2. ACUTE PANCREATITIS
2
Acute pancreatitis (AP) is an inflammatory disorder of
the pancreas characterized by severe pain in the upper
abdomen and increased serum concentrations of
pancreatic lipase and amylase.
In the majority of patients, acute pancreatitis is a self-
limiting disease that resolves spontaneously without
complications.
The risk for progression to chronic pancreatitis after an
initial episode of acute pancreatitis is related to the etiology.
3. ETIOLOGY
3
Common (90%)
Gall stones
Alcohol
Idiopathic
Rare
Metabolic: hypercalcemia, hypertriglyceridemia
Drugs: thiazide, azathioprine, sodium valproate, pentamidine
Infection: mumps, coxsackie virus
Post ERCP (due to back pressure of contrast into ductal system)
Trauma
Organ transplantation
Post GI surgery
5. PATHOPHYSIOLOGY
5
The pathophysiology of acute pancreatitis is based on
events that initiate injury and secondary events that
establish and perpetuate the injury.
Gallstones, alcohol abuse, and other causes of pancreatitis
produce different initial insults to the pancreas.
However, the resulting pathophysiologic process may be
similar and include a combination of autodigestion and
inflammatory response.
The pancreas secretes the digestive enzymes as pro
enzymes which are activated in the intestinal lumen.
Acute pancreatitis may result when activation occurs in
pancreatic duct system or acinar cells.
6. Proenzymes
Activated
proteolytic
enzymes
Defective intracellular
transport and
secretion of pancreatic
zymogens
Pancreatic duct
obstruction (common
bile duct stones,
tumors)
Acute pancreatitis
Hyperstimulation of
pancreas (alcohol,
triglycerides)
Reflux of infectedbile
or duodenalcontents
into pancreatic duct
(sphincter of Oddi
dysfunction)
Pancreatic
secretory
trypsin
inhibitors
++
+ +
-
7. 7
The premature activation of trypsinogen to trypsin
within the pancreas leads to activation of other digestive
enzymes and autodigestion of the gland.
In addition to activation of digestive enzymes within the
pancrease, enzymes are also released into surrounding fat,
vascular endothelium and other surrounding tissues and
structures causing further damage and necrosis.
Lipase damages fat cells, producing noxious substances
that cause further pancreatic and peripancreatic injury.
There may be an independent response from intra-acinar
activation of inflammatory factors.
The release of cytokines by acinar cells directly causes
their injury and enhances the inflammatory response.
8. 8
Injured acinar cells liberate chemo-attractants that
recruit neutrophils, macrophages, and other cells to the area
of inflammation. These immune responses cause a
systemic inflammatory response syndrome (SIRS).
Vascular damage and ischemia causes the release of
kinins, which makes capillary walls permeable and
promotes tissue edema.
The release of damaging oxygen-free radicals appears to
correlate with the severity of pancreatic injury.
Finally, pancreatic infection may result from increased
intestinal permeability and translocation of colonic
bacteria.
9. CLINICAL PRESENTATION
9
• Upper abdominal pain that radiates into the back; it may be
aggravated by eating, especially foods high in fat.
• Swollen and tender abdomen
• Nausea and vomiting
• Fever
• Increased heart rate
• Respiratory distress
• Severe advanced cases may develop bruising and
discoloration in the left flank (Grey Turner’s sign due to
tissue catabolism of Hb) and around the umbilicus
(Cullen’s sign due to hemoperitoneum). These are the rare
and late signs of extensive pancreatic destruction
11. 11
Diagnosis
The diagnosis of acute pancreatitis requires two of the
following three: upper abdominal pain, a serum lipase or
amylase concentration at least three times greater than the
upper limit of normal, or characteristic findings on imaging
studies.
Lipase is more sensitive and specific than amylase and
is the preferred laboratory test. Imaging studies are not
necessary for diagnosis if the other two findings are
positive.
12. 12
Clinical Course and Prognosis
The clinical course of acute pancreatitis varies from a mild
transitory disorder to a severe necrotizing disease.
Mild acute pancreatitis is self-limiting and subsides
spontaneously within 3 to 5 days.
Mortality is influenced by etiology, as idiopathic and
postoperative acute pancreatitis have higher rates than
gallstone- or alcohol-related disease.
First and second occurrences also carry a higher mortality
than subsequent episodes.
13. 13
Complications
Early complications are a result of SIRS and organ failure.
The most common systemic complication of acute
pancreatitis is respiratory failure.
In addition, patients may experience systemic
complications due to exacerbation of pre-existing renal,
lung or heart disease.
A second phase occurs in patients with moderately severe
or severe disease.These patients have persistent organ
failure and may have local complication including fluid
collections that may become necrotic.
14. 14
Long-term complications include glucose intolerance and
recurrence of acute pancreatitis.
There are also local complications that may occur,
including interstitial pancreatitis (acute peripancreatic
fluid collection and pancreatic pseudocysts) and collection
of necrosis. These develop approximately 3 to 4 weeks
after the initial attack.
Pancreatic infections occur in 15% to 30% of those with
pancreatic necrosis and are usually secondary infections of
necrotic tissue.
