acute pancreatitis

ACUTE PANCREATITISACUTE PANCREATITIS
DETAILED PROSPECTS & MANAGEMENT PROTOCOLSDETAILED PROSPECTS & MANAGEMENT PROTOCOLS
Dr sumer yadavDr sumer yadav

PancreasPancreas
Location :- Upper, posterior abdomen, reteroperitonialy,Location :- Upper, posterior abdomen, reteroperitonialy, extendsextends
obliquely from the duodenal C loop to the hilum of theobliquely from the duodenal C loop to the hilum of the
spleen.spleen.
 4 portions: head, neck body and tail.4 portions: head, neck body and tail.
The head is intimately associated with the second portion of theThe head is intimately associated with the second portion of the
duodenum, and they are BOTH supplied by theduodenum, and they are BOTH supplied by the
pancreaticoduodenal arteries.pancreaticoduodenal arteries.
Functions :-Functions :-
1. Endocrine - insulin production (20% of the gross weight)1. Endocrine - insulin production (20% of the gross weight)
2. Exocrine - manufacture and secretion of digestive enzymes for2. Exocrine - manufacture and secretion of digestive enzymes for
carbohydrate, fat, and protein metabolism. (80% of the grosscarbohydrate, fat, and protein metabolism. (80% of the gross
weight)weight)

Exocrine PancreasExocrine Pancreas
 The final product of the exocrine pancreas is aThe final product of the exocrine pancreas is a
clear isotonic solution with a pH in the range ofclear isotonic solution with a pH in the range of
8. The 2 distinct components of exocrine8. The 2 distinct components of exocrine
secretion are enzyme secretion andsecretion are enzyme secretion and
water+electrolyte secretion.water+electrolyte secretion.
 Cholecystokinin is the most potent endogenousCholecystokinin is the most potent endogenous
hormone known to stimulate enzyme secretion.hormone known to stimulate enzyme secretion.
 Secretin is the most potent endogenousSecretin is the most potent endogenous
stimulant of pancreatic electrolyte secretionstimulant of pancreatic electrolyte secretion

Endocrine PancreasEndocrine Pancreas
 The release ofThe release of insulininsulin into the portal blood isinto the portal blood is
controlled by the concentration of blood glucose, vagalcontrolled by the concentration of blood glucose, vagal
interactions, and local concentrations of somatostatin.interactions, and local concentrations of somatostatin.
 The major stimulus forThe major stimulus for glucagonglucagon release is a fall inrelease is a fall in
serum glucose.serum glucose.
 Pancreatic polypeptidePancreatic polypeptide appears to function forappears to function for
regulation of pancreatic exocrine secretion and biliaryregulation of pancreatic exocrine secretion and biliary
tract motility.tract motility.
 SomatostatinSomatostatin has a broad inhibitory spectrum ofhas a broad inhibitory spectrum of
gastrointestinal activitygastrointestinal activity

Normal Pancreatic PhysiologyNormal Pancreatic Physiology
Proteolytic proenzymes such asProteolytic proenzymes such as
trypsinogen convert to activetrypsinogen convert to active
form under the influence ofform under the influence of
ENTEROKINASE,ENTEROKINASE,
luminal HCl and spontaneouslyluminal HCl and spontaneously

EnzymesEnzymes
Pancreatic enzymes:Pancreatic enzymes:
AmylaseAmylase ActiveActive
Proteolytic enzymesProteolytic enzymes InactiveInactive
LipasesLipases InactiveInactive
Inhibitors:Inhibitors:
Alpha1-antitrypsinAlpha1-antitrypsin
Beta2-macroglobulinBeta2-macroglobulin
Pancreatic secretory trypsin inhibitorPancreatic secretory trypsin inhibitor

The pancreas secretes 500-800 ml/day of anThe pancreas secretes 500-800 ml/day of an
alkaline, colorless, odorless, isosmotic fluidalkaline, colorless, odorless, isosmotic fluid
containing large quantity of bicarbonate andcontaining large quantity of bicarbonate and
digestive enzymesdigestive enzymes
Stimulated by secretin, duodenal pH of less than 4.0Stimulated by secretin, duodenal pH of less than 4.0
Vagal stimulation through acetylcholineVagal stimulation through acetylcholine
Inhibited by truncal vagotomy, atropineInhibited by truncal vagotomy, atropine
Contd…

