Acute pancreatitis

Surgical education

1. ACUTE PANCREATITIS Foyez Ahmed Hasan Batch K-68

2. Acute Pancreatitis Acute inflammation of the gland parenchyma of the pancreas Types Mild acute pancreatitis Severe acute pancreatitis Atlanta classification Acute oedematous pancreatitis (80%) Milder form, mortality is <1% Acute necrotising pancreatitis (20%): Characterised by pancreatic and peripancreatic necrosis. Mortality is ≈ 15% - 30% Present Classification of Acute Pancreatitis Interstitial acute pancreatitis with mortality less than 1%. Necrotizing pancreatitis. Sterile necrosis with mortality 10%. Infected necrosis with mortality 30-40%. It is confi rmed by CT guided aspiration and Gram’s stain. When confi rmed , needs pancreatic necrosectomy . Note: In Ulm classii cation pancreatic abscess and pseudocysts are also included. Incidence Acute pancreatitis accounts for 3% of all cases of acute abdomen in UK The disease may occur at any age, with a peak of young men & older women

3. Aetiology MNEMONICS : BAPPI’s SHIT PAD B : Billiary stone A : Alcoholism P : Post ERCP P : Post Operative ( following billiary , upper gastro intestinal or cardiothoracic surgery ) I : Idiopathic S : Scorpion bite H : Hyperparathyroidism, Hypercalcemia , Hereditary pancreatitis I : Infection ( Mumps, Coxsackie B ) T: Tumor ( Ampullary ), Trauma (Abdominal) P : Pancreatic divisum A : Autoimmune pancreatitis D : Drugs ( corticosterooids , Thiazides , valproic acids etc.A )

4. Pathogenesis Pancreatitis is due to enzymatic digestion of the gland Principal injurious agents are phospholipase A , lipase & elastase Phospholipase A in presence of small amounts of bile acids attack phospholipid & capable of producing severe necrotizing pancreatitis Elastase which is both elastolytic & proteolytic can digest walls of blood vessels in Haemorrhagic pancreatitis Autodigestion is the final common pathway of pancreatitis

5. Pathogenesis Pancreatic duct obstruction Gallstones or biliary sludge impacted in the region of the ampulla of Vater ↓ raised intrapancreatic ductal pressure ↓ accumulation of enzyme-rich fluid in the interstitium ↓ Since lipase is one of the few enzymes secreted in an active form, this can cause local fat necrosis ↓ Injured tissues, periacinar myofibroblasts , and leukocytes then release proinflammatory cytokines including IL-1β, IL-6, tumor necrosis factor, platelet-activating factor, and substance P ↓ Initiation of local inflammation ↓ development of interstitial edema through a leaky microvasculature ↓ Edema may further compromise local blood flow ↓ vascular insufficiency ↓ ischemic injury to acinar cells

6. Pathogenesis Primary acinar cell injury viruses (e.g., mumps), drugs, and direct trauma to the pancreas, as well as pancreatitis following ischemia or shock ↓ Direct attack on acinar cells ↓ Release of pro enzymes & lysosomal hydrolases ↓ Activation of the enzymes ↓ Acinar cell injury   

7. Pathogenesis Defective intracellular transport of proenzymes within acinar cells (In normal acinar cells, digestive enzymes and lysosomal hydrolases are transported in separate pathways) Metabolic injury,alcohol,duct obstruction ↓ the pancreatic proenzymes are inappropriately ↓ delivered to the intracellular compartment containing lysosomal hydrolases . ↓ Proenzymes are then activated ↓ the lysosomes disrupted ↓ activated enzymes released ↓ Acinar cell injury (The role of this mechanism in human acute pancreatitis is not clear.)

8. Pathogenesis Proelastase to elastase Prolipase to lipase. ↓ ↓ Causes capillary rupture Metabolises triglycerides to glycerol + fatty acids and fatty acids combine with calcium forming saponified fat. ↓ ↓ Sequestered fl uid , saponifi ed fat, blood, toxins all together forms a chicken broth fl uid .

9. On table photos of acute pancreatitis. Note the typical saponification in the omentum and mesentery.

10. Effects of alcohol on pancreas

11. Clinical Presentation Symptoms Pain develops quickly, reaching maximum intensity within minutes rather than hours and persists for hours or even days The pain is frequently severe,constant and refractory to the usual doses of analgesics. Pain is usually experienced first in the epigastrium but may be localised to either upper quadrant or felt diffusely throughout the abdomen. There is radiation to the back in about 50% of patients, some patients may gain relief by sitting or leaning forwards.

