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Pancreatitis is defined as inflammation of the pancreas. It has several causes and symptoms
and requires immediate medical attention. It may be acutebeginning suddenly and lasting a
few days, or chronicoccurring over many years .Acute pancreatitis is seen infrequently as a
medical or surgical emergency in India. Chronic pancreatitis accounts for a significant
proportion of malabsorption syndrome. Chronic calcific pancreatitis with secondary diabetes is
seen in some endemic areas, especially in Kerala. Pancreatitis is closely associated with
alcoholism and biliary tract disease. Another one type of pancreatitis is autoimmune pancreatitis
it is a form of chronic pancreatitis caused by autoimmune inflammation

Acute pancreatitis has been defined as an acute inflammatory process of the pancreas with
variable involvement of other regional tissues or remote organ systems. In mild disease when organ
dysfunction is minimal prognosis for recovery is good. In severe disease there are local lesions such as
necrosis, abscess or pseudocyst formation and systemic complications such as respiratory distress, shock,
gastrointestinal bleeding, renal failure and others.

Long-standing alcohol consumption and biliary stone disease cause most cases of acute
pancreatitis, but numerous other etiologies are known. In 10-30% of cases, the cause is
unknown, though studies have suggested that as many as 70% of cases of idiopathic pancreatitis
are secondary to biliary microlithiasis.
Biliary tract disease
One of the most common causes of acute pancreatitis in most developed countries (accounting
for approximately 40% of cases) is gallstones passing into the bile duct and temporarily lodging
at the sphincter of Oddi. The risk of a stone causing pancreatitis is inversely proportional to its
It is thought that acinar cell injury occurs secondary to increasing pancreatic duct pressures
caused by obstructive biliary stones at the ampulla of Vater, although this has not been
definitively proven in humans. Occult microlithiasis is probably responsible for most cases of
idiopathic acute pancreatitis.

Alcohol use is a major cause of acute pancreatitis (accounting for at least 35% of cases). At the
cellular level, ethanol leads to intracellular accumulation of digestive enzymes and their
premature activation and release. At the ductal level, it increases the permeability of ductules,
allowing enzymes to reach the parenchyma and cause pancreatic damage. Ethanol increases the
protein content of pancreatic juice and decreases bicarbonate levels and trypsin inhibitor
concentrations. This leads to the formation of protein plugs that block pancreatic outflow.
Most commonly, the disease develops in patients whose alcohol ingestion is habitual over
5-15 years. Alcoholics are usually admitted with an acute exacerbation of chronic pancreatitis.
Occasionally, however, pancreatitis can develop in a patient with a weekend binging habit, and
several case reports have described a sole large alcohol load precipitating a first attack.
Nevertheless, the alcoholic who imbibes routinely remains the rule rather than the exception.
Currently, there is no universally accepted explanation for why certain alcoholics are more
predisposed to developing acute pancreatitis than other alcoholics who ingest similar quantities.
Endoscopic retrograde cholangiopancreatography
Pancreatitis occurring after endoscopic retrograde cholangiopancreatography (ERCP) is
probably the third most common type (accounting for approximately 4% of cases). Whereas
retrospective surveys indicate that the risk is only 1%, prospective studies have shown the risk to
be at least 5%.
The risk of post-ERCP acute pancreatitis is increased if the endoscopist is inexperienced, if
the patient is thought to have sphincter of Oddi dysfunction, or if manometry is performed on the
sphincter of Oddi. No medical measures, with the exception of aggressive preintervention
intravenous (IV) hydration, have been durably shown to prevent post-ERCP pancreatitis in
randomized studies.
Abdominal trauma (approximately 1.5%) causes an elevation of amylase and lipase levels in
17% of cases and clinical pancreatitis in 5% of cases. Pancreatic injury occurs more often in
penetrating injuries (eg, from knives, bullets) than in blunt abdominal trauma (eg, from steering
wheels, horses, bicycles). Blunt injury to the abdomen or back may crush the gland across the
spine, leading to a ductal injury.

Considering the small number of patients who develop pancreatitis compared to the relatively
large number who receive potentially toxic drugs, drug-induced pancreatitis is a relatively rare
occurrence (accounting for approximately 2% of cases) that is probably related to an unknown
predisposition. Fortunately, drug-induced pancreatitis is usually mild.
Drugs definitely associated with acute pancreatitis include the following:

Valproic acid,
5-aminosalicylic acid compounds

In addition, there are many drugs that have been reported to cause acute pancreatitis in
isolated or sporadic cases.

Less common causes

The following causes each account for less than 1% of cases of pancreatitis.


Several infectious diseases may cause pancreatitis, especially in children. These cases of
acute pancreatitis tend to be milder than cases of acute biliary or alcohol-induced

Viral causes include mumps virus, coxsackievirus, cytomegalovirus (CMV), hepatitis

virus, Epstein-Barr virus (EBV), echovirus, varicella-zoster virus (VZV), measles virus,

and rubella virus. Bacterial causes include Mycoplasma pneumoniae, Salmonella,

Campylobacter, and Mycobacterium tuberculosis. Worldwide, Ascarisis a recognized
cause of pancreatitis resulting from the migration of worms in and out of the duodenal

Pancreatitis has been associated with AIDS; however, this may be the result of
opportunistic infections, neoplasms, lipodystrophy, or drug therapies.

