Transfusion Practice Clinical Aspects and Applications

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Transfusion Practice
Clinical Aspects and Applications
10.1 TRAN5FUSION
Transfusion is the process of transfusing blood and its component, which may be between individuals of
the same species (homolog us transfusion) or it may be retransfusion of collected blood into the. same
individual simultaneously or at a later date (autologus transfusion).
Since transfusion is not without hazard, so before administration, we must determine the \VHAT for
any such procedure
W
Whether required
H
How much required
A
Actual component required
T
Time duration of transfusion, i.e. rate at which blood to be administered
To determine WHATindications for transfusion must be known and the particular component required
or suitable for the condition. In this connection, it will be worthwhile to mention that upto a 20% loss of
blood volume can be combated with immediate normal saline transfusion by at least three times of the
amount lost and the patient remains stable fOT twenty four hours provided the PCV does not fall below
30% and in such event administration of blood transfusion has to be considered. Indications given
below are for whole blood and/or c~mponent,
amount (how much) required and time duration (rate of
transfusion) varies from case to case and has to be assessed separately by clinician, each case individually.
The blood component and their indication for usage are given in Table 10.1. There are other uses
also which are not much important. The amount and time duration in respect of each varies from case to
case and has to be assessed by clinician on the merit of each case. However, an outline of general
principle in respect of whole blood and packed cells is given below:
Amount in adults
500 ml of whole blood raises the haemoglobin in an.average adult of 60-70 kg by about 1 gm/dl.
400 ml of packed cells, two such units will raise haemoglobin by 2 to 3 gm in an average adult,
haematocrit by about 7 to 9% and red cell count by 1 million/cmrn approximately.
213

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214
Blood Banking and Transfusion
Table 10.1. Usage of whole blood and blood components
Whole blood -------------+---
I
Exchange
transfusion
~
Brisk active bleeding
~
Routine sutgery
Shock wiilihaernorrhage
~
Bum more than 15to 20%
~
Fresh blood
I
I
Cardiac
surgery
(350ml/unitincludinganticoagulant)
I
Solid
Component/formed elements
(cells and platelet)
r
Liquid
component
(Plasma)
Erythrocyte
Leucocyte
PlateI~t'
I
I
I
I
I
Packed
Washed
Frozen thawed
Leucocyte depleted
(a) Bleeding
I
I
I
I
disorder
reaction
(a) Anemia
(a) Non-
(a) Rare
(a) Intra..
(b) DJ.C.
.(b) Chronic
haemolytic
blood group
uterine
blood
transfusion
(b) Non-haemo-
transfusion
loss
reaction
lytic trans-
(b) Organ
(b) Prevent
fusion
transplant
'sensitisation
reaction
BMT
(i) Protein
(c) Prevent
(c) Prevent
(ii) HLA
HLA
HLA
(c) Dialysis
sensitisation
sensitisation
(d) Dialysis
(1) Granulocytopenia
with associated
infection not
responding to therapy
(2) Cherno-radiotherapy
I
I
I
I
I
I
I
FFP
FP
PRP
PPP
Cryo
Factor IX
Albumin
IMM
(a) Maintain
(a) Maintain
To fulfill
Maintain
(1) Factor
haerno-
~
Serum
blood
blood
platelet
blood
VIII in
philia B
Hypo-
globulin
volume
volume
requirement
volume
haemophilia
volimia
!
(b) Supply
(b) Bum
in case of
(2) Fibrogen
protein
Hypo-
coagulation
nonavailability
deficiency
deficiency
gamaglo-
factor
of platelet
bulinirnia

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Transfusion Practice Clinical Aspects and Applications
215
In India, we are using 350 ml/unit so better guide to estimate rise in haemoglobin is :
(a) 10 ml/kg of whole blood
10% rise in haemoglobin
(b) 5 ml/kg of packed cell
Systolic blood pressure and a full regular pulse is a rough guide for clinical assessment of the
amount ofblood required. The systolic pressure when rises upto level of 100 mm of Hg indicates adequate
restoration of blood volume and depending on condition of the patient transfusion may be continued for
maintenance or discontinue.
Time duration
It depends on the rate of transfusion at which the blood is allowed to flow per minute which is again
dependent on the condition of the patient. Except in severe emergency a rate of 60 to 80 drops/minute is
usually advised (1 ml of blood equals to 15 drops/minute in most of blood administration set available,
it is a rough estimate and may vary) thus 4 ml to 5 ml/minute is the rate of flow. A unit of 350 ml blood
will thus take about 70 to 90 minutes for complete transfusion. A person previously healthy tolerates
well, a flow at rate of 10 ml/minutes this rate is allowed, if the patient is in shock due to haemorrhage etc.
The first 5 to 10 minutes blood is allowed to flow at this rate and later on depending on the condition of
the patient flow rate may be accelerated to reach the 100 mm systolic pressure as early as possible. As
such there is no definite criteria laid down for the rate of transfusion and it is purely dependent on the
condition of patient and clinical assessment. As for example, again in a case of chronic anemia, where
packed cell is advised a rapid flow of blood may lead to circulatory overloading. So a patient with
chronic anemia can at best be given 40 drops/min and in a case of severe anemia associated with CCF
the rate, not to increase more than 1 ml/kg body weight/l hour. The transfusion of blood in cardiac
bypass surgery has its own present guidelines and requires transfusion'at a rapid rate.
So we cannot assume a fixed criteria for rate of transfusion and as such the amount of blood to be
transfused. As has been pointed earlier, it depends mainly on the condition of the patient and clinical
assessment of the case by attending physician/surgeon, which of course, varies from case to case.
10.2 TYPES OF TRANSFUSION AND MAIN OBJECTIVE OF BLOOD TRANSFUSION
Transfusion commonly practiced in human being are mainly of two types:
1. Homologus transfusion
2. Autologus transfusion
Homologus transfusion is the transfusion ofcompatible homologus (different individuals amongstthe
.same species viz.human) storedlbanked blood or the other blood components between different individual
of the same species.
Autologus (auto-self) transfusion is the retransfusion of collected blood simultaneously or at a later
date into the donor himself.
Objectives of transfusion of lH.ood and components :
1. Restoration ofblood volume : A rough guide to this has been given earlier, i.e., relaton of blood
volume to systolic pressure. It has been observed that 100mm of systolic pressure in a previously

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Blood Banking and Transfusion
untransfused case indicates a blood volume of 70% of normal and 140 mm of Hg indicates a
blood volume of at least 800/0 of normal. So restoration of blood volume of cent per cent cannot
be expected immediately after transfusion but a restoration of volume of 70%of normal blood
volume is considered adequate and depending on condition of patient, the transfusion may be
continued or discontinued. Monitoring of CVP is of course a better guide.
2. Enhance the oxygen carrying capacity of blood by maintaining the packed cell volume!
haematocrit (the ratio of volume of erythrocytes tc that of whole blood) and thereby the
haemoglobin percentage (hemoglobin, the main carriers of oxygen), so that the functioning of
vital organs are not disturbed.
3. Maintain haemostasis through supply of platelet and coagulation factor through transfusing
fresh whole blood or the appropriate component.
4. Maintain plasma colJoid cosmotic pressure.
5. Maintain plasma biochemical balance: Acid base equilibrium is disturbed as a sequel to massive
haemorrhage, also there might be some other associated metabolic disturbance and a blood
saline regimen or blood colloid regimen is fruitful in such cases.
6. Maintain uniformity in body temperature through whole blood transfusion which restore the
volume and thereby improves circulation (macro and micro).
Homologus blood transfusion was the sheet anchor for transfusion practice till recently but since
1970, when the autologus transfusion was approved for practice in USA, the homologus transfusion
started loosing its monopolistic control over transfusion practice, particularly due to the associated hazards
of transfusion transmitted disease and transfusion reaction. Autologus is gradually becoming popular
and expected to play a significant role in future transfusion practice. A brief discussion on .autologus
transfusion is thus given below.
Autologus transfusion
The main aim for practicing autologus transfusion are four R's :
(a)
Requirement of rare blood type: Conservation of rare group.
(b)
Reduce the risk of transfusion associated hazard.
(c)
Reduce the workload.
(d)
Religious belief -
Jehovahs witnesses.
Indication
(i) Any elective major surgery
(ii) Preventions of alloimmunisation.
(iii) In case any antibody (unexpected/unidentified) detected in the serum of patient.
Strategies for autoloqus transfusion
A. Selection of donor criteria is almost same as that of donors for homologus transfusion with
certain difference as follows :
(i) Pidonor who has received homologus transfusion during preceding six months is not to be
considered.

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Twentyfirst day
Twentyeighth day
First day
Seventh day
Fourteenth day
Transfusion Practice Clinical Aspects and Applications
217
(ii) Haemoglobin: It should not be lessthan 11 grn/dl.
(iii) Age : No upper age limit provided the patient donor is fit and healthy as per donation
criteria, lower age limit is same as blood donor for homologus transfusion.
(iv) Interval between donation and surgery in predeposit scheme depends on the amount of
blood required, if it is a single unit requirement, than blood can be drawn from the patient
within a week but a 72 hour or three days gap between donation and surgery is always
recommended and be adhered to. In case more than one unit is required, the Leapfrog
technique of collection is to be followed, so time interval win be more.
Leap frog technique
In this method, we collect blood in a gap of seven days, i.e., successive withdrawal of blood is held at an
interval of seven days. On first occasion, we draw an unit of blood say 'X' unit and after seven days, we
retransfuse 'X' and withdraw one extra, Le., 'A' + 1 or two units of blood. Two types of schedule are
followed and dependson choice of transfusionist.
Schedule 1
'X' unit withdrawn
'X' unit retransfused and 'N' + Ywithdrawn
'N' unit retransfused keeping 'Y' in stock and withdrawing 'W' + 'Z'. So
stock becomes Y + W + Z
'Y' unit retransfused keeping Wand Z in stock and withdrawing Q and R.
So stock W + Z + Q+ R
'W' unit retransfused keeping Z + Q+R in stock, and withdrawing K and L,
so we have in our stock Z + Q+ R + K + L - total 5 units.
So out of these five units, Z (two weeks old), Qand R (one week old), K and L (fresh).
Schedule 2 (serial phobotomy)
Day J
Withdrawn 'Q'
Day 2
'Q' retransfused and 'R' and'S' withdrawn
Day 3
Rand S retransfused and 'X', 'Y', 'Z' withdrawn
Day 4
'X', 'Y', 'Z' retransfused and 'X', 'Y', 'Z' and 'M' withdrawn.
Advantage in this method is that all 4 units X, Y, Z and M are fresh.
Relation ofvolume to be withdrawn and weight: An amount 8 mllkg body weight is recommended
and it is well tolerated and accordingly, a person weighing 44 to 45 kg can donate 300 ml of blood and
sample in pilot tube or it can be calculated from the formulae as given below:
v =EBVx HO-Hf
HAV
EBV =Expected blood volume
HO = Initial haematocrit
Hf= minimum allowable haematocrit

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218
Blood Banking and Transfusion
HO+Hf
HAV = Average haematocrit
--2--
V = Volume of blood to be withdrawn
Havingdetermined thevolumeof bloodtobe withdrawn, wemustfindouttheamountofanticoagulant
proportionalto the volume'of blood according to formulae (vide infra) :
V = v. x wt.of patient
1
0
45 kg
VI = amount of anticoagulantrequired
V0 = amount of anticoagulantrequired for 300 mI.
The autologustransfusion can be broadly subdivided into following category
(a) Predeposit scheme: Under this scheme required amount of blood is collectedfrom the patient,
labelledand storedat recommendedtemperatureand is transfusedtothe patientwithinthe period
of shelf life.
(b) Haemodilution : Immediate preoperative withdrawal and short time storage. Basic principle
involved is normovolimic haemodilution. At first the patientis anaesthetised and once he is
under, the required ~ amount of.blood is withdrawn, and replaced with an equal amount of
crystalloidsolution simultaneously. The autologusunit labelled and conservedin anticoagulant
solution at recommended temperature till the completion of surgery. It is transfused after the
completionof surgery. Diuretic mayor may not be administered, it is mainly to reduce plasma
volume.
Advantages :
(i) Blood lost during operation has less haematocrit value, so subsequent requirement for
blood is reduced.
(ii) The administration of simultaneous crystalloid reduces the viscocity of blood allowing
easy perfusion of vital organs during operation.
(iii) Haemodilution increasesthe cardiac output therebycompensatingthe reductionin oxygen
content of blood.
Contraindication : Pre-existing anaemia.
Different techniques ofhaemodilution :Theyarebroadlysubdividedintwo: (i) Normovolemic
haemodilution, and (ii) Hyper volemic haemodilutionas described below.
The Normovolemic Hemodilution (acute/intentional normovolemic hemodilution) i.e. ANH
also known as Isovolemic Haemodilution (IV) may be defined as controlled reduction of
Hematocritby withdrawalof red blood cell mass and simultaneousreplacementwith cell free
substitutes (crystalloids and/or colloids) to maintain isovolemia. This procedure is done
immediately before surgery.
Patient selection : Any patient with adequate Hemoglobin and is expectedto lose more than
25% of estimated blood volume (EBV). Age is not a limiting factor but overall health status
hastobe takenintoconsideration. Patientwith CAD,restrictiveorobstructivepulmonary disease,
pre-existing coagulopathy, decrease renal function and patients with hepatic disease,
thrombocytopenia and impairedplatelet function are not fit cases for IVH.

