Radiology

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Tuesday, 25 November 2008

Strike may cause hospital disruption

Posted on 23:30 by Unknown

  • Nick Miller
  • November 26, 2008

ELECTIVE surgery and outpatient appointments at some Victorian hospitals could be hit by cancellations for the rest of the week, because of industrial action by imaging staff.

Employees of Symbion Imaging, which does X-rays, ultrasounds and other medical imaging for the Northern and Broadmeadows public hospitals, the Epworth in Richmond and 30 other private hospitals and clinics, voted to take industrial action yesterday.

From today until the end of Friday, striking staff will work on imaging only for emergency patients, said Health Services Union national secretary Kathy Jackson. "If it is elective, rather than urgent, it won't be done," she said.

Symbion's staff, including radiographers, administrative workers and technicians, were frustrated by a long-running enterprise bargaining process.

"This is one of the worst employers I have ever dealt with," Ms Jackson said. "For months, they were not prepared to negotiate, then last week they offered a 2 per cent first-and-final offer. They are ripping their staff off." The Age attempted to contact Symbion and its parent, Primary Health Care, but calls were not returned.

However, hospitals contacted by The Age differed on the expected effect of the action.

A spokesman for Northern Health, which includes the Northern Hospital and Broadmeadows, said imaging staff involved in the action had agreed to perform X-rays that were deemed "medically urgent".

"We don't know what will be deemed medically urgent — it will be discussed between medical staff and radiologists," he said. "There will be no impact on emergency or ICU (intensive care) or (operating) theatre. It will be more other inpatient and outpatient services deemed not medically urgent." He believed elective surgery would go ahead.

A spokeswoman for the Epworth said: "We believe there will be no major disruption."

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Wednesday, 19 November 2008

HEALTH & MEDICAL LEGISLATION New South Wales, Australia

Posted on 11:32 by Unknown
 

Civil Liability Act 2002 (NSW)

An Act to make provision in relation to the recovery of damages for
death or personal injury caused by the fault of a person; to amend the
Legal Profession Act 1987 in relation to costs in civil claims; and for
other purposes.


Compensation to Relatives Act 1897 (NSW)

An Act to consolidate enactments relating to compensation to relatives of person's killed by accidents.


Human Tissue Act 1983 (NSW)


Limitation Act 1969 (NSW)

An Act to amend and consolidate the law relating to the limitation of
actions; to repeal section 5 of the Imperial Act known as the Common
Informers Act 1588 and certain other Imperial enactments; to repeal the
unrepealed portion of the Act passed in the fourth year of the ...


Minors (Property and Contracts) Act 1970 (NSW)


Health Administration Act 1982 (NSW)


Health Care Complaints Act 1993 (NSW)


Human Tissue Act 1983


Medical Practice Act 1992 (NSW)


Mental Health Act 2007 (NSW)


Privacy and Personal Information Protection Act 1998 (NSW)



 


 

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Virtual Colonoscopy: A Storm is Brewing

Posted on 10:38 by Unknown

Virtual Colonoscopy: A Storm is Brewing

David J. Vining, MD

Appl Radiol. 2008;37(11):12-16.

Abstract and Introduction

Abstract

The
author performed the first virtual colonoscopy (VC) in 1993. In this
article, he addresses the issues related to the turf battles between
radiologists and gastroenterologists in the use of this technology.
Reviewing common myths associated with VC, he warns that radiologists
must retain expertise in this area.

Introduction

A storm
is brewing around virtual colonoscopy (VC) and whether radiologists or
gastroenterologists will ultimately control this technology. Imagine
the following: in the near future, a patient who requires colorectal
cancer (CRC) screening walks into a local gastroenterologist's office,
obtains a VC examination, which is read by a nurse practitioner, and,
following consultation with a gastroenterologist, undergoes immediate
optical colonoscopy (OC) for evaluation of tiny polyps that either
cannot be found or turn out to be residual feces. Meanwhile, a
radiologist working with this practice interprets the CT data for
extracolonic findings in exchange for a small percentage of the total
professional fee. The patient's insurance (ie, Medicare) is billed for
both the VC and OC, which taxpayers ultimately pay. If this sounds
far-fetched, read on....

Virtual Colonoscopy Development

Colorectal
cancer is the second leading cause of cancer death in the United
States, but it is also one of the most preventable when screening is
used to detect and treat early disease. The 5-year survival rate for
early stage I CRC is 93%, but when it metastasizes to distant organs
and becomes stage IV disease, the survival rate decreases to 8%.[1]
Unfortunately, many adults over the age of 50 do not undergo screening,
and, as a result, CRC is more often diagnosed in advanced stages.[2] Virtual colonoscopy offers the public a more appealing and less invasive alternative for screening.

I
performed the first VC, also known as CT colonography (CTC), at the
Wake Forest University Health Sciences Center in 1993. It has taken
nearly 15 years for VC to mature and gain acceptance by policy makers.
The basic technique consists of: 1) bowel cleansing and stool tagging,
2) gas insufflation of the colon, 3) CT scanning of the abdomen/pelvis,
and 4) 2- and 3-dimensional image analysis of the data to identify
polyps and masses (Figure 1). The first VC examination took 60 seconds
to scan a patient using a single-slice helical CT scanner and nearly 8
hours to process the data for a fly-through, but today multidetector CT
scanners acquire the data in a few seconds, and processing occurs in
real time using inexpensive computers.


