Parenteral
fluid therapy
The rational administration of parenteral fluids is one of the most
significant advances in the care of acutely ill patients in the twentieth
century. However, despite advances
in the monitoring of cardiovascular variables, the questions of what?
when? and how much? remain areas of enormous controversy.
In
the 1930s Blalock suggested that it was the loss of blood rather than the ‘release
of evil humors’ that led to death after major trauma and recommended
treatment by the administration of intravenous fluids. It was not until the
1940s and World War II that blood and plasma were widely used for the treatment
of blood loss. Ironically, the same period highlighted the problems of inducing
anaesthesia in vasoconstricted hypovolaemic casualties. When thiopentone was
used as a sole intravenous anaesthetic agent at Pearl Harbour on 9 December 1941
there were numerous deaths as a result of vasodilatation and cardiovascular
collapse. In the 1940s and 1950s descriptions of postoperative retention of salt
and water as part of the metabolic response to surgery led to a
widespread reluctance amongst surgeons and anaesthetists to administer
crystalloids to their patients. The 1960s brought a swing back the other way
when Shires and others demonstrated an increased survival in experimental
animals that were bled and then reinfused blood plus additional crystalloid.
The ensuing enthusiasm for the infusion of crystalloids led to the publication
of Moore and Shires’ now famous article calling for ‘moderation’.
Colloids
or crystalloids?
The colloid—crystalloid argument rages to this day: if one was clearly
better than the other there would not be a controversy. The common link in the
majority of articles on this subject is the final conclusion that it is dose not
choice of fluid that is the real issue — and ‘the proper dose of any drug
is enough’ (Dr J.H. Drysedale). Certainly if the aim is to restore the
circulating blood volume this will be achieved with a smaller volume and thus
more rapidly by using a colloid.
Diagnosing
hypovolaemia
Hypovolaemia can occur as a consequence of a wide variety of
pathological processes. The nature of the fluid lost should dictate the choice
of replacement fluid. Clinical history, whether first or second hand, in
combination with appropriate laboratory investigations, should be the most
useful guides to a rational fluid regimen. However, hypovolaemia from whatever
cause is an acute medical emergency. Any degree of hypovolaemia jeopardises
oxygen transport and increases the risk of tissue hypoxia and the development of
organ failure. The greater the degree and duration of hypovolaemia the greater the risk. Therefore, the initial treatment is to
restore the circulating volume as quickly and effectively as possible.
Hypovolaemia
may be divided into three categories: covert compensated hypovolaemia, overt
compensated hypovolaemia and decompensated hypovolaemia.
This is the commonest yet least often diagnosed form of hypovolaemia.
It refers to the presence of a reduced circulating blood volume without very
obvious associated physical signs. Price found that healthy volunteers could
have 10—15 per cent of their blood volume removed with no significant change
in heart rate, blood pressure, cardiac output or blood flow to the
splanchnic bed (gut, etc.). However, splanchnic blood volume was reduced
by 40 per cent. The subjects in his study had essentially autotransfused and
were maintaining the systemic circulating volume at the expense of the
splanchnic circulating volume. This same process happens when we donate a unit
of blood with no obvious adverse effects. Over the course of the next few hours
we feel thirsty and therefore drink more, we also ingest salt and at the same
time reduce urine output of salt and water. We make new proteins and blood
cells, and very soon everything has returned to normal with no sequelae. In sick
patients, however, many of the natural compensating mechanisms malfunction
and this, coupled with the fact that fluid intake is being determined by a
second party, namely the physician, makes hypovolaemia common.
Covert
compensated hypovolaemia is extremely difficult to diagnose. In the conscious
patient central nervous system (CNS) symptoms are the best guide. In the
experiments performed above, all of the subjects developed CNS symptoms
ranging from drowsiness and nausea to hiccoughs. Any thirsty patient should be
assumed to be hypovolaemic until proven otherwise. Urinalysis showing an
increased urinary osmolality and decreased sodium concentration is the most
useful laboratory investigation.
Although
covert compensated hypovolaemia is common and probably contributes significantly
to morbidity, the majority of patients withstands the insult. If the
hypovolaemia persists consequent end organ hypoperfusion may be present for many
days before it manifests itself as organ dysfunction. By this time the patient
is usually in a state of overt compensated hypovolaemia.
