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Pancreatitis & Pseudocyst
in
Children
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Anatomy
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Embryology
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PANCREATITIS
Definition and Classification
acute or chronic
clinical characteristics,
pathologic changes, and natural history.
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Pathology
parenchymal and peripancreatic fat necrosis
( severity of an attack)
associated inflammatory reaction.
interstitial edema and infiltration of
inflammatory cells(mild ac pancreatitis)
extensive necrosis, thrombosis of intrapancreatic
vessels, vascular disruption,and intraparenchymal
hemorrhage.(Severe pancreatitis)
infection, intrapancreatic or peripancreatic
abscesses.
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Etiology
Acute PancreatitisBiliary tract stones
Drugs
ERCP
Hypercalcemia
Hyperlipidemia
Idiopathic
Infections
Ischemia
ParasitesPostoperative
Scorpion sting
Trauma
Chronic PancreatitisAutoimmune
Duct obstruction
Hereditary
Hypercalcemia
Hyperlipidemia
Idiopathic
ERCP, endoscopic retrograde
cholangiopancreatography.
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Biliary Tract Stones
Biliary Tract Stones
1901, Opie, a pathologist, Johns Hopkins
University, stone in the terminal bilio pancreatic duct of
a patient who had died of severe pancreatitis.
common biliopancreatic channel, allowing bileto reflux into the pancreatic duct. Opie EL: Theetiology of acute hemorrhagic pancreatitis. Bull Johns Hopkins Hosp
12:182192, 1901.
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DrugsDefinite Cause
5-Aminosalicylate
6-Mercaptopurine
Azathioprine
Cytosine arabinoside
Dideoxyinosine
DiureticsEstrogens
Furosemide
Metronidazole
Pentamidine
Tetracycline
Thiazide
Trimethoprim-
sulfamethoxide
Valproic acid
Probable Cause
Acetaminophen
-Methyl-DOPA
Isoniazid
L-Asparaginase
Phenformin
ProcainamideSulindac
DOPA,
dihydroxyphenylalanine.
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Obstruction
duodenal ulcers, duodenal Crohns disease,
and periampullary tumors, periampullary
diverticulum,
pancreatic duct stricture or
disruption following blunt pancreatic trauma
Parasites such asAs
caris
and Clonorchis
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Hereditary and Autoimmune Pancreatitis
trypsinogen activation
(is protected from injury by the presence of trypsin inhibitors.)
genetic mutations are believed to cause this
protective process to fail (resistant to inhibition)
begin at a young age and lead to chronic
changes including fibrosis, calcifications, and
loss of both exocrine and endocrine fn
cancer is also markedly increased
Autosomal dominant
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autoimmune process,
primary sclerosing cholangitis,
Sjgrens syndrome and
primary biliary cirrhosis
lymphoplasmacytic autoimmune pancreatiti
s.
elevation in the levels ofIgG4.
GatesLD, Ulrich CD, Whitcomb DC, et al: Hereditary pancreatitis gene defects and
theirimplications. Surg Clin North Am 79:711722, 1999.
Hamano H, Kawa S, Horiuchi A, et al: High serum IgG4 concentrationsin patients
with sclerosing pancreatitis. N Engl J Med 344:732738, 2001.
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Miscellaneous
metabolic abnormalities,
hypercalcemia (i.e., hyperparathyroidism)
hyperlipidemia (type I, IV, orV hyperlipoproteinemias).
hyperchylomicronemia interferes with the pancreatic
microcirculation
Trinidad, scorpion stings(excessive pancreatic
stimulation)
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Idiopathic Pancreatitis
20% of patients have pancreatitis without an
identifiable etiology.
gallbladder sludge or microcrystals,
sphincter of Oddi malfunction,
subclinical mutations of the cystic fibrosis
gene.
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Pathophysiology of Acute Pancreatitis
acute pancreatitis is triggered by obstructionof the pancreatic duct
injury begins within pancreatic acinar cells
cathepsin Bmediated intra-acinar cellactivation
colocalization hypothesis,
Steer ML:The early intra-acinar cell events which occur during acute pancreatitis:The
Frank Brooks Memorial Lecture. Pancreas 17:3137, 1998.
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Co Localisation of trypsinogen + cathepsin B (intra cytoplasmic)
Activation of trypsinogen
Trypsin Zymogens
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Symptoms
Abdominal pain, the pain is located in theepigastrium,
pleuritic component and be felt in one or both
shoulders knifelike and radiating straight through to the
mid-central back
nausea, and vomiting.
relieved by leaning forward or lying on the side
Pain persists even after gastric decompression.
