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

VII. Clinical Features of Fluid and Electrolyte Balance
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hyperpolarization block resulting in weakness or paralysis,
whereas hyperkalemia decreases membrane potential causing
hyperexcitability ( Patrick, 1977 ). These features depend
on the state of total body potassium content but also depend
on the speed with which hypokalemia or hyperkalemia
develops ( Saxton and Seldin, 1986 ). As an example, acute
potassium depletion may result in hypokalemia before the
development of marked change in intracellular potassium,
producing a substantial alteration in the ratio of intracellular-to-extracellular
potassium. Acute hypokalemia can produce
a much greater alteration in membrane potential and
thus more marked clinical signs than a gradually developing
hypokalemia of the same magnitude ( Saxton and Seldin,
1986 ). Potassium homeostasis involves regulation of internal
balance (i.e., the distribution of potassium between the
ECF and ICF) as well as external balance (i.e., the relation
of potassium input to output) ( Brobst, 1986 ; Rose, 1984 ).
Internal potassium balance is influenced by changes in acidbase
status, glucose and insulin administration, exercise, and
catecholamine release and will be discussed in greater detail
in the section on factors that influence plasma potassium
concentration.
1 . Potassium Depletion
Potassium depletion is the result of altered external
balance in which potassium losses by all routes exceed
intake. Potassium is present in relatively high concentrations
in most animal feeds. Therefore, dietary deficiency alone is
not a common cause for potassium depletion ( Tasker, 1980 ).
However, dietary factors were associated with hypokalemia
in hospitalized cats, particularly when associated with diseases
linked to increased potassium loss ( Dow et al. , 1987a ).
Herbivores, such as the horse, fed an all-hay diet may have
a daily potassium intake of 3000 to 4000 mEq (3000 to
4000 mmol) per day (Hintz and Schryver, 1976 ; Tasker,
1967a ). Most of this potassium is absorbed in the small
intestine and colon with subsequent renal excretion of more
than 90% of the daily potassium intake ( Hintz and Schryver,
1976 ). These animals are thus highly adept at excretion of a
large daily potassium intake. However, renal compensation
for deficient potassium intake is not efficient, and renal conservation
of potassium may be delayed for several days when
animals normally fed a high-potassium diet are suddenly
taken off feed or develop anorexia ( Tasker, 1967b ) .
Potassium depletion most commonly develops as the
result of gastrointestinal losses from vomiting or diarrhea.
Excessive renal losses can occur as the result of diuretic
usage, mineralocorticoid excess, renal tubular acidosis, and
in the diuresis state that follows relief of urinary obstruction
( Saxton and Seldin, 1986 ). Potassium depletion may result
in decreased ICF volume, altered membrane potential,
altered intracellular pH, and alterations of potassiumdependent
enzymatically mediated reactions ( Elkinton and
Winkler, 1944 ). Clinical features include muscle weakness,
ileus, cardiac arrhythmias, rhabdomyolysis, and renal dysfunction
( Dow et al ., 1987a, 1987b ; Earley and Daugharty,
1969 ; Tannen, 1986 ).
2 . Potassium Excess
Potassium excess occurs relatively rarely and is generally a
consequence of some alteration of renal excretion of potassium.
Potassium excess may be associated with Addison’s
disease, some forms of renal disease, and clinical situations
associated with hypovolemia and renal shutdown ( Rose,
1984 ; Weldon et al. , 1992 ). Care should be taken to avoid
the rapid administration of large amounts of potassium salts
orally or intravenously to patients with severely compromised
renal function. Even normal animals can develop significant
electrocardiographic abnormalities with potassium
( Dhein and Wardrop, 1995 ; Epstein, 1984 ; Glazier et al .,
1982 ) or calcium infusions ( Glazier et al ., 1979 ).
D . Chloride
Modest changes in hydration tend to produce roughly proportional
changes in plasma sodium and chloride relative
to sodium concentration. Acid-base alterations are associated
with disproportionate changes in plasma chloride concentration
( Saxton and Seldin, 1986 ). A disproportionate
hyperchloremia is seen in association with a low to normal
anion gap metabolic acidosis. Chloride concentration
increases in this type of acidosis as the result of proportionately
smaller losses of chloride than bicarbonate and
enhanced renal chloride resorption in response to decreased
bicarbonate ( Saxton and Seldin, 1986 ). Disproportionate
hypochloremia is a consistent feature of metabolic alkalosis
( Rose, 1984 ). Chloride depletion develops in these animals
as a result of excessive loss or sequestration of fluids
with high chloride content. Changes in water balance can
result in modest alterations in the relative concentrations
of plasma sodium and chloride. A pure water deficit produces
increased sodium concentration, which exceeds the
increases in chloride. This contributes to the development
of a contraction alkalosis with an increase in bicarbonate.
A pure water excess has the opposite effect and can result
in an expansion acidosis.
VII . CLINICAL FEATURES OF FLUID AND
ELECTROLYTE BALANCE
It is convenient to discuss the theoretical ramifications of
pure water loss or specific electrolyte deficits. However,
in practical clinical situations, the issue is almost never
so clearly defined, and most often, there is a combination
of fluid, electrolyte, and acid-base alterations. Many
medical problems result in a consistent pattern of fluid
and electrolyte loss with predictable changes in fluid volume,
electrolyte concentration, and acid-base balance.