Acute pancreatitis is inflammation of the pancreas that is usually reversible. It is commonly caused by gallstones or alcoholism. Symptoms include severe abdominal pain, vomiting, and fever. Diagnosis is based on elevated serum amylase and lipase levels. Severity is assessed using scoring systems like Ranson criteria or CT severity index. Mild cases are treated conservatively with IV fluids and analgesics while severe or infected cases require intensive care monitoring, antibiotics, and possibly surgical debridement of pancreatic necrosis.
2. ANATOMY
Soft , lobulated, elongated retroperitoneal organ
Lies transversely across the posterior abdominal wall
posterior to stomach b/w duodenum on right and spleen
on left
At the level of L1 & L2 vertebrae
J shaped or retort-shaped
15-20cm long
PARTS – head, neck, body and tail
3.
4. Ducts of Pancreas
Main pancreatic duct of Wirsung
Begins in the tail of pancreas and runs on the
posterior surface of body and head.
Accessory pancreatic duct of Santorini
Begins in the lower part of head and opens in to the
duodenum.
6. o BLOOD SUPPLY
Pancreatic branch of splenic artery
Superior pancreaticoduodenal artery
Inferior pancreaticoduodenal artery
o VENOUS DRAINAGE
Splenic vein
Superior mesenteric vein
7.
8. NERVE SUPPLY
Parasympathetic by Vagus
Sympathetic by Splanchnic
LYMPHATIC DRAINAGE
Pancreaticosplenic (most)
Pyloric(some)
Coeliac
Superior mesenteric
9. HISTOLOGY
Main pancreatic duct divides into interlobular,
intralobular ducts, ductules & acini
Main duct is lined by columnar cells which becomes
cuboidal in the ductules
Exocrine part- serous compound tubulo-alveolar
gland containing zymogen granules secreted into
lumen of acinar cells which communicates with duct
system
Endocrine part- Islets of Langerhans scattered
throughout the gland
11. It is the acute inflammation of prior
normal gland parenchyma
Usually reversible
With raised pancreatic enzyme level in
blood and urine
Commonly caused by biliary tract d/s
12. Trapnell’s Etiological Classification
MAJOR CAUSES
Biliary tract disease(50-70%)- gallstones
Alcoholism- 25%
OTHER CAUSES
Post-ERCP- duct disruption and enzyme extravasation
Abdominal trauma
Following biliary, upper GI or splenic surgery
Drugs- corticosteroids, INH, azathioprine, valproic
acid, thiazides, oestrogens, tetracycline
Hyperparathyroidism
Hypercalcaemia
Hyperlipidemia
15. ORGANISMS INVOLVED
Commonly Polymicrobial
From gall bladder, colon or small bowel via transmural
migration or by haematogenous spread
E.coli(35%)Klebsiella(25%), Enterococcus(25%)
Others- Staphylococci, Pseudomonas, Proteus,
Enterobacter, Anaerobes, Candida(10%)
16. Normal Physiology
Meal Pancreatic juice with proenzyme
enteropeptidase
Trypsinogen Trypsin
Chymotrypsinogen Chymotrypsin
Procarboxy carboxy
polypeptidase polypeptidase
Proelastase Elastase
Procolipase Colipase
Primarily under hormonal control : CCK,
Secretin
17. Mechanisms of Activation
of Pancreatic Enzymes
Pancreatic Duct Obstruction - raised
intrapancreatic ductal pressure and accumulation
of enzyme-rich fluid in the interstitium
Primary Acinar Cell Injury – release of
intracellular proenzymes and lysosomal hydrolases
which further activate the enzymes
Defective Intracellular Transport of Proenzymes
within Acinar Cells
Germline Mutation in Cationic Trypsinogen
(PRSS1) and Trypsin Inhibitor (SPINK1) genes
19. GROSS
Microvascular leakage causing oedema
Necrosis of fat by lipolytic enzyme(yellow white, chalky)
Destruction of BV & interstitial hemorrhage
MICROSCOPIC
