Acute pancreatitis surgery seminar

pancreatitis

1. ACUTE PANCREATITIS

2. ANATOMY Soft , lobulated , elongated retroperitoneal organ Lies transversely across the posterior abdominal wall posterior to stomach b/w duodenum on right and spleen on left At the level of L1 & L2 vertebrae J shaped or retort-shaped 15-20cm long PARTS – head, neck, body and tail

3. Ducts of Pancreas Main pancreatic duct of Wirsung Begins in the tail of pancreas and runs on the posterior surface of body and head. Accessory pancreatic duct of Santorini Begins in the lower part of head and opens in to the duodenum.

4. Ducts of Pancreas

5. BLOOD SUPPLY Pancreatic branch of splenic artery Superior pancreaticoduodenal artery Inferior pa ncreaticoduodenal artery VENOUS DRAINAGE Splenic vein Superior mesenteric vein

6. NERVE SUPPLY Parasympathetic by Vagus Sympathetic by Splanchnic LYMPHATIC DRAINAGE Pancreaticosplenic (most) Pyloric(some) Coeliac Superior mesenteric

7. HISTOLOGY Main pancreatic duct divides into interlobular, intralobular ducts, ductules & acini Main duct is lined by columnar cells which becomes cuboidal in the ductules Exocrine part- serous compound tubulo -alveolar gland containing zymogen granules secreted into lumen of acinar cells which communicates with duct system Endocrine part- Islets of Langerhans scattered throughout the gland

8. FUNCTIONS EXOCRINE Pancreatic juice Trypsinogen , Chymotrypsinogen,Proelastase , Procarboxypolypeptidase , Pancreatic lipase,Pancreatic α - amylase, Bile salt acid lipase ENDOCRINE α cells- Glucagon β cells- Insulin δ cells- Gastrin , Somatostatin F cells- Pancreatic Polypeptide

9. ACUTE PANCREATITIS It is the acute inflammation of prior normal gland parenchyma Usually reversible With raised pancreatic enzyme level in blood and urine Commonly caused by biliary tract d/s

10. Trapnell’s Etiological Classification MAJOR CAUSES Biliary tract disease (50-70%)- gallstones Alcoholism - 25% OTHER CAUSES Post-ERCP - duct disruption and enzyme extravasation Abdominal trauma Following biliary , upper GI or splenic surgery Drugs - corticosteroids, INH, azathioprine , valproic acid, thiazides , oestrogens , tetracycline Hyperparathyroidism Hypercalcaemia Hyperlipidemia

11. Autoimmune pancreatitis Vascular – shock, atheroembolism , vasculitis Viral infections- mumps, Coxsackie B Porphyria Biliary ascariasis , Clonorchis sinensis Infectious mononucleosis Mycoplasma pneumoniae Scorpion bite Idiopathic

12. ATLANTA CLASSIFICATION A/c edematous pancreatitis (80%) A/c necrotising pancreatitis (20%) PRESENT CLASSIFICATION OF A/C PANCREATITIS Interstitial a/c pancreatitis Necrotising pancreatitis -Sterile necrosis -Infected necrosis( CT guided aspiration and Grams stain – Pancreatic necrosectomy )

13. ORGANISMS INVOLVED Commonly Polymicrobial From gall bladder, colon or small bowel via transmural migration or by haematogenous spread E.coli (35%) Klebsiella (25%), Enterococcus (25%) Others- Staphylococci, Pseudomonas, Proteus, Enterobacter , Anaerobes, Candida(10%)

14. Normal Physiology Meal Pancreatic juice with proenzyme enteropeptidase Trypsinogen Trypsin Chymotrypsinogen Chymotrypsin Procarboxy carboxy polypeptidase polypeptidase Proelastase Elastase Procolipase Colipase Primarily under hormonal control : CCK, Secretin

15. Mechanisms of Activation of Pancreatic Enzymes Pancreatic Duct Obstruction - raised intrapancreatic ductal pressure and accumulation of enzyme-rich fluid in the interstitium Primary Acinar Cell Injury – release of intracellular proenzymes and lysosomal hydrolases which further activate the enzymes Defective Intracellular Transport of Proenzymes within Acinar Cells Germline Mutation in Cationic Trypsinogen (PRSS1) and Trypsin Inhibitor (SPINK1) genes

16. PATHOGENESIS

17. 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

18. Longitudinal section- dark areas of hemorrhage in the head of pancreas and focal area of pale fat necrosis in the peripancreatic fat

