Acute pancreatitis

© S. Barbu 2011

Pancreatic Diseases

Assoc. Prof. S. T. Barbu MD, PhD

IVth Surgical ClinicUniversity of Medicine & Pharmacy “Iuliu Hatieganu” Cluj-Napoca, Romania

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- inflammatory diseases:=> pancreatitis - acute

- chronic

- pancreatic tumors:- benign- malignant

Pancreatic diseases

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Correlationsof

PancreaticDiseases

Acute pancreatitis

Chronic pancreatitis

Pancreatic Cancer

Pancreatic diseases

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Pancreatic anatomy

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Pancreatic anatomy

Pancreas = adnexal gland of the digestive tract

- exocrine function

- endocrine function

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Pancreatic anatomy

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Pancreatic secretion

• The pancreatic gland contains three types of cells.

– The duct cells make up about 10% of the pancreas and secrete solutions rich in bicarbonate.

– The acinar cells comprise over 80% of the pancreas and they synthesize and secrete pancreatic enzymes.

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Pancreatic secretion

• The islet cells make up about 10% of the pancreas and form the endocrine portion of the pancreas.

• The four major types of islet cells secrete the hormones:– insulin,– glucagon,– somatostatin, and– pancreatic polypeptide.

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Pancreatic anatomy

© S. Barbu 2011

Acute Pancreatitis

Assoc. Prof. S. T. Barbu MD, PhD

IVth Surgical ClinicUniversity of Medicine & Pharmacy “Iuliu Hatieganu” Cluj-Napoca, Romania

© S. Barbu 2011

Acute pancreatitis

“the most terrible of all calamities that [affect] the abdominal viscera” –Sir Berkeley Moynihan (Ann Surg1925)

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Acute pancreatitis

- 15 – 20% => necrosis (SAP – severe acute pancreatitis)- 40 – 70% => infection (week 3-4)

- Mortality- Acute Pancreatitis = 10%

- SAP with infected necrosis => up to 50%

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Acute pancreatitis

Course Objectives:– Definitions– Etiology– Pathology– Symptoms– Evolution– Treatment– Indications for Surgery

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Pancreatitis is the inflammation of the pancreas.

Like: - appendicitis- cholecistitis- gastritis- esophagitis

etc

Acute Pancreatitis is an inflammatory process in which pancreatic enzymes autodigest the gland. (autodigestion of the pancreas by its escaped enzymes)

Acute pancreatitis

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√Acute pancreatitis refers to an attack involving a previously normal pancreas.

√Chronic pancreatis is applied to an attack involving a previously, permanently damaged pancreas.

Pancreatitis

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√The gland can sometimes heal without any impairment of function or any morphologic changes. This process is known as acute pancreatitis.

√It can recur intermittently, contributing to the functional and morphologic loss of the gland, the pathological change referred to as chronic pancreatitis.

Pancreatitis

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√Acute pancreatitis is an acute inflammatory process of the pancreas, with variable involvement of:

- other regional tissue or- remote organ systems.

√ Although pancreatic function and structure usually return to normal, the risk of recurrent attacks is 20 to 50% unless the precipitating cause is removed.

√ The disease includes a broad spectrum, which varies from:- mild parenchymal edema to- severe pancreatitis associated with subsequent

gangrene and necrosis (acute necrotizing pancreatitis).

Acute Pancreatitis

© S. Barbu 2011

Epidemiology

• 17 - 19/100,000 per year• Peak incidence in 5th decade• Incidence is Increasing• 180,000 - >200,000 Hospital Admissions/Year

(USA)• 20% have a severe course

– 10-30% mortality for this group, which has not significantly changed during the past few decades despite improvement in critical care and other interventions

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Etiology

• Etiologies: I get smashed– Idiopathic– Gallstones (or other

obstructive lesions)– EtOH– Trauma– Steroids– Mumps (& other viruses)– Autoimmune (SLE,

polyarteritis nodosa)

– Scorpion sting– Hyper Ca, TG – ERCP (5-10% of pts

undergoing procedure)– Drugs (thiazides,

sulfonamides, ACE-I, NSAIDS, azathioprine)

