Comprehensive Understanding of Acute Pancreatitis

This presentation provides a comprehensive discussion on acute pancreatitis, covering the following topics: Definition, Classification, Etiology, Pathogenesis, Clinical Features, Investigations, Severity, Complications, Differential Diagnosis, Treatment, and Clinical Scenarios.

1. Acute Pancreatitis Varun Bansal MBBS

2. Clinical Scenario:- Patient comes with the Pain that is located generally in the epigastrium and radiates to the back in approximately half of cases. Maximum intensity within 30 min, Persists for more than 24 h without relief. Is often associated with nausea and vomiting P/E :- Epigastric tenderness - guarding 2

3. Objectives :- Definition Classification Etiology Pathogenesis Clinical features Investigation Severity Complication Differential diagnosis treatment

4. Definition :- 4 Inflammation in pancreas associated with injury to exocrine parenchyma. Acute pancreatitis is an inflammatory condition of the pancreas Characterized by abdominal pain and increase pancreatic enzymes in the blood. Several conditions are associated with Acute pancreatitis of these Gallstones and Chronic Alcohol abuse accounting for 2/3 rd of cases.

5. Criteria for diagnosis – Symptom – epigastric pain Laboratory findings - serum amylase and/or lipase ≥3 times the upper limit of normal Radiological imaging – consistent finding by CT or mri 5

6. Classification of Acute Pancreatitis :- Atlanta classification : Interstitial oedematous acute pancreatitis- acute inflammation parenchyma and peripancreatic tissues without necrosis Necrotizing acute pancreatitis- inflammation + necrosis of parenchyma Classification according to severity :- 1. Mild Acute Pancreatitis- no organ failure and any complication 2. Moderately Severe Acute Pancreatitis- no organ failure and/or local complications 3. Severe Acute Pancreatitis-persistent organ failure with one or multiple organ failure. 6

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8. Etiology :- 1 . Obstructive causes- Gall stones Obstruction of pancreatic duct system Pancreatic tumour Parasites – ex- Ascaris lumbricoides Developmental anomaly – pancreas divisum , annular pancreas 8 2 . Toxic – Ethyl alcohol Methyl alcohol Scorpion venom Organophosphates Smoking

9. 3. Drugs- Definitive association – Azathioprine, valproic acid, corticosteroids Probable association - thiazides, etc 9 4. Trauma :- Burnt trauma to the abdomen

10. 5. Metabolic causes :- Hyperlipoproteinemia Hypertriglyceridemia Hypercalcemia Hyperparathyroidism Renal failure Postrenal transplantation 10 6. Infection :- Viral – mumps, rubella, viral hepatitis, HIV Bacterial – mycoplasma, TB, leptospirosis 7. Vascular :- Ischemia – hypoperfusion or atherosclerosis emboli Vasculitis – SLE, polyarteritis nodosa, malignant hypertension

11. 8. Miscellaneous Penetrating peptic ulcer Pregnancy associated Reye syndrome 11 9. Idiopathic Pancreas divisum 10. Genetic – Mutation in the pancreatic trypsin inhibitor (SPINK1)

12. Pathogenesis :-

13. Clinical Features :- Abdominal pain - cardinal & major symptom In epigastric and periumbilical region on Lt or Rt side depending on portion of pancreases involved Sudden onset and gradual increase in severity Constant steady and intense (15-60 min) Pain relieves by sitting with trunk flexed and knee drawn up If retroperitoneum is involved, pain radiates to upper back, chest, flank, lower abdomen 2) Anorexia, Nausea, Vomiting 13

14. 14 Trunk Flexed Knee Drawn up

15. Signs :- Early stage : Distressed and anxious patient Marked epigastric tenderness and abdominal distention (due to hypomobility) Rebound tenderness and guarding are absent (inflammation in retroperitoeum ) Tachypnea (d/t ARDS, atelectasis and pleural effusion) Jaundice (d/t gallstone pancreatitis) 15

