Perioperative fluid therapy

Introduction Assessment of fluid requirements in the surgical patient can be complex. Fluid replacement must be based on measurement of plasma electrolytes whilst appreciating that they may be unrepresentative of changes in whole body electrolytes. For instance, in a 70 kg patient only ! mmol of "# is present in the plasma as compared with $!00 mmol in the body as a whole. %a # forms the skeleton to which water is added to form the plasma volume &'(). *igration of %a# intracellularly &accompanied by water), as a result of cellular dysfunction, results in ma+or changes in circulatory homeostasis although the concentration in the plasma is unchanged. ,t is clear, then, that minor changes in serum electrolytes may mask ma+or changes in cellular and total body concentrations that can result in or be the cause of significant cellular dysfunction. ,n addition, although we rely normally on sensors in the -(., -%. and kidneys for maintaining the milieu interieur, following surgical procedures, trauma or severe illness, these control systems are disrupted and act unpredictably. Application of pharmacokinetic principles such as volume of distribution, concentration, redistribution and excretory processes are equally applicable to electrolytes and put changes in plasma electrolytes into context. Normal physiology /ater is the ma+or component of mammalian structure. 0he percentage of total body water &01/) to weight ranges from about !!2 in the adult female, 302 in the adult male, to nearly 402 in the newborn. ,n the adult male of 70 kg, 01/ is equal to about 50 l. 0here are three main compartments through which it is distributed, intracellular fluid &,-F) which contains about 67 l, interstitial fluid &,.F) 0 l and plasma volume &'() of $ l. 0he latter two &,.F and '() constitute extracellular fluid &7-F). '( forms the medium in which red blood cells carrying oxygen can be transported to all cells of the body and together form the circulating volume &-() of ! l. 0ranscellular fluid &0-F) is defined as fluid in transit between various compartments, usually in body cavities such as the gut lumen where it is continuously added to by ingested fluids, secreted and re absorbed. 0he volume at any time is usually not large but may increase markedly in derangement of gut function such as paralytic ileus, diarrhoea and vomiting or is lost iatrogenically as by nasogastric suction. 0-F is extremely difficult to quantify but should always be considered when trying to quantify fluid losses and shifts in the surgical patient. -ontrol of volumes and constituents ,n health, the volume and electrolyte distribution of these compartments of 01/ are controlled by three ma+or processes8 The Na+/K+ pump An active process, relying on A0' and a %a#9"# exchange pump, controls the electrolyte composition of the ,-F and ,.F. 0he ma+or intracellular cation is "# & 50: 30 mmol.l: ) with %a# of 0:50 mmol.l: &depending on the type of cell), whilst in the ,.F and '( the ratios are reversed with %a# being the predominant cation & $6: 5! mmol.l: ) with a "# of $.!:! mmol.l: . 0otal body exchangeable %a# and "# are roughly equivalent to 50 mmol.kg: 1/. ;erangement to this active process in disease results in "# leak from the cells and into the 7-F with %a# &and water) going in the opposite direction. Osmolality and tonicity *aintenance of osmotic balance ensures that the total concentration of osmotically active particles is the same throughout all three compartments. 0he ma+or osmotically active cation in 7-F is %a# whilst in the ,-F it is "#. <smolality is simply the number of osmotically active particles per "g of solvent &in this case water). 0able

Table 1 The major osmotic constituents of plasma

!ation/"nion

!oncentration in mmol#l$1

%a#

$!

"#

-l:

=-<$:

65

>lucose

?rea

0<0A@

645 &mosm.l: )