Despite the technological advances that have occurred during the past decade (eg, CO2
insufflation, multidetector CT scanners, stool tagging,
computer-assisted diagnosis), a strong lobbying effort on the part of
gastroenterologists has delayed the availability of VC in the United
States. Since Congress approved reimbursement for CRC screening in the
1997 Balanced Budget Act, the number of colonoscopies conducted
annually in the United States has increased from 4 million in 2000 to
>14 million in 2002.[3]

Handwriting on the Wall

Clinical
trials that compared VC with OC have shown a dramatic improvement in VC
accuracy in the last few years, culminating in 2 major trials that were
announced in September 2007. The ACRIN National Colonography Trial
enrolled over 2500 patients at 15 sites, and it reported that VC had a
90% sensitivity for the detection of polyps >10 mm.[4] Within a week, Kim[5]
published a study comparing VC screening in 3120 patients with OC
screening in 3163 patients. Remarkably, VC and OC found an equivalent
number of advanced adenomas in each group; more surprisingly, a larger
number of cancers were found in the VC group.[5] These 2
studies plus multiple prior published trials from the United States and
abroad led the American Cancer Society, the American College of
Radiology (ACR), and the United States Multi-Society Task Force to
incorporate VC in its screening recommendations that were published in
March 2008.[6]

As VC has gained acceptance,
gastroenterologists now realize that VC will impact their practice.
After years of bashing VC as not being good enough and requiring more
clinical data, the Future Trends Committee of the American
Gastroenterological Association (AGA) published a report in October
2006 stating that they see the handwriting on the wall.[7]
This Committee proposed that gastroenterologists should position
themselves to play a role in performing and interpreting VC, including
advocating for CPT codes in the 91000 series that will allow
gastroenterologists to be reimbursed for interpreting and providing VC
services, as well as developing specialized training and training
requirements for those interested in performing VC interpretation. In
an effort to make good on its promise, the AGA published a set of
guidelines in 2007 listing the minimum requirements that a
gastroenterologist must satisfy in order to become certified to read VC
examinations.[8]

Battle Lines are Drawn

Currently
the Centers for Medicare and Medicaid Services (CMS) approve
reimbursement for VC only when it follows a failed "diagnostic"
colonoscopy, not a failed "screening" colonoscopy (Figure 2).[9]
Following the inclusion of VC in the American Cancer Society's
screening guidelines, CMS launched a National Coverage Analysis for
Screening Computed Tomography Colonography for Colorectal Cancer
(CAG-00396N) in May 2008. This seeks to expand reimbursement for
screening indications. The final report of this analysis is due in
February 2009.[10] Expanded reimbursement could have a huge
impact on increasing screening and reducing CRC deaths, but it could
also have substantial economic consequences for CMS and taxpayers. A
public comment period held May-June 2008 drew responses from many
individuals and organizations, including the ACR and the AGA. Of
course, the ACR is in favor of expanded reimbursement, but the AGA
stated that it would support VC only if certain conditions were met,[11] including:

1. Reporting of
ALL polyps (which is contradictory to the ACR Practice Guideline for
the Performance of CTC in Adults that states reporting of polyps <5
mm is not recommended because of the low incidence of those lesions
having malignant potential);[12]

2. Allowing patients in consultation with their physician to determine whether or not to remove those polyps; and

3.
Enacting a coverage policy that would encourage rapid follow-up
procedures (ie, colonoscopy) and that correspondingly would not create
a disincentive for physicians (ie, gastroenterologists) who refer those
procedures.

Reading between the lines, if such conditions are
approved by CMS, then the gastroenterologists will have an unrestrained
ability to perform colonoscopy on any little lump or bump that they
might discover if they or their clinical assistant should be allowed to
read VC exams. It is also the position of many prominent
gastroenterologists to create a split-fee arrangement with radiologists
so that radiologists will be relegated to reading only the extracolonic
portions of a CT scan for a small portion of the professional fee, and,
if radiologists refuse to participate, then they will outsource
radiology services, even to foreign providers![13]

Dispelling Popular Myths

Gastroenterologists frequently try to discredit VC with the following myths:

1. Colonoscopy is the "gold standard."
There are no published studies to validate this claim. In fact, studies
comparing back-to-back colonoscopies on the same patients have reported
OC miss rates of 22% for polyps, even in the hands of expert
endoscopists.[14] Studies such as Pickhardt's[15]
landmark VC study have shown VC to outperform OC. Finally, the accuracy
of screening colonoscopy has been shown to be dependent on how much
time a gastroenterologist spends performing the examination.[16]

2. If VC finds a polyp, then colonoscopy is needed for polyp removal, so why not undergo colonoscopy in the first place?
The vast majority of polyps are benign, hyperplastic polyps, and <5%
of the asymptomatic screening population has a significant adenomatous
polyp.[5] Hence, if OC is the primary screening method, then
>95% of the asymptomatic population would under go OC unnecessarily
with its inherent risks of bowel perforation and anesthesia.

3. The radiation dose associated with VC is prohibitive.
Radiation dose is a valid concern, but researchers are striving to
mitigate this risk by using low-dose techniques, even as low as 10 mAs
(compared with a conventional CT scan that might use a dose of 200 mAs).[17]
Hence, the radiation risk from VC with low-dose techniques can be on
the order of 1 to 2 mSv, which is far below the range that has been
associated with potential cancer and multidetector CT use.[18] Alternatively, VC can be performed using MRI, but the availability of MRI scanners is a temporary hurdle, at least for today.

Actions to Take

Radiologists
are already overworked due to the exponential increase in imaging
studies during the past decade, and as a result, we have become
complacent about the ownership of new technologies. In the meantime,
gastroenterologists are purchasing CT scanners and attending training
programs to get ready for CMS approval of reimbursement for VC
screening.[19] However, if radiologists act quickly and take
certain steps to position ourselves to maintain control of VC, we will
not risk losing this technology, as we have done with cardiac imaging.
Some initiatives include:

1. Taking a stronger, vocal interest in
VC. Radiologists are better trained to read an entire CT examination,
especially when disease crosses organ boundaries to involve both the
colon and adjacent anatomy. We need to establish ourselves as the
imaging experts in order to counter claims that endoscopists and nurse
practitioners are as good as radiologists in reading VC exams.[20]

2.
Beginning a dialogue with community gastroenterologists and primary
care physicians. Radiology practices need to be willing to provide
same-day, on-demand VC services for failed "diagnostic" colonoscopy
examinations in advance of the anticipated reimbursement for screening
VC.