Hereditary pancreatitis

Hereditary pancreatitis is an autosomal dominant gain-of-function disorder related to

mutations of the cationic trypsinogen gene (PRSS1), which has an 80% penetrance.
Mutations in this gene cause premature activation of trypsinogen to trypsin.

In addition, the CFTR mutation plays a role in predisposing patients to acute pancreatitis
by causing abnormalities of ductal secretion. At present, however, the phenotypic
variability of patients with the CFTR mutation is not well understood. Certainly, patients
homozygous for the CFTR mutation are at risk for pancreatic disease, but it is not yet
clear which of the more than 800 mutations carries the most significant risk. In addition,
the role of CFTR heterozygotes in pancreatic disease is unknown.

Mutations in the SPINK1 protein, which blocks the active binding site of trypsin,
rendering it inactive, also probably play a role in causing a predisposition to acute

This probably explains the predisposition, rather than the cause, of acute pancreatitis in
these patients. If enough mutant enzymes become activated intracellularly, they can
overwhelm the first line of defense (ie, pancreatic secretory trypsin inhibitor) and resist
backup defenses (ie, proteolytic degradation by mesotrypsin, enzyme Y, and trypsin
itself). Activated mutant cationic trypsin can then trigger the entire zymogen activation


Hypercalcemia from any cause can lead to acute pancreatitis. Causes include
hyperparathyroidism, excessive doses of vitamin D, familial hypocalciuric
hypercalcemia, and total parenteral nutrition (TPN). Routine use of automated serum
chemistries has allowed earlier detection and reduced the frequency of hypercalcemia
manifesting as pancreatitis.

Developmental abnormalities of pancreas

The pancreas develops from 2 buds stemming from the alimentary tract of the developing
embryo. There are 2 developmental abnormalities commonly associated with
pancreatitis: pancreas divisum and annular pancreas.

Pancreas divisum is a failure of the dorsal and ventral pancreatic ducts to fuse during
embryogenesis. Probably a variant of normal anatomy, it occurs in approximately 5% of
the population (see the images below); in most cases, it may actually protect against
gallstone pancreatitis. It appears that the presence of stenotic minor papillae and an
atretic duct of Santorini are additional risk factors that together contribute to the
development of acute pancreatitis through an obstructive mechanism (although this is

Annular pancreas is an uncommon congenital anomaly in which a band of pancreatic

tissue surrounds the second part of the duodenum. Usually, it does not cause symptoms
until later in life. This condition is a rare cause of acute pancreatitis, probably through an
obstructive mechanism.

Sphincter of Oddi dysfunction can lead to acute pancreatitis by causing increased

pancreatic ductal pressures. However, the role of pancreatitis induced by such
dysfunction in patients without elevated sphincter pressures on manometry remains


Clinically significant pancreatitis usually does not occur until a persons serum
triglyceride level reaches 1000 mg/dL. It is associated with type I and type V
hyperlipidemia. Although this view is somewhat controversial, most authorities believe
that the association is caused by the underlying derangement in lipid metabolism rather
than by pancreatitis causing hyperlipidemia. This type of pancreatitis tends to be more
severe than alcohol- or gallstone-induced disease.


Obstruction of the pancreatic ductal system by a pancreatic ductal carcinoma, ampullary

carcinoma, islet cell tumor, solid pseudotumor of the pancreas, sarcoma, lymphoma,
cholangiocarcinoma, or metastatic tumor can cause acute pancreatitis. The chance of
pancreatitis occurring when a tumor is present is approximately 14%. Pancreatic cystic
neoplasm, such as intraductal papillary-mucinous neoplasm (IPMN), mucinous
cystadenoma, or serous cystadenoma, can also cause pancreatitis.


Exposure to organophosphate insecticide can cause acute pancreatitis. Scorpion and

snake bites may also be causative; in Trinidad, the sting of the scorpion Tityus trinitatis is
the most common cause of acute pancreatitis. Hyperstimulation of pancreas exocrine
secretion appears to be the mechanism of action in both instances.

Surgical procedures

Acute pancreatitis may occur in the postoperative period of various surgical procedures
(eg, abdominal or cardiopulmonary bypass surgery, which may damage the gland by
causing ischemia). Postoperative acute pancreatitis is often a difficult diagnosis to
confirm, and it has a higher complication rate than pancreatitis associated with other
etiologies. The mechanism is unclear.

Vascular abnormalities

Vascular factors, such as ischemia or vasculitis, can play a role in causing acute
pancreatitis. Vasculitis can predispose patients to pancreatic ischemia, especially in those
with polyarteritis nodosa and systemic lupus erythematosus.

