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 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


. An opposite effect is seen with a rise in '( %a#. of water has distributed according to the relative volumes of the 7-F and . but in an adult would be 86) and there is an expansion in .! kg infant has 01/ equal to 402 of body weight with the ratio of 7-F to . and an increase in 7-F &and '() %a# up to $$. 0he net result is that the 00 ml. ..-F and vice versa.l: .F.-F is8 . An infusion of 00 ml. 0here is osmotic dysequilibrium that cannot be sustained. 0he overall osmolality of the 7-F &'( and then . /ater will move from '( to . 0hus.. 0his results in an expansion of the .n other words a fall in plasma %a# always results in an increase in . %&ample 0his movement can be seen most clearly in the following Figure 'igure 1# %ffect of addition of 1(( ml# )ater on the relative volumes of %!' and I!' and changes in osmolality *see te&t+ 2 .F in an attempt to equalise the osmotic pressures &osmolality) in the two compartments..F osmolality leads to further movement of water into the . of !2 glucose in water is given over a short period.l: ) 0hus.Table 1 The major osmotic constituents of plasma !ation/"nion !oncentration in mmol#l$1 %a# $! "# ! -l: 0 =-<$: 65 >lucose ! ?rea ! 0<0A@ 645 &mosm. overall osmolality of both compartments is 640 with an 7-F &and '() %a# of 50 mmol..-F of !0 ml.-F &in this case equally. A normal 6.F) is reduced by dilution to 6!5 and the %a# falls to 67. a fall in plasma %a# results in fall in '( osmolality in comparison to that in the .-F. 0he resulting overall fall in .-F by !0 ml. /ater moves from the 7-F to .-F to reestablish osmotic equilibrium.

... is the hydrostatic pressure in the ..per unit pressure gradient in k'a or mm =g. the three compartments are not in a passive state.4 atm or ! 00 mm=g.F. is the oncotic pressure in the .. is the hydrostatic pressure in the capillaries in k'a or mm =g.l: ) divided by the molecular weight. . &%.F in k'a or mm =g.. 0he oncotic pressure gradient between the two compartments that is manifest as solvent drag from . <' pl.F in k'a or mm =g. Albumin also exists in the . is the oncotic pressure in the plasma in k'a or mm =g. 0his hydrostatic pressure is balanced by the presence of colloids in the '(. over two thirds of the bodyAs albumin is in the . <' in. the former is equalised throughout the three main compartments &. 0hus. 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 '().F..ydrostatic and colloid osmotic *oncotic+ balance <bviously. 3 . . the total osmotic pressure of the crystalloid component of the '( is 340 k'a &3.P in+ $ s *OP pl $ OP in+ /here8 • • • • • • • CF is the net outward flow of fluid from the capillaries into the .-F.n man. 0he oncotic pressure of a plasma constituent is proportional to the amount &in g.F to '( is around .. -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.l: ) with a */ of 30.F albumin is mainly in a semisolid gel form.! k'a &60:6! mm =g). 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. At the same time.000 constitutes the most important component of plasma oncotic pressure &$ k'a or 60:6! mm=g).! to 6 k'a & 0: !mm =g).f it is impermeable. &almost entirely due to albumin). K*. hydrostatic pressure and oncotic pressure have been summarised in . due not only to the fact that it is bound to cells.tarlingAs equation which states that8 -' . " is a constant that expresses the flow of fluid outwards in mls. =igh molecular protein constituents of plasma exert Acolloid osmoticA or AoncoticA pressure.P pl $ . 0he reflection coefficient is a measure of the permeability of the capillary to albumin. 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 .. plasma albumin &50 g. 0he effects of these two opposing forces.F. =owever... see later) whilst the colloid oncotic component is only $ to $. 0his oncotic pressure gradient is responsible for maintaining the integrity of the '(. .F and '() whilst the latter is greater in the '( versus the . =' in.F) s is the reflection coefficient of the capillary bed in question. A semi:permeable membrane &the capillary endothelium) represents the barrier between the '( and the . but also that .1..F but its effective concentration is markedly reduced. =' pl.F and eventual depletion of the -(.

