Acute pancreatitis

under graduation level powerpoint presentation

1. Acute Pancreatitis By Orangzeb Khatri (4th year MBBS,Dow Medical College Karachi. )

2. Early medical experts found it extremely difficult to understand the true function of the organ and they actually considered pancreas to be nothing more than a shock absorber.

3. Anatomy overview: Pancreas is a retroperitoneal organ, lying on posterior abdominal wall in the C-shaped curvature of duodenum. Lies at the level of L1 and L2. Posterior to stomach separated from it by lesser sac. Divided into 4 parts: head, neck, body and tail. Around 80g

4. Blood supply: Splenic artery Inferior pancreatic artery Superior pancreaticoduodenal artery Inferior pancreaticoduodenal artery Pancreatica magna artery Caudal pancreatic artery

5. Venous Drainage: Splenic vein SMV Portal vein Lymphatic Drainage: Celiac nodes Superior mesenteric nodes Pancreaticosplenic nodes Nerve Supply: Parasympathetic by vagus Sympathetic by splanchnic plexus

6. Ductal System: Main pancreatic duct (duct of Wirsung ) it joins CBD and empties into major duodenal papilla (ampulla of Vater ) in 2 nd part of duodenum guarded by sphincter of Oddi Accessory pancreatic duct (duct of Santorini) It opens into minor duodenal papilla superior to opening of main pancreatic duct

7. Pancreas is both exocrine and endocrine gland Exocrine portion consists of acinar cells and ductular cells, secretes digestive juices i.e. trypsinogen, lipase, amylase nuclease, elastase, bicarbonate etc. Endocrine portion consists of islets of Langerhans concentrated most in tail, secretes insulin, glucagon, somatostatin and PP

8. Acute Pancreatitis Acute inflammation of pancreas Premature activation of pancreatic enzymes leading to autodigestion Can occur at any age but peak incidence is in young man and older females

9. Types: Mild AP Interstitial inflammation and edema without persistent organ failure or local complications Mortality rate of 1% Severe AP Pancreatic necrosis accompanied by SIRS, multiple-organ failure and local complications Mortality rate of 20-50% Mortality within 1 st week due to multiple-organ failure Mortality after 1 st week is due to septic complication

10. Etiology GET SMASHED Gall stone (MCC in Pakistan) Ethanol (MCC in western world) Trauma Steroids Mumps ( coxsakie B and CMV) Autoimmune Scorpion venom Hyperlipidaemia Hypercalcemia Heredity ERCP induced Drugs (thiazide, furosemide, estrogen , azathioprine, sulphonamide etc. )

11. Diagnosis It requires two of the following three features : Clinical evidence Biochemical Evidence Radiologic Evidence

12. Clinical Presentation Abdominal pain S ite: Epigastric O nset: Sudden C haracter: Stabbing R adiation: Back A ssociated symptom: Nausea and Vomiting T iming: Constant E xacerbating/relieving factor: Movement/Leaning S everity: Very severe

13. Physical Examination General Physical Examination Tachycardia Tachypnea Hypotension Fever Pale Sweating Jaundice

14. Abdominal Examination Inspection Grey-Turner’s sign Cullen’s sign Pandiaraja’s sign (ecchymosis of right axilla) Mild distension Palpation Guarding and Tenderness Auscultation Absent gut sounds

15. One may find pleural effusion in basal part of chest on percussion

16. Biochemical Test Serum amylase 3-5 times above normal limit (<100 U/L) peaks in 1-2 hrs, returns to normal in 3-5 days persistent elevation for greater than 10 days suggests local complication i.e. pseudocyst and abscess Serum lipase 3-5 times above upper normal limit (0-50 IU/L) more sensitive and specific than amylase also helpful in delayed presentation

17. Radiology Abdominal X-ray Sentinel-loop sign colon cut-off sign U/S Does not establish the diagnosis of AP but it must be done within 24hrs to rule out biliary tract pathology

18. Sentinel-loop sign

19. Colon cut-off sign

20. CT scan Best single imaging investigation not done in all pts, its indications are: If the diagnosis is uncertain Progressive clinical deterioration Signs of sepsis Signs of any organ failure Any local complication

21. typical findings focal or diffuse parenchymal enlargement changes in density because of edema indistinct pancreatic margins owing to inflammation surrounding retroperitoneal fat stranding liquefactive necrosis of pancreatic parenchyma lack of parenchymal enhancement often multifocal

22. infected necrosis difficult to distinguish from aseptic liquefactive necrosis presence of gas is helpful FNA helpful abscess formation circumscribed fluid collection little or no necrotic tissues (thus distinguishing it from infected necrosis) hemorrhage high-attenuation fluid in the retroperitoneum or peripancreatic tissues Renal-halo sign

23. Renal-halo sign

24. Prognosis Ranson’s criteria It is the most frequently utilized predictor of mortality Its limitation is that it can not predict severity on admission (requires 48h) Ranson’s score 3 or greater suggests severe Pancreatitis

25. Balthazar CT severity index It is a prognostic scale based on CT findings Renal function should be normal CTSI score: 0-3 ; Mortality 3%, Morbidity 8% CTSI score: 4-6 ; Mortality 6%, Morbidity 35% CTSI score: 7-10 ; Mortality 17%, Morbidity 92%

26. Manegement Mild Pancreatitis NPO Aggressive IV fluid resuscitation Foley’s catheterization and urine output monitoring Analgesics Antiemetics Antibiotics are not indicated Cholecystectomy in case of gall stone pancreatitis CT scan only when condition is deterioration

27. Severe Pancreatitis Admission to HDU NPO Aggressive IV fluid resuscitation Foley’s catheterization and urine output monitoring Analgesics Antiemetics

28. Supplementation SaO 2 >95% Monitoring of vital signs, CVP, urine output and blood gases LFTs, RFTs, serum Ca++, blood glucose, coagulation profile CT scan ERCP within 72h of severe gall stone pancreatitis or sings of cholangitis Supportive therapy for organ failure Antibiotics: Metronidazole + Imipenem not for >14 days Nutritional support Elective cholecystectomy in case of gall stone pancreatitis

29. It can have severe complications and high mortality despite treatment. It is believed that “ Alexander the great ” died of pancreatitis

30. Complications Systemic (common in 1 st week) Shock Arrhythmia ARDS Pleural Effusion Renal Failure DIC Paralytic ileus Encephalopathy Metabolic Hypocalcemia Hyperglycemia Hyperlipedemia

31. Local (common after 1 st week) Acute fluid collection Pancreatic necrosis Pancreatic abscess Pancreatic pseudocyst Pancreatic ascites Pleural effusion portal vein thrombosis Pseudo-aneurysm

32. Pancreatic Pseudocyst Collection of Pancreatic enzymes rich fluid walled off by granulation tissue Psudo because not lined by epithelium Most common cystic lesion (75%) Requires 4 or more weeks to develop Presents with persistent abdominal pain and persistent elevated amylase level A mass may be palpated on abdominal exam

33. Diagnosed by US and CT Differentiated from cystic neoplasm by aspiration CEA level is high in Cystic Neoplasm Amylase level is high in pseudocyst but not diagnostic Cytology reveals inflammatory cells in pseudocyst Management: Indications Symptomatic Complication >6 cm and thick walled Lasting for >12 weeks To differentiate from tumor

34. Lasting for >12 weeks To differentiate from tumor Percutaneous Transgastric cystgastrostomy Endoscopic transgastric cystgastrostomy Surgical approach Cystogastrostomy Cystodudenostomy Roux- en -Y Cystojejunostomy Resection of tail of pancreas