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Complications of plasma exchange in thrombotic thrombocytopenic purpura‐hemolytic uremic syndrome: a study of 78 additional patients
Author(s) -
McMinn J.R.,
Thomas Ira A.,
Terrell Deirdra R.,
Duvall Deanna,
Vesely Sara K.,
George James N.
Publication year - 2003
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1046/j.1537-2995.2003.00336.x
Subject(s) - hematology , thrombotic thrombocytopenic purpura , medicine , family medicine , library science , oncology , computer science , platelet
Complications of plasma exchange in thrombotic thrombocytopenic purpura-hemolytic uremic syndrome: a study of 78 additional patients The frequency of patients treated with plasma exchange (PE) for thrombotic thrombocytopenic purpurahemolytic uremic syndrome (TTP-HUS) increased sevenfold from 1981 to 1997.1 Therefore, the morbidity and mortality due to PE is an increasingly important consideration in management decisions for patients with clinically suspected TTP-HUS. Some studies have described few complications associated with PE,2 but our previous report on 71 consecutive patients with clinically suspected TTP-HUS treated with PE from 1996 to 1999 demonstrated a major complication rate of 30 percent, including two deaths.3 This report describes our experience during the subsequent 3 years, 1999 to 2002, with 78 consecutive patients. From June 25, 1999, to June 25, 2002, a total of 81 consecutive patients were referred to the Oklahoma Blood Institute for PE treatment of their first episode of clinically suspected TTP-HUS. Three patients were excluded because they died before a central venous catheter for PE was inserted. Twenty-one of 78 patients (27 percent) had 27 major complications (Table 1). One patient died immediately after percutaneous insertion of a subclavian central venous catheter from pneumothorax and hemorrhage. Two patients suffered cardiac arrest with pulseless electrical activity: one from an anaphylactic reaction to plasma and the other from pericardial hemorrhage and tamponade, presumably due to cardiac perforation by an internal jugular catheter insertion guidewire. Other major catheter-related complications included one patient with a retroperitoneal hemorrhage following femoral catheter insertion and seven patients with catheter thrombosis that prevented PE and/or required placement of a new central venous catheter; two of these seven patients had catheter-related venous thrombosis requiring systemic anticoagulation. Ten patients developed systemic infection: eight had blood cultures positive for the presence of bacteria (Staphylococcus aureus [five], Staphylococcus epidermidis [three]); the two patients with negative blood cultures were treated with parenteral antibiotics for presumed sepsis. Other major plasma-related complications included hypotension in two patients requiring dopamine, acute hypoxia in two patients, serum sickness in one patient requiring systemic glucocorticoids, and severe vomiting in one patient that prevented completion of PE. Twenty-seven (35 percent) patients developed minor complications, including 10 patients who also had major complications. The majority of the minor complications were urticaria (22 patients); other minor complications included vomiting, tetany, and hypotension responding to intravenous fluids. These data confirm and extend our previous report.3 In summary, over 6 years we have observed 54 major complications, including 3 deaths, related to PE in 42 of 149 (28 percent) consecutive patients treated for clinically suspected TTP-HUS. These observations are essential to understand the risks of PE when evaluating the management of patients who may have TTP-HUS. J.R. McMinn, Jr., MD Ira A. Thomas, BS Deirdra R. Terrell, MPH Deanna Duvall, BSN Sara K. Vesely, PhD James N. George, MD Hematology-Oncology Section The University of Oklahoma Health Sciences Center PO Box 26901 Oklahoma City, OK 73190 e-mail: Jim-George@OUHSC.edu.

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