Acute pancreatitis

surgical

1. Assessment & Management of acute pancreatitis By: R. Nandinii

2. Case study: Mr T, 56 y.o , Indian Male, taxi driver Presented to ED with 8 hours history of epigastric pain that radiates to the back Also complaint of nausea and vomiting Moderate drinker in the past, free of alcohol for the past 3 years No history of gall stone previously No hematemesis, no melena, normal bowel habit PMHx : nil PSHx : nil Meds: nil

3. O/E: BP:110/80, HR:85, RR:18, afebrile Looks distressed, sitting up Resp : normal CVS: normal Abdomen: decreased bowel sound, mildly distended, severe LUQ tenderness, no peritoneal signs, Murphy sign: negative

4. Investigations: Hb : 13.5 HCT: 42 TWC: 6.3 Platelet: 233 DXT: 9.1 Urea:4.9 Creatinine: 97 Abdominal xray : unremarkable USG: pending Amylase: 1164 AST: 77 ALT: 73 ALP: 61 Albumin:35 Calcium: 1.99 LDH: 164 Lactate: 4.6 ABG: 7.336/ 37.4/69.9/20.1/-4.5

5. WHAT IS YOUR WORKING DIAGNOSIS?

6. Pancreas Th e p a nc re a s li e s be h i n d t h e pe ri t on e u m o f th e p os teri o r ab d om i na l wa ll an d is ob li q u e in i t s o r i en ta ti o n. T h e h ea d o f t h e p an c r ea s is o n t h e r i gh t s i d e a n d li e s w it h in t h e “ C ” cu r ve of t h e d u od e nu m a t t h e sec o n d ve r t eb ra l l e ve l ( L2 ) . T h e tip o f t h e p an c r e a s e x t en d s a c r o s s th e a b dom i n a l c a v ity a l m os t to th e s p l e e n . C o ll e c ti n g d u c ts emp ty d i g e s tiv e j u i ce s i n to t h e pa n c re a tic du c t, w h i ch r u n s fro m t h e h ea d to t h e t a il of th e o r ga n.

7. Th e D u c t of W ir su n g is t h e m ain p an c r ea t ic d uc t e x te nd i n g f r o m t h e t a il of th e o r ga n to t h e ma j or d u od e na l pa pilla o r A m p ulla of V at e r . T h e d u c t of W ir s u n g i s c l o se , an d a l m os t pa r a ll e l, to t h e d i s t a l c o m mo n b ile du c t b ef o re co mb i n i n g to fo rm a c o m mo n duc t ch a nn e l p r i o r t o a p p ro ac h i n g t h e d uo d en u m . In a pp ro x i ma t e l y 7 % of p e op l e, a n a c ce s so ry pa n c re a tic du c t o f Sa nt o rin i (d o r s a l pa n c re a tic du c t) is p re se nt . T his d uc t m a y co m m u n ic a te w ith t h e m ain p a nc r ea t i c d u c t.

8. Definition A group of reversible lesions characterised by inflammation of the pancreas Incidence Male:female ratio is 1:3- in those with gallstones and 6:1 in those with alcoholism

9. Etiology: Non-traumatic(75%) Biliary tract diseases Alcohol Viral infection(EBV, CMV, mumps) Drugs(steroid, thiazide, furosemide) Scorpion bites Hyperlipidemia Hyperparathyroidism Traumatic (5%) Operative trauma Blunt/penetrating trauma Lab test(ERCP / angiography) Idiopathic(20%)

10. Pathogenesis of acute pancreatitis Interstitial oedema Impaired blood flow Ischaemia Acinar cell injury Interstitial inflammation oedema Gallstone Chronic alcoholism Release of intracellular proenzymes and lysosomal hydrolases Activation of enzymes ACTIVATED ENZYMES Delivery of proenzymes to lysosomal compartment Intracellular activation of enzymes Proteolysis (proteases ) Fat necrosis (lipase, phospholipase) Haemorrhage (elastase ) Alcohol, drugs trauma, ischaemia, viruses Metabolic injury (experimental) Alcohol, duct obstruction DUCT OBSTRUCTION ACINAR CELL INJURY DEFECTIVE INTRACELLULAR TRANSPORT

11. Clinical manifestation The most common symptoms and signs include: Severe epigastric pain radiating to the back, relieved by leaning forward Nausea, vomiting, diarrhea and loss of appetite Fever/chills Hemodynamic instability, including shock In severe case may present with tenderness, guarding, rebound.

12. Diagnosis AP established by the presence of 2 of the 3 following criteria: ( i ) Abdominal pain consistent with the disease (ii) Serum amylase and / or lipase greater than three times the upper limit of normal (iii) Characteristic findings from abdominal imaging Contrast-enhanced computed tomography (CECT) and / or magnetic resonance imaging (MRI) of the pancreas should be reserved for patients in whom The diagnosis is unclear Who fail to improve clinically within the first 48– 72 h after hospital admission Evaluate complications

13. INITIAL ASSESSMENT AND RISK STRATIFICATION Hemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as Risk assessment should be performed to stratify patients into higher- and lower-risk categories to assist triage, such as admission to an intensive care Patients with organ failure should be admitted to an intensive care unit ICU or intermediary care setting whenever possible

14. INITIAL ASSESSMENT AND RISK STRATIFICATION

15. Clinical findings associated with a SEVERE course for initial risk assessment Age >55 Obesity( BMI>30) Altered mental status Comorbid diseases SIRS (presence of >2) -RR >20 -Pulse> 90 -Temp >38 /<36 -TWC >12000 /<4000 Urea>20 or rising urea HCT> 44 or rising hematocrit Elevated creatinine Radiology findings: -Pleural effusion -Pulmonary infiltrates -Multiple or extensive extrapancreatic collection