19. Symptoms Pain - Sudden onset of upper abdominal,severe Pain agonising , excruciating and constant - in the Epigastrium – tends to pierce to back or left loin, refractory to analgesics and relieves on stooping forward, food & alcohol increases pain Vomiting Hiccough – gastric distension/irritation of diaphragm Fever – Low grade Haemetemesis and malaena (duodenal necrosis, gastric erosion, decreased coagulability )

20. Signs Features of shock – thready pulse, tachycardia, hypotension, cold extremities Cyanosis Tachypnoea Mild Icterus ( biliary obstruction) Temperature : n/l or subnormal Rebound tenderness Muscle guarding in the upper abdomen Abdominal distension Mass in the epigastrium

21. Cullen’s sign – bluish discolouration around the umbilicus Grey turner’s sign – bluish discolouration of the flanks (enzymes sweep across the retroperitoneum causing hemorrhagic spots & ecchymosis) Fox’s sign – bluish discolouration below the inguinal ligament

22. CULLEN SIGN GREY TURNER SIGN

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

24. Investigations SerUM amylase >1000 SU Increase within 24hrs, back to normal within 7 days) Not specific Other conditions where raised: Salivary gland inflammation Upper GIT perforation Mesenteric infarction Torsion of an abdominal viscus Ectopic gestation Salpingitis Retroperitoneal hematoma Renal failure

25. ACR >6% Amylase Creatinine Clearance Ratio Serum lipase - more sensitive and specific, persists for longer period Serum lactescence (TG metabolism) – Most specific in hereditary hyperlipidaemia or alcohol pancreatitis Serum trypsin –(Most accurate) Not commonly done TAP assay in serum & urine – severity Hb % low in haemorrhagic pancreatitis WBC Total count raised >15000/ cumm – inflammation CRP >150mg/L

26. Blood sugar – hyperglycemia Serum Calcium – Hypocalcemia Blood Urea Serum Creatinine Platelet count Coagulation profile LFT - gallstone associated pancreatitis ABG – pulmonary insufficiency Peritoneal tap fluid - high amylase and protein

27. Radiographic Findings Plain X-ray of abdomen ‘ Sentinal loop’ of dilated proximal small bowel Distension of transverse colon with collapse of descending colon (Colon cut off sign) Renal halo sign Calcified gallstones or pancreatic calcification Obliteration – psoas shadow Localised ground class appearance Plain X-ray Chest Pleural effusion Diffuse alveolar interstitial shadowing

28. COLON CUT OFF SIGN

29. USG Abdomen Does not establish a diagnosis of acute pancreatitis Swollen pancreas may be seen Should be done in all patients to detect gallstones, rule out acute cholecystitis , determine dilatation of common bile duct

30. CT SCAN SPIRAL CT – gold standard Pancreatic changes Parenchymal enlargement- diffuse /focal Parenchymal edema Necrosis ( non enhancement area - >30% or 3cm) Peripancreatic changes- Blurring of fat planes, thickening of fascial planes, presence of fluid collections Nonspecific findings - Bowel distention, pleural effusion, mesenteric edema

31. Contrast Enhanced CT (Not necessary for all patients especially mild attacks) Indications - Diagnostic uncertainty Severe - ( necrotising /interstitial) Organ failure, sepsis signs, progressive clinical deterioration Localised complication suspected – fluid, pseudocyst , pseudoaneurysm

32. BALTHAZAR CT SCORING SYSTEM CT Grade: A – normal pancreas – B - oedematous pancreatitis – 1 C -mild extrapancreatic changes – 2 D - Severe extrapancreatic changes with fluid collection – 3 E - Extensive/multiple extrapancreatic collections or gas bubbles in or adjacent to pancreas - 4

33. Necrosis score: None – 0 <1/3 rd – 2 >1/3 rd <1/2 – 4 >1/2 - 6 CT severity index- CT grade + necrosis score 0-3, 4-6, 7-10

34. MRI - similar information to CT EUS, MRCP - stones in CBD, directly assess pancreatic parenchyma ERCP - identification and removal of stones in the CBD in gallstone pancreatitis, recurrent attacks without obvious etiology

35. Differential Diagnosis Perforated duodenal ulcer Cholecystits Mesenteric ischaemia Ruptured aortic aneurysm Ectopic gestation Salpingitis Intestinal obstruction Diabetic ketoacidosis