0hus, a fall in plasma %a# results in fall in '( osmolality in comparison to that in the ,.F. /ater will move from '( to ,.F in an attempt to equalise the osmotic pressures &osmolality) in the two compartments. 0he resulting overall fall in ,.F osmolality leads to further movement of water into the ,-F. An opposite effect is seen with a rise in '( %a#. ,n other words a fall in plasma %a# always results in an increase in ,-F and vice versa. %&ample 0his movement can be seen most clearly in the following example. A normal 6.! kg infant has 01/ equal to 402 of body weight with the ratio of 7-F to ,-F is8 . 0hus, overall osmolality of both compartments is 640 with an 7-F &and '() %a# of 50 mmol.l: . An infusion of 00 ml. of !2 glucose in water is given over a short period. 0he overall osmolality of the 7-F &'( and then ,.F) is reduced by dilution to 6!5 and the %a# falls to 67. 0here is osmotic dysequilibrium that cannot be sustained. /ater moves from the 7-F to ,-F to reestablish osmotic equilibrium. 0his results in an expansion of the ,-F by !0 ml. and an increase in 7-F &and '() %a# up to $$. 0he net result is that the 00 ml. of water has distributed according to the relative volumes of the 7-F and ,-F &in this case equally, but in an adult would be 86) and there is an expansion in ,-F of !0 ml. .ee Figure 'igure 1# %ffect of addition of 1(( ml# )ater on the relative volumes of %!' and I!' and changes in osmolality *see te&t+

,ydrostatic and colloid osmotic *oncotic+ balance <bviously, the three compartments are not in a passive state. 0he dynamics of the circulation and the requirement to transport oxygen and nutrients around the body necessitates the generation of a pressurised flow of blood from left heart to right atrium. 0he hydrostatic pressure generated by this column of blood in the capillaries would inevitably lead to a net loss of fluid from the '( into the ,.F and eventual depletion of the -(. 0his hydrostatic pressure is balanced by the presence of colloids in the '(. A semi:permeable membrane &the capillary endothelium) represents the barrier between the '( and the ,.F. =igh molecular protein constituents of plasma exert Acolloid osmoticA or AoncoticA pressure. -olloids are molecules capable of exerting oncotic pressure and have limited &or Bero) ability to cross a semi: permeable membrane due to their molecular siBe. At the same time, they have the ability to attract solvent &solvent drag) from the other side of the membrane into the compartment in which they are situated &in this case '(). 0he oncotic pressure of a plasma constituent is proportional to the amount &in g.l: ) divided by the molecular weight. ,n man, plasma albumin &50 g.l: ) with a */ of 30,000 constitutes the most important component of plasma oncotic pressure &$ k'a or 60:6! mm=g). Albumin also exists in the ,.F but its effective concentration is markedly reduced, due not only to the fact that it is bound to cells, but also that ,.F albumin is mainly in a semisolid gel form. 0he oncotic pressure gradient between the two compartments that is manifest as solvent drag from ,.F to '( is around .! to 6 k'a & 0: !mm =g). 0hus, the total osmotic pressure of the crystalloid component of the '( is 340 k'a &3.4 atm or ! 00 mm=g, see later) whilst the colloid oncotic component is only $ to $.! k'a &60:6! mm =g). =owever, the former is equalised throughout the three main compartments &,-F, ,.F and '() whilst the latter is greater in the '( versus the ,.F. 0his oncotic pressure gradient is responsible for maintaining the integrity of the '(. 0he effects of these two opposing forces, hydrostatic pressure and oncotic pressure have been summarised in .tarlingAs equation which states that8 -' . K*,P pl $ ,P in+ $ s *OP pl $ OP in+

/here8

CF is the net outward flow of fluid from the capillaries into the ,.F. " is a constant that expresses the flow of fluid outwards in mls.per unit pressure gradient in k'a or mm =g. =' pl. is the hydrostatic pressure in the capillaries in k'a or mm =g. =' in. is the hydrostatic pressure in the ,.F in k'a or mm =g. <' pl. is the oncotic pressure in the plasma in k'a or mm =g. &almost entirely due to albumin). <' in. is the oncotic pressure in the ,.F in k'a or mm =g. &%.1. over two thirds of the bodyAs albumin is in the ,.F) s is the reflection coefficient of the capillary bed in question.

0he reflection coefficient is a measure of the permeability of the capillary to albumin. ,f it is impermeable,

then the full oncotic pressure gradient between plasma and ,.F is experienced, s will be . ,f, on the other hand, the capillary is completely permeable to albumin, then no gradient exists, and fluid leaks out entirely as expressed by the hydrostatic pressure gradient. 0his would result in a s of 0. ,n practice, depending on the capillary bed in question the range is about 0 &liver) to 0.7 &lung).

