Pancretitis

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Pancretitis

  1. 1. PancreatitisDr. Faiez AlhmoudAlbashir HospitalSurg. Department Dr. Faiez
  2. 2. Pancreas.. little anatomy & Physiology• Retroperitoneal organ that extends obliquely from the duodenal C loop to the hilum of the spleen.• It is divided into 4 portions: head, neck body and tail.• The head is 30% of size and intimately associated with the second portion of the duodenum, and they are BOTH supplied by the pancreaticoduodenal arteries.• The aorta and the superior mesenteric vessels lie behind the neck of the gland.• It incorporates endocrine and exocrine function.
  3. 3. Pancreas…….little anatomy & physiology• Behind the neck of the pancreas, near its upper border, the superior mesenteric vein joins the splenic vein to form the portal vein.• The tip of the pancreatic tail extends up to the splenic hilum.• The main pancreatic duct branches into interlobular and intralobular ducts, ductules and, finally, acini.
  4. 4. Pancreas……. little anatomy & physiology• In response to a meal, the pancreas secretes digestive enzymes in an alkaline (pH 8.4) bicarbonate-rich fluid.• The pancreatic enzymes are secreated in an inactive form, the maintenance of this is important in preventing pancreatitis.
  5. 5. Pancreas……. little anatomy & physiology• 1-2 L alkaline, clear, isoosmolar enzyme rich fluid• Na & K at plasma levels• 20 enzymes are secreted• Secretion is regulated by: Secretin, CCK, Vagus n. and low Ph• Proteolytic enzymes (Tryp, Chemotryp, elastase …etc• Lipolytic (lipase, colipase, phospholipase..etc)• amyloytic• Endocrine function: insulin, glucagon, somatostatin..etc) Dr. Faiez
  6. 6. Pancreatitis Inflammation of the pancreatic parenchyma Acute or Chronic Acute pancreatitis represents atransient inflammation that resolveswith or without Complications. Chronic pancreatitis defined ascontinuous inflammation resultingin progressive anatomic andfunctional damage to the pancreas. Dr. Faiez
  7. 7. ?Who gets pancreatitis Biliary tract stones  Idiopathic Ethanol Abuse  Infections Drugs  Ischemia ERCP  Parasites Hypercalcemia  Postoperative Hyperlipidemia  Scorpion sting  Trauma  Pancreatic duct obstruction – Tumour – Pancreas divisum
  8. 8. Pancreatitis..causesGallstone Disease (Alcohol abuse (35% Fewer than 10% of •((45% alcoholics developGallstones impacted at • pancreatitisS.o.OIn general, smaller stones • First attack after 6-10 • more likely to cause yearspancreatitis than larger of beginning alcohol abuseonesmm 5 > Direct effects on •Microlithiasis • pancreatic intracellularMicrolithiasis felt- metabolismresponsible for many“idiopathic” cases Decreased pancreatic • Dr. Faiez
  9. 9. Pancreatitis….causesAlcoholPancreatitis is a consequence of chronic - alcohol abuse; usually 6 to 10 years -Daily consumption averages 100-150 g/day; -10% of heavy drinkers develop pancreatitis -May cause spasm or inflammation of sphincter of Oddi -May decrease solubility of intraductal proteins, promoting stone formation -Decrease in pancreatic blood flow and alterations of lipid metabolism maycontribute as well
  10. 10. Pancreatitis…causes Drugs 5-Aminosalicylate  Furosemide 6-Mercaptopurine  Metronidazole Azathioprine  Pentamidine Cytosine arabinoside  Tetracycline Dideoxyinosine  Thiazide Diuretics  Trimethoprim- Estrogens sulfamethoxide  Valproic acid
  11. 11. Pancreatitis... causesIatrogenic Trauma Accounts for about 1.5% • of acute pancreatitisPost-ERCP( 1) casesPossibly the 3rd most • Abdominal blunt trauma • common cause May crush gland against •Risk approximately 4- • spine8% May disrupt pancreatic • ductPost-surgical( 2 ) Penetrating trauma •Direct injury • Dissection and disruption • of pancreatic duct Dissection of vessels •