EtOH and gallstonesaccount for 70-80% of cases

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Etiology

• Alcohol (30-40%)• Mechanism not fully understood• Alcohol metabolites are toxic

– Not all alcoholics get pancreatitis (only 10 - 15%)• This suggests a subset of the population predisposed

to pancreatitis, with alcohol acting more as a co-precipitant

• Tolerance threshold to alcohol• Alterations of Genes controlling alcohol metabolism

© S. Barbu 2011

Etiology• Gallstones (35%-40%)

– Gallstone pancreatitis risk is highest among patients with small GS < 5mm and with microlithiasis

– GS pancreatitis riskis also increased inwomen > 60 yrs

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Drugs and Toxins (5%)

• Azathioprine• Cimetidine• Estrogens• Enalapril• Erythromycin• Furosemide• Multiple HIV medications• Scorpion Bites• Sulfonamides• Thiazides

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Etiology – Trauma

• Blunt Trauma– Automobile– Bicycle handlebar injuries– Abuse

• Iatrogenic – ERCP (1-7%) – Likely secondary to contrast but also very

operator dependant– Risk is also increased with Sphincter of Oddi

manometry

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Etiology – Trauma

• Iatrogenic – Surgery – Surgery for duodenal ulcer– splenectomy

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Etiology – Multi-System Disease

• Cystic Fibrosis– 2-15% of patients– Ductal obstruction from thickened secretions

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Etiology – Infection• Ascaris• Campylobacter• CMV• Coxsackie B• EBV• Enterovirus• HIV/AIDS• Influenza• MAC• Measles• Mumps Rubella• Mycoplasma• Rubeola• Viral Hepatitis• Varicella

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Etiology-Anatomical Anomalies

• Pancreas Divisum– Failure of dorsal and ventral fusion (5-15% 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– Weight loss– Recent Diabetes mellitus– without other obvious risk factors

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• Pancreas Divisum

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• Annular Pancreas

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Etiology – Idiopathic

• Experts suggest that idiopathic pancreatitis should account for no more than 5-10% of the total cases,

• yet the broadly quoted percentage in the literature at this time in the US is currently 20-25%.

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Trivia

• What is the name of the scorpion that causes pancreatitis?– Hint: you won’t find it in the USA

» Tityus Trinitatis» (Found in Central/ » South America and» the Caribbean)

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PathogenesisPathogenesis1.A complicated 1.A complicated pathophysiologicpathophysiologic processprocess

2.Enzyme 2.Enzyme autoactivationautoactivation and selfand self--digestion digestion

(key point)(key point)

3. Many agents participating in the process3. Many agents participating in the process

4. Complete mechanism remaining unknown4. Complete mechanism remaining unknown

Acute pancreatitis

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Initiation factor in Earlier periodInitiation factor in Earlier periodInitiation factor in Earlier period

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1. 1. Pancreatic Enzyme Abnormally ActivatedPancreatic Enzyme Abnormally Activated⑴⑴Bile refluxBile refluxBile Bile common channelcommon channel pancreatic ductpancreatic duct

1.hypertension in pancreatic duct1.hypertension in pancreatic duct2.premature activation of pancreati2.premature activation of pancreatic c

enzymes enzymes 3.injury to the lining of the pancreatic 3.injury to the lining of the pancreatic

ductsductspancreatic edema or necrosis pancreatic edema or necrosis

MODSMODS

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⑵⑵ Duodenal RefluxDuodenal Refluxduodenal duodenal enterokinaseenterokinase pancreatic pancreatic ductducttrypsinogentrypsinogen trypsintrypsinelastasinogenelastasinogen elastaseelastasephospholipasogenphospholipasogen phospholipasephospholipase

lecithin lecithin lysolecthinlysolecthin

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2.Alcohol Toxicity2.Alcohol Toxicity⑴⑴stimulate the pancreas to secrete stimulate the pancreas to secrete pancreatic pancreatic hypertentionhypertention tiny pancreatic tiny pancreatic duct and duct and acinusacinus rupture pancreatic rupture pancreatic juice spillage juice spillage ⑵⑵spasm of the sphincter of spasm of the sphincter of oddioddi⑶⑶direct injury to pancreasdirect injury to pancreas