In Pancreas acinar cell is highly compartmentalized and is concerned with the secretion of
pancreatic enzymes. Proteins synthesized by the rough endoplasmic reticulum are processed in
the Golgi and then targeted to the appropriate site, whether that be zymogen granules,
lysosomes, or other cell compartments. The pancreas secretes amylolytic, lipolytic, and
proteolytic enzymes. Amylolytic enzymessuch as amylase, hydrolyze starch to oligosaccharides
and to thedisaccharide maltose. The lipolytic enzymes include lipase, phospholipaseA 2 , and
cholesterol esterase.p roteolytic enzymes includeendopeptidases (trypsin, chymotrypsin), which
act on internalpeptide bonds of proteins and polypeptides; exopeptidases
The nervous systeminitiates pancreatic enzyme secretion. The neurologic stimulationis
cholinergic, involving extrinsic innervation by the vagus nerve and subsequent innervation by

intrapancreatic cholinergic nerves.The stimulatory neurotransmitters are acetylcholine and

Normally Autodigestion of the pancreas is prevented by the packaging of pancreatic
proteases in precursor form and by the synthesis of proteaseinhibitor [i.e.,pancreatic secretory
trypsin inhibitor (PSTI)or SPINK1], which can bind and inactivate about 20% of trypsin activity.
Mesotrypsin, chymotrypsin c, and enzyme y can also lyse and inactivate trypsin. These protease
inhibitors are found in the acinar cell, the pancreatic secretions, and the 1 - and 2
-globulinfractions of plasma. In addition, low calcium concentration within the cytosol of acinar
cells in the normal pancreas promotes the destruction of spontaneously activated trypsin
Due to etiological features , The inactive precursors of proteolytic enzymes are activated by
regurgitated bile, viral infections, ischemia, anoxia, trauma or toxins, within the pancreas.the
effects of activated proteolytic enzymes and cytokines, released by the inflamedpancreas, on
distant organs. Activated proteolytic enzymes, especially trypsin, not only digest pancreatic and
peripancreatic tissues but also activate other enzymes such as elastase and phospholipase A 2 .
The active enzymes and cytokines then digest cellular membranes and cause proteolysis, edema,
interstitial hemorrhage, vasculardamage, coagulation necrosis, fat necrosis, and parenchymal cell
necrosis. Cellular injury and death result in the liberation of bradykinin peptides, vasoactive
substances, and histamine that can produce vasodilation, increased vascular permeability, and
edema with profound effects on many organs, most notably the lung. The systemic inflammatory
response syndrome (SIRS) and acute respiratorydistress syndrome (ARDS) as well as
multiorgan failure may occur as a result of this cascade of local as well as distant effects


The cardinal symptom of acute pancreatitis is abdominal pain, which is characteristically
dull, boring, and steady. Usually, the pain is sudden in onset and gradually intensifies in severity
until reaching a constant ache. Most often, it is located in the upper abdomen, usually in the
epigastric region, but it may be perceived more on the left or right side, depending on which
portion of the pancreas is involved. The pain radiates directly through the abdomen to the back
in approximately one half of cases . The pain is frequently more intense when the patient is
supine, and patients may obtain some relief by sitting with the trunk flexed and knees drawn up.
Nausea, vomiting, and abdominal distention due to gastric and intestinal hypomotility and
chemical peritonitis are also frequent complaints
Nausea and vomiting are often present along with accompanying anorexia. Diarrhea can also
occur. Positioning can be important, because the discomfort frequently improves with the patient
in the supine position. The patient adopts a stooping posture with pressure on the abdomen to get
An alcoholic bout or heavy eating may precipitate the attack. f. Nausea, vomiting,
dehydration, and signs of shock occur in severe cases. Mild jaundice may be present in a few
cases. Erythematous skin nodules may form due to fat necrosis. Secondary pleural effusion may
develop on the left side.

Any severe acute pain in the abdomen or back should suggest the possibility acute
pancreatitis. The diagnosis is usually entertained when a patient with a possible predisposition to
pancreatitis presents with severe and constant abdominal pain, frequently associated with
nausea, emesis, fever, tachycardia, and abnormal findings on abdominal examination.
Laboratory studies may reveal leukocytosis, hypocalcemia, and hyperglycemia. The diagnosis of
acute pancreatitis requires two of the following: typical abdominal pain, threefold or greater
elevation in serum amylase and/or lipase level, and/or confirmatory findings on cross-sectional
abdominal imaging. AlthoughM NOT required for diagnosis, markers of severity include
hemoconcentration (hematocrit >44%), azotemia (BUN >22 mg/dL), and signs of organ failure

