Roentgen Ray Reader

High Origin of the Anterior Band of the Inferior Glenohumeral Ligament

2012-02-12T05:47:00.001-06:00

The anterior band of the inferior glenohumeral ligament (aIGHL) usually arises from anteroinferior labrum (below ~4 o’clock), but origins as high as 1 o’clock and from the middle glenohumeral ligament have also been described. These higher origins can mimic labral tears, variants (e.g., sublabral foramen and recess), or normal structures (e.g., spiral glenohumeral ligament) on MR imaging or MR arthrography to the uninitiated.

There may also be a relationship between the sites of attachment of the long head of the biceps tendon and the aIGHL. A study of ~100 cadavers suggested that a long head of the biceps attachment to the posterior labrum was associated with an aIGHL origin below the 4 o’clock position, while a biceps tendon attachment elsewhere was associated with a higher origin of the aIGHL. More recent work (10 cadavers) has not supported these results, however.

References

Merila M, Leibecke T, Gehl HB, Busch LC, Russlies M, Eller A, Haviko T, Kolts I. The anterior glenohumeral joint capsule: macroscopic and MRI anatomy of the fasciculus obliquus or so-called ligamentum glenohumerale spirale. Eur Radiol. 2004 Aug;14(8):1421-6.
Ramirez Ruiz FA, Baranski Kaniak BC, Haghighi P, Trudell D, Resnick DL. High origin of the anterior band of the inferior glenohumeral ligament: MR arthrography with anatomic and histologic correlation in cadavers. Skeletal Radiol. 2011 May 22.
Tuoheti Y, Itoi E, Minagawa H, Yamamoto N, Saito H, Seki N, Okada K, Shimada Y, Abe H. Attachment types of the long head of the biceps tendon to the glenoid labrum and their relationships with the glenohumeral ligaments. Arthroscopy. 2005 Oct;21(10):1242-9.

MRI Staging of Avascular Necrosis

2012-02-11T05:34:00.003-06:00

A staging system has been developed for avascular necrosis based on signal characteristics at the center of the lesion.

Class	T1	T2	Comment
A	High	Intermediate	Fat
B	High	High	Blood
C	Low	High	Fluid
D	Low	Low	Fibrosis

Class A signal intensity is typically seen in early disease, while class D signal intensity is typically seen in late disease. However, more than one class of signal intensity can be found in a single lesion.

References

Mitchell DG, Rao VM, Dalinka MK, Spritzer CE, Alavi A, Steinberg ME, Fallon M, Kressel HY. Femoral head avascular necrosis: correlation of MR imaging, radiographic staging, radionuclide imaging, and clinical findings. Radiology. 1987 Mar;162(3):709-15.

Diffuse Idiopathic Skeletal Hyperostosis: Pelvis

2012-02-10T05:52:00.000-06:00

We're all familiar with the spinal findings of diffuse idiopathic skeletal hyperostosis (DISH). Radiographic manifestations in the pelvis are usually symmetrical and include:

Enthesophytes (yellow arrows): Irregular outgrowths or whiskering seen most commonly at the iliac crests, ischial tuberosities, and the trochanters.
Para-articular osteophytes (red arrows): Broad and well-defined. Seen at the acetabular margins, sacroiliac joints, and pubic symphysis. Sacroiliac osteophytes tend to affect the inferior margins.
Ligamentous ossification: Iliolumbar (black arrows) and sacrotuberous ligaments.

References

Resnick D, Shaul SR, Robins JM. Diffuse idiopathic skeletal hyperostosis (DISH): Forestier's disease with extraspinal manifestations. Radiology. 1975 Jun;115(3):513-24.

KLS Talon Sternal Closure

2012-02-09T06:43:00.004-06:00

The KLS Sternal Talon is a new sternal closure device. The device has two halves that are placed on opposite sides of the sternotomy and snapped together. Each half can can have either one or two legs (or hooks). The single-legged design is shown above.

The device is said to distribute force across a larger area of bone, which can be helpful in patients with morbid obesity, diabetes, chronic obstructive pulmonary disease (forceful coughing), or osteoporosis. The design also allows for rapid opening in case of post-operative complications.

Videos and pictures can be found at the links below.

References

Levin LS, Miller AS, Gajjar AH, Bremer KD, Spann J, Milano CA, Erdmann D. An innovative approach for sternal closure. Ann Thorac Surg. 2010 Jun;89(6):1995-9.
Publicity web site with videos.
Corporate web site with videos.

The Dunn View

2012-02-08T08:00:00.001-06:00

The Dunn view, originally described in 1952 for measuring the anterversion of the femoral neck in children, is now commonly used for assessment of femoral head sphericity in young adults suspected of having cam-type femoroacetabular impingement (FAI).

As originally described (sometimes called the 90° Dunn view), it is an anteroposterior view of the hip with the patient supine and with the hips and knees flexed at 90°, the legs abducted 15°-20° from the midline, and the femur in neutral rotation. The beam is centered at the midway point between the anterior superior iliac spine and the pubic symphysis, and the tube-to-film distance is ~40 in (102 cm). Imagine a patient lying flat on an examination table with the legs in stirrups.

The modified (45°) Dunn view is the same, except that the hip is flexed to 45°. Imagine a patient lying flat on a table with the knee bent and the foot flat on the table. The paper by Clohisy et al has nice pictures of these views.

The Dunn views (45° or 90°) are best at demonstrating femoral head asphericity. A cross-table view in internal rotation can also be used, but anteroposterior or externally rotated cross-table views are likely to miss asphericity.

Using MRI as the standard, and a cut-off alpha angle of 50.5° for diagnosis of cam-type FAI, the 90° Dunn view was found to be 91% sensitive and 88% specific, with a positive predictive value of 93%, negative predictive value of 84%, and accuracy of 90%. There was also strong correlation between alpha angles on the Dunn view and on MRI (Pearson correlation of 0.7).

References

Barton C, Salineros MJ, Rakhra KS, Beaulé PE. Validity of the alpha angle measurement on plain radiographs in the evaluation of cam-type femoroacetabular impingement. Clin Orthop Relat Res. 2011 Feb;469(2):464-9.
Clohisy JC, Carlisle JC, Beaulé PE, Kim YJ, Trousdale RT, Sierra RJ, Leunig M, Schoenecker PL, Millis MB. A systematic approach to the plain radiographic evaluation of the young adult hip. J Bone Joint Surg Am. 2008 Nov;90 Suppl 4:47-66.
Dunn DM. Anteversion of the neck of the femur; a method of measurement. J Bone Joint Surg Br. 1952 May;34-B(2):181-6.
Meyer DC, Beck M, Ellis T, Ganz R, Leunig M. Comparison of six radiographic projections to assess femoral head/neck asphericity. Clin Orthop Relat Res. 2006 Apr;445:181-5.

The Pelvic Digit

2012-02-07T07:53:00.002-06:00

Bony protuberance at the left anterior inferior iliac spine

A pelvic digit is a rare congenital anomaly in which bone develops in soft tissues adjacent to normal skeletal structures. On radiographs it typically appears as a rib- or a phalanx-like bone with a clear cortex and medulla related to the pelvis, often with a characteristic pseudoarticulation at the base. It has been previously reported as an iliac rib or pelvic rib.

It is important to distinguish a pelvic digit from acquired anomalies such as myositis ossificans and avulsion injuries of the pelvis.

This anatomic variant can originate from a displaced costal process, a displaced sternal center, or the ossification center at the anterior superior iliac spine. These explanations, however, do not take into account the varied sites of attachment in the pelvis. As a pelvic digit can be found at the coccyx, the pelvic walls, and the inferior abdominal wall, it must arise from an embryonic mesoderm with rib-forming capacity that is disposed to these regions.

At the end of the third week of embryogenesis, embryonic mesoderm cells, with the potential to form ribs, migrate from the primitive streak and pass around the cloacal membrane, from the region of the future coccyx, through the region of the future pelvic walls, to the region of the lower abdominal wall.

References

Casey MC, Phancao JP, Pressacco J. Answer to case of the month #106. Pelvic Digit. Can Assoc Radiol J. 2006 Feb;57(1):51-3.
Rolando Reyna. MyPacs.net

Diffuse Idiopathic Skeletal Hyperostosis: Hands

2012-02-06T11:35:00.000-06:00

We're all familiar with the spinal manifestations of diffuse idiopathic skeletal hyperostosis (DISH). Findings in the appendicular skeleton are not as well known:

Sites of tendon and ligament attachment: Periosteal enthesophytes and dystrophic calcification can be seen.
Joints: Para-articular osteophytes that can bridge the articulation. The bone underlying the osteophyte can be sclerotic. The involved joint can be radiographically normal, but will usually have degenerative cartilage and bony changes histologically.
Ligaments: Ligamentous mineralization is analogous to the familiar ribbon-like calcifications seen along the anterior aspect of the vertebral bodies. Ranges from minimal involvement to involvement of the entire ligament.

In the hand, DISH can manifest as:

Broadening and arrowheading of the distal phalangeal tufts: Can also be seen in acromegaly. Typically less marked in DISH.
Increased cortical width of tubular bones: Can also be seen in acromegaly.
Enlarged sesamoid bones: Can also be seen in acromegaly. Typically less marked in DISH.
Exostoses: Metacarpal and phalangeal (orange arrow) heads, distal end of the radius (pink arrow). Here we see also one in the left sesamoid (yellow arrow). Can also be seen in acromegaly, but is typically more marked in that condition.
Enthesopathy: At the proximal phalanges (blue arrows). Can also be seen in acromegaly, but is typically mild in that condition.
Joint capsule bone formation: Can also be seen in acromegaly, but is typically more marked in that condition.
Osteoarthritis and osteophyte formation: Interphalangeal joints (green arrow).

Although some of the findings can resemble those of acromegaly, patients with DISH do not have the soft tissue and cartilage hypertrophy that can be seen in acromegaly.

References

Littlejohn GO, Urowitz MB, Smythe HA, Keystone EC. Radiographic features of the hand in diffuse idiopathic skeletal hyperostosis (DISH): comparison with normal subjects and acromegalic patients. Radiology. 1981 Sep;140(3):623-9.
Resnick D, Shaul SR, Robins JM. Diffuse idiopathic skeletal hyperostosis (DISH): Forestier's disease with extraspinal manifestations. Radiology. 1975 Jun;115(3):513-24.
Schlapbach P, Beyeler C, Gerber NJ, van der Linden S, Bürgi U, Fuchs WA, Ehrengruber H. The prevalence of palpable finger joint nodules in diffuse idiopathic skeletal hyperostosis (DISH). A controlled study. Br J Rheumatol. 1992 Aug;31(8):531-4.

Mesenteric Trauma

2012-02-05T07:48:00.007-06:00

CT manifestations of mesenteric trauma can include:

Internal hernia: Secondary sign of a mesenteric tear (difficult to detect on CT). Closed loop bowel obstruction, volvulus, and strangulation can occur.
Increased mesenteric attenuation: Can be a manifestation of isolated mesenteric injury.
Mesenteric hematoma: When seen in the portal venous-phase, should be evaluated on delayed images: Enlargement or increased attenuation is a sign of active bleeding (see below). Small isolated mesenteric hematomas can be managed conservatively with observation. Large hematomas indicated injury to major mesenteric vessels, and are managed surgically to avoid the risk of delayed bowel ischemia.
Beading or abrupt termination of mesenteric vessels: In the setting of trauma, these are signs of significant venous or arterial injury.
Active extravasation: Uncommon, but ~100% specific for a significant vascular injury. Requires operative repair. Endovascular coil embolization is sometimes attempted with injury to smaller vessels; however, patients should be closely monitored for signs of bowel ischemia.

Specific signs of mesenteric trauma include mesenteric hematoma, intraperitoneal extravasation of intravenous contrast, and abrupt termination or unequivocal irregularity of the wall of mesenteric vessels.

When specific signs of mesenteric trauma are encountered, a careful search for associated bowel injury should be initiated.

The image above is from a trauma patient. There is active extravasation of contrast in the right lower quadrant (blue arrows) from injury to iliocolic branch of the superior mesenteric artery (pink arrows). Delayed images show expansion of the extravasated pool of contrast (green arrows). The patient also had a jejunal hematoma (not shown).

References

LeBedis CA, Anderson SW, Soto JA. CT imaging of blunt traumatic bowel and mesenteric injuries. Radiol Clin North Am. 2012 Jan;50(1):123-36.

Anterior Column Acetabular Fracture

2012-02-04T05:05:00.000-06:00

Anterior column fractures make up to 5% of acetabular fractures. These fractures separate the anterior border of the innominate bone from the remaining ilium.

Several types of anterior column fractures have been described based on the location where the fracture plane exits the anterior aspect of the bone. However, all types cross the pelvic brim and result in a fracture of the inferior pubic ramus.

Very low: Exit through the iliopectineal eminence. Can be distinguished from anterior wall fractures by the presence of an inferior pubic ramus fracture and a single break in the iliopectineal line.
Low: Exit just below the anterior inferior iliac spine.
Intermediate: Exit through the anterior superior iliac spine.
High (shown above): Exit through the iliac crest.

Radiographs reveal disruption of the iliopectineal line where the anterior column fracture plane crosses the pelvic brim. This is best seen on the frontal and obturator oblique views. The femoral head moves medially and superiorly with the anterior column fragment.

The images above are from a patient with a high anterior column fracture. The radiograph reveals disruption of the iliopectineal line and a lucency through the iliac wing extending to the iliac crest. The CT images delineate the path of the fracture plane through the iliac crest and inferior pubic ramus.

References

Rockwood and Green's Fractures in Adults (7th ed), pp 1478-1479.
Mack LA, Harley JD, Winquist RA. CT of acetabular fractures: analysis of fracture patterns. AJR Am J Roentgenol. 1982 Mar;138(3):407-12.

Chagas Disease (Chagasic Esophagopathy)

2012-02-03T06:52:00.003-06:00

Chest radiograph: A wide mediastinum with normal heart size.

Contrast series: a dilated esophagus is seen in the AP projection.

CT: The esophagus is seen dilated with fluid in the lumen.

Chagas disease is found only in Latin America. It is named after Carlos Chagas, a Brazilian doctor who first described the disease in 1909. He also described the life-cycle of the parasite, identified the insects that transmit the parasite, identified small mammals that act as reservoir hosts, and suggested means to help prevent its transmission.

Usually a person experiences no immediate symptoms following infection. Ten to 20 years later, however, Chagas disease can appear and bring with it several serious heart disorders.

Chagas disease is a protozoosis caused by the flagellate protozoa Trypanosoma cruzi. The infection is usually transmitted via the feces of blood-sucking insect vectors (reduviid bugs). The infection is mostly found in small mammals (sylvatic cycle), and human disease results from the colonization of the human habitat by some vector species (domestic cycle). Vectorial transmission (via the feces of Triatominae) is responsible for 80% of human infections. The entry of metacyclic trypomastigotes via the mucosal route (oral or ocular) is easy. Direct skin penetration seems more difficult, and generally, the parasite enters via the site of the bite or the microlesions associated with scratching.

Chagas disease results in 45,000-50,000 deaths per year. Mortality is mainly due to chronic chagasic cardiomyopathy. Sudden death, usually due to ventricular fibrillation, is the principal cause of death in 60% of cases. Bradyarrhythmia, thromboembolic phenomena, and, rarely, a ruptured aneurysm, are other causes of sudden death. Congestive heart failure (25-30% of cases), cerebral or pulmonary embolism (10-15% of cases. Symptomatic acute phases mainly occur in newborns (congenital infection) or young children. Chagasic esophagopathy is observed more frequently in the second decade of life, and chronic chagasic cardiomyopathy and colopathy are generally detected later, in the third, fourth, or fifth decade of life.

Radiographic contrast study of the esophagus: Serial radiographs of the esophagus at different times after contrast ingestion allow classification of patients into 1 of 4 evolutive stages of the chagasic esophagopathy.

With stage I, the diameter of the esophagus is normal; emptying is delayed. The organ is sometimes hyperkinetic.

With stage II, the organ is dilated (megaesophagus) and displays irregular motile activity. The gastroesophageal sphincter is hypertonic.

With stage III, dilatation and retention are important, and the motile activity is clearly reduced.

With stage IV, the esophagus is clearly dilated and elongated (dolichomegaesophagus) and atonic.

References

Franquet T, Erasmus JJ, Giménez A, Rossi S, Prats R. The retrotracheal space: normal anatomic and pathologic appearances. Radiographics. 2002 Oct;22 Spec No:S231-46.
Martínez S, Restrepo CS, Carrillo JA, Betancourt SL, Franquet T, Varón C, Ojeda P, Giménez A. Thoracic manifestations of tropical parasitic infections: a pictorial review. Radiographics. 2005 Jan-Feb;25(1):135-55.
Rolando Reyna, mypacs.net.

The Long Plantar Ligament Enthesophyte

2012-02-02T06:22:00.000-06:00

Enthesophytes can arise from several places on the plantar surfaces of the calcaneous. One of these is at the origin of the long plantar ligament, which originates from the plantar aspect of the calcaneus between the posterior and anterior tubercles and inserts into the cuboid, with some fibers continuing on to the second to fourth metatarsal bases. Enthesophytes can also arise from the site of origin of the short plantar (calcaneocuboid) ligament (calcaneocuboid ligament) on the anterior tubercle.

The image above shows two plantar calcaneal enthesophytes, one arising just above the origin of the plantar fascia, and the other arising from the origin of the long plantar ligament (pink arrow).

References

Abreu MR, Chung CB, Mendes L, Mohana-Borges A, Trudell D, Resnick D. Plantar calcaneal enthesophytes: new observations regarding sites of origin based on radiographic, MR imaging, anatomic, and paleopathologic analysis. Skeletal Radiol. 2003 Jan;32(1):13-21.
Ward KA, Soames RW. Morphology of the plantar calcaneocuboid ligaments. Foot Ankle Int. 1997 Oct;18(10):649-53.

Traumatic Pneumatocele

2012-02-01T19:45:00.006-06:00

CT shows two pneumatoceles near the pleural surface with fluid (Traumatic pneumatocele Type I)

A laceration is defined as an abnormal intraparenchymal collection of air resulting from traumatic disruption of the lung architecture.

Types of laceration:

Type 1 is an air-filled cavity with or without an air-fluid level, resulting from sudden compression of a pliable chest wall wherein the air-containing lung ruptures.
Type 2 is an air-containing cavity in a paravertebral location, resulting from severe compression of the more pliable lower chest wall and sudden shifting of the lower lobe across the vertebral body causing a shearing type of injury.
Type 3 is a small peripheral cavity or peripheral linear radiolucency that is always close to the chest wall where a rib has been fractured, resulting from a fractured rib that has punctured the lung.
Type 4 is a result of previously formed, firm pleuropulmonary adhesions causing the lung to tear when the overlying chest wall is violently moved inward or fractures, diagnosed only at surgery or autopsy.

The intraparenchymal collections of air described are also termed pneumatoceles. When traumatic cavities fill with blood, a hematoma forms. Radiographically, traumatic pneumatoceles and hematomas are not usually seen until a few hours or even several days after trauma, initially obscured by surrounding contusion. The size, shape,thickness of the wall, and number of pneumatoceles varies widely from patient to patient.

Unlike a simple contusion, which resolves fairly quickly and completely, a laceration generally takes weeks to months to resolve and may result in residual scarring.

Occasionally, pneumatoceles can become secondarily infected, resembling formation of a hematoma.

References

Collins J and Primack SL. CT of nonpenetrating chest trauma. Applied Radiology. 2001 Feb;30(2):11-21.
Rolando Reyna. Traumatic Pneumatocele. mypacs.net

Heterogeneous Splenic Enhancement in Children

2012-01-31T08:58:00.004-06:00

The spleen commonly has heterogeneous enhancement in the first minute after initiation of contrast injection in both adults and children. This heterogeneity is thought to be due to variable rates of flow through the cords of white and red pulp (lymphoid follicles and vascular sinusoids, respectively). Three enhancement patterns have been described. The archiform pattern is the most commonly seen, followed by focally heterogeneous and diffusely heterogeneous.

Different mechanisms affect the heterogeneity in children and adults. Donnelly et al looked at transient splenic heterogeneity and the variables that affect it in children.

They found transient splenic heterogeneity in about 70% of children. This was maximally visualuzed at ~25 seconds and resolved by 70 seconds in the majority (95%) of cases.

They also found that faster rates of contrast injection (≥ 1.0 cc/sec) were more likely to be associated with transient splenic heterogeneity. The time of visualization and time to resolution, however, did not seem to be affected by the rate of injection.

Children older than 1 year were also more likely to have transient splenic heterogeneity, which was thought to be related to the increasing ratio of white pulp (lymphoid follicles) to red pulp (vascular sinusoids) during the first year of life.

The image above is from a 10-year-old boy. The arterial phase reveals the archiform pattern of enhancement, which resolves on the venous phase image.

References

Donnelly LF, Foss JN, Frush DP, Bisset GS 3rd. Heterogeneous splenic enhancement patterns on spiral CT images in children: minimizing misinterpretation. Radiology. 1999 Feb;210(2):493-7.

Trampoline Fracture of the Proximal Tibia

2012-01-30T20:48:00.005-06:00

A trampoline fracture refers to a transverse or buckle (torus) fracture of the proximal tibial metaphysis that occurs in young children who jump on a trampoline with a heavier person.

The upward recoil of the trampoline after the heavier person jumps can generate a large force. If the child happens to land on the trampoline during the recoil, the force may be sufficient to cause the typical tibial fracture described.

Special thanks to Dr. Hansel Otero for the case and reference.

References

Boyer RS, Jaffe RB, Nixon GW, Condon VR. Trampoline fracture of the proximal tibia in children. AJR Am J Roentgenol. 1986 Jan;146(1):83-5.

Pulmonary Alveolar Microlithiasis

2012-01-29T14:32:00.006-06:00

Pulmonary alveolar microlithiasis is a rare autosomal recessive disease that is caused by impaired transfer of phosphorus ions from the alveolar space into type II pneumocytes. This leads to the development of microliths composed of calcium and phosphorus (calcospherites) in the alveoli.

Men and women are affected at an equal rate, and patients tend to be younger than 50 years of age at diagnosis. Most patients have at least one sibling with the disease, and there is a high rate of consanguineous marriages in affected families.

Patients typically present with progressive dyspnea, which, after a protracted course, progresses to pulmonary fibrosis, end-stage lung disease, and chronic pulmonary heart disease.

Initial laboratory evaluation usually reveals no underlying disorder calcium metabolism, and pulmonary function testing reveals a restrictive pattern of lung disease and decreased diffusion capacity (transfer factor).

Radiographs reveal fine calcific micronodules in a diffuse (sandstorm) pattern, but with a more dense involvement of the lower zones (thought to be due to the larger surface area and greater thickness of this part of the lungs). There is usually silhouetting of the mediastinal and diaphragmatic borders and a linear lucency between the ribcage and parenchyma (reflecting subpleural cystic changes). Small apical bullae with or without an associated pneumothorax may also be present.

The findings are more subtle in children. Nodular calcific densities are less prominent on children’s chest radiographs and the major finding may be ground-glass opacities.

HRCT reveal widespread involvement of both lungs with microliths, with a predisposition for the posterior segments of the lower lobes, anterior segments of the upper lobes, and the medial aspects of the lungs.

Confluent calcifications may also be seen, and are often found in the upper lobes. There is also micronodulation and thickening of the interlobular septa and bronchovascular and subpleural interstitium.

Multiple small, thin-walled subpleural cysts can also be seen and are responsible for the lucent subpleural line seen on radiographs. Pleural calcifications have also been described.

