Pancreatitis

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  • The head lies within the curve of the duodenum, Body overlies the second lumbar vertebra and the vena cava. The aorta and the superior mesenteric vessels lie behind the Neck Tail: extends up to the splenic hilum in the splenorenal (lienorenal) ligament.
  • -The celiac trunk (axis) comes off from the ant surface of the aorta(T12–L1). Trifurcates into the common hepatic artery (CHA), splenic artery, and left gastric artery (LGA). The CHA runs toward the right on the superior border of the proximal body of the pancreas, and the splenic artery runs toward the left on the superior border of the distal body and tail of the pancreas -The gastroduodenal artery (GDA), a branch of the CHA, runs down behind the first part of the duodenum in front of the neck of the pancreas and divides into the right gastro-omental arteryand superior pancreaticoduodenal artery (SPDA), which further bifurcates into anterior and posterior branches. The inferior pancreaticoduodenal artery (IPDA) arises from the SMA and also bifurcates into anterior and posterior branches. -The arterial supply of the pancreas forms an important collateral circulation between the celiac axis and superior mesenteric artery. - Superior pancreaticoduodenal veins (SPDVs) drain into the portal vein and inferior pancreaticoduodenal veins (IPDVs) drain into the superior mesenteric vein
  • The main pancreatic duct (of Wirsung) runs from the tail  body  head of the pancreas where it descends into the lower (inferior) part of the head. There, it joins the duct of the uncinate process coming from left and then the lower part of the CBD to form a common channel ( called the hepatopancreatic ampulla, when dilated) , which runs through the medial duodenal wall A smooth muscle sphincter (of Oddi) is present around the common channel of the pancreatic duct and the common bile duct; this prevents reflux of duodenal juices into the pancreatic duct (and the common bile duct). An accessory pancreatic duct drains the upper (superior) part of the head of the pancreas and opens in the duodenum at the minor duodenal papilla 2 cm anterosuperior to the major papilla The 2 pancreatic ducts (main and accessory) often communicate with each other
  • The pancreas serves two major functions. First, certain cells (i.e., islet cells) dispersed throughout the pancreas play the role of an endocrine gland by producing two crucial hormones that regulate blood-sugar (i.e., glucose) levels: insulin and glucagon. Poorly regulated blood glucose can produce symptoms associated with diabetes. The hormones produced by these cells are released directly into the bloodstream. Second, another specialized group of cells (i.e., acinar cells) secrete digestive enzymes into the small intestine through tubes (i.e., ducts). The exocrine pancreas synthesizes and secretes more protein per cells than any other exocrine organ. -The exocrine pancreas synthesizes and secretes more protein per cells than any other exocrine organ. Much of its protein secretion consists of digestive proenzymes, called zymogens, that require cleavage of an activation peptide by a Protease - . Therefore, under physiological conditions, pancreatic proteases remain inactive during their synthesis, intracellular transport, secretion from acinar cells, and transit through the pancreatic duct. They only become active when reaching the lumen of the small intestine
  • I diopathic G allstone E thanol (alcohol) T rauma (accidental /iatrogenic) S teroids M umps (paramyxovirus) A utoimmune disease/vasculitis S corpion sting H ypercalcemia, hypertriglyceridemia and hypothermia E RCP, estrogens D rugs M umps (paramyxovirus) and other viruses (Coxsackie, hepatitis, EBV, CMV) A utoimmune disease/vasculitis (Polyarteritis nodosa, Systemic lupus erythematosus) S corpion sting (e.g. Tityus trinitatis), and also snake bites H ypercalcemia, hypertriglyceridemia and hypothermia E RCP, estrogens D rugs (SAND - Steroids & sulfonamides, Azathioprine, NSAIDS, Didanosine & diuretics such as frusemide and thiazides), and duodenal ulcers
