Is fresh frozen plasma overtransfused in the United States?

Abstract Objective.—To determine the normative rates of expiration and wastage for units of fresh frozen plasma (FFP) and platelets (PLTs) in hospital communities throughout the United States, and to examine hospital blood bank practices associated with more desirable (lower) rates. Design.—In 3 separate studies, participants in the College of American Pathologists Q-Probes laboratory quality improvement program collected data retrospectively on the numbers of units of FFP and PLTs that expired (outdated) prior to being used and that were wasted due to mishandling. Participants also completed questionnaires describing their hospitals' and blood banks' laboratory and transfusion practices. Setting and Participants.—One thousand six hundred thirty-nine public and private institutions, more than 80% of which were known to be located in the United States. Main Outcome Measures.—Quality indicators of FFP and PLT utilization: the rates of expiration and wastage of units of FFP and PLTs. Results.—Participants submitted data on 8 981 796 units of FFP and PLTs. In all 3 studies, aggregate combined FFP and PLT expiration rates ranged from 5.8% to 6.4% and aggregate combined FFP and PLT wastage rates ranged from 2.0% to 2.5%. Among the top-performing 10% of participants (90th percentile and above), FFP and PLT expiration rates were 0.6% or lower and FFP and PLT wastage rates were 0.5% or lower. Among the bottom-performing 10% of participants (10th percentile and below), expiration rates were 13.8% or higher and wastage rates were 6.8% or higher. We were unable to associate selected hospital characteristics or blood bank practices with lower rates of FFP and PLT utilization. Conclusions.—The rates of FFP and PLT expiration and wastage vary greatly among hospitals in the United States. Hospital blood bank personnel are capable of achieving FFP and PLT expiration and wastage rates below 1%.

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The Recovery of Factor VIII from Fresh-Frozen, Indated and Outdated Human Plasma

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648010 ◽

1976 ◽

Vol 36 (01) ◽

pp. 071-077 ◽

Cited By ~ 2

Author(s):

Daniel E. Whitman ◽

Mary Ellen Switzer ◽

Patrick A. McKee

Keyword(s):

Factor Viii ◽

Polyacrylamide Gel Electrophoresis ◽

Sodium Dodecyl ◽

The United States ◽

Fresh Frozen Plasma ◽

Red Cross ◽

Random Samples ◽

Fresh Frozen ◽

Factor Viii Concentrates ◽

Frozen Plasma

SummaryThe availability of factor VIII concentrates is frequently a limitation in the management of classical hemophilia. Such concentrates are prepared from fresh or fresh-frozen plasma. A significant volume of plasma in the United States becomes “indated”, i. e., in contact with red blood cells for 24 hours at 4°, and is therefore not used to prepare factor VIII concentrates. To evaluate this possible resource, partially purified factor VIII was prepared from random samples of fresh-frozen, indated and outdated plasma. The yield of factor VIII protein and procoagulant activity from indated plasma was about the same as that from fresh-frozen plasma. The yield from outdated plasma was substantially less. After further purification, factor VIII from the three sources gave a single subunit band when reduced and analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis. These results indicate that the approximately 287,000 liters of indated plasma processed annually by the American National Red Cross (ANRC) could be used to prepare factor VIII concentrates of good quality. This resource alone could quadruple the supply of factor VIII available for therapy.

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Hereditary Angioedema: Management of Laryngeal Attacks

American Journal of Rhinology and Allergy ◽

10.2500/ajra.2011.25.3670 ◽

2011 ◽

Vol 25 (6) ◽

pp. 379-382 ◽

Cited By ~ 7

Author(s):

Sandra C. Christiansen ◽

Bruce L. Zuraw

Keyword(s):

Hereditary Angioedema ◽

Treatment Options ◽

The United States ◽

Fresh Frozen Plasma ◽

C1 Inhibitor ◽

Acute Therapy ◽

Fresh Frozen ◽

Life Threatening ◽

Frozen Plasma ◽

Future Management

Background Hereditary angioedema (HAE) patients suffering from laryngeal attacks in the United States faced severely limited treatment options until 2008. These potentially life-threatening episodes occur in over one-half of the patients affected by HAE during their lifetimes. Acute therapy had been relegated to supportive care, intubation, and consideration of fresh frozen plasma (FFP)–-the latter with the potential for actually accelerating the speed and severity of the swelling. Methods In this article we will review the recently approved and emerging HAE treatments that have evolved from the recognition that bradykinin generation is the fundamental abnormality leading to attacks of angioedema. Results Acute therapy for laryngeal attacks will be discussed including purified plasma–derived C1 inhibitor (C1INH), recombinant C1INH, an inhibitor of plasma kallikrein (ecallantide), and a B2 receptor antagonist (icatibant). Prophylactic care has also been transformed from a reliance on attenuated androgens with their attendant side effects to C1INH replacement. Conclusion The arrival of these novel therapies promises to transform the future management of HAE.

