teaching classes for MBBS students.

1. 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.

2. Chronic pancreatitis is defined as a continuing inflammatory disease of the
pancreas characterized by irreversible morphological change typically causing pain
and/or permanent loss of function. Many patients with chronic pancreatitis have
painful exacerbations, but the condition may be completely painless.

3. 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. 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. 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.
Acute pancreatitis

4. Once cellular injury has been initiated, the inflammatory process can
lead to pancreatic oedema, hemorrhage and, eventually, necrosis.
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). Acute
pancreatitis may be categorized as mild (interstitial edematous
pancreatitis) or severe (necrotizing pancreatitis).

6. Management
If after initial assessment a patient is considered to have a mild attack of
pancreatitis, a conservative approach is indicated, guided by frequent
measurement of vital signs, urine output and central venous pressure.
However, if a stable patient meets the prognostic criteria for a severe attack of
pancreatitis, then a more aggressive approach is required, with admission to a
high-dependency or intensive care unit and invasive monitoring

7. If gallstones are the cause of an attack of predicted or proven severe
pancreatitis, or if the patient has jaundice, cholangitis or a dilated
common bile duct, ERCP should be carried out within 72 hours of the
onset of symptoms as sphincterotomy and clearance of the bile duct
can reduce the incidence of infective complications.

8. Clinical presentation
Pain is the cardinal symptom. It characteristically develops quickly, reaching
maximum intensity within minutes rather than hours and persists for hours or
even days. The pain is frequently severe, constant and refractory to the usual
doses of analgesics. Pain is usually experienced first in the epigastrium but may
be localized 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.

9. Pancreatitis can mimic multiple other conditions like peptic perforation, biliary colic
and acute cholecystitis, myocardial infarction, pneumonia or pleuritic pain. In fact,
acute pancreatitis can mimic most causes of the acute abdomen and should seldom be
discounted in differential diagnosis.
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.

10. 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.
Systemic inflammatory reaction syndrome (SIRS) may develop with it’s
consequences.

11. Investigations
Typically, the diagnosis is made on the basis of the clinical presentation
and an elevated serum amylase level. A serum amylase level three times
above normal is indicative of the disease. . If there is doubt, and other
causes of acute abdomen have to be excluded, contrast-enhanced CT is the
best single imaging investigation.

12. Assessment of severity
The Ranson and Glasgow scoring systems are specific for acute
pancreatitis, and a score of 3 or more at 48 hours indicates a severe
attack. Several other systems that are used in intensive care units can
also be applied. These include the APACHE, SAPS, SOFA, MODS and
modified Marshall scoring systems (the latter has the advantage of
simplicity).

13. Regardless of the system used, persisting organ failure indicates a
severe attack. A serum C-reactive protein level >150 mg/L at 48 hours
after the onset of symptoms is also an indicator of severity. Patients
with a body mass index over 30 are at higher risk of developing
complications.

14. Atlanta classification of acute
pancreatitis (1992)
● Mild acute pancreatitis:
● no organ failure;
● no local or systemic complications.
● Moderately severe acute pancreatitis:
● organ failure that resolves within 48 hours (transient
organ failure); and/or
● local or systemic complications without persistent organ
failure.

15. ● Severe acute pancreatitis:
● persistent organ failure (>48 hours).
● single organ failure.
● multiple organ failure.

16. Systemic complications
Pancreatitis may involve all organ systems, (MODS being the end result) and
should be managed by a multidisciplinary team including intensive care
specialists. When there is organ failure, appropriate supportive therapies may
include inotropic support for hemodynamic instability, hemofiltration in the
event of renal failure, ventilatory support for respiratory failure and
correction of coagulopathies (including DIC). Surgery has no role during the
initial period of resuscitation and stabilization and is reserved for the patient
who deteriorates following successful stabilization.

17. Local complications
Acute peripancreatic fluid collection:
Acute peripancreatic fluid collection (APFC) occurs early in the
course of mild pancreatitis without necrosis and is located
adjacent to the pancreas. It has no encapsulating wall (so it is
a pseudocyst). Resolutions may occur spontaneously.

18. Sterile and infected pancreatic necrosis:
The term ‘pancreatic necrosis’ refers to a diffuse or focal area of non-
viable parenchyma. This can be identified by an absence of parenchymal
enhancement on CT with intravenous contrast. Pancreatic necrosis is
typically associated with lysis of peripancreatic fat.

