24.9.09

Dysplasia in Inflammatory Bowel Disease

As we all know, chronic inflammatory bowel disease (IBD) presents a risk for dysplasia and subsequent malignancy in patients with long standing disease.
The risk for adenocarcinoma increases with a number of factors including

  • the linear extent of disease within the bowel,

  • early age at onset of disease,

  • severity of disease and duration of disease.
The pathologic reporting of endoscopic biopsy specimens with inflammatory bowel disease must convey the information the clinician needs in a clear and consistent manner in order to properly manage the patient's disease.
Every biopsy report should, of course, give an assessment of the disease activity and distribution. In addition, the pathologist must render an opinion on the presence or absence of dysplasia. The "second line" diagnosis must reflect one of three choices regarding dysplasia in the biopsy:

1. Negative for dysplasia
2. Indefinite for dysplasia
3. Positive for dysplasia
  • Low grade
  • High grade
Agreeing on the terminology is relatively easy. Agreeing on the morphologic presence or absence of dysplasia is another issue.
Studies have shown poor interobserver reproducibility with regard to recognizing and diagnosing dysplasia. Low grade dysplasia (LGD), as one might guess, suffers from the worst interobserver variability.


The more marked the cytologic changes (high grade dysplasia) the easier it is to recognize and agree upon amongst pathologists.


This variability is one reason that many suggest surveillance for LGD. The histologic parameters which define dysplasia in the colon are consistent regardless of the subtype of IBD - Crohn's colitis or ulcerative colitis.

Negative for dysplasia
The lack of dysplasia in a chronic IBD biopsy is stated as "negative for dysplasia". That phrase should be included in biopsies that are completely normal or indistinguishable from non-IBD biopsies. This could be found in biopsies obtained from an area of the colon that is not affected by the disease or in an area that is completely quiescent perhaps from treatment.


Reactive changes that can and areseen in colitis biopsies are also included in the "negative for dysplasia" category. Some refer to such changes as "baseline atypia"; regardless, that limited spectrum is devoid of dysplasia and falls under the heading of "negative".
Indefinite for dysplasia
This category sometimes suffers from a lack of respect or credibility; however, it is a defined, accepted and even required category in properlyinterpreting dysplasia in IBD.


It is not a crutch upon which uncertain and weak willed pathologists lean. The changes that are included in the indefinite category must be recognized as such lest one either overcalls or undercalls dysplasia when it cannot be unequivocally determined whether it is present or absent. One such example is when dysplasia shows partial surface maturation. That is, the involvement of the surface epithelium by dysplastic change and not just the basal, proliferating portions of crypts is required to make a diagnosis of dysplasia. If the surface is partially involved or shows incomplete maturation then indefinite is the proper designation.
A biopsy that shows marked acute inflammation, erosion or ulceration that has cytologic changes that absent the inflammation would be called dysplastic must be designated as indefinite. This use is intended to recognize that the presence of inflammation makes diagnosing dysplasia with certainty nearly impossible.


Positive for dysplasia- low and high grade .
If there is flat dysplasia present in a biopsy, then one of the above choices (low grade or high grade) ought to appear in the report.
Criterias:
Low grade dysplasia: basally oriented nuclei; mild nuclear enlargement, nuclear crowding and hyperchromasia; decreased intracellular mucin High grade dysplasia: prominent nuclear stratification (compared to low grade) with many nuclei in luminal half of cell; more significant hyperchromasia and pleomorphism; may have marked architectural distortion with a villous or nodular growth pattern resembling adenoma or with cribriforming
The best tool that a pathologist has in effectively interpreting IBD biopsies for dysplasia is the most basic one - the simple hematoxylin and eosin stained tissue section. Ancillary tests such as immunohistochemistry have not proven as effective as the simple histologic evaluation of the H&E stain.
Experience of the pathologist in seeing and appropriately interpreting dysplasia in IBD biopsies is of critical importance.
Proper written and verbal communication between the gastrointestinal pathologist and the endoscopist is essential in going from the correct interpretation to the proper clinical course.
This is of paramount importance in interpreting polypoid dysplasia and distinguishing between a sporadic adenoma and a dysplasia associated lesion or mass (DALM).



SELECTED REFERENCES
  • Riddell RH, Goldman H, Ransohoff DF, et al: Dysplasia in inflammatory bowel disease: Standardized classification with provisional applications. Hum Pathol 14:931-968, 1983.
  • Bernstein CN, Blanchard JF, Kliewer E, et al: Cancer risk in patients with inflammatory bowel disease: A population-based study. Cancer 91: 854-862, 2001.
  • Odze RD, Goldblum JR, Noffsinger A: Interobserver variability in the diagnosis of ulcerative colitis-associated dysplasia by telepathology. ModPathol 15:379-386, 2000.