When extensive, the calcifications can result in interlobular septal thickening. Microliths smaller than 1 mm can produce a ground-glass appearance. Together, these can give an appearance similar to crazy paving.

In children, a ground-glass pattern may predominate, and microliths are seen to a lesser degree.

Differential considerations include:

Metastatic calcification: For example, in chronic renal failure and orthotopic liver transplantation.
Dystrophic calcification: Caused by granulomatous disorders (silicosis, sarcoidosis), DNA viruses, parasitic infections, and pulmonary amyloidosis.
Pulmonary ossification: Multiple causes. Most pimped: chronic chronic mitral stenosis.

References

Chan ED, Morales DV, Welsh CH, McDermott MT, Schwarz MI. Calcium deposition with or without bone formation in the lung. Am J Respir Crit Care Med. 2002 Jun 15;165(12):1654-69.
Gasparetto EL, Tazoniero P, Escuissato DL, Marchiori E, Frare E Silva RL, Sakamoto D. Pulmonary alveolar microlithiasis presenting with crazy-paving pattern on high resolution CT. Br J Radiol. 2004 Nov;77(923):974-6.
Helbich TH, Wojnarovsky C, Wunderbaldinger P, Heinz-Peer G, Eichler I, Herold CJ. Pulmonary alveolar microlithiasis in children: radiographic and high-resolution CT findings. AJR Am J Roentgenol. 1997 Jan;168(1):63-5.
Siddiqui NA, Fuhrman CR. Best cases from the AFIP: Pulmonary alveolar microlithiasis. Radiographics. 2011 Mar-Apr;31(2):585-90.

Tracheal Rupture

2012-01-28T23:16:00.000-06:00

Tracheobronchial injury after blunt or penetrating traumatic chest injury is rare, occurring in less than 2% of cases. The majority of intrathoracic tracheobronchial injuries are within 2.5 cm of the carina and most commonly affect the proximal right main stem bronchus.

Tracheal rupture makes up about 1/4 of all tracheobronchial injuries, and is associated with high morbidity and mortality from ventilatory failure, infection (mediastinitis, sepsis), and intermediate- and long-term complications (airway stenosis, recurrent pulmonary infections, bronchiectasis, and permanent pulmonary function impairment).

Clinical and imaging manifestations are subtle and nonspecific, and can result in delayed or missed diagnosis.

Deep cervical emphysema, pneumomediastinum, and paratracheal gas are seen in the vast majority of cases. The tracheal wall injury can sometimes be directly visualized on CT as a tracheal wall defect of discontinuity. Focal tracheal wall deformity or tracheal ring fracture can be more subtle indications of the location of injury.

In the intubated patient, additional signs of tracheal injury include overdistended, extraluminal, or herniated endotracheal tube balloon cuffs.

Pneumothorax and and pneumoretroperitoneum can be secondary findings, and a persistent pneumothorax despite a well-placed thoracostomy tube suggests a diagnosis of tracheobronchial injury.

Special thanks to Dr. Hansel Otero for the case.

References

Chen JD, Shanmuganathan K, Mirvis SE, Killeen KL, Dutton RP. Using CT to diagnose tracheal rupture. Am J Roentgenol. 2001 May;176(5):1273-80.
Karmy-Jones R, Avansino J, Stern EJ. CT of blunt tracheal rupture. AJR Am J Roentgenol. 2003 Jun;180(6):1670.

Iodine-131: Half-Life

2012-01-27T09:09:00.006-06:00

In the United States, patients treated with ¹³¹I ablation for hyperthyroidism or thyroid carcinoma are sent home with instructions on hygiene and limitations on social interactions. The instructions vary a bit among different centers, but are based on a balance between insurance reimbursement for inpatient isolation, patient comfort, and public safety.

The duration of isolation is usually decided empirically based on the administered dose, ranging from 2-7 days. This is based on the effective half-life of ¹³¹I, which is eliminated mainly through urine, but also in stool.

The physical half-life of ¹³¹I is fixed by nature at approximately 8 days. The effective half-life, however, depends on a number of patient factors. In healthy subjects, the effective half-life for the clearance of ¹³¹I is between 5-7 days. The effective half-life is similar in patients being treated for thyrotoxicosis. In patients with thyroid carcinoma who have been treated with total thyroidectomy, ¹³¹I clears faster because of the absence of significant thyroid tissue. The effective half-life in these patients is between 10 hours - 15 hours.

References

Greenlee C, Burmeister LA, Butler RS, Edinboro CH, Morrison SM, Milas M; American Thyroid Association Radiation Safety Precautions Survey Task Force. Current safety practices relating to I-131 administration for diseases of the thyroid: a survey of physicians and allied practitioners. Thyroid. 2011 Feb;21(2):151-60.
Ravichandran R, Binukumar J, Saadi AA. Estimation of effective half life of clearance of radioactive Iodine (I) in patients treated for hyperthyroidism and carcinoma thyroid. Indian J Nucl Med. 2010 Apr;25(2):49-52.

Paranasal Sinus Osteomas

2012-01-26T10:55:00.006-06:00

Osteomas of the paranasal sinuses are well-defined, slowly growing, non-neoplastic masses that arise from the sinus wall and are covered by the mucoperiosteum of the sinus. Developmental, traumatic, and infective, etiologies have been suggested, but none has been proven.

There is some variability in naming osteomas. Some name them after the sinus invaded by the tumor, while other name then for the sinus of origin.

Osteomas are found in about 3% of the population (more commonly men), and have a peak incidence between the fourth and sixth decades of life. Osteomas can be found sporadically or in association with Gardner syndrome (familial adenomatous polyposis). In the latter case, osteomas tend to be multiple and appear ~15 years before colon polyps. Therefore, gastroenterology referral is suggested when multiple facial or sinonasal osteomas are found.

The majority of patients are asymptomatic, but some can present with sinusitis, headache, and facial pain. Surgery is generally indicated with symptomatic osteomas. The management of asymptomatic osteomas is controversial and variable. Indications for resection of asymptomatic osteomas are not universally accepted and include: Osteomas located near the frontal sinus ostium, frontal osteomas larger than 50% of the volume of the sinus, frontoethmoid osteomas extending beyond the confines of the frontal or ethmoid sinuses, any ethmoid osteoma, and enlarging osteomas.

Recurrence after surgery is rare, even with incomplete resection; however, accelerated growth following incomplete resection has been reported and most will recur if given enough time. Malignant transformation has not been described.

The frontal sinus is most commonly affected, followed by the ethmoid, maxillary, and sphenoid sinuses. In the frontal sinus, there is a predilection to arise at the junction of frontal and anterior ethmoid sinuses. Even a relatively small osteoma in this location can lead to obstruction depending on the drainage pattern of the frontal sinus. The image above shows a relatively large frontal osteoma (pink arrow) leading to obstruction of the drainage pathway of the frontal sinus.

Non-obstructive complications of osteomas are rare, but familiarity with potential problems will help you avoid an incomplete assessment of these often neglected lesions.

Frontal sinus osteomas rarely invade the orbit and cranial fossa. Orbital invasion can cause exophthalmos, proptosis, visual disturbances, or blockage of the nasolacrimal duct. Cranial invasion can lead to pneumocephalus (rarely even tension pneumocephalus), rhinorrhea (from leakage of cerebrospinal fluid), meningitis, and cerebral abscess.

Ethmoid sinus osteomas can extend intracranially through the cribriform plate, laterally into the orbit, or anteriorly to the nasolacrimal duct.

Maxillary sinus osteomas can mimic maxillary antroliths and calcifying odontogenic tumors such as cementomas. An origin from adjacent tooth roots can suggest a calcifying odontogenic tumor such as a cementoma.

Sphenoid sinus osteomas are rare. The major complication of these osteomas is invasion of the sella turcica and associated pituitary issues.

Radiographs are not very sensitive or specific. When seen, osteomas present as well-defined bony lesions within the paranasal sinuses. CT Osteomas can be occult or show increased activity on bone scintigraphy. Lesions with activity have been shown to have potential for growth, while cold lesions tend to remain stable in size.

CT reveals a well-defined mass with attenuation similar to those of normal bone. MRI reveals a mass that is hypointense on all pulse sequences.

References

Chen CY, Ying SH, Yao MS, Chiu WT, Chan WP. Sphenoid sinus osteoma at the sella turcica associated with empty sella: CT and MR imaging findings. AJNR Am J Neuroradiol. 2008 Mar;29(3):550-1.
Earwaker J. Paranasal sinus osteomas: a review of 46 cases. Skeletal Radiol. 1993 Aug;22(6):417-23.
Georgalas C, Goudakos J, Fokkens WJ. Osteoma of the skull base and sinuses. Otolaryngol Clin North Am. 2011 Aug;44(4):875-90, vii.
Sadry F, Hessler C, Garcia J. The potential aggressiveness of sinus osteomas. A report of two cases. Skeletal Radiol. 1988;17(6):427-30.

Calcium Pyrophosphate Dihydrate Deposition around the Dens

2012-01-25T13:14:00.001-06:00

The transverse ligament of the atlas can be involved by calcium pyrophosphate dihydrate (CPPD) deposits in about 6% of the general population and in as many as 2/3 of patients with articular chondrocalcinosis. These deposits can be associated with aging, degenerative disease, or metabolic disorders.

Patients are typically older women, with isolated involvement of the atlanto-axial joints. Crowned dens syndrome refers to acute neck pain due to calcium pyrophosphate dihydrate deposits and calcification surrounding the odontoid process on CT. The neck pain may be accompanied by neck stiffness and fever, and can mimic meningitis. They can be treated with non-steroidal anti-inflammatory medications, and the calcifications usually resorb in about 1-2 weeks.

The deposition can range from linear or stippled calcifications to massive crystal deposition with bone erosion involving the dens. Depending on the extent of CPPD deposition and associated erosions, patients can also be at increased risk for pathologic fracture of the dens.

Radiographs are usually not very sensitive for detection of periodontoid mineralization, and CT is usually needed for characterization. The appearance of the calcifications ranges from curvilinear to stippled, or a mixture of the two. The curvilinear pattern, although less common, is strongly suggestive of calcium pyrophosphate dihydrate deposition. When masslike deposits are present, CT can demonstrate the bony erosions and possible malalignment from associated ligamentous damage and any pathologic fracture of the dens.

MRI, while not as sensitive as CT for the detection of calcification, is better for evaluation of the mass and its effect on the spinal cord, as well as assessment of cartilage, bone, or ligament abnormalities. The retro-odontoid mass is typically hypointense on T2-weighted images and enhances on post-contrast images.

Differential considerations for an extradural mass posterior to the odontoid process include:

Pannus: Seen with rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis. Does not have calcifications.
Os odontoideum:
Neoplasm: Epidural metastases, clivus chordoma, foramen magnum meningioma, aneurysmal bone cyst, osteoblastoma. Neoplasms will typically be T2-hyperintense, while the retro-odontoid mass of CPPD will be T2-hypointense.

References

Baysal T, Baysal O, Kutlu R, Karaman I, Mizrak B. The crowned dens syndrome: a rare form of calcium pyrophosphate deposition disease. Eur Radiol. 2000;10(6):1003-5.
Kakitsubata Y, Boutin RD, Theodorou DJ, Kerr RM, Steinbach LS, Chan KK, Pathria MN, Haghighi P, Resnick D. Calcium pyrophosphate dihydrate crystal deposition in and around the atlantoaxial joint: association with type 2 odontoid fractures in nine patients. Radiology. 2000 Jul;216(1):213-9.

Portal Vein Pulsatility

2012-01-24T05:51:00.007-06:00

The normal flow in the portal venous system is typically continuously hepatopetal, with minimal if any pulsatility in rhythm with the cardiac cycle. Marked portal venous pulsatility can be classified as continuous pulsatile or reversed pulsatile flow.

The continuous pulsatile pattern is continuously hepatopetal, but with marked pulsatility. This pattern can be seen in patients with congestive heart failure, but can also be seen as a normal finding in thin subjects, where there is an inverse correlation of pulsatility to body mass.

The second pattern, reversed pulsatile flow is characterized by marked pulsatility and reversal of flow direction related to the cardiac cycle. There is a strong correlation of reversed pulsatile flow to high (> 20 mmHg) right atrial pressures in patients with chronic heart failure. However, reversed pulsatile flow can also be seen with tricuspid insufficiency, liver disease (cirrhosis, Budd–Chiari syndrome, hepatic outflow obstruction (constrictive pericarditis, mediastinal hematoma, pericardial mass or effusion), and shunts (portal vein–hepatic vein fistula, portocaval shunt). High abdominal pressures during deep inspiration can also cause transient reversal of flow. This is more commonly seen in patients with severe right heart failure or liver disease, but can also be seen in patients without these conditions.

Therefore, pulsatile portal venous flow by itself should not be construed as a sign of cardiac abnormality, especially if there is no reversal of the portal venous flow. The image above, however, shows a reversed pulsatile flow pattern and is from a patient with congestive heart failure.

Special thanks to Dr. Hansel Otero for the case.

References

Gallix BP, Taourel P, Dauzat M, Bruel JM, Lafortune M. Flow pulsatility in the portal venous system: a study of Doppler sonography in healthy adults. AJR Am J Roentgenol. 1997 Jul;169(1):141-4.
Görg C, Riera-Knorrenschild J, Dietrich J. Pictorial review: Colour Doppler ultrasound flow patterns in the portal venous system. Br J Radiol. 2002 Nov;75(899):919-29.
Görg C, Wollenberg B, Beyer J. Reversed portal vein pulsatility on Doppler ultrasound secondary to an iatrogenic mediastinal haematoma. Br J Radiol. 2001 Oct;74(886):962-4.

Lower Limb Skeletal Traction: Proximal Tibia

2012-01-23T05:52:00.008-06:00

Lower limb skeletal traction can be achieved through the proximal tibia, distal tibia, and the calcaneus. Proximal tibial traction is the most frequently used and can be used to reduce and immobilize femoral fractures.

Skeletal traction through the proximal tibia is most commonly achieved under local anesthesia by inserting a pin ~2 cm distal to the tibial tubercle and ~2 cm behind the anterior border of the tibia (measurements are for adults). Ideally, the pin passes through the skin and subcutaneous fat, but will avoid muscle and the common peroneal nerve.

The Steinmann pin (blue bar) is typically used. The pink is usually attached externally to a Böhler-Steinmann stirrup as shown above, which is attached to weights via rope (red arrow) to achieve the desired traction.

The Denham pin can also be used in osteoporotic bone. It is threaded in the middle to engage the cortex and reduce the risk of the pin sliding.

The immediate complication to look for on radiographs is malpositioning of the pin, which can lead to damage to nearby neurovascular bundles. If the traction is maintained for a longer period, radiographs should be inspected for signs of infection. In addition, in cases where the bone is osteoporotic or the applied traction is too heavy, there is a risk of the pin cutting through bone.

References

Cook J, Sankaran B, Wasunna AEO. Chapter 10: Traction. in Surgery at the District Hospital: Obstetrics, Gynaecology, Orthopaedics and Traumatology. WHO(1991).

Cardiac Tamponade: CT Findings

2012-01-22T08:16:00.005-06:00

CT findings of cardiac tamponade can be nonspecific. However, when seen together in the setting of a large pericardial effusion, the following should strongly suggest the diagnosis:

Distention of the superior vena cava: ≥ diameter of the adjacent thoracic aorta.
Distention of the inferior vena cava: ≥ twice the diameter of the adjacent abdominal aorta. Distension of the hepatic and renal veins can also be seen.
Periportal edema: Can also be seen with chronic congestive heart failure, among other conditions.
Reflux of contrast into the azygos vein: Can also be seen with massive pulmonary emboli, cor pulmonale, right-sided heart failure, pulmonary arterial hypertension, obstruction of the main pulmonary artery, bilateral pneumothoraces, and positive pressure ventilation.
Reflux of contrast into the inferior vena cava: Can also be seen with tricuspid regurgitation, hypovolemic or cardiogenic shock, and pulmonary embolism.
Deformity and compression of intrapericardial structures: For example the cardiac chambers (flattened heart sign, shown above), coronary sinus, pulmonary trunk, intrathoracic segment of the inferior vena cava (covered by pericardium anteriorly).
Angulation or bowing of the interventricular septum: Correlates with paradoxical motion of the septum. Can also be seen with pressure and/or volume overload of the right ventricle (constrictive pericardial disease, massive pulmonary embolism).

The image above is a CT pulmonary arteriogram from a young patient with a malignant pericardial effusion. We see the flattened heart sign (black arrow). However, the diameters of the superior and inferior venae cavae were normal, no reflux of contrast into the inferior vena cava or the azygos vein was seen, and no periportal edema was present. Echocardiography showed cardiac tamponade.

References

Restrepo CS, Lemos DF, Lemos JA, Velasquez E, Diethelm L, Ovella TA, Martinez S, Carrillo J, Moncada R, Klein JS. Imaging findings in cardiac tamponade with emphasis on CT. Radiographics. 2007 Nov-Dec;27(6):1595-610.

Transverse Acetabular Fractures

2012-01-21T05:47:00.006-06:00

Transverse fractures of the acetabulum involve both the anterior and posterior aspects of the acetabulum, without involvement of the obturator ring or superior extension into the iliac wing. They comprise between 5% and 20% of acetabular fractures.

The fracture plane is not purely transverse in the anatomic sense, but is transverse relative to the acetabulum. The fracture plane courses superiorly and medially in an oblique plane from the acetabulum and separates the innominate bone into an upper iliac fragment and a lower ischiopubic fragment. The ischiopubic fragment can rotate about the pubic symphysis, and the femoral head moves with the iliac fragment medially and superiorly.

Transverse fractures can be classified as transtectal, juxtatectal, and infratectal based on where the fracture plane crosses the articular surface. Transtectal fractures cross the weight-bearing dome of the acetabulum. Juxtatectal fractures cross the articular surface just superior to the cotyloid fossa. Infratectal fractures cross the cotyloid fossa.

The more superior fracture planes are more vertical in orientation and associated with a smaller intact remaining articular surface, which has implications for treatment.

Radiographs reveal disruption of both the iliopectineal (pink arrow) and ilioischial (blue arrow) lines, as well as interrupted anterior and posterior rim lines. Transtectal fractures will also involve the acetabular roof line without disrupting the relationship of the ilioischial line with the teardrop.

When scrolling down (superior to inferior) on axial CT images, the fracture plane moves medially to laterally. Coronal images reveal involvement of both anterior and posterior aspects of the acetabulum. No superior extension to the iliac wing is seen.

Differential considerations include T-shaped and transverse with posterior wall fractures, both of which have transverse components with added features. The T-shaped acetabular fracture is a transverse fracture with inferior extension into the obturator ring, but no superior extension into the iliac wing. The transverse with posterior wall fracture is a transverse fracture with a comminuted (often displaced) posterior wall fracture and an intact obturator ring.

References

Durkee NJ, Jacobson J, Jamadar D, Karunakar MA, Morag Y, Hayes C. Classification of common acetabular fractures: radiographic and CT appearances. AJR Am J Roentgenol. 2006 Oct;187(4):915-25.
Rockwood and Green's Fractures in Adults (7th ed), p 1479.

Arnold-Hilgartner Staging of Hemophilic Arthropathy

2012-01-20T05:25:00.004-06:00

The Arnold-Hilgartner staging system that describes articular changes as the patient progresses through the stages of the disease.

Stage I: Soft-tissue swelling from hemarthrosis or bleeding into the periarticular soft tissues. No skeletal abnormality.
Stage II: Osteoporosis and overgrowth of the epiphysis without bone cysts or narrowing of the cartilage space.
Stage III: Early subchondral bone cysts, squaring of patella, widening of intercondylar notch of distal femur or humerus, preserved cartilage space. This is the final stage at which hemophilic arthropathy is reversible with treatment.
Stage IV: Characterized by narrowing of cartilage space. More advanced findings of stage III are also seen.
Stage V (shown above): Fibrous joint contracture (as seen in the attempted frontal view), loss of joint cartilage space, marked enlargement of epiphyses, and substantial disorganization of the joint.

References

Arnold WD, Hilgartner MW. Hemophilic arthropathy. Current concepts of pathogenesis and management. J Bone Joint Surg Am. 1977 Apr;59(3):287-305.
Ng WH, Chu WC, Shing MK, Lam WW, Chik KW, Li CK, Li CK, Ling SC. Role of imaging in management of hemophilic patients. AJR Am J Roentgenol. 2005 May;184(5):1619-23.

Denis Classification of Sacral Fractures

2012-01-19T06:38:00.000-06:00

Denis et al classified sacral fractures into three zones. Zone I (extraforaminal) fractures are lateral to the sacral neural foramina. Zone II (transforaminal) fractures extend through the neural foramina, but do not involve the spinal canal. Zone III fractures involve the spinal canal.

They found that zone I fractures were only occasionally associated with partial damage to the L5 nerve root. Zone II fractures were frequently associated with sciatica but rarely with bladder dysfunction. Zone III fractures were frequently associated with saddle anesthesia and loss of sphincter function.

Zone I and II fractures can cause injury to the L5 nerve root in the lumbosacral tunnel (space between the lumbosacral ligament and the S1 sala). Zone II and III fractures can cause injury to the S1 nerve root or pudendal nerve. S1 nerve injury in this setting is usually not isolated and tends to be associated with a lumbosacral plexus injury.

More recent work by Sugimoto et al has found that the incidence of lumbosacral plexus injury was not related to the zone of sacral fracture. Instead they found that risk factors for lumbosacral plexus palsy included longitudinal displacement of the pelvis, transverse sacral fracture, and trauma from a suicidal jump were risk factors.

The image above shows a right zone I sacral fracture (pink arrow). The white arrow indicates the right L5 nerve root/lumbosacral trunk (L4 and L5 nerve roots join up close to this location) is located directly anterior to the fracture.

References

Denis F, Davis S, Comfort T. Sacral fractures: an important problem. Retrospective analysis of 236 cases. Clin Orthop Relat Res. 1988 Feb;227:67-81.
Sugimoto Y, Ito Y, Tomioka M, Tanaka M, Hasegawa Y, Nakago K, Yagata Y. Risk factors for lumbosacral plexus palsy related to pelvic fracture. Spine (Phila Pa 1976). 2010 Apr 20;35(9):963-6.

Flexor Digitorum Accessorius Longus Muscle

2012-01-18T05:58:00.004-06:00

The flexor digitorum accessorius longus muscle (white arrows) is an accessory muscle of the medial compartment of the ankle that is seen in less than 10% of the population. It is more commonly seen in males and is frequenly bilateral.

The muscle arises from variety of structures in the posterior compartment of the calf distal to the soleal line. Its tendon passes posterior to the flexor hallucis longus muscle (pink arrows) and the medial malleolus and inserts into the quadratus plantae muscle (blue arrow) or the flexor digitorum longus tendon. The presence of a flexor digitorum accessorius longus muscle has been associated with tenosynovitis of the flexor hallucis longus tendon.

The relationship of the tendon to the neurovascular structures (yellow arrows) of the ankle is also important, as compression of these structures can lead to tarsal tunnel syndrome. The flexor digitorum accessorius longus tendon is located posterior and superficial to the tibial nerve as it courses deep to the flexor retinaculum through the tarsal tunnel.

On axial MR images, the muscle is seen within the tarsal tunnel, typically superficial to the neurovascular bundle. At this point, the appearance may be similar to the peroneocalcaneus internus muscle. The flexor digitorum accessorius longus muscle, however, may contain fleshy fibers in the tarsal tunnel, which may help in differentiating the two. In addition, unlike the flexor digitorum accessorius longus muscle, the peroneocalcaneus internus muscle insert onto the calcaneus.

