Today we'll discuss even
further disorders of the liver
and we'll specifically learn
about end-stage liver disease.
So let's first begin by
defining what is cirrhosis.
Eventually, with repetitive injury to the liver, you
can develop advanced fibrosis leading to cirrhosis
and ultimately, many of the downstream complications
which include hepatocellular carcinoma.
So there are many common
etiologies of cirrhosis.
The first category we can think
about is inflammatory causes.
So this includes things like chronic viral
hepatitis and autoimmune hepatitis among others.
Recall also that the liver is the place where we
process many of the substances that we ingest,
so any toxins can also lead to cirrhosis.
The most common of which is alcohol and
medications that can be injurious to the liver.
Metabolic disease as we've also
learned can contribute to cirrhosis
in the case of non-alcoholic
fatty liver disease.
And you may have congestion that leads
to eventual scarring of the liver.
So things like congestive heart failure and
veno-occlusive disease such as in Budd-Chiari syndrome.
You may also have congenital
causes of cirrhosis,
so this category includes alpha-1 antitrypsin
deficiency, hemochromatosis and Wilson's disease.
And lastly, we have our last
category of cryptogenic cirrhosis.
This is one we simply don't know the underlying
cause and we just call it cryptogenic.
So now let's go to our cases.
Our first case is a 63-year-old man who presents to
clinic with generalized pruritus for the last 3 months.
He notes yellowing of his eyes, fatigue and
poor appetite for the same time period.
He has a history of hepatitis C for
which he has never undergone treatment.
He has no sick contacts or recent travel.
His vitals are notable for a
blood pressure of 95/53 mmHg.
His physical exam shows jaundice, palmar erythema
and abdominal distention with a fluid wave.
Lab studies are notable for
platelets of 55,000 (x10^9), INR 1.9
and serum albumin 2 (g/dL)
with a bilirubin of 5.7 (mg/dL).
So what is the next step
in confirming his diagnosis?
Let's first go through some
key items in this case.
So he has a nonspecific complaints of pruritus
and yellowing of the eyes with fatigue
that all localizes to the
His history of hepatitis C is a
known risk factor for cirrhosis.
And on exam, he has mild hypotension and physical
exam findings of cirrhosis as we'll discuss later.
In addition, his labs are somewhat
concerning for impaired liver synthetic function,
which we'll also discuss.
So, let's first start with the
clinical manifestations of cirrhosis.
We can break this down into
the effects of portal hypertension,
and effects from hepatocellular
injury or liver cell failure.
So, we'll begin with the
Due to high pressure in
the portal systemic area,
you may develop esophageal
varices and gastropathy
both of which can lead to GI bleeding
as manifested by melena or hematemesis.
Patients may also develop splenomegaly which occurs
after there's back up of flow into the splenic vessels.
Likewise, you may also have dilation
of superficial blood vessels
which then can lead to the typical
appearance of caput medusae
which are just dilated vessels on the
superficial surface of the abdomen.
Patients may also develop ascites
which is free fluid in the abdomen.
And they may have back up of flow into the
rectal vessels leading to varices there
which can manifest with
hemorrhoids and lower GI bleeding.
On the other hand, if we talk about
the effects of liver cell failure,
patients may come in with confusion
or coma from the build up of toxins.
They may also have skin
findings of spider angiomata.
They may develop gynecomastia.
Both of these prior two things
are due to imbalances of estrogen.
They may develop jaundice due
to the build up of bilirubin.
They may develop asterixis
which is also due to toxin build up.
They may have testicular atrophy,
again related to the hormones.
They may have a risk of bleeding
and they may develop ankle edema.
So now that we've gone through all the common
symptoms or manifestations of cirrhosis,
let's talk about what
labs we often see.
So we can think about labs
in 3 different categories:
those that reflect the
liver synthetic function,
those that reflect hepatocellular injury
and then a category of other
labs that are affected.
So we will begin with the
liver synthetic function.
These are the true things that reflect
impaired synthesis within the liver:
So low platelets or thrombocytopenia,
you may have elevated
prothrombin time or coagulopathy
and you may have low albumin.
Now we move to the labs that
reflect hepatocellular injury.
Patients may have elevated AST and ALT although note
that this actually may be normal in certain cases.
They may also have a high alkaline phosphatase
and they often have a high bilirubin.
Other labs that are often
affected in cirrhosis include anemia,
leukopenia - so low white cells, and low
red cells, a reduced creatinine clearance
and patients may develop hyponatremia
from imbalances in free water.
So the diagnosis of cirrhosis is
primarily an imaging diagnosis.
We use abdominal ultrasound as the test of choice
because it is non-invasive and convenient.
There is a newer test called transient elastography
that can be done to detect early fibrosis
before patients have developed cirrhosis but
this is beyond the scope of this lecture.
Liver biopsy is the gold standard for
diagnosis but nowadays is usually not done
because the diagnosis can
be madeP with imaging.
So, some common ultrasound
features as you can see here on the right
are a nodular and coarse echotexture.
You may have reversal of portal
flow which is not shown here
but if you use Doppler with your ultrasound,
you could then see this finding.
Patients may have splenomegaly or
an enlarged spleen on ultrasound.
And shown here is the presence of ascites so that
black-colored fluid above the surface of the liver
is free fluid in the
peritoneum, so ascites.
So now that we've gone through
that, let's go back to our case.
Our 63-year-old man who's coming in with
nonspecific complaints, some findings of jaundice.
He does have history of hepatitis C and he has
physical exam findings now we know of cirrhosis.
In addition, he has impaired
liver synthetic function on his labs
with thrombocytopenia, an
elevated INR and low albumin.
So what is the best next step
in confirming his diagnosis?
We now know the best test would be to do an
abdominal ultrasound to confirm this diagnosis.