HOW to Diagnose and Manage Acute pancreatitis by Dr.Mohammed Hussien

1. Dr/ Mohammed Hussien
Assistant Lecturer of Gastroentrology & Hepatology
Kafrelsheikh University
Acute pancreatitis

2. 2016 By Dr Mohammed Hussien
 Objectives
 Definition
 Pathogenesis
 Diagnosis
 Pervention
 Treatment
Acute pancreatitis

3. Objectives
o Establish the Diagnosis of Acute Pancreatitis
o Establish the Etiology of Acute Pancreatitis
o Initial Management of Acute Pancreatitis
ALL RECOMMENDATIONS ARE BASED ON THE LATEST ACG MANAGEMENT
2016 By Dr Mohammed Hussien

4. Acute pancreatitis
Definition
• Acute pancreatitis (AP) is an inflammatory syndrome initiated by pancreatic
injury and activation of pancreatic digestive enzymes, leading to direct and
indirect activation of the immune system
• ACG ----Acute pancreatitis requires 2 of 3 diagnostic signs
• – Amylase or lipase 3× upper limit of normal values
• – Characteristic sudden onset abdominal pain
• – Characteristic changes on abdominal images
• Contrast-enhanced computed tomographic (CECT) and / or magnetic
resonance imaging (MRI) of the pancreas should be reserved for patients in
whom the diagnosis is unclear or who fail to improve clinically within the fi
rst 48 – 72 h after hospital admission

5. Epidemiology
Mohammed Hussien 2016
 Acute pancreatitis is the third most common inpatient gastrointestinal
diagnosis in the United States.
 While most patients have a benign course, approximately 15% either
present with or develop single or multiple organ involvement and/or
pancreatic necrosis within the first 72 hours, resulting in prolonged
hospitalization and significant morbidity and mortality
 In the United States, more than 80% of the cases of acute pancreatitis
are caused by binge drinking of ethanol or by biliary stones

6. Causes and pathogenesis
• Biliary (eg, gallstones, gallbladder microlithiasis/sludge)
Biliary pancreatitis is most commonly caused by the passage of a
stone from the gallbladder through the cystic duct into the common
bile duct; impaction at the ampulla of Vater causes reflux of bile into
the pancreatic duct.
premature activation of intracellular trypsinogen (which causes acinar
cell injury) and the release of chemokines and cytokines
• Post ERCP Hyperamylasemia and abdominal pain are common
after endoscopic retrograde cholangiopancreatography (ERCP) , but
evidence of significant pancreatitis occurs in less than 5% of
patients undergoing ERCP.
2016

7. 2016
• Alcoholconsume large quantities of alcohol for 5 to 10 years before the first attack. may
occur with as little as 25 g (or two drinks) per day.
• A polymorphism in the detoxifying enzyme uridine 5-diphosphate (UDP) glucuronyl transferase
(UGT1A7★3) confers an increased risk for alcoholic pancreatitis
• Environmental factors or cofactors such as smoking and consumption of a high-fat diet
may also affect a person's susceptibility to the disease.
• Sphincter of Oddi spasm in the presence of stimulated pancreatic secretion, obstruction
of small ductules by proteinaceous plugs,
• oxidative and nonoxidative processes
• Direct toxic effects of alcohol metabolic byproducts
• Alcohol may also change the amounts of potentially damaging proteases in
pancreatic secretions
• Increased amounts of lysosomal enzymes
• increased trypsinogen–pancreatic trypsin ratio have been reported in the pancreatic
juice of alcoholic patients
Mechanism

8. 2016
Autoimmune disease:
Iatrogenic:
Drug-induced:

9. 2016
Surgery (eg, common bile duct exploration, sphincterotomy,
splenectomy, distal gastrectomy)
Idiopathic
Infectious (eg, ascariasis, clonorchiasis, mumps, toxoplasmosis,
coxsackievirus, cytomegalovirus, tuberculosis, Mycobacterium
avium complex)
Inherited (Genetic)
•CFTR (cystic fibrosis transmembrane conductance regulator)
•mutations
•SPINK1 (serine protease inhibitor Kazal type 1) mutations
•PRSS1 (cationic trypsinogen) mutations

