Neonatal Respiratory Distress (NRD):

  • RD in the newborn is usually due to one of 4 disease entities:
1.     Respiratory distress syndrome (RDS; hyaline membrane disease, HMD)

2.     Transient tachypnea of the newborn (TTN)

3.     Meconium aspiration

4.     Neonatal pneumonia

The most common complications of RDS are:

  • Pulmonary interstitial emphysema (PIE)
  • Persistent PDA
  • Bronchopulmonary dysplasia (BPD)

Neonatal Respiratory Distress:

Disease Lung Volume Opacities Time Course Complication
RDS:  Low Granular 4-6 days PIE, BPD, PDA
Transient tachypnea: High or normal Linear, streaky* < 48 hours None
Meconium aspiration:  Hyperinflation Coarse, patchy At birth PFC, ECMO
Neonatal pneumonia:  Anything Granular Variable  

*Ground-glass opacity at birth.

ECMO: extracorporeal membrane oxygenation; PFC : persistent fetal circulation;

RDS/ hyaline membrane disease (HMD):

Evolving Terminology:

  • The term hyaline membrane disease is now less commonly used in clinical practice to describe pulmonary surfactant insufficiency in infants.
  • Hyaline membranes are considered a byproduct, not the cause, of respiratory failure in neonates with immature lungs.
  • The term respiratory distress syndrome is currently used to denote surfactant deficiency and should not be used for other causes of respiratory distress.
  • In recognition of the underlying pathogenesis of the disease process, the alternative term surfactant deficiency disorder has been proposed.


  • RDS is caused by surfactant deficiency. Surfactant diminishes surface tension of expanding alveoli. As a result, acinar atelectasis and interstitial edema occur.
  • Hyaline membranes are formed by proteinaceous exudate.
  • Symptoms occur within 2 hours of life.

The incidence of RDS depends on the gestational age at birth:

Birth at Gestational Age (wk) Incidence (%)
27 50
31 16
34 5
36 1

Radiographic Features:

  • In most cases of RDS, the diagnosis is made clinically but may initially be made radiographically. The role of the radiologist is to assess serial chest films.

CXR signs of premature infants:

  • No subcutaneous fat
  • No humeral ossification center
  • Endotracheal tube present

Any opacity in a premature infant should be regarded as RDS until proven otherwise.

o   Lungs are opaque (ground-glass) or reticulogranular (hallmark).

o   Hypoaeration (atelectasis) leads to low lung volumes à bell-shaped thorax (if not intubated).

o   Bronchograms are often present.

o   Absence of consolidation or pleural effusions

o   In contrast to other causes of RDS in neonates, pleural effusions are uncommon.

o   Treatment with surfactant may result in asymmetric improvement

Treatment complication of RDS:

  • Persistent PDA : signs of congestive heart failure (CHF):
  • The ductus usually closes within 1 to 2 days after birth in response to the high Po2 content.
  • Air-trapping : PIE & acquired lobar emphysema
  • Diffuse opacities (whiteout) may be due to a variety of causes:
  • Atelectasis
  • Progression of RDS
  • Aspiration
  • Pulmonary hemorrhage
  • CHF
  • Superimposed pneumonia

Pulmonary interstitial emphysema (PIE):

  • PIE refers to àaccumulation of interstitial air in peribronchial & perivascular spaces.
  • Most common cause à +ve-pressure ventilation.


  • Pneumothorax
  • Pneumomediastinum
  • Pneumopericardium

Radiographic Features:

  • Tortuous linear lucencies radiate outward from the hilar regions.
  • The lucencies extend all the way to the periphery of the lung.
  • Lucencies do not change with respiration.

Bronchopulmonary dysplasia (BPD)

  • Caused by oxygen toxicity & barotrauma of respiratory therapy.
  • BPD is now uncommon in larger & more mature infants (gestational age > 30 weeks or weighing >1200 g at birth).

Definition of BPD & Diagnostic Criteria:

Diagnostic Criterion Gestational Age < 32 wk Gestational Age > 32 wk
Time point of assessment o   36 wk PMA* or

o   discharge to home, whichever comes first;

o   treatment with >21% oxygen for at least 28 days plus

o   >28 days but <56 days postnatal age or

o   Discharge to home, whichever comes first;

o   Treatment with >21% oxygen for at least 28 days plus

Mild BPD o   Breathing room air at 36 wk PMA or

o   discharge, whichever comes first

o   Breathing room air by 56 days postnatal age or

o   discharge, whichever comes first

Moderate BPD o   Need* for <30% oxygen at 36 wk PMA or

o   discharge, whichever comes first

o   Need* for <30% oxygen at 56 days postnatal age or

o   discharge, whichever comes first

Severe BPD o   Need* for ≥30% oxygen and/or positive pressure (PPV* or nasal CPAP) at 36 wk PMA or

o   discharge, whichever comes first

o   Need* for ≥30% oxygen and/or positive pressure (PPV or nasal CPAP) at 56 days postnatal age or

o   discharge, whichever comes first

*Using a physiologic test (pulse oximetry saturation range) to confirm the oxygen requirement.

  • BPD : bronchopulmonary dysplasia.
  • CPAP: continuous positive airway pressure.
  • PMA : postmenstrual age (gestational age at birth plus chronologic age).
  • PPV : positive-pressure ventilation.
  • There are 4 stages in the development; the progression of BPD àthrough all 4 stages is now rarely seen because of the awareness of this disease entity.
  • Stages of Bronchopulmonary Dysplasia:
Stage Time Pathology Imaging
1 o   < 4 days o   Mucosal necrosis o   Similar to RDS
2 o   1 week o   Necrosis, edema, exudate o   Diffuse opacities
3 o   2 weeks o   Bronchial metaplasia o   Bubbly lungs*
4 o   1 month o   Fibrosis o   Bubbly lungs*

*Bubbly lungs (honeycombing): rounded lucencies surrounded by linear densities; hyperaeration.

Prognosis of Stage 4:

  • Mortality, 40%
  • Minor handicaps, 30%
  • Abnormal pulmonary function tests in almost all in later life
  • Clinically normal by 3 years, 30%

Meconium aspiration syndrome:

  • Meconium (mucus, epithelial cells, bile, debris) à the stool that is evacuated within 12 hours after delivery.
  • In fetal distress, evacuation may occur into the amniotic fluid (up to 10% of deliveries).
  • However, in only 1% does this aspiration cause respiratory symptoms.
  • Only meconium aspirated to below the vocal cords is clinically significant.
  • Meconium aspiration sometimes clears in 3 to 5 days.
  • CXR nearly always returns to normal by 1 year of age.

Radiographic Features:

o   Patchy, bilateral opacities, may be “rope-like”

o   Atelectasis

o   Hyperinflated lungs

o   Pneumothorax, pneumomediastinum, 25%


  • Mortality (25%) from persistent fetal circulation

Neonatal pneumonia (NP):

  • Pathogenesis:

Trans-placental infection: ·        TORCH:

ü Pulmonary manifestation of TORCH is usually less severe than other manifestations.

