Update on managment of Acute Pancreatitis.Practical approach to severity grading, investigations, treatment pathways

1. ACUTE
PANCREATITIS
Dr. K.V.Rajan MS, FRCS
Professor and HOD
Department of Surgery
Mahatma Gandhi Medical College & Research Institute
Puducherry

2. • The leading cause of gastrointestinal-related hospitalization
• 3 lac admissions/year, 822/day across USA
• Varying severity :
Management Mortality
mild disease conservative 1%
severe ICU/Interventions 20-50%
Bimodal Mortality - First 2 weeks - MODS/SIRS
Next 2 weeks - Pancreatic Necrosis/Septic
complications
ACUTE PANCREATITIS

3. • Diagnosis of AP is simple
• Diagnostic Criteria: Acute epigastric Pain radiating to back
Serum amylase/lipase level 3 x normal value
Typical imaging findings
• Major challenge - predicting the progression and outcome
• Severity scoring – Ranson’s, Glasgow, APACHE II etc
Why so many scoring systems?
ACUTE PANCREATITIS

4. ETIOLOGY
Most common causes of AP are
• Gall stones
• Alcohol use 80 - 85%
• Hypertriglyceridemia
ACUTE PANCREATITIS

5. Alcohol-induced pancreatitis
• 2nd most common cause worldwide
• increased, viscous secretions that block small pancreatic ducts
• Activates Inflammatory pathways – NF,TNF, IL-2 --- enzymes leakage
• Mitochondrial dysfunction, cathepsin L and B activation
• Premature activation of digestive and lysosomal enzymes within acinar
cells – Co-Localisation
• Zymogen + lysosomes trypsinogen + cathepsin B
INFLAMMATORY CASCADE ROLLER COASTER
•
ACUTE PANCREATITIS

6. GALL STONES & TRIGLYCERIDES PANCREATITIS HOW?
• Theories:
1.Obstructive
High intraductal pressure
Calcineurin pathway
AP
2. Reflux Theory
Bile salt reflux into MPD
Types I,II,V
TG > 1000mg/dL

7. OTHER CAUSES
• Drug-induced pancreatitis statins, sulfonamides, chemo drugs
• Trauma - Blunt and penetrating
Iatrogenic injury - ERCP, left hemicolectomy,splenectomy
• Congenital : Ampullary stenosis, annular pancreas, pancreas divisum
• Autoimmune pancreatitis: type I (IgG4 disease-related) and type II
• Viral infections: Covid 19, Coxsackie, Cytomegalovirus, Echovirus,
Epstein-Barr virus, Hepatitis A/B/C, HIV, Mumps, Rubella, and
Varicella
• Bacterial infections: Campylobacter jejuni, Legionella,
Leptospirosis, Mycobacterium avium, Mycobacterium tuberculosis,
and Mycoplasma

8. • Genetic disorders: Hereditary pancreatitis
Cystic fibrosis
Alpha 1-antitrypsin deficiency
• Hypercalcemia
• Parasitic infections: Ascaris lumbricoides, Cryptosporidium,
Clonorchis Sinensis, Microsporidia
• Renal disease - Haemodialysis
• Toxins - Scorpion bites, organophosphate poisoning
• Vasculitis - Polyarteritis nodosa
Systemic lupus erythematosus
OTHER CAUSES (CONTD)

9. PATHOPHYSIOLOGY
Calcium homeostasis and pH.
ATP depletion, intra-acinar Ca+
Co-Localisation
Cathepsin B + Trypsinogen
Acinar Cell Death release of IL,TNF alpha etc
SIRS/MODS
Elevation in ductal pressures (such as duct obstruction)
Toxins,Alcohol,Drugs

10. Early activation of trypsinogen to trypsin
Activation of enzymes such as “elastase and
phospholipases.”
“haemorrhagic pancreatitis”
PATHOPHYSIOLOGY

11. Extensive tissue damage
Damage Associated Molecular Patterns (DAMPs) release
Recruiting neutrophils and initiating the
inflammatory cascade.
PATHOPHYSIOLOGY

12. PATHOPHYSIOLOGY

13. PATHOPHYSIOLOGY

14. CLINICAL FEATURES
• Epigastric pain
Sudden onset
Sharp pain
Mostly radiates to the back
• Nausea,vomiting
• History of alcoholism
• Known case of gall stone disease
• History of abdominal trauma
• H/O hyperlipidemia
vs

