acute pancreatitis a thorough review

DR SHAILESH GUPTA
CLINICAL FELLOW
IMAS, SIR GANGARAM HOSPITAL
1

INDEX
Introduction /Etiology
Morphological Classification
Clinical Signs and Symptoms/Complications
Classification of severity
Investigations/Imaging
Assesment of severity
Treatment
Management of Local Complication
2

EPIDEMIOLOGY
 AP Responsible for > 3 lac admissions/year in US 1
 Incidence increased in past 2 decades
 Alcohol-related pancreatitis more common in men, Gallstones related in
Females
 10-20% of AP progressed to severe disease
 1% mortality in mild cases which progressed to10-30% in severe one 2
3
1 Sabiston, D. C., & Townsend, C. M. (2012). Sabiston textbook of surgery: The biological basis of modern surgical practice. Philadelphia, PA: ElsevierSaunders.
2 Yadav D, Lowenfels AB. The epidemiology of pancreatitis and pancreatic cancer. Gastroenterology. 2013;144:1252–1261.

PREREQUISTE OF LABELLING ACUTE
Revised Atlanta classification requires two or more of following
be met for diagnosis of AP 1:
(a) Abdominal Pain suggestive of Pancreatitis,
(b) Serum Amylase or Lipase level Greater than 3 times the upper
normal value, or
(c) Characteristic imaging findings
1 Michael J. Zinner, Stanley W. Ashley, O. Joe Hines , Maingot's Abdominal Operations, 13edition : Mc graw Hill
4

Causes of AP 1
 Metabolic
 Mechanical
 Vascular
 Infection
 Idiopathic ( occult biliary microlithiasis in most cases )
5

Metabolic Causes…
Alcohol
 Second MC Worldwide
 prolonged(10 yrs) heavy consumption
 Smoking Confounding factor
 Trigger Proinflammatory Pathways, increases caspases.
 Causes Sphincter of Oddi Spasm,
 Causes Precipitation of protein in PD
Michael J. Zinner, Stanley W. Ashley, O. Joe Hines , Maingot's Abdominal Operations, 13edition : Mc graw Hill
6
Mechanism
of Action

Metabolic Causes..
Hyperlipoproteinemia
Triglyceride level>1000mg/dl
Common in Type1,2,5 hyperlipidaemia
Hypercalcemia
1.5-13% of Primary Hyperparathyroidism develop AP
7

Metabolic Causes…
 Drugs
2% of AP
corticosteroids, thiazide diuretics, estrogens,
azathioprine, sulphonamides, furosemide
 Genetic
 Scorpion venom
8

Mechanical Causes
Cholelithiasis
 Most common Cause in west
 Obstructive theory 1: injury is the result of excessive pressure in obstructive PD.
 Reflux theory: stone at ampulla of vater common channel allowing bile salt
reflux in pancreas
.
9
1 Sabiston, D. C., & Townsend, C. M. (2012). Sabiston textbook of surgery: The biological basis of modern surgical practice. Philadelphia, PA: ElsevierSaunders

Mechanical Causes…
ERCP
 At least 5% of patients undergoing ERCP develop clinically detectable pancreatitis 1
 More frequent in patients undergoing Therapeutic procedures, had Multiple
attempts of cannulations,and in Sphincter of Oddi Dysfunction
 Mild clinical course in 90 -95% 1
10

Mechanical Causes…
 Postoperative : Excessive Pancreatic Manipulation
 Pancreas Divisum
 Posttraumatic
 Pancreatic duct obstruction: pancreatic tumor, Ascaris
 Pancreatic ductal bleeding
 Duodenal obstruction
11

Vascular Causes
 Postoperative (cardiopulmonary bypass)
 Periarteritis nodosa
 Atheroembolism
12

Infectious Causes
 Mumps
 Coxsackie B
 Cytomegalovirus
 Cryptococcus
13

Morphological Classification of AP ,
Revised Atlanta Classification(RAC) 1
1. Interstitial edematous Pancreatitis: Acute inflammation of pancreatic
parenchyma and peripancreatic tissues without tissue necrosis.
2. Necrotizing Pancreatitis: Inflammation associated with pancreatic
parenchymal necrosis and/or peripancreatic necrosis.
14