Overt
compensated hypovolaemia
Here there is hypovolaemia to an extent that the reflex mechanisms
required to maintain perfusion to vital organs are obvious on clinical
examination but the blood pressure is maintained. As before, clinical history is
essential. On examination the patient will demonstrate the manifestations of
an increased sympathetic drive with tachycardia, a wide arterial pulse pressure,
and typically increased systolic blood pressure and cool clammy skin,
particularly at the hands and feet.
There may be other evidence of an inadequate cardiac output such as
drowsiness, confusion and an increased respiratory rate. If the diagnosis is
uncertain additional dynamic bedside tests can be performed such as gentle
head-down bed tilting, leg raising or the administration of a bolus of
intravenous fluid. If the diagnosis of hypovolaemia is correct then the increase
in venous return may result in a reduction in heart rate, narrowing of pulse
pressure, reduction in respiratory rate and overall improvement in well-being.
If the diagnosis remains uncertain, or coincidental medical problems such as
heart or lung disease make performing or interpreting such tests difficult, then
more complex investigations may be required.
With
the exception of electrolyte and blood gas analysis the majority of laboratory
investigations is of little use in the acute phase. Arterial blood gas analysis
can be performed rapidly; hypovolaemic patients are commonly hypoxaemic and may
have a metabolic acidosis as a consequence of an inadequate cardiac output.
Urinalysis, as described above, may support the diagnosis of hypovolaemia but no
single test is diagnostic. Rapid determinations of total blood volume are not
yet available.
Except
for extreme cases the clinical interpretation of CVP by examination of the
jugular venous waveform is unreliable and has no place in the management of
hypovolaemic patients. If there is any doubt about the diagnosis, particularly
in patients with cardiorespiratory disease, the patient needs a CVP catheter.
The insertion and, indeed, interpretation of the information available from
central venous catheters carries a significant morbidity and mortality so they
should only be inserted and managed by experienced clinicians. For a more
detailed account of central venous catheterisation readers are referred to
Rosen et al. As a general rule the right internal jugular approach is
favoured. The subclavian vein may be particularly difficult to locate in the
hypovolaemic patient and the risk of arterial cannulation, haemorrhage and
pneumothorax is then greatly increased. If during insertion steep head down tilt
produces no adverse effects and it is difficult to visualise or palpate neck
veins, the judicious administration of at least 500 ml of colloid by a
peripheral route before proceeding is sensible and safe. In the unlikely event
that fluid administration produces a deleterious effect the infusion can be
stopped easily, the head-down tilt corrected and the patient sat up.
In
cases of ventricular dysfunction and/or severe pulmonary disease there will be
a misleading discrepancy between right and left atrial filling pressures. If the
information obtained from the CVP catheter is confusing, it may be necessary to
insert a pulmonary artery flotation (Swan-Ganz) catheter. The pulmonary artery
occlusion pressure (PAOP) provides an index of left ventricular filling pressure
and may help to clarify the situation. It is important to realise that right
atrial pressure and PAOP are influenced not only by the circulating volume but
also by the degree to which the circulation is constricted, the compliance of
the right and left heart, as well as pain, agitation, etc., causing increases in
sympathetic tone. Low values are sensitive indicators of hypovolaemia, but high
values do not necessarily mean the patient is well filled. Dynamic tests
using fluid challenges give much more information and should always be
tried in patients with evidence of an inadequate circulation. The administration
of 200—5 00 ml of colloid over 5—10 minutes and comparison of the CVP or
stroke volume (not the cardiac output) before the challenge and 5—10 minutes
after the infusion has finished is the most useful guide. A sustained rise in
CVP or PAOP of 3 mmHg and failure of the stroke volume to increase suggest the
circulation is well filled.
