Doaa Ibrahim, MD

 A 47-year-old female patient complaining from tender mass in upper outer left breast. Clinically cord-like structures were palpable in the upper outer quadrant of her left breast.

 Craniocaudal (Fig. A) and mediolateral oblique (B) mammograms show superficial tubular densities. Breast ultrasound scan (Fig. C) showed a long, superficial, beaded, tubular, hypoechoic structure in the left breast at 3 o’ clock position. Additionally noted low-level echoes were seen within it. It measured 5 mm in its widest diameter and showed no flow on color by spectral Doppler study.

Left breast upper outer subcutaneous thrombophlebitis (Mondor’s disease)

Mondor’s disease of the breast is a benign, self-limiting condition; characterized by thrombophlebitis of the superficial veins of the mammary region (1). Direct trauma and pressure on the superficial veins of the breast leading to stasis has been postulated in the etiopathogenesis of the disease. Breast biopsy and surgery, trauma, infection and breast cancer are risk factors (2).

It commonly affects middle-aged women. Mammogram showed a superficial tubular density in the affected side. The Breast Imaging Reporting and Data System assessment was category 3 for these cases. A short-interval follow-up in six months was recommended.

Mondor's disease presents as a palpable cord or mass in the breast sometimes with pain. Sonographic and mammographic evaluations are indicated in patients with suspected Mondor’s disease. Finding a dilated tubular density may potentially be mistaken for a dilated duct. Mondor’s disease is managed conservatively with treatment of pain using anti inflammatory and analgesic drugs. Biopsy, anticoagulants and antibiotics are unnecessary (3).


1. Pugh CM, DeWitty RL. Mondor’s disease. J Natl Med Assoc 1996;:359–63.
2. Bejanga BI. Mondor’s disease: analysis of 30 cases. J R Coll Surg Edinb 1992;:322–4.
3. Shetty MK, Watson AB. Mondor’s disease of the breast: sonographic and mammographic findings. AJR Am J Roentgenol 2001;:893–6.

Doaa Ibrahim, MD, in radio-diagnosis, Zagazig University Hospitals and TechnoScan Centers in Egypt

Articles

Clinical History: A 47-year-old female patient complaining from tender mass in upper outer left breast. Clinically cord-like structures were palpable in the upper outer quadrant of her left breast.

Mondor’s Disease

 A 48-year-old female presented with vaginal bleeding, urinary frequency and lower abdominal pain.

 A large intra-uterine irregular margin prolapsed pedunculated mass attached to the uterine fundus via broad pedicle , extends down reaching to the upper vagina and the myometrium invaded in the lower part with loss of the characteristic cervical low signal smooth muscle (Fig. A), the mass displacing the urinary bladder anteriorly as well as the rectum posteriorly but still preserved fat planes between them and the outer myometrial layer. The lesion displaying heterogeneous high signal intensity at T2WI (Fig. A) and T2FS (Fig. B), with a small rounded left para-central more high signal intensity area , while in the T1WI (Fig. C) the lesion displaying heterogeneous low signal intensity and high signal intensity within the same left para-central area denoting methemoglobin from subacute hemorrhage. Minimal heterogeneous enhancement noted at the sagittal post contrast T1 WI (Fig. D).

 Pedunculated leiomyoma with sarcomatous changes( leiomyosarcoma).

 Leiomyomas are the most common uterine neoplasm and are composed of smooth muscle with varying amounts of fibrous connective tissue. As leiomyomas enlarge, they may outgrow their blood supply, resulting in various types of degeneration: hyaline or myxoid degeneration, calcification, cystic degeneration, and red degeneration. Leiomyomas are classified as submucosal, intramural, or subserosal (1-3).

Leiomyosarcomas account for one third of uterine sarcomas. Leiomyosarcomas may arise either de novo from uterine musculature or the connective tissue of uterine blood vessels or in a preexisting leiomyoma. The incidence of sarcomatous change in benign uterine leiomyomas is reported to be 0.1-0.8% (4).

Leiomyosarcoma usually presents as a massive uterine enlargement with irregular central zones of low attenuation, suggesting extensive necrosis and hemorrhage. The pattern of tumor spread is to the myometrium, pelvic blood vessels and lymphatics, contiguous pelvic structures, abdomen, and then distantly, most often to the lungs. Although it has been suggested that an irregular margin of a uterine leiomyoma on MRI is suggestive of sarcomatous transformation, the specificity of this finding has not been established (5).

