See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/228542140

Fluid and electrolyte disorders

Article in Indian journal of anaesthesia · January 2003

CITATIONS READS
7 176

5 authors, including:

Chandra Kant Pandey

Institute of Liver and Biliary Sciences
97 PUBLICATIONS 1,609 CITATIONS

SEE PROFILE

All content following this page was uploaded by Chandra Kant Pandey on 04 July 2015.

The user has requested enhancement of the downloaded file.

Indian J. Anaesth. 2003; 47 (5) : 380-387
380
FLUID AND ELECTROLYTE DISORDERS
Dr. Chandra Kant Pandey1 Dr. R. B. Singh2
Preoperative dehydration is common in surgical
patients, and is primarily attributed to prolonged fasting
period and bowel preparation. The symptoms of dehydration
in post-operative fluid may be most evident in minor
surgical procedures, where intraoperative fluid requirements
are low. This is opposed to major surgical procedures,
where large amounts of fluid are often administered intra-
operatively, and therefore may compensate for an initial
fluid deficit. Preoperative fasting of 12 hours or more
may result in a fluid deficit of about one litre in an adult
patient consisting primarily of free water as well as a
small quantity of electrolytes.1,2 The symptoms from this
fluid deficit have not been defined, but may include thirst,
drowsiness and dizziness.3 Apart from subjective patient’s
discomfort, these symptoms of mild dehydration may
contribute to prolonged hospital stay in a review of 17638
patients, where postoperative dizziness and drowsiness were
independent predictors of prolonged hospital stay after
ambulatory surgery.4
The anatomy of body fluids
Fluid balance is often thought of in terms of the
external balance of water and electrolytes between the
body and it s environment. However, it is important to
consider the balance between the fluid compartments within
the body and how these change with diseases. The
Table 1 represents the body fluid compartment in a 70 kg
man. It can be seen that total body water is approximately
60% of the body weight, and that roughly one third of this
is extra-cellular and two third intra- cellular. The two
intra-cellular and extra-cellular are divided by the cell
membrane which, through its sodium pump, maintains the
integrity of the two compartments in which sodium is the
main extra-cellular and potassium the main intracellular
cation, balancing the negative charges on protein and other
molecules within the cells. It is also seen from diagram
that the plasma volume is roughly a quarter of the total
extra cellular fluid volume, the two being separated by the
capillary membrane which, with its restricted pore size,
slows the passage of the large protein molecules from the
vascular to the interstitial space.5 The integrity of the
intravascular volume is therefore maintained by the oncotic
1. M.D., Anaesthesiology, Associate Professor
2. M.D., P.D.C.C. Ex. Senior Resident
Correspond to :
E-mail : ckpandey@sgpgi.ac.in
INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003
380
pressure of the plasma proteins and the functions of the
capillary membrane. Any condition, therefore, which alters
the permeability of the vascular membrane or the level of
plasma proteins, will affect the distribution of fluid between
the intravascular and the interstitial space.5 The integrity
of the intravascular volume is therefore maintained by the
oncotic pressure of the plasma proteins, will affect the
distribution of fluid between the intravascular and the
interstitial space. The intestinal space can be further divided.
Approximately one litre may be transcellular, i.e. secreted
into the gut, and 3-4 litres may be rapidly exchangeable,
the reminder being bound in the matrix of connective
tissue.
Table - 1 : Total body water (70 kg adult) is 60% of the
body weight= 70 × 60/100=42 litres.
Extracellular fluid volume comprises Intracellular water = 40%
interstitial fluid and blood volume body weight = 28 litres.
(20% body weight= 14 litres) Na+ 10 meql-1
Blood volume is approximately 5 litres K+ 150 meql-1
(of which 5% of body weight
is plasma volume equal to 3 litres)
Interstitial fluid = Extracellular
fluid volume – plasma volume (14-3)=11 litres
Na+ 140 meql-1
K+ 4.0 meql-1
The flux of the body fluids :
Through the gut
Approximately 8-9 litres of fluid a day pass the
duodenum, although only 150 ml of water may eventually
appear in the faeces. The reabsorptive capacity of the gut
may fail in various diarrhoeal diseases or with short bowel
or fistulae. In the presence of ileus or intestinal obstruction,
more than 6 litres of water may be pooled in the
gastrointestinal tract and be therefore lost from the
extracellular fluid. It is important therefore, when designing
nutritional support regimens, to be aware of the electrolytes
content of the various gastrointestinal fluids.
Through the kidneys and extracellular fluid volume
regulation
Hundred and eighty litres of water, 25200 mmol of
sodium and 720 mmol of potassium are filtered daily, but
more than 99% of the water and sodium and 86% of the
potassium filtered are reabsorbed. The normal kidney
responds to water or sodium excess or deficit, via osmolality
and volume receptors, acting through anti-diuretic-hormone
PANDEY, SINGH : FLUID AND ELECTROLYTE DISORDERS
(ADH) and the rennin-angiotensin system to restore normal
volume and osmolality of the extracellular fluid.
