CASES Dr HARSHA K J 2ND YR RESIDENT DEPARTMENT OF RADIOLOGY BARODA MEDICAL COLLEGE BARODA 30-01-08

CASE 1

A 64-year-old female with a long-standing history of diabetes mellitus type II and a past surgical history of an open reduction and internal fixation of a right ankle fracture presents with a two day history of increasing right ankle edema, erythema and intermittent drainage from a cutaneous wound.  Upon presentation she has a WBC count of 6,000. 

AP and lateral radiography of the ankle from July AP and lateral radiography of the ankle from October

D/D OSTEOMYELITIS/ SEPTIC ARTHRITIS NEUROPATHIC JOINT

A practical rule of thumb is that IF THERE HAS NOT BEEN A BREAK IN THE SKIN, IT IS LIKELY TO BE CHARCOT’S ARTHROPATHY

IF ULCER PRESENT, LOOK FOR SITE

LOOK FOR WBC COUNT

Three-phase bone scan

Osteomyelitis is not excluded, with additional possibilities to include neuropathic joint, or perhaps, even inflammatory arthropathy

In111 white blood cell study

 Indium WBC Study reveals only mildly increased activity localized to the ankle (red arrows). As a result osteomyelitis is unlikely, and neuropathic change is felt to be more likely.

CASUES OF NEUROPATHIC JOINT

Diabetes mellitus (diabetic charcot foot and ankle)     Tabes dorsalis     Syringomelia     Meningomyelocele     Leprosy     Tumors of the spinal cord     Degenerative spinal disease with nerve root compression     Subacute combined degeneration of the spinal cord     Amyloid neuropathy     Giantism w/ hypertrophic neuropathy     Impaired pain sensitivity due to use of:             intraarticular and systemic steroids             phenylbutazone             indomethacin             excessive ETOH     Congenital insensitivity to pain     Familial hereditary neuropathies             Charcot Marie Tooth disease             Hereditary sensory neuropathy             Hypertrophic intersitial neuropathy (Dejerine-Scottas disease)             Familial dysautonomia (Riley day syndrome)             Familial amyloid neuropathy

Sensory Neuropathy:     - diabetic neuropathy     - paraneoplastic sensory neuropathy     - paraneoplastic mononeuritis multiplex     - neoplastic neuropathy     - chronic inflammatory demyelinating polyneuropathy     - sarcoid neuropathy     - postinfectious small fiber sensory neuropathy     - amyloid neuropathy     - lyme neuropathy     - HIV neuropathy     - leprous neuropathy     - cryoglobulinemic neuropathy (associated with Raynaud's syndrome)     - Vasculitic neuropathy (Sjögren's syndrome)

PATHOGENESIS

NEUROTRAUMATIC THEORY NEUROVASCULAR THEORY Two main theories for neuropathic arthropathy are proposed. NEUROTRAUMATIC THEORY NEUROVASCULAR THEORY

NEUROTRAUMATIC THEORY NEUROVASCULAR THEORY absence of normal protective sensory feedback is the cause for repetitive mechanical trauma which then causes progressive joint destruction which emphasizes on the vascular changes that accompany neuropathic arthropathy This theory is supported by experiments performed by producing anesthesia in the limbs of animals by severing the posterior nerve roots and showing that sensory loss in itself alone did not result in arthropathy. When the anesthetized joints were subjected to trauma, however, typical neuropathic joint lesions occurred Studies have shown that in the absence of a neural stimulus in the limb, sympathetic tone to the limb is lost with resultant vasodilation and hyperemia, which in turn promote bone resorption. Weakened subchondral bone thus results in neuropathic changes.

Both the neurotraumatic and neurovascular theories are supported by clinical and laboratory data, as, it is well known that neuropathic osteoarthropathy may occur in immobilized patients. In these cases, minor trauma inflicted during patient transport, turning in bed, or passive exercise is superimposed on bone weakened by neurovascular mechanisms and is thought to be responsible .