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Physical Findings
rolling or moving around in search of a morecomfortable position
appear ill and anxious.
Hyperthermia is common due to release of
proinflammatory factors, (cytokines and chemokines)
Tachycardia, tachypnea, and hypotension(hypovolemia)
Breath Sounds in the lower lung fields are usuallydiminished and atelectasis ++, pleural effusion
(RDS) acute lung injury
alterations in their mental status
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Jaundice gallstone induced acute pancreatitis,
duct obstruction caused by the inflamed pancreas
cholestasis induced by the severe illness
ileus, bowel sounds are usually diminished duringan attack of pancreatitis and the abdomen maybecome distended
tenderness as well as both voluntary andinvoluntary guarding are common.
flank ecchymoses (Grey Turners sign)
periumbilical ecchymoses (Cullens sign), InguinalInguinal liglig.. FOXSSIGNFOXSSIGN
(retroperitoneal hemorrhage)
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DiagnosisHAEMATOCRIT HYPOVOLEMIA
Hb%DIFFUSE CAPILARY LEAK SYNDROME
BUN RETROPERITONEAL
Cr. (exudation blood & plasma into retroperitoneum)
Albumin FLUID CORRECTION - AIBUMIN FREE CRYSTALLOID
LFTLFTBILIRUBIN
ALKALINE PHOSPHATASE HEPATIC PARENCHYMAL NECROSIS
TRANSAMINASE
TG ETHANOL
ELETROLYTESELETROLYTES
Ca+2 - ALBUMIN
- BINDING IN AREA OF FAT NECROSIS
Mg+2
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AMYLASE 60-180 U/L 3 fold clinch diagnosis
No correlation severeity of pancreatitis &Amylase
Onset 2 12 hrs. 3-6 days after attack normally
Elevation persists > 1 wk Ongoing inflamation
Pseudocyst formationPancreatic abscessPancreatic ascites
Urinary Amylase LONGERLONGER than Serum Amylase
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Amylase Amylase other than pancreatitisother than pancreatitis
Ac.cholecystitisAc.cholecystitis
(( Mild elivation 2-3 fold )) PerforatedPerforated viscusviscus(( PerforatedPerforatedpeptic ulcerpeptic ulcer MC)MC)
Bowel obstruction / infarctionBowel obstruction / infarction
PPancreatitis not associated Amylase
Overhelming necrosis of gland
Ac pancreatitis superimposed onAc pancreatitis superimposed on ch.pancreatitisch.pancreatitis
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LIPASE 0- 160 U/L
More specific
Parallels rise in amylase activity
Elevation persists after amylase
activity returned to normal
Helpful in pts, presents several days
after the attack
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MARKER PREDICTINGSEVERITY OF AN ATTACKTrypsinogen
Procarboxypeptidase URINEURINE
Prophospholipase
Methmalbumin
Inflammatory mediator
IL
-1
,6
SERUM
SERUM
TNF-
CRP
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IMAGINGSTUDIES
Plain ErectAbdominal & Chest RadiographsPlain ErectAbdominal & Chest RadiographsNot helpful inNot helpful in diagonosisdiagonosis,,
Sentinel loop
Dilation of tr. Colon
Epigastric soft tissue density
Obscured psos sign
Colon cut off sign
Renal halo sign
Calcified gall stone
Pancreaticcalcification (ch.pancreatitis,intraductal protein plug)
Left Pleural effusion
Diffuse alveolar interstitial shadow
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USG ABDOMEN
-Limited value:Presennce of intestinal gas inupper abdomen.
