Acute Pancreatitis Managment
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Acute Pancreatitis Managment
- 2. EPIDEMIOLOGY 17 per 100,000 2-3% overall mortality from acute pancreatitis Male: female ratio is 1:3- in those with gallstones and 6:1 in those with alcoholism The median age at onset depends on the etiology AIDS-related - 31 years Vasculitis-related - 36 years Alcohol-related - 39 years Drug-induced etiology - 42 years ERCP-related - 58 years Trauma-related - 66 years Biliary tract–related - 69 years
- 3. CAUSES Obstructive(75%) Operative trauma Blunt/penetrating trauma • • Parasitic • Ascariasis, clonorchiasis • Bacterial • Mycoplasma, C. jejuni, TB • MAI, Leptospirosis, Legionella • Vascular • Ischemia • Embolic • Vasculitis • MISC • • • • • • • • • Lab test(ERCP / angiography) Drugs • Tumor Traumatic (5%) Infection • Viral • HIV/EBV/Coxsackie/Mumps • CMV/Varicella/Hep A&C Gall Bladder stone • 6-mercaptopurine Azathioprine DDI (2 ′ 3 ′ dideoxyinosine) Estrogens Thiazides Sulfa drugs etc Metabolic TG ~ 4% > 1000 mg/dl PTH < 0.5% Toxins Alcohol Scorpion bites Tityus trinitatis & T. serrulatus Hereditary Cystic Fibrosis Idiopathic: 10 to 30% microlithiasis P. divisum Annular pancreas SOD Crohn’s Dz Post Perf DU
- 4. Idiopathic Acute Pancreatitis The etiology of acute pancreatitis should be determined in at least 80% of cases and no more than 20% should be classified as idiopathic Gall stone disease represents approximately half the cases of acute pancreatitis, and 20–25% are related to alcohol abuse The correct diagnosis of acute pancreatitis should be made in all patients within 48 hours of admission. The diagnosis of idiopathic pancreatitis should not be accepted in the absence of a vigorous search for gall stones as a minimum, it is necessary to obtain at least two good quality ultrasound examinations.
- 5. Clinical Presentation Pain (95%) ◦ Acute onset ◦ Mid-abdominal or mid-epigastric ◦ Radiates to the back (50%) ◦ Peak intensity in 30 minutes ◦ Lasts for several hours Nausea and vomiting (80%) Fever Shock Abdominal distension (75%) Abdominal guarding and tenderness (50%) Restlessness and agitation Grey-Turner's sign (hemorrhagic discoloration of the flanks) Cullen's sign (hemorrhagic discoloration of the umbilicus)
- 8. Laboratory Diagnosis BASELINE INVESTIGATION LFT’S Increased amylase and/or lipase >3 times ◦ Amylase levels rise w/in 2-12h Peak w/in first 48hr Remain elevated 3-5days before return to baseline ◦ Lipase much more specific Height of elevation does not correlate with severity No utility in following daily levels after the diagnosis Serum Ca+ LDH VIRAL ANTIBODY TITERS
- 9. Others U/S ABDOMEN CT SCAN EUS MRCP
- 10. PREDICTION OF SEVERITY Available prognostic features which predict complications in acute pancreatitis are clinical impression of severity Obesity APACHE II >8 in the first 24 hours C reactive protein levels >150 mg/l Glasgow score 3 or more Persisting organ failure after 48 hours in hospital
- 11. APACHE II score (Acute Physiology And Chronic Health Evaluation)
- 13. Signs of Organ Failure Cardiovascular ◦ Hypotension ◦ Septic physiology HR, CO and ◦ DIC ◦ Thrombocytosis SVR Respiratory Renal ◦ ATN ◦ Oliguria Hepatic ◦ Encephalopathy ◦ T bili (3 mg/dl) ◦ AST/ALT 2X nl ◦ Hypoxemia ◦ Pleural effusions Hematologic GI ◦ Stress ulcer ◦ Acalculous cholecystitis
- 14. Determining severity Clinical assessment, fluid status vitals UOP pulse oximetry Clinical criteria Radiographic criteria ◦ Ranson criteria ◦ Atlanta criteria ◦ POP score ◦ CT severity index necrosis may not be evident until 48-72h
- 15. Ranson Score At admission age in years > 55 years white blood cell count > 16000 cells/mm3 blood glucose > 11 mmol/L (> 200 mg/dL) serum AST > 250 IU/L serum LDH > 350 IU/L At 48 hours Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hematocrit fall > 10% Oxygen (hypoxemia PO2 < 60 mmHg) BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L
- 16. Atlanta criteria
- 18. When Do I Order A CT? If the patient has….. ◦ ◦ ◦ ◦ ◦ Persisting organ failure Signs of sepsis Deterioration in clinical status after 6-10days Diagnostic dilemma Infection suspected T > 101o F Positive blood cultures What kind of CT? What are you looking for? Follow up scan are recommended only if the patient’s clinical status deteriorates or fails to show continued improvement. ◦ CT scan with pancreatic protocol ◦ Necrosis: Lack of enhancement with contrast ◦ Fluid Collections ◦ Alternate diagnosis
- 19. CT scan with pancreatic protocol 500 ml of oral contrast by mouth or nasogastric tube. An initial scan without iv contrast show extent of peripancreatic change. A post contrast series is obtained aftr iv inj of 100 ml of nonionic contrast delivered at 3 ml/s Images through the pancreatic bed should be obtained with in 40 sec and before 80 sec.
