Help! - Portosystemic shunt vs portal venous congestion

Discussion in 'Medical Students - MD' started by Ezekiel20, Jul 27, 2006.

  1. Ezekiel20

    Ezekiel20 Resident
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    Ok, so this forum likes to discuss issues related to studying medicine, rather than discussing medicine.. So I'm not expecting an enthusiastic response to this question, but here it goes anyway.

    I could ask my profs, but that means I'll have to wait til next week (and I'd rather know sooner than later..)

    I've been trying to understand portosystemic shunts (I mean the acquired pathology due to portal hypertension, NOT the surgical procedure also known as TIPSS).

    I've consulted 3 textsbooks and numerous websites, but the issue is still not resolved to my liking.

    So, basically portosystemic shunts are caused by portal hypertension, which in turn is caused by cirrhosis (the major cause, among other causes).

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    Robbins basic pathology says this (7th ed, p600):

    Portosystemic shunts

    With the rise in portal system pressure, bypasses develop wherever the systemic and portal circulation share capillary beds. Principal sites are veins around and within the rectum (hemorrhoids), the cardioesophageal junction(esophageal varices), the retroperitoneum, and the falciform ligament of the liver (involving periumbilical and abdominal wall collaterals).

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    Harrison's says:

    The major clinical manifestations of portal hypertension include hemorrhage from gastroesophageal varices, splenomegaly with hypersplenism, ascites, and acute and chronic hepatic encephalopathy. These are related, at least in part, to the development of portal-systemic collateral channels. The absence of valves in the portal venous system facilitates retrograde blood flow from the high-pressure portal venous system to the lower-pressure systemic venous circulation. Major sites of collateral flow involve the veins around the cardioesophageal junction (esophagogastric varices), the rectum (hemorrhoids), retroperitoneal space, and the falciform ligament of the liver (periumbilical or abdominal wall collaterals). Abdominal wall collaterals appear as tortuous epigastric vessels that radiate from the umbilicus toward the xiphoid and rib margins (caput medusae).

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    So, both texts are talking about the same thing. Portal hypertension causes a backward congestion, so that all the veins that contribute to the portal vein engorge with blood (varices), some of which may burst. Simple enough.

    Robbin's calls this phenomenon a 'portosystemic shunt' and says that there are 'bypasses'.

    But how is this phenomenon a 'shunt', and where is the 'bypass'? For me, a shunt is when there is an abnormal passage between two points in the vasculature, so that it bypasses its normal route and takes the shortcut, causing various problems in doing so (e.g. right-to-left shunt of blood across a septal defect in the heart).

    Harrison's calls it a 'portal-systemic collateral channel', implying that they are new vessels formed in response to the increased pressure. But where do these new vessels form?

    To me, it seems like what is really happening is that there is a portal venous congestion, leading to engorgement of veins that lie downstream to the portal vein. I can't see any way in which there are any 'shunts', or 'collateral vessel formation' happening.

    Maybe I'm missing the point - so if you understand this better than I do, please share your insight.

    (and also..)

    I googled the term 'portosystemic shunt', and found a whole heap of websites on veterinary medicine (apparently some breeds of dogs commonly have this problem). It defines the term as 'when portal blood bypasses the liver and goes directly to the systemic venous circulation (inferior vena cava)'.

    Now this definition makes sense, but it would not explain any of the symptoms like formation of varices in the esophagus, abdominal wall and rectum. According to the above definition, the pressure in the IVC would increase, and cause congestion in the veins downstream to it (renal veins, common iliac, etc).

    In conclusion, my question boils down to this:

    => The phenomenon described by both Robbins and Harrison's makes sense logically (portal hypertension leads to downstream congestion), but I don't see anyway in which this is a 'shunt', or 'collateral blood flow'. Please shed some light on this issue.

    Thanks in advance
     
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  3. njbmd

    njbmd Guest
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    Hi there,
    Try consulting a medical dictionary, which would have revealed the following:
    Shunt, Bypass 1. To bypass or divert 2. A bypass or diversion.

    Shunt as it applies to the vascular system means a direct connection between the arterial and venous circulation that "bypasses" the capillary bed. To that end, the sites of portosystemic (portocaval) shunts are connections between the portal circulation and the systemic (caval) circulation that "bypass" a capillary bed.

    If you have high pressre in part of the portal circulation i.e. a cirrhotic liver, you tend to have enlargements at the points where the portal system directly connects with the systemic venous system i.e esophageal varices, hemorrhoids, capute medusae and ascites i.e. weeping of fluid from the surface of the liver into the peritoneal cavity.

    I hope that this simplified explanation helps

    njbmd :)
     
  4. Ezekiel20

    Ezekiel20 Resident
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    Thanks for the input

    I actually managed to answer my own question a couple of hours after I posted it.

    It's pretty much like you said, and the answer lies in the anatomy.

    [​IMG]

    Para-umbilical, rectal and esophageal areas apparently have an alternative systemic venous drainage apart from the usual portal vein drainage, and when one has increased pressure, blood is drained by the alternative, systemic veins.

    It's funny how neither Robbins nor Harrison's directly explained this, but rather talked around it.

    Thanks again
     

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