This document discusses complications of acute pancreatitis, with a focus on pseudocyst and pancreatic necrosis. It summarizes that pseudocysts are fluid collections contained by a well-defined capsule that can develop after acute or chronic pancreatitis. Complications include infection, rupture, enlargement, and erosion into blood vessels. Diagnosis involves imaging and labs. Treatment depends on symptoms and includes drainage or resection. Pancreatic necrosis involves death of pancreatic tissue and can become infected. Interventions like drainage may be needed if necrosis is infected or causing other issues. Both conditions are serious complications of acute pancreatitis.

2. THINKING OF COMPLICATIONS ?
 Can we think of life without complications in today’s
life?
 So let us see how Acute Pancreatitis can make the
whole thing complicated

3. COMPLICATIONS OF ACUTE
PANCREATITIS:
WITH SPECIAL EMPHASIS ON
PSEUDOCYST AND ACUTE
PANCREATIC NECROSIS
PREPARED BY: DR. DIPANJAN MANDAL
MALDA MEDICAL COLLEGE & HOSPITAL

4. COMPLICATIONS OF ACUTE PANCREATITIS
LOCAL
• ACUTE FLUID COLLECTIONS
• POSTNECROTIC PANCREATIC & PERIPANCREATIC FLUID COLLECTION
• PSEUDOCYST
• PANCREATIC NECROSIS
• PANCREATIC ABSCESS
REGIONAL
• VASCULAR
• VENOUS THROMBOSIS
• BLEEDING
• INTESTINAL
• PARALYTIC ILEUS
• INTESTINAL ISCHEMIA & NECROSIS
• INTESTINAL OBSTRUCTION
• CHOLESTASIS
SYSTEMIC
•SIRS
•MODS
•RESPIRATORY
•RENAL
•CVS
•METABOLIC
•ENCEPHALOPATHY

5. ACUTE FLUID COLLECTIONS
 30-50% cases
 Content: inflammatory exudates and/or enzyme-rich
pancreatic secretions
 Routes of extension:
 Diagnosis: CECT/MRI/EUS
 Management: wait & watch
• Into lesser sac
• Behind the pancreatic head
• Behind the lt & rt colons on the
psoas muscle
• Into the small bowel mesentry
& buldging through the
transverse mesocolon

6. POSTNECROTIC PANCREATIC &PERIPANCREATIC
FLUID COLLECTION
 Contain both solid & fluid components
 Arise from liquefaction of solid necrosis and/or
pancreatic duct disruption
 Mature lesion has a wall without an epithelial lining
around the collection- “walled off necrosis” (WON)
 Diagnosis:
 Management: same as that for pancreatic necrosis
CECT, MRI, EUS
CECT- Extraluminal gas
Image guided FNA for Gram’s
stain
& culture [Definitive diagnosis]

7. COMPLICATIONS
 Venous thrombosis
 Bleeding
 Paralytic ileus
 Intestinal ischaemia and necrosis
 SIRS
 MODS
 Respiratory complications
 Renal complications
 Cardiovascular complications
 Metabolic complications
 Encephalopathy
 Hypocalcemia
 Hyperglycemia
 DIC
 Protein-energy malnutrition

8. PANCREATIC PSEUDOCYST
 A fluid collection contained within a well-defined capsule.
 Present for > 4 weeks after disease onset
 Doesn’t possess an epithelial lining
 May develop in the context of
Acute pancreatitis(10-15% of cases),
Chronic pancreatitis(20-40% of cases) or
trauma

9.  Location:
• Lesser sac in proximity to the pancreas
• Large pseudocysts can extend into the
Paracolic gutters,
Pelvis,
Scrotum,
Mediastinum or
Thorax

10.  Composition:
• Thick fibrous capsule – not a true epithelial lining
• Pseudocyst fluid: similar electrolyte conc. to that of plasma
high conc. of amylase, lipase & enterokinases such as
trypsin
• Relatively clear watery fluid
• Hemorrhage- may contain clot-become xanthochromic
• Infection-pus

