Now let's move on to our next case.
A 53-year-old woman with a history
of cryptogenic cirrhosis with ascites
is hospitalized for altered mental status.
She has been taking her furosemide,
spironolactone and lactulose as directed.
She's been having 5-7 bowel
movements a day.
Vitals are normal.
She is disoriented.
Physical exam is notable for asterixis
and abdominal distention with a fluid wave.
Her mucus membranes are dry.
Lab studies are notable for BUN of
42 (U/L)and serum creatinine 2.5 (mg/dL).
A urinalysis is normal and
renal ultrasound is unremarkable.
Blood culture results are sent and pending.
Her diuretics are discontinued.
So what is the best next step in
managing her acute kidney injury?
So, she has altered mental status in a
patient with decompensated cirrhosis.
She does have signs of hepatic encephalopathy with
her disorientation, her asterixis and her dehydration.
And she has an evidence of acute
kidney injury with her azotemia.
So, let's discuss hepatorenal syndrome.
This is a particular type of acute kidney
injury in a patrient with liver disease
due to portal hypertension which then
leads to a decline in the renal function.
This is a complicated diagnosis to
make and is a diagnosis of exclusion.
How this forms is first beginning
with portal hypertension.
Portal hypertension leads to
vasodilatation of the splanchnic vessels
which then leads to
effective arterial hypovolemia
and then because the kidneys
are sensing less blood flow,
they then activate the renin-angiotensin-aldosterone
system or the RAAS system.
This leads to increased renal absorption of sodium
and water which in turn leads to buildup of ascites
And on the other hand, this can
also lead to renal vasoconstriction
which leads to acute kidney
injury or hepatorenal syndrome.
So the diagnostic criteria are
quite strict for hepatorenal syndrome.
I must admit this is a very difficult diagnosis
to make because you have to really exclude
anything else that could lead to an AKI.
So it's defined by an
increase in serum creatinine.
You must have no response to
a fluid challenge with albumin.
They must have no other
factors that can lead to an AKI.
So no shock, medications known to be toxic
to the kidneys, the urinalysis must be normal,
they must not have any proteinuria
and you must also make sure the
patient has no chronic kidney disease
or obstruction on the ultrasound,.
both of which may lead to their AKI.
So, just remember that hepatorenal
syndrome is a diagnosis of exclusion.
So you must exclude everything else
that could potentially lead to this picture.
How we manage it depends
on the pathophysiology.
So if you recall that renal perfusion
decreases in the development of HRS
then you now know that to counteract that,
we want to increase perfusion to the kidneys.
We do that by giving
vasoconstricting medications like
terlipressin or octreotide, midodrine or
norepinephrine if the patient is critically ill.
And we also try to increase
blood flow to the kidneys by
increasing the effective blood volume so
that's by colloid resuscitation with albumin.
And if you have done all of these things and
the patient continues to have kidney failure,
you then consider a referral for both a
liver and kidney transplant evaluation.
So now let's go back to our case.
53-year-old woman with new
onset altered mental status.
She has decompensated cirrhosis, signs
of hepatic encephalopathy on her exam
and her labs are concerning
for a new AKI with azotemia.
So now we are asked, what is the
best next step to confirm the diagnosis?
So, recall that her urinalysis
and ultrasound were normal
which helps us rule out other
causes of acute kidney injury.
The next step to confirm the diagnosis would
be to perform a fluid challenge with albumin
to rule out a prerenal AKI.