Ask the patient about recent operative or other invasive procedures (eg, endoscopic
retrograde cholangiopancreatography [ERCP]) or family history of hypertriglyceridemia.
Patients frequently have a history of previous biliary colic and binge alcohol consumption, the
major causes of acute pancreatitis.
Examination of the abdomen shows rigidity, marked tenderness, mild distension due to
ileus of the intestines, and absence of peristaltic sounds. A bluish discoloration may be seen in
the flanks (Turners sign) or around the umbilicus (Cullens sign) due to extravasation of blood
into the abdominal wall. When present, these signs strongly suggest acute necrotising
pancreatitis. Ascites may develop as a complication (pancreatic ascites
The diagnosis of acute pancreatitis is usually established by the detection of an increased
level of serum amylase and lipase. Values threefold or more above normal virtually clinch the
diagnosis if gutperforation, ischemia, and infarction are excluded. However, there appears to be
no definite correlation between the severity of pancreatitis and the degree of serum lipase and
amylase elevations. Afterthree to seven days, even with continuing evidence of pancreatitis, total
serum amylase values tend to return toward normal. However, pancreatic isoamylase and lipase
levels may remain elevated for 7 to14 days. It will be recalled that amylase elevations in serum
and urine occur in many conditions other than pancreatitis
A CT scan can confirm the clinical impression of acute pancreatitis even with less than
a threefold increase in serum amylase and lipase levels. Importantly, CT can be helpful in
indicating the severity of acute pancreatitis and the risk of morbidity and mortality and in
evaluating the complications of acute pancreatitis . However, a CT scan obtained within the first
several days of symptom onset may underestimate the extent of tissue injury. What may appear
to be intestinal pancreatitis on initial CT scan may evolve to pancreatic necrosis on repeat CT
scan three to five days later . Sonography is useful in acute pancreatitis to evaluate the
gallbladder if gallstone disease is suspected
Ultrasonography and CT scan help to assess the morphological abnormality in the pancreaticobiliary system. Endoscopic retrograde cholangiopancreatography performed after subsidence of
the acute phase helps to demonstrate the underlying abnormality. Contrast enhanced CT is a very
good imaging modality to reveal morphological changes in the pancreas. MRI scan gives
additional information

In most patients (8590%) with acute pancreatitis, the disease isself-limited and subsides
spontaneously, usually within three
toseven days after treatment is
instituted. Conventional measures
(1) analgesics for pain,
(2) IV fluids and colloids to
(3) no oral alimentation.
Once it is clear that a patient
will not be able to tolerate oral
feeding (a determination that can
usually be made within 4872
hours), enteral nutrition should be
considered [rather than total
parenteral nutrition (TPN)] since it
maintains gut barrier integrity,
translocation, is less expensive, and
has fewer complications than TPN.
route through which enteral feeding
is administered is under debate.
Nasogastric access is easier to
establish and may be as safe as
However, enteral nutrition
that bypasses the stomach and
duodenum stimulates pancreatic
secretions less and this rationale theoretically supports the use of the nasojejunal route. It has not
been demonstrated whether
either route is superior in altering morbidity and mortality.
When patients with necrotizing pancreatitis begin oral intake of food, consideration should also
be given to the addition of pancreatic enzyme supplementation and proton pump inhibitor
therapy to assist with fat digestion and reduce gastric acid.

The goal of pharmacotherapy is to relieve pain and minimize complications. Currently,

no medications are used to treat acute pancreatitis specifically. Therapy is primarily supportive
and involves intravenous (IV) fluid hydration, analgesics, antibiotics (in severe pancreatitis), and
treatment of metabolic complications (eg, hyperglycemia and hypocalcemia).
ROLE OF ANTIBIOTICS There is currently no role for prophylactic antibiotics in either
interstitial or necrotizing pancreatitis. Although several early studies suggested a role for
prophylactic antibiotics in patients with necrotizing pancreatitis, two recent double-blind,
randomized controlled trials failed to demonstrate a reduction in pancreatic infection with use of
antibiotic prophylaxis. However, it should also be noted that the overall rate of infected necrosis
has been in decline over the past 1015years and currently is found in 20% of patients with
necrotizingpancreatitis. It is reasonable to start antibiotics in a patient who appears septic while
awaiting the results of cultures. If cultures are negative, the antibiotics should be discontinued to
minimize the risk of developing fungal superinfection.
Several drugs have been evaluated by prospective controlled trials and found ineffective in the
treatment of acute pancreatitis. The list, by no means complete, includes glucagon, H 2
blockers, protease inhibitors such as aprotinin, glucocorticoids, calcitonin, nonsteroidal antiinflammatory drugs (NSAIDs), lexipafant, a platelet-activating factor inhibitor. A recent
meta-analysis of somatostatin, octreotide, and the antiprotease gabexate mesylate in the therapy
of acute pancreatitis suggested (1) a reduced mortality rate but no change in complications with
octreotide and (2) no effect on the mortality rate but reduced pancreatic damage with gabexate.
A dynamic contrast-enhanced CT (CECT) scan performed three to five days after hospitalization
provides valuable information on the severity and prognosis of acute pancreatitis ( Fig. 313-1 ).
In particular, a CECT scan allows estimation of the presence and
extent of pancreatic necrosis.
Surgery may be indicated at times in acute pancreatitis.
1. Excision of necrotic tissue (necrosectomy) is needed if there is extensive necrosis as
demonstrated by helical CT with pancreatic protocol.
2. Drainage of pus is required if there is evidence of infection and abscess formation. Gram
staining of FNAC specimen may reveal organisms.
3. Pancreatic ascites may have to be drained at times
4. Relief of biliary obstruction if medical treatment by itself is not successful.
In the presence of biliary stones or other obstructive lesions, surgery is undertaken electively to
prevent relapse of pancreatitis. Necrotic lesions and local fluid collections should be evaluated
by guided needle aspiration. The material should be submitted for microbiological tests. Surgical

