The document discusses acute pancreatitis, defining it as an inflammatory process with varying severity and outlining its major causes (gallstones and alcohol). It describes the pathophysiological mechanisms, clinical features, diagnostic procedures, and management strategies, including both supportive and surgical treatments. Complications, prognosis, and considerations for pancreatic pseudo-cysts and abscesses are also addressed.

1. Acute Pancreatitis
MR. KHALID MOHAMED SALIH SULIMAN
CONSULTANT SURGEON

2. Pancreatitis
Objectives:
 Definition.
 Aetiology.
 Patho-physiology.
 Clinical features.
 Management.
 Complications of Acute Pancreatitis.

3. Acute Pancreatitis
Definition: An inflammatory process of
variable clinical severity range from mild
oedema to pancreatic & peri-pancreatic
necrosis.

4. Acute Pancreatitis
 Aetiology:
 Major Causes (95 %):
A) Gall Stones (40 %).
B) Alcohol (40 %).
C) Idiopathic (10 – 15%).
 Minor Causes (5 %):
1) Trauma: blunt or penetrating abdominal injuries – Iatrogenic (ERCP (5 %) – Surgery (e.g. Gastrectomy –
Splenectomy).
2) Hyperlipidemia (TG – Cholesterol).
3) Hypercalcemia.
4) Infectious diseases (e.g. Mumps, Coxsackie Virus, Rubella, CMV…etc.).
5) Drugs: Isoniazid, Thiazide, Steroids, Estrogen or Lasix.
6) Idiopathic factors – Hypothermia – Scorpion stings – Polyarteritis Nodosa – Pancreatic abnormalities (e.g.
Pancreatic divism & annular pancreas) - Pancreatic Cancer.

5. Pathogenesis of Acute Pancreatitis
Mechanisms of the Pathogenesis:
1) Secretion into an obstructed duct (increase pressure).
2) Bile reflux into the pancreatic duct.
3) Duodenal reflux into the pancreatic duct.
4) Intra-cellular protease activation.

6. Patho-physiology
 Theories behind mechanism of biliary pancreatitis:
 Common channel theory.
 Incompetent sphincter theory.
 Colocolization theory.
 Common channel theory:
 In which a blockage below the junction of the biliary and pancreatic ducts would
cause bile to flow into the pancreas, which could then be damaged by the detergent
action of bile salts.
 Incompetent sphincter theory:
 the passage of a gallstone through the sphincter of Oddi renders it momentarily incompetent,
permitting the reflux of duodenal juice containing activated digestive enzymes into the
pancreatic ductal system leading to premature activation of pancreatic enzymes Acute
Pancreatitis

7. Patho-physiology
 Co-localization theory “Steer & Saluja” 1998:
 A simple mechanical explanation whereby elevated intraductal pressure
causes rupture of the smaller ductules and leakage of pancreatic juice into
the parenchyma. Although the pancreatic duct fluid pH is maintained in
the range of 8 to 9 by the secretion of bicarbonate, the interstitial pH of 7
within the pancreatic tissue favors activation of proteases when trans-
ductal extravasation of fluid occurs. A cascade has been postulated in
which Trypsinogen colocalizes with cathepsin B to produce activated
trypsin, which in turn activates the other digestive zymogens. These active
digestive enzymes then begin auto-digestion within the pancreatic acinar
cells, leading to pancreatitis.

8. Patho-physiology
 How ethanol cause pancreatitis:
 Ethanol causes spasm of sphincter of oddi which leads to obstruction of
pancreatic juice outflow.
 Ethanol increases the concentration of enzyme protein in pancreatic juice
and eventual precipitation of this protein in pancreatic ducts . Calcium
precipitate within the matrix of these protein plugs leading to multiple points of
ductal obstruction randomly scattered throughout the pancreas
 Ethanol increases the permeability of pancreatic ducts .This allows pancreatic
enzymes normally contained within the duct to leak out into surrounding tissue.
If the enzymes are active, they will damage the pancreas.
 Ethanol markedly but transiently depress pancreatic blood flow leading to
cellular damage by ischemia.

9. Patho-physiology
 Triggering factors result in liberation of the digestive enzymes that initiates auto-
digestion.
 Triggering factors e.g. dudeno-pancreatic reflux may result from: ERCP, Surgery,
trauma or small gall stones which splinting Sphincter of oddi. The Duodenal fluids
contains enterokinase which results in liberation & activation of the pancreatic
Proenzymes & Acute pancreatitis.
 N.B. The pancreas is normally protected from auto-digestion that may result from
liberation of digestive enzymes. The pancreas is normally storing its enzymes
in intra-cellular Zymogen granules before secreting them as Proenzymes
e.g. Trypsin is secreted as Trypsinogen & converted to Trypsin by the
action of enterokinase in the gut. Trypsin cleaves others Proenzymes & initiate
cascade of activation and auto-digestion e.g. Phospholipase and Pancreatic
lipase which result in Cell wall damage & necrosis.

