Page 74 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

64 ELECTROLYTE DISORDERS

Initially, TBW content is not altered in the setting of concentration further impairs water excretion. Third,
hyponatremia with hyperosmolality. Rather, there is an the patient is thirsty because of volume depletion and
altered distribution of water between intracellular and continues to drink water if it is available. All of these
extracellular compartments. However, a reduction in factors have a dilutional effect on the remaining body
TBW content develops to the extent that these substances fluids. In one study, approximately 20% of dogs with gas-
cause an osmotic diuresis. trointestinal foreign bodies had hyponatremia. 10
Recall the previous example of the loss of 1 L of fluid
HYPONATREMIA WITH DECREASED with an osmolality of 150 mOsm/kg and consider
PLASMA OSMOLALITY what would happen if the animal in question drinks 1 L

The total body sodium content and ECF volume of of pure water after sustaining the hypotonic loss. The
patients with hyponatremia and hypoosmolality may be added water increases the ECF volume from 1.36 to
normal, decreased, or increased, and hyponatremia may 2.36 L, and the resulting hypotonicity rapidly drives
be classified according to the volume status of the patient water into cells to equalize osmolality:
as hypovolemic, normovolemic, and hypervolemic. In
most instances, nonosmotic stimulation of antidiuretic New ECF osmolality ¼ new ICF osmolality
hormone results in water retention and development of 450 mOsm 1200 mOsm
hyponatremia. Therefore, the second step in the evalua- ¼
ð2:36 xÞ L ð3:64 þ xÞ L
tion of the patient with hyponatremia is to estimate total
body sodium content and ECF volume status. This is best
done by clinical assessment of the patient based on his- where x is the volume of water moving between
tory, physical examination, and a few ancillary tests. A compartments:
good history often indicates a source of fluid loss (e.g.,
vomiting, diarrhea, or diuretic administration), and the 450ð3:64 þ xÞ¼ 1200ð2:36 xÞ
physical examination provides important clues to the x ¼ 0:72 L
patient’s volume status. The following physical findings
should be assessed: skin turgor, moistness of the mucous The new volumes and osmolalities are:
membranes, capillary refill time, pulse rate and character,
appearance of the jugular veins (distended or flat), and 450 mOsm
presence or absence of ascites or edema. Measurements ECF : ¼ 275 mOsm=kg
1:64 L
of hematocrit and total plasma protein concentration,
1200 mOsm
as well as systemic blood pressure and central venous pres- ICF : ¼ 275 mOsm =kg
sure determinations, if available, further clarify the 4:36 L
patient’s ECF volume status.
Note that in this example the intracellular compartment is
Hypovolemic Hyponatremia expanded (4.36 L). The volume of the extracellular com-
(Hyponatremia with Volume Depletion) partment (1.64 L) is greater than it was when the same
For a patient with volume depletion (hypovolemia) to hypotonic loss was not replaced (1.36 L) but still less than
develop hyponatremia, the total body deficit of sodium the previous normal value (2 L). Thus, hypotonic (or iso-
must exceed that of water. Hyponatremic patients with tonic) losses replaced by pure water lead to expansion of
volume depletion have lost fluid by renal or nonrenal the ICF space. These changes are depicted in Figure 3-14.
routes. Gastrointestinal losses (e.g., vomiting, diarrhea) Renal fluid and NaCl losses resulting in hyponatremia
and third-space losses, such as pleural effusion or perito- are usually caused by hypoadrenocorticism or diuretic
neal effusion caused by peritonitis, pancreatitis, or administration. In one study, 81% of 225 dogs with
uroabdomen, are the most important nonrenal losses of hypoadrenocorticism were hyponatremic at presenta-
fluid and NaCl. 19,162 Gastrointestinal losses are often tion. 129 Mineralocorticoid deficiency in hypoadreno-
hypotonic in nature. The question thus arises, “If the corticism results in urinary loss of NaCl and depletion of
losses are hypotonic, how does the patient become ECF volume. Volume depletion in patients with hypoadre-
hyponatremic?” The answer follows from three physio- nocorticismisastrongnonosmoticstimulusfor vasopressin
6
logic events and reflects the body’s tendency to preserve release and impairs water excretion. Hyperkalemia typi-
volume at the expense of tonicity. First, volume depletion cally accompanies hyponatremia in hypoadreno-
decreases GFR, enhances isosmotic reabsorption of corticism. 129,132,144,161 However, some dogs with
sodium and water in the proximal tubules, and decreases hypoadrenocorticism have only glucocorticoid deficiency
delivery of tubular fluid to distal diluting sites. These at the time of presentation and thus have normal serum
events impair excretion of water. Second, volume deple- potassium concentrations. 100,139,156 Glucocorticoids are
tion is a strong nonosmotic stimulus for vasopressin necessary for complete suppression of vasopressin release,
release, and the increased plasma vasopressin and in their absence impaired water excretion and