Radiologic Patterns

As we all know that most important modality for evaluation of the arthritis changes is conventional radiography. Radiographic presentation of any arthritis depends mainly on the 1. type and stage of disease and 2. Site of original insult which is characteristic of various arthritis

Radiographic diagnosis of arthritis is based on the evaluation of two fundamental parameters Morphology of the articular lesion and Its distribution in the skeletal. These findings combined with history, physical examination and laboratory data improve the accuracy of the diagnosis.

In neuropathic osteoarthropathy radiologically, HYPERTROPHIC ATROPHIC.

The classically described hypertrophic joint is manifested radiologically as: joint destruction and fragmentation, osseous sclerosis, and osteophyte formation.

Osteophytes formed in the setting of neuropathic arthropathy may differ from those of osteoarthritis on the basis of: early production ill-defined and rounded margins and later attainment of enormous size. In many cases, however, it is difficult to distinguish neuropathic osteoarthropathy from severe osteoarthritis.

The atrophic form of neuropathic osteoarthropathy has an appearance of osseous resorption that often gives the impression of surgical amputation. Joint disorganization and large persistent joint effusion are features of both atrophic and hypertrophic types of neuropathic osteoarthropathy, and, when severe, both types exhibit disorganization more profound than that seen in other forms of arthropathy. Milder degrees of the disease, however, may be difficult to diagnose.

The atrophic type may appear similar to septic arthritis, and the hypertrophic type, as mentioned earlier, may appear similar to osteoarthritis. The completely resorbed atrophic joint is more common than is the purely productive hypertrophic joint, and mixed patterns are frequently encountered.

The atrophic pattern is more common in the non–weight-bearing joints of the upper extremity and is associated with syringomyelia and peripheral nerve lesions. On the other hand hypertrophic pattern is common in the lower extremities (weight bearing joints ) Either pattern may be seen with central or peripheral neurosensory deficit, but, in some cases an affected joint may exhibit the atrophic pattern early and evolve into the hypertrophic form later.

Fractures are an important although less well-known manifestation of neuropathic osteoarthropathy. These fractures may occur spontaneously or in the presence of minor trauma. In long bones, they are typically transverse in orientation. These fractures are often initially unrecognized and, in the setting of delayed treatment with continued weight bearing and motion at the fracture site, may heal with exuberant callus formation.

Lower Extremity Lower extremtiy >> upper extremity In the past, syphilis was the most common cause and most commonly affected the knee . Today, diabetes mellitus is the most common cause, and most often affects the foot and ankle. It usually occurs with long-term, poorly controlled diabetes.

Although joint changes in the absence of reported trauma is typical, neuropathic changes in the feet of diabetic patients may be precipitated by minor trauma. Clinically, there will be soft-tissue swelling, warmth, and erythema in the early stages, usually with decreased but not absent pain sensation. Neuropathic osteoarthropathy in the diabetic foot often begins in the midfoot, and subluxation usually starts at the second tarsometatarsal joint and proceeds laterally.

Any patient with a Lisfranc fracture, or dislocation in the absence of acute trauma, should undergo evaluation for diabetes mellitus and other causes of sensory neuropathy. Atrophic neuropathic arthropathy of the foot, especially associated with vascular calcifications, is highly suggestive of diabetes mellitus.

However, both atrophic and hypertrophic joints are seen in diabetic patients . The ankle, hindfoot, and forefoot may also show neuropathic changes . Neuropathic fractures that are well known to occur in the diabetic foot are avulsion fractures of the posterior tubercle of the calcaneus and subchondral fracture of the head of the second metatarsal.

Medial oblique radiograph depicts early neuropathic changes at the second tarsometatarsal joint showing Intermetatarsal destruction (arrow) is shown.

Frontal radiograph depicts atrophic neuropathic osteoarthropathy at the tarsometatarsal joints in a 35-year-old diabetic woman. Resorptive changes are present with a Lisfranc pattern of fracture dislocation.

Frontal radiograph depicts Lisfranc fracture dislocation in a 60-year-old diabetic woman. Resorption of the middle cuneiform bone (arrow) is shown without associated bone fragments. Fracture dislocation was unsuspected in this patient, who had undergone a minor trauma.