3. Developing practice guidelines for appropriately
working-up extracolonic findings. Perhaps offering immediate but
limited ultrasound evaluation to resolve indeterminate liver and renal
lesions will help to mitigate the gastroenterologists' cry that they
should be the ones performing VC in their offices.

4. Providing
consistent, high-quality reports of VC findings that can be rapidly
delivered to the patient and referring clinician. Utilization of the CT
Colonography Reporting and Data System (C-RADS) and participation in
the ACR's CTC Registry will help to strengthen our position in the
field.[21,22]

5. Challenging any proposals by
gastroenterologists to split the professional fee for reading colonic
and extracolonic portions of a VC CT scan, including legislative
lobbying if necessary. There are many problems with fee-splitting
arrangements, not the least of which is malpractice
liability—radiologists will certainly be held liable when
gastroenterologists fail to make a correct diagnosis if they should be
allowed to interpret only the intraluminal portion of a VC scan.

All is Not Lost, at Least Not Yet

Much
of the rhetoric coming from the gastroenterology community is coming
from a few but very vocal and rabid gastroenterologists. In fact, a
survey of 2400 AGA members regarding their interest in VC resulted in
only 588 responses, of which one third said that they would want to
perform VC, another third said that they would not perform it but would
support their colleagues, and the final third said that
gastroenterologists should not perform VC.[23] In reality,
radiologists and gastroenterologists will need to work together along
with surgeons and oncologists to provide comprehensive CRC screening
and treatment services. If CRC screening really takes off, then there
will not be enough gastroenterologists available in this country to
perform the necessary therapeutic colonoscopies that will be generated.
Although radiologists specializing in VC may eventually become
employees of large, multispecialty clinics specializing in colorectal
disease, it is paramount that the role and expertise of the radiologist
be maintained.

References

  1. O'Connell
    JB, Maggard MA, Ko CY. Colon cancer survival rates with the new
    American Joint Committee on Cancer sixth edition staging. J Natl Cancer Inst. 2004;96:1420-1425.
  2. Centers
    for Disease Control and Prevention. Colorectal (colon) cancer.
    Available online at:
    http://www.cdc.gov/cancer/colorectal/statistics/screening%5frates.htm.
    Accessed September 15, 2008.
  3. Seeff LC, Richards TB, Shapiro JA,
    et al. How many endoscopies are performed for colorectal cancer
    screening? Results from CDC's survey of endoscopic capacity. Gastroenterology. 2004;127: 1670-1677.
  4. Johnson CD, Chen MH, Toledano AY, et al. Accuracy of CT colonography for detection of large adenomas and cancers. NEJM. 2008;359:1207-1217.
  5. Kim DH, Pickhardt PJ, Taylor AJ, et al. CT colonography versus colonoscopy for the detection of advanced neoplasia. NEJM. 2007;357:1403-1412.
  6. Levin
    B, Lieberman DA, McFarland B, et al. Screening and surveillance for the
    early detection of colorectal cancer and adenomatous polyps 2008: A
    joint guideline from the American Cancer Society, the US Multi-Society
    task force on colorectal cancer, and the American College of Radiology.
    CA Cancer J Clin. 2008;58:130-160.
  7. Regueiro C. Will
    screening colonoscopy disappear and transform gastroenterology
    practice? Threats to clinical practice and recommendations to reduce
    their impact: Report of a consensus conference conducted by the AGA
    Institute Future Trends Committee. Gastroenterology. 2006;131:1287-1312.
  8. Rockey
    DC, Barish M, Brill JV, et al. Standards for gastroenterologists for
    performing and interpreting diagnostic computed tomographic
    colonography. Gastroenterology. 2007;133:1005-1024.
  9. Knechtges
    PM, McFarland BG, Keysor KJ, et al. National and local trends in CT
    colonography reimbursement: Past, present, and future. J Am Coll Radiol. 2007;4:776-799.
  10. Centers
    for Medicaid and Medicare Services. NCA for Screening Computed
    Tomography Colonography (CTC) for Colorectal Cancer (CAG-00396N).
    Available online at: http://www.cms.hhs.gov/ mcd/viewnca.asp?
    where=index&nca_id=220&basket=nca:00396N:220:
    Screening+Computed+Tomography+Colonography+
    %28CTC%29+for+Colorectal+Cancer:Open:New:4. Accessed September 15, 2008.
  11. Sandler
    RS. AGA Institute Comments re: NCA for Screening (CTC) for Colorectal
    Cancer. Available online at: http://www.gastro.org/user-assets/
    Documents/02_Clinical_Practice/CTC/AGA_Institut
    e_comment_ltr_re_CTC_for_CRC_screening_6-18- 08.pdf. Accessed September
    15, 2008.
  12. ACR practice guidelines for the performance of
    computed tomography (CT) colonography in adults. Amended 2006.
    Available online at: http://
    www.acr.org/EducationCenter/ACRFutureClassroom/ct_colonography.aspx.
    Accessed September 15, 2008.
  13. Rex DK. Clinical gastroenterologist's perspective on training in CT colonography. AGA Perspectives. December 2007/January 2008. Available online at: http://www.gastro.org/wmspage.cfm?parm1=4684. Accessed September 15, 2008.
  14. van Rijn JC, Reitsma JB, Stoker J, et al. Polyp miss rate determined by tandem colonoscopy: A systematic review. Am J Gastroenterol. 2006;101: 343-350.
  15. Pickhardt
    PJ, Choi JR, Hwang I, et al. Computed tomographic virtual colonoscopy
    to screen for colorectal neoplasia in asymptomatic adults. N Engl J Med. 2003;349:2191-2200. Comments in: ACP J Club. 2004;141:22-23. CMAJ. 2004;170: 1392. Gastroenterology. 2004;126:1910-1911; discussion 1911-1912. Korean J Gastroenterol. 2004; 43:71-73. N Engl J Med. 2003;349:2261-2264. N Engl J Med. 2004;350:1148-1150; author reply 1148-1150. Rev Gastroenterol Disord. 2005;5: 227-229.
  16. Barclay RL, Vicari JJ, Doughty AS, et al. Colonoscopic withdrawal times and adenoma detection during screening colonoscopy. N Engl J Med. 2006;355;2533-2541.
  17. Iannaccone
    R, Catalano C, Mangiapane F, et. al. Colorectal polyps: Detection with
    low-dose multidetector row helical CT colonography versus two
    sequential colonoscopies. Radiology. 2005;237: 927-937.
  18. Brenner DJ, Hall EJ. Computed tomography—An increasing source of radiation exposure. N Engl J Med. 2007;357:2277-2284.
  19. American
    Gastroenterological Association. CT colonography training for the
    gastroenterologist: A hands-on course. Information available online at:
    http://www.gastro.org/wmspage.cfm?parm1=5599. Accessed September 15,
    2008.
  20. Patrick A, Jackson L, Bell J, Epstein O. High proficiency
    reading of V3D virtual colonoscopy by experienced optical endoscopists
    and endoscopy nurses; A new era in colonoscopy? Gastrointest Endosc. 2007;65:AB129.
  21. Zalis ME, Barish MA, Choi JR, et al. CT colonography reporting and data system: A consensus proposal. Radiology. 2005;236:3-9.
  22. CT Colonography Registry. Available online at: https://nrdr.acr.org/portal/CTC/Main/page.aspx. Accessed September 15, 2008.
  23. Springer J. Members weighing many factors associated with CT colonography. AGA Perspectives. October/November 2006. Available online at: http://www.gastro.org/wmsp. age.cfm?parm1=2788. Accessed September 15, 2008.

