The 'acute abdomen'

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PEDIATRIC ACUTE
ABDOMEN
 The 'acute abdomen' is a clinical condition characterized
by severe abdominal pain, requiring the clinician to make
an urgent therapeutic decision.
This may be challenging, because the differential
diagnosis of an acute abdomen includes a wide
spectrum of disorders, ranging from life-threatening
diseases to benign self-limiting conditions.
Sonography enable an accurate and rapid triage of
patients with an acute abdomen.
INTUSSUSCEPTION
• most common cause of intestinal obstruction
between 3 mo and 6 yr of age
• 60% percent of patients are younger than 1 yr
• 80% of the cases occur before 24 mo
• rare in neonates
• incidence 1-4/1,000 live births
• male:female ratio is 4:1
 If intussusception occurs outside the recognized age range, i.e.
below 6 months and over 6 years of age, then lead points should
be looked for.
 In the very young infant a Meckel diverticulum may
intussuscept, and in the older child, lymphoma
infiltrating the bowel wall is the commonest cause.
 There is an increased incidence of intussusception
in children post-surgery with Peutz–Jaeger syndrome
or with cystic fibrosis.
• cause of most intussusceptions is unknown
• seasonal incidence has peaks in spring and autumn
• correlation with adenovirus infections has been noted
• postulated that swollen Peyer’s patches in the ileum may
stimulate intestinal peristalsis in an attempt to extrude
the mass, thus causing an intussusception
PATHOPYSIOLOGY
• Intussusceptions are most often ileocolic and ileoileocolic, less commonly cecocolic,
and rarely exclusively ileal
• Very rarely, the appendix forms the apex of an intussusception
• The upper portion of bowel, the intussusceptum, invaginates into the lower, the
intussuscipiens, dragging its mesentery along with it into the enveloping loop.
• Constriction of the mesentery obstructs venous return; engorgement of the
intussusceptum follows, with edema, and bleeding from the mucosa leads to a bloody
stool, sometimes containing mucus
• The apex of the intussusception may extend into the transverse, descending, or
sigmoid colon--even to and through the anus in neglected cases. This presentation
must be distinguished from rectal prolapse
• Most intussusceptions do not strangulate the bowel within the first 24 hr but may later
eventuate in intestinal gangrene and shock
CLINICAL PRESENTATION
• “sudden onset, in a previously well child, of severe
paroxysmal colicky pain that recurs at frequent intervals
and is accompanied by straining efforts with legs and
knees flexed and loud cries”
• Vomiting in most cases and is usually more frequent
early
• In the later phase, the vomitus becomes bile stained
• Stools of normal appearance may occur during the first
few hours of symptoms
• then fecal excretions are small or more often do not
occur, and little or no flatus is passed
CLINICAL PRESENTATION
• palpation usually reveals a slightly tender
sausage-shaped mass often in the right upper
quadrant
• about 30% of patients do not have a palpable
mass
• presence of bloody mucus on the finger after
DRE supports the diagnosis
• abdominal distention and tenderness develop as
intestinal obstruction becomes more acute
RADIOGRAPHIC SIGNS OF
INTUSSUSCEPTION
 target sign
(may just resemble a solid
mass) “pseudokidney”
sign because it may have
the shape of an oval mass
in the RUQ
 crescent sign
 absent liver edge
sign (also called
absence of the
subhepatic angle)
 bowel obstruction
KEEP IN MIND…
PLAIN ABDOMINAL FILMS CANNOT BE USED TO
RULE OUT INTUSSUSCEPTION
• Us appearance:
• target, hamburger or doughnut appearance in cross section and
as a pseudo-kidney in longitudinal section.
• Doppler examination should be used to evaluate the vascularity of
the intussusceptum, as a poor vascularity may be associated with
infarction of the bowel .
• In addition, the presence of free fluid trapped between the colon and
intussusceptum has been shown in several studies to be associated
with a significantly lower success rate of reduction and with
ischemia of the bowel.
• The presence of lymph nodes in the intussusceptum also reportedly
reduces the success rate.
• Ultrasonography has a false-negative rate approaching
zero and is a reliable screening tool for children at low
risk for intussusception 5-9.
• Children with classic findings of intussusception,
however, need to be investigated with contrast enema,
which is both diagnostic (the gold standard in the
diagnosis of intussusception) and therapeutic.