Maintenance of volume will always override maintenance
of osmolality if hypovolumaemia and hypo-osmolality
coincide. In the presence of starvation or illness, however,
these normal responses may be altered. Unless such changes
are well understood, the therapeutic errors will be made-
frequently.
Renal adaptation to hypovolumia occurs through
three primary mechanisms: a reduction in renal blood flow,
a reduction in glomerular filtration rate, and increased
tubular reabsorption of sodium and water.6 Initial, renal
blood flow is maintained as perfusion pressure decreases
by decreases in renal afferent arteriolar resistance.
Furthermore decrease in cardiac output may result in
increased renal vascular resistance as blood flow is
redistributed from the kidney to preserve cardiac and
cerebral perfusion.
Renal perfusion during hypovolumia is determined
by balance between renal vasoconstrictor factors and
vasodialtaory mechanism. Autoregualtion may be impaired
or lost during severe acute hypovolumia and may be lost
in the inner-medulla with even reduction in perfusion
pressure7,8 Renal sympathetic stimulation with secretion of
alpha-adrenergic catecholamine and angiotensin II increases
renal vascular resistance.
To preserve plasma volume, reabsorption of filtered
water and sodium is enhanced by antidiuretic hormone and
aldosterone and by reduced secretion of atrial natriuretic
peptide. A 10-20% decrease in blood volume is necessary
before ADH secretion from the posterior pituitary
increases.9 ADH acts primarily on the medullary collecting
ducts to increase water reabsorption and causes excretion
of smaller volumes of more highly concentrated urine.
Sodium conservation results from both decreased filtration
and increased distal tubular reabsorption of sodium,
mediated by aldosterone. Hypoperfusion stimulates
glomerular cells of the renal juxtaglomerular apparatus to
release rennin, which catalyses the conversion of
angiotensionogen to angiotensin I. Angiotensin converting
enzyme converts angiotensin I to angiotensin II, which
stimulates the adrenal cortex to synthesise and release
aldosterone.10 Atrial natriuretic peptide (ANP), which exerts
vasodilatory effects and increases the renal excretion of
sodium and water, is released from the cardiac atria in
smaller quantities in hypovolumia.11 Kidney also synthesizes
vasodilatory prostaglandins that play a critical role in
protecting the kidney from vasoconstrictor hormones and
in maintaining RBF during hypovolumia. The protective
effect of endogenous renal prostaglandin may be
381
antagonized by nonsteriodal anti-inflammatory drugs.12
Response to starvation
Food deprivation and refeeding oedema have been
described. In the semi-starvation in normal volunteers, it
has been shown that although the fat and lean compartments
of the body tissues shrink, the extracellular fluid volume
remains either at its pre-starvation level or decreased very
slightly. In relative terms, therefore, the extracellular fluid
volume occupies an increasing proportion of the body mass
as starvation progress. The degree of oedema may be
related to access to sodium and water and may of course
be exacerbated by refeeding. The sodium and water balance
may also be affected by the diarrhoea which cause problems
in food deprived victims, as well as the cardiovascular
decompensation associated with the effect of starvation on
the myocardium.13
Response to injury and acute illness
It was observed that anaesthesia and surgery produce
oliguria, postoperative patients were unable to excrete the
large amounts of salt and water administered intravenously.
This effect was highlighted by Wilkinson et al who showed
that postoperatively patients were unable to excrete an
excess salt and water load whereas the infusion of saline
solution intravenously into normal subjects resulted in a
diuresis and a restoration of normal salt and water balance
within hours, those suffering from trauma, surgery, or
acute illness were unable to do so. The injudicious
administration of fluids, therefore, results in an increasingly
positive salt and water balance and gross interstitial
overload, manifest as oedema. The presence of oedema
in such patients signify a salt and water overload of at
least 3 litres and often much more. The consequent oedema
of tissue may impair function as well as wound healing.14
The capacity to diurese an excess fluid load returns
as the phase of the injury gives way to the recovery or
anabolic phase. The two terms, sodium retention phase
and sodium diuresis phase has been used to describe two
periods of response to trauma or illness. In fact these
responses are non-specific and occur equally in acute
medical illness and in surgical patients. This is also common
to find a low sodium concentration in sick patients.
This is not, of course, equivalent to salt deficiency, but
merely to the changed proportion of water and sodium
in extracellular space. It often occurs in the presence
of increased body sodium, where hypotonic fluids have
often occurs in the presence of increased body sodium,
where hypotonic fluids have been given in excess to
cause dilution. A limited to dilute the urine may persist
until the convalescence or recovery phase of injury.