Morphological Classification of AP(RAC)…
3. Acute peripancreatic fluid collection(APFC)
 Peripancreatic fluid associated with IEP( Seen in First 3 week)
 No associated peripancreatic necrosis/No well-defined wall
4. Pseudocyst
 a/w IEP ( seen after 4 week)
 Encapsulated collection of fluid /well-defined inflammatory wall.
 Usually outside the pancreas with minimal or no necrosis
15

5. Acute necrotic collection (ANC) :
• a/w Necrotizing Pancreatitis
• Collection containing variable amounts of fluid and necrosis
• Necrosis can involve pancreatic parenchyma and/or the peripancreatic tissues]
6. Walled-off necrosis (WON):
• a/w Necrotizing Pancreatitis(seen after 4 weeks)
• Mature, encapsulated collection of pancreatic and/or peripancreatic necrosis(Well defined
Wall)
16Morphological Classification of AP(RAC)…

Symptoms and Signs
• Severe epigastric pain radiating to the back, relieved by leaning forward
• Nausea, vomiting and loss of appetite
• Fever/chills
• Dehydration, tachycardia, tachypnea
• Hemodynamic instability, including shock
• Abdominal distension with tenderness, guarding, rebound tenderness.
18

Signs and Symptoms..
19
https://consultqd.clevelandclinic.org/images-of-note-grey-turner-and-cullen-signs/
Signs which are less common, and indicate severe disease,include:
Grey-Turner's sign (hemorrhagic discoloration of the flanks)
Cullen's sign (hemorrhagic discoloration of the umbilicus)

Systemic Complication
Shock/Arrythmia
ARDS/Pleural Effusion
DIC
Renal Failure
Ileus
Hyperglycemia/Hypocalcemia/Hyperlipidemia
Confusion/Irritability/Encephalopathy
20

CLASSIFICATION OF LOCAL COMPLICATIONS OF AP
BASED ON CONTENT, CHRONICITY AND INFECTION
(RAC 2013)
21

Classification of Severity
Revised Atlanta Classification(2012)
1. Mild acute pancreatitis: the absence of organ failure and absence of
systemic or local Complications
2. Moderate acute pancreatitis: with transient organ failure and/or local
complications requiring prolonged hospital stay or intervention.
3. Severe acute pancreatitis: with persistent organ failure.
22

Classification of severity..
Determinant-Based Classification (DBC)
(1) Mild AP: no necrosis and no organ failure;
(2) Moderate AP: with sterile necrosis and/or transient organ failure
(3) Severe AP: with infected necrosis or persistent organ failure
(4) critical AP: with infected necrosis and persistent organ failure.
23

Lab investigations
Serum Amylase and Lipase
o Both Amylase /Lipase peak within first 24 hrs of symptoms ,3 fold or
higher Elevation of either of these confirms diagnosis
o Amylase has a slightly shorter plasma half-life. Serum lipase,
therefore, has a slightly higher sensitivity for detection, as elevations
occur earlier and last longer than serum amylase.
25

Lab Investigation…
Serum Amylase and Lipase
• Lipase more specific marker. Hyperamylasemia is also seen in PUD,
Mesenteric ischemia, tumors of the ovaries or even in kidney failure.
• Useful for Diagnosis but not for Prognosis or not for assessment of
Disease Severity
26

Lab investigation……
• Leukocytosis
• Raised blood sugar
• Abnormal elevation of Liver enzymes
• Elevated serum Alanine Aminotransferase(SGPT) in the context of AP confirmed
by high pancreatic enzymes Levels, has a positive Predictive value of 95% for
the diagnosis of acute biliary pancreatitis
27

IMAGING
Abdominal Radiographs
• Cutoff colon sign 1
Colonic spasm at splenic flexure
• Ileus
Air fluid levels
28
1 Sabiston, D. C., & Townsend, C. M. (2012). Sabiston textbook of surgery: The biological basis of modern surgical practice. Philadelphia, PA: ElsevierSaunders.
https://radiopaedia.org/cases/colon-cut-off-sign

Imaging……
USG
 Intra abdominal fat and increase bowel gas limit its usability for diagnosis of AP.
 High Sensitivity (95%) in diagnosis Gall Stones 1
 Combined elevation of liver transaminase and pancreatic enzymes level and Gall
stones on USG has sensitivity of 97 % and specifcity of 100% for diagnosis of
acute biliary pancreatitis 1
29

