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A Presentation on Acute Pancreatitis
Dr. Alim Al Razy
Intern, North East Medical College
Medicine Unit II
Under Prof Dr. Mrinal Kanti Das
• Pancreas is a dual organ having two functions,
namely endocrine function and exocrine
function.
• Endocrine function is concerned with the
production of hormones.
• The exocrine function is concerned with the
secretion of digestive juice called pancreatic
juice.
Acute pancreatitis is reversible
pancreatic parenchymal injury associated
with inflammation.
EPIDEMIOLOGY
• Recent U.S. estimates from the National
Inpatient Sample report that acute pancreatitis is
the most common inpatient principal
gastrointestinal diagnosis.
• The annual incidence ranges fr om 13-
45/100000 persons.
• All pancreatic disorders including acute
pancreatitis affect the black population more
than any other race.
Pathogenesis
• The anatomic changes of acute pancreatitis strongly suggest
autodigestion of the pancreatic substance by inappropriately
activated pancreatic enzymes.
• Thus, the inappropriate activation of trypsinogen is an
important triggering event in acute pancreatitis.
• The mechanisms by which the activation of pancreatic
enzymes is initiated are not entirely clear, but there is
evidence for three possible events.
> Pancreatic duct obstruction.
> Primary acinar cell injury
> Defective intracellular transport of proenzymes
within acinar cells.
Causes of pancreatitis
• Common causes
> Gallstone (including
microlithiasis)
> Alcohol (Acute and chronic
alcoholism)
> Hypertriglyceridemia
> ERCP (specially after biliary
manometry)
> Drug (azathioprim, 6-
mercaptopurine, sulfonamides,
Estrogen, tetracycline, Valporic
acid)
> Trauma (specially blunt
abdominal trauma)
> POST Operative (abdominal or
non-abdominal operation)
• Uncommon causes
> Vuscular causes and
vusculitis (ischemic
hypoperfusion after cardiac
surgery)
> Connective tissue disorder
> Cancer of pancreas
> Hypercalcemia
> Periampullary Diverticulum
> Pancreas Divisum
> hereditary pancreatitis
> Cystic Fibrosis
> Renal failure
> Infection (Mumps, Coxackie
virus, CMV, Echo virus)
Syptoms
• Upper abdominal pain
The pain usually begins in the epigastrium
accompanied by nausea, vommiting,
abdominal distention.
Gradually pain pain become more
intense.
Characteristically, the pain is steady and
boring in character. Located in
epigastrium and periumbilical region.
Involvement of retroperitonium frequenly
leads to back pain.
SINGS
• Distressed and anxious patient.
• Low grade fever, Tachycardia and
hypotension are common.
• There may be features of shock in severe cases.
• Jaundice occurs infrequently.
• Erythematous skin nodules may be found.
• There may be some pulmonary finings like
crackles, atelectesis.
• Bowel sonds are usually diminished or absent.
• A faint blue discoloration around umbilicus
(culen’s sign) may be found.
• Bule-red-purple or green-brown discoloration of
flanks (Turner’s sign) may be present.
• Cullen’s sign • Gray turner’s sign
DIAGNOSIS
• Diagnosis is established by two of the
following criteria:
1) Typical abdominal pain in epigastrium
2) Threefold or greater elevation in serum
lipase and/or amylase. And
3) Confirmatory findings of acute
pancreatitis on cross sectional abdominal
imaging.
LABORATORY DATA
: BLOOD TEST :
• Serum amylase
- Extremely sensitive test if it is three times the upper limit of normal
when measured within 24h of onset of pain
• Urinary amylaseUrinary amylase
- levels may be diagnostic as these remain elevated over a longer
period of time
• Serum lipase
- Rremain elevated for a longer period of time than those of amylase.
- The accuracy of serum lipase is not significantly greater than amylase
• C-reactive protein level
- Useful in assessing disease severity and prognosis.
Other baseline investigations >
• full blood count
• urea and
electrolytes
• blood glucose
• liver biochemistry
• plasma calcium
• arterial blood
gases.
RADIOLOGYRADIOLOGY
• An erect chest X-ray
- Mandatory to exclude gastroduodenal perforation, which also raises the serum
amylase.
• An abdominal ultrasound scan
- used as a screening test to identify a possible biliary (gallstone) cause of
pancreatitis.
• Contrast-enhanced
- CT scanning CT provides very valuable prognostic information.
- Repeated CT scans can detect other complications including fluid
collections, abscess formation and pseudocyst development
• MRI (MRCP)
- Assesses the degree of pancreatic damage and identifies gallstones within
the biliary tree.
• ERCP
- Used as a treatment measure to remove bile duct stones in
selected cases of gallstone-related pancreatitis
> An abdominal CT scan with arterial phase contrast in a patient presenting with
acute pancreatitis 48 h previously.