 1. Parker WH, Fu YS, Berek JS. Uterine sarcoma in patients operated on for presumed leiomyoma and rapidly growing leiomyoma. Obstet Gynecol 1994; 83:414-418.
2. Garcia CR, Tureck RW. Submucosal leiomyomas and infertility. Fertil Steril 1984; 42:16-19.
3. Corson SL. Hysteroscopic diagnosis and operative therapy of submucous myoma. Obstet Gynecol Clin North Am 1995; 22:739-755.
4. Janus CJ, White M, Dottino P, Brodman M, Goodman H. Uterine leiomyosarcoma: magnetic resonance imaging. Gynecol Oncol 1989; 32:79 –81.
5. Pattani SJ, Kier R, Deal R, Luchansky E. MRI of uterine leiomyosarcoma. Magn Reson Imaging 1995; 13:331 –333

Clinical History: A 48-year-old female presented with vaginal bleeding, urinary frequency and lower abdominal pain.

Pedunculated Leiomyoma with Sarcomatous Changes (Leiomyosarcoma)

A 28-year-old man presented with history of pulsing noise in the head and progressive right hemiparesis. 

 Axial, coronal MR T2-WIs images and axial post-contrast MR T1-WI image show multiple flow voids and tubular structures lesion that involves the left tempro-parietal regions . The normal brain parenchyma is interspersed between the abnormal vessels no significant contrast enhancement detected. MRA shows enlarged arteries and draining veins, A-V shunting with early venous filling.

Classic left tempro-parietal arteriovenous malformations

 Vascular lesions of the brain are uncommon lesions that may pose a diagnostic challenge due to their similar clinical manifestations and imaging features. Different classification systems have been put forward. The most commonly used classification system separates vascular lesions into arteriovenous malformations (AVMs), which may be either pial or dural, depending on the location of the shunt; cavernous hemangiomas (or cavernomas); capillary telangiectasia; and developmental venous anomalies (DVAs, formerly known as venous angiomas) (1–3).

However, from a clinical, imaging, and prognostic standpoint, further subclassification of various diseases that were formerly subsumed under the heading “brain AVMs” seems necessary . MRA offers several advantages over conventional angiography. For example, because of its ability to image all vessels in a given volume, an AVM with multiple feeding arteries can be imaged noninvasively in a single study. In addition, 2-dimensional (2D) and 3-dimensional (3D) phase-contrast MRA can be used to examine the direction, rate, and quantity of blood flow. Another advantage of MRA is the ability to retrospectively examine images in any plane. (4–6).


1. Chaloupka JC, Huddle DC. Classification of vascular malformations of the central nervous system. Neuroimaging Clin N Am 1998;8(2):295–321.
2. Wagner BJ, Richardson KJ, Moran AM, Carrier DA. Intracranial vascular malformations. Semin Ultrasound CT MR 1995;16(3):253–268.
3. Zabramski JM, Henn JS, Coons S. Pathology of cerebral vascular malformations. Neurosurg Clin N Am 1999;10(3):395–410.
4. Lasjaunias PL, Landrieu P, Rodesch G, et al. Cerebral proliferative angiopathy: clinical and angiographic description of an entity different from cerebral AVMs. Stroke 2008;39(3):878–885.
5. Hoh BL, Putman CM, Budzik RF,Ogilvy CS. Surgical and endovascular flow disconnection of intracranial pial single-channel arteriovenous fistulae. Neurosurgery 2001;49(6):1351–1363; discussion 1363–1364.
6. Lasjaunias P, Manelfe C, Chiu M. Angiographic architecture of intracranial vascular malformations and fistulas: pretherapeutic aspects. Neurosurg Rev 1986;9(4):253–263.

Doaa Ibrahim, MD in radio-diagnosis, Zagazig University Hospitals and TechnoScan Centers in Egypt 

Case History: A 28-year-old man presented with history of pulsing noise in the head and progressive right hemiparesis.

Classic Left Tempro-parietal  Arteriovenous Malformations

 A 52-year-old female patient complaining from right hypochondrial pain and abdominal swelling for three months, nausea and vomiting.