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Transfusion Practice Clinical Aspects and Applications
219
Technique: The Blood Volume (V) to be removed equals the BBV multiplied by patient initial
HCT (Ho) minus the minimum allowable HCt (Hf) divided by average HCt (Hav) :
V = EBV x (Ho - Ht)/Hav
Let us take an example to explain and apply this formula. Let us take an adult male whose
weight is 50 kg and initial HCt (Ho) is 36. Now, if we aim post-hemodilutional HCt (Hi) of 25,
then the volume of blood withdrawn calculated by above mentioned formula will be :
= 50 x 70 (EBV) 36 - 25/ 36 + 25 = 1262.29 ml
2
During withdrawal, simultaneous infusion of either crystalloid or colloid is done to maintain
isovolemia. The volume of crystalloid or colloid infused to replace blood depends on its physical
properties, for example lactated Ringer's solution should be given 3 times the blood withdrawn,
whereas colloids like polygeline as 1.25 times. Colloids are advantageous over crystalloids,
later moves out of intravascular compartment, whereas former is retained. Hemodynamic studies
comparing albumin of XES have demonstrated no significant differences.
Hemodilution is usually performed in operation theatre following induction of anaesthesia.
Blood is withdrawn from a central or large peripheral vein or radial artery. Blood is collected in
standard blood bags containing anticoagulant. Hemodilution kits are commercially available
(Autologous blood collection Kit 4R5012, Fenawal division, Baxter Health Care, Deerfield,
ill). Intermittent shaking to prevent clotting and weight monitoring is essential part of collection
procedure. All the collected units are to be labelled properly (name, Hospital number, time of
.withdrawal) and is numbered sequentially.
Unit can be kept at room temperature inside or upto 8 hours, but if it is anticipated that more
than 8 hours will elapse before reinfusion, refrigeration of blood (2 to 6°C) is required. The
unit, if not used within 24 hours has to be discarded.
During reinfusion units are reinfused in reverse order of collection so that first unit which has
highest Hct and most clotting factors are administered last. Estimation of blood loss and serial
Hct determinations are used to guide the transfusion therapy. Intensive monitoring of
Hemodynamic parameters during procedure, surgery and post-operative period is done.
The IVH is not free from hazard of transfusion :
(a) Time consuming procedure.
(b) Storage of blood outside body.
(c) Contamination due to outside storage or during withdrawal/transfusion possible.
(d) Mistaken transfusion.
(e) Reduction of red cell mass causes fall in the total oxygen carrying capacity.
To circumvent all these disadvantages, a new technique is being investigated which is called
Hypervoleimic Haemodelution (HVH).
In Lok Nayak Hospital, New Delhi, randomized study comparing IVH and HVH was carried
out. Hypervolemic haemodilution involved rapid infusion ofpre-deteimined volume crystalloid
orcolloid immediately before surgery to temporarily create a state of hypervolemia and reduce
the HCt. This technique of HVH is relatively new.

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Blood Banking and Transfusion
In 1990, the HVH was successfully practiced. and a major surgery wasfacilitated in an anemic
patient belonging to faith of Jehovah's witness. They observed some hours after operation decrease
in Hbconcentration was <5%in spite of blood loss of nearly 50% (Trouwborat et a1.), so by this
method, blood transfusion can be avoided in selected cases and HVH may be of value in anemic
cases, those who declines transfusion or unsuitable for transfusion.
Technique involves infusion of calculated amount of a sanguinous fluid to create a temporary
state of hypervolemia and bringing down the HCt to required level is done by using the formula
suggested by (Kumar et al.) volume of polygeline infused:
= EBV(HO-Hf)100
~
Hf
80
.the increased blood volume termed (EBV post HVH) was sustained throughout surgery. The
allowable blood lossduring surgery is calculated to final Het on this increased HBV.
Intraoperative blood loss is replaced with colloid or crystalloid to maintain Normovolemia. If
bleeding continues' beyond allowable blood loss, allogenic blood is transfused, otherwise, after
a certain period on basis of Hct estimation, decision for transfusion of allogenic blood is done.
Several diluents alone or in combination have been successfully used to create hypervolemia.
HVH is an alternative to IVH has following advantages:
(a) Easy procedure and less time consuming.
(b) Less expensive.
(c) Can be practiced in Jehovas.
(d) HVH is more effective in decreasing the intraoperative haemoglobin loss.
(e) Can-reduce the demand of homologus blood supply in remote areas of country.
(f) HVH is well tolerated in children and adolescent group.
(h) The systemic arterial and mix venous tensions remains unchanged.
(i) Haemodynamic alterations at the beginning of HVH are transient and were observed as
well tolerated in patients.
G) More cost effective.
J'
(k) Minimal clinical staff and thus less clinical error.
Courtesy Prof Rakesh Kumar; Dr. Sunil Kumar; Dr. Dheeraj Kapoor, Department of
Anaesthesiology, MAMC and associated Lok Nayak Hospital (loc cit.).
(c) Intraoperative salvage: Essentially an operation room procedure consisting of salvage,
processing of blood unit a~d
intra- or post-operative autologus transfusion. Salvage is not done
in all cases for fear of reintroduction of infection through retransfusion so avoided in malignancy,
grossly perforated viscera, grossly contaminated wound etc. It is done in some selected surgical
manouver like total hip replacement, ruptured spleen, liver and aneurysm, selective cases of
cardiac surgery. The blood collected in the form of whole blood is processed by washing and
concentrating device in intermittent flow cell separator or continuous flow cell separator machine.
The retransfusion of this unit is done either intraoperatively simultaneously or labelled and
stored to be transfused postoperatively.
Advantages :
(i) Blood is fresh.

[[p.9]]
Transfusion Practice Clinical Aspects and Applications
221
(ii) Different components like RBC concentrate, platelet and leucocytes can be separated and
assessed component required is transfused thereby reducing volume overload.
Contradiction :
(a) Malignancy
(b) Any infections pathology.
Hazards: Air embolism, DJ.C. thrombocytopenia, lysis of red cell.
Hazards in general:
(a) Clerical mistake leading to wrong transfusion.
(b) In predeposit scheme :
~
(i) loss of man days by patient donor in leap frog technique
(ii) anemia in the patient donor.
(c) If surgery is postponed unit is likely to be lost.
(d) In preoperative scheme haemodilution may often lead to hypoximia, if blood in excess is
.withdrawn.
(e) In intraoperative scheme:
(i) Dissemination of undiagnosed malignancy or sepsis.
(ii) Blood collected intraoperatively may contain less platelet.
(iii) Lysis of red cell may ultimately lead to renal failure.
(iv) DJ.C. etc.
To avoid loss of unit in case of postponement of surgery and to avoid any risk involved in
transfusion and other medicolegal complication, it is always better to take a written consent
from patient -
donor for :
(i) Transfusion consent.
(ii) Consent for subsequent homologus use and disposition of such unit.
If thepatient donor is not adult but adolescent; the parent may give the consent.
HOMOLOGUS TRANSFUSION
The commonly practiced mode of transfusion still now, so the procedure normally adopted for transfusion
ofblood into the recipient is described vide infra. The special procedure are described in separate sections
of this Chapter.
Pre-transfusion procedure
(i) An unit of blood bag in India contains 350 ml of whole blood including the anticoagulant and
the component after separation is made up to requirement or as per standard, e.g., platelet 30 to
50 ml, packed RBC 180 ml,70% haematocrit,
(ii) Identification of bag which contains the compatible unit for any particular recipient.
(iii) Physical inspection of bag to rule out any contamination, any discrepancy in temperature of
bag, any leakage, any foreign body or extraneous object change in colour of the content of
blood bag, expiry date compatibility report, and TID clearance report.

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Blood Banking and Transfusion
After observing the pre-transfusion formalities examine the recipient patient and if his temperature
and cardiovascular system, mental condition (physiologically not upset) etc. are conducive for smooth
operation of transfusion, then only, it is undertaken or deferred till the condition of patient permits.
Normally veins in anticubital fossa are selected for transfusion purpose. If veins are not visible, take
the help of tourniquet of cuffof B.P. instrument which is tied above the anticubital fossa, in lower part of
a~ll1
and the veins now becomes prominent, asceptic precautions are taken before venepuncture is
performed. Make a venepuncture with the needle (bevelled end upward) of blood administration set
already connected with the blood bag or bottle. To avoid blood loss an artery forceps may be fixed on
that part of tube which connects between filter and needle. Once the recipient's blood makes a backflow
from veins into the tube of adtninistration set freely, indicates that needle is in the vein proper, now
release the artery forceps to allow passage of blood from bag into the vein. To start with blood is allowed
to flow at a very slow rate and this is maintained for first ten to fifteen minutes because most of reactions
anaphylactic and or haemolytic exhibits their symptoms and signs during this period, once this period is
over, flow rate may be increased under constant monitoring for half an hour, followed by periodic
monitoring till the procedure is over. Flow rate may be increased, decreased, maintained or stopped
depending on the condition of the patient. Transfusion (blood administration) set which is supplied
alongwith blood bag and transfusion report form, is also checked for sterility, date of expiry, batch no.
etc. Disposable sets are recommended. The sets are usually made up of PVC material, sterilised by
gamma irradiation containing inbuilt filter, pore size 170 Jl to retain small clots etc. The needle of the set
is usually 18 to 19 G for adults; it should be sharp, bevelled, made up of stainless steel, should be
covered and protected with sealed plastic tubes. The needle must have uniform internal bore to allow an
unobstructed flow of blood. For paediatric use 230 needles are preferred. Plastic catheters are
recommended in place of needle, if prolonged transfusion is required.
For cardiopulmonary bypass operation, special type of administration set having filters with 20 to
40 1..1., pore size is advised.
'
The importance of filter in transfusion set is essential to filter the fibrin, leucocyte and platelet
aggregates usually found in banked blood more than 5 to 7 days old. This aggregates, if passes into the
circulation of recipient forms leukoagglutinin and lodges into small capillary of lungs finally giving rise
to respiratory distress syndrome.
The physical condition of the blood has to be checked before transfusion. This includes the
temperature of the blood after bringing out of cold is kept in the prevailing environment, so that it
reaches the room temperature usually. takes place within half an hour blood must be brought to room
temperature before it is transfused because administration of cold blood may precipitate:
(i) Reaction with cold agglutinin.
(ii) Infusion of cold blood particularly in infants and massive transfusion may cause ventricular
arrythmia and heart failure.
In a very cold atmosphere, where it takes longer time to reach room temperature, the blood bag may
be placed in water bath with constant monitoring of temperature and position maintained upright, so
water is not in direct contact with portals. The temperature of water bath must ~ maintained at 37°C,
beyond this temperature haemolysis is likely to occur. Now-a-days facility of inline wanner is available,
this warms the blood as it passes through the inline warmer.

[[p.11]]
Transfusion Practice' Clinical Aspects and Applications
223
Controlling the rate of flow
Since the process of transfusioninvolves the principle of gravitation we can increase the rate of flow by
elevatingthe blood bag in case it becomes slower after it has been fixed by regulator at a certain rate, the
needle also has to be checked. This is minor adjustment to increase or maintain the rate of flow. But, if
the rate of transfusion has to be accelerated we can do it by :
(i) Using wider bored needle.
(ii) Mechanical compression device to exert an uniform pressure of 300 mmHg on the blood bag.
The device is fixed with pressure gauge to monitor the pressure applied.
(iii) In case of non-availabilityof such bag, the cuff of BP instrument can be wrappedround the bag
but it exerts irregular pressure and may even cause leaks in the bag sometime.
(iv) Infusion pumps may also be used to control of blood flow.
Procedure
1. Do not add any drug injectable or otherwise to the blood.
2. Always use transfusion set provided alongwith blood bag, it is necessary because to observe
short cut in the procedure some of the operator allows to pass blood through a set previously
used for 5% dextrose,5% dextrose saline, Ringer's lactate or a hypotonic saline. If blood flows
throughthe same set, the red blood cells on coming in contact withdextrose will swell, and then
haemolyse, again lactate in ringers form a compound with calcium which leads to formationof
clot by indirectly effecting the anticoagulant status of stored citrated blood.
3. A written consent for transfusion is necessary.
4. Entryof bloodbag numberas per detailson the stickerof the bag,the batchno. andmanufactures
of administration set used, is to be made on treatment chart. Also mention the amount of units
transfused and see that entries in respect of each unit and set are made.
5. Any reaction,mild.rnoderate and severe,if noted has to be enteredin treatmentchart.If reaction
is observed, then stop the transfusion and proceed as follows :
(a) Fill up transfusion reaction from giving the details as per columns in the form,
(b) Collect a post-transfusion sample of blood and'urine from the recipient.
(c) Despatch the balanceblood in the bag alongwithadministrationset used, the duly filled up
transfusion reaction form and post-transfusion sample of blood and urine immediately to
. blood bank.
(d) Restart transfusion only after receiving report from blood bank.
6. In the event of postponement of transfusion procedure, return the blood to blood bank within
half an hour of issue of blood from the bank, donot ever try to store the bag in other refrigerator
which usually does not provide the required uniform temperature.
7. Do not ever transfuse any unidentified bag or a doubtful bag without further confirmation.
8. Infants are very quickly susceptible to reaction so observe them carefully during the whole
procedure.
9. No warming up of blood by procedures not recommended in the earlier discussion.
10. Though rare now-a-days, keep an observation for any air embolism because it may lead to
instantaneous death.
11. The transfusion procedure should not be prolonged, say more than 4 hours in respect of one
nnir. because in such case likelihood of infection (bacterial) increases.