Imaging..
CECT
 Essential role in evaluation of the progression to severe AP with associated complications.
 Portal Venous phase (65-70 sec after injection of contrast) is most Valuable 1 .
 Viable pancreas will typically enhance by more than 50 HU with the administration of IV
contrast. Nonviable pancreas, will not enhance.
 Findings of simple edematous pancreatitis include enlargement of pancreas with loss of
peripancreatic fat planes, areas of decreased density, and occasional fluid collections
30
Sabiston, D. C., & Townsend, C. M. (2012). Sabiston textbook of surgery: The biological basis of modern surgical practice. Philadelphia, PA: ElsevierSaunders

Timing of CECT in AP
 Necrosis may only become evident 2 -3 days after the onset of symptoms.
 The sensitivity for identifying pancreatic necrosis using CECT approaches 100%
after 4 days from diagnosis
 CECT if performed immediately , severity can be easily underestimated.
 CECT obtained more than 5 d after onset of symptoms that reveals only mild
inﬂammatory changes (fat stranding) surrounding the pancreas virtually excludes
severe form of AP
31

Indication of CECT in AP
CT is not indicated in mild pancreatitis 1 (no clinical signs of severe pancreatitis) and show
rapid improvement with appropriate medical management.
Indication of Initial CECT2
1. Diagnostic uncertainty
2. Patients with hyperamylasemia, severe clinical pancreatitis, abdominal distention a
tenderness, fever >102°, and leukocytosis for the detection of complications .
3. Ranson>3/APACHE2>8
4. Patients who fail to improve after 72 h of conservative medical therapy
5. Acute change in clinical status after initial successful medical therapy
32
2 Kiran K Busireddy, Mamdoh AlObaidy, Miguel Ramalho,etal pancreatitis imaging approachWorld J Gastrointest Pathophysiol. 2014 Aug 15; 5(3)

Indication of CECT in AP..
Indication of Delayed/Follow up CT imaging
1. Change in clinical status ,suggesting complications
2. 7-10 d after presentation if CTSI is 3-10 at presentation1
3. After surgery or intervention radiology procedure to document the
response2
4. Before Discharge of severe AP
33
1 Michael J. Zinner, Stanley W. Ashley, O. Joe Hines , Maingot's Abdominal Operations, 13edition : Mc graw Hil
2 Kiran K Busireddy, Mamdoh AlObaidy, Miguel Ramalho,etal pancreatitis imaging approachWorld J Gastrointest Pathophysiol. 2014 Aug 15; 5(3)

CT Guided Aspiration
 CT-guided aspiration of the necrotic pancreas can be used to diagnose infected
pancreatic necrosis with a high degree of accuracy
 It is reserved for patients with documented pancreatic necrosis who are not
improving clinically or who experience clinical decline (suggestive of Infective
Necrosis).
34

CT Guided Aspiration……
 Areas of non enhancing pancreas are aspirated, with samples sent for aerobic,
anaerobic, and fungal culture
 The sensitivity and specificity for detection of infection with CT-guided
aspiration are reported to be 96% and 99%, respectively, with a positive
predictive value of 99.5% and a negative predictive value of 95% 1
35

CECT in Acute Edematous Pancreatitis
36
Pancreatic parenchyma enhances with IV contrast, no evidence of pancreatic necrosis. Significant fat
stranding of the peripancreatic tissue, with a fluid collection at the tail of the pancreas
Fluid collection at
tail of pancreas
Pancreatic
Enhancement

CECT in Necrotizing Pancreatitis 37
Scan shows near-complete absence of pancreatic enhancement, which is diagnostic of
pancreatic necrosis.
Pancreatic Necrosis

CT in Emphysematous pancreatitis
38
scan demonstrating emphysematous pancreatitis(free gas in pancreatic
parenchyma), which is pathognomonic for infected pancreatic necrosis
Gas in Necrose Pancreatic
tissue

IMAGING..
MRI
 Alternative in patients with moderate renal impairment or allergy to IV contrast.
 Comparable sensitivity and specificity to CT for diagnosis of severe AP1
 MRCP is routinely added to abdominal protocols to assess ductal obstruction,
dilatation or course2
 MRI is less practical for the critically ill patient
39
2 Kiran K Busireddy, Miguel Ramalho,etal pancreatitis imaging approachWorld J Gastrointest Pathophysiol. 2014 Aug 15; 5(3)

