Download weighing up the risks: hazards of anaemia

8 March 2013
No. 9
Perioperative Transfusion
Triggers
P Slabber
Commentator: V Ramson
Moderator: C Evans
Department of Anaesthetics
CONTENTS
INTRODUCTION...........................................................................3
HISTORY OF BLOOD TRANSFUSION........................................3
PHYSIOLOGICAL PRINCIPLES..................................................4
MEASUREMENT OF TISSUE HYPOXIA.....................................7
WEIGHING UP THE RISKS: HAZARDS OF ANAEMIA………..9
WEIGHING UP THE RISKS: HAZARDS OF BLOOD
ADMINISTRATION......................................................................10
WEIGHING UP THE RISKS: CONCLUSION..............................11
EVIDENCE BASED MEDICINE: A STEP CLOSER...................12
CURRENT GUIDELINES............................................................14
METHODS TO DECREASE ALLOGENEIC BLOOD USAGE
PERIOPERATIVELY...................................................................15
CONCLUSION.............................................................................16
Page 2 of 21
PERIOPERATIVE TRANSFUSION TRIGGERS
INTRODUCTION
Many red blood cell transfusions take place in the perioperative period and
as anaesthetists we are intricately involved in this decision making process.
With the rising cost of blood products, critical shortages in blood supplies
and increasing awareness of the complications of blood transfusion, this
decision making process deserves more attention than it is currently
receiving. Appropriately used blood transfusions can be life saving, but
unfortunately many allogeneic blood transfusions administered to our
patients are unnecessary or even harmful.(1) On a daily basis anaesthetists
have to weigh up the risks of transfusion against the risks of anaemia in
their decision to transfuse or not.(2) Evidence is often contradictory or
extrapolated from a different patient group to the one you are faced with.
Guidelines can be vague which leaves the decision up to the discretion of
the often uninformed physician. This booklet aims to shed some light on
these issues faced by anaesthetists, often on a daily basis.
HISTORY OF BLOOD TRANSFUSION
Since the 16th century physicians have shown an interest in blood
transfusions. Jean Denis was the first to transfuse sheep’s blood to a
young boy age 15 years in 1667. The boy survived, but this practise was
outlawed in 1678 due to a very high mortality. Philip Physick was the first
known to transfuse human blood to his patients, but did not publish his
work. James Blundell, an obstetrician, described and published the first
successful transfusion of human blood to a patient after post partum
haemorrhage in 1818. He used the husband’s blood to accomplish this
feat.(3,4) His mortality rate was around 50%. Since then significant advances
has been made in blood transfusion practices with resultant improved
mortality rates.
Historically a transfusion trigger of 10g/dl was proposed as early as 1942.(5)
This number was used for normal, healthy perioperative patients by the
majority of physicians for the next 4 to 5 decades. This so called “10/30”
rule (10g/dl haemoglobin or hematocrit of 30%) was the generally accepted
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minimum level of haemoglobin, particularly in the surgical setting.(6) This led
to unnecessary transfusion of patients and probably to a significant
transfusion related infection rate (10% of HIV infection worldwide is thought
to be transfusion related) as donated blood has only been screened for HIV
since 1985 in US.(7)
The “10/30” rule was challenged in 1988 during the national institutes of
health consensus development conference. It led to a new era in blood
administration practice and it was proposed that otherwise healthy patients
with a haemoglobin of more than 10g/dl rarely require transfusion and
patients with acute anaemia with a haemoglobin less than 7g/dl will
frequently require transfusion.(8) This was a step in the right direction and
sparked new interest in blood transfusion therapy which led to significant
effort being placed on research. The hunt for the universal transfusion
trigger was on. With this, guidelines was being developed and published on
a frequent basis.(9) Despite all this, transfusion practices today still vary
significantly worldwide.(10)
Today around 85 million units are transfused annually worldwide.(11) We are
seeing far fewer transfusions in the 10g/dl range. Unfortunately most
transfusion decisions are still being based on a specific haemoglobin level,
rather than on a combination of physiological signs due to tissue
hypoxia.(12) The reasons for this are multifactorial, but one reason may be
the poor understanding of the physiological principles of oxygen delivery in
the body and the fact that there is currently no simple universally accepted
test to detect regional tissue hypoxia in any given area in the body.