[[p.12]]
224
Blood Banking and Transfusion
12. Platelet are received warm from blood bank and not cold because platelets are stored at room
temperature; unless stated donot transfuse cold platelet.
13. Not more than two units of packed cells are continuously transfused. In case more packed cells
are required, a timesnterval is always recommended. If any packed cell unit is viscous than
addition of 50 to 80 ml of normal saline, unless stated otherwise is recommended.
14. Requirement of blood, if exceeds more than one-third of circulating volume, the transfusion
schedule may be divided in two parts, particularly in cases of chronic anemia and the likes,
where slow transfusion is recommended. This is to prevent overload, patient discomfort and
bacterial contamination.
15. Avoid simultaneous infusion of other fluid unless indicates. After completion of transfusion,
the needle of the administration set is slowly and carefully withdrawn, apply pressure with
cotton and thumbover the venepuncture site, continue pressure for about 4 to 5 minutes,remove
pressure observe for bleeding, if no bleeding or haematoma, then apply bandaid and patient is
asked to relax, if there is oozing from venepuncture site, then milk the site, apply pressure again
and repeat the procedure, if required till oozing is stopped completely.
10.3 SPECIAL PROCEDURE
Apart from from the normalproceduredescribedcertainspecial typeof transfusionneeds to beconsidered-
viz. multiple transfusion, massive transfusion etc. and are described below.
Multiple transfusion
This is a type of transfusion where transfusion is repeated at intervals over a prolonged period for
resurrection and sustenance. Frequency of transfusion and intervals is dependent on the condition of the
patient.
Main indication of multiple transfusion are anemias of chronic nature, the treatment of which varies
widely. Repeated transfusion of blood may be a lifelong commitment, for resurrection and sustenance of
life transfusion is the sheet anchor of treatment in such chronic anemia (Table 10.2)and can be classified
as follows:
Table 10.2. Type of anemia
Anemia
I
I
I
I
I
Idiopathic
Associated with
Haemolytic
Acquired
I
I
I
other disease
I
I
I
Hypoplastic
Aplastic
Thalassemia.
Sickle.
(1) Autoimmune
haemolytic anemia
(2) Paroxysmal
nocturnal
haemoglobinurea
I
I
I
I
I
End stage
End stage
Malignancy
Radiation
Drug
Chronic
renal disease
hepatic disease
induced
induced
induced
infection

[[p.13]]
Transfusion Practice Clinical Aspects and Applications
225
In the anemia due to first three groups, i.e., idiopathic, haemolytic and anemia associated with
diseases, the blood transfusion may be a life long commitment whereas in fourth group of acquired the
blood transfusion required may be multiple, but need not be essentially life long, because in these cases
once the primary cause is treated blood transfusion may be discontinued after a certain period. Homologus
compatible banked blood or component is used for transfusion purpose.
Blood requirement, frequency of transfusion and interval between successive transfusion are
determined on the basis of following :
(i) Initial and the desired level of haemoglobin.
(ii) Clinical assessment of the condition of the patient.
(iii) Level of day to day activity. Sedentary lifestyle the permissible limit for Hb is 7 gm whereas an
~
individual with active life style will require more Hb for sustenance.
(iv) Laboratory report on haemoglobin and haematocrit value and the red cell mass.
(v) Blood loss: In chronic situation the blood volume is usually stable and the red cell mass is thus
reflected by estimation of Hb and haematocrit value
Based on above criteria a workable strategy for multiple transfusion can be recommended (Table 10.3).
This need not necessarily be adhered rigidly and best judgement can be made by physician in charge.
Massive transfusion
This is defined as an administration of blood or its component that equals to the total blood volume of
the patient within a period of 24 hours. Replacement is done by homologus compatible banked blood or
blood component.
Aims and objective
(i) Maintain blood volume.
(ii) Oxygen transporting capacity of red blood cells.
(iii) Maintain haemostasis through platelet and coagulation factors.
Table. 10.3. Transfusion" "in" anemia~
.1
.
Acute blood loss.
I
Immediate trans-
fusion of whole
blood supplement
by colloid and/or
crystalloid
I
Avoid
transfusion
in Hb%·above
lOgm%
I
I
Try to avoid
transfusion by
restricting physical
activity in Hb%
less than 10gm%
butabove 8 gm%
limit for sedentary
life 7 gm%
I
Transfusion
required but
not essentiat
Hb% less than
8 gm% but
above 7 gm%
follow regimen
(i), (iii) and (iv)
I
Chronic blood loss
I
I
Transfusion
essentials in HB%
less than 6 gm%
(i) Packed RBC @
1 ml/kg body wtJhour
(ii) Pretransfusion
Fursemide 40 mg
I.V. may be given
(iii) Constant C.V.P.
monitoring
(iv) 2 (two) units per
sitting

[[p.14]]
226
Blood Banking and Transfusion
(iv) Maintain, correct plasma biochemical balance by avoiding hyperkalemia, hypocalcemia and
acid base disequilibrium.
(v) Colloid osmotic pressure of plasma to be maintained.
(vi) Prevent occurrance of DIC. Indication acute hypovolaemic shock-as a result of accidental/
operative injury.
Strategies of massive blood transfusion : Since massive blood transfusion is required in cases of
acute and rapid haemorrhage resulting in a profound hypovolimia and shock that impairs tissue perfusion.
The management protocol is thus intended to revive the patient immediately from shock so that the
patient does not pass into irreversible shock stage of no return.
Following schedule is recommended:
(a) Ressucitate the patient from shock, simultaneously search for the cause under constant
haematological and other monitoring.
(b) In the meantime arrange for blood, if the bleeding continues switch over to blood transfusion.
(c) Try to achieve target value. Haemoglobin: 10 gm% dl, haematocrit-o.32 and adequate
.restoration of blood volume reflected by rise in systolic blood pressure upto 100 mmHg.
(d) If target value achieved and blood loss is reduced to less than 0.5 litrelhr. Resort to maintenance
therapy, i.e., corrective measures and less aggressive transfusion under constant monitoring.
(e) If the rate of blood loss is not reduced and target value has not been achieved, research for the
. cause of blood loss, monitor platelet count, coagulation factors, prothrombin time and partial
thromboplastin time, fibrinogen etc. Aggressive transfusion with appropriate treatment has to
be undertaken. Our main aim should be to prevent occurrence of DIC.
Reviving the patient from shock at the initial stage includes orderly administration of intravenous
fluid:
(i) Crystalloid are isotonic solution and commonly preferred replacement fluid are normal saline
and Ringer's lactate solution.
(ii) Colloids are solution that contains substances of high molecular weight and are used as synthetic
plasma substitute to provide oncotic pressure, commonly used are Dextran 40.
(iii) Albumin is available as 5% solution in electrolyte, or as salt free albumin. Albumin also helps
in maintaining plasma oncotic pressure once the blood volume is restored, make a search for
the primary cause viz. undetected bleeding point, crush injury etc. and attend t,o the primary
cause.
Blood transfusion In massive transfusion
4 whole blood unit, not more than seven days old, is always preferred for restoration of blood volume.
Blood transfused must be brought at room temperature or in snow bound area, it is made to pass through
inline warmer because rapid transfusion of large amount of cold, whole blood m~y give rise to ventricular
arrythmia and subsequent failure, infants and children are more susceptible to cold refrigerated blood.
Every unit of blood should be properly crossmatched before being issued because successive transfusion
of different homologus unit may give rise to number of unexpected antibodies in the recipient's serum
and after ten units of blood within a period of 24 hours, very little of original blood is left in the patient.
After ten units of homologus blood transfusion, a test for antibody screening is done and if it reveals

[[p.15]]
Transfusion Practice Clinical Aspects and Applications
2~7
nothingand since the blood is to be released immediately, a simple and short procedureis adopted,two
drops of patients serum is taken in a tube and to it is added one drop 5% donor cell suspension,mix and
spin at 3000 rpm for 20 sees. or 4500 rpm for 15 sees. dislodge the button and observe for agglutination
and haemolysis confirm.optically and if compatible,blood is released.Incubatoreffect (ref.Chapter8.4)
isof relevanceto massivetransfusionandtransfusion insuchcasesbecomescounterproductive. Similarly
recommendation for a stock of rare blood group storage is also relevant to massive transfusionviz. Rh
null, Bombayblood groupmay not beavailableall the time so a stock of such group is alwaysneeded to
combat such eventiality. Certain general principles recommendedfor massive transfusionare :
(i) For non-availability of particular group specific blood. '0' negative blood may be used in
emergencysituation (ref. Chapter on "Alternatechoice of blood) after cross matching.
(ii) Use blood less than seven days old and transfusionof cold blood avoided.
(iii) After every ten units of whole blood use two units of FFP.
(iv) Use special filters of 20 to 40 J.1. micron pore size or alternativelytransfusionset to be changed
with every unit of blood.
(v) Sodibicarbone ampoule after every five units of blood.
(vi) For rapid transfusionof blood wide bored needle is more advantageous.
(vii) Next in preferenceto whole blood is packed RBC and FFP for massive transfusion.
SincebothpackedRBC and FFP has its limitationviz. slow rate of infusion,not more than two units
in one sittin~.
In case of FFP thawingrequiresto be done in thermostaticallycontrolledwaterbath at 30°
to 37°C and has to be transfused within two hours of thawing, so the whole blood is always preferred.
Transfusionof homologusstored banked blood has its own problems also. This can be attributedto
the physiochemical changes that occurs due to prolongedstorage at 4° to 6°C, in a closed container with
anticoagulant, broadly that are:
(a) Formationof minute clots - clumps together to form microaggregate.
(b) Reduction in viabilityof erythrocyte, platelet and granulocyte.
(c) Reduction in 2-3 DPG content of RBC·.
(d) Factor V and VIII are also reduced.
(e) In plasma, the lactates, ammonia and potassium shows increase, sodium shows no appreciable
change.
(0 pH becomes acidotic.
These changes are noticed more after seven days of storage. And so transfusion of stored banked
blood with properties described as above certainly induces some biochemicalchange in the recipient's
bloodwhichhasdirectbearingon thewellbeingof thepatient.Topreventthiscertaincorrectivemeasures
are to be undertaken alongwith transfusion so that whole process does not become counter productive,
corrective measures undertaken are : .
(i) Constant haematological monitoring : Hb%, haematocrit value and blood volume. If shows
diminishedvalue can be restored by whole blood or packed RBC transfusion.
(ii) Plateletcountbelow20,000ml warrantsadministration of plateletconcentratealthoughbleeding
time is prolonged at platelet count of lOO,OOO/ml, reflects the qualitative deficiency and is not
indicative of platelet transfusion.

[[p.16]]
228
.1 Blood Banking and Transfusio~
(iii) Coagulation profile -
prothrombin time and partial thromboplastin time should be less than
1.5 times of controls; A safe level is 1.3 X control, if it shows level of 1.5 X control or above
supplement with fresh frozen plasma.
(iv) Diminishing level offibrinogen is an ominous sign and indicative of impending DIC. Fibrinogen
level below 60 to 100 mg/dl should be treated with cryoprecipitate transfusion.
(v) Hypocalcimia due to large amount of banked blood transfusion reported to have no significant
effect on myocardial function. Hyperkalimia due to massive transfusion of banked blood is
counteracted by the alkialosis that results from metabolism ofcitrate to bicarbonate, the potassium
returns to the red cell when banked blood is circulating and eliminated through kidney provided
the urinary output is maintained. For details interested readers may consult clinical practice of
blood transfusion, Petz and Swisher.
(vi) Acid base imbalance may be detected by blood gas analysis and it has already been said that
after every five units of homologus banked blood, one ampoule of sodibicarb 45 meq is
recommended.
(vii) ECG to detect the development ofcardiac overload and ventricular arrythmia commonly observed
in recipient, who has been transfused with large amount cold refrigerated banked blood;
particularly children are more susceptible. Ventricular arrythmia is caused by hypothermia arising
out of transfusion of cold refrigerated banked blood.
(viii) To be on safe side after every 15 units of banked blood, three to five units of platelet transfusion
is recommended.
A massive transfusion of whole blood with sole aim to restore blood volume in patients with acute
uncontrolled bleeding who may easily pass into irreversible shock or DIe is complicated with multiplicity
of problem a short description of which is given above. So strategy for massive transfusion in each
individual case has to be checked out with above background in view. In general the transfusion has to
be carried out under constant laboratory monitoring and wherever all the facilities are not available the
transfusion may be interspersed with intravenous sodibicarb, FFP and platelet as recommended, with
special precaution taken for the temperature of transfused blood, Hb% and systolic blood pressure and
compatibility of transfused blood.
Transfusion in paedeatric age group
Paedeatric age group can be broadly subdivided into:
(i) Neonate
(ii) Infant
(iii) Children.
Being the developmental age group, rapid changes in anatomy physiology and biochemical
composition of body is inevitable. No definite criteria can thus be laid down and parameters for blood
transfusion varies according to changes relevant to that age group. A brief discussion on some of the
important aspect of blood transfusion commonly practiced in paedeatrics is appended below.
A full term neonate has an average blood volume of 85 ml/kg whereas a preterm infant (neonate)
has approximately 100 to 110 mllkg. After birth blood volume reduces as a result of transudation of
plasma. Foetal haemoglobin is the major constituent of cord haemoglobin and has greater affinity for

