Perioperative
Fluid and electrolyte
balance, anaemia and blood
transfusion
David O’Hara
Patricia Richardson
Abstract
An understanding of the basic physiology of fluid and electrolyte balance
and the impact of surgery and anaesthesia on homeostatic mechanisms
is essential to safe patient management in the perioperative period.
Successful fluid management also requires familiarity with both the com-
position and pharmacology of commonly available products for fluid
replacement therapy. A greater awareness of the hazards of blood and
blood components has led to significant changes in practice over the
last 20 years; traditional transfusion triggers have been challenged and
more restrictive strategies adopted.
Keywords blood component transfusion; blood transfusion autologous;
fluid therapy; water–electrolyte balance
An understanding of the basic physiology of fluid and electrolyte
balance and the impact of surgery and anaesthesia on homeo-
static mechanisms is essential to safe patient management in the
perioperative period. The report An Acute Problem, published
in 2005 by the National Confidential Enquiry into Patient Out-
come and Death (NCEPOD), identified poor fluid management
as contributing to preventable morbidity and mortality, echoing
findings of previous reports.
Fluid compartments
Body water is considered to exist in physiologically discrete col-
lections known as compartments. The major division is into
intracellular fluid (ICF) and extracellular fluid (ECF), based on
which side of the cell membrane water lies (Table 1).
A 70 kg adult male body has 42 litres of water (60% of body
weight), of which 28 l is intracellular and 14 l extracellular.
Females, who typically have more body fat than males, have
less water per unit of body weight. Extracellular fluid is further
subdivided into:
• intravascular fluid (plasma), which with blood cells accounts
for a total blood volume of 4.5 litres (6% of body weight).
• interstitial fluid which lies in tissues outside the vascular
­system (9.5 litres; 14% of body weight).
David O’Hara FRCA is a Specialist Registrar in Anaesthesia at the
Broomfield Hospital, Chelmsford, Essex, UK. Conflicts of interest: none
declared.
Patricia Richardson FRCA is a Consultant Anaesthetist at the Broomfield
Hospital, Chelmsford, Essex, UK. Conflicts of interest: none declared.
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Distribution of total body water among body fluid
compartments (70-kg male)
% of body % of total Volume
weight body water (litres)
Extracellular fluid 20 33 14
Plasma 6 9 4.5
Interstitial fluid 14 24 9.5
Intracellular fluid 40 66 28
Table 1
• transcellular fluid (i.e. synovial fluid, cerebrospinal fluid, vit-
reous and aqueous humor).
Fluid movement
Two forces govern the movement and distribution of water be-
tween the intracellular and interstitial spaces:
• osmotic gradients (created by differences in non-diffusible
­solute concentrations)
• hydrostatic pressure gradients, governed by the relationship
­between compartment volume (e.g. circulating volume) and the
tension of the walls of the compartment (e.g. venous tone).
There is a negligible hydrostatic pressure difference between
the ICF and ECF, and so fluid movement is regulated principally
by the osmotic gradients. The cell membrane lipid bilayer, sep-
arating the ICF and ECF is freely permeable to water, but not
solutes. Potassium and sodium are the predominant cations in
the ICF and ECF respectively, and can pass only through spe-
cific voltage or ligand-gated ion channels. The inequality in ion
concentrations create a transmembrane potential, which is main-
tained by the Na-K ATPase pump.
Changes in the ICF and ECF osmolality results in the move-
ment of water from the lower to higher osmalarity compartment.
In contrast, capillary endothelium is non-selective and freely
permeable to both water and ions, thus plasma and interstitial
fluid have similar compositions.
The movement of water between the intravascular and intersti-
tial compartments is governed by hydrostatic and osmotic pressures,
the latter termed colloid oncotic pressure because the vascular endo-
thelium is impermeable to large molecules (colloids). Water flux
between these compartments is governed by Starling’s equation:
Fluid flux = (Pc − Pi) − (πc − πi) σ
where Pc is capillary hydrostatic pressure, Pi is interstitial hydrostatic
pressure, πc is capillary oncotic pressure, πi is interstitial oncotic
pressure and σ is the reflectance coefficient - a constant reflecting
membrane permeability. In hypoprotinaemic states (e.g. hypoal-
buminaemia) the capillary oncotic pressure is reduced, leading to
water movement into the interstitium and oedema formation.
Control of body water
In health, total body water is maintained at a fairly constant level.
In adults daily water intake (dietary, 2200 ml; metabolic, 300 ml)
383 © 2008 Elsevier Ltd. All rights reserved.
 Perioperative