Medial oblique radiograph depicts divergent Lisfranc fracture dislocation in a 62-year-old diabetic woman. Second through fifth tarsometatarsal joints are dislocated dorsally and laterally. The navicular cuneiform joint (arrow) is dislocated medially. The patient reported no history of foot trauma.

Lateral radiograph depicts hypertrophic neuropathic osteoarthropathy of the midfoot in a 63-year-old diabetic woman. Osteophytes (arrow) are larger than those in typical osteoarthritis.

Lateral radiograph depicts neuropathic osteoarthropathy of the ankle in a 27-year-old diabetic woman. Large ankle joint effusion with fragmentation and collapse of the tibiotalar joint. Presence of microvascular calcifications (open arrows) suggests diabetes mellitus as a cause of neuropathic osteoarthropathy.

Lateral radiograph depicts neuropathic osteoarthropathy of the tibiotalar joint in a 60-year-old diabetic woman. Resorption and fragmentation of the distal tibia and talus associated with marked sclerosis, osteophytosis, and periostitis.

Lateral radiograph depicts neuropathic osteoarthropathy of the ankle and hindfoot in a 42-year-old diabetic man. The distal tibia is resorbed and has sharp margins resembling surgical amputation. The talar dome is resorbed. Sclerosis is present, and subtalar joints can no longer be identified.

. Anteroposterior and lateral radiographs of the ankle show disruption of the subtalar joint , talonavicular subluxation, and fracture of the distal fibula

Frontal radiograph depicts collapse of the head of the second metatarsal (arrow). Osseous resorption leads to flattening and fragmentation of metatarsal heads. "Amputations" of the first and fourth toes and vascular calcifications are noted.

Neuropathic changes in the talonavicular joint in a 27-year-old diabetic woman. Lateral radiograph depicts soft-tissue swelling and effusion (arrow) that overlie early osseous fragmentation of the anterior process of the talus.

Lateral radiograph obtained 1 year later shows destruction, sclerosis, and bone fragmentation of the joint. The talonavicular joint is the second most favored site, after the tarsometatarsal joints, of involvement with diabetic neuropathic osteoarthropathy of the foot.

Axial proton-density and sagittal MR images show medial talar dislocation and effusion. Extensive soft-tissue edema is present about the ankle and foot. Soft-tissue edema is commonly seen in neuropathic osteoarthropathy owing to the lack of sympathetic vasoconstriction.

Frontal radiograph depicts neuropathic osteoarthropathy of the forefoot in a 42-year-old diabetic woman. Atrophic changes have resulted in "pointed bones“. The first metatarsophalangeal joint has a mortar-in-pestle configuration . The radiographic pattern is usually of atrophic neuropathic osteoarthropathy in the forefoot.

Lateral radiograph depicts neuropathic destruction of the naviculocuneiform joint in a diabetic man. Neuropathic osteoarthropathy typically involves the medial column of the foot earlier and more frequently than the lateral column.

CASE 2

Screening mammogram. MAMMOGRAPHY: Right MLO view shows extensive, large calcification. These have a smooth needlelike appearance, involve all quadrants, and radiate toward the nipple..

The assessment of calcifications identified on mammography should include the following points of evaluation: morphology, distribution, number, size, variability, Interval stability in comparison with prior exams, associated findings. Morphology of calcifications is the single most important feature, because it is related so closely to the pathologic or histologic finding

Breast Imaging Reporting and Data System (BI-RADS®) of the American College of Radiology provides a lexicon or nomenclature for the description of calcifications on mammography. The lexicon describes calcifications by morphology, distribution, and location and uses the following structure for overall patient assessment: Category 0: needs additional evaluation, i.e., magnification view; Category 1: normal mammogram; Category 2: benign finding, routine follow-up; Category 3: probably benign finding, early follow-up; Category 4: suspicious findings, recommend biopsy; Category 5: highly suspicious for malignancy, recommend biopsy.

