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ACUTE PANCREATITIS

Anatomy & Physiology of Pancreas

Pancreas is a glandular organ of both endocrine & digestive systems;

 Acting as endocrine gland (e.g.: producing several important


hormones such as insulin, glucagon)

 As an exocrine gland secreting pancreatic juice that contains several


digestive enzymes (e.g: trypsin, chemotrypsin, pancreatic lipase &
amylase; which are proenzymes).

It's a retroperitoneal structure that lies in the epigastrium & left upper
quadrant, across the transpyloric line.

It's divided into head, neck, body, & tail that are crossed by the main
pancreatic duct, which in turn receives multiple tributaries. The main
pancreatic duct will open (with the common bile duct) into the
posteromedial aspect of the second part of the duodenum.

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Entrance of fats, proteins, CHO into the duodenum induces it to release


cholecystokinin (CCK) hormone which will stimulate the acinar cells of
pancreas to release pancreatic juice in addition to alkaline water & ions.
CCK also stimulates contraction of the gallbladder releasing bile into the
duodenum. These will act to neutralize the acidity of gastric juice & to
activate pancreatic proenzymes in order to begin digestion.

What we are concerned about here is the activation of pancreatic enzymes


which needs:

Alkaline environment + the presence of Ca+2

ACUTE PANCREATITIS

Acute pancreatitis is an autodigestion of the pancreas by its regurgitated


own enzymes when they are in the active form. It's an inflammatory
process rather than infectious.

It's one of the most common benign diseases that carry high mortality rate
which can reach 20%.

Pancreatic enzymes when they reach the ampulla of Vater, they will be
activated, so if there is any obstruction in this area due to any cause (e.g:
stones, tumor...), then there will be regurgitation of the active enzymes of
pancreas back into it causing autodigestion of it.

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Etiological Factors of Acute Pancreatitis

:
1. Biliary tract disease 50% of pancreatitis cases in Jordan are due to biliary
tract diseases (mainly stones)

2. Alcohol: because it causes edema in the head of pancreas. So if you work in


Adembra or Glasgow in Scotland and you have a patient with acute
pancreatitis, then you should think of alcohol as the cause of pancreatitis;
because habitants of these regions consume excessive amounts of alcohol
daily. 80% of acute pancreatitis cases there is due to alcohol. The same thing
is applied to the west of France (mainly Normandie city)

3. Ischemia: which could be due to hypotension, cardio-pulmonary by pass,


atheroembolism, vasculitis…

4. Trauma: which could be external, operative, ERCP …

5. Pancreatic obstruction: which could be due tumor, pancreatic divisum,


ampullary stenosis…

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ACUTE PANCREATITIS

6. Scorpion venom, which is by a scorpion

7. Metabolic: hypercalcemia, hyperthyroidism, hyperlipidemia

For example, a patient with parathyroid adenoma will have excessive


secretion of parathormone, this will lead to hypercalcemia, hypercalcemia
in turn will lead to calcification of kidney (nephrocalcinosis) & pancreas…So,
the pancreas will be destroyed & thus releasing its pancreatic enzymes.

One of these enzymes is the pancreatic lipase; this enzyme will start
breaking down fatty acids in a process called "saponification process", &
this process actually consumes a lot of calcium, so, as a result leading to
hypocalcemia
Now, calcium is very important for the contraction of the heart. If calcium
levels fall below 8mg/dl (2 mmol/IU) then the heart will stop & your patient
may die from hypocalcemia!

So>> you should supply him with Ca+2 supplement immediately.

ALWAYAS REMEMBER >>> if you have a patient over 70 yrs old with acute
pancreatitis & renal failure >>> then you should examine the neck for any
parathyroid tumor

Another issue concerning Hyperlipidemia…

If a patient has increased levels of lipids (TAG) >> then this will lead to
atherosclerosis >> thus decreased blood supply to different tissues >>
ischemia of pancreas >>> eventually Pancreatitis

Now.. Pancreatitis = destruction of pancreas >> so decreased pancreatic


enzymes production >> thus increased levels of TAG in the serum (due to
decreased production of pancreatic lipase which is responsible for TAG
destruction)

So as a summary…
HYPERcalcemia >>>>>> Pancreatitis >>>>>> HYPOcalcemia
HYPERlipidemia>>>>>> Pancreatitis >>>>>> more HYPERlipidemia

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ACUTE PANCREATITIS

8. Drugs: the most familiar ones are corticosteroids, thiazide diuretics,


furosemide (lazix), & H2- antagonists (e.g: Ranitidine, Cemitidine, &
Famotidine).