- 20. CT Findings Pancreas ◦ ◦ ◦ ◦ Pancreatic enlargement Decreased density due to edema Intrapancreatic fluid collections Blurring of gland margins due to inflammation Peripancreatic ◦ Fluid collections and stranding densities ◦ Thickening of retroperitoneal fat * It may take up to 72h for inflammatory changes to become apparent on CT *
- 23. Balthazar Scoring CT grading of severity POINTS Grade of Acute Pancreatitis A =Normal pancreas B =Pancreatic enlargement C =Pancreatic/peripancreatic inflammation D =Single peripancreatic fluid collection E =Multiple fluid collections 0 1 2 3 4 Grade E = 50% chance of developing an infection and 15% chance of death Degree of Necrosis No necrosis Necrosis of one third of pancreas Necrosis of one half of pancreas Necrosis of more than one half 0 2 4 6 CT Severity Index = Grade + Degree of necrosis
- 24. When can he eat ? TPN vs. enteral feeding In patients with severe disease, oral intake is inhibited by nausea; the acute inflammatory response is associated with impaired gut mucosal barrier function. It has been suggested that nutritional support may help to limit the stimulus to the inflammatory response. Reduce microbial translocation Enhance gut mucosal blood flow Promote gut mucosal surface immunity In these circumstances enteral feeding seems to be safer than parenteral feeding, with fewer septic complications.It is also cheaper
- 25. Contd… Tube feed if anticipate NPO > 1 week. Nasogastric feeding may be feasible in up to 80% of cases. Caution should be used when administering nasogastric feed to patients with impaired consciousness because of the risk of aspiration of refluxed feed. In that case nasojeujunal tube can be used. The use of enteral feeding may be limited by ileus. If this persists for more than five days, and if can’t maintain adequate jejunal access parenteral nutrition will be required.
- 26. Possible pathways for pancreatic infection There are few mechanisms by which bacteria may enter pancreatic and peripancreatic necrosis The haematogenous route via the circulation. Transmural migration through the colonic bowel wall either to the pancreas (translocation),or via ascites to the pancreas, or via the lymphatics to the circulation The biliary duct system from the duodenum via the main pancreatic duct. Intra abdominal fungal infection can also
- 27. Bacteriology in severe acute pancreatic Escherichia coli Staphylococcus aureus Pseudomonas spp Klebsiella spp Proteus spp Candida Streptococcus faecalis Enterobacter spp Anaerobes Monomicrobial Polymicrobial 25% 17% 15% 9% 9% 4% 3% 3% 16% 76% 24%
- 28. Management All patients with acute pancreatitis should receive adequate oxygen Start IV fluids with crystalloid Colloid (blood if Hct <25, albumin if serum alb <2) Rate of fluid replacement should be monitored by frequent measurement of central venous pressure Closely follow input output charting 0.5ml/kg /hr in absence of renal failure Analgseics Opioids Antiemetics NGT decompression if frequent emesis or evidence of ileus on plain films Monitor & correct electrolytes.