A fall in the oncotic pressure gradient, due to loss of albumin or a reduction in the reflection coefficient due to capillary endothelial damage &vide infra), causes a loss of '( and an increased propensity to the development of significant tissue and pulmonary oedema.

<verall, plasma electrolytes represent a dynamic interchange between total body stores, input and output and passive and active movements between compartments as controlled by the processes alluded to above.

Figure 6 shows the effect of the .tarling 7quation and the typical overall pressures in the capillaries and venules and the fluid shifts which occur. 'lease note that as fluid leaves the circulation at the arteriolar end, the hydrostatic pressure gradient gradually diminishes in the capillaries and the oncotic pressure gradient gradually increases. 0hus, by the time we reach the venular end, the pressure gradients have been reversed and fluid reenters the circulation again. 'igure / ,ydrostatic and colloid oncotic pressure gradients in the capillaries#

!onditions causing an increase in capillary endothelial permeability *!%P+

0hree common conditions cause an increase in -7'8

"naphylactic shoc0 &e.g. penicillin allergy) results in increased leakage of fluid leading to sudden hypovolaemia along with peripheral oedema and bronchoconstriction 0he initial treatment for a patient without venous access is i.m. adrenaline &0.! to solution) or in a patient with i.v. access, mg i.e. 0.! to ml. of a 8 000

to 6 ml. boluses of i.v. adrenaline & mg in 0 ml. or

8 0,000). Fluids and oxygen therapy should be used in addition.

1urn injury causes a systemic Acapillary leakA which is proportional to the percentage of the burned area. 0he amount of fluid leakage is massive and is equivalent to 5 ml. of DingerAs @actate per kg. per 2 area burn in 65 hours &'arkland formula). 7.g. in a 30 kg patient with a 502 burn this requires 5 E 30 E 50 F G300 ml, !02 given in the first 4 hours, 6!2 in the next two 4 hour periods) calculated from the time of the burn injury.

2eptic shoc0 or systemic inflammatory response syndrome &.,D.) also leads to loss of -( and this fluid must be replaced in large quantities to maintain -(, despite the inevitable oedema that this causes.

3egulation of blood volume

;ay to day homeostasis

0he factors mentioned above are all designed to maintain the integrity of the '( and -( so that it can form the medium to allow transport of oxygen and nutrients for cellular metabolism. 0his ensures optimal organ function, but in a dynamic process the volumes are not static. Adequate clearance of waste products of metabolism require the kidney to excrete about !00 ml of urine per day containing about 500:400 mmol of urea, !0 to 00 mmol "# and 70 to 50 mmol. %a# &depending on intake). Additional fluid losses are incurred from evaporation, respiratory tract and faeces. 0he total loss of fluid is about 6!00 ml. water plus about 70 mmol %a# and "# in a 70 kg adult per day. 0his has to be replaced to maintain 01/. 0he extent of maintenance fluid requirements is more closely related to body surface area &1.A) than weight. .ince a new born baby of $.! kg. has about 6 96 times the 1.A9wt ratio of an adult & 960th the weight and 94 th the 1.A) it consequently needs 6 96 times the maintenance fluid per unit weight. A common formula used is shown in 0able 6. Table / 4aintenance fluid re5uirements

6eight range $ : 0 kg 0 : 60 kg 60 kg and above 0hus8

'luids per /7 hours 00 ml.kg: 000 ml. for first 0 kg. # !0 ml.kg: for any additional wt. over 0 kg !00 ml. for first 60 kg. # 60 ml.kg: for wt. over 60 kg.

a 8 0g# infant )ould re5uire 8(( mls# per day 18 0g child )ould re5uire 1((( + 9:( . 19:( ml# per day a 8( 0g# adult )ould re5uire 1:(( + 1((( . /:(( ml# per day

