Transfusion reaction identification and management at the bedside.

Blood product transfusion is one of the most common invasive procedures performed in the health care setting. In contrast to pharmaceuticals, blood is actually a liquid transplant. Transfusion complications consequently encompass complex biological processes and infectious possibilities. Changes in vital signs are regularly seen during transfusion. Knowledge of common transfusion reaction signs and symptoms enables the clinical team to differentiate a normal patient response from a life-threatening reaction. Direct care nurses responsible for this procedure play a vital role in its success. Understanding the possible complications of transfusion and how to quickly recognize reactions at the bedside helps ensure the best patient outcomes.

Circulating microparticles in neuropsychiatric systemic lupus erythematosus.

AIM: Phosphatidylserine-rich microparticles derived from endothelial cells, platelets and leukocytes have been implicated as surrogate markers of cellular activation in systemic lupus erythematosus (SLE). Because microparticles have also been associated with many primary neurologic diseases, this study investigated whether cellular-derived microparticles are also implicated in neuropsychiatric SLE (NPSLE). METHOD: Plasma microparticles were measured in 51 SLE patients and 22 age- and gender-matched controls. Acute NPSLE was defined as major NPSLE (acute stroke, transient ischemic attack, psychosis, isolated seizures, major cognitive disorder, or acute confusional state) and NPSLE disease activity was measured with the neurologic components of the SLE Disease Activity Index (Neuro-SLEDAI). RESULTS: Neuro-SLEDAI levels varied widely in SLE patients, consistent with variable NPSLE activity. When considering all patients with SLE, there was no difference in total microparticles relative to matched controls, 2158/µL (interquartile range [IQR] 1214-3463) versus 2782/µL (IQR 1586-2990; P = 0.57) nor differences in microparticles derived from either platelets (P = 0.40), monocytes (P = 0.15) or endothelial cells (P = 0.32). However, levels of circulating monocyte-derived microparticles significantly and independently correlated with NPSLE (r = -0.28; P = 0.045), corticosteroid dosage (r = -0.38; P = 0.006) and levels of circulating C5a (r = 0.54; P < 0.0001). Non-neurologic SLE disease activity was not associated with microparticles. CONCLUSION: Circulating cell-derived microparticles are reduced in active NPSLE, although the relative contribution of reduced microparticle production, increased consumption or intravascular sequestration, remain uncertain.

Milestones for Apheresis education.

Milestones represent the essential knowledge, skills, and attitudes required for the practice of a medical discipline. Defining these milestones for each medical specialty has become a focus for the American Council of Graduate Medical Education (ACGME). Practitioners of Apheresis Medicine come from a variety of medical specialties making it challenging to establish the essential educational milestones for all. The American Society for Apheresis (ASFA) has an interest in promoting standards of excellence for Apheresis Medicine. ASFA's Physician's Curriculum Content Committee is a group of physician educators in the field of Apheresis Medicine, both donor and therapeutic, from across the United States, who have met regularly for several years to discuss the appropriate educational milestones in Apheresis training. The committee members teach residents and fellows from Pathology, Transfusion Medicine, Hematology/Oncology, Nephrology and other specialties. In this document, we have outlined the basic set of Apheresis milestones required in the ACGME defined competency areas of Patient Care and Medical Knowledge. We have also recommended methods of evaluation and estimated the time necessary for the acquisition of these cognitive and behavioral elements.

Teaching and learning apheresis medicine: The Bermuda Triangle in Education.

Apheresis Medicine has evolved markedly due to an explosion of knowledge and technology, whereas the time available for training has shrunk as curricula have become increasingly overloaded. Apheresis teaching has inherited a strong clinical context where real patient problems are used in a hands-on environment. To optimize instruction, those involved in the education of apheresis professionals need to have (1) knowledge of how clinical laboratory medicine education has developed as a field, (2) an understanding of what is known from theory and research about how people learn, and (3) the skills to design teaching/learning activities in ways consistent with literature-based principles of adult education. These developments in education provide a context for curriculum projects currently underway by the American Society for Apheresis. Teachers must determine which competencies are central to the essence of a trained professional. Specific, robust, learning objectives targeted toward the development of higher levels of thinking, professional attitudes, and requisite skills are formulated to guide the learner toward mastering those competencies. Curriculum is developed for each objective, consisting of content and the best teaching/learning methods to help learners attain the objective. Appropriate assessment strategies are identified to determine whether the objective is being achieved. The integration of objectives, curriculum, and assessment creates The Bermuda Triangle of Education (Richter, The Circle of Learning and Bermuda Triangle in Education, University of New Mexico School of Medicine, 2004). When educators do not effectively navigate The Bermuda Triangle of Education, learning may disappear into the murky depths of confusion and apathy. When successfully navigated, the result will be a significant learning experience that leads to transformation through education.

Educating medical students in laboratory medicine: a proposed curriculum.

As the 100th anniversary of the Flexner report nears, medical student education is being reviewed at many levels. One area of concern, expressed in recent reports from some national health care organizations, is the adequacy of training in the discipline of laboratory medicine (also termed clinical pathology). The Academy of Clinical Laboratory Physicians and Scientists appointed an ad hoc committee to review this topic and to develop a suggested curriculum, which was subsequently forwarded to the entire membership for review. The proposed medical student laboratory medicine curriculum defines goals and objectives for training, provides guidelines for instructional methods, and gives examples of how outcomes can be assessed. This curriculum is presented as a potentially helpful outline for use by medical school faculty and curriculum committees.

