ACUTE PANCREATITIS
DR (BRIG) P KRISHNA MURTHY
PROFESSOR OF GENERAL SURGERY
ACUTE PANCREATITIS
PANCREATITIS
● Pancreatitis is inflammation of the pancreatic parenchyma.
● For clinical purposes, it is useful to divide pancreatitis into acute, which presents as an
emergency, and chronic, which is a prolonged and frequently lifelong disorder resulting
from the development of fibrosis within the pancreas. It is possible that acute and chronic
pancreatitis are different phases of the same process
● ACUTE PANCREATITIS:
● Acute pancreatitis is defined as an acute condition presenting with
abdominal pain, a threefold or greater rise in the serum levels of the
pancreatic enzymes amylase or lipase and/or characteristic findings of
pancreatic inflammation on contrast-enhanced CT. Acute pancreatitis
may recur.
PATHOGENESIS OF ACUTE PANCREATITIS
● The underlying mechanism of injury in pancreatitis is thought to be premature activation
of pancreatic enzymes within the pancreas, leading to a process of autodigestion
● Anything that injures the acinar cells and impairs the secretion of zymogen granules or
damages the duct epithelium, and thus delays enzymatic secretion, can trigger acute
pancreatitis.
● Once cellular injury has been initiated, the inflammatory process can lead to pancreatic
oedema , haemorrhage and, eventually, necrosis. As inflammatory mediators are released
into the circulation, systemic complications can arise, such as haemodynamic instability,
bacteraemia (due to translocation of gut flora), acute respiratory distress syndrome and
pleural effusions, gastrointestinal haemorrhage, renal failure and disseminated
intravascular coagulation (DIC).
● Immunolocalization studies have shown that after 15 minutes of pancreatic
injury, both zymogen granules and lysosomes colocalize inside the acinar cells.
● The fact that zymogen and lysosome colocalization occurs before amylase level
elevation, pancreatic edema, and other markers of pancreatitis are evident
suggests that colocalization is an early step in the pathophysiologic process and
not a consequence of pancreatitis.
● Studies also suggest that lysosomal enzyme cathepsin B activates trypsin in these
colocalization organelles. In vitro and in vivo studies have elucidated an intricate
model of acinar cell death induced by premature activation of trypsin. In this
model, once cathepsin B in lysosomes and trypsinogen in zymogen granules are
brought in contact by colocalization induced by pancreatitis-inciting stimuli,
activated trypsin then induces leak of colocalized organelles, releasing cathepsin
B into the cytosol. It is the cytosolic cathepsin B that then induces apoptosis or
necrosis, leading to acinar cell death.
Etiological Factor (Alcohol / Gallstones / Others)
↓
Acinar Cell Injury OR Duct Obstruction
↓
Premature Enzyme Activation (Trypsinogen → Trypsin)
↓
Autodigestion of Pancreas
↓
Local Inflammation + Cytokine Release
↓
Systemic Inflammatory Response (SIRS)
↓
Multi-organ Dysfunction (ARDS, AKI, Shock)
● Acute pancreatitis may be categorised as mild (interstitial oedematous
pancreatitis) or severe (necrotising pancreatitis).
● MILD is characterised by interstitial oedema of the gland and minimal organ
dysfunction. The majority of patients will have a mild attack of pancreatitis,
the mortality from which is around 1%.
● SEVERE acute pancreatitis is seen in 5-10% of patients and is characterised
by pancreatic necrosis, a severe systemic inflammatory response and often
multiorgan failure.
● In those who have a severe attack of pancreatitis, the mortality varies from
20% to 50%.
POSSIBLE CAUSES OF ACUTE PANCREATITIS
1. Gallstones
2. Alcoholism
3. Post ERCP
4. Abdominal trauma
5. Following biliary, upper gastrointestinal or cardiothoracic surgery
6. Ampullary tumour
7. Drugs (corticosteroids, azathioprine, asparaginase, valproic acid, thiazides,
oestrogens)
8. Hyperparathyroidism
9)Hypercalcemia
10)Hypertriglyceridemia
11)Sphincter of Oddi dysfunction
12)Autoimmune pancreatitis
13)Hereditary pancreatitis
14)Viral infection
15)Malnutrition
16)Scorpion bite
17)Idiopathic
ETIOPATHOGENESIS
● The two major causes of acute pancreatitis are biliary calculi, which occur
in 50-70% of patients, and alcohol abuse, which accounts for 25% of cases.
● Gallstone pancreatitis is thought to be triggered by the passage of gallstones
down the common bile duct. If the biliary and pancreatic ducts join to share
a common channel before ending at the ampulla, then obstruction of this
passage may lead to reflux of bile or activated pancreatic enzymes into the
pancreatic duct. Patients who have small gallstones and a wide cystic duct
may be at a higher risk of passing stones.
● The proposed mechanisms for alcoholic pancreatitis include the effects of diet,
malnutrition, direct toxicity of alcohol, concomitant tobacco smoking,
hypersecretion, duct obstruction or reflux, and hyperlipidaemia.
● The remaining cases may be due to rare causes or may be idiopathic.
● Among patients who undergo ERCP, 1-3% develop pancreatitis, probably as
a consequence of duct disruption and enzyme extravasation.
