So now let's go on to our next case.
A 58-year-old man with cirrhosis from
hepatitis C presents to the emergency department
with new confusion for the past 3 days.
He has ascites managed with diuretics and a history
of esophageal varices that were ligated one year ago.
His family notes that he has been sleepy
during the day and having difficulty walking.
Vitals are within normal limits.
On physical exam, he has mild scleral icterus, a
distended abdomen, flapping asterixis and slowed speech.
What is the best next step in management?
So he has cirrhosis with evidence of
decompensation with this presence of ascites.
He has new somnolence
and gait ataxia.
And on exam, he has asterixis which is
an exam finding of a lack of attention.
So let's review the topic
of hepatic encephalopathy.
This is when patients develop
cognitive changes or confusion
due to the build up of the toxins that are
normally cleared and processed by the liver.
There can be many different triggers.
So, infections are number one trigger particularly
with spontaneous bacterial peritonitis or SBP,
GI bleeding can also lead to an
episode of hepatic encephalopathy,
any issues with the kidney or electrolyte
derangement can cause this,
patients who have hypoxemia or hypercapnia
which is the build up of carbon dioxide.
and a procedure such as a TIPS
procedure which we'll discuss later
and portal vein thrombosis can lead to this.
So, the symptoms can range anywhere from
just mild confusion all the way to coma.
Patients also often describe a
disorientation of their sleep-wake cycle.
The diagnosis is made primarily based
on the history and the physical exam.
And treatment is with giving lactulose and we
titrate lactulose to about 3 stools a day.
This ensures that toxins that have built up
with cirrhosis are then cleared in the stool.
For cases that continue to recur, we can
sometimes also give a medication called rifaxamin.
So you may have wondered why are there no labs that
we can check to look for hepatic encephalopathy.
In the past we used to check ammonia levels that
we thought corresponded with encephalopathy.
However, we now know that monitoring
serum ammonia levels is not useful
because levels can be either be high or normal
in an episode of hepatic encephalopathy.
So it is simply a clinical diagnosis and you must
exclude any other things that could lead to confusion.
So now let's return to our case.
Our 58-year-old man with cirrhosis who
now has evidence of decompensation.
He has new somnolence and gait
ataxia and this finding of asterixis
which is an exam finding
of inattention or confusion.
So the best next step in management is first knowing
that he most likely has hepatic encephalopathy.
And then taking the next step to look for
any underlying triggers for this episode.
So rule out infection, bleeding,
any medication changes
and then start treatment with lactulose.