Page 77 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Disorders of Sodium and Water: Hypernatremia and Hyponatremia 67

SIADHisrareindogs.Ithasbeenreportedinassociation evidence of excessive glucocorticoid secretion, and their
with dirofilariasis, undifferentiated carcinoma, neoplasia in response was similar to that previously described for dogs
the region of the hypothalamus, granulomatous amebic with spontaneous hyperadrenocorticism. 8
meningoencephalitis, and hydrocephalus. 12,14,52,77,148 Cerebral salt wasting occurs in critically ill human
Inappropriate vasopressin secretion may have played a role patientswithintracranialinjury,oftensubarachnoidhemor-
inthe pathogenesisofhyponatremiainadogwithglucocor- rhage, but also may be observed after neurosurgical
ticoid deficiency. 28 Idiopathic SIADH also has been procedures. 7,26 Hyponatremia resulting from cerebral salt
characterized indogs. 47,135 Two of the dogs with idiopathic wasting must be differentiated from that caused by SIADH
SIADHhadhyponatremia,hypoosmolality,andinappropri- because patients with the former disorder are volume
ately high vasopressin concentrations (7 to 30 pmol/L). depleted and require NaCl and water replacement, whereas
Urine osmolality was inappropriately high (213 to 535 thosewithSIADHrequirewaterrestriction.Atrialandbrain
mOsm/kg) in one dog in the presence of plasma natriureticfactorslikelyareresponsiblefortheurinarylossof
hypoosmolality. Thethreshold and sensitivity of vasopressin sodium in affected patients. 110 Recognition of volume
secretion were studied by infusion of hypertonic saline. One depletion depends on clinical findings such as changes in
dogdemonstratedapatternofresetosmostatandtheothera skin turgor, systemic blood pressure, central venous pres-
pattern consistent with vasopressin leak. 135 The vasopressin sure, heart rate, and character of peripheral pulses.
receptorantagonistOPC-31260,usedatadosageof3 mg/ Hyponatremia must be corrected slowly (see Treatment
kg orally twice a day for a 3-year period, successfully ofHyponatremiasection),andSIADHshouldbesuspected
increased urine output and decreased USG in a dog with if hyponatremia worsens after saline infusion.
idiopathic SIADH, but serum sodium concentration was Fludrocortisone also has been used in human patients with
47
not normalized. cerebral salt wasting to facilitate sodium retention.
The diagnosis of SIADH must be made by excluding Severe hypothyroidism with myxedema in humans
other causes of hyponatremia. The following criteria can result in hyponatremia, possibly because of decreased
should be met before establishing a diagnosis of SIADH: distal delivery of tubular fluid and nonosmotic stimula-
1. Hyponatremia with plasma hypoosmolality. tion of vasopressin release. Hyponatremia in this setting
is corrected by thyroid hormone replacement. In four
2. Inappropriately high urine osmolality in the presence
reported cases of myxedema coma in dogs, hyponatremia
of plasma hypoosmolality. (Urine osmolality is often
was found in two of three dogs in which the serum
>300 mOsm/kg in human patients with SIADH. 20,83
sodium concentration was measured.
A urine osmolality >100 mOsm/kg should be consid-
Exercise-associated hyponatremia has been reported in
ered abnormal in a patient with hyponatremia and
human athletes during prolonged exertion. It is thought
plasma hypoosmolality. A urine osmolality <100
to be caused by excessive consumption of water or hypo-
mOsm/kg would normally be expected as a result
tonic fluids as well as nonosmotic stimulation of vasopres-
of complete suppression of vasopressin release. Urine
sin release associated with volume depletion that impairs
osmolality is important in distinguishing psychogenic 141
water excretion. Sodium loss in sweat also may play a
polydipsia and SIADH. Urine is maximally diluted in
contributory role. Women, people of low body weight,
psychogenic polydipsia but not in SIADH.)
and those taking nonsteroidal anti-inflammatory drugs
3. Normal renal, adrenal, and thyroid function. 138
are at increased risk. Total body exchangeable cation
4. Presence of natriuresis despite hyponatremia and
content (sodium and potassium) decreases during long-
plasma hypoosmolality as a result of mild volume
distance exercise in Alaskan sled dogs despite no apparent
expansion (urine sodium concentration usually >20
change in TBW, and consequently hyponatremia
mEq/L in human patients). 74
develops. The observed hyponatremia was mild (i.e.,
5. No evidence of hypovolemia, which could result in
139.7 mEq/L after the race as compared with 148.6
nonosmotic stimulation of vasopressin release. 75
mEq/L before the race). Dogs do not sweat apprecia-
6. No evidence of ascites or edema, which could result in
hypervolemic hyponatremia (i.e., no evidence of bly, and the mild hyponatremia was attributed to
severe liver disease, congestive heart failure, or increased urinary losses of sodium in association with
nephrotic syndrome). increased protein catabolism and excretion of large
7. Correction of hyponatremia by fluid restriction. amounts of urea in urine.
Drugs that stimulate the release of vasopressin or
Impaired osmoregulation of vasopressin release was
potentiate its renal effects may lead to normovolemic
observed in 11 dogs with liver disease (7 of which had hyponatremia. Nitrous oxide, barbiturates, isoprotere-
large congenital portosystemic shunts). 143 Either the
nol, and narcotics are drugs used during anesthesia and
threshold for vasopressin release was increased or the
surgery that stimulate vasopressin release from the neuro-
magnitude of response decreased in these dogs, but
hypophysis and may contribute to impaired water excre-
plasma vasopressin and sodium concentrations were
tion in the postoperative period. Anxiety, stress, and pain
within the normal reference range. Affected dogs had
associated with surgical procedures also may contribute