PancreatitisPancreatitis
Pancreatitis is a complex disorder of the exocrinePancreatitis is a complex disorder of the exocrine
pancreas with unclear pathogenic mechanisms,pancreas with unclear pathogenic mechanisms,
which is characterized by acute acinar cell injury andwhich is characterized by acute acinar cell injury and
both regional and systemic inflammatory responses.both regional and systemic inflammatory responses.
Overall mortalityOverall mortality 6.0-20.5%6.0-20.5%
Acute necrotizing pancreatitisAcute necrotizing pancreatitis 50+%50+%

Pancreatitis: ClassificationPancreatitis: Classification
Acute PancreatitisAcute Pancreatitis
Interstitial edematous pancreatitisInterstitial edematous pancreatitis
Sterile necrotizing pancreatitisSterile necrotizing pancreatitis
Infected pancreatic necrosis/abscessInfected pancreatic necrosis/abscess
Hemorrhagic pancreatitisHemorrhagic pancreatitis
Chronic PancreatitisChronic Pancreatitis
Uncomplicated recurrent pancreatitisUncomplicated recurrent pancreatitis
Calcifying chronic pancreatitisCalcifying chronic pancreatitis
Obstructive chronic pancreatitisObstructive chronic pancreatitis

 Nonbacterial inflammatory disease caused byNonbacterial inflammatory disease caused by
activation, interstitial liberation, and autodigestionactivation, interstitial liberation, and autodigestion
of the pancreas by its own enzymes.of the pancreas by its own enzymes.
 Inconclusive evidence regarding pathogenesisInconclusive evidence regarding pathogenesis
 Partial or intermittent ductal obstruction and increasedPartial or intermittent ductal obstruction and increased
ductal pressureductal pressure
 Biliary refluxBiliary reflux
 Duodenal juice refluxDuodenal juice reflux

Common Causes
Gallstones (including microlithiasis)
Alcohol (acute and chronic alcoholism)
Hypertriglyceridemia
Endoscopic retrograde cholangiopancreatography (ERCP),
Trauma (especially blunt abdominal trauma)
Postoperative (abdominal and nonabdominal operations)
Drugs (azathioprine, 6-mercaptopurine, sulfonamides,
estrogens, tetracycline, valproic acid, anti-HIV medications)
Sphincter of Oddi dysfunction
Causes of Acute Pancreatitis

Uncommon causes
Vascular causes and vasculitis
(ischemic-hypoperfusion
states aftercardiac surgery)
Connective tissue disorders
and thrombotic
thrombocytopenic
purpura(TTP)
Cancer of the pancreas
Hypercalcemia
Periampullary diverticulum
Pancreas divisum
Hereditary pancreatitis
Cystic fibrosis
Renal failure
Rare causes
Infections (mumps,
coxsackievirus,
cytomegalovirus, echovirus,
parasites)
Autoimmune (e.g.,
Sjo¨gren’s syndrome)

Causes to consider in patients with recurrent bouts of
acute pancreatitis without an obvious etiology
-Occult disease of the biliary tree or pancreatic ducts,
especially microlithiasis, sludge
-Drugs
-Hypertriglyceridemia
-Pancreas divisum
-Pancreatic cancer
-Sphincter of Oddi dysfunction
-Cystic fibrosis
-Idiopathic

IncidenceIncidence 0.14-1.3%0.14-1.3%
Patients age and gender:Patients age and gender:
Alcohol-inducedAlcohol-induced 30-4030-40
(younger)(younger)
Men >> WomenMen >> Women
Gallstone-inducedGallstone-induced 40-6040-60
(older)(older)
Women >> MenWomen >> Men

Alcohol in Acute PancreatitisAlcohol in Acute Pancreatitis
Acetaldehyde formationAcetaldehyde formation
Microtubular disruptionMicrotubular disruption
Increase in acinar cell membrane permeabilityIncrease in acinar cell membrane permeability
Elevated triglycerides levelElevated triglycerides level
Formation of cytotoxic free fatty acidsFormation of cytotoxic free fatty acids
Increased HCl production stimulates secretinIncreased HCl production stimulates secretin
release and increases pancreatic ductal flowrelease and increases pancreatic ductal flow
Elevation of pancreatic intraductular pressureElevation of pancreatic intraductular pressure

Gallstones in AcuteGallstones in Acute
PancreatitisPancreatitis
Simple cholelithiasisSimple cholelithiasis 72% of patients72% of patients
CholedocholithiasisCholedocholithiasis 20%20%
CholecystitisCholecystitis 8%8%

