative routes through which venous blood can pass between the two circulations.
Under normal conditions, most venous blood from the abdominal gastrointestinal tract, spleen, pancreas, and gallbladder enters the hepatic portal system and passes through the liver before reaching the systemic circulation. When resistance to portal blood flow increases, however, blood may be redirected through pre-existing systemic-portal communications.
The major clinically important sites of systemic-portal anastomosis occur around the lower esophagus, rectum and anal canal, umbilicus, and retroperitoneal regions. Enlargement of these collateral channels can produce characteristic manifestations of portal hypertension, including esophageal and gastric varices, paraumbilical collateral veins, and rectal varices.
Understanding systemic-portal anastomoses requires distinction between the portal and systemic venous systems.
The hepatic portal system collects venous blood from much of the gastrointestinal tract and associated abdominal organs and transports it to the liver. The systemic venous system returns blood from the body directly toward the right atrium through the superior and inferior venae cavae and their tributaries.
The hepatic portal vein carries nutrient-rich venous blood toward the liver.
Its major tributary territories include:
The hepatic portal vein is formed primarily by the union of the superior mesenteric vein and splenic vein.
The inferior mesenteric vein commonly drains into the splenic vein, although its termination is variable.
The systemic venous circulation returns blood toward the heart without first passing through the hepatic sinusoids.
Important systemic pathways involved in portosystemic communications include tributaries of the azygos system, inferior vena cava, abdominal wall veins, and pelvic systemic veins.
A systemic-portal anastomosis occurs where a vein belonging to the portal circulation communicates with a vein belonging to the systemic circulation.
These communications are normally present as relatively small venous channels. They become substantially more important when portal venous pressure rises and collateral flow increases.
The principal anatomical sites of systemic-portal anastomoses include:
| Site | Portal Side | Systemic Side |
|---|---|---|
| Lower esophagus | Left gastric vein | Esophageal veins draining toward azygos system |
| Rectum | Superior rectal vein | Middle and inferior rectal veins |
| Umbilicus | Paraumbilical veins | Superficial veins of anterior abdominal wall |
| Retroperitoneal regions | Portal tributaries of gastrointestinal organs | Retroperitoneal systemic veins |
One of the most clinically important systemic-portal communications occurs in the region of the lower esophagus and gastric cardia.
Portal tributaries associated with the left gastric vein communicate with esophageal veins that drain into the azygos venous system.
The principal portal vessel involved is the left gastric vein.
The left gastric vein drains the lesser curvature of the stomach and receives veins from the lower esophagus before draining into the portal venous system.
Esophageal veins communicate with veins draining toward the azygos and hemiazygos systems.
The azygos system ultimately drains into the superior vena cava.
Within and around the wall of the lower esophagus is a network of venous channels that allows communication between portal and systemic venous territories.
When portal pressure rises, increased blood flow through these channels can cause them to enlarge substantially.
Esophageal varices are abnormally dilated veins, particularly within the submucosal venous plexus of the distal esophagus, associated most importantly with portal hypertension.
Because these veins have relatively thin walls and are exposed to increased venous pressure, they can rupture and cause severe upper gastrointestinal hemorrhage.
Portosystemic collateral circulation can also produce gastric varices, particularly near the gastric cardia and fundus.
Their venous anatomy can involve gastric tributaries of the portal system and collateral pathways connecting with systemic veins.
| Component | Vessel or Pathway |
|---|---|
| Portal side | Left gastric vein and associated tributaries |
| Systemic side | Esophageal veins toward azygos and hemiazygos systems |
| Systemic destination | Superior vena cava |
| Clinical manifestation | Esophageal and related gastric varices |
Another important portosystemic communication occurs within the venous networks of the rectum and anal canal.
The superior rectal venous territory belongs to the portal system, while the middle and inferior rectal venous territories drain predominantly toward the systemic circulation.
The superior rectal vein represents the portal component of the rectal anastomosis.
It drains superiorly into the inferior mesenteric vein and therefore ultimately into the hepatic portal system.
The middle rectal veins drain portions of the rectum toward the internal iliac venous system.
They therefore form part of the systemic side of the rectal portosystemic communication.
The inferior rectal veins drain the inferior anal canal and surrounding region.
They drain through the internal pudendal veins toward the internal iliac veins and ultimately the inferior vena cava.