12. Clinical Presentation The suddenness of onset may simulate a perforated peptic ulcer, biliary colic or acute cholecystitis can be mimicked if the pain is maximal in the right upper quadrant . Radiation to the chest can simulate myocardial infarction, pneumonia or pleuritic pain In fact, acute pancreatitis can mimic most causes of theacute abdomen and should seldom be discounted in differential diagnosis.

13. DD Perforation of peptic ulcer Acute Cholecystitis Cholangitis Myocardial infarction Pneumonia

14. Features of acute pancreatitis with necrosis in the omentum and over pancreas; with haemorrhage .

15. Clinical Presentation Nausea, repeated vomiting and retching Hiccoughs (due to gastric distension or irritation of the diaphragm) SIGN In severely ill patients features of profound shock , toxicity & mental confusion may present Tachypnoea & tachycardia are common.Hypotension may be present. The body Temperature is often normal or even subnormal , but frequently Rises as inflammation develops Mild icterus can be caused by bilIary obstruction in gallstone pancreatitis

16. Clinical Presentation Grey-Turner’s sign : enzymes seep across the retroperitoneum causing haemorrhagic spots and ecchymosis in the flanks Cullen’s sign : enzymes seep through falciform ligament causing discolouration around the umbilicus Haematemesis / malaena due to duodenal necrosis, gastric erosions, decreased coagulability /DIC. Ascites may be present.so abdomen is distended Paralytic ileus is common.

17. Grey-Turner’s sign

18. Clinical Presentation Pleural effusion (20%), pulmonary oedema , consolidation, features of rapid onset ARDS is often observed ( Lecithinase reduces the surfactant in the alveoli of lung, and infection leads to pulmonary insuffi ciency , ARDS and respiratory failure. ) Neurological derangements due to toxaemia , fat embolism, hypoxia, respiratory distress can occur. It may be mild psychosis to coma.

19. Clinical Presentation Tenderness rebound tenderness guarding rigidity

20. So, If a pt comes to us with acute pancreatitis…..what will we Search & what will we find History : Gall stone disease Alcohol Recent surgery or trauma ERCP General exam: Appearance : Toxic Temp : usually increased Pulse : increased BP : Decreased

21. Examination Local examination( Abdomen ) Inspection Abdomen is distended due to paralytic ileus and due to sequestrastion of fluid Grey turner sign Cullen sign Palpation Superficial : localized tenderness,rise of temp,muscle guard,rigidity Deep : epigastric lump due to imflammation

22. Examination Percussion Sign’s of ascitis i.e. shifting dullness and fluid thrill D/R/E : fluid collection in recto-vesicle pouch or pouch of douglas Other sustemic examination: RESPIRATORY SYSTEM Pleural effusion in 10-20 % cae

23. Complications Systemic (More common in first week) Metabolic Hypocalcaemia Hypoglycaemia Hyperlipidaemia Neurological Visual disturbance Confusion, irritability Miscellaneous Subcutaneous fat necrosis Arthralgia Cardiovascular Shock Arrhythmias Pulmonary ARDS Renal failure Haematological DIC Gastrointestinal Paralytic ileus

24. Complications Local (Usually develop after first week) Acute fluid collection Sterile pancreatic necrosis Infected pancreatic necrosis Pancreatic abscess Pseudo cyst Pleural effusion Portal/ Splenic vein thrombosis Pseudo anyurism

25. Pathogenesis of the complications Toxins released may lead to acute tubular necrosis and so acute renal failure. Left sided diaphragm gets elevated and left sided pleural effusion occurs. Lecithinase reduces the surfactant in the alveoli of lung, and infection leads to pulmonary insuffi ciency , ARDS and respiratory failure. Because calcium is utilised for saponifi cation , hypocalcaemia sets in. Diffuse oozing in pancreatic bed occurs which utilizes platelets and causes disseminated intravascular coagulation (DIC). In severe cases, extensive necrosis with haemorrhage occurs causing acute haemorrhagic necrotising pancreatitis ( Fulminant pancreatitis), which has got a high mortality.

26. Pathogenesis of the complications Hypovolemia due to diffuse capillary leak and vomiting causing raised haematocrit , blood urea, serum creatinine levels. Hypoalbuminaemia which is more revealed after fluid correction. Hypocalcaemia is either due to decreased albumin level or specifi c loss of ionized calcium. Hypocalcaemia due to reduced ionised calcium carries poor prognosis. Response of calcium reserve in bone to PTH is also reduced. Total count is raised with neutrophilia . Thrombocytopenia, raised FDP, decreased fibrinogen , prolonged partial thromboplastin time and PT—are common. DIC can develop later.

