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Acute Pancreatitis
• Dr LNR González
• Robert Mangaliso Sobukwe Hospital(Kimberley Hospital)2019
Acute Pancreatitis
Definition
Epidemiology
Aetiology
Signs & Symptoms
Investigations
Management
Complications
Acute Pancreatitis
Definition:
• Acute inflammation of the pancreas(and, sometimes , adjacent
tissues).
• Reversible inflammation .
• Ranges from mild to severe .
Epidemiology
• Acute pancreatitis accounts for 3% of all cases of abdominal pain of
all patients admitted to hospital.
• Affects 2-28 per 100000 population.
• It may occur at any age , peak incidence is between 50-60 years of
age.
• Women are affected more than men , but men are more likely to
suffer from recurring attacks.
Aetiology
Mnemonic : GET SMASHED
• G- allstones (40%)
• E- thanol (40%)
• T- rauma (1.5%)
• S- teroids
• M- umps
• A- utoimmune
• S- corpion venom
• H- yperlipidemia , Hypothermia , Hypercalcemia
• E- RCP (5%), Emboli
• D- rugs
NOTE: Pregnancy , Neoplasia or No Known Cause (10-30%)
Symptoms
• Gradual or sudden severe epigastric or central abdominal pain which
radiates to the back and shoulder tips, relieved by leaning forward.
• Patient tends to lie very still.
• Nausea
• Vomiting
• Retching
• Weakness
Signs
• Tachycardia
• Tachypnoea
• Shallow Breathing
• Diaphoresis
• Hypotension
• Mild Icterus
• Fever
• Shock
• Ileus
• Rigid abdomen +/- local/general tenderness
• Periumbilical bruising (Cullen’s Sign) or on flanks (Grey Turner’s sign) from blood vessel autodigestion and
retroperitoneal haemorrhage.
• Bruising is seen over the inguinal ligament ( Fox’s sign) , occurs in patients with retroperitoneal bleeding,
usually due to acute hemorrhagic pancreatitis.
Differential Diagnosis
• Peptic ulcer
• Perforated Viscus
• Acute Cholecystitis , Biliary Cholic
• Acute Intestinal Obstruction
• Oesophageal Rupture
• Mesenteric Vascular Obstruction
• Renal Colic
• Dissecting Aortic Aneurism
• MI
• Basal Pneumonia
• DKA
Investigations
Should be aimed at answering 3 questions:
1. Is the diagnosis of acute pancreatitis correct?
2. How severe is the attack?
3. What is the aetiology?
Investigations
Blood Tests:
• FBC
• Serum amylase and lipase
• C-reactive protein
• Serum electrolytes
• Blood glucose
• Renal function test
• LFT
• LDH
• Clotting profile
• ABG
Serum Amylase
• Sensitivity: 72% Specificity:99%
• Released with 6-12 hours of the onset & remains elevated for 3-5
days.
• Elevation of >3 x normal is significant.
• Undergoes renal clearance. After its serum level decline , its urine
level remain elevated.
• Its level doesn’t correlate with the disease activity
Serum Lipase
• More pancreatic-specific than Serum Amylase.
• Sensitivity: 100% Specificity: 96%
• Remains elevated longer than amylase ( about 1 week)
• Useful in patients presenting late to the physician.
• S.Amylase tends to be higher in Gall Stone Pancreatitis.
• S.Lipase tends to be higher in Alcoholic Pancreatitis.
Imaging Investigations : X-Rays
Erect CXR :
• Not diagnostic but helps to rule out DDx.
AXR :
• Calcification in the pancreas
• Mass from a pseudocyst
• Sentinel loop: a single dilated jejunal loop in the upper abdomen
• Colon cut off: dilated colon to the mid-transverse colon with no air seen
beyond the splenic flexure. This is due to extension of inflammation along
mesocolon.
• Diffuse ileus (smalll bowel dilatation) is most common
Sentinel Loop Sign
Colon Cut-Off Sign
• Cut off sign and Ileus
• White arrow points to
Transverse Colon cut off
at Splenic flexure. No air
in descending colon.
• TC: Transverse colon
• I: Represents small bowel
loops with air suggestive
of Ileus
Imaging Investigations : Ultrasound
Findings:
• Edematous
pancreas
• Gallstones
• Dilated common
bile duct
• Pseudocyst
• When ileus is
present pancreas Is
poorly defined
Imaging Investigations: CT Scan
Contrast-enhanced CT of the pancreas is diagnostic and can show:
• Enlargement of pancreas due to edema
• Peripancreatic inflammation.
