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.


1. Konno T. Targeting cancer chemotherapeutic agents by use of lipiodol contrast medium. Cancer
1990; 66: 1897–903.
2. Egawa H, Maki A, Mori K, et al. Effects of intraarterial chemotherapy with a new lipophilic
anticancer agent, estradiol-chlorambucil (KM2210), dissolved in lipiodol on experimental liver
tumor in rats. J Surg Oncol 1990; 44: 109–14.
3. Ramsey DE, Kernagis LY, Soulen MC, Geschwind JF. Chemoembolization of hepatocellular
carcinoma. J Vasc Interv Radiol 2002; 13: S211–21.
4. Nakamura H, Hashimoto T, Oi H, Sawada S. Transcatheter oily chemoembolization of hepato
cellular carcinoma. Radiology 1989; 170: 783–6.
5. Sasaki Y, Imaoka S, Kasugai H, et al. A new approach to chemoembolization therapy for
hepatoma using ethiodized oil, cisplatin, and gelatin sponge. Cancer 1987; 60: 1194–203.
6. Kruskal JB, Hlatky L, Hahnfeldt P, et al. In-vivo and in-vitro analysis of the effectiveness of doxorubicin
combined with temporary arterial occlusion in liver tumors. J Vasc Interv Radiol 1993; 4: 741–8.
7. Leung DA, Goin JE, Sickles C, Soulen MC. Determinants of post-embolization syndrome follow
ing hepatic chemoembolization. J Vasc Interv Radiol 2001; 12: 321–6.
8. Marelli L, Stigliano R, Triantos C, et al. Transarterial therapy for hepatocellular carcinoma: which
technique is more effective? A systematic review of cohort and randomized studies. Cardiovasc
Intervent Radiol 2007; 30: 6–25.
9. Varela M, Real MI, Burrel M, et al. Chemoembolization of hepatocellular carcinoma with drug
eluting beads: efficacy and doxorubicin pharmacokinetics. J Hepatol 2007; 46: 474–81.
10. Ono Y, Yoshimasu T, Ashikaga R, et al. Long-term results of lipiodol-transcatheter arterial embo
lization with cisplatin or doxorubicin for unresectable hepatocellular carcinoma. Am J Clin Oncol
2000; 23: 564–8.
11. Takayasu K, Shima Y, Muramatsu Y, et al. Hepatocellular carcinoma: treatment with intraarterial
iodized oil with and without chemotherapeutic agents. Radiology 1987; 163: 345–51.
12. Pelletier G, Roche A, Ink O, et al. A randomized trial of hepatic arterial chemoembolization in
patients with unresectable hepatocellular carcinoma. J Hepatol 1990; 1: 181–4.
13. Madden MV, Krige JE, Bailey S, et al. Randomised trial of targeted chemotherapy with lipiodol and
5-epidoxorubicin compared with symptomatic treatment for hepatoma. Gut 1993; 34: 1598–600.
14. Group d’Etude et de Traitement du Carcinome Hépatocellulaire. A comparison of lipiodol
chemoembolization and conservative treatment for unresectable hepatocellular carcinoma.
N Engl J Med 1995; 332: 1256–61.
15. Lo CM, Ngan H, Tso WK, et al. Randomized controlled trial of transarterial lipiodol chemoem
bolization for unresectable hepatocellular carcinoma. Hepatology 2002; 35: 1164–71.
16. Llovet JM, Real MI, Montana X, et al. Arterial embolization or chemoembolization versus
symptomatic treatment in patients with unresectable hepatocellular carcinoma: a randomized
controlled trial. Lancet 2002; 359: 1734–9.

17. Harada T, Matsuo K, Inoue T, et al. Is preoperative hepatic arterial chemoembolization safe and effective for hepatocellular carcinoma? Ann Surg 1996; 224: 4–9.
18. Majno PE, Adam R, Bismuth H, et al. Influence of preoperative transarterial lipiodol chemoembolization on resection and transplantation for hepatocellular carcinoma in patients with cirrhosis. Ann Surg 1997; 226: 688–701.
19. Lesurtel M, Müllhaupt B, Pestalozzi BC, Pfammatter T, Clavien PA. Transarterial chemoembo
lization as a bridge to liver transplantation for hepatocellular carcinoma: an evidence-based
analysis. Am J Transplant 2006; 6: 2644–50.
20. Maddala YK, Stadheim L, Andrews JC, et al. Drop-out rates of patients with hepatocellular
cancer listed for liver transplantation: outcome with chemoembolization. Liver Transpl 2004;
10: 449–55.
21. Oldhafer KJ, Chavan A, Frühauf NR, et al. Arterial chemoembolization before liver transplanta
tion in patients with hepatocellular carcinoma: marked tumor necrosis, but no survival benefit?
J Hepatol 1998; 29: 953–9.
22. Richard HM 3rd, Silberzweig JE, Mitty HA,etal. Hepatic arterial complications in liver transplant
recipients treated with pretransplantation chemoembolization for hepatocellular carcinoma.
Radiology 2000; 214: 775–9.
23. Di Carlo V, Ferrari G, Castoldi R, et al. Pre-operative chemoembolization of hepatocellular
carcinoma in cirrhotic patients. Hepatogastroenterology 1998; 45: 1950–4.
24. Zhang Z, Liu Q, He J, et al. The effect of preoperative transcatheter hepatic arterial chemoembo
lization on disease-free survival after hepatectomy for hepatocellular carcinoma. Cancer 2000; 89:
25. Wu CC, Ho YZ, Ho WL, et al. Preoperative transcatheter arterial chemoembolization for
resectable large hepatocellular carcinoma: a reappraisal. Br J Surg 1995; 82: 122–6.
26. Schwartz JD, Schwartz M, Mandeli J, Sung M. Neoadjuvant and adjuvant therapy for resectable
hepatocellular carcinoma: review of the randomised clinical trials. Lancet Oncol 2002; 3: 593–603.
27. Vogl TJ, Zangos S, Eichler K, Yakoub D, Nabil M. Colorectal liver metastases: regional che
motherapy via transarterial chemoembolization (TACE) and hepatic chemoperfusion: an update.
Eur Radiol 2007; 17: 1025–34.
28. Martinelli DJ, Wadler S, Bakal CW,etal. Utility of embolization or chemoembolization as second-line
treatment in patients with advanced or recurrent colorectal carcinoma. Cancer 1994; 74: 1706–12.
29. Lang EK, Brown CL. Colorectal metastases to the liver: selective chemoembolization. Radiology
1993; 189: 417–22.
30. Taniai N, Onda M, Tajiri T, et al. Good embolization response for colorectal liver metastases with
hypervascularity. Hepatogastroenterology 2002; 49: 1531–4.
31. Goode JA, Matson MB. Embolisation of cancer: what is the evidence?CancerImaging 2004; 4: 133–41.
32. Hunt TM, Flowerdew AD, Birch SJ, et al. Prospective randomised trial of hepatic arterial
embolization or infusion chemotherapy with 5-fluorouracil and degradable starch microspheres
for colorectal liver metastases. Br J Surg 1990; 77: 779–82.