9. Viral infection: Mumps & Coxaki B4 viruses both can cause pancreatitis.
So, if you have a child that comes to you complaining of severe epigastric
pain, examine his parotid glands, & if you find parotitis then immediately
you should suspect that the cause of pain is pancreatitis due to mumps.
Also, you can check his scrotum for orchitis (e.g: inflammation of the testes);
because mumps causes parotitis, orchitis, & eventually pancreatitis. (So
keep in mind that even children could have pancreatitis, not only adults)

Pathology

Patients with acute pancreatitis will have..

Pancreatic Edema >> leading to Exudation of fluid (& there might be


hemorrhage)

Then >> Suppuration & super added infection >> abcess formation

Then >> there might be pancreatic necrosis (so release of excessive lipase &
other pancreatic enzymes) >> leading to Fat Necrosis esp. around the elbow
(so the patient might be presented with multiple fat nodules around the
elbow)
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ACUTE PANCREATITIS

Then >> due to exudation & hemorrhage there will be loss of large amounts
of fluids >> Hypovolemia >> consequently Hypovolemic Shock

Also the exuded fluids might accumulate in the lesser sac (area between the
stomach & pancreas) >> producing Pseudocyst.

Clinical Picture of Acute Pancreatitis (Signs & Symptoms)

Signs

 Shock: could be: Hypovolemic shock Or Septic shock (if there is super
added infection)
 Jaundice: due to obstruction of the common bile duct by the
enlarged edematous head of pancreas.
 Left pleural Effusion: because the tail of pancreas is located near the
left diaphragm >> so there will be sympathetic effusion & left pleural
effusion (collection of fluid in the left pleural cavity), this in turn will
cause hypoxia to the patient.
 Acute Pulmonary Failure: this is due to:
(lung atelactesis + ischemia of the brain + left pleural effusion)

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ACUTE PANCREATITIS

 Cerebral abnormalities: pO2< 60  decreased O2 to the brain


so, as a consequence of that >> cerebral abnormalities

 Localized Paralytic ileus: because the ileum is near the pancreas,


there will be transcoelomic spread of the infection –in case that there
is super added infection of pancreas- to the ileum >> causing localized
serositis >> then as a consequence of that >> localized paralytic ileus
{Serositis: inflammation of the serous membrane}
 Abdominal mass__ which could be due to:-
o Inflammatory mass of pancreas
o Pancreatic abcess
o pseudocyst

SYMPTOMS
Patient of acute pancreatitis will come to you with very severe sudden
continuous epigastric pain that increase in severity every hour (Crescendo
fashion). This pain radiates to the back; because pancreas is a
retroperitoneal structure. The patient will come to you walking with his back
leaning forward "Hunched/bizarre position" – or as the Dr. said "Hunchow
Position", Sorry but I'm not sure of its spelling -.

Also, the patient will have nausea with vomiting for several times thus
contributing to the hypovolemia that is often caused by acute pancreatitis

So.. Exudation + suppuration + hemorrhage + vomiting lead


to Hypovolemia

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ACUTE PANCREATITIS

Investigations

 CBC to detect leukocytosis & anemia


 Serum amylase we have 2 types of amylase: salivary &
pancreatic. In order to differentiate between them & detect the
pancreatic lipase specifically we do Serum Amylase Isoenzymes.
 Urinary amylase more sensitive than serum amylase because it
stays for longer periods of time, while serum amylase increases
for 2-3 days only then return back to normal
 Serum lipase very sensitive test, but we don't do it routinely
because it's so expensive.
 Peritoneal fluid analysis if the patient has ascitis, you take a
sample from the fluid >> send it for amylase test
 if amylase > 100,000/cm3 (+) for pancreas
so the cause of ascitis is acute pancreatitis
 Chest X-Ray to detect pleural effusion & atelectasis
 Abdominal X-Ray to detect calcification of pancreas
(calcification of it is seen in both chronic & acute cases). Also, we
can see radio-opaque gallstones, & dilated loops of small bowel
due to localized paralytic ileus.
 Barium mealNot used nowadays
 Ultrasoundto detect edema of pancreas and collection of fluid
 CT-scanvery sensitive for the detection of pancreatic necrosis
 MRIalso v. sensitive for the detection of pancreatic necrosis

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ACUTE PANCREATITIS

Note;
Increased serum amylase (hyperamylasemia) does not always mean
pancreatitis, any acute abdominal case can cause hyperamylasemia.

Here are some of the intra-abdominal & extra-abdominal disorders that


might be associated with hyperamylasemia;

Intra-abdominal Disorders associated with Hyperamylasemia

The most condition to cause increased amylase is ruptured aortic aneurysm


which rises it to very high levels

Extra-abdominal Disorders associated with Hyperamylasemia

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ACUTE PANCREATITIS

To diagnose a patient with Acute Pancreatitis, the value of the patient's


serum amylase level must reach the upper limits of your lab's value
according to your unit of measurement.