382
The table 2 shows daily plasma and urine osmolality for
5 days postoperatively in a series of patients who had
undergone uncomplicated abdominal surgery and received
hypotonic fluid postoperatively. Despite increasing
hypotonicity persisting to the seventh day and beyond, the
urine remained relatively concentrated. Severely ill patients
may develop defective cell membrane function such that
sodium may accumulate within the cell. This has been
called the sick cell syndrome.14
Table - 2 : Mean daily plasma and urine osmolalities in 10
patients undergoing abdominal surgery and receiving
hypotonic crystalloids (Allison SP. Metabolic aspect of
intensive care Br I Hosp Med 1974; 661-72).
Osmolalities (in mosmolkg-1) day after operation
Fluid Day 0 Day 1 Day 2 Day 3 Day 4
Plasma Urine 282579 279696 273610 273358 270489
The importance of potassium
Although potassium is lost from the cells as protein
is catabolised, the losses of potassium in the urine
may be disproportionately greater, probably through
mineralcorticoid effects. Even though the total body
potassium may decrease, the serum potassium concentration
may be normal or increase in the catabolic patients,
depending on the presence of other sources of loss, e.g.
urine, fistulae, diarrhoea or nasogastric aspirate. Once
refeeding starts, however, the cells begin to take up
potassium as glycogen and protein are resynthesised. This
may result in abrupt drops in serum potassium
concentration, revealing the underlying potassium deficit.
Careful monitoring of serum potassium and adequate
potassium replacement are important aspect for nutritional
management for such patients. A rise in blood pH or the
use of insulin may precipitate a rapid fall in serum
potassium concentration, not only in the management of
diabetic ketoacidosis, but also in the care of catabolic and
unstable patients.
Effects of feeding
In a series of elegant studies, it has been shown
that starved rabbits tend to retain salt and water when
refed intravenously and that this may lead to increased
lung water.15 This overload was not seen when a low
volume, low sodium feed was given. It was also
demonstrated that a regimen with sole non-protein energy
source was glucose, caused greater water retention than
when half the energy was supplied as fat. Although water
is retained intracellualy as glycogen is reformed, there
was also, in these studies, an increase in extracellular
INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003
water and a dilution of serum albumin concentration.15
Startker et al had reported a series of malnourished patients
who were fed preoperatively. Those who retained fluid
and became hypoalbuminaemic had more complications
postoperatively than those who were able to diurese the
excess fluid and maintain a higher albumin concentration.16
Sitges Serra devised a no sodium, low volume feed for
such patients and showed that this protected against
extracellular fluid expansion and dilution of serum albumin.
This regimen is now used extensively in patients who have
already been overloaded, and restores normal balance over
a period of a week to ten days, with gradual loss of
oedema.
Dissociation between compartmental changes
Feeding of the patients who are unable to eat and
Day 5 have considerable oedema and hypoalbuminaemia
<2.5gdl-1; sepsis, wound breakdown, and fistulae are the
270611 common clinical problems in such groups. Although the
interstitial fluid volume may have been doubled, the plasma
volume is diminished due to gradual plasma loss into
inflamed tissue or from the bowel and, due to increased
capillary permeability elsewhere.
In a recent case, the central venous pressure was
found to be 4 cm in presence of a twelve litre salt and
water overload. Restoration of plasma volume by
administration of concentrated salt poor albumin is
mandatory in such cases to enable the patient to excrete
the excess fluid load, since the kidneys respond to
intravascular volume by albumin infusion also dilates the
subclavian vein allowing easier access for central venous
feeding lines. That’s why not only it is important to council
the external fluid balance, but also of changes in internal
balance between the fluid compartments which may be
altered by disease.
Fluid assessment and monitoring
Fluid balance charts are useful for monitoring
changes in such parameters as fistula or urine output.
These are inaccurate, however, in calculating fluid balance
over a period of days during which the cumulative error
is considerable. The best measure of water balance is
daily weighing. Assuming no pooling in the gut due to
ileus, a change in weight over 24 hours can be interpreted
as an external gain or loss of water by the body tissues.
If change in water balance is known, then any change in
extracellular sodium concentration may be interpreted in
terms of sodium balance. Weighting patients in intensive
care unit may be difficult and one has to depend on
observation of patients for oedema, or salt and water
depletion, monitoring of central venous pressure, and fluid
balance measurements. Two contrasting methods are used
PANDEY, SINGH : FLUID AND ELECTROLYTE DISORDERS
to assess the adequacy of intravascular volume. The first,
conventional clinical assessment, is appropriate for most
patients; the second, goal directed haemodynamic
management, may be superior for high risk surgical
patients. Clinical quantification of blood volume and ECF
is difficult. The clinician must recognize setting in which
deficits; the physical signs of hypovolumia are insensitive
and non-specific. The adequacy of perioperative fluid
resuscitation must be ascertained by evaluating multiple
variables, including heart rate, arterial blood pressure,
urinary output, arterial oxygenation and pH. Tachycardia
is an insensitive and unspecific indicator of hypovolumia.
