ACUTE PANCREATITIS

STRUCTURES
• The pancreas is situated retroperitoneally with
the second part of the duodenum wrapping
around the head. The tail of the pancreas lies
over the spleen.
• The exocrine secretion is drained by a
branching system of ducts, draining into the
main pancreatic duct. This usually enters the
second part of the duodenum together with the
common bile duct at the ampulla of Vater.
There is considerable anatomical variation.
 FUNCTIONS
• The majority of the pancreatic cells are
concerned with its exocrine function.
Release of secretin from acid stimulation of
the duodenum causes production of water ,
electrolytes and bicarbonate from the
pancreas.
• The endocrine function of the pancreas is
served by the islets of Langerhans.Within
these,most cells secrete insulin.
 DEFINITIONS
• Acute pancreatitis is an acute inflammatory
process arising in the exocrine pancreas, with
variable involvement of adjacent and remote
organs.
• The inflammation begins in the perilobular and
peripancreatic fatty tissue, manifested by edema
and spotty fat necrosis.The disease may progress
to the peripheral acinar ce1ls, pancreatic ducts,
blood vessels, and bordering organs.
• In severe cases, patchy areas of the pancreatic
parenchyma become necrotic.
• Although pancreatic function and structure
eventually return to normal, the risk of
recurrent attacks is nearly 50% unless the
precipitating cause is removed.
• Initia1 manifestations and pains of chronic
pancreatitis may be indistinguishable from
attacks of acute pancreatitis. And they
should be treated as such.
 PATHOGENESIS
• Premature activation of zymogens and the escape of activated enzymes
from acinar cells and pancreatic ducts set the stage for the autodigestive
process that represents acute pancreatitis.
• Based on clinical and experimental observations, several mechanisms
have been proposed to initiate acute pancreatitis. Among these, ref1ux
of duodenal contents or bile into the pancreatic duct is no longer
considered to play a role. Obstruction of the pancreatic duct near the
ampulla of Vater remains a plausible mechanism that may explain
many, although not all, episodes of acute pancreatitis 。
 ETIOLOGIC
ASSOCIATIONS
•ASSOCIATED
FACTORS∶
• Clinical conditions, medications, and toxins are
all known to precipitate acute pancreatitis.
Among these, choledocholithiasis and alcohol
abuse account for 70 to 80% of all cases.
• All remaining causes combined account for l0%
or less of the tota1.
• Alcohol.
• Fully 70 to 80% of patients with chronic pancreatitis are chronic alcohol
abusers. Alcoholic pancreatitis, even when if presents as an acute episode, is
a chronic progressive disease. Typically, the initial symptoms appear at ages
35 to 45, but some patients may experience their first attack before age 25.
Alcoho1ic liver disease develops in 40 to 50% of patients and frequently
becomes manifest 5 to 10 years after the onset of pancreatitis.
• Alcohol abstinence offers moderate and unpredictable benefits in terms of
pain relief and 1ater development of diabetes but does not alter the
progression of pancreatic fibrosis and exocrine insufficiency. The
mechanism of alcoho1-induced pancreatic injury remains unknown.
• Hypertriglyceridemia:
• The presence of lipemia ， with serum triglyceride
1evels ＞ 1000mg per deciliter （ 11.29mmol ／
L ）， represents a cause ， not an effect ， of
pancreatitis 。 Causes include estrogen therapy,
alcoholism ， intravenous lipid infusions ， and
primary hyperlipidemias 。
• Multi-ply Factors∶
• Acute hypercalcemia may trigger acute pancreatitis 。 This may occur
with intravenous calcium infusions and with vitamin D poisoning ．
• Blunt abdominal trauma causes pancreatitis by disrupting the duct ； it is
the most common cause of pancreatitis in children 。
• Postoperative pancreatitis may follow intra- and extra-abdomina1 surgery
and carries a high mortality rate of 25 to 50 ％。
• Pancreatitis following endoscopic
retrograde cholangiopancreatography
（ ERCP ） is usually mild unless it is
complicated by duodena1 perforation
during endoscopic sphincterotomy 。
• Pancreatic infections are an exceeding1y
rare and poorly documented cause of
pancreatitis ．
 CLINICAL
PRESENTATIONS
• Steady ， dull ， or boring mid—epigastric pain associated with nausea and
vomiting is the classic presentation of acute pancreatitis 。 The pain reaches
peak intensity within15 minutes to 1 hour from onset ， in contrast to the