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3.Pancreatic Microcirculation3.Pancreatic MicrocirculationDisorderDisorder⑴⑴systemic hypotensionsystemic hypotension⑵⑵hyperlipidemiahyperlipidemia: triglycerides lipase free : triglycerides lipase free acid fatty acids injure pancreatic acid fatty acids injure pancreatic microcirculationmicrocirculation⑶⑶artheroembolismartheroembolism⑷⑷vasculitisvasculitis

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Aggravating factors in later periodAggravating factors in later period⑴⑴Infection: pancreatic abscessInfection: pancreatic abscess⑵⑵Intestinal bacteria translocationIntestinal bacteria translocation⑶⑶Cytokine and systemic inflammation Cytokine and systemic inflammation reaction syndromereaction syndromeTNF ILTNF IL--1 IL1 IL--6 PAF MSOF6 PAF MSOF⑷⑷Free radicalsFree radicals

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Acute pancreatitis• Pathophys- insult leads to leakage of pancreatic

enzymes into pancreatic and peripancreatictissue leading to acute inflammatory reaction

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ACUTE PANCREATITIS Classification of Pancreatitis

• Acute Interstitial edematous pancreatitis (IEP) => Mild acute pancreatitis (clinical)– Homogeneous enhancement of pancreatic parenchyma– No necrosis (pancreatic or peripancreatic)

• Acute Necrotizing pancreatitis (SevereAP)– Non-enhancement of pancreatic parenchyma

and/or peripancreatic necrosis

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Signs & Symptoms

• Severe epigastric abdominal pain - abrupt onset (may radiate to back)

• Nausea & Vomiting• Weakness• Tachycardia• +/- Fever; +/- Hypotension or shock

– Grey Turner sign - flank discoloration due to retroperitoneal bleed in pt. with pancreatic necrosis (rare)

– Cullen’s sign - periumbilical discoloration (rare)

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• Grey Turner sign • Cullen’s sign

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Differential

• Not all inclusive, but may include:– Biliary disease– Intestinal obstruction– Mesenteric Ischemia– Distal aortic dissection– Perforated peptic ulcer (acute peritonitis)– Intestinal oclusion by strangulation

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Evaluation

• ↑ amylase…Nonspecific !!!– Amylase levels > 3x normal very suggestive of

pancreatitis• May be normal in chronic pancreatitis!!!

– Enzyme level ≠ severity– False (-): acute on chronic (EtOH); HyperTG– False (+): renal failure, other abdominal or salivary

gland process, acidemia

• ↑ lipase– More sensitive & specific than amylase

© S. Barbu 2011

Evaluation

• Other inflammatory markers will be elevated– CRP, IL-6, IL-8 (studies hoping to use these markers to aid in

detecting severity of disease)• ALT > 3x normal → gallstone pancreatitis

– (96% specific, but only 48% sensitive)• Depending on severity may see:

– ↓ Ca– ↑WBC– ↑BUN– ↓ Hct– ↑ glucose

© S. Barbu 2011

Radiographic Evaluation

• AXR - “sentinel loop” or small bowel ileus• US or CT may show enlarged pancreas with

stranding, abscess, fluid collections, hemorrhage, necrosis or pseudocyst

• MRI/MRCP newest “fad”– Decreased nephrotoxicity from gadolinium– Better visualization of fluid collections– MRCP allows visualization of bile ducts for stones

– Does not allow stone extraction or stent insertion

• Endoscopic US (even newer but used less)– Useful in obese patients

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CT Scan of acute pancreatitis

• CT showssignificantswellingand inflammationof the pancreas

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Gallstone pancreatitis by ERCP

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Acute Pancreatitis

• Morbidity and mortality highest if necrosis present (especially if necrotic area infected)– Dual phase CT scan useful for initial eval to

look for necrosis • However, necrosis may not be present for 48-72

hours

© S. Barbu 2011

Definitions - Why do we need a classification?

- „Same language“ for all physicians dealing with Pancreatitis=> promote Standardization

- Selection of patients for:- referral to ICU- referral to specialist centers- interventions against complications

- Comparing patients for scientific purposes

- Patients recruitment for clinical trials

- Avoid unneccessary and expensive diagnostic and therapeuticprocedures in mild cases

© S. Barbu 2011

We should Thank…

Bradley EL 3 rd.