27. Pathogenesis of the complications Hypochloraemic metabolic alkalosis is common due to repeated vomiting. Reduced insulin secretion, increased glucagon and catecholamine secretion causes hyperglycaemia , more so in diabetic patients. Hyperbilirubinaemia may be due to biliary stone/obstruction or cholangitis or non-obstructive cholectasis . Hypertriglyceridaemia is common especially in hyperlipidaemic patients. Methemalbuminemia , when it occurs in acute pancreatitis indicates poor prognosis.

28. Investigation Routine Investigation CBC with ESR : Moderate leukocytosis ( 12000/ cumm ) Thrombocytopenia Hematocrit High due to dehydration Low due to blood loss in hemorrhagic pancreatitis Blood urea ,s. creatinine : increased Chest X-ray : for pleural effusion and ARDS

29. Investigations Biochemical For diagnosis Serum lipase: more sensitive & specific Increase several day after an acute attack Serum amylase: Normal : 200-250 IU/L may increases 3 -4 times above normal ( >1000 IU/dl is diagnostic) Increased within 24-48 hours. Decrease in next 4-8 hours

30. Investigation For assessment of severity of disease Blood glucose Serum urea Serum calcium LDH AST/ ALT Arterial oxygen saturation Prognosis scales : Ranson criteria Glasgow score APACHE II scoring system

31. Ranson’s criteria for severity of Acute Pancreatitis On admission “ GA LAW “ A ge >55 years W BC count >16,000/ml Blood g lucose>( 10 mmol /L) Serum L DH >700 Units/L A ST (SGOT) >250 Units/L Disease is severe if 3 or more criteria are present Within 48 hours “ COBBS “ B UN rise > 5 mg/dl Arterial P O 2 <60 mm of Hg Serum Ca <2mmol/L B ase deficit >4 mmol /L Fluid s equestration>6 Litres Mortality rates correlate as follows 0-2 criteria = 2%, 3-4 = 15%, 5-6 = 40%, 7-8 = 100%

32. Glasgow scale On admission Age > 55 years White blood cell count > 15 x 109/ L Blood glucose > 10 mmol /L(no history of diabetes) Serum urea > 16 mmol /L(no response to intravenous fluids ) Arterial oxygen saturation (PaO2) < 8 kPa (60 mmHg) Within 48 hours Serum calcium < 2.0 mmol /L Serum albumin < 32 g/L LDH > 600 units/L AST/ALT > 600 units/L

33. Investigations Imaging study Non invasive Plain radiograph of chest & abdomen USG CT scan ( Best single imaging investigation ) MRI (Cross-sectional MRI can yield similar information to that obtained by CT) MRCP (EUS and MRCP can help in detecting stones in the common bile duct and directly assessing the pancreatic parenchyma , but are not widely available )

34. Minimally invasive Endoscopic USG ERCP ERCP allows the identification and removal of stones in the common bile duct in gallstone pancreatitis In patients with severe acute gallstone pancreatitis and signs of ongoing biliary obstruction and cholangitis , an urgent ERCP should be sought MRI, MRCP—should be done at a later date. ERCP is usually not done in acute phase. Chest X-ray for effusion and ARDS. EUS—to see necrosis, calcifications and to assess CBD . The presentation is so variable that sometimes even an experienced clinician can be mistaken. While this is not desirable occasionally the diagnosis is only made at laparotomy . The appearances at laparotomy are characteristic

35. Balthazar CT Scoring System (Emil Balthazar, 1990) CT grade: A—Normal pancreas—0 B— Oedematous pancreatitis—1 C—B+ mild extrapancreatic changes—2 D—Severe extrapancreatic changes with one fluid collection—3 E—Extensive/multiple extrapancreatic collections or gas bubbles in or adjacent to pancreas—4 Necrosis score: None—0 < 1/3rd—2 More than 1/3rd less than half—4 More than half—6 CT severity index— CT grade + necrosis score 0—3, 4—6, 7—10.

36. CT picture showing features of acute pancreatitis

37. Plain X-ray shows ‘ Sentinel loop ’ of dilated proximal small bowel : Isolated dilatation of a segment of gut consists of jejunum,transverse colon,dudenum ajacent to pancreas. ‘ colon cut off sign’ : Distension of transverse colon with collapse of descen ding colon due to colonic spasm adjacent to pancreatic inflammation Air- fluid level in the duodenum. Renal halo sign : edema around the kidney Obliteration of psoas shadow. Localized ground glass appearance : in acut ehemorrhagic pancreatitis

38. CT 100 % DIAGNOSTIC CT is not necessary for all patients, particularly those deemed to have a mild attack on prognostic criteria. But a contrast-enhanced CT is indicated in the following situations: if there is diagnostic uncertainty in patients with severe acute pancreatitis, to distinguish interstitial from necrotising pancreatitis In the first 72 hours, CT may underestimate the extent of necrosis. The severity of pancreatitis detected on CT may be staged according to the Balthazar criteria in patients with organ failure, signs of sepsis or progressive clinical deterioration when a localised complication is suspected, such as fluid collection, pseudocyst or a pseudoaneurysm .