• Necrosis: On contrast enhanced phases the necrotic pancreatic parenchyma will
show decreased or no enhancement when compared with normally enhancing
viable tissue
• Fluid collections: A simple peripancreatic fluid collection will not have a well-
defined capsule
• Pseudocysts: As liquefaction of necrotic pancreatic tissue progresses it will
gradually take on the appearance of localized fluid collection - pseudocyst
• Abscesses: Diffusely enlarged pancreas with air pockets
• Hemorrhagic pancreatitis: Enlarged pancreas with increased density due to
hemorrhage
Acute Pancreatitis CT
• CT Findings: Post
Contrast
• Diffusely enlarged
pancreas with low
density from
edema
• C: Colon
St: Stomach
P: Pancreas
Acute Haemorrhagic Pancreatitis
• Enlarged tail of
pancreas
• White arrow:
Increased density
in the enlarged tail
of pancreas due to
blood
• Fascial changes
adjacent to tail of
Pancreas due to
inflammation
CT Severity Index
Combines the Balthazar grade
(0-4 points) with the extent of
pancreatic necrosis (0-6 points)
on a 10-point severity scale.
• 0-1 = 0% Mortality
• 2-3 = 3% Mortality
• 4-6 = 6% Mortality
• 7-10 = 17% Mortality
Imaging Investigations : MRI
The advantages of MRI over CT :
• Lack of nephrotoxicity of gadolium.
• Ability of MRI to better categorize
fluid collection as acute fluid
collections, necrosis ,abscess,
haemorrhage, and pseudocyst.
• Greater sensitivity of MRI to
detect mild acute pancreatitis
compared to CT.
• MRI delineates the pancreatic and
bile ducts better and is
comparable to ERCP for the
detection of choledocholithiasis.
Management : Goals of Treatment
• Aggressive supportive care
• Decrease inflammation
• Limit Superinfection
• Identify and treat complications
• Treat cause if possible
Conservative Management
• Gain IV access
• Obtain blood sample
• Rapid fluid resuscitation
• Electrolyte management
• Give analgesics (IM pethidine)
• Give anti-emetics
• Keep patient NPO (until pain free 2-3 days)
• NGT insertion to relieve vomiting
• Urinary catheterization
• Monitor vitals
• PPI IV
Management of Severe Acute Pancreatitis
• Ideally admission to ICU
• Analgesia
• Aggressive fluid resuscitation
• Oxygenation
• Invasive monitoring of vital signs , central venous pressure , urine
output , ABG.
• Frequent parameters of chemical and biological parameters ( Liver
and renal function tests , clotting , serum calcium , blood glucose)
• Nasogastric tube
• CT scan essential if organ failure , clinical deterioration or signs of
sepsis develop
• Supportive failure for organ failure if it develops( inotropes ,
ventilatory support, HD, etc)
• If nutritional support is required, consider enteral feeding.
Role of Antibiotics
 Prophylactic antibiotics have shown NO DECREASE of mortality in
severe acute pancreatitis.
Antibiotics are justified if :
1. Gas in retroperitoneal space
2. Needle aspiration of necrotic material confirms infection
3. Sepsis
4. CRP of >120mg/L
5. Peri-pancreatic fluid collection
6. Organ dysfunction
7. APACHE II Score of >6 ( Estimates ICU mortality based on a
number of laboratory values and patient signs taking both acute
and chronic disease into account)
Operative Management
• Surgery has NO IMMEDIATE ROLE in acute pancreatitis.
• Aggressive surgical pancreatic debridement should be undertaken
soon after confirmation of the presence of infected necrosis.
Systemic Complications
• Cardiovascular : Shock , Arrythmias , Pericardial Effusion.
• Pulmonary: Basal Atelectasis , Pleural Effusion, ARDS.
• Renal: Acute Kidney Injury.
• Haematological: DIC
• Metabolic: Hypocalcaemia , Hyperglycaemia , Hyperlipidaemia.
• GIT: Ileus
• Neurological: Confusion , Irritability , Encephalopathy.
• Miscellaneous: Subcutaneous Fat Necrosis , Arthralgia.