EUS in AP
 Due to probe positioned in close proximity to the pancreas, EUS provides high
resolution images of the PD and parenchyma as well as extra hepatic biliary
system.
 As compared to ERCP, It allows examination of biliary tree and pancreas with no
risk of worsening pancreatitis.
40
1 Sabiston, D. C.etal. Sabiston textbook of surgery: The biological basis of modern surgical practice. Philadelphia, PA: Elsevier
2 Kiran K Busireddy, Miguel Ramalho,etal pancreatitis imaging approachWorld J Gastrointest Pathophysiol. 2014 Aug 15

EUS in AP
Role in AP
1. Assessing and/or confirming choledocholithiasis and subsequent stone
removal(ERCP).1
2. Identifying anatomic abnormalities(pancreas divisum /malignancy) that can
lead to AP2
Disadvantages : Require monitored anaesthesia care, operator dependent
41
1 Sabiston, D. C.etal. Sabiston textbook of surgery: The biological basis of modern surgical practice. Philadelphia, PA: Elsevier
2 Kiran K Busireddy, Miguel Ramalho,etal pancreatitis imaging approachWorld J Gastrointest Pathophysiol. 2014 Aug 15

Assessment of Severity in AP
• Ranson criteria
• Glasgow criteria
• BISAP Score
• CTSI Score
• APACHE 2 Score
• CRP levels
42
Sabiston, D. C.etal. Sabiston textbook of surgery: The biological basis of modern surgical practice. Philadelphia, PA: Elsevier

Ranson Criteria
 Introduce by RANSON and colleague in 1974
 Disadvantage : These systems require 48 hours from admission for full
assessment, therefore it does not predict the severity at the time of admission
 Low positive predictive value (50%) and High Negative Predictive value (90%)
43

RANSON SCORE
Ranson Alcholic AP Ranson Biliary AP
At Admisson At Admisson
Age > 55 years Age > 70 years
TLC >16000/mm3 TLC >18000mm3
LDH > 350 U/L LDH > 250 U/L
AST > 250 U/L AST > 250 U/L
Blood Glucose > 200mg/dl Blood Glucose > 220 mg/dl
At 48 Hours At 48 Hours
Drop in Hematocrit >10% Drop in Hematocrit >10%
BUN Increase > 5mg/dl BUN Increase > 2mg/dl
calcium < 8 mg/dl calcium < 8 mg/dl
PO2 < 60 mm PO2 < 60 mm
Base Deficit > 4 meq/L Base Deficit > 5 meq/L
Fluid Loss > 6l Fluid Loss > 4l
44
• 0 to 2 points: Mortality 0% to 3%
• 3 to 4 points: 15%
• 5 to 6 points: 40%
• 7 to 11: nearly 100%
SCORE > 3 Severe Pancreatitis

Glasgow IMIE Criteria
• P - PaO2 <8kPa
• A - Age >55-years-old
• N - Neutrophilia: WCC >15x10(9)/L
• C - Calcium <2 mmol/L
• R - Renal function: Urea >16 mmol/L
• E - Enzymes: LDH >600iu/L; AST >200iu/L
• A - Albumin <32g/L (serum)
• S - Sugar: blood glucose >10 mmol/L
45
 Predict severity of pancreatitis
but 48 hours after admission.
 scores 3 or more it indicates
severe pancreatitis

BISAP SCORE
• B - BUN >25mg/dl
• I - Impaired Mental status (GCS<15)
• S - SIRS
• A - AGE(>60 Yr)
• P - Pleural effusion
46
BISAP score is calculated at
24 hours
Score of > 3 -severe acute
pancreatitis.
Arif A, Jaleel F, Rashid K. Accuracy of BISAP score in prediction of severe acute pancreatitis. Pak J Med Sci. 2019.