debridement is indicated if there is infection and also in sterile abscesses which fail to improve
with medical therapy. Sometimes biliary obstruction may have to be relieved in the acute phase
of pancreatitis itself if conservative measures fail to resolve the condition.

Surgical Interventions
Surgical intervention, whether by minimally invasive or conventional open techniques, is
indicated when an anatomic complication amenable to a mechanical solution is present (eg,
acute necrotizing pancreatitis in which the necrotic phlegmon is excised to limit a potential site
of sepsis, or hemorrhagic pancreatitis in which surgical control of bleeding is warranted).
Depending on the situation and local expertise, this may require the talents of an interventional
radiologist, an interventional endoscopist, or surgeon (individually or in combination).
The images below provide examples of the treatment of severe acute pancreatitis by means of
minimally invasive techniques.

Gallstone pancreatitis
It is optimal for patients admitted with gallstone pancreatitis to undergo cholecystectomy before
discharge, rather than (for example) being scheduled for a later date as an outpatient. Patients
discharged with gallstone pancreatitis without a cholecystectomy are at high risk for recurrent
bouts of pancreatitis.
Pancreatic duct disruption
Damage to the pancreatic ductal system may allow the pancreatic juice to leak from the gland.
The sudden development of hypocalcemia or a rapid increase in retroperitoneal fluid on
computed tomography (CT) is suggestive of this condition.
When imaging studies provide corroborating evidence, the condition is initially managed by
percutaneous placement of a drainage tube into the fluid collection under the guidance of
ultrasonography or CT scanning.[5] Fluid amylase or lipase levels in the 10,000s strongly suggest
the presence of a ductal disruption.
In the appropriate clinical setting, ERCP confirms the diagnosis and provides a treatment option.
Transpapillary stent placement or, preferably, placement of a 6 French nasopancreatic tube
attached to an external bulb suction device can successfully treat leaks by removing the sphincter

tone and changing the dynamics of fluid flow in favor of ductal healing. Occasionally, leaks are
associated with downstream stenoses that are also amenable to endoscopic treatment.
Refractory cases may warrant surgery. If a persistent leak is present in the tail of the gland, a
distal pancreatectomy is preferred. If the leak is in the head of the gland, a Whipple procedure is
the operation of choice.
Peripancreatic fluid collections persisting for more than 4 weeks are referred to as acute
pseudocysts. Pseudocysts lack an epithelial layer and thus are not considered true cysts. They
also differ from true cysts in that they are usually filled with necrotic debris rather than fluid.
Accordingly, pseudocysts may be better described by the term organized necrosis.
Most pseudocysts can be followed clinically. However, when they are symptomatic (ie,
associated with pain, bleeding, or infection) or are larger than 7 cm and are rapidly expanding in
an acutely ill patient, intervention is indicated. Several different therapeutic approaches may be
implemented, depending on the anatomic relations and on the duration of the natural history of
the complication.
In selected patients with very large fluid collections, percutaneous aspiration of pancreatic
pseudocysts is a reasonable approach. Even though treatment failures are common when the
pseudocyst communicates with the pancreatic ductal system, percutaneous drainage serves as a
temporizing measure that may later lead to successful endoscopic or surgical intervention. Often,
an infected pseudocyst (which by definition is regarded as a pancreatic abscess) can be
successfully managed by means of percutaneous drainage.
Pseudocysts may also be managed endoscopically with transpapillary or transmural techniques.
Transpapillary drainage requires the main pancreatic duct to communicate with the pseudocyst
cavity, ideally in the head or body of the gland. The proximal end of the stent (which should be
smaller than the diameter of the pancreatic duct) is placed into the cavity. The technical success
rate is 83%, the complication rate 12%. Generally, however, pancreatic stents are difficult to
monitor, are prone to obstruction, and carry an increased risk of infection and ductal injury.
Some noncommunicating pseudocysts may be amenable to transmural enterocystostomy.
Technical success requires a mature cyst that bulges into the foregut, and the distance from the
lumen to the cyst cavity should be less than 1 cm. The success rate is 85%, the complication rate
17%. The transduodenal approach is associated with fewer complications and recurrences than
the transgastric approach.