Perineal flora: ·        Group B streptococci, enterococci, Escherichia coli:

ü Ascending infection

ü Premature rupture of membranes

ü Infection while passing through birth canal

Radiographic Features:

  • Patchy asymmetrical opacities in a term infant represent neonatal pneumonia until proven otherwise.
  • Hyperinflation

Transient tachypnea of the newborn (TTN):

  • TTN (wet lung syndrome) is a clinical diagnosis.
  • It is caused by a delayed resorption of intrauterine pulmonary liquids.
  • Normally, pulmonary fluids are cleared by:

Bronchial squeezing during delivery, 30%

Absorption, 30%: lymphatics, capillaries

Suction, 30%


  • Cesarean section, premature delivery, maternal sedation (no thoracic squeezing)
  • Hypoproteinemia, hypervolemia, erythrocythemia

Radiographic Features:

o   Fluid over-load àsimilar appearance as non-cardiogenic pulmonary edema.

o   Prominent vascular markings

o   Pleural effusion

o   Fluid in fissure

o   Alveolar edema

o   Lungs clear in 24 48 hours.

Extracorporeal membrane oxygenation (ECMO):

  • Technique of providing prolonged extracorporeal gas exchange.


  • Any severe respiratory failure with predicted mortality rates of > 80%.

Exclusion criteria for ECMO include:

  • < 34 weeks of age
  • >10 days of age
  • Serious intracranial hemorrhage
  • Patients who require epinephrine


  • Late neurologic sequelae; developmental delay, 50%
  • Intracranial hemorrhage, 10%
  • Pneumothorax, pneumomediastinum
  • Pulmonary hemorrhage (common)
  • Pleural effusions (common)
  • Catheter complications


IMAGING OF PNEUMONIA IN CHILDREN is very important for very doctor to know .

  • Childhood pneumonias are commonly caused by:

– Mycoplasma, 30% àlower in age group < 3 years.

– Viral, 65% àhigher in age group < 3 years)

– Bacterial, 5%

Viral pneumonia:


  • respiratory syncytial virus (RSV), parainfluenza

Radiographic Patterns of Viral Pneumonia:

Pattern Frequency Description

Common o   Normal CXR

o   Overaeration is only diagnostic clue

o   Commonly due to RSV

Bronchiolitis+parahilar, peribronchial opacities:

Most Common o   Dirty parahilar regions caused by:

–         Peribronchial cuffing (inflammation)

–         Hilar adenopathy


Common o   Disordered pattern with:

–         Atelectasis

–         Areas of hyperaeration

–         Parahilar+peribronchial opacities

Reticulonodular interstitial:

Rare o   Interstitial pattern
Hazy lungs:

Rare o   Diffuse increase in density


  • All types of bronchiolitis & bronchitis cause air trapping (over-aeration) with flattening of hemi-diaphragms.
  • RSV, Mycoplasma, & parainfluenza virus : the most common agents that cause radiographic abnormalities (in 10 30% of infected children).
  • Any virus may result in any of the 5 different radiographic patterns.

Bacterial pneumonia:

  • The following 3 pathogens are the most common:

– Pneumococcus (ages 1 to 3)

– Staphylococcus aureus (infancy)

– Haemophilus influenzae (late infancy)

Radiographic Features:

Consolidation: o   Alveolar exudate

o   Segmental consolidation

o   Lobar consolidation

Other findings: o   Effusions

o   Pneumatocele

Complications: o   Pneumothorax

o   Bronchiectasis (reversible)

o   Swyer-James syndrome:

– Acquired pulmonary hypoplasia.

-Radiographically by small, hyperlucent lungs + diminished vessels (focal emphysema).

o   Bronchiolitis obliterans

Round Pneumonia:

  • Usually age < 8 years
  • Pneumococcal pneumonia in early consolidative phase
  • Pneumonia appears round because of poorly developed collateral pathways (pores of Kohn & channels of Lambert).
  • With time the initially round pneumonia develops into a more typical consolidation.

Causes of recurrent Infections:

1-    Cystic fibrosis

2-    Recurrent aspirations

3-    Rare causes of recurrent infection:

o   Hypogammaglobulinemia (Bruton disease):  DDx clue : no adenoids or hilar LNs.

o   Hyperimmunoglobulinemia E (Buckley syndrome)

o   Kartagener syndrome.

o   Other immune-deficiencies

o   Bronchopulmonary foregut malformation


Aspiration pneumonia:

  • Results from inhalation of swallowed materials or gastric content.
  • Gastric acid damages capillaries causing acute pulmonary edema.
  • 2ry infection or acute respiratory distress syndrome (ARDS) may ensue.


aspiration due to :

Swallowing dysfunction:

(most common cause)

o   Anoxic birth injury (common)

o   Coma,

o   Anesthesia.

Obstruction: o   Esophageal atresia or stenosis.

o   Esophageal obstruction.

o   Gastroesophageal reflux (GER),

o   Hiatus hernia.

o   Gastric or duodenal obstruction.

Fistula: o   Tracheoesophageal fistula (TEF)

Radiographic Features:

o   Recurrent pneumonias : distribution:

– Aspiration in supine position: upper lobes, superior segments of lower lobes.

– Aspiration in upright position : both lower lobes

o   Segmental and subsegmental atelectasis

o   Interstitial fibrosis

o   Inflammatory thickening of bronchial walls

Sickle cell anemia:

  • Pulmonary manifestations : are the leading cause of death:
  • Pneumonia, acute chest syndrome, & pulmonary fibrosis.
  • Children with acute chest syndrome may present with one or multiple foci of consolidation, fever, chest pain, or cough.


  • Infection (higher incidence).
  • Fat emboli originating from infracting bone.
  • Pulmonary thrombosis.

Radiographic Findings

  • Consolidation
  • Pleural effusion
  • Fine reticular opacities (pulmonary fibrosis)
  • Large heart in severe anemia
  • H-shaped vertebral bodies
  • Osteonecrosis, bone infarct in visualized humeri


Congenital Pulmonary Abnormalities IMAGING

Congenital cystic adenoid malformation IMAGING IS VERY ESSENTIAL

Bronchopulmonary foregut malformation:

  • Arise from a supernumerary lung bud that develops below the normal lung bud.
  • Location and communication with GIT depend on when in embryonic life the bud develops.
  • Most malformations present clinically when they become infected (communication with GIT).

Overview of Bronchopulmonary Malformations:

Malformation Location

·        Intralobar



60% basilar, left

80% left or below diaphragm

Bronchogenic cyst Mediastinum, 85%; lung, 15%
CCAM All lobes
Congenital lobar emphysema LUL, 40%; RML, 35%; RUL, 20%

Pulmonary sequestration:

Clinical Findings:

  • Recurrent infection
  • Lung abscess
  • Bronchiectasis
  • Hemoptysis during childhood.