is balanced by water lost in urine (1500 ml) and faeces (100 ml),
and insensible losses from skin and lungs (900 ml).
This balance is controlled by the thirst - antidiuretic hormone
(ADH) mechanism, with thirst affecting input and anti-diuretic
hormone (ADH) regulating output.
Thirst is a conscious sensation to drink, originating in the
­hypothalamus, and stimulated by:
• hypertononicity, detected by osmoreceptors in the
­hypothalamus
• hypovolaemia, detected by volume receptors in the right
­atrium and great veins
• hypotension, detected by baroreceptors in the carotid sinus
and aortic arch
• angiotensin II.
ADH (vasopressin) is produced in the hypothalamus and
released into the circulation from the posterior pituitary gland in
response to several stimuli:
• increased plasma tonicity
• hypovolaemia
• hypotension
• angiotensin II
• stress (including the stress response to surgery)
• drugs (such as opiates).
ADH acts on the principal cells of the collecting duct to increase
reabsorption of water via specific ADH-sensitive (aquaporin)
channels.
Electrolyte balance and clinical implications
Sodium
Sodium is the principal intracellular cation, and is the key regula-
tor of water flux. Hyponatraemia (Table 2) in surgical patients is
most commonly caused by inappropriate administration of low
sodium or sodium free solutions, particularly postoperatively,
when increased ADH secretion causes water retention. Acute
hyponatraemia – a medical emergency - is defined as a plasma
sodium concentration <120 mmol l−1 developing over less than
48 hours. Symptoms are those of cerebral oedema; progressing
from nausea and headache to confusion, seizures and finally
brainstem herniation and death. Prompt correction aiming to
increase the plasma sodium concentration by 2 mmol l−1 hr−1
until symptoms resolve can avoid such serious consequences.
Hypernatraemia (Table 3) is less common and is associ-
ated with an increased plasma osmolality and thirst. Symptoms
include nausea, vomiting, confusion, drowsiness, seizures and
coma. Treatment should aim to restore the circulating volume to
normal with isotonic fluids over 48–72 hours.
Potassium
Potassium is predominantly an intracellular cation. Homeostasis
is achieved by matching urinary losses to intake by secretion
of potassium in the distal convoluted tubule. Alterations in the
ECF potassium concentration reflect disturbance of total body
potassium content (intake vs loss) or changes in the ratio of extra­
cellular to intracellular potassium.
Hypokalaemia (Table 4) leads to anorexia, nausea, muscle
weakness, paralytic ileus and cardiac conduction abnormalities.
Treatment requires potassium supplementation and treatment of
the underlying cause.
Hyperkalaemia (Table 5), which may cause life threatening
cardiac arrhythmias, requires immediate treatment. Intravenous
calcium gluconate, glucose and insulin, sodium bicarbonate; rec-
tal calcium resonium or haemodialysis may be used, depending
on the clinical situation and urgency.
Chloride
Chloride, the main anion in ECF, is important in maintaining
normal acid–base status, renal tubular function and formation
of gastric acid. The chloride concentration passively mirrors that
of sodium and is inversely related to plasma bicarbonate. In the
proximal renal tubule, chloride is excreted with ammonium ions
to eliminate hydrogen ions in exchange for sodium and thus acid-
ify urine. Hypochloraemia can occur with loss of gastric, pancre-
atic, bile and intestinal secretions. Excessive infusion of chloride
containing fluids (e.g. saline, gelatins), will lead to hyperchlorae-
mia. This has important implications in acid–base regulation and
Causes of hypernatraemia
Cause Examples

Pure water depletion

Causes of hyponatraemia Extrarenal loss Failure of water intake (postoperative,
coma, elderly)
Hypovolaemia Normovolaemia Hypervolaemia
Mucocutaneous loss
Diarrhoea SIADH Congestive cardiac Fever, hyperventilation, thyrotoxicosis
failure Renal loss Diabetes insipidus (nephrogenic,
Vomiting Hypothyroidism Nephrotic syndrome cranial)
Third-space losses Stress Cirrhosis Chronic renal failure
Diuretic abuse Renal failure Hypotonic fluid loss
Renal tubular Extrarenal loss Gastrointestinal (vomiting, diarrhoea)
Hypoadrenalism Skin (excessive sweating)
Salt-losing Renal loss Osmotic diuresis (glucose, alcohol,
nephropathy mannitol)
Salt gain Iatrogenic (NaHCO3, hypertonic saline)
SIADH, syndrome of inappropriate antidiuretic hormone secretion. Salt ingestion

