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Imaging of Lumps and Bumps in the Pediatric Patient: An Algorithm for Appropriate Imaging and Pictorial Review Michael S. Morrow DO, Amy M. Oliveira MD

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Cite this article as: Michael S. Morrow DO, Amy M. Oliveira MD, Imaging of Lumps and Bumps in the Pediatric Patient: An Algorithm for Appropriate Imaging and Pictorial Review, Semin Ultrasound CT MRI , http://dx.doi.org/10.1053/j.sult.2014.05.005 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Imaging of Lumps and Bumps in the Pediatric Patient: An Algorithm for Appropriate Imaging and Pictorial Review

Michael S. Morrow, DO – Radiology Resident, Clinical Associate of Radiology, Department of Radiology, Tufts School of Medicine, Baystate Medical Center, Springfield, MA.

Amy M. Oliveira, MD – Assistant Professor of Radiology, Musculoskeletal Imaging Division, Department of Radiology, Tufts School of Medicine, Baystate Medical Center, Springfield, MA.

Address manuscript queries and proofs/reprint requests to Michael S. Morrow, DO, Department of Radiology, Tufts School of Medicine, Baystate Medical Center, 759 Chestnut Street, Springfield, MA 01199. Telephone: (413) 794-3521. E-mail: [email protected]

Abstract Superficial lumps and bumps are a common presenting complaint in the pediatric patient population. Although encountered frequently, the path to a definitive diagnosis is not always a straightforward one. Imaging offers a valuable tool to aid in this diagnostic challenge. Radiologists must be familiar with pediatric lumps and bumps, their imaging characteristics, and the best way to further evaluate challenging clinical presentations. This will not only allow the radiologist to serve as a valuable asset to the treating physician in choosing the most appropriate imaging modality, but will also help in accurate diagnosis, all while ensuring the “image gently” principle. An algorithm for imaging in the pediatric patient with lumps and bumps will be presented and a few example entities along with their imaging findings will also be reviewed.

Introduction Pediatric patients with lumps and bumps can be a source of apprehension for parents who typically fear the worst for their child. The differential diagnosis for these types of lesions can be wide-ranging, including both osseous and soft tissue pathology. Although the majority of these presenting complaints are not serious or life threatening, there is the ever-present fear of the “can’t miss” diagnoses and the anxious parent that often propel the physician to make an attempt at a definitive diagnosis. Imaging is often sought to help clear up the clinical picture. Considering the commonality of this presenting

complaint, it is prudent for the radiologist to not only be familiar with the imaging presentation of certain entities to ensure the most accurate diagnosis, but to also be knowledgeable on how to most appropriately image the patient, in order to serve as an effective advisor to the treating physician.

Imaging Modalities In an effort to keep in line with the “image gently” campaign developed by The Alliance for Radiation Safety in Pediatric Imaging, and in order to be a relevant member of the integrated health care team, it is imperative for the radiologist to be able to recommend appropriate imaging for further characterization of pediatric lumps and bumps. Ultrasound, plain radiography, computed tomography (CT), and magnetic resonance (MR) imaging are the currently available imaging modalities that should be used to effectively aid in diagnosing most lesions faced in the clinical setting. CT and MR angiography can also be of value, but will typically be used as a secondary study to further define a known entity (i.e. – completely evaluating the extent of a vascular malformation). Ultrasound is widely available, noninvasive, performed without ionizing radiation and without the need for sedation. Ultrasound is highly user dependent and is best performed where the radiologist is available to personally scan as needed. Plain radiography is also universally available and can be performed quickly, at a relatively low cost. The drawback of plain radiography is the radiation exposure, albeit lower than CT. CT is also widely available, but is more expensive than plain films and requires higher radiation doses. MR not only is the most expensive modality but also is not available in all

locales. However, it does offer excellent soft tissue characterization without any radiation exposure. Other considerations for the use of MR include the potential need for sedation and it untoward effects on a pediatric patient. MR can also be a very lengthy exam, depending on the body part being imaged.

Algorithm The first step in working up a lump or bump is physical examination to determine whether the palpable is bony or soft tissue in origin. Some lesions will be indeterminate. If the lesion feels bony, the first step in the imaging workup would be radiographs to determine if the lesion is calcified or bony in origin and to assess if there is involvement of the underlying bone. Radiographs can in some cases be diagnostic and in others can offer significant information towards the diagnosis. Radiographs can help determine is a bony lesion has an aggressive or nonaggressive appearance. However, associated soft tissue components can be underappreciated with this modality. Depending on the initial radiographic appearance and taking radiation exposure risk into consideration, the next diagnostic choice may be either MR or CT. CT offers excellent evaluation of bone cortex and high-resolution capability. MR offers greater characterization of bone marrow involvement and associated soft tissue components. For palpable lesions thought to be soft tissue, the initial imaging choice would be ultrasound. Upon imaging with grayscale, the solid versus cystic nature of a lesion can be determined, as can be the spatial location and size of the lesion. The vascularity of the lesion can be evaluated with both color and spectral Doppler at the time of ultrasound. The