Venous plexuses within the rectal wall allow communication between superior, middle, and inferior rectal venous territories.
These connections form the anatomical basis of the rectal systemic-portal anastomosis.
Rectal varices are dilated portosystemic collateral veins involving the rectal venous plexus in the setting of portal hypertension.
They should be distinguished anatomically and clinically from ordinary hemorrhoidal disease.
Although both conditions involve veins of the anorectal region, rectal varices are not synonymous with hemorrhoids.
Hemorrhoids are vascular cushions of the anal canal that can become symptomatic for reasons unrelated to portal hypertension. Portal hypertension may produce collateral dilation of rectal veins, but it is not the usual cause of hemorrhoids.
| Component | Vessel or Pathway |
|---|---|
| Portal side | Superior rectal vein |
| Portal pathway | Inferior mesenteric vein toward portal system |
| Systemic side | Middle and inferior rectal veins |
| Systemic pathway | Internal iliac system toward inferior vena cava |
| Clinical manifestation | Rectal varices |
A third major site of systemic-portal communication occurs around the umbilicus.
Small paraumbilical veins associated with the ligamentum teres hepatis communicate with veins of the anterior abdominal wall.
The paraumbilical veins accompany the ligamentum teres within the free margin of the falciform ligament and communicate with the portal venous system.
They also communicate with veins surrounding the umbilicus.
Veins of the superficial anterior abdominal wall ultimately communicate with systemic venous pathways draining toward both the superior and inferior venae cavae.
These veins can enlarge when increased portal pressure drives blood through paraumbilical collateral channels.
The superficial epigastric veins are among the superficial abdominal wall veins that can participate in collateral drainage around the umbilical region.
They communicate with other superficial venous networks of the abdominal wall.
The thoracoepigastric veins form longitudinal venous channels along the lateral trunk and communicate with both superior and inferior systemic venous territories.
They may become more prominent when collateral circulation through the abdominal wall increases.
Caput medusae describes visibly dilated superficial veins radiating from the region of the umbilicus.
It can develop when portal hypertension produces increased collateral flow through paraumbilical and superficial abdominal wall veins.
| Component | Vessel or Pathway |
|---|---|
| Portal side | Paraumbilical veins |
| Anatomical route | Along ligamentum teres and falciform ligament |
| Systemic side | Superficial veins of anterior abdominal wall |
| Clinical manifestation | Dilated abdominal wall collaterals and caput medusae |
Systemic-portal communications also occur where portions of the gastrointestinal tract become secondarily retroperitoneal or lie adjacent to the posterior abdominal wall.
Portal tributaries draining these organs can communicate with systemic veins of the posterior abdominal wall and retroperitoneum.
Portal tributaries involved in these communications may arise from regions of the:
Small systemic veins of the posterior abdominal wall communicate with venous channels associated with retroperitoneal gastrointestinal structures.
These systemic pathways may ultimately drain toward lumbar veins, renal veins, the azygos system, or the inferior vena cava.
Retroperitoneal portosystemic collateral channels are sometimes referred to collectively as veins of Retzius.
They represent communications between veins of portal-drained abdominal viscera and systemic veins of the posterior abdominal wall.
Along the posterior surfaces of the ascending and descending colon, tributaries of the superior or inferior mesenteric venous systems may communicate with retroperitoneal systemic veins.
These pathways can enlarge as collateral channels in portal hypertension.
Venous tributaries from the duodenum and pancreas normally drain into the portal venous system through pancreaticoduodenal, splenic, and mesenteric pathways.
Because portions of these organs lie against the posterior abdominal wall, small communications with systemic retroperitoneal veins can occur.
| Component | Pathway |
|---|---|
| Portal side | Tributaries of mesenteric and related portal veins |
| Systemic side | Retroperitoneal and posterior abdominal wall veins |
| Important regions | Duodenum, pancreas, ascending and descending colon |
| Collateral channels | May include veins of Retzius |
Additional portosystemic communications may occur around the bare area of the liver, where small veins associated with hepatic and diaphragmatic territories can communicate.
These connections are less prominent in basic descriptions than the esophageal, rectal, paraumbilical, and retroperitoneal sites but contribute to the broader network of collateral venous pathways.
Portal hypertension is an abnormal elevation of pressure within the portal venous system.
As portal pressure increases, blood encounters greater resistance to normal passage through the portal circulation and liver. Pre-existing collateral channels between portal and systemic veins may consequently enlarge.
