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Pancreatitis: Brad Brough, DO

Brad Brough, DO provides an overview of pancreatitis including: - Acute pancreatitis is caused by pancreatic enzymes leaking into surrounding tissue due to injury, leading to inflammation. Common causes include gallstones, alcohol, hypertriglyceridemia. - Evaluation involves blood tests like amylase and lipase levels as well as imaging like CT scans. Scoring systems like Ranson and CT severity index can predict prognosis. - Treatment focuses on pain control, IV fluids, removing the cause if possible. Complications can include pseudocysts, infection, necrosis. - Chronic pancreatitis results in permanent damage and dysfunction. It is usually caused by long term alcohol abuse and results

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0% found this document useful (0 votes)
105 views30 pages

Pancreatitis: Brad Brough, DO

Brad Brough, DO provides an overview of pancreatitis including: - Acute pancreatitis is caused by pancreatic enzymes leaking into surrounding tissue due to injury, leading to inflammation. Common causes include gallstones, alcohol, hypertriglyceridemia. - Evaluation involves blood tests like amylase and lipase levels as well as imaging like CT scans. Scoring systems like Ranson and CT severity index can predict prognosis. - Treatment focuses on pain control, IV fluids, removing the cause if possible. Complications can include pseudocysts, infection, necrosis. - Chronic pancreatitis results in permanent damage and dysfunction. It is usually caused by long term alcohol abuse and results

Uploaded by

Lija Manoj
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© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPT, PDF, TXT or read online on Scribd

PANCREATITIS

Brad Brough, DO
Acute pancreatitis
• Pathophys- insult leads to leakage of pancreatic
enzymes into pancreatic and peripancreatic
tissue leading to acute inflammatory reaction
Acute pancreatitis
• Etiologies  Scorpion sting
 Idiopathic  Hyper Ca, TG
 Gallstones (or other  ERCP (5-10% of pts
obstructive lesions) undergoing procedure)
 EtOH  Drugs (thiazides,
 Trauma sulfonamides, ACE-I,
 Steroids NSAIDS, azathioprine)
 Mumps (& other
viruses: CMV, EBV) EtOH and gallstones
 Autoimmune (SLE, account for 60-70%
polyarteritis nodosa) of cases
“Less Common” causes

• Pancreas divisum
• Chinese liver fluke
• Ischemia (bypass surgery)
• Cystic fibrosis
Trivia
• What is the name of the scorpion that
causes pancreatitis?
 Hint: you won’t find it in the USA

• Tityus Trinitatis
• (Found in Central/
• South America and
• the Caribbean)
Signs & Symptoms
• Severe epigastric abdominal pain - abrupt onset
(may radiate to back)
• Nausea & Vomiting
• Weakness
• Tachycardia
• +/- Fever; +/- Hypotension or shock
 Grey Turner sign - flank discoloration due to
retroperitoneal bleed in pt. with pancreatic necrosis
(rare)
 Cullen’s sign - periumbilical discoloration (rare)
• Grey Turner sign • Cullen’s sign
Differential

• Not all inclusive, but may include:


 Biliary disease
 Intestinal obstruction
 Mesenteric Ischemia
 MI (inferior)
 AAA
 Distal aortic dissection
 PUD
Evaluation
•  amylase…Nonspecific !!!
 Amylase levels > 3x normal very suggestive of
pancreatitis
• May be normal in chronic pancreatitis!!!
 Enzyme level  severity
 False (-): acute on chronic (EtOH); HyperTG
 False (+): renal failure, other abdominal or salivary gland
process, acidemia

•  lipase
 More sensitive & specific than amylase
Evaluation
• Other inflammatory markers will be elevated
 CRP, IL-6, IL-8 (studies hoping to use these markers to aid in
detecting severity of disease)
• ALT > 3x normal  gallstone pancreatitis
 (96% specific, but only 48% sensitive)
• Depending on severity may see:
  Ca
 WBC
 BUN
  Hct
  glucose
Radiographic Evaluation
• AXR - “sentinel loop” or small bowel ileus
• US or CT may show enlarged pancreas with
stranding, abscess, fluid collections, hemorrhage,
necrosis or pseudocyst
• MRI/MRCP newest “fad”
 Decreased nephrotoxicity from gadolinium
 Better visualization of fluid collections
 MRCP allows visualization of bile ducts for stones
 Does not allow stone extraction or stent insertion

• Endoscopic US (even newer but used less)


 Useful in obese patients
CT Scan of acute pancreatitis
• CT shows
significant
swelling
and
inflammation
of the
pancreas
Gall stone pancreatitis by ERCP
Acute Pancreatitis