next choice for soft tissue lesions would be MR, which offers excellent tissue characterization. Additionally, MR can evaluate deeper lesions that may not be able to be fully evaluated with ultrasound. Basic MR sequences to obtain when evaluating a lump or bump include imaging in at least two planes and include T1, fat saturated T2 and post contrast images. Additional sequences can be added as needed. Post contrast imaging characteristics offer clues to the diagnosis, demonstrate necrosis and can help guide biopsy. If it is difficult to assess whether the lesion is soft tissue or osseous in origin, then plain radiographs offer the most efficient and cost effective imaging modality to determine the origin. The diagnosis may not always be made on the basis of plain radiographs, but the findings often add sufficient information to guide decisions regarding additional imaging. A summary of these recommendations can be found in Figure 1.

Markers The use of skin surface markers is another thing to bear in mind when imaging pediatric lumps and bumps. The use of these markers helps to alleviate confusion as to where the lesion is, and ensures the radiologist will take special care in evaluating the area of clinical concern. The main consideration when contemplating whether or not to make use of these markers is to ensure that the material being utilized will not interfere with the chosen imaging modality. With readily palpable lesions or lesions that the patient or their parent can identify, a marker may not be necessary for ultrasound examinations. However, when a lesion is palpated by the clinician or is located in a difficult to describe location,

simple demarcation on the skin with a pen line can be of great value. BB markers are commonly used in plain radiography to mark nipples, but can also be used to mark an unknown soft tissue or osseous lesion. We routinely perform tangential views when using plain films to assess a palpable lesion. BB markers can be used in CT exams as well. They are small enough that they typically will not cause streak artifact, which can limit evaluation. Vitamin E capsules are used in MR imaging to help mark palpable abnormalities, and cause limited artifacts.

Example Cases Infantile Hemangioma (Figure 2) Hemangiomas are frequently seen in the pediatric population, occurring in up to 12 % of infants. 1,2 They are seen more frequently in girls, premature infants, twins, caucasians and children of mothers of advanced age or who underwent chorionic villous sampling.1,3 These lesions are true mesenchymal tumors consisting of extensive endothelial lined vascular channels, abundant mast cells and supporting fibrous tissue.1 Superficial infantile hemangiomas often have a characteristic presentation clinically that does not necessitate imaging to make the diagnosis. These lesions are often small, inconspicuous or not present at birth.1 Soon after birth, they enter into a rapid proliferative phase where they increase in size. By approximately 12 months of age, these lesions reach a plateau. Lastly, involution occurs by 3 to 5 years of age. These can either completely resolve or leave a small non-neoplastic fibrous scar.3

Clinical diagnosis can become more challenging when these lesions are located deeper in the tissue planes. Ultrasound is the initial modality of choice to investigate these lesions. They should be studied in gray scale as well as with color and spectral Doppler. A central hyperechoic focus may be seen as the typical feature of a central scar. Color Doppler will show hypervascularity and evaluation with spectral Doppler may depict low resistance waveforms. Enlarged feeding vessels can be seen in the case of shunt vascularity.3 MRI can be used to distinguish these lesions from other high flow lesions malformations. Noncontrast MRI demonstrates T1 isointense to hypointense signal and T2 hyperintense signal. Secondary to their high flow state, infantile hemangiomas often contain flow voids. MRA can be utilized to see the feeding vessels. Routine post contrast MRI images can demonstrate one of the two common enhancement patterns. The pattern is typically either early homogeneous enhancement or centripetal enhancement following early peripheral enhancement of the lesion.3 The same feeding vessels that are seen by MRI would be seen at digital subtraction angiography. Also characteristic at DSA is the parenchymal stain created by enhancement of the masslike soft tissue component.3 Most infantile hemangiomas require no treatment as they typically regress spontaneously and often are only of cosmetic concern. Superficial infantile hemangiomas can undergo ulceration, fissuring on bleeding. Lesions around the orbit can cause longterm problems with visual perception and lesions around the mouth or airway can cause life-threatening impairments. Large lesions can be associated with high output congestive

heart failure.3 Consumptive coagulopathy known as Kasabach-Merritt Syndrome, can be seen with hemangiomas (typically hepatic) though this tends not be seen with infantile hemangiomas.1 Patients may also have hypothyroidism due to the lesion expressing type 3 iodothyronine deiodinase.3 Complications are most frequently seen during the proliferative phase and when they arise, often necessitate treatment.1,3

