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

VIII. Clinicopathological Indicators of Fluid and Electrolyte Imbalance
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TABLE 17-6 Causes of Hypernatremia
Water losses in excess of electrolyte loss
Digestive
Vomiting
Diarrhea
Cutaneous
Burns
Renal
Diuretics
Diabetes mellitus
Mannitol
Intrinsic renal disease
Pure water losses
Insensible
Panting
Diabetes insipidus
Central
Nephrogenic
Inadequate water intake
Water deprivation
Abnormal thirst mechanism
Sodium excess (water restriction)
Hypertonic saline or sodium bicarbonate
Salt poisoning
Mineralocorticoid excess
renal and fecal output ( Brobst and Bayly, 1982 ; Carlson
et al ., 1979b ; Genetzky et al ., 1987 ; Tasker, 1967b ).
However, continued cutaneous and respiratory insensible
water loss may result in hypernatremia ( Carlson et al .,
1979b ; Elkinton and Taffel, 1942 ; Genetzky et al ., 1987 ;
Rumsey and Bond, 1976 ). Abnormal thirst mechanisms
with resultant hypernatremia have been reported in young
dogs ( Crawford et al ., 1984 ; Hoskins and Rothschmidt,
1984). Hypernatremia may occur transiently following
administration of hypertonic saline or sodium bicarbonate
if water intake is restricted or impaired. The hypernatremia
observed with salt poisoning in cattle and swine is, in fact,
triggered by water restriction in animals with a high salt
intake ( Padovan, 1980 ; Pearson and Kallfelz, 1982 ). So
long as adequate water is available, salt poisoning does not
occur. In human subjects, hypernatremia is reported with
mineralocorticoid excess ( McKeown, 1986 ).
C . Serum Potassium
Serum potassium concentration does not always reflect
potassium balance but is influenced by factors that alter
internal balance (i.e., the distribution of potassium across the
cell membrane between the ECF and ICF) as well as factors
that change external balance (i.e., potassium intake and output)
( Brobst, 1986 ; Patrick, 1977 ; Rose, 1984 ). The effective
adjustment of external and internal balance in normal
individuals in response to either large potassium loads or
excessive potassium losses usually maintains serum potassium
concentration within normal limits. However, changes
in potassium concentration occur in a wide variety of clinical
circumstances and have profound neuromuscular effects
largely because of changes in cell membrane potential
( Brobst, 1986 ). The compensating responses to change in
circulating fluid volume distribution and acid-base balance
can result in confusing and contradictory findings. As an
example, calves with acute diarrhea may develop significant
depletion of body potassium stores because of excessive
losses and inadequate intake ( Phillips and Knox, 1969 ).
However, the serum potassium concentration in these calves
may actually be normal to increased as the result of renal
shutdown and the metabolic acidosis induced by dehydration
and sodium depletion with resultant decreases in the effective
circulating fluid volume. Electrolyte replacement fluids given
to these calves should include potassium ( Fettman et al. ,
1986 ). Correct interpretation of serum potassium concentration
thus requires a knowledge of probable intake and
sources of excessive loss as well as the status of renal function
and acid-base balance. Measurement of erythrocyte
potassium concentration has been suggested as an aid in the
assessment of the potassium status of horses with exerciserelated
myopathy ( Bain and Merritt, 1990 ; Muylle et al .,
1984a, 1984b ). However, experimental studies have failed to
demonstrate a close correlation between erythrocyte potassium
concentration and potassium depletion.
1 . Hypokalemia
Hypokalemia occurs relatively frequently in domestic animals
and may result from depletion of the body’s potassium
stores or from a redistribution of potassium from
the ECF into the ICF space ( Brobst, 1986 ), as indicated
in Table 17-7 . Hypokalemia most often is associated with
excessive potassium losses from the gastrointestinal tract
as the result of vomiting or diarrhea ( Tasker, 1967c ).
Excessive renal loss of potassium results from the action
of mineralocorticoid excess, the action of certain diuretics,
and as the result of altered renal tubular function in animals
with renal tubular acidosis or postobstructive states.
Chronic dietary potassium deficiency eventually can lead
to modest hypokalemia even in normal individuals ( Aitken,
1976 ; Dow et al ., 1987a ). A rapidly developing and profound
hypokalemia can occur in animals with reduced
dietary intake as a result of anorexia when coupled with
other causes of excessive potassium loss ( Tasker, 1980 ).
Hypokalemia may develop without potassium depletion
as the result of intracellular movement of potassium
from the ECF space. This situation occurs with an acute
alkalosis ( Burnell et al ., 1966 ) and in patients treated with
insulin and glucose infusions ( Tannen, 1986 ). In fact, medical
management of severe life-threatening hyperkalemia
often involves the administration of glucose, insulin, and,