  • Non-functioning pulmonary tissue ànearly always posteromedial segments of lower lobes.
  • Systemic arterial supply à anomalous arteries from the aorta (less common branch of the celiac artery)
  • No connection to bronchial tree

Types of Pulmonary Sequestration:


Feature Intralobar Sequestration Extralobar Sequestration
Age ·        Older children, adults ·        Neonates
Pleura ·        Inside lung (intralobar) ·        Outside lung àextralobar, own pleura)
Forms ·        Airless (consolidation) and air-containing, cystic type ·        Always airless (pleural envelope) unless à communication with GIT
Venous return: ·        Pulmonary vein ·        Systemic: IVC, azygos, portal
Arterial supply: ·        Thoracic aorta > abdominal aorta
Associations: ·        In 10% of patients:

o   Skeletal anomalies, 5%

o   Foregut anomalies, 5%

o   Diaphragmatic anomalies

o   Other rare associations

·        In 65% of patients:

o   Diaphragmatic defect, 20%

o   Pulmonary hypoplasia, 25%

o   Bronchogenic cysts

o   Cardiac anomalies


Radiographic Features:

  • Large (>5 cm) mass near diaphragm
  • Air-fluid levels if infected
  • Surrounding pulmonary consolidation
  • Sequestration may communicate with GIT.

Bronchogenic cyst:

  • It Results from the abnormal budding of the tracheobronchial tree. Cysts contain respiratory epithelium.


  • Mediastinum, 85% àposterior > middle > anterior mediastinum)
  • Lung, 15%

Radiographic Features:

o   Well-defined round mass in subcarinal / parahilar region

o   Pulmonary cysts commonly located in medial 1/3 of lung

o   Initially no communication with tracheobronchial tree

o   Cysts are thin walled.

o   Cysts can be fluid or air filled.




Congenital cystic adenoid malformation (CCAM):

  • CCAM refers to a proliferation of polypoid glandular lung tissue without normal alveolar differentiation.
  • Respiratory distress occurs during first days of life.


surgical resection (sarcomatous degeneration has been described).



(Stocker types 1 & 2)

o   single cyst or multiple cysts > 5 mm confined to one hemi-thorax.

o    Better prognosis.

o    Common.


(Stocker type 3)

o   Homogeneous echogenic mass without discernible individual cysts.

o   Closely resembles pulmonary sequestration or intrathoracic bowel from a diaphragmatic hernia.

o   Less common.

Radiographic Features:

o   Multiple cystic pulmonary lesions of variable size

o   Air-fluid levels in cysts

o   Variable thickness of cyst wall



Congenital lobar emphysema:

  • Progressive overdistention of one or more pulmonary lobes but usually not the entire lung.
  • 10% of patients have congenital heart disease àpatent ductus arteriosus [PDA] & ventricular septal defect [VSD].


  • Idiopathicà 50%
  • Obstruction of airway with valve mechanismà 50%:
  • Bronchial cartilage deficiency or immaturity
  • Mucus
  • Web, stenosis
  • Extrinsic compression


Radiographic Features:

o   Hyperlucent lobe (hallmark)

o few days of life à alveolar opacification because there is no clearance of lung fluid through bronchi

o   May be asymptomatic in neonate but becomes symptomatic later in life

o   Use CT to àdifferentiate from bronchial obstruction

o   Distribution

§  LUL, 40%

§  RML, 35%

§  RUL, 20%

§  2 lobes affected, 5%


Pulmonary hypoplasia:

Types of Pulmonary Underdevelopment:

  • Agenesis: Complete absence of one or both lungs (airways, alveoli, & vessels).
  • Aplasia: Absence of lung except for a rudimentary bronchus that ends in a blind pouch.
  • Hypoplasia: decrease in number and size of airways and alveoli; hypoplastic PA.
  • Scimitar Syndrome (Hypogenetic Lung Syndrome, Pulmonary Venolobar Syndrome)

– A special form of a hypoplastic lung.

– The hypoplastic lung is àperfused from the aorta & drained by the IVC or portal vein.

– The anomalous vein has a resemblance to a Turkish scimitar (sword).

– Associations include:

   1) Accessory diaphragm, diaphragmatic hernia

   2) Bony abnormalitiesà hemivertebrae, rib notching, rib hypoplasia

   3) CHD: atrial septal defect (ASD), VSD, PDA, tetralogy of Fallot



  • Radiographic Features:
o   Small lung àmost commonly the right lung.

o   Retrosternal soft tissue density à hypoplastic collapsed lung.

o   Anomalous vein resembles a scimitar

o   Systemic arterial supply from aorta

o   Dextroposition of the heart àshift because of hypoplastic lung)


Congenital diaphragmatic hernia (CDH):


  • 1 in 2000 to 3000 births.
  • The mortality rate of isolated hernias is 60% (with postnatal surgery) and higher when other abnormalities are present.
  • Respiratory distress occurs in the neonatal period.
  • Associated abnormalities include:

Pulmonary hypoplasia (common)

CNS abnormalities:

Neural tube defects : spina bifida, encephalocele Anencephaly


Bochdalek’s hernias: Ø 90% of CDH à posterior:

o   75% are on the left, 25% on right

o   Right-sided hernias are more difficult to detect because of similar echogenicity of liver & lung.

o   Contents of hernia:

ü Stomach, 60%.

ü Colon, 55%.

ü Small intestine, 90%.

ü Spleen, 45%.

ü Liver, 50%.

ü Pancreas, 25%.

ü Kidney, 20%.

o   Malrotation of herniated bowel is very common.

Morgagni hernias: Ø 10% of CDH à anterior:

o   Most occur on right (heart prevents development on the left).

o   Most common hernia contents: omentum, colon

o   Accompanying anomalies common

Eventration: o   Due to relative absence of muscle in dome of diaphragm

o   Associated with:

ü Trisomies 13, 18, congenital CMV, rubella arthrogryposis multiplex, pulmonary hypoplasia

  • Radiographic Features:
o   Hemi-diaphragm not visualized

o   Multi-cystic mass in chest

o   Mass effect


Kartagener syndrome (immotile cilia syndrome):

  • Due to the deficiency of the dynein arms of cilia causing immotility of respiratory, auditory, & sperm cilia.

Radiographic Features:

o   Complete thoracic & abdominal situs inversus

o   Bronchiectasis

o   Sinus hypoplasia & mucosal thickening





Primary and secondary liver tumors are a common cause of morbidity and
mortality around the world. While curative therapies for some of these cancers
exist – hepatocellular carcinoma (HCC) can be treated with partial hepatectomy
or liver transplantation – many patients are ineligible for curative liver resection
due to the advanced stage of their cancers; furthermore, widespread implementation of liver transplantation is prevented by a shortage of donor organs.

The same is true for patients with metastatic colorectal or neuroendocrine tumors. Due to these
shortcomings, various palliative therapies have been advanced in the management
of hepatic neoplasms.

These include systemic chemotherapy, radiation therapy, and local and regional percutaneous modalities. The latter group comprises both ablative techniques (chemical and thermal), and the intra-arterial monotherapies.

Unlike healthy hepatocytes, which are supplied largely by the portal venous circulation, both primary and secondary liver tumors receive their vascular supply principally from the hepatic artery.

Thus, occlusion of the hepatic artery would be expected to lead to ischemic necrosis of tumor cells while selectively sparing the native liver. This principle has been exploited in the development of bland transarterial embolization (TAE) and transarterial chemoembolization (TACE).

In both of these approaches, the branches of the hepatic artery that supplies the tumor are occluded with embolic particles.

