Pancreatic Diseases

Assoc. Prof.

S. T. Barbu MD, PhD

University of Medicine & Pharmacy Iuliu Hatieganu Cluj-Napoca, Romania

IVth Surgical Clinic

S. Barbu 2011

Pancreatic diseases

- inflammatory diseases: => pancreatitis - acute

- chronic

- pancreatic tumors: - benign - malignant

S. Barbu 2011

Pancreatic diseases

Acute pancreatitis

Chronic pancreatitis

Correlations of

Pancreatic Diseases
Pancreatic Cancer
S. Barbu 2011

Pancreatic anatomy

S. Barbu 2011

Pancreatic anatomy
Pancreas = adnexal gland of the digestive tract - exocrine function - endocrine function

S. Barbu 2011

Pancreatic anatomy

S. Barbu 2011

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.

S. Barbu 2011

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.
S. Barbu 2011

Pancreatic anatomy

S. Barbu 2011

Acute Pancreatitis
Assoc. Prof.

S. T. Barbu MD, PhD

University of Medicine & Pharmacy Iuliu Hatieganu Cluj-Napoca, Romania

IVth Surgical Clinic

S. Barbu 2011

Acute pancreatitis
the most terrible of all calamities that [affect] the abdominal viscera Sir Berkeley Moynihan (Ann Surg1925)

S. Barbu 2011

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%

S. Barbu 2011

Acute pancreatitis

Course Objectives:
Definitions Etiology Pathology Symptoms Evolution Treatment Indications for Surgery
S. Barbu 2011

Acute pancreatitis

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)
S. Barbu 2011

Pancreatitis

Acute pancreatitis refers to an attack

involving a previously normal pancreas.

Chronic pancreatis is applied to an attack

involving a previously, permanently damaged pancreas.

S. Barbu 2011

Pancreatitis

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.
S. Barbu 2011

Acute Pancreatitis
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).

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

S. Barbu 2011

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 gallstones account for 70-80% of cases

S. Barbu 2011

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 coprecipitant 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 risk is also increased in women > 60 yrs

S. Barbu 2011

Drugs and Toxins (5%)

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

S. Barbu 2011

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
S. Barbu 2011

Etiology Trauma
Iatrogenic Surgery
Surgery for duodenal ulcer splenectomy

S. Barbu 2011

Etiology Multi-System Disease

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

S. Barbu 2011

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

S. Barbu 2011

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

S. Barbu 2011

Etiology-Anatomical Anomalies
Pancreas Divisum

S. Barbu 2011

Etiology-Anatomical Anomalies
Annular Pancreas

S. Barbu 2011

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%.

S. Barbu 2011

Trivia
What is the name of the scorpion that causes pancreatitis?
Hint: you wont find it in the USA

S. Barbu 2011

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

Acute pancreatitis

Pathogenesis
1.A complicated pathophysiologic process 2.Enzyme autoactivation and self-digestion (key point) 3. Many agents participating in the process 4. Complete mechanism remaining unknown
S. Barbu 2011

Initiation factor in Earlier period

S. Barbu 2011

1. Pancreatic Enzyme Abnormally Activated

Bile reflux Bile common channel pancreatic duct

1.hypertension in pancreatic duct 2.premature activation of pancreatic enzymes 3.injury to the lining of the pancreatic ducts pancreatic edema or necrosis MODS

S. Barbu 2011

 Duodenal Reflux
duodenal enterokinase duct trypsinogen elastasinogen phospholipasogen lecithin
S. Barbu 2011

pancreatic

trypsin elastase phospholipase lysolecthin

2.Alcohol Toxicity
stimulate the pancreas to secrete pancreatic hypertention duct and acinus rupture juice spillage spasm of the sphincter of oddi direct injury to pancreas
S. Barbu 2011

tiny pancreatic pancreatic

3.Pancreatic Microcirculation Disorder

systemic hypotension hyperlipidemia: triglycerides lipase free acid fatty acids microcirculation artheroembolism vasculitis
S. Barbu 2011

injure pancreatic

Aggravating factors in later period

Infection: pancreatic abscess Intestinal bacteria translocation Cytokine and systemic inflammation reaction syndrome TNF IL-1 IL-6 PAF Free radicals
S. Barbu 2011

MSOF

Acute pancreatitis
Pathophys- insult leads to leakage of pancreatic enzymes into pancreatic and peripancreatic tissue leading to acute inflammatory reaction

S. Barbu 2011

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

S. Barbu 2011

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) Cullens sign - periumbilical discoloration (rare)

S. Barbu 2011

 Grey Turner sign

Cullens sign

S. Barbu 2011

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

S. Barbu 2011

Evaluation
amylaseNonspecific !!!
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
S. Barbu 2011

CT Scan of acute pancreatitis

CT shows significant swelling and inflammation of the pancreas

S. Barbu 2011

Gallstone pancreatitis by ERCP

S. Barbu 2011

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 therapeutic procedures in mild cases
S. Barbu 2011

We should Thank

Bradley EL 3 rd.
S. Barbu 2011

Goals of Atlanta Symposium

1. 2.