Preservation of blood pressure, accompanied by central
venous pressure of 6-12 mmHg, suggests adequate
replacement. During profound hypovolumia, indirect
measurement of blood pressure may substantially
underestimate true blood pressure.
No intraoperative monitor is sufficiently sensitive
or specific to detect hypoperfusion in all patients. In
comparison to control group that received conventional
monitoring, including central venous catheterisation, a group
of high risk surgical patients treated to achieve oxygen
delivery more than 600 mlmin-1m-2 had greater survival
and decreased complications.17 A second group that
underwent pulmonary artery catheterisation without these
specific management guidelines did not demonstrate better
survival or fewer complications. In a randomized high
risk surgical patients to conventional treatment or oxygen
delivery >600 mlmin-1m-2 demonstrated a decrease in
mortality and in the number of complications in the patient
managed the higher level of oxygen delivery.18 These data
suggest that aggressive, goal directed haemodynamic
support in certain high risk surgical patients may limit the
mortality and morbidity that results from clinically in-
apparent hypoperfusion.
The aims to be achieved with fluid administration
The goals of perioperative fluid administration are to:
1. Maintain adequate oxygen delivery
2. Normal body electrolyte concentrations
3. Normoglycemia.
The total fluid requirements are made up of:
1. Compensatory intra-vascular volume expansion
(CVE)
2. Deficit displacement
3. Maintenance fluids
4. Restoration of losses
5. Substitution for fluid redistribution (third space
losses).
383
1. Compensatory intra-vascular volume expansion (CVE)
Most general and regional anaesthetics cause
arteriolar and venous dilatation, expanding venous capacity
and leading to a reduction in venous return and preload,
and therefore a reduction in cardiac output. Infusing
fluids to increase the preload will most often return the
stroke volume to an acceptable range. CVE requires 5 to
7 mlkg-1 of balanced salt solution just before or during
induction of anaesthesia.
2. Deficits
Fluid deficit is the maintenance fluid requirement
that is 1 to 2 mlkg-1hr-1 multiplied by hours since last
intake PLUS unreplaced PREOPERATIVE external and
third space loss.
When hypovolemia is present, infuse sufficient fluid
to restore mean arterial pressure, heart rate and filling
pressure (preload or CVP) prior to induction. It is also
desirable to establish a normal urine flow rate if time
permits.
3. Maintenance fluids.
Maintenance fluids meet the ongoing basal needs
for water and electrolytes. The surgical stress response
tends to reduce insulin production and leads to
hyperglycemia , therefore fluid use for volume maintenance
should NOT contain dextrose. There are however certain
high risk patients who are in danger of developing
hypoglycemia: premature infants, neonates who are
receiving glucose containing or hyperalimentation solutions
preoperatively, infants of diabetic mothers, neonates who
are small for gestational age and children and adults who
are diabetic. These patients should have their glucose
solution continued in the peri-operative period. They also
require peri-operative blood glucose monitoring. There is
no reason to administer glucose in the routine clinical
situation and there are potential hazards. After surgery,
when the danger of hypoxia and cerebral ischemia is over
or less, glucose solutions can be started.
4. Fluid losses
Any external losses such as blood and ascitic fluid
should be replaced to maintain the normal intravascular
blood volume and composition of the extracellular fluid.
Blood loss is replaced initially with either 3 ml of balanced
salt solution or 1 ml of colloid solution for each ml of
blood loss. Packed red blood cell infusions are used roughly
one ml for each 2 ml of blood loss plus either crystalloid
or colloid as described. Blood transfusion is associated
with certain risks. In patients with reasonable cardiac and
respiratory reserve and without compromised regional
384
circulation (e.g. coronary, cerebral, renal and intestinal)
haemoglobin levels of 7.5 gdL-1 and above are usually
well tolerated provided the intravascular volume is sufficient
(i.e. the CO is maintained). If intravascular volume and
myocardial function are normal, the cardiac output
(specially stroke volume) will increase to maintain the
oxygen delivery. Neonates and small infants are less able
to increase their stroke volume, and are therefore less able
to compensate for a low arterial oxygen content (which is
associated with low haemoglobin).
5. Third space losses
This is primarily caused by tissue oedema and
transcellular fluid displacement. Functionally, this fluid
is not available to the vascular space. The composition
of third space losses is equivalent to the extracellular
fluid and electrolyte composition plus a small amount
of protein. Therefore balanced salt solution is the most
appropriate replacement for third space loss. The volume
distributed correlates roughly with the degree of tissue
damage and manipulation. Intra-abdominal procedures
with small incisions (example hysterectomy) may require
2 mlkg-1hr-1 while major bowel resection will require
4 to 6 mlkg-1hr-1.