• Air/contrast enema
• diagnostic and therapeutic shows a filling defect in
the head of contrast where its advance is obstructed
by the intussusceptum
• “contrast material between the intussusceptum and
the intussuscipiens is responsible for the coil-spring
appearance”
• The treatment of intussusception is to push the
intussusceptum back, usually using air under pressure
via a rectal catheter
• Reduction of the intussusception is generally performed
in the prone position, as it is much easier to maintain a
good seal of the tube in the rectum.
• Ultrasound can be used to monitor pneumatic and
hydrostatic reduction and has the advantage of not using
radiation.
• In patients with prolonged intussusception with signs
of shock, peritoneal irritation, intestinal perforation,
or pneumatosis intestinalis, hydrostatic reduction
should not be attempted
• success rate of hydrostatic reduction under
fluoroscopic or ultrasonic guidance is approximately
50% if symptoms are present longer than 48 hr
• and 75-80% if reduction is done within the first 48
hr
• Bowel perforations occur in 0.5-2.5% of attempted
barium reductions. The perforation rate with air
reduction ranges from 0.1-0.2%
 Small bowel intussusceptions can be found incidentally in
asymptomatic children and in symptomatic pediatric patients
like in this case.
 There is a difference between the small bowel intussusception
and the ileocolic intussusception. The ileocolic intussusception
nearly always needs hydrostatic or even surgical treatment .
The small bowel intussusception in many cases is a self limiting
disease. It is important to look for signs that help differentiating
the self limiting small bowel intussusceptions from the ones that
need surgical treatment.
 Transient small bowel intussusceptions resolve during the
examination or are resolved during a short term follow up
examination.
Signs to look for in a small bowL
intussusception:
Length of the intussusception
Wall thickness
Vascularity of the bowel wall
Identifiable lead point
Signs of obstruction
Signs of peritonitis
• Signs found in intussusceptions that need
surgical treatment are:
Longer length of the intussusception (usually
more than 3,5 cm.)
Bowel wall thickening
Identifiable lead point
Small bowel dilatation
Free peritoneal fluid
Signs of peritonitis
• Signs found in intussusceptions that can
be followed up are :
Shorter length
No bowel wall thickening
Normal vascularity
No signs of obstruction or peritonitis
Fluoroscopy - contrast enema
A contrast enema remains the gold
standard, demonstrating the
intussusception as an occluding mass
prolapsing into the lumen, giving the
"coiled spring” appearance (Barium in
lumen of the intussusceptum and in the
intraluminal space)
The main contra-indication for an
enema is a perforation
• CT
• CT has become the modality of choice for assessment of
acute abdomen in adults, and thus most frequently
images intussusception.
• In addition short length transient intussusception is a
frequent incidental finding.
• Best know is the so-called bowel-within-bowel
configuration, in which the layers of the bowel
are duplicated forming concentric rings (CT equivalent of
the ultrasonographic target sign) when imaged at right
angles to lumen, and a soft tissue sausage when imaged
longitudinally 13.
• Differential diagnosis
• On imaging the appearances on ultrasound and CT are
characteristic. The main differential is that of transient
intussusception, which is an incidental
finding requiring no treatment or follow-up
APPANDICITIS
• The normal appendix is a small tubular structure measuring
no more than 7 mm in diameter and is easily compressible. It
may contain air or fecal material as seen in the proximal
bowel.
• There should be no fatty echogenic mesentery around the
appendix.
• The normal appendix can be differentiated from small bowel
by the absence of peristalsis, and it does not change its
appearance over time.
• It should be distinguishable from ascending colon by its size.
• In children it is easier to visualize the normal appendix
undergoing graded compression than in adults because the
transducer is smaller and hence closer to the region of
interest.
Normal appendix : Longitudinal (A) sonogram depicts a blind-ending
tubular structure (arrowheads) with 'gut-signature', with a maximum
outer diameter of 6 mm, with noninflamed surrounding fat. On an
axial view (B) the appendix can be compressed crossing the iliac
vessels.
Normal appendix: CT shows an aircontaining non-distended appendix
(arrowheads), with homogeneous lowdensity periappendiceal fat.
• Appendicitis
• Appendicitis is one of the common pediatric emergencies,
• occurring primarily in late childhood. While the clinical
diagnosis may be straightforward in some cases, there are
many other causes of an acute abdomen.