Lymphatic and Venous Malformations (Figures 3 and 4) Lymphatic and venous malformations are types of slow flow vascular lesions. Slow flow vascular lesions are non-neoplastic; therefore, terms with the suffix “-oma” (lymphangioma and cystic hygroma) have been removed from the current classifications by the International Society for the Study of Vascular Anomalies.4 Venous malformations are the most common vascular malformations and can range from a single vessel dilated channel (phlebectasia) to multiple extensive spongiform venous lakes. Venous malformations, although congenital, typically do not become clinically apparent until later in childhood or adulthood. They typically grow with the child and due to hormone sensitivity can enlarge during puberty. Clinically, superficial lesions may have a bluish color and are compressible. Dependent positioning or rest may cause local pain.4 Lymphatic malformations are typically composed of cystic spaces, ranging from several millimeters to several centimeters, separated by thin septations (macrocystic subtype). Lesions with much smaller cystic elements can have a more solid appearance

and are referred to as microcystic lymphatic malformations. Macrocystic and microcystic components commonly co-exist in the same lesion. Lymphatic malformations, like all vascular malformations, are congenital and are not mitotically active. However, proportionate growth over time is expected as a child grows. Most, therefore, present early, with 65% present at birth and 90% seen by 2 years of age.1 Those that are found past age two may have become clinically evident secondary to rapid growth related to hemorrhage or infection.5 These can be seen anywhere in the body although the vast majority are seen in the neck and axilla.1,4 The involved portion of the body may aid in diagnosis as lymphatic malformations often cross fascial planes and are often located in the head and neck. Additionally, isolated lesions within a muscle can be seen with venous malformations though would be atypical for a lymphatic malformation.4 Neither plain radiographs nor CT may provide much information in the evaluation of vascular malformations but they may help identify venous calcifications or involvement of bone including expansion, new bone formation or osteolysis. Calcifications are seen with 30% of radiographs of venous malformations and when present are considered pathognomonic. Lymphatic malformations usually measure near water density on CT although they may measure higher density if complicated by hemorrhage or infection.4 Imaging evaluation of slow flow vascular lesions is best performed with ultrasound initially. For optimal ultrasound imaging, the highest frequency probe that can still penetrate to the depth of the lesion should be utilized. Grayscale images of venous malformations and lymphatic malformations may appear similar. Both may show multilocular cystic lesions and may demonstrate fluid levels or contain internal echoes.

The flow in these lesions may be so slow that it is not detectable on spectral Doppler. During the ultrasound examination, there are certain maneuvers that can help differentiate between lymphatic and venous malformations. Venous malformations will change in size with valsalva or positional changes. Flow may be detected with color or spectral Doppler with augmentation or valsalva. The blood filled cystic spaces may also decrease in size with external compression, as blood escapes through the collateral venous channels. Lymphatic malformations may be deformable with compression, but the volume of cystic components will not change with these maneuvers. Solid or nodular components should be sought, as these would suggest an etiology other than a benign vascular malformation.4 If diagnosis is uncertain or treatment is considered, these lesions are commonly further characterized with MR imaging. Both lymphatic and venous malformations both appear as multilocular cystic lesions without flow voids. The channels in venous malformations may have a more serpentine configuration. Fluid-fluid levels can be seen in both due to thrombosis, hemorrhage, or infection. Following contrast administration, the cystic spaces of macrocystic lymphatic malformations show no enhancement, although there is variable enhancement of the septations. The microcystic variant may enhance more heterogeneously. The vascular channels of venous malformations are in continuity with the normal venous system and enhance intensely.1,2,4

Dermoids and Epidermoids (Figure 5) Dermoid and epidermoid cysts are benign, ectoderm-lined inclusion cysts that represent malformations of surface ectoderm, and are closely related in morphology. The

characteristic that distinguishes these two entities is that dermoid cysts contain both ectoderm and skin elements (hair, sebaceous/sweat glands, squamous epithelium), while epidermoid cysts contain only ectoderm. Both lesions are common in the pediatric population, representing possible etiologies for the pediatric patient with unknown lumps and bumps.6,7 Dermoid and epidermoid cysts were originally characterized as congenital epithelial tumors. The most widely accepted current theory is that these occur secondary to failure of the surface ectoderm to separate from underlying structures, and subsequent sequestration implantation of the surface ectoderm. It followed that the cysts originated from these sequestered pouches of ectoderm, or from failure of the surface ectoderm to separate from the underlying structures such as the neural tube.6 Dermoid and epidermoid cysts often arise at sites of embryologic fusion, commonly in the midline. They occur most frequently around the head and neck. Cranial lesions can arise in the soft tissues of the scalp, in diploic space of the calvarium or between the bone and the underlying dura. They are most often seen in the midline and in the frontotemporal region; less frequently they are seen in the parietal regions. In the midline, lesions can occur the anterior fontanelle, glabella, nasion, vertex, and subocciput. They are also known to arise from the cranial sutures.6,7 Dermoid and epidermoid cysts can cause mass effect on surrounding structures, which can be evident on plain radiography. Intraosseous lesions are often expansile, causing bony erosion with sclerotic remodeling, which is best seen on both plain radiography and CT.6 Their appearance on CT and MR follows the internal makeup of the

cyst, and can often have external ostia or underlying sinus tracts associated with them. On CT, epidermoid cysts demonstrate fluid attenuation and dermoid cysts demonstrate a more complex appearance, typically fat attenuation. Epidermoid cysts tend to be low signal on T1-weighted images and high signal on T-2 weighted images (simple fluid intensity characteristics), while dermoid cysts demonstrate high signal on T1-weighted images and low signal on T-2 weighted images.7

