2. 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
3. Anatomy
• Retroperitoneal organ
• In adults- 10-20 cm long & 75-125gm weighs
• 3 portions- head, body and tail
• The uncinate process extends from the head of
the pancreas behind the superior mesenteric
vein and terminates adjactent to the SMA
• The transition point between body and tail is
nebulous.
8. Pancreatitis
Acute
presenting with abdominal pain
and is usually associated with
raised pancreatic enzyme levels in
the blood or urine as a result of
pancreatic inflammation.
Chronic
9. Incidence
• 2 % of all cases of abdominal pain
• Hospital admission rate Worldwide, 50 per 100 000
cases anually.
• The disease may occur at any age, with a peak in
young men and older women.
• Mortality ranges from approximately 1% in mild
cases to almost 30% in severe cases with persistent
organ failure.
10. Etiology
Two major causes are (account for as many as
60% to 80% of all AP cases):
• biliary calculi
• alcohol abuse
The remaining cases may be due to rare causes
(10%) or be idiopathic (30%)
11.
12. 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.
• Between 4% and 8% of patients with gallstones
eventually experience biliary pancreatitis secondary
to migratory gallstones.
• If the patient recovers, endocrine and exocrine
• deficiencies are much less likely than in alcoholic
patients
13. 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
14. 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.
18. History Taking
1) Abdominal Pain
• 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.
19. • 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
25. • 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
26. 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
27. Investigations
• The diagnosis is made on basis of clinical
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
29. Other Blood Tests..
Full Blood
Count
Elevated Leucocytes count for Ranson’s Criteria and
to predict prognosis
LFT To asses cause of Pancreatitis/obstructive jaundice
B.Urea
S.Electrolyte
To determine level of dehydration
Random
Blood
Glucose
Damage to beta cells interferes with insulin
production causing Hyperglycemia (in severe cases)
Serum
Calcium
Hypocalcaemia suggests saponification
30. 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
31. 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
33. 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.
34. 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)
35. 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
36. -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
37. 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
ü In Pt. with severe acute Pancreatitis to distinguish
interstitial from necrotizing pancreatitis.
ü In Pt. with organ failure, signs of sepsis or
progressive clinical deterioration
ü When a localized complication is suspected I.e. fluid
collection, pseudo cyst.
40. Morphologic Types of Acute
Pancreatitis
THE REVISED ATLANTA
CLASSIFICATION
1) Interstitial Edematous Pancreatitis
2) Necrotizing Pancreatitis
• Parenchymal necrosis
• Peripancreatic necrosis
• Combined Type
41. Interstitial Edematous Pancreatitis
• Pancreatic Enlargement
due to edema
• Pancreatic Parenchyma
shows relatively
homogenous enhancement
& peripancreatic fat
stranding
• Outcome : Symptoms
usually resolve within first
week
42. - Inflammation associated
pancreatic parenchymal
necrosis or peripancreatic
necrosis
- Cause impairment of
pancreatic perfusion
- Impairment evolve
over several days
- Early CECT may
underestimate extent
of disease
Necrotizing Pancreatitis
(5-10%)
44. Local Complications should be suspected if :
Persistence or recurrence of abd. pain
Secondary increases in Serum Pancreas activity
ü Increasing organ dysfunction
ü Development of clinical signs of Sepsis i.e. fever,
leucocytosis
Prompt CECT to be done in these cases.
Pancreatic Fluid Collection : REVISED ATLANTA 2012
•Acute Peripancreatic Fluid Collection (APFC)
•Pancreatic Pseudocyst (PP)
•Acute Necrotic Collection (ANC)
•Walled-off Necrosis (WOPN)
45.
46. 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
47. 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
• Appears after 4
weeks of onset IEP
-Note the two round, homogenous fluid
collection with a well defined borders
- White stars denote normal enhancing
pancreas
48. 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)
49. 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
density
-Note the Area of non-liquid components of high
attenuation (black arrows) in the collection
- It has a well defined, enhancing wall (White
arrows)
50. Walled off necrosis in a 27 yr old female patient with air and tip
of PCD inside the necrotic collection (White arrow)
and a very small area of inflammed pancreatic tissue( white star)
DAY 33 OF ONSET
52. Assessment of Severity
Ranson Score
CT severity score
Glasgow Scale
BISAP Score
APACHE II Score
Atlanta classification
Determinant based classification
53. Severity: RANSON’S SCORE
To predict severity of acute pancreatitis.
On Admission
L – Leucocytes >16000
E – Enzyme AST > 250
G – Glucose > 200
A – Age > 55
L – LDH > 350
During Next 48 Hours
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 litres
3 or more factors
present – SEVERE
60. Single parameter biochemical markers
• CRP:-
ü Presently, CRP is frequently considered the “gold
standard” single biochemical marker for the risk
stratifification of AP.
ü It is used as the comparison when assessing new
potential biomarkers.
ü A major limitation of CRP is the relatively long
delay in achieving peak systematic values at 72 to 96
hours after onset of disease, making very early
assessment of severity impossible.
61. Hematocrit
A hematocrit of more than 44% on admission or the absence of a
fall in hematocrit during the fifirst 24 hours after admission was
found to be a clear risk factor for pancreatic necrosis, organ
failure, or pancreatic infection.
ü Hematocrit greater than 50% has also been shown to predict
severe pancreatitis.
Procalcitonin
Blood Urea Nitrogen
IL-6, IL-1
Elastase
63. Mild Acute Pancreatitis
1. Nil by mouth (Enteral nutrition should be
commenced within 24-72 hrs)
2. Fluid resuscitation
3. Analgesia
4. Treat underlying cause
5. No role for antibiotics
64. 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
65. 6. Nasogastric aspiration
7. Antibiotic prophylaxis
8. CT scan after 72 hours
9. Supportive therapy for organ failure
10. Nutritional support
71. Complications & their Management
Acute fluid collection
No intervention unless pressure effect
Aspirate under US or CT guidance OR
Transgastric drainage under EUS guidance
Sterile Pancreatic necrosis
No intervention
73. If patient deteriorates
Necrosectomy
Closed continuous lavage
Closed drainage
Open packing
Closure and relaparotomy
74. § According to Dutch pancreatitis study group (2010)
Step up approach is recommended consisting of PCD
followed by minimal invasive VARD over open
necrosectomy
75. Pancreatic abscess
Percutaneous drainage
Antibiotic cover
Pancreatic effusion
Percutaneous drainage under CT guidance
Portal or systemic vein thrombosis
Aspirin in the early process
76. 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
Normal Amylase : 85
Normal Lipase :
The 3rd criteria is only required to establish diagnosis if the first two criteria are not met. Imaging is of utmost importance for the detection of complications and to help guide the treatment.
Normal Amylase : 85
Amylase /Lipase only 40-60% sensitive for Pancreatitis, Amylase 70-80% specific, 80-90%specific
Assessment of Clinical Parameters ( Vital Signs, Electrolytes, ABG)
Point Allocated in accordance to age
Point added for co-morbid disease or chronic health Pt
A + B + C > 8 : severe acute Pancreatitis