 Large multilocular cyst involving most of the right hepatic lobe with enhanced through transmission. The content of the cysts having low-level echoes and mural nodules with papillary projections project into the cyst lumen.

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Triphasic CT axial images (arterial phase C-G), (portal phase H-K), (delayed phase L-M) showing large partially defined right hepatic cystic lesion, with heterogeneous enhanced soft tissue papillary projections and mural nodules in the arterial phase followed by wash out of contrast at both venous and delayed phases. Displaced surrounding abdominal structures by the large mass.

 A biliary cystadenocarcinoma is a rare cystic hepatic neoplasm. It can be thought of as a malignant counterpart of a biliary cystadenoma. The clinical symptoms are non-specific and are not distinctive from benign cystic liver lesions unless invasive growth of the tumor occurs or distant metastases are present.

The vast majority of these neoplasms are intrahepatic (97 percent) where a small proportion is extrahepatic (3 percent). Some biliary cystadenomas may rarely develop into a cystadenocarcinoma.

The appearance of the cyst fluid on CT is variable depending on its composition. It can range from that of water (HU = 0) to quite hyperattenuating if the cyst has been complicated by recent hemorrhage. Calcifications of septa or cyst wall may be seen. Additionally the septa may enhance following administration of contrast.

The MR signal intensity of biliary cystadenoma is variable on both T1- and T2-weighted images, depending on the content of the cyst fluid.


1. Levy AD, Murakata LA, Abbott RM et-al. From the archives of the AFIP. Benign tumors and tumorlike lesions of the gallbladder and extrahepatic bile ducts: radiologic-pathologic correlation. Armed Forces Institute of Pathology. Radiographics. 22 (2): 387-413.
2. Lewin M, Mourra N, Honigman I et-al. Assessment of MRI and MRCP in diagnosis of biliary cystadenoma and cystadenocarcinoma. Eur Radiol. 2006;16 (2): 407-13.
3. Horton KM, Bluemke DA, Hruban RH et-al. CT and MR imaging of benign hepatic and biliary tumors. Radiographics. 19 (2): 431-51.

Doaa Ibrahim, MD in radio-diagnosis, Zagazig University Hospitals and TechnoScan Centers in Egypt

Biliary Cystadenocarcinoma

A 54-year-old man presented with upper lid swelling, conjunctival chemosis, and proptosis of the right eye.

 MDCT post contrast axial (Figs. A, B), coronal (Figs. C, D) images and CT angiography (MIP Fig. E, VR Fig. F): The axial images show proptosis of the right globe with increased orbital vascularity and dilated enhanced superior ophthalmic vein (Fig. C). Also noted enlarged right enhanced cavernous sinus (Fig. D). Clearly visualized A-V shunting in the CTA MIP & VR images (Figs. E, F).

 Arteriovenous fistulas (AVFs) in the orbit are quite rare, and most are part of facial arteriovenous malformations. Arteriovenous fistulas develop from a single communication between an artery and a vein. Because the bypass of capillary beds results in decreased vascular resistance, regional blood flows preferentially through the fistula, thereby exposing the veins to increased intraluminal pressure.

Advances in spiral CT coupled with continuing progress in 3D imaging have resulted in exciting new applications for CT. In neuroradiology, these techniques can aid in the diagnosis and therapeutic planning of diseases of the neck vessels and of intracranial aneurysms Developments in CT angiography are especially important because they may replace the more invasive conventional angiographic procedures.


1. S. Chakrabortty, T. Nagashima, I. Izawa et al. Intraorbital arteriovenous malformation: case report. Surg Neurol, 40 (1993), pp. 320–325
2. B.H. Hayes, J.W. Shore,
C.T. Westfall et al. Management of orbital and periorbital arteriovenous malformation. Ophthalmic Surg, 26 (1995), pp. 145–152 3. J.W. Kim, W.B. Stewart, W.H. Spencer et al. Acute expansion of an orbital vascular malformation. Arch Ophthalmol, 117 (1999), pp. 844–845
4. M.J. Kupersmith. Neurovascular neuro-ophthalmology, Springer-Verlag, Berlin (1993), pp. 69–108.
5. K. Ohtsuka, M. Hashimoto. Clinical findings in a patient with spontaneous arteriovenous fistulas of the orbit. Am J Ophthalmol, 127 (1999), pp. 736–737
6. J.E. Wright. Orbital vascular anomalies. Trans Am Acad Ophthalmol Otolaryngol, 78 (1974), pp. 606–616.
7. Schwartz RB, Tice HM, Hooten SM, Hsu L, Stieg PE. Evaluation of cerebral aneurysms with helical CT: correlation with conventional angiography and MR angiography. Radiology 1994;192:717-722
8. Alberico RA, Patel M, Casey S, Jacobs B, Maguire W, Decker R. Evaluation of the circle of Willis with three-dimensional CT angiography in patients with suspected intracranial aneurysms. AJNR Am J Neuroradiol 1995;16:1571-1578

