Acute pancreatitis

 
 Acute pancreatitis
An acute inflammatory process of the
pancreas. It is usually associated with
severe acute upper abdominal pain and
elevated blood levels of pancreatic
enzymes. Most cases are associated with
alcoholism or gallstones, but the precise
pathogenetic mechanisms are not fully
understood.
 Acute pancreatitis
Acute pancreatitis can be suspected
clinically, but requires biochemical,
radiologic, and sometimes histologic
evidence to confirm the diagnosis. Clinical,
biochemical, and radiologic features need to
be considered together since none of them
alone is diagnostic of acute pancreatitis
A commonly used classification system (the Atlanta classification) divides AP into two
broad categories:
1. Mild (edematous and interstitial) acute pancreatitis.
2. Severe (usually synonymous with necrotizing) acute pancreatitis.
 Pathophysiology:
• insult leads to leakage of pancreatic enzymes
into pancreatic and peripancreatic tissue leading
to acute inflammatory reaction
 Causes

• Idiopathic • Scorpion sting

• Gallstones (or other • Hyper Ca, TG, hypothermia
• ERCP (5-10% of pts
obstructive lesions) undergoing procedure)
• EtOH • Drugs (thiazides, sulfonamides,
• Trauma ACE-I, NSAIDS, azathioprine)
• Steroids
• Mumps (& other viruses: EtOH and gallstones
CMV, EBV) account for 60-70% of
• Autoimmune (SLE, cases
polyarteritis nodosa)
 “Less Common” Causes
• Pancreas divisum
• Chinese liver fluke
• Ischemia (bypass surgery)
• Cystic fibrosis
 Trivia
• What is the name of the scorpion that
causes pancreatitis?
o Hint: you won’t find it in Australia

 Tityus Trinitatis
 (Found in Central/
 South America and
 the Caribbean)
 Signs and Symptoms
• Acute upper abdominal pain radiating to the back
with nausea and vomiting, relieved with sitting or
leaning forward; epigastric tenderness and
distention
• Tachycardia
• +/- Fever; +/- Hypotension or shock
o Grey Turner sign - flank discoloration due to
retroperitoneal bleed in pt. with pancreatic necrosis
(rare)
o Cullen’s sign - periumbilical discoloration (rare)
 Signs and Symptoms
• Grey Turner sign • Cullen’s sign
 Differential Diagnosis
• Pancreatitis

• Acute cholecystitis • MI

• Ascending cholangitis • Severe

pneumonia
• Perforated viscus

• Intestinal obstructi

• Ruptured AAA

• Appendicitis • Diverticulitis
• Caecal perforation
• Ruptured ectopic • Bowel Ischaemia
 Investigation
Bloods:
• FBC
• U+Es
• LFTs
• CRP
• Glucose
• Amylase/Lipase
• Calcium
 Bloods
•  amylase…Nonspecific !!!
o Amylase levels > 3x normal very suggestive of
pancreatitis
 May be normal in chronic pancreatitis!!!
o Enzyme level  severity
o False (-): acute on chronic (EtOH); HyperTG
o False (+): renal failure, other abdominal or salivary
gland process, acidemia

•  lipase
o More sensitive & specific than amylase
 Bloods
• Other inflammatory markers will be elevated
o CRP, IL-6, IL-8
o C-reactive protein level of >150 mg/L at 48 hours after disease
onset is preferred for discriminating patients with severe
disease
• ALT > 3x normal  gallstone pancreatitis
o (96% specific, but only 48% sensitive)
• Depending on severity may see:
o  Ca
o WBC
o BUN
o  Hct
o  glucose
 Imaging
• When to obtain imaging
o uncertain diagnosis
o Severe disease
 Imaging
• Choice
o U/S – most useful initial test, TOC in gallstone
 Sensitivity 70-80%
o CT abd – if severe acute pancreatitis
 Good for assessing complications
 may show enlarged pancreas with stranding,
abscess, fluid collections, hemorrhage, necrosis or
pseudocyst
 However, necrosis may not be present for 48-72
hours
CT Scan of acute pancreatitis
CT shows significant swelling and inflammation of the pancreas
 Imaging
ERCP and MRCP – duct obstruction
o MRCP is safer, noninvasive and faster than ERCP
but less sensitive
o Decreased nephrotoxicity from gadolinium
o Better visualization of fluid collections
o MRCP allows visualization of bile ducts for stones
o Does not allow stone extraction or stent insertion
o ERCP only if 2 ° to choledocholithiasis
Gallstones pancreatitis by ERCP
 Imaging
• Abd xray – limited
role
 Calcifications 30%
of chronic panc
 Free air–perforation
 “sentinel loop” or
small bowel ileus
Predicting the severity of acute
pancreatitis