Eosinophilic Granuloma (Figure 6) Eosinophilic granuloma is synonymous with Langerhans cell histiocytosis (LCH), a proliferative disorder of the Langerhans cells. The localized form is the most common of the three different forms of the disease and bony involvement is the most common presentation of LCH in children. Osseous lesions are most often seen in the skull, with the femur, maxilla, mandible, orbit, pelvis, and temporal bone being other common sites of involvement. Peak occurrence of LCH is between ages 1 to 4 with a slight predilection for males. Pain and swelling are the usual presenting symptoms, and given the common locations of involvement, there is often overlap with other disease processes like otitis media, mastoiditis, trauma, or even seborrhea. For this reason, it can be misdiagnosed or unrecognized until later in life.7,8 LCH can have an indolent or aggressive appearance. On plain radiography, eosinophilic granulomas are often aggressive with a lytic, “punched-out”, appearance. They can also have a beveled appearance due to uneven destruction of the two osseous tables. At CT, these lesions are soft tissue masses that demonstrate enhancement with surrounding

osseous erosion. On MR, they demonstrate low to intermediate signal intensity on T-1 weighted images, high signal intensity on T-2 weighted images and diffuse enhancement with the administration of contrast. LCH is often followed long term with serial imaging to guide management.7

Desmoid-type Fibromatosis (Desmoid Tumor) (Figure 7) Desmoid-type fibromatosis, also known as desmoid tumor, is a lesion that arises from the fascial sheaths and aponeuroses of striated muscle. Desmoid tumors are classified as a part of the fibromatoses, which is a group of disorders characterized by their similar pathologic features of fibrous tissue proliferation. The fibromatoses are biologically intermediate between benign fibrous lesions and fibrosarcomas, in that they tend to recur and also invade surrounding tissue, but they do not metastasize. The fibromatoses are divided into superficial (fascial) fibromatoses, which are typically small and slow-growing, and deep (musculoaponeurotic) fibromatoses, which are larger and grow relatively quickly. Desmoid tumors make up the deep fibromatoses, which are further divided into extraabdominal, abdominal, and intra-abdominal subgroups.9 In general, desmoid tumors are less common than the superficial fibromatoses, with an annual incidence of two to four individuals per million. They are slightly more common in females, and are more common in adults than in children. The etiology of fibromatoses is felt to be multifactorial and includes genetic, endocrine, and physical factors. In the pediatric population, the extra-abdominal subgroup is the most prevalent type of desmoid tumor, except in Gardner’s syndrome. Extra-abdominal desmoids are deep-seated and

typically solitary in nature. Although they can be located in many different locations on the body, they are most commonly encountered in the head and neck, trunk, and extremitites.8,10 The most common site for lesions in pediatric patients is the head and neck, seen in up to 30% of pediatric desmoid tumors.11,12 These tumors are firm, ill-defined masses that tend to have very few, if any, associated symptoms. Although rare, some of the symptoms that have been reportedly caused by desmoid tumors are neurologic pain and decreased joint mobility.8,10 Given their anatomic origin, in the fascial sheaths and aponeurosis of muscle, and their locally infiltrative nature, it is no surprise that a patient might present with such symptoms if the tumor has infiltrated nerve or bone adjacent to the affected muscle. These tumors have even proven to be fatal in rare circumstances involving the head and neck, where vital structures were infiltrated. On gross appearance, desmoid tumors are solid masses that typically range from 510 cm in maximum diameter, but can exceed 15 cm. They are characteristically firm and can be difficult to penetrate with biopsy needles. On cross section, desmoid tumors are a shiny whitish color and exhibit an internal gritty texture with a coarsely trabeculated surface, similar to that of scar tissue. Given their inherent infiltrative nature, desmoid tumor margins often extend into muscle and subcutaneous tissue and can extend along fascial planes to distant locations relative to the primary tumor site.8,11 Although rare, there are cases of desmoids tumors that spontaneously regress, and due to its relatively benign nature, there is some controversy as to how to best treat desmoids. Most often, treatment for desmoid tumors is based on whether or not symptoms are present and the type of symptoms encountered by the patient. The treatment of choice

in symptomatic patients consists of surgical resection with wide margins, due to their high recurrence rate. Complete surgical excision with clear margins may be difficult to accomplish without causing significant morbidity and/or loss of function, depending on the size and location of the lesion. Nonsurgical treatment includes radiation therapy and chemotherapy.10,11 Imaging is vital in characterizing desmoid tumors preoperatively. With imaging, the number, location, margins, and enhancement patterns of lesions can be assessed, as well as the extent to which local infiltration into adjacent structures may have occurred. At least one study has demonstrated a lower recurrence rate with the advent of advanced imaging modalities (CT and MR), likely on the basis of better surgical planning.9 On plain radiographs, palpable desmoid tumors appear as soft tissue masses without other characteristic features but may demonstrate erosion and/or cortical defects of adjacent bony structures. On ultrasound, desmoid tumors are typically hypoechoic soft tissue masses that are usually ill-defined. They can demonstrate hypervascularity with color flow Doppler examination and larger lesions can demonstrate posterior acoustic shadowing.10,11 On CT, desmoids are characterized as soft tissue masses with poorly defined margins, attributed to their infiltrative nature. They are of variable attenuation, with some lesions demonstrating increased attenuation compared to striated muscle, possibly due to increased collagen deposition. Contrast-enhanced CT imaging of desmoid tumors reveals variable enhancement of the lesions, presumably secondary to the hypervascularity seen in many desmoid tumors.11

