cases

[Hernandez]

So what you're saying is you weren't a bad enough dude to get a BAL! Lol.

Saw more than a few cases like that in fellowship. You just have to ride it out. I mean these folks just used to plain ass die. And this is probably a perfect case for the peanut gallery to see the difference between critical care and the basic resuscitation that happens in the ED.

I still have no takers on my bad liver bad lungs guy.

I'm serious too. Lol. How do I get him off a vent?!? Lol

I'm talking to cards about a potential PFO closure and I'm considering a chest tube even though I know it'll be hell getting it out.

And I'm probably going to try some sildenafil.

No one wants to consider transplant because the guy was drinking three months ago. So wah wah waaaaaahhhhhh.

PFO closure would be no bueno in this guy and could precipitate right heart failure. I'd reiterate fluid management will help you with oxygenation and you likely will need to dry him out till his kidneys aren't working, then dry him out some more, I hate liver, my one attending as a fellow would turn on the damn billboard screaming send me your cirrhotics when he was in the ICU.

You almost talked me into going into a Anesthisia forum style look at the size of my balls tirade...almost.

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[jdh71]

I was referring to pleurx in chest. I think the tunneling of the catheter keeps you from running into problems with leaking after removal like you get with a regular chest tube.

CT has almost nothing to do with diagnosing hepatopulmonary syndrome. The diagnosis is made by demonstrating intrapulmonary shunting in the setting of portal hypertension. This is very difficult to demonstrate with a concurrent right to left intracardiac shunt though could be done with a careful simultaneous right and left heart cath. It doesn't really matter in this case because you're not going to do anything about it anyway.

This is a pt that you might have to extubate on a high fio2 if you have addressed the pneumonia and effusion. The part of the hypoxemia that's due to intracardiac shunt and pulm vascular disease doesn't have anything to do with vent weaning. You can apply 100% fio2 without a ventilator.

Interesting case.

Portal hypertension has nothing to do with the diagnosis of hepatopulmonary syndrome. I know how to diagnose the entity definitively - the CT is consistent.

I appreciate the lecture more when you actually know what you're talking about.

And you are correct will need to extubate to high flow.

 

[jdh71]

PFO closure would be no bueno in this guy and could precipitate right heart failure. I'd reiterate fluid management will help you with oxygenation and you likely will need to dry him out till his kidneys aren't working, then dry him out some more, I hate liver, my one attending as a fellow would turn on the damn billboard screaming send me your cirrhotics when he was in the ICU.

You almost talked me into going into a Anesthisia forum style look at the size of my balls tirade...almost.

His intravascular volume is fine. He doesn't need more diuresus.

 

[bigtuna]

Portal hypertension has nothing to do with the diagnosis of hepatopulmonary syndrome. I know how to diagnose the entity definitively - the CT is consistent.

I appreciate the lecture more when you actually know what you're talking about.

And you are correct will need to extubate to high flow.

Show me some data on diagnosing hepatopulmonary syndrome by CT with concomitant PAH. Maybe the reason you've seen 4 cases with both is because you dont understand the diagnosis?

 

[jdh71]

Show me some data on diagnosing hepatopulmonary syndrome by CT with concomitant PAH. Maybe the reason you've seen 4 cases with both is because you dont understand the diagnosis?

This is priceless. You're the one who tried to tell be you need to have high *portal pressures* for hepatopulmonary syndrome!! Lol.

The reason I've seem four cases is because I trained at one of the highest liver transplant spots in the country. I know how to diagnose BOTH hepatopulmonary syndrome and portopulmonary hypertension. HPS is a much more common phenomenon. This gentleman cannot get a definitive diagnosis by nuc med or echo because of the already existing intracardiac shunt. He has CT findings consistent with the diagnosis (use google to help you out - plenty of literature on the CT findings in HPS) and since I don't think a guy with a bad liver and bad oxygen also has a concomitant ILD (he could), I've made the call. And it makes sense given the amount of shunt I'm dealing with in this patient putting the whole clinical picture together.

I mean you guys act like I told you this guy has kuru. It's a bad liver patient with a common bad liver finding (HPS) and a not so common bad liver finding (PPHTN). Why this surprises anyone is a big guess to me.

****. This is the biggest reason no one posts a lot of cases - too many people go into d-bag mode about silly nonsense.

 

[Hernandez]

His intravascular volume is fine. He doesn't need more diuresus.

I'm thinking this can help with your oxygenation, not just by helping control the effusion, but if you diuresis to decrease the PPH you can decrease some of your right to left shunting with could help with the oxygenation, unless you got massive intrapulmonary AVMs, and if you do IR might also be your friend here.

 

[jdh71]

I'm thinking this can help with your oxygenation, not just by helping control the effusion, but if you diuresis to decrease the PPH you can decrease some of your right to left shunting with could help with the oxygenation, unless you got massive intrapulmonary AVMs, and if you do IR might also be your friend here.

I'll give it a shot.