-Perform within 24 hrs *Pancreatic edema
*Gall stone*AC.cholecystitis
*Dilated CBD
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CECT ( IV+ ORAL)-Diagnostic-Management
Distinguish interstitial from necrotizing pancreatitisLocalised complication Peripancreatic fluid collection
PseudocystPseudoaneurysm
-CT FINDINGSCT FINDINGSPancreatic edemaPeripancreatic fluid collectionMesenteric fat strandingBiliary tract stones
Absence of enhancement(>3 cm or >30% gland)Pancreatic necrosis
< 72 hrs CT underestimates extent of necrosisCRITICAL FINDINGS
Extra visceral gasPneumoperitoneumHemorrhage. Into lesser sac
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timing of CT during an attack of pancreatitis
early performance of contrast-enhanced CT
does not worsen pancreatitis particularly helpful when the diagnosis of
pancreatitis is in doubt
Necrosis, early CT not useful
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y COMBINATION CT SCORE OF UNENHANCED &
CONTRAST-ENHANCED CT ASSESSMENT OF
PANCREAS
A NORMAL
B PANCREATIC EDEMA
C PERIPANCREATIC FATABNORMALITIES
D SINGLE FLUID COLLECTION
E MULTIPLE FLUID COLLECTION OR GAS
Later,Balthazar incorporated pancreatic necrosis into
severity index( 0 10)
CT INDEX >7 MORTALITY 1 7%
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GADOLINIUM & MAGNETICRESONANCE
CHOLANGIOPANCREATOGRAPHY- Alternative to CT
- Use relatively limited
- Not well studied- Where ERCP not technically feasible
associated Gall bladder disease
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ERCP
Gall stone pancreatitis
Biliary obstructionCholangits
REMOVAL OF IMPACTEDSTONE
DECOPRESS BILIARY TREE
DELINEATE PANCRATIC DUCTALANATOMY
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RANSONSCRITERIA NONBILIARYAC. PANCREATITIS BILIARY
AC.PANCREATITIS
ADMISSIONADMISSION
AGE(YRS) >55 > 70
WBC COUNT ( 1000/ cmm) >16 >18
GLUCOSE ( mg/ dl) >200 >220
AST (IU/ L) >250 >250
LDH (IU/
L) >
350
>400
WITHIN 48HRS OFWITHIN 48HRS OF
ADMISSIONADMISSION
HAEMATOCRIT
DECREASE(points)
>10 >10
BUN increase (mg/ dl) >5 >2
BASE deficit (mEq/ L) >4 >5
FLUID replacement(L) >6 >4
PaO2 (mm Hg)
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CRITERIA VALUE
Age(yr)>55
WBC count(1000/ cmm) >15
Glucose(mg/dl) >180
BUN (mg/ dl) >45
LDH(IU/L) >600
Albumin(gm/dl)
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Modified Marshal Score (Excludes Hepatic Index)
forGrading Severe Acute Pancreatitis
SYSTEM 0 1 2 3 4
CVS(SBP) >90
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ACUTE PHYSIOLOGY AND CHRONIC HEALTH EVALUATION(APACHE)-II
SCORING SYSTEM OF DISEASE SEVERITY
(A). PHYSIOLOGIC VARIABLES(A). PHYSIOLOGIC VARIABLES
yTemperature
y Mean arterial pressure(mm Hg)
y Heart rate
y Respiration
y Arterial pH
y PaO2 (mm ofHg)
y Serum sodium
y Serum bicarbonate(mmol/L)
y Serum creatinine(mg/dl)
y Hematocrite(%)
y WBC count
y Glasgow Coma Score
(B). AGE POINTS(B). AGE POINTS
(C). CHRONIC HEALTH POINTS(C). CHRONIC HEALTH POINTS
APACH
E-II SCORE=A+B+C
12 physiologic & laboratory
parametrs + age + comorbid
cond. To estimate severity
Score>9 severe ac.pancreatitis
ADV
On daily basis continuously
quantifying disease severity
DISADV
Somewhat cumbersome
Not specific for ac.pancreatitis
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TREATMENTOF AN ACUTE ATTACK OF PACREATITIS
Evolves in 2 overlapping phases
INITIAL PHASELasts for 2 wks
Acute inflammatory & Autodigestive process
Takes place in & around pancreas
Mayhave systemic effects
LATER PHASEIn SEVERE PANCREATITIS initial phase evolves into this phase
Development of local complications due to Necrosis, Infection,Pancreatic duct rupture
INITIAL TREATMENT
MANAGEMENT OF PAINSevere & difficult tocontrol
Narcoticmedications
MEPERIDINE & its analogue preferable to MORPHINEMophine Sphicterofoddi spasm Biliary pancreatits
Splanchnic block
Continuous epidural anaesthesia
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INTRA VASCULA VOL CRYSTALLOID SOL.
