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BACKGROUND
Pancreatitis is an inflammatory process in
which pancreatic enzymes autodigest the
gland.
The gland sometimes heals without any impairment
of function or any morphologic changes; this process
is known as acute pancreatitis.
Pancreatitis can also recur intermittently,
contributing to the functional and morphologic loss
of the gland; recurrent attacks are referred to as
chronic pancreatitis.
Both forms of pancreatitis present in the (ED)
with acute clinical findings. Recognizing
patients with severe acute pancreatitis as soon
as possible is critical for achieving optimal
outcomes

ANATOMY
Retroperitoneal Organ
Weighs 75 To 100 G
15 To 20 Cm Long
Head
Neck
Body
Tail

PATHOFISIOLOGY OF ACUT PANCREATITIS

 Activated neutrophils then exacerbate the problem by

releasing superoxide (the respiratory burst) or
proteolytic enzymes (cathepsins B, D, and G;
collagenase; and elastase).
Finally, macrophages release cytokines that further
mediate local (and, in severe cases, systemic)
inflammatory responses. The early mediators defined
to date are tumor necrosis factor-alpha (TNF-),
interleukin (IL)-6, and IL-8.
These mediators of inflammation cause an increased
pancreatic vascular permeability, leading to
hemorrhage, edema, and eventually pancreatic
necrosis.
As the mediators are excreted into the circulation,
systemic complications can arise, such as bacteremia
due to gut flora translocation, acute respiratory
distress syndrome (ARDS), pleural effusions,
gastrointestinal (GI) hemorrhage, and renal failure.

 In acute pancreatitis,
parenchymal edema and
peripancreatic fat necrosis occur
first; this is known as acute
edematous pancreatitis. When
necrosis involves the parenchyma,
accompanied by hemorrhage and
dysfunction of the gland, the
inflammation evolves into
hemorrhagic or necrotizing
pancreatitis.
Pseudocysts and pancreatic
abscesses can result from

ETIOLOGY
G: Gallstone
E: Ethanol
T: Trauma
S: Steroid
M: Mump
A :Autoimmune
S: Scorpion bits
H: Hyperlipidemia
E: ERCP
D: Drugs

ETIOLOGY
Biliary tract disease
One of the most common causes of acute pancreatitis in most
developed countries (accounting for approximately 40% of cases) is
gallstones passing into the bile duct and temporarily lodging at the
sphincter of Oddi, although this has not been definitively proven in
humans. Occult microlithiasis is probably responsible for most cases
of idiopathic acute pancreatitis.
Alcohol use
On the cellular level, ethanol leads to intracellular accumulation of
digestive enzymes and their premature activation and release.
On the ductal level, it increases the permeability of ductules,
allowing enzymes to reach the parenchyma and cause pancreatic
damage.
Ethanol increases the protein content of pancreatic juice and
decreases bicarbonate levels and trypsin inhibitor concentrations.
This leads to the formation of protein plugs that block pancreatic
outflow.

 Endoscopic retrograde
cholangiopancreatography
Pancreatitis occurring after ERCP is probably the
third most common type (accounting for
approximately 4% of cases). Whereas
retrospective surveys indicate that the risk is
only 1%, prospective studies have shown the risk
to be at least 5%. .
Trauma
Abdominal trauma (approximately 1.5%) causes
an elevation of amylase and lipase levels in 17%
of cases and clinical pancreatitis in 5% of cases.
Pancreatic injury occurs more often in
penetrating injuries (eg, from knives, bullets)
than in blunt abdominal trauma (eg, from
steering wheels, horses, bicycles).

 Drugs
Considering the small number of patients who
develop pancreatitis compared to the relatively
large number who receive potentially toxic
drugs, drug-induced pancreatitis is a relatively
rare occurrence (accounting for approximately
2% of cases) that is probably related to an
unknown predisposition. Fortunately, druginduced pancreatitis is usually mild.
Drugs definitely associated with acute
pancreatitis include the following:
Azathioprine, Sulfonamides, Sulindac,
Tetracycline, Valproic acid, Didanosine,
Methyldopa, Estrogens, Furosemide, 6Mercaptopurine, Pentamidine, 5-aminosalicylic

LESS COMMON CAUSES

Infection
Hereditery
Hypercalcemia
Hypertrygleceridemia
Tumor
Toxin
Autoimmune

CLINICAL PRESENTATION
Abdominal pain
Epigastric
Radiates to the back
Worse in supine position
Nausea and vomiting
Garding
Tachycardia, Tachypnea,
Hypotension, Hyperthermia
Elevated Hematocrit & Pre renal
azotemia
Cullen's sign
Grey Turner's sign