PHYSIOLOGICAL PRINCIPLES
The reason for red blood cell transfusion is simple. It is to improve oxygen
delivery to cells. Aerobic metabolism and the prevention of hypoxia is
dependent on the continuous delivery of oxygen to tissue. The oxygen flux
equation is a well known physiological principle that describes all the
factors involved in oxygen delivery.(9)
DO2 = CO x CaO2
CO = heart rate x stroke volume
CaO2 = (Hb x 1.34 x SaO2) + (PaO2 x 0.031)
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From the above equation we can see that oxygen delivery (DO2) is
determined by the product of cardiac output (CO) and arterial oxygen
content (CaO2). Cardiac output is determined by the product of heart rate
and ventricular stroke volume. Arterial oxygen content is determined by 3
factors: haemoglobin concentration, haemoglobin saturation with oxygen
(SaO2) and arterial oxygen tension (PaO2).
Global oxygen consumption (VO2) describes the amount of oxygen
consumed by the whole body and is usually around 250mls oxygen/min at
rest. Global oxygen delivery (DO2) as described by the above equation is
usually around 1000mls oxygen/min at rest. The relationship between VO2
and DO2 (VO2/DO2) is known as the oxygen extraction ratio (O2ER) which
is usually around 25% at rest.(18) The relationship is illustrated in figure 1.(19)
Figure 1: The relationship in a healthy adult between VO2 and DO2(19)
It is possible to see from this graph that a normal VO2 can be maintained
for a wide range of DO2 as long as the DO2 is above the critical DO2 point,
therefore the VO2 will be DO2 independent. But at a specific point termed
the critical DO2 (DO2 CRIT) the VO2 starts to decrease (VO2 will be DO2
dependent) in relation to the decrease in DO2 leading to tissue hypoxia,
anaerobic metabolism and lactate formation.
With the above concept in mind we can now look at the body’s
compensatory mechanisms in response to acute anaemia. Acute anaemia
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can lead to decreased DO2. These compensatory mechanisms are aimed
at keeping the DO2 above the DO2CRIT to maintain VO2 and therefore
adequate tissue oxygenation. First there is a change in blood flow
dynamics caused by the decreased viscosity seen in anaemic blood. This
will lead to improved flow characteristics resulting in increased venous
return and decreased systemic vascular resistance, both leading to
increased CO and therefore DO2. Secondly, the anaemia leads to
sympathetic nervous system activation causing increased CO. Third, the
O2ER can be increased leading to increased VO2 for the same DO2. It must
be remembered that this compensatory mechanism is sufficient to maintain
VO2 only as long as the DO2 is above the DO2CRIT and that once the DO2
falls below the DO2CRIT an increase in O2ER will not be sufficient to
compensate and prevent tissue hypoxia.(18)
Of all the determining factors for oxygen delivery, the most important
physiological adaptation during acute normovolaemic anaemia is the
increase in cardiac output and increased oxygen extraction ratio.(2) Due to
these compensatory mechanisms by the body we see healthy patients able
to tolerate haemoglobin levels at 5g/dl by increasing their CO.(13) Reports
on Jehovas Witness patients with haemoglobin levels of 5g/dl or less
showed inconsistent mortality rates related to severe anaemia,
demonstrating adequate compensation is possible.(14) One of the most
extreme examples of anaemia tolerance is that of a 53 year old man that
suffered multiple stab wounds leading to axillary artery injury and significant
bleeding. He’s lowest haemoglobin was 0.7g/dl and he never showed any
signs of myocardial ischemia and survived without any sequelae.(15)
As mentioned before, one of the most important compensatory
mechanisms during acute anaemia is an increase in cardiac output. This
can only occur if there is adequate coronary perfusion to supply the
increased metabolic demands of the myocardium during this stressful
period. With this in mind, it would be obvious that myocardial oxygen
supply is one of the factors involved in determining the physiological limits
to acute anaemia. Therefore adequate coronary perfusion is believed to be
an important limiting factor in the tolerance to acute anaemia.(2,16) This is
probably illustrated in the observation that patients with cardiovascular
disease and perioperative anaemia are more likely to have a worse clinical
outcome.(17) This might also be the reason that a higher transfusion trigger
is often chosen for patients with coronary artery disease.