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Goals of Atlanta Symposium

1. Classification of acute pancreatitis (universally applicable )

2. Nomenclature of pancreatic fluid collections

=> reach “Global consensus”

Comments: “it is easy to discuss Definitions in a hotel-room in Atlanta, but it will be quite difficult to apply them in the emergency room”

=> Laudable+ important Step Forward in 1992

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Atlanta Definitions

Definitions for:

• Mild & Severe acute pancreatitis

• Acute fluid collections

• Pancreatic necrosis (sterile & infected)

• Acute pseudocyst

• Pancreatic abscess (diff from “postop. Abscess”)

(use of terms like “pancreatic phlegmon”, infected pseudocyst”, etc should be discouraged)

© S. Barbu 2011

1992 – 2010 – What we have learned?

• Better understanding of the pathophysiology of acute necrotizing pancreatitis

• Improved diagnostic imaging of thepancreatic parenchyma and peripancreatic collections

• Development of minimally invasive techniques for the management of complications

• Percutaneous (US or CT guided) drainage• Endoscopic drainage• Laparoscopic necrosectomy

© S. Barbu 2011

..…it’s Time for a Revision…..

Spring 2003:- APA, IAP, Pancreas Club, pancreatologists -Circulation of a draft for a revised „Atlanta Classification“Michael Sarr, Rochester/USA

May 2005:Working Group assembled „Revision of the Atlanta Classification“(Acute Pancreatitis Classification Working Group)Christos Dervenis, Athens/GR & Greg Tsiotos, Falirakon/GR –

IAP/EPC

Nov 2005:Decision to establish 2 Sub-Committees (coordinator C.Dervenis):

Clinical (severity) Classification Morphol. (imaged-based) ClassifPeter Banks, Boston/USA Mike Sarr, Rochester/USA

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Approaches to Classification

Clinical

Local / Morphological

No direct correlation exists between clinical severity & morphological characteristics

This revised classification pertains primarily to adults (>18 years old)

(certain definitions and scoring systems may not be applicable to the pediatric population)

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New concepts

• 1st phase (1-2 wks) (early phase)

– “functional” or “clinical” parameters

• 2nd phase (>2wks)

– “morphologic” criteria

The early clinical and the later morphological classification

do not necessarily overlap and do not necessarily correlate with one another

© S. Barbu 2011

New combined Clinical & Image-based Classification 1st Phase: Clinical Classification - 1

Definition of acute pancreatitis (2 of 3 findings)

1. Characteristic abdominal pain

2. Serum amylase / lipase activity >3 times upper normal value

3. Characteristic findings on CECT

© S. Barbu 2011

New combined Clinical & Image-based Classification1st Phase: Clinical Classification - 2

• Definition of onset

=> The time of onset of abdominal pain (not of admission)

(The interval between onset of pain and admission should be noted precisely)

© S. Barbu 2011

Definition of severity*

• Non-severe pancreatitis – no organ failure

• Severe acute pancreatitis –

- persistence of organ failure >48 hr

*Independent of imaging


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Author n Positive Negative

Early Organ Failure (ESAP) *Isenmann et al., 2001 158 n = 47 ESAP + 42% n = 111 SAP only 14%Tao et al., 2004 297 n = 69 ESAP + 42% n = 228 SAP only 3%Poves Prim et al., 2004 112 n = 40 ESAP + 53% n = 17 SAP+late OF 12%

n = 57 OF + 40% n = 55 SAP–OF 0%

Persistent Organ FailureButer et al., 2002 121 n = 20 SAP+OF per 55% n = 33 SAP+OF res 0%Johnson et al. 2004 290 n = 102 SAP+OF per 34% n = 72 SAP+OF res 3%Mofidi et al. 2006 759 n = 89 SAP+OF per 42% n = 120 SAP+OF res 3%

* early organ failure: within 72 hours after disease onset or admissionSAP: severe acute pancreatitis; OF: organ failure; per: persistent; res: resolving