19. This may lead to an acute necrotic collection (ANC). This is typically an
intra- or extra pancreatic collection containing fluid and necrotic
material, with no definable wall. Gradually, over a period of over 4
weeks, this may develop a well-defined inflammatory capsule and
evolve into walled-of necrosis (WON).

20. Collections associated with necrotizing pancreatitis are sterile to
begin with but often become subsequently infected, probably because
of translocation of gut bacteria. Infected necrosis is associated with a
mortality rate of up to 50%. Sterile necrotic material should not be
drained or interfered with..

21. However, if the patient shows signs of sepsis, then one should determine
whether the collection is infected. Aspiration fluid with a fine needle,
percutaneously under CT or ultrasound guidance, can provide the answer.
If the aspirate is purulent, drainage of the infected fluid should be
carried out.

22. Pancreatic necrosectomy should be considered if sepsis worsens despite
conservative measures. This is a challenging operation that carries a high
morbidity and mortality; it is best carried out in a specialist unit and is
necessary only in a very small proportion of patients.

24. Pancreatic abscess:
This is a circumscribed intra-abdominal collection of pus, usually in
proximity to the pancreas. It may be an ANC or a WON that has
become infected. The principles of diagnosis and management are
as outlined above for infected pancreatic necrosis.

25. Pancreatic effusion:
This is an encapsulated collection of fluid in the pleural cavity, arising as a
consequence of acute pancreatitis. Concomitant pancreatic ascites may be
present or there may be a communication with an intra-abdominal
collection. Percutaneous drainage under imaging guidance is necessary.

26. Hemorrhage:
Bleeding may occur into the gut, the retroperitoneum or peritoneal cavity.
Possible causes include bleeding into a pseudocyst cavity, diffuse bleeding from
a large raw surface or a pseudoaneurysm. The last is a false aneurysm of a
major peripancreatic vessel. Recurrent bleeding is common, often culminating
in fatal hemorrhage. CT, angiography or magnetic resonance angiography helps
to make the diagnosis. Treatment involves embolization or surgery.

27. Portal or splenic vein thrombosis:
This may develop silently and is identified on a CT scan. A marked rise in
the platelet count should raise suspicions. In the context of acute
pancreatitis, treatment is usually conservative. If varices or other
manifestations of portal hypertension develop, they will require treatment,
such as endoscopic injection or banding, β-blockade, etc.

28. Pseudocyst:
A pseudocyst is a collection of amylase-rich fluid enclosed in a well-defined
wall of fibrous or granulation tissue. Pseudocysts typically arise following an
attack of mild acute pancreatitis, lie outside the pancreas and represent an
APFC that has not resolved and matured. Formation of a pseudocyst requires
4 weeks or more from the onset of acute pancreatitis. More than half have a
communication with the main pancreatic duct. Pseudocysts are often single
but are occasionally multiple.

29. Pseudocysts usually resolve spontaneously, but complications can develop.
Pseudocysts that are thick walled or large (>6 cm in diameter), have lasted for a
long time (over 12 weeks) or have arisen in the context of chronic pancreatitis
are less likely to resolve spontaneously. Therapeutic intervention is advised only
if the pseudocyst causes symptoms.

30. Outcomes and follow-up of acute pancreatitis:
The overall mortality from acute pancreatitis has remained at 10–15% over
the past 20 years. There is a clear responsibility before the patient is
discharged to determine the etiology of the attack of pancreatitis and the
causes must be looked for and excluded. Failure to remove a predisposing
factor could lead to a second attack of pancreatitis, which could be fatal.

32. Chronic pancreatitis
Chronic pancreatitis is a progressive inflammatory disease in which there is
irreversible destruction of pancreatic tissue. Its clinical course is characterized by
severe pain and, in the later stages, exocrine and endocrine pancreatic
insufficiency. In the early stages of its evolution, it is frequently complicated by
attacks of acute pancreatitis.
In southern India, the prevalence is 100–200 per 100 000. The disease occurs more
frequently in men (male to female ratio of 4:1) and the mean age of onset is about
40 years.