33. Salman HS, Cynamon J, Jagust M, et al. Randomized phase II trial of embolization therapy versus
chemoembolization therapy in previously treated patients with colorectal carcinoma metastatic to
the liver. Clin Colorectal Cancer 2002; 2: 173–9.
34. Kaltsas GA, Besser GM, Grossman AB. The diagnosis and medical management of advanced
neuroendocrine tumors. Endocr Rev 2004; 25: 458–511.
35. Ruszniewski P, O’Toole D. Ablative therapies for liver metastases of gastroenteropancreatic
endocrine tumors. Neuroendocrinology 2004; 80 (Suppl 1): 74–8.
36. Touzios JG, Kiely JM, Pitt SC, et al. Neuroendocrine hepatic metastases: does aggressive management improve survival? Ann Surg 2005; 241: 776–83.
37. Ruutiainen AT, Soulen MC, Tuite CM, et al. Chemoembolization and bland embolization of
neuroendocrine tumor metastases to the liver. J Vasc Interv Radiol 2007; 18: 847–55.
38. Wigmore SJ, Redhead DN, Thomson BN, et al. Postchemoembolisation syndrome: tumour
necrosis or hepatocyte injury? Br J Cancer 2003; 89: 1423–7.
39. Chan AO, Yuen MF, Hui CK, Tso WK, Lai CL. A prospective study regarding the complications of
transcatheter intraarterial lipiodol chemoembolization in patients with hepatocellular carcinoma.
Cancer 2001; 94: 1747–52.
40. Tarazov PG, Polysalov VN, Prozorovskij KV, Grishchenkova IV, Rozengauz EV. Ischemic complications of transcatheter arterial chemoembolization in liver malignancies.ActaRadiol 2000; 41: 156–60.
41. Kim W, Clark TW, Baum RA, Soulen MC. Risk factors for liver abscess formation after hepatic
chemoembolization. J Vasc Interv Radiol 2001; 12: 965–8.
42. Plentz RR, Lankisch TO, Basturk M, et al. Prospective analysis of German patients with hepatocellular carcinoma undergoing transcatheter arterial chemoembolization with or without prophylactic antibiotic therapy. J Gastroenterol Hepatol 2005; 20: 1134–6.
43. Xia J, Ren Z, Ye S,etal. Study of severe and rare complications of transarterial chemoembolization
(TACE) for liver cancer. Eur J Radiol 2006; 59: 407–12.
44. Leung TK, Lee CM, Chen HC. Anatomic and technical skill factor of gastroduodenal complication
in post-transarterial embolization for hepatocellular carcinoma: a retrospective cohort study of
280 cases. World J Gastroenterol 2005; 11: 1554–7.
45. Huo TI, Wu JC, Lee PC, Chang FY, Lee SD. Incidence and risk factors for acute renal failure in
patients with hepatocellular carcinoma undergoing transarterial chemoembolization: a prospective study. Liver Int 2004; 24: 210–15.
46. Roullet MH, Denys A, Sauvanet A, et al. [Acute clinical pancreatitis following selective transcatheter arterial chemoembolization of hepatocellular carcinoma.] Ann Chir 1995; 127: 779–82.
47. Lopez-Benitez R, Radeleff BA, Barragan-Campos HM, et al. Acute pancreatitis after embolization
of liver tumors: frequency and associated risk factors. Pancreatology 2007; 7: 53–62.
48. Pentecost MJ, Daniels JR, Teitelbaum GP, Stanley P. Hepatic chemoembolization: safety with
portal vein thrombosis. J Vasc Intervent Radiol 1993; 4: 347–51.
49. Llado L, Virgili J, Figueras J, et al. A prognostic index of survival of patients with unresectable
hepatocellular carcinoma after transcatheter arterial chemoembolization. Cancer 2000; 88: 50–7.
90 A. T. Ruutiainen, M. Soulen
50. Lewis AL, Gonzalez MV, Lloyd AW, et al. DC Bead: in vitro characterization of a drug-delivery
device for transarterial chemoembolization. J Vasc Intervent Radiol 2006; 17: 335–42.
51. Hong K, Khwaja A, Liapi E, et al. New intra-arterial drug delivery system for the treatment of
liver cancer: preclinical assessment in a rabbit model of liver cancer. Clin Cancer Res 2006; 12:
52. Varela M, Real MI, Burrel M, et al. Chemoembolization of hepatocellular carcinoma with drug
eluting beads: efficacy and doxorubicin pharmacokinetics. J Hepatol 2007; 46: 474–81.
53. Poon RT, Tso WK, Pang RW, et al. A phase I/II trial of chemoembolization for hepatocellular
carcinoma using a novel intra-arterial drug-eluting bead. Clin Gastroenterol Hepatol 2007; 5:
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



Temporal Bone

  • Approach:

  • Soft tissue mass in the middle ear:

ü Cholesteatoma ü Chronic otitis media
ü Granulation tissue ü Cholesterol granuloma
ü Glomus tympanicum tumor ü Aberrant ICA
ü High or dehiscent jugular bulb ü
  • Vascular mass in middle ear:

·        Glomus tympanicum ·        Aberrant carotid artery
·        Carotid artery aneurysm ·        Persistent stapedial artery
·        Exposed jugular bulb ·        Exposed carotid artery
·        Hemangioma ·        Extensive glomus jugulare
  • Intra-canalicular IAC masses:

Exclusively intra-canalicular lesions: §  Acoustic neuroma (CN VIII), common

§  Facial neuroma (CN VII), rare

§  Hemangioma

§  Lipoma

Not primarily intra-canalicular: §  Meningioma

§  Epidermoid


  • Jugular fossa mass:

o   Glomus jugular tumor is the  most common

o   Neurofibroma is the  2nd most common

o   Schwannoma

o   Chondrosarcoma

o   Metastases

  • Mastoid bone defect:

ü Neoplastic bone destruction

ü Cholesteatoma

ü Post-operative simple / radical mastoidectomy

ü Post-traumatic deformity

  • Petrous apex lesions:

§  Cholesterol granuloma which appears T1 hyper-intense

§  Mucocele

   –  T1 hypo-intense

     – but may be T1 hyper-intense if à proteinaceous, then                           indistinguishable from cholesterol granuloma

§  Epidermoid àrestricted diffusion

§  Chondrosarcoma

§  Chordoma à if central extending to petrous

§  Endolymphatic sac tumor:  rare, more posterior; L > R; if bilateral, you think of VHL


  • Approach to orbital masses:


  • Orbital masses by Etiology:

Tumors: o   Hemangioma:  in adults: cavernous, in children: capillary.

o   Lymphoma

o   Metastases

o   Lymphangioma

o   Less common:

     ü Rhabdomyosarcoma

    ü Hemangiopericytoma

    ü Neurofibroma

Inflammatory: o   Pseudotumor is common

o   Thyroid ophthalmopathy is common

o   Cellulitis, abscess

o   Granulomatous is Wegener disease

Vascular: o   Carotid-cavernous fistula

o   Venous varix

o   Thrombosis of superior ophthalmic vein

Trauma: o   Hematoma

o   Foreign body

  • Extra-conal & Intra-conal Disease:

Extraconal disease Intraconal disease
Nasal disease:

·        Infection

·        Neoplasm

Orbital bone disease:

·        Subperiosteal abscess

·        Osteomyelitis

·        Fibrous dysplasia

·        Tumors

·        Trauma

Sinus disease:

·        Mucocele

·        Invasive infections

·        Neoplasm

Lacrimal gland disease:

·        Adenitis

·        Lymphoma

·        Pseudotumor

·        Tumor

Well-defined margins:

·        Hemangioma

·        Schwannoma

·        Orbital varix

·        Meningioma

Ill-defined margins:

·        Pseudotumor

·        Infection

·        Lymphoma

·        Metastases

Muscle enlargement:

·        Pseudotumor

·        Graves disease (thyroid ophthalmopathy)

·        Myositis

·        Carotid cavernous fistula

  • Vascular orbital lesions:

Tumor: ü Hemangioma, hemangioendothelioma, hemangiopericytoma

ü Lymphangioma

ü Meningioma


(with enlarged superior ophthalmic vein):

ü Carotid cavernous fistula

ü Cavernous thrombosis

ü Orbital varix

ü Ophthalmic artery aneurysm

  • Optic nerve sheath enlargement

Tumor o   Optic nerve glioma

o   Meningioma

o   Meningeal carcinomatosis

o   Metastases, lymphoma, leukemia

Inflammatory o   Optic neuritis

o   Pseudotumor

o   Sarcoid

increase intracranial pressure  
Trauma: o   hematoma
  • Tramtrack enhancement of orbital nerve:

§  Optic nerve meningioma

§  Optic neuritis

§  Idiopathic

§  Pseudotumor

§  Sarcoidosis

§  Leukemia, lymphoma

§  Peri-optic hemorrhage

§  Metastases

§  Normal variant

  • Third nerve palsy:

• Compression: ·        Intracranial aneurysm (do not miss)

·        Uncal herniation

·        Tumors  : neurofibroma, metastases, primary

·        Granuloma :Tolosa-Hunt, sarcoid

• Infection: ·        Encephalitis

·        Meningitis

·        Herpes zoster

• Vasculitis, dural cavernous sinus fistula
• Demyelination
• Trauma
• Infiltration (leptomeningeal carcinomatosis)
  • Ocular muscle enlargement:

o   Thyroid ophthalmopathy (most common cause); painless

o   Infection from adjacent sinus

o  Pseudotumor; painful

o   Granulomatous: TB, sarcoid, cysticercosis

o   Rare causes:

High flow: ü Dural AVM,

ü Carotid cavernous sinus fistula (CCF)

ü Lymphangioma

Tumor: ü Lymphoma

ü Rhabdomyosarcoma

ü Leukemia

ü Metastases

Apical mass  
  • Overview of Orbital Masses:

Mass Children Adults
Tumor: ·        Retinoblastoma

·        Rhabdomyosarcoma

·        Optic nerve glioma

·        Lymphoma

·        Hemangioma

·        Hemangioma

·        Schwannoma

·        Melanoma

·        Meningioma

·        Lymphoma

Other: ·        Dermoid cyst ·        Pseudotumor

·        Trauma

  • Mnemonic for childhood orbital masses: “LO VISON:”

o   Leukemia

o   Optic nerve glioma

o   Vascular malformation (hemangioma, lymphangioma)

o   Inflammation

o   Sarcoma, rhabdomyosarcoma

o   Ophthalmopathy, orbital pseudotumor

o   Neuroblastoma

  • Cystic orbital lesions:

·        Dermoid

·        Epidermoid

·        Teratoma

·        Aneurysmal bone cyst

·        Cholesterol granuloma

·        Colobomatous cyst

  • T1W hyperintense orbital masses:

Tumor: §  Melanotic melanoma

§  Retinoblastoma

§  Choroidal metastases

§  Hemangioma

Detachment: §  Coats disease

§  Persistent hyperplastic primary vitreous (PHPV)

§  Trauma

Other: §  Hemorrhage

§  Phthisis bulbi

§  Intra-vitreal oil treatment for detachment

  • Globe calcifications:

Tumor: ü Retinoblastoma à 95% are calcified, 35% are bilateral.

ü Astrocytic hamartoma àassociated with TS, NF.

ü Choroidal osteoma

Infection: (chorioretinitis) ü Toxoplasmosis

ü Herpes


ü Rubella

Other: Phthisis bulbi:

ü Calcification à in end-stage disease

ü Shrunken bulb

Optic nerve drusen:

ü Most common cause of calcifications in à adults

ü Bilateral

  • Sudden onset of proptosis:

·        Orbital varix à worsened by Valsalva maneuver.

·        Hemorrhage into cavernous hemangioma

·        CCF

·        Hemorrhage into lymphangioma

·        Thrombosis of superior orbital vein

  • Lacrimal gland enlargement:

Lymphoid lesions, 50%:  

o   Benign lymphoid hyperplasia

o   Mikulicz disease

o   Lymphoma

o   Pseudotumor

o   Sjögren syndrome

Epithelial neoplasm: o   Pleomorphic adenoma, 75%

o   Adenoid cystic carcinoma


  • Diffuse bone abnormality:


·        bony enlargement (fibrous dysplasia), expansion, sclerosis

ü Fibrous dysplasia

ü Paget disease

ü Thalassemia

ü Congenital (rare):

o   osteopetrosis, craniometaphyseal and diaphyseal dysplasia



  • Radio-opaque sinus:

Normal variant: ü Hypoplasia

ü Unilateral thick bone

Acute à Air-Fluid Level (AFL)

Chronic à mucosal thickening, retention cysts

ü Allergic

ü Fungal à aspergillosis, mucormycosis

ü Granulomatous à sarcoid, Wegener disease

Solid masses: ü SCC

ü Polyp, inverted papilloma

ü Lymphoma

ü Juvenile angiofibroma:

o   Most common tumor in children.

ü Mucocele:

o   Expansile, associated with cystic fibrosis in children.

Post-surgical: ü Caldwell-Luc operation



  • Mucosal space mass:

Tumors: ·        SCC

·        Lymphoma

·        Rhabdomyosarcoma

·        Melanoma

Benign masses: ·        Adenoids

·        Juvenile angiofibroma

·        Thornwaldt cyst

  • Parapharyngeal & carotid space masses:


·   Salivary gland tumors:

       – 80% are à benign,

       – 20% are à malignant

·      Neurogenic tumor àschwannomas, glomus vagale)

·        Nasopharyngeal carcinoma

·        Lymphadenopathy à benign, malignant

Abscess, cellulitis  
  • Pre-vertebral mass:

ü Metastases

ü Chordoma

ü Osteomyelitis, abscess

ü Hematoma



  • Cystic Extra-thyroid / Thyroid lesions:

Cystic extra-thyroid lesions Cystic thyroid lesions

ü Branchial cleft cyst: Lateral to carotid artery.

ü Thyroglossal duct cyst: Midline mass.

ü Ranula:  Retention cyst of sublingual glands.

ü Retention cysts of mucous glands (parotid)

ü Cystic hygroma (lymphangioma):   most common <2 years of age

ü uncommon lesions:

o   Teratoma.

o   Dermoid.

o   Cervical thymic cysts.

o   Hemangioma.


ü Thornwaldt cyst

ü Mucus retention cyst (obstructed glands)

ü Necrotic SCC (thick wall)

Larynx, paralaryngeal space:

ü Laryngocele

ü Mucus retention cyst

ü Colloid cysts

ü Cystic degeneration

ü Cystic tumor:

     – Papillary cancer

     – Cystic metastases (papillary cancer)


  • Solid neck mass:

Tumors: ü SCC of the larynx or Naso-oropharynx  is common.