● Patients with sphincter of Oddi dysfunction or a history of recurrent
pancreatitis, and those who undergo sphincterotomy or balloon dilatation of
the sphincter, carry a higher risk of developing post-ERCP pancreatitis.
● Patients who have undergone upper abdominal or cardiothoracic surgery may
develop acute pancreatitis in the postoperative phase, as may those who have
suffered blunt abdominal trauma
● Hereditary pancreatitis is a rare familial condition associated with mutations of the
cationic trypsinogen gene. Patients have a tendency to suffer acute pancreatitis
while in their teens, progress to chronic pancreatitis in the next two decades and
have a high risk (possibly up to 40%) of developing pancreatic cancer by the age of
70 years. Hypertriglyceridemia should be excluded.
● Occasionally; tumours at the ampulla of Vater may cause acute pancreatitis, It is
important to check the serum calcium level, a fasting lipid profile, autoimmune
markers and viral titres in patients with so-called idiopathic acute pancreatitis.
● It is equally important to take a detailed drug history and remember the association
of corticosteroids, azathioprine, asparaginase and valproic acid with acute
pancreatitis, Statins (taken over a long time) and gliptins have been linked with
pancreatitis, but the evidence is slim.
● It is essential to exclude tiny gallstones.
CLINICAL FEATURES
● Pain is the cardinal symptom. It characteristically develops quickly, reaching
maximum intensity within minutes rather than hours and persists for hours or
even days.
● Pain is usually experienced first in the epigastrium but may be localised to
either upper quadrant or felt diffusely throughout the abdomen. There is
radiation to the back in about 50% of patients, and some patients may gain
relief by sitting or leaning forwards.
● The suddenness of onset may simulate a perforated peptic ulcer, while biliary
colic or acute cholecystitis can be mimicked if the pain is maximal in the
right upper quadrant.
● Radiation to the chest can simulate myocardial infarction, pneumonia or
pleuritic pain. In fact, acute pancreatitis can mimic most causes of the acute
abdomen
● Nausea, repeated vomiting and retching are usually marked. The retching
may persist despite the stomach being kept empty by nasogastric aspiration.
Hiccoughs can be troublesome and may be due to gastric distension or
irritation of the diaphragm
● On examination, the appearance may be that of a patient who is well or, at
the other extreme, one who is gravely ill with profound shock, toxicity and
confusion. Tachypnoea is common, tachycardia is usual and hypotension
may be present.
● The body temperature is often normal or even subnormal, but frequently rises
as inflammation develops.
● It is useful to reiterate here that SIRS is defined by the presence of two or
more of the following criteria: heart rate > 90/min, core temperature <36°C
or >38°C, respirations >20/min or PCO, <32 mmHg, and white blood cell
count <4000 or >12 000/mm3
● Mild icterus can be caused by biliary obstruction in gallstone pancreatitis,
and an acute swinging pyrexia suggests cholangitis.
● Bleeding into the fascial planes can produce bluish discoloration of the flanks
(Grey Turner's sign) or umbilicus (Cullen's sign). Subcutaneous fat necrosis
may produce small, red, tender nodules on the skin of the legs
● Abdominal examination may reveal distension due to ileus or, more rarely,
ascites with shifting dullness. A mass can develop in the epigastrium owing
to inflammation.
● There is usually muscle guarding in the upper abdomen, although marked
rigidity is unusual.
● A pleural effusion is present in 10-20% of patients.
● Pulmonary oedema and pneumonitis are also described and may give rise to
the differential diagnosis of pneumonia or myocardial infarction.
● The patient may be confused and exhibit the signs of metabolic derangement
together with hypoxaemia
Atlanta Classification of Acute Pancreatitis Revised
1. Based on Severity:
MILD- No organ failure, no local or systemic complications
MODERATELY SEVERE - Transient organ failure (<48 hrs), and/or local or
systemic complications without persistent organ failure
SEVERE- Persistent organ failure (>48 hrs), may involve one or more organs
2. Based on Morphology (CT/Imaging):
INTERSTITIAL EDEMATOUS PANCREATITIS :
• Most common form.
• Enlargement of the pancreas due to inflammation and edema.
• No tissue necrosis.
NECROTIZING PANCREATITIS:
• Presence of pancreatic parenchymal necrosis and/or peripancreatic necrosis.
• Usually seen after several days.
3. Local Complications:
ACUTE PERIPANCREATIC FLUID COLLECTION(APFC)-
No necrosis, occurs early (<4 weeks) in interstitial pancreatitis
PANCREATIC PSEUDOCYST -
Encapsulated fluid collection >4 weeks , no necrosis
ACUTE NECROTIC COLLECTION (ANC)-
Seen in necrotizing pancreatitis, unorganized collection (<4 weeks)
WALLED- OFF NECROSIS (WON)-
Organized necrotic collection >4-weeks with well-defined wall
COMPLICATIONS
● Systemic complications
● • Shock
● • Acute lung injury
● • Acute renal failure
● • Disseminated intravascular coagulation
● • Local Complications
● Sterile and infected peripancreatic fluid collections
● • Pancreatic necrosis and infected necrosis
● • Pancreatic abscess
● • Pancreatic pseudocysts
● Pancreatic ascites
On table photos of acute pancreatitis. Note the typical
saponification in the omentum and mesentery.
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