36. ASSESSMENT OF SEVERITY Scoring Systems: Ranson Glassgow APACHE II

37. RANSON SCORE On admission Age >55 years WBC>16×10 9 /L Blood glucose >10 mmol /L LDH >700units/L AST >250 units/L Within 48 hrs BUN rise >5mg% PaO2 <60 mmHg Serum Ca <2mmol/L Base deficit >4 mmol /L Fluid sequestration >6L

38. On admission Age >55 years WBC count >15x10 9 /L Blood glucose >10mmol/L Serum urea >16mmol/L PaO2 <60 mmHg Within 48 hours Serum Ca < 2mmol/L Serum albumin <32g/L LDH >600 units/L AST/ALT>600 units/L GLASGOW SCALE In both systems, disease is classified as SEVERE if 3 or more factors are present

39. APACHE II A/c physiology and c/c health evaluation. age , rectal temperature ,mean arterial pressure ,heart rate ,partial pressure - oxygen ,arterial pH,serum pottasium ,serum sodium, serum creatinine,hematocrit,WBC . APACHE-O-obesity is added . Score >8 -11%-18% mortality.

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

41. MILD ACUTE PANCREATITIS Conservative management IVF(ringer lactate/NS) analgesics, anti-emetics no antibiotics A brief period of fasting if pt is nauseated & in pain If pt deteriorating - ICU admission & invasive monitoring of pt

42. SEVERE ACUTE PANCREATITIS Admission to ICU Analgesia Aggressive fluid rehydration O2 supplementation Invasive monitoring of vital signs, central venous pressure, urine output Frequent monitoring of haematological and biochemical parameters Nasogastric drainage Enteral nutrition if nutritional support necessary Antibiotic prophylaxis Urgent ERCP - for gallstone pancreatitis

43. INDICATIONS FOR ANTIBIOTICS Severe infected necrosis with proved culture Prophylactic Ab therapy in severe pancreatitis Biliary pancreatitis with biliary stone & cholangitis Pancreatic abscess formation Rapidly progressing disease with deterioration CEFUROXIME / IMIPENEM/CIPROFLOXACIN +METRONIDAZOLE

44. 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

45. 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

46. 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.

47. 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.

48. 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

49. COMPLICATIONS Systemic (most common in 1 st week) Shock(large volume of fluid sequestration) Arrhythmias ARDS ( Lecithinase reduces surfactants) RF (toxin ATN) DIC (diffuse oozing in pancreatic bed-utilizes platelets) Paralytic Ileus Hypocalcaemia Hyperglycaemia Hyperlipidaemia Visual disturbances Confusion, irritability, encephalopathy Subcutaneous fat necrosis

50. LOCAL COMPLICATIONS A/c fluid collection Sterile pancreatic necrosis Pancreatic abscess Pseudocyst Pancreatic ascites Pleural effusion Portal/ splenic vein thrombosis Pseudoaneurysm

51. Acute Fluid Collection Occurs in early phase Located in or near the pancreas The fluid is sterile with ill defined wall Most such collections resolve by itself Large collection causing pressure effect - aspirated under US/CT guidance Transgastric drainage under EUS guidance. Can evolve into pseudocyst or abcess if gets infected

52. 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 guidance, needle passed into the area and aspirated- if purulent, do p/c drainage of infected material

53. Appropriate Ab as per the microbiological assessment of aspirate Necrosectomy- thorough debridement of dead tissue Midline laparotomy/ Lt flank incision Further necrotic tissue managed by Closed continuous lavage (Beger) Closed drainage Open packing Closure and relaparotomy(Bradley)

54. CLOSED DRAINAGE – the incision is closed , but the cavity is packed with gauze-filled penrose drains .The penrose drains are brought out through the flank and slowly pulled out and removed after 7 days.

55. Pancreatic Abscess Circumscribed intra-abdominal collection of pus, in proximity to pancreas Acute fluid collection or an infected pseudocyst Treatment - p/c drainage with widest possible drain under image guidance along with antibiotic and supportive care Very occasionally ,open drainage is needed.

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

57. 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

58. H aemorrhage 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.) CT angiography , or magnetic resonance angiography -diagnosis Rx – embolisation or surgery.

59. 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.

60. Pseudocyst Collection of amylase-rich fluid enclosed in a wall of fibrous or granulation tissue in lesser sac of peritoneal cavity. Smooth rounded swelling , fluctuation + Arise following—a/c pancreatitis, c/c pancreatitis, pancreatic trauma Have communication with main pancreatic duct Formation requires 4wks or > from the onset of a/c pancreatitis Identified on CT/USG X-ray with barium meal (lateral)

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