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Acute Pancreatitis-- Radiology
Dr Rekha Khare
MD radiology
Hind institute medical sciences
Safedabad
Pancreas
Acute pancreatitis
ā€¢ Acute pancreatitis (plural: pancreatitides) is
an acute inflammation of the pancreas and is
a potentially life-threatening condition.
Two subtypes
ā€¢ interstitial edematous pancreatitis
ā€“ vast majority (90-95%)
ā€“ most often referred to simply as "acute
pancreatitis" or "uncomplicated pancreatitisā€œ
ā€¢ necrotizing pancreatitis
ā€“ necrosis develops within the pancreas and/or
peripancreatic tissue
Pathology
ā€¢ Mechanism not clear. Activation of pancreatic enzymes within
the pancreas lead to inflammation of the pancreatic tissue,
disruption of small pancreatic ducts, and leakage of
pancreatic secretions
ā€¢ Because the pancreas lacks a capsule, the pancreatic juices
have ready access to surrounding tissues.
ā€¢ Pancreatic enzymes digest fascial layers, spreading the
inflammatory process to multiple anatomic compartments.
Causes of pancreatitis
ā€¢ gallstone passage/impaction: most common
ā€¢ idiopathic: 20%? congenital Duct anomaly
ā€¢ alcohol abuse: most common cause of chronic pancreatitis
ā€¢ metabolic disorders-hypertriglyceridemia-induced pancreatitis
common in prgnancautoimmune pancreatitis
ā€¢ penetrating peptic ulcer
ā€“ viral: mumps, Coxsackievirus, hepatitis, infectious
mononucleosis, HIV/AIDS
ā€“ parasitic: ascariasis 5, clonorchiasis
ā€¢ structural: not a cause, but associated with increased incidence
ā€“ choledochocele
ā€“ pancreas divisum
ā€“ secondarily infected (emphysematous pancreatitis)
Causes
ā€¢ trauma: most common cause in children
ā€¢ Malignancy
ā€¢ Hereditary pancreatitis
ā€¢ malnutrition
ā€¢ Infection
ā€¢ Toxins -scorpion sting: in particular, the Trinidad thick-tailed
scorpion, Tityus trinitatis
ā€“ spider bite,snake bite
ā€¢ drugs: steroids possible cause
ā€¢ Others cystic fibrosis,systemic lupus erythematosus (SLE) 4
ā€“ hemolytic uremic syndrome (HUS)
Complications revised Atlanta
classification
ā€¢ Peripancreatic fluid collection with or without necrosis
ā€“ necrosis absent (i.e. interstitial edematous pancreatitis) in
first 4 weeks
ā€“ After 4 weeks --pseudocysts: encapsulated fluid collections
ā€“ necrosis present (i.e. necrotizing pancreatitis)
ā€¢ acute necrotic collections (ANCs): develop in the first 4
weeks
ā€¢ walled-off necrosis (WON): encapsulated collections
after 4 weeks
Complication
ā€¢ liquefactive necrosis of pancreatic parenchyma
(e.g. necrotizing pancreatitis)
ā€“ emphysematous pancreatitis if infection
ā€“ hemorrhage: resulting from erosion of blood vessels and
tissue necrosis
ā€“ pseudoaneurysm: autodigestion of arterial walls by
pancreatic enzymes results in pulsatile mass that is lined
by fibrous tissue and maintains communication with
parent artery
ā€“ splenic vein thrombosis
ā€“ portal vein thrombosis
ā€¢ pancreatic ascites: leakage of pancreatic secretions into the
peritoneal cavity
ā€¢ abdominal compartment syndrome
Abdominal compartment
syndrome
ā€¢ It occurs when the pressure in abdominal cavity elevates
beyond 20mmHg
ā€¢ Classical triad--A tense distended abdomen, respiratory
distress (or high peak inspiratory pressures if mechanically
ventilation is used), and oliguria and hypotensaion
ā€¢ Signs and Symptoms: The "5 P's" are often times associated
with compartment syndrome:
pain, pallor , paresthesia, pulselessness, and paralysis
Diagnostic criteria
ā€¢ Two of the following three criteria are required for
the diagnosis
ā€¢ acute onset of persistent, severe epigastric pain (i.e.
pain consistent with acute pancreatitis)
ā€¢ lipase/amylase elevation >3 times the upper limit of
normal
ā€¢ characteristic imaging features on contrast-enhanced
CT, MRI, or ultrasound
Phases of acute pancreatitis
Atlanta classification
ā€¢ Early - first weekā€“ only clinical parameter are
needed for management
ā€¢
Late - after the first week
clinical and CT findings combined needed
Severity based on clinical and
morphological findings
ā€¢ Mild- No organ failure and no local or
systemic complication
ā€¢ Moderate - Presence of transient organ failure
less than 48h and/or presence of local
complications.