Classification of acute pancreatitis (universally applicable ) 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

S. Barbu 2011

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 the pancreatic 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

..its 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 Peter Banks, Boston/USA
S. Barbu 2011

Morphol. (imaged-based) Classif Mike Sarr, Rochester/USA

Approaches to Classification
This revised classification pertains primarily to adults (>18 years old) (certain definitions and scoring systems may not be applicable to the pediatric population)

Clinical Local / Morphological

No direct correlation exists between clinical severity & morphological characteristics

S. Barbu 2011

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

1. Characteristic abdominal pain

(2 of 3 findings)

2. 3.

Serum amylase / lipase activity >3 times upper normal value Characteristic findings on CECT

S. Barbu 2011

New combined Clinical & Image-based Classification 1st 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

New combined Clinical & Image-based Classification 1st Phase: Clinical Classification - 3

Definition of severity*
Non-severe pancreatitis no organ failure Severe acute pancreatitis - persistence of organ failure >48 hr *Independent of imaging
S. Barbu 2011

Early & Persistent Organ Failure: Most Important Outcome Determinant

Author

Positive

Negative

Early Organ Failure (ESAP) *

Isenmann et al., 2001 Tao et al., 2004 Poves Prim et al., 2004 158 297 112 n = 47 ESAP + n = 69 ESAP + n = 40 ESAP + n = 57 OF + 42% 42% 53% 40% n = 111 SAP only 14% n = 228 SAP only 3% n = 17 SAP+late OF 12% n = 55 SAPOF 0%

Persistent Organ Failure

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

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

S. Barbu 2011

SEVERE ACUTE PANCREATITIS - scoring Modified Marshall Scoring System 0 1 2 3 4 Respiratory (PO2/FiO2)>400 301-400 201-300 101-200 <101 Renal (serum creatinine) 134 mol/L 1.0 mg% >90 CV (systolic BP) 134-169 170-310 310-439 >440 1.0-1.3 1.3-2.3 2.4-3.3 >3.3 >90 <90 pH<7.3 pH<7.2 81-120 13-15 41-80 10-12 21-50 6-9 <21 <6 Organ system

Coagulation (Plt >120 count) Neurologic (Glasgow 15 coma scale)

S. Barbu 2011

SEVERE ACUTE PANCREATITIS Scoring SOFA Score

0 1 >400 300-400 >150 100-150 None MAP<70 2 <300 3 <200 intubated 4 <100 intubated

Respiratory (PO2FiO2) Hematologic Plt count x 103 CV hypotension

Dopamine Dopamine Dopamine <5 g/ml 15-14 >15 or Dobutamine Epi <0.1 Epi >0.1 or NEp <0.1 NEp >0.1 10-12 171-299 2.0-3.4 6-9 300-440 3.5-4.9 <6 >440 >5

Neurologic Glasgow coma score 15 13-14 Renal (serum creatinine) mol/L <110 100-170 mg% <1.2 1.2-1.9 or urine output
S. Barbu 2011

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

Conclusion:
=> 1st Phase: Severity defined by:
Persistent organ failure >2days death

S. Barbu 2011

New combined Clinical & Image-based Classification 1st Phase: Clinical Classification - 3

Definition of severity*
Non-severe pancreatitis no organ failure Severe acute pancreatitis - persistence of organ failure >48 hr

S. Barbu 2011

SEVERE ACUTE PANCREATITIS Scoring 2nd Phase: > 2 weeks

2nd Phase: Severity defined by:

1. 2. Persistent organ failure Complications of Ac P requiring active intervention (surgical, endocopic, laparoscopic, and/or percutaneous) Need for other supportive mesures (ventilation support, renal dialysis, jejunal feeding Prolonged Hospitalization Death

3.