  • The pathophysiology of acute pancreatitis is generally considered in three phases. In the first phase, there is premature activation of trypsin within pancreatic acinar cells. A variety of mechanisms have been proposed including disruption of calcium signaling in acinar cells (14–18), cleavage of trypsinogen to trypsin by the lysosomal hydrolase cathepsin-B, and decreased activity of the intracellular pancreatic trypsin inhibitor (17, 18). Once trypsin is activated, it activates a variety of injurious pancreatic digestive enzymes. In the second phase, there is intrapancreatic inflammation through a variety of mechanisms and pathways (16, 18–28). In the third phase, there is extrapancreatic inflammation including acute respiratory syndrome (ARDS) (16, 19–21, 29). In both phases, there are four important steps mediated by cytokines and other inflammatory mediators: 1) activation of inflammatory cells, 2) chemoattraction of activated inflammatory cells to the microcirculation, 3) activation of adhesion molecules allowing the binding of inflammatory cells to the endothelium, and 4) migration of activated inflammatory cells into areas of inflammation. Activated proteolytic enzymes  increase capillary permeability, protein exudation, retroperitoneal edema, and peritoneal exudation  macrophage produce cytokines  enter systemic circulation  SIRS, shock, ARDS, renal failure, DIVC
  • requires two of the following three features: (1) abdominal pain consistent with acute pancreatitis (acute onset of a persistent, severe, epigastric pain often radiating to the back); (2) serum lipase activity (or amylase activity) at least three times greater than the upper limit of normal; and (3) characteristic findings of acute pancreatitis on contrast-enhanced computed tomography (CECT) and less commonly magnetic resonance imaging (MRI) or transabdominal ultrasonography Pain: Develop quickly Severe, constant Epigastric  UQ/ diffuse Radiation to back  relief by sitting / leaning forward a/w Nausea & vomiting PE: Well/ ill with profound shock, toxicity & confusion Tachypnoea, tachycardia and hypotension o C  Normal/>> Mild icterus (gallstone pancreatitis) Abdominal distention Mass  epigastrium due to inflammation. Muscle guarding in the upper abdomen Grey Turner sign - flank discoloration due to retroperitoneal bleed in pt. with pancreatic necrosis (rare) Cullen’s sign - periumbilical discoloration (rare) Others: fbc, rp, rbs, calcium, fasting lipid, autoimmune markers and serology. Plain erect chest & abdominal radiographs generalized or local ileus (sentinel loop) colon cut off sign renal halo sign calcified gallstones/ pancreatic calcification may be seen. Chest radiograph pleural effusion Ultrasound Swollen pancreas <24 to detect gallstone Dilated CBD Contrast-enhanced CT scan give clues as to the etiology of acute to diagnose the severity to identify complications of pancreatitis MRCP diagnosis of suspected biliary & pancreatic duct obstruction in the setting of pancreatitis. noninvasive, and fast, ERCP evaluate the biliary & pancreatic ductal system
  • Grey Turner sign - flank discoloration due to retroperitoneal bleed in pt. with pancreatic necrosis (rare) Ecchymosis or discoloration of the flank in patients with retroperitoneal hemorrhage from dissecting blood from the retroperitoneum Cullen’s sign - periumbilical discoloration Bluish discoloration of the periumbilical area from retroperitoneal hemorrhage tracking around to the anterior abdominal wall through fascial planes
  • Severity: Mild: no organ failure, local or systemic complications and usually resolves in the first week. Moderate: presence of transient organ failure, local complications or exacerbation of co-morbid disease. Severe: persistent organ failure, that is, organ failure >48 h. Local complications are peripancreatic fluid collections, pancreatic and peripancreatic necrosis (sterile or infected), pseudocyst and walled-off necrosis (sterile or infected).
  • A 63yold. There is peripancreatic fat stranding (arrows) without an acute peripancreatic fluid collection; the pancreas enhances completely but has a heterogeneous appearance due to oedema.
  • a.The pancreas enhances completely, is thickened, and has a heterogeneous appearance due to oedema. APFC has fluid density without an encapsulating wall.