CTSI..
• 0-3 : Mild acute pancreatitis
• 4-6 : Moderate acute pancreatitis
• 7-10 :Severe acute pancreatitis
48

The Acute Physiology and Chronic Health
Evaluation II(APACHE II)
Calculated from patient's age and 12 routine physiological measurements:
 A-aDO2 or PaO2 (depending on FiO2)/Temperature (rectal)
 Mean arterial pressure/pH arterial
 Heart rate/Respiratory rate
 Sodium (serum)/Potassium (serum)
 Creatinine
 Haematocrit/White blood cell count
 Glasgow Coma Scale
49

APACHE II…
 APACHE II scores of >8 signifies severe pancreatitis.
 APACHE - O (Include obesity).
 Advantage : can be used on admission and repeated at any time.
 Disadvantage: APACHE II is complex ,not specific for AP, and based on the
patient age, limited positive predictive value of only 43% for severe AP
50

CRP
C-reactive protein levels >150 mg/ml, 48 hrs after admission indicates
severe disease
Disadvantage : cannot be used at the time of admission
51

Fluid resuscitation and Monitoring
 Aggressive fluid resuscitation to replace considerable extravascular or “third
space” fluid losses.
 15-20ml/kg bolus (fluid of choice RL, as it reduces SIRS) followed by
3ml/kg/hr. infusion1
 Resuscitation with a goal-directed strategy, with regular assessment: Urine
output > 0.5 mL/kg/h, hematocrit=25% to35%, drop in BUN.2
53
1Aggarwal A, Manrai M, Kochhar R. Fluid resuscitation in acute pancreatitis. World J Gastroenterol 2014;20:18092–103. 10.3748/wjg.v20.i48.18092
2 Wu BU, et al. Lactated Ringer’s solution reduces systemic inflammation compared with saline in patients with acute pancreatitis. Clin Gastroenterol Hepatol. 2011;9 (8):710-717.

Fluid resuscitation and Monitoring..
 Early aggressive intravenous hydration is most beneficial during the first 12 –
24 h.
 Patients who do not respond to initial fluid resuscitation or have significant
cardiorespiratory or renal co morbidities , require CVP and a Foley catheter
 Close monitoring of respiratory,cardiovascular, and renal function is essential
to detect and treat hypovolemia.
54
2 Wu BU, Hwang JQ, Gardner TH, et al. Lactated Ringer’s solution reduces systemic inflammation compared with saline in patients with acute pancreatitis. Clin Gastroenterol
Hepatol.2011;9(8):710-717.

Fluid resuscitation and Monitoring..
 Patients should receive supplementary oxygen to maintain arterial
saturation above 95%
 Patients with severe disease should be admitted to an intensive care unit
for continuous monitoring.
55
2 Wu BU, Hwang JQ, Gardner TH, et al. Lactated Ringer’s solution reduces systemic inflammation compared with saline in patients with acute pancreatitis. Clin
Gastroenterol Hepatol.2011;9(8):710-717.

PAIN MANAGEMENT 56
Schorn, Stephan. Ceyhan etal. Pain Management in Acute Pancreatitis. Pancreapedia: Exocrine Pancreas Knowledge Base,
DOI: 10.3998/panc.2015.15

Pain Management
Thoracic epidural Analgesia 1
 Good analgesia
 TEA also induces a targeted sympathectomy in the anesthetized region, which
results in splanchnic vasodilatation and an improvement in local
microcirculation, resulting in improved pancreatic microcirculation.
57
1 Windisch, Olivier & Heidegger,etal (2016). Thoracic epidural analgesia: A new approach for the treatment of acute pancreatitis?. Critical Care. 20.
10.1186/s13054-016-1292-7

Nutrition Guidelines
 Historically, enteral feeding was limited in the setting of AP for purpose of providing
“pancreatic rest.” it was believed to exacerbate existing inflammatory process through
stimulation of exocrine pancreatic function and release of proteolytic enzymes.
 Limitation of nutritional intake may have serious consequences in setting of critical
illness with enhanced catabolism and negative nitrogen balance 1.
58

Nutrition Guidelines…
 Bowel rest is a/w intestinal mucosal atrophy and increased infectious
complications because of bacterial Translocation from the gut 1.
 TPN should be avoided in patients with mild and severe AP unless ,enteral route
is not available, not tolerated, or not meeting caloric requirements. Multiple RCT
shows that that TPN is a/w infectious and other line-related complications.
59

