Acute pancreatitis DR FRANKLIN IKUNDA.pptx

Internal Medicine

1. Acute pancreatitis

2. ANATOMY & HISTOLOGY OF THE P A N C R E A S 15 cm in length, 60-140 gm, consists of head, body & tail; pancreatic duct empty into duodenum or common bile duct Histologically , consists of 2 components: 1) Exocrine: 80-85%, consists of numerous glands ( acini ) lined by columnar basophilic cells containing zymogen granules, which form lobules; ductal system Trypsin , chemotrypsin , aminopeptidase , amylase, lipase 2) Endocrine: islets of Langerhans , which are invaded by capillaries. Islets consist of: 4 main cell types: B (insulin), A (glucagon), D ( somatostatin ), PP cells (pancreatic polypeptide) 2 minor cell types: D1 (VIP) & enterochromaffin cells (seroton in)

3. Mortality/Morbidity: The overall mortality rate of patients with acute pancreatitis is 10-15%. In patients with severe disease, the mortality rate is approximately 30%. In the first week of illness, most deaths result from multi organ system failure. In subsequent weeks, infection plays a more significant role, but organ failure still constitutes a major cause of mortality. Sex: In general, acute pancreatitis affects males more often than females. The etiology in males is more often related to alcohol; in females, to biliary tract disease.

4. AUTO PROTECTION First, proteins are translated into an inactive form called pro enzymes . The pro enzymes are packaged in a para- crystalline arrangement with protease inhibitors(zymogens granules) Zymogen granules have an acidic pH and a low calcium concentration, which are factors that guard against premature activation

5. Pathology : 4 basic alterations : 1) Proteolytic destruction of pancreatic substance 2) Necrosis of blood vessels & interstitial hemorrhage 3) Fat necrosis by lipolytic enzymes 4) Associated acute inflammatory reaction Pathologic lesions: Acute pancreatic necrosis Acute hemorrhagic pancreatitis Suppurative peritonitis Pancreatic pseudocysts

6. Pathogenesis: Autodigestion of pancreatic tissue by inappropriately activated pancreatic enzymes Trypsin has a major role: Activates other proenzymes ( proelastase , prophospholipase ) Converts prekallikrein to kallikrein ( Kinin system) Hageman factor is activated Mechanisms of pancreatic enzyme activation: Pancreatic duct obstruction Primary acinar cell injury Defective intracellular transport of proenzymes within acinar cells

7. ETIOLOGY REMEMBER -I GET SMASHED- memonic : Although pancreatitis has numerous etiologies, alcohol dependence and biliary tract disease cause most cases. In 10-30% of cases, the cause is unknown, and careful evaluation may identify a rare etiology in 10% of cases . Metabolic: alcohol , hyperlipoproteinemia , hypercalcemia , drugs (e.g. thiazides), genetic Mechanical: gallstones , traumatic & perioperative injury Vascular: shock, atheroembolism , polyarteritis nodosa Infections: Mumps, Coxsackie virus, Mycoplasma Idiopathic : 10-20% ; ? Genetic basis ** I- idiopathic,G -gallstone(the bigger it is the better),E- ethanol,T - trauma,S - mumps,A -autoimmune dse,S -scorpion bite,H -hyperkalemia/ hypertryglyceridaemia,E-ercp (endoscopic retrograde cholangiopancretography ),D-drugs( NRTIS,protease inhibitor)

8. SYMPTOMS History: The cardinal symptom of acute pancreatitis is abdominal pain , which is characteristically dull, boring , and steady . Most often, it is located in the upper abdomen, usually in the epigastric region , but it may be perceived more on the left or right side, depending on which portion of the pancreas is involved. The pain radiates to the back in approximately half of cases. The duration of pain varies but typically lasts more than a day. The pain may be aggravated by eating or lying supine and it may be alleviated by fasting or lying on the left side with the knees and hips flexed . Associated symptoms ( eg , anorexia, nausea, vomiting) are common, and some patients experience diarrhea due to indigestion. Avulsion to fatty foods may be reported

