Management of acute pancreatitis

MANAGEMENT OF ACUTE PANCREATITIS, Cholelithiasis (50%)
Alcoholism (25%)
Post-operative pancreatitis Metabolic disorder
Hyperlipidemia
Diabetes
Nutritional factors
Chemotoxic and iatrogenic causes
Idiopathic pancreatitis
Miscellaneous- scorpion bite, worm infestations

1. MANAGEMENT OF ACUTE PANCREATITIS DR BASHIR BIN YUNUS GENERAL SURGERY UNIT AKTH 26-Feb-16 [email protected] 1

2. OUTLINE INTRODUCTION Definition Epidemiology Etiology PATHOGENESIS CLINICAL FORMS MANAGEMENT Algorithm Investigations and risk assessment Treatment PROGNOSIS COMPLICATIONS CURRENT TRENDS 26-Feb-16 [email protected] 2

3. DEFINITION It is the inflammation with autodigestion of the pancreas often associated with varying degree of pancreatic ductal dilatation. It is an acute condition presenting with abdominal pain and is usually associated with raised pancreatic enzyme levels in the blood or urine as a result of pancreatic inflammation . 26-Feb-16 [email protected] 3

4. EPIDEMIOLOGY World wide the annual incidence is varies from 5-50 per 100,000 10 fold rise in the western world reflect alcohol use. Patients age and gender: Alcohol-induced 30-40years (younger ) Men >> Women Gallstone-induced 40-60 years (older ) Women >> Men 26-Feb-16 [email protected] 4

5. AETIOLOGY Cholelithiasis (50%) Alcoholism (25%) Post-operative pancreatitis Genetic Microbial agents Endocrine factors Cortisone and ATCH Hyperparathyroidism and hypercalcemia Pregnancy Metabolic disorder Hyperlipidemia Diabetes Nutritional factors Chemotoxic and iatrogenic causes Idiopathic pancreatitis Miscellaneous- scorpion bite, worm infestations 26-Feb-16 [email protected] 5

6. PATHOGENESIS Obstruction- Hypersecretion theory Common channel theory Duodenal reflux Acinar cell derangement 26-Feb-16 [email protected] 6

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8. Acinar cell derangement 26-Feb-16 [email protected] 8

9. CLINICAL FORMS OF ACUTE PANCREATITIS Mild form Moderate Severe attack 26-Feb-16 [email protected] 9

10. MILD Epigastric pain may be the only complaint Radiates to the back Relieve by leaning forward ( Van Zant Sign ) Vomiting may be associated with persistent retching and hiccups Constipation is a rule in the initial stage Upper abdominal tenderness and guarding No organ failure , local or systemic complications 26-Feb-16 [email protected] 10

11. MODERATE Local or systemic complications without persistent organ failure Organ failure that resolves within 48 h (transient organ failure) 26-Feb-16 [email protected] 11

12. SEVERE Patient is much iller Pain is severer, Vomiting and retching is more persistent The abdominal tenderness, marked guarding, rebound tenderness and diminished bowel activity Full picture of shock may supervene Persistent organ failure ; single or multiple Other features; left pleural effusion, jaundice 20-30%, carpopedal spasm Could assume fulminating pancreatitis (acute haemorrhagic necrotizing) Shock is profound and coma or diabetic ketosis Retroperitoneal Haemorrhage (revealed as Cullen’s sign and grey Turner’s) 26-Feb-16 [email protected] 12

13. CULLEN’S SIGN 26-Feb-16 [email protected] 13

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15. MANAGEMENT 26-Feb-16 [email protected] 15

16. Management cont …. 26-Feb-16 [email protected] 16

17. Management cont ….. Diagnose Resuscitate Assess severity 26-Feb-16 [email protected] 17

18. INVESTIGATIONS HEMATOLOGICAL investigations RADIOLOGICAL investigations Miscellaneous investigations 26-Feb-16 [email protected] 18