Page 6 of 21
The simplest way to support a patient’s DO2 perioperatively is by increasing
the inspired oxygen fraction (FiO2). It has been argued that by increasing
the FiO2, the DO2 doesn’t increase significantly due to the fact that at an
arterial oxygen tension (PaO2) of 70mmHg the haemoglobin saturation is
90% (deduced from the oxy-haemoglobin dissociation curve).(20) Although
during acute normovoleamic anaemia there is an expansion of the plasma
compartment containing dissolved oxygen. So by hyperoxic ventilation
(FiO2 = 60%) it is possible to saturate this compartment fully causing an
increased gradient for oxygen between plasma and cells and therefore
improving tissue oxygenation.(18) This is partly proven by a study where
healthy volunteers were haemodiluted from 12.7g/dl to 5.7g/dl causing
cognitive and memory impairment which was completely reversed after
breathing oxygen which increased PaO2 levels to approximately
400mmHg.(21)
It is obvious now that there are multiple physiological factors playing a role
in tissue oxygenation. In clinical practice it would be a daunting task to try
and determine which variable is responsible for the tissue hypoxia and
where exactly in the body tissue hypoxia is taking place. It would be of
great value if there was a simple test available to measure the degree of
tissue hypoxia both on a global and regional level. Mixed venous oxygen
saturation has been proposed.
MEASUREMENT OF TISSUE HYPOXIA
In the quest to move away from arbitrary haemoglobin based transfusion
triggers, the concept of physiological transfusion triggers emerged.(22)
Physiological transfusion triggers potentially reflect a reversible limitation of
oxygen delivery to peripheral tissues. The reversal of a physiological
transfusion trigger by a blood transfusion can be seen as an indicator of
transfusion effectiveness. Of course there are prerequisites for the correct
interpretation of these physiological transfusion triggers like normovolaemia
and appropriate depth of anaesthesia.(19)
The limitation of tissue oxygenation can be measured in a variety of regions
in the body. Physiological transfusion triggers for both global (lactate,
mixed venous oxygen saturation, tachycardia, increased catecholamine
Page 7 of 21
demand) and regional (ST segment changes, compromised ventricular
contractility seen on echo, P300 latency test) tissue oxygenation were
proposed to assist in guiding red blood cell transfusion practice.(19) All the
above physiological transfusion triggers have got shortfalls in their
application and will require a fair amount of knowledge for their correct
interpretation. I will only look at the concepts and possible short falls behind
using mixed venous oxygen saturation as a physiological transfusion
trigger.
Mixed venous oxygen saturation (SvO2) is a clinical tool which integrates
the relationship between global VO2 and DO2. It is strictly speaking the
oxygen saturation of haemoglobin taken from the pulmonary artery and is
usually in the range of 70% in healthy adults.(23) Because placing a
pulmonary artery catheter often leads to iatrogeneic complications, a
surrogate for this measurement, the central venous oxygen saturation
(ScvO2) which is taken from the right atrium via a central venous catheter
was suggested. It has been proposed that there is good correlation
between these two measurements with ScvO2 being on average 5% higher
than SvO2.(24) This is due to deoxygenated blood draining into the right
ventricle from the coronary sinus and thebesian veins.
There are 4 main determinants of SvO2 namely haemoglobin, CO, SaO2
(previous 3 factors determine DO2) and VO2. When haemoglobin levels
decrease during anaemia, there is a decrease in DO2 if CO and SaO2 stay
constant, which will lead to a decrease in SvO2 if VO2 stays the same or
increases. This might be seen as a warning sign and prompt sometimes
inappropriate action to increase DO2 by increasing haemoglobin (by giving
blood) or increasing CO (by giving inotropes) to ensure tissue oxygenation.
We assume tissue hypoxia if SvO2 decreases, but this might not be the
case as an increase on O2ER (physiological compensatory mechanism)
can compensate for the decreased DO2 and prevent tissue hypoxia.(23)
When DO2 decreases below DO2CRIT, there is a state of VO2-DO2
dependency, also known as tissue dysoxia. This indicates tissue hypoxia
and increasing lactate (a physiological transfusion trigger) formation.
Dysoxia is usually present in humans when the SvO2 is below 50%. It has
been proposed that measures to increase DO2 (e.g. blood transfusion)
should be followed to increase SvO2 levels above 70% to ensure tissue
oxygenation.(25) Although using SvO2 to guide interventions that increase
Page 8 of 21
DO2 to ensure adequate tissue oxygenation can be falsely reassuring. This
is because in some pathological states where there is low O2ER the SvO2
will seem adequate but the patient is really in a state of hypoxia. This is
where regional oxygenation measurement might be more useful.