A collateral circulation is an alternative vascular route that allows blood to bypass an area of increased resistance or obstruction.
In portal hypertension, systemic-portal anastomoses can function as collateral pathways through which portal blood is redirected toward systemic veins.
The direction and volume of blood passing through these channels depend on pressure gradients between the portal and systemic circulations.
When portal pressure becomes substantially elevated, flow through collateral pathways toward lower-pressure systemic veins increases.
Although collateral vessels provide an alternative route for venous drainage, their enlargement can have important clinical consequences.
These include:
Portal hypertension can result from increased resistance at different levels of the portal circulation.
Causes can be broadly classified as:
Prehepatic portal hypertension results from obstruction before portal blood reaches the liver.
Examples include obstruction or thrombosis involving major portal venous channels.
Intrahepatic portal hypertension results from increased resistance to blood flow within the liver.
Cirrhosis is a major cause because structural remodeling and fibrosis alter the normal intrahepatic vascular architecture.
Posthepatic causes interfere with venous outflow after blood has traversed the liver.
Obstruction involving hepatic venous outflow or elevated pressure downstream from the liver can increase pressure transmitted back toward the portal circulation.
The lower esophageal anastomosis is particularly important because enlarged submucosal veins can rupture.
Bleeding from esophageal varices can result in substantial hematemesis and represents a major complication of portal hypertension.
Gastric collateral veins can enlarge independently or together with esophageal varices.
Fundal gastric varices may be particularly associated with venous pathways involving the short gastric and splenic venous territories.
Increased flow through paraumbilical collateral pathways can produce visible dilation of superficial abdominal wall veins.
The pattern of venous enlargement depends on the collateral pathways recruited and the direction of blood flow.
Increased collateral flow between superior rectal and systemic rectal venous territories can produce rectal varices.
These enlarged collateral vessels represent a direct consequence of the anatomical communication between portal and systemic venous networks.
Retroperitoneal collateral veins can become markedly enlarged in chronic portal hypertension.
Many of these vessels are internal and therefore are identified primarily by cross-sectional imaging or venographic studies rather than external examination.
Some portal collateral blood ultimately reaches the superior vena cava.
The classic example is the esophageal route, where blood can pass from the left gastric venous territory into esophageal veins and then through the azygos system to the superior vena cava.
Other collateral pathways ultimately drain toward the inferior vena cava.
Examples include rectal communications through internal iliac venous pathways and retroperitoneal communications with lumbar and other systemic veins.
When blood bypasses hepatic circulation through collateral vessels or a deliberately created shunt, substances normally processed by the liver can enter the systemic circulation more directly.
This physiological consequence is distinct from the purely mechanical effect of reducing pressure within the portal system.
| Type | Description |
|---|---|
| Natural anastomosis | Pre-existing communication between portal and systemic veins |
| Pathologically enlarged collateral | Natural communication enlarged because of abnormal pressure gradients |
| Therapeutic shunt | Artificially created pathway designed to decompress the portal circulation |
Surgical portosystemic shunts can be constructed to divert portal venous blood into the systemic venous circulation.
Several anatomical configurations have historically been used depending on the underlying disease and vascular anatomy.
A transjugular intrahepatic portosystemic shunt, commonly abbreviated TIPS, creates an artificial channel within the liver between the portal venous circulation and hepatic venous outflow.
The purpose is to reduce the pressure gradient across the portal circulation by providing a lower-resistance pathway for blood flow.
Collateral vessels enlarge when a sustained pressure gradient favors flow from the high-pressure portal system toward lower-pressure systemic veins.
The resulting collateral circulation can partially decompress the portal system but may itself produce significant complications.
Portosystemic collateral vessels can be demonstrated using several imaging techniques.
These include:
Doppler ultrasound can evaluate blood flow within the portal vein and major abdominal vessels.
It can demonstrate changes in flow direction, velocity, portal venous patency, and some collateral vessels.
Contrast-enhanced CT can demonstrate dilated collateral veins throughout the abdomen and lower thorax.
It is particularly useful for mapping paraesophageal, perigastric, retroperitoneal, and abdominal wall collateral pathways.
MRI and MR venographic techniques can demonstrate portal venous anatomy and collateral vessels without ionizing radiation.
They can provide detailed information about the portal vein, splenic vein, mesenteric veins, hepatic vasculature, and collateral pathways.
