AUSTRALASIAN SOCIETY OF BLOOD TRANSFUSION INC

Topics in
Transfusion
Medicine

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September 1994
Vol I, No 2

EDITOR'S NOTE
Two contributions are included in the second edition of "Topics in Transfusion Medicine".
(1)

The Coagulopathy of Massive Blood Transfusion: A Review. From

Michael Harvey (Liverpool Hospital, NSW) and YL Kwan (St George
Hospital, NSW). Originally presented at the NSW ASBT/HSA meeting
in April 1994. Reviewed by David Roxby and John Rowell.

(2)

Transfusion Control: A new concept in nursing management. From

Wedderburn et al (Concord Hospital, NSW). Submitted by Maryann
Nicholls, editorial committee member.

Correspondence is invited.

John Gibson
Editor

All Correspondence
The Australasian Society of Blood Transfusion Inc
145 Macquarie Street, Sydney NSW 2000

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September 1994
Vol I, No 2

Copyright of the Australasian Society of Blood Transfusion

THE COAGULOPATHY OF
MASSIVE BLOOD TRANSFUSION
A REVIEW
MP HARVEY# & Y KWAN*
#HAEMATOLOGY DEPARTMENT, LIVERPOOL HOSPITAL & SOUTH WESTERN AREA PATHOLOGY
SERVICE, *HAEMATOLOGY DEPARTMENT, ST GEORGE HOSPITAL & SOUTHPATH, NSW

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Introduction
The most generally accepted definition of massive transfusion is the replacement of the patient's blood volume in
under 24 hours (1-5). This corresponds to 3,000 ml of red cells or approximately 10 units of packed cells in an
average weight person. The most frequent reasons for massive transfusion include trauma, GIT bleeding, obstetric
bleeding, bleeding abdominal aortic aneurysm, and major elective vascular surgery. Survival in massively
transfused patients will vary depending on the underlying disease process. Overall survivals of 45-67% have been
reported (3, 6, 7)
Of these 90% regain full independence and 75% return to work (7). Massive transfusion
imposes a considerable strain on blood banking resources, and in many centres a relatively small number of
patients consume 10-15% of the total blood supply annually (3). In this review, we will discuss the coagulopathy
of massive blood transfusion and the provision of blood product support.
Hypothermia and Coagulopathy
Many of the coagulation reactions occur inefficiently below 370C and hypothermia contributes to organ dysfunction
with reduced hepatic synthesis of coagulation factors, and impaired platelet function (4, 8). Hypothermia occurs
early, and is related to the volume and rate of blood infused. Most blood warmers in routine use in hospital wards
and intensive care units are not capable of delivering blood at a safe temperature for the speed required. At rapid
rates, these can only deliver an exit temperature of around 200C. The flat plate type of blood warmer is more
efficient and can deliver blood at around 25-280C. The most efficient type in use in a number of trauma centres is
the "Level 1" countercurrent warmer. These have the capacity to warm blood to 370C at a rate of one unit per
minute. One draw-back of these warmers is the high initial cost and the expense of the disposable cartridges
(~ $120). It is important to avoid heat loss during prolonged surgical procedures. Operating rooms should be
maintained, if possible, at 300C. Prolonged laparotomies increase the risk of hypothermia, and it has been
suggested that at the first sign of microvascular ooze or bowel oedema, that the abdomen be packed and the
operation be terminated (7). The definitive procedure may then be performed 24-48 hours later when the
coagulopathy and hypothermia have been corrected.
The Coagulopathy of Massive Transfusion
Without platelet or plasma supplementation, massive transfusion is essentially an exchange transfusion with fluid
devoid of these components. Elements with a purely intravascular distribution will undergo an exponential decay (A
= A0e-bt/v where A is the measured concentration at time t relative to A0 prior to transfusion, b is the quantity of
infused fluid and v is the blood volume)(9). Following single blood volume exchange (10 units of packed cells and
crystalloid), 37% of the original component will remain, and 14% after a two blood volume exchange. This model
is broadly but not totally (vide infra) predictive of the coagulation disturbances that occur during massive
transfusion, and which often become profound between one and two blood volumes replacement. It also suggests
a large absolute loss of a given component during the first volume exchange (63%) as opposed to the second
volume exchange (23%). Thus maintaining absolutely normal levels of coagulation factors and platelets will be far
more costly than accepting, for instance, 50% normal levels. It is thus important to establish the minimum levels
of platelets and coagulation factors required for haemostasis under conditions of massive transfusion.