10. Patho-physiology

11. Patho-physiology
 Microscopic pathology:
1)Blood stained peritoneal fluid (effusion).
2) Fat necrosis are scattered throughout the
peritoneal cavity (N.B. Pancreatic lipase liberate Fatty
acids & glycerol from fat, these fatty acids combine with
calcium to produce insoluble calcium soaps).
3) The pancreas is swollen, hemorrhagic or necrotic.
4) Suppurative pancreatitis.

12. Clinical features:
Minor attacks (75 %)
Major attacks (25 %)
 Epigastric pain (rapid onset. Severe, constant & often radiates into the back). N.B. The patient is
often sits forward.
 Vomiting (early, frequent and profuse).
 Hypovolemic shock.
 Temperature: sub-normal or mild fever.
 Jaundice (usually transient and tinge of jaundice (30 %) due to oedema of the head of the
pancreas obstructing the CBD, but deep jaundice may be stone in the CBD).
 Abdominal examination: reveals abdominal distension, generalized tenderness. Rigidity &
diminished or absent bowel sounds. In severe pancreatitis, the abdominal examination may
reveals bluish discoloration around the umbilicus (Cullen sign) or in the loins (Grey Turner's sign)
which occurs in the severe hemorrhagic pancreatitis and indicates poor prognosis.
 Major attack of Acute pancreatitis are associated with hypoxemia, ARDS, Acute renal
failure, Hyperglycaemia, hypocalcaemia (FAT SAPONOFICATION) & MOSF.
 Tetany due to hypocalcaemia (bad prognosis).

13. Differential diagnosis
 Acute Cholecystitis, Biliary Colic & Cholangitis.
 Peptic ulcer perforation.
 Acute Gastritis & Duodenal Ulcers
 High intestinal obstruction.
 Intestinal Perforation & Intra-abdominal Sepsis - Other causes of Peritonitis
 Mesenteric Artery Thrombosis.
 Dissecting Aortic aneurysm.
 Myocardial Infarction.
 Ectopic pregnancy.
 Acute Appendicitis.

14. Diagnosis
 High index of suspicious: Gall Stone Pancreatitis (previous attacks of
GSD, biliary colic, jaundice & history of fatty dyspepsia) – alcohol
pancreatitis (chronic alcoholism).
 Serum amylase= > 1000 U/L (x 3 folds of the upper limit). N.B. The
differential diagnosis of raised Serum Amylase: Acute cholecystitis,
P.P.U., high intestinal obstruction, bowel strangulation, Mesenteric Vascular
occlusion, ruptured or dissecting AAA, ruptured ectopic pregnancy, Renal
failure, Salivary stones, parotitis, severe DKA & acute alcoholic intoxication.
 Serum Lipase (more specific).
 CBC – RBS – RFT – LFT – Serum calcium – ABGs analysis.

15. INDICATIONS FOR LABORATORY & RADIOLOGICAL
TESTING

16. Diagnosis
Radiology:
 CXR: Left sided pleural effusion – ARDS.
 AXR: Gall stones (10 %). – localized ileus (Sentinel loop of the Jejunum or
Colon cut off sign.
 Abdominal USS: Swelling of the pancreas – peri-pancreatic fluid
collection & oedema – Gall stones.
 Abdominal C.T. Scan: Pancreatic & peri-pancreatic swelling – Peri-
pancreatic fluid collection & oedema – Gall stones.
 MRI – MRCP* – ERCP*.
 Gastrograffin studies: to exclude PPU.

17. Diagnosis
 Serum Amylase:
 Easiest to measure and most widely used
 Rises immediately & Remains for 3-5 days
 Peaks in few hours
 “Three fold rise is diagnostic”
 May be normal in severe attacks
 May be falsely negative in hyperlipidemic patients
 Serum lipase is more specific for pancreatitis than serum amylase

18. Diagnosis
 Radiology:
 Abdominal X-rays.
 Ultrasound of the abdomen & pelvis.
 CT- scan of the abdomen + contrast.
 Abominal X-rays:
 Sentinel loop sign : dilatation of an isolated loop of intestine (duodenum,
jejunum or transverse colon) adjacent to the pancreas
 Colon cutoff sign : A gas filled ascending and right transverse colon that
stops abruptly in the middle or left transverse colon
 All these signs are non specific

19. Diagnosis
Ultrasound can reveal:
Presence of gallstones ,
Pancreatic oedema
Extra-pancreatic duct dilatation,
Peri-pancreatic fluid collection
observation of pseudo-cysts.