• Ultrasound is an excellent technique to aid diagnostic
accuracy in the acute abdomen both to visualize the inflamed
appendix and to exclude other conditions that may mimic
appendicitis.
• Typically in acute appendicitis the child will present clinically
with initial periumbilical pain which moves to the right iliac
fossa and with exquisite tenderness over the inflamed
appendix.
• Then using a technique of what is called ‘graded
compression’, start scanning over the right iliac fossa at
the point of maximum tenderness (generally the site of
the inflamed appendix).
• By gently and progressively compressing over the area,
the surrounding bowel is displaced and th compressibility
of the appendix assessed.
• If the appendix is retrocecal, a lateral and posterior
approach should be used.
• What are the radiological findings of appendicitis in
abdomen ultrasound?
• The most sensitive sign of appendicitis from ultrasound
is a non compressible appendix with a diameter of 7mm
or greater.
• Other findings may include:
•
•
•
•
appendicolith
thickened appendiceal wall
abscess
fluid around the appendix
APPENDICITIS
 The inflamed appendix is non-compressible/ The diameter of the
appendixis over 6 mm and may even be up to 20 mm
 The surrounding mesentery and omentum become highly echogenic
 In 30% of cases a fecolith may be identified
 If the appendix is perforated there may be an associated pelvic
mass which, in a female,usually accumulates in the pouch of
Douglas
 On Doppler examination there is a marked increase in vascularity
 Enlarged lymph nodes may be noted within the abdomen
 An ileus may be present showing nonperistaltic fluid-filled loops of
bowel
 There may be a para-appendiceal abscess and collection of pus
Inflamed appendix at sonography. Longitudinal (A) and transverse (B) crosssection show a distended noncompressible appendix, surrounded bij
hyperechoic inflamed fat (arrowheads).
Appendicitis with an inflamed tip but
normal proximal part
Appendicitis with a 2,2 cm large
appendicolith / fecolith
Appendicitis in a 3 year old boy with a
thickened appendix hyperechoic fat
and hypervascularity
Appendicitis in a 9 year old boy with a thickened vascularized
appendix and hyperechoic mesoappendix
• Appendix abscess. He was treated conservatively and
recovered.
• The main differential diagnoses to look for and
exclude in children are:
• renal abnormalities, ovarian cysts, intussusception,
inflammatory bowel disease
and mesenteric lymphadenitis
• There are no specific signs of appendicitis in plain
films but you may see:
•
•
•
•
ileus
appendicoliths
sentinel loop (dilated adjacent ileum)
evidence for complications like perforation or appendiceal
abscess
• widening and blurring of peritoneal fat line
• right lower quadrant haze due to fluid, edema and mass
• mass indenting the cecum
Plain film showing appendicolith.
Arrow points to ileus.
Appendicolith may be seen without clinical
signs of appendicitis
White arrow points to appendicolith.
D is the diameter of the appendix
measuring more than 7 mm.
Arrowheads point to distended
appendix.
Black arrows point to posterior
shadowing.
• What are the radiological findings of appendicitis in abdomen CT?
• Ileus: Dilated loops of bowel
Appendix > 6mm in diameter
An appendicolith
Failure of the appendix to fill with oral contrast medium
Enhancement of its wall with intravenous contrast medium
Periappendiceal inflammation/inflammatory infiltration of fat
Free fluid in cul de sac
Abscess
• Inflammatory (phlegmon) mass
• Air pockets
• Contrast enhancement
• Extraluminal gas from perforation
• Pericecal lymphadenopathy
• Cecal wall thickening
•
•
•
•
•
•
•
Inflamed appendix at CT. The appendix (arrows) is fluid-filled
and distended with periappendiceal fat-stranding.
Arrows point to the inflammatory mass in the right lower quadrant with an air
pocket, indicating an abscess.
Mass demonstrates contrast enhancement.
• What is the sensitivity and specificity of each imaging
procedure in diagnosing appendicitis?
• CT:
• Spiral CT has a sensitivity of 90-100%, a specificity of 91-99%, a
positive predictive value of 95-97%, and an accuracy of 94100%.
• Ultrasound:
• The limitation to ultrasound is that the appendix is often unseen
due to associated bowel gas.