S. Barbu 2011

SEVERE ACUTE PANCREATITIS Scoring 2nd 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 Severity by 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 Severity by Imaging Procedures

Goldstandard: Contrast-enhanced Computed Tomography (CECT) ERCP not recommended for Dg or Classification
- has No role in this image-based classification

S. Barbu 2011 Department of General, Visceral, and Vascular Surgery, UKS, Homburg/Saar, Germany

CE-CT versus MRI in Acute Pancreatitis

Computed tomography and magnetic resonance imaging in the assessment of acute pancreatitis.
Arvanitakis M et al., Gastroenterol 2004; 126: 715-723
Patients: Results: 39 patients with AP, CE-CT and MRI on admission, after 7 and 30 days. Predicted severe AP in 18% (n=7) Strong correlation between CTSI and MRSI on admission and 7 days later. Prediction of severe AP: MRI CECT Sensitivity 83% 78% Specificity 91% 86%

Conclus.: MRI is a reliable method for staging AP severity and predicting disease prognosis. MRI has fewer contraindications than CT.
Department of General, Visceral, and Vascular Surgery, UKS, Homburg/Saar, Germany S. Barbu 2011

SEVERE ACUTE PANCREATITIS Scoring Classification 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 Scoring Necrotizing 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 Scoring Peripancreatic Fluid Collections

APFC (IEP)

Resolve Pseudocyst Resolve

APNPFC

WOPN

S. Barbu 2011

Acute Peripancreatic collections

They exist predominantly adjacent to the pancreas Have no definable wall Are confined by the normal peripancreatic fascial planes, 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 Scoring Pancreatic/Peripancreatic Fluid Collections Acute peripancreatic fluid collections <4 wk after onset pancreatitis Fluid collection(s) without solid components Occur with IEP Post-necrotic pancreatic/ peripancreatic fluid collections (PNPFCs) Fluid collections containing necrotic components A continuum of liquefaction necrosis Pancreatic and/or peripancreatic necrosis
S. Barbu 2011

Pancreatic pseudocyst APFCs that persists for >4 wk No solid components Thickened wall

Walled off pancreatic necrosis (WOPN) Isolated collection fluid/ necrosis Thickened wall

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

Synthesis
Fluid / necrotic collections Early: <4wks Acute peri-pancreatic fluid collections Post-necrotic pancreatic/ peripancreatic fluid collections (PNPFCs) Late: >4wks Pancreatic pseudocyst

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 relieftextbooks say Meperidine NO conclusive evidence that morphine has deleterious effect on sphincter of Oddi pressure #4- Urgent ERCP and biliary sphincterotomy within 72 hours improves outcome of severe gallstone pancreatitis
Reduced biliary sepsis, not actual improvement of pancreatic inflammation

#5- Dont forget PPI to prevent stress ulcer

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 broadspectrum 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

 S. Barbu 2011

Indication for surgery

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

Indication for surgery

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

S. Barbu 2011

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)

Indication for surgery

When is the best Timing for drainage? = Surgery must be postpone as long as possible => Necrosis must become liquid => efficient drainage Best time = day 28 30 of evolution During the 1st 2 weeks Surgery contra-indicated (mortality >70%)

S. Barbu 2011

Indication for surgery

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

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

Results & Discussions

S. Barbu 2011

Results & Discussions

S. Barbu 2011

Results & Discussions

S. Barbu 2011

Results & Discussions

Lucky situation:
Best time for Drainage
28th day from Acute onset Liquefaction of necrosis

Communicating collections

S. Barbu 2011

Results & Discussions

S. Barbu 2011

Results & Discussions 58 yrs old male

alcoholic CP, PVT cavernoma Acute episode:
associated:
Bilateral subphrenic collections sepsis Low BMI Diabetes mellitus

S. Barbu 2011

Results & Discussions

S. Barbu 2011

Results & Discussions

S. Barbu 2011

Results & Discussions

S. Barbu 2011

Results & Discussions 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

Results & Discussions

S. Barbu 2011

 S. Barbu 2011

 S. Barbu 2011

Pancreatic Pseudocyst

S. Barbu 2011

Pancreatic Pseudocyst
A fluid collection contained within a welldefined 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 S. Barbu 2011 of the International Symposium on Acute Pancreatitis, Arch Surg. 1993;128:586-590

Pancreatic Pseudocyst
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 S. Barbu 2011 543-7 ed.; 2001:

Diagnosis
CT scan MRI / MRCP Ultrasonography Endoscopic Ultrasonography (EUS) ERCP

S. Barbu 2011

Pseudocyst compressing the stomach wall posteriorly

S. Barbu 2011

Sonographic evaluation

S. Barbu 2011

EUS showing pseudocyst

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. S. Barbu 2011 Ann Surg. 2001;233:793800

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
S. Barbu 2011

Enucleation of Pseudocyst

S. Barbu 2011