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Anita Lamichhane Pancreas : Endocrine function Pancreas Exocrine function Insulin production Manufactures & secretes digestive enzymes 20% 80%Slide 3: Retroperitoneal organ Lies between stomach & duodenumSlide 4: CT Scan pic of normal pancreas Acute Pancreatitis : Acute Pancreatitis Single/recurrent episode of Pain abdomen with elevated level of pancreatic enzymes Acute focal/diffuse swelling /inflammation of the pancreas Symptoms resolve After an acute attack; blood biochemistry becomes normalPancreatitis : Pancreatitis Uncommon during childhood Must be considered in every child with unexplained acute or recurrent abdominal pain Good prognosis if not associated with multiorgan failureMortality and morbidity: Mortality and morbidity 10-15% Biliary Pancreatitis – high mortality rate 30% -(with organ failure) 0% -(without organ failure) In the 1 st wk of illness, most deaths - multiorgan system failure. In later wks, infection - multisystem organ failureEtiology : Etiology Drugs & toxins Acetaminophen overdose Sodium valproate Azathrioprine (ischemia) Sulphonamides Corticosteroids (increased viscosity of the pancreatic juice ) Tetracyclins Obstructive Ascariasis Choledocholithiasis Microlithiasis Cholelithiasis Pancreatic ductal abnormalities ERCP complication Pancreatic diversion Ampullary diseaseCauses : Causes Viruses Mumps,measles,varicella Hepatitis A EBV CMV Mononucleosis Coxsackie virus ECHO viruses Bacteria Mycoplasma pneumoniae Legionella Salmonella Campylobacter species TuberculosisContd.: Contd. Systemic disease Cystic fibrosis Diabetes mellitus HUS Malnutrition Hyperparathyroidism Alpha1-antitrypsin deficiency Kawasaki disease Traumatic Blunt injury Burns Child abuse Surgical traumaPathophysiology : Cell membrane superoxide extrusion of the secretory vesicles into the interstitium trypsinogen trypsin macrophages Fusion of the lysosomal and Zymogen compartment Activation of the neutrophils Injury To acinar cell Proteolytic enzymes Zymogen cascade mediate local inflammatory response (TNF-alpha, IL-6, IL-8) PathophysiologyContd…: Contd… TNF-alpha, IL-6,IL_8 Increased pancreatic Vascular permeability hemorrhage bacteremia Necrosis of the pancreas Excreted into the circulation edema Acute respiratory distress syndrome Pleural effusion Renal failure GI hemorrhageSlide 13: Interperitoneal Saphonification Of calcium Altered calcium metabolism Acute Pancreatitis Edema, distension of Capsule, Obstruction of Pancreatic flow Fat necrosis Pain Stress response Release of insulin Obstruction of bile flow Altered glucose metabolism Altered bilirubin metabolism Release of kinins Exudation of blood & protein Into the peritoneal space peritonitis Decrease GI func. Dec. cardiac contractility Vasodilatation shock hypovolemia Summary of the main pathologic events that occur in pancreatitis feverSymptoms : Symptoms Constant & dull aching epigastric pain radiating towards the back Usually worse when the patient is supine Nausea & vomitingSigns : Signs Fever (76%) Tachycardia (65%) Abdominal tenderness/muscular guarding (68%) Distension (65%) Bowel sounds -often hypoactive ( gastric and transverse colonic ileus.) Jaundice (28%)Contd.: Contd. Dyspnea (10%) irritation of the diaphragm (resulting from inflammation) pleural effusion ARDS. Hemodynamic instability (10%) Hematemesis/ melena (5%) Pale, diaphoretic & listlessSome uncommon physical findings: Some uncommon physical findings The Cullen sign - bluish discoloration around the umbilicus resulting from hemoperitoneum The Grey-Turner sign - reddish-brown discoloration along the flanks resulting from retroperitoneal blood dissecting along tissue planesSlide 18: Erythematous skin nodules focal subcutaneous fat necrosis 1 cm in size extensor skin surfaces polyarthritis Purtscher retinopathy (funduscopy ) ischemic injury to the retina causing temporary/permanent blindnessLab studies: Lab studies CBC - Leucocytosis Falling hematocrit Amylase - Increased (>3xnormal) in early phase Persists for 72 hrs Hypoamylasemia < 6 months Lipase - Elevated 8-14 days longer than amylase Trypsin level Not routinely