11. PATHOGENESIS & CLASSIFICATION
 Pancreatic ductal disruption sec. to
1. Acute pancreatitis- Necrosis
2. Chronic pancreatitis- Elevated pancreatic duct
pressures from strictures or ductal calculi
3. Trauma

12. PATHOGENESIS
Acute pancreatitis: Pancreatic necrosis
Ductular disruption
Leakage of enzyme-rich
secretion from inflammed
area of gland
Accumulation in space
adjacent to pancreas
Inflammatory response
induces formation of
distinct cyst wall composed
of granulation tissue,
organizes with connective
tissue & fibrosis

13. THE D’EDIGO CLASSIFICATION
CONTEXT PANCREATIC
DUCT
DUCT-
PSEUDOCYST
COMMUNICATI
ON
Type I Acute
postnecrotic
pancreatitis
Normal No
Type II Acute-on-chronic
pancreatitis
Abnormal (no
stricture)
50:50
Type III Chronic
pancreatitis
Abnormal
(stricture)
Yes

14. PRESENTATION
o Symptoms
1. Persistent abdominal
pain >3 weeks(80-
90%)
2. Nausea/vomiting
3. Early satiety
4. Bloating, indigestion
5. Anorexia, weight loss
6. Abdominal mass
 Signs
1. Tenderness
2. Abdominal fullness

15. COMPLICATIONS (~ 10% CASES)
Process 0utcomes
1.Infection(25% cases) Abscess
Systemic sepsis
2.Rupture
Into the gut Gastrointestinal bleeding
Internal fistula
Into the peritoneum Peritonitis
3. Enlargement
pressure effects Obstructive jaundice from biliary
compression
Bowel obstruction
pain
4. Erosion into a vessel Hemorrhage into the cyst
Haemoperitoneum

16. DIAGNOSIS
 Suspect a pseudocyst
 Acute pancreatitis fails to recover after a week of
Rx
 After initial improvement, symptoms return
 Amylase levels persistently high
 Persistent abdominal pain
 Epigastric mass palpated after pancreatitis

17. DIAGNOSIS
Clinical features: epigastric discomfort or
pain,anorexia, early satiety, nausea, mild fever, back
pain & a palpable mass.
 Labs: persistently elevated serum amylase (>5000U/mL)
 Plain X-ray: not very useful
 Ultrasound: 75-90% sensitive
Advantage:
1) better able to determine the
extent of solid tissue within a fluid
collection
2) often used to guide FNA
Disadvantage: limited by
operator skill, patient’s
habitus, overlying bowel
gas

18.  CECT:
• Most accurate (sensitivity 90-100%)
• Advantages are many
 Triphasic helical CT: delineate the regional
arteries & veins
 MRI: outlines the solid component of the lesions
 ERCP: both diagnostic & therapeutic role
 MRCP: noninvasive
similar diagnostic accuracy to ERCP.

19. MANAGEMENT
Two principal indications for treating pseudocysts
General features of a pseudocyst imp in considering the
most appropriate Rx
 Thickness of the pseudocyst wall
 Location
 Contents
 Number
 Etiology
 Main pancreatic duct anatomy & degree of disruption
To relieve symptoms
To treat complications

21. TREATMENT APPROACHES FOR PANCREATIC PSEUDOCYST
Approaches Examples
Open surgical Cystogastrostomy
Cystoduodenostomy
Roux-en-Y Cystojejunostomy
Distal pancreatectomy +/-splenectomy
External drainage
Laparoscopic Cystogastrostomy
Cystoduodenostomy
Roux-en-Y cystojejunostomy
Distal pancreatectomy +/- splenectomy
External drainage
Radiologic Percutaneous drainage
Percutaneous transgastric drainage
Endoscopic Transpapillary pancreatic duct stent
Transgastric stent
Transduodenal stent

22. DRAINAGE V/S RESECTION
 Drainage procedures are preferred
• Preserve pancreatic function
• Technically easier
• Lower mortality rate
• Complications & mortality rates of int drainage is ½
of ext drainage