33. High alcohol consumption is the most frequent cause of chronic pancreatitis,
accounting for 60–70% of cases, but only 5–10% of people with alcoholism
develop chronic pancreatitis. The exact mechanism of how alcohol causes
chronic inflammation in these patients is unclear; genetic and metabolic
factors may be at play.

34. There are other causes of chronic pancreatitis like stricture formation after
trauma or operations, following acute pancreatitis and congenital causes like
annular pancreas. Other causes are Hereditary pancreatitis, CF, infantile
malnutrition and a large unexplained idiopathic group. Hereditary pancreatitis is
an autosomal dominant disorder with an 80% penetrance; it is associated with a
gain-of function mutation in the cationic trypsinogen gene (PRSS1) on
chromosome 7, which leads to production of a degradation resistant form of
trypsin .

35. Autoimmune pancreatitis has been described relatively recently. Features
include diffuse enlargement of the pancreas and diffuse and irregular
narrowing of the main pancreatic duct. It may occur in association with
other autoimmune diseases, as a multisystem disorder, or may affect the
pancreas alone.

36. At the onset of the disease when symptoms have developed, the pancreas
may appear normal. Later, the pancreas enlarges and becomes hard as a
result of fibrosis. The ducts become distorted and dilated with areas of both
stricture formation and ectasia. Calcified stones weighing from a few
milligrams to 200mg may form within the duct.
Histologically, the lesions affect the lobules, producing ductular metaplasia
and atrophy of acini, hyperplasia of duct epithelium and interlobular
fibrosis.

37. Clinical features
Pain is the outstanding symptom in the majority of patients. The site of pain
depends to some extent on the main focus of the disease. If the disease is
mainly in the head of the pancreas then epigastric and right subcostal pain is
common, whereas if it is limited to the left side of the pancreas left subcostal
and back pain are the presenting symptoms. In some patients, the pain is more
diffuse. Radiation to the shoulder can occur. Nausea is common during attacks
and vomiting may occur. The pain is often dull and gnawing. Severe fare-ups of
pain may be superimposed on background discomfort.

38. All the complications of acute pancreatitis can occur with chronic
pancreatitis. Weight loss is common because the patient does not feel like
eating. The patient’s lifestyle is gradually destroyed by pain, analgesic
dependence, weight loss and inability to work. Loss of exocrine function
leads to steatorrhea in more than 30% of patients with chronic pancreatitis.
Loss of endocrine function and the development of diabetes are not
uncommon, and the incidence increases as the disease progresses.

39. Investigations
Only in the early stages of the disease will there be a rise in serum amylase.
Pancreatic calcifications may be seen on abdominal radiographs. CT or MRI scan
will show the outline of the gland, the main area of damage and the
possibilities for surgical correction. Calcification is seen very well on CT but not
on MRI. An MRCP will identify the presence of biliary obstruction and the state
of the pancreatic duct. The use of intravenous secretin during the study may
demonstrate a pancreatic duct stricture not apparent on standard MRCP, but a
normal-looking pancreas on CT or MRI does not rule out chronic pancreatitis.

40. ERCP is the most accurate way of elucidating the anatomy of the duct and,
in conjunction with the whole organ morphology, can help to determine the
type of operation required, if operative intervention is indicated.
Histologically proven chronic pancreatitis can, however, occur in the
setting of normal findings on pancreatography. Sonographic findings
characteristic of chronic pancreatitis include the presence of stones,
visible side branches, cysts, globularity, an irregular main pancreatic duct,
hyperechoic foci and strands, dilatation of the main pancreatic duct and
hyperechoic margins of the main pancreatic duct.

43. Treatment
Most patients can be managed with medical measures. Endoscopic,
radiological or surgical interventions are indicated mainly to relieve
obstruction of the pancreatic duct, bile duct or the duodenum, or in dealing
with complications. Endoscopic pancreatic sphincterotomy might be
beneficial in patients with papillary stenosis and a high sphincter
pressure and pancreatic ductal pressure.

44. The role of surgery is to overcome obstruction and remove mass lesions. Some
patients have a mass in the head of the pancreas, for which either a
pancreatoduodenectomy or a Beger procedure (duodenum-preserving resection of
the pancreatic head) is appropriate. If the duct is markedly dilated, then a
longitudinal pancreatojejunostomy or Frey procedure can be of value.

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