Acute Pancreatitis

Outline of Presentation
• Anatomy of Pancreas
• Aetiology
• Pathophysiology
• Clinical Approach – History and Physical
Examination
• Differential Diagnosis
• Investigation
• Assessment of Severity
• Management of Acute Pancreatitis
• Complications
ANATOMY OF PANCREAS
 Anatomy
• Retroperitoneal organ
• In adults- 15cm long & 70-100 weighs
• 3 portions- head, body and tail
• Relations:
 Head
 Neck
 Uncinate
 Body
 Tail
• Main pancreatic duct- Wirsung duct
• Acessory duct – Santorini duct
 Pancreatiti
s

Acute Chronic
presenting with abdominal pain and is usually
associated with raised pancreatic enzyme levels
in the blood or urine as a result of pancreatic
inflammation.
 Incidence
• 3 % of all cases of abdominal pain
• Hospital admission rate for is 9.8 per 100 000
population anually
• Worldwide, 50 per 100 000 cases anually.
• The disease may occur at any age, with a peak
in young men and older women.
 Etiology
Two major causes are :
• biliary calculi (50–70%)
• alcohol abuse (25%)

The remaining cases may be due to rare causes

or be idiopathic
 Gallstone Pancreatitis
• Transient blockage of common bile duct 
reflux of bile into pancreatic duct and impair
flow of normal pancreatic juice  premature
activation of pancreatic enzymes within duct
system.
 Alcohol Pancreatitis
• High risk in:
1. Long standing alcohol intake for at least 2
years or single session of heavy drinking
2. Consumption >80g/day
• What Happened ?
1. Direct toxic effect of alcohol in genetically
predisposed individuals
2. Viscid secretion of pancreatic juice  formation
of protein plugs and impairment of flow
 Pathophysiology
• Premature activation of pancreatic enzymes
within the pancreas, leading to a process of
autodigestion.
• Anything that injures the acinar cell and impairs
the secretion of zymogen granules, or damages
the duct epithelium and thus delays enzymatic
secretion, can trigger acute pancreatitis.
• Once cellular injury has been initiated, the
inflammatory process can lead to pancreatic
oedema, haemorrhage and, eventually, necrosis.
• As inflammatory mediators are released into the
circulation, systemic complications can arise.
ACUTE PANCREATITIS
History and Physical Examination
 Purpose of History Taking
• Pain
• Causes
• Complications
 History Taking
1) Abdominal Pain - Remember SOCRATES!
• Site: Diffuse, upper abdominal pain
• Onset: Sudden
• Character: Boring Pain
• Radiation: Radiates to the back
• Associated factor: Nausea, vomiting, dyspnea
• Timing: Pain escalates in intensity and peaks
within 10-20 minutes of onset.
• Aggravating and relieving factor: Aggravated
by breathing with increased chest expansion
and relieved by leaning forward.
• Severity: Depending on severity, patient may
present in shock
2) History of underlying causes

‘I GET SMASHED’

• Idiopathic (10%)
• Gallstone (45%)
• Ethanol (35%)
• Trauma (10%)
• Steroids
• Mumps
• Autoimmune
• Scorpion / Snake
• Hyperlipidemia
• ERCP
• Drugs (10%)
3) History of Complications

Systemic :
• ARDS
• Renal Failure
• Shock, arrythmias
• Metabolic: hypocalcemia, hyperglycemia
• Encephalopathy
Local :
• Mostly develop silently
• Pancreatic abscess – high grade fever
• Pseudocyst
• Pancreatic effusion
 Physical Examination: Acute
Pancreatitis
• Elevation of body temperature is often is
acute pancreatitis
• Abdominal Examination
1. Inspection: abdominal distension
2. Palpation:
• Hepatomegaly
• Tenderness
• Cullen sign
• Gray turner sign
• Peritoneal signs
• Rigidity
• Guarding
• Percussion : Dullness suggesting ascites
• Auscultation: auscultate the abdomen
for hypoactive or an absent bowel sounds
or an abdominal bruit. Ileus is common in
pancreatitis.
• Ausculation of lungs: 10-20% of patients
have pulmonary findings, commonly left sided
findings.
1. Basilar rales
2. Atelectasis
3. Pleural effusion
DIFFERENTIAL DIAGNOSIS

INVESTIGATIONS

SEVERITY SCORING

Presented by Siti Nur Rifhan Kamaruddin

 Differential Diagnosis
For Mild Acute Pain For Severe Acute Pain

Acute Cholecystitis Fecal Peritonitis due to

Perforated Colon
Peptic Ulcer Disease Ruptured Abdominal Aortic
Aneurysm
Inferior Myocardial Infarction Ruptured Ectopic Pregnancy

