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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.
Cullen’s sign
Grey-Turner’s 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.