Recently there has been a trend towards using physiological transfusion
triggers to guide blood administration.(22) The shortfalls of SvO2
measurement, as explained above, has to be remembered especially in the
perioperative period when there are many factors influencing the VO2-DO2
relationship.(23) The maintenance of adequate tissue oxygenation in the
perioperative period is central to our practice, although there are no
universally accepted guidelines or physiological transfusion trigger to
monitor oxygen delivery and tissue oxygenation.(2) This leaves the
physician to weigh up the risks of anaemia against the risks of blood
administration while deciding whether or not to transfuse the patient.
WEIGHING UP THE RISKS: HAZARDS OF ANAEMIA
In healthy patients, mortality significantly increases once their haemoglobin
levels drop below 3.5g/dl.(4) In the perioperative setting it was demonstrated
that there was a correlation between preoperative anaemia and mortality.
This study by Carson in 1988, “Severity of anaemia and operative mortality
and morbidity”, showed a mortality of 7.1% when haemoglobin was above
10g/dl compared to a mortality of 61% when haemoglobin dropped below
6g/dl.(26) In patients with cardiovascular disease (including coronary artery
disease) the presence of a haemoglobin less than 6g/dl let to a significant
increase in 30 day mortality rate compared to those with a haemoglobin
above 12g/dl.(27) In patients with chronic renal disease the presence of
anaemia led to a higher annual mortality.(28) In elderly patients (>65yrs)
even a mild degree of preoperative anaemia led to increased 30 day
mortality rate.(29)
From the above we can deduct that there is sufficient data identifying
anaemia as an independent risk factor for perioperative morbidity and
mortality.(2) The degree of anaemia also seem to correlate with severity of
outcomes. It is also safe to say that in patients with cardiovascular
comorbidities the effect of anaemia on morbidity and mortality is
augmented.
Page 9 of 21
WEIGHING UP THE RISKS: HAZARDS OF BLOOD ADMINISTRATION
The complications associated with blood administration are numerous and
often serious, contributing to patient morbidity and mortality.(34) As outlined
below it can be classified into immunological and non immunological.
Blood
transfusion
complications
Non
immunological
Infection
Viral
Bacterial
Immunological
TACO
Parasite
TRALI
Prion
TRIM
Febrile reaction
Non hemolytic
Anaphylactic
Post
transfusion
purpura
Hemolytic
Graft vs Host
disease
ABO
incompatibility
Infection has originally been the most feared side effect of blood
transfusion.(2) Costly measures has been implemented to minimise this risk
and today especially in first world countries, receiving a unit of blood has
been quoted as being very safe.(4) Although the risk is never zero. Cyto
megalo virus is the most commonly transmitted virus with an incidence of
around 1 in 20. Luckily disseminated infection seems to only develop in
immuno-suppressed patients eg very low birth weight neonates. In South
Africa every unit is routinely tested for HIV 1 and 2, hepatitis B and C virus
and syphilis using tests like hepatitis B surface antigen, hepatitis C
antibody, HIV 1 and 2 antibodies and nucleic acid amplification testing (for
HIV, HBV and HCV).(30) These screening tools adds significantly to the cost
of a unit of packed red blood cells is South Africa so that in 2012 you would
pay R1369.00 in state sector. The incidence of adverse effects to red blood
cell transfusion is well illustrated and compared to other fatal occurences
on a logarithmic scale in figure 2.
Page 10 of 21
Figure 2: Adverse effects of RBC transfusion contrasted with other risks on a logarithmic scale. (12)
Physicians are less aware of the immunological complications of blood
transfusion. Currently one of the most dangerous hazards of blood
transfusion is TRALI (transfusion related acute lung injury).(31) By definition
it is a new acute lung injury occurring within 6 hours of transfusion in
patients without risk factors for acute lung injury.(2) It is manifested by
dyspnoea, fever and hypotension and treatment is supportative, often
requiring intubation and ventilation. One of the differentials for TRALI would
be TACO (transfusion associated circulatory overload). TACO occurs often
in the elderly and is treated with diuretics.(32) It also adds significantly to
length of hospital stay. TRIM (transfusion related immunomodulation)
results in a general increase in post transfusion infection rates. It is
probably one of the reasons for seeing increased postoperative bacterial
infection and cancer recurrence rates in patients receiving allogeneic blood
transfusions.(33)
WEIGHING UP THE RISKS: CONCLUSION
We can now see that both anaemia and blood transfusion hold significant
risks for our patients. As physicians we know that patients presenting with
preoperative anaemia, are at higher risk for worse outcomes than those
Page 11 of 21
without anaemia. But we also know that if you transfuse these anaemic
patients in the perioperative period the outcomes are often worse.