15.9.09

Making Sure Your Lab Reports Are Easy to Understand

A portion of clinical error results from the misinterpretation of laboratory data. Powsner et al reported that surgeons misunderstood 30% of pathology reports.
Whether one communicates test results electronically, by fax, or on paper, one should periodically review the content and layout of the reports to make sure they are as useful as possible. Are the clinicians and caregivers who receive the reports getting the information they need to treat the patient? Is the information clear, accurate, and laid out in such a way that the readers don’t have to struggle to comprehend the data?

Easy Places to Start
Periodically (at a minimum, annually) review all versions of your reports, with the goal of increasing their quality, accuracy, and interpretability. Also review your reports whenever there has been a readability complaint or after a change in testing methodology.
Make the font size large enough. The report should be quickly and easily readable, at arm’s length, in imperfect lighting, by someone wearing bifocals. The smaller the font, the greater the likelihood of misreading the value.
Perform legibility tests:
o Fax a sample of your reports to yourself. Are the numbers and text small and fuzzy or are they clear and legible? To simulate what your customers may see, repeat the test using the fax you just received.
o If your reports are being read via a hospital or practice management computer system, verify that your reports display appropriately and legibly on the systems the physicians are using to read the reports.
Check for complete patient information, including full name, date of birth, and gender.
Check for specimen source/type, reference ranges or target ranges, and flags ( if indicated).
Check that Medical Director, facility name, and contact details are on every page of every report.
Verify any calculated results.
Check for coding and billing information and any pay-for-performance indicators—e.g., PQRI codes.
Review the clarity of the interpretation and any comments—e.g., are interpretations clearly associated with the related result?
Check for reference to prior results, if any. If the result is a critical value, make sure the report includes documentation of appropriate communication—e.g., who notified whom? When? How?

Digging Deeper
There is a lot at stake in one simple lab report. In one study, surgeons misunderstood pathologists’ reports 30% of the time (Powsner). These additional steps can help improve the usability of your reports:
• Standardize the “look and feel” of your results to make them easier to interpret. Putting the same information in the same place, time after time, trains your readers to locate what they are looking for.
• Don’t crowd the data on the page; use sufficient white space to separate columns and lines of numbers.
• All the text should be a good distance from the margins, so no text gets cut off when printing or faxing.
• Enhance your reports with electronic tools such as embedded links to references or other background information—even photos.
• Implement synoptic reports.
• If you use paper charts, consider how you present summary reports and how frequently they are replaced.
• Ask the report recipients for feedback about the information and its presentation. How could you improve the quality and usability of the reports?

Tell the Story
After you have implemented your reporting changes, toot your horn with the administration. Show them the before and after test result reporting formats. Share the metrics of the improvements, including the number of times the improvements will be encountered by clinicians, and the resulting positive impact on patient care.

Reference : College of Americal Pathologist website.(www.cap.org )

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Interesting Case

Clinical History:

53 years male,History of hypertension and tachycardia,MRI abdomen:-Left adrenal mass:- size 5.8 cm Right renal mass:- size-3.0cm Microscopic examination of the renal mass showed vascular tumor with diffuse sheets of clear cells having Fuhrman grade III nuclei. There was no evidence of necrosis within the tumor. There was no evidence of extraparenchymal invasion.
Gross examination of the left adrenal gland revealed cortically centered, solid and multinodular mass measuring 6.5 x 6.0 x 5.0 cm and weighing 122 grams. The tumor was encapsulated but showed evidence of extraparenchymal penetration. The tumor had golden brown cut surface with areas of hemorrhage and necrosis. The partial nephrectomy showed 3.0cm x 3.0cm x 3.0 cm yellow solid mass which did not invade into the perinephric adipose tissue.
Microscopically, the adrenal mass had predominant diffuse sheets and focal trabecular arrangements. The former pattern was present in about third of tumor. The cells had clear cytoplasm and round to ovoid nuclei with conspicuous nucleoli. Mitotic rate was 9/50 HPF and included atypical forms. Gross necrosis and capsular invasion were documented microscopically. There was no evidence of lymphovascular invasion. Considering the above mentioned features, a Weiss histopathologic score2 of 7/9 was applied.



Discussion:

The differential diagnosis included Renal Cell Carcinoma (RCC) with contralateral adrenal metastasis, Adrenocortical carcinoma (ACC) with contralateral renal metastasis, synchronous RCC and ACC or synchronous RCC and adrenocortical adenoma. A panel of immunohistochemical stains was performed to sort out the diagnosis. Adrenal tumor demonstrated strong Vimentin positivity and is negative for CK7, CK20, E1/AE3, EMA, Synaptophysin and S100.Renal cell carcinoma was positive for CK7, AE1/AE3, EMA (weak) and Vimentin. It was negative for CK20, Synaptophysin and S100. The difference of immunoprofile between the two tumors documented that they originated from two different primaries.

Final Diagnosis:

The diagnosis of synchronous RCC and ACC rather than metastasis influences the prognosis.

Prognosis:

The longest disease free interval after removal of contralateral adrenal metastasis was 12.1 years8 and the longest crude survival was 14.3 years. In contrast non metastazing RCC has an excellent prognosis if no metastasis developed.