Friday, May 30, 2008
Diffuse axonal injury (DAI)
Findings
Figure 1 and Figure 3: CT images demonstrate scattered subtle hemorrhages in the interpeduncular cistern and high right frontal white matter.
Figure 2: In the left centrum semiovale is an area of increased lucency representing edema secondary to axonal stretching.
Figure 4, 5, 6 and 7: T2 and FLAIR images demonstrate areas of high signal in the high right frontal white matter consistent with diffuse axonal injury.
Figure 8: Gradient echo image demonstrates areas of increased magnetic susceptibility in the right thalamus and right frontal white matter consistent with small areas of hemorrhage which were not identified on the CT images.
Figure 9, Figure 10, and Figure 11: Diffusion weighted images demonstrate areas of high signal and restricted diffusion in the midbrain, splenium of the corpus callosum and high right frontal white matter.
Diagnosis: Diffuse axonal injury
Diffuse axonal injury (DAI) is the result of severe closed head deceleration injury. The rotational acceleration and deceleration of the brain results in stretching of the axons. Capillaries are disrupted along with axons which produces small petechial hemorrhages. The most commonly involved sites of shear injury are the gray-white junction, corpus callosum (especially the body and splenium), brain stem, superior cerebellar peduncle and internal capsule. The body and splenium of the corpus callosum are most vulnerable because of the broadening of the falx posteriorly which allows the brain to move transiently across the midline anteriorly. Brain stem lesions, lesions within the subcortical white matter and internal capsule are associated with more severe injury. Frontal and temporal lesions at the gray-white junction are associated with more mild injury.
CT is not as sensitive as MRI in detecting lesions in DAI and initial CT examanination is normal in 50-80% of cases. Findings of DAI observed on CT are small hypodense foci which correspond to edema at the site of shearing injury. Hyperdense foci of petechial hemorrhage may be present secondary to capillary disruption. MR findings of DAI are high signal foci on T2 and FLAIR images. Hemorrhagic foci are identified as areas of low signal secondary to increased magnetic susceptibility on gradient echo images. Diffusion weighted imaging demonstrates hyperintense foci reflecting restricted diffusion.
Eighty percent of DAI lesions are microscopic and nonhemorrhagic. The traumatic axonal stretching results in swelling, microglial clusters and eventual wallerian degeneration. The most common signs and symptoms of DAI are loss of consciousness immediately following the injury with coma and persistent vegetative state. Brain stem damage (as in this case) is associated with immediate or early death. There is no treatment for diffuse axonal injury. Supportive therapy is the standard of care.
Tuesday, May 27, 2008
Bilateral parotid hemangiomas
Findings
Figure 1 and Figure 2: Contrast enhanced axial CT images demonstrate bilateral, lobulated, enhancing masses in the expected region of the parotid glands. No cystic areas are seen within the masses. No normal parotid tissue is seen. Prominent enhancing vessels can be seen adjacent to these masses.
Diagnosis: Bilateral parotid hemangiomas
Hemangioma is not only the most common tumor of the parotid glands in childhood, it is also the most common tumor of infancy. The incidence of hemangioma in neonates is 1-2%. 90% of salivary gland hemangiomas occur in the parotid gland, with the remaining 10% occurring in the submandibular gland. 60% of infantile hemangiomas occur in the head and neck, and can involve virtually any space. They can be seen in association with PHACES syndrome.
On noncontrast CT imaging, parotid hemangiomas appear as lobulated, intermediate density masses without calcifications. During the proliferative phase, parotid hemangiomas typically enhance diffusely, with prominent vessels in and adjacent to the mass. As they spontaneously involute, they decrease in size and undergo fatty replacement.
The differential for these lesions includes venous and arteriovenous malformations (typically contain phleboliths), plexiform neurofibroma (look for other stigmata of neurofibromatosis), and sarcoma (tends to occur in older children and are more likely to be invasive and destructive).
In one study of 100 children with parotid hemangiomas, the female-to-male ratio was 4.5:1. Forty-five percent had a cutaneous vascular mark noted at birth. Thirty percent of the patients were asymptomatic and the lesions spontaneously involuted over time. The remaining 70% received therapy for symptomatic lesions. For most, treatment was performed to limit the size of the hemangioma and control ulceration. In the remaining patients, the indication for treatment was related to respiratory distress (26%), potential visual impairment (13%), congestive heart failure (4%), and obstruction of the auditory canal (3%).