• No perfect system exists for predicting which

patients will develop severe pancreatitis
o Ranson (most popular & always taught in med-
school)
 a meta-analysis of 110 studies found the Ranson score to be
a poor predictor of severity
o APACHE II (The acute physiology and chronic
health examination)
o Balthazar CT severity Index
o Imrie Score (Modified Glasgow criteria)
 Ranson Criteria
• Admission • During first 48 hours
o Age > 55 o Hematocrit drop > 10%
o WBC > 16,000 o Serum calcium < 2
o Glucose > 11.1 o Base deficit > 4.0
o LDH > 350 o Increase in BUN > 5
o AST > 250 o Fluid sequestration >
6L
o Arterial PO2 < 60

5% mortality risk with <2 signs

15-20% mortality risk with 3-4 signs
40% mortality risk with 5-6 signs
99% mortality risk with >7 signs
 APACHE II
• Most widely studied severity scoring
system in AP. But complex and
cumbersome to use.
• originally developed for critically ill
patients in intensive care units
 APACHE II

• APACHE II scores on admission and

within 48 hours help distinguish mild from
severe pancreatitis and to predict death.
• Most patients whose APACHE II scores
are 9 or less during the first 48 hours
survive.
• However, patients with APACHE II scores
of 13 or more have a high likelihood of
dying
 CT Severity Index
• CT Grade • Necrosis score
o A is normal (0 points) o None (0 points)
o B is edematous pancreas (1 o < 1/3 (2 points)
point) o > 1/3, < 1/2 (4 points)
o C is B plus extrapancreatic o > 1/2 (6 points)
changes (2 points)
o D is severe extrapancreatic
• TOTAL SCORE =
changes plus one fluid CT grade + Necrosis
collection (3 points)
o E is multiple or extensive
fluid collections (4 points) 0-1 = 0% mortality
2-3 = 3% mortality
4-6 = 6% mortality
7-10 = 17% mortality
Patients with a CT severity index >5 were eight times more likely to die, 17 times
more likely to have a prolonged hospital course, and 10 times more likely to
undergo necrosectomy than the patients with scores <5
 Modified Glasgow criteria
• WCC > 15.0 x 109/L
• Glucose >10 mmol /L
• LDH >600iu/L
• AST >200iu/L
• Urea >16mmol/L
• Serum Ca2+ <2mmol/L
• Serum albumin <32g/L
• PaO2 <60 mmHg
• Greater = poorer prognosis
 Treatment
• varies depending on the severity of the condition
• Remove offending agent (if possible)
• Supportive:
• NPO (until pain free)
o NG suction for patients with ileus or emesis
o Enteral/TPN may be needed (Enteral feeding is used
to avoid central line related infections, maintain gut
barrier integrity, and decrease bacterial translocations)
• Aggressive volume repletion with IVF
 IV access and IDC
 Aggressive fluid resiscitation
 Strict input/output balance
 Treatment continued
• Narcotic analgesics usually necessary for pain
relief…textbooks say Meperidine…
o NO conclusive evidence that morphine has
deleterious effect on sphincter of Oddi
pressure
• Urgent ERCP and biliary sphincterotomy within
72 hours improves outcome of severe gallstone
pancreatitis
o Reduced biliary sepsis, not actual improvement of
pancreatic inflammation
• Don’t forget PPI to prevent stress ulcer
ERCP
 Treatment continued
• Daily FBC, U+Es,LFTS, Ca2+,Glucose, ABGs
• HDU/ICU depending on severity
• Antibiotics:
• If infected pancreatic necrosis
• Antibiotic prophylaxis in severe pancreatitis is
controversial
• Do not forget alcohol withdrawal therapy if due to
excess alcohol
o Diazepam PO/IV
o Pabrinex IV
Managment
algorithm for
severe acute
pancreatitis
 Complications
• Acute fluid collections:
These commonly occur early in the course of
acute pancreatitis. They are primarily
detected by imaging studies and not physical
examination. Because they lack a defined
wall and usually regress spontaneously,
most acute fluid collections require no
specific therapy.
 Complications
• Pseudocyst:
o Peripancreatic fluid
collections for >4wks
o Intervention if:
 >7cm and rapidly
expanding
 Symptomatic (pain,
bleeding, infection)
 Complications