ü Lymphadenopathy:

  • Reactive hyperplasia
  • Malignant

ü Parotid tumors

ü Neural tumors:

  • Neurilemoma
  • Neurofibroma
  • Glomus tumors

ü Other rare tumors:

  • Mesenchymal, dermoid, teratoma
Inflammatory: ü Infection à abscess, fungal, TB

ü Granulomatous inflammation sarcoid, TB lymphadenitis = scrofula.

Congenital: ü Ectopic thyroid
  • Vascular head & neck masses:

Glomus tumor: ü Glomus vagale

ü Glomus jugulare

ü Carotid body tumor

ü Glomus tympanicum



Often ICA:

ü Pseudo-aneurysm

ü Post-traumatic






  • Lateral Film is the best film projection, as Pharynx and Larynx clear of the cervical spine . as in Fig (1). The Film is placed against the shoulder and the incident beam is centered on :
  • Jaw Angle if we want Nasopharynx.
  • Thyroid Cartilage If we want Larynx.


Fig. 1 

(A) Some of the structures demonstrated on a plain lateral view of the neck. Xerography, although giving an excellent demonstration of the air-soft-tissue interface, is no longer available because of the high radiation dose used. 

(B) High-kV lateral neck gives an adequate demonstration of the soft tissue anatomy.


  • More benefit to opacify lesions below the crico-pharyngeus that cannot be assessed with a laryngeal mirror.
  • Tumours of the pharynx will be outlined by barium coating, especially those in the piriform fossae ( difficult to be seen with a mirror).
  • The normal larynx will appear as a `filling defect’ in the frontal projection with contrast in the piriform fossa on either side.
  • This is well shown on the oblique projection, obtained with the patient swallowing while the head is turned to one side.
  • When the larynx fails in its primary function as a protective sphincter for the lungs, ‘spill-over’ will occur to give a `barium laryngogram’.
  • This problem is seen more and more in an aging people, who dysphagia is due to mild stroke.


Fig . 2

Lateral View of normal Barium Swallow. The epiglottis (arrow) folds over the larynx as barium passes down into the esophagus .

Cine Radiology

  • It gives a good demonstration of degustation process.
  •  Passage of the bolus across the back of the tongue with an elevation of the larynx and tilting of the epiglottis down over the closed larynx is shown (Fig. 2).
  • Contrast then passes through the open cricopharyngeus into the esophagus.
  • Minor functional disorders of swallowing can only be shown by this technique (Fig. 3).
  • Videofluoroscopy is an alternative means of assessing swallowing function and a technique for assessment of oral or pharyngeal dysphagia.


Cine barium swallow. Four frames in 1 s, frontal and lateral views. The patient had mild dysphagia due to unilateral vagal paralysis. Various
normal and abnormal features are demonstrated. 
Lateral view. 
1. The vallecula fills with barium and is then partially effaced by the normal backward compression of the tongue. 
2. The epiglottis is partially immobile and only tilts down to the transverse position, not fully covering the laryngeal inlet. 
3. Barium enters the vestibule of the larynx. This may occasionally be observed in asymptomatic subjects but is usually an indication of failure of the laryngeal sphincters ('spill-over'). 
4. At the same time the relation of the postphyaryngeal wall to the cervical spine does not change, indicating paralysis of the middle pharyngeal constrictor. 
5. Cricopharyngeus contracts and relaxes normally. 
AP view. 
6. The epiglottis shows little movement. 
7. The right side of the pharynx contracts normally but the left remains flaccid and filled with barium. 
8. Cricopharyngeus contracts and releases normally.


  • CT is now the optimum method of imaging the outlines of the nasopharynx but also shows the soft-tissue structures of the infratemporal fossa and parapharyngeal space, which lie alongside the Naso- and oropharynx.
  • Formerly this region could be studied radiologically only in an indirect way by examination of surrounding bony structures or by invasive contrast examinations such as sialography and angiography.
  • The infratemporal fossa is situated below the skull base and is bounded by the pharyngeal musculature medially and the mandible laterally.
  • The most prominent and easily recognized structures within the infratemporal fossa are the pterygoid muscles.The anatomy of this region is depicted in Fig. 4.
  • Below, the infratemporal fossa is continuous with the parapharyngeal space.
    The role of CT for lesions in this region may be defined as:
    • To complement direct examination of lesions in the postnasal space
    .• To assess the size and situation and relations of a well-defined
    mass for prospective surgical removal, or the extent of local deep infiltration for radiotherapy planning.
    • To assess the relation of the mass to the great vessels and the parotid gland: by combining CT with contrast enhancement more accurate differentiation becomes possible.Contrast enhancement should be assessed in the vascular phase by intravenous infusion or bolus injection. Further sections in the coronal plane may give more information. Respiratory movement is less of a problem with the new fast scanners.
  • Scanning is begun at the level of the thyroid bone and sequential scans
    of 5 min slices are made in a caudal direction.
  • The shape of the airway alters as sequential scans are viewed. Above the rounded hypopharynx, it is bisected by the crescentic epiglottis.
  • Further down, the median and lateral glossoepiglottic folds delineate the valleculae.
  • Below this, the airway assumes a triangular shape and the piriform sinuses are seen as two lateral appendages separated by the aryepiglottic folds.
  • At the level of the cords the shape changes to the characteristic glottic chink or boat shape with the sharp anterior commissure extending right up to the thyroid cartilage in the midline (Fig. 5).
  • In the subglottic area, there is an even, symmetric oval shape which gives way at the level of the first tracheal ring to an oval flattened posteriorly, which may he likened to the shape of a horseshoe. 
  • CT provides a non-invasive, quick and effective radiological investigation of the larynx, and is not uncomfortable for the patient.
  • It can be done without risk in the face of respiratory obstruction, or after suspected laryngeal injury.
  • It gives an accurate assessment of laryngeal anatomy and involvement by tumor, particularly at the glottic level.
  • The value of such an assessment is greatly increased if partial laryngectomy is contemplated, but this is an unusual operation in the UK where carcinoma of the larynx is treated with radiotherapy and/or total laryngectomy.



Axial CT of soft tissues below the skull base. (A) Normal section through antra and postnasal space. The arrowheads indicate the openings of
the eustachian tubes. m = ramus of mandible; s = styloid process; p = pterygoid muscles. (B) Section at a slightly lower level passes through the soft palate
(sp). Tensor and levator palatini blend with the pharyngeal constrictors (c) to give a dense muscle mass. The enlarged but otherwise normal parotid gland
has a lower attenuation, i.e. appears darker, than the masseter muscle in front of it but not as dark as the fatty tissue in the parapharyngeal space. Thus the
medial limit of the deep parotid lobe can be defined (arrowhead). These features are best shown by MRI.

Axial CT Scan of the normal Larynx at the level of true vocal cords. 
Note the diamond shape of the airway with the cords in abduction.
Contrast is given , so CCA (A) and IJV (I) are shown.


