HISTORY TAKING

Male, 25 y.o.
Present history:
Epigastric pain since 4 days prior admission
On and off constant since 1 day prior admission.

Stabbing pain, pain scale 8/10.

Its getting worse when he lying down or after meal and feels better on
half of sitting.
No radiating pain, no nausea, no vomiting

Diarrhea since 4 days,

Loose stool, no blood no mucous

5 times a day on the first day but its subcide one day prior
consultation.
PMH: pancreatitis 7-8 times, last attack on March 2012.
Social History: one day before the symptom, he drunk 2 small bottle of
alcohol, he is not use to drink alcohol, just sometimes, no smoking.
Family History: His uncle and his brother also has history of recurrent
pancreatitis.
 PE:
BP:127/80 mmHg;Pulse: 68 bpm;Respi: 18x/min;Temp: 36.4;O2 Sat: 99% on
RA
Abd: soft, tender on epigastric and upper right quadrant,
murphy (-), no defans, no mc burney pain, no rebound
tenederness.
Differetial Diagnosis:
Acute Gastritis - Acute Gastroenteritis
Acute Pancreatitis - Acute Cholecystitis
Acute MI

LAB:
AST: 20 ALT: 21 LDH: 295 Gama GT: 17 ALP: 83

CBC: 16.0/46.2/243/6.75 BUN: 8 Crea:0.97

Amylase: 459 Lipase:3733

Ranson Score: 0

Diagnosis: Acute Pancreatitis

Treatment:
NPO
Pain Management

Fluid
On 10 July 2012: On 11 July 2012: On 12 July 2012:
-Fasting Patient still in pain, pain BGA: pH: 7.44 PCO2: 43 PO2: 79
scale 8/10 , gags often, not HCO3-: 29.2 BE: 5 SO2: 96 Ca:9.0
-IVFD Tridex 2500 vomiting abdominal CT Ranson Score 48 hours:2
mls/24 hours Scan:
-Pethidine drip 300 Consistent Acute Pancreatitis
involving pancreatic tail
mg/24 hours extending to peripancreatic cause
-Pethidine 25 mg, the inflammation and free fluid in On 14 July 2012:
perihepatic and perisplenic area. Patient was improving,
IV, PRN epigastric pain was reduced. He
LAB: Amylase: 877
-Fentanyl 25-50 Lipase: 2413 start oral intake with clear foot.
mcg, IV, PRN Refer to internist: He was tolerable.
Sulperazone , 1 gr, IV, BID
Sandostatin 0.2 mg in Dextrose
5% : NaCl 0.9% every 8 hours
Triofusin 500 mls/day On 16 July 2012
He discharged
 Lipase amylase
Amylase
40 10
9
10
35 9
8
8
30 7 7
6 6
25
5 5
20 4 4 amylase
Lipase 3 3
15
2 2
10 1 1
0 0
5
0
Amylase
CBC/ HB Hct PLT WBC
Date

10/7/12 16.0 46.2 243 6.75

12/7/12 12.5 37.1 170 4.74

ACUTE PANCREATITIS
Pathophys: insult leads to leakage of
pancreatic enzymes into pancreatic and
peripancreatic tissue leading to acute
inflammatory reaction
INCIDENCE

Annual incidence of acute pancreatitis has range

from 4.9 to 35 per 100.000 population in various
study.
Advance in diagnosis and therapeutic
intervention have led to decrease in mortality
from acute pancreatitis.
While the overall mortality in all hospitalized
patient with acute pancreatitis is approximately
10% (range2-22%).
The mortality in the subset with severe acute
pancreatitis may be as high as 30%.
ACUTE PANCREATITIS
ETIOLOGY
ETIOLOGY
Gallstones (35%-40%)
Gallstone pancreatitis risk is highest among patients with
small GS < 5mm and with microlithiasis
Male >>Female
Alcohol
Alcohol may act by increasing the synthesis of enzym by
pancreatic acinar cell to synthesize the digestive and
lysosomal enzymes that are thought to be responsible for
acute pancreatitis.
Not all alcoholics get pancreatitis (only about 10%)
Hypertrigliseridemia
Serum trigliseride >1000 mg/dL
Hypretrigliseridemia may account for 1.3 to 3.8 % of cases
of acute pancreatitis.
Impairment of microcirculation in pancreas due to high
level of chylomicron disturb acinar structure and expose
chylomicron to pancreatic lipase.
ETIOLOGY
Hypercalsemia
Deposition calcium in pancreatic duct and calcium activation
trypsinogen within pancreatic parenchyma.
Genetic mutation
Mutation at serine protease 1 (cationic trypsinogen) gene (PRSS1)
Mutation in serine protease inhibitor Kazal type 1 (SPINK1)
Mutation in cystic fibrosis gene (CFTR)
Infection:
Viral: Mumps, coxackievirus, hepatitis B, cytomegalovirus,
varicella zoster, herpes simplex
Bacteria: Mycoplasma, Legionella, Leptospira, Salmonella
Fungi: Aspergillus
Parasite: Toxoplasma, Cryptosporidium, Ascaris
Malnutrition and Re-feeding
Anorexia Nervosa
Pancreatic acinar cells atrophy but true cause of pancreatitis
unknown
ETIOLOGY DRUGS AND TOXINS (5%)
Azathioprine
Cimetidine
Estrogens
Enalapril
Erythromycin
Furosemide
Multiple HIV medications
Scorpion Bites
Sulfonamides
Thiazides
TMP/SMX
ETIOLOGY TRAUMA

