PANCREATITISINTRODUCTION Pancreatitisis defined asinflammationof thepancreas. It has several causes and symptoms and requires immediate medical attention. It may beacutebeginning suddenly and lasting a few days, orchronicoccurring 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 inflammationACUTE PANCREATITIS 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.CAUSESEtiology Long-standing alcohol consumption andbiliary stone diseasecause 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 diseaseOne 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 size.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.AlcoholAlcohol 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 cholangiopancreatographyPancreatitis 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.TraumaAbdominal 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.DrugsConsidering 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: Azathioprine Sulfonamides Sulindac Tetracycline Valproic acid, Didanosine Methyldopa Estrogens Furosemide 6-Mercaptopurine Pentamidine 5-aminosalicylic acid compounds Corticosteroids Octreotide 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. Infection 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 pancreatitis. 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 includeMycoplasma pneumoniae, Salmonella, Campylobacter,andMycobacterium tuberculosis.Worldwide,Ascarisis a recognized cause of pancreatitis resulting from the migration of worms in and out of the duodenal papillae. 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, theCFTRmutation plays a role in predisposing patients to acute pancreatitis by causing abnormalities of ductal secretion. At present, however, the phenotypic variability of patients with theCFTRmutation is not well understood. Certainly, patients homozygous for theCFTRmutation 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 pancreatitis. 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 cascade. Hypercalcemia 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 controversial).

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 controversial. Hypertriglyceridemia 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. Tumors 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. Toxins Exposure to organophosphate insecticide can cause acute pancreatitis. Scorpion and snake bites may also be causative; in Trinidad, the sting of the scorpionTityus trinitatisis 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.PATHOPHYSIOLOGY 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 (carboxypeptidases,aminopeptidases) 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 gastrinreleasingpeptides. 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 effectsPATHOPHYSIOLOGY SIGNS AND SYMPTOMSABDOMINAL PAIN 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 relieF 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.

DIAGNOSIS 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

HISTORY COLLECTION 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.PHYSICAL EXAMINATION 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 ascitesLAB INVESTIGATIONS 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

IMAGING STUDIES 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 pancreatico-biliary 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

TREATMENT 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 include (1) analgesics for pain, (2) IV fluids and colloids to maintainnormal intravascular volume, (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, thereby preventing bacterial translocation, is less expensive, and has fewer complications than TPN. Theroute through which enteral feeding is administered is under debate. Nasogastric access is easier to establish and may be as safe as nasojejunal enteral nutrition. However, enteral nutritionthat 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 whethereither 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.PHARMACOTHERAPY 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 2blockers, protease inhibitors such as aprotinin, glucocorticoids, calcitonin, nonsteroidal anti-inflammatory drugs (NSAIDs), lexipafant, a platelet-activating factor inhibitor. A recentmeta-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 andextent of pancreatic necrosis.

SURGICAL MANAGEMENTSurgery may be indicated at times in acute pancreatitis.Indications 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 InterventionsSurgical 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 pancreatitisIt 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 disruptionDamage 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.Pseudocysts 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 complications.Infected pancreatic necrosisThe 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 CT-guided 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 abscessPancreatic 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 drainageCHRONIC PANCREATITIS 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

ETIOLOGICAL FACTORSThe 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 pancreatitis Other conditions: hyperlipidemia, hyperparathyroidism, uremia, drug use, hereditary causes, autoimmune conditions, congenital causes (a congenital abnormality of fusion, pancreas divisum) TYPESChronic 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.

CLINICAL FEATURES 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%. DiagnosisDiagnosis is based on tests of pancreatic structure and function.Blood testsSerum 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 pancreas.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 disease.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 testsBecause 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 testsImaging 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 cases.Endoscopic retrograde cholangiopancreatographyThe 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 cholangiopancreatographyMRCP 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 ultrasonographyThe 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. Treatment:Approach ConsiderationsThe 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 20-30 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.

AUTOIMMUNE PANCREATITIS (AIP) 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.

NURSING MANAGEMENT

1. Acute PainMay be related to1. Obstruction of pancreatic, biliary ducts2. Chemical contamination of peritoneal surfaces by pancreatic exudate/autodigestion of pancreas3. 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.5.

6. Maintain bedrest during acute attack. Provide quiet, restful environment.7.

8. 2Promote position of comfort on one side with knees flexed, sitting up and leaning forward.9.

10. 3 Provide alternative comfort measures (back rub), encourage relaxation techniques (guided imagery, visualization), quiet diversional activities (TV, radio).11.

12. 4Keep environment free of food odors.13.

14. Administer analgesics in timely manner (smaller, more frequent doses).15.

16. Maintain meticulous skin care, especially in presence of draining abdominal wall fistulas.17.

2. Risk for Deficient Fluid VolumeRisk 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, hemorrhageINTERVENTIONS

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 blood.

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 present.

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 NutritionNursing Diagnosis: Imbalanced Nutrition: Less Than Body RequirementsMay be related to Vomiting, decreased oral intake; prescribed dietary restrictions Loss of digestive enzymes and insulin (related to pancreatic outflow obstruction or necrosis/autodigestion)Nursing Interventions

1. Assess abdomen, noting presence and character of bowel sounds, abdominal distension, and reports of nausea.

2. Provide frequent oral care.

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

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-carbohydrate diet, when indicated.

10. Provide medium-chain triglycerides (MCTs) (MCT, Portagen).

11. Administer medications as indicated:

12. Vitamins: A,D,E,K;

13. Replacement enzymes: pancreatin (Dizymes), pancrelipase (Viokase, Cotazym).

14. Monitor serum glucose.

15 Provide insulin as appropriate.

4. Risk for InfectionRisk factors may include Inadequate primary defenses: stasis of body fluids, altered peristalsis, change in pH of secretions Immunosuppression Nutritional deficiencies Tissue destruction, chronic disease5. Deficient KnowledgeMay be related to Lack of exposure/recall Information misinterpretation; unfamiliarity with information resourcesPossibly 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 factorssuch asexcessive alcohol intake, gallbladder disease, duodenal ulcer, hyper -lipoproteinemias, some drugs (oral contraceptives, thiazides, furosemide [Lasix], isoniazid [INH], glucocorticoids, sulfonamides).

3. Explore availability of treatment programs and rehabilitation of chemical dependency if indicated.

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 tolerance.

6. Instruct in use of pancreatic enzyme replacements and bile salt therapy as indicated, avoiding concomitant ingestion of hot foods and fluids.

CONCLUSION

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.

BIBLIOGRAPHY