  12. 12. Pancreatitis…causesInfections Metabolic:Viral • Hypercalcemia (of any •mumps, coxsackie, measles, ( causevaricella, EBV, CMV Hypertriglyceridemia •: Bacterial• Causes pancreatitis at -TB, mycoplasma, salmonella, levels above 1000campylobacter mg/dL: Helminthic•ascariasis
  13. 13. Pancreatitis…..Pathology Major Pathological Processes Lipolysis Proteolysis Necrosis of blood vessels Inflamation Dr. Faiez
  14. 14. PathogenesisTissue necrosis – activation of several pancreatic enzymes, including trypsin and phospholipase A2. Hemorrhage -extensive activation of pancreatic elastase, which dissolves elastic fibers of blood vessels Exudate containing toxins, activated pancreatic enzymes permeates the retroperitoneum and at times the peritoneal cavity, inducing a chemical burn and increasing the permeability of blood vessels- third space Circulating activated enzymes - may damage tissue directly causing remote systemic effects or generalized systemic inflammatory response (shock, ARDS, multisystem organ failure)
  15. 15. Acute PancreatitisClinical PresentationMid epigastric abdominal pain•Steady, boring pain•Radiation to the back•Anorexia, nausea ± vomiting ± diarrhea•Low grade fever•Presentations associated with complications•Secondary infection-Shock-.Multi-system failure-
  16. 16. Acute PancreatitisExam FindingsAbdominal tenderness•(Fever (66%•(Abdominal guarding (68%•(Abdominal distension (65%•(Tachycardia (75%•Hypoactive bowel sounds•(Dyspnea (10%•(Hemodynamic changes (10%•(Melena or hematemesis (5%•Cullen’s sign•Grey-Turner and Fox sign•Left pleural effusion•(Jaundice (28%•
  17. 17. Cullen’s sign Fox sign Grey-Turner sign Periumbilical ecchymosis usually results from hemoperitoneum, and the diffusion of blood along Periumbilical tissues produces the discoloration around the navel. Diffusion of blood via the falciform ligament may also . produce Periumbilical blood staining
  18. 18. Differential diagnosis Look for other causes of abdominal pain
  19. 19. Differential diagnosis  Biliary System Disease:  Biliary Colic.  Cholangitis.  Cholecystitis.  Cholelithiasis.  Acute Gastritis.
  20. 20. Differential diagnosis  Duodenal Ulcers.  Hollow viscus Perforation.  Myocardial Infarction.  Omental Torsion.  Mesenteric Artery Thrombosis.  Intra-abdominal Sepsis.  Extra-abdominal cuases.
  21. 21. DiagnosisSerum amylase •Not specific for pancreatitis: intestinal ischemia,-,CRFSBO, macroamylasemia, parotitisShort half-life: rise early, returns to normal early (2- -(3 dSerum lipase •More specific to pancreas-Long half-life: rise later, stay elevated longer (7-14 -(dLiver enzymes • Dr. Faiez
  22. 22. Causes of hyperamylasaemia Perforated peptic ulcer Cholecystitis Generalised peritonitis Intestinal obstruction Mesenteric infarction Ruptured AAA Ruptured ectopic pregnancy
  23. 23. Acute pancreatitis amylase - lipaseBoth must be at least 2-3x normal -. valueMagnitude of increase does not -. correlate with disease severityTogether sensitivity increases to -. 94%Persistent hyperamylasemia beyond the initial week may indicate the development of pancreaticpseudocyst ,phlegmon, abscess or ongoing acute.pancreatic inflammation
  24. 24. Diagnosis.. Complete Blood CountHct > 44 risk factor for pancreatic necrosis-Part of Ranson criteria - C-reactive proteinNot specific, but if > 10 mg/dL suggests severe-inflammation serum glucoseelevated level indicate pancreatic endocrine dysfunction - serum calciummaybe decreased - UltrasoundMost useful initial test for gallstone etiology- Dr. Faiez
