This document discusses an approach to evaluating a vomiting infant, including potential causes of vomiting. It covers the relevant anatomy and embryology of the gastrointestinal tract. Specific conditions that can cause vomiting discussed include tracheo-esophageal fistulas, anorectal malformations, malrotation, intestinal atresia, Hirschsprung disease, and hypertrophic pyloric stenosis. The document aims to describe the diagnosis and management of vomiting in infants by understanding the potential anatomical abnormalities and applying the appropriate clinical approach and investigations.

1. EVALUATING A VOMITING INFANT ; TRACHEO-ESOPHAGEAL
FISTULAS & ANORECTAL MALFORMATIONS
BY
Dr SAMEER PEER ( 2ND YEAR PG)

2. OBJECTIVES
• TO DESCRIBE AN APPROACH TO DIAGNOSIS IN A VOMITING
INFANT/CHILD.
• TO UNDERSTAND THE ANATOMY AND EMBRYOLOGY OF
ANORECTAL MALFORMATIONS & TRACHEO-ESOPHAGEAL
FISTULAS.
• TO PRESENT A CASE BASED DISCUSSION.

3. CONFLICT OF INTEREST & FINANCIAL DISCLOSURES
NONE

4. EMBRYOLOGY & RELEVANT ANATOMY
Formation of the Primitive Gut
•The ‘cephalocaudal’ and ‘lateral’
foldings of the embryo will lead to
partial incorporation of endoderm
lined cavity into the embryo to
form the “primitive gut tube”.
•In the cranial & caudal ends of the
embryo the primitive gut forms a
blind ending tube, the ‘foregut’ &
‘Hindgut’, respectively.
•The middle part of the tube,
‘Midgut’ remains temporarily
connected to the yolk sac by means
of a vitelline duct/yolk stalk.

5. As a result of embryonic folding, the dorsal part of yolk sac is enclosed inside the embryo
to form the Gut.
•The gut is endodermal in origin, which is surrounded by splanchno- pleuric mesoderm.
•The Foregut is separated from the stomodeum by the Buccopharyngeal membrane.
•The Hindgut, is separated from the proctodeum by Cloacal membrane.
•The Midgut is connected to definitive yolk sac by Vittellointestinal duct.

7. Derivatives of the Foregut
•Oral cavity (tongue, tonsils,
salivary glands)
•Pharynx
•Esophagus
•Stomach
•Duodenum (Proximal half )
•Liver + Biliary apparatus
•Pancreas
Extent of Foregut
Foregut starts from the Oral
cavity and terminates at the level
of Ampulla of Vater (the point
where common bile duct opens
into Duodenum

8. Development of the
Esophagus
•During the 4th wk., a small
diverticulum appears in the
ventral wall of Pharynx.
•A ‘Tracheoesophageal
Septum’ gradually separates
the ventral Respiratory
diverticulum from the dorsal
part of foregut.
• As a result, the Pharynx is
divided into;
–a ventral portion the
“respiratory primordium”,
–a dorsal portion, the
“esophagus”.

9. Development of the Stomach
•Develops as a fusiform dilatation
of the caudal part of foregut in the
middle of 4th wk.
•Initially oriented in the midline.
•The swelling shows an expansion.
•During the next 2 weeks, the right
wall of the swelling grows more
rapidly than the left wall.
•This leads to the formation of
future ‘greater’ & ‘lesser’
curvatures of the adult stomach.
(The anterior/ventral border
becomes lesser curvature and the
posterior/dorsal border becomes
greater curvature)

10. Rotation of Stomach
Longitudinal axis:
•As the stomach enlarges, it
slowly rotates 90⁰ (clockwise)
around its longitudinal axis. As a
result;
•The ventral border moves to the
right & the dorsal border moves
to the left
•The original left side becomes
ventral surface & the original
right side becomes dorsal surface
( grows faster than the ventral
surface)

11. In Transverse/Horizontal axis:
•The rapidly growing dorsal/posterior
wall of stomach slightly rotates the
stomach on the transverse plane
•As a result, the cranial (esophageal)
end of stomach moves down & to the
left, while, the caudal (duodenal) end
moves up and to the right.

