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Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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VIII. Clinicopathological Indicators <strong>of</strong> Fluid and Electrolyte Imbalance<br />

553<br />

dog ( Jezyk, 1982 ) and certain quarter horses ( Cox, 1985 ;<br />

Pickar et al. , 1991 ; Spier et al. , 1990, 1993 ; Steiss and<br />

Naylor, 1986 ). In the horse, the condition closely resembles<br />

the heritable disease hyperkalemic periodic paralysis,<br />

which has been reported in human subjects and is due<br />

to an alteration in the voltage-regulated sodium chemical<br />

( Rudolph et al ., 1992a, 1992b ). Sudden marked increases<br />

in serum potassium concentration result from the transcellular<br />

movement <strong>of</strong> potassium. Serum potassium concentration<br />

can reach 8 to 9 mEq/l (8 to 9 mmol/l) and is associated<br />

with pr<strong>of</strong>ound electrocardiographic abnormalities and fluid<br />

shifts, which result in marked increases in PCV and protein<br />

concentration. The disease is inherited as an autosomal<br />

dominant, and all affected horses can be traced back to<br />

a common ancestor. A DNA test that can detect the single<br />

base pair substitution responsible for this disease has been<br />

developed (Rudolph et al ., 1992ba). Using this procedure,<br />

it is possible to identify individuals that are heterozygous<br />

or homozygous for this trait.<br />

D . Serum Chloride<br />

It long has been assumed that the anion, chloride, which<br />

combines with sodium to form common salt, simply follows<br />

sodium in the physiological processes that regulate body<br />

fluid and electrolyte balance. It is becoming increasingly<br />

apparent that this may not always be true and that some<br />

<strong>of</strong> the problems ascribed to sodium retention do not occur<br />

unless chloride is present in excess as well ( Kurtz et al .,<br />

1987 ). Causes <strong>of</strong> alterations in chloride concentration are<br />

given in Table 17-9 . The hyperchloremia and hypochloremia,<br />

which are normally seen in association with roughly<br />

proportional changes in sodium concentration, are due to<br />

changes in body water balance.<br />

Changes in chloride concentration that are not associated<br />

with a similar change in sodium concentration are<br />

usually associated with acid-base imbalances ( Divers et al .,<br />

1986 ). Chloride concentration tends to vary inversely with<br />

bicarbonate concentration. A disproportionate increase in<br />

chloride most commonly is associated with a normal to<br />

low anion gap hyperchloremic metabolic acidosis such as<br />

renal tubular acidosis and may be seen as a compensating<br />

response for a primary respiratory alkalosis ( Saxton and<br />

Seldin, 1986 ). Disproportionate decreases in chloride characteristically<br />

are seen in a metabolic alkalosis but also may<br />

be seen as part <strong>of</strong> the compensating response for a chronic<br />

primary respiratory acidosis ( Saxton and Seldin, 1986 ).<br />

E . Osmolality<br />

It has been demonstrated that the concentration <strong>of</strong> sodium<br />

in serum water is closely correlated with the serum osmolality<br />

over an extremely wide range <strong>of</strong> physiological and<br />

pathological states provided appropriate corrections are<br />

TABLE 17-9 Causes <strong>of</strong> Alterations in Chloride<br />

Concentration<br />

Hyperchloremia<br />

With proportional increase in sodium<br />

Dehydration (relative water deficit)<br />

Without proportional increase in sodium<br />

Hyperchloremic metabolic acidosis<br />

Compensation for respiratory alkalosis<br />

Hypochloremia<br />

With proportional decrease in sodium<br />

Overhydration (relative water excess)<br />

Without proportional decrease in sodium<br />

Hypochloremic metabolic alkalosis<br />

Compensation for respiratory acidosis<br />

made for the contributions made by variations in glucose<br />

and urea concentrations ( Edelman et al ., 1958 ). The<br />

measurement <strong>of</strong> serum osmolality has two specific and<br />

very useful purposes ( Gennari, 1984 ): first, to determine<br />

whether serum water content deviates widely from normal<br />

and, second, to screen for the presence <strong>of</strong> foreign lowmolecular-weight<br />

substances in the blood. Interpretation <strong>of</strong><br />

serum osmolality for these purposes requires simultaneous<br />

comparison <strong>of</strong> the measured osmolality and the calculated<br />

osmolality as determined from the measured concentrations<br />

<strong>of</strong> the major solutes in serum (sodium, glucose, and<br />

urea). The difference between the measured and the calculated<br />

osmolality is sometimes referred to as the “ osmolal<br />

gap ” ( Feldman and Rosenberg, 1981 ; Shull, 1978, 1981 ).<br />

Sodium is the principal cation in serum, and sodium is<br />

balanced by a number <strong>of</strong> different anions (chloride, bicarbonate,<br />

protein, sulfate, and phosphate). Sodium concentration<br />

thus provides a reasonable estimate <strong>of</strong> the total<br />

electrolyte concentration (anions and cations) in the sample<br />

and, in this calculation, is usually multiplied by a factor <strong>of</strong> 2.<br />

As mentioned earlier, the water content <strong>of</strong> serum samples<br />

is approximately 94%. Correction for the water content <strong>of</strong><br />

serum is not necessary because, fortuitously, it is counterbalanced<br />

by the fact that sodium chloride does not dissociate<br />

completely and has an osmotic coefficient <strong>of</strong> 0.93 in serum<br />

(Dahms et al ., 1968 ; Rose, 1984 ; Wolf, 1966 ). The osmolality<br />

can thus be calculated using the measured sodium concentration,<br />

and the concentration <strong>of</strong> the two nonelectrolyte<br />

components <strong>of</strong> serum that are normally present in amounts<br />

sufficient to influence osmolality:<br />

mOsm/kg H2O 2<br />

sodium glucose urea (17-15)<br />

This calculation is valid if concentrations <strong>of</strong> sodium, glucose,<br />

and urea are expressed in mmol/l. Conversion <strong>of</strong> glucose<br />

concentration from mg/dl to mmol/l requires division<br />

by 18, and urea concentration in mg/dl can be converted to<br />

mmol/l by dividing by 2.8.

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