%ormally this fluid requirement is regulated both by changes in volume and osmolality in the '( being detected in the hypothalamus. An increase &due to fluid deprivation) stimulates anti: diuretic hormone &A;=) release from the supra optic nucleus which causes thirst and reduces urine output by increasing reabsorption of water from the collecting ducts in the kidney. A decrease in renal perfusion &due to fluid deprivation) increases renin output from the +uxtaglomerular apparatus leads to the formation of angiotensin ,, &A0 ,,). 0his causes thirst, constricts the efferent glomerular artery to maintain glomerular arterial pressure and filtration and also causes release of aldosterone from the adrenal cortex. 0he latter increases renal %a# retention in exchange for "# in the distal tubule.
All these changes are increased by activation of the sympathetic nervous system &.%.). ,f fluid deprivation becomes greater or there are abnormal losses such as diarrhoea, vomiting, ileus or haemorrhage, these processes are amplified. ,t is important to note that volume is usually maintained at the expense of a reduction in osmolality due to hyponatraemia. 0his is due to the more powerful effect of A;= over aldosterone. As plasma %a# concentration falls, proximal tubular reabsorption of %a# &and water) becomes intense, limiting the ability of the kidney to produce dilute urine. Administration of hyponatraemic solutions in the postoperative period in the presence of a low serum %a# further compounds the problem. !2 glucose and 52 glucose 0. 42 saline should never be given if the plasma %a# is low. 0.G2 sodium chloride or DingerAs @actate &=artmannAs) is more appropriate. "cute changes in homeostasis

Acute surgical or traumatic hypovolaemia cannot be compensated for by the more chronic processes mentioned above. Additional mechanisms are brought into play. Acute reduction in -( reduces venous return and cardiac preload so cardiac output and blood pressure &1') fall. Deduction in 1' reduces the afferent activity of the carotid sinus baroreceptors to the ApressorA area in the dorsal hypothalamus, and results in increased .%. discharge. Deduction in venous return leads to a decrease in atrial natriuretic peptide &A%') production &thus reducing urinary sodium loss) and a fall in output from the low pressure

baroreceptors in the atria and great veins to the AdepressorA centre. 0he resultant fall in parasympathetic nervous system &'%.) discharge augments the action of the .%..

The effects of this are summarised as follo)s

;irect neural effects via alpha and beta receptors. !atecholamine release from the adrenal medulla . ,n different shock states, and at different stages of shock, noradrenaline or adrenaline predominates. 3enin release from the +uxtaglomerular apparatus of the kidney &vide infra). Increased Na+ reabsorption in the distal tubule ;ecreased Na+ loss due to a reduction in atrial natriuretic peptide <ascular redistribution of blood in the 0idney from cortex to medulla, the latter being the ma+or site of %a# and water reabsorption

0he ,.F compartment has an important role in maintaining circulating volume. .ympathetic stimulation, particularly to the skin and splanchnic circulation, results in a reduction of flow to these nonessential areas, by alpha adrenergically mediated arteriolar vasoconstriction. 0his results in a reduction of flow to the capillary beds by neuro:humorally mediated increase in the pre:capillary sphincter &'-.) tone. 0he hydrostatic pressure in the capillary beds falls, thus allowing fluid to enter the capillary circulation distal to the '-. as a result of the change in hydrostatic9oncotic pressure gradient &see .tarlingAs equation above). Intravenous perioperative fluid replacement therapy

,nitially, it is pertinent to consider the types of fluids that are available and their uses. Fluids can be conveniently classified into crystalloids, colloids and blood &and blood products). !rystalloids

0hese are solutions containing water and electrolytes and9or glucose made up in a concentration that is usually isotonic with plasma. 0his means that they contain the same number of osmotically active particles as plasma, i.e. about $00 &range 640 to $ 0) mosmol.l: of solute. .everal solutions are available, !2 glucose, 52 glucose 0. 42 saline, %ormal &0.G2) saline and DingerAs lactate &=artmannAs) H see table $).