input and output and passive and active movements between compartments as controlled by the processes alluded to above. and fluid leaks out entirely as expressed by the hydrostatic pressure gradient. then no gradient exists.f. plasma electrolytes represent a dynamic interchange between total body stores. 0hus. Figure 6 shows the effect of the . . 'lease note that as fluid leaves the circulation at the arteriolar end.ydrostatic and colloid oncotic pressure gradients in the capillaries# 4 . the pressure gradients have been reversed and fluid reenters the circulation again. by the time we reach the venular end. on the other hand.F is experienced. . A fall in the oncotic pressure gradient. the hydrostatic pressure gradient gradually diminishes in the capillaries and the oncotic pressure gradient gradually increases. due to loss of albumin or a reduction in the reflection coefficient due to capillary endothelial damage &vide infra). <verall.n practice.7 &lung). s will be . causes a loss of '( and an increased propensity to the development of significant tissue and pulmonary oedema..then the full oncotic pressure gradient between plasma and . 'igure / . the capillary is completely permeable to albumin.tarling 7quation and the typical overall pressures in the capillaries and venules and the fluid shifts which occur. 0his would result in a s of 0. depending on the capillary bed in question the range is about 0 &liver) to 0.

. but in a dynamic process the volumes are not static.A) it consequently needs 6 96 times the maintenance fluid per unit weight. 6!2 in the next two 4 hour periods) calculated from the time of the burn injury. 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. of a 8 000 to 6 ml. • 2eptic shoc0 or systemic inflammatory response syndrome &.! to ml. • 1urn injury causes a systemic Acapillary leakA which is proportional to the percentage of the burned area.D. 0his ensures optimal organ function. 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. of DingerAs @actate per kg. 0he amount of fluid leakage is massive and is equivalent to 5 ml. Additional fluid losses are incurred from evaporation..A9wt ratio of an adult & 960th the weight and 94 th the 1. %a# &depending on intake).000). Fluids and oxygen therapy should be used in addition. 0his has to be replaced to maintain 01/.g. per 2 area burn in 65 hours &'arkland formula). water plus about 70 mmol %a# and "# in a 70 kg adult per day. in a 30 kg patient with a 502 burn this requires 5 E 30 E 50 F G300 ml. !0 to 00 mmol "# and 70 to 50 mmol. boluses of i. adrenaline & mg in 0 ml. adrenaline &0.ince a new born baby of $.m. 3egulation of blood volume . Table / 4aintenance fluid re5uirements 5 . 0. 7.! to solution) or in a patient with i.A) than weight. 0he total loss of fluid is about 6!00 ml. has about 6 96 times the 1.g.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.!onditions causing an increase in capillary endothelial permeability *!%P+ 0hree common conditions cause an increase in -7'8 • "naphylactic shoc0 &e. respiratory tract and faeces. or 8 0. 0he extent of maintenance fluid requirements is more closely related to body surface area &1. !02 given in the first 4 hours. mg i. access.v.! kg. A common formula used is shown in 0able 6. despite the inevitable oedema that this causes.) also leads to loss of -( and this fluid must be replaced in large quantities to maintain -(.e.v.

. All these changes are increased by activation of the sympathetic nervous system &. # 60 ml. and results in increased . limiting the ability of the kidney to produce dilute urine.). these processes are amplified. discharge. !2 glucose and 52 glucose 0. vomiting. A decrease in renal perfusion &due to fluid deprivation) increases renin output from the +uxtaglomerular apparatus leads to the formation of angiotensin . constricts the efferent glomerular artery to maintain glomerular arterial pressure and filtration and also causes release of aldosterone from the adrenal cortex. a 8 0g# infant )ould re5uire 8(( mls# per day 18 0g child )ould re5uire 1((( + 9:( . "cute changes in homeostasis Acute surgical or traumatic hypovolaemia cannot be compensated for by the more chronic processes mentioned above. Acute reduction in -( reduces venous return and cardiac preload so cardiac output and blood pressure &1') fall. ileus or haemorrhage. /:(( ml# per day %ormally this fluid requirement is regulated both by changes in volume and osmolality in the '( being detected in the hypothalamus. Additional mechanisms are brought into play. As plasma %a# concentration falls. .= over for any additional 000 ml. 0his causes thirst. for wt. over 0 kg !00 ml. over 60 kg.f fluid deprivation becomes greater or there are abnormal losses such as diarrhoea.. Deduction in 1' reduces the afferent activity of the carotid sinus baroreceptors to the ApressorA area in the dorsal hypothalamus.6eight range $ : 0 kg 0 : 60 kg 60 kg and above 0hus8 'luids per /7 hours 00 ml.%.%. 42 saline should never be given if the plasma %a# is low. An increase &due to fluid deprivation) stimulates anti: diuretic hormone &A. 0his is due to the more powerful effect of A.t is important to note that volume is usually maintained at the expense of a reduction in osmolality due to hyponatraemia. 0he latter increases renal %a# retention in exchange for "# in the distal tubule. for first 60 kg. . # !0 ml.G2 sodium chloride or DingerAs @actate &=artmannAs) is more appropriate. &A0 . Administration of hyponatraemic solutions in the postoperative period in the presence of a low serum %a# further compounds the problem.=) 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. proximal tubular reabsorption of %a# &and water) becomes intense.). for first 0 kg. 19:( ml# per day a 8( 0g# adult )ould re5uire 1:(( + 1((( . 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 6 .