> The pancreas is swollen with very little uptake of contrast suggesting a severe
necrotizing process. There are peri-pancreatic inflammatory changes.
A coronal view of a CT scan in the same patient carried out in second week after
presentation.
There is now a large fluid collection with debris within. This is a precursor of a large
pseudocyst, which extends down the left paracolic gutter into the pelvis. This has
occurred as a consequence of a pancreatitis-induced ductal leak
MANAGEMENT
PRINCIPLES of MANAGEMENT
• Aggressive fluid resuscitation
• Search for etiology for proper care
• Management of pain
• Prevent other organ failure
• Strict monitoring of vital signs.
Fluid resuscitation
• Nothing should be given by mouth.
• The most important treatment intervention
for acute pancreatitis is aggressive
intravenous fluid resuscitation.
• Fuid choice: Ringer lactate or normal
saline
• Requirement: 15-20 cc/kg followed by
3mg/kg/hr.
Pain management
• Tramadol or other opiates are the drugs of
choice for immediate post-presentation
pain control.
Prophylactic antibiotics.
• Controlled data for the use of antibiotics
are available but the results are not
uniform in showing benefit, particularly in
showing improved mortality. There is
evidence that the beta lactam imipenem
reduces the incidence of infected
pancreatic necrosis
MONITORING
Special attention should be given on-
• Pulse
• BP
• Urine output
• Resp Rate
• Temperature
• WBC count
• BUN
• ABG
• S. Creatinine
• S. Electrolytes
COMPLICATIONS
LOCAL
• Necrosis
- Sterile
- Infected
• Pancreatic fluid
collections ancreatic
pseudocyst
• Disruption of main
pancreatic duct or
secondary branches
• Pancreatic ascites
• Involvement of
contiguous organs by
necrotizing pancreatitis
• Thrombosis of blood
vessels (splenic vein,
portal vein)
• Pancreatic enteric fistula
• Bowel infarction
• Obstructive jaundice
SYSTEMICSYSTEMIC
• PULMONARY
- Pleural effusion
- Atelectasis
- Mediastinal fluid
- Pneumonitis
• CARDIAC
- Hypotension
- Hypovolemia
- Non-specific ST-T
changes in ECG
(simulating MI)
- Pericardial effusion
• HAEMATOLOGIC
- DIC
• GIT
- PUD
- Erosive gastritis
• RENAL
- Oliguria
- Azotemia
- Renal artery/vein
thrombosis
- ATN
• METABOLIC
- Hyperglycemia
- Hypocalcemia
- encephalopathy
- Sudden blindness
• CNS
- Psychosis
- Fat emboli
THANK YOU
Acute pancreatitis

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Acute pancreatitis

  • 1. A Presentation on Acute Pancreatitis Dr. Alim Al Razy Intern, North East Medical College Medicine Unit II Under Prof Dr. Mrinal Kanti Das
  • 2.
  • 3. • Pancreas is a dual organ having two functions, namely endocrine function and exocrine function. • Endocrine function is concerned with the production of hormones. • The exocrine function is concerned with the secretion of digestive juice called pancreatic juice.
  • 4.
  • 5. Acute pancreatitis is reversible pancreatic parenchymal injury associated with inflammation.
  • 6. EPIDEMIOLOGY • Recent U.S. estimates from the National Inpatient Sample report that acute pancreatitis is the most common inpatient principal gastrointestinal diagnosis. • The annual incidence ranges fr om 13- 45/100000 persons. • All pancreatic disorders including acute pancreatitis affect the black population more than any other race.
  • 7. Pathogenesis • The anatomic changes of acute pancreatitis strongly suggest autodigestion of the pancreatic substance by inappropriately activated pancreatic enzymes. • Thus, the inappropriate activation of trypsinogen is an important triggering event in acute pancreatitis. • The mechanisms by which the activation of pancreatic enzymes is initiated are not entirely clear, but there is evidence for three possible events. > Pancreatic duct obstruction. > Primary acinar cell injury > Defective intracellular transport of proenzymes within acinar cells.
  • 8.
  • 9. Causes of pancreatitis • Common causes > Gallstone (including microlithiasis) > Alcohol (Acute and chronic alcoholism) > Hypertriglyceridemia > ERCP (specially after biliary manometry) > Drug (azathioprim, 6- mercaptopurine, sulfonamides, Estrogen, tetracycline, Valporic acid) > Trauma (specially blunt abdominal trauma) > POST Operative (abdominal or non-abdominal operation) • Uncommon causes > Vuscular causes and vusculitis (ischemic hypoperfusion after cardiac surgery) > Connective tissue disorder > Cancer of pancreas > Hypercalcemia > Periampullary Diverticulum > Pancreas Divisum > hereditary pancreatitis > Cystic Fibrosis > Renal failure > Infection (Mumps, Coxackie virus, CMV, Echo virus)
  • 10. Syptoms • Upper abdominal pain The pain usually begins in the epigastrium accompanied by nausea, vommiting, abdominal distention. Gradually pain pain become more intense. Characteristically, the pain is steady and boring in character. Located in epigastrium and periumbilical region. Involvement of retroperitonium frequenly leads to back pain.