• Surgical Treatment of
Pseudocysts
o Percutaneous
aspiration
 Very large fluid
collections
• Pancreatic abcess
o Also responds to
percut drainage
 Complications
• Surgical Treatment of
Pseudocysts
o Transpapillary
drainage
 If pancreatic duct
communicates with
pseudocyst, can place
stent
 Complications
• Surgical Treatment of
Pseudocysts
o Transmural
enterocystostomy
 Endoscopic if distance
between lumen and
pseudocyst is <1cm
 Complications
• Surgical Treatment of
Pseudocysts
o Transmural
enterocystostomy
 Complications
• Intra-abdominal infections: Within the first 1-3
weeks, fluid collections or pancreatic necrosis
can become infected and jeopardize clinical
outcome.
• Intestinal florae are the predominant source of
bacteria causing the infection. The usual
suspects are
• Escherichia coli (26%)
• Pseudomonas species (16%)
• Staphylococcus species (15%)
• Klebsiella species (10%)
• Proteus species (10%)
• Streptococcus species (4%)
 Complications
• Pancreatic necrosis:
This is a nonviable area of pancreatic parenchyma
that is often associated with peripancreatic fat
necrosis and is principally diagnosed with the aid of
dynamic spiral CT scans. Sterile pancreatic
necrosis is usually treated with aggressive medical
management, whereas almost all patients with
infected pancreatic necrosis require surgical
debridement or percutaneous drainage if they are to
survive
Approach to
pancreatic
necrosis in
severe acute
pancreatitis
(SAP)
 Various
therapeutic
approaches in
pancreatic
necrosis
 Complications
• Pancreatic ascites
• Disruption of main pancreatic duct     
• Leaking pseudocyst   
• Involvement of contiguous organs by necrotizing
pancreatitis     
• Massive intraperitoneal hemorrhage     
• Thrombosis of blood vessels (splenic vein, portal
vein)
• Bowel infarction
• Obstructive jaundice
 Systemic Complications

• Pulmonary:
• Pleural effusion
• Atelectasis  
• Mediastinal abscess   
• Pneumonitis   
• Adult respiratory distress syndrome
• Cardiovascular:
• Hypotension   
• Hypovolemia   
• Sudden death   
• Nonspecific ST-T changes in electrocardiogram simulating
myocardial infarction
• Pericardial effusion
 Systemic Complications
• Hematologic
• Disseminated intravascular coagulation
• Gastrointestinal hemorrhage
• Peptic ulcer disease
• Erosive gastritis
• Hemorrhagic pancreatic necrosis with erosion into major blood
vessels
• Portal vein thrombosis
• variceal hemorrhage
• Renal
• Oliguria   
• Azotemia   
• Renal artery and/or renal vein thrombosis   
• Acute tubular necrosis
 Systemic Complications
• Metabolic   
• Hyperglycemia   
• Hypertriglyceridemia   
• Hypocalcemia   
• Encephalopathy
 Systemic Complications
• Sudden blindness (Purtscher's retinopathy):
this ischemic injury to the retina appears to be caused by
activation of complement and agglutination of blood cells
within retinal vessels. It may cause temporary or
permanent blindness.

• Central nervous system:

• Psychosis   
• Fat emboli

• Fat necrosis:
• Subcutaneous tissues (erythematous nodules)   
• Bone   
• Miscellaneous (mediastinum, pleura, nervous system)
Pancreatitis in Patients with AIDS
• The incidence of acute pancreatitis is increased
in patients with AIDS for two reasons:

• The high incidence of infections involving the

pancreas, such as infections with
cytomegalovirus, Cryptosporidium and the
Mycobacterium avium complex.

• The frequent use by patients with AIDS of

medications such as didanosine, pentamidine,
trimethoprim-sulfamethoxazole and protease
inhibitors.
 Prognosis
• 85-90% mild, self-limited
o Usually resolves in 3-7 days
• 10-15% severe requiring ICU admission
o Mortality may approach 50% in severe cases
 Conclusion
• Pancreatitis is common
• Mild pancreatitis is treated for several days with supportive
care including pain control, intravenous fluids, correction of
electrolyte and metabolic abnormalities, and nothing by
mouth. The majority of patients require no further therapy,
and recover and eat within three to seven days
• In severe pancreatitis, intensive care unit monitoring and
support of pulmonary, renal, circulatory, and hepatobiliary
function may minimize systemic sequelae
• pancreatic infection is a leading cause of morbidity and
mortality in acute necrotizing pancreatitis
• In gallstone pancreatitis, early ERCP and sphincterotomy for
those who have a high suspicion of cholestasis and those
with cholangitis
• Cholecystectomy should be performed after recovery in all
 References

• www.uptodate.com
• Leung TK et al. “Balthazar CT severity index is superior to Ranson
criteria and APACHE II scoring system in predicting acute
pancreatitis outcome.” World J Gastroenterology. 2005; 11:6049-52.
• Hatzicostas C et al. “Balthazar CT severity index is superior to
Ranson criteria and APACHE II and II scoring systems.” J Clin
Gastroenterology. 2003;36:253-60
• Vriens PW et al. “CT severity index is an early prognostic tool for
acute pancreatitis.” J Am Coll Surgery. 2005; 201:497-502.
• http://www. emedicine .com
• http://hopkins- gi.nts.jhu.edu/pages/latin/templates/index.cfm?
pg=disease4&organ=4&disease=24&lang_id=1