 Enteral feeding maintain mucosal barrier, prevents disruption, and prevents translocation of
bacteria that seed pancreatic necrosis, may prevent infected necrosis(shorter stay, decrease
morbidity and mortality)
 In mild AP, oral feedings can be started immediately if there is no nausea and vomiting, and the
abdominal pain has resolved , initiation of feeding with a low-fat solid diet appears as safe as a
clear liquid diet .
T Tenner, Scott MD,etal FACG4 American Journal of Gastroenterology: September 2013 - Volume 108 - Issue 9 - p 1400-1415
60

Route of Enteral Feed (Nasogastric vs Nasojejunal)
Both are comparable in safety and efficacy
 Nasojejunal : avoids gastric stimulation, lesser risk of aspiration, Require IR or
endoscopy
 Nasogastric : easier to place, risk of aspiration, Gastric stimulation
61
Tenner, Scott MD,etal FACG4 American Journal of Gastroenterology: September 2013 - Volume 108 - Issue 9 - p 1400-1415

Antibiotic Therapy
Recommendation
1. Antibiotics should be given for an extra pancreatic infection, such as cholangitis,
catheter-acquired infections, bacteremia, urinary tract infections, pneumonia2
2. Routine use of prophylactic antibiotics in patients with severe AP is not
recommended1
3. The use of antibiotics in patients with sterile necrosis to prevent the development
of infected necrosis is not recommended.1
62
2 Tenner, Scott MD etal,American Journal of Gastroenterology: March 2014 - Volume 109 - Issue 3 - p 444

Antibiotic Recommendations…
4. Infected necrosis should be considered in patients with pancreatic or extra
pancreatic necrosis who deteriorate or fail to improve after 7 – 10 days of
hospitalization.1
In these patients, either (i) initial CT-guided FNA for Gram stain and culture to
guide use of appropriate antibiotics or (ii) empiric use of antibiotics without CT
FNA, Can be done . 2
2 Tenner, Scott MD etal,American Journal of Gastroenterology: March 2014 - Volume 109 - Issue 3 - p 444
63

Antibiotic Recommendations….
5, In patients with infected necrosis, antibiotics known to penetrate pancreatic
necrosis, such as carbapenems, quinolones, and metronidazole, may be useful in
delaying or sometimes totally avoiding intervention, thus decreasing morbidity
/mortality.1,2
64
2 Tenner, Scott MD etal, American Journal of Gastroenterology: March 2014 - Volume 109 - Issue 3 - p 444

ERCP Guidelines in AP
1. Early ERCP (24 hr of admission) should be reserved for patients with acute
cholangitis superimposed to acute pancreatitis1;
2. There is no indication for urgent ERCP in patients with mild pancreatitis without
cholangitis; who lack laboratory or clinical evidence of ongoing biliary
obstruction2
65

ERCP Guidelines in AP…..
3. In cases with severe biliary pancreatitis the differential diagnosis between
acute cholangitis and pancreatitis with SIRS may be difficult.
In these patients every effort should be made to identify biliary obstruction, by
MRCP and EUS when accessible, before resorting to ERCP3
66
3 Kapetanos DJ. ERCP in acute biliary pancreatitis. World J Gastrointest Endosc. 2010;2(1):25–28.

ERCP Guidelines..
4. In the absence of cholangitis and / or jaundice, MRCP or EUS rather than
diagnostic ERCP, should be used to screen for choledocholithiasis, if highly
suspected1
5. Pancreatic duct stents and / or post procedure rectal NSAID suppositories should
be utilized to lower the risk of severe post-ERCP pancreatitis in high-risk patients.2
67

Cholecystectomy in AP
Mild Pancreatitis
• In patients with mild AP, found to have gallstones , cholecystectomy should be performed
before discharge to prevent a recurrence of AP 1,2
• Cholecystectomy reduces the percentage of hospital readmissions and overall cost, due
to recurrent biliary events.
Severe Pancreatitis
In a patient with necrotizing biliary AP, in order to prevent infection, cholecystectomy is to be
deferred until active inflammation subsides and fluid collections resolve or stabilize.1,2
68
2 Bouwense, Stefan A. van Baal,ETAL. (2015). Timing of cholecystectomy after acute biliary pancreatitis. Pancreapedia: Exocrine Pancreas Knowledge Base,
DOI: 10.3998/panc.2015.23