15. PHYSICAL EXAMINATION
• General Examination Dehydration, Tachycardia, tachypnea ( SIRS)
Hypotension
Gallstone AP Icterus, S/O Cholangitis
• Abdomen Epigastric tenderness
guarding/rigidity – severe AP
Grey Turner sign / Cullen sign/Fox Sign
• Respiratory System – Left Pleural effusion

16. SCIENCE BEHIND SIGNS
Identify the signs and explain
the reason for the signs.

17. PRACTICAL EVALUATION OF ACUTE PANCREATITIS
• DIAGNOSIS Clinical
Laboratory
Imaging
• SEVERITY GRADING Clinical
Laboratory
Imaging

18. EVALUATION
• How to diagnose ACUTE PANCREATITIS
Revised Atlanta Classification(Banks et al 2013)
The diagnosis of acute pancreatitis requires at least 2 of 3 criteria:
1.A lipase or amylase level is three times the normal upper limit.
2.Abdominal pain is consistent with pancreatitis.
3.Abdominal imaging is consistent with acute pancreatitis.
Serum Values:
Amylase normalises by 3-5 days
Lipase normalises by 8-14 days

19. LABORATORY EVALUATION
• Hemogram-Hb, Hct, WBC
• S.amylase, Lipase
• serum triglyceride
• serum calcium
• liver function tests ALP, AST,ALT, Bilirubin
• genetic testing in patients with strong family history

20. CxR
Read the X-ray images and identify
the signs
AxR
IMAGING

21. USG : edematous pancreas, FF, CBD dilated, GB stones,pleural effusion
CECT: Timing – >72 hrs of onset of pain
Early Scan - only if other dx can’t be excluded
mesenteric ischemia/bowel perf
Late Phase - detection of complications
Indications: 1.Uncertain Dx
2.Severity grading
3.Failure to respond to Rx
4.Dx infected necrosis/WON etc
4.Interventions – pigtail etc
Balthazar CTSI staging the severity of the disease(necrosis)
IMAGING

22. CECT
IMAGING
Whats the precise diagnosis and the next step of treatment?

23. SEVERITY OF ACUTE PANCREATITIS
Revised Atlanta Classification – Banks et al 2013, APA

24. SCORING SYSTEMS TO PREDICT THE COURSE OF AP

25. SCORING SYSTEMS TO PREDICT THE COURSE OF AP

26. CT SEVERITY INDEX

27. PREDICTIVE FACTORS FOR SEVERE ACUTE PANCREATITIS
• Obesity
• CRP ≥ 150mg/L at 48 hours post-admission
• Procalcitonin >1.8 ng/ml
• Evidence of organ dysfunction on admission
• Glasgow score >3 at 48 hours post-admission
• APACHE II score ≥8 on admission
• Evidence of necrosis on contrast-enhanced CT
Recent Recommendation : SIRS scoring System
Constant SIRS Transient SIRS No SIRS
25% 8% 0%

28. PRACTICAL APPROACH TO MANAGING AP
• Ascertain the Severity Grading of AP – FIRST STEP
• Resuscitation
• Analgesics - opioids
• Nutrition
• Manage Complications Local Early and Late
Systemic – RS/Renal/Cardiac/Hematologic
Local Complications :
Early – Acute Fluid collections, ANC
Necrosis – Infected/Sterile
Abdominal Compartment syndrome
Late – Pseudocyst Pancreatic Fistula Pancreatic abscess
WOPN Pseudoaneurysm

29. ARDS
HYPOVOLEMIC
SHOCK
ACUTE FLUID
COLLECTION
NECROSIS
ACUTE
NECROTIC
COLLECTION
ABDOMINAL
COMPARTMENT
SYNDROME
PSEUDOCYST
WALLED-OFF
PANCREATIC
NECROSIS
4 WEEKS 8 WEEKS
DAY 0
24 HRS
TIMELINE OF EVENTS IN ACUTE PANCREATITIS
5 DAYS

30. TREATMENT OF ACUTE PANCREATITIS
The initial management of acute pancreatitis is largely supportive
• Fluid replacement and electrolyte balance
• O2 to maintain SpO2 – 95%
• Optimization of calories support
• Preventing, identifying and treating local and systemic
complications.
• Antibiotics
• Octreotide NO ROLE
• Other drugs
When will you give antibiotics?