Inflammatory infiltration, interstitial oedema, focal areas
of fat necrosis, granular blue appearance of fat cells( FA
+Ca)
PATHOLOGY
20. Longitudinal section- dark areas of hemorrhage in
the head of pancreas and focal area of pale fat
necrosis in the peripancreatic fat
21. Symptoms
Pain-Sudden onset of upper abdominal,severe Pain
agonising, excruciating and constant - in the
Epigastrium – tends to pierce to back or left loin,
refractory to analgesics and relieves on stooping
forward, food & alcohol increases pain
Vomiting
Hiccough–gastric distension/irritation of diaphragm
Fever – Low grade
Haemetemesis and malaena (duodenal necrosis, gastric
erosion, decreased coagulability)
22. Signs
Features of shock –
thready pulse, tachycardia, hypotension, cold
extremities
Cyanosis
Tachypnoea
Mild Icterus (biliary obstruction)
Temperature : n/l or subnormal
Rebound tenderness
Muscle guarding in the upper abdomen
Abdominal distension
Mass in the epigastrium
23. Cullen’s sign – bluish discolouration around
the umbilicus
Grey turner’s sign – bluish discolouration of
the flanks (enzymes sweep across the
retroperitoneum causing hemorrhagic spots &
ecchymosis)
Fox’s sign – bluish discolouration below the
inguinal ligament
26. FLUID, METABOLIC,
HAEMATOLOGIC &
BIOCHEMICAL CHANGES
Hypovolemia
Hypoalbuminaemia
Hypocalcemia
TC is raised with neutrophilia
Thrombocytopaenia with raised FDP
Hypochloraemic metabolic alkalosis
Hyperglycaemia
Hyperbilirubinaemia
Hypertriglyceridaemia
Methemalbuminaemia
27. Investigations
SerUM amylase >1000 SU
Increase within 24hrs, back to normal within 7
days)
Not specific
Other conditions where raised:
Salivary gland inflammation
Upper GIT perforation
Mesenteric infarction
Torsion of an abdominal viscus
Ectopic gestation
Salpingitis
Retroperitoneal hematoma
Renal failure
28. ACR >6%
Amylase Creatinine Clearance Ratio
Serum lipase - more sensitive and specific, persists
for longer period
Serum lactescence (TG metabolism) – Most
specific in hereditary hyperlipidaemia or alcohol
pancreatitis
Serum trypsin –(Most accurate) Not
commonly done
TAP assay in serum & urine – severity
Hb% low in haemorrhagic pancreatitis
WBC Total count raised >15000/cumm–
inflammation
CRP >150mg/L
29. Blood sugar – hyperglycemia
Serum Calcium – Hypocalcemia
Blood Urea
Serum Creatinine
Platelet count
Coagulation profile
LFT - gallstone associated pancreatitis
ABG– pulmonary insufficiency
Peritoneal tap fluid - high amylase and protein
30. Radiographic Findings
Plain X-ray of abdomen
‘Sentinal loop’ of dilated proximal small bowel
Distension of transverse colon with collapse of
descending colon (Colon cut off sign)
Renal halo sign
Calcified gallstones or pancreatic calcification
Obliteration –psoas shadow
Localised ground class appearance
Plain X-ray Chest
Pleural effusion
Diffuse alveolar interstitial shadowing
32. USG Abdomen
Does not establish a diagnosis of acute pancreatitis
Swollen pancreas may be seen
Should be done in all patients to detect gallstones, rule
out acute cholecystitis, determine dilatation of
common bile duct
33. CT SCAN
SPIRAL CT– gold standard
Pancreatic changes
Parenchymal enlargement- diffuse /focal
Parenchymal edema
Necrosis ( non enhancement area - >30% or 3cm)
Peripancreatic changes- Blurring of fat planes, thickening
of fascial planes, presence of fluid collections
Nonspecific findings - Bowel distention, pleural
effusion, mesenteric edema
34. Contrast Enhanced CT
(Not necessary for all patients especially mild
attacks)
Indications -
1. Diagnostic uncertainty
2. Severe - (necrotising/interstitial)