=ow do we make an isotonic solutionI From first principles, if

gram molecular weight of solute is placed

in a flask containing

kg. of solvent &i.e.

litre of water) it will form a molar solution. 0hus, 40g of glucose mol. or 000 mmols.l: . 1y definition, if one mole of

& 40 F the m.w. of glucose) in a kg. of water will have

glucose is dissolved in 66.5 litres of solution at %0' &i.e. 0 deg -) it will exert an osmotic pressure of one atmosphere & 00 k'a or 730 mm =g). 0hus, a molar solution will exert an osmotic pressure of 66.5 atmospheres &6600 k'a or !600 mm =g) at %0' or 6!.5 atmospheres &6!50 k'a or G$50 mm =g) at $7 deg -. 0his amount is referred to as osmol or 000 mosmol. <ne mosmol at $7 deg - thus generates an

osmotic pressure of 6.! k'a & G mm=g), thus in total the osmotic pressure of plasma is equal to $00 E 6.! F 7!0 k'a &!700 mm=g). 0hus, this molar solution of 42 glucose & 40g per litre or 4 g per 00 ml) is hypertonic & 000 versus $00 mosmol.l: ). 7ach g per litre therefore gives about !.! mosmol.l: , so !0g &!2 solution of glucose) will produce an isotonic solution of !0 times !.! or 67! mosmol.l: .

/ith an electrolyte such as sodium chloride, the molar solution &!4.! g of sodium chloride) will contain nearly 6000 mosmol. l: as in solution it is almost completely dissociated into sodium and chloride ions. 0hus, roughly 93th. of !4.!g.l: is required, i.e. Gg per litre &0.G g. 00 ml: or 0.G2 saline) with !0 mmol. of %a# and !0 mmol. of -l:. ,n a similar manner, 52 glucose and 0. 42 %a-l will give $0 mosmol. of both %a# and -l: per litre plus 660 mosmol.l: from glucose making 640 in all. ,t can be seen that normal &0.G2) saline is hardly physiological as it contains excess %a# & !0 vs $!) and excess -l: & !0 vs 0!). 7xcess -l: administration can result in retention of =# and urinary loss of =-<$: and a dilutional acidosis if administered in excess. 0hus, ideally, a AbalancedA salt solution &1..) should be used. .uch a solution is DingerAs lactate &also called =artmannAs solution). 0his contains in mmol.l: , %a# $0, "#$.!, -l 0!, -a 6, @actate 6G. 0he latter is a =# acceptor and is metabolised by the liver with net formation of one molecule of =-<$: and one molecule of pyruvate which can be utilised as an energy source in the "rebs cycle. ,t does not cause a dilutional or lactic acidosis provided that liver perfusion is adequate. ,t is worth noting that a fall in serum %a# of ! mmol.l: &accompanied by a change in -l: of the same amount) will result in a pressure dysequilibrium between the '(, ,.F and ,-F of 9$0th & 09$00) of total plasma osmotic pressure or about G0 mm =g & 9$0th of !G00). 0his large pressure difference, should it occur rapidly, results in water leaving the '( into the ,.F and then into the ,-F in an attempt to restore osmotic balance between the fluid compartments. ,f this occurs acutely, as in excess absorption of non: sodium containing irrigation fluid during transurethral resection of prostate &0?D'), cerebral oedema and raised intracranial pressure may occur. 0he latter occurs in the TURP syndrome. =owever, it should be noted that glycine .!2, the irrigation fluid traditionally used during 0?D', is hypotonic. 0he molecular weight of glycine is 7!, so 7! g dissolved in a kg. of solvent &i.e. a litre of water) would be a molar solution and would contain 000 mosmol.l: . 0hus .!2 glycine &or ! g. l: ) has an osmolality of 600 mosmol.l: . 0o aid detection of excess absorption of fluid, ethanol & 2) is usually added as a marker. ,f a significant amount of irrigation fluid is absorbed, the ethanol component will be detectable in the breath &cf a AbreathalyBerA). 0he concentration of ethanol thus reflecting the extent of absorption. 0he addition of ethanol 2 to the .!2 glycine affects its osmolality. 0he */ of ethanol is 53, thus 0 g per litre &i.e. a 2 solution) will increase osmolality by 6 7 thus making the total osmolality of the irrigating solution 5 7 i.e. hypertonicJ .ince this combined solution is now commonly used it may account for the diminished incidence of 0?D' syndrome.

