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

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Chapter | 17 Fluid, Electrolyte, and Acid-Base Balance
exchangeable ( McKeown, 1986 ). The ECF volume thus
contains essentially all of the body’s readily available and
exchangeable sodium. The exchangeable sodium content
is the principal determinant of ECF volume, and sodium
deficits are the principal causes of decreased ECF volume
( Saxton and Seldin, 1986 ). Increases in sodium content result
in expansion of ECF volume, which may lead to the development
of hypertension or edema formation ( Dow et al .,
1987b ; McKeown, 1986 ). In either instance, the observed
plasma sodium concentration will primarily depend on relative
water balance. Because monitoring daily electrolyte
balance is difficult in most animal species, urinary fractional
excretion or creatinine clearance ratios have been useful
to provide an index of daily intake or potential deficits of
sodium, potassium, chloride, and other electrolytes. Normal
values have been established for dogs, cats, horses ( Morris
et al. , 1984 ), and cattle ( Fleming et al. , 1992 ).
1 . Sodium Depletion
Sodium depletion is rarely the result of dietary sodium deficiency
( Aitken, 1976 ). This is true even for herbivores whose
feedstuffs are normally very low in sodium. Chronic sodium
depletion has been reported in lactating dairy cows on a low
salt diet ( Whitlock et al ., 1975a ), but the sodium deficit was
most probably the result of sodium losses in milk ( Michell,
1985 ). Mastitis markedly enhances sodium loss in milk
and could play a role in sodium depletion in lactating cows
maintained on a low-salt diet ( Michell, 1985 ). Sodium depletion
almost invariably is associated with excessive losses of
sodium-containing fluid ( McKeown, 1986 ; Rose, 1984 ),
most often occurring as the result of gastrointestinal losses
through vomiting or diarrhea ( Fisher and Martinez, 1976 ;
Lakritz et al. , 1992 ). Excessive renal sodium losses can occur
with intrinsic renal disease or as the result of diuretic therapy
( Rose, 1984 ; Rose and Carter, 1979 ; Rose et al ., 1986 ).
Cutaneous losses via sweating are important in the exercising
horse and may occur in any animal with extensive exfoliative
dermatitis or burns. Salivary losses as the result of esophagostomy
have been reported as a cause of sodium depletion
in horses ( Stick et al ., 1981 ). A history suggestive of excessive
loss of sodium-containing fluid is thus an extremely
important criterion for the diagnosis of sodium depletion in
domestic animals. The foregoing discussion applies indirectly
to the so-called third space problems associated with
a sequestration or compartmentalization of a portion of the
ECF volume ( Rose, 1984 ). This situation can occur with
obstructive bowel disease or with the sudden accumulation
of fluid within the abdomen or thorax resulting from peritonitis,
ruptured bladder, ascites, or pleural effusion. These fluids
have an electrolyte composition similar to the ECF and
initially are drawn from the plasma volume and interstitial
fluids. The resultant change in plasma volume and effective
circulating fluid volume produce the same clinical and
clinicopathological changes as those observed with excessive
external losses of sodium containing fluid ( Billig and Jordan,
1969 ). In these cases, fluids have not been lost from the body,
but there has been an internal sequestration of fluid which
can be mobilized if treatment is effective.
2 . Sodium Excess
Sodium excess occurs most often in association with an
increase in body water leading to an isotonic expansion of ECF
volume and the development of hypertension or generalized
edema ( Saxton and Seldin, 1986 ). Congestive heart failure,
hypoalbuminemia, and hepatic fibrosis may lead to a failure
to maintain effective circulating volume, which then, in turn,
results in compensating renal sodium retention ( Rose, 1984 ).
In these cases, expanded ECF volume represents an attempt to
restore effective circulating fluid volume, and, at least initially,
plasma volume may decrease whereas ECF volume expands.
An expansion of ECF volume of 20% to 30% may be necessary
before edema is first evident ( Scribner, 1969 ). Sodium
excess and edema can develop iatrogenically as the result
of the excessive administration of sodium-containing fluid to
patients with severely compromised renal function.
Most domestic animals can tolerate a large sodium
intake provided they have adequate drinking water
( Aitken, 1976 ; Buck et al ., 1976 ; Pierce, 1957 ). Excessive
salt intake may occur when animals that had been on
salt-restricted diets are first allowed free access to salt
( Michell, 1985 ). Salt intoxication can occur in cattle that
are feeding in reclaimed salt water marshes or on pastures
contaminated by oil field wastes when they are deprived
of fresh water ( Aitken, 1976 ; McCoy and Edwards, 1979 ;
Michell, 1985 ; Pierce, 1957 ; Sandals, 1978 ). Salt poisoning
in swine also occurs in association with water restriction
followed by access to water ( Aitken, 1976 ; Buck
et al ., 1976 ). Salt intoxication is generally associated with
increases in plasma or cerebrospinal fluid sodium concentrations.
Neurological signs associated with excessive salt
consumption coupled with water restriction are related to
development of cortical edema and, in swine, a characteristic
eosinophilic meningoencephalitis ( Aitken, 1976 ).
C . Potassium
Potassium is largely an intracellular ion with over 98% of
the exchangeable potassium located intracellularly ( Brobst,
1986 ; Strombeck, 1979 ). This distribution of potassium is
coupled with the active extrusion of sodium from the cells,
which is maintained by an energy-dependent sodium:potassium
pump at the cell membrane ( Brobst, 1986 ; Tannen,
1986 ). Potassium distribution across the cell membrane
plays a critical role in the maintenance of cardiac and neuromuscular
excitability. Changes in potassium concentration
that alter the ratio of intracellular to extracellular potassium
alter membrane potential ( Tannen, 1986 ). In general,
hypokalemia increases membrane potential, producing a