Clinical History: A 54-year-old man presented with upper lid swelling, conjunctival chemosis, and proptosis of the right eye.

Orbital Arteriovenous Fistula

A 54-year-old female complaining of left parotid swelling for three months

 MDCT contrast enhanced axial (Figs. A, B, C)and coronal (Figs. D, E) images showing ill defined heterogeneous enhanced soft tissue density mass involving both lobes of the left parotid gland. The lesion extending antero-medially inseparable from the pterygoid muscles (Fig. B - black arrow), with loss of the surrounding fat planes, additionally noted erosion of the medial superior aspect of the left mandible body (Fig. E - black arrow).

Neoplastic left parotid mass pathologically proven as squamous cell carcinoma

 About 70 percent of all salivary gland neoplasms occur in the parotid gland. Several studies have investigated the value of computed tomography (CT) in distinguishing parotid gland tumours. The results of some documents have demonstrated that CT could identify patients with pleomorphic adenomas, Warthin’s tumors and malignant tumors, and evaluate the extent of parotid gland tumors.

Squamous cell carcinoma of the salivary glands represents a rare neoplasm that constitutes 0.3 percent to 1.5 percent of salivary gland tumors. This malignancy occurs more often in the submandibular gland than the parotid gland. Proper diagnosis of squamous cell carcinoma requires exclusion of contiguous spread of a squamous cell carcinoma into the gland, metastases to the gland, and high-grade mucoepidermoid carcinoma.

These tumors usually present as firm indurated masses and occur more commonly in males, usually in the seventh decade of life. Histologically, these tumors reveal intracellular keratinization, intercellular bridges, and keratin pearl formation. However, they do not produce mucus.PET scans may play a role but not in the initial diagnosis. False positives seen in inflammatory process limits its usefulness in distinguishing benign from malignant. PET scan cannot reliably distinguish benign from malignant process.


1. Nagler RM, Laufer D. Tumors of the major and minor salivary glands: review of 25 years of experience. Anticancer Res. 1997;17:701–707.
2. Pinkston JA, Cole P. Incidence rates of salivary gland tumors: results from a population-based study. Otolaryngol Head Neck Surg. 1999;120:834–840. doi: 10.1016/S0194-5998(99)70323-2.
3. McGahan JP, Walter JP, Bernstein L. Evaluation of the parotid gland. Comparison of sialography, non-contrast computed tomography, and CT sialography. Radiology. 1984;52:453–458.
4. Choi DS, Na DG, Byun HS, et al. Salivary gland tumors: evaluation with two-phase helical CT. Radiology. 2000;214:231–236.
5. Lev MH, Khanduja K, Morris PP, et al. Parotid pleomorphic adenomas: delayed CT enhancement. AJNR Am J Neuroradiol. 1988;19:1835–1839.
6. Yerli H, Aydin E, Coskun M, et al. Dynamic multislice computed tomography findings for parotid gland tumors. J Comput Assist Tomogr. 2007;31:309–316.
7. Current controversies in the Management of Malignant Parotid Tumors SOURCE: Grand Rounds Presentation, The University of Texas Medical Branch (UTMB), Dept. of Otolaryngology DATE: February 25, 2011

Case History: A 54-year-old female complaining of left parotid swelling for three months

Neoplastic Left Parotid Mass Proven as Squamous Cell Carcinoma  

 A 3-month-old make presented with marked skull enlargement and widening sutures and fontanelles.

 MDCT (Figs. A, B, C) showing marked dilatation of the ventricular system of the brain. Reduced brain mantel effaced against the skull. 3D reconstructed images (Figs. D, E) showing thinning expanded skull bone with very widened sutures and fontanelles.