12. Development of the distal part of Foregut (Duodenum)
With the 90⁰clockwise
rotation the greater
posterior wall of stomach
moves to the left in
abdomen & the C-shaped
Duodenum moves to the
right

13. Derivatives of Midgut:
•Distal half of the Duodenum
•Entire Small Intestine
– Jejunum,
– Ileum
•2/3rd of Large Intestine
– Cecum,
– Appendix,
– Ascending Colon,
– Transverse Colon (proximal 2/3rd )
EXTENT OF MIDGUT Starts from below the Major duodenal papilla and terminates at
the junction of the proximal two-third of the Transverse Colon with the distal one-third.

14. Dual origin of Duodenum:
As the Midgut starts from the point of Ampulla of Vater, therefore, the
upper half of Duodenum is a part of Foregut, while, the lower half of
Duodenum is a part of Midgut)

15. The Midgut;
•dorsally is suspended in the midline by a
double-layered ‘Dorsal mesentery’
•ventrally communicates with the yolk
sac by way of a wider Vitelline duct/Yolk
stalk

16. Development of Primary intestinal loop
•The middle wider part of the primitive gut tube which is in communication with the yolk sac
elongates and forms a u-shaped loop, the Primary intestinal loop/Midgut loop.
•The loop is suspended from dorsal abdominal wall by an elongated mesentery.
Physiological Herniation of gut:
•There is a rapid growth of the loop & as there is very little space available with in the
abdomen (because of massive Liver & a pair of Kidneys), the midgut loop herniates into the
connecting stalk/Umbilical cord.
•Herniation starts from the 6th wk and the loop keeps on growing in length with in the
umbilical cord
Reduction of physiological hernia:
•By the end of 10th wk, as the abdominal cavity increases in size, the developed loops of
Midgut start re-entering the abdominal cavity and by 12th wk all of the Midgut re-enters &
settled in the abdominal cavity
The tip of the loop is connected with the yolk sac by a Vitelline duct & this connection
persists till the end of 10th wk.

17. Rotation of Midgut with in the Umbilical cord
•When the Midgut loop enters the cord, it has a ‘Cranial limb’ & a ‘Caudal limb’ and the
“superior mesenteric artery”(SMA) is the axis of the loop.
•The caudal limb soon develops a swelling at its end, the ‘Cecal bud’. This bud acts like a
marker throughout the rotation.
•Immediately after entering the cord, the loop rotates 90⁰ counterclockwise on the axis of
artery. Therefore, the cranial limb comes to lie on the right & caudal to the left.
•The original cranial limb shows a rapid growth in its length as compare to the caudal
limb.
•Then another 90⁰ counterclockwise rotation happens and as a result, the original cranial
limb will become caudal and the original caudal limb will become cranial
Total 180⁰ counterclockwise rotation along the axis of SMA takes place with in the
cord

20. EMBRYOLOGY OF ANORECTAL REGION FROM THE POINT OF
VIEW OF ARMs
• In early embryonic life, the terminal portion of the hindgut—the primitive cloaca—is
divided into dorsal and ventral parts by a coronal sheet of mesenchyme—the
urorectal septum—and separated from the amniotic cavity by the cloacal membrane.
Most ARMs result from abnormal development of the urorectal septum.
• Between weeks 4 and 6 of gestation, both the yolk sac or primitive hindgut and the
allantois or primitive urogenital sinus enter into the cloaca
• The urorectal septum then develops forklike infoldings (Tourneux and Rathke folds)
of the lateral cloacal walls; at the same time, the embryo starts to curve as a result of
the longitudinal growth of the developing neural tube and the mesodermal
compartment.
• With these morphologic changes, the distance between the cloacal membrane and the
tip of the urorectal septum is progressively reduced.

21. • At the end of week 7, the urorectal septum and the cloacal membrane are located at
the same level. The cloaca is thus divided into a ventral part (the urogenital sinus) and
a dorsal part (the rectum and proximal anal canal). Between them, the tip of the
urorectal septum becomes the perineal area .
At this time, the cloacal membrane ruptures by apoptosis, thus opening two orifices in
the perineum: one ventral or urogenital and one dorsal or anal.
Also at the end of week 7, a secondary occlusion of the anorectal canal takes place,
initially by adhesion of the walls and later by formation of an epithelial “plug” at the
anal level. This secondary closed anal orifice will rupture and recanalize by apoptosis at
the end of week 8
Embryologic basis of ARMs. (a) Evolution of the cloaca at day 32. (b, c) Subdivision of the
cloaca and the beginning of formation of the perineum at day 36 (b) and day 56 (c). 1 = allantois,
2 = cloacal membrane, 3 = cloaca, 4 = urorectal septum, 5 = Rathke fold, 6 = Tourneux fold, 7 =
primitive urogenital sinus, 8 = anus, 9 = rectum, 10 = perineal area.