MR imaging is the best modality to definitively characterize and differentiate desmoid fibromatoses from other soft tissue masses. On MR, the borders may be well or non-circumscribed, once again attributable to the tumor’s infiltrative characteristics. Linear extension of tumor along fascial planes is a common characteristic finding of desmoid tumors on MR, and can further serve to aid in staging disease and in surgical planning. The signal characteristics of desmoid tumors on MR are heterogeneous and felt to be related in large part to the cellular make-up of the lesion. The signal seems to vary depending on the degree of collagen, spindle cells, and mucopolysaccharides present in the tumor. In general, MR characteristics of desmoid tumors most include intermediate to low signal intensity relative to muscle on T1-weighted images, and high intensity signal mixed with bands of low intensity signal relative to muscle on T2-weighted images. These bands of low signal intensity can also be seen on T1-weighted contrast enhanced images, and are helpful in differentiating desmoid tumors from other neoplastic lesions. After administration of contrast material, most desmoid tumors demonstrate heterogeneous enhancement on MR imaging. Ultimately, confirmation with tissue biopsy is necessary for a definitive

diagnosis.10,11,13

Myositis Ossificans (Figure 8) Myositis ossificans (MO) is a benign soft tissue mass composed of reactive hypercellular fibrous tissue and bone, usually found in skeletal muscle. The name of this entity is misleading, as it does not involve primary inflammation of muscle. It is also known as pseudomalignant osseous tumor of soft tissue, extraosseus localized nonneoplastic bone

and cartilage formation, myositis ossificans circumscripta, myositis ossificans traumatica, pseudomalignant myositis ossificans, and hypertrophic ossification. These lesions are typically solitary, self-limiting, and reparative. They are fast-growing lesions that often cause concern given their histological appearance of hypercellularity, cytological atypia, and mitotic activity. Occurrence in infants is rare and there is a predilection for males. Most patients with MO are physically active, and there seems to be an antecedent traumatic event associated with these lesions in most patients. Patients often present with pain, a palpable mass and decreased range of motion.2 MO can occur anywhere in the body, but is most often seen in the extremities, trunk, and head and neck.8,14 In the first week or two, the imaging characteristics are nonspecific, showing an intramuscular mass. Plain radiographs and CT scans in patients with MO can exhibit soft tissue fullness and swelling in the area of the abnormality. On MR, MO demonstrates heterogeneous signal intensity and high signal intensity on T2-weighted images. In the next several weeks, the lesions begin to ossify, eventually developing dense peripheral calcifications, and ultimately demonstrate eggshell-like/lacy appearance of bone deposition in the periphery.8,14 This appearance is best appreciated with plain films and CT. Mineralization will present as low signal on MR and may not be recognized as ossification without a high index of suspicion and correlation with other imaging.

Muscle Hernia (Figure 9) Muscle hernias are bulges of skeletal muscle through an overlying fascial defect. These most commonly are found in the lower extremity typically involving tibialis anterior.

These most often present as a painless mass, though occasionally can cause pain. Muscle contraction, exercise and upright positioning cause enlargement. Many causes including prior trauma, athletic and work related activities, chronic compartment syndrome and fascial weakness due to perforating vessels have been associated with muscle hernias.15 At ultrasound, a muscle hernia can be seen as a protrusion of muscle through a defect in the overlying echogenic fascia or bulging of a region of thinned fascia. The herniated muscle and adjacent nonherniated muscle appear less echogenic than normal muscle.15 The herniating muscle may extend out of the fascial defect in a mushroom like fashion and can sometimes be seen with an adjacent vessel. Active muscle contraction or upright positioning during the examination may make apparent or increase the size of the hernia. With MRI, a muscle hernia can be seen as a focal bulge or contour abnormality at the site of the palpable abnormality. The overlying fascia defect may or may not be seen. Axial imaging utilizing rapid sequences with the foot held in plantar and dorsiflexion may increase the conspicuity of the hernia.16

Popliteal (Baker’s) cyst (Figure 10) Popliteal cysts are synovial lined cysts arising in the medial popliteal fossa, located between the tendons of the semimembranosus and medial head of gastrocnemius. In adults, these reflect a communication of joint fluid with the normally occurring gastrocnemius-semimembranosus bursa.17 Since they communicate with the joint, the

same processes can affect them, such as synovitis, hemarthrosis or loose bodies. In children, these are less prevalent than in adults. The pathogenesis of Baker’s cysts in children is postulated to be caused by direct trauma to the popliteal fossa and in turn to the normally occurring bursa, since a direct communication between the bursa and the joint is found in less than half of cases.18-20 Popliteal cysts can extend both superiorly and inferiorly from the joint line and can be multilobulated. Partial rupture can be seen as fluid extending from the cyst, often inferiorly due to positioning. With radiographs, a popliteal cyst may be seen as soft tissue fullness in the popliteal fossa. At ultrasound, a cystic structure is seen in the medial aspect of the popliteal fossa. The fluid may appear complex if there is synovitis or hemorrhage. With MR, the exact position of the cyst as it relates to the two tendons can be discerned, as can any complexities to the fluid.