Upper gastrointestinal endoscopy provides direct visualization of esophageal and gastric varices protruding into the gastrointestinal lumen.
Endoscopy therefore assesses the luminal consequences of collateral venous enlargement rather than the entire portosystemic vascular network.
Venographic techniques can demonstrate the anatomy and direction of flow within portal and collateral venous channels.
Detailed vascular mapping can be particularly important when planning interventional procedures.
Rupture of an esophageal varix can produce severe gastrointestinal bleeding because the dilated submucosal veins are exposed to elevated pressure and have relatively fragile walls.
The anatomical location of these veins in the distal esophageal wall explains why bleeding enters the gastrointestinal lumen.
Gastric varices can also rupture and produce significant upper gastrointestinal bleeding.
Their vascular anatomy differs according to their location and the collateral pathways responsible for their formation.
In portal hypertension, venous channels associated with the ligamentum teres and falciform ligament can become markedly enlarged.
Imaging may demonstrate a prominent paraumbilical vein extending from the left portal venous territory toward the anterior abdominal wall.
Not every connection between two abdominal veins is a systemic-portal anastomosis.
For the term to apply, one side of the communication must belong to the portal venous circulation and the other must drain through the systemic venous circulation.
Communications between two veins that both ultimately drain into the portal system are portal-portal communications, not systemic-portal anastomoses.
The distinction depends on the ultimate drainage territory of each vessel.
Caval-caval anastomoses connect systemic venous territories, such as tributaries of the superior and inferior venae cavae.
They do not involve the portal venous system and therefore are anatomically distinct from portosystemic communications.
| Anastomosis | Systems Connected |
|---|---|
| Systemic-portal | Portal circulation and systemic venous circulation |
| Portal-portal | Two portal venous territories |
| Caval-caval | Systemic venous territories, often SVC and IVC tributaries |
| Location | Portal Vessel | Systemic Vessel | Potential Manifestation |
|---|---|---|---|
| Lower esophagus | Left gastric vein | Esophageal veins toward azygos system | Esophageal varices |
| Rectum | Superior rectal vein | Middle and inferior rectal veins | Rectal varices |
| Umbilicus | Paraumbilical veins | Superficial abdominal wall veins | Caput medusae and abdominal wall collaterals |
| Retroperitoneum | Mesenteric and related portal tributaries | Retroperitoneal systemic veins | Deep abdominal collateral veins |
| Site | Representative Collateral Route |
|---|---|
| Esophagus | Left gastric vein → esophageal veins → azygos system → SVC |
| Rectum | Superior rectal territory ↔ middle/inferior rectal veins → internal iliac system → IVC |
| Umbilicus | Portal territory → paraumbilical veins → superficial abdominal wall veins → systemic circulation |
| Retroperitoneum | Mesenteric tributaries ↔ retroperitoneal veins → lumbar/renal/caval pathways |
| Feature | Key Point |
|---|---|
| Definition | Communication between portal and systemic venous territories |
| Normal state | Usually relatively small venous communications |
| Major trigger for enlargement | Portal hypertension |
| Esophageal portal vessel | Left gastric vein |
| Esophageal systemic pathway | Azygos venous system |
| Rectal portal vessel | Superior rectal vein |
| Rectal systemic vessels | Middle and inferior rectal veins |
| Umbilical portal vessels | Paraumbilical veins |
| Retroperitoneal collaterals | Communications between portal visceral and systemic posterior abdominal wall veins |
| Major clinical risk | Variceal hemorrhage |
Systemic-portal anastomoses form an important anatomical interface between the hepatic portal and systemic venous circulations. Although normally small, these communications provide potential alternative routes for venous return when resistance within the portal circulation increases.
The lower esophagus contains communications between the left gastric and azygos venous territories, the rectum contains communications between superior rectal and systemic rectal veins, the umbilical region connects paraumbilical veins with superficial abdominal wall veins, and retroperitoneal gastrointestinal structures communicate with systemic veins of the posterior abdominal wall.
In portal hypertension, increased flow through these pathways can enlarge the collateral veins. The resulting anatomy explains the development of esophageal and gastric varices, rectal varices, paraumbilical collateral veins, and deep retroperitoneal collaterals. These pathways are therefore important not only in normal venous anatomy but also in understanding the clinical manifestations, imaging findings, and interventional management of portal hypertension.