The laboratory approach to inherited and acquired coagulation factor deficiencies.

Besides the long-recognized hemophilias, there are many other factor deficiencies. Some also are inherited, but others are acquired because of both immune and nonimmune etiologies. Understanding the optimal laboratory approach to evaluating factor deficiency will aid physicians and laboratory scientists in obtaining a prompt diagnosis and in avoiding pitfalls in coagulation testing.

HBOC-201 use in traumatic brain injury: case report and review of literature.

BACKGROUND: The first use of HBOC-201 in severe traumatic brain injury (TBI) is presented. The use of noninvasive cerebral oximetric devices to follow clinical progress in a patient infused with HBOC-201 is reported and the literature of hemoglobin-based oxygen carriers (HBOCs) in brain injury is reported. CASE REPORT: A 21-year-old Jehovah's Witness who was hit and dragged by a motor vehicle was admitted to the University of New Mexico Hospital Level 1 Trauma Center Trauma Surgical Intensive Care Unit with severe TBI and extensive soft tissue loss resulting in profound anemia. The patient received infusion of HBOC-201 with regional and global oximetric monitoring. RESULTS: Chart abstraction was performed to identify clinically relevant physiologic markers of patient progress. We observed a marked increase in brain tissue oxygen saturations, central venous oxygen saturation, and hemodynamic variables after administration of HBOC-201. The patient subsequently suffered massive cerebral edema and died. CONCLUSIONS: Major HBOC trials to date have excluded severe TBI. We report the first use of an HBOC in severe TBI to correct profound anemia. The HBOC-201 rapidly corrected cerebral venous and central venous oxygen saturations. The patient's death may have been due to massive reperfusion injury from delayed repayment of cerebral oxygen debt in a severely ischemic brain.

A randomized, controlled Phase III trial of therapeutic plasma exchange with fresh-frozen plasma (FFP) prepared with amotosalen and ultraviolet A light compared to untreated FFP in thrombotic thrombocytopenic purpura.

BACKGROUND: Photochemical treatment of fresh-frozen plasma (FFP) with amotosalen and ultraviolet (UV) A light (PCT FFP) results in inactivation of a broad spectrum of pathogens while retaining coagulation factor activity, antithrombotic proteins, and von Willebrand factor-cleaving protease (VWF-CP) activity. STUDY DESIGN AND METHODS: A randomized, controlled, double-blind Phase III trial was conducted with PCT FFP or control FFP for therapeutic plasma exchange (TPE) in patients with thrombotic thrombocytopenic purpura (TTP). Owing to the rarity of this diagnosis, the trial was not powered to demonstrate small differences between treatment groups. Patients were treated with study FFP for a maximum of 35 days until remission was achieved (for a maximum of 30 daily study TPEs with no remission) plus an additional 5 days after remission. RESULTS: Among the 35 patients treated, the primary endpoint, remission within 30 days, was achieved by 14 of 17 (82%) PCT patients and 16 of 18 (89%) control patients (p = 0.658) The 90 percent confidence interval for treatment difference in remission rate for test - control was (-0.291 to 0.163). Time to remission, relapse rates, time to relapse, total volume and number of FFP units exchanged, and number of study TPEs were not significantly different between groups. Improvement in VWF-CP and inhibitors was similar for both groups. The overall safety profile of PCT FFP was similar to control FFP. No antibodies to amotosalen neoantigens were detected. CONCLUSION: The comparable results between treatment groups observed from this small trial suggest that TPE with PCT FFP was safe and effective for treatment of TTP.

Recombinant factor VIIa in management of spontaneous subcapsular liver hematoma associated with pregnancy.

BACKGROUND: Spontaneous subcapsular liver hemorrhage is a rare but life-threatening complication of pregnancy. Optimal management of an expanding hematoma or ruptured capsule has not been established. CASES: We report 3 patients with preeclampsia and hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome with spontaneous subcapsular liver hematomas. The first 2 patients with ruptured liver hematomas experienced life-threatening hemorrhage. The third patient experienced uncontrollable vaginal bleeding, liver hemorrhage, and was in imminent danger of capsule rupture. Despite aggressive surgical intervention and traditional blood component therapy, adequate hemostasis could not be achieved in any of these patients. Recombinant factor VIIa was used to achieve hemostasis in all three patients. CONCLUSION: Recombinant factor VIIa is an effective adjunct in the treatment of preeclamptic patients with expanding or ruptured subcapsular liver hematoma.

Three cases of massive fetomaternal hemorrhage presenting without clinical suspicion.

Fetomaternal hemorrhage (FMH) is a common obstetrical occurrence most often associated with small volumes of blood transferred across the placenta. Fetomaternal hemorrhage leads to alloimmunization of Rh D-negative mothers, resulting in an increased risk of hemolytic disease of the newborn. Massive FMH involving volumes of blood greater than 30 mL can cause substantial fetal morbidity and mortality. Massive FMH may present with signs and symptoms such as decreased movement, sinusoidal heart rhythms, or fetal anomalies. We present 3 cases of clinically unexpected massive FMH of 206, 88, and 155 mL. The treating clinicians were unaware of any fetal or maternal signs or symptoms of FMH until contacted by the laboratory. These cases illustrate the necessity for FMH quantitation, even in the absence of clinical suspicion. Additional studies are needed to find better ways to identify these patients in advance. Development of criteria allowing identification of patients at risk would be of benefit to both mother and baby.