Soft tissue abscess (Figure 11) Soft tissue infection can manifest as cellulitis, phlegmon or discrete abscess. Soft tissue abscesses can be located either superficially or deep, can cross multiple spaces, and can arise due to direct trauma or hematogenous spread. Radiographs may demonstrate a soft tissue lump or diffuse swelling. CT with intravenous contrast will usually show peripheral rim enhancement and low-density nonenhancing central cavity. The density of the fluid can vary dependent upon the proteinaceous composition of the fluid. Without contrast, the extent of an abscess may be

difficult to fully appreciate as many abscesses are surrounded by inflammatory edema and phlegmonous change, which may appear indistinguishable from the abscess without contrast. Post contrast imaging also helps to identify septations or loculations within the collection that may alter the approach for surgical or percutaneous drainage. Similarly, MR can resolve septations and dependent on the protein content of the fluid and its related signal differences, can often distinguish an abscess from surrounding edema.

Osteochondroma (Figure 12) Osteochondromas are the most common bone tumor, representing 10-15% of all bone tumors and 20-50% of benign bone tumors. However, they are a developmental lesions rather than true neoplasms (21). They are most commonly seen as a solitary finding or can be associated with the autosomal dominant syndrome known as hereditary multiple exostoses (HME) or diaphyseal aclasis, which can show incomplete penetrance in females. They result from the separation of a piece of epiphyseal growth plate cartilage which then extrudes through the periosteal bone cuff, which normally surrounds the growth plate.21 Osteochondromas can be either pedunculated or sessile. The lesions are composed of cortical and medullary bone with an overlying cartilaginous cap. They must also have cortical and medullary continuity with the underlying bone. Osteochondromas can occur in any bone that undergoes enchondral ossification. The most frequently involved sites are the long bones of the lower extremity with most lesions seen found around the knee and humerus. Lesions in the small bones of the hands and feet, scapula, pelvis and spine are

seen less commonly seen. Long bone lesions typically involve the metaphysis and the pedunculated variety tends to point away from the nearest joint.21 The radiographic appearance is often pathognomonic though sometimes the contiguity with the marrow cavity can be difficult to discern on radiographs necessitating cross sectional imaging. CT can accurately depict this connection. The mineralized portion of the cartilage cap can be seen on CT; however, measurement of nonmineralized portions of the cap can be challenging with CT, as it can be difficult to distinguish this from a possible overlying bursa. The cartilage cap in benign lesions typically measures a few millimeters in thickness or may be absent in adults, with greater thickness up to 1-3 cm seen in children. Once skeletal maturity has occurred, these lesions should cease growing. Increased thickness of the cartilage cap or continued growth after skeletal maturity suggests possible malignant transformation, which is seen in approximately 1% of solitary lesions and 3%-5% in HME.21 MRI also can demonstrate the contiguity with the underlying medullary bone and remains the best modality to demonstrate the mass effect on adjacent structures. When contrast is administered, septal and peripheral enhancement of the cartilage cap can be seen.21 With HME, approximately 2/3rds of patients have a positive family history. This in combination with the multiplicity of lesions and their associated deformity, lower the age at diagnosis, with most diagnosed by age 5 and virtually all by age 12. The osteochondromas in HME are identical to the solitary variety though in HME, sessile lesions are more common and may be up to 90% of the total lesions.21,22

Bony deformation in HME is most commonly manifested as bowing deformity. Uncovering of the femoral heads can be caused by coxa valga of the proximal femurs. Bowing and growth disturbances in the forearm can lead to Madelung deformity. Synostoses can occur when large lesions grow together.22 Osteochondromas can also cause pressure erosions of adjacent bones, restrict motion, and lead to tendon snaping, tenosynovitis and premature osteoarthritis. Irritation, compression, or displacement of adjacent soft tissues can lead to formation of bursitis, neuropathy, pseudoaneurysms and thrombosis. Fracture can occur through the stalk of pedunculated lesions. As mentioned previously, the lesions can also undergo malignant transformation, almost invariably to chondrosarcoma. Murphey et all suggest using a cutoff of 1.5 cm in thickness for a benign cartilage cap in a skeletally mature patient with greater thicknesses concerning for transformation.21