Common Channel ConceptCommon Channel Concept

Initial triggering event in
development of acute pancreatitis
is
DUCTAL HYPERTENSION

PathogenesisPathogenesis
Fundamental pathologic eventFundamental pathologic event
is injury to acinar cellis injury to acinar cell
Process begins within minutesProcess begins within minutes

contd..contd..
-Autophagic cytoplasmic vacuoles-Autophagic cytoplasmic vacuoles
(zymogen lakes) formation(zymogen lakes) formation
-Elevated levels of TNF-alpha, IL-1,-Elevated levels of TNF-alpha, IL-1,
-IL-6-IL-6
-Hypoxia-Hypoxia
-Loss of normal cell polarity-Loss of normal cell polarity
-Basolateral disordered discharge-Basolateral disordered discharge

Cardinal symptom ofCardinal symptom of
acute pancreatitis isacute pancreatitis is
epigastric abdominalepigastric abdominal
PAINPAIN
Symptoms and signsSymptoms and signs

 Midepigastric abdominal painMidepigastric abdominal pain
 Radiating to the backRadiating to the back
 Nausea and vomitingNausea and vomiting
 Fever and tachycardiaFever and tachycardia
 Abdominal distentionAbdominal distention
 IleusIleus
 Abdominal tenderness/massAbdominal tenderness/mass
 Bluish discoloration in the flankBluish discoloration in the flank ((Grey Turner’s sign)Grey Turner’s sign)
 Bluish discoloration periumbilicallyBluish discoloration periumbilically ((Cullen’s sign)Cullen’s sign)
All non-specificAll non-specific
Contd..Contd..

DiagnosisDiagnosis
 It is supported by appropriate laboratoryIt is supported by appropriate laboratory
determinations and radiographic findingsdeterminations and radiographic findings
 Serum amylase is the most widely used lab testSerum amylase is the most widely used lab test
 Hyperamylasemia is commonly observed within 24Hyperamylasemia is commonly observed within 24
hrs. of the onset and gradually returns to normalhrs. of the onset and gradually returns to normal
 Persistent hyperamylasemia beyond the initial weekPersistent hyperamylasemia beyond the initial week
may indicate the development of pancreaticmay indicate the development of pancreatic
pseudocyst, phlegmon, abscess or ongoing acutepseudocyst, phlegmon, abscess or ongoing acute
pancreatic inflammation.pancreatic inflammation.

Contd..Contd..
 Elevated amylase levels may occur in other acuteElevated amylase levels may occur in other acute
abdominal conditions, though levels rarely exceed 500abdominal conditions, though levels rarely exceed 500
IU/dLIU/dL
 Urinary amylase excretion is increased and this may beUrinary amylase excretion is increased and this may be
very helpful in cases where the serum amylase levelvery helpful in cases where the serum amylase level
has returned to normal.has returned to normal.
 Other lab. FindingsOther lab. Findings
 Moderate leukocytosisModerate leukocytosis
 Mild bilirubin elevation (<2mg/dL)Mild bilirubin elevation (<2mg/dL)
 Raised HaematocritRaised Haematocrit
 Hypocalcaemia (Calcium being complexed with fatty acids)Hypocalcaemia (Calcium being complexed with fatty acids)

Radiographic findingsRadiographic findings
 CXR and PFA non-specific findingsCXR and PFA non-specific findings
 Sentinel loopSentinel loop
 Pleural effusion (Left)Pleural effusion (Left)
 Abdominal UltrasonographyAbdominal Ultrasonography
 Lithiasis of biliary tractLithiasis of biliary tract
 Pancreatic swellingPancreatic swelling
 Computed Tomography with iv contrastComputed Tomography with iv contrast

Ultrasound of the PancreasUltrasound of the Pancreas

CT ScanCT Scan
CT scanning is the BESTCT scanning is the BEST
imaging study in evaluationimaging study in evaluation
of acute pancreatitisof acute pancreatitis

On admission : Note the mildly decreased density of the body of the
pancreas to the left ofthe midline (arrow).
There are a few linear strands in the peripancreatic fat, suggesting inflammation (open
arrows).
A small amount of fluid is seen in the anterior pararenal
space (arrowhead).

