Acute pancreatitis

Pancreatic Diseases

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

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

- inflammatory diseases:=> pancreatitis - acute

- chronic

- pancreatic tumors:- benign- malignant

Pancreatic diseases

Correlationsof

PancreaticDiseases

Acute pancreatitis

Chronic pancreatitis

Pancreatic Cancer

Pancreatic diseases

Pancreatic anatomy

Pancreas = adnexal gland of the digestive tract

- exocrine function

- endocrine function

Pancreatic anatomy

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.

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.

Pancreatic anatomy

Acute Pancreatitis

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

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

Acute pancreatitis

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

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%

Acute pancreatitis

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

Pancreatitis is the inflammation of the pancreas.

Like: - appendicitis- cholecistitis- gastritis- esophagitis

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

Acute 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.

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.

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).

Acute Pancreatitis

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

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

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

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

Drugs and Toxins (5%)

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

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

Etiology – Trauma

• Iatrogenic – Surgery – Surgery for duodenal ulcer– splenectomy

Etiology – Multi-System Disease

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

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

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

• Pancreas Divisum

• Annular Pancreas

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%.

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)

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

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

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

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

lecithin lecithin lysolecthinlysolecthin

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

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

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

Acute pancreatitis• Pathophys- insult leads to leakage of pancreatic

enzymes into pancreatic and peripancreatictissue leading to acute inflammatory reaction

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

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)

• Grey Turner sign • Cullen’s sign

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

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

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

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

CT Scan of acute pancreatitis

• CT showssignificantswellingand inflammationof the pancreas

Gallstone pancreatitis by ERCP

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

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

We should Thank…

Bradley EL 3 rd.

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

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)

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

..…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

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)

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

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

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)

Definition of severity*

• Non-severe pancreatitis – no organ failure

• Severe acute pancreatitis –

- persistence of organ failure >48 hr

*Independent of imaging

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

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

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

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

• Persistent organ failure – >2days

• death

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

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

failure

• Severe acute pancreatitis –

- persistence of organ failure >48 hr

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

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

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)

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

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

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

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)

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

Necrosis - Infection

• Depending on the stage (time from onset)

– Primarily solid– Semi-solid– Liquefaction

Varying amount of suppuration

SEVERE ACUTE PANCREATITIS – ScoringPeripancreatic Fluid Collections

APFC(IEP)

APNPFC

Resolve

Pseudocyst

Resolve

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

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.

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

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

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

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

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

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

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

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

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

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

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)

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)

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%)

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

Surgical procedures

Open Surgical treatment = Necrozectomy, followed by

-abdominal wall closure & Continous lavage

-laparostomy

Surgical procedures

Open Surgical treatment = Necrozectomy, followed by

-abdominal wall closure & Continous lavage

-laparostomy

Minimal invasive procedures

- Drainage by Laparoscopy (retroperitoneal, posterior)

-Endoscopic drainage (trans-gastric)

-Percutaneous US or CT guided drainage

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

Lucky situation:– Best time for Drainage

• 28th day from Acute onset• Liquefaction of necrosis

– Communicating collections

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

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

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

Pancreatic Pseudocyst

• 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

• 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

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

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

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

Diagnosis

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

Pseudocyst compressing the stomach wall posteriorly

Sonographic evaluation

EUS showing pseudocyst

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

Treatment

• Initial– Treat pain– TPN– Octreotide

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

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

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

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

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

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

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

Enucleation of Pseudocyst

Acute pancreatitis

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