0hus, absorption of irrigation solution will increase overall osmotic pressure in the '( but still result in a fall in plasma %a#. ,n fact, the 0?D' syndrome is more to do with fluid overload and the possible cerebral effects of glycine than the effect of the drop in plasma %a#. ,n the same way, infusion of !2 glucose will cause a fall in plasma %a# due to a dilutional effect but osmotic pressure will remain the same as the solution is isotonic. As the glucose is metabolised &the glucose concentration in !2 glucose is about 67! mmol.l: whilst in plasma it is !), the osmotic pressure in the plasma will fall and water will go into the cells. 0he effect on cellular overhydration will depend on the rate of administration of !2 glucose. 0hus, although non:sodium containing isotonic solutions will eventually result in increased cellular water they do not do so rapidly enough in most circumstances to cause problems of dysequilibrium between the body compartments.

,n chronic hyponatraemia, as in patients on diuretic therapy, there is time to restore osmotic equilibrium without ma+or pressure differences occurring between compartments. =owever, use of hypertonic saline may result in too rapid correction of %a# in the plasma will cause rapid reversal of the above process and cerebral dehydration which can be equally dangerous. 0hus, it is much easier to raise %a# concentrations rapidly than to cause a fall. 0he commonest cause of excess hypertonic %a# adminstration is the use of %a#=-<$: solutions &see 0able $).

7lectrolyte concentrations of commonly used crystalloid solutions are shown in the 0able $. Table 9 !ontent of !rystalloid solutions

!ontent of crystalloid solutions

Name %a-l 0.G2 Kno)n as %ormal .aline !5 DingerAs @actate =artmannAs $ >lucose !2 !2 dextrose $0 G7 ! 50E 000 000 amounts in mmol.l: 6!6 643 !!6 6000 !5 ! 6 6G 640 Na+ !l$ K+ !a== 4g++ ,!O9$ >actate$ mosmol#l$1 $04

>lucose 52 # %a-l 0. 42 ;extrose saline $0 'lasmalyte 54 # glucose .odium 1icarbonate 4.52 'lasmalyte 54

E &as gluconate9actetate)

-rystalloid solutions containing isotonic concentrations of %a# do not remain in the '( following i.v. administration. 0he (olume of ;istribution &(d) of these fluids is 7-F and thus they only

provide a short term expansion of the -(. Approximately three times the volume of estimated blood loss must be given to maintain -(. ,n severe blood loss, massive doses of crystalloid for resuscitation &together with blood) have been implicated in the formation of pulmonary and generalised tissue oedema due to the large volumes required for resuscitation. Although this has not been substantiated in clinical trials, many anaesthetists employ colloid containing solutions for resuscitation as lower volumes are required.
!olloids

Also known as Aplasma expandersA, these solutions contain high molecular weight substances such as dextrans, gelatins and starch which exert oncotic pressure and thus retain fluid in the circulating volume as stated above. ,n addition, naturally occurring colloid solutions such as !2 albumin and plasma protein fraction &''F) can be used but they are expensive and have no advantages over the other synthetic colloid solutions &0able 5).
Table 7 !ommonly used colloid solutions

!ontent of !olloid solutions

From Aveling (1992) -ost & GG0) K50 platelet

%ame

Avge. */

*/ range

t 96 in '(

7ffect on coagulation

''F

3G,000

3G,000

60 days

none ;ecreased

;extran 70

$4,000

0:6!0,000

6 hr.

aggregation, reduced K5 Factor (,,,

=aemaccel >elofusinE

65,!00 66,300

!:!0,000 0: !0,000

6.! hr. 5 hr.

none none Mes, if N than ml.kg: !

K5 K$.!0

=espan

70,000

0,000 to 0L3

6! hr.

K !