  25. 25. Diagnosis.. CXR and PA non-specific findings – Sentinel loop – Ileus – Cutoff sign – Pleural effusion (Left) – Calcifications
  26. 26. Cutoff sign Sentinel loop Dr. Faiez
  27. 27. Diagnosis Dynamic Contrast CT Scan( May help identify etiology (e.g. pancreatic tumor -Useful to assess grade or complications, especially -afterinitial 72 hours as fluid collections or pancreaticnecrosis MRCPNon invasive
  28. 28. Pancreatitis SeverityAcute Mild – interstitial edema and response ofinflammatory cells with little necrosis Severe – necrosis, thrombosis, vascular disruption, hemorrhage.Chronic – fibrosis, loss ofexocrine/endocrineelements, perineural inflammation, neuralenlargement; may have superimposed acutechanges
  29. 29. Severity - ScoringRanson Criteria - > 3 indicates severe APAt Admission:Age > 55; WBC > 16K; Glucose > 200; •;AST > 250 LDH >350During first 48 hours:Hct decrease by > 10% with hydration •BUN increase > 5 mg/dL •Calcium < 8 mg/dL •pO2 < 60 mm Hg • Evidence of fluid sequestration •( 6L replacement )<
  30. 30. Markers of Severity within 24 HoursSIRS [temperature >38° or < 36°C, Pulse > 90,[ Tachypnea > 24, WBC > 12,000( Hemoconcentration (Hct >44%(BISAP (Bedside Index of Severity in Acute Pancreatitis% B) Blood urea nitrogen (BUN) >22 mg)I) Impaired mental status)S) SIRS: 2/4 or more present)A) Age >60 years)P) Pleural effusion)Organ FailureCardiovascular: systolic BP <90 mmHg, heart rate >130Pulmonary: Pao2 <60 mmHg%Renal: serum creatinine >2.0 mgGastrointestinal: bleeding >500 ml/24 hours
  31. 31. Pancreatitis….SeverityRisk FactorsAge > 60 yearsObesity & overweight, BMI > 30Comorbid diseaseMarkers during HospitalizationPersistent organ failurePancreatic necrosisHospital-acquired infection
  32. 32. Contrast-enhanced CT scoring system A Normal B • Focal or diffuse glandular enlargement . • Small intra-pancreatic fluid collection C • Any of the above • Peripancreatic inflammatory changes • Less than 25% gland necrosis D • Any of the above • Single extrapancreatic fluid collection • 25-50% gland necrosis E •Any of the above •Extensive extrapancreatic fluid collection •Pancreatic abscess •More than 50% gland necrosis
  33. 33. Ranson Criteria PrognosisMortality correlates with number of criteria1% 0-2 •15% 3-4 •40% 5-6 •100% 7-8 •
  34. 34. Severe Acute Pancreatitis Definition Organ failure. 1 ,Shock, pulmonary insufficiency • renal failure, GI bleeding Local complications. 2 Pseudocyst, abscess, pancreatic • necrosis Ranson criteria 3< . 3
  35. 35. Edematous acute pancreatitis
  36. 36. Necrotizing acute pancreatitis
  37. 37. How do you treat acute pancreatitis Pain control Fluid and electrolyte management Lots of fluid Foley’s catheter Supplemental oxygen NGT??? Mechanical ventilation, inotropes Eliminate cause (i.e. gallstones, hypoperfusion ,scorpions, etc.) Dr. Faiez
  38. 38. What is the Target for .treatment Pain control Correction of fluid and electrolyte derangement  Reduction of pancreatic secretory stimuli
  39. 39. Mild Acute PancreatitisManagementMild AP (Ranson score 2) = 85% patients•Most cases will resolve in several days•NPO, IV fluids, Analgesia•Advance diet as tolerated•Gallstone pancreatitis = cholecystectomy•Failure to improve, status worsens•.CT abdomen -
  40. 40. Severe ACUTE PANCREATITSManagementSevere AP (Ranson score 3) 15% patients•ICU with close monitoring, strict VS charting•NPO, NGT?, aggressive IV fluid replacement, • analgesiaEarly ERCP + sphincterotomy if due to gallstone • diseasePancreatic necrosis on CT = start IV antibiotics•Maintain nutrition•Enteral nutritional support•NJ tube within 3-4 days•
  41. 41. ACUTEPANCREATITS COMPLICATION S