  • MRI is superior over CT for neck masses.
  • MRI show neck vessels without the need to contrast.
  • T1WI gives the best spatial resolution.
  • T weighted Protocols give the best view of muscle invasion by carcinoma esp in Tongue base.
  • CT with contrast is superior over MRI in the evaluation of Neck Lymph Nodes, however, none of them can differentiate neoplastic from inflammatory hyperplasia, yet metabolic techniques like FDG-PET, SPECT is promising in that.
  • Sometimes the presence of Fat can obscure lesions, so fat saturation techniques are very useful, STIR protocol the most dependent one show increase signal intensity from most of the tumors especially Parotid Tumors. But It can’t be used with gadolinium contrast.
  •   Chemical Shift fat saturation techniques can show recurrent tumor after gadolinium injection.
  • Now Fat Saturation Techniques, used with T1 fast spin echo OR Post-gadolinium T protocols are more useful in defining Neck Lesions .   


Fig.6 (A) upper image: Sagittal MRI, T 1 -weighted, shows good differentiation between the tongue muscles, the genioglossi in the floor of the mouth and the surrounding fat, especially in the pre-epiglottic space (arrow).  (B) lowe image : Sagittal film in a child revealing subglottic stenosis (arrow)


Chordoma. Sagittal MR section, T,-weighted, shows a nonhomogeneous mass in the nasopharynx and replacing the basisphenoid.The tumor has burst out of its capsule and is displacing the brainstem posteriorly.




The Sonographic Revolution

For many years the rheumatologist adopted to fight against time to diagnose and follow most of the rheumatic diseases, this fighting continues to occur with no winners until the sonographic revolution has occurred in rheumatology.

Ultrasonography has been shown to be capable of substantially changing the traditional approach to most clinical problems in daily rheumatological practice because of its ability to allow a quick, safe and inexpensive access to otherwise undetectable anatomical information on the early targets of most rheumatic diseases.

Ultrasonography completes the physical examination in a rapid and accurate manner and allows the very early detection of a wide spectrum of pathological findings involving different anatomical structures in the musculoskeletal system.1


Although musculoskeletal ultrasound may be considered as one of the latest developments in ultrasound applications, it was first used, as far back as 1958, in the assessment of the acoustic attenuation of musculoskeletal tissues by K.T Dussik et al.2, 3

Dussik had also been the first to use ultrasound as a medical imaging modality in 1942. 2, 4

Ultrasound developed slowly until 1960 when Donald and colleagues produced the first automatic scanner.2

For the next decade, ultrasound was predominantly limited to the evaluation of abdominal and pelvic diseases.

By 1972 the first B-scan image of a joint was reported in the differentiation of a Baker’s cyst and thrombophlebitis.5

Graf, in 1980, published his landmark paper on the use of ultrasound in the diagnosis of congenital hip joint dislocation.6

In 1988, L. De Flaviis described ultrasound of the hand in rheumatoid patients including erosions, 10 years after Cooperberg described features of synovial thickening and joint effusion in the rheumatoid knee.7, 8

Since this time, particularly in the past decade, there has not only been a rapid development in ultrasound technology, but also widespread use of ultrasound in the investigation of musculoskeletal disorders to the point where it is now firmly established as a key imaging modality.


Ultrasound uses high-frequency sound waves to acquire images for the soft tissues, bones, and nerves of the body.

The ultrasound machine sends an electrical signal to the transducer, which is connected (via a cable) to the monitor and computer processing unit.

This system results in the production of sound waves that are transmitted from the transducer to the soft tissues of the body through acoustic transmission gel.9

The sound waves interact with the tissue interfaces and some reflect back toward the transducer on the surface of the skin.

The ultrasound image is produced from this reflection, which converts sound waves to an electrical current.9

The ultrasound machine then measures the amplitude of the returning electrical signal and records its travel time to determine the depth of the reflected structure.

As the machine generates and records the amplitudes and travel times of the sound beams, it uses the computer software to produce a two-dimensional image of the scanned structures.10

Transducer Selection:

The transducer is an essential element of US equipment, responsible for the generation of a US beam and the detection of returning echoes.

It greatly influences spatial resolution, penetration and signal-to-noise ratio, and in turn its selection affects the quality of the US image.9

Frequency of the Transducer:

To produce an image of optimal quality, it is important to select the proper transducer for the area of interest.

A transducer is described by the range of sound wave frequencies it can produce (MHz).

Higher-frequency transducers produce higher resolution images, but at the expense of beam penetration, because higher-frequency sound is more rapidly absorbed by the tissues.

Lower-frequency transducers are more capable of assessing deeper structures, but they have lower resolution.9

Shape of the Transducer foot plate:

Transducers also can be described as linear or curvilinear.

Linear transducers produce a sound wave that is propagated in a straight line perpendicular to the transducer surface (Fig.1).

Such transducers are best for evaluating linear structures like tendons.

Curvilinear transducers produce an arched beam and are less commonly used, but have some advantages in evaluating deeper structures (Fig. 2) and the small-footprint linear array L shaped transducer (hockey-stick transducer) which is suitable for evaluation of the small joints (Fig. 3).

Commonly used transducers in musculoskeletal ultrasound include the high frequency (20–7 MHz), linear transducer, and the low- to medium frequency (5–2 MHz) curvilinear array transducer.

The examiner should choose the highest-frequency transducer that can adequately image the target structure at the appropriate depth.9

Fig.1: Linear transducers are best for evaluating linear structures like tendons (coated from Jacobson JA, 9).

Fig.2: Curvilinear transducers are used for evaluating deeper structures such as hip, piriformis muscle, and sciatic nerve (coated from Jacobson JA, 9).

Fig.3: The small-footprint linear array transducer is also called a hockey-stick transducer and has higher frequency compared with other transducers. This transducer is used for evaluating small superficial structures such as peripheral nerves (coated from Jacobson JA, 9).


Reducing the width and thickness of the US beam to be limited to the area of interest has definite advantages in terms of contrast and spatial resolution.

In modern linear-array transducers’, focusing is currently not obtained by means of a fixed lens as in the old mechanical sector probes in which degrading of the image quality occurred at a short distance from the focal zone.

Focusing is now produced electronically by activating a series of elements in the array with appropriate delays, so that the trigger pulses to the inner elements are delayed with respect to the pulses to the outer ones.

In this way a curved wave front results from constructive interference bringing the US beam toward a focus. Recently, the introduction and refinement of matrix (1.5D probes) transducers led to further progress.

In these transducers, the single row of long piezoelectric elements found in a conventional probe is replaced by more layers (three to seven) incorporated into a single thin layer to produce parallel rows of short elements.

The slice thickness of the US image is improved by performing dynamic focusing in the elevation plane.

This leads to better spatial and contrast resolution and reduction of partial- volume averaging artifacts.11 A less expensive alternative to 1.5D probes is the use of peculiar acoustic lenses – Hanafy lenses –placed in front of the piezoelectric elements.

The Hanafy lens has nonuniform thickness and resonance properties: it produces a narrow and uniform image slice thickness and, simultaneously, a very broad bandwidth pulse.

The inner portion of the lens is thinner, resonates at higher frequencies and focuses in the near field, whereas its outer portions resonate at lower frequency and are focused in both transmission and reception at the deepest part of the image providing better penetration.12

Fig 4: Hanafy lens (Acuson-Siemens) coated from Claudon et al., 12.

Basic Scanning Techniques:

At first it is important to use enough acoustic transmission gel.

After that the examiner should begin by holding the transducer between the thumb and fingers of their dominant hand, positioning the end of the transducer near the ulnar side of the hand.

It is essential to securely stabilize the transducer on the patient’s body, with either the palm of the imaging hand or the small finger.

After the transducer is properly placed on the patient’s skin, a rectangular image is produced on the monitor.