19. HEMATOLOGICAL BASELINES CBC: Low Hb : prolonged hemetemesis /melena, internal hemorrhage Leucocytosis (10,000-30,000/ mcL )-infection, non infectious inflammation Low platelets-DIC Hct –raised in hemoconcentration LFT’s: raised bilirubin, AST/ALT/LDH, ALP, GGTP- gall stone pancreatitis RFT’s: raised BUN/ cretainine - ATN  ARF Coagulation profile: increased INR-DIC BSR: > 180 mg/dl-diabetes as a sequelae or cause Serum electrolytes: Low sodium/potassium: persistent vomiting Hypocalcemia - saponification/fat necrosis Serum Protein: low protein/ albumin Diabetes Mellitus AP

20. HEMATOLOGICAL ABG’s Etiology specific investigations Serum fasting lipid profile Viral titers Serum Calcium ( Hypercalcemia APHypocalcemia ) Autoimmune markers increased serum levels of IgG4 serum autoantibodies such as anti-nuclear antibody (ANA), anti- lactoferrin antibody, anti-carbonic anhydrase II antibody, and rheumatoid factor (RF), Acid-Base Disturbance Etiology Metabolic (Lactic) acidosis with high anion gap Hypovolemic shock Cholride -responsive Hypokalemic Hypochloremic metabolic alkalosis (Urine chloride < 20 mEq /L) persistent vomiting Respiratory acidosis ARDS/ resp failure

21. HEMATOLOGICAL Pancreatic Enzymes’ Assays Serum Amylase: ONSET: almost immediately PEAK: within several hours 3-4 times upper limit of normal within 24 hrs (90%) RETURN to normal depends on severity(3-5 days ) normal at time of admission in 20% cases Compared with lipase, returns more quickly to values below the upper limit of normal. Serum Lipase: more sensitive/specific than amylase Remains elevated longer than amylase(12 days) Useful if late presentation

22. Pancreatic Enzymes’ Assays Urine Amylase More sensitive than serum levels Remain elevated for several days after serum levels returned to normal Pancreatic-specific amylase(p-amylase) Measuring p-amylase instead to total amylase(also includes salivary amylase) makes diagnosis more specific(88-93%)

23. CONDITIONS ASSOCIATED WITH RAISED SERUM AMYLASE ABDOMEN Small bowel obstruction strangulation ileus mesenteric ischemia Acute appendicitis Cholecystitis Perforated Duodenal Ulcer Gastroenteritis Biliary peritonitis Spasm of sphincter of Oddi GYNE Ruptured Ectopic pregnancy T orsion of an ovarian cyst OTHERS Parotitis (Mumps) Macroamylasaemia Opioids administration Low GFR Brain injury(CVA)- hyperstimulation of pancreas

24. Plain CXR-PA view Left sided Pleural effusion : blunting of costophrenic and cardiophrenic angles + haziness in lower zones Elevated diaphragm on left side Linear focal atelactasis of lower lobe of lungs ARDS: diffuse alveolar interstitial shadowing Pulmonary edema : prominent vascular markings _________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis

25. Plain X-ray abdomen erect AP view Sentinel* loop sign Localized isolated Distended gut loop (Ileus) seen near the site of injured viscus or inflamed organ RATIONALE : body's effort to localize the traumatic or inflamed lesions ETIOLOGY : Localized paralysis followed by accumulation of gas SITE : Acute Pancreatitis  Left hypochondrium (PROXIMAL JEJUNUM) Acute Appendicitis Right iliac fossa Acute Cholecystitis  Right Hypochondrium Diverticulitis Left iliac fossa *SENTINEL: A soldier stationed as a guard to challenge all comers and prevent a surprise attack _______________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis

26. SENTINEL LOOP SIGN

27. Plain X-ray abdomen erect AP view Colon cut-off sign Gas filled (Distended) segment of proximal(mainly transverse) colon associated  with narrowing of the splenic flexure abruptly ending at the area of pancreatic inflammation with collapse of descending colon RANTIONALE : Extension of inflammatory process from the pancreas into the phrenicocolic ligament  via the transverse mesocolon r esulting in functional spasm and/or mechanical narrowing of the splenic flexure at the level where the colon returns to the retroperitoneum . Differential DIAGNOSIS : IBD Carcinoma of colon Mesenteric Ischemia ____________________________________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis

28. COLON CUT-OFF SIGN

29. Plain X-ray abdomen erect AP view Renal halo sign RATIONALE: peripancreatic inflammatory reaction extension into pararenal space ETIOLOGY : water-density (radiolucent-halo)of inflammation in anterior pararenal space contrasts with perirenal fat; more common on left side OTHERS _______________________________________________________________ Not diagnostic of Acute Pancreatitis; useful in differential diagnosis Air in the duodenal C-loop increased gastrocolic separation G astric curvature distortion To rule out perforated DU(gas under diaphragm) Obliteration of psoas shadow Localized ground glass appearance ( localized increased high soft tissue density) Calcified gall stones Pancreatic calcification(chronic pancreatitis)

30. Renal Halo Sign NORMAL RENAL HALO SIGN

31. Transcutaneous Abdominal Ultrasonography Not diagnostic Should be performed within 24 hours in all patients to detect gall stones* as a potential cause Rule out acute cholecystits as differential diagnosis Detect dilated CBD sensitivity-(70-80%) DEMERIT: overlying gas shadows 2ndary to bowel distension THERAPEUTIC: USG-guided aspiration for gram staining and culture USG-guided pig tail catheter insertion ______________________________________________________________________________ * Identification of gallstones as the etiology should prompt referral for cholecystectomy to prevent recurrent attacks and potential biliary sepsis. Gallstone pancreatitis is usually an acute event and resolves when the stone is removed or passes spontaneously.

32. IV Contrast enhanced Computed Tomography Scan Provides over 90 % sensitivity and specificity for the diagnosis of AP….. BUT Routine use in patients with AP is unwarranted, as the diagnosis is apparent in many patients and most have a mild, uncomplicated course .

33. IV Contrast enhanced Computed Tomography Scan* INDICATIONS-DIAGNOSTIC Diagnostic uncertainty (differentiating pancreatitis from other possible intra-abdominal catastrophes) Severe acute pancreatitis- distinguish interstitial from necrotizing pancreatitis Necrosis( non enhancement area > 30 % or 3 cm) done at 72 hrs * Systemic complications: Progressive deterioration, MOF, sepsis Localized complications: Altered fat and fascial planes, Fluid collection, pseudocyst , psduoaneurysm , Bowel distension, mesenteric edema, hemorrhage _____________________________________________________________ *INVESTIGATION OF CHOICE **Seldom needed within first 72 hrs after symptom onset unless the diagnosis is uncertain, because inflammatory changes are often not radiological present until this time

34. IV Contrast* enhanced Computed Tomography Scan INDICATIONS-DIAGNOSTIC Initial assessment of prognosis(CT severity index) Perfusion CT at 3 rd day  area of ischemia predict pancreatic necrosis INDICATIONS-THERAPEUTIC: CT-guided aspiration of fluid collection/necrotic tissue for gram staining and culture(sterile vs infected necrosis) specimen should be delivered to the laboratory within an hour and interpreted promptly CT-guided pig tail catheter insertion ______________________________________________________________ *Use of IV contrast may increase risk of complications of pancreatitis and AKI *Avoided if serum creatinine >1.5 mg/ dL *MRI suitable alternative

35. BALTHAZAR CT severity index(CTSI)-1994 ___________________________________________________________________ Mild (0-3) moderate (4-6) severe (7-10) CT Severity Index Inflammation score + Necrosis score

36. M agnetic R esonant I maging Suitable alternative to CT in patients with a contrast allergy and renal insufficiency where T2-weighted images without gadolinium contrast can diagnose pancreatic necrosis

37. M agnetic R esonant C holangio p ancreatography INDICATION: diagnosis of suspected biliary and pancreatic duct obstruction in the setting of pancreatitis . Repeated attacks of idiopathic acute pancreatitis Merit used if choledocholithiasis is suspected but there is concern that pancreatitis might worsen is ERCP is performed Provide non-invasive/fast/safe high-quality (Heavily T2–weighted) imaging for diagnostic and/or severity purposes

38. E ndoscopic U ltra S onography INDICATIONS Repeated idiopathic acute pancreatitis* occult biliary disease- small stones/sludge secretin-stimulated EUS study may reveal resistance to ductal outflow at the level of the papilla, as evidenced by dilatation of the pancreatic duct to a greater extent and longer duration than in a healthy population Age >40 to exclude malignancy especially those with prolong or recurrent course RATIONALE: 5 % CA pancreas present as AP _________________________________________ *Endoscopic investigation in patients with acute idiopathic pancreatitis should be limited, as the risks and benefits of investigation in these patients are unclear and should be referred to centers of expertise.