For example.. In KAUH the used unit is the international unit (IU). Normally
this value must be 2-27. If you have a patient with serum amylase 270 IU (10
times the upper limit of your lab), then he's certainly positive for having
acute Pancreatitis

Other hospitals use King Armstrong Unit (KAU). Normally this value must be
1-13 KAU. So if they have a patient with serum amylase 130 KAU (10 times
the upper limit of their lab), then he's certainly having acute Pancreatitis

Differential Diagnosis of Pancreatitis

- MI >> inferior MI esp. in elderly patients have similar pain to acute


Pancreatitis

- Perforated peptic ulcer

- Acute cholecystitis

Mortality & Prognosis

Mortality rate is 6-20%

#Causes of death:

1- Hypovolaemic shock
2- Electrolyte disturbances esp. hypocalcemia
3- Toxemia
4- Renal failure
5- Respiratory failure (collapse, consolidation, effusion)

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ACUTE PANCREATITIS

In summary, although acute Pancreatitis is a disease of single organ, but


usually it leads to multi organ failure (MOF), & that's why it has a high
mortality rate.

Determination of the way of treatment & mortality rate


of acute Pancreatitis patient
Suppose that you have a patient with acute Pancreatitis

-Where would you admit him; ICU or normal ward? –taking in consideration
that normal ward entrance costs the pt 16 JD, while ICU entrance costs him
600 JD-
-How would you determine the mortality rate of him?..

It's your duty to determine the prognosis of your patient in addition to


diagnosis & treatment
In order to answer these two questions we have 2 criteria that could be
followed;

1- Emrie Scale (Glasgow Pancreatic Scale)


2- Ranson's criteria (you are required to know this only)

Ranson's criteria

When you admit a patient with


Pancreatitis, there are 5 criteria
that you can know it immediately,
& there is another 6 criteria that
you know it during the initial 48
hours of admission

Every criteria of these will be


considered as one point if it's
present, then according to the
number of points calculated we can
determine the mortality rate &

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ACUTE PANCREATITIS

consequently his need to the ICU or not.

- Glucose level is high because the pancreas is destroyed, so no insulin >>


thus increased Glucose

- LDH & SGOT >> these are liver function tests that don't need more than 10
minutes to get their results

- Hematocrite fall

Suppose that you admit a patient with Hct (or PCV) of 42, & in the next day
his Hct becomes 35.

10% of 42 = 4.2, the decrease in Hct in the previous case is 5  so more


than 10% of Hct so we give this patient 1 point due to Hct fall > 10%

Or in another way.. if you admit a patient with Hb = 14, & next day his Hb
becomes 10

10% of 14 = 1.4, the decrease in Hb is 4  so more than 10%

- Blood Urea Nitrogen rise 5 mg/dl

Suppose that we have a patient with BUN = 16mg/dl in the first 24 hours, &
in the next day it rises into 25

There is a rise of 6 mg/ dl which is more than 5 , so we give him one point
due to BUN rise > 5 mg/dl

- Base Deficit >> if there is decrease of HCO3 of more than 4 meq; that is
acidosis of more than 4  positive result so you give the patient one point.

- Fluid sequestration >> when a patient with acute Pancreatitis comes with
hypovolemic shock, we supply him with large amounts of fluid to correct his
situation, large portion of this fluid will be found in the intestine not
absorbed; mainly due to localized paralytic ileusin surgery we call this
"loss of third space". If we need more than 6 liters to correct the patient's
pressure so fluid sequestration is positive & you give the patient 1 point
for it.

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ACUTE PANCREATITIS

If your patient has:

< 2 points no mortality, & he will go home safely (insha2allah

3-4 points 15% mortality rate

5-6 points50% mortality rate

> 7 points test the limits of modern medicine; so your patient will
inevitably die!

If you have a patient with 3 points or more, you should immediately admit
him to the ICU

Treatment of Acute Pancreatitis

We call it "R-Regimen"

Rest the pain (Relieve Pain)>> Pethidine 100mg/4hr + antispasmodic


We use antispasmodic with pethidine because Pethidine alone can cause
spasm of sphincter of oddi.

Rest the pancreas>> NPO, IV fluid, electrolytes replacement.


So you should keep the patient without food in order to rest the Pancreas

Rest the bowel >> NG tube


The bowel is filled with fluid in addition to third fluid space, both will cause
distension of the bowel _ so we use NG tube to decompress it.

Resuscitation>> Replacement therapy for fluids & electrolytes


Resist enzymatic activity>> Using protease inhibitors, Trasylol , H2
antagonist, glucagon ?

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ACUTE PANCREATITIS

Resist infection>> Antibiotics?


