Page 166 - Basic Monitoring in Canine and Feline Emergency Patients

weakness and lethargy. In general, the more chronic and muscular tone) and intracellular signaling, and
the change in sodium, the less severe the clinical is a cofactor for many enzyme systems including
VetBooks.ir signs directly attributable to the sodium abnormal- the coagulation system.
The largest proportion of calcium is stored in the
ity since the brain has more time to adapt.
Sodium loss or a gain in water leads to hypona-
tremia and in turn a hypo-osmolar plasma. If this skeleton (99% of all calcium) with the remaining
1% (i.e. the extracellular calcium) free and able to
happens acutely, the cells in the brain are relatively exchange between the blood and the extracellular
hyperosmolar compared to the plasma, and the bony matrix. This extracellular calcium is found in
excess water will shift from the plasma into the three forms – ionized (iCa), complexed (i.e. bound
cytoplasm. This in turn can lead to cellular swell- to phosphate, bicarbonate, sulfate, citrate, and lac-
ing, causing cerebral edema and signs ranging from tate), and protein bound (primarily to albumin).
lethargy and vomiting to changes in mentation, Typically, since iCa is the fraction of calcium that is
seizures, and even death. If the hyponatremia is the most important in cellular functions, it is the
more chronic, the brain cells have a chance to calcium that should be monitored clinically rather
adapt and will reduce their own osmolality through than total calcium. See Fig. 8.2 for basic calcium
the loss of intracellular potassium and other intra- metabolism and regulation by the body.
cellular organic osmoles such as amino acids. This In general, extremes of calcium will be clinically
reduces the difference in osmolality between the important. Ionized hypercalcemia (usually accom-
brain cells and the hypo-osmolar plasma, leading panied by total hypercalcemia) can lead to cell
to less movement of water from the plasma into the death secondary to the toxic effects of excessive
brain cells, less cerebral edema, and blunting of calcium. While all cells can be affected, central
clinical signs. nervous system, renal, cardiac, and gastrointestinal
Conversely, hypernatremia – whether from gain (GI) tract cell death lead to the most obvious clini-
of sodium particles or loss of plasma water – leads cal signs. Clinical signs include polyuria and poly-
to a hyperosmolar plasma. Acutely, plasma that is dipsia as the body tries to reduce the higher
hyperosmolar compared to cellular fluid will draw calcium concentration by diluting the calcium, as
water out of the cells of the brain, leading to shrink- well as increasing urinary excretion. Some animals
age of those cells. This can lead to an overall become lethargic and weak, and concurrent ano-
decrease in brain volume that, in the most severe rexia and vomiting often occur. The latter clinical
cases, can cause rupture of blood vessels in the brain signs are likely due to impaired muscle contraction
and sudden intracerebral hemorrhage. Less acutely, of smooth muscle in the GI tract leading to ileus, in
the dehydrated nerves can become demyelinated. addition to death of gastrointestinal tract cells. As
Signs of demyelination can take up to 72 hours or with sodium, the faster the hypercalcemia develops,
more to become clinically apparent. If the hyperna- the more severe the clinical signs. However, the
tremia is more chronic, the cells of the central nerv- more chronic the hypercalcemia, the more likely
ous system will have a chance to adapt, accumulating that mineralization of soft tissues will occur due to
and producing ‘idiogenic osmoles’ (intracellular a high phosphorus × calcium product (greater than
solutes such as amino acids and electrolytes) to raise 60–70 predisposes to mineralization), resulting in
their own osmolality closer to that of the plasma. organ dysfunction. While mineralization can occur
This will reduce the movement of water out of the in any tissue, clinical signs usually manifest first in
cells, ensuring that the cells are protected and result- the kidneys as progressive renal failure.
ing in fewer or less obvious clinical signs. Ionized hypocalcemia (usually accompanied by
total hypocalcemia) causes a variety of clinical
signs including muscle tremors that often appear
Calcium
seizure-like, facial/muzzle pruritus resulting in facial
Calcium volumes in the body are relatively small, rubbing, a stiff gait, or even behavioral changes
especially as compared to sodium. However, like including restlessness, disorientation, or hypersen-
sodium, calcium is found in many locations in the sitivity to stimuli. Changes in electrical activity of
body and is integral to many cellular functions. the heart (arrhythmias) can also occur and rarely
Calcium is incorporated and stored in body tissues these animals display polyuria or polydipsia. Both
(bones, teeth) and plays a crucial role in electro- extremes – hypocalcemia and hypercalcemia – can
physiology (nerve conduction, cardiac conduction, potentially be fatal if untreated.

158 E.J. Thomovsky