chapter 3 fluids and electrolytes asli
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CHAPTER 3
FLUIDS AND ELECTROLYTES
Fluid and electrolyte management in the surgical patient has become increasingly
important over the last several decades. The advance of medical science and improved
surgical techniques have allowed us to operate on higher risk patients; close attention to fluid
balance constitutes a critical aspect ofthe care ofthese patients. This chapter focuses on the
changes in fluid homeostasis and electrolyte balance that occur in the peri- and postoperative
period. We will also review treatment options.
NORMAL FLUID SPACES AND DYNAMICS
In critically ill patients the alteration in fluid balance is a d!"namic process
characteri#ed by ma$or hemodl"namic changes and fluid shifts between body compartments.
The e%tent of these changes is a function of the severity of the underlying disease process.
&lose monitoring of these fluid shifts helps the clinician to gauge the clinical course of the
patient. 'nowledge of the normal fluid distribution of the body is necessary to understand
these changes. In a normal human appro%imately ())*o of the total body weight is water
+e.g., in a /)-kg man and slightly less in women0. 1ppro%imately fivo thirds of this fluid
resides inside cells and is called intracellular fluid +l&F0. The remaining one third of the
water the e%tracellular fluid +2&F0 is outside the cells. The 2&F is further separated into two
compartments; the vascular compartment +plasma fluid0 constitutes appro%imately one third
of the 2&F and the fluid present between cells +interstitial fluid0 constitutes appro%irrrately
two thirds of the 2&F. Within the vascular compartment +e.g. ,.( in the /)-kg man0
appro%imately 34olo of the fluid resides in the venous side of the circulation and l4o*o in the
arterial side. 1 number of forces govern the movement of fluid befiveen and the relative
volumes of the interstitial space and the vascular compartment. In the capillaries a balance
of forces e%ists between hydrostatic and oncotic pressure. This concept is e%pressed
mathematically by the 5tarling equation6
7f6 'f % +8v- 8t0 - ( % +&98 - T980
where 7f is fluid flu% 'f is capillary filtration coefficient 8v is vascular hydrostatic
pressure 8t is interstitial hydrostatic pressure ( is a reflection toefficient +which defines the
effectiveness of the membrane in preventing solute flow0 &98 is colloid osmotic pressure
and T98 is tissue osmotic pressure +!0. Fluid leaves the capillary at the arterial end because
hydlbstatic pressure e%ceeds oncotic pressure. 1s blood continues to flow down the capillary
hydrostatic pressure falls and oncotic pressure increases as a result of increasing protein
concentration. When the oncotic pressure e%ceeds the hydrostatic pressure-in the venous end
of the capillary-fluid returns from the interstitium to the capillary. 5ome of the fluid that is
not returned to the venous end of the capillaries by virtue of the 5tarling forces is eventually
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returned to the vascular compartment by lymphatic drainage. :nder some circumstances
li.rnphatic flow can be massive. For e%ample in cirrhotic patients hepatic fibrosis leads to
high capillary hydrostatic pressures which in con$unction with low capillary oncotic
pressures due to hypoalbuminemia cause a 9-fold increase in daily lymphatic flow +from I
to ) ld0 +0. 5erum albumin is the ma$or determinant of capillary &98 andhypoalbuminemia can lead to e%cess transudation of fluid from the vascular to the interstitial
compartment. 1s discussed later this is one of the more important factors contributing to the
development of interstitial edema and e%pansion of 2&F volume in the surgical patient.