22. APPROACH TO A VOMITING INFANT
Vomiting, or the forceful extrusion of gastric contents, is never normal in the
infant and usually occurs because of complete or partial obstruction
somewhere along the course of the gastrointestinal (GI) tract between the
stomach and cecum.
Clinically, vomiting is categorized as being nonbilious or bilious; the latter
suggests the point of obstruction is distal to the ampulla of Vater. Most
commonly, nonbilious “vomiting” is actually regurgitation (gastroesophageal
reflux [GER]). The clinical differentiation between vomiting and regurgitation
may be challenging.
Regurgitation, or GER, is normal in the first 3 months of life and resolves in
time. It usually has no definitive pathologic cause and is unrelated to a
functional defect. Rarely, regurgitation may be due to displacement of a
portion of the stomach into the chest (ie, hiatal hernia). In other cases, low
esophageal sphincter pressures or delays in gastric emptying have been
implicated as causative and typically resolve in time.

23. Infants with normal weight gain tend not to have disease as the cause of their
vomiting.
However, bilious emesis or repeated forceful vomiting
should be evaluated for underlying pathology.
When evaluating a neonate who presents in the first week of life with vomiting, a
congenital GI tract abnormality is a primary consideration.
Upper or lower tract abnormalities can cause vomiting with the possible etiologies
including
• malrotation with or without volvulus,
• atresia of the antropyloric region, atresia/stenosis of the small bowel or
colon,
• functional obstructions caused by Hirschsprung disease,
• functional immaturity of the colon, and meconium ileus.
Importantly, although malrotation most commonly presents in newborns, it can
present at any time during life with decreasing frequency with age

24. Several GI pathologies to consider in a vomiting infant outside of the
newborn time period include hypertrophic pyloric stenosis (HPS),
pylorospasm, formula intolerance, and gastroenteritis
In a young infant, less common GI etiologies include neonatal appendicitis,
intussusception, gastric ulcer disease, gastric volvulus, and lactobezoar.
Medical causes to consider include sepsis, enteritis, pneumonia, otitis
media, meningitis, raised intracranial pressure (from tumor, trauma, or
hydrocephalus), kernicterus, metabolic disorders (phenylketonuria,
hyperammonemia, maple syrup urine disease, galactosemia, diabetes,
adrenocortical hyperplasia, methylmalonic acidemia), diencephalic
syndrome, and rarely drugs or toxic agents.

25. Diagnostic workup :
• History
• Clinical examination
• Labs
RADIOLOGY
• ALARA PRINCIPLE
• ACR APPROPRIATENESS CRITERIA

29. CASE STUDIES
CASE 1
2 month old infant presents with bilious vomiting
and abdominal distention. Patient is very sick

30. BARIUM – UPPER GI SERIES
AP LATERAL

31. COMPANION IMAGE

32. COLOR DOPPLER

33. DIAGNOSIS
Intestinal Malrotation with midgut volvulous
SURGICAL EMERGENCY !!!

34. The normal position of the duodenojejunal junction is to the left of the left-sided
pedicles of the vertebral body at the level of the duodenal bulb on frontal views
and posterior on lateral views.
ANATOMICAL VARIATIONS
Inferior displacement of DJ
flexure

35. Wandering Duodenum- mimics Midgut volvulous
Normal DJ flexure location

36. Problem solving approach to upper GI series
• First, the initial passage of barium through the duodenum should be
observed directly with fluoroscopy to confirm the course of the duodenum
and the position of the duodenojejunal junction.
• Second, the position of the duodenojejunal junction should be
documented with the acquisition of both frontal and true lateral
projections.
• Third, the stomach should not be overfilled with barium
• Fourth, manual palpation may be used to determine the mobility of the
duodenum.
• Fifth, other imaging studies should be reviewed.
• Sixth, if the diagnosis remains in doubt or the upper GI tract findings are
equivocal , delayed abdominal radiographs should be acquired to identify
the position of the cecum.
• Seventh, if the clinical manifestations do not correspond to the upper GI
tract findings, the upper GI series should be repeated on a subsequent
day