available Is specific Pancreatic isoenzyme determination – Differentiates between pancreatic & non pancreatic causesSlide 20: Blood glucose - hyperglycemia Alkaline phosphatase Total bilirubin Increase in gall bladder disease ALT AST Sr calcium – hypocalcaemia (Saphonification of fats in the retroperitoneum)Slide 21: Sr Magnesium ,sr. cholesterol Serum triglycerides ( falsely lowered during an episode of acute pancreatitis ) Serum electrolytes Renal function tests Hemoconcentration at admission (an admission hematocrit value > 47%) - a sensitive measure of more severe diseaseSlide 22: Leukocytosis represents inflammation /infection C-reactive protein Arterial blood gases –dyspneic patient IgG4 levels - autoimmune pancreatitis not specific elevated in 10% of pts with acute pancreatitisOther conditions of hyperamylasemia: Other conditions of hyperamylasemia Parotitis Sialadenitis Anorexia nervosa Biliary tract disease Peptic ulcer Peritonitis Intestinal obstruction Acute appendicitis Diabetes mellitus Burns Renal insufficiencyImaging Studies : Imaging Studies Abdominal X-ray- localized ileus sentinel loop USG abdomen- decreased echodensity of the pancreas Pseudocyst formation ERCP/MRCP- patency of the main pancreatic duct done in recurrent Acute pancreatitis/ stones /stricturesSlide 25: Abdominal CT scan severe acute pancreatitis provide prognostic information based on the following grading scale developed by Balthazar: A - Normal B - Enlargement C - Peripancreatic inflammation D - Single fluid collection E - Multiple fluid collectionsSlide 26: Grades A &B - the chances of infection & death are virtually nil Grades C,D&E - increase Grade E - 50% chance of developing an infection 15% chance of dying.Slide 27: Dynamic spiral CT scanning determine the presence & extent of pancreatic necrosis (loss of enhancement in at least 30% of the pancreatic parenchyma) Magnetic resonance cholangiopancreatography (MRCP) Endoscopic retrograde cholangiopancreatography (ERCP) Endoscopic ultrasonography (EUS)Slide 28: Severe acute pancreatitis evidence of organ failure SBP <90 mm Hg PaO2 <60 mm Hg Serum creatinine >2 mg/dL GI bleeding >500 mL/24 h Local complications ( necrosis, abscess, pseudocyst)Differential diagnosis: Differential diagnosis Lesions of the stomach and duodenum Atypical appendicitis Volvulus IntussusceptionComplications : Complications Shock Fluid & electrolyte imbalance Ileus ARDS Hypocalcaemia 3 rd – 5 th day – ATN Pseudocyst- 5-10% (resolve spontaneously in 60- 70 % of cases)Slide 31: Infection Hemorrhage Rupture Fistula formation Phegmon formation Rare sequelae Chronic pancreatitis Exocrine pancreatic insufficiency Endocrine insufficiencyGoals of medical management: Goals of medical management Aggressive supportive care Decrease inflammation Limit infection / superinfection Identify/treat complications as appropriate.Slide 33: Clinical improvement Mild pancreatitis Severe pancreatitis Clinical assessment of severity No necrosis CT with contrast of the abdomen sterile necrosis Clinical deteoration/ no improvement Supportive therapy Iv fluids Analgesia Nutrition identify the cause Antibiotics for 2 weeks. nutrition Antibiotics , Enteral nutrition (or TPN) Clinical deteoration CT guided aspiration for Gram stain & culture Presentation of acute pancreatitis No clinical improvement infected necrosis necrosis present Surgical debridement Supportive care Elective surgical debridementtMedical treatment: Medical treatment NPO IV fluids-hydration/correction of electrolyte imbalance Gastric decompression Analgesics-meperidine (Demerol) + an antiemetic is preferred over morphine ( morphine may cause spasm of the sphincter of Oddi) Synthetic Opiod narcotic analgesicSlide 35: Acid suppression (PPI) Nutrition- Enteral /Parenteral Broad spectrum antibiotics-in necrotizing pancreatitis ,not routinely for fever in early disease ( it is secondary to inflammatory response to cytokines )Slide 36: The use of gabexate & somatostatin (Zecnil) Decrease pancreatic secretions Shows a trend towards favorable outcomes in small, uncontrolled studies But not routinely used in acute pancreatitisEmerging