ā€¢ Severe - Persistent organ failure > 48 hour.
Morphological types
ā€¢ Acute oedematous or interstitial pancreatitis/
collection/pseudopancreatic cyst
ā€¢ Acute necrotizing pancreatitis
ā€¢ Usually the necrosis involves both the
pancreas and the peri pancreatic tissues.
Clinical out come
ā€¢ Mild pancreatitis
These patients have no organ failure, no fluid collections and no
necrosis.
These patients usually recover by the end of the first week.
ā€¢ Moderate severe and severe pancreatitis
Cytokine cascades result in a systemic inflammatory response
syndrome (SIRS), which increases the risk of organ failure.
ā€¢
The presence of organ failure is determined by respiratory (pO2ā†“),
renal (creatinineā†‘) and cardiovascular failure (blood pressureā†“).
ā€¢
Many of these patients however will have necrotizing pancreatitis and
the mortality increases when the necrosis becomes infected.
Role of imaging
ā€¢ to clarify the diagnosis when the clinical
picture is confusing
ā€¢ to assess severity (e.g. Balthazar score) and
thus to determine prognosis
ā€¢ to detect complications
ā€¢ to determine possible causes
CT for acute pancreatitis
ā€¢ CT is the imaging modality of choice for the
diagnosis and staging of acute pancreatitis
and its complications.
ā€¢
Ultrasound and ERCP with sphincterotomy
and stone extraction play an important role in
biliary pancreatitis.
X-ray --insensitive
ā€¢ Abdominal radiographs-
ā€¢ localized ileus of the small intestine (sentinel loop)
ā€¢ spasm of the descending colon (colon cut-off sign)
ā€¢ Chest radiographs-
ā€¢ Pleural effusion, usually left-sided
ā€¢ hemidiaphragm elevation
ā€¢ basal atelectasis
ā€¢ pulmonary edema /ARDS
Ultrasoundā€”main role
ā€¢ To identify gallstones as a possible cause
ā€¢ Diagnosis of vascular complications, e.g. thrombosis
ā€¢ Identify areas of necrosis that appear as hypoechoic / cystic
regions
ā€¢ Assessment of clinically similar etiologies of an acute
abdomen
ā€¢ Increased pancreatic volume with a marked decrease or
heterogenous echogenicity
ā€¢ Displacement of the adjacent transverse colon and/or
stomach secondary to pancreatic volume expansion
CT imaging
ā€¢ Typical findings
ā€“ focal or diffuse enlarged hypodense parenchymal
enlargement with retroperitoneal fat stranding
ā€¢ LIquefactive necrosis of pancreatic
parenchyma usually after 1 week no contrast
enhancement
ā€¢ Infected necrosis with gas( emphysematous)
ā€¢ Abscess formation
ā€¢ Haemorrhage or Calcification
Atlanta classification of fluid
collection
ā€¢ Contents
ā€“ Fluid only in acute peripancreatic fluid collection and
Pseudocyst.
ā€“ Mixture of fluid and necrotic material in acute necrotic
collection and walled-off-necrosis
ā€¢ Degree of capsulation
ā€“ Complete encapsulation in pseudocyst and walled off
necrosis
ā€¢ Time Within 4 weeks
- acute peripancreatic and necrotic fluid collection only
after 4 week for a capsule to form
Nature of collection
ā€¢ All these collections may remain sterile or
become infected.
ā€¢ Infection is rare during the first week.
CT severity index
ā€¢ The CT severity index (CTSI) combines the
Balthazar grade (0-4 points) with the extent of
pancreatic necrosis (0-6 points) on a 10-point
severity scale.
