Acute pancreatitis

Acute pancreatitis

1. Acute pancreatitis Dr Lalit K Shah Resident 1st year General Surgery

2. Anatomy Pancreas is derived from Greek word ‘pan’ (all) and ‘kreas’ (flesh) Pancreas is situated in the retroperitoneum The average pancreas weighs beween 75 g to 125 g and measures 10 cm to 20 cm Anatomically divided into five sections, the head; uncinate; neck; body and tail

3. The head, which occupies 30% of the gland by mass lies to right of midline within the C loop of the duodenum, overlying the body of second lumbar vertebra and vencava Uncinate process extends from the head of the pancreas behind the SMV and terminates adjacent to the SMA

4. Behind the neck of the pancreas, near its upper border, the SMV joins splenic vein to form the portal vein The body and tail of the pancreas extend across the midline slightly cephald terminating within the splenic hilum

5. Arterial Supply The head and uncinate process are supplied by the pancreaticoduodenal arteries (superior and inferior) The neck, body, and tail receive arterial supply from the splenic arterial system (several small branches, including the dorsal pancreatic artery and greater pancreatic artery)

6. Venous Drainage Head of the pancreas draining into the anterior and posterior pancreaticoduodenal veins The posterosuperior pancreaticoduodenal vein enters the SMV laterally at the superior border of the neck of the pancreas. The anterior superior pancreaticoduodenal vein enters the right gastroepiploic vein just before its confluence with the SMV at the inferior border of the pancreas The body and tail are drained through the splenic venous system

7. Lymphatic Drainage

8. Definition Pancreatitis is inflammation of the pancreatic parenchyma Acute pancreatitis is defined as an acute condition presenting with abdominal pain, a threefold or greater rise in the serum levels of the pancreatic enzymes amylase or lipase, and/or characteristic findings of pancreatic inflammation on contrast-enhanced CT

9. Classification Two classification system have been proposed : on the basis of severity 1. Three grades (mild, moderately severe and severe ) of Revised Atlanta classification 2. Four catagories (mild, moderate severe and critical) of Determinant based classification Schwartz 11 th ed

10. Epidemiology In context of Nepal, incidence of AP ranges from 10 to 50 per 100,000 per annum Overall mortality of approximately 4-6% and increases to 17-39 %in severe cases In Nepal exact data are yet to be discovered But study claims alcoholic pancreatitis as the leading cause,accounting for 66 % of all causes

11. Etiology

12. Gallstones : Are the most common cause (worldwide) Accounts for 40 to 70% of cases However only 3 -7 % of patients with gallstones develop pancreatitis

13. Three possibilities have been suggested Common channel hypothesis : Reflux of bile into the pancreatic duct due to transient obstruction of ampulla during passage of stone Edema resulting from the passage of a stone Obstruction of pancreatic duct and leading to ductal hypertension Small gallstones are associated with increase risk of pancreatitis

14. Alcohol : responsible for approximately 25 to 35 % of cases of acute pancreatitis ,worldwide 1. Act by increasing the synthesis of enzymes by pancreatic acinar cells to synthesize the digestive and lysosomal enzymes 2. Sensitization of acinar cells to cholecystokinin induced premature activation of zymogens 3. Ethanol induces ductal permeability which cause prematurely activated enzyme to cause damage to the pancreatic parenchyma 4. Decreases the level of trypsin inhibitor concentration

15. Hyper lipidemia : Lipase liberates toxic fatty acid into pancreatic micro circulation Leads to impairment of pancreatic microcirculation and ischemia

16. Hereditary pancreatitis : Autosomal dominant disease related to mutation of trypsinogenic gene Drugs : Thaizides diuretics, frusemide, Estrogen replacement therapy,steroid therapy , propofol

17. Pathophysiology Pancreatitis begins with : Premature activation of pancreatic enzymes within pancreas Activation of digestive zymogen inside acinar cells Causes injury to acinar cells

18. Events subsequent to acinar cell injury : Inflammatory cell activation and recruitment Generation and release of cytokines and other chemical mediators That causes systemic inflammation and multiple organ dysfunction

19. Diagnosis Modalities of diagnosis 1.Detailed history 2.Thorough examination 3.Appropriate investigations

20. Detailed History Clinical Presentation Pain is the cardinal symptom Characteristically develops quickly, reaching maximum intensity within minutes Pain is severe , constant and refractory to the usual dose of analgesics Usually experienced in the epigastrium, but may be localized to the upper quadrant or diffused throughout abdomen

