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

VIII. Clinicopathological Indicators of Fluid and Electrolyte Imbalance
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TABLE 17-5 Causes of Hyponatremia
False hyponatremia
Hyperlipidemia
Hyperproteinemia
Hyperglycemia
Hyponatremia (relative water excess)
Decreased effective circulating volume
Vomiting
Diarrhea
Excessive sweating
Cutaneous loss—burns
Blood loss
Repeated pleural drainage
Pleuritis, chylothorax
Adrenal insufficiency
“ Third space problems ”
Sequestration of fluid
Peritonitis
Ascites
Ruptured bladder
Excess circulating volume
Congestive heart failure
Chronic liver failure
Nephrotic syndrome
Normal effective circulating volume
Psychogenic water drinking
Renal disease
Inappropriate ADH secretion
mechanics of this process are complicated by the fact that
cells and tissues are variably permeable to glucose, and
thus the glucose space clearly exceeds the ECF volume.
For practical purposes, it can be anticipated that serum
sodium concentration will decline 1.6 mEq/l (1.6 mmol/l)
for each 100 mg/dl (5.55 mmol/l) increase in glucose concentration
( Saxton and Seldin, 1986 ). Serum osmolality
may be increased by hyperglycemia, but this should not
cause a large disparity between the measured and calculated
serum osmolality.
Changes in water balance are principally responsible
for changes in serum sodium concentration ( Leaf, 1962 ).
Hyponatremia should be considered as an indication of a
relative water excess ( Scribner, 1969 ). Hyponatremia is
often, but not invariably, associated with conditions that
cause sodium depletion and resultant decreases in effective
circulating volume. These conditions include vomiting,
diarrhea, excessive sweat losses, and adrenal insufficiency.
Dehydration and volume depletion induce neurohormonal
responses that result in increased water consumption via
increased thirst and enhanced renal conservation of water
as well as sodium ( Rose, 1984 ). Fluid losses in these forms
of dehydration are most often hypotonic or isotonic, and
initial fluid and electrolyte deficits do not result in hyponatremia
until water intake or renal water retention disturbs
the balance between the remaining exchangeable cations
and the total body water. Thus, whereas substantial sodium
and potassium deficits are associated with these conditions,
plasma sodium concentration does not always reflect
these deficits, and a diagnosis of sodium depletion should
be based on other grounds ( Scribner, 1969 ).
The accumulation of sodium-containing fluid within
body cavities as a result of ascites, peritonitis, or a ruptured
bladder is referred to as a “ third space problem ” ( Rose,
1984 ). The fluid that accumulates in the “ third space ” has a
composition similar to the ECF. When this accumulation of
fluid occurs rapidly, plasma volume is reduced, and serum
sodium concentration then may decrease as the compensating
responses result in water retention. A classic example
of this situation is the marked hyponatremia associated
with ruptured bladder in neonatal foals. As the dilute urine
of the neonate accumulates in the abdomen, osmotic equilibrium
is established first with the ECF and then with all
of the body fluid compartments. Sodium and chloride as
well as other ions are drawn from the rest of the ECF into
this progressively expanding fluid compartment, and hyponatremia
develops despite the fact that there has been no
appreciable loss of sodium from the body. The severe neurological
signs associated with ruptured bladder in foals
are related in large part to the effects of the sudden and
marked hypotonic hyponatremia on the central nervous system.
Hyponatremia associated with excessive retention of
water also can occur without the development of significant
sodium depletion or decreases in effective circulating fluid
volume. Hyponatremia may be observed with psychogenic
polydipsia if the rate of water consumption exceeds renal
capacity for free water clearance because of intrinsic renal
disease or renal medullary washout ( Tyler et al ., 1987 ). This
condition also may occur in patients with impaired free
water clearance resulting from renal disease or when under
the influence of inappropriate release of ADH ( McKeown,
1986 ). Hyponatremia and associated neurological disturbances
can develop with naturally occurring disease ( Lakritz
et al ., 1992 ) or iatrogenically if excessive amounts of free
water are administered to patients with altered renal function
( Arieff, 1986 ; Sterns et al ., 1986 ).
Urine sodium concentration can be useful in the differentiation
of the causes of hyponatremia as indicated in
Figure 17-6 . Renal adaptive responses normally result in
sodium retention and production of urine with very low
sodium concentration in patients with sodium depletion
resulting from vomiting, diarrhea, excessive sweat loss,
or third space problems ( Rose, 1984 ). Hyponatremia and
hypokalemia of adrenal insufficiency are generally associated
with a relatively high urine sodium concentration
( Rose, 1984 ). With the syndrome of inappropriate secretion
of antidiuretic hormone (SIADH), urine sodium tends
to be high in the presence of hyponatremia, whereas urine
sodium concentration tends to be low in animals with psychogenic
polydipsia. Urine sodium concentration in animals
with renal failure can be quite variable.