37. In subltle cases, delayed films for caecal position is useful, caecal position is a
predictor of volvulous

38. RELATIONSHIP BETWEEN SMA & SMV

39. CASE 2
A 1 yr old child presented with history of recurrent chest
infections, breathlessness, wheeze with vomiting after feeds, more
in lying down posture and after nocturnal feeds.
O/E- child is well hydrated with normal weight for age
Labs – unremarkable
Upper GI series – normal
Plan – 24 hr pH monitoring, EGD, Esophageal manometry, Tc-99m
antimony sulphur colloid scan

40. Tc-99m antimony Sulphur Colloid Scan
A B

41. DIAGNOSIS
Gastro-Espohageal Reflux Disease
Diagnostics of the gastrointestinal reflux is not always required. Very often, the
diagnosis can be based on typical clinical symptoms. Only after introducing a
proper treatment, if there is no therapeutic effect, the patient should be referred for
diagnostic tests.
Diagnostics is required in cases with symptoms suggestive of esophageal
inflammation, children with impaired physical development, patients suspected
of atypical reflux disease, and especially those with symptoms referable to the
respiratory tract, e.g. recurrent infections of the lower respiratory tract,
refractory asthma, apnea

42. CASE 3
SPOT DIAGNOSIS
A B C

43. DIAGNOSIS – HIATUS HERNIA
A. moderate-sized sliding hiatal hernia
(arrow). The gastroesophageal junction
(arrowheads) has slid superiorly into the
chest.
B. a small paraesophageal hernia (arrow).
The gastroesophageal junction
(arrowhead) is seen in its normal location
below the diaphragm
C. show an intrathoracic stomach (ST) with a
short esophagus ( Es)

44. CASE 4
A 2yr old child presenting with multiple episodes of non
bilious vomiting associated with cyanosis and apnea. NG
tube could not be passed into the stomach. Patient not
allowing to touch abdomen

46. DIAGNOSIS –
ORGANO-AXIAL GASTRIC VOLVULOUS
• stomach is rotated along its long axis (along the
cardiopyloric line, which is drawn between the
cardia and the pylorus)
• mirror image of normal anatomy can occur with
reversal of the greater and lesser curves
• antrum rotates anterosuperiorly
• fundus rotates posteroinferiorly
• incomplete (<180º) also called organo-axial position
of the stomach, usually asymptomatic
• complete (>180º) present with obstruction or
ischemia

47. COMPANION CASE

48. DIAGNOSIS –
MESENTRO-AXIAL GASTRIC VOLVULOUS
• rotation around short axis from the
lesser to greater curvature (i.e.
perpendicular to the cardiopyloric
line)
• usually incomplete, <180°)
• displacement of antrum
above gastro-oesophageal
junction; stomach appears upside-
down with the antrum and pylorus
superior to the fundus and proximal
body
• coincides with the axis of
mesenteric attachment and is
associated with severe obstruction
and strangulation
• less associated with diaphragmatic
defect

49. CASE 5
2 month old male infant with recent onset of non-bilious
projectile vomiting.
O/E – dehydrated. No mass palpable P/A
Labs – Hypokalemia, hypochloremia, metabolic alkalosis,
aciduria

50. PLAIN X-RAY ABDOMEN

51. USG

52. Barium UGI series

53. DIAGNOSIS - HYPERTROPHIC PYLORIC STENOSIS
• Easy ultrasound technique is to find gallbladder then turn the probe
obliquely sagittal to the body in an attempt to find pylorus
longitudinally.
• pyloric muscle thickness, i.e. diameter of a single muscular wall on a
transverse image: <3 mm (most accurate )
• length, i.e. longitudinal measurement: <15 mm
• With the patient right side down the pylorus should be watched and
should not be seen to open.