HAEMATOCRIT BLOOD TRNSFUSION
H YPOALBUMINEMIA ALBUMIN TRANSFUSION
ALBUMIN FREE CRYSTALLOID
H YPOMAGNESEMIA ADMINISTRATION OF Mg+2
HYPOCALCEMIA(IN SEVERE ATTACK)
IONIZED CALCIUM
LOW CIRCULATING ALBUMIN
(N) - TETANY
NOTHING TO DO CARPOPEDAL SPASM
ADMINISTRATION OF Ca+2 WITH
CAUTION,SINCE Ca+2
IMPLICATED IN GENESIS OF
PANCREATITIS
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y CADIOVASCULARSYSTEM
Meticulousreplacement of fluid & eletrolyte losses
Placement of a Central venous orSwan-Ganz catheter
Fluid balance flow sheet
PR,BP,O2 saturation,UOP- unreliable for determining fluid needs
Haematocrit -Accurateindicators ofmagnitude ofextra cellular fluid loss
- In a setting of bl.loss or hemolysis Haehatocrit measurementmay
loose their
valuein fluid management
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y RESPIRATORY MONITORING & SUPPORT
ABGABG (At diagonosis & at intervals 12hrs.for initial 48-72 hrs.
Early Arterial HypoxemiaEarly Arterial Hypoxemia Close monitaringAdministrating o2
Progressive Resp. FailureProgressive Resp. Failure IVF administration + UOP
maintained/ by diuresis
SevereSevere PulPul. Insufficiency. Insufficiency Endotracheal intubation
+
PEEP( Positive End Expiratory Pressure) ventilation
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ROLEOF NASOGASTRICDECOMPRESSION
Aspiration of gastric acid Secrretin release Pancreatic secretion
Not alter course or outcome of pancreatic attack
Provide greater pt.comfort during early stage from
Nausea
Vomiting
Retching MALLLORY- WEISSSYNDROME
Abdominal distention
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ROLEOF PROPHYLACTIC ANTIBIOTIC
PANCREATIC INFECTION
TRANSLOCATION OF GUT BACTERIAACROSSTHEINJUREDTRANSLOCATION OF GUT BACTERIAACROSSTHEINJURED
BOWEL WALL ADJACENTTO ARES OF PANCREATIC INJURYBOWEL WALL ADJACENTTO ARES OF PANCREATIC INJURY
MILD PANCREATITIS NOBENEFIT
SEVERE PANCREATITIS CONTROVERSIAL
BENEFIT OBSERVEDBENEFIT OBSERVED IMIPENEM
IMIPENEM + CILASTATATINIMIPENEM + CILASTATATINCEFUROXIMECEFUROXIMECIPROFLOXACIN +CIPROFLOXACIN +METRONIDAZOLEMETRONIDAZOLE
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NUTRITIONALSUPPORTTHEORETICAL FEAR OF STIMULATING ANALREADY INFLAMMED PANCREASTHEORETICAL FEAR OF STIMULATING ANALREADY INFLAMMED PANCREASWITH ORAL ORWITH ORAL OR ENTERALNUTRITIONNOT FOUNDEDINEVIDENCEDMEDICINE.NUTRITIONNOT FOUNDEDINEVIDENCEDMEDICINE.
MILD PANCREAITIS IF PT.UNABLETO MEETADEQUATE PROTEINIF PT.UNABLETO MEETADEQUATE PROTEIN& CALORIC NEEDS PER OS WITHIN 5& CALORIC NEEDS PER OS WITHIN 5--1010
DAYSDAYSOF ONSETOF ONSET
SUPPLEMENTAL FEEDING VIANASOENTERICSUPPLEMENTAL FEEDING VIANASOENTERICFEEDING TUBEFEEDING TUBE(NEED FOR PARENTERALNUTRITION RARE.)(NEED FOR PARENTERALNUTRITION RARE.)
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SEVERE PANCREATITIS
MOST CATABOLIC COND.