  • -About 5-10 % pt develop necrosis of the pancreatic parenchyma -Mostly involve both parenchymal n peripancreatic tissueas -The diagnosis of infected pancreatic necrosis is important  need for antibiotic treatment and likely active intervention. The presence of infection can be presumed when there is extraluminal gas in the pancreatic and/or peripancreatic tissues on CECT (figure 6) or when percutaneous, image-guided, fine-needle aspiration (FNA) is positive for bacteria and/or fungi on Gram stain and culture
  • -Local complications should be suspected when there is persistence or recurrence of abdominal pain, secondary increases in serum pancreatic enzyme activity, increasing organ dysfunction, and/or the development of clinical signs of sepsis, such as fever and leucocytosis. - Exacerbation of pre-existing co-morbidity, such as coronary artery disease or chronic lung disease, precipitated by the acute pancreatitis is defined as a systemic complication Cardiovascul ar Shock Arrhythmias Pulmonary ARDS Renal failure Haematological DIC Metabolic Hypocalcaemia Hyperglycaemia Hyperlipidaemia Gastrointestinal Ileus Neurological Visual disturbances Confusion, irritability Encephalopathy Miscellaneous Subcutaneous fat necrosis Arthralgia
  • -Early: During the early phase, systemic disturbances result from the host response to local pancreatic injury. This early phase is usually over by the end of the first week but may extend into the second week. Cytokine cascades are activated by the pancreatic inflammation which manifest clinically as the systemic inflammatory response syndrome (SIRS) When SIRS is persistent,41 42 there is an increased risk of developing organ failure . The determinant of the severity of acute pancreatitis during the early phase is primarily the presence and duration of organ failure. This is described as ‘transient organ failure’ if the organ failure resolves within 48 h or as ‘persistent organ failure’ if organ failure persists for >48 h. If organ failure affects more than one organ system, it is termed multiple organ failure (MOF). -Late: The late phase is characterised by persistence of systemic signs of inflammation or by the presence of local complications, the late phase occurs only in patients with moderately severe or severe acute pancreatitis. Local complications evolve during the late phase
  • urgent ERCP  jaundice, cholangitis or dilated CBD, w/in 72 hours Sphincterotomy & clearance bile duct reduce incidence of infective complication The fi rst approach, and the more widely utilized, is performed while using a standard pull-type sphincterotome. The second approach uses an endoscopic needle-knife to cut the sphincter muscle after placement of a pancreatic duct stent
  • Pancreatic duct obstruction trauma (post surgery or ERCP) After acute pancreatitis Occlusion by tumour (pancreatic cancer) Congenital abnormalities Pancreas divisum and annular pancreas Hereditary pancreatitis Autosomal dominant disorder with 80% penetrance Mutation in the cationic trypsinogen gene on chromosome 7 Idiopathic chronic pancreatitis Divided in to early and late onset Most patient live in warm climates (Kerala India) Occur at young age
  • Pain: -Depending on the main focus of disease and it may be diffuse Head of pancreas : epigastric and right subcostal pain Left side of pancreas : left subcostal and back pain -Chronic or recurrent -Dull and gnawing -To the back or shoulder -Nausea and vomiting Exocrine failure (>30%) Anorexia and weight loss : protein malabsoprtion Steatorrhea : fat malabsorption *soft, greasy, foul smelling stools that float on water Endocrine failure Insulin dependant diabetis melitus : loss of β islets cells Loss of appetite and loss of weight
  • serum amylase & lipase LFT  bilirubin & ALP Se Ca &triglycerides RBS/OGTT  f(X) Test of pancreatic F(X) Plain abdominal xray  pancreatic calcification Endoscopic Ultrasound  > 4 features (+)stones, visible side branches, cysts, lobularity, an irregular main pancreatic duct, hyperechoic foci and strands,dilation of the main pancreatic duct Hyperechoic margins of the main pancreatic duct. Pancreatic CT scan/MRI Identify the cause Main area of damage Extent of disease ERCP  anat of the duct & in conjunction w whole organ morphology MRCP  biliary obstruction & state of pancreatic duct
  • Treat addiction Pain management Nutritional & digestive measures Treat DM Help the patient to stop alcohol consumption and tobacco smoking Involve a dependency counsellor or a psychologist Eliminate obstructive factors (duodenum, bile duct, pancreatic duct) Escalate analgesia in a stepwise fashion Refer to a pain management specialist For intractable pain, consider CT/EUS-guided coeliac axis block Diet: low in fat and high in protein and carbohydrates Pancreatic enzyme supplementation with meals Correct malabsorption of the fat-soluble vitamins (A, D, E, K) and vitamin B12 Medium-chain triglycerides in patients with severe fat malabsorption (they are directly absorbed by the small intestine without the need for digestion) Reducing gastric secretions may help
  • Severity: Mild: no organ failure, local or systemic complications and usually resolves in the first week. Moderate: presence of transient organ failure, local complications or exacerbation of co-morbid disease. Severe: persistent organ failure, that is, organ failure >48 h.