Early & Persistent Organ Failure:Most Important Outcome Determinant

© S. Barbu 2011

SEVERE ACUTE PANCREATITIS - scoring

Organ systemRespiratory (PO2/FiO2)

Renal (serum creatinine)µmol/Lmg%

CV (systolic BP)

Coagulation (Pltcount)Neurologic (Glasgow

coma scale)

>120 81-120 41-80 21-50 <21

15 13-15 10-12 6-9 <6

Modified Marshall Scoring System

0 1 2 3 4>400 301-400 201-300 101-200 <101

134 134-169 170-310 310-439 >4401.0 1.0-1.3 1.3-2.3 2.4-3.3 >3.3>90 >90 <90 pH<7.3 pH<7.2

© S. Barbu 2011

SEVERE ACUTE PANCREATITIS – ScoringSOFA Score

0 1 2 3 4Respiratory (PO2FiO2) >400 300-400 <300 <200 <100Hematologic intubated intubatedPlt count x 103 >150 100-150CV – hypotension None MAP<70 Dopamine Dopamine Dopamine

<5 µg/ml 15-14 >15or Dobutamine Epi <0.1 Epi >0.1

or NEp <0.1 NEp >0.1Neurologic – Glasgow

coma score 15 13-14 10-12 6-9 <6Renal (serum creatinine) µmol/L <110 100-170 171-299 300-440 >440mg% <1.2 1.2-1.9 2.0-3.4 3.5-4.9 >5or urine output

© S. Barbu 2011

Conclusion:=> 1st Phase: Severity defined by:

• Persistent organ failure – >2days

• death

New combined Clinical & Image-based Classification1st Phase: Severity defined by:

© S. Barbu 2011

Definition of severity*• Non-severe pancreatitis – no organ

failure

• Severe acute pancreatitis –

- persistence of organ failure >48 hr


© S. Barbu 2011

SEVERE ACUTE PANCREATITIS – Scoring2nd Phase: > 2 weeks

2nd Phase: Severity defined by:

1. Persistent organ failure

2. Complications of Ac P requiring active intervention (surgical, endocopic, laparoscopic, and/or percutaneous)

3. Need for other supportive mesures (ventilation support, renal dialysis, jejunal feeding

• Prolonged Hospitalization

• Death

© S. Barbu 2011

SEVERE ACUTE PANCREATITIS – Scoring2nd Phase: Imaging-Based Concerns

1. Presence/absence of necrosis(pancreatic and/or peripancreatic)

2. Presence/absence of infection

3. Pancreatic/peripancreatic fluid collection– Persistence >4 wk– Presence/absence of necrosis

• Pancreatic parenchymal necrosis• Peripancreatic necrosis

© S. Barbu 2011

Stratification of Morphological Severityby Imaging Procedures

Goldstandard:Contrast-enhanced Computed Tomography (CECT)

Magnetic Resonance Imaging (MRI)(MRCP – best used when CECT cotraindicated – allergy to IV contrast, etc -)

Transabdominal US and/or EUS – can also be used (not so good) (may help to clarify the type of peripancreatic collection)

© S. Barbu 2011

Stratification of Morphological Severityby Imaging Procedures

Goldstandard:Contrast-enhanced Computed Tomography (CECT)

ERCP – not recommended for Dg or Classification- has No role in this image-based classification

Department of General, Visceral, and Vascular Surgery, UKS, Homburg/Saar, Germany

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Computed tomography and magnetic resonance imaging in the assessment of acute pancreatitis.Arvanitakis M et al., Gastroenterol 2004; 126: 715-723

Patients: 39 patients with AP, CE-CT and MRI on admission, after 7 and 30 days.

Results: Predicted severe AP in 18% (n=7)Strong correlation between CTSI and MRSI on admission and 7 days later.

Prediction of severe AP: Sensitivity SpecificityMRI 83% 91%CECT 78% 86%

Conclus.: MRI is a reliable method for staging AP severity and predicting diseaseprognosis. MRI has fewer contraindications than CT.