References

Cheung YY, Rosenberg ZS, Colon E, Jahss M. MR imaging of flexor digitorum accessorius longus. Skeletal Radiol. 1999 Mar;28(3):130-7.
Sookur PA, Naraghi AM, Bleakney RR, Jalan R, Chan O, White LM. Accessory muscles: anatomy, symptoms, and radiologic evaluation. Radiographics. 2008 Mar-Apr;28(2):481-99.

Fibrosarcoma of Bone

2012-01-17T05:15:00.002-06:00

Fibrosarcomas of bone are typically seen between the third and sixth decades of life, most commonly in the metaphysis or metadiaphysis of the long tubular bones. Fibrosarcomas can be intramedullary (most common) or periosteal (rare, but better prognosis). They can also be categorized as primary or secondary.

Secondary fibrosarcoma of bone can arise from benign bone lesions (Paget disease, bone infarction, fibrous dysplasia, chronic osteomyelitis, giant cell tumor), malignant bone lesions (e.g., chondrosarcoma), or irradiated bone. Fibrosarcomas occurring in the spine or the flat bones are usually secondary lesions.

Radiographs typically reveal a large aggressive lytic lesion with cortical destruction and soft tissue extension. The location is typically metaphyseal and extension into the diaphysis and epiphysis is common.

Differential considerations for high-grade fibrosarcomas include:

Multiple myeloma:
Metastasis:
Lymphoma:
Malignant fibrous histiocytoma:

Low-grade fibrosarcomas can have more sclerotic and better-defined borders, and can be similar to:

Desmoplastic fibroma:
Chondromyxoid fibroma:
Giant cell tumor:

References

Koplas M and Sundaram M. Fibrogenic and Fibrohistiocytic Tumors. in Imaging of Bone Tumors and Tumor-Like Lesions. Davies AM, Sundaram M, and James SLJ (eds). Springer-Verlag Berlin Heidelberg (2009); pp 310-311.

Isolated Tibial Diaphysis Fractures

2012-01-16T12:35:00.002-06:00

An isolated tibial fracture with an intact fibula is the most common tibial fracture pattern seen in children. Displaced fractures can be difficult to reduce because of the splinting effect created by the intact fibula. In addition, the splinting effect of the fibula is though to produce a bending moment that results in varus angulation on healing.

Discussion on whether or not the presence of an intact fibula results in delayed union with non-operative management has been made irrelevant, as the overwhelming majority of surgeons prefer to treat both low-energy and high-energy closed fractures of the tibial diaphysis with intramedullary nailing.

References

Bhandari M, Guyatt GH, Swiontkowski MF, Tornetta P 3rd, Hanson B, Weaver B, Sprague S, Schemitsch EH. Surgeons' preferences for the operative treatment of fractures of the tibial shaft. An international survey. J Bone Joint Surg Am. 2001 Nov;83-A(11):1746-52.
O'Dwyer KJ, DeVriese L, Feys H, Vercruysse L. Tibial shaft fractures with an intact fibula. Injury. 1993 Oct;24(9):591-4.
Sarmiento A, Sharpe FE, Ebramzadeh E, Normand P, Shankwiler J. Factors influencing the outcome of closed tibial fractures treated with functional bracing. Clin Orthop Relat Res. 1995 Jun;(315):8-24.
Yang JP, Letts RM. Isolated fractures of the tibia with intact fibula in children: a review of 95 patients. J Pediatr Orthop. 1997 May-Jun;17(3):347-51.

Central Venous Obstruction in the Chest

2012-01-15T11:13:00.008-06:00

Collateral vessels can be recruited to bypass central venous obstruction in the chest via three routes. More central obstructions (superior vena cava) tend to recruit more inferior collaterals, while the more peripheral obstructions (subclavian or brachiocephalic veins) tend to recruit more superior collaterals.

The three routes are:

Superior route: Seen with subclavian or brachiocephalic vein obstruction. Blood flows via through the ipsilateral external jugular vein into horizontal veins that communicate across the midline via the transverse arch of the anterior jugular venous system. Once on the contralateral side, blood flows into the external jugular vein into the subclavian vein, and finally into the superior vena cava.
Posterior route: Seen in cases of obstruction at the level of the supraazygos superior vena cava. This leaves the azygos vein as a conduit for blood to get into the superior vena cava. Blood from the head and neck flows through paravertebral collaterals into intercostal and paravertebral veins and then the superior intercostal vein, which drains into the azygos vein.
Anterolateral: Seen in cases of central superior vena cava obstruction (shown above). Blood flows through anterior intercostal, internal mammary (pink arrow), and long thoracic veins, which, flow to the inferior vena cava (green arrow) via pericardiophrenic (yellow arrow), musculophrenic (blue arrow), lumbar, and hepatic veins. The internal mammary vein can also connect to the left portal vein via the paraumbilical vein and result in increased activity or enhancement in segment IV of liver (white arrow) and is the basis of the focal hepatic hot spot sign on ^99mTc sulfur colloid "liver and spleen" scans. IN the image above, we also see aortopulmonary window collaterals (red arrow) that drain into the infraazygos superior vena cava(S), in this patient with combined infraazygos superior vena cava and azygos vein obstruction.

References

Dickson AM. The focal hepatic hot spot sign. Radiology. 2005 Nov;237(2):647-8.
Gosselin MV, Rubin GD. Altered intravascular contrast material flow dynamics: clues for refining thoracic CT diagnosis. AJR Am J Roentgenol. 1997 Dec;169(6):1597-603.
Lee KR, Preston DF, Martin NL, Robinson RG. Angiographic documentation of systemic-portal venous shunting as a cause of a liver scan ""hot spot'' in superior vena caval obstruction. AJR Am J Roentgenol. 1976 Oct;127(4):637-9.
Godwin JD, Chen JT. Thoracic venous anatomy. AJR Am J Roentgenol. 1986 Oct;147(4):674-84.

Button Sequestrum

2012-01-14T14:40:00.002-06:00

The button sequestrum is a lucent bony lesion with an internal opacity. It is a nonspecific finding that is an uncommon/rare manifestation of the following conditions:

Langerhans cell histiocytosis of bone:
Osteomyelitis:
Fibrous sarcomas of bone: Includes fibrosarcoma, desmoplastic fibroma and malignant fibrous histiocytoma of bone.
Lymphoma:
Intraosseous Lipoma: Lucent lipoma with partial calcification.
Tuberculous osteitis:
Radiation necrosis:
Metastatic carcinoma:
Fibrous dysplasia:
Epidermoid and dermoid cyst:
Hemangioma:
Meningioma:

References

Krasnokutsky MV. The button sequestrum sign. Radiology. 2005 Sep;236(3):1026-7.

Modified Eichenholtz Classification of Neuropathic Joints

2012-01-13T18:37:00.002-06:00

Neuropathic (Charcot) arthropathy of the foot and ankle has been divided into three stages by Eichenholtz (1966) and modified by Johnson (1998). The classification is based on the natural history of the disease.

Stage I (Dissolution): 2-6 months. Patients present with an acutely inflamed and hyperemic foot that can be mistaken for an infection. Pain is present in most patients, in spite of the underlying sensory neuropathy.

Radiographs typically reveal periarticular soft-tissue swelling, regional demineralization, periarticular fragmentation, and dislocation. This demineralization is why operative treatment of fractures that occur in this stage have higher rates of failure of fixation, recurrent deformity, and infection.
Stage II (Coalescence): Patients present with decreased inflammation and swelling.

Radiographs reveal absorption of bony debris, organization and early healing of fracture fragments, and periosteal new-bone formation.
Stage III (Resolution): The inflammation and swelling are minimal, and there is permanent enlargement of the foot and ankle with fixed deformity.

Radiographs reveal smoothing of edges of large fragments of bone, sclerosis, and osseous or fibrous ankylosis.

References

Johnson JE. Operative treatment of neuropathic arthropathy of the foot and ankle. J Bone Joint Surg. 1998;80:1700–1709.

Mirels Classification for Risk of Pathological Fracture

2012-01-12T05:14:00.018-06:00

The Mirels system classifies the risk of pathologic fracture based on scoring four variables on a scale of 1-3: location of lesion, radiographic appearance, size, and pain. An overall score is calculated, and a recommendation for or against prophylactic fixation is made.

	1	2	3
Location	Upper extremity	Lower extremity	Intertrochanteric
Radiographic appearance	Blastic	Mixed	Lytic
Size^a	< 1/3	1/3 - 2/3	>2/3
Pain	Mild	Moderate	Functional^b
^a Size is determined as a fraction of the diameter of the bone. ^b Functional pain is defined as severe pain or pain aggravated by limb function.

Score	Fracture Risk	Recommendation
≥9	33%-100%	Prophylactic fixation is recommended
=8	15%	Clinical judgement should be used
≤7	<4%	Observation and radiation therapy can be used

As an example, the lytic, intertrochanteric lesion shown above takes up >2/3 of the diameter of bone, getting an overall score of 9 in the absence of any clinical information about the degree of pain.

References

Mirels H. Metastatic disease in long bones. A proposed scoring system for diagnosing impending pathologic fractures. Clin Orthop Relat Res. 1989 Dec;(249):256-64.

Cartilage Lesions by Age and Location

2012-01-11T21:26:00.006-06:00

Image of the humerus from Human skeleton front en.svg

Once you've made the determination that a long bone lesion is a cartilage tumor, age and location can help narrow your differential diagnosis.

Chondroblastoma and clear-cell chondrosarcoma are epiphyseal lesions that can be indistinguishable. While chondroblastomas tend to affect a younger age group than clear-cell chondrosarcomas, there is some overlap.

Chondromyxoid fibromas are rare metaphyseal lesions that may not have an obvious chondroid matrix on radiography. They most commonly occur in the proximal tibia.

Enchondromas and chondrosarcomas are diaphyseal lesions that have characteristic appearances at their extremes. However, there can be significant overlap, especially between enchondromas and low-grade chondrosarcomas.

Please note that these are rough guidelines: Tumors don't read this blog.

References

Greenspan A, Jundt G, Remagen W. Cartilage (Chondrogenic) Lesions. In Differential Diagnosis of Orthopaedic Oncology, 2nd Edition. 2007 Lippincott Williams & Wilkins; pp 162-255.
Kindblom LG. Bone Tumors: Epidemiology, Classification, Pathology. in Imaging of Bone Tumors and Tumor-Like Lesions. Davies AM, Sundaram M, and James SLJ (eds). Springer-Verlag Berlin Heidelberg (2009); pp 1-4.

Unicameral Bone Cyst of the Long Bones

2012-01-10T17:55:00.006-06:00

Unicameral bone cysts (simple bone cystss) are tumor-like lesions of unknown etiology that make up about 3% of all primary bone lesions. They are thought to represent a local reactive or developmental growth disturbance. They are more commonly found in boys in the first 2 decades of life, in the proximal diaphyses of the humerus and femur.

Unicameral bone cysts are well-defined, lucent lesions with sclerotic margins that are located centrally in the metaphysis or diaphysis of long bones. There is frequently cortical thinning and expansion, but the width of the cyst is typically less than that of the nearby physis. Epiphyseal extension is not typical, and periosteal reaction is not seen unless the cyst is complicated by a pathologic fracture.

In about 20% of cases of fractures through unicameral bone cysts, a fallen fragment sign is present, representing a fragment of fractured cortex laying in the dependent portion of the fluid-filled lesion. The forme fruste of the fallen fragment sign is the trap door sign, which represents an infolded fragment of cortex that remains attached to the periosteum.

Radiography is usually diagnostic, and CT can be used in equivocal cases. The cyst fluid has attenuation of 15-20 HU and the radiographic findings noted above can be seen to better advantage. Bone scintigraphy may reveal a nonspecific halo of increased uptake around the photopenic cyst, but can also be normal.

MRI reveals a fluid-filled lesion that is low to intermediate signal on T1-weighted images and homogeneously hyperintense on T2-weighted images.

The main differential consideration in the long bones is an aneurysmal bone cyst. Aneurysmal bone cysts almost invariably have some degree of periosteal reaction (usually solid), are eccentrically located, and can have significant cortical expansion.

The radiograph above is from a 4-year-old boy. There is a central, well-defined lucent lesion in the proximal metadiaphysis of the humerus that results in mild cortical thinning and mild expansion. Pseudoseptations can be seen within the lesion. No periosteal reaction is present.

References

Greenspan A, Jundt G, Remagen W. Miscellaneous Tumors And Tumor-like Lesions. In Differential Diagnosis of Orthopaedic Oncology, 2nd Edition. 2007 Lippincott Williams & Wilkins; pp 400-410.

Compress Compliant Pre-Stress Implant

2012-01-09T18:25:00.008-06:00

The Compress Compliant Pre-Stress Implant makes use of stored energy to snap the extramedullary portion of the prosthesis to the native bone. Proximally, an anchor plug is fixed to the native bone via transverse pins and connected to an intramedullary traction bar. The bar extends out through the spindle and is loaded with Belleville washers (washer-shaped springs). A nut is tightened at the end of the traction bar to achieve the desired compression of the spindle against the bone.

This compression acts to induce bone hypertrophy, reduce stress shielding seen in stem prostheses, and seal the medullary canal from particulate debris that can cause osteolysis.

The short length of the device allows placement of a prosthesis with as little as 46 mm of bony canal.

References

Bhangu AA, Kramer MJ, Grimer RJ, O'Donnell RJ. Early distal femoral endoprosthetic survival: cemented stems versus the Compress implant. Int Orthop. 2006 Dec;30(6):465-72.

Signs of Malignancy in Ovarian Teratomas

2012-01-08T21:45:00.000-06:00

Malignant transformation is seen in about 1% of ovarian teratomas and can occur in any of the three germ cell layers that make up the teratoma: ectoderm, mesoderm, and endoderm.

The most common type of malignant transformation is squamous cell carcinoma, seen in 80% of reported cases. Increased risk of transformation is seen in patients older than 45 years of age, tumors larger than about 10 cm, and serum squamous carcinoma antigen level greater than 2 ng/mL.

Imaging findings can be nonspecific. Invasion of adjacent structures and lymph node and distant metastases are obviously signs of malignancy. Other findings can suggest malignancy: A complex, predominantly solid tumor, significant areas of necrosis, and poor definition of adjacent soft-tissue planes all suggest malignancy.

The Rokitansky nodule or dermoid plug of ovarian teratomas is a frequent site of malignant transformation and imaging findings suggestive of malignant transformation have been proposed. Transmural growth of the Rokitansky nodule should raise concern for malignant transformation. Softer signs of malignant transformation include contrast enhancement of the Rokitansky nodule and an obtuse angle between the nodule and the inner wall of the cyst.

References

Park SB, Kim JK, Kim KR, Cho KS. Imaging findings of complications and unusual manifestations of ovarian teratomas. Radiographics. 2008 Jul-Aug;28(4):969-83.
Park SB, Kim JK, Kim KR, Cho KS. Preoperative diagnosis of mature cystic teratoma with malignant transformation: analysis of imaging findings and clinical and laboratory data. Arch Gynecol Obstet. 2007 Jan;275(1):25-31.

Neurocutaneous Melanosis

2012-01-07T23:47:00.003-06:00

Neurocutaneous melanosis is one of the less common phakomatoses. It is a rare, noninherited dysplasia of neuroectodermal cells, which give rise to melanocytes and the basal leptomeninx.

Patients present with large or multiple congenital melanocytic nevi with benign or malignant proliferation of melanocytes in the leptomeninges. The classic appearance is a large melanocytic nevus in a posterior axial location with satellite melanocytic nevi. Leptomeningeal involvement can result in hydrocephalus, spinal cord compression, or other mass effect, usually in the first 2 years of life. Neurological symptoms are usually progressive and rapidly fatal.

MR reveals thickened and enhancing leptomeninges (predominantly over the cerebral convexity and quadrigeminal plate cistern), ventricular dilatation, and inferior vermian hypoplasia. Focal parenchymal melanocytomas can also be seen, sometimes in the absence of leptomeningeal involvement. Leptomeningeal T1-hyperintensity has been reported, but it is not unusual to have amelanotic melanocytoma or amelanotic melanocytosis, so contrast-enhanced images are necessary for full evaluation.

The post-contrast images of the brain and spine above reveal diffuse meningeal enhancement and mild residual dilatation of the ventricles post ventriculoperitoneal shunt (not shown). The enhancement is both leptomeningeal (predominantly on the left) and pachymeningeal. The imaging findings are not pathognomonic. Differential considerations for leptomeningeal enhancement include chronic meningitis (tuberculosis or coccidioidomycosis), and leptomeningeal metastases (e.g., medulloblastoma, ependymoma, high-grade astrocytoma, pineoblastoma and choroid plexus carcinoma).

References

Byrd SE, Darling CF, Tomita T, Chou P, de Leon GA, Radkowski MA. MR imaging of symptomatic neurocutaneous melanosis in children. Pediatr Radiol. 1997 Jan;27(1):39-44.
Pavlidou E, Hagel C, Papavasilliou A, Giouroukos S, Panteliadis C. Neurocutaneous melanosis: report of three cases and up-to-date review. J Child Neurol. 2008 Dec;23(12):1382-91.

Lymph Node Metastases in Soft Tissue Sarcomas

2012-01-06T07:43:00.001-06:00

Lymph node metastases are uncommon in soft tissue sarcomas, occurring in about 5% of cases. The sarcomas that most frequently metastasize to lymph nodes in adults include: Angiosarcoma, rhabdomyosarcoma (embryonal variant), and epithelioid sarcoma (the order varies depending on the study).

Synovial, clear cell, and alveolar soft part sarcomas were previously thought to have high rates of lymph node metastases, but this has not found to be the case in larger case series.

The sarcomas that account for the most lymph node metastases due to their relatively higher prevalence are leiomyosarcoma and pleomorphic undifferentiated sarcoma (formerly malignant fibrous histiocytoma).

Regional lymph node involvement is a poor prognostic factor. In addition, patients with isolated regional lymph node involvement at diagnosis have a poorer outcome than patients who develop isolated regional lymph node involvement later in the course of their disease.

References

Behranwala KA, A'Hern R, Omar AM, Thomas JM. Prognosis of lymph node metastasis in soft tissue sarcoma. Ann Surg Oncol. 2004 Jul;11(7):714-9.
Fong Y, Coit DG, Woodruff JM, Brennan MF. Lymph node metastasis from soft tissue sarcoma in adults. Analysis of data from a prospective database of 1772 sarcoma patients. Ann Surg. 1993 Jan;217(1):72-7.

Girdlestone Resection Arthroplasty

2012-01-05T05:29:00.002-06:00

The Girdlestone procedure is a resection arthroplasty of the hip that involves removal of portions of the proximal femur. It is named after Gathorne Robert Girdlestone, who popularized the procedure for treatment of late septic arthritis.

Two main types of the procedure have been described: primary and secondary. A primary Girdlestone resection arthroplasty is performed for primary hip disorders (e.g., septic and tuberculous hip and rarely osteoarthritis and rheumatoid arthritis). The secondary or modified Girdlestone resection arthroplasty is used for failed hip replacement or failed construction after hip trauma.

The primary procedure is rarely used in modern practice. The majority of Girdlestone resection arthroplasties performed today are the secondary type and performed in patients who are not healthy enough for further major interventions (e.g., one- or two-stage reimplantations) after failed primary total hip replacement. It is also performed as the first stage of a two-stage revision in selected patients.

References

Girdlestone GR. Acute pyogenic arthritis of the hip: an operation giving free access and effective drainage (1943). Clin Orthop Relat Res. 2008 Feb;466(2):258-63.
Sharma H, De Leeuw J, Rowley DI. Girdlestone resection arthroplasty following failed surgical procedures. Int Orthop. 2005 Apr;29(2):92-5.

Multiple Biliary Hamartomas

2012-01-04T05:23:00.002-06:00

Multiple biliary hamartomas of the liver (also known as von Meyenburg complexes) are mulitiple tiny (1 mm - 10 mm), well-circumscribed foci of disorganized bile ductules surrounded by fibrous stroma. It is thought that they are caused by failure of involution of embryonic bile ducts (the same mechanism for polycystic liver disease).

Ultrasound will show multiple irregular hypoechoic lesions are seen throughout the liver. Smaller ductules may cause crowding of the interfaces, leading to hyperechoic lesions.

CT reveals multiple, irregular, low-attenuation lesions throughout the liver. On MRI, the lesions are well-defined, T1-hypointense, and T2-hyperintense (T2 hyperintensity is slightly less than that of water). There are usually mural nodules that are isointense on T1-weighted images and intermediate signal on T2-weighted images and which are between 1-2 mm. These nodules enhance.

Differential considerations include:

Metastases: Lesions are usually not as uniform in shape and size as in multiple biliary hamartomas
Microabscesses: Usually in immunosuppressed patients
Cysts:

References

Juchems MS, Jeltsch M, Brambs HJ. Multiple cystic liver lesions on CT: multiple biliary hamartomas. Gut. 2008 Feb;57(2):144, 251.
Tohmé-Noun C, Cazals D, Noun R, Menassa L, Valla D, Vilgrain V. Multiple biliary hamartomas: magnetic resonance features with histopathologic correlation. Eur Radiol. 2008 Mar;18(3):493-9.

Metallosis

2012-01-03T05:53:00.001-06:00

Metallosis is the infiltration of periprosthetic soft tissues and bone by metallic debris. The debris is most commonly from wear of metallic prosthesis (usually of the metal-backed polyethylene patellar prosthesis), but metallic debris can also be generated from hinged prostheses and, as in the case shown above, repetitive contact of fractured prosthesis components.

The particles can lead to metal-induced synovitis, and the release of cytokines by histiocytes stimulated by the metallic debris can lead to significant osteolysis.

Patients often present with pain and a joint effusion, usually 1-2 years after surgery.

Radiographs reveal periprosthetic metallic debris, and sometimes a dense joint effusion is seen. In more than half of patients, a thin opaque line outlines the periprosthetic pseudocapsule: The so-called metal-line sign or bubble sign. (The metal-line sign can also be seen after intraarticular injection of gold salts and dissolution of migrated lead bullets into the joint). Osteolysis may complicate the picture, and a high index of suspicion is appropriate.

References

Heffernan EJ, Alkubaidan FO, Nielsen TO, Munk PL. The imaging appearances of metallosis. Skeletal Radiol. 2008 Jan;37(1):59-62.

Rheumatoid Arthritis and Lymphoma

2012-01-02T07:05:00.001-06:00

Patients with longstanding rheumatoid arthritis have been shown to have an increased risk for non-Hodgkin lymphoma in large population-based studies. The mechanism is thought to be related to chronic inflammation and the resultant chronic antigenic stimulation of B-cells by rheumatoid factors, which leads to an increased risk for B-cell transformation. Methotrexate treatment has also been implicated in the development of lymphoma in patients with rheumatoid arthritis, but this has been contested in more recent work.

The Epstein-Barr virus has also been implicated in the past. Recent work, however, suggests that it may only be associated with an increased risk of Hodgkin lymphoma.

The images above are from a patient with longstanding rheumatoid arthritis who developed B-cell lymphoma. The radiograph of the hand reveals severe joint space narrowing and erosions and subluxations that predominantly involve the radiocarpal, intercarpal, and carpometacarpal joints. Axial CT image in mediastinal window reveals an enlarged left internal mammary lymph node (pink arrow). Lung windows reveal multiple pulmonary nodules (blue arrows) in a perilymphatic distribution.