David J. Vining, MD
is a Professor of Diagnostic Radiology and the Medical Director of the
Image Processing and Visualization Laboratory, University of Texas M.D.
Anderson Cancer Center, Houston, TX

Disclosure:
Dr. Vining discloses that he has received royalties from Wake Forest
University and Bracco, Inc., for virtual colonoscopyrelated products.
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Tuesday, 11 November 2008

SUPRATENTORIAL BRAIN TUMORS

Posted on 19:10 by Unknown
SUPRATENTORIAL BRAIN TUMORS

John R. Hesselink, MD, FACR and Richard J. Hicks, MD

In the diagnostic work-up of intracranial tumors, the primary goals of the imaging studies are to detect the abnormality, localize and determine its extent, characterize the lesion, and provide a list of differential diagnoses or, if possible, the specific diagnosis. Correlative studies have proved that MR is more sensitive than CT for detecting intracranial masses. Moreover, the multiplanar capability of MR is very helpful to determine the anatomic site of origin of lesions and to demarcate extension into adjacent compartments and brain structures. The superior contrast resolution of MR displays the different components of lesions more clearly. MR can assess the vascularity of lesions without contrast infusion. On the other hand, CT detects calcification far better than MR, a useful finding for differential diagnosis. Gradient-echo techniques improve MR detection of calcification by accentuating the diamagnetic susceptibility properties of calcium salts, but the observed low signal on T2-weighted images is nonspecific, in that any accompanying paramagnetic ions would produce the same effect.

br-300a.gif
br-300a1.gif

Contrast enhancement with gadolinium increases both the sensitivity and specificity of MR. Endnote Gadolinium is a blood-brain barrier (BBB) contrast agent like iodinated agents for CT. It does not cross the intact BBB, but when the BBB is absent or deficient, gadolinium enters the interstitial space to produce enhancement (increased signal) on T1-weighted images. All the collective knowledge learned from contrast-enhanced CT can be applied directly to the gadolinium-enhanced MR images. Although the enhancement patterns are not tumor specific, the additional information is often helpful for diagnosis. Lesions can be classified as homogeneous or heterogeneous, and necrotic and cystic components are seen more clearly. The margins of enhancement provide a gross measure of tumor extension. Endnote Contrast MR is particularly valuable for extra-axial tumors because they tend to be isointense to the brain on plain scan.


CEREBRAL GLIOMAS


Gliomas are malignant tumors of the glial cells of the brain and account for 30-40% of all primary intracranial tumors. They occur predominantly in the cerebral hemispheres, but the brain stem and cerebellum are frequent locations in children, and they are also found in the spinal cord. The peak incidence is during middle adult life, when patients present with seizures or symptoms related to the location of the gliomas and the brain structures involved.

Astrocytomas are graded according to their histologic appearance. Grade 1 astrocytomas have well-differentiated astrocytes and well-defined margins. The clinical course often proceeds over many years and complete cures are possible. The pilocytic variant is a low-grade tumor with a distinct capsule that is commonly found in children. The giant cell astrocytoma is a specialized tumor that develops from pre-existing hamartomas in patients with tuberous sclerosis. Grade 2 astrocytomas are well-differentiated but diffusely infiltrating tumors. The fibrillary type is most common, and although initially benign, they may evolve into a higher grade tumor over time. This changing character of gliomas makes histological classification difficult from sample biopsies, because different parts of the tumor often exhibit varying degrees of malignancy. The higher grade astrocytomas are very cellular and pleomorphic. Anaplastic astrocytomas (Grade 3) are very aggressive tumors, readily infiltrate adjacent brain structures, and have a uniformly poor prognosis. Glioblastoma multiforme (Grade 4) has the added histologic features of endothelial proliferation and necrosis. Multicentric foci of tumor may be seen in 4 to 6% of glioblastomas. Gliomatosis cerebri is an unusual condition with diffuse contiguous involvement of multiple lobes of the brain.