20. Diagnosis
 CT-scan (signs observed in acute pancreatitis):
 focal or diffuse enlargement of the pancreas
 heterogeneous enhancement of the gland
 shaggy contour of the pancreatic margins
 thickening of fascial planes
 Intra-peritoneal or retroperitoneal fluid collections.
 Retroperitoneal air

21. USS IMAGE

22. C.T.Scan images

23. C.T.Scan images

24. ERCP IMAGES

25. MRCP IMAGES

26. IMAGINGS OF THE PANCREAS

27. Abdominal X-rays:

28. Prognosis
 Prognostic indicators:
 Serum markers: e.g. CRP***= > 140 (Severe Pancreatitis).
 C.T.Scan.
 Systemic complications.
 Prognostic scores:
 Ranson Score.
 Apache II (acute physiological and chronic health evaluation )
 Modified Glasgow Score.***

29. Glasgow Criteria for Severe Acute
Pancreatitis
 1) Age < 55 years.
 2) Glucose > 10 mmol / L. (not diabetic).
 3) TWBCC > 15.OOO .
 4) Blood Urea > 16 mmol / L. (no response to I.V. Fluid).
 5) PaO2 < 60 mmHg (respiratory insufficiency).
 6) Serum Calcium < 2 mmol / L.
 7) Albumin < 32 g / L.
 8) Lactate Dehydrogenase (LDH) > 600 I.U. / L.
 9) Aspartate Transaminase (AST) > 100 I.U. / L.
 Factors assessed within 48 hours of admission.
 3 or more positive criteria indicates Severe Pancreatitis.

30. Modified Glasgow Severity scoring system of acute
pancreatitis & RANSON SCORING SYSTEM

31. Supportive treatment
 Identification of the high risk cases, allows aggressive intensive
management in early stage.
 1) NPO & NGT aspiration (resting of the pancreas by removing stimuli of
secretion).
 2) Analgesia e.g. Pethidine (avoid Morphine= spasm of sphincter of oddi).
 3) Fluid replacement: electrolytes & fluid replacement – Colloids or Blood
transfusion (shock).
 4) Antibiotics: Gall stone Pancreatitis.
 5) PPIs (prophylaxis against stress ulcer).
 6) Nutrition.
 7) ERCP & endoscopic Sphincterotomy (Gall stone pancreatitis).

32. Surgical Treatment
 Surgery should be avoided in the early stage of the acute pancreatitis.
 Indications:
1) Infected pancreatic necrosis: Per-cutaneous drainage of the collections
or abscess (multiple drains), failure to resolve, then, operative debridement of
the necrotic pancreas (Necrosectomty) is indicated, often multistage procedure.
2) Pancreatic pseudo-cyst: operative (external or internal) drainage may
required at later stage. (N.B. SMALL PANCREATIC PSEUDO-CYST < 3 cm usually
resolves spontaneously without intervention).
3) Gall stone pancreatitis: Cholecystectomy during the same admission.
4) Laparotomy to confirm the diagnosis.
 Prognosis: mortality 10 %.

33. Complications:
 1) Abscess formation with pancreatic necrosis: (fever + persistent
Leucocytosis).
 2) Pancreatic pseudo-cyst: persistently raised serum amylase & pain +
Epigastric Swelling (usually in the 2nd
week).
 3) Hypovolemic Shock – Septic Shock – M.O.S.F.
 4) Acute renal failure.
 5) Acute pulmonary insufficiency (ARDS).
 6) G.I.T. bleeding (acute gastric erosion – P.U.).
 7) Relapsing pancreatitis – chronic pancreatitis.
 8) Diabetes mellitus.

34. Complications of Acute PANCREATITIS
Local complications
 Pancreatic phlegmon
 Pancreatic abscess
 Pancreatic pseudocyst
 Relapsing Pancreatitis - Chronic
Pancreatitis
 Pancreatic ascites - DM.
 Involvement of adjacent organs, with
hemorrhage, thrombosis, bowel infarction,
obstructive jaundice, fistula formation, or
mechanical obstruction.
Systemic complications
Pulmonary Pneumonia , atelectasis
Acute respiratory distress syndrome
Pleural effusion
Cardiovascular Hypotension
Hypovolemia
Sudden death
Non-specific ST-T wave changes
Pericardial effusion
Gastrointestinal system Gastrointestinal hemorrhage
Peptic ulcer
Erosive gastritis
Portal vein or splenic vein thrombosis with varices
Renal Oliguria
Azotemia
Renal artery/vein thrombosis
Metabolic Hyperglycemia
Hypocalcemia
Hypertriglyceridemia
Central nervous system Psychosis
Sudden blindness (Porsche's retinopathy)
Alcohol withdrawal syndrome

35. Complications of Acute PANCREATITIS

36. PANCREATIC ABSCESS & PSEUDO-CYST

37. Pancreatic Pseudo-cyst
 DEFNATION:
 A chronic collection of pancreatic fluid surrounded by a
nonepithelialized wall of granulation tissue and fibrosis is referred
to as a pseudo-cyst.
 Pseudo-cysts occur in up to 10% of patients with acute pancreatitis,
and in 20 to 38% of patients with chronic pancreatitis, and thus they
comprise the most common complication of chronic pancreatitis. In
chronic pancreatitis ((disruption of the Pancreatic duct, leads to
pancreatic duct leak with extravasation of pancreatic juice and this
results in a peri-pancreatic fluid collection (PFC))). Over a period of 3
to 4 weeks, the PFC is sealed by an inflammatory reaction that leads
to development of a wall of granulation tissue without much fibrosis.

