Kimura's disease (KD) is a rare, benign disorder characterized by subcutaneous masses with regional lymph-node enlargement. It is considered to be due to chronic inflammation of unclear etiology. Most cases have been reported in young, 20-30-year-old men of Asian descent. The diagnosis of KD is based on pathological features and elevated immunoglobulin E levels. Characteristic pathological features include intact lymph-node architecture, florid germinal center hyperplasia, extensive eosinophilic infiltrates, and proliferation of postcapillary venules. However, these features can also be seen in Hodgkin's disease or T-cell lymphoma, therefore, cases presenting as KD pose a diagnostic challenge. We report a case series of two cases with suspected KD at initial presentation, with one patient eventually diagnosed with Hodgkin's disease after clinical progression. The first case was a 45-year-old Asian man who presented with bilateral thigh masses and significantly enlarged inguinal lymph nodes. The histopathology was characteristic and the patient had stable disease on treatment with cetirizine for 20 months. The second case was a 29-year-old African-American man who had progressive enlargement of the right neck lymph nodes extending into the mediastinum, with the original biopsy suggestive of KD. An initial search for Reed-Sternberg cells using immunohistochemical staining for CD15 and CD30 was negative. However, the patient developed neurological symptoms corresponding to tumor extension to the cervical and thoracic neural foramina. A repeat biopsy showed a lack of nodal structure and atypical large cells that were positive for CD30 staining. The patient was treated with chemotherapy with good response. We emphasize the importance of following the clinical course to render an accurate diagnosis. Both cases showed extensive eosinophilic infiltration and other KD-like pathological features. However, KD is rare; not missing a malignant diagnosis lies in high clinical suspicion and repeated exhaustive work up.

3703 Introduction: Heparin induced thrombocytopenia (HIT) has been reported to occur in up to 3% patients undergoing Cardiopulmonary Bypass (CPB) surgery by using clinical criteria. However, the accurate diagnosis of HIT in this setting is very difficult due to underlying thrombocytopenia related to the mechanical consumption of platelets by the bypass machine. This study aims to evaluate (1) the clinical and laboratory characteristics of thrombocytopenia after CPB, its temporal evolution and recovery, to aide in the differential diagnosis of thrombocytopenia after CPB, and (2) the incidence of HIT in our database. Methods: A retrospective study was conducted. CPT codes for coronary artery bypass graft surgery and valve surgery were used to search the 2008 hospital data base, and patients were eligible if they underwent “on-pump” surgery with the use of heparin during procedure. A total of 450 patients were randomly selected, medical records on thrombocytopenia, evaluation for HIT and Doppler tests for DVT were reviewed. Initial platelet decrease was defined as a greater than 33% drop from baseline and an absolute value below 100,000 up to 10 days. The time from surgery to when platelet nadir was reached was recorded as time to nadir (in days). The initial recovery was defined as platelet count reaches 50 % above the nadir, and the final recovery was defined as 75% of the normal baseline or above 150,000, or upward trend in those who were discharged before full recovery. The second platelet drop was defined as any degree of platelet fall after initial recovery. Results: Among 450 patients, 142 demonstrated thrombocytopenia after surgery, 47 of them also received platelet transfusion during the surgery. There were 93 males and 49 females, with median age 71 years (range 41 to 90 years). The platelet nadir was recorded in 28% of patients on day0, 32% of patients on day1, 21% of patients on day2, 14% of patients on day3, 5% of patients on day4, median time to nadir was 1 day. Initial platelet recovery started on day 0 and all patients showed final recovery by day 10, with a median of 5 days. The median degree of platelet drop was 61% (range 34% to 97%). HIT PF4 antibody ELISA test was sent on 37 patients, four had positive results but no Doppler evidence of DVT, and one had negative serotonin release assay (SRA) test. No direct thrombin inhibitors treatment was started, and all four patients demonstrated spontaneous platelet recovery. Four cases of DVT were found in the HIT PF4 ELISA negative group, while none was found in the rest of the thrombocytopenia patients who were not tested for HIT. Nine patients showed a steep decrease in platelet count after recovery from the first drop, 6 of them due to sepsis and 3 of unknown causes. The nadir was from post-op days 2 to 25 and recovery started after 1 day and was completed in all patients by day 29 except one patient whose platelet count did not recover. HIT PF4 ELISA test were sent on five patients, and all were negative; two of those patients also had negative DVT studies. The only possible case of thrombosis in this group was arterial occlusion in a patient with sepsis who had spontaneous platelet recovery, no HIT test was done. Conclusions: Thrombocytopenia is a common phenomenon after CPB, which could nadir in 0–4 days from surgery and takes up to 10 days for recovery. The average magnitude of the drop is more than 50%. These characteristics share many overlapping features with that identified and used as clinical criteria for the diagnosis of HIT. Three suspicious but not confirmed cases of HIT were found in our series of 450 randomly selected patients, suggesting a much lower incidence (0.66%) than previously reported. The accurate and prompt diagnosis of HIT after CPB is extremely challenging, calling for the development of more specific and convenient laboratory tests. Disclosures: No relevant conflicts of interest to declare.