.ympathetic stimulation.) tone. colloids and blood &and blood products). i.. 42 saline. =ow do we make an isotonic solutionI From first principles.baroreceptors in the atria and great veins to the AdepressorA centre. . the latter being the ma+or site of %a# and water reabsorption 0he . thus allowing fluid to enter the capillary circulation distal to the '-. 0his means that they contain the same number of osmotically active particles as plasma.ecreased Na+ loss due to a reduction in atrial natriuretic peptide <ascular redistribution of blood in the 0idney from cortex to medulla. 0his results in a reduction of flow to the capillary beds by neuro:humorally mediated increase in the pre:capillary sphincter &'-. Fluids can be conveniently classified into crystalloids. as a result of the change in hydrostatic9oncotic pressure gradient &see . it is pertinent to consider the types of fluids that are available and their uses.e. !atecholamine release from the adrenal medulla . Intravenous perioperative fluid replacement therapy . noradrenaline or adrenaline predominates.G2) saline and DingerAs lactate &=artmannAs) H see table $). 0he resultant fall in parasympathetic nervous system &'%.nitially. Increased Na+ reabsorption in the distal tubule . particularly to the skin and splanchnic circulation. 0he hydrostatic pressure in the capillary beds falls.) discharge augments the action of the . if gram molecular weight of solute is placed 7 . 3enin release from the +uxtaglomerular apparatus of the kidney &vide infra).everal solutions are available.n different shock states.tarlingAs equation above). !2 glucose.%. %ormal &0. !rystalloids 0hese are solutions containing water and electrolytes and9or glucose made up in a concentration that is usually isotonic with plasma. and at different stages of shock.. results in a reduction of flow to these nonessential areas. 52 glucose 0. . about $00 &range 640 to $ 0) mosmol.F compartment has an important role in maintaining circulating volume. by alpha adrenergically mediated arteriolar vasoconstriction.irect neural effects via alpha and beta receptors.l: of solute. The effects of this are summarised as follo)s • • • • • • .

