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Acute
pancreatitis
PRESENTED BY: IRFAN UL HAQ
MBBS FINAL YEAR.
GMC SRINAGAR.
Definition
 Acute pancreatic inflammation associated with little or
no fibrosis.
 It ranges from a mild self-limiting inflammation
of the pancreas to critical disease characterized by infected
pancreatic necrosis, multiple organ failure and a high risk of mortality.
Pancreas with biliary tree
Epidemiology
 Worldwide annual incidence of acute pancreatitis may range from 5 to 50 per 100,000 with
highest incidence in Finland and US.
 The disease may occur at any age , with peak in young men and older women.
 Smoking is an independent risk factor for acute pancreatitis.
Aetiology
 There are two major causes of acute pancreatitis which are
 Gallstones and
 Alcohol abuse.
 Gallstone pancreatitis is seen in 50-70% of cases whereas due to alcohol
abuse it is 25%.
 The other possible causes of acute pancreatitis are:
 Biliary tract disease
 Hyperlipidemia
 Hereditary
 Hypercalcemia
Aetilogy (contd)
 Trauma:
 External
 Surgical
 Endoscopic retrograde cholangiopancreatography.
 Ischemia:
 Hypoperfusion
 Atheroembolic
 Vasculitis
 Pancreatic duct obstruction:
 Neoplasms
 Pancreas divisum
 Ampullary and duodenal lesions
 Infections.
 Venom.
 Drugs.
 Idiopathic.
Pathophysiology
 Acute pancreatitis occurs in various degrees of severity, the
determinants of which are multifactorial.
 The generally prevalent belief today is that pancreatitis begins with the activation
of digestive zymogens inside acinar cells, which cause acinar
cell injury.
 Studies suggest that the ultimate severity of the
resulting pancreatitis may be determined by the events that
occur subsequent to acinar cell injury.
 These include inflammatory cell recruitment and activation, as well as generation
and release of cytokines and other chemical mediators of inflammation.
Pathogenesis (contd.)
Clinical features
 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 .
Clinical features(contd)
 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)
 Abdominal examination reveals distention due to ileus or more rarely, ascites
with shifting dullness.
 A mass can develop in epigastrium due to inflammation.
 A pleural effusion is present in 10-20% of patients.
Cullens sign
Grey-Turners Sign
Investigations
 Full blood count: neutrophil leukocytosis.
 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).
Investigations(contd)
Amylase and lipase :
 Elevated serum amylase and lipase levels, in combination with
severe abdominal pain, often trigger the initial diagnosis of acute
pancreatitis.
 Serum lipase rises 4 to 8 hours from the onset of symptoms
and normalizes within 7 to 14 days after treatment.
 Marked elevation of serum amylase level during first 24 hours
 Reasons for false positive elevated serum amylase include
salivary gland disease (elevated salivary amylase) and
macroamylasemia.
 If the lipase level is about 2.5 to 3 times that of Amylase, it is
an indication of pancreatitis due to Alcohol or gallstone
 The degree of amylase/lipase elevation does not correlate
with severity of acute pancreatitis.
Assesment of severity of AP.
 Different scoring systems have been applied to asses the severity and prognosis of acute
pancreatitis viz:
 Ranson Score.
 APACHE II Score.
 Balthazar Score.
Ranson score
Ranson Score(contd)
APACHE II Score(Acute Physiology And Chronic
Health Evaluation)
Score 0 to 2 : 2% mortality. Score 3 to 4 : 15% mortality.
Score 5 to 6 : 40% mortality. Score 7 to 8 : 100% mortality.
1) Hemorrhagic peritoneal fluid.
2) Obesity.
3) Indicators of organ failure.
4) Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min.
5) PO2 <60 mmHg.
6) Oliguria (<50 mL/h) or increasing BUN and creatinine.
7) Serum calcium < 1.90 mmol/L (<8.0 mg/dL).
8) Serum albumin <33 g/L (<3.2.g/dL).
Balthazar scoring
Complications
 Immediate:
 Shock.
 DIVC.
 ARDS.
 Late:
 Pancreatic pseudocyst.
 Pancreatic abscess.
 Pancreatic necrosis.
 Pancreatic jaundice.
 Persistant duodenal ileus.
 G I bleed.
 Pancreatic ascites.
Management
 IV fluid replacement (normal saline).
 Bowel rest (NG tube, NPO) in severe case.
 Administration of meperidine/pethidine as pain killer.
 Antiemetic if necessary.
