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Syndrome of Inappropriate Antidiuretic Hormone Secretion: Recognition and Management.


This educational activity is designed for nurses and other health care professionals who care for and educate patients regarding the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The multiple choice examination that follows is designed to test your achievement of the following educational objectives. After studying this offering, you will be able to:

1. Cite risk factors associated with the development of SIADH.

2. Describe the pathophysiology that occurs in SIADH.

3. Examine laboratory data of a client who has SIADH.

4. Explain treatment modalities for SIADH and the rationale for their uses.

Older persons are at greater risk for developing hyponatremia. Structural changes in aging kidneys cause alterations in the functional balance of fluid and electrolytes, and sodium regulation is less effective (Larsen & Martin, 1994). When serum sodium values for 139 healthy persons were analyzed, an age-related decrease of 1 mEq/L/decade from a mean value of 141 [+ or -] 4 mEq/L in younger persons was noted (Abrams, Beers, & Berkow, 1995). In one study of elderly persons in long-term care facilities, 18% to 22% had serum sodium levels [is less than or equal to] 135 mEq/L, and over a 12-month period, the incidence of hyponatremia among this group was about 50% (Abrams, Beers, & Berkow, 1995).

In one form of hyponatremia found among the elderly, total body sodium content is normal, but water is retained because of increased antidiuretic hormone (ADH) secretion. This condition, referred to as the syndrome of inappropriate secretion of ADH or SIADH, has many causes including chronic illnesses and various medications. Its development can be insidious, but SIADH can lead to dangerously low serum sodium levels. A high degree of suspicion for this disorder can help lead to early recognition and appropriate treatment. To understand what causes SIADH, a brief review of related physiology is necessary.


There are several homeostatic mechanisms involved in maintaining fluid balance. One such mechanism, the hypothalamus-neurohypophyseal system, is responsible for the neural control of bodywater balance. Special neurosecretory cells in the hypothalamus' supraoptic and paraventricular nuclei synthesize ADH. Axons from these nuclei in the hypothalamus extend through the pituitary stalk to the pituitary gland's posterior lobe. ADH is stored in the pituitary's posterior lobe in resting conditions. Strategically located near the supraoptic nuclei of the hypothalamus are osmoreceptors which create a feedback control system for ADH secretion. These osmoreceptors respond to very minute changes (1% to 2%) in the osmolality of the extracellular fluid which can result from changes in sodium ion concentration. Normal osmolality is maintained in a very narrow range (between 280 mOsm/kg and 295 mOsm/kg). When it reaches 295 mOsm/kg, osmosis of water out of the osmoreceptor cell causes the cell to shrink. This shrinkage increases the cell's firing rate, and, in turn, increases the secretion of ADH. Conversely, when extracellular osmolality is low ([is less than] 280 mOsm/kg), osmosis of water into the osmoreceptor causes the cell to swell. Swelling decreases the firing rate of the osmoreceptor cells which slows the production of ADH (Germon, 1987).

In the kidney, circulating ADH attaches to receptor sites on the nephron in the distal tubule and collecting duct and increases the permeability of these sites to water (Batcheller, 1994). Hence, when the osmoreceptors in the hypothalamus sense an increase in plasma osmolality, ADH is released, and the kidney reabsorbs solute-free water into the capillary network. A smaller volume of concentrated urine is excreted. In contrast, when plasma osmolality is reduced to below 280 mOsm/kg, ADH release is inhibited, no water reabsorption by the kidney occurs, and a large volume of dilute urine is excreted (Tang & Lau, 1995).

In addition, stretch receptors in the left atrium and baroceptors in the aortic arch and carotid sinus sense shifts in effective circulating blood volume and changes in blood pressure. These receptors provide information to the hypothalamus as well via ascending neural fibers. Inhibitory or facilitory impulses from the hypothalamus to the pituitary can then be initiated which either decrease or increase the excretory rate of ADH (Patterson & Noroian, 1989; Germon, 1987). Limbic stimulation may also lead to an increase in ADH production, and a systemic response to stress is the most likely cause. Stimuli which may activate the limbic system include pain, nausea, fear, and major trauma (for example, surgery) (Poe & Taylor, 1989).


SIADH results from an abnormal production or sustained secretion of ADH, and it has been associated with many clinical states or syndromes as well as a variety of drugs. The most frequent cause is a cancer, particularly small cell or oat cell carcinomas of the lung (Batcheller, 1994; Poe & Taylor, 1989). Malignant lung cells obtained from patients with SIADH are capable of synthesizing, storing, and releasing ADH. Chemical and biologic analyses of tumor cells have demonstrated that this cellularly derived ADH is identical to the hormone produced by the neurophypophyseal system (Poe & Taylor, 1989). Since this syndrome can precede the diagnosis of a tumor, it should always be viewed as a potential marker of an underlying malignancy (Germon, 1987).

Other pulmonary conditions associated with SIADH include bacterial pneumonias, chronic obstructive pulmonary disease (COPD), tuberculosis (TB), and lung abscesses. The most likely source of ADH in these conditions is also endogenous release; TB lesions, for example, may synthesize and release the hormone in a manner similar to that of malignancies (Batcheller, 1994). Malignancies of the pancreas, duodenum, colon, lymphoid tissue, and thymus can also produce this syndrome Batcheller, 1994; Lindaman, 1992; Poe & Taylor, 1989).