CT severity index
CT imaging
ā€¢ Since the diagnosis of acute pancreatitis is usually
made on clinical and laboratory findings
ā€¢ an early CT is only recommended when the diagnosis
is uncertain, or in case of suspected early
complications such as bowel perforation or ischemia
ā€¢ Sometimes an early CT may be misleading regarding
the morphologic severity of the pancreatitis, because
it may underestimate the presence and amount of
necrosis.
Case
ā€¢ Pic1ā€“ normal enhanced
pancrease
Pic2ā€“ condition gets
worsen so ct done again
Major part of pancreas
involved
Patient died on 5th day
due to SIRS and multi
organ failure
Meaning CT on 1st day was
under estimate
SIRSā€”systemic inflammatory response
syndrome
CT criteria
ā€¢ 1--Acute peri pancreatic fluid collection only
sometimes not or partially encapsulated seen
within 4 wks in interstitial pancreatitis/APPF
ā€¢ 2--Acute Necrotic Collections/ANC contain a
mixture of fluid and necrotic material. They
are not or only partially encapsulated. They
are seen within 4 weeks in necrotizing
pancreatitis
CT criteria
ā€¢ 3ā€“ After 4 weeks pseudocyst in interstitial
pancreatitis. This fluid collection is
encapsulated. Pseudo cysts are uncommon in
acute pancreatitis. Most persistent fluid
collections may contain some necrotic
material also.
ā€¢ 4--After 4 weeks most necrotic collections are
fully encapsulated and are called Walled-off
Necrosis (WON)
Interstitial
pancreatitis
ā€¢ Here an example of
interstitial pancreatitis.
There is normal
enhancement of the
entire pancreatic gland
with only mild
surrounding fatty
infiltration.
ā€¢ There are no fluid
collections and there is
no necrosis of the
pancreatic parenchyma.
CTSI: 2 points
Acute necrotizing
pancreatitis
ā€¢ The CT shows an acute
necrotizing pancreatitis.
The body and tail of the
pancreas do not
enhance.
There is normal
enhancement of the
pancreatic head (arrow)
ā€¢ More than 50% of the
pancreas is necrotic and
there are at least two
collections
CTSI: 4 + 6 = 10 points.
Necrotizing pancreatitis
ā€¢ Necrosis of pancreatic parenchyma or
peripancreatic tissues occurs in 10-15 % of
patients.
It is characterized by a protracted clinical
course, a high incidence of local
complications, and a high mortality rate
Necrotizing pancreatitis-3 subtypes
1. Commonly--Necrosis of both pancreatic and
peripancreatic tissues (most common).
2. Less commonly--Necrosis of
only extrapancreatic tissue without necrosis
of pancreatic parenchyma
3. Rarely--Necrosis of pancreatic parenchyma
without surrounding necrosis of
peripancreatic tissue
Necrotizing pancreatitis on CT
ā€¢ Necrosis of the pancreatic parenchyma can be
diagnosed on a contrast-enhanced CT ā©¾ 72
hours.
ā€¢
Necrosis of peripancreatic tissue can be vary
difficult to diagnose, but is suspected when
the collection is inhomogeneous,
i.e. various densities on CT
MRI for Acute pancreatitis
ā€¢ Contrast-enhanced MR is equivalent to CT in
the assessment of pancreatitis
ā€¢ Diffusion-weighted imaging shows
hyperintense signal of the involved
parenchyma with decreased ADC values
CT versus MRI
ā€¢ MRI is superior to CT in
differentiating between fluid
and solid necrotic debris
ā€¢ Here a patient with several
homogeneous peripancreatic
collections on CT.
ā€¢ These collections also show
homogeneous high signal
intensity on a fat-suppressed
T2-weighted MRI image, are
fully encapsulated and
contain clear fluid (i.e.
pseudocysts).
CT versus MRI
caseā€“2 mths ago pt had necrotizing
pancreatitis
ā€¢ The CT-image shows a
homogeneous peripancreatic
collection in the transverse
mesocolon (arrow).
ā€¢ A T2-weighted MRI sequence
shows that the collection has a
low signal intensity (arrow).
Most likely this is necrotic fat
tissue (i.e. sterile necrosis or
walled-off necrosis).
This patient had no fever or
signs of sepsis.