For chemoembolization, chemotherapeutic agents are added to the embolization mixture for delivery directly into the tumor.

In principle, chemoembolization targets liver lesions by a multifaceted attack. First, embolization of the vascular supply triggers localized tissue ischemia. Second, since the chemotherapeutic agents are delivered directly into the ischemic tumor, their local concentrations and tissue dwell times can be significantly increased [1–5].

Equally importantly, the ischemia induced by chemoembolization may counteract
drug resistance by causing metabolically active cell membrane pumps to fail, thereby
increasing intracellular retention of the chemotherapeutic agents [3,6].

Technique of chemoembolization

Pretreatment assessment

Preoperative evaluation for chemoembolization includes imaging, serology, and counseling. A patient should have either a definitive tissue diagnosis or a compelling clinical diagnosis, such as a markedly elevated serum alpha-fetoprotein (AFP) level associated with an HCC-like mass in a cirrhotic liver [3].

The patient must have a dynamic gadolinium-enhanced MRI or triple-phase CT of the liver.

The extrahepatic disease should be excluded by a bone scan and cross-sectional imaging of the chest, abdomen, and pelvis. Serological studies should include CBC, PT,
PTT, creatinine, liver function tests, and AFP levels. Due to the demanding nature
of this palliative treatment, patients should receive thorough counseling about
their regimens. In particular, this discussion should mention the common postembolization syndrome, the 5–7% risk of serious complications, and the 1–4%
chance of periprocedural mortality. The patient and family members should clearly
understand that chemoembolization is a palliative regimen with the potential for
significant discomfort, risk, and expense.

Embolization procedure

Patients need not be routinely admitted until the morning of their procedure, but they should be advised to fast overnight.

On the morning of the procedure, patients are hydrated with 0.9% NSS at 200–300 cm3 h−1. Prophylactic medications are administered intravenously, including antibiotics (cefazolin 1 g, metronidazole 500 mg) and antiemetics (odansetron 24 mg, decadron 10 mg, diphenhydramine
50 mg).

The evidence for antibiotic prophylaxis is not compelling except for patients without a functioning sphincter of Oddi (e.g., post-Whipple or biliary stent), and not all practitioners administer them routinely.

The patient is sedated, prepped, and draped. Before any embolization is performed, diagnostic angiography of the celiac and superior mesenteric arteries is performed to determine the arterial supply to the liver and to confirm the patency of the portal vein.

Because non-target embolization of the gut or gallbladder is a significant cause of morbidity, the origins of the right gastric, supraduodenal, cystic, and other potential extrahepatic arteries must be clearly identified [7].

Once the arterial anatomy has been mapped, a catheter is advanced super selectively into a lobar or segmental branch of the right or left hepatic artery.

Typically, the lobe with the greatest tumor burden is embolized first, with subsequent treatments
targeting the contralateral side.

The chemo-embolic mixture is injected into the segmental artery until nearly complete stasis of blood flow is achieved. Intra-arterial lidocaine (30mg boluses, up to a total of 200mg) and intravenous fentanyl and midazolam should be used to alleviate discomfort during the procedure

Post-procedure care

Antibiotics, antiemetics, and intravenous hydration are continued after the embolization (3L of 0.9% NSS over 24h).

The common post-embolization syndrome must be managed aggressively with palliation of pain, nausea, and fever.

Specifically, narcotics, perchlorpromazine, odansetron, decadron, and acetaminophen should
be liberally administered.

The patient can be discharged with the resumption of oral intake and the cessation of parenteral narcotic therapy.

Typically, half of the patients are discharged on the first postoperative day, while most of the remainder leave after 2 days [3].

Oral home medications include antibiotics (5 days), antiemetics, and narcotics when needed. Laboratory studies are repeated in 3 weeks to ensure the normalization of liver enzymes. Depending upon the tumor burden and arterial anatomy, a cycle of chemoembolization will include between one and four procedures. Thus, the patient will return for the next embolization in about 4 weeks; treatments alternate between the left and right lobes, as well as any parasitized

Following completion of the treatment cycle, responseis assessed with repeat cross-sectional imaging and tumor marker serology. If the response has been inadequate, further rounds of chemoembolization can be administered.

Embolic materials

Choice of embolic particles

Variousembolicparticlesareavailableon the market.Thoughtheydifferinstructure, no agent has been conclusively demonstrated to be superior to any other.

The first embolic particle to be developed, the gelatin sponge (Gelfoam; Upjohn, Kalamazoo,
MI) has been used in the majority (71%) of chemoembolization trials [8].

Historically it has been available in various formulations – particles, cubes, pellet, powder,
fragments, and strips – the size of the particles determining how distal the embolization would take place [8].

Notably, use of the powder formulation has been discontinued because of an unfavorable side-effect profile. In all of these formulations, the gelatin causes only temporary devascularization, allowing recanalization to take place in about 2 weeks.

A similar temporary occlusion agent has also been developed from cross-linked bovine collagen (Angiostat; Regional Therapeutics, Pacific Palisades, CA).

More permanent embolic particles include polyvinyl alcohol (PVA; several vendors) and trisacryl gelatin spheres (Embosphere microspheres; BioSphere Medical, Rockland, MA).

Both of these come in a range of sizes (40–1000 μm), allowing the clinician to select the level of embolization. Less commonly, reports exist of the use of steel coils, starch microspheres, autologous blood clots, and even the herb Bletilla striata to embolize the hepatic artery [8]. Recent studies have begun to assess the feasibility of drug-eluting beads, a new approach that may
offer an improved pharmacokinetic profile compared to traditional chemoembolization [9].

Choice of chemotherapeutic agents

Several chemotherapeutic agents are available for chemoembolization, for use as monotherapy or in combination.

Doxorubicin and cisplatin are the most commonly used single agents [8]. Most reports from Europe and Asia use doxorubicin or epirubicin, whether alone or in combination with mitomycin-C.

Centers in the United States prefer cisplatin monotherapy or a combination of 100–150 mg
cisplatin, 40–60 mg doxorubicin, and 10–20 mg of mitomycin-C (CAM).

Although at least one case series suggested that cisplatin may confer a survival benefit over doxorubicin [10], no randomized trial has shown the superiority of any of these agents [8].

In fact, apparent differences between these agents may be driven by the ability to administer more embolizations in patients treated with cisplatin [10].In any case, no clear consensus has yet emerged for the superiority of any chemotherapeutic agent or combination.

Choice of emulsion: transarterial oily chemoembolization

The observation that iodized poppyseed oil (Ethiodol; Savage Laboratories, Melville, NY) selectively accumulated in hepatocellular carcinomas led to the incorporation of lipiodol (Guerbet, Aulnay-sous-Bois, France) into chemo-embolic regimens.

This technique, now known as transarterial oily chemoembolization, has the potential to more accurately target the chemotherapeutic drugs.

When iodized oil is injected into the hepatic artery, it travels to the distal arterioles, where it shunts
into the terminal portal venules at the pre-sinusoidal level.

From there, the oil slowly moves into the sinusoids and becomes trapped in the tumor vessels. In
theory, any chemotherapeutic agents suspended in this oily phase would thus be targeted to the liver.