38. Pancreatic Pseudo-cyst
 Acute pseudo-cysts may resolve spontaneously in up to
50% of cases, over a course of 6 weeks or longer.
Pseudo-cysts larger than 6 cm resolve less frequently
than smaller ones, but may regress over a period of
weeks to months. Pseudo-cysts are multiple in 17% of
patients, or may be multi-lobulated. They may occurs
intra-pancreatic or extend beyond the region of the
pancreas into other cavities or compartments.

39. Definitions of Pancreatic Fluid Collections:
 Peri-pancreatic fluid collection:
 A collection of enzyme-rich pancreatic juice which occurs early in the
course of acute pancreatitis, or which forms after a pancreatic duct leak;
located in or near the pancreas, it lacks a well organized wall of
granulation or fibrous tissue
 Early pancreatic (sterile) necrosis:
 A focal or diffuse area of non-viable pancreatic parenchyma, typically
occupying more than 30% of the gland, and containing liquefied debris
and fluid.

40. Definitions of Pancreatic Fluid Collections:
 Late pancreatic (sterile) necrosis:
 An organized collection of sterile necrotic debris and fluid with a well-
defined margin or wall within the normal domain of the pancreas
 Acute pseudo-cyst:
 A collection of pancreatic juice enclosed within a perimeter of early
granulation tissue, usually as a consequence of acute pancreatitis which
has occurred within the preceding 3–4 weeks
 Chronic pseudo-cyst:
 A collection of pancreatic fluid surrounded by a wall of normal granulation
and fibrous tissue, usually persisting for more than 6 weeks
 Pancreatic abscess:
 Any of the above in which gross purulence (pus) is present, with bacterial or
fungal organisms documented to be present

41. Pancreatic abscess:
 Pseudo-cysts may become secondarily infected, in
which case they become abscesses. They can
compress or obstruct adjacent organs or
structures, leading to superior mesenteric-portal
vein thrombosis or splenic vein thrombosis. They
can erode into visceral arteries and cause intra-
cystic hemorrhage or pseudo-aneurysms . They also
can perforate and cause peritonitis or intra-
peritoneal bleeding.

42. treatment of pancreatic pseudo-cyst:
 Pseudo-cysts usually cause symptoms of pain, fullness, or early
satiety. Asymptomatic pseudo-cysts can be managed expectantly, and
may resolve spontaneously or persist without complication. Symptomatic or
enlarging pseudo-cysts require treatment. Pseudo-cysts can resemble
Cysta-denoma and cyst-adenocarcinoma radio- graphically thus, an
incidentally discovered cystic lesion should be examined by EUS and
aspirated to determine whether it is a true neoplasm or a pseudo-cyst.
 If infection is suspected, the pseudo-cyst should be aspirated (not
drained) by CT- or US-guided fine-needle aspiration, and the contents
examined for organisms by Gram's stain and culture. If infection is
present, and the contents resemble pus, external drainage is
employed using either surgical or percutaneous techniques.

43. treatment of pancreatic pseudo-cyst:
 If the pseudo-cyst has failed to resolve with
conservative therapy and symptoms persist,
internal drainage is usually preferred to
external drainage, to avoid the complications of a
pancreatico-cutaneous fistula. Pseudo-cysts
communicate with the pancreatic ductal system in
up to 80% of cases, so external drainage creates a
pathway for pancreatic duct leakage to and
through the catheter exit site.

44. treatment of pancreatic pseudo-cyst:
 Internal drainage may be performed with either percutaneous
catheter-based methods (trans-gastric puncture and stent placement to
create a Cysto-gastrostomy), endoscopic methods (trans-gastric or trans-
duodenal puncture and multiple stent placements, with or without a Naso-
cystic irrigation catheter), or surgical methods (a true cysto-enterostomy,
biopsy of cyst wall, and evacuation of all debris and contents).
 Because pseudo-cysts often communicate with the pancreatic ductal
system, two newer approaches to pseudo-cyst management are based on
main duct drainage, rather than pseudo-cyst drainage per se. Trans-
papillary stents inserted at the time of ERCP may be directed into a
pseudo-cyst through the ductal communication itself.