ā€¢ Endoscopic or percutaneous
drainage would have little or
no effect on its size, but
increases the risk of infection
Caseā€”acute peri pancreatic collection
ā€¢ In early phase of ac. Pancreatitis
Intra abdominal fluid collection and
of necrotic tissue with no wall/
capsule
ā€¢ (lesser sac ,ant post renal space of
retroperitoneum, transverse
mesocolon and small bowel
mesentry are preferred sites)
ā€¢ Collection and necrosis is due to
release of activated pancreatic
enzmes They may remain sterile or
develop infection.
ā€¢ The images show spontaneous
regression of an acute
peripancreatic fluid collection
(APFC).
Caseā€“ acute necrotic collection
ā€¢ The findings are:
ā€¢ Necrosis of the
pancreas
ā€¢ Inhomogeneous
collection in the
peripancreatic tissue
ā€¢ No wall
ā€¢ We can conclude that
this is an acute necrotic
collection - ANC.
Case -- collections
Day 5--Normal enhancement
of the entire pancreas.
ā€¢ Extensive peripancreatic
collections, which have
liquid and non-liquid
densities on CT.
ā€¢ There are at least two
collections, but no
pancreatic parenchymal
necrosis (CTSI: 4).
ā€¢ Day 18- expansion of the
peripancreatic collections
and an incomplete wall is
present.
Pseudocyst
2mts after acute pancreatitis c/o gastric outlet obstruction with no fever
There is a homogeneous
well-demarcated
peripancreatic
collection in the lesser
sac, which abuts the
stomach and the
pancreas. Clear fluid
with high amylase
The collection
underwent successful
percutaneous drainage,
Pseudocyst
ā€¢ A Pseudocyst is a collection of pancreatic juice or
fluid enclosed by a complete wall of fibrous tissue
It occurs in interstitial pancreatitis and the absence
of necrotic tissue is imperative for its diagnosis.
ā€¢ Communication with the pancreatic duct may be
present
ā€¢
A pseudocyst requires 4 or more weeks to develop
D/D pseudocyst
ā€¢ . True pseudocysts are uncommon, since most
acute peripancreatic fluid collections resolve
within 4 weeks
ā€¢ The differential diagnosis includes walled-off
necrosis and sometimes a pseudo aneurysm
or even a cystic tumor.
Most often, they occur in the lesser sac.
ā€¢ Most collections that persist after 4 weeks are
walled-of-necrosis.
Walled off necrosis
ā€¢ Based on CT alone it is sometimes impossible
to determine whether a collection contains
fluid only or a mixture of fluid and necrotic
tissue.
Consequently it is sometimes better to describe
these as
'indeterminate peri pancreatic collections'.
Walled off necrotic collection
ā€¢ On the upper image is a
collection in the area of
the pancreatic head in
the right anterior
pararenal space.
ā€¢ At this stage, it is not
possible to distinguish
between an acute
peripancreatic fluid
collection and acute
necrotic collection.
Won at CT
.
Sometimes at surgery, the collection
contained much necrotic debris, which was
not depicted on CT.
ā€¢ that at times CT cannot reliably differentiate
between collections that consist of fluid only
and those that contain fluid and solid necrotic
debris with or without infection.
Central gland
necrosis
It is specific form of necrotizing
pancreatitis- full thickness
necrosis between the pancreatic
head and tail with disrupted
pancreatic duct
it leads to to persistent collections
as the viable pancreatic tail
continues to secrete pancreatic
juices
These collections may react poorly
to endoscopic or percutaneous
drainage.
Definitive treatment may require
distal pancreatectomy
PANCODE SYSTEM
Limitation of imaging
Management acute pancreatitis
Management Acute pancreatitis
Fine needle aspiration
ā€¢ Important remarks concerning Drainage:
ā€¢ Indications for intervention of evolving peri
pancreatic collections should be based on full
evaluation of clinical, lab, and imaging
ā€¢ No role for drainage in early collections
ā€¢ Can be used as a guide for surgical approach
Preferred approach for FNA
ā€¢ The retroperitoneal approach has some
advantages:
ā€¢ Same compartment as the pancreas.
ā€¢ No contamination with intestinal flora.
ā€¢ Gravity.
ā€¢ Drain runs parallel to pancreatic bed
ā€¢ Same route for minimal invasive surgery
Take home message
ā€¢ Morphologic severity of acute pancreatitis (including
pancreatic parenchymal necrosis) can only be reliably
assessed by imaging 72 hours after onset of
symptoms.