Studies in rabbits [1] and humans [11] have demonstrated that the combination of oily chemoembolization with a particulate agent is superior to oily chemoembolization alone [11].

Such an effect is probably caused by the fact that most chemotherapeutic drugs remain in the aqueous phase of the emulsion. When chemoembolization is performed exclusively with an oily emulsion, continuous arterial inflow elutes out the aqueous drug, even though the oil itself remains
suspended in the liver.

Particulate-only chemoembolization causes relatively proximal occlusion, allowing continued inflow into the tumor from the portal venules, again diluting the chemotherapeutic drugs and resulting in reduced ischemia.

Thus the combination of oil and particles allows the occlusion of both distal arterioles and
portal venules – effectively sandwiching the drugs and maintaining tumor ischemia. Additionally, since this technique increases hepatic drug retention, it has the benefit of reduced systemic toxicity

Efficacy of chemoembolization

Historically, the efficacy of the transarterial embolo- therapies has been somewhat controversial. For example, early studies were inconclusive about the efficacy of chemoembolization in the treatment of hepatocellular carcinoma.

Nevertheless, evidence has emerged during this decade from several randomized trials that a role
exists for chemoembolization in the management of HCC.

Though the evidence is slightly less clear for the management of colorectal and neuroendocrine metastases, chemoembolization has nonetheless become established as an important palliative
therapy in the oncologist’s armamentarium.

Role of chemoembolization in unresectable hepatocellular carcinoma

Initial retrospective cohort studies in the Orient, Europe, and the United States suggested that chemoembolization was effective in the palliation of unresectable  HCC: rates of tumor necrosis ranged from 60% to 100% [3].

Cumulative probability of survival in these studies was 54–88% at one year, 33–64% at 2 years, and 18–51% at 3 years, with the best results obtained by repeated embolizations with a combination
of iodized oil, gelfoam, and chemotherapeutic drugs.

Survival varied directly with oil uptake and retention, and inversely with tumor volume, stage, and Child class.

Nevertheless, early randomized controlled trials failed to demonstrate a survival benefit for patients with unresectable HCC. Chemoembolization with gelfoam/doxorubicin (n = 42 patients) [12], lipiodol/5-epidoxorubicin (n = 50) [13], and gelfoam/lipiodol (n = 96) [14] did not increase survival compared to control subjects who received only palliation of pain.

Interestingly, however, two of these studies [13,14] did demonstrate non-significant trends towards increased survival from chemoembolization, suggesting that they may have been underpowered to
answer this question.

Since that time, however, evidence has begun to mount in favor of chemoembolization in the management of unresectable HCC. In 2002, two randomized studies demonstrated a clear survival benefit from chemoembolization.

In the first study, of 80 patients from Hong Kong, survival in patients treated with cisplatin/
lipiodol/gelatin-sponge chemoembolization was 57%, 31%, and 26% at 1, 2, and 3
years, compared with 32%, 11%, and 3% in those receiving conservative management [15].

In the second study, of 112 patients from Barcelona, 1-year and 2-year survival was 82% and 63% in patients receiving doxorubicin/gelatin-sponge chemoembolization, 75% and 50% in those treated only with gelatin-sponge bland TAE, and 63% and 27% for those receiving conservative management [16].

The authors hypothesized that the results of these trials may have differed from earlier studies because of differences in patient demographics and tumor background [15].

In particular, the studies from Hong Kong and Barcelona were conducted in patients whose HCC arose in the presence of viral hepatitis in 80% of cases, compared to a higher preponderance of alcohol-induced liver disease in the earlier French studies [14].

The tolerance of patients with alcohol-induced cirrhosis for chemoembolization may have been lower than that of those with viral hepatitis [15].

A recent meta-analysis of 175 cohort studies and randomized controlled trials (RCTs) of chemoembolization in the treatment of unresectable HCC concluded that chemoembolization does provide a significant survival benefit when compared to conservative therapy (631 patients in nine RCTs, p = 0.0025) [8].

Interestingly, a sub-analysis of studies comparing chemoembolization to bland TAE (412 patients,
3 RCTs) failed to demonstrate a survival benefit for either methodology, though
chemoembolization trended towards an improved outcome (p = 0.052).

Lastly, chronologically later studies demonstrated improved outcomes in comparison to
earlier trials [8]; this finding could be partially explained as a result of the improving
proficiency of clinicians.

In summary, evidence indicates that patients with unresectable hepatocellular carcinomas benefit from transarterial chemoembolization, though the benefit of specific choices of chemoembolic combinations remains unproven.

Disagreements between early randomized trials of chemoembolization and newer studies may have
resulted from differences in the patient populations or from the improving proficiency of clinicians.

Role of chemoembolization as a neoadjuvant therapy in HCC

While chemoembolization has become well established as a palliative therapy in the management of unresectable hepatocellular carcinomas, its role as a neoadjuvant therapy for HCC has been more controversial.

In theory, chemoembolization could prevent tumor growth in patients awaiting orthotopic liver transplants, thus decreasing attrition from the transplant waiting list due to tumor progression: as
such, chemoembolization could serve as a bridge to transplantation.

Alternatively, preoperative chemoembolization might be expected to improve outcomes after
partial hepatic resection, and might even convert some unresectable lesions into resectable tumors.

Early support for the role of chemoembolization as a neoadjuvant came from retrospective cohort studies showing that neoadjuvant chemoembolization could induce a reduction in tumor size and thus a downstaging of HCC before hepatic resection or liver transplantation [17,18].

Similarly, while the 6-month drop-out rate from the transplant waiting list is typically between 23% and 46% [19], those patients who receive neoadjuvant chemoembolization have been reported to have a drop-out rate of only 15% [20].

Nevertheless, while such early studies were encouraging, it is unclear whether their conclusions can translate to improved outcomes.

For example, the aforementioned study [18] failed to demonstrate a statistically significant improvement in patient survival, thus calling into question the clinical relevance of the findings.

In fact, the results of later retrospective cohort studies of chemoembolization as a bridge to transplant have been contradictory [19,21], and no RCT has yet been conducted on the issue.

In fact, a recent systematic evidence-based review of the available studies concluded
that at present there is insufficient evidence to claim that chemoembolization could be used as a bridge to transplant, that it would decrease transplant waiting list drop-out rates, or that preoperative chemoembolization could improve posttransplant survival in patients with HCC [19].

Perhaps the most relevant confounding variable is wait times for listed patients. In regions with short wait times (< 3 months), the drop-out rate is low, so neoadjuvant therapy is not

When wait times are very long, approaching the median time to-progression after image-guided therapy, the benefit from neoadjuvant stabilization is lost.

The wide geographic and temporal variation in wait times makes analysis of the benefit of neoadjuvant therapy from prior literature difficult.

Nevertheless, in the absence of any randomized trials, chemoembolization continues to be used in a non-palliative role in the pre-transplant setting, largely because it at least has not been shown to increase postoperative complications in transplant patients [22].

The effectiveness of preoperative chemoembolization in patients receiving hepatic resection has been similarly controversial. In theory, the combination of chemoembolization with curative surgery might be expected to improve patient outcomes.