  • Pancreatitis

    1. 1. PANCREATITISR. NANDINIIGroup K1
    2. 2. Overview: Acute Pancreatitis  Chronic Pancreatitis Anatomy of pancreas Physiology of pancreas Pancreatitis : - Definition- Classification
    3. 3. ANATOMY
    4. 4. ANATOMY
    5. 5. Duct of Wirsung (Main pancreatic duct)
    6. 6. PHYSIOLOGY
    7. 7. Acute pancreatitis: Epidemiology Incidence about 50 per 100,000 population per year 80% have mild disease 40% with severe disease dev. infected pancreatic necrosis The mortality ass. with infected necrosis is about 40% 50% of deaths occur within first week due to MOF This usually occurs in the absence of local complicationsSource: Surgical Tutor co.uk
    8. 8. Most Common etiologies: Idiopathic Obstruction Choledocolithiasis Ampullary or pancreatic tumours AlcoholSource: Surgical Tutor co.uk
    9. 9. Pathophysiology acute pancreatitis
    10. 10.  Symptoms Abdominal pain Laboratory Elevated amylase or lipase > 3x upper limits of normal Radiology Abnormal CECT, Abd USG / MRIDiagnosisDiagnosis
    11. 11.  Grey Turner sign  Cullen’s sign
    12. 12. CT Scan of acute pancreatitis CT showssignificantswellingandinflammationof thepancreas
    13. 13. CONSENSUS CLASSIFICATION(Revision of the Atlanta 1992 classification)
    14. 14. Morphologic Types of Acute Pancreatitis1992 ATLANTA Interstitial edematouspancreatitis Acute necrotizingpancreatitisREVISED Interstitial edematouspancreatitis Acute necrotizingpancreatitis-parenchymal necrosis alone-peripancreatic necrosis alone-combined type
    15. 15. Interstitial edematous pancreatitis Localized / diffuse enlargementof the pancreas Normal homogenous / slightlyheterogenous enhancement Mild inflammatory changes inthe peripancreatic soft tissue :i.e: strandingFigure 1 A 63yold. There is peripancreatic fat stranding(arrows) without an acute peripancreatic fluid collection.
    16. 16. Interstitial edematous pancreatitisFigure 2 (A) Acute interstitial oedematous pancreatitis and acute peripancreatic fluid collection(APFC) in the left anterior pararenal space (white arrows showing the borders of the APFC). (B) Afew weeks later, a follow up CT shows complete resolution of the APFC with minimal residualperipancreatic fat stranding.
    17. 17. Acute necrotizing pancreatitis Inflammation associated withpancreatic parenchymalnecrosis and/orperipancreatic necrosis Lack of pancreaticparenchymal enhancementby intravenous contrast agentand/or Presence of findings ofperipancreatic necrosis Sterile /InfectedFigure 3 Acute necrotic collection (ANC) in a 47-year-oldwoman involving the pancreatic parenchyma alone. Thinwhite arrows denote a newly developed, slightlyheterogeneous collection in the region of the neck andbody of the pancreas, without extension in theperipancreatic tissues.