Management of Local Symptoms
69

CLASSIFICATION OF LOCAL COMPLICATIONS OF ACUTE
PANCREATITIS BASED ON CONTENT, CHRONICITY AND
INFECTION (RAC 2013)
70

Management of acute peripancreatic fluid
collection
 The presence of acute peripancreatic fluid is seen in 30-57% of AP Patients
 APFC usually Asymptomatic, usually remain sterile and resolve spontaneously.
 Large collections, are more likely to be due to disruption of the MPD and likely to
persist several weeks .
 An asymptomatic fluid collection is managed by observation alone, and only when
infection is present , drainage necessary(Endoscopic,radiolological,sx).
71

Acute Peripancreatic Fluid collection…
 There is no role for diuretics or peritoneal lavage.
 Rarely, leakage from a disrupted main pancreatic duct can be treated by
endoscopic intervention.1
 Endoscopic pancreatic duct stenting can be used to decrease ductal pressure and
facilitate drainage of collection across the damaged duct to duodenum and
also reduce the risk of stricture formation.1
72

Management of Infective Necrosis
 20% of AP patients develop necrosis(80% of patients who died after AP)
 Main complication of pancreatic necrosis is infection(directly proportional to
amount of necrosis)
 Bacterial translocation usually involving gram negative rods(E coli, klebsiella,
and pseudomonas) and enterococcus
 Infective necrosis should be suspected in patients with prolonged fever,
elevated WBC or progressive clinical deterioration
73

Management of Infective Necrosis
Timing of Intervention
 In general, longer patient can be medically optimized and managed with enteral nutrition and
antibiotics, more mature a fluid collection ,and therefore extent of endoscopic or operative
debridement will be better delineated and tolerated .
 Early surgery is more difficult and dangerous because necrotic tissue is immature, poorly demarcated,
not easily separated from viable tissue, resulting in a significant risk of bleeding.
 inflammatory cascades are not easily switched off, and increase by the surgical procedure
 With mortality rates of up to 65%, trend toward early intervention has curtailed
74

Surgical Intervention in Infected Necrosis
Open Surgery Approaches
 Necrosectomy + wide tube drainage
 Necrosectomy + closed packing
 Necrosectomy +drainage+ relaparotomy (staged re exploration)
 Necrosectomy + laparostomy ± open packing
 Necrosectomy + drainage + closed continuous lavage
75

Surgical Intervention in Infected Necrosis..
Minimally Invasive Approaches
• Endoscopic Transgastric necrosectomy
• Gastro colic/infra meso colic Laparoscopic Necrosectomy
• Laparoscopic transgastric necrosectomy
• Laparoscopic-assisted percutaneous drainage
• Translumbar extraperitoneal retroperitoneoscopy
• Video-assisted retroperitoneal debridement(VARD)
76

STEP UP Approach
This advocates the use of less invasive interventions initially (eg, percutaneous or
endoscopic drainage), and then stepping up to minimally invasive surgical
interventions and only employing open surgical techniques later in the disease
course in those who fail to respond.
PANTER Trial ,demonstrated that the step-up approach reduced the rate of the
composite endpoint of major complications and/or death
77

Endoscopic Transgastric Necrosectomy
necrosectomy imasendoscpic transgastric necrosectomy.mp4
78

Lap Transgastric Necrosectomy
 necrosectomy imaslap transgastric necrosectomy.mp4
79

Lap Infra Mesocolic Necrosectomy
 necrosectomy imaslap infra mesocolic necrosectomy.mp4
80

Lap Assisted Retroperitoneoscopy with
Percutaneous Drainage
 necrosectomy imaslaproscopic assisted retropertinoscopy with
percutaneous drainage.mp4
81

VARD
 necrosectomy imasVARD.mp4
82

D’EGIDIO Classification of Pseudocyst
TYPE CONTEXT Pancreatic DUCT Duct-Pseudocyst
communication
Primary
Treatment
1 Acute Post
Necrotic
Pancreatitis
Normal NO Percutaneous
drainage
2 Acute on Chronic
Pancreatitis
Abnormal(no stricture) 50:50 Internal drainage
or resection
3 Chronic
Pancreatitis
Abnormal(stricture) yes Internal drainage
with duct
decompression
84

Treatment Approaches to Pseudocyst
85

Treatment Algorithm for Pseudocyst 86

THANK YOU !!
87
What you are will show in what you do!!
Thomas Edison

acute pancreatitis a thorough review

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