Table 2 Table 3

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 Perioperative

vasoconstriction secondary to catecholamines. ADH concentra-

Causes of hypokalaemia tions may increase by 50–100 fold, and do not return to normal
for 3–5 days, accounting for postoperative period of oliguria.
Cause Examples The cytokine response is stimulated by local tissue damage
at the site of surgery in proportion to the extent of damage and
Abnormal gastrointestinal loss Vomiting is unaffected by neural blockade. It leads to increased capillary
Diarrhoea membrane permeability and third space fluid losses.
Villous adenoma
Increased renal loss Drugs (diuretics), metabolic
acidosis, magnesium depletion Assessment of hydration
ECF–ICF shift Drugs (insulin, b-agonists), Accurate clinical assessment of intravascular volume is often
metabolic alkalosis difficult and laboratory investigations are invariably required to
guide perioperative fluid therapy. Thirst, skin turgor, hydration
ECT, extracellular fluid; ICF, intracellular fluid.
of mucous membranes, core-periphery temperature gradient, res-
piratory rate, pulse rate and volume, orthostatic hypotension and
Table 4
urine output are valuable signs of hydration. Unfortunately there
are many confounding factors that may influence these, such as
will lead to a hyperchloraemic metabolic acidosis. Infusion of a drugs, surgical stress, age and underlying disease. Laboratory
large volume of normal saline can precipitate a metabolic acido- signs of dehydration include:
sis because renal sodium excretion occurs in preference chloride • hypernatraemia
and hydrogen ion excretion (Table 6). • rising haematocrit
• progressive metabolic acidosis
• rising lactate
Anaesthesia, surgery and fluid balance
• increased serum urea to creatinine ratio
The impact of the physiological response to surgical stress, along • urinary sodium <20 mmol/litre
with the various fluid shifts that may occur mean that accurate • Urine osmolality approaching 1200 mosmol/kg.
assessment of hydration is paramount. Many patients are dehy- In more complex cases central venous pressure (CVP) may
drated before surgery due to prolonged fasting, bowel prepara- be required. Observation of the haemodynamic and clinical
tion or diuretics. Perioperative losses are often underestimated, response to the rapid intravenous infusion of a small volume
with fluid loss from drains and sequestration of fluid in tissues of fluid (e.g. 250–500 ml over 20–30 minutes) permit assess-
and the gastrointestinal tract (third space losses) persisting into ment of the compliance of the circulation and intravascular vol-
the postoperative period. ume status. Such fluid challenges may be repeated successively
The stress response to surgery has two main components - if there is no, or a transient change in CVP. A sustained rise
neuroendocrine and cytokine. The neuroendocrine response is in CVP of 3 cmH2O is considered evidence of adequate fluid
stimulated initially by afferent nociceptive stimuli reaching the administration.
central nervous system and may be blunted by regional anaes-
thesia and opioids. It is characterized by an increase in ADH,
A practical approach to clinical fluid prescribing
adrenocorticotropic hormone (ACTH), growth hormone (GH),
cortisol and aldosterone secretion, and activation of the sympa- Intravenous fluid administration has two goals: meeting daily
thetic nervous system and renin-angiotensin system. This results maintenance requirements, and correct existing and ongoing
in sodium and water retention, the magnitude of which is modu- water and electrolyte losses. In the adult, the daily maintenance
lated by factors such as the effects of anaesthetic agents on renal requirements (water 35 ml kg−1, sodium 2 mmol kg−1, potas-
blood flow and glomerular filtration rate, hypotension, and renal sium 1 mmol kg−1) can be provided by 1000 ml normal saline
and 1500 ml 5% glucose with the addition of potassium 20 mmol
l−1 to each litre of fluid. Correction of ongoing extracellular fluid
losses, which have a composition similar to that of plasma, is
Causes of hyperkalaemia best achieved with lactated Ringer’s (Hartmann’s) solution. It is
important that the volume of intravenous drugs and nutrition is
Cause Examples
taken into account.
Decreased renal Renal failure, drugs (b-blockers, ACE inhibitors)
clearance Metabolic acidosis Osmolarity, osmolality and tonicity
Adrenocortical failure
ICF–ECF shift Tissue damage (burns, crush injury, haemolysis
The terms osmolarity, osmolality and tonicity are often and
Metabolic acidosis
incorrectly used interchangeably. Osmolarity (expressed in mil-
liosmoles per litre of solution) and osmolality (expressed in mil-
ACE, angiotensin converting enzyme; ECT, extracellular fluid; ICF, liosmoles per kilogram of solvent) describes the number of all the
­intracellular fluid. solutes that contribute to a solution’s osmotic pressure. Plasma
osmolarity, which is normally 280–300 mOsm l−1, can be esti-
Table 5 mated using the formula:

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 Perioperative

Electrolyte composition, pH and osmolality of body compartments, secretions and commonly used intravenous fluids

Fluid Na+ K+ Ca2+ Mg2+ Cl– HCO3−1 pH Osmolality Plasma volume

T½ (min)