Many hemangiomas will involute spontaneously, and watchful waiting is recommended in these cases. Symptomatic lesions or lesions causing significant cosmetic deformity can be treated. About 10-20% of hemangiomas present with indications for prompt therapy, such as expansion, destruction, obstruction, or life-threatening complications. Possible treatment options include corticosteroid or interferon injections, surgical excision, laser ablation, and embolization.
Monday, May 26, 2008
Synovial Osteochondromatosis
Consultant Radiologist ,VIMHANS and CEO-Teleradiology Providers
Editor-in-chief, The Internet Journal of Radiology
Director, DAMS (Delhi Academy of Medical Sciences
ACL Tear
Normally ACL may show a striated signal distally caused by interspersed fat and synovium between the 2 bundle and proximal ligament appears. Any discontinuity or signal change in the ligament is indicative of ACL tear. There are some indirect signs of ACL tear like focal areas of increased signal in the lateral tibial plateau and femoral condyle, pivot shift injury (combination of signal changes in lateral femoral condyle and posteror lateral tibial plateau, abnormal slope of ACL, avulsion of the anterior tibial spine, segond fractur (capsular avulsion fracture of the lateral tibial plateau and kissing contusions involving the anterior tibia and femur resulting from hyperextension injury. This case shows ACL avulsion tear on MRI image.
Dr.Sumer K Sethi, MD
Consultant Radiologist ,VIMHANS and CEO-Teleradiology Providers
Editor-in-chief, The Internet Journal of Radiology
Director, DAMS (Delhi Academy of Medical Sciences
Saturday, May 24, 2008
A Little Boy
I would have loved to interview this boy but the traffic suddenly moved on and the jeepneys and cars began to rush forward. The intrepid child beat a hasty retreat and scampered in between vehicles trying his best to avoid the rushing automations. In a minute he was gone, lost from my view and into the murky jungle of vehicles and automobiles of Avenida Rizal.
Thursday, May 22, 2008
75,000 People In Love With Obama
Interesting Note: Oregon is, according to the U.S. Census Bureau, more than ninety percent white. Interestingly, that is 40% more white than Mr. Obama is.
Cat scratch disease
Additional clinical information: Six-year-old boy with swollen lymph glands under right-side of jaw. Concern for peritonsillar abscess.
Findings
CT shows a heterogeneously enhancing, right submandibular level I lymph node with several additional smaller, scattered enhancing subjacent lymph nodes. There is overlying infiltration of the subcutaneous fat consistent with cellulitis.
Differential Diagnosis:
- Lymphoma
- Sarcoid
- Cat scratch disease
- TB/histoplasmosis
- Mononucleosis
- Metastatic disease
- Other bacterial infectious processes
Diagnosis: Cat scratch disease
Further clinical probing subsequently revealed recent, unmonitored contact with a cat.
Discussion
Self-limiting infectious disease characterized by painful regional lymphadenopathy following the scratch of a cat (typically a kitten).
Bartonella henselae, (gram-negative bacillus) - determined to be nearly exclusively responsible for CSD.
Epidemiology:
- 22,000 cases of CSD diagnosed annually in US (1993 data).
- 70-90% of CSD cases occur in the fall and early winter months. (presumed to be due to a midsummer rise in kitten births accompanied by increased flea infestation).
- M:F 3:2
- < 21 years of age (80% of cases)
Clinical:
- >90% of patients with the disease report recent contact with a cat, usually a kitten.
- Incubation period of 3-12 days is followed by the development of one or more cutaneous papules or pustules at the inoculation site.
- Primary lesion lasts for 1-3 weeks then recedes as regional lymphadenopathy appears, generally immediately proximal to the inoculation site.
- Regional lymphadenopathy, (approx. 90%) - most notable manifestation (usually prompts medical evaluation).
- Lymphadenopathy primarily involves axillary >cervical > inguinal regions.
- Lymph nodes are often painful and spontaneously suppurate in 25-30% of cases.