Osgood-Schlatter (Figure 13) Osgood-Schlatter disease is defined by abnormal growth and development of the tibial apophysis at the site of the attachment of the patellar tendon, secondary to chronic fatigue injury and traction microtrauma. It is most common in adolescents between 10 and 15 years of age, with a predilection for males. It is typically seen in patients who are physically active, especially in sports that require jumping, squatting, or kneeling. The typical presentation is unilateral or bilateral anterior knee pain and tenderness. Physical exam reveals soft tissue swelling and tenderness over the anterior tibial tubercle. It is

typically a clinical diagnosis that is self-limited. When the diagnosis is in question, imaging can be performed to help rule out other etiologies.23,24 The anterior tibial tubercle is a downward protruding extension of the proximal tibial epiphysis. Like other immature epiphyseal equivalents, the periphery is initially cartilaginous with an underlying ossification center that eventually grows to replace the epiphyseal cartilage. Repetitive microtrauma can involve only the superficial cartilage or also involve the ossification center. Early in the process, plain radiography will show only soft tissue swelling. As the process progresses, there may by irregularity and fragmentation of the anterior cortex of the tibial tubercle. At this point, the process can heal with no longterm sequellae. However, chronic cartilaginous avulsion can also lead to development of accessory ossicles or a bony tibial protruberance at the attachment of the patellar tendon. It is important to note that the tibial tubercle itself may ossify in a fragmented fashion. These normal growth centers should be seen within the contour of the normal anterior tibia. The accessory ossicles due to cartilage avulsion will be positioned anterior to the normal bone cortex. Ultrasound and MR are usually unnecessary. The most common findings on MR including soft tissue swelling over the tibial tubercle, hypertrophy or fragmentation of the tibial tubercle, loss of the sharp inferior angle of the infrapatellar fat pad and surrounding soft tissues, thickening and edema of the inferior patellar tendon, and infrapatellar bursitis. Ultrasound reveals thickening and heterogeneous echogenicity of the patellar tendon. Echogenic fragments representing bone and hypervascularity can also been seen in the patellar tendon with ultrasound.23-25

Conclusions Given the prevalence of palpable abnormalities in the pediatric patient, and the need to help narrow the differential diagnosis based upon imaging, it is essential for radiologists to have a wide-range of knowledge of many frequently encountered causes. Having a general understanding of the possible entities, their imaging findings, and which imaging modalities are best suited for further evaluation, will not only enable the radiologist to be a valuable member of the medical team, but will also help to avoid unnecessary radiation exposure in such a sensitive patient population.

Citations: 1. Donnelly LF, Adams DM, Bissett GS: Vascular Malformations and Hemangiomas: A Practical Approach in a Multidisciplinary Clinic. AJR 174: 597-608, 2000

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FIGURE CAPTIONS

Fig. 1. Imaging Algorithm. A systematic approach to image evaluation of the pediatric patient with a palpable abnormality is presented.

Fig. 2. Infantile hemangioma. MR imaging of an 11 month old female with a posterior neck mass shows a multilobulated mass in the subcutaneous fat of the posterior neck. The mass is mildly hyperintense on noncontrast T1 (A) and STIR (B). Note flow voids on the coronal STIR image (arrow). Postcontrast T1 axial (C) and coronal (D) images show intense uniform enhancement.

Fig. 3. Lymphatic malformation. Prenatal ultrasound transverse (A) and 3-D surface rendering (B) images performed at 33 weeks and 6 days gestational age show a left axillary septated, cystic mass that is confined to the subcutaneous tissues. No flow was seen with color Doppler (not shown). (C) Postnatal chest radiograph of the same patient at 30 days of age shows a large left axillary soft tissue mass. (D) Ultrasound on the same day confirms the thin-walled, septated cystic morphology. Diagnosis was confirmed histologically after surgical excision.

Fig. 4. Venous malformation. Grayscale ultrasound image (A) demonstrating a lobulated, septated anechoic lesion within the biceps muscle with internal flow noted on color Doppler (B). Note that not all of the anechoic spaces show flow on color Doppler, likely reflecting slow flow. Upon external compression with the transducer (C), there is near complete effacement of the anechoic spaces. Coronal STIR (D), axial fat suppressed T2 (E), axial fat suppressed T1 pre-contrast (F) MR images in the same patient demonstrate the T2 hyperintense and mildly T1 hyperintense mass located within

the biceps muscle. Post contrast T1 (G) shows near-uniform enhancement of the cystic spaces, characteristic of venous malformations. Note the use of a skin marker (*) to delineate the region of the palpable mass.

Fig. 5. Dermoid cyst. Axial (A) and sagittal (B) CT with contrast in a 3 year old female with a palpable scalp mass demonstrate a sharply circumscribed lytic lesion with sclerotic borders that abuts the underlying superior sagittal sinus (arrow) without compression, thrombosis, or intracranial extension. Coronal T2 (C), sagittal fat suppressed, contrast–enhanced T1 (D) and sagittal MR venogram (E) in the same patient, confirm a non-enhancing mass without vascular or intracranial extension. The lesion abuts the flow-void of the superior sagittal sinus, without extension into the sinus. Diagnosis was confirmed histologically after surgical excision.