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Thrombocytopenia and Massive Transfusion

Thrombocytopenia occurs in the majority of patients who have received more than 10 units of blood in 24 hours
and is generally accepted to be a major contributor to the haemostatic defect in massively transfused patients (9,
10, 11, 12, 13, 14). There is an inverse relationship between the number of units transfused and the platelet count
but with a high degree of variability (6). Mild thrombocytopenia (50-100 X 109/l) occurs in virtually all patients given
more than 15 units of blood and severe thrombocytopenia (<50 x 109/l) is very common after 20 units of blood (15).
Interestingly, the counts observed are higher than one would expect on just the basis of blood volume exchange
(9). It is possible that there is release of platelets from splenic and bone marrow pools to counteract this effect
(6). The platelets drop early after trauma, usually continuing to fall for another 24 hours after the sites of bleeding
have been controlled and remain low for the first four days after injury. During the convalescent phase, a reactive
thrombocytosis is common (average of 563 X 109/l at 25 days), (2). It appears that the thrombocytopenia after the
initial phase of haemodilution has a complex multifactorial origin which includes consumption, underproduction,
and disseminated intravascular coagulation (2). A platelet function defect is almost universal - 19 of 22 massively
transfused patients had a bleeding time of > 15 minutes in one study, as well as a high incidence of impaired
aggregation with ADP and collagen (2). Impaired platelet aggregation correlated with shock time in the latter
study.
Depletion of Coagulation Factors During Massive Transfusion
An analogous situation exists for the coagulation factors, with an early acute drop due to haemodilution, and then
the subsequent effects of consumption. A coagulopathy (>1.5 X normal APTT or PT) occurs in virtually all
patients given >12 plasma free units of blood and in 1/3 of patients given <12 units of blood (15). Beck et al made
the observation that transfusion of over 15 units of blood was always associated with an abnormal PT and APTT
(16). Consumption of coagulation factors seems to play an important part as there is a poor correlation between
the number of units transfused and the levels of factors (9, 17). One blood volume replacement without
supplemental plasma may be expected to drop fibrinogen levels to <50% baseline, and two blood volumes to
<25% (17). Levels of fibrinogen commonly drop below 1.0 g/l at between one and two blood volumes transfused.
Ciavarella et al. (18) observed that in the massive transfusion setting, the major contributors to the prolongation in
PT and APTT, apart from fibrinogen, are reduced V and VIII levels. Factors V and VIII are labile, and are sensitive
to thrombin, activated protein C and plasmin degradation which are likely to be involved in the setting of a
consumptive coagulopathy (18). Factor VIII levels vary considerably and levels >50% are common despite a
greater than one blood volume replacement, suggesting release from endothelial stores (17). Factor IX levels also
drop with increasing transfusion (17). Ciavarella et al. (18) found that prolongation of the PT and APTT to >1.8X
normal was associated with clotting factor levels <20%, and was highly correlated with microvascular bleeding,
whilst lesser degrees of prolongation correlated poorly.
Duration of shock plays a major role in coagulopathy. Patients who receive >50% haemodilution with crystalloid
during elective surgery develop a transient elevation in PT/APTT which corrects back to normal within 12 hours
(19). Hewson et al. (19) studied 64 patients receiving more than 10 units of packed cells in 12 hours and found a
biphasic phenomenon. The early rise in APTT appeared dilutional and correlated closely with the volume of fluid
received. The elevation in APTT occurring after four hours, however, correlated poorly with the total volume of fluid
and best with the period of hypotension during resuscitation. This has been documented in other studies (9, 1214). Similarly, in a dog model of massive haemorrhage, coagulation factors continue to drop after resuscitation
until day two, and were not affected by FFP replacement (20). This may reflect shock-related impairment of
production of coagulation factors, shock initiated disseminated intravascular coagulation, or shifts of coagulation
factors and water between the interstitial and intravascular spaces (19). Thus aggressive volume replacement and
maintenance of perfusion early on plays a significant role in the prevention of subsequent coagulopathy.
A syndrome of microvascular bleeding (MVB) occurs in approximately 18-30% of patients who are recipients of
massive transfusion (7, 17, 18, 21). The duration of shock and prior liver disease are probably as important as the
actual volume of blood transfused (13, 19). MVB has been defined as bleeding from cannula sites, endotracheal
tubes, or persistent ooze from wound sites which is not felt to be "surgical" in origin. Obviously the last of these
criteria is often the most difficult to judge, and there are only loose associations between coagulopathy and
clinically observed bleeding. Good predictors of MVB in the study of Ciavarella (18) were: APTT/PT >1.8X normal;
fibrinogen <0.5 g/l; and platelets <50 X 109/l. Murray et al. have suggested elsewhere that fibrinogen < 0.75g/l and
PT/APTT >1.5 X normal are the levels at which clinical bleeding is likely to occur (17). Wilson et al. found that
fibrinogen of <1.0 g/l, platelets < 50 X 109/l and PT prolonged more than five seconds were significantly associated
with MVB (13). These are probably broad levels to aim at when determining coagulation factor and platelet