  • 11. SINGS • Distressed and anxious patient. • Low grade fever, Tachycardia and hypotension are common. • There may be features of shock in severe cases. • Jaundice occurs infrequently. • Erythematous skin nodules may be found. • There may be some pulmonary finings like crackles, atelectesis. • Bowel sonds are usually diminished or absent. • A faint blue discoloration around umbilicus (culen’s sign) may be found. • Bule-red-purple or green-brown discoloration of flanks (Turner’s sign) may be present.
  • 12. • Cullen’s sign • Gray turner’s sign
  • 13. DIAGNOSIS • Diagnosis is established by two of the following criteria: 1) Typical abdominal pain in epigastrium 2) Threefold or greater elevation in serum lipase and/or amylase. And 3) Confirmatory findings of acute pancreatitis on cross sectional abdominal imaging.
  • 15. : BLOOD TEST : • Serum amylase - Extremely sensitive test if it is three times the upper limit of normal when measured within 24h of onset of pain • Urinary amylaseUrinary amylase - levels may be diagnostic as these remain elevated over a longer period of time • Serum lipase - Rremain elevated for a longer period of time than those of amylase. - The accuracy of serum lipase is not significantly greater than amylase • C-reactive protein level - Useful in assessing disease severity and prognosis.
  • 16. Other baseline investigations > • full blood count • urea and electrolytes • blood glucose • liver biochemistry • plasma calcium • arterial blood gases.
  • 17. RADIOLOGYRADIOLOGY • An erect chest X-ray - Mandatory to exclude gastroduodenal perforation, which also raises the serum amylase. • An abdominal ultrasound scan - used as a screening test to identify a possible biliary (gallstone) cause of pancreatitis. • Contrast-enhanced - CT scanning CT provides very valuable prognostic information. - Repeated CT scans can detect other complications including fluid collections, abscess formation and pseudocyst development • MRI (MRCP) - Assesses the degree of pancreatic damage and identifies gallstones within the biliary tree. • ERCP - Used as a treatment measure to remove bile duct stones in selected cases of gallstone-related pancreatitis
  • 18. > An abdominal CT scan with arterial phase contrast in a patient presenting with acute pancreatitis 48 h previously. > The pancreas is swollen with very little uptake of contrast suggesting a severe necrotizing process. There are peri-pancreatic inflammatory changes.
  • 19. A coronal view of a CT scan in the same patient carried out in second week after presentation. There is now a large fluid collection with debris within. This is a precursor of a large pseudocyst, which extends down the left paracolic gutter into the pelvis. This has occurred as a consequence of a pancreatitis-induced ductal leak
  • 21. PRINCIPLES of MANAGEMENT • Aggressive fluid resuscitation • Search for etiology for proper care • Management of pain • Prevent other organ failure • Strict monitoring of vital signs.
  • 22. Fluid resuscitation • Nothing should be given by mouth. • The most important treatment intervention for acute pancreatitis is aggressive intravenous fluid resuscitation. • Fuid choice: Ringer lactate or normal saline • Requirement: 15-20 cc/kg followed by 3mg/kg/hr.
  • 23. Pain management • Tramadol or other opiates are the drugs of choice for immediate post-presentation pain control.
  • 24. Prophylactic antibiotics. • Controlled data for the use of antibiotics are available but the results are not uniform in showing benefit, particularly in showing improved mortality. There is evidence that the beta lactam imipenem reduces the incidence of infected pancreatic necrosis
  • 25. MONITORING Special attention should be given on- • Pulse • BP • Urine output • Resp Rate • Temperature • WBC count • BUN • ABG • S. Creatinine • S. Electrolytes
  • 27. LOCAL • Necrosis - Sterile - Infected • Pancreatic fluid collections ancreatic pseudocyst • Disruption of main pancreatic duct or secondary branches • Pancreatic ascites • Involvement of contiguous organs by necrotizing pancreatitis • Thrombosis of blood vessels (splenic vein, portal vein) • Pancreatic enteric fistula • Bowel infarction • Obstructive jaundice
  • 28. SYSTEMICSYSTEMIC • PULMONARY - Pleural effusion - Atelectasis - Mediastinal fluid - Pneumonitis • CARDIAC - Hypotension - Hypovolemia - Non-specific ST-T changes in ECG (simulating MI) - Pericardial effusion • HAEMATOLOGIC - DIC • GIT - PUD - Erosive gastritis • RENAL - Oliguria - Azotemia - Renal artery/vein thrombosis - ATN
  • 29. • METABOLIC - Hyperglycemia - Hypocalcemia - encephalopathy - Sudden blindness • CNS - Psychosis - Fat emboli