Oligodendrogliomas are the most benign of the gliomas. Calcification is common, and they occur predominantly in the frontal lobes. Endnote The mixed neuronal and glial tumors are found mostly in children and young adults. They are slow-growing and are found predominantly in the temporal lobes and around the third ventricle. Intratumoral cysts and calcification are common. Endnote

The common signal characteristics of intra-axial tumors include high signal intensity on T2-weighted images and low signal on T1-weighted images, unless fat or hemorrhage is present. Fat and subacute hemorrhage (methemoglobin) exhibit high signal on T1-weighted images, and acute hemorrhage (deoxyhemoglobin) and chronic hemorrhage (hemosiderin/ferritin) show low signal intensity on T2-weighted scans. Gliomas have poorly defined margins on plain MR. They infiltrate along white matter fiber tracts, and the deeper lesions have a propensity to extend across the corpus callosum into the opposite hemisphere. They are often quite large by the time of clinical presentation.

The higher grade gliomas, particularly glioblastomas, appear heterogeneous due to central necrosis with cellular debris, fluid, and hemorrhage. Peritumoral edema and mass effect are common features. Following injection of gadolinium, T1-weighted images show irregular ring enhancement, with nodularity and nonenhancing necrotic foci. Endnote As mentioned above, gliomas are infiltrative lesions, and microscopic fingers of tumor usually extend beyond the margin of enhancement. Enhanced scans are particularly helpful to outline subependymal spread of tumor along a ventricular surface, as well as leptomeningeal involvement. Endnote Although highly malignant, anaplastic astrocytomas may or may not exhibit breakdown of the blood-brain barrier. In general, the presence or lack of enhancement alone is not helpful in grading astrocytomas.

The lower grade astrocytomas tend to be more homogeneous without central necrosis. Large cystic components may be present. The cysts have smooth walls, and the fluid is of uniform signal, to distinguish them from necrosis. Enhancement is variable, depending on the integrity of the blood-brain barrier.

Perfusion imaging has shown promise as a technique for determining the grade of intracranial mass lesions. Perfusion imaging relies on a first-pass susceptibility-related signal loss on T2*-weighted images, from which relative cerebral blood flow and volume can be calculated. Several studies have shown a correlation between relative cerebral blood volume and tumor grade, likely due to the relationship of blood volume to vascular proliferation in high-grade gliomas. Endnote


MR Spectroscopy

MR spectroscopy provides a measure of brain chemistry and can help characterize tumors and and grade the degree of malignancy. As a general rule, as malignancy increases, NAA and creatine decrease, and choline, lactate, and lipids increase. NAA decreases as tumor growth displaces or destroys neurons. Very malignant tumors have high metabolic activity and deplete the energy stores, resulting in reduced creatine. Very hypercellular tumors with rapid growth elevate choline. Lipids are found in necrotic portions of tumors, and lactate appears when tumors outgrow their blood supply and start utilizing anaerobic glycolysis. To get an accurate assessment of the tumor chemistry, the spectroscopic voxel should be placed over an enhancing region of the tumor, avoiding areas of necrosis, hemorrhage, calcification, or cysts.

Multi-voxel spectroscopy is best to detect infiltration of malignant cells beyond the enhancing margins of tumors. Particularly in the case of cerebral glioma, elevated choline levels are frequently detected in edematous regions of the brain outside the enhancing mass. Endnote Finally, MRS can direct the surgeon to the most metabolically active part of the tumor for biopsy to obtain accurate grading of the malignancy.

br-300a2.gif

A common clinical problem is distinguishing tumor recurrence from radiation effects several months following surgery and radiation therapy. Elevated choline is a marker for recurrent tumor. Radiation change generally exhibits low NAA, creatine, and choline on spectroscopy. If radiation necrosis is present, the spectrum may reveal elevated lipids and lactate.

MRS cannot always distinguish primary and secondary tumors of the brain from one another. As mentioned above, one key feature of gliomas is elevated choline beyond the margin of enhancement due to infiltration of tumor into the adjacent brain tissue. Most non-glial tumors have little or no NAA. Elevated alanine at 1.48 ppm is a signature of meningiomas. They also have no NAA, very low creatine, and elevated glutamates. Endnote


LYMPHOMA


Primary malignant lymphoma is a non-Hodgkin's lymphoma that occurs in the brain in the absence of systemic involvement. These tumors are highly cellular and grow rapidly. Favorite sites include the deeper parts of the frontal and parietal lobes, basal ganglia, and hypothalamus. Most occur in patients who are immunocompromised secondary to chemotherapy or acquired immunodeficiency syndrome (AIDS) or in organ transplant recipients who are on immunosuppressant drugs. Cerebral lymphomas are very radiosensitive and respond dramatically to steroid therapy.

Lymphomas typically appear as homogeneous, slightly high signal to isointense masses deep within the brain on T2-weighted images. The observed mild T2 prolongation is probably related to dense cell packing within these tumors, leaving relatively little interstitial space for accumulation of water. They are frequently found in close proximity to the corpus callosum and have a propensity to extend across the corpus callosum into the opposite hemisphere, a feature that mimics glioblastoma. Multiple lesions are present in as many as 50%. Despite their rapid growth, central necrosis is uncommon. They are associated with only a mild or moderate amount of peritumoral edema. By time of presentation they can be quite large and yet produce relatively little mass effect, a feature that sets lymphoma apart from glioblastoma and metastases. Intratumoral cysts and hemorrhage are unusual. Most lymphomas show bright homogeneous contrast enhancement. Endnote

The pattern is modified somewhat in AIDS patients. Multiplicity seems to be more common. Moreover, lymphomas exhibit more aggressive behavior and readily outgrow their blood supply. As a result, central necrosis and ring enhancement are often seen in lymphomatous masses in AIDS patients. Endnote On MR spectroscopy, lymphomas exhibit elevated choline little or no NAA.