3. Organ failure, sepsis signs, progressive clinical
deterioration
4. Localised complication suspected – fluid,
pseudocyst, pseudoaneurysm
35. BALTHAZAR CT SCORING
SYSTEM
CT Grade:
o A – normal pancreas – 0
o B - oedematous pancreatitis – 1
o C -mild extrapancreatic changes – 2
o D - Severe extrapancreatic changes with fluid
collection – 3
o E - Extensive/multiple extrapancreatic collections
or gas bubbles in or adjacent to pancreas - 4
36. Necrosis score:
o None – 0
o <1/3rd – 2
o >1/3rd <1/2 – 4
o >1/2 - 6
CT severity index-
CT grade + necrosis score
0-3, 4-6, 7-10
37. MRI - similar information to CT
EUS, MRCP - stones in CBD, directly assess
pancreatic parenchyma
ERCP - identification and removal of stones in
the CBD in gallstone pancreatitis, recurrent
attacks without obvious etiology
40. RANSON SCORE
o On admission
Age >55 years
WBC>16×109/L
Blood glucose >10 mmol/L
LDH >700units/L
AST >250 units/L
o Within 48 hrs
BUN rise >5mg%
PaO2 <60 mmHg
Serum Ca <2mmol/L
Base deficit >4 mmol/L
Fluid sequestration >6L
41. o On admission
Age >55 years
WBC count >15x109/L
Blood glucose >10mmol/L
Serum urea >16mmol/L
PaO2 <60 mmHg
o Within 48 hours
Serum Ca < 2mmol/L
Serum albumin
<32g/L
LDH >600 units/L
AST/ALT>600 units/L
GLASGOW SCALE
In both systems, disease is classified as SEVERE if 3 or more
factors are present
42. APACHE II
A/c physiology and c/c health evaluation.
o age , rectal temperature ,mean arterial pressure
,heart rate ,partial pressure - oxygen ,arterial
pH,serum pottasium ,serum sodium, serum
creatinine,hematocrit,WBC.
o APACHE-O-obesity is added .
o Score >8 -11%-18% mortality.
44. MILD ACUTE PANCREATITIS
Conservative management
IVF(ringer lactate/NS)
analgesics, anti-emetics
no antibiotics
A brief period of fasting if pt is nauseated & in pain
If pt deteriorating - ICU admission & invasive
monitoring of pt
45. SEVERE ACUTE PANCREATITIS
Admission to ICU
Analgesia
Aggressive fluid rehydration
O2 supplementation
Invasive monitoring of vital signs, central venous
pressure, urine output
Frequent monitoring of haematological and
biochemical parameters
Nasogastric drainage
Enteral nutrition if nutritional support necessary
Antibiotic prophylaxis
Urgent ERCP - for gallstone pancreatitis
46. INDICATIONS FOR ANTIBIOTICS
Severe infected necrosis with proved culture
Prophylactic Ab therapy in severe pancreatitis
Biliary pancreatitis with biliary stone &
cholangitis
Pancreatic abscess formation
Rapidly progressing disease with deterioration
CEFUROXIME / IMIPENEM/CIPROFLOXACIN
+METRONIDAZOLE
47. SURGERY
INDICATIONS
Condition of pt deteriorates
Formation of pancreatic absess or infected
necrosis
In severe necrotising pancreatitis
Diagnosis in doubt
OPEN SURGERY – gold std for infected pancreatic
necrosis
48. CONVENTIONAL CLOSED METHOD
Open abdomen - necrotic tissue, pus, infected fluid and
toxins removed
NS wash (10-20 L ).
Drainage tubes placed .
Abdomen closed in layers
OPEN METHOD.
Laprotomy - necrosectomy - wide debridement
wash - wide packing.
wound left open –
SEMI OPEN METHOD.
Laprotomy - necrosectomy
closure with drain
Then relaprotomy later
49. ZIP technique
used for repeated wash to remove toxins and
necrotic tissues until healthy granulation tissue
develops in pancreatic bed
BRADLEY’S REPEATED LAPROTOMIES AND
WASH.
CLOSED CONTINOUS LAVAGE
(BEGER’S LAVAGE)
panceatic bed and lesser sac
10-20L(NS/ hyperosmolar K+ free dialysate)
fluid 2L /hr( after initial debridement) to remove
toxic material in peritoneal cavity/ retroperitoneal
area until return fluid becomes clear.