Moreover, since chemoembolization has been shown to be capable of downstaging tumors [18], it might be able to convert some patients with unresectable lesions into surgical candidates. Indeed, some studies have shown just this, with preoperative chemoembolization significantly improving the 5-year survival of patients undergoing hepatic resection from 19% to 39% [23].

These findings have been further supported by a large retrospective cohort analysis

However, other prospective trials have failed to show a benefit from neoadjuvant chemoembolization before hepatic resection; one prospective study actually demonstrated worsened actuarial survival in chemoembolized patients due to the delay in curative resection [25].

A review of various adjuvant and neoadjuvant therapies in HCC has concluded that there is insufficient evidence to claim that neoadjuvant chemoembolization improves patient survival before resection [26].

Still, in the absence of definitive randomized controlled trials, the issue remains unresolved.

In summary, the role of chemoembolization as a neoadjuvant before liver transplantation or hepatic resection has been rather controversial.

Despite positive findings from some studies, the preponderance of evidence has not yet supported
such an indication. In fact, where the administration of chemoembolization may delay a definitive therapy, chemoembolization may actually worsen patient survival [25].

Clearly, randomized controlled studies are needed to further clarify these questions.

Toxicity of Chemoembolization

Despite having a more favorable side-effect profile than conventional chemotherapy, chemoembolization is not free of complications.

Thirty-day mortality ranges from 1% to 4%; chemoembolization in the treatment of HCC had a median mortality of 2.4% in a recent meta-analysis of 2858 patients [8].

Severe complications of chemoembolization occur in 5–7% of subjects, though these rates can be
reduced to 3–4% when patients are properly selected.

Most patients suffer from a self-limited post-embolization syndrome. Major complications of chemoembolization include hepatic insufficiency, abscesses, ischemic complications (cholecystitis,
bile duct necrosis, perforation of the alimentary tract), and renal dysfunction.

Less commonly, chemoembolization can also lead to tumor rupture, occlusion of the hepatic artery, and clinically significant pancreatitis.

Post-embolization syndrome

The majority of patients (40–86%) [14,38] suffer from a condition termed post-embolization syndrome (PES).

This is generally characterized by fever (74% of patients), abdominal pain (45.2%), nausea/emesis (58.9%), and a transaminitis (54%) [39].

In most cases PES is self-limited, though its palliation does necessitate hospitalization. On average, patients defervesce within 3 days, their nausea and pain can be medically managed, and their hepatic function gradually returns to normal [39].

Though previously thought to be indicative of tumor necrosis and thus a successful treatment, neither the presence nor the severity of PES has been shown to correlate to positive patient outcomes [38].

While reliable clinical predictors of the severity of PES have not yet been identified,PES does trend towards a more indolent course when embolization of the gall bladder is avoided, and when the patient is receiving repeat embolization to previously treated territory [7].

Major complications

Acute irreversible hepatic decompensation has been reported to occur in 3% of patients [8,39]. It should be distinguished from the transient and self-limited transaminitis that occurs with post-embolization syndrome.

Irreversible decompensation is more common with the use of high doses of cisplatin and poor
pretreatment hepatic function (high bilirubin, prolonged PT, and advanced cirrhosis) [39].

Abscess formation affects between 0.2% and 2.5% [40,43] of patients receiving chemoembolization.

The majority of these infections occur in the liver, though 0.4% of patients may suffer from a splenic abscess [40].

While their proximate cause is an infectious process, their formation is ultimately permitted by local ischemic necrosis.

Abscesses present with localized pain, fever, and leukocytosis,and can be definitively diagnosed by ultrasound or CT [40].

The likelihood of abscess formation has been strongly linked to a history of a Whipple procedure:
the presence of a bilioenteric anastomosis increases the incidence of a hepatic abscess by an odds ratio of 894 [41].

Attempts at prophylaxis against the formation of abscesses have led many clinicians to treat patients with broadspectrum antibiotics peri- and postoperatively [8]; others have even advocated
the addition of antibiotics to the embolic mixture.

However, a recent prospective cohort study from Germany casts doubt on these practices: patients who  did not receive treatment with antibiotics had no more infections or other complications than those who received 3 days of intravenous and 7 days of oral broad-spectrum antibiotics [42].

Severe ischemic complications, other than abscesses, have been reported to occur in 2.1% of patients receiving chemoembolization: these consist of ischemic cholecystitis (1.1%), bile duct necrosis (1.1%) [40], and perforation of the duo denum (0.05%) [43].

However, several other studies have quoted the incidence of gastroduodenal erosions and ulcerations to be significantly higher: one retrospective analysis of 280 cases demonstrated an endoscopy-proven incidence of 5.3% [44].

Since such lesions can result from the reflux of embolic material into the gastric circulation, the importance of meticulous attention to anatomic variants and adherence to selective or superselective embolization is the primary safeguard against this possibility [44].

Alternatively, at least some of these lesions could be the result of stress ulceration. Similarly, embolization distal to the cystic artery is the primary way of avoiding ischemic cholecystitis [40].

Nevertheless, since chemoembolization purposefully causes tissue ischemia, some damage to structures that are dependent on the hepatic artery is unavoidable (e.g., the intrahepatic bile

Renal failure has also been documented as a complication of chemoembolization, though its reported incidence varies between 0.05% [43] and 13%, averaging 1.8% in the aforementioned meta-analysis [8].

A prospective cohort study revealed an incidence of 8.6%, with 2.9% developing irreversible renal impairment [45].

Independent risk factors for the development of acute renal failure are the number of chemoembolization sessions, high Child–Pugh class, and a severe course of post-embolization syndrome; irreversible renal dysfunction was predicted only by the presence of diabetes [45].

The proximate causes of such kidney damage may be
the use of arterial contrast agents, the nephrotoxicity of the chemotherapeutic drugs, and inflammatory factors released from tumor necrosis [8,45].

The less common complications of chemoembolization include tumor rupture, occlusion of the hepatic artery, and clinically significant pancreatitis.

Spontaneous rupture of the treated tumor occurs in 0.15% of patients, most often after the
embolization of a large neoplasm [43].

Occlusion of the hepatic artery is a complication of repeated embolizations, occurring in 2% of patients following their second or third round of chemoembolization [43].

Though clinically significant pancreatitis is generally considered a rare complication – Roullet et al. report an incidence of 1.7% [46] – subclinical elevations in pancreatic enzymes may occur in as many as 15.2% of patients [47].

Patient selection

The likelihood of suffering severe side effects from chemoembolization is attenuated by both meticulous technique and proper patient selection. In principle, patients must be selected to include only those who will both benefit and tolerate the embolization procedure.

Selecting patients for optimum efficacy

Patients with multiple or unresectable lesions located exclusively or predominantly in the liver are ideal candidates for chemoembolization.

Since liver embolization only targets intrahepatic lesions, patients whose hepatic tumor burden is the primary driver of their symptoms and survival are the most likely to benefit from chemoembolization.

Nevertheless, the presence of some extrahepatic disease is not an absolute contraindication to chemoembolization; some patients whose metastatic disease is minimal or indolent may still be candidates for this therapy.

