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Information

Synonym/Acronym

Vasopressin, arginine vasopressin hormone, ADH.

Rationale

To evaluate disorders that affect urine concentration related to fluctuations of ADH secretion, such as diabetes insipidus and syndrome of inappropriate ADH secretion.

Patient Preparation

There are no food, fluid, or medication restrictions unless by medical direction. The patient should be encouraged to be calm and in a sitting position for specimen collection.

Normal Findings

Method: Radioimmunoassay.

AgeAntidiuretic Hormone*SI Units (Conventional Units × 0.923)
NewbornLess than 1.5 pg/mLLess than 1.4 pmol/L
Child (normally hydrated)0.5–1.7 pg/mLLess than 0.5–1.6 pmol/L
Adult (normally hydrated)1–5 pg/mL0.9–4.6 pmol/L

*Conventional units.

Recommendation

This test should be ordered and interpreted with results of a serum osmolality.

Serum Osmolality*Antidiuretic HormoneSI Units (Conventional Units × 0.923)
270–280 mOsm/kgLess than 1.5 pg/mLLess than 1.4 pmol/L
280–285 mOsm/kgLess than 2.5 pg/mLLess than 2.3 pmol/L
285–290 mOsm/kg1–5 pg/mL0.9–4.6 pmol/L
290–295 mOsm/kg2–7 pg/mL1.8–6.5 pmol/L
295–300 mOsm/kg4–12 pg/mL3.7–11.1 pmol/L

*Conventional units.

Critical Findings and Potential Interventions

Effective treatment of the syndrome of inappropriate antidiuretic hormone production (SIADH) depends on identifying and resolving the cause of increased ADH production. Signs and symptoms of SIADH are the same as those for hyponatremia, including irritability, tremors, muscle spasms, convulsions, and neurological changes. The patient has enough sodium, but it is diluted in excess retained water. Failure to treat can be life threatening as water intoxication with sodium deficit leads to free water movement to cerebral cells, cerebral edema, coma, and death.

Overview

Study type: Blood collected in a prechilled lavender-top [EDTA] tube; related body system: Endocrine system.

Instructions regarding appropriate handling and transport of the specimen should be obtained from the testing facility prior to specimen collection. ADH is formed by the hypothalamus and stored in the posterior pituitary gland. ADH is important in the regulation of water reabsorption and is released in response to increased serum osmolality or decreased blood volume. ADH secretion exhibits diurnal variation; the highest levels occur at night, which helps prevent the need for urination during the night. When the hormone is active, water is reabsorbed by the kidneys into the circulating plasma instead of being excreted, and small amounts of concentrated urine are produced; in its absence, large amounts of dilute urine are produced. Although a 1% change in serum osmolality stimulates ADH secretion, blood volume must decrease by approximately 10% for ADH secretion to be induced. Psychogenic stimuli, such as stress, pain, and anxiety, may also stimulate ADH release, but the mechanism is unclear.

The ADH suppression, or water load, test is used in the differential diagnosis of SIADH from other causes related to sodium imbalances (e.g., adrenal insufficiency, excessive loss of sodium) or conditions that result in the development of edema (e.g., heart failure, myxedema, nephrosis). The suppression test is performed over a 6-hr period, in the fasting state, by administration of water at the initiation of the test (20 mL/kg of body weight to a maximum of 1,500 mL) followed by hourly measurements of serum and urine osmolality. The idea of osmolality being increased or decreased can be confusing in disease states because blood and urine levels vary in response to each other’s compensatory mechanisms in maintaining water balance. Normal serum osmolality is 275 to 295 mOsm/kg; urine osmolality is 250 to 900 mOsm/kg; and the normal ratio of serum osmolality to urine osmolality is 1:3. Urine and serum values should be evaluated together.