9. Physical exam: Distressed anxious patient Low grade fever Tachycardia Shock- ( i )due to exudation of blood and plasma proteins into retroperitoneal space. (ii) kininins - vasodilation , increased vascular permeability (iii)systemic effects of lipolytic enzymes released into circulation Jaundice-infrequent-edema of head of pancreas Erythematous skin nodules- subcut fat necrosis 10-20 % → pulmonary findings- rales , atelectasis , pleural effusions Decreased bowel sounds Pancreatic pseudocyst -palpable in upper abdomen Cullens sign -faint blue discolouration around umblicus due to hemoperitoneum Turner”s sign → blue-red-purple discolouration or green brown discolouration in the flanks-Tissue catabolism of hemoglobin-Latter 2 rare. If present- necrotising pancreatitis

10. Diagnosis of acute pancreatitis Amylase and lipase -elevations of 3 times above reference range considered diagnostic Amylase not specific for pancreatic dis-can occur in small intestine obstruction , mesenteric ischaemia , tubo -ovarian disease , renal insufficiency, parotitis Serum T ½ of amylase is short -elevations return to ref range within a few days. Lipase-longer half life more specific to the pancreas. Note-levels of the two do not correlate with prognosis REF-Lipase-56-239 -Amylase-0-260U/L(under 18 years) -35-115U/L(over 18years)

11. ….Diagnosis Liver enzymes-ALP , total bil , AST, Alanine aminotransferase-search for gall stone pancreatitis if elevated Alanine aminotransferase >150U/L-gallstone pancreatitis Calcium levels - hypercalcemia as aetiolgy or saponification if hypocalcemia - correlates well with severity of disease. Levels lower than 7 mg/ dL (when serum albumin is normal) are associated with tetany and an unfavorable prognosis. Cholestero l, TGs, if elevated search for aetiology ( Hyperlipidimia ) -fasting triglyceride levels above 1000 mg/ dL . Baseline TGs can be lower in acute pancreatitis

12. ….Diagnosis… C.B.C – Hct >47 proposed as a sensitive measure of more severe disease, however this has subsequently been shown to have value only as a negative predictor of severe disease i.e. lack of severe hemoconcentration rules out severe disease Leukocytosis-inflammation or infection CRP-higher levels-organ failure. CRP not specific. BGAs if patient is dyspnoic Trypsin and its precursor trypsinogen 2 in both urine and peritoneal fluid-not widely used

13. ….DIAGNOSIS Imaging-Radiologic findings are inconstant and non-specific. CXR, K.U.B- exclude other diagnosis CT scan may confirm impression of acute pancreatitis and severity (esp. Contrast Enhanced CT-CECT) . Abdominal ultrasonography -detects gall stones-Sensitivity in acute pancreatitis 70-80 % M RCP -emerging role.T2 weighted images provide a non invasive image of the biliary and pancreatic ducts Endoscopic ultrasonography-more details than transcutaneous U/S-Principal role –evaluating microlithiasis , biliary sludge, periampulary lesions

14. Diagnostic procedures ERCP - evaluates biliary and pancreatic ductal system. Should be used with caution in pts with acute pancreatitis.Never to be used as a first line tool in this disease. Used in suspected choledocholithiasis and biliary pancreatitis with worsening jaundice CT-guided needle aspiration-diff sterile from infected necrosis. Evaluate specimen for culture and sensitivity and gram stain

15. complications

16. Factors affecting survival

17. ASSESSMENT OF SEVERITY Ranson's criteria- are generally used in assessing the severity of acute alcoholic pancreatitis on presentation (pancreatitis due to other causes is assessed by similar criteria). 1. When three or more of the following are present on admission, a severe course complicated by pancreatic necrosis can be predicted with a sensitivity of 60–80%: Age over 55 years. White blood cell count over 16,000/mcL. Blood glucose over 200 mg/dL. Serum LDH over 350 units/L. AST over 250 units/L.

18. 2. Development of the following in the first 48 hours indicates a worsening prognosis: Hematocrit drop of more than ten percentage points. BUN rise greater than 5 mg/ dL . Arterial Po 2 of less than 60 mm Hg. Serum calcium of less than 8 mg/ dL . Base deficit over 4 mEq /L. Estimated fluid sequestration of more than 6 L.

