Acute pancreatitis copy and complications.pptx

acute pancreatitis presentaton a, CT findings , complications and management

1. Acute pancreatitis Lujain Malkawi & ali al- sou’b

2. Outlines • Anatomy • Definition • Etiology. • Presentation, history and physical exam. • Diagnosis. • Classification. • Management. • Other DDx .

3. Anatomy of the Pancreas The pancreas is retroperitoneal organ located at the level of L1-L2 vertebra ,it lies posterior to the stomach between the duodenum on the right and the spleen on the left . Parts : 1)Head : Lies within the C-shaped-concavity of the duodenum 2) Neck : anterior to superior mesenteric vessels 3) Body & Tail : posterior to the stomach with the end of the tail reaching splenic hilum. 5) uncinate process :posterior to superior mesenteric vein.

4. Blood supply of the pancreas Blood supply of the head of pancreas : Variety of major arterial sources (Celiac & SMA) • Celiac —> Common Hepatic Artery —> Gastroduodenal Artery —> Superior pancreaticoduodenal artery which divides into anterior and posterior branches • SMA —> Inferior pancreaticoduodenal artery which divides into anterior and posterior branches Blood supply of body and tail : The body and tail of the pancreas are mainly supplied by branches of the splenic artery, including the dorsal pancreatic, great pancreatic, and caudal pancreatic arteries

5. Venous Drainage of Pancreas Venous Drainage of Pancreas • Follows arterial supply. • Ultimately, into portal vein. The splenic vein leaves the hilum and runs behind the tail and the body of the pancreas. Behind the neck of the pancreas, the splenic vein joins the superior mesenteric vein to form the portal vein.

6. Pancreatic Ducts The main pancreatic duct begins in the tail and runs the length of the gland. It joins the bile duct to form hepatopancreatic ampulla (ampulla of Vater ) that--opens into the second part of the duodenum at the summit of the major duodenal papilla. The accessory pancreatic duct usually opens into the minor duodenal papilla .

7. Acute pancreatitis Acute pancreatitis is acute inflammatory disorder of the pancreas , characterised by auto-digestion of pancreatic tissue due to premature activation of pancreatic enzymes It range from mild , self limiting edema to severe necrosis and multi- organ damage Pathophysiology The key idea: premature activation of pancreatic enzymes → auto-digestion of pancreatic tissue → inflammation Trigger: Obstruction (e.g., stone) or acinar cell injury (e.g., alcohol, drugs). Premature enzyme activation: Trypsinogen → trypsin inside the pancreas Activates lipase, amylase, elastase → tissue destruction Inflammatory cascade: Cytokine release → local edema, necrosis Severe cases → systemic inflammatory response syndrome (SIRS) → multi-organ failure

8. Etiology I GET SMASHED. I: Idiopathic • G: Gallstones: ( the most common cause) Two factors, 1) Reflux of bile into the pancreatic duct: Transient obstruction of the ampulla by a passing gallstone increases biliary pressure, causing bile to flow backward into the pancreatic duct, which injures pancreatic cells and activates enzymes prematurely. 2) Obstruction at the ampulla of Vater : A gallstone may lodge at the ampulla or cause edema after passage, blocking pancreatic juice outflow and leading to enzyme activation and inflammation • E: Ethanol (Alcohol): Usually occurs after prolonged heavy alcohol use. The exact mechanism is unclear, but proposed factors include increased pancreatic secretion, spasm of the sphincter of Oddi , and direct toxic effects of alcohol and its metabolites on acinar cells, leading to enzyme activation and inflammation.

9. Cont • T: Trauma : Blunt abdominal trauma or iatrogenic injury (e.g., after ERCP or surgery) can damage pancreatic tissue or ducts. • S: Steroids. • M: Mumps (viral infection) . • A: Autoimmune. • S: Scorpion sting bite . • H: Hypercalcemia , Hypertriglyceridemia . • E: ERCP(Endoscopic retrograde cholangiopancreatography ) : Post-procedural inflammation due to mechanical or chemical irritation of the pancreatic duct • D: Drugs : ( steroids, thiazides, diuretics, azethioprine ) .

10. presentation S ymptoms :- Sudden severe Epigastric abdominal pain, radiating to the back, worse lying supine and relieved by leaning forward (because it’s a retroperitoneal organ and leaning forward pulls the peritoneum anteriorly, decreasing the pressure on retroperitoneal organs and relieving the pain).- Nausea, vomiting, bloating, low grade fevers, and anorexia ● Signs:- tachycardia, epigastric tenderness , rigidity , distention , jaundice , ileus (decrease bowel sounds) , flank ecchymosis (Grey–Turner sign), peri - umbilical ecchymosis (Cullen sign), bluish discoloration of the inguinal ligament (Fox’s sign), and shock.