E -ontains no "# or -a##

Intraoperative fluids

%ot all patients undergoing surgery need intravenous fluid therapy. ,ndeed, intravenous fluid administration is not devoid of risks &air embolism, deep vein thrombosis, overloading, discomfort to the patient, infection risk and considerable cost), so it should not be undertaken lightly. 0here are three components to fluid therapy in the surgical patient. Firstly, as it is customary to deprive patients of fluids for at least 5 hours prior to a surgical procedure under general anaesthesia, there is an element of maintenance fluid deficit. .econdly, depending on

10

the site and severity of the operative procedure, there will be an element of compartmental fluid shift due to tissue trauma &the so:called Athird space lossA). 0hirdly, there will be the additional losses of blood and other fluids such as excessive urine output, ascites and fluid collections in the peritoneal or pleural cavities.
4aintenance fluid

0he average daily requirements stated above correspond to the normal physiological losses &70 kg patient) through the urine & .! l), faeces & 00:600 ml), perspiration &$00:!00 ml) and respiration &!00 ml). ,t is not necessary to replace this loss intravenously for many minor procedures where the preoperative period of fluid deprivation has been short and it is expected that oral fluids can be commenced within hours of the procedureAs termination. ,f maintenance fluids are required then the aim should be to replace the preoperative deficit and then provide the requirements on an hourly basis until oral fluids are tolerated. <n a 65 hour basis, 52 glucose 0. 42 %a-l provides a suitable solution as 6!00 ml &for a 70kg patient) provides 7! mmol. %a#. <n an hourly basis this equates to 00 ml. 500 ml. will compensate for the preoperative deficit and then 00 ml. thereafter &see formula above). Addition of "# is not required for short term &less than 54 hours) therapy.
?nphysiological losses

0hese may arise from surgical drains, nasogastric tubes or vomiting, diarrhoea, excessive body temperature and excessive urinary output due to diuretic drugs. @osses arising from nasogastric tubes, drains and urine output can be accurately measured whilst losses due to high body or ambient temperatures can only be roughly estimated. 0he measurable losses must always be replaced as accurately as possible in volume, %a# and "# content8 note that diarrhoea has a high "# content &60:!0 mmol: ) and vomit has a high chloride content &40: 00 mmol: ). 'atients on thiaBide diuretics or frusemide may lose !0:70 mmol of "# per litre of urine. 7levation of body temperature is reasonably compensated for by an increase in the normal water, %a# and "# intake of !2 for each degree - above the normal $7.
Third space losses

0his only becomes relevant during ma+or surgery &or trauma) where there is extensive tissue damage, e.g. ma+or abdominal and thoracic surgery. -ellular damage results in an inability to maintain the %a#9"# pump, so %a# and water leak into the cells which become swollen and oedematous. 0he ma+or loss of fluid, however, is from the '( into a non:exchangeable compartment of the ,.F &the so:called Athird spaceA). 0his is due to alterations in the oncotic9osmotic balance between the '( and ,.F, again as a result of tissue damage. ,n extensive surgery these losses can be considerable, although estimates which have been made of !ml.kg: hr: are now thought too high. A more reasonable figure is !: 0 ml.kg: hr: , nevertheless, this may represent a five fold increase over basic maintenance requirements. 0his loss of functional extracellular fluid volume &F7-(), if not replaced in adequate quantities, leads to further activation of A;= and aldosterone secretion as well as inhibition of atrial natriuretic peptide &A%'). ,t is not surprising that there is marked water and sodium retention with oliguria in the post operative period. 0his fluid should be replaced with adequate quantities of a 1.. such as DingerAs lactate.
1lood loss

11

*aintenance of adequate oxygen delivery &;<6) should be the primary aim rather than simply considering blood replacement. ;<6 F -ardiac output &l.min: ) E Arterial oxygen content &Arterial oxygen content F .a<69 00 E =b &g.l: ) E .$5), ignoring the small amount dissolved in the plasma. Although the latter is not numerically important, it does form the all important interface between oxygen bound to haemoglobin and cells which require it.) 0hus, at a normal cardiac output of ! lpm, oxygen saturation of GG2 and =b of 5! g.l: 8 ;<6 F ! E &.GG E 5! E .$5) F 000 ml.min: ,n considering when blood loss should be replaced, it is pertinent to consider that a !02 fall in =b can be compensated by a doubling of cardiac output, provided circulating volume is maintained. ,n addition, although similar big swings in .a<6 are rarely observed, a !2 reduction to 4!2 is not uncommon in the postoperative period and would have the same effect as the loss of to 6 units blood. ,t is therefore important to maintain &or increase) cardiac output and oxygenation, as a priority, in patients experiencing blood loss. <nly when blood loss is likely to result in a fall in =b to below 40g.l: , or when there are limitations on the ability of the patient to increase cardiac output should it be replaced. Although blood may not be required until 602 or more of the blood volume is lost &in a healthy patient) it is obviously necessary to replace the fluid component so that preload and thus cardiac output can be maintained. 'lease also note that 000 ml.min: of oxygen can only be delivered to the tissues if a similar amount is being delivered to the alveoli. 0his is normally achieved by an alveolar ventilation of ! l.min: and an oxygen concentration of 6 2. ,f oxygen demand is increased then more oxygen will have to be delivered to the alveoli. 0his can be achieved by increased ventilation, increased oxygen concentration &<6 supplementation) or a combination of the two. Three 2pecial Problems
;ehydration