more abrupt onset of pain with a perforated viscus 。 It radiates straight to
the midline of the lower thoracic vertebral region in about 50 ％ of patients
and is usually worse in the supine position.
• Painless acute pancreatitis is very rare but carries a grave prognosis because
the patients frequently present in shock 。
• Initial physical examination reveals mild fever and tachycardia ；
hypotension is present in 30 to 40% of patients 。
• There is marked tenderness to deep palpation of the upper
abdomen ， but signs of peritoneal irritation such as abdominal wall
rigidity and rebound tenderness are absent 。
• Bowel sounds are diminished ； paralytic ileus with abdominal
distention may develop during the first few days, signifying
extension of the inflammatory process into the small intestinal and
colonic mesentery.
• One to two weeks after the onset, large ecchymosis rarely
appear in the f1anks(Grey Turner's sign) or the umbilical
area(Cullen's sign).
• These represent blood dissecting from the
retroperitoneal1y located pancreas along fascial planes.
• Similarly, inflammatory masses, large fluid collections, or
a pancreatic abscess may become palpable later in the
course of the disease.
DIAGNOSIS
• The diagnosis of acute pancreatitis rests on a
combination of clinical, laboratory, and radiologic
findings, none of which is infallible. The goals of
diagnostic studies are
• (1) to exc1ude other acute conditions that may
require urgent surgical management;
• (2) to assess the prognosis;
• (3) to detect local and systemic complications early;
• (4) to identify a precipitating cause
LABORATORY TESTS
• Amylase.
• Total serum amylase activity is the test most frequently used to diagnose acute pancreatitis. The
level rises 2 to l2 hours after onset of symptoms and remains e1evated for 3 to 5 days in most
cases. Va1ues>5 times the upper limit of normal are highly specific for acute pancreatitis, but these
are found in only 80 to 90% of cases.
• The magnitude of the rise in serum amylase does not correlate with the severity of the attack, nor
does prolonged hyperamylasemia indicate developing complications. Marked hypetriglyceridemia,
sufficient to give the serum a lipemia appearance ， masks elevations in serum amylase and
lipase ； dilution of these sera leads to a paradoxical rise in the reported enzyme values 。
• Separation of total serum amylase into its pancreatic (P) and
salivary （ S ） isoenzymes and measurements of urinary amylase
output add 1ittle to the diagnostic information 。
• Serum amylase may be elevated in many other clinical
conditions ， such as chronic pancreatitis ， perforation of
viscus ， mesenteric infarction ， metabolic acidosis ；
carcinoma of the pancreas ， illustrating the fact that the diagnosis
of acute pancreatitis should not be based so1ely on laboratory
results 。
• Lipase.
• Serum lipase assays ， have similar
specificity ， and sensitivity as serum
amylase 。 The serum lipase tends to remain
e1evated longer than amylase during the healing
phase of pancreatitis.
• Combinations of Serum Enzyme
Tests∶
• The combination of serum amylase and lipase
determinations is more accurate than either test
alone 。 The diagnostic accuracy can be
improved further by ca1culating cut-off values
that lie above the upper limit of normal.
• Other B1ood Tests:
• Leukocytosis of up to 25000 cells per cubic mi1limeter is present in 80% of
patients.
• Hypocalcemia occurs in up to 30% of patients due to a combination of
hypoalbuminemia and calcium precipitation in areas of fat necrosis. The
ionized calcium concentration remains norma1, and symptoms of tetany are
extremely rare;Pre-existing hypercalcemia may, however, be obscured by
the ca1cium-lowering effect of pancreatitis.
• Transient mi1d hyperg1ucemia is common and does not require insulin
treatment.
• Elevation of serum triglyceride leve1s should be obtained in all patients
with liver disease or to the pancreatic inf1ammation itself because of
their etiologic imp1ications and to help interpret unexpectedly normal
serum amy1ase and lipase levels.
• Elevated alanine aminotransferase (ALT) and a1kaline phosphatase
(ALP) va1ues suggest ga1lstone-associated pancreatitis. The serum
aspartate aminotransferase (AST) is elevated in approximately 50% of
patients owing to alcoho1ic abuse.
• A positive score consists of three or more of the
fo1lowing tests exceeding the stated limit:
（ 1 ） alkaline phosphatase ＞ ULN （ upper limit of
normal ）；

