CHAPTER 3 FLuids and Electrolytes Asli

8/19/2019 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.

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CHAPTER 3 FLuids and Electrolytes Asli