Fig. 6. Langerhans Cell Histiocytosis. Lateral skull radiograph (A) in a 15 year old male with a painless right frontal scalp mass reveals a 2.5 cm lytic lesion in the right frontal bone without sclerotic margins. A cutaneous BB marker lies over the lesion. (B) Bone window from axial CT image shows a scalp mass with fairly aggressive bone destruction. (C) Axial T2 MR image shows a high signal scalp mass. (D) Coronal T1 contrast enhanced image with fat suppression shows an enhancing mass in the right frontal region that extends through the full thickness of the calvarium, contacting the dura without epidural extension. (E) Whole body planar Tc99m bone scan shows an area of increased activity in the right frontal bone but no other lesions. The patient had biopsyproven Langerhans Cell Histiocytosis.

Fig. 7. Desmoid tumor. (A) Lateral radiograph of the right lower extremity in a 13 year old male with a palpable mass above the ankle, reveals soft tissue prominence anterior to the distal tibia (arrow) with no evidence of internal calcification or erosion of the underlying bone. (B) Coronal T1weighted MR image shows a low signal mass in the anterolateral aspect of the leg, originating from the extensor digitorum longus muscle. (C) Axial fat suppressed proton density and (D) coronal contrast-enhanced, fat suppressed T1-weighted MR images show intense, slightly heterogeneous enhancement of the mass. A vitamin E marker (*) is used to delineate the area of the palpable abnormality. The mass was later proven to represent a desmoid fibromatosis.

Fig. 8. Myositis ossificans. Serial lateral radiographs of the left femur in a 16 year old male after a football injury with thigh pain and swelling. (A) Initial radiograph shows no osseous or soft tissue abnormality. (B) Approximately one month after initial injury there is a peripherally calcified soft tissue lesion overlying the anterior mid femoral shaft. Subsequent imaging at three (C), five (D), and eleven months (D) after initial presentation, show progressive ossification and incorporation into the femoral cortex.

Fig. 9. Muscle hernia. (A) Transverse ultrasonography image of the anterior right leg of a 16 year old female with a palpable nodule demonstrates a defect in the anterior fascial plane of the tibialis anterior muscle (arrows). (B) A protrusion of striated soft tissue is demonstrated traversing this defect (arrow), consistent with a muscle hernia.

Fig. 10. Baker’s cyst. (A) Lateral radiograph of the right lower extremity in a 6 year old male with a palpable, soft, non-tender posterior right knee mass, shows soft tissue fullness in the popliteal fossa

that extends dorsal to the distal femur (arrow). (B) Sagittal ultrasound image shows a septated cystic mass of the right posterior thigh, extending inferiorly into the popliteal fossa. (C) Fat suppressed axial T2 (C), sagittal proton density (D) and T1 contrast-enhanced MR images show a multi-septated fluid collection in the popliteal fossa. The collection arises from the knee joint and exits between the tendons of the medial head of gastrocnemius (long arrow) and semimembranosis (short arrow) muscles. (E) Sagittal post contrast fat saturated T1 only shows enhancement of the thin wall and septations.

Fig. 11. Pretibial hematoma. (A) Gross photograph of the leg of a 12 year old male with posttraumatic anterior leg pain shows swelling, ecchymosis and mild erythema. (B) Transverse and (C) longitudinal ultrasound images demonstrate a complex, partially septated cystic collection, with dependent layering debris. No foreign body was seen. The sagittal image shows apparent elevation of the periosteum (arrows). There was no internal flow on color Doppler (not shown). (D) Lateral plain film obtained immediately after the ultrasound shows no foreign bone destruction or calcified periosteal reaction. Incision and drainage revealed 20 cc blood clot that was culture negative.

Fig. 12. Osteochondroma. 14 year old male with leg pain and swelling and known history of multiple hereditary exostosis. Frontal and lateral radiographs of the left femur (A, B) demonstrate multiple exostoses projecting from the distal femur. The largest is posterior and has a broad based attachment with a pedunculated contour. There is an associated abnormal contour to the overlying soft tissues. There is also an exostosis arising from the fibula posteriorly. There is no evidence of pathologic fracture. CT images in the same patient, including 3D reconstructions (C-E), reveal multiple, circumscribed pedunculated and sessile metadiaphyseal exostoses of both lower

extremities. They project from the bony cortex and demonstrate continuity with the marrow cavity. There are no aggressive features.

Fig. 13. Osgood Schlatter disease. (A) Lateral radiograph of the right lower extremity in a 12 year old female with anterior knee pain shows fragmentation of the anterior tibial tubercle (arrow). Sagittal fat suppressed T2-weighted and proton density MR images of the right knee (B, C) in the same patient also demonstrates osseous fragmentation of the tibial tubercle and increased signal in the lower patellar tendon, consistent with tendinopathy. (D and E) Lateral views of the knee in a different patient requested to assess painful swelling. (D) The initial film at 15 years old shows soft tissue swelling and irregular ossification of the anterior cortex of the tibial tubercle. (E) Repeat film 2 years later shows complete ossification of the tubercle and an accessory ossicle at the attachment site of the patellar tendon.