 Congenital marked communicated hydrocephalus

 Hydrocephalus occurs in approximately one out of 500 births. The following are the primary reasons why hydrocephalus occurs:
• Blockage of the CSF flow inside of the head
• Problems absorbing the CSF
• Overproduction of CSF (rare)

Hydrocephalus can occur either as a condition present at birth (congenital), or it can be acquired later in life. When hydrocephalus isn't related to a known genetic cause, it's thought that many factors, both genetic and environmental, contribute to the condition. In a small percentage of babies, a single gene defect on the X chromosome, or another chromosome, is responsible for the condition. If a child has been born with hydrocephalus not known to be caused by a single gene defect, the chance of it occurring in another child is 1 to 5 percent.

Causes of acquired hydrocephalus may include the following:
• Tumor
• Infection
• Prematurity
• Bleeding inside the head
• Birth injury
• Abnormal blood vessel formation inside of the head
• Trauma


1. Hydrocephalus. American Association of Neurological Surgeons. 

http://www.aans.org/Patient%20Information/Conditions%20and%20Treatments/Hydrocephalus.aspx

. Accessed June 11, 2011.
2. Hydrocephalus fact sheet. National Institute of Neurological Disorders and Stroke. 

http://www.ninds.nih.gov/disorders/hydrocephalus/detail_hydrocephalus.htm

. Accessed June 10, 2011.
3. Fishman MA. Hydrocephalus. http://www.uptodate.com/home/index.html. Accessed May 10, 2011. 4. Diagnosis of hydrocephalus. Hydrocephalus Association. 

https://www.hydroassoc.org/hydrocephalus-education-and-support/learning-about-hydrcephalus/diagnosis-of-hydrocephalus

Congenital Marked Communicated Hydrocephalus

 A 12-year-old male complaining of skull expansion, facial deformity, nasal stuffiness, proptosis and visual impairment.

 MDCT axial images (Figs. A, B) with sagittal (Fig. C), axial (Fig. D) bone window images and 3D reformatted images (Fig. E) show thick expanded all skull bones (sphenoid, frontal, maxillary, ethmoid bones, occipital, temporal bones) effacing the brain tissue and facial bones (mandible and maxilla), with diffuse ground glass appearance of the bones on bone window (Figs. C, D). Additionally noted encroachment upon the cranial nerves foraminae and orbital proptosis. Widened diploic space. Obliteration of paranasal sinuses. 3D reconstructed images show lion face appearance (Figs. E, F)

 Fibrous dysplasia of the skull (Leontiasis Ossea)

 Fibrous dysplasia is an abnormal bone growth where normal bone is replaced with fibrous bone tissue. The skull is a frequent site of the pathologic process now known as fibrous dysplasia and the skull changes are often the only manifestation of the disease.

Fibrous dysplasia is a largely historical term used to describe a number of conditions which result in the affected patient's face resembling that of a lion. Although it is most frequently associated with craniofacial fibrous dysplasia, it has a broader meaning encompassing other lesions that have similar appearance.

In general the distinction is made between true leontiasis ossea (craniofacial fibrous dysplasia) and other conditions having similar external appearance (mimics), however it would be safe to say that as a term it is no longer of clinical use and should be avoided.

In addition to craniofacial fibrous dysplasia the following conditions may mimic leontiasis ossea:

• Paget disease
• gigantism
• craniosysonstosis
• tumours of the paranasal sinuses
• syphilitic osteoperiostitis
• ureamia with secondary hyperparathyroidism


1. EVANS J. “Leontiasis ossea; a critical review, with reports of four original cases.” The Journal of Bone and Joint Surgery. British Volume 35-B, no. 2 (May 1953): 229-243.
2. Classic Radiologic Signs: An Atlas and History. M.E. Mulligan. Informa Healthcare; 1st edition (November 15, 1996) 3. Maramattom Boby. “Leontiasis ossea and post traumatic cervical cord contusion in polyostotic fibrous dysplasia.” Head & Face Medicine 2, no. 1 (2006): 24.

Case History: A 12-year-old male complaining of skull expansion, facial deformity, nasal stuffiness, proptosis and visual impairment.

