DI vs SIADH: Overview Notes
Diabetes Insipidus (DI); DRY
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Hyposecretion of ADH/Vasopressin secondary to strokes, trauma, idiopathic causes
kidney tubules fail to reabsorb water.
Diabetes insipidus (DI) is associated with a deficiency (lack) of production or secretion of
ADH/Vasopressin or decreased renal response to ADH. Depending on cause, DI may be
transient or a chronic lifelong condition.
There are three types of DI: Central (Neurogenic) ADH not produced by posterior pituitary,
which is most common, nephrogenic (Renal tubules desensitized to effects of ADH, and
primary.
o Central (Neurogenic)- usually occurs due to severe head trauma, brain or pituitary
tumors. Posterior pituitary unable to secrete vasopressin (ADH), leading to inability to
concentrate urine
DI is characterized by polydipsia and polyuria. If oral fluid intake cannot keep up with urinary
losses, severe fluid volume deficit results as manifested by hypotension and hypovolemic
shock. The increased urinary output and plasma osmolality can cause severe fluid and
electrolyte imbalances.
DI is characterized by dilute urine with urine output greater than 200 mL per hour and specific
gravity < 1.005 (Dilute). Identification of cause as central neurogenic DI often requires a water
deprivation test.
For central DI, fluid and hormone therapy is the cornerstone of treatment.
Nursing care includes early detection, maintenance of adequate hydration, and patient teaching
for long-term management.
Assessment
Polyuria, 4 to 24 L/day
Polydipsia
Dehydration
Decreased skin turgor, dry mucus membranes
Inability to concentrate urine
Low urinary specific gravity, below 1.005
Elevated plasma osmolality >295 mOsm/kg (Dry)
Decreased urine osmolality <500 mOsm/kg (Dilute)
Hypernatremia (Na high = serum dry)
Fatigue
Muscle pain/weakness
Headache
Postural hypotension that may progress to vascular collapse
Tachycardia
Hemo-concentration (electrolyte, etc.)
Interventions – Nursing Care
Monitor vital signs/cardiovascular/neurological status.
Provide safe environment.
Monitor electrolyte levels as prescribed (BMP, UA)
Strict I&O, foley catheter
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Monitor for signs dehydration (Decreased urine output, loss of weight, decreased specific
gravity, dry skin, dry mucus membranes, lack of tears, if infant, sunken fontanel)
Maintain adequate intake of fluids (Volume replacement)
Administer chlorpropamide as prescribed for mild DI.
Administer vasopressin (ADH) tannate or desmopressin acetate
(DDAVP) IV/SQ initially as prescribed for severe or chronic deficiency in ADH.
Instruct client in administration of medications as prescribed.
Desmopressin acetate (DDAVP) may be administered intranasally,
by injection, or orally.
Educate client to obtain and wear at all times Medic-Alert bracelet.
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
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Excess ADH/Vasopressin released, but not in response to bodily need for it. Causes include
trauma, stroke, malignancies, especially lungs/pancreas, medications (antineoplastics), stress.
Results in hyponatremia. Excessive release of ADH→ decreases urine volume → urine very
concentrated → Can progress to water intoxication, cerebral edema and death.
Syndrome of inappropriate antidiuretic hormone (SIADH) results from abnormal production or
sustained secretion of ADH. The most common cause is a hormone-secreting tumor, such as
lung cancer.
SIADH is characterized by fluid retention, serum hypoosmolality, dilutional hyponatremia,
hypochloremia, concentrated urine in presence of normal or increased intravascular volume,
and normal renal function.
Treatment is directed at the underlying cause with a goal to restore normal fluid volume and
osmolality. Fluid restriction results in gradual, daily weight reductions, progressive rise in
serum sodium concentration and osmolality, and symptomatic improvement. With chronic
SIADH, patients must learn self-management.
Low sodium levels must be normalized very carefully and in a measured manner. The level
should not increase by more than 8 to 12 mEq/L in the first 24 hours.
Sodium levels of less than 120 mg/dL are considered critical and require the implementation of
seizure precautions and hourly neuro checks.
Assessment
Signs of fluid overload, including bounding pulse, hypertension, distended
neck veins, dyspnea, crackles, pitting dependent
edema, ascites
Weight gain
Tachycardia
Early signs: Anorexia/nausea/vomiting, HA, Fatigue, Dyspnea
Late signs: Decreased LOC, Coma, Seizures
Hyponatremia (Na+ <135 mEq/dL)
Blood Serum Osmo < 280 mOsmo/kg (Dilute)
Very concentrated urine
Urine Osmo >500 mOsmo/kg
Interventions – Nursing Care
Monitor vital signs/cardiac/neurological status.
Provide safe environment.
Strict I&O
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Daily weighing, if in hospital.
Monitor serum electrolytes, especially sodium.
Restrict fluid intake (Free water restriction)
Administer diuretics (Loop diuretics; Furosemide, Bumetadine)
Administer IV fluids; If severe, 3% saline infusion + diuretic
Monitor infusions carefully because of risk of water intoxication.
Administer demeclocycline (tetracycline antibiotic): Increases urinary water
excretion, Inhibits ADH (ADH release) induced water reabsorption/produces
water diuresis
Normal Labs
Serum Osmolality 285-295 mOsm/kg
Sodium 136-145 mEq/L
Urine osmolality 500-1200 mOsm/kg
Urine specific gravity 1.005-1.030
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