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Das Smith-Lemli-Opitz-Syndrom

Kinder- und Jugendmedizin ◽

10.1055/s-0037-1617867 ◽

2005 ◽

Vol 5 (04) ◽

pp. 178-182

Author(s):

Wieland Kiess ◽

Manuela Schulz ◽

Sabine Liebermann ◽

Roland Pfäffle ◽

Peter Bührdel ◽

...

Keyword(s):

Fresh Frozen Plasma ◽

Therapeutische Möglichkeiten ◽

Fresh Frozen ◽

Frozen Plasma

ZusammenfassungDas Smith-Lemli-Opitz-Syndrom wird durch einen Defekt des letzten Schrittes der Cholesterolbiosynthese, den Mangel an 7-Dehydrocholesterolreduktase, verursacht. Die Akkumulation der Metaboliten 7-Dehydrocholesterol und 8-Dehydrocholesterol, die die wichtigsten biochemischen Marker für die Diagnose der Erkrankung darstellen, sowie der Mangel an Cholesterol können zu multiplen kongenitalen Anomalien führen. Die Ursache des Enzymmangels sind Mutationen innerhalb des DHCR7-Gens, welches auf Chromosom 11q13 lokalisiert ist. Therapeutische Möglichkeiten bestehen in der Gabe von Cholesterol und im Notfall Fresh Frozen Plasma (FFP); der therapeutische Nutzen von Statinen befindet sich zurzeit in der klinischen Erprobung.

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Haemophilia in a Female

Thrombosis and Haemostasis ◽

10.1055/s-0038-1653669 ◽

1971 ◽

Vol 26 (02) ◽

pp. 205-210

Author(s):

J. A McBride ◽

J Hunter ◽

Elizabeth Pearse ◽

Yvette Sultan ◽

J. P Caen

Keyword(s):

Fresh Frozen Plasma ◽

Plasma Fibrinogen ◽

Fresh Frozen ◽

Frozen Plasma

SummaryA case of haemophilia in a female is described together with the response of the patient’s level of antihaemophilic factor in the plasma following transfusion of fresh frozen plasma, fibrinogen and cryoprecipitate.

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Severe Inherited “Homozygous” Protein C Deficiency in a Newborn Infant

Thrombosis and Haemostasis ◽

10.1055/s-0038-1661136 ◽

1984 ◽

Vol 52 (01) ◽

pp. 053-056 ◽

Cited By ~ 77

Author(s):

A Estellés ◽

I Garcia-Plaza ◽

A Dasí ◽

J Aznar ◽

M Duart ◽

...

Keyword(s):

Newborn Infant ◽

Protein C ◽

Skin Lesions ◽

Fresh Frozen Plasma ◽

Clinical Syndrome ◽

Assay Method ◽

Enzyme Linked Immunosorbent Assay ◽

Protein C Deficiency ◽

Fresh Frozen ◽

Frozen Plasma

SummaryA relapsing clinical syndrome of skin lesions and disseminated intravascular coagulation (DIC) that showed remission with the infusion of fresh frozen plasma is described in a newborn infant with homozygous deficiency of protein C antigen.This patient presented since birth a recurrent clinical picture of DIC and ecchymotic skin lesions that resembled typical ecchymosis except for the fact that they showed immediate improvement with the administration of fresh frozen plasma. Using an enzyme linked immunosorbent assay method, the determination of protein C antigen levels in the patient, without ingestion of coumarin drugs, showed very low values (<1%).No other deficiencies in the vitamin-K-dependent factors or in anti thrombin III, antiplasmin, and plasminogen were found. Seven relatives of the infant had heterozygous deficiency in protein C antigen (values between 40-55%), without clinical history of venous thrombosis. The pedigree analysis of this family suggests an autosomal recessive pattern of inheritance for the clinical phenotype, although an autosomal dominant pattern has been postulated until now in other reported families.We conclude that our patient has a homozygous deficiency in protein C and this homozygous state may be compatible with survival beyond the neonatal period.

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