[[p.17]]
Transfusion Practice. Clinical Aspects and Applications
229
oxygen. A situation which is advantageous for a foetus in development stage but it may not be of same
advantage after the birth of foetus, i.e., neonate. And a new borncan not compensate for volumedepletion
like the adults, the bone marrow response is very slow, the immune system is immature so the new born
are easily susceptible to vagaries and variability. Because of the reasons stated a person must be extra
careful while transfusing the blood even if it is for benefit and treatment of patient.
Protocol for donation, preservation and transfusion is paedeatric age group :
A major hurdle is supplying of small volume of blood for transfusion purpose and several options
were tried like :
(i) withdraw a small volume required, from a unitlbottle and transfuse the same, expiry time of
such blood is limited to 24 hours only.
.. (ii) walk in donor programme all these were found unsatisfactory till the discovery of multiple
plastic bag like triple bag or quad bags. In this system blood is collected, i.e., total volume.350
ml in the parent bag with anticoagulant and later on transferred to satellite bag distributing them
equally amongst all the bags.
The whole process is carried out asceptically and blood is tested for mandatory tests and kept at
recommended temperature after separating them from one another.
Before issue blood is thoroughly cross matched. In new born upto the age 3 to 6 months, the blood
for transfusion should be cross matched with mother's blood, and grouping is done only by cell grouping
technique in infant's blood. This is because of immature immune system in new born, who develops
antibody usually after six months. Thorough crossmatching including antibody screening for unexpected
antibody and clearance by all mandatory test (as per recommendation byDrugController, G.O.l.) including
CMV and HbS, if possible is to be ensured, to avoid haemolytic transfusion reaction and occurrence of
transfusion transmitted disease. Another precaution of immense importance that usually escapes our
notice is vertical transmission and subsequent vehicle transmission of disease, viz. AIDS etc., the hosts
are easily susceptible in this age group.
Clinical conditions commonlyencountered in paedeatric age group with successful application of
transfusion are : .
{~'
(a) Exchange transfusion in haemolytic disease of new born
(b) Septicimia
(c) Neonatal purpura
(d) Haemorrhagic disease of new born
(e) Anemia
(f) Haernoglobinopathy, Thallasemia
(g) Coagulation factor deficiency, Haemophilia and others.
.
Exchange transfusion is by far the most successful clinical application of transfusion which involves
replacement of equal volume of fluid by another homogenous fluid either through continuous or
intermittent infusion. In exchange transfusion of new born, the fluid in'volved is bl~Od
and in actual
practice, there is slightly difference between the replacing (transfused blood being stored bank blood)
fluid and replaced (human blood in vivo intravascular) fluid. So all the time, we may not get exactly
homogenous fluid for replacement. However, the mechanism involved is that of exchange that may be
again partial or total.

[[p.18]]
230
Blood Banking and Transfusion
Indications
(a) Haemolytic disease of newborn
(b) Sickle cell anemia
(c) Respiratory distress syndrome
(d) DIe
(e) Some uncommon conditions polycythemia, foetal hydrops and removal of toxic material viz.
drugs or otherwise.
The first two indications are commonly encountered and exchange transfusion in these cases are
frequently' practiced..In other cases the application is still in experimental stage and results though
arbitrary, has been observed to improve survival,
In respiratory distress syndrome, it probably acts by replacing foetal haemoglobin having greater
affinity for oxygen, by adult haemoglobin having lesser affinity for oxygen. The adult haemoglobin
releases more oxygen to tissues, and thereby, counteracting the effect of less oxygen in tissues induced
by foetal haemaglobin.
In DIC, it probably acts by replacing the circulating fibrin degradation product by fresh whole blood
containing all necessary factors required to control DIC.
In sickle cell anemia partial exchange transfusion is employed, the red blood cells containing HbS is
replaced by normal RBC containing HbA. In neonatal polycythemia partial exchange with FFP and in
foetal hydrops partial exchange with packed RBC are employed.
In haemolytic disease of newborn the exchange transfusion aims at :
(a) Removal of antibody coated red cells that on destruction helps in developrit'erit of kernicterus.
(.b) Correct anemia.
(c) Remove bilirubin.
(d) Reducing the amount of antibody that mayform complex (antigen antibody) withnewly formed
cells.
. (e) Compatible fresh red cell substitute having optimal oxygen transport function is provided.
There is no universally acceptable and non-controversial laid down criteria for application ofexchange
transfusion but a guideline can be suggested ~n the basis of cord haemoglobin and cord bilirubin.
Cord haemoglobin: At 13 gmldl consider exchange transfusion and below 12 gm/dl exchange to be
undertaken.
Cord bilirubin : Above 5 gmldl exchange tQbe undertaken at 4 gmldl exchange to be considered.
Figures given above are just guidelines and a neonatologist is' the right person to-offer the direction
for application of exchange transfusion.
Technique
(a) Arrangement of blood and cross matching etc. :
(i) Cross match the blood (to be transfused) against maternal serum.
(ii) For Rh HDN choice of blood given in order as below:
Rh" red blood cells and infants ABO group--compatibility checked, is first choice. In
case of non-availability, orr blood is the second choice-compatibility checked. .

[[p.19]]
Transfusion Practice Clinical Aspects and Applications
231
(iii) For ABO HDN use 0 group red blood cells with infants Rh group compatibility checked.
(iv) First preference given to frozen washed red cell, followed by washed red cells and then to
whole blood.
(v) If washed, red cell or whole blood is used, give fresh whole blood, not older than 72 hours.
(vi) CPD blood preferred to ACD blood to prevent citrate toxicity.
(vii) Blood or component used must pass all mandatory tests including test for CMV and
screening for HbS.
(viii) Blood transfused must be warmed upto 37°C (body temperature) and cold refrigerated
blood is not to be transfused.
(ix) Requirement of blood in severe Rh HDN, where main aim is to remove bilirubin, a 90%
replacement is recommended. This can be achieved by replacing 200 ml/kg of volume @
1.8 ml/kg/minute, transfusion time is 2 hours at this rate. For 70% volume replacement
recommended is 100 mllkg and for 45% exchange, volume replacement recommended is
50 ml/kg, Calculation of percentage for volume replacement is done according to the
formulae given below :
%R =(V -S)O
V
where R is percentage of infants blood remaining, V - estimated blood volume, S - volume
of each aliquot of blood removed and replaced, N - number of times syringe filled or
cycles performed.
(b) Start exchange transfusion :
(i) A nasogastric suction tube is passed and gentle aspiration is done, the tube is kept in place
and intermittent suction as per requirement is done till the transfusion is over.
(ii) Whole procedure is covered with constant ECG monitoring.
(iii) Proper placement of umbilical catheter is the key to success. Catheter is placed in the
umbilical vein gently manipulated through ductus into the inferior vena cava. Forcing is
not advocated. A ligature around umbilical stump pulled caudally may help advancement
of catheter.
(iv) Once catheter is in the inferior vena cava indicated by free flow of blood, the procedure for
exchange transfusion may be started. Recommended removal and replacement for term
infants is 20 ml and 10 rnl/cycle for preterrn infants.
(v) Time for one sitting of exchange should not be more than 2 hours.
Two methods are usually followed :
1.. Isovolumetric method: In this method, two catheters are used. Catheters used must be same
size. One is introduced into umbilical vein through which blood is transfused and another in
umbilical artery through which blood is withdrawn. Single peristaltic pump acts as regulator.
2. Push and pull technique : Single catheter is used which is fixed with three way stop cock
connecting the blood bag, baby through the catheter and extension tube to the discard container.
The discard container is graduated. In this method limitation is a very small volume about 5 ml
can be exchanged in one cycle.

[[p.20]]
232
Blood Banking and Transfusion
Exchange transfusion is not a danger free procedure and there may be several complication viz.
infections, cardiac and vascular complication, haematologicaI and other complications are also reported.
Among the complications, the important ones are ventricular arrythmia leading to cardiac arrest or
myocardial infarction, volume overload, perforation ofvessels andthrombosis, air emboli, TfD, intestinal
perforation and haemoperitoneum, portal hypertension, Necrotising enterocolitis. The newer method of
exchange transfusion via peripheral vessels has been tried successfully and it has a definite edge on the
above two methods. It has been proved successful in both partial and double volume exchange transfusion
in neonates, the later is applied in cases of neonatal hyperbilirubinimia.
In partial exchange transfusion the radial or posterior tibial artery is canulated and calculated volume
of blood withdrawn and an equal volume of saline infused simultaneously at the same rate of withdrawal
through peripheral vein of another extremity.
In double volume exchange transfusion radial artery is percutaneously cannulated with 24 gauge
neoflon, A syringe with three way stop cock to withdraw and discard blood in aliquot of 5 to 10 ml while
simultaneously replacing equal volume of blood through a peripheral vein. This is done under cover of
prophylactic antibiotic and intermittent flushing of arterial line with 1 ml of heparinised saline.
Precondition for this procedure is to confirm adequacy of collateral circulation.
(a) In order to avoid complication with conventional technique or where due to infection, the
conventional technique falls, the peripheral technique is a useful procedure.
(b) Scepticimia in neonate is a very grave condition and transfusion of fresh whole blood with
antibiotic cover is given to prevent the neonate to pass into DIC. Granulocyte transfusion is
recommended in refractory or gram negative sceptimia since large volume has to beadministered,
it has the disadvantage of giving in divided doses at an interval of 6 to 12 hours which also
covers the intravascular life span of 6 hours in case of neutrophil.
(c) Neonatal purpura is not a very comnlon condition and the causes may be immunologic.
autoimmunisation or alloimmunisation in mother, infectious causes are usually associated with
hepatosplenomegaly and may be viral (CMV, Rubella), bacterial, spirochaetal, protozoal
(toxoplasma). Among the other causes, acute leukaemia, drug induced and multiple exchange
transfusion are important.
The neonatal alloimrnune thrombocytopenic purpura is a rare entity, its pathogenesis is similarto
HDN. Most frequently involved is PLAI antigen. A platelet count below 20,000 ml warrants
platelet transfusion. PLAI negative donors are very rare and in such cases washed maternal
platelet suspended in AB neutral serum from Rh negative donor is advocated. In neonatal·
autoimmune thrombocytopenic purpura, the platelet antibody adheres to almost all the platelet,
it will be rational to reduce antibody first by exchange transfusion followed by platelet
concentrate.
In other cases basic pathology is treated first which is later supplemented by platelet transfusion.
Platelet from random donors are choosen unless otherwise indicated.
(d) In haemorrhagic disease of new born commonly due to vitamin K deficiency and or deficiency
of coagulation factor is treated with adequate doses of vitamin K, to start with inject 1 mg IV
and in the meantime try to establish the cause and when deficient factor is detected appropriate
treatment is instituted.
Thallasemia and haemophilia is.dealt separately in appropriate section.
(e) Anemia in infants deserves special mention in Indian paediatric age group patient, this apart

[[p.21]]
Transfusion Practice Clinical Aspects and Applications
233
from sickle cell anemia and autoimmune haemolytic anemia. Most of infant and children hailing
from low socioeconomic status sufferers from anemia due to variety of reasons. So all these
cases are to be treated for basic pathology supplemented by blood or component transfusion.
Anemia, a vast subject is beyond the scope of this book, so will restrict only to recommended
guideline for blood transfusion.
Severe anemia
(i) Fresh whole blood less than 72 hours is recommended.
(ii) Partial exchange transfusion with compatible substitute viz., washed packed RBC, frozen thawed
washed red cells.
Anemia not so severe
Amount of transfusate (blood or blood product) can be calculated for exact requirement and transfused
as per recommendation viz., instruction for red cell transfusion (packed) or washed frozen thawed red
cells to be followed. Instead of transfusing large volume in one sitting several small transfusion is
always better.
Calculation
(Circulating blood volume) x (Incremental increase in haemoglobin)
Haemoglobin per dI of blood or blood product
e.g., assuming 85 mllkg is the volume, so in a patient 'X' kg circulating volume is "X", X85 =85X.
Assuming 16 gm is limit for haemoglobin and patient has 'Y' gm in blood so incremental increase is
16-Y.
Assuming that haemoglobinldl of blood product is 'Z' :
..
(85X) x (16 - Y)
Equation IS thus
Z
=N
So, 'N' of blood or blond product is required.
Anemia due to acute haemorrhage resulting in hypovolemic shock
This is an emergency in neonate and infants. The regimen usually followed is rapid infusion of colloid
and/or crystalloid to restore blood volume till blood is arranged, if group specific blood is not available
orr blood is preferred and transfused at the rate of 10 to 20 mllkg depending on the gravity of shock. This
is done under constant haematological monitoring and ECG (ref. massive transfusion). In the meantirne,
search for primary cause. If condition does not improve and venous pressure warrants another whole blood
transfusion (repeat transfusion) at 10 to 20 mllkg and research for the primary cause.
Obstetrics and transfusion
1. Pregnancy with severe anemia posed problem for obstetrician :
(i) Risk of cardiac failure during delivery may be accentuated due to postpartum transfusion
to restore blood loss in PPH because labour imposes a great strain on heart.
(ii) Pre-operative transfusion at a rapid rate cannot be done where immediate surgery is required,
because heart may fail to take the cardiac overload.