Nine days after admission: - there is a marked worsening with
severe inflammation of the pancreas evidenced by anterior displacement
of the posterior gastric wall (arrows),
- Increased inflammation of the peripancreatic fat, increased pancreatic
effusion in the anterior perirenal space and around the splenic vein (open

Acute Fluid CollectionAcute Fluid Collection

Risk Factors That Adversely Affect Survival in
Acute Pancreatitis
1. Organ failure
a. Cardiovascular: hypotension (systolic blood pressure < 90 mmHg)
or tachycardia > 130 beats/min
b. Pulmonary: PO2 < 60 mmHg
c. Renal: oliguria (<50 mL/h) or increasing BUN or creatinine
d. Gastrointestinal bleeding
2. Pancreatic necrosis
3. Obesity (BMI > 29); age > 70
4. Hemoconcentration ( hematocrit > 44%)
5. C-Reactive protein > 150 mg/L
6. Trypsinogen activation peptide
7a. >3 Ranson criteria (not fully utilizable until 48 h)
7b. Apache II score > 8 (cumbersome)

Clinical courseClinical course
 Early identification of patients at greater risk ofEarly identification of patients at greater risk of
complications allows them to be managed morecomplications allows them to be managed more
aggressively, which appears to decrease the mortality rate.aggressively, which appears to decrease the mortality rate.
 The severity and prognosis of an attack of acuteThe severity and prognosis of an attack of acute
pancreatitis can be predicted by use of routinely availablepancreatitis can be predicted by use of routinely available
laboratory determinations.laboratory determinations.
 Just the single finding of fluid sequestration exceeding 2Just the single finding of fluid sequestration exceeding 2
L/d for more than 2 days is reasonably accurate dividingL/d for more than 2 days is reasonably accurate dividing
line between severe and mild to moderate diseaseline between severe and mild to moderate disease..

Ranson’s CriteriaRanson’s Criteria
On admissionOn admission
Age >55 yearsAge >55 years
WBC >16,000WBC >16,000
Glucose >200Glucose >200
LDH >350LDH >350
AST >250AST >250
After 48 hoursAfter 48 hours
Drop in Hct >10%Drop in Hct >10%
Increase in BUN >5Increase in BUN >5
Ca <8.0Ca <8.0
Arterial PaO2 <60 mm HgArterial PaO2 <60 mm Hg
Base deficit >4Base deficit >4
Fluid deficit >6 LFluid deficit >6 L
Total Ranson score of 3 or more indicates severe acute pancreatitisTotal Ranson score of 3 or more indicates severe acute pancreatitis

APACHE-IIAPACHE-II
A Total Acute Physiology ScoreA Total Acute Physiology Score
Temperature (Rectal)Temperature (Rectal)
MAP (mmHg)MAP (mmHg)
Heart rateHeart rate
Respiratory RateRespiratory Rate
Oxygenation (PaOOxygenation (PaO22 - mmHg)- mmHg)
Serum Na, K, Cre, Hct, WBCSerum Na, K, Cre, Hct, WBC
Glasgow Coma ScoreGlasgow Coma Score
B Age pointsB Age points
C Chronic health pointsC Chronic health points
Total APACHE II score of 8 or more indicatesTotal APACHE II score of 8 or more indicates
severe acute pancreatitissevere acute pancreatitis

Glasgow prognostic systemGlasgow prognostic system

Severity Index in Acute Pancreatitis Points
Grade of acute pancreatitis
Normal pancreas 0
Pancreatic enlargement alone 1
Inflammation compared with pancreas
and peripancreatic fat 2
One peripancreatic fluid collection 3
Two or more fluid collections 4
Degree of pancreatic necrosis
No necrosis 0
Necrosis of one-third of pancreas 2
Necrosis of one-half of pancreas 4
Necrosis of more than one-half of pancreas 6
CT severity index (CTSI) CT grade necrosis score (0–10)

TreatmentTreatment
Goals of medical treatmentGoals of medical treatment
 Reduction of pancreatic secretory stimuliReduction of pancreatic secretory stimuli
 Correction of fluid and electrolyte derangementsCorrection of fluid and electrolyte derangements

Medical TreatmentMedical Treatment
 Gastric suctionGastric suction
 Fluid and electrolyte replacementFluid and electrolyte replacement
 Antibiotics (+/-)Antibiotics (+/-)
 OxygenOxygen
 Octreotide, PPIsOctreotide, PPIs
 Endoscopic sphincterotomy (ERCP)Endoscopic sphincterotomy (ERCP)

Role of AntibioticsRole of Antibiotics
- Local & systemic infections may complicate
pancreatitis.
-Organisms : Most commonly E.coli, Klebsiella,
Streptococcus, Staphylococcus, Pseudomonas.
-Prophylactic antibiotic are to be given early in the
course
Of acute necrotizing pancreatitis particularly in pts
with signs of organ falure and sepsis.
-At the present time administration of Imipenem-
Cilastatin is recommended.
-Start as soon as the diagnosis is made and continue
for 2-4 weeks.