On the basis of prospective studies in the 1970s, surgery was recommended for persistent large
(> 7 cm) pancreatic pseudocysts because complications developed in 41% of patients, 13% of
whom died. Internal pseudocyst-enteric anastomosis became the standard of care, with an
operative mortality of 3-5%. This dogma was subsequently challenged by 2 retrospective studies
in which patients with smaller (ie, < 5 cm) asymptomatic pseudocysts rarely (< 10%) developed
Infected pancreatic necrosis
The clinician cannot rely on clinical findings alone to differentiate infected and sterile pancreatic
necrosis. When clinical signs of infection or SIRS are present in the setting of necrotizing
pancreatitis, CT-guided needle aspiration is indicated.
Surgery is recommended when large areas of the pancreas are necrotic and percutaneous CTguided aspiration demonstrates infection on the basis of a positive Gram stain. Antibiotic therapy
alone is not sufficient to achieve a cure. Aggressive surgical gdebridement and drainage are
necessary to remove dead tissue and to clear the infection.
A study of patients with necrotizing pancreatitis and infected necrotic tissue determined that a
step-up approach to treatment (consisting of percutaneous drainage followed, if necessary, by
minimally invasive retroperitoneal necrosectomy) yielded better results than standard care with
open necrosectomy.[26] Patients who received step-up treatment had a lower rate of major
complications (new-onset multiorgan failure, multiple systemic complications, perforation of a
visceral organ, enterocutaneous fistula, or bleeding) and death.
Pancreatic abscess
Pancreatic abscesses generally occur late in the course of pancreatitis. Many of these respond to
percutaneous catheter drainage and antibiotics. Those that do not respond require surgical
debridement and drainage

Chronic pancreatitis represents a continuous, prolonged, inflammatory and
fibrosing process of the pancreas with irreversible morphologic changes resulting in
permanent endocrine and exocrine pancreatic dysfunction
.it is a disease process characterized by irreversible damage to the pancreas as distinct from the
reversible changes noted in acute pancreatitis. The condition is best defined by the presence of
histologic abnormalities, including chronic inflammation, fibrosis, and progressive destruction
of both exocrine and eventually endocrine tissue. A number of etiologies may result inchronic

The main causes of chronic pancreatitis include the following:
Alcoholism: Alcoholism is associated with chronic pancreatitis in 60-90% of patients.
Cholelithiasis: Cholelithiasis is a common cause of acute pancreatitis, but it probably is
associated with chronic pancreatitis in 20-25% of patients.
cysticfibrosis is the most frequent cause in children
Idiopathic: Etiology is idiopathic in 10-40% of patients.
Cystic fibrosis: This disease is associated with pancreatic atrophy and chronic
Other conditions: hyperlipidemia, hyperparathyroidism, uremia, drug use, hereditary
causes, autoimmune conditions, congenital causes (a congenital abnormality of fusion,
pancreas divisum)
Chronic pancreatitis can be classified into 3 categories:
1. Chronic calcifying pancreatitis is invariably related to alcoholism.
2. In chronic obstructive pancreatitis, the prominent histologic changes are periductal
fibrosis and subsequent ductal dilatation. These changes are much more focal than those
in the other forms, and in most patients, the changes involve only the portion of the
pancreas in which ductal drainage is impaired. Diffuse changes may occur, in which the
main pancreatic duct or ampulla is obstructed.
3. Chronic inflammatory pancreatitis is rare and can affect elderly persons without a
previous history of alcohol excess.
Chronic pancreatitis is more common in the fourth and fifth decades. It presents with
recurrent upper abdominal pain following alcoholic bouts or dietary excesses. The pain may be
referred to the back between T10 and T12 segments. These patients adopt a characteristic
squatting posture with pressure applied to the abdomen. When present, this feature may suggest
the diagnosis. Overt diabetes develops in one-fifth of the cases. Except for vague tenderness over
the epigastrium, physicalexamination may not reveal much. Less commonly, enlarged pancreas,
pseudocyst or pancreatic abscess may be palpable. Course and prognosis:
Chronic pancreatitis tends to be persistent or recurrent, especially if accompanied by biliary
tract disease. Complications include malabsorption state, malnutrition, obstructive jaundice,
diabetes mellitus and higher risk of malignancy. Chronic pancreatitis carries a mortality of 50%
in 20-25 years. Malabsorption develops when the exocrine function falls by 80%.

Diagnosis is based on tests of pancreatic structure and function.

Blood tests
Serum amylase and lipase levels may be slightly elevated in chronic pancreatitis; high levels are
found only during acute attacks of pancreatitis. In the later stages of chronic pancreatitis, atrophy
of the pancreatic parenchyma can result in normal serum enzyme levels because of significant
fibrosis of the pancreas, resulting in decreased concentrations of these enzymes within the
While low concentrations of serum trypsin are relatively specific for advanced chronic
pancreatitis, they are not sensitive enough to be helpful in most patients with mild to moderate
Laboratory studies to identify causative factors of chronic pancreatitis include serum calcium
and triglyceride levels. When common etiologies are not found, research protocols are available
to test for genetic mutations in cationic trypsinogen andCFTR.
Fecal tests
Because maldigestion and malabsorption do not occur until more than 90% of the pancreas has
been destroyed, steatorrhea is a manifestation of advanced chronic pancreatitis. Neither
qualitative nor quantitative fecal fat analysis can detect early disease.Assays of fecal
chymotrypsin and human pancreatic elastase 1 have the same limitations but are useful in
confirming advanced chronic pancreatitis with exocrine insufficiency.