CE-CT versus MRI in Acute Pancreatitis

Department of General, Visceral, and Vascular Surgery, UKS, Homburg/Saar, Germany

© S. Barbu 2011

SEVERE ACUTE PANCREATITIS – ScoringClassification of Pancreatitis

• Acute Interstitial edematous pancreatitis (IEP)– Homogeneous enhancement of pancreatic parenchyma– No necrosis (pancreatic or peripancreatic)

• Acute Necrotizing pancreatitis– Non-enhancement of pancreatic parenchyma

and/or peripancreatic necrosis

© S. Barbu 2011

Necrotizing Pancreatitis

• Site:– Pancreatic + peripancreatic necrosis– Peripancreatic alone (20%) – better prognosis

– Pancreatic alone (rare)

• Infection– Sterile necrosis– Infected necrosis(bubble gas inside the collection + Clinical signs of sepsis)

© S. Barbu 2011

SEVERE ACUTE PANCREATITIS – ScoringNecrotizing Pancreatitis

• Non-enhancement (necrosis) of pancreatic parenchyma– Extent: <30%, 30-50%, >50%<30% +No peripancreatic = possible fluid – repeat CECT after 5-7 days

• Necrosis of peripancreatic tissue (evolving continuum –initially solid necrosis liquefies)– Suggestive findings (MRI ?)

• Thickening of retroperitoneal tissues• Non-homogeneous

© S. Barbu 2011

Necrosis - Infection

• Depending on the stage (time from onset)

– Primarily solid– Semi-solid– Liquefaction

Varying amount of suppuration

© S. Barbu 2011

SEVERE ACUTE PANCREATITIS – ScoringPeripancreatic Fluid Collections

APFC(IEP)

APNPFC

Resolve

Pseudocyst

Resolve

WOPN

© S. Barbu 2011

Acute Peripancreatic collections

• They exist predominantly adjacent to the pancreas

• Have no definable wall

• Are confined by the normal peripancreatic fascialplanes, primarily the anterior pararenal fascia.

• May be Sterile (most of them) or Infected

• Almost 90% will resolve spontaneously during evolution

© S. Barbu 2011

Postnecrotic Pancreatic Fluid Collections

• Fluid collections arising in patients with acute necrotizing pancreatitis are termed PNPFCs to distinguish them from APFCs and => pseudocysts.

• PNPFCs contain both fluid and necrotic contents to varying degrees.

• In PNPFCs, there exists a continuum from the initial solid necrosis to liquefaction necrosis and eventually infection.

© S. Barbu 2011

SEVERE ACUTE PANCREATITIS – ScoringPancreatic/Peripancreatic Fluid Collections

Acute peripancreatic fluid collections

<4 wk after onset pancreatitisFluid collection(s) without

solid componentsOccur with IEP

Pancreatic pseudocyst APFCs that persists for >4 wk

No solid componentsThickened wall

Post-necrotic pancreatic/peripancreatic fluid collections(PNPFCs)Fluid collections containing

necrotic componentsA continuum of liquefaction

necrosisPancreatic and/or peripancreatic

necrosis

Walled off pancreatic necrosis (WOPN)

Isolated collection fluid/ necrosis

Thickened wall

© S. Barbu 2011

Synthesis

Acute pancreatitis • Acute Interstitial edematous pancreatitis (IEP)• Acute Necrotizing pancreatitis

– Pancreatic + peripancreatic necrosis– Peripancreatic alone (20%)– Pancreatic alone (rare)

(sterile or Infected)

2 Phases of evolution• 1st Phase – 1-2 wks –

– best described by Clinical parameters• 2nd Phase - >2wks –

– Best described by Morphology image-based + Clinical parameters

© S. Barbu 2011

SynthesisFluid / necrotic collections

Early: <4wks

Acute peri-pancreatic fluid collections

Late: >4wks

Pancreatic pseudocyst

Post-necrotic pancreatic/peripancreatic fluid collections(PNPFCs)

Walled off pancreatic necrosis (WOPN)

• All of them May be Sterile or Infected

© S. Barbu 2011

Therapy

• Remove offending agent (if possible)• Supportive !!!• #1- pain killers (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