0his is a common situation meaning depletion of water, nearly always accompanied by %a# depletion. -linically, the symptoms and signs are8 0hirst, dry mucosae, loss of elasticity of the skin, fall in urine output, collapsed veins, cold extremities and tachycardia. 0his is a common situation in the postoperative patient after ma+or surgery. ,t is usually due to inadequate quantities of isotonic %a# containing fluids being given to compensate for continuing Athird spaceA losses. 0he important findings are8
a low urine output of O 0.! ml.kg: per hour in the adult low plasma %a# &e.g. 6! to $0 mmol.l: ) high urine osmolality &N 300 or at least 68 urine9plasma osmolality ratio) low urinary %a# &less than 60 mmol.l: ) due to %a# retention as a result of continuing Athird spaceA

12

loss

a low central venous pressure &-(') the =b concentration may be relatively normal due to haemoconcentration

;o not give diuretics in this situation &unless the patient is on regular diuretic therapy) as it will only exacerbate the hypovolaemia. %ormal saline or DingerAs @actate should be used for initial replacement. 1egin with a 0 : 60 ml.kg: bolus over ! minutes and follow this with a rate of 0 ml.kg: per hour monitoring the signs listed above at hourly intervals. Deduce to maintenance levels when the above signs are reversed. 52 glucose 0. 42 %a-l may be used in addition if the blood %a# concentration is higher than 50 mmol.l:
Potassium depletion

-hronic depletion is commonly seen in the ageing hospital population who have been chronically treated with diuretics for hypertension or cardiac failure. 'lasma "# starts to fall below the normal minimum of $.! mmol l: only after 02 of total body "# has been lost &500 mmol). A good additional indicator of depletion is a high plasma bicarbonate value &N64 mmol l: ), associated with acid urine. ;epletion of 500:300 mmol causes intracellular acidosis as hydrogen ions enter the cells to maintain ionic equilibrium. @osses should be replaced over several days with oral supplements, and the underlying cause corrected. ,f the patient is unable to take oral supplements "# must be given intravenously. ,t is administered as "-l, and concentrations of more than 60 mmol l: in %ormal saline or !2 glucose cause pain and thrombosis in peripheral veins. Dapid replacement is rarely advisable. ,f absolutely necessary, it is given through a -(' line &preferably in the =igh ;ependency or ,ntensive -are ?nit, with continuous 7-> monitoring and frequent plasma "# measurements.
6ater into&ication

0his rarely occurs, but has dramatic consequences due to hyponatraemia. 0he cause is usually iatrogenic. <ther causes include compulsive water drinking, transurethral resection of the prostate with excessive absorption of glycine irrigation fluid, inappropriate secretion of A;= and a few rare medical disorders. <ver prescription of intravenous !2 glucose and 52 glucose 0. 42 %a-l solutions is the main iatrogenic cause. 0his was a not infrequent in labour wards. A fall in plasma %a#, as stated above, leads to a movement of water from the hypotonic '( into the ,.F and ,-F to maintain osmotic equilibrium. 0his expansion of ,-F can lead to cerebral oedema, mental disturbances and convulsions if plasma %a# falls rapidly. Frusemide &0.! mg kg: ) followed by 0.G2 or .42 %a-l intravenously is an effective treatment of this emergencyP a urinary catheter is needed. 0he speed of correction must be tailored to the speed on onset, chronic changes being corrected slowly.

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