Selecting patients for optimum tolerability

The fundamental principle underlying the intra-arterial embolo-therapies is the differential blood supply of the hepatic neoplasms (supplied via the hepatic artery) and hepatocytes (supplied via the portal vein). Thus, if the native hepatocytes were to become more dependent on the blood flow from the hepatic artery,embolization of this vessel would be expected to lead to increased side effects.

This has in fact been demonstrated. Conditions that predispose the healthy liver to injury by increasing the relative contribution of blood from the arterial circulation include portal vein thrombi and superimposed liver disease.

Thus, occlusion of the portal vein is a relative contraindication to chemoembolization, though small
case series suggest that patients with the significant collateral flow can still be embolized
safely [48].

Patients with significant liver disease, such as those of Child-Pugh class C, with tumor replacing > 50% of liver [49], alpha-fetoprotein > 400 U L−1 [49], lactate dehydrogenase > 425 IU L−1, aspartate aminotransferase > 100 IU L−1, or total bilirubin ≥ 2 mg dL−1, are also at increased risk. Severe liver disease, as indicated by hepatic encephalopathy or jaundice, is an absolute contraindication to embolization.

Biliary pathology is another relative contraindication. Biliary obstruction predisposes patients to biliary necrosis even in the absence of hyperbilirubinemia.

As discussed previously, a surgical biliary anastomosis or stent virtually guarantees the development of a hepatic abscess, at least in the absence of prophylactic antibiotics [41].

Last, since the chemoembolization procedure must include angiography, patients with contraindications to this procedure cannot be embolized. All of the contraindications for chemoembolization also apply to bland embolization.

New developments in chemoembolization technology

The latest generation of embolic particles are polyvinyl alcohol polymeric beads specifically designed to load chemotherapeutic drugs and elute them over time into the tumor tissue following embolization.

Preclinical bench-top and animal studies have confirmed the ability of these drug-eluting beads to provide enhanced local drug delivery over a prolonged period with minimal systemic exposure

Phase I/II clinical trials for hepatoma in Europe and Asia have shown promising 1-year and 2-year survivals in the 85–90% range, but a disturbing incidence of major complications at around 10%, with a surprising frequency of hepatic abscess [52,53].

Randomized trials against conventional oily chemoembolization have not been completed. These beads are available as bland embolics in the USA and can be loaded with one or more drugs, but such off-label use is discouraged until their safety and efficacy is established in clinical trials, particularly given their high cost.


Transarterial chemoembolization is a powerful and well-established tool in the palliative management of both primary and secondary liver tumors.

While future randomized trials are still needed to unequivocally prove the survival benefits of
chemoembolization in some cancers, its effects on the management of symptoms have been clearly demonstrated.

When performed with meticulous technique, chemoembolization can be efficacious while still maintaining a side-effect profile superior to that of conventional therapies.

Though patient selection remains crucial, the transarterial embolotherapies can be offered to many more patients than traditional hepatic resection or transplantation.

Therefore, familiarity with chemoembolization is essential for any clinician involved in the care of patients with primary or secondary liver tumors.


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Transarterial chemoembolization 91
High-intensity focused ultrasound (HIFU)
treatment of liver cancer




Upper Airway:


  • Inspiratory stridor : is the most common indication for radiographic upper airway evaluation.
  • The main role of imaging is to identify conditions that need to be treated emergently & /or surgically (e.g., epiglottitis, foreign bodies).
  • Technique:
  1. Physician capable of emergency airway intervention should accompany child
  2. Obtain 3 films:

– Lateral neck: full inspiration, neck extended

– Anteroposterior (AP) and lateral chest: full inspiration, include upper airway.


  1. Fluoroscope the neck if radiographs are suboptimal or equivocal
  2. Primary diagnostic considerations:
  • Infection : epiglottitis, croup, abscess.
  • Foreign body : airway or pharyngo-esophageal.
  • Masses : lymphadenopathy, neoplasms.
  • Congenital abnormalities : webs, malacia
  1. If upper airway is normal, consider:
  • Pulmonary causes : foreign body, bronchiolitis.
  • Mediastinal causes: vascular rings, slings.
  • Congenital heart disease (CHD)


Normal appearance:

  • 3 anatomic regions:

– Supra-glottic region

– Glottic region : ventricle & true cords

– Sub-glottic region

  • Epiglottis & aryepiglottic folds are thin structures.
  • Glottic shoulders are seen on AP view.
  • Adenoids are visible at 3 to 6 months after birth.
  • Normal retropharyngeal soft tissue thickness (C1 C4) = three-fourths vertebral body width.


  • A common cause of stridor in the 1st year of life.
  • Immature laryngeal cartilage leads to supra-glottic collapse during inspiration.
  • Stridor improves with activity & is relieved by prone positioning or neck extension.
  • Self-limited course.
  • Diagnosis is established by fluoroscopy àlaryngeal collapse with inspiration.


  • Collapse of trachea with expiration.
  • May be focal or diffuse.
  • Focal type is usually Secondary to congenital anomalies that impress on the trachea, such as a vascular ring.



  • Most common in the larynx.

Tracheal stenosis:

  • Diffuse hypoplasia, 30%
  • Focal ring-like stenosis, 50%
  • Funnel-like stenosis, 20%

Subglottic stenosis:

  • Fixed narrowing at level of cricoid. Failure of laryngeal recanalization in utero.


  • Life-threatening bacterial infection of the upper airway.
  • Most commonly caused by Haemophilus influenzae.
  • Age: 3 to 6 years (older age group than with croup).
  • ttt is with àprophylactic intubation for 24 48 hours & antibiotics.
  • Clinical Findings




Sore throat

  • Radiographic Features:

Thickened aryepiglottic folds (hallmark)

Key radiographic view: lateral neck

Thickened epiglottis

Subglottic narrowing due to edema, 25%: indistinguishable from croup on AP view

Distention of hypopharynx


  • Pearls:
  • Other causes of enlarged epiglottis or aryepiglottic folds:

o   Caustic ingestion

o   Hereditary angioneurotic edema

o   Omega-shaped epiglottis : normal variant with normal aryepiglottic folds.

o   Stevens-Johnson syndrome


  • Sub-glottic laryngotracheobronchitis.
  • Most commonly caused by parainfluenza virus.
  • Age: 6 months to 3 years (younger age group than epiglottitis).
  • Clinical Findings:

Barking cough

Upper respiratory tract infection


  • Radiographic Features:

Subglottic narrowing: inverted “V” or “steeple sign”.

Key view: AP view

Lateral view should be obtained to exclude à

Steeple sign : loss of subglottic shoulders.

  • Pearls:

Membranous croup:

Uncommon infection of bacterial origin Staphylococcus aureus.

Purulent membranes in subglottic trachea.

Epiglottitis may mimic croup on AP view.


Retropharyngeal abscess:

  • Typically due to the extension of a suppurative bacterial lymphadenitis, most commonly S. aureus, group B streptococci, oral flora.
  • Age  < 1 year.
  • Other causes include foreign body perforation and trauma.
  • Clinical Findings


Stiff neck


Stridor (uncommon)

Most cases present as àcellulitis rather than a true abscess.

  • Radiographic Features:
o   Plain film findings : usually nonspecific.

o   Widened retropharyngeal space : most common finding

o   Air in soft tissues is specific for abscess.

o   Straightened cervical lordosis

o   CT is helpful to define superior & inferior mediastinal extent.