© S. Barbu 2011

Therapy continued

• #3- Narcotic analgesics usually necessary for pain relief…textbooks say Meperidine…– NO conclusive evidence that morphine has

deleterious effect on sphincter of Oddipressure

• #4- Urgent ERCP and biliary sphincterotomywithin 72 hours improves outcome of severe gallstone pancreatitis – Reduced biliary sepsis, not actual improvement of

pancreatic inflammation• #5- Don’t forget PPI to prevent stress ulcer

© S. Barbu 2011

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

© S. Barbu 2011

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

© S. Barbu 2011

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

© S. Barbu 2011

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

© S. Barbu 2011

Indication for surgery

Mild acute pancreatitis = No indication for surgery.A correct conservative treatment needed (prevent evolution to SAP)

Severe acute nectorizing pancreatitis, Surgery indications:

-Infected necrosis (or infected pancreatic fluid collections)

-Extension of necrosis to neighbouring organs => acute abdomen-intestinal infarction,- perforation of colon, stomach, duoenum, etc - hemorrhage that can not be resolved by embolization

- Abdominal Compartment syndrome – resistant to conservative treatment

© S. Barbu 2011


Infected pancreatic and peri-pancreatic necrosis= Most frequent Indication for surgery.

1 When do we suspect infected necrosis presence?- Septic Syndrome: fever, bad general condition- + cultures from blood- CECT = air in the fluid collections

2 How do we have a Confirmation of Infected necrosis?-Fine needle aspiration (US or CT guided) + culture-(sensitivity > 90%; can produce iatrogenic infection)

© S. Barbu 2011


How do we Treat Sterile necrosis= No indication for surgery(unless, conservative treatment no efficient = persistent MSOF, abdominal compartment syndrome).

How do we Treat Infected necrosis- Percutaneous US or CT guided drainage- endoscopic drainage- Surgical drainage

- laparoscopy- open surgery

Patients with Infected necrosis, but:- good general condition- reduced signs of sepsis

=> Can be treated conservatively as long as possible (Antibiotics according to the antibiogram)

© S. Barbu 2011


When is the best Timing for drainage?= Surgery must be postpone as long as possible=> Necrosis must become liquid => efficient drainageBest time = day 28 – 30 of evolution

During the 1st 2 weeks – Surgery contra-indicated(mortality >70%)

© S. Barbu 2011

Surgical procedures

Surgical treatment = Necrozectomy- aims:

- extirpation of all (almost all) necrotic tissue- drain infected collections- minimize the risk of complications

(hemorrhage, digestive fistulas)- ensure a solid abdominal wall

© S. Barbu 2011

Surgical procedures

Open Surgical treatment = Necrozectomy, followed by

-abdominal wall closure & Continous lavage

-laparostomy

© S. Barbu 2011

Minimal invasive procedures

- Drainage by Laparoscopy (retroperitoneal, posterior)

-Endoscopic drainage (trans-gastric)

-Percutaneous US or CT guided drainage

© S. Barbu 2011

Results & Discussions

62 yrs old male– Hyper-triglyceridemic CP– Acute severe episode:

• associated:– Chronic pulmonary lung disease– Myocardial insufficiency– Portal vein thrombosis

(cavernoma)– Diabetes mellitus

© S. Barbu 2011


Lucky situation:– Best time for Drainage

• 28th day from Acute onset• Liquefaction of necrosis

– Communicating collections

© S. Barbu 2011


58 yrs old male– alcoholic CP, PVT cavernoma– Acute episode:

• associated:– Bilateral subphrenic collections– sepsis– Low BMI– Diabetes mellitus

© S. Barbu 2011


58 yrs old male– alcoholic CP, PVT cavernoma– Acute episode:

– Bilateral subphrenic collections– Treatment:

» Both collections drained percutaneously» Left collection proved to be a Pseudocyst» => external pancreatic fistula (left)

» => distal pancreato-splenectomy +» + pancreatico-jejunal anastomozis T-L

© S. Barbu 2011


• A fluid collection contained within a well-defined capsule of fibrous or granulation tissue or a combination of both

• Does not possess an epithelial lining• Persists > 4 weeks• May develop in the setting of acute or

chronic pancreatitis

Bradley III et al. A clinically based classification system for acute pancreatitis: summary of the International Symposium on Acute Pancreatitis, Arch Surg. 1993;128:586-590

© S. Barbu 2011


• Most common cystic lesions of the pancreas, accounting for 75-80% of such masses