Local Complications
Occur after 1st week :
• Acute fluid collection
• Sterile pancreatic necrosis
• Infected pancreatic necrosis
• Peripancreatic
Pseudoaneurysm
• Pancreatic abscess
• Splenic vein thrombosis
References
• Harrison’s , Merck Manual, WSES guidelines, UpToDate, etc
Acute Pancreatitis
THANK YOU

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Acute pancreatitis

  • 1. Acute Pancreatitis • Dr LNR González • Robert Mangaliso Sobukwe Hospital(Kimberley Hospital)2019
  • 2. Acute Pancreatitis Definition Epidemiology Aetiology Signs & Symptoms Investigations Management Complications
  • 3. Acute Pancreatitis Definition: • Acute inflammation of the pancreas(and, sometimes , adjacent tissues). • Reversible inflammation . • Ranges from mild to severe .
  • 4. Epidemiology • Acute pancreatitis accounts for 3% of all cases of abdominal pain of all patients admitted to hospital. • Affects 2-28 per 100000 population. • It may occur at any age , peak incidence is between 50-60 years of age. • Women are affected more than men , but men are more likely to suffer from recurring attacks.
  • 5. Aetiology Mnemonic : GET SMASHED • G- allstones (40%) • E- thanol (40%) • T- rauma (1.5%) • S- teroids • M- umps • A- utoimmune • S- corpion venom • H- yperlipidemia , Hypothermia , Hypercalcemia • E- RCP (5%), Emboli • D- rugs NOTE: Pregnancy , Neoplasia or No Known Cause (10-30%)
  • 6. Symptoms • Gradual or sudden severe epigastric or central abdominal pain which radiates to the back and shoulder tips, relieved by leaning forward. • Patient tends to lie very still. • Nausea • Vomiting • Retching • Weakness
  • 7. Signs • Tachycardia • Tachypnoea • Shallow Breathing • Diaphoresis • Hypotension • Mild Icterus • Fever • Shock • Ileus • Rigid abdomen +/- local/general tenderness • Periumbilical bruising (Cullen’s Sign) or on flanks (Grey Turner’s sign) from blood vessel autodigestion and retroperitoneal haemorrhage. • Bruising is seen over the inguinal ligament ( Fox’s sign) , occurs in patients with retroperitoneal bleeding, usually due to acute hemorrhagic pancreatitis.
  • 8. Differential Diagnosis • Peptic ulcer • Perforated Viscus • Acute Cholecystitis , Biliary Cholic • Acute Intestinal Obstruction • Oesophageal Rupture • Mesenteric Vascular Obstruction • Renal Colic • Dissecting Aortic Aneurism • MI • Basal Pneumonia • DKA
  • 9. Investigations Should be aimed at answering 3 questions: 1. Is the diagnosis of acute pancreatitis correct? 2. How severe is the attack? 3. What is the aetiology?
  • 10. Investigations Blood Tests: • FBC • Serum amylase and lipase • C-reactive protein • Serum electrolytes • Blood glucose • Renal function test • LFT • LDH • Clotting profile • ABG
  • 11. Serum Amylase • Sensitivity: 72% Specificity:99% • Released with 6-12 hours of the onset & remains elevated for 3-5 days. • Elevation of >3 x normal is significant. • Undergoes renal clearance. After its serum level decline , its urine level remain elevated. • Its level doesn’t correlate with the disease activity
  • 12. Serum Lipase • More pancreatic-specific than Serum Amylase. • Sensitivity: 100% Specificity: 96% • Remains elevated longer than amylase ( about 1 week) • Useful in patients presenting late to the physician. • S.Amylase tends to be higher in Gall Stone Pancreatitis. • S.Lipase tends to be higher in Alcoholic Pancreatitis.