Cullen's sign is yellow blue discolouration of the

skin around the umbilicus. commonly
associated with severe, acute pancreatitis.It is
caused by pancreatic enzymes that have
tracked along the falciform ligament and
digested subcutaneous tissues around the
umbilicus

Grey Turner's sign refers to bruising of the

flanks, appearing as a blue discoloration.[1]This
sign takes 2448 hours. It can predict a severe
attack of acute pancreatitis, It is a sign of
retroperitoneal hemorrhage. It may be
accompanied by Cullen's sign, which may then
be indicative of pancreatic necrosis with
retroperitoneal or intraabdominal bleeding.

LABORATORY
serum amylase
Nonspecific
Returns to normal in 35 days
Normal amylase does
not exclude
pancreatitis
Level of elevation
does not predict
disease severity
Urinary amylase
P-amylase
Serum Lipase

CBC
Increased Hb
Thrombocytosis
Leukocytosis

Liver Function Test

Serum Bilirubin
elevated
Alkaline Phosphatase
elevated
Aspartate
Aminotransferase
elevated

RANSON CRITERIA
CRITERIA FOR ACUTE GALLSTONE
PANCREATITIS
Admission
Age > 70
WBC > 18,000
Glucose > 220
LDH > 400
AST > 250

During first 48
hours

Hematocrit drop
> 10 points
Serum calcium <
8
Base deficit > 5.0
Increase in BUN >
2
Fluid
<2 pos sign: mortality rate is 0
3-5 pos sign: mortalitysequestration
rate is 10 to 20% >
>7 pos sign: mortality
4Lrate is >50%

TREATMAENT OF MILD
PANCREATITIS
Pancreatic rest
Supportive care
fluid resuscitation watch BP and urine output
Pain Control
NG tubes and H2 blockers or PPIs are usually not helpful
Refeeding (usually 3 to 7 days) If:
Bowel Sounds Present
Patient Is Hungry
Nearly Pain-free (Off IV Narcotics)
Amylase & Lipase Not Very Useful

TREATMENT OF SEVERE
PANCREATITIS
Pancreatic Rest & Supportive Care
Fluid Resuscitation may require 5-10
liters/day
Careful Pulmonary & Renal Monitoring ICU
Maintain Hematocrit Of 26-30%
Pain Control PCA pump
Correct Electrolyte Derangements (K+, Ca++,
Mg++)
Contrasted CT scan at 48-72 hours
Prophylactic antibiotics if present
Nutritional support
May be NPO for weeks
TPN

GUIDELINES FOR THE MANAGEMENT OF

ACUTE PANCREATITIS
Because acute pancreatitis can usually be diagnosed based
on clinical symptoms and laboratory testing, contrastenhanced computed tomography (CT) scanning and/or
magnetic resonance imaging (MRI) of the pancreas should
performed only in the absence of clinical improvement or a
clear diagnosis
Assessment of the patients hemodynamic status should
occur immediately upon presentation, with resuscitative
measures initiated as necessary
Patients with systemic inflammatory response syndrome
(SIRS) and/or organ failure should, if possible, be admitted
to an intensive care unit (ICU) or an intermediary care
setting
All patients should receive aggressive hydration, unless
this is precluded by cardiovascular and/or renal
comorbidities; aggressive intravenous (IV) hydration is
most effective within the first 12-24 hours, with possibly
little benefit derived from its administration after this point

 Within 24 hours of admission, patients with concurrent acute

cholangitis should undergo endoscopic retrograde
cholangiopancreatography (ERCP); in high-risk patients, the risk
of severe post-ERCP pancreatitis should be reduced through the
use of postprocedure rectal nonsteroidal anti-inflammatory drug
(NSAID) suppositories and/or pancreatic duct stents
The guidelines recommend against routinely using prophylactic
antibiotics in cases of severe acute pancreatitis and/or sterile
necrosis; however, intervention in patients with infected
necrosis may be delayed through the use of antibiotics that
penetrate the necrosis
In mild cases of acute pancreatitis with no nausea and vomiting,
oral feeding can be initiated immediately; enteral nutrition
should be used in severe cases to prevent infectious
complications, and parenteral nutrition should be avoided
Regardless of lesion size, location, and/or extension,
intervention is not necessary for asymptomatic pancreatic
and/or extrapancreatic necrosis and/or pseudocysts
Surgical, radiologic, and/or endoscopic drainage in stable
patients with infected necrosis should be postponed (for 4
weeks if possible) to permit a wall to develop around the
necrosis

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