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replacement. It is possible that other factors contribute, and it has certainly been noted that correction of the
laboratory coagulopathy does not always correct the bleeding tendency (16).
Coagulopathy and Microvascular Bleeding: Preventable with Replacement?
Although coagulopathy is a well established complication of massive transfusion, it is less evident that it is
preventable. There are data from a dog haemorrhagic shock model (20) to suggest that prophylactic replacement
with fresh frozen plasma is not significantly more effective in preventing coagulation disturbances than balanced
electrolyte solutions. Mannucci et al. also found that the routine administration of one unit of FFP per three units
of packed cells during massive transfusion did not result in any reduction in the amount of blood transfused (21).
In a randomised study of 33 massively transfused patients (average 20 units per patient) Reed et al. investigated
whether the prophylactic administration of six units of platelets vs two units of FFP with every 12 units of modified
whole blood was effective in preventing microvascular bleeding (6). Patients were transfused with modified whole
blood (platelets and cryoprecipitate removed before storage) and an incidence of approximately 18% microvascular
bleeding was found in both groups. This compares with an incidence of 20% in a previous study from the same
institution in which no prophylactic treatment was given (22). In addition there were no statistical differences in the
platelet count between the two groups. The major drop, due to platelet washout, occurred before 10 units were
transfused with much smaller drops after 10 units, as predicted on the basis of exponential decay. The predicted
drop, however, was less than expected for pure platelet washout, suggesting perhaps release from sites of pooling.
By contrast the seven patients who developed microvascular bleeding in this study, required large and repeated
doses of platelets to stop bleeding and maintain platelet counts, suggesting that consumption played a major part
in this subgroup. These authors concluded that prophylactic platelet transfusions were not indicated.
Protocols for Massive Transfusion: Formula or Ad Hoc Replacement?
A number of different replacement formulae have been proposed (reviewed Nolan & Gallup, 4). Early
recommendations from the 1970's which suggested one unit of FFP per every four units of blood have largely been
abandoned (13, 14, 23), particularly because of the lack of correlation between the amount of FFP given and the
observed coagulopathy. Some workers have suggested that 25% of volume be replaced with FFP (1); or even a
1:1 ratio of transfused packed cells to FFP (19). Other groups have advised against prophylactic use of FFP
unless measured defects of coagulation are observed (4, 5, 14, 21). As noted above, the routine use of platelets is
also controversial. This approach is recommended by some authors (9, 22) but is not supported by an early
randomised prospective trial of prophylactic platelet transfusions (24) or by the experience of other groups (2).
There does however seem to be agreement that platelet counts should be maintained above 50 X 109/l during
massive transfusion (1, 4, 14) and many trauma units would aim for counts of >100 X 109/l. Because of the larger
initial absolute drops with exponential decay, however, maintaining levels of >100 X 109/l will be a more costly
exercise than accepting a lower count. Reasonable thresholds to be aimed for in the massive transfusion setting
are PT/APTT < X1.5 normal, fibrinogen >0.75 g/l and platelets >75 X 109/l. As mentioned, fibrinogen levels of <0.5
g/l correlate highly with microvascular bleeding and it has been suggested that in this situation, or when the
thrombin time is twice normal, cryoprecipitate (0.15 units/kg) is of benefit (4, 5). Similarly, two British Committee
for Standardization in Haematology (BCSH) Task Forces have recommended the use of cryoprecipitate when there
is continued bleeding, marked abnormalities of coagulation (fibrinogen < 0.8 g/l) or laboratory evidence of DIC (1,
14).
Both crystalloids and colloids have been used in the resuscitation of shocked patients. The theoretical advantage
of colloids is the maintenance of plasma oncotic pressure, and in general a smaller quantity is required to maintain
intravascular volume. Large initial volumes of crystalloid solutions are however well tolerated. There was a
suggestion from the North American literature that albumin resuscitation leads to greater drops in coagulation
proteins and a higher incidence of subsequent adult respiratory distress syndrome (25-30). More recent reviewers,
however, have concluded that either crystalloids or colloids may be safely given as resuscitative fluids (31).
Finally, there has been some recent interesting work suggesting that initial infusion of hypertonic (7.5%) saline
250 ml is an efficient, safe and rapid method of restoring circulating blood volume in shocked patients (32)
Fresh Blood
There is still considerable debate and interest surrounding the use of fresh, whole blood which ideally would be
fully tested but <24 hours old (1, 33). A study during Israeli-Arab Six Day War demonstrating that in combat
casualties massively transfused with whole blood less than 24 hours old (46 patients received an average of 15
units) there was no clinically evident coagulopathy (34). Probably equally relevant in this study was very
aggressive crystalloid resuscitation prior to arrival in hospital, with many patients volume overloaded with
haematocrits as low as 10%. It has been suggested that blood products contribute to a consumptive

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coagulopathy by introducing partially broken down cellular elements plus partially activated coagulation factors (5).
The degree of thrombocytopenia in massively transfused patients in one study correlated with the age of the blood
transfused (2). Transfusion of stored erythrocytes also places a considerable metabolic burden on the already
stressed patient. It has been estimated that the expenditure of up to 16,000 mmol of ATP is required to restore
one unit of red cells to the appropriate metabolic composition plus clear waste products (35, 36). Thus there
appears to be a good basis for attempting to use the "freshest blood possible" during massive transfusion
episodes, although this will be limited by logistical constraints. The use of uncrossmatched blood from walk in
donors is clearly a dangerous practice and impossible to justify (5). It seems desirable to give blood less than
three days old and certainly less than 14 days old (20) .