 

[bigtuna]

The reason I've seem four cases is because I trained at one of the highest liver transplant spots in the country. I know how to diagnose BOTH hepatopulmonary syndrome and portopulmonary hypertension. HPS is a much more common phenomenon. This gentleman cannot get a definitive diagnosis by nuc med or echo because of the already existing intracardiac shunt. He has CT findings consistent with the diagnosis (use google to help you out - plenty of literature on the CT findings in HPS) and since I don't think a guy with a bad liver and bad oxygen also has a concomitant ILD (he could), I've made the call. And it makes sense given the amount of shunt I'm dealing with in this patient putting the whole clinical picture together.

Sorry about continuing on with the "silly nonsense" but the CT findings in HPS and "ILD" have nothing in common. Interested in how you can gauge the amount of shunt attributed to HPS when you have PFO, PPH, pneumonia, effusion, COPD, ascites, rib fx, pna.

 

[jdh71]

Sorry about continuing on with the "silly nonsense" but the CT findings in HPS and "ILD" have nothing in common. Interested in how you can gauge the amount of shunt attributed to HPS when you have PFO, PPH, pneumonia, effusion, COPD, ascites, rib fx, pna.

What kind of doctor are you anyway?

Rericulonodular opacities can be the manifestation if many kinds of ILD. Much in common. So. Sorry bigT.

Are you even a pulmonologist?

I'm gauging the amount of shunt by clinical gestalt and experience. It all makes sense.

I am *obviously* silly to give this diagnosis to the patient with consistent CT findings when 1/5 bad liver patients will have HPS.

 

[bigtuna]

What kind of doctor are you anyway?

Rericulonodular opacities can be the manifestation if many kinds of ILD. Much in common. So. Sorry bigT.

Are you even a pulmonologist?

I'm gauging the amount of shunt by clinical gestalt and experience. It all makes sense.

I am *obviously* silly to give this diagnosis to the patient with consistent CT findings when 1/5 bad liver patients will have HPS.

Yes I'm pulm/cc - the abnormalities in HPS on CT are distal vessel based versus ILD being parenchymal based, no?

 

[jdh71]

Yes I'm pulm/cc - the abnormalities in HPS on CT are distal vessel based versus ILD being parenchymal based, no?

The CT findings in HPS syndrome are reticulonodular and at the bases mostly. Plenty of ILD has reticulonodular changes. If you are pulmonary you got dick for ILD training.

 

[bigtuna]

The CT findings in HPS syndrome are reticulonodular and at the bases mostly. Plenty of ILD has reticulonodular changes. If you are pulmonary you got dick for ILD training.

Well I can tell the difference between a vascular abnormality and a parenchymal abnormality on a chest CT….Why do you get so butt hurt over this stuff?

 

[jdh71]

Well I can tell the difference between a vascular abnormality and a parenchymal abnormality on a chest CT….Why do you get so butt hurt over this stuff?

I'm not butthurt. The most common CT finding in HPS is reticulonodular opacities not vascular malformation. It is not common to see large vascular malformations on ct. You have simply been making ignorant statements in here while at the same time deigning to lecture me. You've been incorrect. I think you need to get back into your books before you starting trying to make authoritative statements.

 

[PlutoBoy]

 

[bigtuna]

I'm not butthurt. The most common CT finding in HPS is reticulonodular opacities not vascular malformation. It is not common to see large vascular malformations on ct. You have simply been making ignorant statements in here while at the same time deigning to lecture me. You've been incorrect. I think you need to get back into your books before you starting trying to make authoritative statements.

This is a direct quote from The Hepatopulmonary Syndrome: Radiologic findings in 10 Patients AJR 1996; 166:1379-1385

CT scans (n = 8) showed distal vascular dilatation in all eight cases (Figs. 1C, 1D, and 2). Dilated vessels were always associated with an abnormally large number of visible terminal branches (Figs. 1C, 1D, and 2). The vascular cause of the opacities was better appreciated on scans of 10-mm-thick sec- tions than on scans of 1.0- on 1.5-mm-thick sections in all cases (Fig. 2). Abnormal vessels were bilateral in seven cases and unilateral in one and were always concentrated in the lower lung zones. These findings varied from mild (few vessels) to severe (multiple vessels).

...High-resolution CT scans (n = 8) showed no evidence of fibrosis (Figs. 1C, 1D, and 2A) as the cause of abnormal opacities on chest radiographs.

 

[jdh71]

This is a direct quote from The Hepatopulmonary Syndrome: Radiologic findings in 10 Patients AJR 1996; 166:1379-1385

CT scans (n = 8) showed distal vascular dilatation in all eight cases (Figs. 1C, 1D, and 2). Dilated vessels were always associated with an abnormally large number of visible terminal branches (Figs. 1C, 1D, and 2). The vascular cause of the opacities was better appreciated on scans of 10-mm-thick sec- tions than on scans of 1.0- on 1.5-mm-thick sections in all cases (Fig. 2). Abnormal vessels were bilateral in seven cases and unilateral in one and were always concentrated in the lower lung zones. These findings varied from mild (few vessels) to severe (multiple vessels).

...High-resolution CT scans (n = 8) showed no evidence of fibrosis (Figs. 1C, 1D, and 2A) as the cause of abnormal opacities on chest radiographs.

So?