10. 2016
Metabolic (eg, hypercalcemia, hypertriglyceridemia)
Serum triglyceride levels higher than 1000 mg/dL may precipitate attacks of acute pancreatitis, and
lowering serum triglyceride levels to less than 200 mg/dL can prevent pancreatitis. It is currently believed
that pancreatitis occurs as a result of the harmful effects of fatty acids released into the pancreatic
circulation or parenchyma by the action of pancreatic lipase.
Hypercalcemia secondary to hyperparathyroidism, immobilization, multiple myeloma, or total parenteral
nutrition has been linked to hyperamylasemia but probably causes pancreatitis infrequently.
Malignancy (eg, pancreatic or ampullary tumors)
Structural (eg, pancreatic divisum Pancreas divisum results from failure of the ventral and dorsal ducts
to join during fetal development; the small accessory duct of Santorini and minor papillae may produce
high outflow resistance, Sphincter of Oddi dysfunction or pancreas divisum has been reported in more
than 25% of patients with idiopathic pancreatitis in some series, although whether this association is
causal or coincidental is difficult to determine, annular pancreas, sphincter of Oddi dysfunction,
periampullary diverticula, duodenal duplication cysts, choledochocele, anomalous pancreaticobiliary
junction, regional enteritis
Toxic (eg, organophosphates, scorpion venom)
Traumatic (especially motor vehicle accidents)----- Reduced vascular perfusion (e.g., shock), as may
occur when surgical procedures are associated with hypotension or hypoperfusion.
Vascular : hypotension or hypoperfusion.

11. 2016
Pathobiology
Pathologically, two morphologic classifications are recognized: acute
interstitial pancreatitis and acute hemorrhagic pancreatitis. The latter
type is associated with much higher morbidity and mortality.
The fundamental mechanism for transformation of the initial injury
into pancreatitis appears to be intracellular activation of digestive
enzymes and autodigestion. The complex cascade of cellular events
leading to acute pancreatitis begins in the pancreatic acinar cells.
Intracellular conversion of pancreatic zymogens into active enzymes
most likely involves several pathways, including
(1) cleavage of trypsinogen to trypsin by the lysosomal hydrolase
cathepsin B,
(2) disruption of intracellular Ca2+ signaling, and
(3) trypsinogen autoactivation.

12. 2016
Clinical Manifestations
The typical symptoms of acute pancreatitis are abdominal pain, nausea, and vomiting.
Pain usually develops first and remains constant, without the waxing and waning
pattern typical of intestinal or renal colic). The pain is frequently located in the
epigastrium with radiation to the midback region; it typically lasts for hours to days
and is not relieved by vomiting. Increased pain when supine prompts many patients to
sit leaning forward in an effort to minimize discomfort. However, 5% of patients with
acute pancreatitis present without abdominal pain.
vary with the severity of the attack, from minimal
local tenderness to marked generalized rebound tenderness, guarding, and
abdominal distention. Bowel sounds are frequently diminished or absent because of
intestinal ileus.
Jaundice can occur even without stone-induced pancreatitis as a result of compression
of the common bile duct by the edematous pancreas. With severe attacks,
hypotension, tachypnea, tachycardia, and hyperthermia may be noted.
Fever is usually less than 38.5° C.
large ecchymoses may occasionally appear in the flanks (Grey Turner's sign) or the
umbilical area (Cullen's sign);
Abdominal findings

13. 2016
Common complications in acute pancreatitis
Pancreatic Ductal
• Duct disruption
_ With fluid collections
– Unorganized (previously called phlegmon)
– Organized (pseudocysts)
_ With fistula
– Pancreatic ascites
– Pleural effusion
• Duct obstruction
_ Pancreatic Stone, stricture, or other with upstream ductal dilation
– Stone, stricture, or other with upstream fluid leak
_ Biliary Stone, stricture, or other with abnormal liver injury tests
– Stone, stricture, or other with bacterial cholangitis

