Anatomy Physiology Definition Etiology Pathophysiology Clinical Presentation Investigations Differentials Diagnosis Severity Scoring System Treatment Complications.

Presentation on theme: "Anatomy Physiology Definition Etiology Pathophysiology Clinical Presentation Investigations Differentials Diagnosis Severity Scoring System Treatment Complications."— Presentation transcript:

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2 Anatomy Physiology Definition Etiology Pathophysiology Clinical Presentation Investigations Differentials Diagnosis Severity Scoring System Treatment Complications

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4 Pyhsiology

5 Definition

6 Etiology Biliary tract diseases Alcohol Non-traumatic(75%)
Viral infection(EBV, CMV, mumps) Drugs(steroid, thiazide, furosemide) Scorpion bites Hyperlipidemia Hyperparathyroidism Traumatic (5%) Operative trauma Blunt/penetrating trauma Lab test(ERCP / angiography) Idiopathic(20%)

7 DUCT OBSTRUCTION ACINAR CELL INJURY DEFECTIVE INTRACELLULAR TRANSPORT Alcohol, drugs trauma, ischaemia, viruses Gallstone Chronic alcoholism Metabolic injury (experimental) Alcohol, duct obstruction Interstitial oedema Release of intracellular proenzymes and lysosomal hydrolases Delivery of proenzymes to lysosomal compartment Impaired blood flow Activation of enzymes Intracellular activation of enzymes Ischaemia Acinar cell injury ACTIVATED ENZYMES Haemorrhage (elastase) Interstitial inflammation oedema Proteolysis (proteases) Fat necrosis (lipase, phospholipase)

8 PATHOPHYSIOLOGY TRYPSINOGEN  TRYPSIN Activation of prekallikrein Activation of kinin system Activation of Hageman factor-XII Activation of clotting and complement systems thrombosis and inflammation Activation of Phospholipase Activation of Prostaglandins and Bradykinins Lipase activation Triglycerides Glycerol + Fatty acids Fatty acids+ calcium saponified fat Hypocalcemia Elastase activation Digestion of elastic fibers Capillary leak/rupture/ Pseudoaneurysm 3rd space Sequestration of blood/fluid Hemorrhage+ Hypovolemic shock Activation of Lysolecithinase (derived from bile) Membrane damage Necrosis Release of inflammatory mediators into circulation systemic complications

9 Symptoms and signs The most common symptoms and signs include:
Severe epigastric pain radiating to the back, relieved by leaning forward Nausea, vomiting, diarrhea and loss of appetite Fever/chills Hemodynamic instability, including shock In severe case may present with tenderness, guarding, rebound. Signs which are less common, and indicate severe disease, include: Grey-Turner's sign (hemorrhagic discoloration of the flanks) Cullen's sign (hemorrhagic discoloration of the umbilicus) Pulmonary involvement – HypoxemiaARDS

10 Cullen sign – discolouration around umbilicus

11 Cullen sign

12 Grey-Turner sign- discolouration in the flanks

13 Investigation Full blood count: neutrophil leukocytosis Amylase & Lipase levels elevated. Electrolyte abnormalities include hypokaemia, hypocalcemia Elevated LDH in biliary disease Glycosuria ( 10% of cases) Blood sugar: hyperglycaemia in severe cases Ultrasound look for stones in biliary tract diseases. Abdominal CT scan may reveal phlegmon(inflammatory mass), pseudocyst or abscess(complications of acute pancreatitis)

14 Pancreatic Enzymes’ Assays
Serum Amylase: ONSET: almost immediately PEAK: within several hours 3-4 times upper limit of normal within 24 hrs (90%) RETURN to normal depends on severity(3-5 days) normal at time of admission in 20% cases Compared with lipase, returns more quickly to values below the upper limit of normal. Serum Lipase: more sensitive/specific than amylase Remains elevated longer than amylase(12 days) Useful if late presentation

15 Differentials Abdomen Thorax Pelvic

16 Diagnosis Characteristic pain S.Amylase & S.Lipase Imaging

17 Ranson Score predicting the severity of acute pancreatitis
At admission age in years > 55 years white blood cell count > cells/mm3 blood glucose > 11 mmol/L (> 200 mg/dL) serum AST > 250 IU/L serum LDH > 350 IU/L At 48 hours Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL) Hematocrit fall > 10% Oxygen (hypoxemia PO2 < 60 mmHg) BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration Base deficit (negative base excess) > 4 mEq/L Sequestration of fluids > 6 L

18 Balthazar scoring Balthazar Grade
Balthazar Grade Appearance on CT CT Grade Points Grade A Normal CT points Grade B Focal or diffuse enlargement of the pancreas 1 point Grade C Pancreatic gland abnormalities and peripancreatic inflammation points Grade D Fluid collection in a single location points Grade E Two or more fluid collections and / or gas bubbles in or adjacent to pancreas4points Necrosis Score Necrosis Percentage Points No necrosis 0 points 0 to 30% necrosis 2 points 30 to 50% necrosis 4 points Over 50% necrosis 6 points

19 APACHE II score (Acute Physiology And Chronic Health Evaluation)

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21 management Iv fluid replacement(normal saline)
Bowel rest (NG tube, NPO) in severe case Administration of parenteral narcotics to control pain. Antiemetic if necessary Monitor hematocrit,glucose level,calcium & albumin levels. Antibiotics Determine & treat specific etiology(avoid alcohol) Indication to surgery if pancreatitis not respond to treatment.

22 complications Immediate Late Pancreatic pseudocyst Pancreatic abscess
Pancreatic necrosis Progressive jaundice Persistent duodenal ileus GI bleeding Pancreatic ascites

23 progression

24 Thank you..