[[p.22]]
234
Blood Banking and Transfusion
Different regimen were tried viz. transfusion of washed packed RBC under cover of diuretics
though simple and less blood is required to be transfused, it could not meet the specific target
for rapid rise in PCV, so this small volume multiple transfusion is not considered.
After much trial, it was found that exchange transfusion in such cases are quiet useful. The
procedure by Fullerton and Turner (loc cit) demonstrates withdrawal of 1100 to 1700 ml of
blood from the femoral vein and transfusion of washed packed RBC 1000 to 1500 ml in an arm
vein. Volume withdrawn is more but in packed RBC, we can provide red cell even upto 90%
(depending on how it is manufactured). So, by this method, we reduce volume overload and
provide packed RBC that raises PCV directly needed by anemics fixed for emergency surgery.
Heparinisation is not required.
2. Intra-uterine transfusion is another type of transfusion practiced in the field of obstetrics with
sole aim to treat a foetus in utero diagnosed to be a case of severe haemolytic disease of new
born. It has been observed that .imrauterine transfusion has improved the survival and reduced
mortality due to severe haemolytic disease of newborn. The severity of disease can be estimated
by analysing the amount of bilirubin present in amniotic fluid and putting the observation in
Liley's chart, we will find a bilirubin bulge at an optical density of 450 to 460 nm. Appearance
of bilirubin bulge is indicative of severe haemolytic diseases, the foetus is suffering from, and if
the mother has a previous history of affected infant, the intrauterine transfusion is recommended
to improve the survival rate. The blood transfused in this type of transfusion should pass all
mandatory test, tests for CMV and screening for HbS and properly crossmatched with maternal
serum. Main aims of such transfusion is to replace foetal Rh 'D' positive RBC with Rh 'D'
negative RBC to invalidate the action of maternal antibody (anti-'D'). There are two types of
intrauterine transfusion intravascular and intraperitoneal. The former is usually practiced during
23rd to 26th week of pregnancy, in earlier days, it used to be conducted under foetoscopic cover
and considered difficult in unexperienced hand; since it involves special skill, the later method
of intraperitoneal transfusion is commonly practiced. With advent of ultrasonography the
intraperitoneal transfusion has become more easier. The blood of choice is orr packed RBC
with 70 to 80% haematocrit preferably irradiated to prevent GVHD. The blood required is
determined from the age of gestation and varies from 20 ml at twenty week of gestation to 70 ml
at 33 weeks of gestation, is placed in peritoneal cavity. The tafton catheter used may be left in
situ for subsequent repetition at interval of two weeks. Hydrops foetus is a contraindication for
such transfusion. Complication that may accompany are :
(a) 'Perforation of various adjacent maternal structure.
(b) Perforation of vessels and adjacent structures in foetus, even cranium or pericardium may
be perforated.
(c) GVHD in foetus.
(d) Potassium intoxication of foetus.
(e) Transfusion transmitted disease in foetus.
(f) Infection in both mother and foetus, if sterility is not observed properly.
The intravascular procedure is known as cordocentisis, with advent in technology and ultrasound
guidance, even in the skilled, 'experienced hand, rate of foetal mortality and attendant risks viz.
foetomaternal haemorrhage etc. is higher. In, cordocentesis, at first; a cord blood sample is obtained and
the tip of needle is kept in situ and if Hb% is belownormal, the volume required is calculated and the

[[p.23]]
Transfusion Practice Clinical Aspects and Applications
235
amount that will correct anemia is transfused. Blood transfused is fresh packed RBC, Rh negative
compatible with mother. The procedure may be repeated after one to three weeks, ifnecessary. Transfusion
can be performed as early as 17weeks and repeated upto 35-38 weeks. Success was reported in intrauterine
bone marrow transplant where maternal T-cell depleted bone marrow was injected into foetal peritoneal
cavity followed by subsequent intrauterine blood transfusion. A normal baby unaffected with GVHD at
34 weeks was delivered.
Surgery and transfusion
The intimate relationship of surgery and blood transfusion is universally recognised. Central to this
relationship is the clinical application of transfusion of blood and/or component which is again determined
by the nature of requirement.
A careful analysis of Table 10.4 infer:
(i) Requirement of blood can be planned or controlled in emergency or planned surgery.
(ii) Requirement cannot be controlled, if it is due to loss of.blood, component and/or products, and
if the condition is attended or treated immediately, patient survives, untreated cases may have
fatal outcome.
Table 10.4. Nature of. requirement
I
.Emergency
I
Loss of blood or its component
. I
I .
Emergency
surgery
•
I
Planned
Judicial administration
of blood according to
MSBOS (maximum
surgical blood order
schedule)
Treated (by replacement),
restore volume, oxygen
carrying capacity and
peifusion
J,
Resusscitation
J,
Survival
I
Deep (Liquid + RBC)
full thickness bum
I
I
Superficial
(liquid lost mainly)
I
I
+---- Shock------+
I
Hypovolimia
Hypovolemia
1_---.--_1
Untreated
J,
Renal and cardiovascular failure
J,
Irreversible shock I
Other organ
failure
Death f-(---

[[p.24]]
236
Blood Banking and Transfusion
So the situation as in second above is of utmost importance for clinician. The amount of replacement
(cystalloid, colloid, blood or blood product) fluid is directly proportional to the percentageofloss. Clinical
assessment ofthe loss can be roughly made from patients response to such loss. Since blood transfusion
is not infrequently accompanied by transfusion associated harzard (TAH) viz., volume overload,
haemolytic transfusion reaction anaphylaxis etc., a judicious combination to minimise or avoid whole
blood is always preferable and this is exactly where a transfusionist may be called on for advise.
Hereinbelow, a brief description of percentage loss, patients response, symptomatology and guideline
for treatment which a reader may appreciate to chalk out the strategy for infusion/transfusion.
In general the blood loss in a human being is usually attended with three types of responses namely
vascular, endocrine and metabolic, the symptomatology also varies accordingly in mild, moderate and
severe blood loss.
Mild haemorrhage: A loss of 15 to 20% of total blood volume is categorised as mild haemorrhage
is usually responded by venous contractions of larger vein. No appreciable change in metabolism and
endocrine system is observed.
Shift of extracellular fluid occurs and body tries to adjust the blood loss. Symptomatology are also
mild. But above 15% sometimes, adjustment may fail in undernourished or individual already diseased.
In such cases treatment with crystalloid infusion is recommended. Crystalloid solution in common use
are 0.9% sodium chloride and Ringers lactate and the usual recommendation is 1 : 3 i.e, one volume of
blood loss to be replaced by three volumes of crystalloid.
Moderate: A bloodloss of 20 to 300/0 is categorised as moderate and is characterised by reduced
peripheral blood flow, increased cardiovascular activity reflected by tachycardia and reduced pulse
pressure. Increase in metabolism is reflected by hyperglycemia, free fatty acid may show an increase,
and increased consumption of oxygen. Retention of salt and water, reduced urinary output can be
appreciated by increase in aldostome and ADH excretion. Symptomatology are tachycardia, reduced
pulse pressure, hypotension, cold clammy skin, hyperventilation etc., variable from person to person.
The treatment usually recommended are crystalloid followed by colloid. Colloids are available as HMD
(Dextran 70), LMD (Dextrans 40), HES (hydroxyethyl starch) and albumin. The last one is preferable
because it has no risk forTl'D (Transfusion transmitted disease, hepatitis and HIV) and no effect on
clotting time. The albumin is used after 15 to 20% of loss is made up with crystalloid and if the bleeding
still continues, albumin is used. Albumin is available as 5% and 25%, this is diluted in N/I0 saline
before intravenous use.
'Moderately severe: An.amount of 30 to 500/0 loss of total blood volume is categorised as moderately
severe and is characterised by hypotension, systolic blood pressure is below 100 mmHg, rapid thready
pulse, pallor and cold periphery and is due to reduced blood flow even the visceral flow' is reduced, the
flow diverted to maintain vital cerebral and cardiac function. Renovascular resistance increases with
reduced renal flow. Increase in catecholamine and 17-hydroxysteroid. Lactic acidosis occurs heralding
the shock, if untreated. Symptomatology includes thirst, air hunger, rapid thready pulse, appreciable
oliguria, cold clammy skin are all indicative of impending shock. Treatment is by replacement, by a
judicious combination of crystalloid, colloid and red blood cell concentrate.
Severe : A blood loss of more than 50% of total blood volume is half of total blood volume is
categorised as severe. This situation may arise due to continued blood loss and at this stage, the
compensatory mechanism falls to make any more adjustment, and is attended with all type ofexaggerated
response, profound metabolic acidosis, central. aortic pressure falls and is insufficient to maintain the

[[p.25]]
Transfusion Practice Clinical Aspects and Applications
237
coronary perfusion resulting in fall of cardiac output that leads to further fall in central aortic pressure.
The endocrine system already strained fails to make any further allowance and the pressure falls further,
coronary perfusion is further reduced vicious cycle ensues. Immediate replacement of loss can save the
patient from passing into irreversible state with anuria etc. Recommended treatment is with red cell
concentrate. Albumin solution or liquid stored plasma. Unattended the patient passes into stage of
irreversible shock, anurea usually with fatal outcome. If patient is brought at, when the loss approximates
60 to 70%, then fresh whole blood to be started first followed- by red cell concentrate and FFP or
cryoprecipitate (determined by haematological monitoring) to be infused and patient treated vigorously
to prevent any fatal outcome.
As a precautionary measure, it is always advisable to conduct all the infusions and transfusions
under constant monitoring (haematological and others) particularly to prevent volume overload in infusions
with crystalloid and colloid. The CVP which is central to the monitoring system is not truly reflective of
volume overload caused by crystalloid and colloid. CVP gives the measure of interaction of blood
volume, venous tone and pumping status of right heart but does not reflects the change in volume of
fluid at interstitial space, the space where the crystalloid and colloid exerts their initial effect. And since
.volume overload may cause problems such as pulmonary oedema etc., a multiple monitoring system is
advised.
(i) Haemoglobin percentage.
(ii) Haematocrit value of 30% requires transfusion of 'RBC for maintenance of oxygen carrying
capacity.
(iii) Systolic blood pressure 100 mm of systolic pressure indicates adequate restoration.
(iv) CVP normal is 5 to 8 cm of water a value above 15em of water indicates volume overload or
insufficient cardiac output.
(v) Measurement of pulmonary capillary wedge pressure is more informative of fluid overload due
to crystalloid and colloid in pulmonary interstitial space.
(vi) Urine flow : In abscence of any disease of kidney, the urinary output is truly reflective of
perfusion in vital organs. A urinary outflow of 50 ml/hour is considered normal, whereas, an
output below 25 mllhour indicates reduced renal circulation.
(vii) Measurement of mixed venous oxygen tension: At rest the true venous oxygen tension is 40
mmHg. Arising P02 indicates that patients circulatory status is improving.
(viii) Urinary sodium, less than 20 mEq/litre and urinary plasma creatinine more than 30, suggests
that oliguria is due to hypovolimia.
(ix) Hyperventilation is commonly associated with haemorrhagic shock which results in alkalemia
reflected by change in pH above 7.4 and PaC02less than.36 mmHg. In normal ventilation, the
range of pH is between 7.3 to 7.4 so measurement of blood pH also gives an idea of true status
of patient.
Other bedside monitoring includes a full volume regular pulse, systolic BP of 100 mmHg or
above. Normal skin temperature etc. suggests adequate restoration of blood volume.
Factors influencing the recovery: Blood pH less than 7.3, PaC02 more than 45 mmHg and serum
lactate 2 mMflitre exerts a negative influence on the recovery. Advanced age more than 70 years, previously
diseased heart, kidney, liver or any other associated infectious pathology is unfavourable for the prognosis.

[[p.26]]
238
Blood Banking and Transfusion
In planned surgery or even in emergency surgery the transfusion of blood or other fluid could be
anticipated or controlled and transfusion of blood could be minimised until and unless there is any major
mishap during the operation, maximum surgical blood order schedule is the guideline for surgeon and
transfusionist regarding the maximum amount of blood required for a particular surgical procedure and
accordingly the blood to be arranged, Le., ordered by surgeon and supplied by transfusionist. These
restrictions, if adhered to, will keep the use of blood limit to minimum. But where excess blood is
required, it has to be notified to the blood bank in advance and such excess requirement is countersigned
by the surgeon incharge of the patient. Unfortunately in India, we donot have any MS BOS and thus a
foreign model can be adopted.
Cardiovascular surgery is a major surgical procedure that consumes several units ofblood particularly
the open cardiac surgery. The consumption blood and/or its component was very high in earlier days.
But with recent advancement, the requirement has been tremendously reduced mainly because :
(i) Cardiopulmonary bypass machine of improved variety requires a less amount of blood to be
transfused.
(ii) Cell saver machine are employed to reuse the blood shed in mediastinum.
(iii) Needs for homologus transfusion is reduced after introduction of haemodilution technique. A
few words about the mechanical damage caused by the cardiopulmonary bypass machine.
Observed effects were :
(a) damage of circulating red cells
(b) platelet dysfunction
(c) coagulation defects.
With introduction of haemodilution, these effects became less remarkable.
But to conduct a prolonged bypass surgery, it requires further perfection. And so effort is on to
further improve the extracorporeal device by a refined pumping system or a membrane oxygenator etc.
Nevertheless a transfusionist may be called on postoperatively for any unexpected change in
haemodynamics of circulation which can be effectively treated by suitable replacement therapy.
Anaesthesia and blood transfusion
Anaesthesiology, an integer in modern medical system is a discipline based on scientific principle and
artistic application. It came into being in 1772 with Prestly's discovery of Nitrous oxide 'gas and subsequent
discovery of its analgesic property by Davy..On October 16, 1846, the first public demonstration of
anaesthetic application in surgery was done by Morton in Masachusetts General Hospital, Boston, USA,
following which started the era of clinical application of anaesthesia which culminated in development
of Anaesthesiology. If we recognise the blood line as one -of the key component in practice of major
surgery conducted under anaesthesia, then anaesthetist becomes the person 'logically responsible to keep
the flow continued till required by patient, irrespective of intraoperative or postoperative resusscitative
phase. Not being a casual relationship, it needs to be viewed in the overall perspective of its application
in differing clinical situation and has to be redefined accordingly. For example, the application in planned
surgery, emergency surgery and resusscitation of critically ill and terminal cases will certainly differ
from each other. Variability in application of blood transfusion, component transfusionor a combination
of volume expanders and blood in different clinical situation and the resultant success depends on clinical
acumen of anaesthetist, this is beyond the scope of this book. Hereinbelow, we confine to commonly

