00:01
The clinical presentation
is going to be related
to what stage we're in
if it's fatty liver disease
that's going to be
somewhat different
than if we're at
steatohepatitis,
than if we're at cirrhosis.
00:11
With alcoholic steatosis
or just fatty liver.
00:13
It's largely asymptomatic.
00:15
There may be vague
abdominal discomfort,
the liver is actually
somewhat expanded
by the accumulation of fat
and by stretching glistens
capsule around the liver,
you may have that vague sense
of, I don't feel so good.
00:28
And we may actually formally
be able to distinguish
that there is
hepatomegaly on exam,
we'll be able to
feel the liver edge
below the right costal margin.
00:39
With more severe disease,
now alcoholic hepatitis.
00:42
It's inflammation, so
there'll be a low grade fever.
00:45
There'll be a lot of other
systemic manifestations
including anorexia and nausea.
00:50
There will be that right
upper quadrant discomfort,
the patient may be jaundice
because we are impacting the ability
of the hepatocytes to function,
So we may not be metabolizing
bilirubin appropriately.
01:02
There'll be the
same hepatomegaly
that we saw with
fatty liver disease.
01:05
And depending on the
extent of inflammation,
we may be starting to see the
beginning of portal hypertension
with associated ascites
and addition, we may be
able to see some effects
on the CNS
with hepatic encephalopathy.
01:21
And then frank
alcoholic cirrhosis
that's in stage disease,
and I would actually refer
you to the entire talk
in the Lecturio files
that's all about cirrhosis.
01:33
But we'll see as indicated here,
fatigue, malaise, weight
loss, severe jaundice.
01:38
Pruritus from deposition
of bile salts,
so the patient
becomes quite itchy.
01:42
With alcoholic cirrhosis,
we'll see hepatic encephalopathy
including signs like asterixis,
where you have the
patient close their eyes
and try to stop traffic
and their palms do that
they have a flap.
01:54
They may be tired, confused,
even be in a frank coma.
01:59
Ascites occurs due to portal
hypertension and decreased albumin
and we may have GI bleeding
because of esophageal varices
associated with the
portal hypertension.
02:11
Skin changes will include things
related to elevated estrogen
such as telangiectasias.
02:18
We may also have other
portosystemic shunts
so that you have
a Caput Medusae.
02:24
Palmar erythema is associated
with elevated estrogens.
02:27
Clubbed nails may be a
secondary and rare manifestation
and then patients will get
into patrons contracture
usually have the ring finger
where they have
abnormal fibrosis
and holds that finger
in that position.
02:40
Dupuytren's contractures are
associated with other entities
and can be completely
idiopathic,
but our seem at a certain
frequency and alcoholic cirrhosis.
02:49
And then other hyper
estrogenic effects.
02:52
Gynecomastia,
hypogonadism,
reduced libido, erectile
dysfunction, infertility,
and amenorrhea.
03:01
Finally, there may be alopecia
and or the effects of
diminished vitamin.
03:06
So if the individual is drinking
more than they're actually eating
and not getting
adequate nutrition,
they may have B12, or
folate deficiencies,
they have iron deficiencies
and then we'll see a glossitis,
a smooth and inflamed tongue.
03:21
Or you may have an anemia
associated with vitamin deficiency.
03:26
In making the diagnosis,
clearly it's related to history.
03:30
How much alcohol?
How frequently do you do it?
What's the duration of that?
Keep in mind that with
alcohol disorders,
anything else that potentially
causes injury to the liver
is going to exacerbate the
alcohol related injury.
03:46
So we want to assess
and see whether there are other
causes such as hemochromatosis,
abnormal copper, metabolism,
Wilson's disease,
Alpha-1 antitrypsin,
viral hepatitis,
or other medications that
may synergize with alcohol.
04:00
In terms of laboratory studies,
classically, the AST is
more elevated than the ALT
in terms of identifying
enzyme elevation
with abnormal liver function.
04:13
And the gamma
glutamyl transferase
is also a very sensitive
indicator of alcohol intake.
04:21
Typically, classically, the AST
to ALT ratio is greater than 2.
04:25
And that's something you can tuck
away in the back of your head
because that's frequently
asked on rounds.
04:32
Any AST or any ALT that
is greater than 500 says,
as something else
is going on here.
04:37
We usually don't see elevations,
more than 500 and pure
alcoholic disease.
04:44
And the alkaline phosphatase is
certainly going to be elevated
when there's a lot
of inflammation.