14. 2016
Vascular
• Pancreatic necrosis
• Portal vein thrombosis
• Splenic vein thrombosis
• Hemorrhage from
pseudoaneurysms
– Hemosuccus pancreaticus
– Pseudocysts
– Retroperitoneal Inflammatory
• Pancreatic abscess
• Pseudocysts
• Post-necrotic fluid collections
– Sterile pancreatic necrosis
– Infected pancreatic necrosis
• Inflammatory mass
Peripancreatic
• Peripancreatic fat necrosis
• Duodenal stenosis – obstruction
• Colonic stenosis – obstruction
Extrapancreatic
• Abdominal compartment syndrome – (intra-abdominal
pressure of
20–25 mmHg or higher)
• Systemic inflammatory complications
– Systemic inflammatory response syndrome (SIRS)
– Compensatory anti-inflammatory response syndrome
(CARS)
– Infections
• Distant organ dysfunction/failure
_ Vascular leak syndrome
_ Cardiovascular
– Hypotension
– Shock
_ Pulmonary
– Pulmonary edema (capillary leak rather than heart failure)
– Adult respiratory distress syndrome
_ Intestine
– Ileus
– Leaky gut syndrome
_ Renal
– Pre-renal azotemia
– Acute tubular necrosis

15. 2016
Laboratory Findings
Serum Amylase
Typically, the serum amylase level rises rapidly over the initial 2 to 12
hours of an attack and then slowly declines to its normal values over the
next 3 to 5 days.
Hyperamylasemia is not specific to pancreatitis, but marked elevations
in serum amylase (more than three times the upper limit of normal)
The magnitude of hyperamylasemia has no prognostic value
Hyperamylasemia may result from small bowel obstruction,
perforation, or infarction; a perforated duodenal ulcer; or liberation of
amylase into the circulation from nongastrointestinal sources such as the
lung, fallopian tubes, and salivary & release of amylase from certain
tumors or be caused by reduced renal clearance of amylase secondary to
renal failure
Diagnosis

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Macroamylasemia, an unusual but not rare condition, can occasionally
cause isolated elevation of the serum amylase level. In this condition,
amylase is bound to an abnormal serum protein; the complex is not
cleared by the kidney and results in hyperamylasemia..
Differentiation from pathological hyperamylasemia relies on
calculating the amylase-to-creatinine clearance ratio (ACCR), which
equals (serum creatinine × urine amylase)/(urine creatinine × serum
amylase) × 100. An ACCR less than 1% suggests macroamylasemia.
Amylase activity in blood is composed of isoenzymes from both the
pancreas and salivary glands. Pancreatic isoamylase normally accounts
for approximately 40% of total serum amylase activity. In acute
pancreatitis, serum pancreatic isoamylase increases substantially.
Unfortunately, such increases can also occur in conditions other than
acute pancreatitis, including intestinal injury and renal insufficiency,
thereby rendering its measurement nonspecific.

17. 2016
Serum Lipase
During acute pancreatitis, serum lipase levels increase in parallel with serum
amylase levels. The lipase level remains elevated longer and thus may help
diagnose pancreatitis after an attack has passed. Additionally, lipase levels are
normal in patients with macroamylasemia and parotitis.
Routine laboratory tests in patients with moderate to severe acute pancreatitis
usually reveal leukocytosis. Transient mild hyperglycemia is common and occurs
when excess glucagon is released from alpha cells of the islets of Langerhans.
Hypocalcemia is generally caused by extravasation of nonionized, albumin-bound
calcium from inflamed retroperitoneal and, at times, peritoneal surfaces; this form of
hypocalcemia is common, usually causes no symptoms, and requires no treatment. In
necrotizing pancreatitis, hypocalcemia can be more severe because of loss of ionized
calcium within areas of fat necrosis in the pancreas and peripancreatic tissue.
Correlates with severity of the disease. Levels lower than 7 mg/dL (1.75 mmol/L)
(when serum albumin is normal) are associated with tetany and an unfavorable
prognosis.
Hyperbilirubinemia and elevations in serum aminotransferase and alkaline
phosphatase levels are seen in up to 50%