Imaging tests
Imaging studies such as abdominal radiography and CT scanning can show inflammation or
calcium deposits of the pancreas or changes in the pancreatic ducts. Pancreatic calcifications,
often considered pathognomonic of chronic pancreatitis, are observed in approximately 30% of
Endoscopic retrograde cholangiopancreatography
The endoscopic retrograde cholangiopancreatography (ERCP) test provides the most accurate
visualization of the pancreatic ductal system and has been regarded as the criterion standard for
diagnosing chronic pancreatitis. It combines the use of endoscopy and fluoroscopy to visualize
and treat problems of the bile and pancreatic ducts.
Magnetic resonance cholangiopancreatography

MRCP provides information on the pancreatic parenchyma and adjacent abdominal viscera, and
it uses heavily T2-weighted images to visualize the biliary and pancreatic ductal system. This
procedure is relatively safe, reasonably accurate, noninvasive, fast, and very useful in planning
surgical or endoscopic intervention.
Endoscopic ultrasonography
The most predictive endosonographic feature of chronic pancreatitis is the presence of stone

Chronic pancreatitis should be suspected clinically in any alcoholic patient complaining of

epigastric pain referred to the back.

Approach Considerations
The goals of medical treatment are as follows:

Modify behaviors that may exacerbate the natural history of the disease
Enable the pancreas to heal itself
Determine the cause of abdominal pain and alleviate it
Detect pancreatic exocrine insufficiency and restore digestion and absorption to normal
Diagnose and treat endocrine insufficiency
Abstinence from alcohol and smoking and reduction of weight help to reduce exacerbations.
Analgesics and antispasmodics may be necessary to relieve pain. Reduction of dietary fat to 2030 g/day helps to reduce the abdominal discomfort and relieve steatorrhea in mild cases. Fat
soluble vitamins have to be supplemented orally or parenterally as required. Digestion can be
aided by the administration of pancreatic enzymes or enzymes derived from fungal or other plant
sources given orally after food. Pancreatic extract (Pankreon, Pancreatin) is available
commercially. Four to six tablets (2-3 g) have to be given with meals or more frequently. This
measure helps in digestion, corrects the steatorrhea, and also ameliorates pain. Vitamin B12
malabsorption is also corrected. Though this is generally safe, excessive use of pancreatic
extracts leads to hyperuricemia. In moderate and severe cases H2 receptor blocker drugs such as
ranitidine 150 mg bd or a proton pump inhibitor such as omeprazole 20 mg bd are given orally
to reduce gastric acidity and thereby limit the inactivation of pancreatic enzymes in the intestine.
Medium chain triglycerides are useful to reduce diarrhea. They require only small amounts of
pancreatienzymes for digestion. Moreover bile salts are not required for their absorption.
Medium chain triglycerides are contained in oils such as coconut oil. Diabetes has to be treated
on its own merits. Surgery: Intractable pain, pancreatic cysts, pseudocysts and neoplasms are
indications for surgery. In many cases, relief of obstruction and withdrawal of alcohol results in

improvement of pancreatic function. In some cases removal of the affected portion of the
pancreas may be required.


Syn: Autoimmune related pancreatitis This was first described in 1955 by Yoshida et al to
describe the form of pancreatitis that is associated with autoimmune manifestations revealed by
clinical and laboratory parameters. AIP is a form of chronic pancreatitis caused by autoimmune
inflammation. This leads to lymphocytic infiltration with associated fibrosis of the pancreas
leading to organ dysfunction. AIP forms 5-11% of the total cases of chronic pancreatitis. Male to
female ratio is 2:1 the disease is present in India and formed 1% of a serious from Vellore. Ref:
Etiology and clinical profile of chronic pancreatitis the CMC Vellore experience. Ashok Chacko
and Shajan Peter in chronic pancreatitis and pancreatic diabetes in India. Edited by V.
Balakrishnan and others published by The Indian Pancreatitis Study Group 2006. Some cases
show association with other autoimmune diseases such as rheumatoid arthritis, Sjgrens
syndrome and inflammatory bowel disease. Clinical features: A wide variety of symptoms may
occur. Jaundice and mild to moderate abdominal pain are frequent. Imaging studies shows
biliary duct strictures which may resemble those of primary sclerosing cholangitis. Histology
helps to confirm the diagnosis. Diagnosis: The CT scan image is characteristic. Endoscopic
ultrasonography is an important tool to diagnose AIP. AIP has to be differentiated from alcohol
induced pancreatitis and pancreatic cancer. Treatment: Corticosteroids form the mainstay of
treatment. Prednisolone in a dose of 40 mg/day/should be started orally and continued for a
week, before tapering the dose.