31. RULES OF FLUID RESUSCITATION?
• Moderate and severe AP
• Mild interstitial pancreatitis – conservative, allowed early oral fluids
• Choice of fluid Crystalloids – Ringer Lactate( balanced RL),
Plasmalyte
Avoid Normal saline
Aggressive vs Controlled Fluids
6L in 24 hrs titrated to fluid deficit and response
15ml/kg/hr 5-10ml/kg/hr, 4L/24hr
organ perfusion better, pancreas ischemia less (IPA/APA Guidelines 2013)
A/R: Edema, ACS, ileus
• Central Line – non-responders, cardiac, renal, respiratory comorbs

32. PROBLEMS OF AGGRESSIVE FLUID THERAPY

33. RESUSCITATION
GOALS
• To prevent
hypovolemia
• To preserve organ
perfusion
END POINTS
Central venous pressure
8 – 12 mm Hg
Mean arterial pressure
65 mm Hg
CV oxygen saturation
>=70%
IVC compression test

35. FLUID PROTOCOL IN SEVERE ACUTE PANCREATITIS
Parameter Recommendation
Fluid resuscitation
Necessary: the earlier the resuscitation, the better
the outcome
Type of fluid
Colloids and/or crystalloids: Among crystalloids,
lactate Ringer’s better than normal saline Use
colloids especially when albumin < 2.0 g/dL or
hematocrit < 35%
Amount of fluid
Total fluid in first 24 h: between 3 and 4 L, Not to
exceed 4 L
Rate of infusion
Initial bolus 1000 mL over one hour followed by 3
mL/kg per hour (200 mL/h) for 24-48 h
Monitoring
Urine output > 0.5 mL/kg/h, hematocrit = 25% to
35%, drop in BUN. CVP: Not good for monitoring
Duration of resuscitation 24-48 h, until signs of volume depletion disappear

36. PROPHYLACTIC ANTIBIOTICS IN AP
Recent ACG and AGA guidelines have recommended against the
routine use of prophylactic antibiotics in AP patients
Cochrane Review 2010
Meta-analysis
Problems: resistance bacteria
increased fungal co infection
Main Indications: Infected necrosis -- CECT/FNA Gm stain/Cult
Blood culture +
Pre-existing infections

37. THE ROLE
FOR
ANTIBIOTICS
IN AP ??
Carbapenems
Quinolones
Metronidazole
PSEUDO
CYST-----
-----NO
PERI-
PANCREATIC
COLLECTION
NO
STERILE
NECROSIS-
-------------
NO
INFECTED
NECROSIS-
---------- YES
Why do we prefer these antibiotics as first choice?

38. NUTRITION - EARLY OR DELAYED
• Early enteral nutrition -protect the gut mucosal barrier
reduce bacterial translocation.
Reduce infected pancreatic necrosis.
(Cochrane Review 2013, Al-Omran et al 2010)
Enteral TPN
Gut barrier mucosal atrophy
NG /NJ feeding line complications
metabolic problems

39. GALLSTONE PANCREATITIS
• ERCP/ES - AP with cholangitis
Elderly with comorbidities to prevent recurrent AP
(Working Group IAP/APA Guidelines 2013)
• Laparoscopic Cholecystectomy
Mild AP Same admission
Severe AP 6 weeks later
(PONCHO Trial , de Costa et al 2015 – Timing of Cholecystectomy in
AP)

40. COMPLICATIONS OF
ACUTE PANCREATITIS

41. COMPLICATIONS OF AP

42. LOCAL COMPLICATIONS REVISED ATLANTA OF AP

43. PERIPANCREATIC FLUID COLLECTIONS
• Acute fluid Collection - 30-60%
• No epithelium or fibrotic capsule
• Sterile fluid collection: spontaneously reabsorbed
• Infected Fluid Collection (ANC – acute necrotic collection)
Fever, elevated WBC, abdominal pain
CECT – gas bubbles or FNA is confirmatory
Percutaneous drainage and IV antibiotics

44. NECROTIZING PANCREATITIS
• Definition - presence of greater than 30% of nonenhancement of the
pancreas on CECT
• High morbidity and mortality rate
• Sterile or infected