18. 2016
Imaging
Chest radiographs may show pleural effusions and basilar atelectasis. Bilateral
pulmonary opacification with a normal-sized heart is the hallmark of adult respiratory
distress syndrome (ARDS;
Abdominal radiographs should be obtained to exclude nonpancreatic diseases
such as intestinal perforation. Intestinal gas patterns may indicate ileus, which may
sometimes appear as an isolated dilated loop of small bowel overlying the pancreas (a
sentinel loop) or dilation of the transverse colon with abrupt termination of the gas
column at the splenic flexure (colon cutoff sign) when the inflammatory process
affects the phrenicocolic ligament.
Ultrasound and Computed Tomography
US is the single best noninvasive test for detecting cholelithiasis ,although it is less
reliable for direct visualization of a bile duct stone. An inflamed pancreas
CT is the primary modality for evaluating the extent and local complications of
pancreatitis. Pancreatic inflammation may be seen as pancreatic enlargement,
inhomogeneity of the pancreatic parenchyma, or fluid infiltrating the peripancreatic fat
in 90% of patients

19. 2016
Magnetic Resonance Imaging and Endoscopic Retrograde Cholangiopancreatography
Magnetic resonance imaging (MRI)
MRI is better than CT for distinguishing between an uncomplicated pseudocyst and one that
contains necrotic debris. Though more expensive and less accessible, MRI is preferred in
patients who are pregnant or have contrast allergies. In patients with suspected biliary
pancreatitis, magnetic resonance cholangiopancreatography (MRCP) may identify more than
90% of bile duct stones.
ERCP is not useful for establishing the diagnosis of acute pancreatitis
very useful to diagnose and treat persistent bile duct stones in acute pancreatitis. It should also
be used in the investigation of patients with unexplained recurrent pancreatitis. It is especially
useful for the diagnosis of mild chronic pancreatitis, pancreas divisum, or sphincter of Oddi
disease. However, it should be noted that pancreatitis occurs in about 5% of patients undergoing
ERCP. This risk for pancreatitis increases significantly in female patients with normal serum
bilirubin, patients suspected of sphincter of Oddi dysfunction, and those with a previous history
of post-ERCP pancreatitis. In fact, patients with the lowest probability of harboring truly
obstructive pathology are at the highest risk for the development of pancreatitis after ERCP, even
if the procedure is performed for diagnosis alone.
Endoscopic ultrasound (EUS) have accuracy rates rivaling that of ERCP, they may be preferable
to ERCP for patients with equivocal evidence of biliary obstruction, especially those at high risk
for post-ERCP pancreatitis.

20. 2016
Scoring systems (Evaluation of Severity)

21. 2016
Prognostic Criteria for Acute Pancreatitis (Ranson Criteria)
Ranson Criteria
At admission 48 hr after admission
 Age >55
 Hematocrit decrease >10%
 Leukocyte count
>16,000/µL
 Serum urea nitrogen
increase >5 mg/dL
 Lactate
dehydrogenase
>350 IU/L
 Calcium <8 mg/dL
 Glucose >200
mg/dL
 Arterial PO2 <60 mm Hg
 Aspartate
aminotransferase
>250 IU/L
 Base deficit >4 meq/L
 Estimated fluid
sequestration >6 L

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Simplified Glasgow Criteria
Within 48 hr of admission
 Age >55
 Leukocyte count >15,000/µL
 Lactate dehydrogenase >600 IU/L
 Glucose >180 mg/dL
 Albumin <3.2 g/dL
 Calcium <8 mg/dL
 Arterial PO2 <60 mm Hg
 Serum urea nitrogen >45 mg/dL
The Acute Physiology and Chronic Health Evaluation (APACHE) II system uses
14 routinely measured parameters to produce a numerical score based on a patient's
deviation from the normal range; however, it is more complex and difficult to use
outside an intensive care unit.

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Harmless Acute Pancreatitis Score

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(BISAP)

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Atlanta Classification

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Balthazar Scoring

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Initial assessment and risk stratification
 Hemodynamic status should be assessed immediately upon presentation and resuscitative
measures begun as needed Risk assessment should be performed to stratify patients into
higher- and lower-risk categories to assist triage, such as admission to an intensive care
setting
 Patients with organ failure should be admitted to an intensive care unit or intermediary
care setting whenever possible
Initial management
 Aggressive hydration, defined as 250-500 ml per hour of isotonic crystalloid solution
should be provided to all patients, unless cardiovascular and / or renal comorbidities exist.
Early aggressive intravenous hydration is most beneficial the first 12 – 24 h, and may have
little benefit beyond
 In a patient with severe volume depletion, manifest as hypotension and tachycardia, more
rapid repletion (bolus) may be needed
 Lactated Ringer’s solution may be the preferred isotonic crystalloid replacement fluid
 Fluid requirements should be reassessed at frequent intervals within 6 h of admission and
for the next 24 – 48 h. The goal of aggressive hydration should be to decrease the blood
urea nitrogen
Treatment (According to ACG)