- Constitutional symptoms (usually mild); include malaise, low-grade fever, anorexia, nausea, fatigue, or headache.
- Erythematous, tender papules or pustules at inoculation site.
- Tender unilateral lymphadenopathy (>90%); 50% have involvement of a single node, 30% have involvement of nodes in multiple sites, and 20% with involvement of several nodes in the same region.
- Routine laboratory tests are usually unremarkable and unlikely to aid in diagnosis. Mild leukocytosis and elevated ESR are common but nonspecific.
- Indirect fluorescent antibody (IFA) for Bartonella (84-88% sensitive and 94-96% specific), and rising immunoglobulin G (IgG) titers (titers above 1:64 supportive) provide laboratory confirmation of diagnosis. PCR from lymph node biopsy provides even more sensitive detection of disease.
- Self-limiting disease with excellent prognosis, even in patients with profound manifestations - usually resolves spontaneously over 2-5 months with rare permanent sequelae. However, immunocompromised patients may experience a dramatic and potentially life-threatening course of disease.
- Management primarily symptomatic. Antibiotics not indicated in most cases, but may be considered for severe or systemic disease.
Radiographic Overview of Diagnosis:
- Non-specific unilateral regional lymphadenopathy at/proximal to the site of inoculation.
Monday, May 19, 2008
Hepatocellular Carcinoma with Inferior vena cava invasion
Sunday, May 18, 2008
Aneurysmal Bone Cyst of Talus
Saturday, May 17, 2008
CT scan findings in Otzi the Iceman-Radiology providing insight into archaeology
“lesion of a close-to-the-shoulder artery has been found… lesion of the dorsal wall of the left subclavian artery, the artery underneath the clavicle, caused by an earlier, already-detected arrowhead that remains in the back. In addition, a large haematoma could be visualized in the surrounding tissue. By incorporating historic as well as modern data on the survival ship of such a severe lesion, the scientists concluded that the Iceman died within a short time due to this lesion.”
Images and details here-
Anthropology.net
Avascular Necrosis of the Hip
T1-weighted images: A peripheral band of low signal is present in the superior portion of the femoral head outlining a central area of bone marrow.
T2-weighted images: The inner border of the peripheral band demonstrates high signal. This is termed the double-line sign and is pathognomonic for AVN.
Classification of the AVN lesion
Class A: Central osteonecrotic focus signal analogous to that of fat.
Class B: Central osteonecrotic focus signal analogous to that of blood.
Class C: Central osteonecrotic focus signal analogous to that of fluid.
Class D: Central osteonecrotic focus signal analogous to that of fibrous tissue
Thursday, May 15, 2008
Pneumothorax after Central Line Placement
Dr.Sumer K Sethi, MD
Consultant Radiologist ,VIMHANS and CEO-Teleradiology Providers
Editor-in-chief, The Internet Journal of Radiology
Director, DAMS (Delhi Academy of Medical Sciences
Wednesday, May 14, 2008
Brain metastasis
Additional clinical history: The patient has lung cancer and recently developed severe headaches.
Findings
CT shows a hyperdense lesion in the suprasellar region with significant ventriculomegaly. Intraventricular air. Right frontal approach ventriculostomy tube also present. MR shows lesion is localized to pituitary stalk and hypothalamus without definite extension into body of pituitary gland. There is extension into the third ventricle causing hydrocephalus. No restricted diffusion. Lesion enhances and shows posterior hemorrhage on gradient sequences.
Differential Diagnosis:
- Pituitary adenoma
- Meningioma
- Lymphoma
- Metastatic lesion
- Thrombosed basilar tip aneurysm
- Colloid cyst
Diagnosis: Brain metastasis (CSF cytology consistent with metastatic disease)
Key Points
Metastases to the pituitary gland as a whole are rare.
Most commonly breast and lung cancer (2/3) as part of widespread metastases.
Usually to posterior lobe of the pituitary.
Most common presenting symptom is diabetes insipidus, however most are clinically silent.
Often indolent course.
Mimic pituitary adenoma, abscess, aneurysm, and any other variety of suprasellar lesions.
On CT, iso- or hyper dense mass with some enhancement. On MR, iso- or hypo intense on T1 and hyper intense on T2-weighted images with homogeneous post-gado enhancement (clearly not specific).