Decompensated
hypovolaemia
This is what many people refer to as shock. The degree of hypovolaemia
is such that reflex redistribution of blood flow is insufficient to compensate
and vital organs are no longer adequately perfused. The mean arterial
blood pressure falls and may be difficult to record as peripheral pulses are
often impalpable. The blood supply to the heart and lungs is compromised, which
further reduces cardiac output, causes ventilation/perfusion (V/Q) mismatching
and compounds the problem. Tachycardia changes to bradycardia as myocardial
oxygenation becomes critical and the conscious level is severely obtunded. If
untreated this clinical state rapidly progresses to total circulatory arrest. No
special equipment or investigations are needed to make the diagnosis of
decompensated
hypovolaemia and to start aggressive volume replacement therapy. Misdiagnosis
and inappropriate over transfusion is an overrated problem. Delay in the
treatment of hypovolaemic shock greatly reduces the chances of successful
resuscitation. Most causes of hypovolaemic shock carry a far better prognosis
than any condition that presents in a similar fashion but would be made worse by
a fluid challenge.
The
consequences of hypovolaemia
Decompensated hypovolaemia will result in endorgan damage and death if
it is not treated rapidly and completely. Probably a far more common and
insidious source of morbidity and mortality is the compensated hypovolaemias. As
described above, a small reduction in circulating blood volume rapidly results
in a far more significant reduction in splanchnic blood volume and in particular
the supply to the innermost layer of the gut lumen, the mucosa. It is becoming
increasingly clear that hypoperfusion of the gut mucosa is of fundamental
importance in the pathogenesis of multiple organ dysfunction (see below).
Therefore,
hypovolaemia is a potential killer in any disease process. The manifestations of
persistent covert compensated hypovolaemia may not be seen for many days. Once a
patient has overt hypovolaemia the chances of successful treatment are already
significantly reduced with the exception of simple acute haemorrhage. Most
patients are referred to intensive care units once they have progressed to
decompensated shock with established organ failure. By that stage it is probably
too late to make a significant difference to outcome. The early recognition and
treatment of hypovolaemia is essential in any disease process.
Treatment
of hypovolaemia
Very few patients benefit from fluid restriction; if there is evidence
of hypovolaemia it should be treated. Ionotropes should be used only when the
circulating volume has been corrected.
Occult
hypovolaemia is very difficult to diagnose. Therefore, in conscious patients
who can drink the most rational approach is to be generous with fluids. Access
is important, as is strength and volition. The patient with a full water jug and
a raging thirst is commonplace. The aim should be an asymptomatic patient (i.e.
no thirst) with good urine volumes (in excess of 0.5 mI/kg/hour) and normal
urinalysis. The overriding principle is that fluid overload is easy to treat,
whereas fully established organ failure is incurable.
Overt
hypovolaemia should be considered a medical emergency and treatment is
required urgently. The intravascular space must be resuscitated in minutes to
hours not hours to days, as is currently common practice. Restoration of
total body water and electrolytes will he slower. Treatment should be started
following a presumptive diagnosis of hypovolaemia; by all means send
laboratory investigations but do not wait for the results before starting
treatment.
High-flow
oxygen therapy should be given to all hypovolaemic patients until arterial
blood gas analysis confirms normoxia. A pulse oximeter is useful if available.
Venous access should be secured with short, large-bore cannulae, allowing large
volumes to be infused rapidly. Ideally a 14G cannula in an arm vein should be
used. These allow flow rates twice those of a 16G cannula. CVP catheters are of
very limited use in the early phase of resuscitation, and are difficult and
hence more dangerous to place. They should only be used if the diagnosis of
hypovolaemia is in doubt or if no other access is available.
The
initial choice of fluid in overt hypovolaemia should be a colloid for the
reasons stated above. The need for blood (see below) should not delay initial
resuscitation. Cardiac arrest due to a low haemoglobin concentration is very
unusual; cardiac arrest due to hypovolaemia is relatively common. Resuscitation
should he a continuous process with the doctor at the bedside re-evaluating the
patient. Failure of a fluid challenge to secure improvement requires the use of
more invasive monitoring. Each fluid challenge must be seen to produce a
definite improvement. Precharted fluid regimens and remote management cost
lives.
Just
as patients compensate for volume loss in the early stages of hypovolaemia, so
an apparently resuscitated patient may still have a significant volume deficit.