• When carefully performed it has a sensitivity of 75-90 percent, a
specificity of 86-100 percent, and a positive predictive value of
89- 93 percent for the diagnosis of appendicitis.
• It is operator dependent
• What are the potential complications of acute
appendicitis?
• Perforation (most serious)
• Pyelophlebitis with thrombosis of the portal vein
• Liver abscess
• Mesenteric lymphadenitis.
• Mesenteric lymphadenitis is a common mimicker of
appendicitis.
It is the second most common cause of right lower quadrant
pain after appendicitis.
It is defined as a benign self-limiting inflammation of rightsided mesenteric lymph nodes without an identifiable
underlying inflammatory process, occurring more often in
children than in adults..
This diagnosis can only be made confidently when a normal
appendix is found, because adenopathy also frequently
occurs with appendicitis.
Key finding: Lymphadenopathy with a normal appendix and
normal mesenteric fat.
Normal appendix (green arrow) and enlarged
mesenteric lymphnodes (yellow arrows).
• Bacterial ileocecitis
• Infectious enterocolitis may cause mild symptoms
resembling a common viral gastroenteritis, but it
may also clinically present with features
indistinguishable from appendicitis especially in
bacterial ileocecitis, caused by Yersinia,
Campylobacter, or Salmonella.
Key finding: ileocecal wall thickening without
inflamed fat, adenopathy, normal appendix
US typically shows submucosal wall thickening (arrowheads) of
the terminal ileum and cecum without inflammation of the
surrounding fat
MALROTATION
MALROTATION
• Intestinal maltoration
• is a congenital anatomical anomaly which results from an
abnormal rotation of the gut as it returns to the abdominal cavity
during embryogenesis. Although some individuals live their entire
life with malrotated bowel without symptoms, the abnormality
does predispose to midgut volvulus and internal hernias, with the
potential for life threatening complications
• Midgut malrotation has been estimated to occur in approximately
one in 500 live births . However, it is difficult to ascertain the true
incidence
• It is also frequently (~ 50%) associated with other abdominal
anomalies, some of which are causative and others merely
associated:duodenal atresia / stenosis / web /congenital
diaphragmatic herniation /gastroschisis /omphalocele heterotaxy
: 70% of individuals will have a malrotation /choanal atresia
• Clinical presentation
• correlates to the age of presentation 5.
• In the infant the most common presentation is with / midgut
volvulus.
• In the older child or even adult presentation is more frequently
intermittent with episodes of spontaneously resolving
duodenal obstruction. This is thought to be due to kinking of
the duodenum by Ladd bands rather than a volvulus 5.
Internal hernias are also encountered.
• In some individuals, presentation is very non-specific with
episodes of abdominal pain, weight loss, melaena, or even
chronic pancreatitis
• Pathology
• During normal embryogenesis the bowel herniates into the
base of the umbilical cord and rapidly elongates. As it returns
to the abdominal cavity it undergoes complex ~270 degree
counter clockwise rotation resulting in the duodeno-jejunal
(DJ) flexure normally located to the left of the midline, at the
level of L1 verterbal body and the terminal ileum located in the
right iliac fossa. This results in a broad mesentery running
obliquely down from the DJ flexure to the caecum, and
prevents rotation around the superior mesenteric artery (SMA)
1-6.
• In malrotation this does not occur and as a result the
mesentery has a short root, which allows it to act as a pedicle
(through which the SMA and SMV pass) around which
volvulus can occur.
• Plain film
• Abdominal radiographs, in the absence of midgut
volvulus, are neither specific nor sensitive 2.
• They may show:
right sided jejunal markings
absence of stool filled colon in right lower quadrant
29-year-old woman with chronic
intermittent abdominal pain. Supine
frontal abdominal radiograph shows
small bowel with jejunal markings on
right (arrowheads) and colon
predominately on left. Note absence of
colon in right lower quadrant (arrow).
• Ultrasound
• May show and inversion in the SMA /SMV
relationship with the SMA on the right and the SMV
on the left.
Transverse sonogram obtained through
upper abdomen in 11-year-old girl with
malrotation shows vertical or slightly
inverted orientation between superior
mesenteric artery (arrowhead) and
superior mesenteric vein (v
• CT
• may again show abnormal SMA (smaller and more
circular) / SMV relationshipvein (SMV) is a useful
indicator of malrotation .
