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955.e2 Syndrome of Inappropriate Antidiuretic Hormone Secretion

Syndrome of Inappropriate Antidiuretic Hormone Secretion
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medical conditions (e.g., hydrocephalus,
BASIC INFORMATION
meningoencephalitis, putative cystic Rathke’s antagonists of the renal ADH receptor may
also be effective but are expensive.
Definition pouch, aspiration pneumonia).
Syndrome of inappropriate antidiuretic Acute General Treatment
hormone secretion (SIADH) is a disorder DIAGNOSIS • Severe hyponatremia (<120 mEq/L) should
caused by release of antidiuretic hormone (ADH be corrected with IV fluid therapy using
[vasopressin]) in the absence of normal osmotic Diagnostic Overview conventional crystalloid solutions (e.g.,
or nonosmotic stimuli. SIADH is rarely diagnosed but should be 0.9% saline) to raise plasma sodium con-
considered in patients with hyponatremia for centration at a rate of less than 12 mEq/L/
Synonyms which other differentials have been excluded day. Hypertonic saline (3%-5%) should be
Syndrome of inappropriate antidiuresis (SIAD); by clinical signs, complete database (CBC/ avoided because it may raise the plasma
vasopressin excess biochemistry profile/urinalysis), adrenocortico- sodium concentration too rapidly in cases
tropic hormone (ACTH) stimulation testing, of chronic hyponatremia.
Epidemiology and thyroid testing. Paired urine and plasma • After plasma sodium concentration has been
SPECIES, AGE, SEX osmolality measurements may help to confirm corrected to > 125 mEq/L, water may be
Rare in dogs and cats; no sex or age the diagnosis. offered orally at a volume less than urine
predisposition output to promote free water loss and restore
Differential Diagnosis normal body fluid volume.
RISK FACTORS Hyponatremia (pp. 518 and 1241):
Pituitary surgery • Primary hypoadrenocorticism Chronic Treatment
• Diabetes mellitus/glucosuria • Chronic management of SIADH is directed
ASSOCIATED DISORDERS • Gastrointestinal (GI) sodium loss (vomiting, at treating the underlying cause. If this is
Hyponatremia and cerebral edema diarrhea) not possible, plasma hypoosmolality and
• Chronic congestive heart failure hyponatremia should be prevented by water
Clinical Presentation • Primary polydipsia restriction.
HISTORY, CHIEF COMPLAINT • Artifact (hyperlipidemia) • A selective ADH receptor antagonist, OPC-
• Lethargy and nausea • Acute kidney injury/anuria 31260 (Otsuka Pharmaceutical, Tokyo), has
• Neurologic signs: tremors, generalized • Severe liver disease been reported to palliate signs in a dog with
seizures, and coma • Nephrotic syndrome SIADH over a 3-year treatment period with
• Hypothyroidism a dosage of 3 mg/kg PO q 12h.
PHYSICAL EXAM FINDINGS • Recent use of diuretics • Other selective (nonpeptide) ADH receptor
• Weakness • Hospital-acquired fluid imbalance antagonists (e.g., tolvaptan, conivaptan) are
• Tremors, seizures, or coma available for human patients, but their use
• No evidence of peripheral (extracellular) Initial Database in dogs with clinical hyponatremia remains
edema or ascites • CBC, serum biochemical profile, urinalysis: poorly described.
hyponatremia, normal renal parameters
Etiology and Pathophysiology • ACTH stimulation test: normal response Possible Complications
• Normally, ADH is released by the • Total thyroxine (T 4 ) concentration: normal • Rapid correction of chronic hyponatremia
neurohypophysis (posterior pituitary) in or low can result in osmotic demyelination
response to increased plasma osmolality • Further testing to exclude primary hypothy- syndrome due to brain dehydration as free
and, to a lesser degree, to reduced blood roidism may be required (p. 525). water moves out of the brain and into the
volume. relatively hypertonic plasma.
• In SIADH, inappropriate ADH release Advanced or Confirmatory Testing • Clinical signs of osmotic demyelination
occurs independent of normal stimuli from • Plasma osmolality: decreased (<280 mOsm/ syndrome occur 3-4 days after rapid cor-
osmoreceptors or baroreceptors. kg) rection of hyponatremia, are neurologic in
• Inappropriate ADH release results in • Urine osmolality: inappropriately high nature (lethargy, ataxia, hypermetria, paresis),
increased water resorption by the renal urine concentration (>1000 mOsm/kg) in and may be fatal.
collecting ducts, which leads to volume the presence of plasma hypo-osmolality and
expansion and plasma hypotonicity and hyponatremia Recommended Monitoring
subsequently to hyponatremia. • Plasma ADH concentration inappropriately • During the correction phase, patients should
• With hyponatremia, two-thirds of the rela- high relative to plasma osmolality; unfor- be monitored closely and plasma sodium
tive water surplus is intracellular, making tunately, circulating ADH concentrations concentration (using minimal amounts of
generalized (intra)cellular edema the hallmark can be measured only in a few research blood), fluid balance, and neurologic status
of SIADH. laboratories. should be checked q 1-2h.
• Unlike extracranial tissues that can expand • Improvement after water restriction • Chronic management requires periodic
freely, a distending brain is compressed monitoring of plasma sodium concentration.
against an unyielding cranium, provoking the TREATMENT
syndrome of cerebral edema. This syndrome PROGNOSIS & OUTCOME
includes weakness, lethargy, and nausea and Treatment Overview
may culminate in resting tremors, generalized Therapy for SIADH focuses on correction of Prognosis depends on the underlying cause of
seizures, and coma. hyponatremia and treatment of the underly- SIADH. In idiopathic forms of SIADH, water
• Although SIADH may be idiopathic, it has ing disease if identified. Fluid restriction is restriction may allow the animals to live an
also been related to a variety of drugs or an important part of the therapy. Selective almost normal life for several years.

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