EARLY NUTRITION IMPERATIVE
ACHIVED INITIALLY WITH TPN THROUGH CENTRAL VENOUS CATHETERTIME TO START
WITHIN 1 OR DAY 2 DELAY STARTING UNTIL EARLY PHASE
OF PANCREATITIS(EXTENSIVE FLUID SHIFT+
HIGH FLUID REQUIREMENTS)COMPLETED
PREFERRED ONE
USE OF LIPIDS IN TPN NOT SHOWN TO WORSEN THE COURSE OF AC.PANCREATITIS
RESUMPTION OF ENTERAL INTAKE OR ORAL FEEDING SHOULD COINCIDE WITH
RESOLUTION OF GASTRIC ILEUS
(1).NASOGASTRIC TUBE ADVANTAGE
ENTERAL INTAKE ENTERAL NUTRITION EXERTS A TROPHIC
(2).NASO JEJUNAL TUBE EFFECT ON INJURED BOWEL WALL THAT
COULD REDUCE THE BACTERIAL
TRANSLOCATION & THUS REDUCE THE
INCIDENCE OF TIONPANCREATIC INFECTION
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TREATMENT OFLIMITEDOR UNPROVEN VALUE
PERITONEAL DIALYSISPERITONEAL DIALYSISTO ELIMINATE THE PROI NFLAMMATORY FACTORS NO BENIFITTO ELIMINATE THE PROI NFLAMMATORY FACTORS NO BENIFITRELEASED INTO ABDOMEN DURING PANCREATITISRELEASED INTO ABDOMEN DURING PANCREATITIS
ATTEMPTS TO PANCREATIC SECRETIONATTEMPTS TO PANCREATIC SECRETIONNASOGASTRIC DECOMPRESSIONNASOGASTRIC DECOMPRESSIONH2 BLOCKERH2 BLOCKERPPIPPIATROPINEATROPINEANTACIDSANTACIDS NONO
BENIFITBENIFITSOMATOSTATINSOMATOSTATIN
GLUCAGONGLUCAGONCALCITONINCALCITONINPEPTIDEYYPEPTIDEYYCHOLECYSTOKININ RECEPTOR ANTAGONISTCHOLECYSTOKININ RECEPTOR ANTAGONIST
(MORE RECENT STUDY DID NOT DEMONSTRATE ANY BENEFIT OF(MORE RECENT STUDY DID NOT DEMONSTRATE ANY BENEFIT OF OCTREOTIDE.)OCTREOTIDE.)
ANTI INFLAMMATORY AGENTSANTI INFLAMMATORY AGENTSSTEROIDSSTEROIDS
PGsPGs NONOBENIFITBENIFITINDOMETHACININDOMETHACIN
CYCLOOXYGENASECYCLOOXYGENASE --22INHIBITOR MAY BE BENEFICIALINHIBITOR MAY BE BENEFICIAL
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Reginald Fitz 1889Reginald Fitz 1889
It is fascinating toIt is fascinating to cojecturecojecture how anhow aninflammatory process in a retroperitoneal glandinflammatory process in a retroperitoneal gland
can produce an abnormalities in so many organscan produce an abnormalities in so many organs..
SirSir BerkelyBerkely moynihan1925moynihan1925
Acute pancreatitis is the most terrible of all theAcute pancreatitis is the most terrible of all thecalamities occurring in conjunction with thecalamities occurring in conjunction with theabdominalabdominal viscerviscer
PANCREATIC ABSCESSPANCREATIC ABSCESS
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PANCREATIC ABSCESSPANCREATIC ABSCESS CIRCUMSCRIBED INTRACIRCUMSCRIBED INTRA--ABDOMINALCOLLECTION OFABDOMINALCOLLECTION OF
PUS,CLOSE PROXIMITY TO PANCREAS.PUS,CLOSE PROXIMITY TO PANCREAS.
DEVELOPED AS A CONSEQUENCEOFDEVELOPED AS A CONSEQUENCEOF
INFECTED PSEUDOCYSTINFECTED PSEUDOCYSTACUTEFLUIDCOLLECTIONACUTEFLUIDCOLLECTION
CONTAIN LITTLEOR NO NECROTIC TISSUECONTAIN LITTLEOR NO NECROTIC TISSUE
INFECTED PANCREATIC NECROSIS (NECROSISINFECTED PANCREATIC NECROSIS (NECROSIS
PREDOMINATESPREDOMINATES MATERIAL PASTELIKE/ PUTTY LIKE)MATERIAL PASTELIKE/ PUTTY LIKE)
PERCUTANEOUSDRAINAGE WITH WIDEST POSSIBLEPERCUTANEOUSDRAINAGE WITH WIDEST POSSIBLE
DRAINS PLACED IMAGEGUIDANCEDRAINS PLACED IMAGEGUIDANCE
++
ANTIBIOTIC THERAPYANTIBIOTIC THERAPY
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PSEUDOCYST
COLLECTION OF AMYLASE RICH FLUIDENCLOSED
BY NONEPITHELIALIZED WALL (FIBROUS & GRANULATIONTISSUE).