Acute Appendicitis Massive Bowel Infarction

INVESTIGATION
S
 Investigation
• s on basis of clinical
The diagnosis if made
presentation, an elevated serum Amylase level and
characteristic Imaging features.
• Biological :
- Serum Amylase increase 3x than
normal or more than 1000IU/mL (Peak
within the first 24hours after onset of
Symptom)
- Serum Lipase has longer half life thus
more useful in delayed cases.
- Serum Lipase: more sensitive &
specific for Pancreatitis than Amylase
Other Causes of Increased Serum Amylase :
• Renal Failure
• Liver Cirrhosis
• Peritonitis
• GIT Inflammation
• Ruptured Ectopic Pregnancy/Salphingitis
• Salivary Gland Inflammation (Parotitis)
 Other Blood Tests..
Full Blood Elevated Leucocytes count for Ranson’s Criteria and
Count to predict prognosis
LFT To asses cause of Pancreatitis/obstructive jaundice

BUSE To determine level of dehydration

Random Damage to beta cells interferes with insulin
Blood production causing Hyperglycemia (in severe cases)
Glucose

Serum Hypocalcaemia suggests saponification

Calcium
 Role of Imaging in Acute
Pancreatitis

• To clarify diagnosis when the clinical picture is

confusing
• To determine possible causes
• To assess severity (Balthazar Score) and thus
to determine prognosis
• To detect complications
 Imaging : Ultrasound
• Trans abdominal USG : Does not establish a diagnosis.
• USG should be performed within 24 hours in ALL
patients
- To detect gallstones
- To rule out Acute Cholecystitis
- To determine whether the common bile duct is
dilated
• To evaluate change on pancreas i.e. edema, mass in
Pancreas
• Transverse
Transbadominal
Ultrasound shows a
swollen pancreatic
body with ill-
defined
heterogeneous
hypoechoic
pattern.
 ERCP
• Diagnostic and therapeutic
• To look for Gallstones, CBD stones or CBD
dilatation
• In patient with severe acute gallstone
pancreatitis & signs of on going biliary
obstruction and cholangitis – an urgent ERCP
should be sought.
ERCP : Gallstone Pancreatitis
 Plain Abdominal X-Ray
• Plain erect chest & abdominal X-ray are not diagnostic
of Acute Pancreatitis but are useful in differential
diagnosis.
• Non specific findings in Pancreatitis : Generalized
or local ileus (Sentinel Loop), a colon cut off sign, and
calcified gallstones.
• Erect CXR. Look for pleural effusion. In severe cases,
a diffuse alveolar shadowing (Acute Respiratory
Distress Syndrome)
A focal dilated proximal jejunal loop in the left upper quadrant. A focal
area of adynamic ileus close to an intraabdominal inflammatory process
The sentinel loop sign may aid in localizing the source of inflammation.
Sentinel Loop in upper abdomen may indicate Pancreatitis
-Colon Cut-off Sign describes gaseous distension seen in proximal colon
-Associated with narrowing of splenic flexure in cases of Acute
Pancreatitis
-This Appearance results from inflammatory process extending from
Pancreas into the phrenicolic ligament via transverse mesocolon
 CT Scan
• Not necessary for all patients.
• May reveal pseudo cyst or abscess (complication
of acute pancreatitis)
• A contrast-enhanced CT is indicated in
following :
 If there is diagnostic uncertainty
 In Pt. with severe acute Pancreatitis to distinguish
interstitial from necrotizing pancreatitis.
 In Pt. with organ failure, signs of sepsis or
progressive clinical deterioration
 When a localized complication is suspected I.e. fluid
CT Anatomy Pancreatic Level
CT shows significant swelling &
Inflammation of the Pancreas
 Morphologic Types of Acute
Pancreatitis
THE REVISED ATLANTA CLASSIFICATION
1) Interstitial Edematous Pancreatitis
2) Necrotizing Pancreatitis
• Parenchymal necrosis
• Peripancreatic necrosis
• Combined Type
 Interstitial Edematous Pancreatitis
• Pancreatic Enlargement
due to edema
• Pancreatic Parenchyma

shows relatively
homogenous enhancement
& peripancreatic fat
stranding
• Outcome : Symptoms
usually resolve within first
week
Necrotizing Pancreatitis
(5-10%)

- Inflammation
associated pancreatic
parenchymal necrosis
orperipancreatic
necrosis
- Cause impairment of
pancreatic perfusion
- Impairment
evolve over
several days
- Early CECT may
underestimate extent
Pancreatic Fluid Collection : Revised Atlanta 2012

85% 15%
 Pancreatic Fluid Collection : REVISED ATLANTA 2012
•Acute Peripancreatic Fluid Collection (APFC)
•Pancreatic Pseudocyst (PP)
•Acute Necrotic Collection (ANC)
•Walled-off Necrosis (WOPN)

Local Complications should be suspected if :