16. Severe disease : Low grade fever, tachycardia, & hypotension Shock with oliguria Abdominal examination – tenderness + guarding + diminished or absent bowel sound RS: basal rales, atelectasis & pleural effusion Skin : erythematous skin nodules d/t focal subcutaneous fat necrosis Purtscher retinopathy: Ischemic injury to retina (on fundus examination) Cullen's sign: Faint bluish discoloration (bruising) around the umbilicus d/t hemoperitoneum Grey Turner's sign: Blue-red-purple or green-brown discoloration of the flanks d/t tissue catabolism of hemoglobin Fox's sign: Bluish discoloration over the inguinal ligament 16

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18. Laboratory Investigation :- Serum Amylase : Levels markedly (three times the upper limit of normal) raised during the first 24 hours and then decline to normal within 3-5 days If persistent indicates complications such as pancreatic abscess or pseudocyst formation. Amylase levels may be spuriously normal in 20% patients with alcoholic pancreatitis and 50% patients with hypertriglyceridemia. Peritoneal amylase is massively raised in pancreatic ascites. 18

19. Urinary amylase: Levels may be diagnostic because they remain elevated over a longer period of time Serum lipase: It is raised within 72-96 hrs and remains elevated for 8-14 days (hence preferred over amylase) Greater diagnostic accuracy and is a more useful indicator of acute pancreatitis Marked elevation of lipase in pleural or peritoneal fluid (> 5000 IU/dL) suggests acute pancreatitis C-reactive protein : assessing severity and prognosis 19

20. Other blood investigation :- Leukocytosis : in : Moderate to severe acute pancreatitis (in infection & inflammation) Hyperglycemia and glycosuria: in 10% cases d/t hyperglucagonemia or hypoinsulinemia Hypocalcemia Low Hb – P rolonged hematemesis/ melena, internal haemorrhage Urea and electrolytes Liver biochemistry Triglycerides, and Arterial blood gases . 20

21. Radiological Investigation

22. Plain X-Ray Abdomen and Chest :- It is useful for excluding other causes of acute abdominal pain(gastroduodenal obstruction or perforation). Non specific signs like colon cutoff sign & sentinel loop sign can be seen 22

23. USG Abdomen – Used as a screening test to evaluate gallbladder and biliary tree, to identify gallstones, biliary obstruction or pseudocyst formation. It may show pancreatic swelling, necrosis and peripancreatic fluid collections. 23

24. CT Abdomen – It shows swollen pancreas phlegmon, pseudocyst or pancreatic abscess. Helpful in assessing the severity and complications. CECT: - Should be performed after 72 hours of onset of symptoms to know extent of pancreatic necrosis MRI & MRCP:- assessing the degree of pancreatic damage and necrosis, to identify gall stones within biliary tree 24

25. Severity of Acute Pancreatitis 25

26. Modified Glasgow /Pancreas score Pao2 < 8kpa (60 mm hg) Age >55 years Neutrophils :WBC > 15x10 9 /L Calcium < 2 mmol/L Renal function ( Urea > 16 mmol/L Enzymes ( AST/ALT > 200 IU/L OR LDH > 600 IU/L) Albumin <32 g/Dl Sugar ( Glucose > 10 mmol/L) Applicable for both gall stone and alcohol induced pancreatitis within 48 hrs of admission

27. Differential Diagnosis 29

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29. MANAGEMENT Establish the diagnosis and assess the severity of acute pancreatitis. Resuscitation and early treatment Detection and treatment of complications. Treatment of underlying cause General supportive care IV fluids Feeding : Nil per oral in severe cases .TPN associated with high risk of infection .Nasogastric tube feeding to be started by gradual oral intake.

30. Opiate analgesia should be given to treat pain and hypovolemia should be corrected by using normal saline or crystalloids . Urinary catheter should be inserted in patients with shock,with central venous catheter if required. Tramadol or other opiates are drug of choice. Nasogastric aspiration –To prevent abdominal distension,vomiting and aspiration pneumonia ( only if paralytic ileus is present) Prophylactic antibiotics : Carbapenems or quinolones and metronidazole may reduce the incidence of infected pancreatic necrosis. Anticoagulation : LMWH to prevent DVT.

31. Endoscopic Retrograde Cholangiopancreatography Indications Severe gall stone AP or AP with concurrent cholangitis/biliary obstruction /biliary sepsis ERCP Within 24 -72 hrs of admission

32. Indications of Surgery in acute pancreatitis

33. Complications 35

34. Systemic+Local Complications

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