CALCIFICATION MALIGNANT INDETERMINATE BENIGN

BENIGN skin, vascular, coarse, dystrophic, large rodlike, eggshell or rimlike, lucent-centered or spherical, sutural, milk of calcium, round, and punctate.

SKIN CALCIFICATIONS

They typically occur in sebaceous glands and are related to chronic inflammation. Because of their location within the interconnecting lumina of the sebaceous glands, their pattern may be in the form of a PAW PRINT

Dermal calcifications: small, very-well-defined, round, and lucent shapes

Bilateral MLO views (A) show multiple very-well- circumscribed masses in both breasts (arrows), as well as extensive regional calcifications. On the CC views (B), the masses are not identified; however, there is very prominent skin thickening medially (arrows). On an enlarged image (C), the skin thickening with associated lucent-centered calcification is noted. Keloids appearing as pseudomasses with dystrophic calcification in the scars

TATTOO SIGN The calcifications lie in a fixed orientation relative to each other on two different views, indicating a superficial location

VASCULAR CALCIFICATIONS

Magnified image of left breast Magnified image of left breast. Circuitous vessels are associated with calcification in the walls, typical of arterial calcification. - Arterial calcifications.

Early arterial calcifications may be stippled and fine, and the observation of the vessel corresponding to their path is key in suggesting the proper diagnosis Magnification mammography is often essential in this situation for differentiating early vascular calcifications from clustered fine microcalcifications of ductal or lobular origin

COARSE CALCIFICATIONS

Left MLO (A) and CC (B) views show very dense and glandular tissue. In the 12 o'clock position, there is a very-well-defined mass with a fatty halo around most of its margin. Dense popcornlike calcifications are present in the mass and are typical of a degenerated fibroadenoma. Other scattered benign calcifications are also seen. - Degenerated calcified fibroadenoma.

Bilateral MLO views. The breasts are glandular for the age of the patient. There are multiple, popcornlike, very coarse, dense calcifications in both breasts. These have almost totally replaced the soft tissue masses from which they originated, except for a few partially calcified nodules (arrows). The appearance of these lesions is characteristic of degenerated fibroadenomas.

Right magnification view. There is a 1 Right magnification view. There is a 1.5-cm well-defined ovoid mass in the right outer quadrant. This lesion contains coarse peripheral macrocalcifications typical of a degenerating fibroadenoma.

Right CC view. There is a large well-defined mass in the subareolar area that contains coarse bizarre macrocalcifications. The mass has smooth, lobulated margins. The findings are typical of a fibroadenoma with coarse calcifications.

Left (A) and right (B) CC views show dense parenchyma and extensive coarse and vascular calcifications in a bilateral pattern that suggests a systemic etiology. The extensive nature of the calcifications is typical of tumoral calcinosis secondary to hypercalcemia.

Left MLO view shows extensive very-high-density nodules throughout the breast. These represent silicone droplets that have been injected, some of which are calcifying

Left CC view (A) and magnified image (B) Left CC view (A) and magnified image (B). There is a high-density spiculated mass typical of malignancy. There are relatively coarse dense calcifications, 3 - 4 mm in diameter, within the mass (B), and larger than are generally considered to be associated with carcinoma. Occasionally, malignancies may contain larger calcifications, and their presence should not alter a diagnosis of carcinoma based on the morphology of the mass.

Dystrophic Calcifications

Left CC magnification views (A, B) Left CC magnification views (A, B). There are two groups of dystrophic calcifications that are smoothly marginated. The pattern is suggestive of a benign etiology, such as a fibroadenoma, because of the smoothness of the edges of individual calcifications. These had been stable for 4 years

Left (A) and right (B) bilateral CC views and magnified right CC image. There are numerous coarse irregular calcifications that are oriented in a linear arrangement and that were situated directly beneath the surgical scars. A right magnified view (C) shows the calcifications to be more coarse and pleomorphic. The findings are typical of fat necrosis, and the extent and distribution are seen after reduction mammoplasty.