Post-operative fluid therapy
Haemoglobin should be maintained at an acceptable
level. Urine output should be above 0.5 mlkg-1hr-1 and
administration of 1.5 mlkg-1hr-1 of balanced salt solution
will provide replacement of insensible loss, and maintain
urine output.
Which fluids?
Hypotonic intravenous fluid in the immediate
postoperative period, coupled with the loss of sodium that
is not being replaced by intravenous fluid, potentially leads
to the development of dilutional hyponatremia. This may
occur 2 to 24 hours after surgery. Acute dilutional
hyponatremia is a potential problem in almost every
post-operative patient who has undergone any degree of
tissue trauma or has been placed on hypotonic fluids post-
operatively. Vomiting results in loss of fluid which is high
in sodium i.e. balanced salt solution. Vomiting, coupled
with small bowel losses and / or third space losses can
result in the need for post-operative sodium. Sodium in
hypotonic solutions is often inadequate and acute dilutional
hyponatremia results. The problem is that while the
extracellular fluid becomes hypotonic, the intracellular fluid
remains isotonic, so there is a transfer of water from the
extracellular fluid to the intracellular fluid, resulting in
cerebral edema. This leads to central nervous system
depression, irritability, and vomiting and seizure activity.
INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003
Hyponatremia is the most frequent electrolyte disorder in
the perioperative period. Acute symptomatic hyponatremia
is a medical emergency which requires immediate therapy.
Because of its availability, 4.2 % NaHCO3, which is 3 %
sodium solution is the drug of choice to correct the problem.
The empirical dose is 2 ml per kilogram of 4.2 % NaHCO3
over 1 to 2 hours. This should raise the serum sodium
by 6 meqL-1. NaHCO3 should be administered to any
patient with seizures who is receiving a hypotonic solution
post-operatively, along with the normal treatment of the
seizure. When the seizure has abated, balanced salt solutions
can be given as the appropriate fluid.19
Duration of intravenous therapy
This should be continued as long as gastrointestinal
function is inadequate to meet metabolic and caloric
requirements.
Fluid management in perioperative period
Trauma and surgery alters the volumes and
composition of the intracellular and extra cellular spaces.
Therapeutic infusion of fluids further alters compartmental
volumes and composition. Appropriate management of fluid
may limit surgical morbidity and mortality.
Accurate replacement of fluid deficits requires an
understanding of the distribution spaces of water, sodium,
and colloid. Sodium concentration is equal in plasma volume
and interstitial fluid. Albumin is unequally distributed in
plasma volume (4g mdL-1) and IF (1g mdL-1). The IF
concentration of albumin varies greatly among tissues. ECV
is the distribution volume for colloid, although the
concentration in PV and IF are unequal.
Physiology and pharmacology of colloid, crystalloids,
and hypertonic solutions and its clinical implication
Osmotically active particles attract water across
semipermeable membranes until equilibrium is attained. If
membrane permeability is intact, colloids such as albumin
or hydroxyl starch preferentially expand plasma volume
rather than interstitial fluid volume. Concentrated colloid
solutions may translocate interstitial fluid into the plasma.
Plasma expansion unaccompanied by interstitial expansion
offers apparent advantages: lower fluid requirements, less
peripheral and pulmonary oedema accumulation, and
reduced concern about later fluid mobilization.
Exhaustive research has failed to establish the
superiority of either colloid-containing or crystalloid
containing fluids. Much of the debate has centred on the
relative risk of pulmonary oedema. Crystalloid solutions
are associated with pulmonary oedema. In disease states
associated with increased pulmonary capillary permeability,
infusion of colloids may aggravate pulmonary oedema. In
PANDEY, SINGH : FLUID AND ELECTROLYTE DISORDERS
the absence of oncotic pressure gradient, small increase in
the hydrostatic gradient can result in pulmonary oedema.