Body compartment
Plasma 142 4 2.5 1 100 25 7.4 280
Interstitial fluid 145 4 2.4 0.9 118 27 7.4 280
Intracellular fluid 12 155 0 15 8 10 7.2 280
Secretions
Saliva 50–70 15–20 – – 10–15 30–50 6–7
Gastric juice 150 5–10 – – 100–160 10–20 1–3.5
Bile 180–220 6–8 – – 60–70 60–70 7–8
Pancreatic juice 160 4 – – 30–60 80–120 8–8.3
Small bowel 140 4 – – 100 25 7.8–8
Crystalloids
Normal saline (0.9% NaCl) 154 – – – 154 – 5 300 80
Hartmann`s solution 131 5 2 – 111 6.5 275 68
Dextrose 4% saline 0.19% 31 – – – 31 – 4.5 286
Dextrose 5% – – – – – – 4.2 278 19
Bicarbonate 8.4% 1000 – – – – 1000 8 2000 –
Colloids
Gelofusine 154 0.4 0.4 0.4 120–125 – 7.4 274 180
Hydroxyethyl starch (450/0.7) 154 – – – 154 – 5.5 300–310 75
Hydroxyethyl starch (130/0.4) 154 – – – 154 – 5.0 308 700
Dextran 40 154 – – – 154 – 3.5–7.0 280–324 180
Dextran 70 154 – – – 154 – 5.0 280–324 1500
HAS 4.5% 100–160 <2.25 – – 100–160 – 5.5 200–310 1000

HAS, human albumin solution; HCO3–, bicarbonate. Reproduced from Mackenzie I. Fluid and electrolyte balance. Surgery 2005; 23: 453–60.

Table 6

Osmolarity = (1.86×[Na+])+[glucose]+[urea]+9 mOsm l−1
Fluids such as normal saline and 5% glucose (300 mOsm l−1) are
iso osmolar, whereas 10% glucose and 1.8% saline (600 mOsm l−1)
are hyperosmolar. In contrast, tonicity describes only the number
of solutes that cannot cross cell membranes. Thus normal saline is
described as being isotonic whereas 4% glucose in 0.18% saline
(300 mOsm l−1) is hypotonic because membranes are permeable
to glucose.
Intravenous fluids
In most territories fluids for intravenous infusion are classed as
‘prescription only medicines’ and should, therefore, be regarded
as ‘drugs’ – each having pharmacokinetic and pharmacodynamic
properties, interactions and side-effect profiles. For this reasons
fluids must be prescribed with the same care and attention as
any other drug.1,2
Crystalloids
Crystalloids are simple electrolyte solutions, whose distributon
within the body is governed by their osmolarity and tonicity. Flu-
ids such as saline and Hartmann’s solution, which have a sodium
concentration similar to that of ECF, remain within the ECF. If
used to replace blood loss, 3 to 4 times the volume lost must be
administered as only 25–30% will remain in the intravascular
compartment.
Following the administration of hypotonic solutions, such as
5% glucose, the membrane permeable solute (i.e. glucose) is
readily taken up by cells. The net effect is that of administering
pure water, which distributed throughout each compartment in
proportion to its contribution to total body water.
Synthetic colloids
Derived from the Greek word for glue, the term colloid refers to
the dispersion – as apposed to solution - of one substance within
another. Macromolecules suspended in water are known as
hydrocolloids. Synthetic colloids for clinical use are iso osmolar
crystalloid or glucose solutions containing a suspension of semi-
synthetic polypeptides or polysaccharides with molecular weight
>30,000 kDa, which exert an osmotic force across capillary walls.
Because they tend to remain in the circulation for longer than crys-
talloid solutions, blood replacement can be achieved with smaller
volumes of colloid and without the infection transmission risk
of blood products. Colloids are more costly than crystalloids and
have a small but significant risk of adverse allergic reactions.
Gelatins
Modified gelatins (e.g. Gelofusine, Haemaccel, Volplex), which
are derived from animal skin and bone, are the most commonly