The aim for immediate resuscitation should he normal measures of pulse, blood
pressure and CVP, urine output > 0.5 mI/kg/hour with normal urinary
osmolality and sodium concentration. Any metabolic acidosis should be seen to be
correcting. Thereafter, one must try to maintain normovolaemia. This is a
continuous process. Critically ill patients may have capillary leak and will
therefore have a continuing colloid requirement. Gelatins, being small molecules, are poorly retained and can be
replaced by hydroxyethyl starch, plasma or blood at this stage. In sepsis this
requirement may be very large (see below).
The
importance of blood in immediate resuscitation, the threshold at which one
should transfuse urgently (i.e. consider using group compatible,
uncross-matched blood or even Group 0 blood) and even the target haemoglobin
level are controversial. Resuscitation should not be delayed whilst waiting for
blood to be grouped; if acute anaemia is secondary to the bleeding
resuscitation should be with Group 0 blood or group-compatible blood as it
becomes available. Otherwise colloid should be used initially and cross-matched
blood and relevant blood products should be used when they are ready. Packed
cells are not colloid and have little plasma expanding effect; transfusions with
large amounts of packed cells will require supplementation with colloid. The age
of the blood is important (old blood is acidic, with decreased oxygen-carrying
capacity and poor red cell deformability) —use the youngest possible blood and
whole blood if it is available.
Hypovolaemia
and the surgical patient
Hypovolaemia is extremely common among patients undergoing surgery. It
remains standard practice in the UK to deny patients food or drink for a minimum
of 6 hours prior to elective surgery in an attempt to reduce the risk of
pulmonary
acid aspiration syndrome. It is not uncommon for this to extend to 10 or even 20
hours due to unforeseen delays. Preoperative fluid restriction is currently a
matter of debate. Indeed, there is evidence suggesting that the administration
of oral fluids to patients until 2 hours prior to elective surgery has produced
a more favourable effect on gastric contents than total starvation. Yet no
attempt is routinely made to maintain normal hydration in preparation for
surgery, despite numerous previous studies demonstrating the benefits of fluid
administration for even the most minor surgical procedures. Recently a study on
fit young patients having elective laparoscopic sterilisation under general
anaesthesia demonstrated a reduced morbidity by the administration of
crystalloid during the operation. It is commonly taught that as part of the
stress response to surgery patients have increased levels of ADH and aldosterone
postoperatively and thus retain salt and water. As a result of this the
overzealous administration of intravenous fluids is feared. Whilst it is
probably true that ADH levels do rise in all postoperative patients, the
presence of hypovolaemia per se may be responsible for much of the increase. A
reduction in urine output in the first 24 hours after surgery may be acceptable,
but a fall to oliguric levels (<0.5 ml/kg/hour) is not. Using the gastric
tonometer, reduced splanchnic perfusion as a consequence of hypovolaemia has
been demonstrated to be common during major surgery and associated with the
development of postoperative organ failure. It is difficult to find any
objective evidence to support the hypothesis that peripheral oedema or the
accumulation of extravascular lung water, as opposed to
pulmonary oedema due to left ventricular failure, has any significant
adverse effects. On the contrary, the evidence supporting the prophylactic
administration of intravenous fluids to patients having major surgery is
impressive.
Hypovolaemia
and cardiogenic shock
Conventional management of the patient with acute pulmonary oedema is
still all too often based on diuretics. Unlike congestive cardiac failure, the
usual problem in acute left ventricular failure is not an excess of total body
salt and water but an acute redistribution of a normal quantity. This leads to
an effectively hypovolaemic patient, particularly if they have been treated
enthusiastically with diuretics. The most appropriate treatment is to reduce
pre- and after-load with infused vasodilators such as GTN to encourage
redistribution of fluid in a more normal fashion and to consider using ionotropes
and even judicious colloid challenges guided by a pulmonary artery catheter if
vasodilators do not produce a rapid improvement. This is particularly important
in right ventricular infarction, where the effect of hypovolaemia and poor right
ventricular function is to underfill the left ventricle which in itself is
usually underperforming.
The
treatment of patients with congestive cardiac failure is more difficult. The
basic principle should remain the maintenance of an adequate circulation with
the use of vasodilators to improve overall haemodynamics supplemented with
diuretics as necessary. The fact that so many patients tolerate diuretic-based
regimens so well reflects the inherent robustness of the average human being!