Hypoproteinaemia in critically ill patients has been
associated with development of pulmonary oedema and
with increased mortality. However either crystalloid or
colloid administration may precipitate pulmonary oedema
in patients who have valvular heart diseases and decreased
left ventricular compliance. After experimentally increasing
microvascular permeability, no difference was found
between increase in extravascular lung water induced by
colloid or crystalloid.20 In surgical patients at risk for the
development of pulmonary oedema, pulmonary artery
catheterisation may facilitate management. Part of the
difficulty in defining the superiority of crystalloid or colloid
fluids is directly attributable to the difficulty of defining
comparable end points in clinically relevant experimental
models21. More recently developed models replicate clinical
situations, permitting more accurate comparison of
crystalloid and colloid solutions. In animals infused with
E.coli lipopolysaccharide, which mimics some aspects of
clinical sepsis, lactated ringers solutions or 6.0%
hydroxyethyl starch produced comparable effects on the
critical end point of oxygen delivery while producing the
expected differences in extravascular fluid accumulation.22
Fluid replacement therapy
Two simple formulas are used interchangeably to
estimate maintenance water requirement. Combining the
predicted daily maintenance requirement for water, sodium,
and potassium in healthy, 70 kg adult results in an estimated
2500 mlday-1 of a solution containing a Na of 30 meqL-1
and K of 15-20 meqL-1 intraoperatively, fluids containing
sodium free water are rarely employed in adults because
most surgical losses are isotonic. Postoperatively, lactated
Ringer’s solution or 0.9% saline commonly is used until
patients are haemodynamically stable. Subsequently,
patients can tolerate fluids containing either more free
water or containing Na+ in excess for maintenance
requirements if cardiac and renal function is satisfactory.19
Dextrose
Traditionally, physicians have infused glucose-
containing intravenous fluids perioperatively in an effort
to prevent hypoglycemia and limit protein catabolism.
However, due to the hyperglycemic response associated
with surgical stress, only infants and patients receiving
insulin or drugs that interfere with glucose synthesis are
at risk for hypoglycemia. Iatrogenic hyperglycemia can
induce an osmotic diuresis and may aggravate ischemic
and traumatic brain injury. 23,24 The type of fluid
administered may be of importance because preoperative
administration of glucose-containing fluid has in several
385
studies been found to reduce postoperative insulin
resistance25. In one randomized study, administration of
1200 ml 12.5% glucose solution preoperatively led to
improvements in preoperative hunger, thirst and anxiety.22
Another study compared administration of 20 mlkg-1 lactated
ringer with 20 mlkg-1 lactate/glucose intra operatively in
minor gynaecological surgery and the improvements in the
fitness for discharge, and the late outcome evaluations
dizziness, faintness, headache, drowsiness and throat pain
were only seen in the patients receiving solutions containing
glucose.20 Further studies are needed with regard to
postoperative effects of pre and intraoperative glucose
administration.
Surgical fluid requirements
Surgical patients require replacement of plasma
volume and extracellular losses secondary to wound or
burn oedema, ascitis and gastrointestinal secretions. Wound
and burn oedema and ascetic fluid are protein rich and
contain electrolytes in concentrations similar to those found
in plasma. If extracellular volume is adequate and renal
and cardiovascular functions are normal, all gastrointestinal
secretions can be replaced using lactated ringer’s solution
or 0.9% saline; if renal or cardiovascular function is
compromised, more precise replacement is necessary.
Substantial loss of gastrointestinal fluids requires
replacement of other electrolytes. Chronic gastric losses
may produce hypochloremic metabolic alkalosis that can
be corrected with 0.9% saline; chronic diarrhoea may
produce hyperchloremic metabolic acidosis that may be
prevented or corrected by infusion of fluid containing
bicarbonate or bicarbonate substrate.
Guidelines have been developed for replacement of
fluid shift during surgical procedures. The simplest formula
provides, in addition to maintenance fluids and replacement
of estimated blood loss, 4 mlkg-1hr-1 of lactated ringer’s
solution or 0.9% saline for procedures involving minimal
trauma, 6 mlkg-1hr-1 for those involving moderate trauma,
and 8 mlkg-1hr-1 for those involving extreme trauma.
Clinical implications of hypertonic fluid administration
An ideal alternative to conventional crystalloid and
colloid fluid would be hypertonic fluid which is inexpensive,
produce minimal peripheral or pulmonary oedema, generate
sustained hemodynamic effects, and be effective even if
administered in small volumes. Hypertonic, hypernatremic
solutions combined with colloid appear to fulfil some of
these criteria. In an experimental study small volumes
6 mlkg-1 of 7.5 hypertonic saline restored blood pressure
and cardiac output and increased mesenteric blood flow to
greater than control values in haemorrhaged dogs and all
animals survived.26 Although posttreatment serum
386
osmolality exceeded 330 mmolkg-1, no animal showed
adverse effects.
Hypertonic solutions exerts favourable effects on
cerebral haemodynamics because the in-permeability of
sodium to the blood-brain barrier in uninjured brain causes
the brain to shrink in response to acute increases in serum
sodium. In dogs with intracranial mass lesions and
haemorrahgic shock, intracranial pressure increased during
resuscitation from with 0.8% saline but remained unchanged
if 7.2% saline was infused in a sufficient volume to a
comparably improved systemic haemodynamics.27
Hypertonic solutions restored regional cerebral blood flow
better than did slightly hypotonic solutions. 26 In
haemorrhaged rats subjected to mechanical brain injury,
brain water content was lower in uninjured brain after
resuscitation with hypertonic saline. If fluid resuscitation
continues after immediate stabilization, difference between
fluids of varying tonicity become negligible.28,29
Conclusion
Careful fluid management is essential in limiting
morbidity and mortality in critically ill surgical patients.