45. Infected Necrosis
• Occurs usually after 10th day of AP
• Risk of infection – 70% of gland necrosis – 50 % chance
30% of gland necrosis – 20% risk
• Suspect when signs of sepsis, with fever, pain and leucocytosis,
organ failure
• Diagnosis: CT shows air in necrosis,
guided FNA, Gram stain, Culture
• Treatment: Antibiotics - fluoroquinolones, imipenem/meropenem
Organ support and Delayed Intervention for drainage
NECROTIZING PANCREATITIS

46. INFECTED PANCREATIC NECROSIS
• TIMING OF INTERVENTION
Mortality
< 2 WEEKS 75%
2-4 WEEKS 45%
> 4 WEEKS 8%
Practice Pearl – Delay as much as possible – 8 weeks
Less is Better Minimal Routes vs Open/Lap Necrosectomy

47. INFECTED PANCREATIC NECROSIS
STRATEGIES FOR NECROSECTOMY
Open approach Minimally invasive
1. Open necrosectomy with closed packing A. Endoscopic approach
2. Open necrosectomy with open packing B. Laparoscopic approach
3. Open necrosectomy with continuous C. Radiological approach
post op packing D. Step up Approach
4. Programmed open necrosectomy

48. RATIONALE FOR NECROSECTOMY
• a) removal of necrotic intrapancreatic and extra pancreatic tissue
interrupt the inflammatory process , systemic release of
mediators for remote organ failure.
• b) The prevent long-term endocrine and exocrine functional
impairment
• c) Remove only free floating necrotic tissue

49. Open necrosectomy
• Laparotomy through a bilateral subcostal incision.
• After blunt removal of all necrotic tissue, two large-bore drains for postoperative
lavage were inserted, and the abdomen closed.
• After surgical debridement an extensive intraoperative lavage is performed using
6–12 L of isotonic saline in order to clear the surface of the pancreatic bed and
the extra pancreatic spaces affected by fatty tissue necrosis.
• For postoperative continuous local lavage large-bore single lumen (24–28F) and
double lumen (16–18F) catheters are placed into the lesser sac and brought out
through either side of the lateral abdominal wall at the level of the retroperitoneal
spaces

50. Debridement and open packing/staged
laparotomy
• The abdomen is entered through a midline or bilateral subcostal incision and
the pancreas is approached by dividing the gastrocolic ligament.
• After opening the peritoneum overlying the pancreas, peripancreatic and
pancreatic necrosectomy is performed by careful blunt finger dissection,
extensive lavage, and aspiration of debris.
• The abdomen is temporarily closed using a zipper, a prosthesis, or adhesive
plastic sheeting sewn to the fascial edges. Operative evaluation and
debridement of ongoing necrosis is repeated every 48–72 hours until
devitalized tissue is removed and granulation tissue starts to develop
NECROTIZING PANCREATITIS

51. MINIMALLY INVASIVE TECHNIQUES
ENDOSCOPIC
1.Trans gastric
2.With SEMS
3.Through PEG

52. LAPAROSCOPIC APPROACH
• 1. VARD ( Video assisted retroperitoneal debridement)
• 2. MIRP
• 3. Retro gastric approach
• 4. Trans gastric
• 5. Trans mesocolic
• 6. Hand assisted
• 7.Robotic necrosectomy
Access Routes : Lesser Sac
Trans-mesocolon
(MIRP – Minimally Invasive RetroPeritoneal necrosectomy)

53. VARD PROCEDURE
• Part of a ‘‘step-up approach’’ consisting of percutaneous
retroperitoneal catheter drainage (PCD)
• Drain is used as guide
• Laparoscope inserted and under vision necrosectomy done
• Two large bore surgical drains are placed into the collection
NECROTIZING PANCREATITIS

54. VARD PROCEDURE
• Part of a ‘‘step-up approach’’ consisting of percutaneous
retroperitoneal catheter drainage (PCD)
• Drain is used as guide
• Laparoscope inserted and under vision necrosectomy done
• Two large bore surgical drains are placed into the collection
NECROTIZING PANCREATITIS

56. VARD ENDOSCOPIC

57. MIRP PROCEDURE
• A percutaneous retroperitoneal catheter placed in left flank space
between spleen, colon and kidney
• Drain is exchanged with guide wire--- dilated to 30Fr
• Access maintained by Amplatz sheath
• Nephroscope with lap graspers to debride under vision
• Sump drain placed and post op lavage with warm saline
• Replaced with simple drain
• Check CT confirms resolution and drain removed
NECROTIZING PANCREATITIS

