Diagnostic Imaging in Children (Abdominal cavity (Indications for…
Diagnostic Imaging in Children
Congenital heart lesions
Clinically classified into cyanotic and acyanotic lesions,which forms the starting point for interpreting the radiologic findings:
Cyanotic lesions are usually subdivided into those with decreased pulmonary vascularity (oligemia) and those with increased pulmonary vascularity (plethora)
Acyanotic lesions are generally the left to right shunts that produce pulmonary plethora or increased flow.
With plethora include:
Truncus arteriosus, Total anomalous pulmonary venous return, Single ventricle
With oligaemia include: Teralogy of Fallot, Simple pulmonary stenosis or atresia, Tricuspid atresia, Ebstein’s anomaly
Atrial septal defect (ASD), Ventricular septal defect (VSD), Atrioventricular canal (AVC), Patent ductus arteriosus, Cardiac failure from lesions such as coarctation of the aorta
Teralogy of Fallot, showing the typical upturned cardiac apex lifted off the diaphragm (arrow) and oligaemic lungs.
Oligaemia. Decreased pulmonary vascularity in „lucent” lungs- i.e. „black” lungs with few vascular markings- can be confused with either hyperinflation or pneumothorax. In pneumothorax there is usually a margin which can be seen representing the edge of collapsed lung.
Indications for diagnostic imaging of GI tract in neonates
GI tract obstructions diagnosed directly after birth:
Oesophageal atresia (EA), Imperforate anus
GI tract obstructions diagnosed few hours after birth:
Duodenal obstruction, Small intestinal obstruction, Meconium ileus, Meconium peritonitis, Intestinal malrotation
Necrotizing enterocolitis Enterocolitis necroticans NEC, Congenital megacolon Hirschsprung's disease, Paralytic ileus
Tumors of abdomen
Respiratory and swallowing disorders:
Vascular rings, Tracheoesophageal fistula
Oesophageal atresia (EA)
The most common oesophageal atresia type is that with tracheoesophageal fistula (85-93%)
Entrance to the lower gastrointestinal tract is blocked , air reaches the lower oesophageal pouch via the fistula with the trachea or bronchi
The first clinical indication is excessive secretion of saliva in the mouth of neonate and problems with passing naso-duodenal tube into the stomach
In neonates who are suspected of oesophageal atresia no contrast medium is administrated!
In suspected cases a soft, opaque catheter is passed through the nose and anteroposterior and lateral film are exposed
Findings on posteroanterior and lateral chest images confirm a diagnosis of EA by displaying a coiled nasogastric tube (placed for determination of EA) in the proximal oesophageal pouch of a child.
Lateral chest image shows blind end lower oesophageal pouch distended with air
The presence of fistula is established by visualisation of air in the stomach and intestines
Chest films must be carefully examined for aspiration pneumonia, (especially in the right upper lobe) and patchy atelectasis which may be frequently present
Duodenal and small intestinal obstruction
Duodenal atresia is present in 20-30% infants with Down syndrome
High complete or almost complete obstruction: atresia, annular pancreas, duodenal bands (narrowing lumen of duodenum) associated with malrotation of the colon
An upright plain film of chest and abdomen shows two fluid levels present in dilated stomach and proximal duodenum (double bubble sign)
If the obstruction is partial some air may be visualized in the distal gut
In small intestine obstruction plain films show fluid levels in gas distended intestinal loops above the place of obstruction and absence of gas distally in lower abdomen
(Passage of gas through the intestinal tract of healthy neonate is rapid, after six hours the head of the air column reaches the rectum)
anomalies associated with rectal abnormalities are malformations of the urinary tract and oesophagus and, less often, the small bowel
May be complicated with fistulas between rectum and genitourinary tract
Abnormality diagnosed early after birth
Imperforate anus is broadly classified by its relation to the levator ani muscles.
Atresia at or above the levator muscle complex are defined as high anomalies , below as low anomalies- each needs different surgical treatment
A lateral film of the inverted patient (head down position) with beam horizontal may help to outline the distance between bowel filled with gas and marked anal dimple (lead marker or cotton pad with barium)
10-20%neonates suffering from mucoviscidosis
Thick viscid meconium fills loops of intestine causing obstruction
on plain radiographs:
soap bubble mass (meconium mixed with gas) is visible on the righ
there may be no present fluid levels in small intestine in upright position due to tenacious nature of meconium
loops are distended like in obstruction
sometimes granular calcifications are present in the peritoneal cavity (prior prenatal rupture of bowel and meconium peritonitis)
therapy and diagnosis is made by water soluble contrast enema (!warm the contrast to body temperature!).
CM makes fluid pass through the bowel wall into the lumen
examination shows microcolon- narrow lumen of the colon
contrast enema results in immediate passage of meconium and resolution of intestinal dilatation
(Current practice uses low-osmolar contrast, no evidence exists that the newer low-osmolar agents are less therapeutic than hyperosmolar media)
Necrotizing enterocolitis (Enterocolitis necroticans, NEC)
Commonly affects premature infants and low weight full-term infants
Precise ethiology is unknown although three most important factors are:
intestinal ischemia and hypoperfusion leading to altered mucosal integrity
bacterial overgrowth with gas formation in the bowel wall
Irritation of the bowel by oral feeding
generalized intestinal distension due to paralytic ileus walls may be thickened and indistinct (due to oedema)
The most pathognomonic and late finding:
pneumatosis interstitialis (linear, curvilinear collection of gas bubbles- intramural gas)
presence of gas in portal vein system– gas enters vascular channels in the affected intestine
The most commonly affected parts of GI tract are colon and distal loops of intestine (any region of the bowel can be involved, the stomach can be involved as well)
horizontal-beam radiograph – perforation of the intestinal wall –some quantity of free air may be seen (pneumoperitoneum)
radiograph - gas in portal venous system -parallel streaks of air density in the liver
US of the abdomen - thick-walled loops of bowel with hypomotility. intraperitoneal fluid , pneumatosis intestinalis and gas in the portal venous circulation within the liver.