11. Clinical suspicion + lab + imaging Labs: Serum amylase ↑ (3x normal, rises in 6–12h, normalizes in 3–5 days) Serum lipase ↑ (more specific and sensitive than amylase , rises faster, remains elevated longer) LFTs: may indicate gallstone etiology CBC, CRP, electrolytes, calcium Diagnosis

12. Diagnosis (Revised Atlanta Criteria) Diagnosis: 2 of 3 criteria • Pain (persistent, epigastric, ± back radiation) • Lipase/amylase >3x upper limit • Imaging consistent with pancreatitis

13. Imaging Abdominal and chest radiographs: range from unremarkable in mild disease to localized ileus of a segment of small intestine (sentinel loop) sign or the colon cutoff sign in more severe disease which is distention of the transverse colon and collapse of the descending colon . • Abdominal ultrasound in a cute pancreatitis : the pancreas appears diffusely enlarged and hypoechoic on abdominal ultrasound. Gallstones may be visualized in the gallbladder or the bile duct, in case of pancreatic necrosis: Peripancreatic fluid appears as an anechoic collection on abdominal ultrasound

14. Cont Abdominal CT with contrast: findings of acute interstitial edematous pancreatitis, include focal or diffuse enlargement of the pancreas with heterogeneous enhancement with intravenous contrast, Necrosis of pancreatic tissue is recognized as lack of enhancement after intravenous contrast administration. • If performed three or more days after the onset of abdominal pain, contrast-enhanced CT scan can reliably establish the presence and extent of pancreatic necrosis and local complications and predict the severity of the disease.

15. Classification ( Revised Atlanta classification of acute pancreatitis  ) Severity based: Mild acute pancreatitis: absence of organ failure and local or systemic complications. Moderately severe acute pancreatitis is characterized by transient organ failure (≤48 hours) and/or the development of local complications. Severe acute pancreatitis is characterized by persistent organ failure (>48 hours) of one or multiple organs, defined as shock, respiratory failure, or kidney failure; or modified Marshall score of ≥2 in at least one of the three accepted organ systems

16. M odified Marshall score : Modified Marshall score: provide a simple and objective way to assess organ failure

17. Classification ( Revised Atlanta classification of acute pancreatitis  )

18. Classification, cont. Morphology based: Interstitial edematous acute pancreatitis : characterized by acute inflammation of the pancreatic parenchyma and peripancreatic tissues , but without recognizable tissue necrosis. Necrotizing acute pancreatitis : inflammation associated with pancreatic parenchymal necrosis and/or peripancreatic necrosis . Note: Necrotizing pancreatitis often correlates with moderately severe and severe disease , and In the absence of organ failure and pancreatic necrosis, interstitial edematous acute pancreatitis correlates with mild disease

19. Cont. Necrotizing acute pancreatitis interstitial edematous acute pancreatitis Necrotizing = non-enhancing areas = dead tissue . Interstitial = edema , uniform enhancement , no necrosis .

20. Ranson Criteria?? According to the Revised Atlanta Classification (2012) for acute pancreatitis , the Ranson criteria were not included or recommended as part of the classification anymore. Ranson’s criteria were developed in the 1970s as one of the earliest scoring systems to predict severity and mortality in acute pancreatitis. They require 11 parameters measured over 48 hours , which delays early decision- making.

21. Management - Initial Management

22. Cont. Pain Control: Mild pain: Oral opioids ± NSAIDs, Moderate/severe pain: IV opioids Monitoring : Vitals & O2 sats : Keep SpO₂ >95% Labs: Electrolytes, BUN, Cr (q12h x 72h) Glucose (hourly if >180–200 mg/dL) Ca²⁺, Mg²⁺ (correct if low) Watch for: Acute kidney injury, ARDS, Abdominal compartment syndrome (measure bladder pressure

23. Cont. Antibiotics: Not used prophylactically even in necrotizing pancreatitis Only if infection suspected (e.g., pneumonia, UTI, cholangitis) Empiric: Vancomycin + Cefepime → De- escalate if cultures are negative. Nutrition: Early oral feeding : low-fat, solid diet as soon as tolerated, ideally within 24 hours  Enteral tube (nasogastric or nasojejunal ) : preferred over parenteral nutrition if patients cannot tolerate oral intake Parenteral nutrition (total or partial) : only in patients who cannot tolerate enteral feeds (e.g., those with persistent paralytic ileus)

