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  1. 1. Acute Pancreatitis By: Amina A. Al-Qaysi
  2. 2. Objectives • Introduction • Definition • Epidemiology • Aetiology & Pathogenesis • Signs & Symptoms • Investigations • Management • Complications • Mortality
  3. 3. Pancreatitis • Inflammation of the pancreatic parenchyma. • Types: 1. Acute: Emergency condition. 2. Chronic: Prolonged & frequently lifelong disorder resulting from the development of fibrosis within the pancreas.
  4. 4. Acute Pancreatitis • Definition: Acute condition of diffuse pancreatic inflammation & autodigestion, presents with abdominal pain, and is usually associated with raised pancreatic enzyme levels in the blood & urine. • Reversible inflammation of the pancreas • Ranges from mild to severe.
  5. 5. Epidemiology • Acute pancreatitis accounts for 3% of all cases of abdominal pain among patients admitted to hospital in the UK. • Affect 2 – 28 per 100 000 of population. • It may occur at any age, peak incidence is between 50 and 60 years. • Women are affected more the men, but men are more likely to suffer recurrent attacks.
  6. 6. Etiology • 80% of the cases are due to gallstones & alcohol. • The remaining 20 % of cases are due to: 1. Congenital: Pancreatic divisum 2. Metabolic: Hyperlipidemia, Hypercalcemia. 3. Toxic: Scorpion venom 4. Infective: Mumps, Coxsackie B, EBV, CMV.
  7. 7. 5. Drugs: Azathioprine, Sulfonamides, Steroids, Thiazides, Estrogens. 6. Vascular: Ischemia, Vasculitis (SLE, PAN). 7. Autoimmune: Hereditary pancreatitis. 8. Traumatic. 9. Miscellaneous: CF, Hypothermia, Periampullary Tumors. 10. Idiopathic.
  8. 8. • Mnemonic for the causes of Acute Pancreatitis: ‘I get smashed‘ Idiopathic Gallstones Ethanol Trauma Steroids Mumps Autoimmune Scorpion / Snakes Hyperlipidaemia / Hypercalcaemia ERCP Drugs
  9. 9. • Biliary Pancreatitis: 1. Common channel theory 2. Incompetent sphincter of Oddi 3. Obstruction of the pancreatic duct
  10. 10. Alcoholic Pancreatitis: - Direct toxic effect on the pancreatic acinar cells - Stimulation of the pancreatic secretion - Constriction of the sphincter of Oddi
  11. 11. Symptoms • Upper Abdominal pain, sudden onset, sharp, severe, continuous, radiates to the back, reduced by leaning forward. Generalized abdominal pain, radiates to the shoulder tips. Patient lies very still. • Nausea, non-projactile vomiting, retching • Anorexia • Fever, weakness
  12. 12. Signs • Distressed, moving continuously, or sitting still • Pale, diaphoretic. Confusion • Low grade fever • Tachycardia, Tachypnea • Shallow breathing • Hypotension • Mild icterus • Abdominal distension (Ileus, Ascites) • Grey Turner’s sign, Cullen’s sign, Fox’s sign • Rebound tenderness, Rigidity • Shifting dullness, reduced bowel sounds
  13. 13. Cullen’s Sign Grey Turner’s Sign Fox’s Sign
  14. 14. Panniculitis • Subcutaneous nodular fat necrosis • Tender red nodules • Usually measures 0.5 – 2 cm • Usually over the extremities
  15. 15. Differential Diagnosis  Perforated viscus (DU)  Acute cholecystits, Biliary colic  Acute intestinal obstruction  Esophageal rupture  Mesenteric vascular obstruction  Renal colic  Dissecting aortic aneurysm  Myocardial infarction  Basal pneumonia  Diabetic ketoacidosis
  16. 16. Investigations Should be aimed at answering three questions: 1. Is a diagnosis of acute pancreatitis correct ? 2. How severe is the attack ? 3. What is the aetiology ?
  17. 17. Investigations Blood tests: • Complete Blood Count • Serum amylase & lipase • C-reactive Protein • Serum electrolytes • Blood glucose • Renal Function Tests • Liver Function Tests • LDH • Coagulation profile • Arterial Blood Gas Analysis
  18. 18. Serum Amylase: • Sensitivity: 72% Specificity: 99% • Released within 6-12 hours of the onset, & Remains elevated for 3-5 days. • Elevation ˃ 3X normal is significant. • Undergoes renal clearance. After its serum levels decline, its urinary level remains elevated. • Its level doesn't correlate with the disease activity.
  19. 19. Serum Lipase: • More pancreatic-specific than s. Amylase. • Sensitivity: about 100% Specificity: 96% • Remains elevated longer than amylase (up to week). • Useful in patients presenting late to the physician. • S. Amylase tends to be higher in gallstone pancreatitis • S. Lipase tend to be higher in alcoholic pancreatitis
  20. 20. Imaging Investigations: • Plain erect chest X-ray: not diagnostic on pancreatitis, but to rule out other D/D • Pleural effusion, diffuse alveolar infiltrate (ARDS)
  21. 21. Sentinel Loop Sign
  22. 22. Colon cut-off sign