ERCPERCP
 Diagnostic as well as therapeutic modalityDiagnostic as well as therapeutic modality
 Role in patients having obstructiveRole in patients having obstructive
choledocholithiasischoledocholithiasis
 Less obvious role acute biliary pancreatitisLess obvious role acute biliary pancreatitis
without obstructive choledocholithiasiswithout obstructive choledocholithiasis
 Significant reduction in morbidity but notSignificant reduction in morbidity but not
mortalitymortality
 Not a routine procedureNot a routine procedure
 MRCP –MRCP – Non-invasive diagnostic modality,Non-invasive diagnostic modality,
avoid post procedure pancreatitis riskavoid post procedure pancreatitis risk

Surgical TreatmentSurgical Treatment
Indicated in specific circumstancesIndicated in specific circumstances
 Uncertainty of Clinical DiagnosisUncertainty of Clinical Diagnosis
 Intra-abdominal catastrophe unrelated toIntra-abdominal catastrophe unrelated to
necrotizing pancreatitis such as perforated viscusnecrotizing pancreatitis such as perforated viscus
 Infected necrosesInfected necroses
 Severe sterile necrosisSevere sterile necrosis
 Symptomatic organised pancreatic necrosisSymptomatic organised pancreatic necrosis
 Treatment of Pancreatic SepsisTreatment of Pancreatic Sepsis
 Abscess up to 5%Abscess up to 5%
 Correction of Associated Biliary Tract DiseaseCorrection of Associated Biliary Tract Disease
 Deterioration of Clinical StatusDeterioration of Clinical Status

Acute Pancreatic NecrosisAcute Pancreatic Necrosis
Acute necrotizing pancreatitis - process whenAcute necrotizing pancreatitis - process when
one or more diffuse or focal areas ofone or more diffuse or focal areas of
nonviable pancreatic parenchyma are present.nonviable pancreatic parenchyma are present.
Pancreatic glandular necrosis usuallyPancreatic glandular necrosis usually
associated with necrosis of peripancreatic fatassociated with necrosis of peripancreatic fat

Acute necrotizing pancreatitis - affected portions do not showAcute necrotizing pancreatitis - affected portions do not show
normal contrast enhancementnormal contrast enhancement
Contrast-enhanced dynamic CT scanning - GOLD standardContrast-enhanced dynamic CT scanning - GOLD standard
(accuracy 90% if more than 30% of the gland is affected)(accuracy 90% if more than 30% of the gland is affected)
Patients with necrosis have 82% morbidity and 23% mortalityPatients with necrosis have 82% morbidity and 23% mortality
Patients without 6% and 0%Patients without 6% and 0%

-Infected necrosis-Infected necrosis develops in 30-70% of patientsdevelops in 30-70% of patients
with acute necrotizing pancreatitis and accounts forwith acute necrotizing pancreatitis and accounts for
more than 80% of deaths from acute pancreatitismore than 80% of deaths from acute pancreatitis
-- Sterile necrosisSterile necrosis mortality - 10%mortality - 10%
-Deaths occur in two phases:-Deaths occur in two phases:
Early - 1-2 weeks due to multisystem organ failure dueEarly - 1-2 weeks due to multisystem organ failure due
to release of inflammatory mediators and cytokinesto release of inflammatory mediators and cytokines
Late - due to systemic infectionsLate - due to systemic infections

Pancreatic AbscessPancreatic Abscess

Infected Pancreatic NecrosisInfected Pancreatic Necrosis

General Treatment IssuesGeneral Treatment Issues
Patients need to be placed in intensive care environment
with constant monitoring
Aggressive fluid resuscitation
Nasogastric suction is appropriate in patients with ileus
and vomiting for symptomatic relief
Administration of Imipenem-Cilastatin is recommended.
Start as soon as the diagnosis is made and continued for
2-4 weeks.