• Morbidity and mortality highest if necrosis


present (especially if necroctic area
infected)
 Dual phase CT scan useful for initial eval to
look for necrosis
• However, necrosis may not be present for 48-72
hours
Prognosis
• Many different scoring systems
 Ranson (most popular & always taught in med-school)
• No association found with score, and mortality or length of
hospitalization
 APACHE II
 CT severity Index
• Recent studies show this to be most predictive of adverse outcomes
 CT score > 5 associated with 15x mortality rate
 Problem is 1 CT study showing this was conducted 72 hours after
admission (Ranson/Apache are 24 & 48 hours)
 Imrie Score
• Atlanta Classification used to help compare various
scores (clinical research trials)
Ranson Criteria
• Admission • During first 48 hours
 Age > 55  Hematocrit drop > 10%
 WBC > 16,000  Serum calcium < 8
 Glucose > 200  Base deficit > 4.0
 LDH > 350  Increase in BUN > 5
 AST > 250  Fluid sequestration >
6L
 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
CT Severity Index
• CT Grade • Necrosis score
 A is normal (0 points)  None (0 points)
 B is edematous pancreas  < 1/3 (2 points)
(1 point)  > 1/3, < 1/2 (4 points)
 C is B plus extrapancreatic  > 1/2 (6 points)
changes (2 points)
 D is severe extrapancreatic • TOTAL SCORE =
changes plus one fluid CT grade + Necrosis
collection (3 points)
 E is multiple or extensive 0-1 = 0% mortality
fluid collections (4 points)
2-3 = 3% mortality
4-6 = 6% mortality
7-10 = 17% mortality
Therapy

• Remove offending agent (if possible)


• Supportive !!!
• #1- NPO (until pain free)
 NG suction for patients with ileus or emesis
 TPN may be needed
• #2- Aggressive volume repletion with IVF
 Keep an eye on fluid balance/sequestration
and electrolyte disturbances
Therapy continued
• #3- Narcotic analgesics usually necessary for pain
relief…textbooks say Meperidine…
 NO conclusive evidence that morphine has
deleterious effect on sphincter of Oddi pressure
• #4- Urgent ERCP and biliary sphincterotomy
within 72 hours improves outcome of severe
gallstone pancreatitis
 Reduced biliary sepsis, not actual improvement of
pancreatic inflammation
• #5- Don’t forget PPI to prevent stress ulcer
Complications
• Necrotizing pancreatitis
 Significantly increases morbidity & mortality
 Usually found on CT with IV contrast
• Pseudocysts
 Suggested by persistent pain or continued high
amylase levels (may be present for 4-6 wks afterward)
 Cyst may become infected, rupture, hemorrhage or
obstruct adjacent structures
• Asymptomatic, non-enlarging pseudocysts can be watched
and followed with imaging
• Symptomatic, rapidly enlarging or complicated pseudocysts
need to be decompressed
Complications continued #2
• Infection
 Many areas for concern: abscess, pancreatic necrosis,
infected pseudocyst, cholangitis, and aspiration
pneumonia -> SEPSIS may occur
 If concerned, obtain cultures and start broad-spectrum
antimicrobials (appropriate for bowel flora)
 In the absence of fever or other clinical evidence for
infection, prophylactic antibiotics is not indicated
• Renal failure
 Severe intravascular volume depletion or acute tubular
necrosis may lead to ARF
Complications continued #3
• Pulmonary
 Atelectasis, pleural effusion, pneumonia and
ARDS can develop in severe cases
• Other
 Metabolic disturbances
• hypocalcemia, hypomagnesemia, hyperglycemia
 GI bleeds
• Stress gastritis
 Fistula formation
Prognosis

• 85-90% mild, self-limited


 Usually resolves in 3-7 days
• 10-15% severe requiring ICU admission
 Mortality may approach 50% in severe cases
Chronic pancreatitis
• Pathophys - irreversible parenchymal
destruction leading to pancreatic dysfunction

• Persistent, recurrent episodes of severe pain


• Anorexia, nausea
• Constipation, flatulence
• Steatorrhea
• Diabetes
Chronic pancreatitis
• #1- etiology is chronic EtOH abuse (90%)

• Gallstones
• Hyperparathyroidism
• Congenital malformation
(pancreas divisum)
• Idiopathic

• MRCP of pancreas
divisum
Evaluation

•  or normal amylase and lipase


• Plain AXR / CT may show calcified
pancreas
• Pain management critical
 EtOH cessation may improve pain
 Narcotic dependency is common
CT - chronic pancreatitis
Complications
• Exocrine insufficiency typically manifests
as weight loss and steatorrhea
 If steatorrhea present, a trypsinogen level < 10
is diagnostic for chronic pancreatitis
 Manage with low-fat diet and pancreatic
enzyme supplements (Pancrease, Creon)
• Endocrine insufficiency may result from
islet cell destruction which leads to
diabetes
Conclusion

• Pancreatitis is common
 YOU WILL SEE IT!!!
• 10-15% are severe = ICU admission
 Mortality may approach 50% in severe cases
• These are the cases where knowing future
complications would be great (ie finding a marker
that correlates with severity…and that’s what the
clinical researchers are attempting to do)
References
• “The Washington Manual of Medical Therapeutics.” 32nd edition. 2007.
Department of Medicine, Washington University School of Medicine.
• Caroll JK, et al. “Acute Pancreatitis: Diagnosis, Prognosis and Treament.”
American Family Physican. 2007; Vol. 75/No 10:1513-1522
• 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.

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