References

Naschitz JE, Rosner I. Musculoskeletal syndromes associated with malignancy (excluding hypertrophic osteoarthropathy). Curr Opin Rheumatol. 2008 Jan;20(1):100-5.

Differentiation Syndrome

2012-01-01T09:38:00.005-06:00

(image by A. Rad)

Acute promyelocytic leukemia is caused by a chromosomal translocation of the promyelocytic leukemia gene to the retinoic acid receptor-alpha gene, which blocks terminal granulocytic differentiation at the promyelocytic stage. Treatment with all-trans retinoic acid (ATRA) relieves this blockage and the promyelocytes go on to differentiate into granulocytes. This treatment results in complete remission in > 90% of patients.

The differentiation syndrome (also know as retinoic acid syndrome and ATRA syndrome) is a cytokine release syndrome that is seen in ~1/4 of patients after induction chemotherapy with ATRA or arsenic trioxide (ATO) for acute promyelocytic leukemia. The symptoms of this potentially fatal syndrome are related to the effects of cytokines released from malignant promyelocytes.

Patients have weight gain, fever, hypoxemia, respiratory distress, hypotension, renal and hepatic dysfunction, serositis (resulting in pleural and pericardial effusions), alevolar infiltrates (hemorrhage and myeloid cells), interstitial infiltrates (edema and myeloid cells), and peripheral edema. The portable chest radiograph above reveals bilateral airspace opacities and bilateral pleural effusions. These findings are nonspecific, but in the patient with acute promyelocytic leukemia on induction therapy with ATRA or ATO, differentiation syndrome should be considered.

Patients are treated with dexamethasone until symptoms resolve. In severe cases (patients with respiratory distress or acute renal failure) ATRA and ATO are stopped until the patient recovers.

References

Rego EM, De Santis GC. Differentiation syndrome in promyelocytic leukemia: clinical presentation, pathogenesis and treatment. Mediterr J Hematol Infect Dis. 2011;3(1):e2011048.
Luesink M, Jansen JH. Advances in understanding the pulmonary infiltration in acute promyelocytic leukaemia. Br J Haematol. 2010 Nov;151(3):209-20.

Kump's Hump

2011-12-31T05:08:00.007-06:00

Kump's hump, also known as kump's bump, is named after the radiologist Warren Kump, who described an undulation of the anteromedial aspect of the distal tibial physis.

Kump's hump is the site of first closure of the physis and should not be mistake for a fracture. On MRI, the normal loss of cartilaginous signal intensity of the physis begins at Kump's hump.

Kump's hump can also present a pitfall on MRI. The undulation at this location can simulate physeal closure on T1-weighted images, a phenomenon that is due to partial volume averaging of the physis with the adjacent epiphysis and metaphysis.

References

Chung T, Jaramillo D. Normal maturing distal tibia and fibula: changes with age at MR imaging. Radiology. 1995 Jan;194(1):227-32.
Keats TE and Anderson MW. Atlas of Normal Roentgen Variants That May Simulate Disease. 8th edition, page 812; Mosby (2004).
Kump WL. Vertical fractures of the distal tibial epiphysis. Am J Roentgenol Radium Ther Nucl Med. 1966 Jul;97(3):676-81.

Osteoarthritis and the Metabolic Syndrome

2011-12-30T05:21:00.001-06:00

The metabolic syndrome is a complex of disorders that includes abnormalities in triglycerides, high-density lipoprotein, blood glucose, systolic and diastolic blood pressure, and body mass index. Patients with metabolic syndrome have an increased lifetime risk for cardiovascular disease and diabetes.

Osteoarthritis, which is commonly thought of as a degenerative joint disease related to mechanical factors and/or age-related changes in articular cartilage, has recently been shown to be associated with the metabolic syndrome.

For example, patients who develop osteoarthritis at the mean age of the general population have a ~5-fold increased risk of metabolic syndrome even when controlling for obesity. An association has also been found between popliteal artery wall thickness and generalized osteoarthritis, even after controlling for sex, age, and body mass index. In addition, knee osteoarthritis is more common in obese women with metabolic syndrome than in obese women without metabolic syndrome.

Several mechanisms have been put forward for this association: Impaired expression of genes regulating cholesterol metabolism in cartilage, impaired blood flow to bone from endothelial cell damage caused by hypertension, high glucose concentrations leading to reactive oxygen species in chondrocytes, and abnormalities in leptin production by osteoblasts leading to cartilage destruction.

These findings suggest that a common set of factors underlies the development of both osteoarthritis and the metabolic syndrome, and that the development of osteoarthritis isn't simply due to the repetitive microtrauma from obesity. Some have even suggested that the finding of osteoarthritis should prompt a cardiovascular workup.

References

Katz JD, Agrawal S, Velasquez M. Getting to the heart of the matter: osteoarthritis takes its place as part of the metabolic syndrome. Curr Opin Rheumatol. 2010 Sep;22(5):512-9.
Kornaat PR, Sharma R, van der Geest RJ, Lamb HJ, Kloppenburg M, Hellio le Graverand MP, Bloem JL, Watt I. Positive association between increased popliteal artery vessel wall thickness and generalized osteoarthritis: is OA also part of the metabolic syndrome? Skeletal Radiol. 2009 Dec;38(12):1147-51.

Denticulate Ligaments

2011-12-29T05:08:00.004-06:00

The denticulate ligaments, also known as dentate ligaments, are pia-arachnoid covered thick collagenous bundles that extend from spinal cord to the dura mater. The 20-21 pairs of denticulate ligaments are located between the dorsal and ventral rootlets and divide the spinal canal into posterior and anterior compartments. They are thought to stabilize the cord within the spinal canal and are used by surgeons as landmarks to localize spinal pathways during cordotomy.

The most cephalad denticulate ligaments attach intracranially. They are located just posterior to the vertebral artery and the ventral rootlets of C1 and anterior to the branches of the posterior spinal artery, spinal accessory nerve and, dorsal rootlets of C1.

The dentate ligaments get denser in the lower thoracic spine and tend to attach to the dura mater closer to the exiting nerve roots compared to those of the cervical and upper thoracic spine.

The most caudal of the denticulate ligaments merge with the pia mater surrounding the filum terminale.

References

Epstein BS. Cinemyelographic examination of the cervical spinal canal and the craniovertebral junction: the dentate ligaments. Br J Radiol. 1967 Mar;40(471):195-200.
Kershner DE, Binhammer RT. Lumbar intrathecal ligaments. Clin Anat. 2002 Mar;15(2):82-7.
Sigmund EE, Suero GA, Hu C, McGorty K, Sodickson DK, Wiggins GC, Helpern JA. High-resolution human cervical spinal cord imaging at 7 T. NMR Biomed. 2011 Dec 20. [Epub ahead of print]
Tubbs RS, Mortazavi MM, Loukas M, Shoja MM, Cohen-Gadol AA. The intracranial denticulate ligament: anatomical study with neurosurgical significance. J Neurosurg. 2011 Feb;114(2):454-7.
Tubbs RS, Salter G, Grabb PA, Oakes WJ. The denticulate ligament: anatomy and functional significance. J Neurosurg. 2001 Apr;94(2 Suppl):271-5.

FDG-PET Appearance of Rectus Femoris Origin Injuries

2011-12-28T05:05:00.005-06:00

Strain or avulsion injury of the proximal tendon of the rectus femoris muscle can lead to increased FDG activity at the level of the anterior inferior iliac spine and superior acetabular ridge. Recognition of this entity can help avoid confusion for neoplasm on PET and offer a non-neoplastic etiology for pain in this region.

References

Sopov V, Bernstine H, Stern D, Yefremov N, Sosna J, Groshar D. Spectrum of focal benign musculoskeletal 18F-FDG uptake at PET/CT of the shoulder and pelvis. AJR Am J Roentgenol. 2009 Apr;192(4):1029-35.

Pinch-off Syndrome

2011-12-27T05:47:00.002-06:00

Pinch-off syndrome occurs when a subclavian central venous catheter gets compressed between the clavicle and the first rib. This can result in anything from transient obstruction of the catheter to complete transsection and embolization of the catheter.

The imaging appearance of subclavian central venous catheters can be graded from 0-3 based on the severity of the compression. A normal catheter that runs a smooth curved course in the region of the clavicle and first rib without luminal narrowing is considered grade 0. Grade 1 refers to an abrupt change in course of the catheter without luminal narrowing. This can be seen in up to 1/3 of asymptomatic control patients.

Grade 2 is considered when luminal narrowing is present. This has been referred to as the "pinch-off sign" on chest radiography: indentation of the catheter as it passes deep to the clavicle. This findings represents significant catheter compression and should raise concern for serious catheter complications.

Finally, complete catheter fracture is referred to as grade 3.

The radiograph on the left was obtained 6 months after port placement. The catheter was non-functional. The inset reveals a small indentation (black arrows) as the catheter passes between the clavicle and the first rib, consistent with the pinch-off sign. Contrast injection into the port 5 days later revealed fracture of the catheter at the site of the indentation, with extravasation of contrast at the fracture site (white arrows).

References

Hinke DH, Zandt-Stastny DA, Goodman LR, Quebbeman EJ, Krzywda EA, Andris DA. Pinch-off syndrome: a complication of implantable subclavian venous access devices. Radiology. 1990 Nov;177(2):353-6.
Yeung CW, Cheung WW, Leung AY, Kwong YL. Spontaneous central venous catheter fracture: relevance of the pinch-off sign. J Hosp Med. 2010 Apr;5(4):E33.

Klippel-Trenaunay Syndrome

2011-12-26T11:27:00.005-06:00

Klippel-Trenaunay syndrome is a congenital disorder of limb asymmetry associated with vascular abnormalities. It is also known as nevus vasculosus osteohypertrophicus and Parkes Weber syndrome (after Frederick Parkes Weber).

Diagnosis requires 2 or more of the following three classic characteristics:

Cutaneous vascular lesions: Port-wine stain (nevus flammeus). These are mostly capillary malformations and usually involve the affected limb. Most common manifestation (seen in 98% of patients). Unlike hemangiomas, the cutaneous vascular lesions don't evolve with time.
Abnormal venous and lymphatic structures : Varicosities and venous malformations can be superficial, deep, or perforating.
Enlargement of an extremity: Least common of the three abnormalities. Usually unilateral involvement of a lower extremity. Enlargement of the extremity can be caused by circumferential soft-tissue hypertrophy, bone elongation, or both. The bony and soft-tissue enlargement may be due to local hyperemia and venous stasis from the aforementioned venous abnormalities.

The images above are from a patient with left leg hypertrophy, nevi predominantly on the left foot, and varicose veins throughout the left lower extremity.

References

Elsayes KM, Menias CO, Dillman JR, Platt JF, Willatt JM, Heiken JP. Vascular malformation and hemangiomatosis syndromes: spectrum of imaging manifestations. AJR Am J Roentgenol. 2008 May;190(5):1291-9.
Mavili E, Ozturk M, Akcali Y, Donmez H, Yikilmaz A, Tokmak TT, Ozcan N. Direct CT venography for evaluation of the lower extremity venous anomalies of Klippel-Trenaunay Syndrome. AJR Am J Roentgenol. 2009 Jun;192(6):W311-6.

Dysgerminoma

2011-12-25T23:04:00.005-06:00

Dysgerminomas are the ovarian counterpart of testicular seminoma. Dysgerminomas are the second most common ovarian germ cell tumor and the most common malignant germ cell tumor. They are most commonly seen in girls and young women in the 2nd and 3rd decades of life.

The majority of tumors are pure dysgerminomas, which do not secrete any hormones. About 5%, however, contain syncytiotrophoblastic giant cells and produce β−hCG.

Dysgerminomas are multilobulated, usually unilateral, solid masses that can contain speckled calcifications (pink arrow), prominent fibrovascular septa, and central low-attenuation areas representing necrosis and hemorrhage (white arrow).

The differential diagnosis for ovarian neoplasms with calcification was covered earlier.

References

Jung SE, Lee JM, Rha SE, Byun JY, Jung JI, Hahn ST. CT and MR imaging of ovarian tumors with emphasis on differential diagnosis. Radiographics. 2002 Nov-Dec;22(6):1305-25
Shanbhogue AK, Shanbhogue DK, Prasad SR, Surabhi VR, Fasih N, Menias CO. Clinical syndromes associated with ovarian neoplasms: a comprehensive review. Radiographics. 2010 Jul-Aug;30(4):903-19.

Flexion-Extension Radiography in Evaluation of Suspected Cervical Spine Trauma

2011-12-24T10:41:00.004-06:00

The clinical utility of flexion-extension radiography for diagnosing ligamentous injury in patients with suspected cervical spine trauma is questionable. The rate of technically inadequate studies, low sensitivity, and high false-positive rate make the technique too unreliable. In addition, the risk of inducing spinal cord injury makes flexion and extension radiography contraindicated until other imaging studies have been performed.

Flexion and extension radiography and dynamic fluoroscopy can be useful in assessing the significance of equivocal MR findings such as abnormal ligamentous signal without definite disruption and in patients with a normal MR and continued clinical concern for ligamentous injury.

References

Daffner RH, Hackney DB. ACR Appropriateness Criteria on suspected spine trauma. J Am Coll Radiol. 2007 Nov;4(11):762-75.

Thorotrast Accumulation in the Spleen

2011-12-23T10:50:00.006-06:00

Thorotrast (Thorium dioxide) was used as an intravenous contrast agent during World War II. It is taken up by the reticuloendothelial system and is slowly excreted by the kidneys.

Radiographs reveal increased density of a small or normal-sized (depending on how long ago the injection was), granular spleen with a fine mottled appearance. The splenic capsule is not abnormally dense. The liver may also be denser, but this is not as pronounced on radiographs.

On CT scan, the liver and abdominal lymph nodes have slightly higher attenuation, although not to the extent of that of the spleen. The Thorotrast deposits are not seen on conventional MRI or on ultrasound.

The problem with Thorotrast is that it is an alpha-emitter and can cause liver tumors (intrahepatic cholangiocarcinoma and angiosarcoma), decades after injection.

The main differential consideration is gold deposition from prolonged treatment of rheumatoid arthritis, which can look identical across all imaging modalities discussed above. Miliary calcification from miliary tuberculosis or a vascular disorder that results in multiple calcifications can be similar on radiographs, but will have imaging characteristics of calcium on ultrasound and MRI. In addition, on radiography, miliary calcifications are generally coarser in appearance, larger, and fewer in number. Some people mention capsular calcifications and calcifications in splenic cysts in the differential, but these are pretty easy to differentiate from thorotrast spleen.

The image above shows a patient with a history of Thorotrast injection. The chest radiograph shows fine granular densities within the spleen. The CT image with bone windows show the granularity as well. The liver on this non-contrast study has a higher attenuation than normal (70 HU, compared to about 55 HU for normal). The ultrasound shows a small spleen, but is otherwise normal.

Special thanks to Dr. Tommaso Bartalena for adding gold deposition to the differential diagnosis.

References

Bartalena T, Rinaldi MF. Hyperdense spleen after prolonged gold therapy. CMAJ. 2010 Dec 14;182(18):E858.
Ono N, Hirai K, Ijyuin H, Itano S, Noguchi H, Sakata K, Aoki Y, Aritaka T, Abe H, Tanikawa K. MRI in thorotrastosis. Clin Imaging. 1995 Oct-Dec;19(4):229-33.
Samuel E. Thorotrast spleen. Br J Radiol. 1955 Apr;28(328):204-5.
Yamamoto Y, Chikawa J, Uegaki Y, Usuda N, Kuwahara Y, Fukumoto M. Histological type of Thorotrast-induced liver tumors associated with the translocation of deposited radionuclides. Cancer Sci. 2010 Feb;101(2):336-40.

Ossification of the Sacrotuberous Ligaments

2011-12-22T10:40:00.000-06:00

Ossification of the sacrotuberous ligaments has a caudocranial direction of growth. On frontal radiographs, pencil-like opacities project over the obturator foramina and extend cephalad and medially towards the sacrum. On cross-sectional imaging, the ossifications have a ventrodorsal flattened appearance and extend cephalad from the ischial tuberosities medially and posteriorly.

It has been suggested that ossification of the sacrotuberous ligaments is a good indicator of diffuse idiopathic skeletal hyperostosis (DISH), although others have contested this association. For what it's worth, our patient, a 50-year-old man, had no manifestations of DISH in the spine. Ossification of the sacrotuberous ligaments has also been associated with pudendal nerve entrapment.

Atherosclerotic calcifications can mimic the appearance of ossified sacrotuberous ligaments, but recognition of the course and tubular nature of these calcifications should be sufficient to avoid confusion.

References

Arora J, Mehta V, Suri RK, Rath G. Unilateral partial ossification of sacrotuberous ligament: anatomico-radiological evaluation and clinical implications. Rom J Morphol Embryol. 2009;50(3):505-8.
Prescher A, Bohndorf K. Anatomical and radiological observations concerning ossification of the sacrotuberous ligament: is there a relation to spinal diffuse idiopathic skeletal hyperostosis (DISH)? Skeletal Radiol. 1993 Nov;22(8):581-5.
Robert R, Prat-Pradal D, Labat JJ, Bensignor M, Raoul S, Rebai R, Leborgne J. Anatomic basis of chronic perineal pain: role of the pudendal nerve. Surg Radiol Anat. 1998;20(2):93-8.

Malignant Peripheral Nerve Sheath Tumors

2011-12-21T15:27:00.002-06:00

Malignant peripheral nerve sheath tumors make up about 10% of all soft-tissue sarcomas. These are highly highly malignant tumors that tend to recur locally and to metastasize.

Up to half of all cases of malignant peripheral nerve sheath tumors are associated with neurofibromatosis type 1, and deep plexiform neurofibromas have an even higher risk of malignant transformation that superficial or solitary neurofibromas.

It can be difficult to differentiate malignant peripheral nerve sheath tumors from neurofibromas, a task that is even more difficult in patients with neurofibromatosis type 1.

Imaging features can help. A recent study by Wasa et al reviewed 41 cases of malignant peripheral nerve sheath tumor and 20 cases of neurofibroma, about half of whom had neurofibromatosis type 1. They found four statistically significant features that were useful in differentiating malignant peripheral nerve sheath tumors from neurofibromas, and suggest that a tumor with two or more of these features can be considered highly suspicious for malignancy. They also found an additional feature that was useful in patients with neurofibromatosis type 1.

The four (plus 1) features in their study were:

Large long-axis dimension: Malignant lesions tend to be larger than about 5 cm in largest dimension.
Peripheral enhancement: Focal central enhancement is usually seen in benign neurogenic tumors. Although neurofibromas can also show a peripheral enhancement pattern, this is more commonly seen in malignant peripheral nerve sheath tumors.
A perilesional edema-like zone:
Intratumoral cystic areas: Can be commonly seen in schwannomas and malignant peripheral nerve sheath tumors, but rarely in neurofibromas. Often is seen in association with peripheral enhancement
Heterogeneity on T1-weighted images (in neurofibromatosis type 1): Can be helpful in differentiating malignant peripheral nerve sheath tumors from neurofibromas in patients with neurofibromatosis 1, but doesn't seem helpful in the general population.

The case above doesn't really present a diagnostic dilemma. This is an enhancing soft tissue lesion that is malignant until proven otherwise. I'll try to find a case that better presents the challenge of differentiating a malignant peripheral nerve sheath tumor from a neurofibroma.

References

Wasa J, Nishida Y, Tsukushi S, Shido Y, Sugiura H, Nakashima H, Ishiguro N. MRI features in the differentiation of malignant peripheral nerve sheath tumors and neurofibromas. AJR Am J Roentgenol. 2010 Jun;194(6):1568-74.

Retractile and Ascending Testes

2011-12-20T05:14:00.010-06:00

A retractile testis is a normally developed testis that can be brought into a stable position at the bottom of the scrotum during physical examination, but can also move into the groin by the cremasteric reflex.

As many as 35% of children's testes are thought to be retractile, with a peak incidence between the ages of 5 and 6 years. A retractile testis can transiently lie between the inguinal canal and scrotum and appear as a lump on physical examination and on imaging. Retractile testes usually descend completely by puberty, and there are no implications for fertility.

An ascending testis, also known as an ascended testis, ascensus testis, secondary cryptorchidism, and acquired cryptorchidism, is one that had previously been in the scrotum, but which can now be classified as undescended. Ascending testes are more frequently seen on the left, and many patients have associated disorders.

The majority of patients with an ascending testis can be shown to have had a history of a retractile testis and about 1/3 of boys with retractile testes go on to have ascending testes. The high position of the testis causes the same damage as seen with congenitally undescended testes and can lead to adverse effects on germ cell development and fertility.

Physical examination criteria have been proposed to differentiate an incompletely descended testis from a retractile testis on a single examination:

An incompletely descended testis is smaller than the contralateral testis
The incompletely descended testis rapidly retracts out of the scrotum when it is released.
Pain is elicited when the incompletely descended testis is manipulated into the scrotum.

Of these, only the first can be applied to imaging, and may be helpful in differentiating an incompletely descended testis from a retractile or ascending testis on a single imaging study. Physical examination is then needed to differentiate a retractile testis from an ascending testis.

The images above are from a 7-year-old boy who in 2010 had descended testes bilaterally. His most recent MRI (in 2011) reveals that the left testis (pink arrow) has moved up into the inguinal canal. Note that the testes are about the same size.

References

Guven A, Kogan BA. Undescended testis in older boys: further evidence that ascending testes are common. J Pediatr Surg. 2008 Sep;43(9):1700-4.
Kidney DD, Cohen AJ, Seville P. Retractile testis: an incidental CT finding in trauma patients. AJR Am J Roentgenol. 1997 May;168(5):1233-4.
Shadbolt CL, Heinze SB, Dietrich RB. Imaging of groin masses: inguinal anatomy and pathologic conditions revisited. Radiographics. 2001 Oct;21 Spec No:S261-71.
Shapiro E. The risk of retractile testes becoming ascending testes. Rev Urol. 2006 Fall;8(4):231-2.
Yoshida T, Ohno K, Morotomi Y, Nakamura T, Azuma T, Yamada H, Hayashi H, Suehiro S. Clinical and pathological features of ascending testis. Osaka City Med J. 2009 Dec;55(2):81-7.

Rosai-Dorfman Disease

2011-12-19T12:31:00.003-06:00

Rosai-Dorfman disease, also known as sinus histiocytosis with massive adenopathy, is a macrophage-related histiocytic disorder of varied biological behavior.

Rosai-Dorfman disease predominantly affects children and adolescents, who most commonly with bilateral painless cervical lymphadenopathy and fever. There is a slight male predominance.

Extranodal involvement, seen in about 40% of cases, can occur with or without lymphadenopathy and can be solitary or multiple. Common extranodal sites include the nasal cavity and paranasal sinuses (shown above), although involvement has also been reported of the soft tissue, central nervous system, orbit, skin, oral cavity, bone, kidneys, upper respiratory tract, gastrointestinal tract, testicles and salivary glands.

The image above is from an atypical presentation in a middle-aged woman who presented with isolated paranasal sinus involvement. Biopsy of the left maxillary sinus lesion revealed the characteristic histopathologic feature of emperipolesis: Histiocytes with intracytoplasmic lymphocytes, plasma cells, erythrocytes, and/or polymorphonuclear leukocytes (from phagocytosis by the histiocytes). Another feature that can be seen is intracytoplasmic eosinophilic globules (Russell bodies) in the phagocytized plasma cells. These features are usually less prominent in extranodal Rosai-Dorfman disease, which was the case in this patient, who required a surgical biopsy for definitive diagnosis.