METASTATIC DISEASE


Metastases to the brain occur by hematogenous spread, and multiple lesions are found in 70% of cases. The most common primaries are lung, breast, and melanoma, in that order of frequency. Other potential sources include the gastrointestinal tract, kidney, and thyroid. Metastases from other locations are uncommon. Clinical symptoms are nonspecific and no different from primary brain tumors. If a parenchymal lesion breaks through the cortex, tumor can extend and seed along the leptomeninges.

Metastatic lesions can be found anywhere in the brain but a favorite site is near the brain surface at the corticomedullary junction of both the cerebrum and cerebellum. They are hyperintense on plain T2-weighted images. Areas of necrosis are prevalent in the larger lesions, accounting for their heterogeneous internal texture. Peritumoral edema is a prominent feature, but multiplicity is the most helpful sign to suggest metastatic disease as the likely diagnosis. Correlative studies have shown MR to be more sensitive than CT for detecting metastases, particularly lesions near the base of the brain and in the posterior fossa. One limitation of plain MR is the frequency of periventricular white matter hyperintensities found in the same older age group at risk for metastatic disease.

Gadolinium enhanced MR has resulted in improved delineation of metastatic disease compared with nonenhanced scans. Moderate to marked enhancement is the rule, nodular for the smaller lesions and ringlike with central nonenhancing areas for the larger ones. Endnote Controlled clinical trials have also shown that contrast-enhanced MR is more sensitive than both plain MR and contrast-enhanced CT for detecting cerebral metastases. In patients with a known primary, T1-weighted enhanced MR is probably sufficient to screen the brain for metastatic disease.

Hemorrhage is present in 3 to 14% of brain metastases, mainly in melanoma, choriocarcinoma, renal cell carcinoma, bronchogenic carcinoma, and thyroid carcinoma. The presence of nonhemorrhagic tissue and pronounced surrounding vasogenic edema are clues to the underlying neoplasm.

Metastatic melanoma has been a topic of special interest in the MR literature because of the presence of paramagnetic, stable free radicals within melanin. The MR appearance is variable depending on the histology of the melanoma and the components of hemoglobin. Most are hyperintense to white matter on T1-weighted scans and hypointense on T2-weighted scans. Atlas and coworkers Endnote observed three distinct signal intensity patterns. Nonhemorrhagic melanotic melanoma was markedly hyperintense on T1-weighted images and isointense or mildly hypointense on T2-weighted images. Nonhemorrhagic amelanotic melanoma appeared isointense or slightly hypointense on T1-weighted scans and isointense or slightly hyperintense on T2-weighted scans. The signal pattern for hemorrhagic melanoma was variable depending on the components of hemoglobin. Some uncertainty remains as to whether the predominant effect on signal intensity within melanomas is due to stable free radicals, chelated metal ions, or hemoglobin.


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INTRAVENTRICULAR TUMORS


The intraventricular location is unique in that many of the tumor types are more commonly associated with extra-axial locations. Patients often present with obstructive hydrocephalus. Most intraventricular tumors are relatively benign and have well-defined margins. As they grow, the tumors expand the ventricle of origin. With malignant degeneration, extension into the brain parenchymal occurs. The primary blood supply to intraventricular lesions is derived from the choroidal arteries.


MENINGIOMA


Meningiomas account for 15% of all intracranial tumors and are the most common extra-axial tumor. They originate from the dura or arachnoid and occur in middle-aged adults. Women are affected twice as often as men. Meningiomas are well-differentiated, benign, and encapsulated lesions that indent the brain as they enlarge. They grow slowly and may be present for many years before producing symptoms. The histologic picture shows cells of uniform size that tend to form whorls or psammoma bodies.

The parasagittal region is the most frequent site for meningiomas, followed by the sphenoid wings, parasellar region, olfactory groove, cerebello-pontine angle, and rarely the intraventricular region. Meningiomas often induce an osteoblastic reaction in the adjacent bone, resulting in a characteristic focal hyperostosis. They are also hypervascular, receiving their blood supply predominantly from dural vessels.

Most meningiomas are isointense with cortex on T1- and T2-weighted images. A heterogeneous internal texture is found in all but the smallest meningiomas. The mottled pattern is likely due to a combination of flow void from vascularity, focal calcification, small cystic foci, and entrapped CSF spaces. Hemorrhage is not a common feature. An interface between the brain and lesion is often present, representing a CSF cleft, a vascular rim, or a dural margin. MR has special advantages over CT in assessing venous sinus involvement and arterial encasement. Occasionally, a densely calcified meningioma is encountered that is distinctly hypointense on all pulse sequences.

Meningiomas show intense enhancement with gadolinium and are sharply circumscribed. Endnote They have a characteristic broad base of attachment against a dural surface. Associated hyperostosis may result in thickening of low signal bone as well as diminished signal from the diploic spaces. Although meningiomas are not invasive, vasogenic edema is present in the adjacent brain in 30% of cases. Contrast scans are especially helpful for imaging the en plaque meningiomas that occur at the skull base. MR spectroscopy shows elevated alanine and glutamates, no NAA, and markedly decreased creatine.


