Acute Pancreatitis It's Management and Complications .pptx

Acute pancreatitis is treated in hospital, where you'll be closely monitored for signs of serious problems and given supportive treatment, such as fluids and oxygen.

1. Acute Pancreatitis Presenter Dr. Ajinkya Patil (PG 1 st Year) Guide Dr. Arvind Diwaker (Asso. Professor General Surgery)

2. Pancreatitis Pancreatitis is inflammation of the pancreatic parenchyma. For clinical purposes, it is useful to divide pancreatitis into Acute , which presents as an emergency with inflammatory changes which are reversible. Chronic , which is a prolonged and frequently lifelong disorder resulting from the development of fibrosis within the pancreas.

3. Acute Pancreatitis An acute condition presenting with Abdominal pain, A threefold or greater rise in the serum levels of the pancreatic enzymes' amylase or lipase And/or characteristic findings of pancreatic inflammation on contrast-enhanced CT.

4. Trapnell’s Etiological Classification MAJOR CAUSES Gallstones (50-70%) Alcohol (25%) OTHER CAUSES Post-ERCP (1-3%) - duct disruption and enzyme extravasation Abdominal trauma Following biliary, upper GI or splenic surgery Drugs - corticosteroids, INH, azathioprine, valproic acid, thiazides, estrogens, tetracycline, Metronidazole Hypertriglyceridemia, Hypercalcemia, Hyperlipidemia Viral infections (mumps, coxsackie B) Scorpion bite Idiopathic

5. Pathophysiology Premature activation of pancreatic enzymes within the pancreas, leading to a process of autodigestion. Anything that injures the acinar cells and impairs the secretion of zymogen granules or damages the duct epithelium, and thus delays enzymatic secretion, can trigger acute pancreatitis.

6. PATHOGENESIS

7. ATLANTA CLASSIFICATION Acute edematous pancreatitis (80%) Acute necrotizing pancreatitis (20%) PRESENT CLASSIFICATION OF ACUTE PANCREATITIS Interstitial Acute pancreatitis Necrotizing pancreatitis Sterile necrosis Infected necrosis (CT guided aspiration and Grams stain – Pancreatic necrosectomy)

8. GROSS Microvascular leakage causing oedema Necrosis of fat by lipolytic enzyme (yellow white, chalky) Destruction of BV & interstitial hemorrhage MICROSCOPIC Inflammatory infiltration, interstitial oedema, focal areas of fat necrosis, granular blue appearance of fat cells( FA +Ca) Pathology

9. Symptoms Sudden onset severe upper abdominal relieves on stooping forward Nausea, repeated vomiting and retching, hiccough (gastric distension/irritation of diaphragm) Fever – Low grade Jaundice (in cases of choledocholithiasis and cholangitis)

10. Signs Features of shock - thready pulse, tachycardia, hypotension, cold extremities Cyanosis Tachypnoea Mild Icterus (biliary obstruction) Temperature : normal or subnormal Muscle guarding in the upper abdomen Abdominal distension (due to ileus or, more rarely, ascites with shifting dullness) Mass in the epigastrium (due to inflammation) A pleural effusion is present in 10–20% of patients.

11. Bleeding into the fascial planes can produce Cullen’s sign – bluish discoloration around the umbilicus Grey turner’s sign – bluish discoloration of the flanks (enzymes sweep across the retroperitoneum causing hemorrhagic spots & ecchymosis) Fox’s sign – bluish discoloration below the inguinal ligament

12. CULLEN SIGN GREY TURNER SIGN

13. FLUID , METABOLIC , HAEMATOLOGIC & BIOCHEMICAL CHANGES Hypovolemia Hypoalbuminaemia Hypocalcemia TC is raised with neutrophilia Thrombocytopaenia with raised FDP Hypochloraemic metabolic alkalosis Hyperglycaemia Hyperbilirubinaemia Hypertriglyceridaemia Methemalbuminaemia

14. Diagnosis Typically, the diagnosis is made on the basis of the clinical presentation and an elevated serum amylase level (3x Normal)

15. Investigations Serum Amylase >1000 SU Increase within 24hrs, back to normal within 7 days Not specific Amylase Creatinine Clearance Ratio Serum Lipase

16. Investigations Plane Xrays Sentinel loop of dilated proximal small Bowel Colon Cut Off Sign ( Distention of transverse colon with collapse of descending colon) Air fluid level in Duodenum Renal halo sign Obliteration of psoas shadow

17. Investigations USG should be performed within 24 hours in all patients to detect gallstones as a potential cause, rule out acute cholecystitis as a differential diagnosis and determine whether the common bile duct is dilated. CECT Gold Standard Done after 72 hrs The severity of pancreatitis detected on CT staged according to the Balthazar criteria.

18. Investigations CECT is indicated in the following situations: If there is diagnostic uncertainty. In patients with severe acute pancreatitis to distinguish interstitial from necrotizing pancreatitis. (In the first 72 hours, CT may underestimate the extent of necrosis.) In patients with organ failure, signs of sepsis or progressive clinical deterioration. When a localized complication is suspected, such as fluid collection, pseudocyst or a pseudoaneurysm.