  • Main DDs:

Retropharyngeal hematoma

Neoplasm àe., rhabdomyosarcoma.


Tonsillar hypertrophy:

  • The tonsils consist of lymphoid tissue that encircles the pharynx.
  • 3 groups:

Pharyngeal tonsil (adenoids).

Palatine tonsil.

Lingual tonsil.

  • Tonsils enlarge secondary to infection and may obstruct nasopharynx & /or eustachian tubes.
  • Rarely, bacterial pharyngitis can lead to àa tonsillar abscess (quinsy abscess), which requires drainage.
  • Specific causes include:


o   Mononucleosis (Epstein-Barr virus)

o   Coxsackievirus (herpangina, hand-foot-mouth disease)

o   Adenovirus (pharyngoconjunctival fever)

o   Measles prodrome (rubeola)

o   Beta-Hemolytic Streptococcus (quinsy abscess)

  • Radiographic Features:
o   Mass in posterior nasopharynx (enlarged adenoids)

o   Mass near end of uvula (palatine tonsils)

o   CT is useful to determine the presence of a tonsillar abscess.


Airway foreign body (FB):

  • Common cause of respiratory distress.
  • Age à 6 months to 4 years.
  • Acute aspiration results in cough, stridor, wheezing; chronic FB causes à hemoptysis or recurrent pneumonia.
  • Location à right bronchi > left bronchi > larynx, trachea.
  • Radiographic Features:
Bronchial FB: o   Unilateral air tapping causing hyperlucent lung à 90%

o   Expiratory film or lateral decubitus àmakes air trapping more apparent.

o   Atelectasis is uncommon, 10%

o   Only 10% of FBs are radio-opaque.

o   Chest fluoroscopy or CT should be performed if plain film findings are equivocal.

Tracheal FB:


o   FB usually àlodges in sagittal plane

o   CXR is usually ànormal.




  • The ratio of thymus to body weight â with age.
  • Thymus is routinely identified on CXR from birth to 2 years of age.
  • Size & shape of the thymus are highly variable from person to person.

Common mediastinal tumors:

Anterior: o   Thymic hyperplasia & thymic variations in shape & size (most common)

o   Teratoma

o   T-cell lymphoma

o   Cystic hygroma

o   Thymomas are extremely rare.

Middle: o   Adenopathy (leukemia, lymphoma, TB)

o   Bronchopulmonary foregut malformation

Posterior: o   Neuroblastoma

o   Ganglioneuroma

o   Neurofibromatosis

o   Neurenteric cysts

o   Meningoceles


  • Any pediatric anterior mediastinal mass is considered thymus until proven otherwise.
  • Posterior mediastinal masses are the most common abnormal chest masses in infants

If you want to view Real Case Imaging of each disease , this link will be very helpful :




IMAGING ANATOMY OF PHARYNX & LARYNX is essential to understand subsequent pathology,  The upper aerodigestive tract consists of the pharynx and the larynx. The larynx connects pharynx and trachea.

The pharynx is divided into:

Nasopharynx: extends to inferior portion of  soft palate
Oropharynx: extends from soft palate to hyoid bone
Hypopharynx (laryngeal part of the pharynx): contains pyriform sinuses and posterior pharynx.

The larynx contains:

• The laryngeal surface of epiglottis.                                                                                          • Aryepiglottic folds
• Arytenoid cartilage
• False cords
• True cords (glottis is the space between vocal cords)
• Subglottic larynx

Para-pharyngeal Space    (Fig. 1)

  • it’s Potential space filled with loose connective tissue.
  • A pyramidal Space , with the apex directed toward the lesser cornua of the hyoid bone and the base toward the skull base.
  • It Extends from skull base to mid-oropharynx.
    Lateral: mandible, medial pterygoid muscle
    Medial: superior constrictor muscles of pharynx, tensor and levator veli palatini
    Anterior: buccinator muscle, pterygoid, mandible
    Posterior: carotid sheath.

FIG (1)
  • CONTENTS(Fig. 2)

           • Anterior (prestyloid) compartment : – Internal maxillary artery  – Interior alveolar, lingual, auriculotemporal nerves.

           • Posterior (retrostyloid) compartment:   – ICA, internal jugular vein (IJV) -CNs IX, X, XII -Cervical sympathetic chain lymph nodes.

        • Medial (retropharyngeal) compartment:  Lymph nodes (Rouvière)

FIG (2)
  • Lymphatics (Fig. 3)
    The parapharyngeal space has abundant lymph node groups.
    Lateral pharyngeal node (Rouvière)
    Deep cervical nodes
    Internal jugular chain, including jugulodigastric node
    • Chain of spinal accessory nerve
    • Chain of transverse cervical artery

FIG (3)

Paraganglia (Fig. 4)

Cells of neuroectodermal origin that are sensitive to changes in oxygen and CO2.


• Carotid body (at carotid bifurcation)
• Vagal bodies
Neoplastic transformation of the jugular bulb ganglion produces the glomus jugulare.

FIG (4)

Fluoroscopic Vocal Cord examination (Fig. 5)

Occasionallyperformedtoevaluatethesubglotticregion (Valsalva maneuver), invisible by laryngoscopy.
• Phonation of “E” during expiration: adducts cords.

• Phonation of “reversed E” during inspiration; distends laryngeal ventricles
• Puffed cheeks (modified Valsalva): distends pyriform
• Valsalva: distends subglottic region
• Inspiration: abducts cords.

FIG (5)

Nodal Stations (Fig. 6)

• IA: between anterior margins of the anterior bellies of the digastric muscles, above the
hyoid bone and below the mylohyoid muscle (submental)
• IB: below mylohyoid muscle, above hyoid bone, posterior to anterior belly of digastric muscle,
and anterior to a line drawn tangential to the posterior surface of the submandibular gland
Levels II, III, IV: internal jugular nodes       II: (jugulodigastric) from skull base to lower body of the hyoid bone, through posterior edge of the sternocleidomastoid muscle and posterior edge of the submandibular gland.
Note: A node medial to the carotid artery is classified as a retropharyngeal node.
III: hyoid bone to cricoid cartilage
IV: cricoid to clavicle
Level V: skull base to clavicle, between anterior edge of trapezius muscle and posterior edge of
sternocleidomastoid muscle.

• Level VI: visceral nodes; from hyoid bone, top of manubrium, and between common carotid arteries on each side
• Level VII: caudal to top of the manubrium in superior mediastinum (superior mediastinal

FIG (6)

Pathologic Adenopathy Size Criteria:

Neck lymphadenopathy by size has poor specificity, and no universal standard exists for determination of adenopathy. Nonetheless, two methods are commonly used:
• Long axis: 15mm in levels I and II, 10mm elsewhere
• Short axis: 11mm in level II, 10mm elsewhere Retropharyngeal nodes should not exceed 8mm
(long) or 5mm (short).

Emerging technologies such as MRI lymph node imaging with iron nanoparticles or PET may prove to be more specific and sensitive.


THANKS TO PROF.DR. Ralph Weissleder, MD, PhD