23. CYSTOGASTROSTOMY
 Ideal when pseudocyst adherent to post stomach &
indenting it
 Disadvantage: not a dependent stoma, may act as
sump when pseudocyst is large can accumulate
gastric debris

27. PANCREATIC NECROSIS
 Approx 20% of pts with acute pancreatitis
 25-70% develop infected necrosis
 Risk higher when involvement is more extensive(>30% of
the gland) & with time( 24% by end of 1st wk; 36% by end
of 2nd wk;71% beyond of 3rd wk)
 Clinical features: same as that of acute pancreatitis

28. Pathogenesis
Early/vasoactive
phase
Late/septic
phase

29. PATHOPHYSIOLOGY

30. FATE
 <1cm : resolve spontaneously.
 2-4 cm :demarcated by macrophages that slowly
phagocytose the necrotic material; inner content of
foci become liquified
 >5cm :macrophages rich in hemosiderin+ other
immune cells form a thin layer of granulation tissue
by 10-20 days of disease onset, after 20-30 days
become a fibrous capsule increasing in thickness .
Necrotic areas slowly resolved& replaced by fibrotic
scar tissue (necrosis-fibrosis sequence)

31. MICROBIOLOGY
 Routes of entry
1. Hematogenous
2. Transpapillary reflux of duodenal content into pancreatic
duct
3. Translocation of intestinal bacteria & toxins via
mesenteric lymphatics to systemic circulation via
thoracic duct
4. Reflux of bacteriobilia via a distrupted pancreatic duct
into necrotic parenchyma
5. Transperitoneal spread

32. ORGANISMS INVOLVED:
1. Polymicrobial 1/3rd ;monomicrobial 2/3rd
2. Gram –ve aerobic bacteria: most common; E.coli ,
Proteus, Pseudomonas, Klebsiella
3. Gram +ve bacteria: Enterococcus, Staph aureus
4. Anaerobic bacteria: 5%
5. Fungi :more common after prophylactic antibiotic

33. DIAGNOSIS
 Ranson, Glascow, APACHE ,BISAP used for severity
stratification
 CECT:
a. Gold standard
b. Disadvantage: contrast used might worsen necrosis
and/or exacerbate existing renal failure
c. Useful to grade the severity by CTSI
 MRI
 EEU
 Prognostic markers:
a) CRP: 85% accurate; requires 3-4 days to reach a
diagnostic level; threshold value>120 mg/dl

34. a) Other prognostic markers
• IL-6( threshold>14pg/ml)
• Polymorphonuclear elastase( threshold >120µ/l)
• Phospholipase A2 ( threshold>15U/L)
• Urinary trypsinogen activating peptide
• Procalcitonin

35.  Image guided( CT or ultrasound) FNA : Indications
a. >30% necrosis+ persistent symptoms
b. Smaller areas of necrosis+ clinical suspicion of
infected necrosis

36. INDICATIONS OF INTERVENTIONS
1) Infected necrosis, confirmed by culture +ve FNA
2) Persistent sepsis from infected necrosis
3) Failure of attempted radiological drainage
4) Massive hemorrhage or bowel perforation
5) Pts with sterile necrosis, those clinically
deteriorating & who have a clear target lesion.

37. EARLY SURGERY V/S LATE INTERVENTION
 Early surgery : more difficult & dangerous —significant
risk of bleeding
 There may be infection of sterile necrosis
Current concept: intervention
should be as late as possible after
disease onset( preferably >4 wks)
because necrosis has stopped
extending, clear demarcation b/w
viable & non-viable tissues, infected
necrotic tissues have become
organized & “walled-off”

38. TYPE OF INTERVENTION

39. Factors to determine the type of intervention:
1. Anatomical location
2. Infection status
3. Complexity of target lesion(s)
4. Physiological status
5. Comorbidity of an individual patient
6. Availbility of expertise with the type of intervention

40. PRINCIPLES FOR INTERVENTION
 Removal of all infected & necrotic tissue and fluid
 Preservation of vital tissues
 Avoidance of intraoperative hemorrhage

41. OPEN AND MINIMALLY INVASIVE APPROACHES TO THE
TREATMENT OF PANCREATIC NECROSIS