POSTOPERATIVE CHANGES IN BODY FLUID COMPARTMENTS
1 number of perioperative events contribute to 2&F volume e%pansion. These
nonspecific events also occur with many other pathologic conditions such as sepsis e%tensive
burns multiple trauma pancreatitis bone marrow transplants and so on. 1 ma$or stimulus to
2&F e%pansion is a reduced intravascular volume. First hemorrhage may directly reduce
blood volume. 5econd a generali#ed increase in capillary permeability occurs in many
patients especially after ma$or abdominal and chest surgery. This results from a loss of
endothelial integrity and the opening of intercellular clefts. The mediators that cause
increased capillary permeability are probably identical to those responsible for some elements
of the inflammatory response. These include but may not be limited to cytokines
+interleukin l interleukin ( tumor necrosis factor0 integrins thrombin bradykinin and
platelet-activating factor +!0. 1s a result of increased capillary permeability protein-rich fluid
escapes from the vascular compartment and e%pands the interstitial fluid. Third negative
interstitial fluid hydrostatic pressure may develop and increase the intravascular to interstitial
pressure gradient generating interstitial edema +0. The above alterations lead to reducedcardiac output and decreased effective blood volume. The sensors for effective blood volume
are in the intra-arterial side of the intravascular compartment. In response to these signals
volume is regulated by modulation of renal sodium and water reabsorption. 1 decrease in
cardiac output increase in peripheral arterial vasodilation or any combination thereof leads
to arterial underfilling and thereby initiates and sustains a sodium- and water-retaining state
+,0. Failure to maintain adequate intravascular volume leads to systemic hypoperfusion
decreased o%ygen delivery lactic acidosis and ultimately tissue death. Therefore it is
imperative to replace intravascular volume with appropriateamounts of colloid and
crystalloid. The aim is to maintain a systolic blood pressure above !)) mm
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their underlying illness the @capillary leak@ resolves. 1lthough substances that counteract the
proinflammatory mediators could theoretically attenuate this pathologic state none have
proved to be effective. 1s long as clinical parameters suggest low effective intravascular
volume the best approach is the $udicious administration of balanced electrolyte solutions
and colloid to e%pand this compartment. 1cceptable cardiac output and tissue perfusionremain the paramount concerns even at the price of a marked increase in 2&F and total body
weight. In the severely anemic or bleeding patient blood transfusions are used to e%pand
intravascular volume and improve tissue o%ygen delivery. To optimi#e intravascular volume
replacement pulmonary arterial pressure monitoring can be accomplished through a 5wan-
>an# catheter which measures pulmonary capillary wedge pressure and cardiac output. 1
pulmonary capillary wedge pressure of !( to !3 mm
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Table .! depicts the electrolyte composition and osmolality of various intravenous solutions.
1lthough it is tempting to use diuretics during the early phase ofresuscitation ofoliguric
critically ill patients oliguria in this early phase may be appropriate and may simply reflectdecreased intravascular volume and cardiac output. In that case diuretics are contraindicated
because they could further reduce circulatoryvolume peripheral perfusion and thereby
contribute to the development of lactic acidosis and acute renal failure. Biuretics are
appropriate when cardiogenic pulmonaryedema develops following aggressive fluid
resuscitation or when progressive 1AB5 occurs. 1lso during the ecovery phase a large
amount of interstitial fluid may reenter the intravascular compartment leading to pulmonary
edema. Biuretics may then be required.
>enerally loop diuretics are selected because they are most potent. oop diuretics
have several important beneficial effects6 +i0 they inhibit active sodium absorption in the thick
ascending limb of
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There is also a strong tendenry by some clinicians to use low-dose dopamine therapy
to try to prevent postoperative acute renal failure.
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Hyponatrema
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perfusion is likely to retain hypotonic intravenous fluids and thereby develop hyponatremia.
Women in their reproductive years seem to be unusually susceptible to the neurologic
complications of hyponatremia. 1s little as of intravenous water over ( hours can lead to
devastating symptoms of hyponatremia severe neurologic morbidity and death +!!,0.
1lthough the e%act mechanism responsible for this unusual syndrome has not been fullyelucidated the administration of hypotonic fluid perioperatively has clearly played a ma$or
role. In high-risk patients only isotonic fluids should be used and the serum sodium should
be evaluated frequently.
1nother important often overlooked hyponatremic syndrome occurs in patients
undergoing a transurethral prostateresection +!40. Buring this procedure the prostatic bed
isirrigated with large volumes of hlpotonic glycine-containingsolutions. 1bsorption ofthis
fluid into theintravascular spacecan generate hyponatremia whereas the plasma
osmolalitymay only be reduced slightly +as a result of the glycine0.When the s!"ndrome is
severe these men become hypertensiveconfused dyspneic and nauseated.