Maintenance of systemic perfusion is a critical strategy in
avoiding shock and the late consequences of the multiple
system organ failure syndromes.
Acknowledgement
We acknowledge and thanks for the efforts and
support provided by Dr. Mehdi Raza, Dr. Devendra Gupta,
Dr. Sanjay Dhiraj and Dr. Sandeep Pawar in preparation
of this manuscript.
References
1. Holte K, Kehlet H. Compensatory fluid administration for
preoperative dehydration-does it improve outcome? Acta
Anaesthesiol Scand 2002; 46: 1089-93.
2. Keane PW, Murray PF. Intravenous fluids in minor surgery.
Their effect on recovery from anaesthesia. Anaesthesia 1986;
41: 635-7.
3. Yogendran S, Asokumar B, Cheng DC, Chung F. A prospective
randomized double-blinded study of the effect of intravenous
fluid therapy on adverse outcomes on out patient’s surgery.
Anesth Analg 1995; 80: 682-6.
4. Chung F, Mezei G. Factors contributing to a prolonged stay
after ambulatory surgery. Anesth Analg 1999; 89: 1352-9.
5. Allison SP. Dehydration. In: Macrae R, Robinson RK, Sadler
MJ (eds). Encyclopedia of food science, food technology ad
nutrition. London Academic Press 1993; 457-72.
6. Badr KF, Ichikawa I. Prerenal failure: a deleterious shift
from renal compensation to decompensation. N Eng J Med
1988; 319: 623-9.
7. Henrich WL, Pettinger WA, Cronin RE. The influence of
circulating catecholamine and prostaglandins on canine renal
hemodynamics during hemorrhage. Circ Res 1981; 48: 424-9.
INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003
8. Lerman LO, Bentley MD, Fiksen-Olsen MJ, Strick DM, Ritman
EL, Romero JC. Pressure dependency of canine intrarenal
blood flow within the range of autoregulation. Am J Physiol
1995; 268: F 404-9.
9. Hall J, Robertson G. Diabetes insipidus. Problems in Critical
Care 1990; 4: 342-54.
10. Laragh JH. The endocrine control of blood volume, blood
pressure and sodium balance: atrial hormone and rennin system
interactions. J Hypertens 1986; 4(suppl 2): S143-56.
11. Needleman P, Greenwald JE. Atriopeptin: a cardiac hormone
initimately involved in fluid, electrolyte, and blood pressure
homeostasis. N Eng J Med 1986; 314: 828-34.
12. Murray MD, Brater DC. Adverse effect of nonsteriodal anti-
inflammatory drugs on renal function. Ann Intern Med 1990;
112: 559-60.
13. Winick M (ed). Hunger disease: studies by the Jewish
Physicians in the Warsaw Ghetto. New York, Wiley 1979.
14. Allison SP. Metabolic aspect of injury. In: Tubbs N, London
PS (eds). Topical reviews in accident surgery. Bristol, John
Wright 1980; 1: 11-32.
15. Stiges SA, Arcas G, Guirao X, Garcia-Dominho M, Gil MJ.
Extracellular fluid expansion during parenteral feeding. Clin
Nutr 1992: 11: 63-8.
16. Starker PM, Lasala PA, Forse RA, Askanzi J, Elwyn DH,
Kinney JM. Response to total parenteral nutrition in the
extremely malnourished patient. JPEN 1985; 9: 300-302.
17. Shoemaker WC, Appel PL, Kram HB, Waxman K, Lee TS.
Prospective trial of supranormal values of survivors as
therapeutic goals in high risk surgical patients. Chest 1988;
94: 1176-86.
18. Boyd O, Grounds RM, Bennett ED. A randomized clinical
trail of the effect of deliberate perioperative increase of oxygen
delivery on mortality in high risk surgical patients. JAMA
1993; 270: 2699-2707.
19. Prough DS, Mathru M. Fluid management in critically ill
patients. In: Murray MJ, Coursin DB, Pearl RG, Prough DS,
editors. Critical Care Medicine: Perioperative management.
Philadelphia, Lippincott-Raven, 1997: 99-108.
20. Pearl RG, Halperin BD, Mihm FG, Rosenthal MH. Pulmonary
effects of crystalloid and colloid resuscitation from hemorrhagic
shock in the presence of oleic acid-induced pulmonary
capillary injury in the dog. Anesthesiology 1988; 68: 12-20.
21. Prough DS, Johnston WE. Fluid resuscitation in septic shock:
no solution yet. Anesth Analg 1989; 69: 699-704.