 Persistence or recurrence of abd. pain
 Secondary increases in Serum Pancreas activity
 Increasing organ dysfunction
 Development of clinical signs of Sepsis i.e. fever,
leucocytosis
Prompt CECT to be done in these cases.
1) Acute Peripancreatic
Fluid Collection (APFC)
• Peripancreatic Fluid
associated with IEP with
no necrosis
• Usually seen within first 4
weeks
• Homogenous collection of
fluid
• Usually resolve
spontaneously
• When a localised APFC
persists > 4 weeks –
develop into a Pseudocyst
 2) Pancreatic
Pseudo cyst
• Encapsulated
collection of fluid
with a well defined
inflammatory wall
usually outside the
pancreas
• With minimal or no
necrosis
• Usually round or
oval -Note the two round, homogenous fluid
• Appears after 4 collection with a well defined borders
- White stars denote normal enhancing
weeks of onset IEP pancreas
3) Acute Necrotic
Collection (ANC)
• A collection
containing of both
fluid & necrosis
• < 4 weeks
• Occurs only in
setting of NP
• Single or multiple
heterogeneous
collection
• No defined wall -Note enhancement of entire pancreatic
Parenchyma (Whitestars)
- Note the heterogeneous, non-liquid component
in retroperitoneum (White arrows pointing at the
borders of ANC)
4) Walled-off
Necrosis (WON)
• A mature, encapsulated
collection of pancreatic
/peripancreatic necrosis
• that has developed a
well-defined
inflammatory wall
• Appears >4 weeks after
onset of NP
• Heterogeneous with
liquid & non-liquid -Note the Area of non-liquid components of
density high attenuation (black arrows) in the collection
- It has a well defined, enhancing wall (White
arrows)
 Pseudocyst (PC) vs. Walled-off Necrosis (WON)

- Homogenous, -Heterogeneous with liquid

low attenuation fluid density and solid densities
- NO solid component
SUMMARY: Local Complications of AP
CT Severity Index: Balthazar + Necrosis Score

E
 Assessment of
Severity
 Ranson Score
 Glasgow Scale
 APACHE II Score
 Severity: RANSON’S SCORE
To predict severity of acute pancreatitis.
On Admission (LEGAL)
L – Leucocytes >16000
E – Enzyme AST > 250
3 or more factors
G – Glucose > 200
A – Age > 55
present –
L – LDH > 350 SEVERE
During Next 48 Hours (C.HOBBS)
C – Calcium 8mg/dl
H – Hematocrit fall of >10%
O2– Pa02 < 60mmHG
B – Base deficit > 4mmol/L
B – BUN rise > 5
S – Sequestration (Fluid) > 6
Glasgow Scale

3 OR MORE FACTORS
PRESENT - SEVERE
APACHE II SCORE

Score > 8 : Severe

Acute Pancreatitis
 Management of Acute
Pancreatitis

Presented By Fariza Asilah Ahmad Rahim

 Mild Acute Pancreatitis
1. Nil by mouth
2. Fluid resuscitation : 4 pints
3. Analgesia : IM Tramal 50mg TDS
4. Treat underlying cause
5. No role for antibiotics
 Severe Acute Pancreatitis
• Admission to intensive care or high-
dependency unit
1. Oxygen supplementation
2. Analgesia
3. Aggressive fluid rehydration
4. Monitor vital signs
5.Monitor haematological & biochemical
parameters
6. Nasogastric drainage
7. Antibiotic prophylaxis –imipenem, cefuroxime
8. CT scan
9. ERCP within 72 hours
10. Supportive therapy for organ failure
11. Nutritional support
Complications of Acute
Pancreatitis
 SYSTEMIC
• Cardiovascular - shock
- arrhythmia
• Pulmonary - ARDS
• Renal failure
• Haematological - DIC
• Gastrointestinal - Ileus
 SYSTEMIC
• Metabolic - Hypocalcaemia
- Hyperglycaemia
- Hyperlipidaemia
• Neurological - Visual disturbance
- Confusion
- Encephalopathy
• Miscellaneous - Arthralgia
 LOCAL
• Acute fluid collection
• Sterile pancreatic necrosis
• Infected pancreatic necrosis
• Pacreatic abscess
• Pseudocyst
 LOCAL
• Pancreatic ascites
• Pleural effusion
• Portal or systemic vein thrombosis
• Pseudocyst
 Complications & their Management
 Acute fluid collection
 No intervention unless pressure effect
 Aspirate under US or CT guidance OR
 Transgastric drainage under EUS guidance

 Pancreatic necrosis
 No intervention
 Infected pancreatic necrosis
 Aspirate under CT guidance
 Percutaneous drainage
 Prophylactic antibiotic
If patient deteriorates
 Necrosectomy
 Closed continuous lavage
 Closed drainage
 Open packing
 Closure and relaparotomy
 Pancreatic abscess
 Percutaneous drainage
 Antibiotic cover

 Pancreatic ascites
 Drainage
 Parenteral or jejunal feeding
 Pancreatic effusion
 Percutaneous drainage under CT guidance

 Portal or systemic vein thrombosis

 Aspirin in the early process
 Pseudocyst
Percutaneous transgastric cystogastrotomy
and place double-pigtail drain
 Endoscopic under EUS guidance and place
tube drain
 Surgical drainage – internal drainage into
gastric or jejunum lumen
Cystogastrotom
y
 Reference
 BAILEY, H., LOVE, R. J. M., MANN, C. V., & RUSSELL, R. C. G.
(1992). Bailey and Love's short practice of surgery. London,
Chapman & Hall Medical.
 COLLEDGE, N. R., WALKER, B. R., RALSTON, S., &
DAVIDSON, S.
(2010). Davidson's principles and practice of medicine.
Edinburgh, Churchill Livingstone/Elsevier.