39. E ndoscopic R etrograde C holangio p ancreatography INDICATION Severe gallstone AP or AP with concurrent acute cholangitis/biliary obstruction/ biliary sepsis/jaundice (due to persistent stone) E RCP within 24(-72) h of admission Sphincterotomy /stent and bile duct clearance reduces infective complications/mortality NOT INDICATED N ot needed early in most patients with gallstone pancreatitis who lack laboratory or clinical evidence of ongoing biliary obstruction As most of gallstones causing AP readily pass to duodenum and are lost in stool MRCP or EUS recommended if CBD stone still suspected as risk of post-ERCP pancreatitis is greater with normal calibre bile duct and normal bilirubin MRCP /EUS as accurate as diagnostic ERCP

40. ASSESSMENT OF SEVERITY Early identification of patient at risk of severe pancreatitis and serious complication thereby decrease mortality. Haemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as needed Ranson’s scoring system Glasgow scoring system Apache II scoring system Contrast enhance CTScan C-reactive protein 26-Feb-16 [email protected] 40

41. RANSON’S SCORING SYSTEM 11 Parameters, 5 on admission, 6 within 48hours. ≥3 factors indicate severe acute pancreatitis ON ADMISSION 26-Feb-16 [email protected] 41

42. RANSON SCORE-1974 (for alcohol pancreatitis) ON ADMISSION Age > 55 yrs TLC > 16,000/mm3 BSR> 200 mg/ dL AST > 250 IU/L LDH > 350 IU/L WITHIN 48 HOURS BUN rise >5 mg/ dL Pa0 2 < 60 mmHg ( 8 KPa ) Serum Calcium < 8 mg/ dL Base deficit > 4 meq /L Fluid Sequestration > 6000 mL Hct fall > 10 % NOTE: Disease classified as SEVERE when 3 or more factors are present

43. Revised RANSON SCORE-1979 (for Gallstone pancreatitis) ON ADMISSION Age > 70 years TLC > 18000/mm 3 BSR > 220 mg/ dL AST> 250 IU/L LDH >400 IU/L WITHIN 48 HOURS BUN rise >5 mg/ dL Pa0 2 < 60 mmHg ( 8 KPa ) Serum Calcium < 8 mg/ dL Base deficit > 5 meq /L Fluid Sequestration > 4 litres Hct fall > 10 % NOTE : Disease classified as SEVERE when 3 or more factors are present

44. RANSON SCORE Ranson score Mortality rate SEVERITY Interpretation 0-2 ≈ 0-2 % i.e. minimal mortality Mild AP Admit in regular ward 3-5 10-20 % Severe AP Admit in ICU/HDU 6-7 40 % Associated with more systemic complications >7 >50 % Same as above SCORING SYSTEM SENSITIVITY SPECIFICITY Ranson Criteria 73% 77% APACHE II 77% 84% CRP 73% 71%

45. RANSON SCORE……. DRAWBACKS One has to measure all 11 signs to achieve the best predictability of prognosis 2 full days are needed to complete the profile . A delay of 48 hours after admission merely for assessment may squander a valuable opportunity to prevent a complication during this time . Best used within the initial 48 hours of hospitalization and have not been validated for later time intervals . Threshold for abnormal valve depends on whether cause is gallstone or alcohol Only 73 % sensitive and 77 % specific in predicting mortality