If you are asked in the Oral exam about giving antibiotics you can answer by
either YES or NO & it will be considered correct for both answers IF you give
the correct explanation for your answer

 Why "YES"? Because mortality of Pancreatitis is related to septic


shock, so I should give him antibiotics to prevent its occurrence
 Why "NO"? Because it's an inflammatory process rather than
infectious, so I'll keep them in my pocket & use them whenever there
is super added infection

Repeated examination>> General features, abdominal signs, fluid balance


every 2 hours

Repeated serum estimations>> Daily Ca+2, WBC (fibrinogen,


methaemalbumin, Mg+2)

Respiratory support>> O2, assisted respiration, so you might need to put


the patient on a ventilator

When diagnosis is uncertain…

1-Peritoneal lavage

2-Laparotomy

NOTE… In surgery, when you are in doubt about your patient's case it's
better to open & see rather than to wait.

Treatment when complications become apparent

1-Toxic patient (septic)

2-Abdominal mass

3-Persistently high gastric aspiration

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ACUTE PANCREATITIS

R-Regimen is used for all cases of Pancreatitis except the serous one which
is associated with pancreatic necrosis, treatment of this case will be
discussed at the end of the lecture

Complications:

1. MOF >> multi organ failure

2. Abscess formation

3. Cyst formation >> these often form in the third week

Rx you follow up your patient with ultrasound. In most of the cases the
cyst regresses & disappears spontaneously, but if you notice that the cyst is
increasing in size, then you should do "CT-scan guided aspiration" –this is
the one used nowadays-, or you can do laparotomy>> then open the cyst
into the stomach or jejunum to empty there (e.g: gastrocystostomy or
jejunocystostomy)

4. Recurrent acute attacks

5. Chronic Pancreatitis >> here the patient will lose both the exocrine &
endocrine functions, so the patient will have DM & steatorrhea due to
malabsorbtion syndrome caused by loss of pancreatic enzymes.

Treatment of Pancreatic Necrosis

If you see that your patient is so tired (severely hypoxic, septic,


tachycardia…), then you must send him to CT-scan to detect Pancreatic
Necrosis. This is catastrophe in surgery so you put him on ventilator and you
need to do surgical treatment.

In the past they used to do total pancreatictomy, which has 100% mortality
rate within 2 days.

In the world the most experienced hospital in treatment the cases of


Pancreatitis is a hospital in Paris.

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ACUTE PANCREATITIS

If necrosis occurs in the pancreas:-

We open the abdomen (laparotomy)>> we will find a lot of fluid which


represents the pancreatic juice & toxins so we aspirate it immediately 
then we do peritoneal lavage; which is washing of the abdomen by 10-20 ml
of normal saline then we raise the stomach to see the lesser sac and
observe the pancreas, which is now black (because of necrosis).

You obtain a knife and start to peel the pancreas until blood appear (this
means that you reach the living tissue), this is very bloody operation

After finishing this stage you bring a roll of gauze of 15 m., and immersed
it in aseptic solution, and then you make it as a ball and put it inside the
abdomen

After that you cover the abdomen with dressing (gauze) and send him to
the ICU (his abdomen is still opened) >> this operation called

Laparostomy (open , send to ICU , with opened abdomen ) rather than

Laparotomy (open abdomen then close)

 After 48 hours, you bring your patient back to the theater remove the
ball of gauze look at the pancreas, you'll find it black again >> so you peel
it another time

 You repeat this 4-5 times every other day


by this operation you can save 60% of patients

As a summary, this process involves three steps:-

 Laparostomy
 Pancreatic necrosictomy
 Peritoneal lavage

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ACUTE PANCREATITIS

Chronic pancreatitis

It is a long-standing inflammation and of the pancreas with destruction


of the exocrine pancreas, in its late stages, the endocrine parenchyma is
also lost. Although chronic pancreatitis can result from recurrent bouts
of acute pancreatitis, the chief distinction between acute and chronic
pancreatitis is the irreversible impairment in pancreatic function in the
latter.

Patients with chronic pancreatitis usually present with persistent


abdominal pain or steatorrhea resulting from malabsorption of the fats
in food. Diabetes is a common complication due to the chronic
pancreatic damage and may require treatment with insulin.

Causes are similar to that of acute pancreatitis, with alcohol and


gallstones being the most common ones in developed countries. On the
other hand, malnutrition and dietary factors are the most common ones
in the rest of the world.

Put in mind that almost all patients with cystic fibrosis develop chronic
pancreatitis.

Treatment of chronic pancreatitis is directed, when possible, to the


underlying cause, and to relieve pain and malabsorption. Replacement
pancreatic enzymes are often effective in treating the malabsorption
and steatorrhea.

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