PINEAL REGION TUMORS


Tumors in the pineal region can be classified into three major groups based on their origin: germ cell, pineal parenchyma, and parapineal. Germinoma is the least differentiated of the germ cell group. It occurs in children and young adults and accounts for more than 50% of all pineal region tumors. The other germ cell tumors include embryonal carcinoma, yolk-sac tumor, and choriocarcinoma. Differentiation along three germ layers results in a teratoma. The true pinealomas consist of pineoblastoma and pineocytoma. Pineoblastoma is an embryonal tumor of neuroectoderm, related to neuroblastoma and medulloblastoma, and is found primarily in young children. Pineocytomas are less cellular and exhibit benign behavior. The parapineal lesions include gliomas of the tectum and posterior third ventricle, meningiomas arising within the quadrigeminal cistern, and developmental cysts (epidermoid, dermoid, arachnoid cyst). Endnote

The clinical expression of these tumors is usually related to mass effect upon adjacent brain structures. Hydrocephalus secondary to aqueductal obstruction is a common presentation. Compression of the tectum of the midbrain can produce paralysis of upward gaze, the classic Parinaud's syndrome. Germinomas and gliomas have a propensity to grow into the third ventricle and compress the hypothalamus, resulting in endocrine dysfunction. Dissemination through the CSF pathways is a known complication of pineoblastoma and germinoma.

Pineal germinomas and primary pineal tumors are most often isointense with the brain on T1- and T2-weighted images. A few lesions exhibit long T1 and T2, which may correlate with embryonal cell elements. Despite this relative lack of contrast, with multiplanar imaging plain MR delineates pineal region masses better than CT, showing the relationships of the tumor to the posterior third ventricle, vein of Galen, and aqueduct. Endnote These tumors are well defined and enhance to a moderate degree, usually without central necrosis, cystic change, or hemorrhage. Enhanced scans are essential to assess CSF spread of tumor. In young patients with germinoma, the difficulty of visualizing calcium is a disadvantage of MR, as this may be the only evidence of tumor. Endnote

Meningiomas can appear very similar on plain scan, but their intense enhancement may set them apart from other lesions. Gliomas infiltrate the tectum and posterior walls of the third ventricle. They tend to be poorly circumscribed and produce symptoms earlier. Edema is not a consistent finding, and enhancement is variable. Larger gliomas in the splenium of the corpus callosum may present as pineal region masses.

Teratomas are of mixed signal intensity, frequently with calcification. They may also have cystic components and fat. Arachnoid cysts, epidermoid and dermoid tumors can usually be distinguished from other pineal region tumors by their increased signal on T2-weighted images.

Pineal cysts were visualized in 4.3% of normal patients in one MR study. Endnote These apparently benign lesions are seen best as areas of high signal on intermediate T2-weighted images. They are not associated with hydrocephalus or a pineal mass and are not clinically significant.


BENIGN CYSTIC MASSES


Cystic lesions occur most often in the basal cisterns, a midline location or within the ventricular system. They include arachnoid cyst, dermoid, epidermoid, and neuroepithelial cysts, including colloid cyst. These lesions are interesting in that their MR appearance is quite distinct from solid masses. Their signal characteristics depend to a large extent on the cyst contents, but associated solid components may also have specific features.


Arachnoid Cyst

Arachnoid cysts are CSF-containing cysts that are found in the middle fossa, posterior fossa, suprasellar cistern, or near the vertex. They are benign but slowly grow as they accumulate fluid, compressing normal brain structures. Remodeling of the adjacent skull is an important clue for a benign expansile process.

Arachnoid cysts are smoothly marginated and homogeneous. They are not calcified and do not enhance. The multiplanar capability of MR is particularly helpful in establishing the exact location, and the diagnosis is supported by the cyst fluid being isointense with CSF on all pulse sequences. Endnote The cysts may appear higher signal than CSF on intermediate T2-weighted images. The exact reason for this is uncertain, although it may reflect dampening of the CSF pulsations that normally results in signal loss in the ventricles and cisterns. This effect will be less apparent with pulse sequences that incorporate flow compensation techniques.


Epidermoid Cyst

Epidermoid cysts are referred to as "pearly tumors" because of their glistening white appearance at surgery. They arise from epithelial cell rests in the basal cisterns. They are benign and grow slowly along the subarachnoid spaces and into the various crevices found at the base of the brain. Intradural epidermoids are usually quite large with lobulated outer margins and an insinuating pattern of growth. They have a heterogeneous texture and variable signal intensity on MR. Endnote Most are slightly higher signal than CSF on both T1 and T2-weighted images. An occasional epidermoid has a very short T1 and appears bright on T1-weighted images. The heterogeneous signal pattern is likely related to varying concentrations of keratin, cholesterol, and water within the cyst, as well as the proportion of cholesterol and keratin in crystalline form. Calcification is sometimes present. Epidermoid tumors do not enhance with contrast.


Dermoid Cyst

Dermoid cysts have both dermal and epidermal derivatives, accounting for their more varied histologic and MR appearance. They are primarily midline lesions, occurring in the pineal and suprasellar regions. Dermoids have some distinctive features on MR. They tend to be heterogeneous owing to the multiple cell types within them. Fatty components are common, producing high signal on T1-weighted images. On axial and sagittal scans, a fat-fluid level may be seen, or a level between fat and matted hair within the cyst. Rupture of a dermoid and leakage of cyst contents into a ventricle or subarachnoid space may produce an ependymitis or meningitis, respectively.

Lipomas are also midline lesions and are often associated with partial or complete agenesis of the corpus callosum. Occasionally, an incidental lipoma will be found in the region of the quadrigeminal plate or cerebellopontine angle.


Colloid Cyst

Colloid cysts originate from primitive neuroepithelium within the roof of the anterior third ventricle. They are positioned just posterior to the foramina of Monro between the columns of the fornix. Histologically, they consist of a thin, fibrous capsule with an epithelial lining. The cysts contain a mucinous fluid with variable amounts of proteinaceous debris, blood components, and desquamated cells.