  • 13. Imaging Investigations : X-Rays Erect CXR : • Not diagnostic but helps to rule out DDx. AXR : • Calcification in the pancreas • Mass from a pseudocyst • Sentinel loop: a single dilated jejunal loop in the upper abdomen • Colon cut off: dilated colon to the mid-transverse colon with no air seen beyond the splenic flexure. This is due to extension of inflammation along mesocolon. • Diffuse ileus (smalll bowel dilatation) is most common
  • 15. Colon Cut-Off Sign • Cut off sign and Ileus • White arrow points to Transverse Colon cut off at Splenic flexure. No air in descending colon. • TC: Transverse colon • I: Represents small bowel loops with air suggestive of Ileus
  • 16. Imaging Investigations : Ultrasound Findings: • Edematous pancreas • Gallstones • Dilated common bile duct • Pseudocyst • When ileus is present pancreas Is poorly defined
  • 17. Imaging Investigations: CT Scan Contrast-enhanced CT of the pancreas is diagnostic and can show: • Enlargement of pancreas due to edema • Peripancreatic inflammation. • Necrosis: On contrast enhanced phases the necrotic pancreatic parenchyma will show decreased or no enhancement when compared with normally enhancing viable tissue • Fluid collections: A simple peripancreatic fluid collection will not have a well- defined capsule • Pseudocysts: As liquefaction of necrotic pancreatic tissue progresses it will gradually take on the appearance of localized fluid collection - pseudocyst • Abscesses: Diffusely enlarged pancreas with air pockets • Hemorrhagic pancreatitis: Enlarged pancreas with increased density due to hemorrhage
  • 18. Acute Pancreatitis CT • CT Findings: Post Contrast • Diffusely enlarged pancreas with low density from edema • C: Colon St: Stomach P: Pancreas
  • 19. Acute Haemorrhagic Pancreatitis • Enlarged tail of pancreas • White arrow: Increased density in the enlarged tail of pancreas due to blood • Fascial changes adjacent to tail of Pancreas due to inflammation
  • 20. CT Severity Index Combines the Balthazar grade (0-4 points) with the extent of pancreatic necrosis (0-6 points) on a 10-point severity scale. • 0-1 = 0% Mortality • 2-3 = 3% Mortality • 4-6 = 6% Mortality • 7-10 = 17% Mortality
  • 21. Imaging Investigations : MRI The advantages of MRI over CT : • Lack of nephrotoxicity of gadolium. • Ability of MRI to better categorize fluid collection as acute fluid collections, necrosis ,abscess, haemorrhage, and pseudocyst. • Greater sensitivity of MRI to detect mild acute pancreatitis compared to CT. • MRI delineates the pancreatic and bile ducts better and is comparable to ERCP for the detection of choledocholithiasis.
  • 22. Management : Goals of Treatment • Aggressive supportive care • Decrease inflammation • Limit Superinfection • Identify and treat complications • Treat cause if possible
  • 23. Conservative Management • Gain IV access • Obtain blood sample • Rapid fluid resuscitation • Electrolyte management • Give analgesics (IM pethidine) • Give anti-emetics • Keep patient NPO (until pain free 2-3 days) • NGT insertion to relieve vomiting • Urinary catheterization • Monitor vitals • PPI IV
  • 24. Management of Severe Acute Pancreatitis • Ideally admission to ICU • Analgesia • Aggressive fluid resuscitation • Oxygenation • Invasive monitoring of vital signs , central venous pressure , urine output , ABG. • Frequent parameters of chemical and biological parameters ( Liver and renal function tests , clotting , serum calcium , blood glucose) • Nasogastric tube • CT scan essential if organ failure , clinical deterioration or signs of sepsis develop • Supportive failure for organ failure if it develops( inotropes , ventilatory support, HD, etc) • If nutritional support is required, consider enteral feeding.
  • 25. Role of Antibiotics  Prophylactic antibiotics have shown NO DECREASE of mortality in severe acute pancreatitis. Antibiotics are justified if : 1. Gas in retroperitoneal space 2. Needle aspiration of necrotic material confirms infection 3. Sepsis 4. CRP of >120mg/L 5. Peri-pancreatic fluid collection 6. Organ dysfunction 7. APACHE II Score of >6 ( Estimates ICU mortality based on a number of laboratory values and patient signs taking both acute and chronic disease into account)
  • 26. Operative Management • Surgery has NO IMMEDIATE ROLE in acute pancreatitis. • Aggressive surgical pancreatic debridement should be undertaken soon after confirmation of the presence of infected necrosis.
  • 27. Systemic Complications • Cardiovascular : Shock , Arrythmias , Pericardial Effusion. • Pulmonary: Basal Atelectasis , Pleural Effusion, ARDS. • Renal: Acute Kidney Injury. • Haematological: DIC • Metabolic: Hypocalcaemia , Hyperglycaemia , Hyperlipidaemia. • GIT: Ileus • Neurological: Confusion , Irritability , Encephalopathy. • Miscellaneous: Subcutaneous Fat Necrosis , Arthralgia.
  • 28. Local Complications Occur after 1st week : • Acute fluid collection • Sterile pancreatic necrosis • Infected pancreatic necrosis • Peripancreatic Pseudoaneurysm • Pancreatic abscess • Splenic vein thrombosis
  • 29. References • Harrison’s , Merck Manual, WSES guidelines, UpToDate, etc Acute Pancreatitis