Conclusions
It is difficult to be dogmatic about replacement protocols based on the available literature, much of which suffers
from the retrospective design of studies and the heterogeneity of patient groups. What practical recommendations
can one deduce from the literature? Firstly, aggressive resuscitation with crystalloid or colloid plus the prevention
of hypothermia make major contributions to the prevention of subsequent coagulopathy. Secondly, microvascular
bleeding is likely to occur if platelets fall below 50 X 109/l, fibrinogen < 0.5 g/l and coagulation times >1.8 X
normal. These thresholds are likely to be attained following infusion of between 10 and 20 units of packed cells in
under 24 hours. The platelet count, PT and APTT should be followed closely in massively transfused patients, and
component therapy targeted on this basis. Because of the initial steep absolute drop in factors during the
exponential decay of "exchange transfusion", attempts to maintain normal levels of platelets and clotting factors
are likely to be costly in the use of blood components. Reasonable targets would appear to be the maintenance of
a platelet count >75 X 109/l, fibrinogen >0.75 g/l and PT and APTT <1.5X prolonged compared to normal controls.
There will be situations where rapid, catastrophic bleeding does not allow sufficient time for serial monitoring of
coagulation and platelets (e.g. >10 units of blood per hour). In this situation, a "best guess" replacement of up to
five units FFP and 10 units platelets per 10 units of packed cells, after the initial 10 units have been transfused,
may be justified to prevent microvascular bleeding from potentially dangerous sites, such as closed head injuries
in multitrauma patients. Cryoprecipitate has a role in patients with measured plasma fibrinogen of <1.0 g/l. The
freshest blood available, which has been fully screened, should be used.

References:
1.
Anonymous. Guidelines for transfusion for massive blood loss. A publication of the British Society for
Haematology. British Committee for Standardization in Haematology Blood Transfusion Task Force. Clinical &
Laboratory Haematology 1988;10(3):265-73.
2.
Harrigan C, Lucas CE, Ledgerwood AM, Walz DA, Mammen EF. Serial changes in primary hemostasis
after massive transfusion. Surgery 1985;98(4):836-44.
3.
Sawyer PR, Harrison CR. Massive transfusion in adults. Diagnoses, survival and blood bank support. Vox
Sanguinis 1990;58(3):199-203.
4.
Nolan TE, Gallup DG. Massive transfusion: a current review. [Review]. Obstetrical & Gynecological Survey
1991;46(5):289-95.
5.
Hewitt PE, Machin SJ. ABC of transfusion. Massive blood transfusion. [Review]. British Medical Journal
1990;300(6717):107-9.
6.
Reed R, Ciavarella D, Heimbach DM, et al. Prophylactic platelet administration during massive
transfusion. A prospective, randomized, double-blind clinical study. Annals of Surgery 1986;203(1):40-8.
7.
Wudel JH, Morris JJ, Yates K, Wilson A, Bass SM. Massive transfusion: outcome in blunt trauma
patients. Journal of Trauma 1991;31(1):1-7.
8.
Rohrer MJ, Natale AM. Effect of hypothermia on the coagulation cascade. Critical Care Medicine
1992;20(10):1402-5.
9.
Collins JA. Problems associated with the massive transfusion of stored blood. Surgery 1974;75:274-295.
10.
McNamara JJ, Burran EL, Stemple JF, Molto MD. Coagulopathy after major combat injury: occurrence,
management and pathophysiology. Annals of Surgery 1972;176:243-6.
11.
Lim RC, Olcott CI, Robinson AJ, Blaisdell FW. Platelet response and coagulation changes following
massive blood replacement. Journal of Trauma 1973;13:577-82.

