Acute pancreatitis

1. ACUTE
PANCREATITIS

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

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.

5. Ducts of Pancreas

6. o BLOOD SUPPLY
Pancreatic branch of splenic artery
Superior pancreaticoduodenal artery
Inferior pancreaticoduodenal artery
o VENOUS DRAINAGE
Splenic vein
Superior mesenteric vein

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

10. FUNCTIONS
o EXOCRINE
Pancreatic juice
Trypsinogen,
Chymotrypsinogen,Proelastase,
Procarboxypolypeptidase,
Pancreatic lipase,Pancreatic α- amylase,
Bile salt acid lipase
o ENDOCRINE
α cells- Glucagon
β cells- Insulin
δ cells- Gastrin, Somatostatin
F cells- Pancreatic Polypeptide

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

13.  Autoimmune pancreatitis
 Vascular – shock, atheroembolism, vasculitis
 Viral infections- mumps, Coxsackie B
 Porphyria
 Biliary ascariasis, Clonorchis sinensis
 Infectious mononucleosis
 Mycoplasma pneumoniae
 Scorpion bite
 Idiopathic

14. ATLANTA CLASSIFICATION
 A/c edematous pancreatitis (80%)
 A/c necrotising pancreatitis (20%)
 PRESENT CLASSIFICATION OF A/C PANCREATITIS
 Interstitial a/c pancreatitis
 Necrotising pancreatitis
-Sterile necrosis
-Infected necrosis( CT guided aspiration
and Grams stain – Pancreatic necrosectomy)

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

18. PATHOGENESIS

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

24. CULLEN SIGN GREY TURNER SIGN

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

31. COLON CUT OFF SIGN

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

38. Differential Diagnosis
Perforated duodenal ulcer
Cholecystits
Mesenteric ischaemia
Ruptured aortic aneurysm
Ectopic gestation
Salpingitis
Intestinal obstruction
Diabetic ketoacidosis

39. ASSESSMENT OF SEVERITY
Scoring Systems:
Ranson
Glassgow
APACHE II

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.

43. MANAGEMENT
Conservative(70-90%)
Surgical Rx- when indicated(10-30%)
Management of complications

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

52. COMPLICATIONS
Systemic (most common in 1st week)
 Shock(large volume of fluid sequestration)
 Arrhythmias
 ARDS (Lecithinase reduces surfactants)
 RF (toxin ATN)
 DIC (diffuse oozing in pancreatic bed-utilizes
platelets)
 Paralytic Ileus
 Hypocalcaemia
 Hyperglycaemia
 Hyperlipidaemia
 Visual disturbances
 Confusion, irritability, encephalopathy
 Subcutaneous fat necrosis

53. LOCAL COMPLICATIONS
A/c fluid collection
Sterile pancreatic necrosis
Pancreatic abscess
Pseudocyst
Pancreatic ascites
Pleural effusion
Portal/splenic vein thrombosis
Pseudoaneurysm

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)