[[p.27]]
Transfusion Practice Clinical Aspects and Applications
239
practiced anaesthetic perspective of transfusion of blood and itscomponent is planned surgery. From
anaesthesia point of view a planned surgery is broadly subdivided in :
0
(i) Preoperative phase
(ii) Intraoperative phase
(iii) Postoperative phase
Preoperatlve phase
Here the patient is checked up before operation and i~
recommended for build up, if haemoglobin is
below 10 gm/dl, but it has no scientific explanation rather a preset standard of practice because it pas
been observed that a sedentary person with 7 gm/dl does not produce symptom. It is below 7 gm/dl, then
the vital organ starts showing symptoms due to deficiency of oxygen. It is rather effort tolerance of
patient, i.e., cardiac and pulmonary status, duration of surgery, blood volume, peripheral resistance,
haemoglobin level, all should be correlated before considering fitness and or recommending for correction
ofpreoperative anemia. We can use autologus blood collected under predeposit scheme or we can transfuse
the homologus stored banked blood. The rise in haemoglobin level occurs (ref. 10.1 section) and
preoperative anemia once corrected, patient is considered for surgery.
Intraoperative phase
The aim is to maintain the intravascular volume of blood giving due regards to its physiochemical
property, functional ability of red cells and other solid component so that vital functions are continued
undisturbed. This is done by volume replacement of blood lost during surgery. To monitor exact volume
lost is difficult °in a patient under anaesthesia. One of my anaesthetist friend has likened it to bikini.
"Concealing mor~
than what it is revealing", e.g., a retroperitoneal bleeding may not be visualised or a
internal bleeding in thigh due to a fracture femur or a bleeding inside the thoracic cavity etc. they are
very much deceptive bleeding.
So any unexplained sudden hypotension associated with bradycardia (at initial stage of blood loss)
in a patient undergoing operation under general anaesthesia is to be attended with utmost care. A patient
with 15to 20%of volume loss may be apparently normal, goes into decompensation suddenly with little
more blood loss (ref. surgery and transfusion). If the condition is not. attended immediately, patient may
pass into shock. The pulse rate, urinary output even CVP may be seriously misleading. Much more
informative is "pulmonary capillary pressure". It reflects the pressure in the left atrium. Measurement of
central mixed venous tension showing rise in central P02 reflects improvement in circulatory status. So
there is no fixed parameter to know the hidden blood loss under anesthesia but an anesthetist should get
alerted with sudden unexplained hypotension and if it is associated with oozing from different sites.
Replenishment of volume lost could be autologus, homologus or a combined therapy of component
with artificial volume expanders.
I. Autologus :
(a) Haemodilution
(b) Intraoperative salvsage (ref. autologus donation).
II. Homologus:
(a) Whole blood for rapid loss of blood here the whole blood acts as volume expander and
RBC provides the enhancement of oxygen carrying capacity.

[[p.28]]
240
Blood Banking and Transfusion
(b) In case of non-availability whole of blood a combination of RBe component alongwith
artificial volume expander may be transfused while transfusing stored homologus banked
blood we must ensure that :
(i) Blood is a compatible unit.
(ii) Within limit of expiry.
(iii) Blood bag/unit has to be identified and cross-checked with the attached label.
(iv) It has passed all the mandatory test.
(v) It is provided with an administration set fitted with filter as per specification.
(vi) Blood is warm but not haemolysed and/or contaminated.
(vii) No leakage in bag or administration set. Administration set should be properly packed
and no nick in the pack.
'
Similar precautions are to be observed with components also, and while transfusing see that with
each unit the administration set is' provided, use the set for transfusion purpose. If multiple/massive
transfusion is needed single administration set can be used for two or three bags but observe for any
sediment or collection in the filter, discard the set if it is present and do not add any drug to the blood or
to the transfusate,
Homologus stored banked blood possess some abnormality commonly called "storage lesion" which
needs due consideration when the homologus blood is transfused.
(i) Increased potassium content: Potassium concentration in banked blood is more and it may rise
upto 25 meq/litre by third week, this might be a cause of concern in patients receiving more
than ten units of blood but below that, it is not of much concern because the potassium
concentration referred to, reflects the potassium that has come out in plasma during storage and
they return to the red cells after transfusion. But rapid transfusion of ten units as done in massive
transfusion where hyperkalemia may occur transiently, this is counteracted by alkalosis that
results from metabolism of citrate and with adequate urinary output, gain in potassium will be
excreted through kidney.
(ii) Citrate toxicity: Citrate is used an an anticoagulant for storing the blood unit, citrate exerts its
anticoagulant effect by binding of ionised calcium in stored blood but on transfusion, this effect
is reversed by ionised calcium present in the patient. Citrate is metabolised 'in nucleated cells
and excretion takes place through kidney. But in rapid and massive transfusion at the rate of 1
litre/If min., citrate induced lethal effect due to decrease in ionised calcium may be observed
but to counteract with 10% calcium gluconate practiced earlier has now 'been discontinued in
view of fatal cardiac arrestoccurred in good number of cases. Experimental research on citrate
toxicity due to homologus banked blood transfusion was done by several workers but their
research failed to reveal any significant relationship between transfused volume of blood and
citrate level in,the recipient. Impaired liver function has an unfavourable influence on citrate
toxicity whereas warming probably has a favourable influence.
(iii) Acidosis: It is a common problem faced with homologus stored bank blood transfusion. It has
been observed by workers that fresh ACD stored blood has a,base deficiency of 20-25 mEq/l
which increases further proportionate to the duration of storage. This is attributed to lactate
accumulation in stored blood. This effect or acid load in CPD stored blood is less in comparison
to ACD stored blood. So massive transfusion of stored blood may fraught with deleterious

[[p.29]]
Transfusion Practice Clinical Aspects and Applications
241
effect of acidosis. This may be counteracted by 40 to 45 mEq of sodium bicarbonate given IV
after every 5 units of homologus blood transfusion or as determined by blood gas analysis.
(iv) 2-3 diphosphoglycerate : This is an intracellular organic phosphate and this exerts influence on
oxygen dissociation, dissociation curve and the value of P50. The increase in DPG leads to
decrease in oxygen affinity and increase in release of oxygen to tissue that means there is a shift
of oxygen to the right. whereas there is a shift of oxygen dissociation curve to the left with
decrease in DPG levels as observed in banked blood resulting in increase of oxygen affinity by
haemoglobin and less release of oxygen to tissues. However after transfusion in vivo the red
cell DPG level is restored to 25% of normal in about three to four hours but takes longer time to
reach a 50% level,
(v) Progressive loss ofplatelet occurs in storedlbanked blood: The platelets are best preserved at
room temperature of 20 to 24°C'- to be more specific at 22°C for 72 hours only. At the
recommended temperature for storage of blood, it has been observed that most of platelets
suffers from storage lesion -
microtubules of platelets breaks up resulting in shortening of
their life span and s~ after transfusion of homologus banked blood of 72 hours age the platelet
recovery is only 20%.
(vi) Factor VIII and factor V also shows declined level at the recommended temperature of storage.
Initially there is rapid drop during first 24 hours and later on, it remains stable for about three
weeks after initial decline.
(vii) ATP also shows a declined level in stored blood resulting in loss of viability of red cells and
rigidity of cell membrane occurs and below a certain critical level phosphorylation of glucose is
adversely affected. This occurs in storage at the temperature recommended for red blood cell
preservation. It has been observed that addition ofAdenine to anticoagulant preservative solution
restore the level of ATP in vitro.
(ix) Thebanked blood shows increase in screen filtration pressure required to force a given volume
at a fixed rate through 20 m mesh screen and is thought to be due to formation of microaggregates
ofplatelet, fibrin and leucocyte. This, ifpasses unfiltered may cause respiratory distress syndrome
in a patient under anaesthesia, characterised by decrease in PA02 and responds well to positive
end expiratory pressure ventilation.
The "storage lesion" that occurs in a homologus banked blood tempts one to think more in favour of
autologus transfusion - haernodilution technique which has the added advantage of reduced viscosity of
blood and better perfusion of vital organs also no haemolytic reaction. But intraoperative transfusion is
exclusively at the discretion of surgeon and anaesthetist, the choice of blood and type of transfusion to
be adopted is guided by their mutual consent.
For intraoperative volume loss of moderate severity whole blood is a better choice but in case of
non-availability of whole blood a combination of packed RBC with artificial volume expanders viz.
crystalloid or colloid is preferred. The type of combination, i.e., packed RBC with crystalloid or packed
RBe with colloid or a combination of all three has to be decided by anaesthetist. When the volume loss
is of severe in nature and transfusion of ITIOre than 5 units is required, it is to be interspersed by
administration of sodibicarb. Fresh frozen plasma and platelet (ref. section on massive transfusion in
this chapter), Red blood cells and component be made available to the anaesthetist on demand:
(a) Packed RBC or concentrated RBe 200 ml in each unit ± 10has haematocrit value ranging 70 to
85% whereas whole blood has an haematocrit value of 38%, packed RBC can be produced hy

[[p.30]]
242
Blood Banking and Transfusion
sedimentation or centrifugation method. It has the advantage of having less blood group antibody
due to removal of plasma. In case of emergency issue, 0 negative packed cells can be issued.
Anaphylactic reaction commonly associated with protein is inconspicuous by its abscence. The
only disadvantage is increased viscosity in packed RBC unit, this reduces the rate of flow but it
can be overcome by addition of·50 mI to 100 ml of normal saline. Sometimes, it may have to be
reconstituted with albumin, if whole blood is not available. Transfusion depends on the condition
of patient and clinical accumen of anaesthetist.
(b) Leukocyte poo~
red cells are recommended for patients having previous history of white cell
sensitivity and can be transfused through a specially available leucocyte filter leucoguard etc.
or leucocyte depleted red cell can be produced by inverted centrifugation of 7 to 10 days old
blood. It is also preferred in case of multi-transfused patient or multiparous patient.
(c) Washed red cells ~an
~e
produced manually or by using haemonetic cell washing machine.
Saline washing of red cells removes a major portion of white cells. This is recommended in
patients showing anaphylactoid reactions to IGA or in those patients having history of febrile
episode, commonly attributed to leucocytes. Manually prepared washed red cell has to be used
within 24 hours of preparation.
(d) Fresh frozen plasma is separated from whole blood within six hours of collection and stored at
a temperature below 30°C. It consists of a wide spectrum of coagulation factor and is
recommended in case where bleeding is thought to be due to deficiency of coagulation factor
but the specific factor has not been identified. Some prefers to use it as volume expander in
cases having more than 10 gmldl of haemoglobin. This also provides Albumin, FFP unit of 250
ml contains 175 to 250 units of coagulation factors (labile and stable) and Fibrinogen about.400
mg.
(e) Platelet rich plasma (PRP) and platelet concentrate (PC) are two produced automatically by
machine from pooled platelets of random donors, the platelet concentrate so produced should
contain 5.5 x 1010 of platelet at its minimum in a 50 ml platelet pack. PRP is produced by
centrifugation and has the advantage of containing both platelet and coagulation factor.
Recommended in patients with unexplained haemorrhagic diathesis or in Aspirin induced platelet
disorder or in those cases where DIe has set in.'Anticipated platelet increment is calculated for
the patient and transfusion of platelet is done accordingly.
(f) Albumin is one of the safe volume expander produced by plasma fractionation employing Cohn's
filteration method. ~~e
finished product is heat inactivated at 60°C to make it virus free (HbsAg,
, HCV, HIV) and PKA free. Available in bottle as 25 gm albumin (to be reconstituted in 500 ml
of distilled water) as 5% to 25% preparation. Also available as salt poor preparation of albumin
and as plasma protein fraction. Main indications are :
(i) Blood volume expansion - severe trauma, extensive bum, major intraoperative blood loss.
(ii) Albumin loss: It has been estimated that for each unit of blood loss approximately 15 gm of
albumin is lost; malabsorption viz. protein losing enteropathy, nephrotic syndrome, ascites and
sepsis.
(iii) Other uses : Cardiopulmonary bypass pump priming. Resuspension of packed RBC before
transfusion. In plasmapheresis as replacement colloid (still under experiment), chemical buffer
in hyperbillirubinimia, used as a component in solution for preservation of organ meant for
transplantation.