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12.
Lucas CE, Ledgerwood AM. Clinical significance of altered coagulation tests after massive transfusion for
trauma. American Surgeon 1981;47(3):125-30.
13.
Wilson RF, Mammen E, Walt AJ. Eight years of experience with massive blood transfusions. Journal of
Trauma 1971;11(4):275-85.
14.
Contreras M, Ala FA, Greaves M, et al. Guidelines for the use of fresh frozen plasma. British Committee
for Standards in Haematology, Working Party of the Blood Transfusion Task Force [see comments]. Transfusion
Medicine 1992;2(1):57-63.
15.
Leslie SD, Toy PT. Laboratory hemostatic abnormalities in massively transfused patients given red blood
cells and crystalloid. American Journal of Clinical Pathology 1991;96(6):770-3.
16.
Beck EA, Bove JR, Hogman CF, Langdell RD, Schorr JB, Tullis JL, Veltkamp JJ. International forum.
Which is the factual basis, in theory and clinical practice, for the use of fresh frozen plasma? Vox Sanguinis
1978;35(6):426-435.
17.
Murray DJ, Olson J, Strauss R, Tinker JH. Coagulation changes during packed red cell replacement of
major blood loss. Anesthesiology 1988;69(6):839-45.
18.
Ciavarella D, Reed RL, Counts RB, et al. Clotting factor levels and the risk of diffuse microvascular
bleeding in the massively transfused patient. British Journal of Haematology 1987;67(3):365-8.
19.
Hewson JR, Neame PB, Kumar N, et al. Coagulopathy related to dilution and hypotension during massive
transfusion. Critical Care Medicine 1985;13(5):387-91.
20.
Martin DJ, Lucas CE, Ledgerwood AM, Hoschner J, McGonigal MD, Grabow D. Fresh frozen plasma
supplement to massive red blood cell transfusion. Annals of Surgery 1985;202(4):505-11.
21.
Mannucci PM, Federici AB, Sirchia AB. Haemostasis during massive blood replacement. Vox Sanguinis
1982;1982(42):113-123.
22.
Counts RB, Haisch C, Simon TL, Maxwell NG, Heimbach DM, Carrico CJ. Hemostasis in massively
transfused trauma patients. Annals of Surgery 1979;190:91-99.
23.
Consensus Conference . Fresh-frozen plasma: indications and risks. Journal of the American Medical
Association 1985;253:551-553.
24.
Heimbach DM. Hemostasis in massively transfused trauma patients. In: Fresh Frozen Plasma:
Indications and Risks. National Institutes of Health Consensus Development Conference, Bethesda, 1984.
25.
Virgilio RW, Rice CL, Smith DE, et al. Crystalloid vs. colloid resuscitation: is one better? A randomized
clinical study. Surgery 1979;85(2):129-39.
26.
Lucas CE, Ledgerwood AM, Higgins RF, Weaver DW. Impaired pulmonary function after albumin
resuscitation from shock. Journal of Trauma 1980;20(6):446-51.
27.
Weaver DW, Ledgerwood AM, Lucas CE, Higgins R, Bouwman DL, Johnson SD. Pulmonary effects of
albumin resuscitation for severe hypovolemic shock. Archives of Surgery 1978;113(4):387-92.
28.
Leibold WC, Lucas CE, Ledgerwood AM, et al. Effect of albumin resuscitation on canine coagulation
activity and content. Annals of Surgery 1983;198(5):630-3.
29.
Lucas CE, Ledgerwood AM, Mammen EF. Altered coagulation protein content after albumin resuscitation.
Annals of Surgery 1982;196(2):198-202.
30.
Johnson SD, Lucas CE, Gerrick SJ, Ledgerwood AM, Higgins RF. Altered coagulation after albumin
supplements for treatment of oligemic shock. Archives of Surgery 1979;114(4):379-83.
31.
Giesecke AJ, Grande CM, Whitten CW. Fluid therapy and the resuscitation of traumatic shock. Critical
Care Clinics 1990;6(1):61-72.
32.
Younes RN, Aun F, Accioly CQ, Casale LP, Szajnbok I, Birolini D. Hypertonic solutions in the treatment
of hypovolemic shock: a prospective, randomized study in patients admitted to the emergency room. Surgery
1992;111(4):380-5.
33.
Isbister JP. Haemotherapy for acute haemorrhage. Anaesthesia & Intensive Care 1984;12(3):217-28.
34.
Pfeffermann R, Rozin RR, Durst AL, Marin G. Modern war surgery: operations in an evacuation hospital
during the October 1973 Arab-Israeli war. Journal of Trauma 1976;16(9):694-703.
35.
Wilson RF, Binkley LE, Sabo FJ, et al. Electrolyte and acid-base changes with massive blood
transfusions. American Surgeon 1992;58(9):535-44.
36.
Sohmer PR, Scott RL. Metabolic burden of massive transfusions. Progress in Clinical and Biological
Research 1982;108:273-283.

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Table 1: A Suggested Protocol for Support of the Massively Transfused Patient.