Normally we associate low values with small concentrations and high values with large concentrations. In the case of SIADH, urine osmolality values decrease in response to an abnormal increase in ADH secretion, telling the kidneys to retain water, concentrate the urine, and dilute the blood volume. A smaller urine osmolality number indicates highly concentrated urine, and a larger number indicates more dilute urine. Patients with SIADH excrete none or a very small amount of the water and have a more concentrated urine that measures a higher urine osmolality than expected if ADH was being properly suppressed (greater than 100 mOsm/kg, is an indication of the kidneys’ inability to dilute the urine), whereas patients with an imbalance of sodium or significant edema excrete some water and have a relatively more dilute or decreased urine osmolality than patients with SIADH (less than 300 mOsm/kg). Patients should be closely monitored and educated regarding the signs and symptoms of water intoxication, a potential complication of the suppression test.

Indications

Interfering Factors

Factors That May Alter the Results of the Study

  • Drugs and other substances that may increase ADH levels include acetaminophen, barbiturates, estrogen, furosemide, lithium, narcotics, sulfonylureas, and thiazides.
  • Drugs and other substances that may decrease ADH levels include chlorpromazine, ethyl alcohol, and phenytoin.
  • Recent radioactive scans or radiation within 1 wk before the test can interfere with test results when radioimmunoassay is the test method.
  • ADH exhibits diurnal variation, with highest levels of secretion occurring at night; first morning collection is recommended.
  • ADH secretion is also affected by posture, with higher levels measured while upright.

Potential Medical Diagnosis: Clinical Significance of Results

Increased In

  • Acute intermittent porphyria (speculated to be related to the release of ADH from damaged cells in the hypothalamus and effect of hypovolemia; the mechanisms are unclear)
  • Brain tumor (related to ADH production from the tumor or release from damaged cells in an adjacent affected area)
  • Disorders involving the central nervous system, thyroid gland, and adrenal gland (numerous conditions influence the release of ADH)
  • Ectopic production (related to ADH production from a systemic tumor)
  • Guillain-Barré syndrome (relationship to SIADH is unclear)
  • Hypovolemia (potent instigator of ADH release)
  • Nephrogenic diabetes insipidus (related to lack of renal system response to ADH stimulation; evidenced by increased secretion of ADH)
  • Pain, stress, or exercise (all are potent instigators of ADH release)
  • Pneumonia (related to SIADH)
  • Pulmonary tuberculosis (related to SIADH)
  • SIADH (numerous conditions influence the release of ADH)
  • Tuberculous meningitis (related to SIADH)

Decreased In

Decreased production or secretion of ADH in response to changes in blood volume or pressure.

Nursing Implications, Nursing Process, Clinical Judgement

Before the Study: Planning and Implementation

Teaching the Patient What to Expect

  • Discuss how this test can assist in providing information about effective urine concentration.
  • Explain that a blood sample is needed for the test.

After the Study: Implementation & Evaluation Potential Nursing Actions

Avoiding Complications

  • Observe for signs and symptoms of hyponatremia (low sodium) and fluid retention.
  • Frequently monitor input and output, vital signs, weight, and results of other laboratory values to include Na+, urine specific gravity, and osmolality.
  • Manage medications, understanding both purpose and observed effect.
  • Monitor for CNS changes; orientation, alertness, confusion, seizure activity, or coma related to decreased sodium.
  • Maintain an open airway for those who are CNS compromised.

Treatment Considerations

  • Inform the patient, as appropriate, that treatment for fluid retention may include diuretic therapy and fluid restriction to successfully eliminate the excess water. Ideally, the patient should be in a quiet environment with as little environmental stimulation as possible.
  • Discuss the importance of adhering to fluid restrictions to overall health.

Nutritional Considerations

  • Add dietary sodium to assist in reversal of hyponatremia as appropriate.
  • Review specific fluid limitations for those at risk for fluid overload.

Clinical Judgement

  • Consider how altered electrolytes can damage normal body function and what can be said to the patient to convince them to adhere to treatment options.

Follow-Up and Desired Outcomes

  • Acknowledges education regarding reportable initial SIADH symptoms; fatigue, weakness, nausea, anorexia, headaches. This includes late symptoms such as irritability, muscle weakness, vomiting, decreased reaction time, altered level of consciousness, or seizures.
  • Understands the therapeutic goal is to normalize fluid and electrolyte balance.