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 Perioperative
used colloids in the UK. Gelatin molecules have a wide range of
sizes and each solution is described as the weight-average molec-
ular weight (Mw) - typically 30 kDa. Most of the administered
dose is excreted unchanged in the urine, 10% excreted in faeces
and 3% metabolised. There is no long-term retention.
Starches
Starches are produced from amylopectin, which has been stabi-
lised by hydroxylation to prevent rapid hydrolysis by amylase.
Solutions are fractionated to yield the desired ranges of molec-
ular weights (e.g. hydroxyethyl starch Mw 200 kDa). Starches
are thought to reduce capillary leak by ‘plugging’ holes in the
endothelial basement membrane, but their use in sepsis has been
shown to be an independent risk factor for renal failure. Starches
have a longer plasma half-life than gelatins and this has lead to
their popularity. However, there is no evidence base to suggest
any outcome benefit over gelatins.
Dextrans
Dextrans are highly branched polysaccharide molecules synthe-
sized from sucrose by the bacterium Leuconostoc mesenteroides.
The formulations currently available are Dextran 40 (Mw 40 kDa)
and Dextran 70 (Mw 70 kDa). The rate and extent of renal elimi-
nation is a function of molecular weight, with half of Dextran
40 being excreted within a few hours of administration, whilst
Dextran 70 has a duration of action of 6–8 hours. Dextrans are
used to improve microcirculatory flow by reducing erythrocyte
aggregation and leucocyte plugging, but interfere with platelet
aggregation, by reducing concentrations of von Willebrand fac-
tor and enhance fibrinolysis. Dextrans cause severe anaphylactic
reactions more frequently than gelatins or starches.
Natural colloids
Human albumin solution (HAS): albumin makes up 60% of
plasma protein and contributes to 80% of plasma colloid osmotic
pressure. It has additional functions as a carrier in the blood.
Human albumin solution (HAS, 66 kDa) is harvested and pooled
from blood donors for use either as a dilute (4.5–5%) or con-
centrated, or salt-poor (20–25%) solution. HAS has an excellent
safety record and pasteurisation has been shown to be highly
effective at inactivating viruses such as hepatitis A, B and C and
human immunodeficiency virus (HIV). Concerns about varient
Creutzfeld-Jacob disease (vCJD) transmission has led to HAS
used in the UK being sourced from USA.
A meta-analysis, published in 2004 by the Cochrane Review
Group, controversially claimed that, when used for resuscitation
and volume expansion in critically ill patients, HAS was associ-
ated with an excess mortality of 6%. The reputation of HAS was
partially restored following subsequent publication of the saline
versus albumin fluid evaluation (SAFE) study, which showed
clinically equivalent outcomes in intensive care patients.
Despite the high cost of HAS, it still has a role in the restoration
of plasma volume following the acute phase of critically illness in
situations of sodium and water overload. Concentrated solutions
may promote diuresis in cirrhotic, hypoalbuminaemic patients.
Controversy still exists as to which is the most appropriate
fluid for use in the perioperative period. Systematic reviews
show no significant differences in pulmonary oedema, mortality
or length of stay between colloid or crystalloid resuscitation.
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Blood transfusion
An awareness of the potentially devastating effects of disease
transmission resulting from blood product use has brought about
significant changes in transfusion medicine in the last 20 years.
The development of clotting factor concentrates pooled from up
to 30,000 donors initially liberated haemophiliacs from frequent
periods of hospitalisation. Sadly, this led to widespread exposure
of patients to hepatitis B (HVB) and C (HVC), and subsequently
HIV. By the time viral inactivation processes were introduced in
1985 it was estimated that in the UK 4,800 haemophiliacs had
been infected with HVC and of these 1,200 with HIV.
Four cases of vCJD have been reported in the UK following
blood transfusion; the first case being identified in December
2003. In all cases the donor developed symptoms of the disease
18 months or later after donating blood. As a response to this
rare but devastating risk, blood in the UK is now supplied ‘leu-
cocyte deplete’ to minimise prion transmission. The risk of cyto-
megalovirus (CMV) transmission is similarly minimised by this
precaution. Leucocyte depleted blood contains <5 × 106 leuco-
cytes per unit of red cells.
Every unit of blood donated in the UK is tested for hepatitis
B surface antigen, hepatitis C antibody and RNA, HIV antibody,
HTLV antibody, and syphilis antibody.
Perioperative anaemia and transfusion triggers
For many years it was thought that patients should be trans-
fused to achieve a haemoglobin concentration of 10 g dl−1 and a
haematocrit of 30%. The publication in 1999 of the Transfusion
Requirements in Critical Care (TRICC) study showed that a hae-
moglobin target of 7–9 g dl−1 in critically ill patients was associ-
ated with no worse 30 day mortality and morbidity than a more
liberal target of 10–12 g dl−1. Subgroup analysis of patients with
known coronary artery disease echoed this finding of reduced
complications and indeed the liberal transfusion strategy group
had a higher incidence of pulmonary oedema. Only those with
severe ischaemic heart disease showed a non-statistically signifi-
cant difference in absolute survival rates.
The indications for blood transfusion detailed in the 2002
Department of Health (UK) circular (HSC2002/09) are sum-
marised in Table 7. The decision to transfuse should be made
by senior clinicians aware of the risks and benefits. The justifica-
tion for transfusion must be discussed with the patient whenever
possible and documented. HSC2002/09 sets out a target haemo-
globin concentration of 7 g dl−1 for patients undergoing surgery.
This may be most appropriately achieved without transfusion
with dietary supplementation such as vitamin B12, folate and
iron. It should be noted that such therapies only reduce the rate
of transfusion where haematinic deficiency is the cause of the
anaemia. There is no standard transfusion trigger that will pro-
vide an optimal risk-benefit profile in all preoperative patients
and the justification for transfusion must take into account the
urgency of surgery, cause anaemia and medical condition of the
patient.
Donor red blood cells
Donor blood is immediately cooled to and stored at 4°C which
produces erythrocyte changes or ‘storage lesions’. These include
an increase in extracellular potassium concentration (20 mmol l−1
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 Perioperative