Therefore the ideal would be to have all patients presenting to theatre with
normal haemoglobin levels. This might not be a viable option as patients
would have to be seen months in advance, with frequent follow up, to
monitor the treatment effects to anaemia.
Therefore in our daily practice a trade-off between the effects of anaemia
and those of red blood cell administration has to be made while calculating
our decision whether to transfuse or not.(2) Having an approach to this
problem, that is easy to follow, would make decisions regarding
perioperative blood administration easier. Not surprisingly, there is no
universally accepted approach to this complicated dilemma.
EVIDENCE BASED MEDICINE: A STEP CLOSER
Because it is a complicated process to weigh up the risks of anaemia
against the risks of blood transfusion in our every day decision making
process, maybe there is a better approach to this issue. By comparing
patient outcomes through reliable evidence in specific patient groups,
randomized to a restrictive (7-9 g/dl) and liberal (>9 g/dl) transfusion groups
we might find a simpler approach to our practice. If the outcomes are the
same, the restrictive group will not be harmed by infectious and noninfectious complications of unnecessary blood transfusions and a
significant cost saving will incur as less blood units will be administered.(12)
There have been multiple studies investigating the above research
hypothesis. Some of them were small retrospective studies in burns
patients with various flaws in study design.(35) Others were adequately
powered randomised controlled trials of specific patient groups e.g. the
TRACS (transfusion requirements after cardiac surgery) trial.(36) Although,
to get the best overall view of the literature, systematic reviews that
incorporate randomized controlled trials with specific exclusion criteria
should be looked at. Two such reviews have been published by the
Cochrane database, one in 2002 and the other in 2010.(37,38) The similarity
in certain outcomes between these two reviews were striking:
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 40% decreased risk of receiving RBC in the restrictive group vs
liberal group
 30-day mortality and rate of cardiac events unaffected in restrictive
group vs liberal group
 Length of hospital/ICU stay unaffected in restrictive group vs liberal
group
Subsequent to these reviews the FOCUS (Liberal or restrictive transfusion
in high risk patients after hip surgery) trial was published.(39) They enrolled
2016 patients of age 50 yrs or older who either had a history of
cardiovascular disease or had risk factors for it. After randomization, results
similar to the above reviews were found:
 An average of 2 units more transfused in the liberal group
 Death or inability to walk across a room unassisted after 60 days, no
difference between liberal and restrictive groups
 Rate of in hospital acute coronary syndrome 4.3% in liberal and 5.2%
in restrictive groups (no statistically significant difference)
The most recent systematic review of the literature was published in 2012
by the AABB (American association of blood banks).(12) Like the systematic
reviews in the Cochrane database they used specific criteria for selection of
trials from the 1950s until 2011. Based on high quality evidence they made
very specific recommendations:
1. In hospitalized haemodynamically stable adult and paediatric patients
only consider transfusion when Haemoglobin is <7g/dl.
2. In hospitalized heamodynamically stable postoperative surgical
patients or patients with pre-existing cardiovascular disease consider
transfusion when Haemoglobin is <8g/dl
Or
when they are symptomatic (angina, hypotension, tachycardia).
Page 13 of 21
CURRENT GUIDELINES
There are multiple recommendations and practice guidelines in the
literature with regards to blood transfusion practices. For us as
anaesthetists, the most practical and relevant guidelines was published in
2006 by the American Society of Anaesthesiologists Task Force.(40) These
are most likely the guidelines that will be referred to in a court case if
negligence with regards to transfusion practice is suspected. For simplicity I
will summarise only what is relevant to us.
ASA Practice guidelines for perioperative blood transfusion:
1. Monitor for inadequate perfusion and oxygenation of vital organs:
 Conventional methods - Blood pressure
- Heart rate
- Oxygen saturation of blood
- Urine output
- Electrocardiography
 Special methods - Echocardiography
- Mixed venous oxygen saturation
- Blood gasses (? lactate levels)
Note: In the guideline it states that the literature is insufficient to evaluate the efficacy of these special
methods for detecting inadequate perfusion/oxygenation of tissue or organs.
