1. ACUTE PANCREATITIS

2. INTRODUCTION
the evaluation of the patient of suspected pancreatitis begin with detail history to symptom onset , proior pancreatitis ,alchohol abuse, gallstone disease & review of medications. On physical examination , tender epigastric region or diffusely tender whole abdomen is present .bowel sound may be absent indicative of ileus . SIRS with fever, tachycardia & tachypnea may be present.Diminised bowel sound ,hypoxia & altered mental status suggest severe disease. Gall stone & alcohol are the common causes of pancreatitis & other rare cause include autoimmune , post ERCP, medications, malignancy, hereditary & trauma.
As per the atlanta symposuium, it is diagnosed with abdominal pain , 3 times greater value of amylase & lipase from the upper normal limit & pancreatic imflammation on crosssectional imaging. .serum lipase is more sensitive in the diagnosis of [pancreatitis & remain elevated for longer than serum amylase. elevation in liver enzymes ( particularly liver transaminases with or without hyperbilirunemia suggest the presence of bile duct stones or compression of common bile duct by pancreatic edema. An abdominal ultrasonography should be done in suspected gall stone pancreatitis to assess for cholelithiasis or choledocolithiasis .CECT is the best modality for evaluating pancreatic necrosis , inflammation & peripancreatic fluid collection. CECT should be delayed upto 72 hours to avoid missing necrosis unless there is concern for other complications or when diagnosis in doubt.for recurrent acute pancreatitis (two or more episodes) a detailed workup (IgG4, triglyceride, calcium) is warranted.
Management: As early prediction of severity is difficult, all cases to be treated as severe until proven otherwise the treatment includes IVF , pain control ,nutritional support , role of ERCP, use of antibiotics, & management of peripancreatic fluid collection.

3. INTRODUCTION
Acute pancreatitis is frequent cause of gastrointestinal related critical illness.
The overall mortality among pts with acute pancreatitis is aroun 5 % but pts who develop severe acute pancreatitis have mortality rateas high as 15%

4. PATHOPHYSIOLOGY
Triggered by an increase in indraductal pressure & direct injury to acinar cells from metabolic or toxic stimuli .
Leads to breakdown of junctional barrier & leakage of pancreatic fluid & enzymes into instertial space.
Intrapancreatic activation of proteolytic enzymes leads to autophagy & autodigestion of acinar cells

5. The acinar tissue death leads to intense SIRS caused by the release of activated pancreatic enzymes, mediated by cytokines,immunocytes & complement system.
Inflammatory cytokines such as TNF cause macrophage to migrate into tissues distant from the pancreas, including lungs & kidneys.
Result is tissue destruction, fluid & electrolyte loss, hypotension, renal & pulmonary complications & in severe cases MOF & death.

6. ETIOLOGY Most common – alcohol & gall stone.
Others --- hypertryglyceridemia,post ERCP panceatitis, hypercalcemia , trauma, infection, drug injury.
Anatomic variants --- pancreas divisum & idiopathic pancreatitis.
Several studies say smoking to be an independent risk factor for acute pancreatitis in dose dependent manner.

7. DIAGNOSIS & ASSESSMENT OF SEVERITY.
2 of the following 3 criteria:
Sudden onset of characteristic abdominal pain
Elevation of serum amylase &/or lipase above 3 times normal.
Findings of pancreatic inflammation noted in imaging.
* imaging is not required for diagnosis in pts who present with characteristic abdominal pain & elevated sr amylase & lipase.

8. TYPES OF ACUTE PANCREATITIS
Acute fluid collection --<4 wks—homogenous with fluid density/ no encapsulation /interstitial edematous pancreatitis.
Acute necrotic collection -- < 4 wks—heterogenous ( both fluid & solid component)/ no encapsulation / acute necrotising pancreatitis.
Pseudocyst(PP)4 wks– homogenous with fluid density/ well defined wall/ after interstitial edematous pancreatitis.
Walled off necrosis4 wks-- heterogenous with fluid density/ well defined wall/ after acute necrotising pancreatitis.

9. INITIAL RESUSCITATION & MANAGEMENT.
Starts in emergency department.
“GOLDEN HOUR”– ist 24 hrs.
Close monitoring is needed as both under as well as over resuscitation can lead to worse outcome.
Ringer’s lactate should be the initial choice for fluid resuscitation in all pts with acute pancreatitis except those with hypercalcemia since it contains 3meq/l of calcium.

10. Monitoring done by clinical(vitals, urine output) & lab(BUN/ hematocrit)
A general approach is to start with 1 to 2 litre crystalloid fluid bolus followed by fluid resuscitation at a rate of ml/hr for 1-3L to target a urine output0.5ml/kg/hr.

11. NUTRITION IN ACUTE PANCREATITIS
EVOLVED from the concept of ‘PANCREAS REST” to efforts directed to early resumption of enteral nutrition with aim to maintain the gut integrity & prevent bacterial translocation & associated complications.
Enteral nutrition should be started as soon as possible.
Associated with lower rate of systemic infections , multiorgan failure & mortality in comparision to parenteral nutrition.

12. Pts with acute pancreatisis should be fed as soon as they are hungry, without any restriction of consistency of food.
A low fat solid diet seems to be as safe as clear liquid diet.
Nutritional support should be started within 24 to 48 hrs of presentation in moderate to severe cases.
No data strongly favour between nasogastric or nasojejunal feeding.

13. ROLE OF PROPHYLACTIC ANTIBIOTICS
Approx one- fourth of the pts with acute pancreatitis develop infectious complications & those with severeidsese are particularly at high risk.
As per study, use of prophylactic antibiotic is not associated with decreased incidence of infected pancreatic necrosis, mortality or need for surgical intervention, even though a decresed incidence of infection in pancreatic necrosis & a trend toward lower mortality were noted in pt reciving imipenam.

14. Recent guideline from american college of gastroenterology suggest that when infection is suspected , it is justifiable to start empiric antibiotic , covering with both gram negative & gram positive organisms, antibiotics can be discontinued if cultures are negative & no definite source is identified.

15. ROLE OF ERCP IN ACUTE PANCREATITIS
It can be used in pts with acute gallstone pancreatitis with cholangitis & those with pancreatic duct disruption.
Should be performed within 24 hrs of admission since it is associated with decreased morbidity & mortality.
Benefits in pts with gallstone pancreatitis without cholangitis is not clear.

16. When acute pancreatitis is mild intestinal & billary in origin , cholecystectomy is preffered before discharge.
When moderate to severe, reimaging after 1 month to exclude any fluid collection, if present , both can be removed simultaneously during surgery.