Immunophenotyping by flow cytometry is well established as an ancillary technique in the diagnosis of hematopoietic neoplasms. However, flow cytometry is rarely performed on cytologic specimens because most cytologist are more comfortable with direct microscopy and believe that there is inadequate cellularity for analysis. Paradoxically, cytologic material is usually cell suspensions making it ideal for flow cytometry. In order to evaluate the usefulness of immunophenotyping cytologic specimens by flow cytometry, we retrospectively reviewed all cytologic specimens submitted to our flow cytometry unit from 1988 to 1991. Thirty-one cerebrospinal fluid specimens were analyzed. There were inadequate cells for analysis in 15 cases. Five showed a monoclonal proliferation; 11 were nondiagnostic. A range (r) of one to six cell surface markers were performed. Thirty-two body cavity fluids were analyzed: 7 peritoneal, 19 pleural, 2 pericardial, and 4 bronchoalveolar lavage. There were cells to analyze in all cases. Seven had a monoclonal proliferation; 25 were nondiagnostic (r = 4-21 markers performed). One hundred eighteen fine needle aspirates (FNA) were reviewed; 58 FNA were radiologically guided, 60 were superficial lesions. There were inadequate cells for analysis in two cases. Sixty-one demonstrated a monoclonal proliferation; 55 were nondiagnostic (r = 1-22 markers performed). We conclude that immunophenotyping by flow cytometry is of limited value for cerebrospinal fluid analysis and that knowledge of previous immunophenotyping studies is essential for correct analysis; analysis of body cavity fluids is easily performed but less often demonstrates a monoclonal proliferation. Immunophenotyping by flow cytometry is a valuable adjunctive technique for FNA and yields adequate cells for analysis.

To determine the reliability of infarct measurements on hard-copy computed tomography (CT) images the in vivo (IV) infarct volumes of 20 CT-detected infarcts were estimated and divided into four size groups with 5 infarcts in each group: Group A, less than 0.5 ml; Group B, 0.5 to 5.0 ml; Group C, 5 to 50 ml; and Group D, more than 50 ml. Seventeen infarcts were measured once and 3 infarcts three times to the nearest 0.5 mm by each of two neurologists and two neuroradiologists using a ruler on hard-copy CT images. The longest diameter (designated AP), the greatest diameter at right angles to AP (designated LAT), and the number of slices showing the infarct were recorded and multiplied by the hard-copy minification factor to give IV dimensions. Volume (VOL) was calculated according to a previously published method. Interrater intraclass correlation coefficients for all infarcts combined were 0.98 (AP), 0.91 (LAT), and 0.97 (VOL). Using all raters' measurements for any single infarct, the difference between the largest and the smallest measurement of AP and LAT was smallest (< 6 mm IV) for Group A and largest (< 31 mm IV) for Group D. This difference was largest relative to the dimension being measured in Groups A and B, where it reached 101% of the mean of the four raters' measurements for the AP dimension being measured in Group B, and 70% of the dimension being measured in Group A. With all raters' measurements for any single infarct, the difference between the largest and smallest measurement of VOL was smallest (< 0.5 ml) for Group A and largest (< 260 ml) for Group D. This difference was largest relative to the mean volume of the infarct being measured in Group B, where it reached 153% of the mean of the four raters' measurements for VOL and reached 115% of the mean of the four raters' measurements for VOL in Group A. The authors conclude that infarcts can be measured on hard-copy images with good interrater agreement. When infarcts with a volume smaller than 5 ml are measured, differences between raters' measurements may exceed the size of the dimensions being measured.

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