Why is sinusoidal hypertension necessary for ascites?

[GomerPyle]

Uworld question regarding portal vein thrombosis says that you don't get ascites because there's no sinusoidal hypertension (obviously because the the obstruction is before the liver)..but I guess I don't understand the pathophysiology of ascities. So why is "sinusoidal hypertension" necessary for development of ascites?

Thanks!

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[dorster]

increased lymph formation in the liver causes "transcapsular weeping" which means the extra lymphatic fluid leaks out of the liver capsule so if the thrombus is in the portal vein the pressure will move backwards and it doesn't reach the liver. The pressure in the sinusoids of the liver is normal so theres no transcapsular weeping so theres no ascites.

 

[zhopv10]

^good point I wasn't thinking about that/had forgotten that before. The altered starling forces force more fluid into the space of disse where it is removed from by hepatic lymphatics via the hypoalbuminemia (robins says that normal hepatic lymph flow is 800-1000mL's per day and with cirrhosis that may reach 20L, wild!!). The other aspect to ascites/portal HTN that is commonly accepted (see up to date, surgwiki, etc) is basically the idea that the backing up of portal blood flow leads to dilation and increased flow through splanchnic collaterals. Now the kicker is that this leads to release of fairly local vasodilator that dilate the splanchnic vasculature and decrease the TPR. This then leads to compensatory increased CO activation of the renal RAAS and sodium and water retention leading to an overloaded state. Now uptodate mentions the fact that sinusoidal HTN/liver damage is required for ascites but unfortunately doesn't list a source so here is what I think: the other part of maintaining fluid in the vasculature and not in the abdomen is oncotic pressure (that is actually established I'm not hypothesizing yet haha). So I think that perhaps portal HTN itself is not enough of a factor to lead to ascites itself (since pre-sinusoidal pathology like a portal thrombosis clearly can lead to portal HTN) but you need the damage to the liver which deceases albumin production, decreases the intravascular oncotic pressure and leads to loss of fluid into the abdomen (where the pressure is already high so there is even more driving force). Just my 2 cents, hope it's helps.


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[zhopv10]

*oops sorry forgot a key thing there, so the release of the vasodilatory compounds is actually key in the splanchnic arterioles. This increases flow to the portal vasculature that is downstream this accentuating the problem. Sorry that wasn't clear above.


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[dorster]

^good point I wasn't thinking about that/had forgotten that before. The altered starling forces force more fluid into the space of disse where it is removed from by hepatic lymphatics via the hypoalbuminemia. The other aspect to ascites/portal HTN that is commonly accepted (see up to date, surgwiki, etc) is basically the idea that the backing up of portal blood flow leads to dilation and increased flow through splanchnic collaterals. Now the kicker is that this leads to release of fairly local vasodilator that dilate the splanchnic vasculature and decrease the TPR. This then leads to compensatory increased CO activation of the renal RAAS and sodium and water retention leading to an overloaded state. Now uptodate mentions the fact that sinusoidal HTN/liver damage is required for ascites but unfortunately doesn't list a source so here is what I think: the other part of maintaining fluid in the vasculature and not in the abdomen is oncotic pressure (that is actually established I'm not hypothesizing yet haha). So I think that perhaps portal HTN itself is not enough of a factor to lead to ascites itself (since pre-sinusoidal pathology like a portal thrombosis clearly can lead to portal HTN) but you need the damage to the liver which deceases albumin production, decreases the intravascular oncotic pressure and leads to loss of fluid into the abdomen (where the pressure is already high so there is even more driving force). Just my 2 cents, hope it's helps.


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that all might be true but the initial mechanism of ascites is liver cirrhosis which leads to sinusoidal hypertension and that is due to hepatic venous blockage secondary to liver cirrhosis aka fibrosis. The reason you would not get ascites if there is a thrombus in the portal vein is because its before the liver, that would be a blockage of blood trying to get from the portal venous system into the liver. Its the same reason why right heart failure alone wouldn't lead to pulmonary edema. The pressure buildup is moving backwards.

 

[zhopv10]

Agreed, I'm glad you pointed that out because looking back I definitely did not make my point clear (and it was a pretty terrible post in general haha). In my mind for some reason i was thinking the fluid was coming from the splanchnic vasculature into the abdomen (and it actually does somewhat, see Robbins, uptodate etc.) but for some reason I was thinking it did more. And so the point I was wanting to connect was if both sinusoidal and presinusoidal HTN lead to portal hypertension what's the difference, or what causes ascites in one and prevents it in the other? So anyway I meant to point out first off that your point was the key I was missing, the problem starts with the liver like you said and you get huge lymph output (which explains the decently high albumin count in fluid from ascites) and that pathology in the liver is of course the driving factor. My other point was to say I think the lower levels of albumin and the pathophysiology of portal HTN might accentuate the issues in the splanchnic vascular and contribute but it really shouldn't have been the focus of my post, just made things unclear (and pretty much wrong haha). Hopefully that clears things up a little bit, thank you for the clarification and pointing that out.


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