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Letters to the Editor LETTERS TO THE EDITOR Complications of plasma exchange in after percutaneous insertion of a subclavian central ve- thrombotic thrombocytopenic nous catheter from pneumothorax and hemorrhage. Two purpura-hemolytic uremic syndrome: patients suffered cardiac arrest with pulseless electrical a study of 78 additional patients activity: one from an anaphylactic reaction to plasma and The frequency of patients treated with plasma exchange the other from pericardial hemorrhage and tamponade, (PE) for thrombotic thrombocytopenic purpura- presumably due to cardiac perforation by an internal hemolytic uremic syndrome (TTP-HUS) increased seven- jugular catheter insertion guidewire. fold from 1981 to 1997.1 Therefore, the morbidity and Other major catheter-related complications included mortality due to PE is an increasingly important consid- one patient with a retroperitoneal hemorrhage following eration in management decisions for patients with clini- femoral catheter insertion and seven patients with cath- cally suspected TTP-HUS. Some studies have described eter thrombosis that prevented PE and/or required place- few complications associated with PE,2 but our previous ment of a new central venous catheter; two of these seven report on 71 consecutive patients with clinically sus- patients had catheter-related venous thrombosis requir- pected TTP-HUS treated with PE from 1996 to 1999 dem- ing systemic anticoagulation. Ten patients developed sys- onstrated a major complication rate of 30 percent, in- temic infection: eight had blood cultures positive for the cluding two deaths.3 This report describes our experience presence of bacteria (Staphylococcus aureus [five], Staph- during the subsequent 3 years, 1999 to 2002, with 78 con- ylococcus epidermidis [three]); the two patients with secutive patients. negative blood cultures were treated with parenteral an- From June 25, 1999, to June 25, 2002, a total of 81 tibiotics for presumed sepsis. consecutive patients were referred to the Oklahoma Other major plasma-related complications included Blood Institute for PE treatment of their first episode of hypotension in two patients requiring dopamine, acute clinically suspected TTP-HUS. Three patients were ex- hypoxia in two patients, serum sickness in one patient cluded because they died before a central venous cath- requiring systemic glucocorticoids, and severe vomiting eter for PE was inserted. in one patient that prevented completion of PE. Twenty-one of 78 patients (27 percent) had 27 major Twenty-seven (35 percent) patients developed minor complications (Table 1). One patient died immediately complications, including 10 patients who also had major complications. The majority of the minor complications were urticaria (22 patients); other minor complications TABLE 1. Major complications of PE in 78 included vomiting, tetany, and hypotension responding consecutive patients treated for clinically to intravenous fluids. suspected TTP-HUS* These data confirm and extend our previous report.3 Number Complications of patients In summary, over 6 years we have observed 54 major Catheter-related complications complications, including 3 deaths, related to PE in 42 of Pulmonary hemorrhage and pneumothorax 149 (28 percent) consecutive patients treated for clini- resulting in death 1 Cardiac tamponade with arrest 1 cally suspected TTP-HUS. These observations are essen- Retroperitoneal hemorrhage 1 tial to understand the risks of PE when evaluating the Thrombosis 7 management of patients who may have TTP-HUS. Catheter obstruction† 5 Venous thrombosis systemic anticoagulation 2 J.R. McMinn, Jr., MD Systemic infection 10 Ira A. Thomas, BS Documented bacteremia 8 Deirdra R. Terrell, MPH Suspected bacteremia‡ 2 Deanna Duvall, BSN Plasma-related complications Sara K. Vesely, PhD Anaphylaxis with cardiac arrest 1 Hypotension requiring dopamine 2 James N. George, MD Serum sickness 1 Hematology-Oncology Section Hypoxia§ 2 The University of Oklahoma Health Sciences Center Vomiting࿣ 1 PO Box 26901 * The classification of complications as central venous cath- eter-related or plasma-related and the definition of major Oklahoma City, OK 73190 complications has been previously described.3 e-mail: [email protected]. † Required placement of a new catheter and/or prevented PE. ‡ Negative blood cultures but systemic symptoms present and treated with a full course of parenteral antibiotics for pre- REFERENCES sumed sepsis. 