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

COMPLICATIONS OF ACUTE PANCREATITIS: WITH SPECIAL EMPHASIS ON PSEUDOCYST AND ACUTE PANCREATIC NECROSIS

PREPARED BY: DR. DIPANJAN MANDAL MALDA MEDICAL COLLEGE & HOSPITAL

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

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

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, EUSCECT- Extraluminal gas Image guided FNA for Gram’s stain & culture [Definitive diagnosis]

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

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

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

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

PATHOGENESIS & CLASSIFICATION Pancreatic ductal disruption sec. to 1. Acute pancreatitis- Necrosis2. Chronic pancreatitis- Elevated pancreatic duct

pressures from strictures or ductal calculi3. Trauma

PATHOGENESIS

Acute pancreatitis: Pancreatic necrosis

Ductular disruptionLeakage 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

THE D’EDIGO CLASSIFICATION

CONTEXT PANCREATIC DUCT

DUCT-PSEUDOCYST COMMUNICATION

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

PRESENTATION

o Symptoms1. Persistent

abdominal pain >3 weeks(80-90%)

2. Nausea/vomiting3. Early satiety4. Bloating,

indigestion5. Anorexia, weight

loss6. Abdominal mass

Signs1. Tenderness2. Abdominal fullness

COMPLICATIONS (~ 10% CASES)Process 0utcomes1.Infection(25% cases) Abscess

Systemic sepsis2.Rupture Into the gut Gastrointestinal bleeding

Internal fistula Into the peritoneum Peritonitis3. Enlargement pressure effects Obstructive jaundice from

biliary compressionBowel obstruction

pain4. Erosion into a vessel Hemorrhage into the cyst

Haemoperitoneum

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

DIAGNOSISClinical 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 collection2) often used to guide FNA

Disadvantage: limited by operator skill, patient’s habitus, overlying bowel gas

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.

MANAGEMENTTwo 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 symptomsTo treat complications

TREATMENT APPROACHES FOR PANCREATIC PSEUDOCYST

Approaches ExamplesOpen surgical Cystogastrostomy

CystoduodenostomyRoux-en-Y CystojejunostomyDistal pancreatectomy +/-splenectomyExternal drainage

Laparoscopic CystogastrostomyCystoduodenostomyRoux-en-Y cystojejunostomyDistal pancreatectomy +/- splenectomyExternal drainage

Radiologic Percutaneous drainagePercutaneous transgastric drainage

Endoscopic Transpapillary pancreatic duct stentTransgastric stentTransduodenal stent

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

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

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

Pathogenesis

Early/vasoactive phase

Late/septic phase

PATHOPHYSIOLOGY

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)

MICROBIOLOGY

Routes of entry1. Hematogenous2. Transpapillary reflux of duodenal content into

pancreatic duct3. 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

ORGANISMS INVOLVED:

1. Polymicrobial 1/3rd ;monomicrobial 2/3rd 2. Gram –ve aerobic bacteria: most common;

E.coli , Proteus, Pseudomonas, Klebsiella3. Gram +ve bacteria: Enterococcus, Staph

aureus4. Anaerobic bacteria: 5%5. Fungi :more common after prophylactic

antibiotic

DIAGNOSIS Ranson, Glascow, APACHE ,BISAP used for severity

stratification CECT: a. Gold standardb. 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

a) Other prognostic markers• IL-6( threshold>14pg/ml)• Polymorphonuclear elastase( threshold

>120µ/l)• Phospholipase A2 ( threshold>15U/L)• Urinary trypsinogen activating peptide• Procalcitonin

Image guided( CT or ultrasound) FNA : Indications

a. >30% necrosis+ persistent symptomsb. Smaller areas of necrosis+ clinical suspicion

of infected necrosis

INDICATIONS OF INTERVENTIONS1) Infected necrosis, confirmed by culture +ve

FNA 2) Persistent sepsis from infected necrosis3) Failure of attempted radiological drainage4) Massive hemorrhage or bowel perforation5) Pts with sterile necrosis, those clinically

deteriorating & who have a clear target lesion.

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”

TYPE OF INTERVENTION

Factors to determine the type of intervention:

1. Anatomical location2. Infection status3. Complexity of target lesion(s)4. Physiological status5. Comorbidity of an individual patient6. Availbility of expertise with the type of

intervention

PRINCIPLES FOR INTERVENTION Removal of all infected & necrotic tissue and

fluid Preservation of vital tissues Avoidance of intraoperative hemorrhage

OPEN AND MINIMALLY INVASIVE APPROACHES TO THE TREATMENT OF PANCREATIC NECROSIS

THANK YOU ALL