1. Acute Pain
May be related to
1. Obstruction of pancreatic, biliary ducts
2. Chemical contamination of peritoneal surfaces by pancreatic exudate/autodigestion of
3. Extension of inflammation to the retroperitoneal nerve plexus
4. Investigate verbal reports of pain, noting specific location and intensity (010 scale). Note factors that
aggravate and relieve pain.
6. Maintain bedrest during acute attack. Provide quiet, restful environment.

8. 2Promote position of comfort on one side with knees flexed, sitting up and leaning forward.
10. 3 Provide alternative comfort measures (back rub), encourage relaxation techniques (guided imagery,
visualization), quiet diversional activities (TV, radio).
12. 4Keep environment free of food odors.
14. Administer analgesics in timely manner (smaller, more frequent doses).
16. Maintain meticulous skin care, especially in presence of draining abdominal wall fistulas.
2. Risk for Deficient Fluid Volume
Risk factors may include

Excessive losses: vomiting, gastric suctioning

Increase in size of vascular bed (vasodilation, effects of kinins)
Third-space fluid transudation, ascites formation
Alteration of clotting process, hemorrhage

1. Measure I&O including vomiting, gastric aspirate diarrhea. Calculate 24-hr fluid balance.
2. Note decrease in urine output (less than 400 mL per 24 hr).
3. Record color and character of gastric drainage, measure pH, and note presence of occult
4. Weigh as indicated. Correlate with calculated fluid balance.
5. Note poor skin turgor, dry skin and mucous membranes, reports of thirst.
6. Observe and record peripheral and dependent edema. Measure abdominal girth if ascites
7. Investigate changes in sensorium (confusion, slowed responses).
8 Auscultate heart sounds; note rate and rhythm. Monitor and document rhythm, changes.
9 Inspect skin for petechiae, hematomas, and unusual wound or venipuncture bleeding. Note
hematuria, mucous membrane bleeding, and bloody gastric cont

3. Imbalanced Nutrition
Nursing Diagnosis:

Imbalanced Nutrition: Less Than Body Requirements

May be related to

Vomiting, decreased oral intake; prescribed dietary restrictions

Loss of digestive enzymes and insulin (related to pancreatic outflow obstruction or

Nursing Interventions
1. Assess abdomen, noting presence and character of bowel sounds, abdominal distension, and reports of
2. Provide frequent oral care.

3. Assist patient in selecting food and fluids that meet nutritional needs and restrictions when diet is resum

4. Observe color, consistency and amount of stools. Note frothy consistency and foul odor.
5. Note signs of increased thirst and urination or changes in mentation and visual acuity.
6. Test urine for sugar and acetone.
7. Maintain NPO status and gastric suctioning in acute phase.
8. Administer hyperalimentation and lipids, if indicated.

9. Resume oral intake with clear liquids and advance diet slowly to provide high-protein, high-carbohydra
diet, when indicated.
10. Provide medium-chain triglycerides (MCTs) (MCT, Portagen).
11. Administer medications as indicated:
12. Vitamins: A,D,E,K;

Nursing Interventions
13. Replacement enzymes: pancreatin (Dizymes), pancrelipase (Viokase, Cotazym).
14. Monitor serum glucose.
15 Provide insulin as appropriate.
4. Risk for Infection
Risk factors may include

Inadequate primary defenses: stasis of body fluids, altered peristalsis, change in pH of



Nutritional deficiencies

Tissue destruction, chronic disease

5. Deficient Knowledge
May be related to

Lack of exposure/recall
Information misinterpretation; unfamiliarity with information resources

Possibly evidenced by

Questions, request for information; statement of misconception

Inaccurate follow-through of instructions/development of preventable complicatio

1. Review specific cause of current episode and prognosis.

2. Discuss other causative and associated factors such as excessive alcohol intake,
gallbladder disease, duodenal ulcer, hyper -lipoproteinemias, some drugs (oral
contraceptives, thiazides, furosemide [Lasix], isoniazid [INH], glucocorticoids,
3. Explore availability of treatment programs and rehabilitation of chemical dependency if
4. Stress the importance of follow-up care, and review symptoms that need to be reported

immediately to physician (recurrence of pain, persistent fever, nausea and vomiting,

abdominal distension, frothy and foul-smelling stools, general intolerance of food).
5. Review importance of initially continuing bland, low-fat diet with frequent small feedings
and restricted caffeine, with gradual resumption of a normal diet within individual
6. Instruct in use of pancreatic enzyme replacements and bile salt therapy as indicated,
avoiding concomitant ingestion of hot foods and fluids.

Pancreatitis some times act as a medical emergency otherwise it can treated
through bedrest and nil per oral,alchoholism is the major factor that cause the disease condition
so avoidance of alchohol is must to prevent the risk of infection.