•（ 2 ） total bilirubin ＞ ULN ；

（ gallstones or bile duct dilatation with a positive

biochemical score is indicative of this situation)

•（ 3 ） gamma glutamyltransferase ＞ 2× ULN ；

•（ 4 ） ALT ＞ 1.5×ULN ；

•（ 5 ） ALT ／ AST ＞ 1.0

• Abdominal Ultrasonography (US) and Computed Tomography (CT)
Scan.
• These two imaging modalities play important and complementary roles in
diagnosing and managing acute pancreatitis.
• US is the method of choice for detecting cholelithiasis and for determining the
diameter of the extrahepatic and intrahepatic bile ducts. Di1atation of these
ducts suggests recent or persisting impaction of a stone in the distal common
bile duct or the ampulla of Vater.
• US also very accurate1y detects acute cholecystitis.
• The CT scan is the primary modality for assessing the extent and local
complications of pancreatitis. It is far superior to US in this regard. The
examination shou1d be performed with rapid intravenous bo1us injection of
contrast material (dynamic CT scan).
• The CT scan revea1s extension of peripancreatic inflammation, involvement of
adjacent organs,venous thrombosis(splenic vein) , and f1uid co1lections. Most
importantly, pancreatic necrosis can be identified and quantitated by the lack of
contrast enhancement following the bolus injection.
• The abdominal CT scan may be normal, however, in about 10% of patients with
ear1y, mi1d pancreatitis.
• Differentia1 Diagnosis∶
• There is no sing1e absolute criterion for the diagnosis of acute
pancreatitis 。 The differential diagnosis shou1d focus on other
conditions presenting with acute upper abdominal pain which require
specific therapy 。
• These include perforated peptic ulcer ， acute cholecystitis ， and
mesenteric vascular occlusion.
• A ga11stone impacted in the ampulla of Vater may not only delay the
resolution of bi1iary pancreatitis but a1so cause combination of
positive US findings.
CLINICAL COURSE
AND THERAPY
• Mild Pancreatitis
• Mi1d acute pancreatitis is defined by the absence of systemic and local
complications. About 80% of patients belongs to this category and
require<1 week of hospitalization.
• Treatment consists of general supportive care and close monitoring for
signs of systemic complications; local complications tend to manifest
during the second and third week of illness. There is no evidence that any
medication is specifical1y beneficial.
• The intravascular volume deficit may exceed 30% due to
peripancreatic fluid sequestration and vomiting. Volume
restoration must be rapid and efficient in order to
maintain regularly monitored urine output of 40 ml per
hour.
• The patient receives nothing by mouth, with the goal of
resting the pancreas. Nasogastric aspiration is indicated
in the presence of vomiting or developing ileus; this need
not be initiated routine1y.
• The patient should receive sufficient analgesic
medications to alleviate pain.
• Systemic Complications
• Most systemic complications occur during the first week of illness.
They are treated by standard medica1 measures. Close patient
monitoring is the key to their timely recognition.
• 1.Circulatory shock arises by a combination of volume depletion and
a hyperdynamic circu1atory state with decreased peripheral vascular
resistance. The management includes transfer to an ICU, volume
replacement, and vasopressor substances. The occurrence of shock is
frequently followed by pancreatic necrosis.
• 2. Acute renal failure may be caused by circu1atory
shock and a selective increase in renal vascular resistance.
The treatment is that of acute tubular necrosis arising in
any setting.
• 3.The 1eading cause of respiratory insufficiency during
acute pancreatitis is the adult respiratory distress
syndrome(ARDS). A1though respiratory depression
caused by opiate medications, p1eural effusions, involves
damage to the pulmonary surfactant layer by circulating