 Monitor & correct electrolytes.
 Prevent infection by antibiotic prophylaxis.
 Determine & treat specific etiology(avoid alcohol).
 Indication to surgery if pancreatitis not respond to treatment.
Acute pancreatitis

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Acute pancreatitis

  • 1. Acute pancreatitis PRESENTED BY: IRFAN UL HAQ MBBS FINAL YEAR. GMC SRINAGAR.
  • 2. Definition Acute pancreatic inflammation associated with little or no fibrosis. It ranges from a mild self-limiting inflammation of the pancreas to critical disease characterized by infected pancreatic necrosis, multiple organ failure and a high risk of mortality.
  • 4. Epidemiology Worldwide annual incidence of acute pancreatitis may range from 5 to 50 per 100,000 with highest incidence in Finland and US. The disease may occur at any age , with peak in young men and older women. Smoking is an independent risk factor for acute pancreatitis.
  • 5. Aetiology There are two major causes of acute pancreatitis which are Gallstones and Alcohol abuse. Gallstone pancreatitis is seen in 50-70% of cases whereas due to alcohol abuse it is 25%. The other possible causes of acute pancreatitis are: Biliary tract disease Hyperlipidemia Hereditary Hypercalcemia
  • 6. Aetilogy (contd) Trauma: External Surgical Endoscopic retrograde cholangiopancreatography. Ischemia: Hypoperfusion Atheroembolic Vasculitis Pancreatic duct obstruction: Neoplasms Pancreas divisum Ampullary and duodenal lesions Infections. Venom. Drugs. Idiopathic.
  • 7. Pathophysiology Acute pancreatitis occurs in various degrees of severity, the determinants of which are multifactorial. The generally prevalent belief today is that pancreatitis begins with the activation of digestive zymogens inside acinar cells, which cause acinar cell injury. Studies suggest that the ultimate severity of the resulting pancreatitis may be determined by the events that occur subsequent to acinar cell injury. These include inflammatory cell recruitment and activation, as well as generation and release of cytokines and other chemical mediators of inflammation.
  • 9. Clinical features 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 .
  • 10. Clinical features(contd) 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) Abdominal examination reveals distention due to ileus or more rarely, ascites with shifting dullness. A mass can develop in epigastrium due to inflammation. A pleural effusion is present in 10-20% of patients.
  • 13. Investigations Full blood count: neutrophil leukocytosis. 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. Investigations(contd) Amylase and lipase : Elevated serum amylase and lipase levels, in combination with severe abdominal pain, often trigger the initial diagnosis of acute pancreatitis. Serum lipase rises 4 to 8 hours from the onset of symptoms and normalizes within 7 to 14 days after treatment. Marked elevation of serum amylase level during first 24 hours Reasons for false positive elevated serum amylase include salivary gland disease (elevated salivary amylase) and macroamylasemia. If the lipase level is about 2.5 to 3 times that of Amylase, it is an indication of pancreatitis due to Alcohol or gallstone The degree of amylase/lipase elevation does not correlate with severity of acute pancreatitis.
  • 15. Assesment of severity of AP. Different scoring systems have been applied to asses the severity and prognosis of acute pancreatitis viz: Ranson Score. APACHE II Score. Balthazar Score.
  • 18. APACHE II Score(Acute Physiology And Chronic Health Evaluation) Score 0 to 2 : 2% mortality. Score 3 to 4 : 15% mortality. Score 5 to 6 : 40% mortality. Score 7 to 8 : 100% mortality. 1) Hemorrhagic peritoneal fluid. 2) Obesity. 3) Indicators of organ failure. 4) Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min. 5) PO2 <60 mmHg. 6) Oliguria (<50 mL/h) or increasing BUN and creatinine. 7) Serum calcium < 1.90 mmol/L (<8.0 mg/dL). 8) Serum albumin <33 g/L (<3.2.g/dL).
  • 20. Complications Immediate: Shock. DIVC. ARDS. Late: Pancreatic pseudocyst. Pancreatic abscess. Pancreatic necrosis. Pancreatic jaundice. Persistant duodenal ileus. G I bleed. Pancreatic ascites.
  • 21. Management IV fluid replacement (normal saline). Bowel rest (NG tube, NPO) in severe case. Administration of meperidine/pethidine as pain killer. Antiemetic if necessary. Monitor & correct electrolytes. Prevent infection by antibiotic prophylaxis. Determine & treat specific etiology(avoid alcohol). Indication to surgery if pancreatitis not respond to treatment.