References

La Barge DV 3rd, Salzman KL, Harnsberger HR, Ginsberg LE, Hamilton BE, Wiggins RH 3rd, Hudgins PA. Sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease): imaging manifestations in the head and neck. AJR Am J Roentgenol. 2008 Dec;191(6):W299-306.
Gupta P, Babyn P. Sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease): a clinicoradiological profile of three cases including two with skeletal disease. Pediatr Radiol. 2008 Jul;38(7):721-8; quiz 821-2. Epub 2008 Feb 2.

Response Evaluation Criteria in Solid Tumors (RECIST) 1.1: Imaging Basics

2011-12-18T10:16:00.004-06:00

RECIST guidelines exist to standardize objective response to therapy on imaging and clinical examination. We focus here on the basics of imaging criteria. Special cases will be covered in a later post.

Baseline assessment

A tumor lesion or soft tissue component of a bony lesion are measurable if they are:
- ≥ 10 mm on CT (slice thickness ≤ 5 mm).
- ≥ 20 mm on chest radiography.
- Lesions with cystic components are considered measurable; however, if non-cystic lesions are present in the same patient, these should be used as target lesions.
A lymph node is pathologically enlarged and measurable if it is:
- ≥ 15 mm in short-axis dimension on CT (slice thickness ≤ 5 mm).
Non-measurable lesions include:
- Small lesions (longest diameter <10 mm, pathological lymph nodes ≥ 10 to < 15 mm in short-axis dimension)
- Blastic bone lesions
- Leptomeningeal disease
- Ascites
- Pleural or pericardial effusion
- Inflammatory breast disease
- Lymphangitic involvement of skin or lung
- Abdominal masses or organomegaly on physical exam not measurable by reproducible imaging techniques

The lesions should lend themselves to reproducible repeated measurements (i.e., the largest lesion is not necessarily the one that should be selected if it does not lend itself to reproducible measurement).

Measurable disease is defined by the presence of at least one measurable lesion as defined above. A maximum of five total lesions and a maximum of two lesions per organ are identified as target lesions and recorded and measured at baseline.

Overall tumor burden at baseline is then determined as the sum of the longest diameters of non-nodal lesions added to the sum of the short-axis dimension of nodal lesions (if nodal lesions are used as target lesions).

The sum at baseline will be used as a comparator for subsequent measurements. The same target lesions will be recorded and evaluated on subsequent imaging. Based on the behavior of these target lesions, objective tumor response is defined as:

Complete Response: Disappearance of all target lesions. Pathological lymph nodes (target or non-target) reduced in short=axis diameter to < 10 mm.
Partial Response: At least a 30% decrease in the sum of diameters of target lesions, taking as reference the baseline sum diameters.
Progressive Disease: At least a 20% increase in the sum of diameters of target lesions AND an absolute increase of at least 5 mm in the sum of diameters of target lesions, taking as reference the smallest sum on prior studies (can include the baseline sum if that is the smallest). The appearance of one or more new lesions is also considered progression.
Stable Disease: Neither sufficient shrinkage to qualify for partial response nor sufficient increase to qualify for progressive disease, taking as reference the smallest sum of diameters while on the study.

References

Chalian H, Töre HG, Horowitz JM, Salem R, Miller FH, Yaghmai V. Radiologic Assessment of Response to Therapy: Comparison of RECIST Versions 1.1 and 1.0. Radiographics. 2011 Nov;31(7):2093-105.
Eisenhauer EA, Therasse P, Bogaerts J, Schwartz LH, Sargent D, Ford R, Dancey J, Arbuck S, Gwyther S, Mooney M, Rubinstein L, Shankar L, Dodd L, Kaplan R, Lacombe D, Verweij J. New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1). Eur J Cancer. 2009 Jan;45(2):228-47.

Hydroxyapatite Ocular Implants

2011-12-17T07:23:00.006-06:00

Hydroxyapatite ocular implants are porous implants that are derived from sea coral. The porous structure of these implants allows ingrowth of host fibrovascular tissue, which reduces the risk of migration, extrusion, and infection. In addition, the extraocular muscles can be more securely attached to the implants, allowing the implant to move synchronously with the other eye.

An understanding of the sequence of events after enucleation can reduce confusion when evaluating the post-operative eye. In addition, MRI and nuclear medicine may be requested to confirm vascularization of the implant, although this is no longer universally used.

Patient information and surgical demonstration videos for one type of ocular implant provide a good overview of the procedure.

The ocular implant is placed immediately after enucleation and a temporary ocular conformer is placed on top of the implant. This conformer stays in place for about 4 to 8 weeks after surgery, at which point an ocularist fits, shapes, and paints an ocular prosthesis to match the patient's other eye. The prosthesis sits on top of the implant like a large contact lens.

We can sometimes be a bit loose in terminology, but there is a distinction between implant and prosthesis.

Mechanical coupling between the implant and the prosthesis can be improved with a second procedure where a round-headed peg or screw is inserted into the implant (the back of the prosthesis is also modified to accommodate this peg). The hole for the peg is usually not drilled until 6 months after enucleation: Enough time to allow for implant vascularization.

Radiologists used to be called upon to confirm vascularization of the implant by bone scintigraphy or contrast-enhanced MRI prior to drilling the hole for the peg, but this is no longer routinely done. Bone scintigraphy can show increased activity within the implant starting 1 to 6 months after surgery, indicating fibrovascular ingrowth. Contrast-enhanced MRI can also reveal the extent of fibrovascular ingrowth.

The images above are from a patient 4 years post left eye enucleation. CT shows the implant with a high-attenuation prosthesis anterior to it. FDG/PET shows no activity in the implant. The MR images show the attachment of the extra-ocular muscles to the implant. Anterior to the implant is the prosthesis, which is low signal intensity on all pulse sequences. Both CT and MR show linear striations in the implant, which is presumably due to the channels in these implants, although I can't find a reference in this regard. Enhancement along the periphery of the implant indicates fibrovascular ingrowth. No peg was placed in this patient.

References

Custer PL, Kennedy RH, Woog JJ, Kaltreider SA, Meyer DR. Orbital implants in enucleation surgery: a report by the American Academy of Ophthalmology. Ophthalmology. 2003 Oct;110(10):2054-61.
De Potter P. Advances in imaging in oculoplastics. Curr Opin Ophthalmol. 2001 Oct;12(5):342-6.
Domange-Testard A, Papathanassiou D, Menéroux B, Amans J, Liehn JC. SPECT-CT images of an ocular coralline hydroxyapatite implant visible on bone scintigraphy. Clin Nucl Med. 2007 Feb;32(2):132-4.
Hamilton HE, Christianson MD, Williams JP, Thomas RA. Evaluation of vascularization of coralline hydroxyapatite ocular implants by magnetic resonance imaging. Clin Imaging. 1992 Oct-Dec;16(4):243-6.
Shields CL, Shields JA, De Potter P, Singh AD. Problems with the hydroxyapatite orbital implant: experience with 250 consecutive cases. Br J Ophthalmol. 1994 Sep;78(9):702-6.

Annular Pancreas

2011-12-16T05:45:00.003-06:00

Annular pancreas is the second most common congenital pancreatic anomaly (after pancreas divisum), occurring in 1 in 2000 people. Its embryogenesis is unclear, but the end result is pancreatic tissue surrounding the second portion of the duodenum. This may be partial or complete.

Annular pancreas can be extramural or intramural. In the extramural type, the ventral pancreatic duct encircles the duodenum to join the main pancreatic duct. In the intramural type, the pancreatic tissue is intermingled with the duodenal wall muscle and small pancreatic ducts drain directly into the duodenum.

Patients with extramural annular pancreas can present with high gastrointestinal obstruction, sometimes with pancreatitis. Patients with intramural annular pancreas can present with symptoms of duodenal ulceration.

Contrast fluoroscopy can suggest the diagnosis by revealing narrowing at the level of the major papilla. ERCP or MRCP can show the duct of Wirsung encircling the duodenum in the patient with extramural annular pancreas. Cross sectional imaging will show pancreatic tissue around the second portion of the duodenum, as shown above in two patients with annular pancreas.

References

Johnston DW. Annular pancreas: a new classification and clinical observations. Can J Surg. 1978 May;21(3):241-4.
Mortelé KJ, Rocha TC, Streeter JL, Taylor AJ. Multimodality imaging of pancreatic and biliary congenital anomalies. Radiographics. 2006 May-Jun;26(3):715-31.
To'o KJ, Raman SS, Yu NC, Kim YJ, Crawford T, Kadell BM, Lu DS. Pancreatic and peripancreatic diseases mimicking primary pancreatic neoplasia. Radiographics. 2005 Jul-Aug;25(4):949-65.

Benign Notochordal Cell Tumors

2011-12-15T05:52:00.003-06:00

Benign notochordal cell tumors are recently discovered intraosseous lesions of notochordal cell origin that are usually asymptomatic or indolent. Synonyms for this tumor include benign chordoma, giant notochordal rest, giant notochordal hamartoma of intraosseous origin, notochordal hamartoma, ecchordosis physaliphora vertebralis,

These tumors can have histologic findings that overlap with those of chordomas. It has been suggested that benign notochordal cell tumors may be precursors of chordomas, but the evidence for this seems to be lacking at this point.

Like chordomas, benign notochordal cell tumors are most commonly found at the midline in the sacro-coccygeal region and the base of the skull.

On radiography, these are ill-defined and sclerotic lesions, sometimes with the appearance of an ivory vertebra. Radiographs can be normal, however. Regardless of the visibility of these lesions on radiographs, bone expansion should not be seen.

CT can also be normal or reveal sclerosis ranging from mild to severe. Trabecular and cortical destruction should not be seen. The lesions can be central in the vertebral body, extend to the cortex, or occupy the entirety of the vertebral body, resulting in an ivory vertebra.

The lesions are homogeneously hypointense on T1-weighted images, and homogeneously iso- to hyperintense on T2-weighted images. No significant enhancement is typically seen, although the lesion in our case has mild enhancement. Extraosseous extension should not be seen.

Chordomas may resemble benign notochordal cell tumors with cellular atypia on biopsy. Imaging can help in differentiating the two by remembering that in contrast to chordomas, benign notochordal cell tumors are not typically osteolytic and may have sclerosis. In addition, chordomas can have a soft tissue mass, while benign notochordal cell tumors typically do not.

References

Kyriakos M. Benign notochordal lesions of the axial skeleton: a review and current appraisal. Skeletal Radiol. 2011 Sep;40(9):1141-52. Epub 2011 Aug 17.
Yamaguchi T, Iwata J, Sugihara S, McCarthy EF Jr, Karita M, Murakami H, Kawahara N, Tsuchiya H, Tomita K. Distinguishing benign notochordal cell tumors from vertebral chordoma. Skeletal Radiol. 2008 Apr;37(4):291-9.

Autoimmune Pancreatitis

2011-12-14T05:29:00.003-06:00

Autoimmune pancreatitis is caused by periductal infiltration with IgG4-positive plasma cells, which leads to periductal and interlobular fibrosis, causing diffuse narrowing of the pancreatic duct and acinar atrophy. Autoimmune pancreatitis may be responsible for up to 10% of cases of chronic pancreatitis. Men are more commonly affected. Patients typically present with fluctuating obstructive jaundice, abdominal pain, weight loss, steatorrhea, and diabetes (~50% of patients).

The Mayo Clinic diagnostic criteria require one or more of the following findings:

Histologic findings diagnostic of autoimmune pancreatitis
Characteristic CT and pancreatographic findings with elevated serum IgG4 levels
Response to steroid therapy

The role of the radiologist is in identifying the characteristic imaging findings and differentiating them from those of acute pancreatitis and pancreatic carcinoma (up to ~10% of pancreatectomy patients for presumed carcinoma actually have autoimmune pancreatitis).

The affected area(s) of the pancreas are typically hypoechoic, hypoattenuating, T1-hypointense, and mildly T2-hyperintense. Decreased enhancement is usually seen during early dynamic imaging, and moderate enhancement is seen in the late phases. A capsule-like rim or halo of low attenuation or intensity is common and is thought to represent fluid, phlegmon, or fibrous tissue. ERCP or MRCP typically reveals a narrow and irregular pancreatic duct in the affected portion(s) of the pancreas.

Three patterns of autoimmune pancreatitis have been recognized

Diffuse: Most common type. The pancreas is sausage-like: diffusely enlarged with a sharp margin and loss of the normal lobular contour and pancreatic clefts.

This form can mimic the appearance of acute pancreatitis. Unlike acute pancreatitis, there is minimal or no peripancreatic stranding and no peripancreatic fat necrosis.
Focal: Looks like a relatively well-demarcated focal mass, often involving the pancreatic head.

This form Can mimic pancreatic carcinoma, but upstream dilatation of the main pancreatic duct is typically milder than in patients with carcinoma (usually smaller than 5 mm). In addition, while the peripancreatic veins may be involved in patients with focal autoimmune pancreatitis and in those with pancreatic cancer, involvement of the peripancreatic arteries is unlikely in the former.

On ERCP patients with focal autoimmune pancreatitis usually have a stenosed main pancreatic duct longer than 30 mm and an upstream main pancreatic duct that is smaller than 6 mm in diameter.
Multifocal: Self explanatory.

The pancreas and pancreatic duct usually return to normal on imaging within 4–6 weeks after initiation of steroid therapy. However, there is atrophy of the affected areas of the pancreas in the burnt-out phase of the disease in about half of patients. Spontaneous regression is can also occur. Diabetes may also resolve following treatment.

Two cases of autoimmune pancreatitis are shown above. The left image has a sausage-like pancreas that is diffusely enlarged with a sharp margin and loss of the normal lobular contour and pancreatic clefts. The pancreas in the right image has a low-attenuation peri-pancreatic halo. Peripancreatic stranding is minimal to absent in both cases.

References

Vlachou PA, Khalili K, Jang HJ, Fischer S, Hirschfield GM, Kim TK. IgG4-related sclerosing disease: autoimmune pancreatitis and extrapancreatic manifestations. Radiographics. 2011 Sep-Oct;31(5):1379-402.
Yang DH, Kim KW, Kim TK, Park SH, Kim SH, Kim MH, Lee SK, Kim AY, Kim PN, Ha HK, Lee MG. Autoimmune pancreatitis: radiologic findings in 20 patients. Abdom Imaging. 2006 Jan-Feb;31(1):94-102.

Aortitis: Differential Diagnosis

2011-12-13T05:18:00.007-06:00

Aortitis, the inflammation of the aortic wall, can be due to infectious or noninfectious conditions. Patients present with nonspecific signs, symptoms, and laboratory findings that can include pain, fever, vascular insufficiency, and elevated levels of acute phase reactants.

Differential considerations include:

Noninfectious

Large-vessel vasculitides (shown above):
- Giant cell arteritis: Affects large and medium-sized vessels. Often involves the superficial cranial arteries.
- Takayasu arteritis: Abdominal aorta most commonly affected. Descending thoracic aorta and aortic arch can also be involved. Look for stenosis or luminal narrowing of aorta and branch vessels. Aneurysmal dilatation less common, but can be seen after destruction of media. Arterial wall calcification (can be seen in chronic cases) is typically linear and spares the ascending aorta.
- Rheumatoid arthritis: Aortitis is rare. Heart, aortic valve, and great vessels can be affected.
- Systemic lupus erythematosus: Aortitis uncommon.
- Ankylosing spondylitis: Aortic root and valve disease seen in 80% of cases. Aortic wall thickening is seen in 60% of affected patients.
- Reiter syndrome:
Medium- and small-vessel vasculitides:
- Wegener arteritis:
- Polyarteritis nodosa:
- Behçet disease: Wall-enhancing saccular pseudoaneurysms can be seen in the aorta and branch vessels in 20% of patients.
- Relapsing polychondritis: May manifest as aortic root dilatation and aortitis.
- Cogan syndrome: Ocular, inner ear, and vascular inflammation. Patients are usually white young adults. Aortitis and valvulitis seen in ~10% of patients.
Isolated aortitis: Isolated idiopathic (thoracic) aortitis, Chronic periaortitis (Idiopathic retroperitoneal fibrosis, inflammatory abdominal aortic aneurysm, perianeurysmal aortitis, idiopathic isolated abdominal periaortitis).
Radiation-induced: Usually years after exposure to high-dose radiation. Can manifest as thrombosis, pseudoaneurysm, rupture, stenosis, and accelerated wall calcification.

Infectious

Bacterial: Salmonella, Staphylococcus, Streptococcus pneumoniae
Syphilis: The typical calcification of the ascending aorta is uncommon.
Mycobacterial: Mycobacterium tuberculosis
Viral: HIV.

References

Gornik HL, Creager MA. Aortitis. Circulation. 2008 Jun 10;117(23):3039-51.
Restrepo CS, Ocazionez D, Suri R, Vargas D. Aortitis: imaging spectrum of the infectious and inflammatory conditions of the aorta. Radiographics. 2011 Mar-Apr;31(2):435-51.

Metformin and 18F-FDG PET

2011-12-12T06:44:00.006-06:00

Metformin has been shown to significantly increase ¹⁸F-FDG uptake in the colon and, to a lesser extent, the small bowel.

Cells of the intestinal wall are exposed to much higher concentrations of metformin for much longer times compared to other cell types. In addition, animal studies have shown that metformin increases glucose transfer into intestinal mucosal cells and can increase glucose utilization by up to 60%.

This results in intense, diffuse, and continuous uptake along the bowel on ¹⁸F-FDG PET imaging. The uptake is seen in both the wall and within the lumen (likely due to excretion of ¹⁸F-FDG into the stool).

The pattern is fairly characteristic and confusion with malignant focal bowel uptake is rare. The problem is that this diffuse uptake can mask an existing bowel malignancy and lead to a false-negative result.

References

Gontier E, Fourme E, Wartski M, Blondet C, Bonardel G, Le Stanc E, Mantzarides M, Foehrenbach H, Pecking AP, Alberini JL. High and typical 18F-FDG bowel uptake in patients treated with metformin. Eur J Nucl Med Mol Imaging. 2008 Jan;35(1):95-9.

Fibrous Hamartoma of Infancy

2011-12-11T07:08:00.005-06:00

Fibrous hamartoma of infancy is a rare benign fibrous tumor found in early childhood, more commonly in boys. More than 90% occur during the 1st year of life, and about 25% are congenital. They can be rapidly growing, but are cured by local excision. Recurrence is rare, but also cured by excision.

These are superficial tumors that are usually painless and freely movable, but may also be attached to the underlying fascia. Involvement of the skeletal muscle is rare. They are most commonly located in the axilla, followed by the upper arm and shoulder, thigh and groin, back, and forearm.

Fibrous hamartomas of infancy are poorly circumscribed masses that consist of a mixture of fibrocollagenous tissue, immature -appearing primitive mesenchymal cells, and mature fat.

Ultrasound is usually the first modality used for evaluation of these lesions, but I can't find a reference for the appearance of these lesions on sonography. MR characteristics reflect the different components discussed above: The fibrocollagenous component is low signal intensity on both T1- and T2-weighted images and the mature fat component is hight signal intensity on both T1- and T2-weighted images. Organized trabeculae of fibrous tissue interspersed with fat should suggest the diagnosis.

When fat is identified in these lesions, the differential diagnosis should include lipoma, lipoblastoma, and an involuting hemangioma.

The images above are from a 1-year-old boy with a right forearm mass (pink arrow). The lateral radiograph reveals an ill-defined mass along the volar surface of the proximal forearm. Ultrasound reveals a heterogeneous, predominantly hyperechoic lesion without significant vascularity on Doppler. MRI reveals a lobular, ill-defined mass that is predominantly isointesnse to skeletal muscle on the T1-weighted image and hyperintense on the T2-weighted image, but has internal areas of fat signal. Thin fibrous sepata are seen on the T1-weighted image (black arrow). Mild enhancement is seen.

References

Hashimoto H. Fibrous hamartoma of infancy. in Pathology and Genetics of Tumours of Soft Tissue and Bone. Fletcher CDM, Unni KK, Mertens F (eds). IARCPress Lyon, 2002. pp 58-59.
Laffan EE, Ngan BY, Navarro OM. Pediatric soft-tissue tumors and pseudotumors: MR imaging features with pathologic correlation: part 2. Tumors of fibroblastic/myofibroblastic, so-called fibrohistiocytic, muscular, lymphomatous, neurogenic, hair matrix, and uncertain origin. Radiographics. 2009 Jul-Aug;29(4):e36.

Renal Leiomyoma

2011-12-10T06:54:00.000-06:00

Renal leiomyomas are benign tumors of the kidneys that most commonly arise from smooth muscle cells of the renal capsule. Other origins include the muscularis of the renal pelvis and cortical vascular smooth muscles. The tumors contain areas of hemorrhage and irregular calcification.

They are relatively uncommon, being found in ~5% of subjects in autopsy series, more commonly in white women.

Most renal leiomyomas are small and asymptomatic, but larger lesions can cause pain or even be palpable.

The imaging appearance of renal leiomyoma is nonspecific. They tend to be well-circumscribed and peripherally located lesions that cause buckling of the renal cortex. Non-contrast CT reveals a high-attenuation mass that can have areas of hemorrhage and cystic degeneration (larger lesions). Calcification is uncommon. Contrast enhanced CT images reveal relatively homogeneous enhancement.

MRI typically reveals a lesion with homogeneously low signal intensity on T1- and T2-weighted images. As on CT, larger lesions can have a complex appearance due to calcifications, hemorrhage, and cystic or myxoid degeneration. The appearance of these large tumors can be identical to that of renal cell carcinoma.

The images above are from a renal tumor protocol CT in a patient with an incidentally detected left renal lesion. The lesion is peripheral, relatively small, and has foci of calcification (uncommon in leiomyomas) as well as an area of low-attenuation/non-entrancement. The lesion is hypervascular. The imaging findings are nonspecific and the lesion should be thought of as renal cell carcinoma until proven otherwsie. Core biopsy prior to radiofrequency ablation revealed a diagnosis of leiomyoma.

References

Prasad SR, Surabhi VR, Menias CO, Raut AA, Chintapalli KN. Benign renal neoplasms in adults: cross-sectional imaging findings. AJR Am J Roentgenol. 2008 Jan;190(1):158-64.

Li-Fraumeni Syndrome

2011-12-09T07:41:00.006-06:00

Li-Fraumeni syndrome is an autosomal-dominant familial cancer syndrome that results in an increased lifelong risk of what are considered Li-Fraumeni syndrome spectrum tumors (e.g., soft tissue sarcoma, osteosarcoma, brain tumor, premenopausal breast cancer, adrenocortical carcinoma, leukemia, lung bronchoalveolar cancer), among others. About 3/4 of patients have a mutation in the gene encoding the p53 tumor suppressor protein (TP53). The cancers aren't limited to those listed above, however, and patients can have a wide range of malignancies, including melanoma, germ-cell tumors, gastric carcinoma, Wilms tumor, lymphoma, and lung, laryngeal, prostate, and pancreatic cancers.

The 2009 Chompret (after Agnès Chompret) criteria for germline TP53 mutation screening are as follows:

[A Li-Fraumeni syndrome spectrum tumor before age 46 years.] AND [At least one first- or second-degree relative with a Li-Fraumeni syndrome spectrum tumor (except breast cancer if the proband has breast cancer) before the age of 56 years or with multiple tumors.]
OR
[Multiple tumors (except multiple breast tumors), two of which belong to the Li-Fraumeni syndrome tumor spectrum.] AND [The first tumor occurred before the age of 46 years.]
OR
[Adrenocortical carcinoma or choroid plexus tumor (irrespective of family history).]