The top of the image represents the tissues in contact with the transducer; the bottom of the image displays the deeper structures.

The left-to right orientation of the image can be altered using a button on the machine or by rotating the transducer 180 degree (fig 5).9

The image on the screen can be further adjusted and optimized by changing the sound-beam penetration using the depth controls.

Selection of the proper transducer is also critical in evaluating the depth of a structure.

There is an inverse relation between the frequency of the transducer and its depth of penetration, such that higher-frequency transducers are usually best to view superficial structures, whereas lower-frequency transducers are used for deeper structures.10, 13

Fig.5: (A, B) Orientation of the image. The top of the image usually shows the shallow structures and the bottom of the image, the deeper structures. The notch (arrow) of the probe usually represents the left side of the image (asterisk), but an image can be inverted by controls on the machine and it is important to confirm the side of the transducer with the side of the image on the screen. During examinations, t is important to be consistent. Many find it helpful to align the left side of the image with the examiner’s left side, coated from Jacobson JA, 2007.9 

The next step in imaging is adjusting the focal zone of the ultrasound beam.

The number of focal zones should be reduced to span the area of interest.

The zone feature is usually displayed on the side of the image as a series of cursors or symbols.

The depth and length of the focal zone position should match the position of the structure of interest.

The examiner may adjust the gain to either increase or decrease the brightness of the echo image.

A standardized approach to the study of the various anatomical regions is advisable even if the choice of the acoustic window is conditioned by the specific diagnostic need.14

Each anatomical area should be explored on various scan planes so as to obtain all of the necessary information.

An in-depth knowledge of the anatomy of the region examined is required for the musculoskeletal US. 14

Advantages and Disadvantages of Musculoskeletal Ultrasound:

When comparing US with other musculoskeletal imaging techniques (radiography, computed tomography, and magnetic resonance imaging), ultrasound offers numerous advantages.

Perhaps the most important of these is that ultrasound offers a hands-on, dynamic examination, allowing the clinician to image in real-time, while interacting with the patient.15

The clinician can ask the patient for assistance during the examination and may accurately localize painful areas by palpating with the transducer and seeking patient feedback.16

The sonographer can also ask the patient to reproduce the abnormal or painful event while scanning dynamically.

Furthermore, ultrasound is less expensive when compared to CT or MRI, can be repeated, and US can be used to compare the finding in the diseased side with the normal side of the same patient in the same session.

Ultrasound transmits no radiation to the patient or user, and thus may be used in special populations, including pregnant women and those with metal implants or other sources of imaging artifacts. 16

In addition, the enhanced sensitivity for detecting low-velocity flow in small tendon and synovium vessels achieved by recent colour Doppler and power Doppler techniques has led to the incorporation of Doppler US in rheumatology.

US allows an immediate correlation between imaging findings and clinical data, which improves diagnosis and management of patients with a range of rheumatic diseases from inflammatory arthritis, vasculitis or osteoarthritis to soft-tissue diseases.16-20

US has demonstrated more sensitivity than clinical evaluation in assessing joint inflammation.21-26

In addition, ultrasound is a bedside tool for performing accurate and safe musculoskeletal injections.27

On the other hand, the primary disadvantage of ultrasound is that it is operator dependent and there is a steep learning curve. Numerous examinations must be performed to establish a reliable diagnostic algorithm.28

Ultrasonographic Tissue Appearance:

Musculoskeletal ultrasound can be used to identify muscles, tendons, ligaments, nerves, bone surface and vessels, at a resolution of less than0.1 mm.

These structures can be characterized and described by their echogenicity. 29

When there is a large difference in impedance at the interface between tissues the sound beam is strongly reflected, creating a bright echo on the image. This process is described as hyperechoic.

If an image displays no echo and is black, it is referred to as anechoic, and when a weak or low echo is produced, it is termed hypoechoic.

When the echogenicity of a structure appears equal to an adjacent structure, it can be described as isoechoic or of equal echogenicity. 29

In general, when interpreting musculoskeletal ultrasound, a practical order of echogenicity is: bone/ligament/tendon/nerve/muscle.

In addition to their echogenicity, tissues are also described by their echotexture, which refers to their internal echo pattern.

Echotexture varies based on whether a structure is imaged longitudinally or transversely.30, 31

Definitions of Basic ultrasound terminology:

Echotexture refers to the coarseness or non-homogeneity of an object.
Echogenicity refers to the ability of tissue to reflect ultrasound waves back toward the transducer and produce an echo. The higher the echogenicity of tissues, the brighter they appear on ultrasound imaging.
Hyperechoic structures are seen as brighter on conventional US imaging relative to surrounding structures due to higher reflectivity of the US beam.
Isoechoic structures of interest are seen as bright as surrounding structures on conventional US imaging due to similar reflectivity to the US beam.
Hypoechoic structures are seen as darker relative to the surrounding structures on conventional US imaging due to the US beam being reflected to a lesser extent.
Anechoic structures that lack internal reflectors fail to reflect the US beam to the transducer and are seen as homogeneously black on imaging.
Longitudinal structure is imaged along the long axis.
Transverse structure is imaged perpendicular to the long axis.