50. Extra peritoneal lavage through b/l flank incisions
is also done
Laproscopy
necrosectomy ,wash and drainage
Jejunostomy is often done with these procedures
to have early enteral nutrition.
Endoscopic necrosectomy
early endoscopic intervention ( within 48 hrs)
with ERCP
biliary stone removal and stenting in biliary
pancreatitis can be done.
51. Further management
to prevent recurrence of gallstones
by laproscopic cholecystectomy
2 wks after a/c attack during same admission
period.
Endoscopic spincterectomy (ERCP) and often
stenting may be needed if there are CBD stones
54. Acute Fluid Collection
o Occurs in early phase
o Located in or near the pancreas
o The fluid is sterile with ill defined wall
o Most such collections resolve by itself
o Large collection causing pressure effect -
aspirated under US/CT guidance
o Transgastric drainage under EUS guidance.
o Can evolve into pseudocyst or abcess if gets
infected
55. Sterile and Infected Pancreatic
Necrosis
o Diffuse or focal area of non-viable parenchyma
that is typically associated with peripancreatic fat
necrosis
o Identified by absence of contrast enhancement on
CT
o Sterile to begin with, but can become
subsequently infected, probably due to
translocation of gut bacteria
o If signs of sepsis, under CT guidance, needle
passed into the area and aspirated- if purulent,
do p/c drainage of infected material
56. o Appropriate Ab as per the microbiological assessment of
aspirate
o Necrosectomy- thorough debridement of dead tissue
Midline laparotomy/ Lt flank incision
o Further necrotic tissue managed by
Closed continuous lavage (Beger)
Closed drainage
Open packing
Closure and relaparotomy(Bradley)
57. CLOSED DRAINAGE – the incision is closed , but the cavity
is packed with gauze-filled penrose drains .The penrose
drains are brought out through the flank and slowly pulled
out and removed after 7 days.
58. Pancreatic Abscess
o Circumscribed intra-abdominal collection of pus, in
proximity to pancreas
o Acute fluid collection or an infected pseudocyst
o Treatment - p/c drainage with widest possible drain
under image guidance along with antibiotic and
supportive care
o Very occasionally ,open drainage is needed.
59. Pancreatic Ascites
o Chronic, generalised, peritoneal, enzyme-rich
effusion usually associated with duct disruption
o Paracentesis – turbid fluid with high amylase
levels
o Rx- drainage with wide bore drains placed
under imaging guidance
o To supress pancreatic secretion:
parenteral/nasojejunal feeding
administration of octreotide
o ERCP- demonstration of duct disruption &
placement of pancreatic stent
60. Pancreatic Effusion
o Encapsulated collection of fluid in pleural cavity,
arising as a consequence of acute pancreatitis
o Concomitant pancreatic ascites or communication
with an intra-abdominal collection
o Rx- p/c drainage under image guidance
61. Haemorrhage
o Into gut ,retroperitoneum or peritoneal cavity.
o Causes – bleeding into a pseudocyst cavity ,diffuse
bleeding from a large raw surface, or a
pseudoaneurysm( false aneurysm of a major
peripancreatic vessel confined as a clot by the
surrounding tissue and often associated with
infection.)
o CT angiography , or magnetic resonance
angiography -diagnosis
o Rx –embolisation or surgery.
62. Portal or splenic vein thrombosis
o Identified on a CT scan.
o A marked raise in platelet count should raise
suspicions.
o Usually conservative Rx.
o If varices or manifestations of portal HTN develop
– endoscopic injection or banding , beta blockers ,
etc…
o Thrombocytosis – aspirin or other anti platelet
drugs.
63. Pseudocyst
o Collection of amylase-rich fluid enclosed in a wall of
fibrous or granulation tissue in lesser sac of peritoneal
cavity.
o Smooth rounded swelling , fluctuation +
o Arise following—a/c pancreatitis, c/c pancreatitis,
pancreatic trauma
o Have communication with main pancreatic duct
o Formation requires 4wks or > from the onset of a/c
pancreatitis
o Identified on CT/USG
o X-ray with barium meal (lateral)