19. Severity index in acute pancreatitis

20. TREATMEMT OF ACUTE PANCREATITIS 85 -90 % of patients the disease is self limited, subsides in 3 to 7 days of rx Conventional measures ( i ) analgesics- meperidine , up to 100–150 mg intramuscularly every 3–4 hours as necessary (ii) IV fluids and colloids (iii) no oral intake (iv) NG suction to decrease gastrin release and prevent gastric contents from entering duodenum. Anticholinergics -no therapeutic advantage Antibiotics-used but RCTs have shown no benefit in mild to moderate severity disease Current evidence- prophylactic antibiotics in necrotizing acute pancreatitis-decreases sepsis and mortality

21. ….TREATMENT… Surgery-infected pancreatic necrosis. Data support delaying surgical debridement of necrotic tissue for at least 2 weeks for viable pancreatic tissue to become evident Patients with severe gall stone induced pancreatitis may improve if papillotomy is done within 36 to 72 hours Studies show that only those pts with gall stone pancreatitis who are in the very severe group should be considered for ERCP

22. …TREATMENT… Hypertryglyceridemia associated acute pancreatitis- (i)wt loss (ii)Lipid restricted diet (iii)exercise (iv)avoid alcohol and drugs e.g. vitamin A, thiazides, beta blockers (v) control DM

23. INFECTED PANCREATIC NECROSIS Diffuse infection of acutely inflamed, necrotic pancreas occurs in the first 1 to 2 weeks of onset of acute pancreatitis Treated by surgical debridement. Mostly gram negative bacteria of gut origin. Early diagnosis-CT guided needle aspiration Imipenem-cilastatin 500 mg TID for 2 weeks-prophylactic

24. Pancreatic abscess Ill defined collection of pus, evolves over longer period 4 to 6 weeks Life threatening but lower rate of surgical mortality Treated surgically or in selected cases percutaneous drainage

25. PANCREATIC PSEUDOCYST Collection of tissue, fluid, debris, pancreatic enzymes, and blood. Develops over 1-4 weeks. Forms in 15% of patients Wall consists of necrotic tissue, granulation tissue, fibrous tissue Preceded by pancreatitis in 90% of cases, trauma in 10% of cases May be two or more. 85% located in body or tail.15% head

26. … Pseudocyst … Abdominal pain with or without radiation to the back. Palpable tender mass in the middle or left upper abdomen Serum amylase elevated in 75% of patients at some point during illness Sonography reliable in detecting pseudocysts . Serial u/s indicates resolution or not CT complements U/S in diagnosis Recent studies show non interventional, expectant management is the best course in pts with minimal symptoms with no alcohol use

27. Pseudocyst…. Complications-pain caused by expansion, rupture, hemorrhage, abscess Increase in size, localized bruit over mass, sudden drop in Hb/Hct-possibility of hemorrhage from pseudocyst U/S or CT guided repeated needle aspiration/ catheter drainage-success rate 45-75 % success rate

28. Pseudoaneurysm- In 10% of pts. Reflects distribution of pseudocyst and fluid collections. Splenic artery most commonly involved, followed by inferior and superior pancreatico duodenal arteries Thin cut CT usually reveals a contrast enhanced lesion within or adjacent to suspected pseudocyst. Arteriography is necessary to confirm diagnosis

29. Spiral CT- Pseudoaneurysm(small arrow) within pseudocyst and duct

30. CT- Lobulated pseudocyst

31. Acute pancreatitis with necrosis: Lack of enhancement of the body and most of the tail

32. THANK YOU let meet in surgery References: HARRISON’S PRINCIPLES OF INTERNAL MEDICINE . ROBBINS AND COTRAN PATHOLOGICAL BASIS OF DISEASES 9 TH EDITION William F. Ganong eMedicine

33. I- idiopathic G-gallstones-the bigger it is the lesser it cause and vice versa E- ethanol T- trauma S-mumps M- auto immune dise A- autoimmune S-scorpion bite H- hyperkalemia/ hypertryglyceridaemia E- ercp (endoscopic retrograde cholangiopancreatography ) D-drugs-NRTI and protease inhibitors