CAUSE 1.AC.PANCREATITIS2.CH.PANCREATITIS
3.PANCREATIC TRAUMA
SITE 1.EXTRAPANCREATIC(LESSER SAC)-MC
2.INTRAPANCREATIC
TIME TO DEVELOP
4-6 WKS AFTER AN ACCUTE ATTACK
BEFORE THAT LACKS A DEFINED WALL- ACUTE FLUID COLLECTION
- LOCALIZED AREA OF NECROSIS
NO. SINGLE(MC)
MULTIPLE
>1/2 COMMUNICATION WITH MAIN PANCREATIC
DUCT
COMPLICATIONABSCESS
INFECTIONINFECTION
SYSTEMIC SEPSISSYSTEMIC SEPSIS
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RUPTURE GI BLEEDING
INTO GUT
INTRNAL FISTULA
INTO PERITONEUM PERITONITIS
ENLARGEMENT BILLIARY COMPRESSION
OBSTRUCTIVE JAUNDICE
PRESSURE EFFECT
BOWEL COMPRESSION
GASTRIC OUTLET
OBSTRUCTIONEARLY SATIETY
PAIN
BLEED INTO CYST
EROSION INTO VESSEL
HEMOPERITONEUM
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DIAGONOSIS ULTRASOUND
CT SCAN
ERCP COMMUNICATION Between.
MRCP CYST & DUCT
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yDIAGONOSTICCONFUSION
CYSTIC NEOPLAS
M
EUS & ASPIRATION
CEA LEVEL >400 ng/ ml
AM
YLASE
LEVE
L
INFLAMMATORY CELLS
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y MANAGEMENTRESOLVE SPONTANEOULY MOST LY
BUT, THICK WALLED
> 6 cm IN DIAMETER
DURATION> 12 WKS
ARISEN IN THE CONTEXT OF CH.PANCREATITIS
ASSOCIATED WITHSYMTOMATIC
ENLARGING
ASSOCIATED WITH COMPLICATION
- NEEDS SURGICAL INTERVENTION
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POOR SURGICAL RISK PATIENTS
PERCUTANEOUS CATHETER DRAINAGE
DISADV: RECURRENCE
CATHETER INDUCED INFECTION
EXTERNAL PANCREATIC FISTULA
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INTRNALDRAINAGEINTRNALDRAINAGE
ENDOSCOPICALLY DOUBLE PIGTAILCATHTERDRAINAGE
CYSTOGASTROSTOMY/ CYSTODUODENOSTOMY TRNS PAPILLARY DRAINAGEBY PUTTING A
STENT
SURGICALLY CYSTOGASTROSTOMYCYSTODUODENOSTOMY
CYSTOJEJUNOSTOMY
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PANCREATIC ASCITES MECH
(1).PANCREATICDUCT RUPTURE
(2).LEAKING PSEUDOCYST
PANCREATIC JUICEGAINSENTRY INTO
PERITONEALCAVITYDIAGONOSIS AMYLASE IN ASCITIC
FLUID
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TREATMENTNONOPERATIVE
ELIMINATION ENTERAL FEEDINGSECRETION NASOGASTRIC DRAINAGE
SOMATOSTATIN
REPEAT PARACENTESIS
RESOLUTION WITHIN 2-3 WKS(50-60%).
PERSISTENT/ RECURRENT ASCITESPERSISTENT/ RECURRENT ASCITES
ENDOSCOPIC PANCREATIC SPHINTEROTOMY WITH/ENDOSCOPIC PANCREATIC SPHINTEROTOMY WITH/
WITHOUT PLACEMENT OF TRANSPAPILLARY PANCREATICWITHOUT PLACEMENT OF TRANSPAPILLARY PANCREATIC
DUCTSTENT.DUCTSTENT.DOES NOT RESPOND to ERCPDOES NOT RESPOND to ERCP
LEAKIN PANCREATIC TAIL RESECTIONLEAKIN PANCREATIC TAIL RESECTION
LEAKIN HEAD &NECK RouxLEAKIN HEAD &NECK Roux--enen--YY
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MANAGEMENT OF PANCREATIC FISTULA
CAUSE: CONSEQUENCE OF NECROSECTOMY
SEVERE NECROTIZING PANCREATITIS
FLUID ISSUING FROM A DRAIN SITE OR WOUNDMEASUREMENT OF AMYLASE DIAGNOSTIC
MANAGEMENT- CORRECT FLUIDAND ELECTROLYTE BALANCE
-PROTECT THE SKIN(ADEQUATE DRAINAGE OF FISTULA INTO STOMA BAG)-DRAINADEQUATELY
-PARENTERAL / NASOJEJUNAL FEEDINGAS OPPOSED TO NASOGASTRICOR ORAL FEEDING
- OCTREOTIDE
MOST FISTULA MAY SEAL SPONTANEOUSLY WITH THIS
NOT RESOLVE
1.ERCP(BEST)
ANATOMY OF FISTULA 2.MRI3.FISTULOGRAPHY
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