Indications for blood transfusion

Indication Details

Acute blood loss Blood volume loss (%) Fluid Role of blood transfusion
15–30 Crystalloid/colloid Unlikely
30–40 Crystalloid/colloid Probable
> 40 Crystalloid/colloid Required
The aim is to maintain circulating blood volume and Hb concentration above 7 g/dl in fit patients,
and above 9 g/dl in elderly patients and those with cardiovascular disease
Perioperative transfusion Most patients should not require transfusion. Use Hb to guide blood transfusion
Healthy patient: aim for Hb 7 g/dl
Cardiovascular disease or significant risk factors (elderly, hypertension, diabetes mellitus, peripheral
vascular disease): aim for Hb 9 g/dl
Critical care Transfuse to Hb > 7 g/dl
Post-chemotherapy No evidence base to guide transfusion trigger
Radiotherapy Transfuse to maintain Hb above 10 g/dl
Chronic anaemia Transfuse to lowest Hb concentration to alleviate symptoms
Other Transfusion may also be indicated in the management of inherited and acquired red blood cell
disorders and in cases of marrow failure. Seek specialist haematological advice

Hb, haemoblobin concentration.

Table 7

after 3 weeks of storage) and decreased triphosphate and 2,3
diphosphoglycerate levels, the latter hindering oxygen binding.
After 3 weeks stored blood has a pH of 6.9 and bicarbonate con-
centration of 10 mmol l−1. Erythrocyte membranes become rigid
and fragile resulting in enhanced haemolysis. Clotting factor activ-
ity in whole blood decreases rapidly and is significantly reduced
after 7 days of storage. For this reason plasma is separated from
erythrocytes and administered separately as fresh frozen plasma
(FFP). Erythrocyte have a shelf life of 35 days and are usually
supplied as concentrated cells with a haematocrit of 55–75%.
In the UK erythrocytes are usually suspended in saline, adenine,
glucose and mannitol (SAG-M); the plasma having been removed
and used for other blood components. The use of SAG-Mannitol
makes the resulting suspension less viscous. Red cell blood is leu-
codepleted to minimise transmission of infections (CMV, vCJD).
Gamma irradiation is performed to reduce lymphocyte transmis-
sion and is required solely for immunological reasons in patients
with inherited or acquired immunodeficiency states.
Complications of blood transfusion
Despite major advances in blood transfusion safety, hazards
associated with blood transfusion do exist, and prompt recogni-
tion and treatment is essential (Table 8).
Transfusion-related acute lung injury (TRALI)
TRALI remains a rare complication of the transfusion of any blood
component that is believed to be significantly under reported.
The clinical picture is one of a severe acute pulmonary reaction
clinically indistinguishable from acute respiratory distress syn-
drome (ARDS). However, improvement usually occurs within
48–96 hours provided timely supportive treatment is initiated.
The mortality rate is 5% in contrast to 30–60% seen in ARDS.
In cumulative analyses of Serious Hazards of Transfusion
(SHOT) data (see below) TRALI remains a leading cause of
transfusion-related mortality and morbidity, second only to ABO
incompatibility. It is difficult to accurately quote an incidence.
One US hospital with a particular interest in TRALI quotes 0.02%
(1 in 5000 units of blood), whereas the 2006 UK SHOT report
quotes an incidence of 0.004% (1 in 200,000 units).
TRALI occurs 5–6 times more frequently following the admin-
istration of platelets and FFP than erythrocytes and in 90% of
cases donor leucocyte antibodies, reacting with patient leuco-
cytes can be detected. The resultant complement-mediated leu-
cocyte activation leads to pulmonary endothelial damage. Blood
donors subsequently shown to have human leucocyte antigen
(HLA) or granulocyte-specific antibodies should not be used
again as donors. Multiparous women are more likely to fall into
this group. All FFP (a pooled product) in the UK now comes from
male donors.
Massive blood transfusion
Massive blood transfusion is defined as the complete replace-
ment of the entire blood volume within a 24-hour period. This is
associated with additional risks to those related to smaller trans-
fusions, which result from metabolic alterations in the blood as
a result of cooling and storage. The adverse consequences are
shown in Table 9.
Serious Hazards of Transfusion
The Serious Hazards of Transfusion (SHOT) scheme is a UK
based organisation established in 1996 with the aim of collect-
ing and investigating reports of major adverse events following
blood transfusion and focuses on particular predefined catego-
ries. Although reporting remains voluntary, all UK hospitals are
actively encouraged to report and engage in ‘haemovigilance’.