22. Baum TD, Wang H, Rothschild HR, Gang DL, Fink MP.
Mesentric oxygen metabolism, ileal mucosal hydrogen ion
concentration, and tissue edema after crystalloid or colloid
resuscitation in porcine endotoxic shock: comparison of
Ringer’s lactate and 6% hetastarch. Circ Shock 1990; 30:
385-97.
23. Lanier WL, Stangland KJ, Scheithauer BW, Milde JH,
Michenfelder JD. The effects of dextrose infusion and head
position on neurologic outcome after complete cerebral
ischemia in primates: examination of a model. Anesthesiology
PANDEY, SINGH : FLUID AND ELECTROLYTE DISORDERS 387

1987; 66: 39-48.
24. Lam AM, Winn HR, Cullen BF, Sundling N. Hyperglycemia
and neurological outcome in patients with head injury. J
Neurosurg 1991; 75: 545-51.
25. Traber LD, Brazeal BA, Achmitz M, et al. Pentafraction
reduces the lung lymph response after endotoxin administration
in the ovine model. Circ Shock 1992; 36: 93-103.
26. Velasco IT, Pontieri V, Rocha e Silva M Jr, Lopes OU.
Hyperosmotic NaCl and severe hemorrhagic shock. Am J
Physiol 1980; 239: H664-73.
27. Prough DS, Whitley JM, Taylor CL, Deal DD, DeWitt DS.
Regional cerebral blood flow following resuscitation from
hemorrhagic shock with hypertonic saline. Influence of a
subdural mass. Anesthesiology 1991; 75: 319-27.
28. Wisner DH, Schster L, Quinn C. hypertonic saline resuscitation
of head injury: effects on cerebral water content. J Trauma
1990; 30: 75-8.
29. Whitley JM, Prough DS, Brockschmidt JK, Vines SM< DeWitt
DS. Cerebral hemodynamic effects of fluid resuscitation in
the presence of an experimental intracranial mass. Surgery
1991; 110: 514-22.

CONFERENCE CALENDER 2003 - 2004

1) 25th Annual UP State Chapter 5) XIX Annual Conference of the Indian Society for
1st and 2nd November 2003 study of pain (IASP–Indian Chapter) ISSPCON 2004,
Contact : Dr. Mukesh Tripathi 23rd, 24th, 25th January 2004
Organising Secretary Contact : Dr. S. Sen
UPISACON-2003 Pacific Point-57/14, Ballygunj Circular Road,
Dept. of Anaesthesiology, Kolkata – 700 019.
Sanjay Gandhi Postgraduate Institute of Email : ssen@vsnl.com
Medical Sciences, Lucknow – 226 014.
E-mail: upsilverjublee@email.com 6) 5th Annual Conference of Indian Society of
Neuroanaesthesiology and Critical Care
2) Post-Graduate Assembly, Anaesthesiology 6th 8th February 2004.
& Critical Care, 2003 Contact : Dr. G.S. Umamaheshwara Rao
8th–15th November 2003 Organising Secretary
Contact : Prof. A. K. Sethi 5th Annual Conference of Mental Health
Organizing Chairman and Neurosciences (NIMHANS)
Head, Dept. of Anaesthesiology & Critical Care, Bangalore – 560 029 KARNATAKA
University College of Medical Sciences & GTB Hospital, E-mail: isnacc2004@himhans.kar.nic.in
Shahdara, Delhi-110 095
7) 7th Annual Conference of Indian Association
3) Asian Society of Paediatric Anaesthesiologists of ISA. of Cardiovascular and Thoracic
22-23rd November 2003 Anaesthesiologists (IACTA)
Contact : Dr. Dilip Pawar 19th and 21st February 2004.
Dept. of Anaesthesiology, Contact : Dr. Suresh G. Nair
All India Institute of Medical Sciences, Oranising Secretary
New Delhi – 110 029. Anaesthesia House, Shopping Complex,
Email: dkpawar@hotmail.com Panampilly Nagar, Cochin – 682 036
Tel : 0484-2322251
4) 51st Annual Conference of ISA ISACON 2003 E-mail : anaesthesia@vsnl.net
26th- 30th December. 2003
Contact : Dr. Narayan Acharya 8) 13th World Congress of Anaesthesiologists
Organising Secretary 2004 Paris (France)
IMA House Medical Road, 18th -23rd April, 2004
Ranihat, Cuttack – 753 007 Orissa. Contact : Prof. Philippe Scherpereel
Mobile.: 0-9437053586 / 0-9861053586 President, WCA 2004
Email.: drnacharya@isacon2003. Congress Office, COLLOQUIM-12
Reu-dela-Croix-Faubin – 75557, Paris-cedex-11-France
Tel. : 33(0)144-64-1515
E-mail: wca2004@colloquim.fr

View publication stats