1. Volume resuscitation
A sample is taken, wherever possible, on arrival for an urgent group & crossmatch plus
baseline FBC, PT, APTT.
Initial aggressive resuscitation with crystalloid or synthetic colloids to maintain systolic BP
>100 mm Hg and good perfusion.
All fluids should be infused through a "level one" countercurrent blood warmer and the
patient well insulated, as far as possible, in a warm environment. Avoid intraoperative heat
loss. Microaggregate filters are not routinely recommended.
2. Packed Cells
Transfuse to maintain Hb >80g/l and HCT >25%. If crossmatched or group compatible
blood are not available, use uncrossmatched group O (O positive for males and
postmenopausal females, O negative for females of child bearing age).
Continue using group O blood until group compatible (confirmed on saline "immediate
spin" against the donor units) or fully crossmatched blood available. If greater than 4 units
of group O blood has been given, a current specimen should establish that passive
haemolysins are not detectable on a normal group and crossmatch.
Transfuse with the freshest fully screened blood available (ideally < 3 days old, and
certainly less than 14 days old).
3. Platelets and Coagulation Factors
Transfusion of under 10 units in under 24 hours usually requires no platelet or FFP support
unless clinically indicated or measured abnormalities.
Measure FBC, PT, APTT regularly (every 1-2 hours until haemostasis obtained). Give
aliquots of 4 units FFP replacement if PT and APTT rise to > 1.5X normal. Check
fibrinogen in patients with persistent microvascular bleeding, despite FFP and platelet
replacement. Supplement with aliquots of 10 units cryoprecipitate if the fibrinogen falls
<1g/l .
Give platelets if measured count is <75 X109/l, or at lesser degrees of thrombocytopenia if
microvascular bleeding is noted. Aim to maintain platelet counts >50 X109/l.
If rapid, catastrophic blood loss associated with multiple trauma (e.g. >10 units per hour)
makes serial monitoring impossible, consider giving up to 10 units of platelets and 5 units
of FFP for every 10 units of blood starting after the initial 10 packed cell transfusion, until
serial monitoring allows more accurately guided therapy.

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TRANSFUSION CONTROL
A NEW CONCEPT IN NURSING MANAGEMENT
WEDDERBURN C, AU-YEUNG D, ROWLEY-BATES M, DAVIES V J, AND NICHOLLS M D., HAEMATOLOGY
DEPT, CONCORD HOSPITAL, NSW

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INTRODUCTION
As hospital transfusion practice becomes increasingly focused on the appropriate use of blood and blood products
and reducing transfusion risk, it is important to be able to identify and monitor indicators of quality of care in that
transfusion practice. It is essential that these indicators be measurable, relevant to laboratory and clinical practice
and supervised by a hospital transfusion specialist or committee.
Just as the role of infection control nurse has become recognised and its importance acknowledged in infection
control programs, the role of a transfusion control nurse has begun to emerge as a key factor in the process of
improving transfusion practices.
Such a position was created in January 1988 at Concord Repatriation General Hospital, a 750 bed teaching
hospital of the University of Sydney. Primary objectives were to review transfusion administration practices, to
optimise patient care and to undertake the opportunities for one-on-one education with nursing and medical staff
involved in all transfusion episodes. This involved a prospective transfusion surveillance and a follow up of all
transfused patients within 24 - 72 hours. All reactions were then appropriately documented, investigated and
followed up to ensure appropriate management. Blood transfusion administration was gradually optimised by
assessing all transfusion practices and by initiating appropriate responses.
In an attempt to liaise between "demand" and "supply" and to inform hospital staff about the necessity of
transfusion "risk and benefit" assessment, transfusion practices were audited and targeted education then
delivered. This was important to establish standards of transfusion practice and to format on-going education for
both medical and nursing staff. In cases where incorrect procedures are identified, inservice is delivered. In
addition to key interfaces and activity profiles (Table 1), registered nurses must attend a Blood Administration
workshop before being accredited to administer the first and subsequent units of blood and are invited to attend a
more formal three day course in Transfusion Medicine, held twice yearly. The autologous predeposit program
commenced in 1983 with the aim of maximising autologous opportunities and has been previously reported (1).
This program was also expanded to include intraoperative haemodilution and salvage and involved liaison with the
hospital's blood bank, surgical and anaesthetic staff.
The purpose of this paper is to demonstrate the advantages of creating a position of Transfusion Control Nurse to
co-ordinate a Transfusion Surveillance Program.
TRANSFUSION SURVEILLANCE
The transfusion surveillance program commenced in 1988 and has enabled all patients to be followed up within 2472 hours of transfusion. All documented transfusion reactions were referred to a Haematologist for clinical
assessment and were recorded on a Transfusion Reaction Investigation Form. The surveillance program has
provided accurate information on the prevalence of transfusion reactions and appropriate management and
education strategies have been instituted. From 1988 - 1991 Concord Hospital's transfusion surveillance program
followed up the transfusions of 30,000 red cells, FFP and platelets. Morbidity occurred in 1 in 29 episodes (1). By
1993, we had followed up 47,700 transfusions and morbidity had been reduced in total to 1 in 80 transfusion
episodes (Table 2). This improvement can be attributed primarily to appropriate planning of transfusion therapy in
patients who are transfusion dependent, (eg the use of blood warmers and filters), to better ward nursing
transfusion practices (Table 1), increased transfusion medicine education and maximisation of autologous usage
in patients facing elective surgery. All data collected is entered into individual patient records in the Blood Bank
computer re future transfusion requirements and in the Blood Donor Centre for statistical reference and research
purposes.