  42. 42. Local Complications Pseudocyst Pancreatic necrosisSterile – treat with antibioticsInfected – urgent surgical debridementIf infection suspectedCT-guided needle aspiration to decide Peri-pancreatic fluid collectionsof patients 57% •Initially ill-defined •Usually managed conservatively • Dr. Faiez
  43. 43. Pseudocyst The most common complication of acute pancreatitis (occurring in approximately 25% of patients). Pseudocyst is a collection of pancreatic juice enclosed in a wall of fibrous or granulation tissue. Formation of Pseudocyst require 4 weeks or more from the onset of acute pancreatitis. Dr. Faiez
  44. 44. PseudocystClassification of Investigation of Pseudocyst Pseudocyst• Type 1 - normal duct • Ultrasound will allow anatomy. No fistula assessment of changes between duct and in the size of the cyst cyst • Endoscopic ultrasound• Type 2 - abnormal increasingly used duct anatomy - No • CT to define fistula relationship to adjacent• Type 3 - abnormal organs duct anatomy and fistula
  45. 45. :Pancreatic necrosisPancreatic necrosis is a significant complicationof acute pancreatitis, and may result in mortalityrates as high as 15%. Whatever the mechanism ofacute pancreatitis, in necrotizing pancreatitis,there is obstruction of the pancreaticmicrocirculation Dr. Faiez
  46. 46. Pancreatic Infections Ideal culture media Pathways of contamination : -Hematogenous spread -Duodenal reflux via pancreatic duct -Biliary contamination -Colonic translocation Dr. Faiez
  47. 47. Systemic Complications  CV collapse, pulmonary and renal compromise ( Due to significant third spacing and hypovolemia )  DIC and GI bleeding ( Proinflammatory mediators activate coagulation cascade )  Retinopathy and Encephalopathy ( Pathogenesis unknown )  Hypocalcaemia ( Due to extravasation of albumin into
  48. 48. ?What bugs are we talking aboutPancreatic infections are nearly always bacterial,are commonly polymicrobial, and are most oftendue to gut floraAerobic gram negative bacilli Enterococcus Staphylococcus Increasing fungus Similar in pancreatic necrosis and abscesses
  49. 49. The Role of Antibiotic Prophylaxis“ in Severe Acute PancreatitisAntibiotic prophylaxis appeared to be associated with-significantly decreased mortality but not infected pancreaticnecrosisAntibiotics are sometime prescribed to prevent infection of-dead tissue (pancreatic necrosis) in acute pancreatitis (aserious acute abdominal disease) because this complication. carries a high risk of death. Their role is unprovenNon-protocol antibiotic-
  50. 50. ?What should we use…Don’t use …Use Aminopenicillins  3rd generation 1st generation cephalosporins cephalosporins  Piperacillin Aminoglycosides  Mezlocillin  Quinolones  Imipenem  Metronidazole
  51. 51. …Conclusions Give prophylactic antibiotics to:Severe acute pancreatitis with necrosis -Disruption of the pancreatic ductal system - Antibiotic must pass blood-pancreas barrier and achieve minimum inhibitory concentration Give antibiotics early; duration yet to be determined
  52. 52. …When Rushing tosurgery
  53. 53. Indicated in 4 specific circumstances Uncertainty of Clinical Diagnosis (rare) Treatment of Pancreatic Sepsis Abscess up to 5% Correction of Associated Biliary Tract Disease Deterioration of Clinical Status (controversial)
  54. 54. Treat complicationsEarly Late• Bleeding • Endo or exocrine• Fluid collection insufficiency• Sepsis • Pseudocyst• Colon ischemia • Recurrent pancreatitis• Pancreatic fistula • Sinistral hypertension• Intestinal fistula• Renal dysfunction Dr. Faiez
  55. 55. ?What is role of endoscopy in acute pancreatitis
  56. 56. Prevention of pancreatitis
  57. 57. Thank you finished !!
  58. 58. Dr. Faiez

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