• In most patients with quiescent malrotation, the SMA
and SMV will assume a vertical relationship or show
left—right inversion .
• large bowel predominantly on left and small bowel
predominantly on the right
• inspection of the pancreas in malrotation will reveal
underdevelopment or absence of the uncinate
process .
32-year-old man with left flank
pain. Axial contrast-enhanced CT s
shows inverted relationship
between superior mesenteric
artery (arrowhead) and superior
mesenteric vein (v). Note absence
of pancreatic uncinate process.
Axial contrast-enhanced CT
scan obtained through mid
abdomen shows
characteristic appearance of
small bowel on right and
colon on left
—22-year-old man with episodic
colicky abdominal pain. Axial contrastenhanced CT scan shows vertical
orientation of superior mesenteric
artery (arrowhead) and superior
mesenteric vein (v).
show bowel dilatation and mucosal hyperattenuation, findings indicative of global
small-bowel ischemia. There is a twist at the root of the small-bowel mesentery,
and an abnormal relationship between the superior mesenteric artery (long arrow)
and the superior mesenteric vein (short arrow) is seen.
Appendicitis in patients with
malrotation.
Axial contrast-enhanced CT scans in
56-year-old woman with left lower
quadrant abdominal pain, vomiting,
and leukocytosis show abnormal
dilated appendix with marked
periappendiceal stranding extending
from left-sided cecum. Note also
superior mesenteric artery—superior
mesenteric vein inversion
Appendicitis in patients with malrotation. Axial contrast-enhanced CT scan in woman
with left-sided abdominal pain and clinical diagnosis of diverticulitis shows enlarged
appendix (A) with periappendiceal inflammation on left. Note terminal ileum (asterisks)
crossing to left-sided cecum.
• Fluoroscopy
• paediatric upper gastrointestinal contrast study is the
examination of choice when the diagnosis is suspected. The
key findings of malrotation are:
• abnormal duodeno-jejunal (DJ) junction location
• duodenum fails to cross the midline
• DJ flexure lies inferior to the duodenal bulb
• Contrast enema has historically also been used, the theory
being that in malrotation the large bowel will also be
malrotated. Unfortunately in 20 - 30% of cases with
malrotation the caecum is normally located. The converse is
also true, with position of the caecum in normal individuals
being variable 4.
• Malrotation Presenting with Acute Symptoms
• Midgut volvulus is a complication of malrotation in which
clockwise twisting of the bowel around the SMA axis occurs
because of the narrowed mesenteric attachment .
• The clinical diagnosis of midgut volvulus in adolescents and
adults is difficult because the presentation is usually
nonspecific and malrotation is rarely considered. Recurrent
episodes of colicky abdominal pain with vomiting over a
period of months or years are typical and may eventually lead
to imaging .
• Diarrhea and malabsorption from chronic venous and
lymphatic obstruction may also occur .
• Findings
• on abdominal radiographs in midgut volvulus are usually abnormal
but non-specific .
• Upper gastrointestinal examination (the study of choice in
neonates) shows the typical corkscrew appearance of the proximal
small bowel.
• However, in older patients with acute symptoms, CT is generally
performed instead of a barium examination. . The CT whirl or
whirlpool sign describes the swirling appearance of bowel and
mesentery twisted around the SMA axis. A similar appearance can
be seen on sonography.
• Additional CT findings include duodenal obstruction,
congestion of the mesenteric vasculature, and evidence of
underlying malrotation .
• The presence of intestinal ischemia or necrosis is an ominous sign
6-day-old girl with malrotation and
midgut volvulus
Midgut volvulus in an infant Lateral upper GI image obtained in a different
patient also shows the classic corkscrew-like
• Barium study showing the typical twisted ribbon appearance of the proximal
small bowel in malrotation and volvulus.
29-year-old man with acute abdominal pain and vomiting His history was
significant for similar prior episodes without diagnosis. Axial contrastenhanced CT scans show characteristic whirllike appearance of bowel and
mesentery wrapping around superior mesenteric artery (arrowheads,). Note
dilated duodenum /engorged mesenteric vessels
12-year-old girl with acute abdominal pain from malrotation with midgut
volvulus. Axial contrast-enhanced CT scans show characteristic
clockwise twisting of bowel, mesentery, and superior mesenteric vein
(arrowheads) around axis of superior mesenteric artery.