15. TREATMENT
15
Desired Outcomes
Treatment of acute pancreatitis is aimed at relieving
abdominal pain and nausea, replacing fluids, correcting
electrolyte, glucose, and lipid abnormalities, minimizing
systemic complications, and managing pancreatic necrosis
and infection.
Management varies depending on the severity of the attack.
Patients with mild acute pancreatitis respond very well to
the initiation of supportive care.
Patients with severe acute pancreatitis should be treated
aggressively and monitored closely.
16. 16
General Approach to Treatment
All patients with acute pancreatitis should receive
supportive care, including IV fluid resuscitation, adequate
nutrition, and effective relief of pain and nausea.
Patients should be evaluated for admission to the intensive
care unit.
Patients predicted to follow a severe course may require
treatment of systemic complications.
Fluid therapy is recommended and may help prevent organ
failure.
17. 17
Patients with pancreatitis and SIRS should be treated
according to SIRS guidelines.
IV potassium, calcium, and magnesium are used to correct
electrolyte deficiency states.
Insulin is used to treat hyperglycemia.
Local complications resolve as the inflammatory process
subsides.
However, patients with necrotizing pancreatitis may require
antibiotics and procedural intervention.
18. 18
Non pharmacologic Therapy
Nonpharmacologic therapy includes ERCP(endoscopic
retrograde cholangio pancreatography) for removal of any
underlying biliary tract stones, procedural interventions,
and nutritional support.
Advances in minimally invasive surgical techniques are
changing practice with respect to timing and approach to
managing infected necrotizing pancreatitis, and may help
lower the risk of mortality in the most critical patients.
19. 19
Nutrition
Nutritional support plays an important role in the
management of patients with mild or severe disease as
acute pancreatitis creates a catabolic state that promotes
nutritional depletion. This can impair recovery, increase the
risk of complications, and prolong hospitalization.
Patients with mild acute pancreatitis can begin oral feeding
when pain is decreasing and inflammatory markers are
improving. It is not necessary to withhold oral nutrition
until lipase normalizes.
20. 20
In severe or complicated disease, nutritional deficits
develop rapidly and are complicated by tissue necrosis,
organ failure, and surgery.
If enteral feeding is not possible or if the patient is unable
to obtain sufficient nutrients, total parenteral nutrition
should be implemented before protein and calorie depletion
become advanced.
ASPEN guidelines state that IV lipids are considered safe
unless the serum triglyceride concentration is greater than
400 mg/dL (4.52 mmol/L) and the patient has a history of
hyperlipidemia.
21. 21
Pharmacologic Therapy
Patients with acute pancreatitis often require IV antiemetics
for nausea.
Those requiring ICU admission should be treated with
antisecretory agents (such as famotidine or pantoprazole) if
they are at risk of stress-related mucosal bleeding.
Patients also require appropriate fluid resuscitation and pain
management.
22. 22
Fluid Resuscitation
Vasodilation from the inflammatory response, vomiting,
and nasogastric suction contributes to hypovolemia and
fluid and electrolyte abnormalities, thus necessitating
replacement.
Patients with acute pancreatitis should receive aggressive
fluid replacement to reduce the risks of persistent SIRS
and organ failure.
The IAP/APA guidelines recommend goal directed
intravenous fluid with lactated Ringer’s at an initial rate of
5 to 10 mL/kg/h while the ACG guidelines recommend 250
to 500 mL/h with crystalloids.
23. 23
Goals for fluid therapy are one or more of the following:
Heart rate less than 120/min
Mean arterial pressure 65 to 85 mm Hg,
Urinary output greater than 0.5 to 1 mL/kg/h,
Invasive measures of stroke volume or intrathoracic blood
volume, or
Hematocrit 35% to 44% (0.35-0.44) with transfusion of
blood.
Patients with SIRS or sepsis should be resuscitated according
to sepsis guidelines
24. 24
Relief of Abdominal Pain
Parenteral opioid analgesics are used to control
abdominal pain associated with acute pancreatitis despite a
lack of high quality evidence to support the practice. A
Cochrane review found a lack of studies to support any
specific agent or class of agents for pain management in
acute pancreatitis.
Parenteral morphine is often recommended for pain
control because it provides a longer duration of pain
relief than other opioids.
Although morphine increases biliary pressure, there is no
evidence to indicate that it is contraindicated for use in
acute pancreatitis.
25. 25
Antimicrobial use in Acute Pancreatitis
Use of prophylactic antibiotics is not recommended in
patients with acute pancreatitis without signs or symptoms
of infection, including those with necrosis.
However, empiric antimicrobial therapy may be considered
in patients with necrosis who deteriorate or fail to improve
with in 7 to 10 days.
Because the source of bacterial contamination is most
likely the colon, the antibiotic regimen for patients with
known or suspected infected pancreatitis should be broad-
spectrum, covering the range of enteric aerobic gram-
negative bacilli and anaerobic microorganisms.
26. 26
Antibiotics of choice are CARBAPENAMS.
IMIPENAM 500 mg 8th hourly given.
Patients with infected necrotic pancreatitis are generally
treated with a combination of invasive interventions and
antibiotics.
Antibiotics alone may be sufficient in some cases or at least
delay the need for an invasive procedure long enough for
the necrotic areas to be walled off.