the irrigation fluid traditionally used during 0?D'.w.!2.e. 0he latter occurs in the TURP syndrome..e. of -l:. .F and . 0hus.G g. -a 6. 0he concentration of ethanol thus reflecting the extent of absorption.f this occurs acutely. or 000 mmols. .l: . 0his amount is referred to as osmol or 000 mosmol. of glucose) in a kg.e.5 atmospheres &6!50 k'a or G$50 mm =g) at $7 deg -. -l 0!.!. hypertonicJ .l: . 0hus. 8 .G2) saline is hardly physiological as it contains excess %a# & !0 vs $!) and excess -l: & !0 vs 0!). of solvent &i. /ith an electrolyte such as sodium chloride.l: . %a# $0. this molar solution of 42 glucose & 40g per litre or 4 g per 00 ml) is hypertonic & 000 versus $00 mosmol. 40g of glucose mol. . as in excess absorption of non: sodium containing irrigation fluid during transurethral resection of prostate &0?D'). a molar solution will exert an osmotic pressure of 66. of %a# and !0 mmol. so !0g &!2 solution of glucose) will produce an isotonic solution of !0 times !. 0hus . of water will have glucose is dissolved in 66. 00 ml: or 0. ideally. the ethanol component will be detectable in the breath &cf a AbreathalyBerA).l: . thus in total the osmotic pressure of plasma is equal to $00 E 6.l: is required. . results in water leaving the '( into the . 0 deg -) it will exert an osmotic pressure of one atmosphere & 00 k'a or 730 mm =g). . a AbalancedA salt solution &1.l: . if one mole of & 40 F the m.G2 saline) with !0 mmol. it should be noted that glycine .l: from glucose making 640 in all. a 2 solution) will increase osmolality by 6 7 thus making the total osmolality of the irrigating solution 5 7 i. ethanol & 2) is usually added as a marker. 0his contains in mmol. 0he addition of ethanol 2 to the . 52 glucose and 0.-F of 9$0th & 09$00) of total plasma osmotic pressure or about G0 mm =g & 9$0th of !G00).l: . Gg per litre &0. 0he */ of ethanol is 53. should it occur rapidly.t is worth noting that a fall in serum %a# of ! mmol. roughly 93th.f a significant amount of irrigation fluid is absorbed. "#$. so 7! g dissolved in a kg. =owever. 0he molecular weight of glycine is 7!. a litre of water) would be a molar solution and would contain 000 mosmol.! or 67! mosmol.l: ). thus 0 g per litre &i.t can be seen that normal &0.! g of sodium chloride) will contain nearly 6000 mosmol. 7xcess -l: administration can result in retention of =# and urinary loss of =-<$: and a dilutional acidosis if administered in excess.uch a solution is DingerAs lactate &also called =artmannAs solution)..thus generates an osmotic pressure of 6.! F 7!0 k'a &!700 mm=g). 0o aid detection of excess absorption of a flask containing kg.) should be used. . cerebral oedema and raised intracranial pressure may occur.n a similar manner.e.! mosmol. 42 %a-l will give $0 mosmol. . 0hus. 1y definition. l: ) has an osmolality of 600 mosmol.e. .5 atmospheres &6600 k'a or !600 mm =g) at %0' or 6!.F and then into the . i.ince this combined solution is now commonly used it may account for the diminished incidence of 0?D' syndrome.-F in an attempt to restore osmotic balance between the fluid compartments. litre of water) it will form a molar solution. 7ach g per litre therefore gives about !.! k'a & G mm=g).!2 glycine affects its osmolality. the molar solution &!4. of both %a# and -l: per litre plus 660 mosmol. 0hus.!2 glycine &or ! g. l: as in solution it is almost completely dissociated into sodium and chloride ions. is hypotonic. 0he latter is a =# acceptor and is metabolised by the liver with net formation of one molecule of =-<$: and one molecule of pyruvate which can be utilised as an energy source in the "rebs cycle. of !4. <ne mosmol at $7 deg . of solvent &i. 0hus. @actate 6G.l: &accompanied by a change in -l: of the same amount) will result in a pressure dysequilibrium between the '(..t does not cause a dilutional or lactic acidosis provided that liver perfusion is adequate.!g. 0his large pressure difference.5 litres of solution at %0' &i.

n the same way. . As the glucose is metabolised &the glucose concentration in !2 glucose is about 67! mmol. Table 9 !ontent of !rystalloid solutions !ontent of crystalloid solutions Name %a-l 0.l: whilst in plasma it is !). =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. 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#. 42 .aline !5 DingerAs @actate =artmannAs $ >lucose !2 !2 dextrose $0 G7 ! 50E 000 000 amounts in mmol.G2 Kno)n as %ormal .istribution &(d) of these fluids is 7-F and thus they only 9 .n chronic hyponatraemia. 0hus.extrose saline $0 'lasmalyte 54 # glucose .0hus. there is time to restore osmotic equilibrium without ma+or pressure differences occurring between compartments.l: 6!6 643 !!6 6000 !5 ! 6 6G 640 Na+ !l$ K+ !a== 4g++ . as in patients on diuretic therapy. absorption of irrigation solution will increase overall osmotic pressure in the '( but still result in a fall in plasma %a#. 0hus. it is much easier to raise %a# concentrations rapidly than to cause a fall. 7lectrolyte concentrations of commonly used crystalloid solutions are shown in the 0able $.v. the osmotic pressure in the plasma will fall and water will go into the cells. 0he (olume of .odium 1icarbonate 4. infusion of !2 glucose will cause a fall in plasma %a# due to a dilutional effect but osmotic pressure will remain the same as the solution is isotonic.52 'lasmalyte 54 E &as gluconate9actetate) -rystalloid solutions containing isotonic concentrations of %a# do not remain in the '( following i. although non:sodium containing isotonic solutions will eventually result in increased cellular water they do not do so rapidly enough in most circumstances to cause problems of dysequilibrium between the body compartments. . 0he commonest cause of excess hypertonic %a# adminstration is the use of %a#=-<$: solutions &see 0able $).n fact. 0he effect on cellular overhydration will depend on the rate of administration of !2 glucose.!O9$ >actate$ mosmol#l$1 $04 >lucose 52 # %a-l 0. administration.

