Page 1134 - Clinical Small Animal Internal Medicine

1072 Section 10 Renal and Genitourinary Disease

A correction factor can be applied to correct the serum in neurologic or oncologic patients as well as after major
VetBooks.ir sodium concentration in diabetic patients. Traditionally, surgery (Table 118.2). The syndrome refers to secretion
of ADH that is inappropriate for the physiologic state
that correction factor has been reported to be 1.6–
1.7 mEq/L, such that for each 100 g/dL increase in blood
It is characterized clinically by normovolemia, low serum
glucose concentration above normal, the serum sodium (i.e., not secondary to hypovolemia or hyperosmolality).
concentration will decrease by 1.6–1.7 mEq/L. This cor- sodium concentration, and decreased urine output. The
rection factor has been challenged in human medicine, urine osmolality is high and urine sodium concentration
and the correction factor may be closer to 2.4 mEq/L, is >20 mEq/L, indicating that the patient is not in a
and also the association between sodium and glucose sodium‐retaining state (i.e., not hypovolemic) and
concentrations is nonlinear, with a correction factor that that the ADH secretion is in fact inappropriate (see
can be up to 4.0 mEq/L if blood glucose concentration is Table 118.2). The decreased urine output will not respond
above 400 mg/dL. The appropriate correction factor for to fluid administration, which is the first indication for
dogs and cats is unknown. the clinician faced with a patient with decreased urina-
For example, a patient with a blood glucose concentra- tion, and measurements of urine sodium concentration
tion of 1100 g/dL and serum sodium concentration and osmolality are necessary for the diagnosis of SIADH.
between 105 and 125 mEq/L would have a “corrected The usual treatment for SIADH is fluid restriction and
serum sodium” concentration of 145 mEq/L (i.e., nor- treatment of the primary cause, allowing the body to
mal) if a correction factor of 2–4 mEq/L is used. This reset its ADH trigger (usually within 24–72 hours). Most
patient therefore is actually not suffering from hypona- criticalists will treat patients with SIADH using a low
tremia. Alternatively, the same patient with a measured dosage (e.g., 0.2–0.5 mg/kg) of furosemide.
serum sodium concentration of 135 mEq/L would have a
“corrected serum sodium” concentration between 155 Clinical Manifestations of Hyponatremia
and 175 mEq/L. Thus, such a patient actually is suffering
from free water loss and should be treated accordingly. It is not possible to predict serum sodium concentration
Similarly, when monitoring the changes in serum sodium based on history and physical examination. Measurement
concentration in diabetes mellitus, the “corrected serum of serum sodium concentration is needed as well as some
sodium” concentration should be used to judge the risk other clinicopathologic data to rule out pseudohypona-
of overly rapid osmotic shifts of water, because these tremia. Clinical signs of hyponatremia are nonspecific
shifts are due to changes in osmolality and should take (e.g., nausea, vomiting), and related to dysfunction of the
into account the blood glucose concentration. central nervous system, such as lethargy, disorientation,
The syndrome of inappropriate ADH secretion and diminished reflexes. Most human patients do not
(SIADH) is a common disorder in critically ill human manifest clinical signs until serum sodium concentration
patients and also has been described in dogs. It is common is below 125 mEq/L, although rapid decrease in serum

Table 118.2 Syndrome of inappropriate ADH secretion summary

Identify appropriate trigger Diagnosis
● Postoperative nausea ● Plasma hypoosmolality
a
● Pain or stress ● Normovolemia (i.e., absence of hypovolemia)
● Neoplasia (common) ● Increased urine specific gravity/osmolality (>100 mOsm/kg)
● Pulmonary disease ● Urine sodium concentration >20–40 mEq/L indicating absence of an RAAS trigger (i.e.,
b
● Neurologic disease absence of hypovolemia)
● Trauma
● Drugs (e.g., NSAIDs, narcotics,
vincristine)
Treatment Notes
● Stop/decrease fluid therapy ● Low urine output not responsive to fluid therapy
● Treat primary trigger ● Age is a risk factor in humans
● May provide small dose of ● Case reports of SIADH have been published in veterinary medicine
furosemide
NSAID, nonsteroidal antiinflammatory drug; RAAS, renin‐angiotensin‐aldosterone system; SIADH, syndrome of inappropriate ADH.
a Spot urine sodium concentration can be influenced by administration of steroids or diuretics, osmotic diuresis (e.g., glucosuria, mannitol
administration, postobstructive diuresis), chronic kidney disease and bicarbonaturia (e.g., proximal renal tubular acidosis).
b A weight gain is common in SIADH (author’s personal observation).