1. Clark WF, Rock GA, Buskard N, et al. Therapeutic plasma § Required treatment with glucocorticoids and/or stopping PE. ࿣ Required stopping PE. exchange: an update from the Canadian Apheresis Group. Ann Intern Med 1999;131:453-62. Volume 43, March 2003 TRANSFUSION 415 LETTERS TO THE EDITOR 2. McLeod BC, Sniecinski I, Ciavarella D, et al. Frequency of immediate adverse effects associated with therapeutic TABLE 1. Flow cytometric data of fluorescence of RBCs labeled with a panel of blood apheresis. Transfusion 1999;39:282-8. group antibodies 3. Rizvi MA, Vesely SK, George JN, et al. Complications of Median fluorescence plasma exchange in 71 consecutive patients treated for Antibody Clone (MoAb) Control RBCs Patient’s clinically suspected thrombotic thrombocytopenic specificity or serum (O R1R2 or O rr) RBCs purpura-hemolytic uremic syndrome. Transfusion 2000; Negative control 4 5 D FITC-BRAD-3*† 191 167 40:896-901. D BRAD-5*† 743 661 C MS257* 57 36 C HMR7† 118 109 Quantitation and phenotyping of fetal RBCs c MS37* 29 19 c MS51* 85 93 in maternal blood by flow cytometry E HIRO-18* 79 76 Flow cytometry may be used to detect and quantitate E HIRO-91† 34 32 fetal D+ RBCs in fetomaternal hemorrhage (FMH) to cal- E 907* 41 51 e MS70* 4 5 culate the dose of Rho (D) immune globulin required to K Serum 43 54 and 4 prevent maternal alloimmunization and protect against k Serum 12 27 a subsequent HDN. Fetal RBCs may be detected with an- Fy Serum 33 50 Fyb Serum 19 44 tibodies to fetal Hb (anti-HbF) or to the D antigen (anti- Jka Serum 7 12 D), either by indirect labeling or, more recently, by using Jkb Serum 12 5 directly conjugated MoAbs.1,2 Antibodies to additional * The MoAbs were submitted to the Third International Work- RBC blood group antigens have been used to phenotype shop on Monoclonal Antibodies Against Human Red Blood Cells and Related Antigens held in 1996. 3 RBCs after transfusion and to monitor chimerism after † The MoAbs were submitted to the Fourth International Work- marrow transplantation.4,5 shop on Monoclonal Antibodies Against Human Red Blood We report the case of a woman whose fetus died in Cells and Related Antigens held in 2001. utero at 35 weeks of gestation following trauma. The woman’s RBCs were Group A, D+, and the antibody screen was negative. The Kleihauer-Betke test demon- Using adult RBCs alone or with added cord RBCs, a strated a 50-mL FMH. Cord blood was not available for marker was set to encompass strongly fluorescent fetal phenotyping. It was therefore not known whether she RBCs on histograms of FITC-anti-HbF–stained RBCs. The could be immunized to antigens (other than D) expressed percentage of events under this marker in the adult on fetal RBCs. Fetal and maternal RBCs were phenotyped sample (0.09%) was subtracted from that of the patient’s by flow cytometry, the large FMH was confirmed, and an sample (2.59%), that is, 2.5 percent (Fig. 1A). Using the antigen mismatch was identified. formula FMH (mL of packed fetal RBCs) = percentage of the FMH in the patient’s sample 22,6 ן RBCs from the patient, two adult donors (controls, positive events phenotypes O R1R2 and O rr K+ k+ Fy(a+b+) JK(a+b+)), was calculated to be 55 mL. and cord blood were washed, and a mixture of cord and The median fluorescence of RBCs obtained with the adult RBCs was made; 20-␮L aliquots of 5 percent sus- blood group-specific antibodies is listed in Table 1. O ␮ pensions were labeled with 10 L of FITC-conjugated R1R2 RBCs were tested with the MoAbs and O rr RBCs anti-HbF (Silenus, Boronia, Victoria, Australia), 5 ␮Lof with the antisera; the patient’s RBCs were tested with all FITC-conjugated anti-D (BRAD-3),2 200 ␮L of MoAb, or antibodies. All samples, except three, exhibited fluores- 50 ␮L of antiserum (Table 1). RBCs were incubated either cence, as the patient’s RBCs were negative with anti-Jkb at room temperature for 30 minutes (anti-HbF) or at 37ЊC and anti-e did not show binding. For most antibodies, the for 1 hour (blood group antibodies). Before labeling with median fluorescence of RBCs was similar between the anti-HbF, RBCs were fixed (in 1 mL of 0.05 percent glu- controls exhibiting a single dose of antigen (O R1R2 and O taraldehyde in PBS), washed, permeabilized (in 0.5 mL of rr) and the patient, indicating that similar amounts of 0.1% Triton X-100 in PBS with 0.1% BSA), and washed.1 antibodies were bound. Only one sample showed two Unlabeled primary antibodies were detected with 100 ␮L populations; this occurred when the patient’s RBCs were of 1-in-100 FITC-conjugated anti-human IgG (F(ab); incubated with anti-K. The major population (97.7%) was Jackson ImmunoResearch, West Grove, PA). Samples K+ (median fluorescence, 54), but a minor population of were analyzed with a flow cytometer (FACSCalibur, Bec- 2.2 percent of events was K– (median fluorescence, 4) ton Dickinson, Oxford, UK),6 collecting 50,000 events and (Fig. 1B). Subtracting the background of unlabeled events placing markers as appropriate on histograms of log- under this marker (0.2%) gave 2 percent K– cells or a integrated FL1 fluorescence. The percentage of gated 44-mL FMH. events and the median fluorescence of events under the Some examples of anti-C, anti-c, and anti-E gave markers were computed. greater fluorescence than others (Table 1). It was ob- 416 TRANSFUSION Volume 43, March 2003 LETTERS TO THE EDITOR binding fluorescent microspheres10 (sensitive but te- dious).
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