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AUDITS
As part of the transfusion surveillance program, the appropriateness of blood transfusions was assessed by
several transfusion audits. In January 1990 a retrospective audit was carried out on 246 transfusion episodes in
178 patients to determine the appropriateness of red cell, platelet and FFP transfusion practices. Criteria for
appropriate red cell, FFP, platelet and single unit transfusions were formulated. Forty-six percent of the red cell
transfusions were considered appropriate consequent to active bleeding, with or without hypovolaemia or with a
documented fall in Hb within the preceding 48 h. Similarly, a red cell transfusion was considered appropriate in
the presence of anaemia if the Hb was <8.5g/dL or if the Hb was between 8.5 and 10.0g/dL in the presence of
cardiovascular instability or ongoing chemotherapy; 54% of the transfusions were given for this indication. In total,
98.3% of these red cell transfusions were considered justified. There were only 10 units, transfused to six
patients, considered inappropriate.
Platelet transfusion criteria were also established. Prophylactic platelet transfusion was considered appropriate if
the platelet count was <20 x 109/L and 33% of the platelets were transfused for this indication. Since 1992, the
threshold would be 15 x 109/L if this audit were repeated (NSW Blood Transfusion Service Guidelines). Platelet
transfusions were considered appropriate if the platelet count was <50 x 109/L in the presence of bleeding or
disseminated intravascular coagulopathy (DIC) and if given prophylactically to prevent bleeding with invasive
procedures or surgical events; 47% of platelets were transfused for this indication. In the remaining 20% of
cases, platelet transfusions were given if the platelet count was >50 x 109/L in the presence of bleeding, laboratory
evidence of platelet dysfunction or in association with a massive transfusion event, as defined by the transfusion of
greater than one blood volume in 24hr. In all, 89 units of platelets were transfused and all were considered
appropriate. This figure is consistent with our policy of concurrent vetting of all platelet transfusion requests by an
on-call haematologist.
Audit criteria for FFP transfusions were also developed. FFP administration was considered appropriate
prophylactically or therapeutically in three situations consequent to chronic or acute hepatic dysfunction (68%),
warfarin-related bleeding (5%), and in massive transfusion cases (26%). In all, only 43 units of FFP were
transfused during the audit period which was unrepresentatively low. Of these, 88.4% were considered
appropriate. Between 1988 to 1992 there has been a 42% reduction in the hospital's usage of FFP and a further
FFP audit (1992) showed 98.7% of units transfused to be appropriate to the clinical circumstances. In all cases
pre and post FFP, PT, APTT tests were performed (3).
Another audit, conducted from August 1991 to January 1992, focused on the appropriateness of single unit red cell
transfusions as defined by a one unit transfusion within a 72hr period. Single unit transfusions accounted for 1.5%
of units and 3.8% of patients transfused. In all, 60% of the single unit transfusions were justified (36 units
transfused to 36 patients). In this group the pre-transfusion Hb was 8.7g/dL, which was much lower than the mean
pre-transfusion Hb (11.1g/dL) in the 40% of unjustified single unit transfusions. Of this latter group (25 units
transfused to 25 patients), 80% were administered in the presence of acute blood loss in the operating room
complex. It is of interest that the mean pre-op Hb in the 13 autologous patients receiving a single unit transfusion
was 11.6g/dL, obviously indicating a higher transfusion trigger. A consequent recommendation of this audit to the
hospital transfusion committee was that a facility to assess intra-operative Hb be provided to assist in the
transfusion decision. The single unit, single transfusion event in particular must be critically reviewed to assess
the transfusion risk-to-benefit relationship in these transfusion decisions.
DAY ONLY TRANSFUSIONS
Data collected during our transfusion surveillance revealed that the length of stay for transfusion dependent
patients ranged between 2 and 3 days. After investigating the then current admission and transfusion processes,
it became clear that the transfusion period could be reduced. A more streamlined procedure is now completely
co-ordinated by the Transfusion Surveillance Team and calls for the patient to be brought in the day before
admission and blood sample taken for cross matching. By 7.30 the next morning the patient is admitted and the
first unit of blood commenced. A further 2 units can be safely administered during the day allowing the patient to
be discharged by early to late afternoon. Transfusion dependent patients admitted as inpatients are also
coordinated by the Transfusion Surveillance Team in order to minimise their length of stay.
FIBRIN GLUE
Since 1992 the transfusion surveillance program has also been involved, in certain clinical circumstances, in the
preparation of cryoprecipitate for fibrin glue. Using the Double-Freeze thaw method of Wan et al 1989 (2), 6