ā€¢ CT can not reliably differentiate between collections
that consist of fluid only and those that contain solid
necrotic debris.
In these cases MRI can be of additional value.
ā€¢ Avoid early drainage of collections and avoid
introducing infection.
THANK YOU
Have a nice day

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Acute pancreatitis.ppt

  • 1. Acute Pancreatitis-- Radiology Dr Rekha Khare MD radiology Hind institute medical sciences Safedabad
  • 3. Acute pancreatitis ā€¢ Acute pancreatitis (plural: pancreatitides) is an acute inflammation of the pancreas and is a potentially life-threatening condition.
  • 4. Two subtypes ā€¢ interstitial edematous pancreatitis ā€“ vast majority (90-95%) ā€“ most often referred to simply as "acute pancreatitis" or "uncomplicated pancreatitisā€œ ā€¢ necrotizing pancreatitis ā€“ necrosis develops within the pancreas and/or peripancreatic tissue
  • 5. Pathology ā€¢ Mechanism not clear. Activation of pancreatic enzymes within the pancreas lead to inflammation of the pancreatic tissue, disruption of small pancreatic ducts, and leakage of pancreatic secretions ā€¢ Because the pancreas lacks a capsule, the pancreatic juices have ready access to surrounding tissues. ā€¢ Pancreatic enzymes digest fascial layers, spreading the inflammatory process to multiple anatomic compartments.
  • 6. Causes of pancreatitis ā€¢ gallstone passage/impaction: most common ā€¢ idiopathic: 20%? congenital Duct anomaly ā€¢ alcohol abuse: most common cause of chronic pancreatitis ā€¢ metabolic disorders-hypertriglyceridemia-induced pancreatitis common in prgnancautoimmune pancreatitis ā€¢ penetrating peptic ulcer ā€“ viral: mumps, Coxsackievirus, hepatitis, infectious mononucleosis, HIV/AIDS ā€“ parasitic: ascariasis 5, clonorchiasis ā€¢ structural: not a cause, but associated with increased incidence ā€“ choledochocele ā€“ pancreas divisum ā€“ secondarily infected (emphysematous pancreatitis)
  • 7. Causes ā€¢ trauma: most common cause in children ā€¢ Malignancy ā€¢ Hereditary pancreatitis ā€¢ malnutrition ā€¢ Infection ā€¢ Toxins -scorpion sting: in particular, the Trinidad thick-tailed scorpion, Tityus trinitatis ā€“ spider bite,snake bite ā€¢ drugs: steroids possible cause ā€¢ Others cystic fibrosis,systemic lupus erythematosus (SLE) 4 ā€“ hemolytic uremic syndrome (HUS)
  • 8. Complications revised Atlanta classification ā€¢ Peripancreatic fluid collection with or without necrosis ā€“ necrosis absent (i.e. interstitial edematous pancreatitis) in first 4 weeks ā€“ After 4 weeks --pseudocysts: encapsulated fluid collections ā€“ necrosis present (i.e. necrotizing pancreatitis) ā€¢ acute necrotic collections (ANCs): develop in the first 4 weeks ā€¢ walled-off necrosis (WON): encapsulated collections after 4 weeks
  • 9. Complication ā€¢ liquefactive necrosis of pancreatic parenchyma (e.g. necrotizing pancreatitis) ā€“ emphysematous pancreatitis if infection ā€“ hemorrhage: resulting from erosion of blood vessels and tissue necrosis ā€“ pseudoaneurysm: autodigestion of arterial walls by pancreatic enzymes results in pulsatile mass that is lined by fibrous tissue and maintains communication with parent artery ā€“ splenic vein thrombosis ā€“ portal vein thrombosis ā€¢ pancreatic ascites: leakage of pancreatic secretions into the peritoneal cavity ā€¢ abdominal compartment syndrome
  • 10. Abdominal compartment syndrome ā€¢ It occurs when the pressure in abdominal cavity elevates beyond 20mmHg ā€¢ Classical triad--A tense distended abdomen, respiratory distress (or high peak inspiratory pressures if mechanically ventilation is used), and oliguria and hypotensaion ā€¢ Signs and Symptoms: The "5 P's" are often times associated with compartment syndrome: pain, pallor , paresthesia, pulselessness, and paralysis
  • 11. Diagnostic criteria ā€¢ Two of the following three criteria are required for the diagnosis ā€¢ acute onset of persistent, severe epigastric pain (i.e. pain consistent with acute pancreatitis) ā€¢ lipase/amylase elevation >3 times the upper limit of normal ā€¢ characteristic imaging features on contrast-enhanced CT, MRI, or ultrasound
  • 12. Phases of acute pancreatitis Atlanta classification ā€¢ Early - first weekā€“ only clinical parameter are needed for management ā€¢ Late - after the first week clinical and CT findings combined needed
  • 13. Severity based on clinical and morphological findings ā€¢ Mild- No organ failure and no local or systemic complication ā€¢ Moderate - Presence of transient organ failure less than 48h and/or presence of local complications. ā€¢ Severe - Persistent organ failure > 48 hour.