Metastases to the pituitary infundibulum are especially rare and also usually of lung or breast origin. They invade locally and are also indolent.
Primary tumors of the infundibulum are rare, but include pituicytomas, other astrocytomas, ependymomas, and pleomorphic xanthoastrocytomas.
Metastatic lesions to pituitary stalk have been described extending superiorly into the hypothalamus.
Metastases to the hypothalamus alone without pituitary involvement is almost never described.
Persistent hypoglossal artery
Findings
Axial images demonstrate abnormal bifurcation of the right internal carotid artery, giving rise to a persistent hypoglossal artery, which is seen entering the hypoglossal canal.
Figure 1: Abnormal bifurcation of the right internal carotid artery.
Figure 2: Abnormal bifurcation of the right internal carotid artery.
Figure 3: Persistent right hypoglossal artery entering through the hypoglossal canal.
Figure 4: Persistent right hypoglossal artery entering through the hypoglossal canal and forming the right vertebral artery.
Sagittal images demonstrate abnormal bifurcation of the right internal carotid artery, giving rise to a persistent hypoglossal artery, which is seen entering the hypoglossal canal.
Figure 5: Abnormal bifurcation of the right internal carotid artery.)
Figure 6: Persistent right hypoglossal artery entering through the hypoglossal canal.
Figure 7: Bifurcation of ICA and persistent hypoglossal artery.
Figure 8: Persistent hypoglossal artery entering hypoglossal canal at the occipital condyle.
Figure 9: Angiogram from a different patient. Arrow points to the origin of the presistent hypoglossal artery. Please note the absence of vertebral arteries originating from the subclavian arteries.
Figure 10: Injection of left ICA opacifies a large persistent hypoglossal artery, shown to pass through the hypoglossal canal. It perfuses the entire posterior circulation.
Diagnosis: Persistent hypoglossal artery
Persistent carotid-basilar artery anastomosis occurs when there is failure of regression of the otic, hypoglossal, trigeminal and proatlantal intersegmental segments formed early during embryogenesis at day 24-28. These connections form to provide blood to the hindbrain while the posterior circulation and vertebral arteries develop.
The otic artery regresses first at the 4th week of gestation. The hypoglossal, trigeminal and proatlantal intersegmental arteries all regress by the 7th to 8th week of gestation.
Persistent trigeminal artery is the most common persistent carotid-basilar anastomosis with an incidence of 0.1-0.2% Persistent hypoglossal artery is the second most common with an incidence of 0.03-0.26%. Approximately 40 cases of persistent proatlantal intersegmental artery have been reported. Most rare is the persistent otic artery, of which there are only two well documented cases.
Persistent hypoglossal artery typically originates from the cervical portion of the ICA at the C1–C2 level and continues medially and posteriorly to enter the skull through the hypoglossal canal in conjunction with the XII nerve. With persistent carotid-basilar anastomoses the vertebral arteries are usually absent or severely hypoplastic, and there are no posterior communicating arteries. Persistent hypoglossal artery is associated with aneurysms due to the abnormal flow dynamics that often accompany this anatomical variant. They are also associated with arteriovenous malformations. It is also important to identify this anatomical variant before any endarterectomy or skull base surgery is performed as the posterior circulation is dependent on the anterior circulation.
At the 4–5mm embryonic stage bilateral longitudinal neural arteries (arrows)—one set of longitudinal neural arteries, dorsal aorta, and cervical intersegmental arteries is shown—are supplied by trigeminal artery (TA), otic artery (OA), hypoglossal artery (HA), proatlantal intersegmental artery (PA), and cervical intersegmental arteries. Internal carotid artery (ICA), external carotid artery (ECA), aortic arch (AA), dorsal aorta (DAo) and ventral aorta (VAo) are also labeled.
Basilar Artery Dissection-MRA
Reference- Z Han et al China. In Hongkong med journal Vol 13 No 2, Apr 2007
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Dr.Sumer K Sethi, MD
Consultant Radiologist ,VIMHANS and CEO-Teleradiology Providers
Editor-in-chief, The Internet Journal of Radiology
Director, DAMS (Delhi Academy of Medical Sciences