  23. 23. • CT Scan: not indicated in every patient, only in: 1. Diagnostic uncertainty. 2. Severe acute pancreatitis. 3. Clinical deterioration, with multi-organ failure, sepsis, progressive deterioration. 4. Local complications occurs (fluid collection, pseuodocyst, pseudo-aneurysm).
  24. 24. Axial CT Scan: Peripancreatic stranding (arrow). Multiple gallstones in the gallbladder
  25. 25. Contrast-enhanced CT: acute necrotising pancreatitis. Pancreatic area of reduced enhancement, peripancreatic edema and stranding of the fatty tissue
  26. 26. Pancreatic pseudocyst occupying the head of the pancreas. The pancreatic duct (arrow) is dilated
  27. 27. CT Severity Index = Balthazar Grade + Necrosis Score
  28. 28. MRCP
  29. 29. • Endoscopic Ultrasound, MRCP: CBD stones detection, assessment of pancreatic parenchyma. Not widely available. • ERCP: CBD stones identification & removal. Urgent ERCP in severe acute gallstone pancreatitis & signs of ongoing biliary obstruction & cholangitis.
  30. 30. ERCP
  31. 31. ERCP in Acute Pancreatitis
  32. 32. Biliary sphincterotomy with stone removal
  33. 33. Goals of Treatment • Aggressive supportive care • Decrease inflammation • Limit superinfection • Identify and treat complications (of pancreatitis & its treatment) • Treat cause if possible
  34. 34. Conservative Management • Gain IV access, obtain blood sample, rapid fluid resuscitation & electrolytes replacement. • Give analgesics (IM pethidine). • Give Anti-emetics. • Keep the patient NPO (until pain free/2-3 days). • NGT insertion to relieve vomiting.
  35. 35. • Urinary catheterization is done. • Monitor the vital signs.
  36. 36. • Injection Ranitidine 50 mg IV 8 hourly, or Omeprazole 40 mg IV BD. • Somatostatin or octreotide (pancreatic secretions inhibitors). • Respiratory support: oxygen supplementation, or Venti mask • ICU admission if severe acute pancreatitis.
  37. 37. Role of Antibiotics • Prophylactic antibiotics have shown No decrease in mortality in severe acute pancreatitis. • Antibiotics are justified if: 1. Gas in retroperitoneal space 2. Needle aspiration of necrotic material confirms infection 3. Sepsis 4. CRP of ˃ 120 mg/L 5. Peri-pancreatic fluid collection 6. Organ dysfunction 7. APACHE II Score of ˃ 6
  38. 38. Operative Management • Surgery has no immediate role in acute pancreatitis. • Aggressive surgical pancreatic debridement (Necrosectomy) should be undertaken soon after confirmation of the presence of infected necrosis. • Pseudocyst: Cystogastrostomy, Cystodudenostomy, Roux-en-Y cystojejunostomy.
  39. 39. Complications
  40. 40. Complications Systemic Complications: • Cardiovascular: Shock, Arrhythmias, Pericardial effusion • Pulmonary: Basal atelactasis, pleural effusion, ARDS • Renal: ATN, Renal failure • Haematological: DIC • Metabolic: Hypocalcemia, Hyperglycemia, Hyperlipidemia • GIT: Ileus • Neurological: Confusion, Irritability, Encephalopathy • Miscellaneous: Subcutaneous fat necrosis, Arthralgia
  41. 41. Local Complications Acute fluid collection: • Occurs early in the course of acute pancreatitis • Located in or near the pancreas, the wall encompassing the collection is ill defined, the fluid is sterile. • Most of such collections resolve, & no intervention is necessary unless a large collection causes symptoms or pressure effects, in which case it can be percutaneously aspirated under ultrasound or CT guidance. • Transgastric drainage under EUS guidance is another option. • An acute fluid collection that does not resolve can evolve into a pseudocyst or an abscess if it becomes infected.
  42. 42. Pancreatic Pseudocyst: • Wall formed by granulation tissue & fibrosis • typically presents as abdominal pain, abdominal mass, & persistent hyperamylasemia in a patient with prior pancreatitis.
  43. 43. Transgastric Endoscopic Pseudocyst Drainage
  44. 44. Sterile and infected pancreatic necrosis: • Diffuse or focal area of non-viable parenchyma, typically associated with peripancreatic fat necrosis. These areas can be identified by an absence of contrast enhancement on CT. • They’re sterile to begin with, but can become subsequently infected, due to the gut bacterial translocation. • Sterile necrotic material should not be drained or interfered with. • If the patient shows signs of sepsis, then one should determine whether the necrosis is infected.
  45. 45. Mortality • Mild acute pancreatitis: Mortality rate of 1% • Severe pancreatitis: Mortality rate of 75-90% • Overall mortality rate of 15-20% • First week of illness -> MODS • Subsequent weeks -> infection
  46. 46. References • Bailey’s & Love’s Short Practice of Surgery, 25th Edition, Page 1138 – 1146. • Essential Surgery, Burkitt, 4th Edition, Page 380 – 388. • Robbins & Cotran Pathologic Basis of Disease, 8th Edition. • •