2. Monitor for transfusion indications:
 Hb < 6 g/dl (especially in acute anaemia)
 Hb between 6 – 10 g/dl the decision should be based on:
- Ongoing indications of organ ischemia
- Potential or actual ongoing bleeding (rate and magnitude)
- Assessment of intravascular volume status
- Risk factors for inadequate oxygenation (eg patients with
cardiorespiratory disease or high oxygen consumption)
Page 14 of 21
METHODS TO DECREASE ALLOGENEIC BLOOD USAGE
PERIOPERATIVELY
Considerable research has been done on methods to decrease allogeneic
blood usage worldwide. Not all these options (like erythropoietin) are
practical in the South African setting for various reasons like cost and time
factor. Below I will shortly mention the most appropriate methods for
anaesthetists to decrease allogeneic blood usage in the perioperative
period.
1. Decreased “transfusion triggers”
Decrease your transfusion trigger in stable healthy patients to 7 g/dl,
being vigilant in observing for signs of tissue hypoxia. Restrictive
transfusion strategies have been shown by Carless et al in a
systematic review, “Transfusion thresholds and other strategies for
guiding allogeneic red blood cell transfusion”, to reduce the risk of
receiving a red blood cell transfusion by a relative 37%.(38) This
equates to an average absolute risk reduction of 33% (95% CI 21%45%).(38) It is probably the most effective and safest method to
decrease allogeneic blood usage. There is no additional costs
involved and in only requires a change in mindset.
2. Cell salvage
Usage of this technique has become more popular with advances in
technology. It is considered a viable option in specific settings.
Relative contra-indications and indications have to be considered to
be able to benefit maximally from this technique.(41) If the mean
transfusion requirement for the specific procedure exceeds 1 unit it
should be considered.
3. Acute normovolemic haemodilution
The literature supports the efficacy in reducing the number of
allogeneic units transfused per patient. But there is controversy with
regards to the efficacy to reduce the number of patients receiving
allogeneic blood.(42) It does seem to be safe and effective in centres
that make routine use of this technique.(4)
Page 15 of 21
4. Pharmacological interventions
The use of antifibrinolytics (tranexamic acid and aprotinin) have been
shown to decrease perioperative blood loss and allogeneic blood
requirements in certain surgical procedures such as major
orthopaedic surgery.(43) Tranexamic acid seems to be associated with
less adverse events than aprotinin.
5. Induced hypotensive anaesthesia
This has been shown to be effective in decreasing blood loss and
requirements of allogeneic blood especially in orthognathic
surgery(44), although it has been associated with it’s own side effects.
Patient selection and appropriate monitoring is vital.
CONCLUSION
Around 700 000 units are transfused annually in South Africa.(30) As
perioperative physicians we are faced with making decisions regarding
blood administration almost on a daily basis. Blood should only be
administered if it improves patient outcome. This is easier said than done
as there are so many variables to consider.
As each of our patients physiological limits to anaemia differ (depending on
their state of health) the idea of a universal transfusion trigger has been
correctly scrutinized in the literature as being too a simplistic approach.
Although the use of physiological transfusion triggers e.g. mixed venous
oxygen saturation has been suggested to guide management, they are not
without limitations which need to be taken into consideration when used.
Evidence based medicine has been invaluable in guiding our practice. The
use of a liberal transfusion trigger (>9 g/dl) doesn’t have a better outcome
for the majority of patients compared to a restrictive transfusion trigger (7-9
g/dl).(38) In specific high risk patient groups like those with acute coronary
syndrome, the literature is insufficient to make recommendations with
regards to transfusion guidelines.(12) In these groups vigilance with regards
to monitoring for signs of tissue hypoxia is imperative to guide our decision.
Page 16 of 21
The resistance to change in blood transfusion practice by doctors is
affecting patient’s lives. I suggest following the ASA guidelines of 2006(40)
as these are the most applicable to us as anaesthetists. I would encourage
you to not only remember a specific number, but to use wisely all methods
available to you and to take into consideration all variables known by you,
to ensure tissue oxygenation and improve patient outcome. So before you
administer the next bag of blood to your patient, ask yourself this: If this
was me, would I want to receive this blood??
Page 17 of 21
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