• Internal hernia
• caused by abnormal peritoneal bands is an underrecognized
complication of malrotation after childhood .
• This condition may also be life-threatening because of the risk
of bowel obstruction and strangulation.
• CT findings of malrotation and small-bowel obstruction
(without volvulus) may be seen in patients having this
complication .
• Evidence of ischemic bowel again portends a poor prognosis .
• Some patients may present with a combination of midgut
volvulus and internal hernia .
23-year-old man with acute abdominal pain from malrotation with internal
hernia and partial midgut volvulus.
Axial contrast-enhanced CT scans show dilated duodenum (D, A), small whirl
sign involving more distal superior mesenteric artery (arrowheads, B), and
malpositioning of bowel. Localized cluster of unopacified bowel or fluid is
present inferiorly (arrows, C). Internal hernia with encapsulated appearance
was found at surgery
MESENTERIC LYMPHADENOPATHY
• Mesenteric lymphadenopathy is a common finding when
examining the abdomen in children and is generally
reactive.
• It can be found in the folds of the small bowel mesentery
around the superior mesenteric artery and vein and in
the arteries supplying the jejunum and ileum.
• They are normally less than 5 mm in diameter .
ACUTE PANCREATITIS
 Normal dimensions of the pancreas as a function of
age in children
• Maximal anteroposterior diametera (cm)
0–6yr:head 1.6cm (1.0–1.9)/ body 0.7cm (0.41.0)
/tail 1.2cm (0.8–1.6)
7–12yr :head1.9cm (1.7–2.0) /&body0.9cm (0.6–1.0)
& tail 1.4 (1.3–1.6)
13–18yr: head2.0cm (1.8–2.2) /&body1.0cm(0.7-1.2)
tail1.6cm(1.3-1.8)
 The commonest cause of acute pancreatitis in pediatrics
is blunt abdominal trauma, most commonlyfrom road traffic accidents or
non-accidental injury.
 ther causes include infection such as mumps, drug toxicity and biliary
and pancreatic anomalies
 .Biliary lithiasis is a rare cause in children.
 Acute pancreatitis is uncommon in childhood,and when it does occur no
obvious precipitating cause can be found. Trauma as a result of child
abuse is one of the commonest causes,
 whereas hereditary causes are most common for chronic pancreatitis.
 . when pancreatitis is prolonged, pleural effusions and pancreatic
pseudocysts may occur.
The diagnosis is confirmed by markedly raised amylase levels.
• Pediatric Pancreatitis cause:
•
•
•
•
•
•
•
Inflammation / Infection
–Trauma
–Cholelithiasis
–Familial
–Congenital –Pancreas Divisum
–Medications
–Viral (mumps, coxsackie, CMV, EBV)
•
•
•
•
•
•
Pancreatitis: Imaging Findings Ultrasound
“normal”
Focal / diffuse enlargement
Peripancreatic fluid
+/-gallstones, Biliary ducts
Vascular thrombosis
• Pancreatitis Imaging Findings CT:
•
•
•
•
•
Focal / diffuse enlargement
Peripancreatic fluid / stranding
Necrosis (↓density, enhancement)
Vascular thombosis
Pseudocysts
o In the diagnosis and staging of acute pancreatitis and its
complications CT is the imaging modality of choice.
o Ultrasound is important in determining whether gallstones are
the cause of the acute pancreatitis (i.e. biliary pancreatitis).
o ERCP with sphincterotomy and stone extraction should only
be used if a patient has biliary pancreatitis and signs of biliary
obstruction.
o MRI is as sensitive as CT, but not as practical or accessible.
• The diagnosis is usually made on clinical and laboratory
findings.
• There is no additional value of an early CT (within 72 hours) in
patients with acute pancreatitis.
• An early CT may be misleading concerning the severity of the
pancreatitis, since it can underestimate the presence and
amount of necrosis.
• Early CT is only recommended when the diagnosis is
uncertain, or in case of suspected early complications such as
perforation or ischemia.
• In mild pancreatitis the gland may appear normal but usually
there is evidence of edema with an enlarged gland which appears
hypoechoic.
• The ultrasound findings are diverse and may be diffuse
or focal gland enlargement. The borders of the
gland may be poorly defined and there may be dilation of the duct.