kg: ! K5 K$.econdly. !olloids Also known as Aplasma expandersA.. .ndeed.n severe blood loss. K ! E -ontains no "# or -a## Intraoperative fluids %ot all patients undergoing surgery need intravenous fluid therapy.000 6 hr. reduced K5 Factor (.000 6.300 !:!0.000 to 0L3 6! hr. discomfort to the patient.! hr. =aemaccel >elofusinE 65.000 0: !0. depending on 10 . these solutions contain high molecular weight substances such as dextrans. if N than ml. */ */ range t 96 in '( 7ffect on coagulation ''F 3G. Although this has not been substantiated in clinical trials.!00 66.000 60 days none . none none Mes.. Table 7 !ommonly used colloid solutions !ontent of !olloid solutions From Aveling (1992) -ost & GG0) K50 platelet %ame Avge. 0here are three components to fluid therapy in the surgical patient. .n addition. so it should not be undertaken lightly. gelatins and starch which exert oncotic pressure and thus retain fluid in the circulating volume as stated above. there is an element of maintenance fluid deficit. 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.provide a short term expansion of the -(.ecreased .!0 =espan 70.000 0. intravenous fluid administration is not devoid of risks &air embolism. Approximately three times the volume of estimated blood loss must be given to maintain -(. . . 5 hr. overloading. aggregation.extran 70 $4. as it is customary to deprive patients of fluids for at least 5 hours prior to a surgical procedure under general anaesthesia.000 0:6!0. infection risk and considerable cost). Firstly. deep vein thrombosis.000 3G. 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). many anaesthetists employ colloid containing solutions for resuscitation as lower volumes are required.

the site and severity of the operative procedure. excessive body temperature and excessive urinary output due to diuretic drugs.= and aldosterone secretion as well as inhibition of atrial natriuretic peptide &A%'). ascites and fluid collections in the peritoneal or pleural cavities. 0his is due to alterations in the oncotic9osmotic balance between the '( and . so %a# and water leak into the cells which become swollen and oedematous. perspiration &$00:!00 ml) and respiration &!00 ml).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. diarrhoea. drains and urine output can be accurately measured whilst losses due to high body or ambient temperatures can only be roughly estimated..above the normal $7. .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. 500 ml. e.F. . there will be the additional losses of blood and other fluids such as excessive urine output. although estimates which have been made of !ml. %a#.. 'atients on thiaBide diuretics or frusemide may lose !0:70 mmol of "# per litre of urine. 4aintenance fluid 0he average daily requirements stated above correspond to the normal physiological losses &70 kg patient) through the urine & .g. 0he ma+or loss of fluid. thereafter &see formula above). nevertheless. again as a result of tissue damage. A more reasonable figure is !: 0 ml. is from the '( into a non:exchangeable compartment of the .kg: hr: . 1lood loss 11 . -ellular damage results in an inability to maintain the %a#9"# pump. faeces & 00:600 ml). . ma+or abdominal and thoracic surgery. this may represent a five fold increase over basic maintenance requirements. such as DingerAs lactate.n extensive surgery these losses can be considerable.! l). %a# and "# content8 note that diarrhoea has a high "# content &60:!0 mmol: ) and vomit has a high chloride content &40: 00 mmol: ). leads to further activation of A. 7levation of body temperature is reasonably compensated for by an increase in the normal water. . Third space losses 0his only becomes relevant during ma+or surgery &or trauma) where there is extensive tissue hr: are now thought too high.t is not surprising that there is marked water and sodium retention with oliguria in the post operative period. 52 glucose 0. 42 %a-l provides a suitable solution as 6!00 ml &for a 70kg patient) provides 7! mmol. @osses arising from nasogastric tubes. will compensate for the preoperative deficit and then 00 ml. <n an hourly basis this equates to 00 ml. 0hirdly. 0he measurable losses must always be replaced as accurately as possible in volume. %a# and "# intake of !2 for each degree . ?nphysiological losses 0hese may arise from surgical drains.. if not replaced in adequate quantities. there will be an element of compartmental fluid shift due to tissue trauma &the so:called Athird space lossA). nasogastric tubes or vomiting. however.F &the so:called Athird spaceA). 0his loss of functional extracellular fluid volume &F7-(). 0his fluid should be replaced with adequate quantities of a 1. <n a 65 hour basis. Addition of "# is not required for short term &less than 54 hours) therapy.