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 Perioperative

Complications of blood transfusion

Complication Details

Febrile non-haemolytic
transfusion reactions
Acute haemolytic
transfusion reactions
Delayed haemolytic
transfusion reactions
Urticarial and
anaphylactic reactions
Bacterial contamination
Post-transfusion purpura
Immunomodulation
Transfusion-associated
graft vs host disease
Transfusion-transmitted
infections
Transfusion-related
acute lung injury
Common, especially in parous women and after previous transfusions
Mediated by donor leucocytes
Benign but must be differentiated from life-threatening haemolytic reactions
Flushing, fever, tachycardia, rigors
Treat by slowing transfusion rate and with paracetamol
Abandon transfusion if >1.5°C temperature rise and consult laboratory
Intravascular haemolysis owing to ABO compatibility, resulting from ‘wrong’ blood to ‘wrong’ patient
Small (20 ml) inoculation causes symptoms of fever, substernal/loin pain, hypotension, dyspnoea, flushing,
haemoglobinuria, DIC
STOP TRANSFUSION
Maintain renal perfusion with fluids (35% risk of renal failure), oxygen therapy
Supportive treatment. Transfer to HDU/ITU and seek specialist help
Haemolysis generally extravascular owing to Kidd and Duffy incompatibility
Fever, jaundice, haemoglobinuria presenting 5–10 days after transfusion
Less commonly hypotension and renal failure
Rarely fatal
Reactions may be anaphylactic or anaphylactoid and should be managed according to standard allergic reaction
protocols. Investigation of the cause will guide subsequent management
Endogenous contamination due to a bacteraemia donor may lead to infections such as Treponema pallidum
(syphilis)
Exogenous contamination of blood pack during processing risks transfusion of Pseudomonas and Staphylococcus
This rare cause of immune destruction of both transfused and host platelets occurs 7–10 days after transfusion. It
is usually self-limiting but plasma exchange ± immunoglobulin may be needed
Transfusion results in both temporary and long-term stimulatory and suppressive changes in immune function in
the recipient
Recurrent spontaneous abortions rates are increased in females
Colorectal tumour recurrence may be increased by as much as 37%. This may occur, but is less well defined in
other tumours
Although rare, this is almost always fatal as there is no effective treatment
Immunodeficient patients develop a rash, diarrhoea, liver failure, leading to marrow failure and pancytopenia
Death occurs within 3–4 weeks following infection
γ-irradiation of blood reduces the risk
Infectious agents of several types reported to have been transmitted
Viral: HIV, hepatitis A, B, C and D, CMV, HTLV I and II, EBV
Bacterial: syphilis, Lyme disease, brucellosis, salmonella
Protozoan: malaria, toxoplasmosis
See text

CMV, cytomegalovirus, DIC, disseminated intravascular coagulation; EBV, Epstein–Barr virus; HDU, high-dependency unit; HTLV, human T-lymphotropic virus.

Table 8

Reports are published annually detailing causes of mortality
and morbidity and the data are used to make evidence-based
and targeted recommendations or improvements in transfusion
practice.
The 2006 SHOT report: In the financial year April 2005-6 2.5 mil-
lion units of blood were issued from transfusion services in the UK.
There was a 13% reduction in the number of reports in existing
SHOT categories compared with 2005. ABO incompatible transfu-
sions were lower than ever recorded; 8 cases with no fatalities.
Prescription errors by doctors were prominent with 125
reported incidences; 2 resulting in death. As a consequence it
has been recommended that transfusion medicine becomes part
of core UK medical school curriculum.
Two other deaths occurred - one following administration
of platelets infected with Klebsiella pneumoniae and one from
TRALI. 400 events of incorrect blood component transfusion
were reported. This represents an incidence of 10.6 reports per
100,000 components transfused, verses a rate of 12.8 in 2005
report.

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 Perioperative

and shivering may occur in up to 12% cases as a consequence of

Complications of massive blood transfusion inefficient blood washing.
Cell salvage is contraindicated in the presence of sepsis and
Complication Details from contaminated surgical fields (e.g. bowel surgery). Its suit-
ability for use in malignant disease remains unclear because of
Hyperkalaemia Arrhythmias concerns that transfused malignant cells may disseminate the
Hypocalcaemia due Abnormal liver function/perfusion slows malignancy. The consequence of transfusing amniotic fluid and
to citrate toxicity citrate metabolism foetal cells to obstetric patients is similarly undefined.
Monitor ionized calcium on blood gas
analyser Preoperative autologous donation
Treat with 10 ml of 10% calcium chloride Preoperative autologous donation (PAD) is a less common prac-
(not gluconate which requires hepatic tice in the UK. Patients donate blood for blood bank storage and
metabolism for calcium liberation) for their exclusive use in advance of planned surgery. Donations
Hypothermia Warm blood, especially in massive are usually given over a 5 week period with 400–500 ml being
transfusions harvested on each occasion. Blood can only be stored for 5 weeks
Impaired oxygen Right shift of the oxygen dissociation
and the last donation must be no less than 72 hours - preferably
delivery curve is effected by acidosis and
no less than 7 days - before surgery.
hypothermia
It has been shown that oral iron supplements will increase
Acidosis Control with bicarbonate only in extreme
the blood yield even in non-iron deficient patients and is recom-
cases
mended. While erythropoetin is licensed for use in this indication
Coagulopathy PT and APTT should be maintained at
its use is limited by high cost and the increased thrombotic risk.
< 1.5 × control
PAD has been shown to reduce the number of allogeneic units
Consider FFP after 1 × blood volume
used, but is associated with an increased likelihood of transfu-
replacement
sion, which exposes patients to risks such as administrative
Maintain fibrinogen at >1.0 g/litre
errors, fluid overload and sepsis. Difficulty in predicting blood
Thrombocytopenia Maintain at >75 × 109/litre
requirements leads to high blood wastage rates.
Anticipate transfusion after two blood
volume replacements.
Acute normovolaemic haemodilution
Clerical error Emergency situation increases risk of
Venous blood is drained into bags containing citrate immediately
wrong blood to wrong patient
prior to surgery and replaced with crystalloid or colloid infusion.
Transfusion-related Rare. See text
Consequently, blood shed during surgery will have a lower hae-
acute lung injury
matocrit. The harvested blood is returned to the patient towards
APTT, activated partial thromboplastin time; FFP, fresh frozen plasma; PT,
the end of the operative procedure. The units are not subject to
prothrombin time. microbiological tests and should be treated and labelled as being
‘high risk’; they must not to be stored in blood bank refrigerators
Table 9 for risk of them entering the hospital blood pool. Unused blood
is discarded at the end of the procedure.