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patients undergoing Free Flap reconstructive surgery for Head and Neck cancer were treated with autologous or
directed fibrin glue. A cost comparison study of these patients and 6 controls was performed which showed
savings in dressing costs of between 37% and 78% as well as savings in nursing opportunities which amounted to
22 - 60hrs/patient. The 3-day preparation time for all freeze-thaw manipulations occupied only 1 hour labour of
Blood Bank staff. The hospital length of stay was shorter in the fibrin glue group providing additional potential
savings occupied bed day. In addition the post hospital phase required no additional dressings. In comparison,
the control group required community nursing services for up to 2 months.
ALLOGENEIC PROGRAM
An allogeneic program linked to the Red Cross Transfusion Service was established at CRGH in 1989 as part of a
comprehensive transfusion service and to enable staff donors to donate at more convenient times with no intrusion
on the Hospital workload. This program has enabled us to recruit donors for a Special Donor Panel for single
donor platelets and for the very occasional requirement of super fresh blood. In addition, the on-site allogeneic
program has provided constancy of blood supplies at times of intermittent NSW BTS shortages with supply and
has prevented the unnecessary postponement of some surgery.
From January 1989 to June 1994 a total of 8009 allogeneic donations have been collected. Of this, 23.7% were
staff, 32.2% from Donor Centre recruitment drives and 41.5% were self referred. Overall, donations have
increased at a rate of 10% per annum and the program has proved to be successful with many advantages for
patient care and in promoting local community links and support.

CONCLUSION
Transfusion Control Nursing or Transfusion Surveillance, as described during this article forms a basis for
monitoring and evaluating hospital transfusion practices and subsequently for initiating a directed education
program. The objectives for this role encompass the optimisation of transfusion practices, an active transfusion
program for the identification and management of transfusion reactions, an interactive predeposit autologous blood
collection program and a pro-active transfusion medicine education policy for medical officers and registered
nurses. In the context of hospital transfusion practices, the indications of quality of care must be measurable and
therefore available for systematic and on-going monitoring. The net result of transfusion control nursing is an
incremental improvement in patient care.

Correspondence: Dr MD Nicholls, Haematology Department, Concord Hospital, NSW 2139

REFERENCES:
1. Nicholls M, Predeposit Autologous Blood - How far can we go? in Australia Anaesthesia 1992.
Kerr D and Thirlwell J, Australian and New Zealand College of Anaesthetists, 152-158
2.

Wan H-L, Huang ST, Floyd DM, McGowan EI, Feldman DS. Is the amount of fibrinogen in cryoprecipitate
adequate for fibrin glue? Introduction of an improved recycled cryoprecipitate method.
Transfusion
1989;29:Oct (Suppl); Abstract S143;p41S.

3.

Nicholls MD, Au-Yeung D, Iannella M, Fresh Frozen plasma use in a tertiary-referral hospital,
J Qual Clin Practice (1984), 14, 77-84

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Table 1 - Activity Profile of Nursing Transfusion Control and Surveillance Function

ACTIVITY
NIGHT TRANSFUSIONS

TRANSFUSION NOTES
CROSS MATCH REQUEST FORM

OUTPATIENT TRANSFUSIONS

PLASMA THAWING PROCEDURE

PLATELET TRANSFUSION AND

POOLING

PATIENT IDENTIFICATION

LIAISON WITH HAEMATOLOGY

TEAM

TRANSFUSION CONTROL
NURSE MONITERING

TRANSFUSION CONTROL
NURSE LIAISON

ACTION
Wards identified and inserviced;
Flyer attached to all units of blood despatched after 10pm
highlighting safety issues;
Followup medical team to ensure transfusion clinically
indicated.
Ensure nursing reports correctly documented.
Refer noncountersigned request forms to Transfusion
Specialist/Committee.
Reduce length of stay of transfusiondependent patients to day
only.
Overcame incorrect ward thawing by thawing FFP in monitored
water bath in blood bank.
Prospective vetting of all platelet transfusions;
Enhance customer service by pooling platelets in Blood Bank
immediately pretransfusion.
Wards and units with inadequate identification of patients
transfused identified and inserviced;
Inadequate identification data referred to Transfusion
Specialist/Committee;
Data issued to Nursing Quality Assurance.
Coordinate transfusion dependent inpatients to minimise
length of stay;
For special requirements, eg single donor platelets, HLA
matched platelets:
- screen family members for group compatibility and
serology for infectious markers, or
- select donors from special panel.
All documented reactions are referred to a Haematologist for
clinical assessment;
Reaction details on patients all entered on Blood Bank
Computer;
Registered nurses are educated on appropriate management
eg. Leucocytes filters;
All data is stored in Blood Donor Centre for statistical
research.
Staff Haematologist re unsafe Transfusion Practices;
NSWBTS Metro and Country to Link Autologous and
Allogenic Collections;
Director of Nursing for staffing, equipment, etc
Quality assurance staff re improvement in transfusion
practices;
Surgeons, anaesthetists, etc

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Table 2 - Transfusion Reactions

1988 - 1993

RED CELLS

No. of Units Transfused

PLATELETS

FFP

39,239

1,747

6,667

No. of Transfusion Reactions

465

95

33

Prevalence of TxR/Tx * episode

1:84

1:18

1:202

Febrile

72%

69%

30%

Overload

14%

6%

Allergic

9%

7%

52%

Histamine

12%

Haemolytic

10%

Infective/Contaminated

1%

2%

2%

12%

Anaphylactic

*TxR

- Transfusion Reaction, Tx - Transfusion

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