- 29. When Do I Start Antibiotics? Acute pancreatitis is c/b infection ~ 10% 30-50% of those with necrosis get infection Prophylactic antibiotics ◦ Controversial No benefit in mild EtOH pancreatitis Selective gut decontamination may be beneficial General recommendations for use: ◦ Biliary pancreatitis with signs of cholangitis ◦ > 30% necrosis on CT scan
- 31. A final word on antibiotics Do not use empirically early in mild pancreatitis Fever early in the disease process is almost universally secondary to the inflammatory response and NOT an infectious process
- 32. When Do I Consult GI ? Evidence of biliary pancreatitis ◦ Elevated LFTs + pancreatitis No matter what the US shows Severe pancreatitis Recurrent unexplained pancreatitis Rule out infected necrosis EUS FNA sampling of fluid collections Endoscopic treatment of necrosis/abscess
- 33. GALL STONE PANCREATITIS AND TREATMENT OF GALL STONES Q: When should I suspect it ? ◦ A: Always Q: How do I evaluate for it ? ◦ A: (E)US and LFTs Q: When is ERCP indicated ?
- 34. Contd…. Urgent therapeutic ERCP should be performed in patients with acute pancreatitis of gall stone etiology who satisfy the criteria for severe pancreatitis, or when there is cholangitis, jaundice, or a dilated common bile duct. The procedure is best carried out within the first 72 hrs after the onset of pain. All patients undergoing early ERCP for severe gall stone pancreatitis require endoscopic sphincterotomy whether or not stones are found in the bile duct. Patients with signs of cholangitis require endoscopic sphincterotomy or duct drainage by stenting to ensure relief of biliary obstruction
- 35. Timing of cholecystectomy All patients with biliary pancreatitis should undergo definitive management of gall stones during the same hospital admission. For unfit patients, endoscopic sphincterotomy alone is adequate treatment
- 36. Complications of AP Immediate Shock DIC ARDS Late Pancreatic pseudocyst Pancreatic abscess Pancreatic necrosis Progressive jaundice Persistent duodenal ileus GI bleeding Pancreatic ascites
- 37. Management of Pancreatic Complications Acute fluid collections ◦ Occur early, seen but not felt ◦ No defined wall usually resolve spontaneously ◦ No routine percutaneous or operative drainage require Infected pancreatic necrosis Pancreatic abscess Pseudocysts
- 38. Infected necrosis All patients with persistent symptoms and greater than 30% pancreatic necrosis, and those with smaller areas of necrosis and clinical suspicion of sepsis, should undergo image guided FNA to obtain material for culture 7–14 days after the onset of the pancreatitis. Patients with infected necrosis will require intervention to completely debride all cavities containing necrotic material.
- 39. Contd… Radiological percutaneous wide bore drainage Surgical Debridement of necrotic tissue following this abdomen can be closed in three ways Closed ovr drain Packed and left open Closed over drain and irrigated A new approach for surgical debridement of infected necrosis offers the potential to debride necrotic tissue with minimal systemic disturbance, by approaching the cavity along the track of a percutaneously placed drain.The cavity is then debrided piecemeal with an operating nephroscope. Several sessions may be required in order to achieve complete debridement. Postoperatively the cavity is continuously irrigated
- 41. Pseudocysts Collection of pancreatic fluid enclosed by non-epithelialized wall of granulation tissue Complicates 5-10% cases of AP ~ 4 weeks after insult 25-50% resolve spontaneously
- 42. Complications of Pseudocyst Infection - 14% Rupture - 6.8% Hemorrhage - 6.5% Common bile duct obstruction - 6.3% GI obstruction - 2.6%
- 43. Pseudocyst Management Old thought ◦ Pseudocysts > 5 cm that have been present > 6 weeks must be drained Current practice ◦ Asymptomatic pseudocysts, regardless of size, do not require treatment
- 45. Pseudocyst Drainage Techniques Endoscopic Surgical Radiologic
- 51. Pancreatic abscess ◦ CT or EUS guided drainage Walled collection of pus Similar to management of pseudocyst
- 52. Closing Points Patients with severe acute pancreatitis have an increased risk of death. Patients who die usually have evidence of organ failure. All patients with severe acute pancreatitis should be managed in a high dependency unit or intensive therapy unit with full monitoring and systems support The pancreas is mean