These criteria result in a mutation detection rate of ~30-35% and sensitivity and specificity of ~80-90% and ~50-60%, respectively.

These screening criteria and the availability of genetic testing raise the question of how best to manage patients, asymptomatic carriers, and relatives of patients with Li-Fraumeni syndrome.

Regarding the patient with Li-Fraumeni syndrome and a known malignancy: Radiation must be carefully applied (if at all), as second malignant tumors frequently arise in the radiotherapy field in these patients.

It has been suggested that women begin breast cancer screening in their mid-20s (the average age of onset is ~30 years in these patients). Beyond that, there are currently no clear clinical surveillance, preventive, or treatment recommendations for patients with Li-Fraumeni syndrome.

The situation seems even less clear when it comes to management of asymptomatic relatives of patients with p53 germline mutations. This is because of the variable expressivity of the mutation, the diverse range of tumors, and, as noted above, absence of clear surveillance, preventative, and treatment recommendations.

PET-CT has been put forward as a surveillance modality for identifying presymptomatic malignancies. In a study of members of Li-Fraumeni syndrome families with germline TP53 mutations, FDG-PET/CT screening resulted in cancer detection in 20% (3 out of 15 subjects).

Prenatal genetic testing can also be offered after careful screening and thorough counseling of parents.

The images above are from a patient with a history of right adrenal cortical carcinoma (note the clips on the right, pink arrow), who developed an anterior mediastinal sarcoma. A p53 mutation was found.

References

Chompret A. The Li-Fraumeni syndrome. Biochimie. 2002 Jan;84(1):75-82.
Malkin D. Li-fraumeni syndrome. Genes Cancer. 2011 Apr;2(4):475-84.
Masciari S, Van den Abbeele AD, Diller LR, Rastarhuyeva I, Yap J, Schneider K, Digianni L, Li FP, Fraumeni JF Jr, Syngal S, Garber JE. F18-fluorodeoxyglucose-positron emission tomography/computed tomography screening in Li-Fraumeni syndrome. JAMA. 2008 Mar 19;299(11):1315-9.
Tinat J, Bougeard G, Baert-Desurmont S, Vasseur S, Martin C, Bouvignies E, Caron O, Bressac-de Paillerets B, Berthet P, Dugast C, Bonaïti-Pellié C, Stoppa-Lyonnet D, Frébourg T. 2009 version of the Chompret criteria for Li Fraumeni syndrome. J Clin Oncol. 2009 Sep 10;27(26):e108-9.

Cystic Retroperitoneal Masses: Differential Diagnosis

2011-12-08T12:20:00.003-06:00

Epithelial neoplasms: Mucinous cystadenoma or cystadenocarcinoma, serous cystadenocarcinoma, perianal mucinous cystadenocarcinoma (rare, associated with history of anal fistula).
Mesothelial neoplasms: Mesothelioma.
Germ cell neoplasms: Cystic teratoma.
Neuroendocrine neoplasms: Paraganglioma.
Neural neoplasm: Schwannoma.
Sarcoma: Necrotic areas can appear cystic.
Lymphovascular: Lymphangioma, lymphangiomatosis, lymphangioleiomyoma.
Developmental: Müllerian cyst, epidermoid cyst, tailgut cyst, bronchogenic cyst (subdiaphragmatic location).
Miscellaneous fluid collections: Hematoma, urinoma, abscess, lymphocele (shown above in a patient with testicular cancer, post lymph node dissection), pseudocyst (pancreatic, and nonpancreatic), pseudomyxoma retroperitonei (caused by a ruptured mucocele of the appendix).

References

Rajiah P, Sinha R, Cuevas C, Dubinsky TJ, Bush WH Jr, Kolokythas O. Imaging of uncommon retroperitoneal masses. Radiographics. 2011 Jul-Aug;31(4):949-76.

Kikuchi-Fujimoto Disease

2011-12-07T05:03:00.003-06:00

Kikuchi-Fujimoto disease, also known as Kikuchi disease and histiocytic necrotizing lymphadenitis lymphadenitis, is a rare, self-limiting condition characterized by characterized by lymphadenopathy, fever, and neutropenia.

Its cause is unknown. Viral etiologies have been proposed, with the usual suspects (EBV, HHV 6 and 8) included in the lineup. An autoimmune mechanism has also been suggested, supported by a strong association with systemic lupus erythematosus and mixed connective tissue disorders.

Patients are typically girls or young women under 30 years of age. The most common presentation is firm, tender, unilateral cervical lymphadenopathy. Patients may also have more generalized adenopathy, low-grade fever, malaise, fatigue, diarrhea, weight loss, nausea, and vomiting. Kikuchi-Fujimoto disease generally has a benign, self-limited course with symptoms lasting between 1–2 months.

Patients can have nonspecific laboratory findings such as neutropenia with atypical lymphocytes, anemia, and elevated rythrocyte sedimentation rate (ESR), lactogen dehydrogenase (LDH), and transaminases. Diagnosis, however, can be made with biopsy revealing effaced nodal architecture with islands of hyperplasia and zonal necrosis. Fine needle aspiration can also be used.

Imaging findings overlap with those of lymphoma, and biopsy cannot be avoided. As noted above, the lymphadenopathy is more commonly found in the neck, where it is more often unilateral. Cervical lymph nodes range in size from 0.5–3.5 cm and the majority of patients show perinodal fatty infiltration and homogeneous nodal contrast enhancement. A minority of cases have lymph nodes with low-attenuation areas, sometimes resulting in ring-shaped lymph nodes mimicking tuberculosis or metastatic lymphadenopathy.

The images above are from a 50-year-old woman with diffuse lymphadenopathy and "mildly positive ANA." Cervical, mediastinal, hilar, and axillary lympahdenopathy was noted, without evidence of retroperitoneal or pelvic lympahdenopathy. Nodal enhancement was homogeneous. Mild perinodal infiltration is well seen in a left level IIA lymph node (red *)

References

Hasan M, Zaheer S, Sofi LA, Parvez A. Fine-needle aspiration cytology of Kikuchi Fujimoto disease. J Cytol. 2009 Jan;26(1):43-5.
Kim TA, Lupetin AR, Graham C. CT appearance of Kikuchi-Fujimoto disease. Clin Imaging. 1995 Jan-Mar;19(1):1-3.
Kwon SY, Kim TK, Kim YS, Lee KY, Lee NJ, Seol HY. CT findings in Kikuchi disease: analysis of 96 cases. AJNR Am J Neuroradiol. 2004 Jun-Jul;25(6):1099-102.

Subcutaneous Granuloma Annulare

2011-12-06T05:58:00.005-06:00

[No Image Available]
Granuloma annulare is an uncommon, benign inflammatory papular eruption. Granuloma annulare is classified as localized, generalized (disseminated), perforating, erythematous, or subcutaneous. The first four types are cutaneous and are diagnosed and managed by dermatologists.

Subcutaneous granuloma annulare, because of its deeper location, can present a diagnostic challenge, leading to multiple referrals and imaging evaluation. Indeed, subcutaneous granuloma annulare is the most frequently biopsied benign soft tissue mass in the lower extremity of children under the age of 5, and is susceptible to inappropriate and sometimes repeated surgical intervention before the correct diagnosis is determined.

Synonyms for subcutaneous granuloma annulare include benign rheumatoid nodule, pseudorheumatoid nodule, deep granuloma annulare, subcutaneous palisading granuloma, palisading granuloma nodosum, and isolated subcutaneous nodule.

Subcutaneous granuloma annulare typically presents as a rapidly growing, firm, painless, subcutaneous mass in children younger than 5 years of age. A pretibial location is typical and lesions along the extensor aspects of forearms and feet, and within the occipital scalp are also common. Atypical presentations with pain and multiple soft lesions have also been reported.

Radiographs reveal a dense subcutaneous mass without calcifications. The lesions are hypoechoic on ultrasound. MRI reveals a subcutaneous lesion with indistinct margins and signal abnormality extending into the adjacent subcutaneous fat. The lesions are iso- or slightly hyperintense to muscle on T1-weighted images and heterogeneously hyperintense on T2-weighted images. Enhancement can be variable.

The imaging findings are nonspecific, but the age and location can suggest the diagnosis. Differential considerations include:

Subcutaneous nodules of rheumatoid arthritis: Imaging findings can be identical, and pathological findings can be very similar.
Foreign-body reactions:
Post-traumatic lesions: Fat necrosis, hematoma,
Infectious lesions: Abscess, inflammatory granuloma

References

Chung S, Frush DP, Prose NS, Shea CR, Laor T, Bisset GS. Subcutaneous granuloma annulare: MR imaging features in six children and literature review. Radiology. 1999 Mar;210(3):845-9.
Jang EJ, Lee JY, Kim MK, Yoon TY. Erythematous granuloma annulare. Ann Dermatol. 2011 Aug;23(3):409-11.
Vandevenne JE, Colpaert CG, De Schepper AM. Subcutaneous granuloma annulare: MR imaging and literature review. Eur Radiol. 1998;8(8):1363-5.
Wollina U. Granuloma annulare disseminatum responding to fumaric acid esters. Dermatol Online J. 2008 Dec 15;14(12):12.

Alkaptonuria, Ochronosis, and Ochronotic Arthropathy

2011-12-05T07:36:00.009-06:00

Alkaptonuria (also known as alcaptonuria) is an autosomal recessive condition caused by homogentisate 1,2-dioxygenase deficiency in the liver. The consequence of this deficiency is homogentisic aciduria (alkaptonuria), which is followed by ochronosis and ochronotic arthropathy.

Ochronosis

Ochronosis is caused by deposition of homogentisic acid as a polymer in collagenous tissues, resulting in a dark blue discoloration of sclera, cornea, cartilage, and heart valves. Ochronosis is seen on physical exam and on biopsy by noting the dark blue discoloration.

Not all cases of ochronosis are genetic. Exogenous ochronosis, which is clinically and histologically similar, is differentiated by its lack of systemic effects. It is most commonly caused by hydroquinone-containing products such as skin lightening creams, which paradoxically cause skin hyperpigmentation in these patients. Exogenous ochronosis can also occur following the use of antimalarial medications and products with resorcinol, phenol, mercury or picric acid.

Ochronotic Arthropathy

Longstanding ochronosis can lead to joint destruction. The mechanism is thought to be a positive feedback loop initiated by pigment deposition, which makes adjacent tissue susceptible to pigmentation and leads to progressive tissue destruction.

Ochronotic arthropathy can be seen on imaging as joint destruction and mineral deposition. Characteristic imaging findings of ochronotic arthropathy include involvement of the thoracic and lumbar spines with relative sparing of the cervical spine. In the thoracolumbar spine, one may see osteopenia, loss of lumbar lordosis, multilevel calcification of the annulus fibrosus, vacuum phenomenon, and progressive narrowing of intervertebral spaces. Patients with longstanding ochronosis can have severe kyphosis, obliteration of the intervertebral spaces, and marginal osteophytes that can look like syndesmophytes.

Findings in the appendicular skeleton are nonspecific and resemble osteoarthritis, except that there is less pronouced ostephyte formation than would be expected for the degree of joint space narrowing. Chondrocalcinosis can be seen. In the knee, which is typically involved, the lateral compartment is more severely affected.

Differential considerations for disk calcifications of ochronotic arthropathy include:

Calcium pyrophosphate dihydrate deposition disease
Degenerative or post-traumatic osteoarthritis
Ankylosing spondylitis
Hemochromatosis
Hyperparathyroidism
Acromegaly
Amyloidosis

Differential considerations for chondrocalcinosis include:

Calcium pyrophosphate dihydrate crystal deposition disease (CPPD)
Degenerative or post-traumatic osteoarthritis
Hemochromatosis
Hyperparathyroidism
Idiopathic

References

Aquaron RR. Alkaptonuria in France: past experience and lessons for the future. J Inherit Metab Dis. 2011 Dec;34(6):1115-26.
Baeva M, Bueno A, Dhimes P. AIRP best cases in radiologic-pathologic correlation: ochronosis. Radiographics. 2011 Jul-Aug;31(4):1163-7.
Bongiorno MR, Aricò M. Exogenous ochronosis and striae atrophicae following the use of bleaching creams. Int J Dermatol. 2005 Feb;44(2):112-5.
Taylor AM, Boyde A, Wilson PJ, Jarvis JC, Davidson JS, Hunt JA, Ranganath LR, Gallagher JA. The role of calcified cartilage and subchondral bone in the initiation and progression of ochronotic arthropathy in alkaptonuria. Arthritis Rheum. 2011 Dec;63(12):3887-96.

Sphenooccipital Synchondrosis

2011-12-04T07:50:00.000-06:00

The sphenooccipital synchondrosis is the cartilagenous space between the basal portion of the sphenoid and occipital bones. Radiographs of the open synchondrosis reveal a lucent band 1 to 3 mm in width across the clivus at the level of the petrous apex. It usually closes by the age of 25. Ossification starts above and proceeds down, and is usually evident on radiographs as superior narrowing around the age of 13.

References

Irwin GL. Roentgen determination of the time of closure of the spheno-occipital synchondrosis. Radiology. 1960 Sep;75:450-3.

Diaphyseal Dysplasias

2011-12-03T05:39:00.007-06:00

We'll be dealing with two possibly related disorders: Progressive diaphyseal dysplasia (Camurati-Engelmann disease, Engelmann disease) and hereditary multiple diaphyseal sclerosis (Ribbing disease, shown above). The arguments for and against the relatedness of these disorders are not convincing one way or the other and will not be discussed.

Both are disorders of intramembranous ossification, primarily affecting the diaphysis and sparing the metaphysis and epiphysis, which are formed by endochondral ossification. Both conditions manifest radiographically as periosteal and endosteal hyperostosis of the long bones. Bone scintigraphy can be positive in both. The clinical and imaging presentations diverge after this:

	Camurati-Engelmann	Ribbing
Patient age	Children	Young adults to middle aged
Disease course	Progression or regression	Slow progression followed by stabilization
Symptoms	Waddling gait, bone pain, myopathy, and weakness	Bone pain in the affected extremities
Patient appearance	Elongated long bones (Marfanoid)	Non-Marfanoid
Distribution	Bilateral and symmetric	Unilateral or asymmetrically and asynchronously bilateral (usually lower extremities)
Skull base involvement	Sometimes	No

Other conditions can mimic these diaphyseal dysplasias. Medullary osteosclerosis, like Camurati-Engelmann and Ribbing diseases can present radiographically as increased bone formation within the medullary cavity of the long bones of the lower extremities. Like Ribbing disease, the onset is usually in adulthood. Unlike the two diaphyseal dysplasias that are the subject of this post, The sclerosis in medullary osteosclerosis is limited to the medullary space, minimal or no cortical thickening.

Melorheostosis can also present with both peri- and endosteal hyperostosis, but the endosteal hyperostosis, if present, is usually seen in later stages of the disease and is less advanced than the characteristic periosteal hyperostosis.

Finally, Erdheim-Chester disease may have cortical thickening, narrowing of the medullary cavity, sparing of the epiphyses, and a symmetric lower extremity dominant distribution. In addition to the above, radiographs of patients with Erdheim-Chester disease can show bone infarctions and periostitis.

The images above from a 50-year-old man show asymmetric right lower extremity endosteal and mild periosteal hyperostosis. The skull is normal. The age, skeletal distribution, and skull findings suggest Ribbing disease. Mild periosteal sclerosis is seen, helping differentiate this case from medullary osteosclerosis.

The Ribbing in Ribbing disease is not a gerund, but is the last name of the Swedish radiologist (Seved Ribbing) who described the condition in 1949.

References

Ihde LL, Forrester DM, Gottsegen CJ, Masih S, Patel DB, Vachon LA, White EA, Matcuk GR Jr. Sclerosing bone dysplasias: review and differentiation from other causes of osteosclerosis. Radiographics. 2011 Nov;31(7):1865-82.
Ribbing S. Hereditary, multiple, diaphyseal sclerosis. Acta radiol. 1949 Jun 30;31(5-6):522-36.
Seeger LL, Hewel KC, Yao L, Gold RH, Mirra JM, Chandnani VP, Eckardt JJ. Ribbing disease (multiple diaphyseal sclerosis): imaging and differential diagnosis. AJR Am J Roentgenol. 1996 Sep;167(3):689-94.
Shier CK, Krasicky GA, Ellis BI, Kottamasu SR. Ribbing's disease: radiographic-scintigraphic correlation and comparative analysis with Engelmann's disease. J Nucl Med. 1987 Feb;28(2):244-8.
Ziran N, Hill S, Wright ME, Kovacs J, Robey PG, Wientroub S, Collins MT. Ribbing disease: radiographic and biochemical characterization, lack of response to pamidronate. Skeletal Radiol. 2002 Dec;31(12):714-9.

Birt-Hogg-Dubé Syndrome

2011-12-02T04:56:00.005-06:00

Birt-Hogg-Dubé syndrome is a rare autosomal-dominant multiorgan disorder that affects the skin, kidneys, and lungs.

Skin lesions include the characteristic triad of fibrofolliculomas (hamartomas of the hair follicles, 2- to 4-mm, smooth, dome-shaped papules), trichodiscomas (tumors of the hair disk), and acrochordons (skin tags).

Renal involvement includes a predisposition to hybrid chromophobe oncocytomas, chromophobe carcinomas, clear cell carcinomas, oncocytomas, and papillary renal cell carcinomas.

Pulmonary involvement manifests as cystic lung disease and spontaneous pneumothorax. The cysts are variable in shape and size, but are discrete and thin-walled. Larger cysts are usually multiseptated. The cysts tend to be larger and more numerous in the lower lobes, a distribution that can help differentiate Birt-Hogg-Dubé syndrome from other causes of multiple cystic lung lesions such as Langerhans cell histiocytosis and lymphangioleiomyomatosis (see below).

Patients present with the characteristic skin lesions in the 3rd–4th decades of life. Spontaneous pneumothorax occurs in about 1/4 of patients, and renal cancer develops in 15%–30% of patients with skin lesions.

The images above reveal a solid left renal lesion that turned out to be an oncocytoma, as well as cystic lung disease. Note that the typical cysts described are usually larger and more irregular in shape (see the article by Agarwal et al for the full spectrum).

Differential Diagnosis

The main differential consideration in a patient with a solid renal tumor and cystic lung disease is tuberous sclerosis. Sclerotic bone lesions, renal angiomyolipoma, and brain lesions support the latter diagnosis. The pattern and appearance of the cystic lung disease (see below) is also helpful.

The presence of pulmonary cysts without a solid renal tumor widens the differential diagnosis to include other causes of cystic lung disease:

Langerhans cell histiocytosis: Upper lung–predominant distribution of irregularly shaped cysts and nodules.
Lymphangioleiomyomatosis: Cysts are typically round, more uniform in size, and diffuse in distribution. Cysts are not as large as those in Birt-Hogg-Dubé syndrome.
Lymphocytic interstitial pneumonia: Characterized by ground-glass opacities, often in combination with cystic lesions. Typically seen in in patients with Sjögren syndrome, human immunodeficiency virus infection, and variable immunodeficiency syndromes.
Pneumocystis jiroveci pneumonia: Typically seen in immunocompromised patients. Look for associated ground-glass opacities.

References

Agarwal PP, Gross BH, Holloway BJ, Seely J, Stark P, Kazerooni EA. Thoracic CT findings in Birt-Hogg-Dube syndrome. AJR Am J Roentgenol. 2011 Feb;196(2):349-52.
Choyke PL, Glenn GM, Walther MM, Zbar B, Linehan WM. Hereditary renal cancers. Radiology. 2003 Jan;226(1):33-46.
Mueller-Mang C, Grosse C, Schmid K, Stiebellehner L, Bankier AA. What every radiologist should know about idiopathic interstitial pneumonias. Radiographics. 2007 May-Jun;27(3):595-615.

Melorheostosis

2011-12-01T04:56:00.005-06:00

Melorheostosis, a combination of the Greek words melos (limb), rhein (to flow), and ostos (bone), is a rare form of mixed sclerosing dysplasia affecting the skeleton and adjacent soft tissues. In fact, soft-tissue abnormalities such as osseous, chondroid, vascular, and fibrocartilaginous masses can be seen in about 75% of cases

Melorheostosis, also known as candle disease of the bone, Leri disease, and osteosis eburnisans monomelica, has an incidence of fewer than 1 case per one million. It begins in early childhood and is evident by 20 years of age in about half of the cases. It follows a chronic course punctuated with periods of exacerbations and arrest, slowing down as the patient gets older.

The cause is unknown, but various theories have been proposed. The observation that the lesions appear in a monomelic sclerotomal distribution (areas of bone innervated by an individual spinal sensory nerve) has linked melorheostosis to an early somatic mutation, infection, or injury to a segment or segments of the neural crest during embryogenesis. Co-occurrence of melorheostosis. osteopoikilosis, and and osteopathia striata (overlap syndrome) has led some to suggest a genetic cause; however, definitive evidence is lacking.

Histologically, melorheostosis is characterized by thickened trabeculae containing irregularly arranged Haversian canals surrounded by cellular fibrous tissue. While a benign condition, skin and soft tissue involvement can cause fibrosis and joint contractures, leading to deformity and limb-length discrepancies. Heterotopic bone formation and soft-tissue calcification can be seen in association with joint ankylosis.

Commonly one or several adjacent bones are affected in a sclerotomal distribution. The long tubular bones of the lower extremity are more frequently affected, with a predilection for the diaphyseal and the epiphyseal regions. However, any bone or any region of bone can be affected, including (rarely), the spine, skull and facial bones.

Para-articular soft-tissue masses seen in melorheostosis are not necessarily contiguous with the bony abnormalities. The masses can be mineralized or non-mineralized and are more commonly found medial to the hip joint and in the popliteal fossa. The case above has an irregular mineralized soft tissue mass lateral to the left greater trochanter.

Characteristic imaging findings include flowing periosteal hyperostosis along the cortex of a long bone that has a linear, segmental distribution. As mentioned above, one or more bones can be involved. Endosteal hyperostosis may be seen in later stages of the disease, obliterating the medullary cavity.

Less characteristic imaging findings include hyperostosis on the outer or inner aspect of the affected bone resembling an osteoma, an osteopathia striata-like pattern with long dense hyperostotic intramedullary striations near the inner cortex (second case, shown below), and nodular soft tissue calcifications that may resemble myositis ossificans.

As seen in the case below, bone scintigraphy can be positive, reflecting the increased bone turnover that is characteristic of melorheostosis. Mineralized soft tissue masses can also have increased uptake, but nonmineralized or minimally mineralized soft tissue masses can be occult on bone scintigraphy.

References

Judkiewicz AM, Murphey MD, Resnik CS, Newberg AH, Temple HT, Smith WS. Advanced imaging of melorheostosis with emphasis on MRI. Skeletal Radiol. 2001 Aug;30(8):447-53.
Janousek J, Preston DF, Martin NL, Robinson RG. Bone scan in melorheostosis. J Nucl Med. 1976 Dec;17(12):1106-8.
Suresh S, Muthukumar T, Saifuddin A. Classical and unusual imaging appearances of melorheostosis. Clin Radiol. 2010 Aug;65(8):593-600.

The Yune Soft Tissue Index

2011-11-30T05:28:00.007-06:00

The Yune soft tissue index is used to assess the amount of soft tissue at the tips of the distal phalanges. This can help in early detection of acral soft-tissue atrophy (for example, in patients with scleroderma).