    18. 18. Acute necrotizing pancreatitisFigure 4 (A) Acute necrotic collections (ANC) in a 44-year-old man with acute necrotising pancreatitis involving only theperipancreatic tissues. Note enhancement of the entire pancreatic parenchyma (white stars) and the heterogeneous,non-liquid peripancreatic components in the retroperitoneum (white arrows pointing at the borders of the ANC). (B) TheANC in the same patient as (A) but imaged a few weeks later demonstrate a heterogeneous collection with areas of fat(black arrowheads) surrounded by fluid density. This finding is typical for peripancreatic necrosis. White arrows denoteborder of ANC; white stars denote enhancement
    19. 19. Gall stone pancreatitis by ERCP
    20. 20. ComplicationComplication
    21. 21. PhasesEarly Occurs within 1stweek Involves early inflammation withvariable degree of pancreaticedema & ischemia Leads to resolution / permanentnecrosis & liquefaction Severity is entirely based on clinicalparametersLate Begins after the first week, canextend to weeks or months Characterized by increasingnecrosis, infection & MOF Imaging becomes moreimportant for detecting localcomplications & directingtreatment
    22. 22. Modified Marshall Scoring System for Organ Dysfunction
    23. 23. Grades of Severity: ▸ Mild acute pancreatitis▸ No organ failure▸ No local or systemic complications ▸ Moderately severe acute pancreatitis▸ Organ failure that resolves within 48 h (transient organ failure) and/or▸ Local or systemic complications without persistent organ failure ▸ Severe acute pancreatitis▸ Persistent organ failure (>48 h)–Single organ failure–Multiple organ failure
    24. 24. Management Mild pancreatitis-Fasting-Fluid restriction-Analgesia-Treat underlying cause-No role for antibiotic Severe pancreatitis-Admission to ICU-Monitoring-Supportive therapy-Nutritional support-CT scan-ERCP (in 72hours or ASAP)
    25. 25. ERCP : Endoscopic retrograde cholangiopancreaticography
    26. 26. Chronic Pancreatitis
    27. 27. Etiology
    28. 28. Pathology
    29. 29. 31 Pain Exocrine failure Endocrine failure Loss of appetite & loss of weight Intermittent jaundice
    30. 30. Investigations:32
    31. 31. CT - chronic pancreatitis
    32. 32. MANAGEMENT Conservatively Endoscopic & Radiological Surgical
    33. 33. Glasgow (Imrie) prognostic score PO2<60mmHg Age>55y Neutrophils + all WBC>15 x109/L Calcium<2mmol/L Raised urea>16mmol/L Enzymes AST>200U/L, LDH >600U/L Albumin<32g/L Sugar, glucose>10mmol/L
    34. 34. Summary: Common causes of acute pancreatitis are idiopathic, gallstones &alcohol. Diagnosed if patient has 2 of the following: abdominal pain, serumamylase > 3 times of upper limit or abnormal imaging finding. Revised Atlanta classification is useful in determining the prognosis &chances for patient to develop MOF. Always assess severity of patients upon admission & 48 hours later todetermine prognosis. Management is supportive & treat underlying cause.
    35. 35. References: Banks, P. et al. Classification of acute pancreatitis—2012: Revision of theAtlanta classification and definitions by international consensus, 2012.Gut;62:102–111. Kumar, V., Abbas, AK., Fausto, N. & Mitchell, R., Basic Pathology 7thed, 2007.Elsevier Ltd, Philadelphia, 1121. Lichtman, MA., Shafer, JA., Felgar, RE. & Wang, N., Lichtmans Atlas ofHematology, 2007, McGraw Hill, Canada, 215-216. Surgical-Tutor, http://www.surgical-tutor.org.uk/default-home.htm, AcutePancreatitis, [Accessed on: 26thMarch 2013.] Williams, NS. et al. Bailey & Loves Short Practice of Surgery 25thedition, 2008.Edward Arnold Ltd, Great Britain, 816-820.

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