19. Balthazar Grading

20. A revision in 2013 of the Atlanta classification of acute pancreatitis Mild acute pancreatitis: no organ failure; no local or systemic complications. Moderately severe acute pancreatitis: organ failure that resolves within 48 hours (transient organ failure); and/or local or systemic complications without persistent organ failure. Severe acute pancreatitis: persistent organ failure (>48 hours); single organ failure; multiple organ failure.

21. Criteria for Assessment of severity Glasgow Score - for both Gall Stone & Alcohol Induced Pancreatitis Ranson Score – for Alcohol Induced Pancreatitis BISAP (Bed Side Index for Severity of Acute Pancreatitis) Score

22. RANSON SCORE On admission Age >55 years WBC >16×10 9 /L Blood glucose >11 mmol/L (>200 mg/dl) LDH > 350 units/L AST >250 units/L Within 48 hrs BUN rise > 5mg /dL (1.8 mmol/L) PaO2 <60 mmHg (<8kPa) Serum Ca <8 mg/dL (<2mmol/L) Base deficit >4 mmol /L Fluid sequestration >6L

23. Within 48 hours Age >55 years White blood cell count >15 × 109/L Blood glucose >10 mmol/L (no history of diabetes) LDH >600 units/L or AST >200 units/L Serum urea >16 mmol/L (no response to intravenous fuids ) Arterial oxygen saturation (PaO2) <8 kPa (60 mmHg) Serum Ca < 2mmol/L Serum albumin <32g/L GLASGOW SCALE In both systems, disease is classified as SEVERE if 3 or more factors are present

24. MANAGEMENT Conservative Management (70-90%) Surgical Management when indicated (10-30%) Management of complications

25. MILD ACUTE PANCREATITIS Conservative management IVF (RL/NS) and Non Invasive Monitoring like Brief period of fasting With RT in Pt With N&V (No prolonged NBM) Analgesics, Anti-emetics No antibiotics If pt deteriorating - ICU admission & invasive monitoring of Pt.

26. SEVERE ACUTE PANCREATITIS Admission to ICU Analgesia Aggressive fluid rehydration guided by frequent measurement of vital signs, urine output and central venous pressure O2 supplementation Frequent monitoring of ABG, Hematocrit, clotting profile, blood glucose and serum levels of calcium and magnesium

27. SEVERE ACUTE PANCREATITIS Nasogastric drainage Enteral nutrition if nutritional support necessary Antibiotic prophylaxis CT scan essential if organ failure, clinical deterioration or signs of sepsis develop ERCP within 72 hours for severe gallstone pancreatitis or signs of cholangitis Supportive therapy for organ failure if it develops (inotropes, ventilatory support, hemofiltration, etc.)

28. Role of Antibiotics Prophylactic antibiotics in patients with severe acute pancreatitis to prevent local and other septic complications. Severe infected necrosis with or without proved culture If, there is evidence of cholangitis or concomitant respiratory or urinary infection Pancreatic abscess formation Rapidly progressing disease with deterioration Regime Cefuroxime / Imipenem/Ciprofloxacin + Metronidazole

29. SURGERY INDICATIONS Condition of pt deteriorates Formation of pancreatic absess or infected necrosis In severe necrotising pancreatitis Diagnosis in doubt OPEN SURGERY – gold std for infected pancreatic necrosis

30. CONVENTIONAL CLOSED METHOD Open abdomen - necrotic tissue, pus, infected fluid and toxins removed NS wash (10-20 L ). Drainage tubes placed . Abdomen closed in layers OPEN METHOD. Laprotomy - necrosectomy - wide debridement wash - wide packing. wound left open – SEMI OPEN METHOD. Laprotomy - necrosectomy closure with drain Then relaprotomy later

31. ZIP technique used for repeated wash to remove toxins and necrotic tissues until healthy granulation tissue develops in pancreatic bed BRADLEY’S REPEATED LAPROTOMIES AND WASH. CLOSED CONTINOUS LAVAGE (BEGER’S LAVAGE) panceatic bed and lesser sac 10-20L(NS/ hyperosmolar K+ free dialysate ) fluid 2L /hr( after initial debridement) to remove toxic material in peritoneal cavity/ retroperitoneal area until return fluid becomes clear.

32. Extra peritoneal lavage through b/l flank incisions is also done Laproscopy necrosectomy ,wash and drainage Jejunostomy is often done with these procedures to have early enteral nutrition. Endoscopic necrosectomy early endoscopic intervention ( within 48 hrs) with ERCP biliary stone removal and stenting in biliary pancreatitis can be done.