Fibrous Dysplasia of the Skull (Leontiasis Ossea)

 A 74-year-old male complaining of from difficulty swallowing, fever and neck pain.

 Lateral X-ray of the neck showing widening of the pre-vertebral soft tissue shadow with multiple air densities inside.

 Axial CT images showing prevertebral cystic lesion with jet black air densities , abutting the vertebral bodies and effacing the pharyngeal air way which displaced anteriorly.

 Retropharyngeal abscess (RPA) produces the symptoms of sore throat, fever, neck stiffness, and stridor. Retropharyngeal abscess occurs less commonly today than in the past because of the widespread use of antibiotics for suppurative upper respiratory infections. Early recognition and aggressive management of retropharyngeal abscess are essential because it still carries significant morbidity and mortality.

The incidence of RPA in the United States is rising, however. Retropharyngeal abscess, once almost exclusively a disease of children, is observed with increasing frequency in adults. Retropharyngeal abscess poses a diagnostic challenge for the emergency physician because of its infrequent occurrence and variable presentation.

CT and MRI are ideal for characterizing and delineating collections. In this pictorial essay, we present the anatomy of the retropharyngeal space and offer a practical approach to evaluating retropharyngeal collections on multiplanar imaging. Important points to remember are that one, a suppurative retropharyngeal node is contained by the nodal capsule; two, a retropharyngeal space abscess is contained only by the fascia of the retropharyngeal space and has the potential for devastating complications from mass effect and the spread of infection; and three, retropharyngeal space edema is noninfectious and resolves spontaneously as its cause is treated.


1. Abdel-Haq N, Quezada M, Asmar BI. Retropharyngeal Abscess in Children: The Rising Incidence of Methicillin-Resistant Staphylococcus aureus. Pediatr Infect Dis J. Jul 2012;31(7):696-9.
2- Lander L, Lu S, Shah RK. Pediatric retropharyngeal abscesses: a national perspective. Int J Pediatr Otorhinolaryngol. Dec 2008;72(12):1837-43.
3-Multiplanar CT and MRI of Collections in the Retropharyngeal Space: Is It an Abscess? Jenny K. Hoang, Barton F. Branstetter, IV, James D. Eastwood and Christine M. Glastonbury. AJR. 2011;Vol.196

Case history: A 74-year-old male complaining of from difficulty swallowing, fever and neck pain.

Cervical Prevertebral Abscess

A 55-year-old woman presented to the surgical emergency unit with symptoms of acute intestinal obstruction for the last three days and worsening over the last 24 hours.

Findings: Marked distention of the stomach, small bowel loops and irregular heterogeneous mass involving both the cecum and the terminal ileum with abrupt transition on the right colon, mild fat stranding, and small mesenteric lymph nodes.

Diagnosis: Ileocecal adenocarcinoma with subsequent intestinal obstruction.

Discussion: Adenocarcinomas of the cecum account for one-fourth of all colic adenocarcinomas. They have the same general and multi-detector row CT features as all other colic adenocarcinomas, including marked asymmetric colic wall thickening, short segment involvement, and abrupt change from normal to abnormal segments of colon.

However, cecal adenocarcinomas have a tendency to be large, polypoid, and bulky and may act as the lead point for an intussusception. Although they may occupy a large proportion of the colic lumen, they rarely cause obstruction and often grow without clinical manifestations for long periods of time. Cecal adenocarcinomas may demonstrate mild local infiltration, even without perforation. However, wall thickening is more severe relative to pericolic infiltration than in most acute inflammatory diseases, particularly diverticulitis.

The distal ileum may be affected and abnormally thickened in up to 10 percent of patients with right colic cancer as a result of tumor extension or, less commonly, a nontumoral process (congestion and edema).

1. GoreRM. Colorectal cancer: clinical and pathologic features. Radiol Clin North Am1997;35:403–429.
2. JangHJ, Lim HK, Lee SJ, Lee WJ, Kim EY, Kim SH. Acute diverticulitis of the cecum and ascending colon: the value of thin-section helical CT findings in excluding colonic carcinoma. AJR Am J Roentgenol2000;174:1397–1402. 
3. KimAY, Ha HK, Seo BK, et al. CT of patients with right-sided colon cancer and distal ileal thickening. AJR Am J Roentgenol2000;175:1439–1444.