Pancreatitis & Pseudocyst

8/8/2019 Pancreatitis & Pseudocyst

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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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