[[p.31]]
Transfusion Practice Clinical Aspects and Applications
243
The abovementioned components are commonly practiced by anaesthetist iritroperatively and/or
postoperatively as well as in the resusscitation of the critically or terminally ill patient.
Hypotension in patient under general anaesthesia can be due to so many causes and needs to be
differentiated before arriving into any conclusion. According to cause, it can be broadly subdivided as
given in Table 10.5.
(a) Hypovolimia is due to fall in total circulatory volume. It may occur as a result of loss of blood
or plasma from the circulation. Commonly observed in :
(i) haemorrhage which could be traumatic, operative or internal bleeding viz. gastrointestinal
haemorrhage, ruptured varices etc.
(ii) loss of red cell mass .alongwith fluid may occur in extensive and full thickness bum needs
resusscitation prior to surgery and maintenance intraperatively.
(iii) undetected loss in retroperitoneal space and or other serous spaces.
(b) Cardiac causes may include both intrinsic and extrinsic causes. Amongst the intrinsic causes :
(i) Due to decreased myocardial contractibility.
(ii) Precipitation of myocardial infarction.
~-'
(iii) Arrythmias, ventricular arrythmia commonly observed in massive and rapid transfusion of
refrigerated/cold blood. The extrinsic cause is pulmonary embolism.
(c) Vascular reas~ns
for hypotension is due to expanded vascular bed resulting from dilatation of
artery and arterioles, venous pooling, arterio-venous shunt etc., wherethe existing circulatory
volume becomes inadequate to cope up with the. situation. In overwhelming bacterimia
particularly gram negative bacterimia, the bacterial endotoxin cause initial vasoconstriction
followed by vasodilation. se unattended infection in elderly, diabetics and immunocompromised
patients taken for immediate emergency surgery, may sometime manifest hypotension under
general anaesthesia and is usually precipitated by operative manipulation oforgans and visceras.
Table 10.5
I
Others
(a) Acute femoral
venous thrombosis
(b) Tension
pneumothorax
(c) Pericardeal
temponade
(d) Acute spinal
injury
(e) Accidental injection
of distilled water
I
Vascular
Transfusion
reaction
I
Hypotension
I
Leucocyte and
platelet related
I
Plasma
,--I
lOA deficient
Protein
1---1
Injection of
Administration
immunoglobulin
of PPF
I
Immune
haemolysis
I
Cardiac
I
Hypovolimia

[[p.32]]
244
Blood Banking and Transfusion
(d) Transfusion reaction and its clinical expression are markedly masked in recipient under general
anaesthesia. Morphin has a modifying effect on transfusion reaction. The two signs that should
attract immediate attention of anaesthetist are:
(i) Hypotension despite adequate .volume replacement.
(ii) Abnormal bleeding, haemoglobinurea (unexplained).
Oozing from different sites unrelated to surgical field. Transfusion reaction could be due to
components shown in the table, brief discussion follows. Immune haemolysis occurs as a result of
antigen and antibody reaction in vivo, consequent upon an incompatible transfusion. Two types of
haemolysis occurs:
(i) Intravascular haemolysis usually complement mediated commonly met with IgM antibody with
thermal range of 37°C.
(ii) Extravascular haemolysis mechanism involved is phagocytosis commonly met with IgG antibody
usually exhibits a mild or delayed reaction.
The immediate intravascular haemolysis is of relevance to patient under G.A. who has been transfused
with incompatible blood is manifested by hypotension of persistent nature gradually proceeding to shock,
if the cause is not attended, laboratory parameter - Haemoglobinurea, high plasma haemoglobin and a
positive direct Coomb's test, hyperbilirubiminia, leucocyte and platelet related reactions are mostly febrile
reactions of varying severity and attributed chiefly to leukoagglutinin more commonly observed in
multitransfused and multiparous women. Cytotoxic antibodies were also observed in such cases.
Additionally, the pulmonary infiltration, dyspnoea and hypotension were observed in cases where
leukoagglutinins were demonstrated.
Some of transfusion reactions are due to antibodies present in plasma or due to plasma protein
fractions (PPF) and these are usually not detected by cross matching. The blood thus transfused when.
provokes reaction becomes a matter of concern for anaesthetist and like all other transfusion reactions,
these reactions are also masked by general anaesthesia. And the conditions associated with hypotension
due to antibody or PPF in plasma are found in (i) IgA deficient individual, approximate incidence being
1 : 600. Reaction occurs when IgA is present in donor plasma and transfused to an IgA deficient individual.
The reaction at its severest produces anaphylactic reaction characterised by flushing of face and skin,
substernal discomfort with breathlessness and severe hypotension. Mild or intermediate reactions are
observed and are called anaphylactoid reaction characterised by appearance of hives, nausea, flushing
of skin, light headedness with hypotension. Short lived symptom and signs are usually followed by chill
and rigor. The former reaction are said to be due class specific antibody where total deficiency of IgA
have been found. The later is due to antibody with limited specificity. Reactions occurring due to plasma
protein fraction are usually acquired and are observed in the recipients when he or she has earlier been
injected by immunoglobulin. Injection of immunoglobulin per se consists of more than 95% of IgG but
it also contains very small amount of IgA. And IgA deficient individuals on receiving this injection
develops anti-IgA who when subsequently transfused IgA positive donor plasma develops reaction.
Prekallikrein activator (PKA) : Though it is not clearly established but has been accepted that factor
xii (Hageman factor) plays an important role in triggering the initial process of blood coagulation.
Activated Hageman factor once formed acts through feedback mechanism that involves prekallikrein
and HMWK, generating more activated Hageman factor. PKA is also activated and Kallikrein isformed
which after l1:i action with HMWK produces Bradykinin. It was previously thought that Bradykinin, so

[[p.33]]
Transfusion Practice Clinical Aspects and Applications
245
formed isresponsible for hypotension produced by transfusion of PPF, but later on it was confirmed by
further research that it is Prekallikrin activator (PKA) is responsible for hypotension. This PKA is found
in plasma protein fraction and in some of human albumin. So transfusion of PPF or albumin may cause
hypotension suddenly but with variability of individual response and with improved manufacturing
process by which PKA content is taken care of in the finished product, these adverse reaction are seldom
observed now-a-days.
The other causes that may produce hypotension are, e.g., in acute ileo femoral venous thrombosis
large volume of fluids collects distal to the thrombus reflected clinically by unilateral swelling of thigh
and leg leads to fall in total circulatory volume and thus hypotension. The pericardial tamponade resulting
from trauma or operative injury showing simultaneous elevated C.V.P. with systemic hypotension in
presence of chest injury should arouse suspension of increased pressure in pericardial sac. Tension
pneumothorax may also be associated with hypotension. High intrapleural pressure impedes venous
return producing shock, hypotension and cyanosis. It can be confirmed by X-ray and clinically by hyper-
resonant percussion note with diminished breath sound on affected side. Commonly observed in injury,
chest and occasionally as a complication to continuous positive pressure ventilatory support. Acute
spinal injury acts through sudden loss of inhibitory control over vasomotor tone-resulting in dilatation
and rapid pooling of blood in periphery or splanchic pooling resulting in decreased cardiac output with
systemic hypotension. Again accidental infusion of large volume of distilled water is also associated
with hypotension.
Postoperative phase: Resusscitation is the main aim at this phase, it may be done as follows:
(i) Replace operative blood loss by volume replacement through whole blood, RBC and or
components.
(ii) Reverse coagulation defects that might have occurred during the course of operation.
(iii) Other ancillary measures deemed necessary.
Replacement of operative loss by whole blood, RBC and or components or with artificial volume
expanders has already been discussed.
The coagulation defects can be treated with FFP and PRP which were already been described.
Disruption of normal haernostasis is a common problem faced by anaesthetist during postoperative
period. This is usually observed in cases undergoing prolonged surgery with involvement of mechanical
devices and operative manipulation of organs and viscera. Let us consider one such operation -
cardiopulmonary bypass surgery, higher incidence of kidney and lung failure has been reported in the
past. With advent in technology, the situation has greatly improved at present but it is still far from being
satisfactory and needs alert attention of anaesthetist in postoperative period. No definite cause has still
been identified but in summation, three different factors are said to be responsible and they are mechanical
cause, platelet dysfunction and coagulation defects. And treatmentlresusscitation varies from patient to
patient and has to be decided by anaesthetist on the spot. Similarly in other such case of prolonged
surgery, postoperative management by transfusion has to be done depending on the condition of patient.
A broad outline for therapy has already been given. The ancillary measures are beyond the scope of
present communication.
In some postoperative cases DIe becomes a problem to be dealt with. The next communication in
this chapter is DIC. The transfusion therapy under intensive care for critically ill or terminal patient is
beyond the scope of present discussion.

[[p.34]]
246
Blood Banking and Transfusion
10.'4 DISSEMINATED INTRAVASCULAR COAGULATION
DIe is a syndrome characterised by a reduced level of fibrinogen and widespread deposition of fibrin
thrombi in microcirculation commonly associated with haemorrhage due to thrombocytopenia and
diminished factor V and VIII.
Aetiopathogenesis : It is an acquired coagulopathy manifested by its consumptive
thrombohaemorrhagic nature. Events following a wide variety of primary pathological process that leads
to activation of coagulation and/or fibrinolysis are presented below:
(a)
~elease
of thromboplastic material into circulation that activates the coagulation system.
(b) Deposition of fibrin thrombi in smaller vessels.
(c) Intravascular coagulation leads to production offibrin degradation production (FDP) that interfere
with fibrin polymerisation and platelet function.
(d) Utilisation of coagulation factors: Factor V, VIII and platelet eventually leads to haemorrhage,
A wide variety of primary pathological process giving rise to DIe, if not attended properly is.
listed in Table 10.6.
Laboratory. parameters as observed in ole
Platelet count
Diminished
Fibrinogen
Diminished
Fibrin degradation product (FOP)
Elevated
Plasminogen
Low or normal
Factor V
Low
Factor VIII
Low
AP7T: Prolonged indicates deficiency of factors involving "intrinsic pathway" XII, XI, IX, VIII, X,
V, II and fibrinogen, prekallekrin and HMWK' (high molecular weight kinnogen).
PT : Prolonged, indicates deficiency of factors involving "Extrinsic pathway" VII, X, V, II and
fibrinogen.
17': Prolonged, indicates deficiency offibrinogen, presence ofFibrin degradation product or heparin.
DIe commonly associated with fibrinolysis..This secondary fibrinolysis sometimes clinically
resembles a rarer condition of primary pathological fibrinolysis and needs to be differentiated before
Table 10.6. AetiopathologyDIC
ole
I
Surgery and related
(a) Heart and lung
surgery
(b) Pulmonary
embolism
(c) Single giant
haernangeiona
I
Obstetrics and related
(a) Major obstetric and
gynaecological
surgery
(b) Abortion
(c) Abruptio placenta
(d) IUFD
(e) Amniotic fluid
embolism
I
Blood related
(a) Acute leukaemia
(b) Thrombotic
thrombocytopenic
purpura (TIP)
(c) Haemolytic
transfusion
reaction
Other
(a) Malignancy
(b) Scepticimia gram
negative
(c) Snake bite
(d) Hypersensitivity
reaction

[[p.35]]
Transfusion Practice Clinical Aspects and Applications
247
arriving at a diagnosis for DIC. In the primary pathological fibrinolysis the oozing of blood is less
diffuse and laboratory parameters that strikingly differs are :
(i) Platelet count and fibrinogen both diminished in DIC whereas in PPF the platelet count is
normal and fibrinogen may-below or normal.
(ii) FDP are markedly elevated in ~PF
but in DIe, it is moderately elevated.
(iii) Increased plasmin level and low plasminogen in PPF.
(iv) Factor V and VIII less decreased in PPF.
Management
(i) Treatment of primary cause is the basic approach to management of DIC.
(ii) Supportive therapy includes restoration of blood volume and correction of haemostatic defect
preferably by replenishment. These two combined hastens the recovery.
The former is beyond the scope of this book. Regarding correction of haemostatic defect the use of
heparin is controversial except in cases of persistent thrombosis, where it acts through inhibition of
fibrin formation. The advocated dose for intravenous heparin is 5000 units I.V. followed by maintenance
dose 1500 unitslhour continuously for 12 hours in adults. In case of children 100 units per kg initially
followed 50 unitslkg every 4 to 6 hours. Restoration of blood volume by whole blood which may be
interspersed according to necessity or as determined by laboratory parameter, with FfP (advocated dose
15 to 20 mllkg) and/or cryoprecipitate. The use of platelet concentrate is to be restricted to those cases
where it is indicated. The commonly used FFP gives a wide spectrum of coverage and a single donor
FFP usually contains the following clotting factors approximately ranging between 0.7 to 1.0 unit/ml.
FFP contains factor V, VIII, II, VII, IX, X, XI. Cryoprecipitate is more specific in the sense that it
contains factor VIII C (80 to 120 units/IO to 20/ml). Fibrinogen (150 to 2501mg) factor VIII R : AG,
factor VIII : VWF, XIII, II, V and IX, it also contains Fibronectin. The transfusion of cryoprecipitate to
raise the level of fibrinogen approximately to level of 100 mg/dl may require minimal transfusion of 16
units of CPPT. In addition to Fibrinogen CPPT provides factor VIII and fibronectin. Fibronectin is a
glucoprotein that provides opsonin. It has been observed that sceptic states are associated with fall in
opsonin, so in DIe due to scepticimia, it may proved to be useful adjunct to the therapy. The platelets are
not commonly used unless it is indicated as, e.g., dilutional thrombocytopenia, haematological malignancy
etc.
Above description is a general guideline for management of a case of DIe but there are certain
conditions where situation is slightly different and accordingly management also varies and as such
deserves attention (i) DIC due to haemolytic transfusion reaction; (ii) ole due to snake bite.
The former is of special relevance to transfusionist and the later is no less important particularly in
tropical country like India. Hereinbelow is a brief discussion on both the conditions :
(i) DIC due to haemolytic transfusion reaction is a known hazard of mismatched transfusion.
Development of DIC in ABO incompatible blood transfusion has been observed and all such
cases has ultimately expired. Occurrence of DIC is mostly seen in mismatched blood transfusion
more than 180 ml to 210 ml and in ABO incompatible transfusion. Strategies for management
could thus be prophylactic and/or management when DIe has made its appearance, determined
by laboratory parameter. Heparin is the recommended drug of choice but since heparin itself
may sometime cause bleeding and contraindicated intraoperatively and immediate postoperative