Bilateral MLO (A) and CC (B) views show extensive, somewhat coarse calcifications bilaterally. On the enlarged image (C), the plaquelike appearance of these dystrophic calcification is seen. The calcifications are located superficially in the subcutaneous area and extend beyond the breast toward the axilla. The diffuse, bilateral appearance suggests the possibility of a systemic etiology

Eggshell or Rimlike Calcifications

Right CC view (A) and magnified image (B). There is a well-defined, 1-cm eggshell calcification in the periphery of a radiolucent mass, characteristic of a calcified oil cyst. Other smaller, dense, round, and circular calcifications of fat necrosis (liponecrosis microcystica) are seen. The changes are related to the previous surgery

Round calcifications

These are often multiple and may be 1 to 3 mm in diameter. may occur in multiple conditions, including fat necrosis, in which the central lucency of the oil cyst is not evident; in secretory disease, in which they are mixed with rodlike calcifications; and in areas of fibrocystic change, in which small cysts are completely calcified. This pattern is usually not problematic in characterizing as clearly benign on mammography. Round calcifications represent one of the patterns that may disappear on subsequent mammography

changes with round lobular An 83-year-old nulliparous woman with a pleural effusion and no palpable breast abnormalities. MAMMOGRAPHY: Bilateral oblique views (A) and magnification image of the right breast (B). The breasts are dense and diffusely nodular, as may be seen in an elderly nulliparous woman. The snowflake pattern of nodularity suggests fibrocystic changes with adenosis. There are also innumerable round pearllike microcalcifications distributed evenly throughout both breasts. The smooth-bordered, rounded shapes of the micro calcifications and the similarity in appearance suggest a lobular origin and are consistent with adenosis. IMPRESSION: Diffuse fibrocystic changes with round lobular calcifications, BI-RADS® 2.

Sutural Calcifications

A 56-year-old woman with a history of surgical biopsy in left breast for benign disease. MAMMOGRAPHY: Left MLO (A) and BB (B) views show a surgical site marked with BBs. There is a somewhat coarse calcification located centrally. On the enlarged MLO image (C), the knotlike shape of this sutural calcification is evident. IMPRESSION: Sutural calcification.

Large Rodlike Calcifications

Bilateral MLO (A) and CC (B) views show scattered fibroglandular densities. There are extensive rodlike calcifications oriented toward the nipples in both breasts. The pattern and distribution of calcifications is typical of secretory disease or plasma cell mastitis.

SECRETORY DISEASE CALCIFICATION IN OUR CASE LARGE RODLIKE CALCIFICATION HENCE BENIGN TYPE OF CALCIFICATION SECRETORY DISEASE

SIGN

MRI FADING SIGN

T1-weighted sequence demonstrates multiple rounded masses within the adnexa bilaterally.  Some of these are hyperintense, consistent with multiple endometrial implants containing blood products.  The presence of methemoglobin accounts for the striking T1-hyperintensity.

Single-shot T2-weighted sequence shows loss of signal intensity within those lesions which demonstated hyperintensity on T1-weighted sequence, the so-called MR shading sign.   The crescent of hyperintensity lateral to the endometrioma in the right ovary is consistent with a compressed simple follicular cyst.  

Endometriomas represent focal collections of concentrated blood products secondary to endometriosis, most commonly within the adnexa.  There are two main hypotheses as to how this abnormality arises.    retrograde passage of sloughing endometrial tissue through the fallopian tubes and onto the surface of the ovary and other peritoneal surfaces. Alternately rests of tissue may be left behind during development of the Mullerian system.

On MR endometriomas demonstrate signal intensity of concentrated blood products.  Classically they are bright on T1 weighted sequences, reflecting the presence of concentrated methemoglobin, and demonstrate darkening or loss of signal on T2-weighted sequences (the so-called MRI shading sign). Chemical shift fat suppression allows for differentiation from a dermoid cyst, which contains macroscopic fat which is bright on conventional T1 weighting without fat suppression.  Differential for endometrioma also includes hemorrhagic ovarian cyst, which can also appear bright with T1 weighting.  Hemorrhagic cysts are usually at least partially bright on T2-weighted images, but may be T2 isointense to hypointense.  Bilaterality is more common with endometrioma.

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