Colloid cysts are smoothly marginated spherical lesions without surrounding brain reaction. Two signal patterns have been reported on MR scans and correlated with their CT features. Those that are low density on CT are isointense on T1-weighted images and hyperintense on T2-weighted images, probably indicating a fluid composition similar to CSF. Most colloid cysts are isodense or slightly hyperdense on CT. The MR counterpart is a high signal capsule and a hypointense center on T2-weighted images. The signal characteristics of the fluid depend on the protein content of the cyst fluid and is similar to that observed in sinonasal secretions. Endnote

Dilatation of the lateral ventricles is a common finding, and the enlargement may be unequal owing to asymmetric positioning of the cyst at the foramina of Monro. The expanding cyst also enlarges the anterior third ventricle, but the posterior third, aqueduct, and fourth ventricle should be normal. Following contrast infusion, colloid cysts may show ring enhancement, due to either enhancement of the cyst wall or choroid plexus draped around the cyst.


REFERENCES

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Thursday, 6 November 2008

ESGAR CT COLONOGRAPHY WORKSHOP FEB 2-4 HARROGATE, UK

Posted on 04:15 by Unknown
Preliminary Programme

Group I: Monday, February 2, 2009 Day 1

Group II: Tuesday, February 3, 2008 Day 1





08:00 – 08:25 Registration



08:25 – 08:30 Introduction: Presentation of the workshop programme

A. Laghi (Latina/IT)



08:30 – 08:45 Introduction State-of-the-art CT-Colonography

D. Burling (London/UK)



08:45 – 09:10 Polyps and Colorectal Cancer (Gastroenterologist’s view)

James East (London/UK)



09:10 – 10:30 Technical basis of CTC: Preparation, image acquisition, complications

Chairman: S.Taylor (London, UK)



09:10 – 09:30 Bowel preparation and faecal tagging

P. Lefere (Roeselare/BE)



09:30 – 09:50 Practical Issues (technique, insufflation)

J. Stoker (Amsterdam/NL)



09:50 – 10:10 Image acquisition: technical parameters

P. Rogalla (Berlin/DE)



10:10 – 10:30 Complications (Perforation, cardiovascular effects)

S. Taylor (London/UK)



10:30 – 11:00 Coffee



11:00 – 12:40 2D - 3D First approach: face to face

Chairman: S. Halligan (London/UK)



11:00 – 11:20 Basic reading technique, primary 2D and 3D, normal anatomy,

C. Kay (Bradford/UK)



11:20 – 11:40 Pitfalls in interpreting CTC

S. Gryspeerdt (Roeselare/BE)



11:40 – 12:00 Teaching on workstation – easy case (based on ESGAR study)

A. Lowe (Bradford/UK)



12:00 – 12:45 Panel discussion: Q&A

Moderator: A. Laghi (Latina/IT)

Panellists: all speakers of previous three sessions.



12:45 – 14:15 Lunch



14:15 – 16:15 CTC: clinical application

Chairman: R. Frost (Salisbury/UK)



14:15 – 14:35 Study results and indications

A. Laghi (Latina/IT)



14:35 – 14:55 Extra-colonic findings

M. Hellström (Göteborg/SE)



14:55 – 15:15 How to report CTC

E. Neri (Pisa/IT)



15:15 – 15:30 How to set up a CTC service

M. Morrin (Dublin/IRE)



15:30 – 16:15 Panel discussion: Q&A

Moderator: R. Frost (Salisbury/UK)

Panellists: All speakers



16:15 – 17:00 Coffee





17:00 – 18:00 TWO PARALLEL SESSIONS:





17:00 – 18:00 CAD

Moderator: S.Halligan (Harrow/UK)



Technique and results (17:00 – 17:20)

D Regge (Turin/IT)



Integration of CAD in the workflow (17:20 – 17:40)

A. Graser (Munich/DE)



Panel discussion: CAD (17:40 – 17:50)



17:00 – 18:00 Basic teaching on workstation in hands-on workstation room

(in parallel to CAD Session)

Lead: T. Mang (Vienna/AT), A. Gupta (London/UK)







18:00 – 19:00 Moderator: D.Tolan (Leeds/UK)



Workstations are available for participants for individual familiarisation

(Application Specialists are available for questions)

Workstation Room









Group I: Tuesday, February 3, 2009 Day 2

Group II: Wednesday, February 4, 2009 Day 2




08:30 – 09:30 Familiarisation with the different workstations available for the hands-on sessions

Moderator: D.Tolan (Leeds/UK)

Introduction of the tutors and the application specialists



Introduction of each vendor by application specialists. Explanation of workflow



Teaching on workstations

(20 min for cases review on workstation + 10 min for review with faculty)



09:30 – 10:30 Cancer cases



09:30 – 10:15 Cancer cases for review

Participants to review specific cases



10:15 – 10:30 Case review and discussion

D. Hock (Liege/BE)



10:30 – 11:00 Coffee



11:00 – 12:00 Polyp cases



11:00 – 11:45 Polyp cases for review

Participants to review specific cases



11:45 – 12:00 Case review and discussion

F. Iafrate (Rome/IT)



12:00 – 13:00 Difficult cases



12:00 – 12:45 Difficult cases for review

Participants to review specific cases



12:45 – 13:00 Case review and discussion

A. Gupta (London/UK)



13:00 – 14:15 Workstations face to face (Lunch Symposium)

Moderation: G. Maskell (Truro/UK)



14:15 – 15:15 “Blind” case reviews



14:15 – 15:00 “Blinded” Cases

Participants to review specific cases



15:00 – 15:15 Case review and discussion

P. Wylie (London/UK)



15:15 – 16:15 Hands-on session: free

(Participants to use syllabus for findings and to address queries to faculty)



16:15 – 16:45 Coffee



16:45 – 17:15 2 cases prize competition

F.Iafrate/ S.Taylor (Berlin/DE)



17:15 – 17:25 Complete evaluation forms and submit them at the registration desk
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