1. Grassi W., Filippucci E., and Busilacchi P. Musculoskeletal ultrasound Best Practice & Research
Clinical Rheumatology 2004; 18: No. 6, pp. 813–826.
2. Kane D, Grassi W, Sturrock R et al. A brief history of musculoskeletal ultrasound: ‘From bats and
ships to babies and hips.’ Rheumatology 2004;43:931–933.
3. Dussik KT, Fritch DJ, Kyriazidou M et al. Measurements of articular tissues with ultrasound. Am
J Phys Med 1958;37:160–165.
4. Dussik KT. On the possibility of using ultrasound waves as a diagnostic aid. Z Neurol Psychiatr
5. McDonald DG, Leopold GR. Ultrasound B-scanning in the differentiation of Baker’s cyst and
thrombophelebitis. Br J Radiol 1972;45:729–732.
6. Graf R. The diagnosis of congenital hip-joint dislocation by the ultrasonic combound treatment.
Arch Orthop Trauma Surg 1980;97:117–133.
7. De Flaviis L, Scaglione P, Nessi R et al. Ultrasonography of the hand in rheumatoid arthritis. Acta
Radiol 1988;29:457–460.
8. Cooperberg PL, Tsang I, Truelove L et al. Gray scale ultrasound in the evaluation of rheumatoid
arthritis of the knee. Radiology 1978;126:759–763.
9. Jacobson JA. Fundamentals of musculoskeletal ultrasound. Philadelphia: Saunders Elsevier; 2007.
p. 1–38.
10. Smith J, Finnoff JT. Diagnostic and interventional musculoskeletal ultrasound: Part 1.
Fundamentals. PM R 2009;1(1):64–75.
11. Rizzatto G. Evolution of US transducers: 1.5 and 2D arrays. Eur Radiol1999;9:304–306
12. Claudon M, Tranquart F, Evans DH et al. Advances in ultrasound. Eur Radiol 2002;12:7–18
13. Kremkau F. Diagnostic ultrasound. Principles and instruments. 6th edition. Philadelphia: WB
Saunders; 2002. p. 428.
14. Backhaus M, Burmester GR, Gerber T, et al. Guidelines for musculoskeletal ultrasound in
rheumatology. Annals of the Rheumatic Diseases 2001; 60: 641–649.
15. O’Neill J. Introduction to musculoskeletal ultrasound. In: O’Neill J, editor. Musculoskeletal
ultrasound. New York: Springer; 2008. p. 3–17.
16. Grassi W, Cervini C. Ultrasonography in rheumatology: an evolving technique. Ann Rheum Dis
17. Wakefield RJ, Brown AK, O´ Connor PJ, et al. Musculoskeletal ultrasonography: what is it and
should training be compulsory for rheumatologists? Rheumatology 2004;43:821–2.
18. Kane D, Grassi W, Sturrock R, Balint PV. Musculoskeletal ultrasoundda state of the art review in
rheumatology. Part 2:
19. Clinical indications for musculoskeletal ultrasound in rheumatology. Rheumatology 2004;43:829–
20. Schmidt WA, Seifert A, Gromnica-Ihle E, et al. Ultrasound of proximal upper extremity arteries to
increase the diagnostic yield in large-vessel giant cell arteritis. Rheumatology 2008;47:96–101.
21. Backhaus M, Kamradt T, Sandrock D, et al. Arthritis of the finger joints: a comprehensive
approach comparing conventional radiography, scintigraphy, ultrasound, and contrast-enhanced
magnetic resonance imaging. Arthritis Rheum 1999;42:1232–45.
22. Kane D, Balint PV, Sturrock RD. Ultrasonography is superior to clinical examination in the
detection and localization of knee joint effusion in rheumatoid arthritis. J Rheumatol
23. Wakefield RJ, Green MJ, Marzo-Ortega H, et al. Should oligoarthritis be reclassified? Ultrasound
reveals a high prevalence of subclinical disease. Ann Rheum Dis 2004;63:382–5.
24. Karim Z, Wakefield RJ, Quinn M, et al. Validation and reproducibility of ultrasonography in the
detection of synovitis in the knee: a comparison with arthroscopy and clinical examination.
Arthritis Rheum 2004;50:387–94.
25. Szkudlarek M, Narvestad E, Klarlund M, et al. Ultrasonography of the metatarsophalangeal joints
in rheumatoid arthritis: comparison with magnetic resonance imaging, conventional radiography,
and clinical examination. Arthritis Rheum 2004;50:2103–12.
Chapter One Principles of ultrasound
26. Naredo E, Bonilla G, Gamero F, et al. Assessment of inflammatory activity in rheumatoid
arthritis: a comparative study of clinical evaluation with grey scale and power Doppler
ultrasonography. Ann Rheum Dis 2005;64:375–81.
27. Koski JM. Ultrasound-guided injections in rheumatology. J Rheumatol 2000;27:2131–8.
28. Nofsinger C, Konin JD. Diagnostic ultrasound in sports medicine: current concepts and advances.
Sports Med Arthrosc 2009;17(1):25–30.
29. Smith J, Finnoff JT. Diagnostic and interventional musculoskeletal ultrasound: Part 2. Clinical
applications. PM R 2009;1(2):162–77.
30. Lew HL, Chen CP, Wang TG, and Chew KT. Introduction to musculoskeletal diagnostic
ultrasound: Part 1: examination of the upper limb. Am J Phys Med Rehabil. Apr 2007. 86(4):310-
31. Chew KT, Stevens KJ, Wang TG, Fredericson M, and Lew HL. Introduction to musculoskeletal
diagnostic ultrasound: Part 2: examination of the lower limb. Am J Phys Med Rehab. Mar 2008.






Tendons are characterized by their parallel course with respect to the skin surface and by a typical fibrillar echotexture that is clearly detectable in longitudinal scans.

The fibrillar echotexture is generated by parallel running fascicles of collagen fibres, which appear as closely positioned, fine hyperechoic lines with even finer anechoic thin lines in between, corresponding to inter-fascicular ground substance. Fig.6

On tendons with a synovial sheath, a subtle anechoic rim interposed between the sheath and the tendon margin can be detected.1

Fig.6: Tendon longitudinal:
A: sonographic picture,T= tendon, F= fat pad, C= cartilage, I.P=Proximal phalanx, I.MC=
metacarpal head, JS= joint space.
B: Tissue specimen of the same picture, T= tendon, S= subcutaneous fat, B= bone.

Fig.7: Tendon transverse:
A: sonographic picture,T= tendon, B= bone.
B: Tissue specimen of the same picture, T= tendon,B= bone.

In transverse scans, tendons appear as round or oval structures, characterized by numerous closely joined dots that are homogeneously distributed and correspond to the intra-tendinous connective fibers.

The tendon’s sonographic characteristics in healthy subjects are fairly homogeneous and have limited intra- and inter-individual variability.1 Fig.7


They are made up of two components: the muscle fibers, which are long and cylindrical in structure, representing the cellular unit of muscle, and stromal connective tissue.

Individual muscle fibers are grouped together in bundles, which are commonly known as fascicles, and several fascicles join together to form an individual muscle (Fig. 8).

Thin connective tissue strands – the endomysium – separate the individual muscle fibers; a more substantial connective sheath with small vessels and nerve endings, the perimysium (also referred to as fibroadipose septa), envelops individual fascicles; a thick fibrous layer, the epimysium, surrounds the entire muscle. 2,3 , Fig.8.

Fig.8: Muscle fiber: cross-section (coated from van Holsbeeck and Introcaso, 2001).3

The fasciculi can be identified as separate structures on ultrasound.2, 3 They are best identified in the longitudinal plane as hypoechoic cylindrical structures, separated by the hyperechoic intervening connective tissue, the perimysium (fig 9,10).

Individual fibers and the endomysium are not individually discernible. The epimysium, fascia, and intermuscular fat are all thin, linear hyperechoic structures on ultrasound.

During contraction of a muscle, the fibers shorten, causing an apparent increase in muscle bulk. When the muscle is contracted, the fascicles have a thicker and more hypoechoic appearance.3

Fig.9: Muscle longitudinal: A: sonographic picture F = fascia, M = muscle. B: Tissue specimen of the same picture, F = fascia, M = muscle. (coated from van Holsbeeck and Introcaso, 2001).3

Fig.10: Muscle Transverse: A: sonographic picture F = fascia, M = muscle. B: Tissue specimen of the same picture, F = fascia, M = muscle. (coated from van Holsbeeck and Introcaso, 2001).3


Ligaments are fibrous structures appearing similar to tendons. However, they are less compact and are composed of a more diverse pattern of collagen bundles.4

Ligaments are usually well defined and easily visible on ultrasound examination. However, when they occur as a focal thickening of a joint capsule, they may not be distinguishable as distinct structures.

Ligaments display a hyperechoic, linear appearance on ultrasound and are optimally evaluated when they are stretched.5, Fig.11

Similar to tendons, ligaments appear fibrillar during longitudinal scanning and have a broom-end appearance on transverse scans.

However, ligaments can be distinguished from tendons by tracing them back to the bony structures to which they attach.4

Fig.11: Ultrasound image of medial collateral ligament reveals the superficial ligament (arrows) and meniscofemoral ligament (mf) and meniscotibial ligament (mt) attached to the meniscus (asterisk).


A peripheral nerve is a cordlike structure containing a large number of individual nerve fibers.

The nerve fibers are grouped together into bundles known as fascicles Fig.12. The fascicles are enclosed in a connective tissue sheath or membrane known as the epineurium.