21. Radiates to back in 50% of the patient In some ,relieved by leaning forward Nausea ,repeated vomiting and retching are marked Retching may persists even if stomach is kept empty by nasogastric aspiration

22. Thorough Examination Can be fair looking or at the extreme, gravely ill look with profound shock toxicity and confusion Tachypnea and tachycardia is usual, hypotension can be present Body temperature is often normal, but rises as inflammation develops Mild icteric due to biliary obstruction in gall stone pancreatitis

23. Bleeding into fascial plane can produce bluish discoloration Flanks (Grey turner’s sign) or umbilicus ( cullen’s sign) Usually muscle guarding in upper abdomen Pleural effusion present in 10-20% of patients Another rare sign is tetany due to hypocalcemia

24. Appropriate Investigations Investigations of acute pancreatitis must be based on : 1. Is a diagnosis of acute pancreatitis correct ? 2. How severe is the attack ? 3. What is the etiology ?

25. Laboratory Serum amylase or lipase (> 3 times upper limit of normal) Serum amylase concentrates rises immediately with onset of disease Peaks within several hours and remains elevated for 3-5 days No correlation between extent of serum amylase elevation and severity Serum lipase if available, is more sensitive and specific then amylase

26. Imaging Non specific sign on abdominal radiographs : Colon cut off sign Generalised or localized illeus (sentinel loop) Renal halo sign Chest radiograph may reveal a pleural effusion

27. USG doesnot establish the diagnosis of acute pancreatitis Should be performed : To detect gallstone,as a potential cause To rule out acute cholecystitis

28. CECT is indicated in following : 1. If there is diagnostic uncertainty . 2. In patients with severe acute pancreatitis, to distinguish interstitial from necrotising pancreatitis 3. S everity of pancreatitis detected on CT be staged a/c to balthazar score 4. In patients with organ failure, signs of sepsis and clinical deterioration 5.When localized collection is suspected, fluid collection, psuedocyst

29. MRI and MRCP ,are used increasingly to diagnose and assess severity MRI appears to be comparable to CT : As effective as CT in demonstrating presence and extent of pancreatic necrosis and fluid collection Regarding the severity of the disease Probably superior for indicating the suitability of collections for non surgical drainage

30. Severity scoring system Ranson’s criteria Glass gow score SOFA score CT severity index ( balthazar score) Apache II score Systemic inflammatory response syndrome score BISAP score Harmless acute pancreatitis score

31. Harmless Acute Pancreatitis Score Assess for the following features : . No sign of peritonitis Normal serum creatinine Normal Hematocrit If all three features are present ,it is 98% accurate at identifying patients with a non severe disease

32. CT severity index : 23 % mortality with any degree of pancreatic necrosis 0 % with no necrosis

33. Treatment After initial assessment if a patient is considered to have mild acute pancreatitis A conservative approach is indicated with IV fluids and frequent observation Brief period of fasting for patient who is nauseated, prolonged Nil by mouth has got little physiological justification Antibiotics are not indicated Apart from analgesic and anti emetics ,No drugs and intervention are warranted

34. Early Management of Severe acute Pancreatitis Admission to HDU/ICU Analgesia Aggressive fluid rehydration Supplemental oxygen Invasive monitoring of vital signs, central venous pressure, urine output, blood gases Frequent monitoring of haematological and biochemical parameters (including liver and renal function, clotting, serum calcium, blood glucose)

35. Nasogastric drainage (only initially) Antibiotics if cholangitis suspected; prophylactic antibiotics can be considered CT scan essential if organ failure, clinical deterioration or signs of sepsis develop ERCP within 72 hours for severe gallstone pancreatitis or signs of cholangitis Supportive therapy for organ failure if it develops (inotropes, ventilatory support, haemofiltration ,)

36. Local complications Acute (< 4 weeks, No defined walls) Acute pancreatic fluid collection Acute necrotic collection Chronic ( > 4 weeks, Defined walls) Pancreatic pseudocyst Walled of necrosis

37. Systemic complications 1.Cardiovascular Shock, Arrhythmias 2. Pulmonary ARDS ,Pulmonary Effusion 3.Renal failure 4.Haematological

38. 5. Metabolic Hypocalcaemia Hyperglycaemia Hyperlipidaemia 6. Gastrointestinal Ileus ,GI hemmorrhage 7. Neurological Visual disturbances Confusion, irritability Encephalopathy 8. Miscellaneous Subcutaneous fat necrosis, Arthralgia