• Severe acute pancreatitis may be complicated by
complete gland necrosis, which is best demonstrated
by CT.
This may become infected in a significant proportion, and the
presence of air either from a fistula or the infection means that this
needs to be drained.
• Fluid collections arise in or adjacent to the pancreas in
acute pancreatitis, and the majority will resolve
spontaneously.
• Some may persist, but others may develop into
pseudocysts.
• Pancreatic pseudocysts have fibrous capsules.
Pseudocysts evolve from an acute collection and may
take several weeks to develop.
• CT Severity Index
• It is critical to identify patients who are at high risk for
severe disease, since they require close monitoring and
possible intervention.
• Early staging is based on the presence and degree of
systemic organ failure (cardiovascular, pulmonary, renal)
and on the presence and extend of pancreatic necrosis.
• Balthazar et al constructed a CT severity index (CTSI)
for acute pancreatitis that combines the grade of
pancreatitis (A-E) with the extent of pancreatic necrosis.
• Mild pancreatitis
• Patients with pancreatitis but no collections or necrosis
(i.e. Balthazar grade A-C) have a mild pancreatitis.
This is also called 'edematous or interstitial pancreatitis'
(no pancreatic necrosis).
• It is a self-limiting disease with an uneventfull recovery
occurring in 80% of patients with acute pancreatitis.
• There is an intermediate form of pancreatitis without
pancreatic necrosis with an intermediate clinical course.
• This is called extrapancreatic necrosis (EXPN) .
Sometimes the term exudative pancreatitis is used.
• These patients have Balthazar grade D or E.
• These patients have a relatively mild course because there is
no pancreatic necrosis, but there is higher morbidity than in
interstitial pancreatitis, because they have peripancreatic
collections, that can become infected
• Severe pancreatitis or necrotizing pancreatitis
• Severe pancreatitis, also called 'necrotizing pancreatitis'
occurs in 20% of patients.
It is characterized by a protacted clinical course, a high
incidence of local complications and a high mortality
rate.
Interstitial pancreatitis
On the left there is normal enhancement of the entire pancreatic gland with only
mild surrounding fatty infiltration.
There are no fluid collections or necrosis
(Balthazar grade C, CTSI: 2).
• Exudative Pancreatitis
• In exudative pancreatitis, or better called EXPN, there is
normal enhancement of the entire pancreas associated with
extensive peripancreatic collections.
These are often heterogeneous in appearance and may be
progressive.
• EXPN consists of necrosis of peripancreatic fat, extravasated
pancreatic fluid and inflammatory and hemorrhagic
components.
When peripancreatic collections persist or increase, it is
usually due to the presence of fat necrosis (i.e. EXPN).
Since fat does not enhance on CT, we cannot diagnose fat
necrosis.
In the case on the left on day 18 there is expansion of the peripancreatic
collections.
There are two or more collections, but no pancreatic necrosis.
(Balthazar grade E, CTSI: 4)
• Central gland necrosis
• Central gland necrosis is a subtype of necrotizing
pancreatitis.
It represents necrosis between the pancreatic head and
tail and is nearly always associated with disruption of the
pancreatic duct.
This leads to persistent collections as the viable
pancreatic tail continues to secrete pancreatic juices.
These collections react poorly to endoscopic or
percutaneous drainage.
Definitive treatment often requires distal pancreatectomy
PERIPANCREATIC COLLECTIONS
• Intraabdominal fluid collections and collections of necrotic tissue are
common in acute pancreatitis.
• These collections develop early in the course of acute pancreatitis.
In the early stage such a collection does not have a wall or capsule.
Preferred locations are the omental bursa and the retroperitoneal space
(anterior and posterior pararenal space).
• These collections are the result of the release of activated pancreatic
enzymes (namely lipase, trypsin and amylase) which also causes
necrosis of the surrounding tissues.
This explains why a lot of these collections contain solid debris.
• 50% of these collections show spontaneous regression
The other 50% either remain stable or increase and undergo
organization and demarcation with liquefaction.
They may remain sterile or develop infection
There is a fluid collection in the
omental bursa, adjacent to the
stomach.
Notice the normal enhancement
of the pancreatic head and tail,
but the lack of enhancement of
the majority of the pancreatic
body.
Spontaneous regression of peripancreatic collection
Pancreas surrounded by fat stranding due to exsudative pancreatitis.
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