[[p.36]]
248
Blood Banking and Transfusion
period, its prophylactic use in anticipation to DIe is not rational and as such itsuse intraoperatively
is not advised. But in immediate postoperative period where DIe has set in due to a haemolytic
transfusion reaction and unless strongly contraindicated. Heparin may be used at a rate of 5000.
IV LV. stat followed by 1500 IUlhour by continuous iv drib, this maintains heparin level for 6 to
24 hours. This is to be done under constant haematological monitoring.andtransfusion controlled
accordingly or stopped when not required. In case of recurrence, Heparin with protamin may be
tried.
The use of whole blood in such cases though ideal for volume restoration is not recommended by
clinician, but if the cause for haemolytic transfusion reaction has been identified and taken care of, then
transfusion of a unit of compatible whole blood is worth consideration, otherwise we can use 5% albumin
for volume restoration. FFP or platelet can be transfused according to necessity as determined by laboratory
parameter.
Snake bite and ole
India being a tropical country, a good number of snake bite cases occurs every year. Approximately
15,000 deaths occurs in India every year from snake bite. Out of total 3500 species of snakes, about 300
species are found in India (Table 10.7).
Table 10.7. Signs and symptoms of Indian snake poison
Type of snakes
Family
Toxin or
Target organ
Common sign symptom
commonly founo in
venom·
India
1. Kratts (Naja-Naja)
Elapidae
Neurotoxin
Neuromuscular
Ptosis, resp. failure,
(Predominant)
junction, eNS,
comma, ophthalmoplegia
spinal cord,
palatal and pharyngeal
respiratory paralysis
paralysis. Flaccid limb
paralysis
2. Cobra (Bangrus)
Cardio toxin
Heart cardiovascular
hypotension, cardiac
failure
arrest convulsion
3. Russel's viper
Viparidae
Capillary endothelium
Bleeding from site of bite,
and haernostatic
and gum, maJena purpura,
4.
Saw scaled viper
Haemorrhagin
system, renal failure
haernatorna, oliguria
(Echis carianatus)
In neurotoxic and cardiotoxic group two modality :
1. Conventional: ASV (antevenin) and supportive measure, electrolyte infusion and corticosteroid.
2. Trial group: Specific therapeutic agent in addition to conventional treatment.
Snake venom, a mixture ofenzymes, peptides and low molecular weight protein. The venom produced
by members of viperidae family again differs according to species of different subfamily and as such the
symptoms produced by viper bite may slightly differ from each other depending on predominance of a
particular component in the venom in crotalus admantus of crotaline subfamily, collagenases produces
local haemorrhage by attacking basement membrane of capillary. Again anticoagulant phospholipase A2
was observed in venom of vipera berusorientalis by M.e. Boffa et a1. (loc cit.). The anticoagulantactivity

[[p.37]]
Transfusion Practice Clinical Aspects and Applications
249
on plasma was explained by antagonism to phospholipid procoagulant activity. Ecarin, a prothrombin
converting enzyme from Echis carinatus cause rapidly developing defibrination of prolonged duration.
A comparative study ofhaemolysis ofRBC by M.A. Gomez, venom of vipera Russelli is most indirectly
haemolytic. Venoms from crotalean subfamily are more haemolytic than ,those obtained from Bothrops
Asper. In India, defibrination state caused by toxins which are thrombin like in action is restricted to
crotaline subfamily (Himalayan pit viper and humpnosed viper of western ghat hills of south). Russel
viper acts by activation of factor X, platelet consumption and factor V and calcium causing
thrombocytopenia.
Pathogenesis ofthe killer effect of viperine venom differs from species according to the predominance
of a particular component in the venom and is a moot point. Upon the whole, the effect is on haemostatic
system, capillary endothelium, erythrocytes-haemolysis. This results in abnormal haemorrhage due to
fibrinolysis, thrombocytopenia and defibrination. Shock may supervene due to exudation of blood and
plasma. Renal failure may occur at end stage which usually terminates fatally. Morbid- pathology in
viperine bites (E. Carinatus and Russel viper). The lesions in kidney glomerulonephritis and interstitial
nephritis - haemorrhagic (differentiated from cortical necrosis) and, cortical necrosis (patchy and diffuse).
Tubular necrosis is alsocommon. Lesions in brain are cerebral haemorrhage, subarachnoid haemorrhage
cerebral edema, patchy demyelination and occasional neuronal degeneration.
Laboratory parameters show coagulation defect with prolonged ciotting time, prothrombin time,
partial thromoplastin time and thrombin time, haemoglobin and plasma fibrinogen reduced, platelet
count may be reduced or normal, bleeding time is nonna!. Urine output may be reduced and change in
colour of urine due to haematurea or microscopic haematurea may be observed.
10.5 HAZARDS OF TRANSFUSION
Genetic make up differs from individual to individual, be it in human or animal, identical twins being
the exception to this principle. Homologus blood is, therefore, expected to be fraught with deleterious
effect of introduction of foreign antigen that could be potentially immunogenic in a recipient negative to
the particular antigen protein. Depending mainly on the immunogenecity and of course influenced by
synergism (good responders etc.) and antagonism (immunological tolerance etc.), the recipient develops
antibody immediately or at a delayed period. Failure to recognise this is fraught with possibility of
immune haemolysis oftransfused blood in vivo. Apart from this, there could be non-immunologic reaction
and transfusion transmitted disease in the recipient of whole blood or its component. Taken altogether,
they are known as transfusion associated hazard or TAH. An accepted therapeutic modality, blood
transfusion thus has to be evaluated and considered in terms of risk involved, preferably restricted to
where it is clearly indicated and/or avoided with safer alternatives if possible. Transfusion of one unit of
blood does not have much therapeutic value. TAH that broadly includes HTR (immunologic/and non-
immunologic) and TfD (bacteria virus, parasites, neoplasia) could not be accounted for in terms of
percentage because of the variability in response by recipients. The adverse effects could thus be mild,
moderate, severe, overt or covert and a good number of cases may escaped unnoticed. Causative agents
are numerous and actiopathogenesis varies, the table 10.8 gives a brief account of classification ofTAH,
an' attempt is made to place them aetiological-wise.
The conditionslhazards listed in the table and the in vivo unpredictable immunohaematological,
biochemical and pathophysiological changes which often terminate fatally tempts one to think on the
negative aspect of blood transfusion. Such situation may even arise following compatible blood

[[p.38]]
250
Blood Banking and Transfusion
INCOMPATIBLE
.TRANSFUSION
Cortical necrosis
(irreversible)
+
Detomatlon of
Renal profile
~
.
Coma (uremic?)
+
Death
~nVagination
~
Phagocytosed
1. Acute transient shut down
2. Bilateral cortical necrosis
3. Tubular necrosis
l
HypotenSiO)n
/
"-...SHOCK
I
I
/
1
1/ t::\
~
IgG coated RBC
I
_
CHEMO @
I
e
TAXIS
<QjI-- Opsonin
Tuftsin
Hb
-,
<,-,,
Haerne+ Globin
-,
MethemalbuminHaempaxine
FreeSerum HaemOgl~bin
.
e
\
~
\
A«:-t- \)~
\ -,-, r-V
'F"
\~~J
~~~
\ 4
fS'0
\
~'lJ.e
/
\
Ruptured
\
RBC
\
\
\
\
I
\
0
I
\
0
I
\
~
I
, "
\
In
I ~
\
m~
/
't)
,
I ¥
~,
~
/
~
«> \
I g'
(.\l
,
I
~,
I
%'
I
,
8\1 I
JlI
-------
___ - - - - - -
RENAL
- -
-
FAILURE
Clinical manifestation
Fever, Chill, Rigor,
Pain Chest and Back
Flushing Face
Hypotension
SHOCK
Tubular necrosis
(Reversible)
~
Improvedby 8 to
12 days glomerular
filtrate contain low urea
i
Diuresis (with loss of 'K')
+
Recovery
Haemolysis
c
~.E0"8
.90
0.-0,
~
C
<,
J:t13
, ,
<,
Haptoglobin&}'"
Haemoglobin
"
Complex
ole
Fig. 10.1. Pathogenesis of haemolytic transfusion reaction (HTR).

[[p.39]]
Table 10.8.
Transfusion Associated hazard
I
~c.n
~
~
iiJ
:::J
~c-
(/)
5'
:::J
\J;n2
Qs-
~
»
(/)
"'Ca
Dl
::1
Q.
»
-0
~
~cf
:J
(/)
HBV,HCV
NonA,NonB
BBV
CMV
HIV 1 and 2
HTLVI
herpes
Toxoplasma
Malaria
Kalazar
Filaria
Trypanosoma
pallidum
other bacteria
(gram
negative
Rare-
brucella
albortus
Yersinia
Trypano-
somiasis
(chaggas
disease)
Babeseosis
Accidental
Transfusion of
Cancerous blood
I
I
Haemolytic transfusion reaction
Transfusion transmitted disease
1----------,
Immunological
Non-inm!unologiCal
I
I
I
I
Immediate
Delayed
-.JL.-
__
I
I
I
I
I
Primary
Secondary
Internal
External
(a) Delayed
(a) Anamnestic
(a) Fever
induced
reaction
response
(b) Cardiac
(a) Asymptomatic
due to
resulting in
failure due
haemo
weak
haemolysis
to volume
globinuria
antibody
overload
(transfusion
in serum
(c) Haemosiderosis
of haemolysed
of reci-
(iron overload
blood, induced
pients
multiple
by physical,
against
transfusion and
chemical or
trans-
thalassemia)
other agents.
fused
(d) DIC
(b) Cardiac
cells
.(dilutional
arrythmia
(b) Purpura
thrombocytopenia
(transfusion
(anti-
FDP, lack of
of cold
platelet
factor V and Vill)
refrigerated
antibody)
(e) Fever with
blood-massive
(d) GVHD
shock
transfusion
(engraft-
(bacterial
and in infant,
ment of
endotoxin)
neonate).
leucocyte
(e) Thrombo-
immuno-
phlebitis
compro-
mised
patient)
Cell related
Plasma related
(a) Haemolysis
(a) Urticaria
(incompatible
. (antibody
redcell)
to plasma
(b) Fever
protein)
(antibody to
(b) Anaphylac-
leucocyte
tic reaction
antigen)
(antibody
(c) Pulmonary
to IgA)
odema
(c) High titre
(leucoagglu-
antibody
tinin
(dangerous
(d) Incubator
universal
effect
dono~

[[p.40]]
252
Blood Banking arid Transfusion
transfusion, the compatibility test is not always cent per cent foolproof. As such, it is always better to
avoid transfusion unless the patient care would be seriously compromised or preferably restricted to the
needs according to the necessity, i.e., a minimal use of a particular componentlblood that serves the
purpose should be adhered to in principle in order to avoid/minimise the HTR and TID.
Mechanisnl of TID and Hl'R
TID : In transfusion transmitted disease through blood transfusion, the underlying mechanism that leads
to production of sign, symptoms andthe disease chiefly depends on the offending agent namely bacteria,
virus and others and the important ones are discussed separately later in this section. Main reason is, of
course, transfusion of unscreened blood or blood products or postscreening contamination viz. bacterial
contamination during storage, contamination during transport and immediate pretransfusion period.
HTR : In haemolytic transfusion reaction adverse effects are broadly classified into two main
headings:
(i) Immunological
(ii) Non-immunological
The immunological effects could be immediate and delayed and the immediate effects could be cell
related or plasma related, the delayed effect which are also immunological, could be' due to delayed
effect ofpresent transfusion - primary, or itcould be due to revival of immunological memory or secondary
anamnestic reaction.
The immunological effect is mainly due to antigen antibody reaction in vivo, induced by mismatched
transfusion and manifested by haemolysis, urticaria, fever, anaphylactic reaction etc. The haemolysis,
which is immune mediated is also known as immune haemolysis may have fatal outcome, if not contained
either by withdrawal of offending agent or arrest by therapeutic measure. The pathophysiology ofimmune
haemolysis constitutes of acute intravascular haemolysis and/or extravascular haemolysis. The former is
due to complement activation by IgM type of antibody - anti-A', anti-B, anti-Le, anti-P and anti-I and
they are also haemolytic in vivo. The extravascular haemolysis is usually caused by.IgG type of antibody.
The antibody coated red cells are phagocytosed in liver and spleen. Antibodies belonging mainly to Rh
system, Kell system, duffy.and S of MNS system takes part in extravascular haemolysis. Unlike IgM
type, they are not haemolytic in vivo. IgG molecules particularly IgG 1 and IgG 3 subclass shows better
binding to the receptors on monocyte and macrophage through its Fe region which leads to phagocyto.sis,
the anti-D commonly belongs to IgG, whereas C and E components are sometimes IgM. Boorman and
Dodd (loc cit.) observed that red cell sensitised by IgM Rh antibody are removed predominantly by
liver, whereas, red cells sensitised by IgG Rh antibody are removed by spleen.
Sequal to haemolysis some biochemical'changes takes place which are reflected in the laboratory
investigation and are helpful in diagnosis of haemolytic transfusion reaction. The red cell ruptures and
releases haemoglobin which combines with haptoglobin and in the liver, the haptoglobin haemoglobin
complex is splitted into bilirubin and iron. Alternatively the heme part combines with albumin
(methemalbumin) or with hemopaxin, they too are tackled in the liver. The whole process is reflected by
rise in bilirubin and plasma haemoglobin, fall in the haptoglobin and hemopaxin associated with
haemoglobinuria and positive direct Comb's test. Histamin, serotinin etc. are released consequent to
complement activation. The extravascular haemolysis is tackled by reticuloendothelial system, mainly
in the spleen, through phagocytosis of IgG coated red cells, releasing iron and bilirubin.
Opsonin and tuftsin are said to enhance the process of phagocytosis opsonin coats the target particle
and probably acts alone or in combination with complement. The exact mechanism of action of opsonin

[[p.41]]
Transfusion Practice Clinical Aspects and Applications
2'53
and tuftsin are yet to be explored. The target particle gets attached to phagocyte through chemotoxis
mainly acted on by opsonin and tuftsin, this is followed by invagination and phagocytosis. If the process
continues unchecked, then renal failure develops. The kidney damage occurs due to combined effect of
free serum haemoglobin DIC, complement and hypotension and may exhibit as :