t is therefore important to maintain &or increase) cardiac output and oxygenation. increased oxygen concentration &<6 supplementation) or a combination of the two.l: ) high urine osmolality &N 300 or at least 68 urine9plasma osmolality ratio) low urinary %a# &less than 60 mmol. 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. 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.l: . Three 2pecial Problems . .! ml.g. -linically. it does form the all important interface between oxygen bound to haemoglobin and cells which require it.min: ) E Arterial oxygen content &Arterial oxygen content F .f oxygen demand is increased then more oxygen will have to be delivered to the alveoli.l: ) due to %a# retention as a result of continuing Athird spaceA 12 .t is usually due to inadequate quantities of isotonic %a# containing fluids being given to compensate for continuing Athird spaceA losses. collapsed veins. nearly always accompanied by %a# depletion.ehydration 0his is a common situation meaning depletion of water. provided circulating volume is maintained. <nly when blood loss is likely to result in a fall in =b to below 40g.n considering when blood loss should be replaced.min: and an oxygen concentration of 6 2. Although the latter is not numerically important.*aintenance of adequate oxygen delivery &.<6 F -ardiac output &l. .n addition. 0he important findings are8 • • • • a low urine output of O 0.a<69 00 E =b &g.min: .a<6 are rarely observed.min: of oxygen can only be delivered to the tissues if a similar amount is being delivered to the per hour in the adult low plasma %a# &e. fall in urine output. 0his is normally achieved by an alveolar ventilation of ! l.l: 8 . 0his can be achieved by increased ventilation. the symptoms and signs are8 0hirst.) 0hus. loss of elasticity of the skin. .<6) should be the primary aim rather than simply considering blood replacement. . or when there are limitations on the ability of the patient to increase cardiac output should it be replaced. oxygen saturation of GG2 and =b of 5! g. it is pertinent to consider that a !02 fall in =b can be compensated by a doubling of cardiac output. . ignoring the small amount dissolved in the plasma. 'lease also note that 000 ml. dry mucosae.$5) F 000 ml. although similar big swings in .<6 F ! E &. cold extremities and tachycardia. as a priority. in patients experiencing blood loss.$5).l: ) E . at a normal cardiac output of ! lpm. 6! to $0 mmol. 0his is a common situation in the postoperative patient after ma+or surgery.GG E 5! E .

ntensive -are ?nit.loss • • a low central venous pressure &-(') the =b concentration may be relatively normal due to haemoconcentration .ependency or . A fall in plasma %a#. 'lasma "# starts to fall below the normal minimum of $. and concentrations of more than 60 mmol l: in %ormal saline or !2 glucose cause pain and thrombosis in peripheral veins. associated with acid urine.o not give diuretics in this situation &unless the patient is on regular diuretic therapy) as it will only exacerbate the hypovolaemia.! mmol l: only after 02 of total body "# has been lost &500 mmol). Deduce to maintenance levels when the above signs are reversed. and the underlying cause corrected. @osses should be replaced over several days with oral supplements. . leads to a movement of water from the hypotonic '( into the . . transurethral resection of the prostate with excessive absorption of glycine irrigation fluid.epletion of 500:300 mmol causes intracellular acidosis as hydrogen ions enter the cells to maintain ionic equilibrium. Dapid replacement is rarely advisable. 0he speed of correction must be tailored to the speed on onset. 42 %a-l solutions is the main iatrogenic cause.f absolutely necessary. 0his expansion of .= and a few rare medical disorders. 0he cause is usually bolus over ! minutes and follow this with a rate of 0 ml. inappropriate secretion of A. it is given through a -(' line &preferably in the =igh .kg: per hour monitoring the signs listed above at hourly intervals. mental disturbances and convulsions if plasma %a# falls rapidly. %ormal saline or DingerAs @actate should be used for initial replacement.G2 or . 1egin with a 0 : 60 ml. as stated above. <ver prescription of intravenous !2 glucose and 52 glucose 0.t is administered as "-l. .! mg kg: ) followed by 0. ..42 %a-l intravenously is an effective treatment of this emergencyP a urinary catheter is needed. 13 . 6ater into&ication 0his rarely occurs.f the patient is unable to take oral supplements "# must be given intravenously. A good additional indicator of depletion is a high plasma bicarbonate value &N64 mmol l: ). chronic changes being corrected slowly. 0his was a not infrequent in labour wards.F and . <ther causes include compulsive water drinking.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. 52 glucose 0. Frusemide &0. 42 %a-l may be used in addition if the blood %a# concentration is higher than 50 mmol. with continuous 7-> monitoring and frequent plasma "# measurements.-F to maintain osmotic equilibrium.-F can lead to cerebral oedema. but has dramatic consequences due to hyponatraemia.