46. TREATMENT OF MILD/MODERATE 26-Feb-16 [email protected] 46

47. Mild/moderate Acute Pancreatitis mild and self-limiting, needing only brief hospitalization . Rehydration by IV fluids Frequent non-invasive observation/monitoring( atleast 8 hrly ) Brief period of fasting till pain/vomiting settles Little physiological justification for prolonged NPO No medication required other than analgesics(important) and anti-emetics Antibiotics not indicated in absence of signs or documented sources of infection Pain results in ongoing cholinergic discharge, stimulating gastric and pancreatic secretions Analgesics: WHO analgesic ladder-1986 Avoid Morphine-cause sphincter of Oddi spasm Metabolic support Correction of electrolyte imbalance

48. Severe Acute Pancreatitis P: Pain relief Proton pump inhibitors-omeprazole Peritoneal lavage A Admit in HDU/ICU Antibiotics N Nasogastric intubation(if vomiting) Nasal oxygen Nutrition support C Calcium gluconate CVP line Catherisation - Foley R Rehydration by IV fluids,plasma,blood Ranitidine(for stress ulcer) Radiology: CT scan, USG Resuscitation when required E Endotracheal intubation Electrolytes management ERCP A Antacids S Swan- Ganz catheter for CVP and TPN Suction-in case of aspiration Steroids in case of ARDS Supportive therapy for organ failure Inotropes Hemofiltration Ventilator(PEEP)

49. Monitoring CLINICAL Vitals UOP CV pressure INVESTIGATIONS Baselines Serial ABGs Serial BSR Serum calcium/magnesium

50. Role of Surgery in AP In case of mild gallstone AP, cholecystectomy should be performed before discharge to prevent a recurrence of AP Within 48-72 hour od admission or briefly delay intervention(after 72 hrs but during same admission Along with intraoperative cholangiography and any remaining CBD stones can be dealt with intra/post operative ERCP or Along with preoperative EUS or MRCP In case of necrotizing biliary AP, in order to prevent infection, cholecystectomy is to be deferred until active inflammation subsides and fluid collections resolve or stabilize Cholecysectomy done for recurrent AP (IAP) with no stones/sludge on USG and no significant elevation of LFTs is associated with >50 % recurrence of AP _________________________________________________________ If patient unfit for surgery(comorbid/elderly), biliary sphincherotomy alone may be effective to reduce further attacks of AP

51. Sterile necrosis infected necrosis Asymptomatic doesnot mandate intervention regardless of size, location and extension surgical, radiologic, and/or endoscopic drainage should be delayed preferably for more than 4 weeks to allow liquefaction of the contents and the development of a fibrous wall around the necrosis Initially treated with antibiotics Stable Symptomatic (associated with GOO or bile obstruction) minimally invasive methods of necrosectomy are preferred to open necrosectomy Urgent debridement unstable Minimally invasive approach: laparoscopic surgery(ant or retroperitoneal approach), percutaneous radiologic catheter drainage or debridement, video-assisted or small incision-based left retroperitoneal debridement, and endoscopy

52. When to Discharge Pain is well controlled with oral analgesia Able to tolerate an oral diet that maintains their caloric needs, and all complications have been addressed adequately Follow up Routine clinical follow-up care (typically including physical examination and amylase and lipase assays) is needed to monitor for potential complications of the pancreatitis, especially pseudocysts . Within 7-10 days

53. PROGNOSIS Mortality rate for all patient with acute pancreatitis is about 10% Necrotizing pancreatitis associated with infection has mortality of 20% Earlier diagnosis of infection and aggressive intervention may lower this figure. 26-Feb-16 [email protected] 53

54. COMPLICATIONS Pancreatic abscess Pancreatic pseudocyst Pancreatic fistula Acute renal failure Diabetic ketosis Gastric erosion Intestinal obstruction Splenic rupture Hypocalcaemia and tetany Hypomagnesaemia 26-Feb-16 [email protected] 54

55. CURRENT TREND Treatment with platelet-activating factor (PAF) antagonists appears to ameliorate the severity of acute pancreatitis and reduction in organ failure. Lexipafant Interleukin 1 antagonist and IL-10 administration may prove beneficial to patient with severe disease, still under trial. 26-Feb-16 [email protected] 55

56. REFERENCES 26-Feb-16 [email protected] 56