In this lecture, we’ll be discussing acute
pancreatitis and cholecystitis in children.
Let’s start with pancreatitis.
So here, you have a 17-year-old male who’s
coming in with abdominal pain and vomiting.
He admits to drinking alcohol
with his friends after school
and has been feeling
nauseous and vomiting a lot,
but was attributing these
symptoms to his alcohol use.
On physical exam, he has abdominal tenderness,
fever, and decreased bowel sounds.
You notice he has an upper abdominal
pain that radiates up to his back.
He’s feeling worse after eating,
maybe a half hour to
an hour after eating.
And then you notice the lab work
shows an elevated lipase level.
This is a classic case of pancreatitis.
Let’s look at what pathologic processes
might have led to this problem.
So, pancreatitis is an acute or chronic
inflammatory process of the pancreas.
Generally, in acute disease, it’s a reversible
injury associated with inflammation.
In chronic disease, there is irreversible
destruction from prolonged inflammation.
Keep in mind, pancreatitis is much
more common in adults and children.
But likewise, children are more likely to
have acute rather than chronic pancreatitis
with the exception of
those children with
underlying significant systemic
disease such as say cystic fibrosis.
Metabolic disorders and
anatomic or mechanical problems
can increase your risk of problems
in the pancreas in children.
Examples are pancreas divisum,
which is a congenital
where there might be impairment of
drainage of the pancreatic fluid.
Choledochal cyst are
common in children,
and we’ve talked about
them in our GI lectures.
This choledochal cyst can cause a backup
in some cases and a pancreatitis.
Or in some cases, patients may have a
dysfunction of the Sphincter of Oddi.
Remember, that’s the sphincter
that might constrict and prevent
release of pancreatic juices
into the intestinal vault.
So, let’s drill down into the pathophysiologic
mechanisms of acute pancreatitis.
First, a patient may have duct obstruction,
a gallstone, for example, that could
stack in the common bile duct
and prevents exocrine
function of that pancreas
causing a backup of
Or a patient may ingest a
substance such as alcohol,
which could cause a
direct acinar cell injury
so the cells of the pancreas themselves
are actually being directly damaged.
Or a patient may have some defective
intracellular transport of enzymes
within the cell that then
escape and cause damage.
All of these things will lead
to an acinar cell injury,
and that will result in activated
enzymes, which autodigest the pancreas.
This is acute pancreatitis.
Let’s go through these three
major causes one at a time,
starting with duct obstruction.
The most common cause of duct obstruction
is gallstones or biliary sludging.
We see this more commonly in
patients with sickle cell disease.
This is because these patients have a
high rate of red blood cell turnover
requiring more bilirubin
to be excreted,
and they can get sludging
in their gallbladder.
Patients with cystic fibrosis
often have pancreatic problems
because the chloride channel is defective
and they have thicker
secretions inside the pancreas.
Very rarely in children,
there can be neoplasms
which might obstruct flow
of pancreatic fluids.
Choledochal cyst, and there are several
types, can involve the pancreas.
And so, this cyst may obstruct
outflow of pancreatic enzymes.
Very rare but you can see
especially Ascaris lumbricoides
cause obstruction of the
And lastly, congenitally, pancreas
divisum can cause it as well.
All of these causes can result in an
interstitial edema within the pancreas,
an impaired blood flow and
an ischemia to the pancreas,
which results in
acinar cell injury.
Thus, the enzymes that the pancreas
is producing become activated.
There is an autodigestion of the
pancreas resulting in acute pancreatitis.
Patients can rarely have
direct acinar cell injury
that’s not from an obstruction of
the pancreatic drainage system.
Examples would be alcohol or drugs,
direct trauma to the pancreas,
an ischemic process in the pancreas.
Viruses can rarely cause this.
Patients with diabetes because
of the autoimmune process
occurring in their pancreas may have
impairment of exocrine function
as well as endocrine
function of the pancreas.
Also, hypercalcemia is associated
with acute pancreatitis.
These acinar cell injuries
cause release of pro-enzymes
resulting in acinar cell
injury that further occurs.
These enzymes are activated
just like in ductal obstruction
resulting in the
Patients may also have some
problems with intracellular
transport of some of
these digestive enzymes.
This happens during metabolic
injury through exposure to alcohol,
and also as a response to duct obstruction.
This further enhances the
auto-wide digestion phenomenon.
This interruption of delivery of
proenzymes to the lysosomal compartment
can result in intracellular
activation of the enzymes
so these cells aren’t essentially
eaten from the inside.
This acinar cell injury, again, results in
activated enzymes and acute pancreatitis.