39. USG OF HBS WITH PANCREAS USG can detect Swollen pancreas Free peritoneal fluid GSD Dilatation of CBD Occasionally abdominal aortic aneurism Ultrasound does not establish a diagnosis of acute pancreatitis. ultrasonography should be performed within 24 hours in all Patients to detect gallstones as a potential cause rule out acute cholecystitis as a differential diagnosis determine whether the common bile duct is dilated.

40. TREATMENT If after initial assessment a patient is considered to have a mild attack of pancreatitis, a conservative approach is indicated with intravenous fluid administration and frequent, but non-invasive, observation Treatment of acute pancreatitis Conservative, 70-90% Surgical treatment when indicated, 10-30% Management of complications like acute pseudocyst , Abscess fistula , haemorrhage systemic complications like ARDS, renafailure , MODS

41. Treatment Medical treatment of severe acute pancreatitis Immediate hospitalization and resuscitation N/P/O and NG tube Intubation and suction IV access with wide bore cannula Rehydration is essential (250-400 ml / hour) as there is lot of fluid sequestration and 3rd space fluid loss. It is done by using ringer lactate, normal saline, dextrose saline , plasma and fresh blood transfusion/packed cells. Pain relief by pethidine and other analgesics. Morphine is not used as it causes spasm of sphincter of Oddi .

42. Treatment In severe haemorrhagic episodes, fresh frozen plasma and platelet concentrate may be required in anticipation of DIC and haemorrhage . urinary catheterisation to maintain and monitor urine output 50 ml hourly. ( maintain input output chart ) Antibiotics like third generation cephalosporins , imipenem , meropenem , cefuroxime are used even though its role is not clear but it is commonly used to reduce the anticipated sepsis.

43. Treatment Calcium gluconate 10 ml 10% IV 8th hourly is given as patient will be hypocalcaemic . CVP line is essential to monitor, for rapid fluid therapy and for Total Parenteral Nutrition (TPN) using carbohydrate,amino acids, vitamins, essential elements. IV Ranitidine 50 mg 6th hourly or IV omeprazole 40 mg BD or IV pantoprazole 80 mg BD to prevent stress ulcers and erosive bleeding . Proper electrolyte management with monitoring is needed. Oxygen: if PaO2 levels falls bellow 70mm Hg that occurs in 30 % pt Parenteral nutrition to avoid stimulating pancreas

44. It is always better to manage the patient in an intensive care set up so that when needed endotracheal intubation, ventilatory support, tracheostomy can be done as an emergency basis. In case of renal failure haemodialysis is required. Somatostatin / octreotide is often used to reduce pancreatic secretion. Anticholinergics , protease inhibitors and calcitonin are other agents used. Their effiicacy is not sure. Steroid injection in initial phase of shock is beneficial . It is also useful in respiratory distress and ARDS.

45. Nebulisation , bronchodilators are also tried. Nasojejunal tube placement and feeding should be started as early as possible once ileus subsides so that it reduces the infection rate by transmucosal migration of bacteria and it also improves nutritional status. During recovery period nasogastric feeding or jejunostomy feeding can be undertaken. Repeated calcium estimation, U/S examination to see the response is useful. Dopamine or low molecular weight dextran (to improve renal perfusion) somatostatin / octreotide (to reduce pancreatic secretion) are also often used. Management of complications like acute lung injury, atelectasis , renal failure, GI bleeding, metabolic encephalopathy, electrolyte deficiency as and when needed by repeated observation and evaluation.

46. Surgery Indications for Surgical Intervention (10% cases) If condition of patient deteriorates in spite of good conservative treatment. If there is formation of pancreatic abscess, or infected necrosis. When diagnosis is in doubt. In severe necrotising pancreatitis as a trial to save the life of the patient which has got very high mortality

47. Treatment Procedures Cholecystectomy , Choledocotomy , Sphincteroplasty in gallstone pancreatitis Debridement of dead pancreatic tissue Surgery for complications Minimally invasive Endoscopic sphincterotomy