16. INITIAL MANAGEMENT Aggressive hydration, defined as 250-500ml per hour of isotonic crystalloid solution should be provided to all patients, unless cardiovascular, renal, or other related comorbid factors exist Early aggressive intravenous hydration is most beneficial during the first 12 – 24 hr , and may have little benefit beyond this time period Adequate prompt fluid resuscitation Fluids are given intravenously Aim to maintain urine output >0.5 ml/kg body weight

17. Nutrition in acute pancreatitis In mild AP, oral feedings can be started immediately if there is no nausea and vomiting, and the abdominal pain has resolved In mild AP, initiation of feeding with a low-fat solid diet appears as safe as a clear liquid diet

18. Management in a nutshell. Fluid resuscitation and correction of electrolyte imbalance Analgesia Bowel rest Strict urine output measuring DXT monitoring Stress ulcer prophylaxis ** Ryles tube **Antibiotic

19. Case study: Mr T (Day 2) Overnight patient was oliguric ++, tachypneic , hypotensive IV infusing around 300 cc/H –over 7L of fluid given Transferred to ICU for intensive monitoring, fluid resuscitation & was subsequently intubated Blood works were repeated

20. Investigations : Adm 48H Hb : 13.5 13.0 HCT: 42 39 TWC: 6.3 15.4 Platelet: 233 170 DXT: 9.1 13.4 Urea: 4.9 16.2 Creatinine: 97 260 Adm 48H Amylase: 1164 746 AST: 77 43 ALT: 73 32 ALP: 61 31 Albumin: 35 33 Calcium: 1.99 1.19 LDH: 164 254 Lactate: 4.6 3.0 ABG: 7.286/33.6/80.3/16.1/-8.9

21. CT abdomen: Acute pancreatitis with peripancreatic fluid with no necrotic pancreatic tissue. Patient was started on IV Carbenem after having repeated temperature.

22. Complication: Acute pancreatic collection Pancreatic necrosis (sterile or infected) Pseudocyst Walled off necrosis

23. 39-year and 43-year-old men with acute pancreatitis and pseudocysts formation. a) Axial contrast-enhanced CT scan shows ovoid shape peripheral rim enhancing lesion (arrowhead), indicative of pseudocyst, in lesser sac and detectable peripancreatic fluid collection and fat infiltration (arrows). b) Axial contrast-enhanced (b) CT scan shows two pseudocysts (arrowhead) in head of pancreas and pancreaticoduodenal groove, respectively.

24. THE ROLE OF ANTIBIOTICS IN AP Infected necrosis should be considered in patients with pancreatic or extrapancreatic necrosis who deteriorate or fail to improve after 7– 1 0 days of hospitalization Once blood and other cultures are found to be negative and no source of infection is identified, antibiotics should be discontinued. In stable patients with infected necrosis, surgical, radiologic, and/ or endoscopic drainage should be delayed by preferably 4 weeks to allow the development of a wall around the necrosis (walled-off pancreatic necrosis).

25. Management of pancreatic necrosis when infection is suspected

26. TREATMENT OF STERILE NECROSIS Sterile necrosis is best managed medically during the first 2–3 wk After this interval, if abdominal pain persists and prevents oral intake, debridement should be considered. This is usually accomplished surgically, but percutaneous or endoscopic debridement is a reasonable choice in selected circumstances with the appropriate expertise .

27. TREATMENT OF STERILE NECROSIS When sterile necrosis is debrided surgically, a common sequela is the development of infected necrosis and the need for additional surgery Patients with sterile necrosis, there was a trend to greater mortality among those operated on within 4 days If surgery is delayed for at least 2-3 wk ,the diffuse inflammatory process in the retroperitoneum resolves considerably, and gives rise to an encapsulated structure that envelops the necrotic pancreas and peripancreatic area This structure has frequently been called organized necrosis . By this time, organ failure has usually subsided, and many patients are now asymptomatic and do not require additional therapy.

28. Indication of ERCP ERCP is indicated for clearance of bile duct stones in patients with : - Severe worsening biliary pancreatitis Cholangitis Poor candidates for cholecystectomy Post cholecystectomy Strong evidence of persistent biliary obstruction

29. ERCP E R C P is a n e n do s co pic te ch n i qu e f o r v i s u a liz a ti o n o f t h e b ile an d p a nc re a tic du c t s . P hy si c i a n i n se r t s a s i d e- v i e w i n g e n do s co p e in t h e d uo d en u m fa c i n g th e ma j o r pa pilla . Th e s i d e - vi ew i n g e nd o sc o p e ( du o de n osc o pe ) is s pe ci a lly d e s i g n e d t o fa c ilit a te p l ac e m e n t of e n do s cop i c ac c es s o rie s i n to th e b i le a n d p an c r e atic d uc t. Th e e n dos c op i c a c ce s so r i e s ma y b e p as s e d t h r o u g h t h e b i o p s y c ha n ne l i n to t h e b ile a n d p a nc r ea t i c d u c t s . A c a t h et e r is u sed to i n j e c t dye i n t o b o th p an c r e atic a n d b ili a r y d u c ts to o b tain x - r a y i m a ge s us i n g f l uo ro sc o p y Du r i n g t h is p r o c ed ur e , t h e ph y s i c i a n is ab l e to s e e t w o se ts o f i m a g es : t h e en d os c op ic i mag e o f th e d uo d en u m a n d ma j or p a p ill a, a n d th e fl u o ro sc o p ic i m a g e of t h e b i l e a n d p a nc r ea t i c d u c t s .

30. THANK YOU