treatments: Emerging treatments Cytokines (role in systemic inflammatory response syndrome) A recent large clinical trial of lexipafant ( a platelet-activating factor antagonist) has shown no benefit in patients with severe acute pancreatitis. Anti-TNF alpha therapy - recently been targeted as a potential therapeutic in acute pancreatitis; however, clinical trials have not begun.Surgical Care : Surgical Care Reserved for traumatic disruption of the gland Intraductal stone Unresolved/infected pseudocyst/abscess An interventional radiologist, interventional endoscopist, and/or surgeon (alone or in combination). Early Endoscopic decompression of the biliary systemSlide 39: Fine needle aspiration - tap necrotic tissue & peri-pancreatic fluid Early ERCP with sphincterotomy & stone extraction – done in gall stones pancreatitis Pseudocysts ( peripancreatic fluid collections persisting >4 wks, lack an epithelial layer, not a true cyst, contains organized debris & not fluid)-intervention indicated when becomes symptomaticSlide 40: Pancreatic abscesses: Occur late Percutaneous catheter drainage & antibiotics Require surgical debridement & drainageSlide 41: Intestinal florae are the predominant source of bacteria causing the infection Escherichia coli (26%) Pseudomonas species (16%) Staphylococcus species (15%) Klebsiella species (10%) Proteus species (10%)Slide 42: Streptococcus species (4%) Enterobacter species (3%), Anaerobic organisms(16%) Fungal superinfection may occur weeks /months into the course of severe necrotizing pancreatitis.Prognosis : Prognosis Clinical assessment and severity of the disease Several clinical scoring systems genetic markers Recovery within 2- 5 days – uncomplicated casesChronic Pancreatitis: Recurrent episodes of upper abdominal pain Chronic Pancreatitis varying degrees of pancreatic endocrine & exocrine dysfunction progressive & irreversible structural changes in the pancreas Malabsorption (diarrhea, fatty stool)Causes : Causes Hereditary Congenital anomalies of the pancreas / biliary system Hyperlipidemia CRF Hypercalcemia Idiopathic Autoimmune- autoimmune pancreatitis IBD associated chronic pancreatitis Recurrent & severe acute Pancreatitis Post necrotic ( severe acute pancreatitis ) Obstructive PancreatitisCauses : Causes Endoscopy (ERCP) Sphincterotomy Stenting of the bile duct Stenting of the pancreatic duct Gallstone removal Pancreas stone removal Cyst/pseudocyst operation Drainage operation Partial or complete removal of pancreasSlide 47: Genetic Cationic trypsinogen mutation CFTR mutations SPINK1 mutations 1-Antitrypsin deficiency Medical therapies Octreotide Pancreatic enzymes Vitamins and antioxidantsSigns & symptoms: Signs & symptoms Prolonged h/o upper abdominal pain of variable severity; radiates towards the back Fever& vomiting-not common Malnutrition (secondary to failure of pancreatic exocrine secretions may also occurLaboratory findings: Laboratory findings Blood biochemistry Pancreatic enzymes Stool tests - pancreatic enzymes fecal fat Pancreatic stimulation (secretin) tests Diagnostic imaging X-rays abdomen- pancreatic calcification (30%) diagnostic of chronic pancreatitis even in absence of clinical diseaseSlide 50: USG abdomen Dilatation of the pancreatic/biliary tracts may be noted Calcification Complications - Pseudocysts abscess calculi ascites ERCP MRCPTreatment : Treatment Medical Easing the pain High carbohydrate diet Enzyme supplementation Low fat diet SurgicalSurgery in chronic pancreatitis: Surgery in chronic pancreatitis To relieve pain, treat complications or both Types of surgery Sphincteroplasty Pancreatic drainage via pancreaticojejunostomy /end to end pancreaticojejunostomy Pancreatogastrotomy and pancreatectomyRecurrent acute pancreatitis can be a challenging clinical problem: Recurrent acute pancreatitis can be a challenging clinical problem CT scan abdomen MRCP EUS Better sensitivity for detecting biliary sludge & microlithiasis Detects peri Ampullary lesions Missed by CT/MRCP CT scan abdomenSlide 55: THANK YOU You do not have the permission to view this presentation. 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