In case of perforation surgical treatment must be involved - surgical exploration and resection of necrotic bowel
Congenital megacolon -Hirschsprung's disease
intramural ganglion cells in the Meissner (submucosal) and Auerbach (myenteric) plexuses are absent.
the disease results in decreased motility in the affected bowel segment
the anus is always involved
a variable length of colon may be involved as well.
the aganglionic, aperistaltic bowel segment is contracted
the normal proximal colon is dilated and hypertrophied
Mostly in boys with a ratio of 4:1
5% neonates with Down syndrome are affected
Symptoms in newborns are : failure to pass meconium within the first 48 hours of life, abdominal distension that is relieved by rectal stimulation or enemas, vomiting , constipation and diarrhoea
A diagnostic evaluation should begin with plain abdominal radiography followed by a contrast (barium) enema examination of the colon to confirm the diagnosis
Radiographs of the neonatal abdomen may show multiple loops of dilated small bowel with air-fluid levels that can usually be determined to be a distal bowel obstruction, an empty rectum is a common finding, a cut-off sign in the rectosigmoid region, with an absence of air distally is found
Contrast (barium) enema examination can show the presence of a transition zone, irregular contractions, mucosal irregularity
The hallmark of the diagnosis is demonstration of the transition zone from the dilatated normal colon above to the reduced-calibre, aganglionic bowel segment
delayed evacuation of contrast material after contrast enema is a typical finding.
rectal mucosal biopsy is required for accurate diagnosis
When Hirschprung disease is suspected enema emptying bowel of its contents mustn’t be done prior barium enema examination
Congenital uterine abnormalities are a result of developmental problems in the Muellerian ducts
The incidence rate is between 0.1 and 12%.
Some abnormalities can have a major impact on infertility and pregnancy outcome
Class I: Segmental Muellerian agenesis or hypoplasia
Class II: Unicornuate uterus
Class III: Uterine didelphis
Class IV: Bicornuate and septate uterus
The best screening method for detecting uterine anomalies has been HSG, but it is unable to delineate the external uterine surface.
currently the golden standard for presurgical evaluation of uterus cavity and fallopian tubes (mostly in management of infertility)
allows for visualization of uterine cavity,
documents tubal patency and provides information about tubal mucosa and size.
intraperitoneal adhesions can be also visualized
The HSG is usually done in a radiology lab and takes between 10 to 30 minutes. A speculum will be inserted vagina (after having a Pap smear), and then place a thin plastic tube inside the cervix that will lead to your uterus and fallopian tubes. A special dye will be injected through the plastic tube. The dye should fill the uterus and fallopian tubes, and spill out of each fallopian tube. Next, x-rays is taken to evaluate uterus and fallopian tubes.
Many women feel some cramping, especially when the dye is injected. Women who have a blocked fallopian tube may feel intense pain. Over-the-counter pain medicines such as ibuprofen can help relieve this pain or discomfort. The risks of the HSG include pain or discomfort, infection, and vaginal spotting or bleeding. The test should be scheduled after period ends, usually between days 6 to 10 of the menstrual cycle.
Coronal T2 weighted MR image in patient with uterus didelphys demonstrates splayed, duplicated uterine horns (asterisks).
Central Nervous System
sonography through the anterior fontanelle as an ultrasound window.
5-7,5 MHz transducers for far imaging and 10MHz to evaluate near field pathology
Sector and linear transducers
non-invasive, with no radiation portable imaging
Scanning- rocking transducer back and forth in the coronal and sagittal projections
intraventricular haemorrhages, subependymal haemorrhages, hematomas, abscesses, posthemorrhagic hydrocephalus, porencephalic cysts and other changes due to hypoxia and ischemia, congenital defects and malformations, neoplasmatic tumours.
Time guidelines of ‘routine’ US screening in preterm infants
Early Ultrasound scans are needed in following situations :
gestational age less than 32 weeks and infant’s weight below 1500g – a scan on day 1, repeated by day 7, will pick up most antenatal lesions and all new cases of intracranial haemorrhage (45%)
Late Ensure that follow-up US scans are completed by the time of discharge from the neonatal intensive care unit and/or at the corrected gestational age of 36 weeks. If the first scan is abnormal, repeat as required.
If head growth is excessive or too little- scan weekly or more frequently. Normal head growth is about 1 mm per day.
Use ultrasonography as a guide to surgical postoperative management of shunt insertion and its efficiency.
Scan following acute severe hypoxemia and recovery, at about 5-7 days for cystic lesions
Indications for intracranial sonography in full-term infant
2500gm birth weight or less , perinatal asphyxia, neurologic abnormality, circulatory and pulmonary failure, congenital defects of skull and spinal column
Most common pathology of CNS in premature infants prior 32w ga
In 45% of cases intracranial haemorrhage (IVH intraventricular haemorrhage) occurs
Hypoxic-ischemic changes in the white matter
Predisposing factors include:
prematurity- immaturity of central nervous system
respiratory distress syndrome (RDS),
increased or decreased cerebral blood flow,
increased venous pressure
pneumothorax, and hypertension
These factors result in rupture of the germinal matrix blood vessels