• Location– Lesser peritoneal sac in proximity to the

pancreas– Large pseudocysts can extend into the

paracolic gutters, pelvis, mediastinum, neck or scrotum

• May be loculated

© S. Barbu 2011

Composition

• Thick fibrous capsule – not a true epithelial lining

• Pseudocyst fluid– Similar electrolyte concentrations to plasma– High concentration of amylase, lipase, and

enterokinases such as trypsin

© S. Barbu 2011

Pathophysiology

• Pancreatic ductal disruption 2° to– Acute pancreatitis – Necrosis – Chronic pancreatitis – Elevated pancreatic

duct pressures from strictures or ductal calculi – Trauma– Ductal obstruction and pancreatic neoplasms

© S. Barbu 2011

Presentation

• Symptoms– Abdominal pain > 3 weeks (80 – 90%)– Nausea / vomiting– Early satiety– Bloating, indigestion

• Signs– Tenderness– Abdominal fullness

Cohen et al: Pancreatic pseudocyst. In: Cameron JL, ed. Current Surgical Therapy. 7th ed.; 2001: 543-7

© S. Barbu 2011

Complications

• Infection– S/S – Fever, worsening abd pain, systemic signs of

sepsis – CT – Thickening of fibrous wall or air within the cavity

• GI obstruction• Perforation• Hemorrhage• Thrombosis – SV (most common)• Pseudoaneurysm formation – Splenic artery

(most common), GDA, PDA

© S. Barbu 2011

Treatment

• Initial– Treat pain– TPN– Octreotide

• Antibiotics if infected• 1/3 – 1/2 resolve spontaneously

© S. Barbu 2011

Intervention

• Indications for drainage– Presence of symptoms (> 6 wks)– Enlargement of pseudocyst ( > 6 cm)– Complications– Suspicion of malignancy

• Intervention – Percutaneous drainage– Endoscopic drainage– Surgical drainage

© S. Barbu 2011

Percutaneous Drainage

• Continuous drainage until output < 50 ml/day + amylase activity ↓– Failure rate 16% – Recurrence rates 7%

• Complications– Conversion into an infected pseudocyst (10%)– Catheter-site cellulitis– Damage to adjacent organs– Pancreatico-cutaneous fistula– GI hemorrhage

Gumaste et al: Pancreatic pseudocyst. Gastroenterologist 1996 Mar; 4(1): 33-43

© S. Barbu 2011

Endoscopic Management• Indications

– Mature cyst wall < 1 cm thick– Adherent to the duodenum or posterior gastric wall– Previous abd surgery or significant comorbidities

• Contraindications– Bleeding dyscrasias– Gastric varices– Acute inflammatory changes that may prevent cyst

from adhering to the enteric wall– CT findings

• Thick debris • Multiloculated pseudocysts

© S. Barbu 2011

Endoscopic Drainage

• Transenteric drainage– Cystogastrostomy– Cystoduodenostomy

• Transpapillary drainage– 40-70% of pseudocysts communicate with

pancreatic duct– ERCP with sphincterotomy, balloon dilatation

of pancreatic duct strictures, and stent placement beyond strictures

© S. Barbu 2011

Surgical Options

• Excision– Tail of gland & a/w proximal strictures – distal

pancreatectomy & splenectomy– Head of gland with strictures of pancreatic or bile

ducts – pancreaticoduodenectomy• External drainage• Internal drainage

– Cystogastrostomy– Cystojejunostomy

• Permanent resolution confirmed in b/w 91%–97% of patients*– Cystoduodenostomy

• Can be complicated by duodenal fistula and bleeding at anastomotic site

Nealon et al, Analysis of surgical success in preventing recurrent acute exacerbations in chronic pancreatitis. Ann Surg. 2001;233:793–800

© S. Barbu 2011

Laparoscopic Management

• The interface b/w the cyst and the enteric lumen must be ≥ 5 cm for adequate drainage

• Approaches– Pancreatitis 2° to biliary etiology →

extraluminal approach w/ concurrent laparoscopic cholecystectomy

– Non-biliary origin → intraluminal (combined laparoscopic/endoscopic) approach

Acute pancreatitis

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