  • 14. Morphological types ā€¢ Acute oedematous or interstitial pancreatitis/ collection/pseudopancreatic cyst ā€¢ Acute necrotizing pancreatitis ā€¢ Usually the necrosis involves both the pancreas and the peri pancreatic tissues.
  • 15. Clinical out come ā€¢ Mild pancreatitis These patients have no organ failure, no fluid collections and no necrosis. These patients usually recover by the end of the first week. ā€¢ Moderate severe and severe pancreatitis Cytokine cascades result in a systemic inflammatory response syndrome (SIRS), which increases the risk of organ failure. ā€¢ The presence of organ failure is determined by respiratory (pO2ā†“), renal (creatinineā†‘) and cardiovascular failure (blood pressureā†“). ā€¢ Many of these patients however will have necrotizing pancreatitis and the mortality increases when the necrosis becomes infected.
  • 16. Role of imaging ā€¢ to clarify the diagnosis when the clinical picture is confusing ā€¢ to assess severity (e.g. Balthazar score) and thus to determine prognosis ā€¢ to detect complications ā€¢ to determine possible causes
  • 17. CT for acute pancreatitis ā€¢ CT is the imaging modality of choice for the diagnosis and staging of acute pancreatitis and its complications. ā€¢ Ultrasound and ERCP with sphincterotomy and stone extraction play an important role in biliary pancreatitis.
  • 18. X-ray --insensitive ā€¢ Abdominal radiographs- ā€¢ localized ileus of the small intestine (sentinel loop) ā€¢ spasm of the descending colon (colon cut-off sign) ā€¢ Chest radiographs- ā€¢ Pleural effusion, usually left-sided ā€¢ hemidiaphragm elevation ā€¢ basal atelectasis ā€¢ pulmonary edema /ARDS
  • 19. Ultrasoundā€”main role ā€¢ To identify gallstones as a possible cause ā€¢ Diagnosis of vascular complications, e.g. thrombosis ā€¢ Identify areas of necrosis that appear as hypoechoic / cystic regions ā€¢ Assessment of clinically similar etiologies of an acute abdomen ā€¢ Increased pancreatic volume with a marked decrease or heterogenous echogenicity ā€¢ Displacement of the adjacent transverse colon and/or stomach secondary to pancreatic volume expansion
  • 20. CT imaging ā€¢ Typical findings ā€“ focal or diffuse enlarged hypodense parenchymal enlargement with retroperitoneal fat stranding ā€¢ LIquefactive necrosis of pancreatic parenchyma usually after 1 week no contrast enhancement ā€¢ Infected necrosis with gas( emphysematous) ā€¢ Abscess formation ā€¢ Haemorrhage or Calcification
  • 21. Atlanta classification of fluid collection ā€¢ Contents ā€“ Fluid only in acute peripancreatic fluid collection and Pseudocyst. ā€“ Mixture of fluid and necrotic material in acute necrotic collection and walled-off-necrosis ā€¢ Degree of capsulation ā€“ Complete encapsulation in pseudocyst and walled off necrosis ā€¢ Time Within 4 weeks - acute peripancreatic and necrotic fluid collection only after 4 week for a capsule to form
  • 22. Nature of collection ā€¢ All these collections may remain sterile or become infected. ā€¢ Infection is rare during the first week.
  • 23. CT severity index ā€¢ The CT severity index (CTSI) combines the Balthazar grade (0-4 points) with the extent of pancreatic necrosis (0-6 points) on a 10-point severity scale.