04:50
Other findings with
alcoholic hepatitis,
we'll see abnormal
bilirubin metabolism
and or release,
we will see diminished
albumin synthesis,
we will see diminished
coagulation factor synthesis
and we will may or may
not see evidence of anemia
either macrocytic
from B12 or folate
or microcytic due to iron
and iron and blood loss occurs
also with alcoholic gastritis.
05:18
With alcoholic cirrhosis now,
at the end stage,
you may actually not see
an elevation in AST or ALT.
05:24
At that point,
the hepatocytes are
no longer susceptible
to any further damage.
05:29
They're in stage.
05:31
So it's usually a
modest elevation.
05:34
Bilirubin will certainly
be elevated because
we are not metabolizing or
releasing bilirubin appropriately,
the gamma glutamyl
transpeptidase
still ends up being a
relatively sensitive marker.
05:44
And alkaline phosphatase
will be quite elevated
because the fibrosis
in the cirrhotic state
is markedly impacting the
ability of the biliary tree
to do its appropriate actions.
05:58
And as a manifestation of
that alkaline phosphatase
is markedly elevated.
06:02
Other laboratory
studies with cirrhosis,
elevated ammonia,
markedly diminished
protein synthesis.
06:09
The PT is down.
06:11
Platelets are down for a
combination of reasons.
06:14
One is you have hypersplenism
due to portal hypertension,
and that sucks up platelets,
but also the liver
makes thrombopoietin
and thrombopoietin is
going to be necessary
for getting the bone marrow
to synthesize and
make new platelets.
06:27
You may have anemia
and hyponatremia.
06:31
The hyponatremia is because of
the effects of chronic alcohol
and cirrhotic disease altering
the normal renal cycle
that is responsible for maintaining
water and sodium within limits.
06:48
Imaging to make a diagnosis,
ultrasound is quite good.
06:51
It shows an irregular
trunk and liver.
06:54
CT scan can also be employed.
06:56
And then the gold standard
overall is to do a liver biopsy.
07:00
How do you manage this?
Well, you know, basically
stopped drinking.
07:05
Okay, that's easier
said than done.
07:07
Also want to make sure the
patients are in a healthy diet.
07:09
So they're getting
adequate nutrition
and an adequate vitamin intake.
07:13
In alcoholic hepatitis,
it's the same story,
stop drinking.
07:17
Make sure that there
is adequate hydration
and normal electrolyte
correction,
supplement the nutrition,
and make sure that there's
not something else concurrent
that is exacerbating the injury.
07:30
Additional treatments for
alcoholic hepatitis include:
glucocorticoids to
limit inflammation.
07:35
And pentoxifylline
is another drug
that is used for patients
who can't have steroids.
07:41
And what this does
is start to do
is limit the production of
various pro-inflammatory mediators
such as tumor necrosis factor.
07:49
So with cirrhosis
at the end stage,
it's going to be
largely supportive.
07:55
You will do similar
things that you've done
for a patient as
alcoholic hepatitis,
you just don't want the
disease to get any worse.
08:03
So you want to
minimize any damage.
08:05
So you want to quit drinking,
you may have to salt
and water restrict
because of the aberrations
in the normal renal function.
08:12
You give diuretics and or
a therapeutic paracentesis
to remove the excess
fluid from the ascites.
08:19
For the hepatic encephalopathy,
you restrict protein intake.
08:22
So you need to have
a low protein burden.
08:26
The more protein you have,
the greater the severity
of the encephalopathy.
08:31
And similarly, you can
reduce the microbiota,
which is a major source of
protein as well in the GI tract
by giving oral
lactulose oral neomycin.
08:41
And finally, for patients
who have quit drinking,
then you can offer the
possibility of a liver transplant,
but with a limited resource
and if a patient is not able to
abstain forever from alcohol,
then they are not a candidate
for that for that procedure.
09:00
So what's the outlook
for these patients?
If the patient has
alcoholic hepatitis,
they tend to progress at a rate
of about 10 to 20%
per year to cirrhosis.
09:10
In most cases, that's because
they continue to drink,
abstinence reduces that
risk substantially.
09:17
The median survival for
compensated cirrhosis
without significant
complications
such as bleeding without
hepatic encephalopathy,
without hepatorenal syndrome,
with the renal aberrations
is about 12 years.
09:32
The median survival when
there is really severe disease
is much less on the
order of months.
09:37
And the model for assessing,
whether a patient has
really severe liver disease
or moderate or mild
is this model for end
stage liver disease,
otherwise called the MELD score.
09:50
We're not going
into the details.
09:52
But when you become
a hepatologist
or a liver transplanter,
you will use the MELD score
to determine where on the transplant
list your patient will be.
10:04
With that,
we have finally come to the
end of alcoholic liver disease.
10:10
Go have a drink.