phospholipase A and free fatty acids.
• 4. Sepsis is most commonly caused by infection of the bile
ducts, of areas of pancreatic necrosis, or of peripancreatic
f1uid collections .
• 5. Ascending cholangitis and severe bi1iary pancreatitis
present over1apping features and may coexist. Gram-
negative bacteremia and spiking fevers are more common
with infection of the biliary tract, whereas
hyperbilirubinemia may be mild or absent in this
situations. Appropriate antibiotic therapy should be
instituted.
LOCAL COMPLICATIONS
• Pancreatic Necrosis (or abscess) ：
• Pancreatic necrosis(PN) is found by dynamic CT
scanning in approximately 80% of patients with
clinically severe disease ( 6% of the tota1),
usually during the second or third week of
illness. PN, however, is present in approximately
40% of patients within 4 days of symptom onset.
It fo11ows that PN resolves without incident in
nearly 60% of patients who develop it.
• Therapy and prognosis of the severely patients with PN depend
crucia1ly on the presence of necrotic tissue. This question
should be answered by fineneedle aspiration of necrotic areas
under CT guidance before the patient leaves the CT suite.
• A Gram stain of the aspirate is>95% accurate in predicting the
final results of bacterial cu1tures.
• Antibiotics with high penetration into pancreatic tissue include
the fluroquinolones, imipen/cilastatin and metronidazole.
• The morta1ity of patients with infected PN treated
conservatively is 60 to l00%. Immediately removing
necrotic tissue (necrosectomy), combined with continued
1avage of the necrotic space, lowers the morality to about
20%.
•The patients frequently require re-operation for
continuing necrosis and other local complications, such as
bleeding and fistula formation.
•The management of patients with sterile PN remains
controversial.
• Fluid Collections ：
• These occur within or around the pancreas is up to 50% of patients
with severe pancreatitis. The majority resolve spontaneous1y;
collections that persist for>6 weeks develop a wall of granulation
tissue and are then called pseudocysts . Collections that continue to
expends or become infected require drainage.
• Pancreatic abscesses contain 1iquid pus and may be considered to
represent infected fluid collections.
• Pancreatic ascites reflects involvement of peritoneal surfaces by the
inf1ammatory process and, rarely, the rupture of a pancreatic duct with
pancreatic juice entering into the peritoneal cavity.
• BLEEDING:
• There are several causes of b1eeding during acute
pancreatitis.
• Hemorrhage may occur into necrotic intrapancreatic and
peripancreatic tissue and into f1uid co1lections.
• Brisk hemorrhage occurs with erosion of the splenic or
gastroduodenal arteries. At times, the blood gains access
to a disrupted pancreatic duct and empties into the
duodenum. Diffuse mucosa1 bleeding from antrum and
duodenum is common but rarely severe.
• Final1y, bleeding may signal perforation of
peripancreatic inflammation into any portion of
the gastrointestinal tract from esophagus to colon.
• The spleen may become involved by direct
extension of the inflammatory process or,
secondarily, by splenic vein thrombosis. The latter
complication leads to gastric fundic varices.
 PREVENTING
RECURRENCES
• The search for the precipitating cause begins during the
acute attack.
• Serum calcium and triglyceride leve1s are determined.
• An abdominal US examination is performed routinely. If
gallstones are detected, the patient should undergo early
cholecystectomy, preferably before discharge from the
hospital. The absence of choledocholithiasis must be
ascertained before or during this surgical procedure
• At this stage, approximately 20% of patients are assumed to
have idiopathic pancreatitis.
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