54. Case 6
15 month old infant with irritability and few episodes of
bilious vomiting. Parents give history of recent fever, cough
and running nose with eruption of rash on buttocks
O/E – Abdomen is guarded, rash on buttocks is purpuric and
palpable. DRE – Blood mixed with mucus
Labs – urine – RBC casts

55. PLAIN X-RAY ABDOMEN

56. USG

57. REDUCTION WITH CONTRAST ENEMA

58. DIAGNOSIS –
INTUSUSSCEPTION IN SETTING OF HENOCH-
SCHONLEIN PURPURA

59. TAKE HOME MESSEGE……
1. Age of presentation
2. Bilious v/s non-bilious vomiting
3. General condition of the patient
4. Labs
5. UGI series in most cases
6. Ultrasound/doppler
7. Nuclear Scan
8. ACR appropriateness criteria
9. ALARA

60. TRACHEO-ESOPHAGEAL FISTULA
Congenital tracheo-oesophageal fistula is a congenital pathological
communication between the trachea and oesophagus.
Epidemiology
Tracheo-oesophageal fistula and oesophageal atresia have a combined
incidence of approximately 1 in 3500 live births. There is only a minimal
hereditary/genetic component with an incidence in twins and those with
family history being only approximately 1% . There is no convincing gender
or racial predilection .

61. TYPES

62. Clinical presentation
Clinical presentation is similar for all types except for type E (H-type).
Antenatally polyhydramnios may be present due to inability to adequately swallow
fluid, and it is found in up to 90% of cases , but is, unfortunately, a non-specific sign.
The diagnosis is usually made in the neonate, as they experience feeding difficulties
and respiratory compromise due to repeated aspiration.
In cases where oesophageal atresia is present (i.e. again, all but H-type), then
attempted the passage of a nasogastric tube will not be successful. Only with H-type
fistulae, which can be very small, and typically slant down from the trachea toward the
oesophagus, may presentation be delayed, sometimes for many years

63. Associations
In just over half of cases, there are other associated congenital abnormalities, including:
cardiac anomalies: 15-19%
PDA
ASD
VSD
right sided aortic arch
VATER/VACTERL
gastrointestinal anomalies: 22%
imperforate anus
malrotation
intestinal atresia
aneuploidic chromosomal abnormalities
trisomy 21
trisomy 18
trisomy 13
non-aneupliodic syndromic associations
Feingold syndrome
CHARGE syndrome
Pallister-Hall syndrome

64. Pathology
The trachea is an out-budding from the ventral foregut, and tracheo-oesophageal
fistulae represent incomplete/abnormal division. They are very closely related to
oesophageal atresia, and represent a spectrum of disease. As such, the types of
oesophageal atresia/tracheo-oesophageal fistula can be divided into:
proximal atresia with distal fistula: 85%
isolated oesophageal atresia: 8%
isolated fistula (H-type): 4%
double fistula with intervening atresia: 1%
proximal fistula with distal atresia: 1%

65. Radiologic features
Plain radiograph
Demonstration of the nasogastric tube curled in the proximal oesophagus in a child
where the passage of the tube has been unsuccessful is usually sufficient for
diagnosis. The proximal oesophageal stump may be distended with air (types A and
C).
The presence of air in the stomach and bowel in the setting of oesophageal atresia
implies that there is a distal fistula.
Often the lungs demonstrate areas of consolidation/atelectasis due to recurrent
aspiration.

66. Fluoroscopy (Barium studies)
H-type fistulas can be difficult to diagnose and may require contrast studies,
looking for contrast passing into the tracheobronchial tree.
Barium is usually the contrast medium of choice, a non-ionic iodinated
contrast medium can be used alternatively. Ionic iodinated contrast medium
should not be used as they can cause chemical pneumonitis
Ultrasound
Antenatal ultrasound may demonstrate polyhydramnios or even in some
cases a distended proximal blind ending oesophagus
CT
In some instances, CT and virtual bronchoscopy may be of benefit in preoperative planning .
This is especially the case in patients with long segment atresia who may require a staged
operation

67. CASES
TYPE D/C

68. Type A Type C with Anal atresia Type E ( H-shaped)

69. Treatment and prognosis
Prior to surgical correction, bronchoscopy is frequently performed.
In infants who are deemed unable to tolerate emergency repair, then a
gastrostomy and sump drainage catheter may be performed to allow feeding
and weight gain.
Another reason for a delay is in patients who have a 'long-gap' atresia
precluding primary anastomosis repair. In most cases, however, the defect is
corrected immediately.
Prognosis is often most affected by the presence of associated congenital
anomalies.
For example in one study (albeit from 1979) the mortality for infants with just
oesophageal atresia / tracheo-oesophageal fistula was 23% versus 79% in those
with associated cardiac anomalies

70. ANO-RECTAL MALFORMATIONS
• Anorectal malformations (ARMs) are a complex group of congenital anomalies
involving the distal anus and rectum, as well as the urinary and genital tracts
in a significant number of cases.
• The prevalence is approximately one per 5000 live births, with a slight male
preponderance . In most ARMs, the anus is not perforated and the distal
enteric component may end blindly (ie, atresia) or as a fistula into the urinary
tract, genital tract, or perineum.
• ARMs are associated with other congenital anomalies in up to 70% of
cases. The final prognosis and quality of life for children with ARMs will
depend, to a large extent, on the presence and gravity of these associated
anomalies.

