Tasty Morsels of Critical Care 073 | Hepatorenal syndrome

18 Sep

Welcome back to the tasty morsels of critical care podcast.

Following hot on the heels of tasty morsel number 72 on cardio renal syndrome is its partner in nephron injury: hepatorenal syndrome. This gets covered in a sub section of Oh’s manual chapter 44 on liver issues but there are a variety of other sources mentioned at the end that are worth a read.

It can be a little tricky to pin down this diagnosis. A lot of that comes because it is a “syndrome”, ie a collection of clinical findings that someone has put into a big bucket and mixed around without paying too much attention to hard core diagnostic information like histology or a true pathological diagnosis.

To start with we need context. We should have an AKI in the setting of advanced chronic liver disease and portal hypertension ie cirrhosis. But of course there are multiple reasons for AKI in this context so we have to work through them a little before the label of hepatorenal gets attached. Our friends in the international club of ascites (yes that’s a thing, i didn’t make it up) suggest that you need an AKI with a failure to respond to simple things like withdrawal of nephrotoxic agents, treatment of infection and, importantly a decent trial of albumin. You also have to exclude intrinsic renal diseases that lose protein and blood but this is usually fairly straightforward to exclude. However you can quickly see that a lot of this is pretty nebulous and it can be hard to really draw a line under. As such it’s fair to say that your patient may have several causes for their AKI in cirrhosis and hepatorenal may only be part of the problem.

To take hepatorenal per se, what’s the purported pathogenesis? Well we think that increasing portal venous pressures and cirrhosis leads to splanchnic vascular vasodilation. The vessels in our gut lose tone and we develop this chronic high output, low SVR state. This state of reduced pressure leads to activation of the RAAS causing increased resistance in the renal arteries (in distinction to the very low resistance state of the splanchnic vasculature). As such, perfusing pressure to the glomerulus falls and GFR falls. This is reflected in oliguria and the usual renal response to a crisis of hanging onto Na for all its worth with a urine Na typically <10 if you do go looking for it. In the background you’ve got all this chronic ascites that is adding to the compartment pressure in the abdomen making things worse. That’s the basic bedtime story version of the pathophys that i received, I understand there’s a competing theory where the chronic bacterial translocation of a leaky liver leads to a chronic inflammatory process buggering the kidneys but i digress.

At this stage, it’s worth noting that just like our cardiorenal syndrome we can split hepatorenal into a couple of types. This is all about timing of onset. The in-patient with a rapidly rising creatinine in the hospital setting is more likely to have type I or acute HRS while the stable out patient cirrhotic with a gradually rising creatinine is going to have the type II or chronic HRS.

HRS itself can be precipitated by the usual chronic liver disease decompensations – ie , bleeding, infection, SBP and also large volume paracentesces without appropriate albumin replacement.

How should we treat. First off an important reminder that cirrhosis is not a reversible pathology and if you’re decompensating then the only real treatment to turn the whole thing around is a transplant. All the rest of it is a little bit like rearranging the deck chairs on the Titanic. I don’t mean to imply that the deck chairs should not be rearranged; rearranging the deck chairs may well lead to some meaningful short term outcomes and quality of life improvement but the hole in the hull from the iceberg isn’t going to get any better without the transplant.

As mentioned in the diagnostic bit, they probably should’ve got some albumin. I don’t deny that albumin has a limited role in the ICU, gone are the days where we could make bold assertions about colloid osmotic pressures and how albumin was better than crystalloid. We studied it and it turns out it doesn’t seem to be any better than salty water. But i still think that in the livers it still has an important role and HRS is probably one of those scenarios. The data for its use in HRS is not exactly stellar, and no where near as good as it is say for albumin in ascites drainage in SBP where it has a mortality benefit.

I confess i have done the sneaky move “push the MAP up to 75 mmHg” for a few days to see if that makes a difference but i can’t say I’m standing on solid ground doing that but it does get a mention in the relevant UpToDate article.  Of course given that we have access to terlipressin in Ireland and the UK, these types of haemodynamic manipulations could even be done on the ward before rushing to commit yourself to CRRT and an ICU admission.

TIPS has been described to be helpful in improving renal function in HRS but only on a very limited basis so probably worth a discussion with your local liver experts but not something you can use evidence to make a compelling argument for.

If the HRS fails to respond to such therapies then the option of CRRT is usually raised. This will indeed replace the failing kidney but like many things in intensive care, there’s not much point in starting it if there’s no chance of reversibility. Some HRS may be in the context of something like acute alcoholic hepatitis where the chance of recovery of some hepatic function is reasonable and hence a trial of the CRRT while the liver settles is reasonable. In addition if the patient is already on the transplant list then keeping them going with CRRT pending the transplant would also be reasonable. However the more common scenario is the burnt out cirrhotic who is having increasing frequency of decompensations. The prognosis here is dismal and adding more machines at the end of life is probably not going to help. The tricky bit for us is teasing out so much of what we’ve discussed above, eg is this one of the many other eminently reversible causes of AKI in the context of cirrhosis or is this all driven by the chronic progressive liver failure. This as you’ve probably discovered by now is a core part of ICM and best learnt in the unit and on the wards rather than on the podcast.


ICA Guidelines

Deranged Physiology


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