Case

54yo man with h/o HCV cirrhosis who has been lost to follow up for the last 3yrs presents to the emergency department accompanied by a friend of his who says that he's been increasingly confused over the last couple days and this morning was difficult to arouse. His friend says that for the last couple months he's noticed that the patient's abdomen has been more distended and that his eyes have been yellow. A week ago his friend told him that he felt like he had a cold and may have had a fever.

98.5 102/67 92 24 86%RA
Difficult to arouse, A&Ox1, PERRLA, icteric sclera, 2/6 holosystolic murmur at LSB, Lungs CTAB, abd distended with a fluid wave, 2 spider angiomata on torso, pitting lower extremity edema, lower extremity clonus

What do you think is going on?

What needs to be done now?

What initial work up needs to be done?

A patient with known cirrhosis is coming in with new development of ascites and a change in mental status concerning for HE who recently may have had a URI or febrile episode.

Lactulose and antibiotics (either rifaximan, flagyl or neomycin) are usually used for HE --> but how would you decide how to administer? What used Flagyl and titrated Lactulose by giving it to him every hour until he made 3-5 loose stools. Key point is this --> make sure they can protect their airway. Some times these folks need to be intubated for airway protection. Also, they may not be able to swallow or be a bit confused/combative so you often have to drop an NGT in order to give the lactulose and pills. He was unable to cooperate to assess for asterix, but he did have clonus in the lower extremities and had a positive milkmaids sign, so those were 2 good physical findings for hepatic encephalopathy

Any other causes of AMS that you might want to rule out in a cirrhotic? Tests/studies to confirm and/or work up HE?

You mentioned a GI bleed, but what are other causes of HE that must be ruled out? What GIB's do cirrhotics often have? What labs, studies and/or imaging would order?

By my exam, he had ascites (new per his friend). Do you tap him right away? If so, what do you send the fluid for?

What to make of his hypoxia and a relatively normal pulm exam? What is the differential for hypoxia in someone with cirrhosis?

JP,

PERRLA and his lungs were CTAB. My intern and my medical student (not to mention my attending) agreed. But thanks for the advice.

The lung volumes were slightly decreased but they were clear. His primary problem was hypoxia. There are other causes of hypoxia in a cirrhotic aside from volume overload. He has ascites and lower extremity edema mainly 2/2 to his portal hypertension. Our initial thoughts were to get an ABG to see if he had an elevated A-a gradient and grab a chest Xray.

The CXR was read as low lung volumes and a ? of atelectasis at the bases. His ABG showed a respiratory alkalosis and gap acidosis along with an elevated A-a gradient (I can't remember his initial gas).

So, as far as his hypoxia was concerned -> we were concerned about hepatopulmonary syndrome (hypoxia didn't fully correct with O2 either) but were also thinking about bad portopulmonary hypertension. He had a couple spider angiomata, which actually raises the pretest probability of hepatopulmonary syndrome. The other thing that can happen in cirrhotics with ascites is hepatohydrothorax, but he had nothing going for him on exam for that. And of course, they can get all the other causes of hypoxia i.e. PNA, PE, CHF, etc.

To answer some of the other questions -> we grabbed the sonosyte in the ED and found a nice pocket of ascites for a diagnostic para and sent it for cell count and culture. His gram stain was negative. His cell count showed 750 PMN's and his ascites culture grew out Klebsiella. The tap looked cloudy and we emperically started him on cefepime along with 1.5g/kg albumin. We did not do a large volume paracentesis initially.

We also did the rest of the infectious w/u and blood cultures, U/A and Ucx were negative.

He had an elevated anion gap, a creatinine of 1.4, an INR of 1.4, platelets of 80 and a Tbili of 4.2. K was normal as was his sodium. The ED sent a lactate, but you can't make much of that in the setting of liver disease.

By the time he we admitted him, he was on IV abx and periodic boluses for MAPS < 60, getting lactulose and flagyl through an NGT, had gotten albumin and was put no PPI BID.

By the next morning he had had 8 bowel movements and his mental status had dramatically improved. He did not have any fevers and his bx cultures continued to be negative. His ascites cultures wound up being a Klebsiella senstive to Levo and his antibiotics were tailored.

Are you guys comfortable with SBP as the explanation for his HE? Any other labs or studies you'd want to be more comfortable?

How do you want to work up his hypoxia? I'll tell you that his O2 sat was better laying down than when he would sit up. His tachypnea improved somewhat by the next day to about 12-14 laying down. Sitting up he'd get more SOB. He was able to say that his shortness of breath has been this way for months.

What's up with his creatinine? He initially got some fluids in the ED for a couple MAPS <60 and his creatinine the following day was unchanged. How would you work that up?

JPHazelton said:

Then I would question your interns', students' and attendings' capabilities...as well as your own.

With a palpable fluid wave in the abdomen and perfectly clear lungs...I have a very hard time believing that.

What I have an even HARDER time believing is that a 54 year old male still has his ocular accomodation reflex...commonly lost by most after age 40. This is even more amazing since this is a gentleman who is systemically sick, difficult to arouse and encephalopathic.

If you got this guy to ocularly accomodate I suggest you video tape it and submit it to the Opthalmologic literature...then congratulate the student, intern and attending for all being witness to a truly amazing medical marvel.

Oh...and get someone with better ears to listen to the lungs as well, because if you can see accomodation in this guy you might have a hard time with reality...like bibasilar crackles or rales.

Click to expand...

Fair enough, he did not accomodate. Shall I be more specific and say that his pupils were not fixed and they were reactive to light?

As far as his lung exam is concerned, it is what it is and it was correct. Sorry if you are skeptical.

I admire your convictions and your trust no one expect sabotage approach. I'm the same way. But the dude had no crackles, period. Perhaps if he was a bit more cooperative on exam and was able to pull nice huge tidal volumes I might have heard some thing different, but not every one's a text book.