Autologous blood transfusion Blood transfusion and the Jehovah’s Witness

Concerns over transmission of infection following allogeneic
blood transfusion have led to interest in this area. It is also a
useful practice for managing patients with rare blood groups and
demand on allogeneic transfusion services can be reduced. This
approach is not without risk and administration of a safe and
efficient service is costly. Its use should be restricted to situations
of anticipated blood loss of >20% blood volume. Unused blood
is not suitable for return to the national donor pool and there-
fore must be discarded. Three methods are currently available
for autologous transfusion.
Cell salvage
Cell salvage is the most commonly used method in the UK. Shed
blood is collected during and after surgery, ‘washed’ with saline
and separated from debris by centrifugation to form a concen-
trated transfusable product.
Cell salvage has an excellent safety record and blood loss is
virtually matched with supply. Complications can arise from
electrolyte disturbances and dilutional coagulopathy. Pyrexia
Every competent adult is entitled to refuse medical treatment.
Allogeneic blood transfusions (whole blood, packed red cells,
FFP and platelets) and preoperative autologous blood collec-
tion are regarded as unacceptable to Jehovah’s Witnesses. Each
patient may make a personal choice regarding blood salvage,
plasma fractions (albumin, immunoglobulins, clotting factors)
and organ transplantation.
The key to successful management of this group is good com-
munication between senior staff involved in the care, the patient
and their community elders, who can be invaluable in provid-
ing guidance. Discussions should be fully documented and the
patient’s views must be explicitly recorded and witnessed. Flout-
ing documented wishes may place a clinician at risk of disci-
plinary action and may be considered a criminal offence. Many
Witnesses carry advanced directives, or lodge them with their
general pratctioner, which may help guide emergency treatment.
The situation for the children of Jehovah’s Witnesses is com-
plex and there are minor variations in the procedure required
between England and Wales and both Scotland and Northern

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 Perioperative

I­reland. In most cases application for a court order will be made.
It is worth noting that in each of these countries, a child over 16
may override the wishes of their parents with regard to their own
treatment. In the emergency situation, where it can be convinc-
ingly shown that a child will die without immediate blood admin-
istration, the courts are likely to uphold the decision of a doctor
in doing so. The situation in other countries will vary and each
clinician should be aware of local and national guidance. ◆
References
1 Choi P, Yip G, Quinonez L, Cook D. Crystalloids versus colloids in
fluid resuscitation: a systematic review. Crit Care Med 1999; 27:
200–10.
2 Schierhout G, Roberts I. Fluid resuscitation with colloid or crystalloid
solutions in critically ill patients: a systematic review of randomised
trials. BMJ 1998; 316: 961–4.
Further reading
Guyton AC, Hall JE. Textbook of medical physiology, 11th edn.
Saunders, Elsevier Health Sciences, 2005.
Murphy M, Pamphilon, eds. Practical transfusion medicine. London:
Blackwell Science, 2001.
Serious Hazards of Transfusion (SHOT). Also available from:
http://www.shotuk.org June 2008.
The Albumin Reviewers (Alderson P, Bunn F, Li Wan Po A, Li L, Roberts
I, Schierhout G). Human albumin solution for resuscitation and
volume expansion in critically ill patients. Cochrane Database Syst
Rev 2004, Issue 3. Art. No.: CD001208. DOI: 10.1002/14651858.
CD001208.pub2.
The SAFE Study Investigators. A comparison of albumin and saline for
fluid resuscitation in the intensive care unit. N Engl J Med 2004;
350: 2247–56.
William F, Ganong MD. Review of medical physiology, : McGraw-Hill,
2005.

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