You take the amount of soft tissue at the tip of the finger (A) and compare it to the width of the base of the distal phalanx (B). If A is larger than B/4, then the amount of soft tissue is normal. If A is less than B/5, then the amount of soft tissue is abnormal.

The case above in a patient with scleroderma seemed borderline by eye. Let's see if the Yune soft tissue can help.
A = 2.9 mm
B = 13.4 mm

2.9 [?] (13.4/4)
2.9 < 3.35
∴ Not normal

2.9 [?] (13.4/5)
2.9 > 2.68
∴ Not abnormal

∴ Borderline.

References

Freyschmidt J, Brossmann J, Wiens J, Sternberg A. The Hand - Distal Phalanges. In Freyschmidt's Köhler and Zimmer: Borderlands of normal and early pathologic findings in skeletal radiography. Fifth revised edition. Thieme (2003). P 81.

Histiocytic Disorders

2011-11-29T07:20:00.015-06:00

A new classification scheme for histiocytic disorders has been promulgated by the World Health Organization's Committee on Histiocytic/Reticulum Cell Proliferations and the Reclassification Working Group of the Histiocyte Society.

The new classification scheme is based on the biological behavior of the disease and the lineage of the predominant cell type.

A very cursory review of immunology is helpful before proceeding to the classification. A histiocyte is a cell of the mononuclear phagocyte system (formerly the reticuloendothelial system). The histiocytes we'll be concerned with are monocytes, macrophages, and dendritic cells. Precursor cells in the marrow give rise to circulating monocytes, which differentiate into the tissue-resident phagocytes, macrophages and dendritic cells under the proper cytokine milieu. Langerhans cells are a class of dendritic cells that typically reside in the epidermis.

Under the new classification scheme, histiocytic disorders are classified based on biologic behavior into those with malignant behavior and those with varied biological behavior, and based on predominant cell type into monocyte-, dendritic cell-, or macrophage-related disorders. The term varied biological behavior is meant to convey the spectrum of behavior in this class, which can range in severity from self-limited to lethal.

Langerhans cell histiocytosis, the most well known of the histiocytic disorders by radiologists, is classified as a dendritic cell-related histioctyic disorder of varied biological behavior. Terms such as eosinophilic granuloma, Hand-Schüller-Christian disease, and Letterer-Siwe disease are now (> 10 years) considered obsolete or unnecessary, and should be avoided unless you're trying to be difficult during case conference.

Erdheim-Chester disease, an extremely rare disorder that somehow pops up during radiology residency and on boards, is classified as part of Juvenile xanthogranuloma and related disorders.

The outline below summarizes the current classification scheme:

Disorders of Varied Biological Behavior

Dendritic cell-related
- Langerhans cell histiocytosis
- Secondary dendritic cell processes
- Juvenile xanthogranuloma and related disorders
  - Erdheim-Chester disease
  - Solitary histiocytomas with juvenile xanthogranuloma phenotype
- Solitary histiocytomas of various dendritic cell phenotypes
Macrophage-related
- Hemophagocytic syndromes
- Primary hemophagocytic lymphohistiocytosis (familial , sporadic)
- Secondary hemophagocytic syndromes (infection-associated, malignancy-associated, other)
- Rosai-Dorfman disease (sinus histiocytosis with massive adenopathy)
- Solitary histiocytoma with macrophage phenotype

Malignant Disorders

Monocyte-related
- Leukemias (Monocytic leukemia M5A and B, acute myelomonocytic leukemia M4, chronic myelomonocytic leukemia)
- Extramedullary monocytic tumor or sarcoma
Dendritic cell-related histiocytic sarcoma (localized or disseminated) based on phenotype
- Langerhans cells
- Follicular dendritic cell
- Interdigitating dendritic cell
- Others
Macrophage-related histiocytic sarcoma (localized or disseminated)

References

Chow A, Brown BD, Merad M. Studying the mononuclear phagocyte system in the molecular age. Nat Rev Immunol. 2011 Oct 25;11(11):788-98.
Favara BE, Feller AC, Pauli M, Jaffe ES, Weiss LM, Arico M, Bucsky P, Egeler RM, Elinder G, Gadner H, Gresik M, Henter JI, Imashuku S, Janka-Schaub G, Jaffe R, Ladisch S, Nezelof C, Pritchard J. Contemporary classification of histiocytic disorders. The WHO Committee On Histiocytic/Reticulum Cell Proliferations. Reclassification Working Group of the Histiocyte Society. Med Pediatr Oncol. 1997 Sep;29(3):157-66.
Lieberman PH, Jones CR, Steinman RM, Erlandson RA, Smith J, Gee T, Huvos A, Garin-Chesa P, Filippa DA, Urmacher C, Gangi MD, Sperber M. Langerhans cell (eosinophilic) granulomatosis. A clinicopathologic study encompassing 50 years. Am J Surg Pathol. 1996 May;20(5):519-52.

Bifid Ribs

2011-11-28T07:55:00.003-06:00

A bifid rib, also known as a forked or bifurcated rib, is a relatively common anatomic variant where the sternal end of a rib divides into upper and lower divisions. It is thought that the lower division represents the intended development of the rib, and the upper division represents the anomalous development.

Bifid ribs are more common in males, slightly more common on the right, and occur most frequently in the third and foruth ribs, followed by the fifth, sixth, and second ribs. Both divisions have their own costal cartilage, which may fuse before joining with the sternum.

The space between the upper division and the rib above (white *) is usually narrowed, while the lower intercostal space (red *) is wider than normal.

Familiarity with the underlying muscular, vascular, and neural anatomy may be important for planning surgical and percutaneous procedures.

The intercostal muscles traverse the space between the upper and lower divisions.
Intercostal nerves run their normal course along the inferior margin of the parent rib and then usually along the inferior margin of the lower division. At least one case of a pair of intercostal nerves traveling along both the upper and lower margins of the parent rib has been reported.
I assume that the intercostal arteries take the same course as the nerves, but can't find any supporting evidence.

Bifid ribs are usually isolated, unilateral, and asymptomatic. They may, however, present as a palpable abnormality on physical examination or an asymmetric opacity on chest radiography.

Bifid ribs can also be seen in association with other conditions, most famously with basal cell nevus syndrome, where they may be multiple and bilateral.

References

Osawa T, Sasaki T, Matsumoto Y, Tsukamoto A, Onodera M, Nara E, Chen JK, Fujimura A, Nozaka Y. Bifid ribs observed in the third and the fourth ribs. Kaibogaku Zasshi. 1998 Dec;73(6):633-5.
Song WC, Kim SH, Park DK, Koh KS. Bifid rib: anatomical considerations in three cases. Yonsei Med J. 2009 Apr 30;50(2):300-3.

Imaging Features of Fanconi Anemia

2011-11-27T10:36:00.006-06:00

Fanconi anemia is a genetically and phenotypically heterogeneous recessive disorder of progressive pancytopenia, various congenital malformations, and predisposition to hematologic and solid malignancies.

Many of the congenital anomalies can be detected on imaging studies. These include:

Growth disturbances: Intrauterine growth retardation, short stature, delayed ossification.
Central nervous system: Hydrocephalus, single ventricle, absent septum pellucidum/corpus callosum, vascular malformations, moyamoya, Chiari malformations/absent septum pellucidum/corpus callosum.
Skull: Microcephaly, craniosynostosis, micrognathia, frontal bossing, small or absent external auditory canal, absent tympanic membrane, microtia, fused ossicles.
Spine: Spina bifida, Klippel-Feil anomaly, vertebral body anomalies, sacral agenesis or hypoplasia, kyphosis, scoliosis.
Radial ray anomalies: Thenar hypoplasia; dislocation of the radial head; radioulnar synostosis; absence or hypoplasia of the radius, scaphoid, trapezium, and/or thumb; floating thumb; bifid thumb; digitalized thumb; and abnormal thumb placement.
Extremities (other): Brachydactyly, arachnodactyly clubfoot, dysplastic or absent ulna, humeral abnormalities, absent clavicles, Sprengel deformity, congenital hip dysplasia/dislocation, Legg-Calve-Perthes disease, leg length discrepancy, soft-tissue syndactylism of the toes, metatarsus varus, medial deviation of the toes, hammer toes.
Gastrointestinal: Esophageal atresia, tracheoesophageal fistula, duodenal atresia, duodenal web, malrotation, foregut duplication cyst, anal atresia. Biliary atresia, annular pancreas.
Renal anomalies: Renal aplasia, horseshoe kidney, low-lying kidney(s), renal ectopy, hydronephrosis, hydroureter, urethral stenosis, reflux.
Genital anomalies: Hypogenitalism, cryptorchidism, hypospadias, bicornate uterus, aplasia or hypoplasia of vagina and uterus, atresia of vagina, hypoplasic uterus, hypoplastic/absent ovary.
Cardiopulmonary: Patent ductus arteriosis, ventricular septal defect, pulmonic or aortic stenosis, coarcation of the aorta, double aortic arch, cardiomyopathy, tetralogy of Fallot, pulmonary atresia.
Osteoporosis:

References

Auerbach AD. Fanconi anemia and its diagnosis. Mutat Res. 2009 Jul 31;668(1-2):4-10.
Juhl JH, Wesenberg RL, Gwinn JL. Roentgenographic findings in Fanconi's anemia. Radiology. 1967 Oct;89(4):646-53.
De Kerviler E, Guermazi A, Zagdanski AM, Gluckman E, Frija J. The clinical and radiological features of Fanconi's anaemia. Clin Radiol. 2000 May;55(5):340-5.

The Dot-in-Circle Sign

2011-11-26T22:20:00.003-06:00

The dot-in-circle sign refers to the appearance of mycetoma on T2-weighted and post-contrast images. It consists of a tiny hypointense focus within a high-intensity spherical lesion. Numerous lesions are typically seen, separated by a low-signal intensity matrix. It is thought that the small central hypointense focus represents the fungal ball or granule and the surrounding hyperintense area represents the inflammatory granuloma. The intervening tissue of low signal intensity represents the fibrous matrix.

The mycetomas can be found in the soft tissues or bone and can represent infection by fungi (eumycetoma) or aerobic actinomycetes (actinomycetomas). Recall from medical school that actinomycetes have microscopic characteristics similar to those of fungi, and were formerly classified as fungi.

Patients present with a history of a firm, painless nodule that follows an indolent but progressive course. The initial infection may communicate with the skin with discharge of fungal granules. Alternatively, the infection may fester internally and even lead to osteomyelitis and significant destruction and deformity. Definitive diagnosis may be provided by biopsy, or be elusive in cases of fastidious organisms.

The case above is a STIR image of the foot, revealing multiple round hyperintense lesions with central hypointense foci along the dorsum of the foot. The patient had a 10-year history a slowly growing foot mass following trauma and presented to us after biopsy (unknown) and unspecified treatment and at an outside facility. Biopsy at our facility revealed no evidence of fungal infection but was positive for bacteria. This complicated picture was suspected to be due to actinomycetoma.

Geography trivia: Mycetomas are more commonly found in the dry topics. The entity of Madura foot (mycetoma of the foot) was first described in the Madura district of Southern India in 1846. The infection usually starts with penetrating injury to the foot (e.g., thorn prick) with inoculation of organisms that are normal inhabitants of the soil.

References

Cherian RS, Betty M, Manipadam MT, Cherian VM, Poonnoose PM, Oommen AT, Cherian RA. The "dot-in-circle" sign -- a characteristic MRI finding in mycetoma foot: a report of three cases. Br J Radiol. 2009 Aug;82(980):662-5.
Kumar J, Kumar A, Sethy P, Gupta S. The dot-in-circle sign of mycetoma on MRI. Diagn Interv Radiol. 2007 Dec;13(4):193-5.
Sarris I, Berendt AR, Athanasous N, Ostlere SJ; OSIRIS collaborative study group. MRI of mycetoma of the foot: two cases demonstrating the dot-in-circle sign. Skeletal Radiol. 2003 Mar;32(3):179-83.

Ischiofemoral Impingement

2011-11-25T10:25:00.004-06:00

Normally the femur can rotate without contacting the ischium or proximal hamstring tendons. Abnormal contact between the ischium and femur is referred to as ischiofemoral impingement and can cause hip pain. The abnormal contact can be due to congenital narrowing of the space between the ischial tuberosity and lesser trochanter or be the result of abnormal positioning following hip arthroplasty.

Radiographs may reveal sclerosis and cystic change at the lesser trochanter and ischium. On MRI, one can see crowding of the fibers of the quadratus femoris muscle belly as it passes between the ischium or hamstring tendons and the posteromedial femur. Edema can also be seen, centered in the muscle belly at the site of maximal impingement.

The main differential consideration is quadratus femoris strain, which presents with edema along the distal myotendinous junction near the posteromedial aspect of the proximal femur.

Two spaces have been defined for the purposes of assessing the free rotation of the femur without contacting the ischium or proximal hamstring tendons. The ischiofemoral space is "the smallest distance between the lateral cortex of the ischial tuberosity and medial cortex of the lesser trochanter." The quadratus femoris space is "the smallest space between the superolateral surface of the hamstring tendons and the posteromedial surface of the iliopsoas tendon or lesser trochanter" (this delimits the space for passage of the quadratus femoris muscle). Unfortunately, these measurements depend on the degree of hip rotation during imaging, and the validity of exact numbers remains unclear.

References

Kassarjian A, Tomas X, Cerezal L, Canga A, Llopis E. MRI of the quadratus femoris muscle: anatomic considerations and pathologic lesions. AJR Am J Roentgenol. 2011 Jul;197(1):170-4.
Patti JW, Ouellette H, Bredella MA, Torriani M. Impingement of lesser trochanter on ischium as a potential cause for hip pain. Skeletal Radiol. 2008 Oct;37(10):939-41.
Torriani M, Souto SC, Thomas BJ, Ouellette H, Bredella MA. Ischiofemoral impingement syndrome: an entity with hip pain and abnormalities of the quadratus femoris muscle. AJR Am J Roentgenol. 2009 Jul;193(1):186-90.

Parietal Thinning

2011-11-24T07:04:00.001-06:00

Biparietal thinning (previously known as involutionskrankheit, malum senile biparietale, senile atrophy, biparietal thinness, and biparietal osteodystrophy) is thought to represent a manifestation of osteoporosis in the skull. Histologically it represents loss of the external table and compensatory remodeling of the diploe. It occurs in about 0.5% of the population, more commonly in women and in older people.

Radiographically, it manifests as a sharp lucency in the parietal region on lateral skull radiographs and flattening or grooving in the parietal regions on frontal views.

References

Bruyn GW. Biparietal osteodystrophy. Clin Neurol Neurosurg. 1978;80(3):125-48.
Cederlund CG, Andrén L, Olivecrona H. Progressive bilateral thinning of the parietal bones. Skeletal Radiol. 1982;8(1):29-33.
Epstein BS. The concurrence of parietal thinness with postmenopausal, senile, or idiopathic osteoporosis. Radiology. 1953 Jan;60(1):29-35. No abstract available.
Phillips RC. Cranial anomaly, pathology, or normal variant? Thin parietal bones in ancient Egyptian human remains. (January 1, 2007). Dissertations available from ProQuest. Paper AAI3292064.

Ankylosis

2011-11-23T07:10:00.000-06:00

Ankylosis is rigidity across a joint and can be classified as extra-articular and intra-articular based on the level of fusion. Ankylosis can occur following trauma and electrical and thermal injury.

Extra-articular ankylosis is due to bridging heterotopic ossification. The underlying joint is preserved. The elbow, shoulder and hip are most commonly affected. Interestingly, these joints can be affected regardless of the site of injury.

The earliest radiographic manifestation of extra-articular ankylosis is periarticular calcification that may progress to heterotopic ossification. Extra-articular ankylosis usually responds to physical therapy and surgical excision.

Intra-articular ankylosis (shown above) occurs within the joint and most commonly occurs at the interphalangeal joints. Intra-articular ankylosis results in serious functional and cosmetic problems and is not as easily treated as the extra-articular type. Treatment options include arthrodesis, osteotomy, arthroplasty, or amputation.

References

Balen PF, Helms CA. Bony ankylosis following thermal and electrical injury. Skeletal Radiol. 2001 Jul;30(7):393-7.
Tomak Y, Piskin A, Gulman B, Tomak L. Treatment of U-shaped bone ankylosis of the knee with the Ilizarov method. A case report. J Bone Joint Surg Am. 2005 May;87(5):1104-7.

Ulnar Attachment of the Annular Ligament

2011-11-22T04:13:00.002-06:00

A small fossa can be seen in the proximal ulna at the attachment of the annular ligament. The size of this fossa ranges from a small notch, as seen above, to a wider saucer. It should not be mistaken for a pathological process.

References

Keats TE and Anderson MW. Atlas of Normal Roentgen Variants That May Simulate Disease. 8th edition, page 556; Mosby (2004).

Superior Sublabral Recess

2011-11-21T04:01:00.003-06:00

The superior sublabral recess is a synovial recess between the superior labrum and the glenoid rim created by the attachment of the biceps tendon on the supraglenoid tubercie. Because of this recess, the labrum does not attach to the glenoid rim at the 12 o'clock position.

The size of this recess is variable, and has been classified into various types by different authors. One scheme divides the sublabral recess into 3 types. In a type 1 attachment, the labral-bicipital complex is firmly attached to the glenoid rim and an arthroscopic probe cannot be inserted between the labrum and the glenoid. A type 2 attachment has a small sulcus between the labrum and the glenoid rim, while a type III attachment has a deep sulcus between the labrum and the glenoid rim that allows a probe to be inserted between the two.

The superior sublabral recess can be continuous with the sublabral foramen.

References

Cooper DE, Arnoczky SP, O'Brien SJ, Warren RF, DiCarlo E, Allen AA. Anatomy, histology, and vascularity of the glenoid labrum. An anatomical study. J Bone Joint Surg Am. 1992 Jan;74(1):46-52.
De Maeseneer M, Van Roy F, Lenchik L, Shahabpour M, Jacobson J, Ryu KN, Handelberg F, Osteaux M. CT and MR arthrography of the normal and pathologic anterosuperior labrum and labral-bicipital complex. Radiographics. 2000 Oct;20 Spec No:S67-81.
Kreitner KF, Botchen K, Rude J, Bittinger F, Krummenauer F, Thelen M. Superior labrum and labral-bicipital complex: MR imaging with pathologic-anatomic and histologic correlation. AJR Am J Roentgenol. 1998 Mar;170(3):599-605.
Kwak SM, Brown RR, Resnick D, Trudell D, Applegate GR, Haghighi P. Anatomy, anatomic variations, and pathology of the 11- to 3-o'clock position of the glenoid labrum: findings on MR arthrography and anatomic sections. AJR Am J Roentgenol. 1998 Jul;171(1):235-8.
Smith DK, Chopp TM, Aufdemorte TB, Witkowski EG, Jones RC. Sublabral recess of the superior glenoid labrum: study of cadavers with conventional nonenhanced MR imaging, MR arthrography, anatomic dissection, and limited histologic examination. Radiology. 1996 Oct;201(1):251-6.

POEMS Syndrome

2011-11-20T04:23:00.005-06:00

POEMS syndrome is a paraneoplastic syndrome related to a plasma cell dyscrasia that is also known as Crow-Fukase syndrome, Takatsuki syndrome. The acronyms POEMS (Polyneuropathy, Organomegaly, Endocrinopathy, M protein and Skin changes) and PEP (Plasma cell dyscrasia, Endocrinopathy and Polyneuropathy), capture some—but not all—of the associated manifestations. Other manifestations include sclerotic bone lesions, Castleman disease, papilledema, thrombocytosis, erythrocytosis, pleural effusions, edema, and ascites.

Given this potential variability in presentation, Dispenzieri et al. proposed major and minor criteria for the diagnosis of POEMS syndrome. The major criteria are polyneuropathy and monoclonal plasmaproliferative disorder.

Minor criteria include sclerotic bone lesions, Castleman disease, Organomegaly (splenomegaly, hepatomegaly, or lymphadenopathy), Edema (edema, pleural effusion, or ascites), endocrinopathy (adrenal, thyroid, pituitary, gonadal, parathyroid, pancreatic), skin changes (hyperpigmentation, hypertrichosis, plethora, hemangiomata, white nails), papilledema.

They proposed that two major criteria and at least one minor criterion differentiate POEMS syndrome from neuropathy associated with monoclonal gammopathy of undetermined significance, myeloma, and Waldenström disease.

The vast majority of POEMS syndrome patients have radiographic evidence of bone lesions at presentation. Slightly less than half of these lesions are purely sclerotic (well-defined or fluffy), approximately half are mixed sclerotic and lytic, and a small number (2%) are purely lytic bone lesions, which tend to have scelrotic margins giving them a unique ring-like appearance. More than half of patients with bone lesions had more than one lesion.

Resnick has described a pattern of bony proliferation that is pathognomonic for POEMS syndrome: irregular and spiculated bone contours at areas of tendinous and ligamentous attachment, posterior elements of the spine (facet joints, laminae, transverse processes, and costovertebral articulations).

Differential considerations for the sclerotic bone lesions include:

Tuberous sclerosis:
Mastocytosis:
Sclerotic metastases:
Cystic angiomatosis:

Differential considerations for the proliferative spine lesions include:

Diffuse idiopathic skeletal hyperostosis (DISH): Also has flowing anterior ossifications.
Seronegative spondyloarthropathy: Look for syndesmophytes, sacroiliac joint ankylosis.
Fluorosis: Also has increased bone density.
Hypoparathyroidism:
X-linked hypophosphatemia:

The images above are from a patient with POEMS syndrome. We see sclerotic lesions in the humerus, pelvis, and proximal femur, some of which have the typical ring-like appearance (e.g., the left intertrochanteric region). Looking through our 20 or so cases of POEMS here, I wasn't able to find any with the pathognomonic proliferative changes described by Resnick, so a look at the original paper is worthwhile to get familiar with this appearance.

Special thanks to Dr. James Dimaala for the case.

References

Chong ST, Beasley HS, Daffner RH. POEMS syndrome: radiographic appearance with MRI correlation. Skeletal Radiol. 2006 Sep;35(9):690-5.
Dispenzieri A, Kyle RA, Lacy MQ, Rajkumar SV, Therneau TM, Larson DR, Greipp PR, Witzig TE, Basu R, Suarez GA, Fonseca R, Lust JA, Gertz MA. POEMS syndrome: definitions and long-term outcome. Blood. 2003 Apr 1;101(7):2496-506.
Owens CL, Weir EG, Ali SZ. Cytopathologic findings in "POEMS" syndrome associated with Castleman disease. Diagn Cytopathol. 2007 Aug;35(8):512-5.
Resnick D, Greenway GD, Bardwick PA, Zvaifler NJ, Gill GN, Newman DR. Plasma-cell dyscrasia with polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes: the POEMS syndrome. Distinctive radiographic abnormalities. Radiology. 1981 Jul;140(1):17-22.

Myxoinflammatory Fibroblastic Sarcoma

2011-11-19T06:29:00.000-06:00

Myxoinflammatory fibroblastic sarcoma is a low-grade sarcoma with myxoid stroma and a mixed acute and chronic inflammatory infiltrate. Three main types of neoplastic cells are seen: spindled cells, large polygonal and bizarre ganglion-like cells, and variably sized multivacuolated lipoblast-like cells. All three types also have features of fibroblasts. The lesion predominantly affects the extremities, usually the hands and feet.

MRI findings are variable. The lesions can be well-defined or poorly defined. The signal characteristics are also variable. They can be low signal intensity on T1-weighted images and high signal intensity on T2-weighted images, mimicking a cyst on unenhanced imaging. Post-contrast imaging reveals these to be solid lesions with avid enhancement ranging from mildly heterogeneous to homogeneous.