Blunt Trauma
Iatrogenic ERCP (5-25%)
Likely secondary to contrast but also very operator
dependant
Risk is also increased with Sphincter of Oddi manometry
studies
Etiology Idiopathic
Experts suggest that idiopathic pancreatitis should
account for no more than 30% of the total cases.
ETIOLOGY ANATOMICAL ANOMALIES
Pancreas Divisum
Failure of dorsal and ventral fusion (7% of population )
Annular Pancreas
Any Ductal Anomalies
Sphincter of Oddi dysfunction
Always consider a primary malignancy as a possible
cause of new onset pancreatitis in older patients
without other obvious risk factors
\
ACUTE PANCREATITIS
Clinical Presentation
CLINICAL PRESENTATION
Clinical
Continuous mid-epigastric / right upper quadrant diffuse
Radiating to back
Nausea/ Vomiting
Restlessness, agitation and relief on bending foward
Fever
Aggravated by eating
Progressive
Physical examiantion:
Tachycardia
+/- Fever; +/- Hypotension or shock
Tenderness on epigastric area
DyspneaPleural effusions generally left-sided
Guarding sometimes
Grey Turner sign - flank discoloration due to
retroperitoneal bleed in pt. with pancreatic necrosis
(rare)
Cullens sign - periumbilical discoloration (rare)
 Grey Turner sign Cullens sign
LAB AMYLASE
Elevates within 6-12 hours and can remain
elevated for 3-5 days
High specificity when using levels >3x normal

Many false positives (see next slide)

Most specific = pancreatic isoamylase

(fractionated amylase)
LAB AMYLASE ELEVATION
Pancreatic Source Unknown Source
Biliary obstruction Renal failure
Bowel obstruction Head trauma
Perforated ulcer Burns
Appendicitis Postoperative
Mesenteric ischemia
Peritonitis
Salivary
Parotitis
DKA
Anorexia
Fallopian tube
Malignancies
LAB LIPASE
The preferred test for diagnosis
Begins to increase 4-8H after onset of symptoms
and peaks at 24H
Remains elevated for days

Sensitivity 86-100% and Specificity 60-99%

>3X normal S&S ~100%

LAB
Elevated ALT > 3x normal (in a non-alcoholic)
has a positive predictive value of 95% for GS
pancreatitis
Other Nonenzymatic pancreatic secretory
product:
Trypsinogen activation protein
C Reactive protein > 150mg/ dL at 48hours
discriminate severe from mild disease.
DIAGNOSIS IMAGING
Plain Abdomen: sentinel loop or small bowel
ileus
USG or CT Scan Abdomen: may show enlarged
pancreas with stranding, abscess, fluid
collections, hemorrhage, necrosis or pseudocyst
MRI/MRCP newest fad
Better visualization of fluid collections
MRCP allows visualization of bile ducts for stones
Does not allow stone extraction or stent insertion
ERCP / EUS
Diagnostic and Therapeutic
Can see and treat:
Ductal dilatation
Strictures
Filling defects / GS
Masses / Biopsy
ACUTE PANCREATITIS
Prognosis
PROGNOSIS RANSONS (SEVERE > 3)
Ransons Score
5 on Admission
Age > 55 y
Glucose >200

WBC > 16000

LDH > 350

ALT > 250

6 after 48 hours from presentation

Hct > 10% decrease
Calcium < 8

Base Deficit > 4

BUN > 5

Fluid Sequestration > 6L

PaO2 < 60
PROGNOSIS CT SEVERITY INDEX
CT Grade
Normal 0 points
Focal or diffuse enlargement 1 point
Intrinsic change or fat stranding 2 points
Single ill-defined fluid collection 3 points
Multiple collections of fluid or gas 4 points
Necrosis Score
None 0 points
1/3 of pancreas 2 points
1/2 of pancreas 4 points
> 1/2 of pancrease 6 points
Severe = Score > 6 (CT Grade + Necrosis)
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
5% mortality risk with <2 signs Arterial PO2 < 60
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 < 1/3 (2 points)
pancreas (1 point)
> 1/3, < 1/2 (4 points)
C is B plus
extrapancreatic > 1/2 (6 points)
changes (2 points) TOTAL SCORE =
D is severe
extrapancreatic CT grade + Necrosis
changes plus one fluid 0-1 = 0% mortality
collection (3 points) 2-3 = 3% mortality
E is multiple or 4-6 = 6% mortality
extensive fluid 7-10 = 17% mortality
collections (4 points)
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 relieftextbooks 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- Dont 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
CONCLUSIONS
Do not assume alcohol is the primary cause of
pancreatitis
Always consider further work-up for idiopathic
pancreatitis
Severe acute pancreatitis should be managed in
ICU/SD
Infected necrosis carries a high mortality
Antibiotics for suspected infected necrosis
Tube feedings preferred, post ligament of Triez
Always look for the myriad of complications