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Inappropriate lack of thirst or no access to water. 2%cessive water loss or salt intake
may contribute as well. The2&F volume status of hlpernatremic patients is high whenthey
have e%cess total body solute; normal when total bodysolutes are normal but water isinadequate or low whentotal body solutes are low and water is reduced even more.For
e%ample %cessive sweating and large evaporative lossesfrom the skin and lungs especially
with fever or high environmentaltemperatures may cause a disproportionate lossof water
compared with the loss of salt from the body. Thiscan generate severe h0ernatremia. In such
instances bothsolute and water are depleted but water loss e%ceeds soluteloss. Initial therapy
with isotonic saline is usually indicatedto restore normal intravascular volume before
addressing thefree water deficit.5imilarly when diarrhea is induced by osmotic catharticssuch
as lactulose sorbitol or by carbohydrate malabsorptionlarge quantities ofh;potonic fluid will
be lost in the stool and can cause severe h!!Jernatremia.
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water deficit 6 total body water % +l - !,) K serum sodium0
:sually the rate of correction of hypernatremia should not e%ceed ! m=+ld +!/0.
The aim should be to correct appro%imately half the deficit over the first , hours. Toorapid a
orrection of hypernatremia may lead to cerebraledema and sei#ures.
Hypo!a"ema
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inflammatory drugs and ryclosporine are otherconditions and drugs that reduce renal
potassium e%cretion.5everal circumstances may cause a shift of potassiumout of cells into the
2&F compartment. The cells maybe damaged or destroyed with hemolysis or
rhabdomyolysisfor e%ample.
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Gost of the body"s calcium is contained within the bone matri%; appro%imately ).!L
of body calcium is in the 2&F.?ormally the serum calcium concentration is maintainedat a
level between E.) and !)., mg*dl or .4 and.( mmoll. &alcium in the ierum is found in
three forms6appro%imately ,)o*o is protein bound !))*o is comple%ed to phosphate and other
anions and 4)o*o e%ists in the ioni#edform. ?ormally the concentration of ioni#ed calcium is remarkably constant despite marked
variations in the levelof total calcium concentration. 1 fall in serum albumin ofI g d usually
is associated with a ).3 mg*dl fall in totalcalcium concentration yet the ioni#ed calcium may
remainnormal. 1lterations in systemic p< will affect albuminbinding of calcium. Getabolic
acidosis decreases proteinbinding and increases the ioni#ed calcium concentrationwhereas
metabolic alkalosis has the opposite effect. Birectmeasurement of the ioni#ed calcium can be
done with specialelectrodes and is often helpful.9f clinical importance hypocalcemia may be
defined asa reduction in the ioni#ed component of serum calcium.8atients with
hypoalbuminemia and a low total serumcalcium concentration may or may not have a
reductionin ioni#ed calcium. &onsequently the clinical presentationof the patient with
hypocalcemia is crucial when decidingwhether therapy is indicated.The principal clinical
manifestations of hypocalcemiaare neurologic and include in order of increasing
severity6perioral paresthesias carpal pedal spasm tetany andgenerali#ed sei#ures. &hvostek
sign +twitching of the corner of the mouth produced by tapping over the facial nerve0
andTrousseau sign +spasm ofthe fingers produced by inflatinga blood pressure cuff above
systolic0 are also manifestationsof neuromuscular irritability. lectrocardiographic
changesinclude prolonged corrected 7T and 5T intervals and peakedT waves. Aarely heart
block may develop.8erioperative hypocalcemia may be the result of hypomagnesemiaacute
renal failure septic shock rhabdomyolysisor acute pancreatitis.
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thatcontain sodium citrate a bicarbonate precursor.The kidneys have an enormous capacity to
rapidly e%cretelarge quantities of bicarbonate. &onsequently for metabolicalkalosis to persist
impaired renal corrective mechanismsor strong signals to the kidney to retain bicarbonate
must e%ist. If renal function is impaired markedly thekidney cannot e%crete the generated
bicarbonate load. Ifrenal function is preserved then three ma$or stimuli actto enhance bicarbonate reabsorption6 +i0 effective arterialvolume depletion +ii0 mineralocorticoid e%cess
and +iii0hypokalemia. Becreased effective arterial volume increasespro%imal tubular
bicarbonate reabsorption.