33. Further management to prevent recurrence of gallstones by laproscopic cholecystectomy 2 wks after a/c attack during same admission period. Endoscopic spincterectomy (ERCP) and often stenting may be needed if there are CBD stones

34. COMPLICATIONS Systemic (more common in 1 st week) CVS – Shock (due to large volume of fluid sequestration) & Arrhythmias Pulmonary - ARDS RF (toxin ATN) Hematological - DIC (diffuse oozing in pancreatic bed-utilizes platelets) GIT - Paralytic Ileus Metabolic – Hypocalcaemia , Hyperglycaemia , Hyperlipidaemia Neurological - Visual disturbances, Confusion, irritability, encephalopathy Subcutaneous fat necrosis

35. COMPLICATIONS Local Complications Acute peripancreatic fluid collection (APFC) Sterile pancreatic necrosis Infected Pancreatic Necrosis Pancreatic abscess Pseudocyst Pancreatic ascites Pleural effusion Portal/splenic vein thrombosis Pseudoaneurysm

36. Acute Peripancreatic Fluid Collection Occurs in early phase Located in or near the pancreas Sterile and most such collections resolve by itself Large collection causing pressure effect - aspirated under US/CT guidance or Transgastric drainage under EUS guidance. Can evolve into pseudocyst or abscess if gets infected

37. Sterile and Infected Pancreatic Necrosis Diffuse or focal area of non-viable parenchyma that is typically associated with peripancreatic fat necrosis Identified by absence of contrast enhancement on CT Sterile to begin with, but can become subsequently infected, probably due to translocation of gut bacteria If signs of sepsis, under CT/US guidance, needle passed into the area and aspirated to determine infected collection - if purulent, drainage of infected fluid

38. Sterile and Infected Pancreatic Necrosis Internal drainage into the stomach under EUS Guidance Percutaneous Drainage Pancreatic necrosectomy should be considered if sepsis worsens despite conservative measures. After Necrosectomy Further necrotic tissue managed by Closed continuous lavage ( Beger ) Closed drainage Open packing Closure and relaparotomy(Bradley)

39. Pancreatic Abscess Circumscribed intra-abdominal collection of pus, in proximity to pancreas Can be Acute Necrotic Collection or Walled Off Necrotic Collection that get infected. Management are as outlined above for infected pancreatic necrosis Endoscopic internal drainage or, failing that, percutaneous drainage with the widest possible drains along with appropriate antibiotics and supportive care Very occasionally, open drainage is needed.

40. Pancreatic Ascites Chronic, generalized, peritoneal, enzyme-rich effusion usually associated with pancreatic duct disruption Paracentesis – turbid fluid with high amylase levels Rx- drainage with wide bore drains placed under imaging guidance To suppress pancreatic secretion: Parenteral/ nasojejunal feeding Administration of octreotide ERCP- demonstration of duct disruption & placement of pancreatic stent

41. Pancreatic Effusion Encapsulated collection of fluid in pleural cavity, arising as a consequence of acute pancreatitis Concomitant pancreatic ascites or communication with an intra-abdominal collection Rx- p/c drainage under image guidance

42. Hemorrhage Can occur into gut, retroperitoneum or peritoneal cavity. Causes - bleeding into a pseudocyst cavity, diffuse bleeding from a large raw surface, or a pseudoaneurysm (false aneurysm of a major peripancreatic vessel confined as a clot by the surrounding tissue and often associated with infection.) Dx - CT angiography , or magnetic resonance angiography Rx - embolisation or surgery.

43. Portal or splenic vein thrombosis Identified on a CT scan. A marked raise in platelet count should raise suspicions. Usually conservative Rx. If varices or manifestations of portal HTN develop – endoscopic injection or banding , beta blockers , etc… Thrombocytosis – aspirin or other anti platelet drugs.

44. Pseudocyst Collection of amylase-rich fluid enclosed in a well-defined wall of fibrous or granulation tissue Smooth rounded swelling , fluctuation + Arise following – Mild Acute Pancreatitis, Chronic Pancreatitis, Pancreatic Trauma Have communication with main pancreatic duct Formation requires 4 wks or > from the onset of a/c pancreatitis Identified on CT/USG X-ray with barium meal (lateral) Pseudocysts usually resolve spontaneously Therapeutic intervention is advised only if the pseudocyst causes symptoms, complications develop or distinction has to be made between a pseudocyst and a tumour.

45. Pseudocyst Management There are three possible approaches to draining a pseudocyst: percutaneous, endoscopic and surgical A percutaneous trans gastric cyst gastrostomy can be performed under imaging guidance, and a double-pigtail drain placed with one end in the cyst cavity and the other end in the gastric lumen. Endoscopic puncture of the cyst through the stomach or duodenal wall under EUS, and placement of a tube drain with one end in the cyst cavity and the other end in the gastric lumen Surgical drainage involves internally draining the cyst into the gastric or jejunal lumen

46. The fluid should be sent for measurement of carcinoembryonic antigen (CEA) levels, amylase levels and cytology. Fluid from a pseudocyst typically has a low CEA level, and levels above 400 ng/mL are suggestive of a mucinous neoplasm