  • 25. CT imaging ā€¢ Since the diagnosis of acute pancreatitis is usually made on clinical and laboratory findings ā€¢ an early CT is only recommended when the diagnosis is uncertain, or in case of suspected early complications such as bowel perforation or ischemia ā€¢ Sometimes an early CT may be misleading regarding the morphologic severity of the pancreatitis, because it may underestimate the presence and amount of necrosis.
  • 26. Case ā€¢ Pic1ā€“ normal enhanced pancrease Pic2ā€“ condition gets worsen so ct done again Major part of pancreas involved Patient died on 5th day due to SIRS and multi organ failure Meaning CT on 1st day was under estimate SIRSā€”systemic inflammatory response syndrome
  • 27. CT criteria ā€¢ 1--Acute peri pancreatic fluid collection only sometimes not or partially encapsulated seen within 4 wks in interstitial pancreatitis/APPF ā€¢ 2--Acute Necrotic Collections/ANC contain a mixture of fluid and necrotic material. They are not or only partially encapsulated. They are seen within 4 weeks in necrotizing pancreatitis
  • 28. CT criteria ā€¢ 3ā€“ After 4 weeks pseudocyst in interstitial pancreatitis. This fluid collection is encapsulated. Pseudo cysts are uncommon in acute pancreatitis. Most persistent fluid collections may contain some necrotic material also. ā€¢ 4--After 4 weeks most necrotic collections are fully encapsulated and are called Walled-off Necrosis (WON)
  • 29. Interstitial pancreatitis ā€¢ Here an example of interstitial pancreatitis. There is normal enhancement of the entire pancreatic gland with only mild surrounding fatty infiltration. ā€¢ There are no fluid collections and there is no necrosis of the pancreatic parenchyma. CTSI: 2 points
  • 30. Acute necrotizing pancreatitis ā€¢ The CT shows an acute necrotizing pancreatitis. The body and tail of the pancreas do not enhance. There is normal enhancement of the pancreatic head (arrow) ā€¢ More than 50% of the pancreas is necrotic and there are at least two collections CTSI: 4 + 6 = 10 points.
  • 31. Necrotizing pancreatitis ā€¢ Necrosis of pancreatic parenchyma or peripancreatic tissues occurs in 10-15 % of patients. It is characterized by a protracted clinical course, a high incidence of local complications, and a high mortality rate
  • 32. Necrotizing pancreatitis-3 subtypes 1. Commonly--Necrosis of both pancreatic and peripancreatic tissues (most common). 2. Less commonly--Necrosis of only extrapancreatic tissue without necrosis of pancreatic parenchyma 3. Rarely--Necrosis of pancreatic parenchyma without surrounding necrosis of peripancreatic tissue
  • 33. Necrotizing pancreatitis on CT ā€¢ Necrosis of the pancreatic parenchyma can be diagnosed on a contrast-enhanced CT ā©¾ 72 hours. ā€¢ Necrosis of peripancreatic tissue can be vary difficult to diagnose, but is suspected when the collection is inhomogeneous, i.e. various densities on CT
  • 34. MRI for Acute pancreatitis ā€¢ Contrast-enhanced MR is equivalent to CT in the assessment of pancreatitis ā€¢ Diffusion-weighted imaging shows hyperintense signal of the involved parenchyma with decreased ADC values
  • 35. CT versus MRI ā€¢ MRI is superior to CT in differentiating between fluid and solid necrotic debris ā€¢ Here a patient with several homogeneous peripancreatic collections on CT. ā€¢ These collections also show homogeneous high signal intensity on a fat-suppressed T2-weighted MRI image, are fully encapsulated and contain clear fluid (i.e. pseudocysts).
  • 36. CT versus MRI caseā€“2 mths ago pt had necrotizing pancreatitis ā€¢ The CT-image shows a homogeneous peripancreatic collection in the transverse mesocolon (arrow). ā€¢ A T2-weighted MRI sequence shows that the collection has a low signal intensity (arrow). Most likely this is necrotic fat tissue (i.e. sterile necrosis or walled-off necrosis). This patient had no fever or signs of sepsis. ā€¢ Endoscopic or percutaneous drainage would have little or no effect on its size, but increases the risk of infection
  • 37. Caseā€”acute peri pancreatic collection ā€¢ In early phase of ac. Pancreatitis Intra abdominal fluid collection and of necrotic tissue with no wall/ capsule ā€¢ (lesser sac ,ant post renal space of retroperitoneum, transverse mesocolon and small bowel mesentry are preferred sites) ā€¢ Collection and necrosis is due to release of activated pancreatic enzmes They may remain sterile or develop infection. ā€¢ The images show spontaneous regression of an acute peripancreatic fluid collection (APFC).