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ERCP in acute pancreatitis
 Patients with acute pancreatitis and concurrent acute cholangitis should undergo ERCP
within 24 h of admission
 ERCP is not needed in most patients with gallstone pancreatitis who lack laboratory or
clinical evidence of ongoing biliary obstruction
 In the absence of cholangitis and / or jaundice, MRCP or endoscopic ultrasound (EUS)
rather than diagnostic ERCP should be used to screen for choledocholithiasis if highly
suspected.
 Pancreatic duct stents and / or postprocedure rectal nonsteroidal anti-infl ammatory
drug (NSAID) suppositories should be utilized to prevent severe post-ERCP pancreatitis
in high-risk patients
The role of antibiotics in acute pancreatitis
 Antibiotics should be given for an extrapancreatic infection, such as cholangitis, catheter-
acquired infections, bacteremia, urinary tract infections,
pneumonia
 Routine use of prophylactic antibiotics in patients with severe acute pancreatitis is not
recommended
 The use of antibiotics in patients with sterile necrosis to prevent the development of
infected necrosis is not recommended

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 Infected necrosis should be considered in patients with pancreatic
or extrapancreatic necrosis who deteriorate or fail to improve after
7 – 10 days of hospitalization. In these patients, either
(i) initial CT-guided fineneedle aspiration (FNA) for Gram stain and
culture to guide use of appropriate antibiotics or
(ii)empiric use of antibiotics without CT FNA should be given
 In patients with infected necrosis, antibiotics known to penetrate
pancreatic necrosis, such as carbapenems, quinolones, and
metronidazole, may be useful in delaying or sometimes totally
avoiding intervention, thus decreasing morbidity and mortality
 Routine administration of antifungal agents along with
prophylactic or therapeutic antibiotics is not recommended

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Nutrition in acute pancreatitis
 In mild AP, oral feedings can be started immediately if there is no nausea and
vomiting, and abdominal pain has resolved (conditional recommendation,
 moderate quality of evidence).
 In mild AP, initiation of feeding with a low-fat solid diet appears as safe as a clear
liquid diet (conditional recommendations, moderate quality of
 evidence).
 28. In severe AP, enteral nutrition is recommended to prevent infectious
complications. Parenteral nutrition should be avoided unless the enteral route is not
available, not tolerated, or not meeting caloric requirements
 Nasogastric delivery and nasojejunal delivery of enteral feeding appear comparable
in efficacy and safety

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The role of surgery in acute pancreatitis
 In patients with mild AP, found to have gallstones in the gallbladder, a
cholecystectomy should be performed before discharge to prevent a recurrence of
AP
 In a patient with necrotizing biliary AP, in order to prevent infection,
cholecystectomy is to be deferred until active inflammation subsides and fluid
collections resolve or stabilize
 The presence of asymptomatic pseudocysts and pancreatic and / or
extrapancreatic necrosis do not warrant intervention, regardless of size, location,
and / or extension
 In stable patients with infected necrosis, surgical, radiologic, and / or endoscopic
drainage should be delayed preferably for more than 4 weeks to allow liquefaction
of the contents and the development of a fibrous wall around the necrosis (walled-
off necrosis)
 In symptomatic patients with infected necrosis, minimally invasive methods of
necrosectomy are preferred to open necrosectomy

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Prognosis
 The natural history of pancreatitis is unpredictable and depends on
the cause. In gallstone pancreatitis, cholecystectomy will prevent
further attacks.
 Hyperparathyroidism, hyperlipidemia, and implicated drugs may
cause or contribute to pancreatitis; elimination of these precipitants
should prevent reoccurrence. With the exception of alcoholic
pancreatitis, progression from acute to chronic pancreatitis is rare.
 In most cases of alcoholic pancreatitis, structural and functional
abnormalities have generally already occurred, so pancreatic
structure and function may continue to deteriorate despite alcohol
abstinence, albeit at a slower pace. Nevertheless, alcohol abstinence
will decrease the risk for future episodes