Interventions for PancreaticInterventions for Pancreatic
NecrosisNecrosis
Aggressive surgical pancreatic debridment (necrosectomy)
is the standard of care if drainage is undertaken and may
require multiple abdominal operations. This is gold standard
treatment.
Options for laparotomy:
-Debridement with wide sump drainage ( closed)
-Debridement with open packing
-Debridement and continuous closed post operative
lavage of lesser sac.
Overall mortality with closed or open techniques is
approximately 20%

Acute Pancreatitis:Acute Pancreatitis:
NecrosectomyNecrosectomy

Alternative Methods ofAlternative Methods of
DebridementDebridement
Minimally invasive approaches:
-Percutaneous Therapy (Interventional
radiology)
-Endoscopic Therapy
-Laproscopic technique
-Great technical expertise required
-Team approach is necessary
-Combination of methods can be used
-Used to prevent the need for laprotomy during
the most acute phase of illness.

ComplicationsComplications
EarlyEarly
SystemicSystemic LocalLocal
ARDSARDS GI bleedingGI bleeding
ARFARF Adjacent bowel necrosis/fistulaAdjacent bowel necrosis/fistula
HypocalcemiaHypocalcemia formationformation
ShockShock HydronephrosisHydronephrosis
CoagulopathyCoagulopathy Splenic rupture or hematomaSplenic rupture or hematoma
HyperglycemiaHyperglycemia Splenic vein thrombosisSplenic vein thrombosis
Infected necrosis/abscessInfected necrosis/abscess

Late
Pseudocyst (1-4%)
Duct obstruction
Endocrine insufficiency
Diabetes

 AbscessAbscess
 Pseudocyst formationPseudocyst formation
 Pancreatic ascitesPancreatic ascites
 Chronic pleural effusionChronic pleural effusion
 Gastrointestinal bleedingGastrointestinal bleeding
 Acute splenic vein thrombosisAcute splenic vein thrombosis
 Chronic PancreatitisChronic Pancreatitis

Pancreatic PseudocystPancreatic Pseudocyst
 The term pseudocyst denotesThe term pseudocyst denotes absence of an epithelialabsence of an epithelial
lininglining in contrast to true cystsin contrast to true cysts
 Encapsulated collections of fluid with high enzymeEncapsulated collections of fluid with high enzyme
concentrations that arise from the pancreas.concentrations that arise from the pancreas.
 They are usually located either within or adjacent to theThey are usually located either within or adjacent to the
pancreas in the lesser sac.pancreas in the lesser sac.
 The walls of a pseudocyst are formed by inflammatoryThe walls of a pseudocyst are formed by inflammatory
fibrosis of the peritoneal, mesenteric and serosalfibrosis of the peritoneal, mesenteric and serosal
membranes which limits spread of the pancreatic juice asmembranes which limits spread of the pancreatic juice as
the lesion develops.the lesion develops.

 Early or late presentationEarly or late presentation
 Pain is the most common findingPain is the most common finding
 Fever, weight loss, tenderness, palpable massFever, weight loss, tenderness, palpable mass
 Jaundice rarelyJaundice rarely
 Elevated amylase and WBC in ~ 50%Elevated amylase and WBC in ~ 50%
 CT scan is the investigation of choiceCT scan is the investigation of choice
 D/D Abscess, phlegmon, neoplastic cystsD/D Abscess, phlegmon, neoplastic cysts

 InfectionInfection
 > Abscess> Abscess
 RuptureRupture
 Severe chemical peritonitisSevere chemical peritonitis
 HaemorrhageHaemorrhage

Pseudocyst DrainagePseudocyst Drainage

Nutritional SupportNutritional Support
Total enteral nutrition delivered through a
JEJUNAL feeding tube is preferable in
patients with AP in the absence of
substantial ileus and can be started within
first 48 hours of onset of illness.
It is well tolerated, cheaper, less total risk
and a lower risk of developing infectious
complications.

ConclusionsConclusions
1. Aggressive critical care with antibiotics, pain control, fluid
resuscitation and nutrition is the mainstay of management
of acute necrotizing pancreatitis, with surgery or other types
of debridement limited to patients with infected necrosis.
2. Hyperamylasemia, if present, probably, indicates acute
pancreatitis, if absent it proves nothing.
3. Ultrasound should be used within first 24 hours of
admission. Look for gallstones.
4. ERCP is neither required for diagnosis, nor provides
prognostic information. It is needed urgently in patients with
gallstones.

ConclusionsConclusions
5. Pseudocysts. Asymptomatic require no treatment,
Symptomatic can be decompressed by surgical
(open or endoscopic) and radiologic methods.
Consider timing.
DO NOT DRINK !!!

acute pancreatitis

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