  • 38. Caseā€“ acute necrotic collection ā€¢ The findings are: ā€¢ Necrosis of the pancreas ā€¢ Inhomogeneous collection in the peripancreatic tissue ā€¢ No wall ā€¢ We can conclude that this is an acute necrotic collection - ANC.
  • 39. Case -- collections Day 5--Normal enhancement of the entire pancreas. ā€¢ Extensive peripancreatic collections, which have liquid and non-liquid densities on CT. ā€¢ There are at least two collections, but no pancreatic parenchymal necrosis (CTSI: 4). ā€¢ Day 18- expansion of the peripancreatic collections and an incomplete wall is present.
  • 40. Pseudocyst 2mts after acute pancreatitis c/o gastric outlet obstruction with no fever There is a homogeneous well-demarcated peripancreatic collection in the lesser sac, which abuts the stomach and the pancreas. Clear fluid with high amylase The collection underwent successful percutaneous drainage,
  • 41. Pseudocyst ā€¢ A Pseudocyst is a collection of pancreatic juice or fluid enclosed by a complete wall of fibrous tissue It occurs in interstitial pancreatitis and the absence of necrotic tissue is imperative for its diagnosis. ā€¢ Communication with the pancreatic duct may be present ā€¢ A pseudocyst requires 4 or more weeks to develop
  • 42. D/D pseudocyst ā€¢ . True pseudocysts are uncommon, since most acute peripancreatic fluid collections resolve within 4 weeks ā€¢ The differential diagnosis includes walled-off necrosis and sometimes a pseudo aneurysm or even a cystic tumor. Most often, they occur in the lesser sac. ā€¢ Most collections that persist after 4 weeks are walled-of-necrosis.
  • 43. Walled off necrosis ā€¢ Based on CT alone it is sometimes impossible to determine whether a collection contains fluid only or a mixture of fluid and necrotic tissue. Consequently it is sometimes better to describe these as 'indeterminate peri pancreatic collections'.
  • 44. Walled off necrotic collection ā€¢ On the upper image is a collection in the area of the pancreatic head in the right anterior pararenal space. ā€¢ At this stage, it is not possible to distinguish between an acute peripancreatic fluid collection and acute necrotic collection.
  • 45. Won at CT . Sometimes at surgery, the collection contained much necrotic debris, which was not depicted on CT. ā€¢ that at times CT cannot reliably differentiate between collections that consist of fluid only and those that contain fluid and solid necrotic debris with or without infection.
  • 46. Central gland necrosis It is specific form of necrotizing pancreatitis- full thickness necrosis between the pancreatic head and tail with disrupted pancreatic duct it leads to to persistent collections as the viable pancreatic tail continues to secrete pancreatic juices These collections may react poorly to endoscopic or percutaneous drainage. Definitive treatment may require distal pancreatectomy
  • 51. Fine needle aspiration ā€¢ Important remarks concerning Drainage: ā€¢ Indications for intervention of evolving peri pancreatic collections should be based on full evaluation of clinical, lab, and imaging ā€¢ No role for drainage in early collections ā€¢ Can be used as a guide for surgical approach
  • 52. Preferred approach for FNA ā€¢ The retroperitoneal approach has some advantages: ā€¢ Same compartment as the pancreas. ā€¢ No contamination with intestinal flora. ā€¢ Gravity. ā€¢ Drain runs parallel to pancreatic bed ā€¢ Same route for minimal invasive surgery
  • 53. Take home message ā€¢ Morphologic severity of acute pancreatitis (including pancreatic parenchymal necrosis) can only be reliably assessed by imaging 72 hours after onset of symptoms. ā€¢ CT can not reliably differentiate between collections that consist of fluid only and those that contain solid necrotic debris. In these cases MRI can be of additional value. ā€¢ Avoid early drainage of collections and avoid introducing infection.
  • 54. THANK YOU Have a nice day