Editor's Notes

  • Disorder of the exocrine pancreas
    Predominantly d/t activation of intracelluler trypsinogen to trypsin
  • peak in young men and older women.
  • Gallstones: females Alcohol: males
  • Widespread fat necrosis of the omentum. A test tube has been filled with blood-stained peritoneal fluid. This specimen was rich in amylase. Fat necroses are dull, opaque, yellow-white areas suggestive of drops of wax. They are most abundant in the vicinity of the pancreas, but are widespread in the greater omentum and the mesentery.
    At necropsy, they can sometimes be demonstrated beneath the pleura and pericardium, and even in the subsynovial fat of the knee joint. Fat necroses consist of small islands of saponification caused by the liberation of lipase, which splits into glycerol and fatty acids. Free fatty acids combine with calcium to form soaps (fatty necrosis)

    Acute pancreatitis. The microscopic field shows a region of fat necrosis on the right and focal pancreatic parenchymal necrosis (center).
  • pancreatic position
  • Jaundice: obstruction of CBD d/t pancreatic head edema or cholidocholithiasis
  • d/t fat necrosis & retroperitoneal bleeding
    Severe necrotizing pancreatitis
    Fox’s sign: bruising over the inguinal ligament
  • Esophageal rupture: HX of emesis
  • Leukocytosis, hemoconcentration (elevated hgb & hct)
    Hyperglycemia: reduced insulin release, increase glucagon release, increase adrenal corticosteroids & catecholamines
    Ionized Ca
    ECG: abnormalities simulating MI

    Dx: 1. typical abdominal pain, with 2. increased amylase or lipase (3X normal), or 3. imaging finding compatible with pancreatitis
  • Half life in the blood is about 10 hrs
    Renal failure: reduced renal clearance
    Normal serum amylase level doesn't rule out Acute pancreatitis, and the level poorly correlates with the severity.
    Prolonged amylase elevation (>1 week) may be a clue to the presence of pancreatic abscess, pseudocyst, or ascites.
  • Slightly greater sensitivity, specially when measured after 24 hrs of the presentation
  • d/d esophageal rupture
  • Calcified gallstones
  • Doesn’t establish the Dx.
    Edematous pancreas, extra-pancreatic fluid collection, gallstones, dilated CBD.
    To be done in the first 24 hrs.
    Limited value d/t presence of intestinal gas.
  • CT is the most important imaging investigation in A.P. It assess severity, complications
    Areas of necrosis: non enhancing regions more than 3 cm, on IV contrast if renal function permits
    CT or US guided aspiration to differentiate sterile from infected pancreatic necrosis or pseudocyst

    CRP ˃110 mg/L
    Ranson’s score ˃ 3, APACHE II score ˃8
  • Early intervention (˂72 hrs) is favoured in severe biliary pancreatitis
    In acute biliary pancreatitis but without obstructive jaundice, early ERCP & papillotomy are not beneficial
  • If 3 or more factors are present in the patient, it indicates severe pancreatitis.
  • Gain IV access, rapid fluid resuscitation & electrolytes replacement (key factor in the tt of acute pancreatitis).
    Pancreatic rest
  • Hourly urine output
  • Somatostatin or octreotide: reduce mortality rate but no change in the complications
  • Cefuroxime : 2nd generation cephalosporin
    Enteral nutrition is preferred to parental nutrition for improving patient outcomes
  • Purtscher retinopathy (funduscopy ) ischemic injury to the retina causing temporary/permanent blindness
  • CT of pancreatic pseudocyst. A large pseudocyst is seen in the head of the pancreas. A nasojejunal feeding tube is seen anterolaterally.
  • MC cause of early death in A. P. Patients is hypovolemic shock
  • ×