Each fascicle is in turn covered by a sheath of connective tissue, the perineurium. The individual nerve fibers within the fascicle are also enclosed by a sheath of connective tissue, the endoneurium.

Extending inward from the epineurium is the interfascicular epineurium, which is thin septae adding further support to the nerve bundles and their vascular supply. 6, 7.

Fig.12: Peripheral nerve: cross section (coated from van Holsbeeck and Introcaso, 2001).3 

Ultrasound, in the longitudinal axis of the nerve, demonstrates a fascicular pattern of uninterrupted hypoechoic bands with intervening linear interrupted hyperechoic bands Fig.13.

The hypoechoic bands represent the fasciculi and the hyperechoic bands the supporting interfascicular epineurium.

The epineurium is hyperechoic and of similar appearance to perineural fat and may not be separable on ultrasound.

In the axial study, the nerve is composed of fasciculi seen as multiple hypoechoic dots, which may be of varying size, intermingled in a hyperechoic background of the supporting connective tissue.2, 8–10

Fig.13: Ultrasound image of median nerve (A= long axis, B= short axis) shows hypoechoic nerve
 fascicles (arrowheads). t = flexor digitorum tendon, p = palmaris longus tendon, R = radius, L = lunate.


Ultrasound provides limited views of bones. It can display vivid anatomic details of the cortical surfaces of the superficial bone.5

Bones appear with well-defined, linear, and smooth hyperechoic borders. This hyperechoic appearance is caused by the high reflectivity of the acoustic interface.

Because nearly the entire sound beam is reflected, ultrasound is unable to image beyond the bone surface or that of other calcified structures, so the image beyond the interface appears black; this is referred to as posterior acoustic shadowing.4

Because of this phenomenon, Ultrasound can provide information only about the superficial portion of bones Fig.14.

Fig.14: US appearance of normal bone: surface echotexture. a Longitudinal 12–5 MHz US image obtained over the diaphysis of the radius demonstrates the bone surface as a continuous straight hyperechoic line (arrows) produced by a strong reflection of sound due to the marked difference in acoustic impedance of the soft tissues and bone. Reverberation artifact (arrowheads) projecting in the shadow beyond the bone can be seen.


Synovial joints are the most common joints examined with ultrasound. They are formed by articulating bone surfaces, fibrous capsules, and ligaments, and other intraarticular structures (ligaments, menisci, labra, and fat pads) 2, Fig.15.

Ultrasound examination of joint surfaces reveals a homogeneously smooth hypoechoic smooth linear band (the hyaline cartilage).11,12

The joint capsule appears as a hyperechoic line merging with the para-articular tissues.2 The deeper subchondral bone is a regular, continuous, bright, hyperechoic line.

Fig (15): Elbow joint anterior longitudinal veiw:
 A: sonographic picture, M= muscle, F= fat pad, CA= cartilage, R=Radius phalanx, H= humerus,
 JS= joint space. B: Tissue specimen of the same picture. (coated from van Holsbeeck and Introcaso, 2001).3


Cartilage can be divided into hyaline cartilage, white fibrocartilage, and elastic or yellow fibrocartilage.

The latter is present in only select regions, e.g., the auricle of the external ear.

Articular hyaline cartilage is of varying thickness, being thicker in points of greater stress and on convex rather than concave surfaces.

It provides a degree of elasticity and shock absorption, as well as helping to dissipate stress across a joint.6,7 On ultrasound, it has a smooth, well-defined surface and border and is uniformly hypoechoic. 3, Fig.17.

Fig.17: Articular hyaline cartilage:
 A: sonographic picture, S= Skin, C= cartilage, B=bone. B: Tissue specimen of the same picture
 (coated from van Holsbeeck and Introcaso, 2001).3


It’s a variable mixture of white fibrous tissue and cartilaginous tissue with a large component of collagen fibrils.

It provides elasticity and flexibility. The menisci of the knee, temporomandibular and sternoclavicular joints, the glenoid and hip labra, and the triangular fibrocartilage of the wrist are composed of fibrocartilage.

On ultrasound, fibrocartilage is hyperechoic with well-delineated borders. Because of its position within joints, it is not always fully accessible to a full ultrasound examination.3, Fig.18

Fig.18: Fibrocartilage. The posterior glenoid labrum (arrow) is demonstrated here as a well-defined, hyperechoic triangular structure between the articulating surfaces of the glenoid (G) and humerus (H).


Normal bursae in healthy subjects are not always easily visualized. They appear as a thin hypoechoic space delimited by echoic borders corresponding to the tissue–fluid interface.

Bursitis is characterized by an increase in the synovial fluid that usually appears as a sharply defined anechoic area.13, Fig.16.

Fig.16: Retrocalcaneal bursa: + bursa , t, Achilles tendon; c, calcaneal bone.



1. Martinoli C, Derchi LE, Pastorino C, et al. Analysis of echotexture of tendons with US. Radiology
1993; 186: 839–843.
2. Martinoli C, Bianchi S, Dahmane M. Ultrasound of tendons and nerves. Eur Radiol 2002; 12:44–
3. van Holsbeeck M, Introcaso J. Sonography of tendons. In: Musculoskeletal Ultrasound, 2nd ed, St.
Louis: Mosby, 2001, pp. 77–81
4. Smith J, Finnoff JT. Diagnostic and interventional musculoskeletal ultrasound: Part 2. Clinical
applications. PM R 2009;1(2):162–77.
5. Lew HL, Chen CP, Wang TG, and Chew KT. Introduction to musculoskeletal diagnostic
ultrasound: Part 1: examination of the upper limb. Am J Phys Med Rehabil. Apr 2007. 86(4):310-
6. Gray H. General anatomy or histology. In: The Complete Gray’s Anatomy, 16th ed.,: Longman,
Green, and Co., 1995, pp. 1–72. London.
7. Snell R. Basic anatomy. In: Clinical Anatomy, 7th ed, Philadelphia: Lippincott Williams &
Wilkins, 2004, pp. 1–48.
8. Silvestri E, Martinoli C, Derch L et al. Echotexture of peripheral nerves: Correlation between US
and histologic findings and criteria to differentiate tendons. Radiology 1995;197(1):291–296.
9. Gruber H, Kovacs P. Sonographic anatomy of the peripheral nervous system. In: Peer S, Bodner G
(eds.). High Resolution Sonography of the Peripheral Nervous System, 1st ed. New York:
Springer, 2003 , pp. 28–32.
10. Peer S. High-resolution sonography anatomy of the peripheral nervous system: General
considerations and technical concepts. In: Peer S, Bodner G (eds.). High Resolution Sonography
of the Peripheral Nervous System, 1st ed., NewYork: Springer, 2003, pp. 1–11.
11. 24. Martino F, De Serio A, Macarini L, et al. Ultrasonography versus computed tomography in
evaluation of the femoral-trochlear groove morphology: a pilot study on healthy, young
volunteers. Eur Radiol 1998;8:244–7.
12. 25. Grassi W, Lamanna G, Farina A, et al. Sonographic imaging of normal and osteoarthritic
cartilage. Semin Arthritis Rheum 1999; 28:398–403.
13. 10. Zamorani MP, Valle M. Bone and joint. In: Bianchi S, Martinoli C, editors. Ultrasound of the
musculoskeletal system. Berlin: Springer; 2007. p. 137–85.