24. Cont. Avoid early surgery in necrotizing pancreatitis — early debridement worsens outcomes. Use step- up approach : supportive care → antibiotics → drainage → surgery only if needed . Surgery is typically last resort , not first-line. Surgery usually delayed ≥4 weeks to allow walling-off (↓ risk of bleeding & complications). Abdominal compartment syndrome - Urgent decompressive laparotomy if bladder pressure is high and organ dysfunction is worsening. Gallstone pancreatitis - Cholecystectomy during same admission if mild pancreatitis Delayed until recovery if severe or necrotizing:

25. Cont. Management of the underlying cause: Biliary pancreatitis : Therapeutic ERCP . Indication: biliary pancreatitis associated with cholangitis or persistent CBD obstruction Cholecystectomy : Indicated for All patients with biliary pancreatitis to prevent recurrence

26. Management of the underlying cause: Hypertriglyceridemia-induced pancreatitis : Initiate measures to rapidly decrease triglyceride levels alongside fluid resuscitation and analgesia Long-term managementInitiate long-term lipid-lowering therapy

27. Local Complications: Early complications (<4 weeks after onset of pancreatitis): Acute peripancreatic fluid collection: usually remain asymptomatic and usually resolve spontaneously without the need for drainage . Acute necrotic collection: Necrotizing pancreatitis most commonly manifests as necrosis involving both the pancreas and peripancreatic tissues. Less than 4 weeks and unstable: drainage if infected ; avoid surgery if possible. more than 4 weeks: Consider minimally invasive or surgical necrosectomy if symptomatic or infected. acute necrotic collection

28. Cont. Late complications (>4 weeks after onset of pancreatitis) Pancreatic pseudocyst: pancreatic pseudocyst is an encapsulated collection of fluid with a well-defined inflammatory wall usually outside the pancreas with minimal or no necrosis. usually occur more than four weeks after the onset of interstitial edematous pancreatitis (it is also rare, most acute peripancreatic fluid collections resolve spontaneously). Walled- off necrosis: mature, encapsulated collection of pancreatic and/or peripancreatic necrosis that has developed a well- defined inflammatory wall

29. Complications of necrotizing pancreatitis Infected necrosis: Occurs in ~1/3 of patients with pancreatic necrosis, usually after 10 days. Common pathogens: gut-derived bacteria (E. coli, Klebsiella, Pseudomonas) and rising multidrug- resistant organisms. Suspect infection with clinical deterioration, fever, leukocytosis, or gas on CT. Diagnosis: clinical + imaging; procalcitonin and cultures support diagnosis. Empiric antibiotics targeting pancreatic tissue penetration are started (e.g., piperacillin/tazobactam). Management algorithm is in the slides below.

30. Cont. Sterile Necrosis: No infection signs; antibiotics and intervention usually unnecessary. Intervention considered if: Persistent obstruction (gastric, intestinal, biliary) after 4 weeks. Persistent symptoms >8 weeks. Disconnected duct syndrome with symptomatic collections after 4 weeks.

31. Peripancreatic vascular complications Splanchnic Venous Thrombosis (SVT): Involves: splenic, portal, or superior mesenteric veins . Common in necrotizing pancreatitis. Management : Anticoagulation if clot extends to portal or SMV . No anticoagulation for isolated splenic vein thrombosis . Duration: 3–6 months ; start with heparin → switch to DOAC upon stability. Possible sequelae: segmental portal hypertension , gastric varices, hypersplenism . Rare bleeding → treat with endoscopic therapy or splenectomy if needed. No prophylactic splenectomy is recommended

32. Cont. Pseudoaneurysm : A pancreatic pseudoaneurysm usually occurs when there is an erosion of a peripancreatic or pancreatic artery into a pseudocyst Suspect if: Unexplained GI bleeding , drop in Hct, or Sudden expansion of a fluid collection. Requires urgent diagnosis and angiographic management . Abdominal Compartment Syndrome: Defined as: Intra- abdominal pressure >20 mmHg + organ failure . Risk factors: severe pancreatitis, aggressive fluids, ascites, ileus. Monitor with bladder pressure in ICU. Requires urgent decompression if diagnosed.

33. Thank you!