Professional Documents
Culture Documents
digestive
enzymes
hormones
Exocrine Function
common bile
duct
BODY
TAIL
HEAD
pancreatic duct
ampulla
UNCINATE
pancreatic enzymes
Enzyme Secretion
acinus
pancreatic duct
microscopic view
of pancreatic acini
duodenum
Enzyme Secretion
Neural
acetylcholine
VIP
GRP
Hormonal
CCK
gastrin
Secretin (hormonal)
H2O
bicarbonate
LIPOLYTIC ENZYMES
Lipase
Prophospholipase A2
Carboxylesterase lipase
NUCLEASES
Deoxyribonuclease (DNAse)
Ribonuclease (RNAse)
OTHERS
Procolipase
Trypsin inhibitor
trypsinogen
chymotrypsinogen
proelastase
prophospholipase
procarboxypeptidase
duodenal lumen
trypsin
chymotrypsin
elastase
phospholipase
carboxypeptidase
Exocrine Stimulation
Protective Measures
Acute Pancreatitis
Definition
Acute Pancreatitis
Etiology
Acute Pancreatitis
Associated Conditions
Cholelithiasis
Ethanol abuse
Idiopathic
Medications
Pancreas divisum
Hyperlipidemia
ERCP
Trauma
Hereditary
Hypercalcemia
Viral infections
- Mumps
- Coxsackievirus
Acute Pancreatitis
Causative Drugs
Pancreas divisum
Hereditary Pancreatitis
Autosomal dominant with 80% phenotypic
penetrance
Acute Pancreatitis
Pathogenesis
acinar cell
injury
premature
enzyme activation
failed protective
mechanisms
Acute Pancreatitis
Pathogenesis
local
vascular
insufficiency
local
complications
activation
of white
blood cells
release of
enzymes into
the circulation
distant
organ failure
Acute Pancreatitis
Pathogenesis
SEVERITY
Mild
- Retroperitoneal edema
- Ileus
Hypotension/shock
Metabolic disturbances
Sepsis/organ failure
Acute Pancreatitis
Clinical Presentation
Abdominal pain
-
Epigastric
Radiates to the back
Worse in supine position
Acute Pancreatitis
Differential Diagnosis
Choledocholithiasis
Perforated ulcer
Mesenteric ischemia
Intestinal obstruction
Ectopic pregnancy
Acute Pancreatitis
Diagnosis
Symptoms
- Abdominal pain
Laboratory
Radiology
- Abnormal sonogram or CT
Causes of Increased
Pancreatic Enzymes
Amylase
Lipase
Intestinal injury
Tubo-ovarian
disease
Normal
Renal failure
Pancreatitis
Parotitis
Biliary stone
Macroamylasemia
Normal
Normal
Acute Pancreatitis
Diagnosis
EtOH: history
Gallstones: abnormal LFTs & sonographic
evidence of cholelithiasis
Acute Pancreatitis
Clinical Manifestations
PANCREATIC
PERIPANCREATIC
SYSTEMIC
Cardiovascular: hypotension
Pulmonary: pleural effusions, ARDS
Renal: acute tubular necrosis
Hematologic: disseminated intravascular coag.
Metabolic: hypocalcemia, hyperglycemia
Acute Pancreatitis
Time Course
ER presentation
cytokine release
organ failure
Predictors of Severity
Which is best?
Ranson Criteria
Alcoholic Pancreatitis
AT ADMISSION
WITHIN 48 HOURS
1.
2.
3.
4.
5.
1.
2.
3.
4.
5.
6.
Number
Mortality
<2
3-4
1% 16%
5-6
40%
7-8
100%
Glasgow Criteria
Non-alcoholic Pancreatitis
1.
2.
3.
4.
5.
6.
7.
8.
CT Severity Index
appearance
normal
enlarged
inflamed
1 fluid
collection
2 or more
collections
grade
score
necrosis
none
< 33%
33-50%
> 50%
score
score
morbidity
mortality
1-2
4%
0%
7-10
92%
17%
Balthazar et al. Radiology 1990.
Scoring systems
3 Ranson criteria
8 APACHE II points
5 CT points
Organ failure
- shock (SBP < 90 mmHg)
- pulmonary edema / ARDS (PaO2 < 60 mmHg)
- renal failure (Cr > 2.0 mg/dl)
Local complications
- fluid collections pseudocysts
- necrosis (mortality 15% if sterile, 30-35% if
infected)
- abscess
Goals of Treatment
Limit systemic injury
harmful?
- inhibit inflammatory mediators ineffective
- inhibit circulating trypsin ineffective (too late)
- removing gallstones mostly ineffective
Treatment of Mild
Pancreatitis
Pancreatic rest
Supportive care
Treatment of Severe
Pancreatitis
Rule-out necrosis
- contrasted CT scan at 48-72 hours
- prophylactic antibiotics if present
- surgical debridement if infected
Nutritional support
- may be NPO for weeks
- TPN vs. enteral support (TEN)
Role of ERCP
Gallstone pancreatitis
- Cholangitis
- Obstructive jaundice
Structural abnormalities
Neoplasm
Bile sampling for microlithiasis
Nutrition in Acute
Pancreatitis
Metabolic stress
- catabolism & hypermetabolism seen in 2/3 of
patients
- similar to septic state (volume depletion may
be a major early factor in the above
derangements)
Micronutrient alterations
- calcium, magnesium, potassium, etc
Hypermetabolism
Catabolism
Severe
Pancreatitis
Pancreatitis
Admissions
80%
20%
Pancreatic
necrosis
No
Yes
80%
0%
Morbidity
8%
38%
Mortality
3%
27%
Parameter
Benefit or harm?
- early uncontrolled studies suggested benefit
- two retrospective studies (70s & 80s) showed
no benefit with TPN in pancreatitis
- 1987 randomized study of early TPN vs. IVF
alone showed more sepsis, longer stays, & no
fewer complications with TPN
studies
- late 80s patients who received jejunal feeding tubes at
the time of surgery, did well with early
post-op enteral support
- 1991 randomized study of early TPN vs. early TEN
post-op showed no short-term difference
- 1997 early TPN vs. early TEN (Peptamen) via
nasojejunal tube in 32 patients showed no difference
except 4x less cost & less hyperglycemia
- 1997 similar study showed fewer complications and
lower cost without change in length of stay
- 1998 similar study showed more sepsis and organ
failure in the TPN group
1997
1997
1998
No of patients
32
38
34
Etiology
EtOH 19/32
--
Biliary 23/34
Severe
pancreatitis
19%
100%
38%
Enteral
formula
Semi-elemental
Semi-elemental
Polymeric
Cost
5x less
3x less
--
Outcome
No difference
Fewer comp
Less SIRS
Conclusions
Acute pancreatitis is a self-limited disease in
which most cases are mild.