Differential considerations include much more common entities, such as ganglion cyst (in cases of predominantly myxoid lesions), giant cell tumor of the tendon sheath (in cases of well-defined heterogeneous lesions near tendon sheaths), and tenosynovitis (in cases of poorly defined lesions near tendon sheaths), nodular fasciitis (for lesions occurring in the subcutaneous tissues), and other soft tissue sarcomas.

The case above is from a 50-year-old woman who palpated a nodule in her right knee. The images reveal a heterogeneous, poorly defined lesion in the subcutaneous tissues abutting the vastus medialis muscle. The lesion is predominantly T1- and T2- hypointense with central areas of T2 hyperintensity and a peripheral T2-hyperintense rim. Post-contrast imaging was not performed.

References

Kindblom LG and Meis-Kindblom JM. Myxoinflammatory fibroblastic sarcoma. in Pathology and Genetics of Tumours of Soft Tissue and Bone. Fletcher CDM, Unni KK, Mertens F (eds). IARCPress Lyon, 2002. pp 96-97.
Narváez JA, Martinez S, Dodd LG, Brigman BE. Acral myxoinflammatory fibroblastic sarcomas: MRI findings in four cases. AJR Am J Roentgenol. 2007 May;188(5):1302-5.
Tateishi U, Hasegawa T, Onaya H, Satake M, Arai Y, Moriyama N. Myxoinflammatory Fibroblastic Sarcoma: MR Appearance and Pathologic Correlation. AJR Am J Roentgenol. 2005 Jun;184(6):1749-53.

Implantable Spinal Fusion Stimulator

2011-11-18T10:50:00.001-06:00

The implantable spinal fusion stimulators by Biomet consist of a direct current generator (pink arrow) in a titanium shell with a focal coating of platinum (serves as the anode) connected to insulated nonmagnetic steel leads (white arrows) that in turn connect to bare wire cathodes (blue arrows). The cathodes get embedded in pieces of bone graft by the surgeon and are thought to stimulate fusion of the allograft. The SpF-XL IIb Spinal Fusion Stimulator model is shown in the image above.

The generator is powered by a lithium iodine battery that is capable of delivering 20-μA of current for about 6 months. After that, the device is non-functional.

The device can be safely used in magnets with static field strengths of 1.5 T or less. The cathodes should ideally be placed at least 1 cm from nerve roots (to reduce the possibility of nerve excitation during MR imaging). It would also be nice if the stimulator is placed as far as possible from the spinal canal and bone graft to decrease the effect of artifact.

In addition,

Radiographs should be obtained prior to MRI to verify that the leads are intact. Broken leads can lead to excessive heating during imaging. If radiographs cannot make this determination, the risk of heating should be discussed with the patient prior to the study.
MRI should be performed in magnets with static fields of 1.5 T or less.
Spin-echo, fast spin-echo, and gradient echo pulse sequences are permissible.
Echo planar techniques, conditions that produce exposures to high levels of RF energy (exceeding a whole-body averaged specific absorption rate of 1.0 W/kg), exposure to gradient fields that exceed 20 T/sec, or unconventional MR sequences should be avoided.
Patients should be continuously observed during the study and instructed to report any unusual sensations including any feelings of warming, burning, or neuromuscular excitation or stimulation.

References

Biomet. MRI Safety Information - SpF®-XL IIb.
Schwardt JD, Jankowski GB. Preformed extendable mesh cathode for implantable bone growth stimulator. US Patent 6,112,122
Shellock FG, Hatfield M, Simon BJ, Block S, Wamboldt J, Starewicz PM, Punchard WF. Implantable spinal fusion stimulator: assessment of MR safety and artifacts. J Magn Reson Imaging. 2000 Aug;12(2):214-23.
Tejano NA, Puno R, Ignacio JM. The use of implantable direct current stimulation in multilevel spinal fusion without instrumentation. A prospective clinical and radiographic evaluation with long-term follow-up. Spine (Phila Pa 1976). 1996 Aug 15;21(16):1904-8.

The J Sign

2011-11-17T04:24:00.000-06:00

The intact inferior glenohumeral ligament normally extends from the glenoid labrum to the anatomic neck of the humerus, forming a U shape on oblique coronal images. Avulsion of the right inferior glenohumeral ligament from the neck of the humerus results in its humeral end falling inferiorly forming a J shape. This J-shaped appearance of the torn right inferior glenohumeral ligament in cases of humeral avulsion of the glenohumeral ligament (HAGL) is referred to as the J sign. On the left side, the J is reversed.

Special thanks to Dr. David Wells for the case.

References

Carlson CL. The "J" sign. Radiology. 2004 Sep;232(3):725-6.

Brachymesophalangia

2011-11-16T04:24:00.001-06:00

Brachymesophalangia is the most common hereditary anomaly of the middle phalanges. It is more common in the small finger (brachymesophalangia-5 or brachymesophalangia-V) and is seen in up to 20% of the Japanese population and about 1% of the European population. About 2/3 of patients with Down syndrome have brachymesophalangia.

As seen in the image above, the short, often trapezoidal middle phalanx can result in angular deviation of the distal phalanx (clinodactyly).

In 1951, Bell classified brachydactyly into types A-E.

Type	Description
A1	Brachymesophalangia II-IV with brachybasophalangia I
A2	Brachymesophalangia II with absent epiphyses, delta phalanx, and radial clinodactyly
A3	Brachymesophalangia V with radial clinodactyly (case shown above)
A4	Brachymesophalangia II-V with bifid distal phalanx of thumb and dystelephalangia V
B	Brachymesophalangia with brachytelephalangia II-V (or absent distal phalanges)
C	Brachymesophalangia II, III, and V with hyperphalangia of index and middle finger proximal phalanges
D	Brachytelephalangia I with broadening
E	Brachymetacarpia III-V

Brachybasophalangia: Short proximal phalanges
Brachymetacarpia: Short metacarpals
Brachytelephalangia: Short distal phalanges
Dystelephalangia: Deformed terminal phalanx (Kirner deformity)

References

Bell J. On brachydactyly and symphalangism. Treasury of human inheritance. Vol 5, part 1. London: Cambridge University Press, 1951.
Freyschmidt J, Brossmann J, Wiens J, Sternberg A. Chapter 2 - Upper Extremity. In Freyschmidt's Köhler and Zimmer: Borderlands of normal and early pathologic findings in skeletal radiography. Fifth revised edition. Thieme (2003). Pp 85-86.

Medial Meniscus Root Tears

2011-11-15T04:06:00.005-06:00

Circumferential collagen fibers in menisci absorb compressive forces, resisting longitudinal loading (hoop stress) and meniscal extrusion. The normal hoop tension for the meniscus is reduced by radial tears that extend to the capsular margin of the meniscus. Functionally speaking, the loss of hoop tension of a meniscus is equivalent to total meniscectomy and leads to early degenerative change.

Root tears are more commonly seen in the posterior horn of the medial meniscus. Complete radial tear of the medial meniscus root leads first to meniscal extrusion and subsequently to the development of osteoarthritis. The image above shows a complete radial tear of the posterior root of the medial meniscus on the coronal image (pink arrow) with a ghost meniscus on the sagittal image (white arrow held by Casper) and meniscal extrusion (blue arrow). Bone marrow T2 hyperintensity is seen in the medial femoral condyle and the medial tibial plateau, with loss of articular cartilage at the medial compartment and a small subchondral fracture at the medial tibial plateau.

References

Lerer DB, Umans HR, Hu MX, Jones MH. The role of meniscal root pathology and radial meniscal tear in medial meniscal extrusion. Skeletal Radiol. 2004 Oct;33(10):569-74.

Accessory Epiphysis (Pseudoepiphysis)

2011-11-14T04:12:00.002-06:00

A pseudoepiphysis is an accessory epiphysis that does not significantly contribute to the longitudinal growth of a tubular bone. One or more can occur in the same patient as normal variants, but they have also been associated with Down syndrome and hypothyroidism (~80% of patients with Down syndrome have pseudoepiphyses).

When found incidentally in patients without chromosomal and metabolic abnormalities, they they are most common in the distal thumb metacarpal followed by the proximal index finger metacarpal. In patients with Down syndrome, they are more common in the proximal index finger metacarpal followed by the distal thumb metacarpal (i.e., the order of the two most common sites is reversed).

References

Freyschmidt J, Brossmann J, Wiens J, Sternberg A. The Hand-General Aspects. In Freyschmidt's Köhler and Zimmer: Borderlands of normal and early pathologic findings in skeletal radiography. Fifth revised edition. Thieme (2003). Pp 23-24.
Kozin SH and Waters PM. Fractures and dislocations of the hand and carpus in children. In Rockwood and Wilkins' Fractures in Children. Seventh edition. Wolters Kluwer (2010). P 227.
Ogden JA, Ganey TM, Light TR, Belsole RJ, Greene TL. Ossification and pseudoepiphysis formation in the "nonepiphyseal" end of bones of the hands and feet. Skeletal Radiol. 1994 Jan;23(1):3-13.

Os Carpi Centrale

2011-11-13T05:12:00.007-06:00

The os carpi centrale (os centrale) is an uncommon accessory carpal bone that is located dorsally between the first and second carpal rows and articulates with the scaphoid, capitate, and trapezoid, but not with the trapezium. It can have the appearance of a segment cut out of the scaphoid that has ossified independently of it. The os carpi centrale is usually round and dense, and lacks an internal trabecular architecture. It can be bilateral and duplicated.

When the os carpi centrale is unossified, it is radiographically occult and can present as a large gap between the distal scaphoid and a groove in the capitate. On the other extreme, the os carpi centrale can fuse with the adjacent scaphoid, capitate, or trapezoid

A similar bone is found in the writs of of the Orangutan, but the os centrale in these primates articulates with the trapezium.

Because of its location, it may be confused with a scaphoid fracture. Patients are usually asymptomatic; however, some may present with painful clicking or pain from osteonecrosis.

The main differential considerations are bipartite scaphoid, scaphoid fracture, and an unfused scaphoid ossification center. Dysplasia epiphysealis hemimelica and congenital hypothyroidism can also be considered but the appearance of these conditions is usually distinct.

References

Abascal F, Cerezal L, del Piñal F, García-Valtuille R, García-Valtuille A, Canga A, Torcida J. Unilateral osteonecrosis in a patient with bilateral os centrale carpi: imaging findings. Skeletal Radiol. 2001 Nov;30(11):643-7.
Freyschmidt J, Brossmann J, Wiens J, Sternberg A. Carpus-Scaphoid. In Freyschmidt's Köhler and Zimmer: Borderlands of normal and early pathologic findings in skeletal radiography. Fifth revised edition. Thieme (2003). Pp 155-157.
Turner W. Some Variations in the Bones of the Human Carpus. J Anat Physiol. 1883 Jan;17(Pt 2):244-9.

Wrisberg Rip

2011-11-12T06:29:00.005-06:00

Wrisberg rip is a term coined by the folks at RadSource for a longitudinal tear in the posterior horn of the lateral meniscus that extends laterally from the Wrisberg ligament attachment. They feel that the tear is the result of traction from the ligament of Wrisberg in cases of anterior cruciate ligament tears.

The Wrisberg rip should be differentiated from the normal appearance of the so-called Wrisberg pseudo-tear: A vertical/oblique signal intensity region at the junction of the a meniscofemoral ligament (most commonly the ligament of Wrisberg) with the posterior horn of the lateral meniscus. When seen on only one sagittal slice, the pseudotear is thought to be caused by a volume averaging of the ligament connection with the meniscus. It can also be seen on multiple slices depending on the angle of insertion of the meniscofemoral ligament.

The case above shows a Wrisberg rip. The sagittal images A-C are from lateral to medial. The pink and white arrows indicate the posterior horn of the lateral meniscus on either side of a tear extending laterally from the attachment of the ligament of Wrisberg (blue arrow). The axial images (D, E) show the same thing from a different perspective. Panel F shows the anterior cruciate ligament tear that is seen in association with this meniscal tear pattern.

References

de Abreu MR, Chung CB, Trudell D, Resnick D. Meniscofemoral ligaments: patterns of tears and pseudotears of the menisci using cadaveric and clinical material. Skeletal Radiol. 2007 Aug;36(8):729-35.
Vahey TN, Bennett HT, Arrington LE, Shelbourne KD, Ng J. MR imaging of the knee: pseudotear of the lateral meniscus caused by the meniscofemoral ligament. AJR Am J Roentgenol. 1990 Jun;154(6):1237-9.

Low-Lying Peroneus Brevis Muscle Belly

2011-11-11T08:10:00.013-06:00

A low-lying peroneus brevis muscle belly is one that has muscle tissue extending beyond the retromalleolar groove and the distal tip of the fibula. Between ~10%-25% of patients with a peroneus longus or brevis tendon tear have a low-lying peroneus brevis muscle belly when examined by MRI, suggesting that this variant can predispose the muscle and tendon to tears. It is thought that increased muscle mass in the retromalleolar groove causes overcrowding and results in peroneal tendon injury. A similar mechanism is thought to underlie the association of the presence of a peroneus quartus muscle to peroneal tendon tears.

The main differential consideration for the appearance of a low-lying peroneus brevis muscle belly is an accessory muscle, such as the peroneus quartus.

References

Freccero DM, Berkowitz MJ. The relationship between tears of the peroneus brevis tendon and the distal extent of its muscle belly: an MRI study. Foot Ankle Int. 2006 Apr;27(4):236-9.
Geller J, Lin S, Cordas D, Vieira P. Relationship of a low-lying muscle belly to tears of the peroneus brevis tendon. Am J Orthop (Belle Mead NJ). 2003 Nov;32(11):541-4.
Khoury NJ, el-Khoury GY, Saltzman CL, Kathol MH. Peroneus longus and brevis tendon tears: MR imaging evaluation. Radiology. 1996 Sep;200(3):833-41.
Rosenberg ZS, Beltran J, Cheung YY, Colon E, Herraiz F. MR features of longitudinal tears of the peroneus brevis tendon. AJR Am J Roentgenol. 1997 Jan;168(1):141-7.

Fredericson Grading of Tibial Stress Reaction

2011-11-10T04:34:00.007-06:00

Fredericson system is a 5-level grading scheme for tibial stress reactions developed by studying symptomatic runners. In symptomatic patients, it correlates with the time for return to full impact activity.

The MRI findings have to be correlated to symptoms, as a follow-up study showed that almost half of asymptomatic college distance runners had signs of tibial stress reaction on MRI. In addition, these changes did not predict future tibial stress reactions or stress fractures.

Grade	MRI Findings	Time to full-impact activity^*
0	Normal MRI findings.
1	Increased periosteal T2 signal. Normal marrow signal intensity on all images (shown here)	2 to 3 weeks
2	Grade 1 plus bone marrow signal changes on T2-weighted images	4 to 6 weeks
3	Grade 2 plus bone marrow signal changes on T1-weighted images (shown above)	6 to 9 weeks
4	Grade 3 plus a clearly visible fracture plane
^*Full impact activity: Ablility to return to running on grass or a soft dirt track

References

Bergman AG, Fredericson M, Ho C, Matheson GO. Asymptomatic tibial stress reactions: MRI detection and clinical follow-up in distance runners. AJR Am J Roentgenol. 2004 Sep;183(3):635-8.
Fredericson M, Bergman AG, Hoffman KL, Dillingham MS. Tibial stress reaction in runners. Correlation of clinical symptoms and scintigraphy with a new magnetic resonance imaging grading system. Am J Sports Med. 1995 Jul-Aug;23(4):472-81.

Aggregoma

2011-11-09T04:27:00.004-06:00

Deposition of monoclonal light chains in B-cell dyscrasias can be systemic or localized, and fibrillar and non-fibrillar, and can be categorized under the broad definition of monoclonal immunoglobulin deposition diseases: "monoclonal expansion of a B-cell and plasma-cell population producing an excess immunoglobulin polypeptide with structural characteristics predisposing to tissue deposition in either the fibrillar or nonfibrillar state."

Systemic forms of amyloid (fibrillar) deposition include light chain (AL) and heavy chain (AH) amyloidosis, while systemic forms of non-amyloid (non-fibrillar) deposition include light chain deposition disease (LCDD), heavy chain deposition disease (HCDD) and light–heavy chain deposition disease (LHCDD).

The localized form of amyloid deposition is known as an amyloidoma. By analogy, aggregomas are localized tumoral masses of monoclonal light chain deposition, consisting of nonfibillar and Congo-red-negative proteins.

Imaging findings have not been described, but are presumably similar to those of amyloidomas.

References

Rostagno A, Frizzera G, Ylagan L, Kumar A, Ghiso J, Gallo G. Tumoral non-amyloidotic monoclonal immunoglobulin light chain deposits ('aggregoma'): presenting feature of B-cell dyscrasia in three cases with immunohistochemical and biochemical analyses. Br J Haematol. 2002 Oct;119(1):62-9.
Buxbaum J, Gallo G. Nonamyloidotic monoclonal immunoglobulin deposition disease. Light-chain, heavy-chain, and light- and heavy-chain deposition diseases. Hematol Oncol Clin North Am. 1999 Dec;13(6):1235-48.

Meniscal Cysts

2011-11-08T11:52:00.013-06:00

Meniscal cysts are seen in about 5%-10% of knee MRIs. Meniscal cysts are more commonly parameniscal (perimeniscal), but can also be intermeniscal or both. The majority, though not all, of meniscal cysts are associated with meniscal tears. Conversely, parameniscal cysts are seen in less than 10% of cases of meniscal tears.

Meniscal cysts are thought to arise from dissection of synovial fluid through meniscal tears, and entrapment through a one-way valve mechanism.

On MRI, they are more commonly seen in the medial compartment. Earlier studies, however, reported a ration of lateral to medial cysts of up to 7:1. The discrepancy is thought to be related to the higher sensitivity of MRI for the detection of meniscal cysts compared to physical examination (which is better at detecting lateral cysts due to the smaller amount of fatty soft tissue on the lateral aspect of the knee), conventional knee arthrography, and arthroscopy (due to the difficult surgical approach to the posterior horn of the medial meniscus, where most medial cysts are located).

Parameniscal cysts typically present as loculated fluid signal with a connection to the adjacent meniscus. Intrameniscal cysts present as increased signal within an enlarged meniscus with an expanded contour. The T2 signal of intrameniscal cysts may not be as high as that of parameniscal cysts.

When located medially, parameniscal cysts are usually adjacent to the posterior horn. The majority also extend anteriorly adjacent to the body. Cysts can also extend centrally and end up posterior to or surrounding the posterior cruciate ligament, simulating a ganglion.

When located laterally, parameniscal cysts are usually adjacent to the anterior horn, with half of the cysts extending posteriorly adjacent to the body. The image above shows a cyst adjacent to the body of the lateral meniscus in communication with a horizontal tear.

The majority of medial parameniscal cysts, as well as parameniscal cysts overlying the body or posterior horn of the lateral meniscus are associated with meniscal tears. By comparison, only about 2/3 of cysts adjacent to or extending to the anterior horn of the lateral meniscus are associated with meniscal tears. It is not clear why these cysts are less likely to have an underlying meniscal tear.

References

Anderson JJ, Connor GF, Helms CA. New observations on meniscal cysts. Skeletal Radiol. 2010 Dec;39(12):1187-91.
Bergin D, Hochberg H, Zoga AC, Qazi N, Parker L, Morrison WB. Indirect soft-tissue and osseous signs on knee MRI of surgically proven meniscal tears. AJR Am J Roentgenol. 2008 Jul;191(1):86-92.
Campbell SE, Sanders TG, Morrison WB. MR imaging of meniscal cysts: incidence, location, and clinical significance. AJR Am J Roentgenol. 2001 Aug;177(2):409-13.
De Smet AA, Graf BK, del Rio AM. Association of parameniscal cysts with underlying meniscal tears as identified on MRI and arthroscopy. AJR Am J Roentgenol. 2011 Feb;196(2):W180-6.

Clear Cell Variant of Chondrosarcoma

2011-11-07T18:03:00.002-06:00

Clear cell chondrosarcoma is a low-grade malignancy that behaves less aggressively than conventional chondrosarcoma. It accounts for about 2% of all cases of chondrosarcoma, is more commonly seen in men, and usually affects patients in their 20s to 40s.

It tends to affect the epiphyses of long tubular bones, most commonly the femur and humerus. In such cases, patients can present with joint pain and effusion and limited range of motion.

Radiographs typically reveal a predominantly lytic lesion with a narrow zone of transition sometimes with a sclerotic margin. The lesion may be expansile, have central calcifications and ossifications, and demonstrate endosteal scalloping. Periosteal reaction and soft tissue extension are rare. The imaging appearance can mimic chondroblastoma, especially when seen in younger patients: While clear cell chondrosarcoma has homogeneous intermediate signal intensity on T1-weighted images and heterogeneous high signal intensity on T2-weighted images, chondroblastoma usually has low signal intensity on T1- and T2-weighted images.

References

Greenspan A, Jundt G, Remagen W. Cartilage (Chondrogenic) Lesions. In Differential Diagnosis of Orthopaedic Oncology, 2nd Edition. 2007 Lippincott Williams & Wilkins; pp 222-224.

Inverted Napoleon's Hat Sign

2011-11-06T09:06:00.004-06:00

The inverted Napoleon's hat sign refers to the appearance of the L5 vertebra on frontal radiographs in patients with anterolisthesis of L5 on S1. It is formed by overlap of L5 on the sacrum on the frontal radiograph, with the vertebral body forming the dome of Napoleon's hat and the transverse processes forming tapered brim of the hat.

References

Talangbayan LE. The inverted Napoleon's hat sign. Radiology. 2007 May;243(2):603-4.

Metal Artifact Reduction Sequence (MARS)

2011-11-05T07:35:00.000-05:00

The metal artifact reduction sequence (MARS) is a modified spin-echo pulse sequence that uses view angle tilting (application of the slice-select gradient at the same time as the frequency encoding gradient). Additional modifications are also made to optimize imaging.

All together, the MARS technique involves:

View angle tilting: Used to remvoe geometric distortion. The slice-select gradient is applied at the same time as the frequency encoding gradient (i.e., during signal readout), giving the spins the same narrow frequency band and removing distortion due to magnetic field inhomogeneity. This comes at the cost of introducing blurring in the frequency encode direction.
Increasing the slice-select gradient strength: This makes the imaging gradients as large as possible relative to the susceptibility-induced gradients produced by metal. Increasing the slice-select gradient strength also results in a decrease in slice thickness.
Increasing the frequency encoding gradient strength: This makes the imaging gradients as large as possible relative to the susceptibility-induced gradients produced by the metal implants. Also decreases geometric distortion in the image. Increasing the frequency encoding gradient strength, however, requires a larger bandwidth, which reduces the signal-to-noise ratio (30% to 50% lower, depending on the field-of-view).

References

Cho ZH, Kim DJ, Kim YK. Total inhomogeneity correction including chemical shifts and susceptibility by view angle tilting. Med Phys. 1988 Jan-Feb;15(1):7-11.
Lee MJ, Janzen DL, Munk PL, MacKay A, Xiang QS, McGowen A. Quantitative assessment of an MR technique for reducing metal artifact: application to spin-echo imaging in a phantom. Skeletal Radiol. 2001 Jul;30(7):398-401.
Olsen RV, Munk PL, Lee MJ, Janzen DL, MacKay AL, Xiang QS, Masri B. Metal artifact reduction sequence: early clinical applications. Radiographics. 2000 May-Jun;20(3):699-712.