58. MIRP

59. ENDOSCOPIC NECROSECTOMY THROUGH PERCUTANEOUS SEMS
• Access – left lateral subcostal
retroperitoneal route
• Guide wire, dilators and
deployment of SEMS
• Endoscope through stent and
necrosectomy

60. RADIOLOGICAL TECHNIQUES
• 1. Trans peritoneal drainage
• 2. Retroperitoneal drainage
• 3. Trans mural drainage- Stomach/duodenum

61. STEP UP APPROACH
• The first step - percutaneous or endoscopic trans gastric
drainage. The preferred route is - the left retroperitoneum
• No clinical improvement after 72 hours ----- a second drainage
procedure is performed
• If this is not possible
or if there is no clinical improvement next 72 hours
• the second step --- VARD with postoperative lavage
• Stepwise retraction of the drains
(PANTER Trial – van Santvoort et al 2010 – Dutch Trial)

62. CURRENT RECOMMENDATIONS - PANCREATIC NECROSIS
ENDOSCOPIC DRAINAGE WITH SEMS
ADD ON – RADIOLOGICAL DRAIN
VARD /MIRP
LAPAROSCOPIC NECROSECTOMY

63. LONG TERM COMPLICATIONS OF NECROSECTOMY
• 1. Diabetes
• 2. Exocrine insufficiency
• 3. Fistula- panc-Cutaneous, Ent-Cutaneous, colonic
• 4. Wound complications – SSI, dehiscence, incisional hernia

64. WALLED OF PANCREATIC NECROSIS
• Infection with systemic signs
• Abdominal Pain
• Nutritional Failure
TREATMENT
1.Endoscopic Drainage
EUS guided drainage
OGD guided drainage
Cystotome to enter cyst – dilated –pigtail
catheters placed
Naso-cystic catheter and lavage
2.Laparoscopic cystogastrostomy

65. PSEUDOCYST PANCREAS
• 5-15 % of AFC patients
• By definition, the capsule of a
pseudocyst is composed of collagen
and granulation tissue and is not
lined by epithelium.
• Duration to develop: 4-8 weeks
CT showing a pancreatic pseudocyst with acute
hemorrhage. A 10-cm pancreatic pseudocyst.
The pseudocyst is compressing the stomach.

66. • high concentration of pancreatic enzymes
• Most are sterile.
• Complications – Pain, satiety, GOO, infection, CBD obstruction
hemorrhage, rupture leading to pancreatic ascites.
• USG/CECT
• EUS and FNA – amylase rich, nil CEA and mucin
• Treatment : Asymptomatic - No treatment – esp. <4cm, in panc. tail
no MPD communicn
Symptomatic - Surgical,
Radiologic
Endoscopic drainage.
PSEUDOCYST PANCREAS

67. Surgical drainage of a pseudocyst
Cysto-gastrostomy
Cysto-duodenostomy
Roux-en-Y cysto-jejunostomy
Resection of pancreatic tail with cyst
Radiological drainage
Infected pseudocysts - Percutaneous catheter drainage
ERCP – cyst communicates with MPD
MPD stricture – dilatation and stent
PSEUDOCYST PANCREAS

68. PANCREATIC ASCITES AND PANCREATICOPLEURAL FISTULAS
• Complete disruption of pancreatic duct .
• Very rare
• Diagnostic paracentesis - elevated amylase(50000) and lipase levels.
• Treatment : TPN
abdominal drainage
ERCP and stenting
• Surgical treatment: Distal resection and closure of the proximal stump
Roux-en-y pancreaticojejunal anastomosis

69. GI BLEEDING, SPLENIC AND VASCULAR COMPLICATIONS
Elastase
Pressure necrosis
High mortality Treatment - embolization

70. KEY POINTS – PRACTICE PEARLS
• Prompt diagnosis and ascertain the severity of Acute Pancreatitis
• Triage patients into mild or severe AP – severe patients admitted in HDU
• Goal directed fluid resuscitation, O2 therapy, Analgesics
• Establish and treat the etiology – USG to rule out gallstones
• Promote early enteral nutrition
• Antibiotics ONLY in proven infected complications
• Timing of cholecystectomy in Gallstone AP
• Delaying surgical intervention for necrosectomy 8-12 weeks
• Less is more – Step Up Approach Drains RP drainage Lapscopic