72. Classification of ARMs
• The best-known classification of ARMs is the Wingspread
classification of 1984.
• It divides ARMs into three types—low, intermediate, and high—
depending on whether the rectal pouch is located below, at the level
of, or above the puborectal sling, respectively, with special categories
for cloacal and rare malformations.
• More recently, the Krickenbeck Conference of 2005 established a
new classification, which is based mainly on the presence or absence
of fistulas and their type and location, as well as the position of the
rectal pouch.

76. Role of Imaging in Initial Evaluation of ARMs
Imaging studies play a key role in initial evaluation of ARMs. They not only allow
classification of the ARM but also facilitate identification and determination of the
severity of associated anomalies.
Imaging studies in the first 2 days of life should include radiography of the
thorax, spine, and pelvis along with cardiac, perineal, abdominal, pelvic,
and spine US to detect possible associated anomalies

78. Associated anomalies detected on x-ray

79. Pelvic Muscle Anatomy: MR Imaging Correlation
Pelvic MR imaging is used in children with ARMs to evaluate both the real
position of the rectal pouch and the size, morphology, and grade of
development of the sphincteric muscles before definitive surgical correction.
The final prognosis of ARMs depends significantly on the grade of
development of these muscles.

80. Two important reference transverse planes are used with MR imaging for
evaluation of ARMs.
The first is the pubococcygeal plane, which extends from the upper border of
the os pubis to the os coccyx . As described by Stephens et al , this plane
corresponds to the attachment level of the levator ani muscle to the pelvic
wall
The second relevant transverse plane follows a line joining the lowest points
of the ischial tuberosities (ischial plane) and represents the deepest point of
the funnel of the levator ani muscles in healthy patients. The ischial plane
includes the base of the penis in males and, posteriorly, the oval EAS
Coronal images should be obtained perpendicular to the pubococcygeal plane
to allow correct identification of the levator hammock and the anal canal inside
the EAS

83. Pelvic MR Imaging in Boys with ARMs
CASES
Low ARM without fistula

84. Low ARM with Perineal Fistula

85. Intermediate or High ARM with recto-
urethral Bulbar fistula.

86. High ARM with
partial sacral
agenesis and
fistulous
communication with
UB

87. Pelvic MR Imaging in Girls with ARMs
CASES
Low ARM with a rectovestibular fistula in a girl

88. Cloacal anomaly in a girl.

89. Caudal regression syndrome
(cloacal anomaly with genital
duplication, partial sacral
agenesis, spinal cord
anomalies, horseshoe kidney,
and vesicoureteral reflux) in a
girl.

90. Currarino triad
a very rare disorder.
It was described in 1981 and consists of
ARM (commonly anal stenosis or agenesis),
sacrococcygeal defect, and
presacral mass (most often an anterior meningocele; teratoma; or
neurenteric, dermoid, or epidermoid cyst), which causes secondary
tethered cord syndrome
Currarino triad results from a common developmental defect of the notochord in
the early phases of embryogenesis, with incomplete separation of the
endodermal and ectodermal layers, ventral failure of vertebral fusion, and
consequent persistence of an open communication between the gut and
sacral spine
Children with the Currarino triad present with intractable constipation.

91. Currarino triad
(high ARM with
recto–urethral
prostatic fistula
confirmed at
surgery, partial
sacral agenesis,
tethered cord,
and anterior
lipomyelomenin
gocele) in a boy

92. CONCLUSION
• History and clinical examination
• Knowledge of Embryology and Anatomy
• Plain films and Conventional procedures are invaluable for
Diagnosis in most cases and could be therapeutic in some
conditions.
• USG in neonates and infants – associated anomalies
• MR very useful in evaluation and classification of ARMs.
• ALARA principle and ACR appropriateness criteria

93. ACKNOWLEDGEMENTS
CASES CTSY : RADIOPAEDIA.ORG