SIADH is a potential untoward effect of a number of medications. This is particularly problematic for frail elderly persons who consume the largest number of medications. A typical nursing home patient receives an average of seven drugs, and the medications most commonly prescribed are antipsychotics, sedative-hypnotics, diuretics, antihypertensives, analgesics, cardiac drugs, and antibiotics (Abrams et al., 1995). Many of these commonly prescribed drugs have been tied to SIADH (see Table 1).

Table 1. Causes of SIADH
Drugs                   Malignancies            Conditions

Morphine                Bronchiogenic           Hypothyroidism
Barbiturates            Pancreatic              Tuberculosis
Vincristine             Duodenal                Lung abscess
Carbamazepine           Lymphoid tissue         Pneumonia
General anesthetics     Prostate                COPD
Nicotine                Thymus                  Status asthmaticus
Clofibrate              Colon                   Lupus erythematous
Chlorpropamide          Brain                   Acute intermittent
Tolbutamide                                     Porphyria
Thiazide diuretics
Beta adrenergic

                        Neurovascular           Miscellaneous
Drugs                   Disorders               Conditions

Morphine                Skull fracture          Severe pain
Barbiturates            Subdural hematoma       Stress
Vincristine             Subarachnoid hem-       Nausea
Carbamazepine           orrhage                 Trauma
General anesthetics     CV thrombosis           Anxiety
Nicotine                Cerebral atrophy
Clofibrate              Acute encephalitis
Chlorpropamide          TB meningitis
Tolbutamide             Purulent meningitis
Acetamide               Guillian-Barre
Thiazide diuretics
Beta adrenergic

Drugs such as chlorpropamide and carbamazepine either increase or potentiate the action of ADH. To illustrate, chlorpropamide enhances the release of ADH from the posterior pituitary lobe and potentiates the action of ADH on the collecting duct, thereby causing an iatrogenic form of SIADH. Most instances of SIADH related to diuretics have occurred with the use of thiazides (for example, hydrochlorthiazide, metolazone, chlorthalidone, and chlorothiazide). These drugs (a) act on the distal nephron to decrease free water excretion, (b) result in drug-induced volume depletion, and (c) increase renin production. Antineoplastic drugs, such as vincristine, tricyclic antidepressants, and nicotine, the primary ingredient in tobacco, have all been associated with increased amounts of circulating ADH (Batcheller, 1994; Poe & Taylor, 1989).

Patients on ventilators with positive end expiratory pressure (PEEP) may exhibit a form of SIADH. The PEEP may decrease venous return thereby reducing volume and atrial stretch. Baroceptors are then stimulated and ADH secretion is enhanced. Fluid is retained because the body is misreading its own signal and responding as if blood volume is low (Batcheller, 1994; Germon, 1987).

Psychologic stimuli via the limbic system to the hypothalamus may result in overproduction of ADH. Examples of such stimuli may include trauma, pain, stress, and acute psychosis (Batcheller, 1994; Poe & Taylor, 1989; Germon, 1987). Nausea is another potent stimulator of ADH release that may be a cause of the hyponatremia often seen in patients experiencing nausea and vomiting. In such cases, volume depletion stimulates ADH release so that water is retained in excess of sodium. The hyponatremia which results is usually mild and is rarely [is less than] 125 mEq/L (Abrams et al., 1995; Poe & Taylor, 1989).

Signs and Symptoms

Excessive secretion of ADH results in unchecked water reabsorption from the distal renal tubules and collecting ducts of the kidney. The posterior pituitary becomes unresponsive to the normal feedback mechanisms and water conservation continues despite decreasing serum osmolality. With the continuing absorption of fluid, blood volume increases, and the kidneys attempt to compensate for this by actively excreting sodium. Urine osmolality becomes inappropriately high compared to serum osmolality, and urine sodium levels increase (Brunner & Suddarth, 1988; Isley, 1990; Patterson & Noroian, 1989).

The severity of signs and symptoms depends on both the degree of hyponatremia and how rapidly the syndrome develops (Batcheller, 1994; Poe & Taylor, 1989). Table 2 displays common signs and symptoms. Neurologic sequelae are often the result of cerebral edema which occurs when the low serum osmolality disrupts the normal intracellular-extracellular osmotic gradient and water moves into brain cells. When hyponatremia develops quickly (in less than 48 hours) and plasma sodium levels dip below 120 mEq/L, more serious neurologic signs and symptoms such as seizures and coma may occur and mortality rates can rise as high as 50% (Batcheller, 1994). With coexisting alcoholism or cachexia, the rate reaches about 70% (Abrams et al., 1995).

Table 2. Signs and Symptoms of SIADH
Cardiovascular          Neurological          Gastrointestinal

Increased blood         Decreased level of    Anorexia
 pressure                consciousness        nausea/Vomiting
Weight gain without     Headache              Decreased bowel
 edema                  Impaired memory        sounds
                        Confusion/            Abdominal cramps
                        Muscle cramps
                        Psychotic behavior

Cardiovascular          Urinary               Respiratory

Increased blood         Decreased urine       Adventitious breath
 pressure                output                sounds
Weight gain without

When hyponatremia evolves more slowly (over more than 48 hours), the movement of solutes such as sodium and potassium ions and amino acids out of brain cells can help to normalize brain water content by eliminating the osmotic gradient between intracellular and extracellular compartments. Then too, cerebral overhydration increases hydrostatic pressure in the cerebral interstitium. This results in the movement of fluid from the cerebral interstitial space to the cerebral spinal fluid (Tang & Lau, 1995). These adaptive mechanisms may prevent some patients with chronic hyponatremia from developing cerebral edema, and they remain relatively symptom free (Batcheller, 1994).


The diagnosis of SIADH involves excluding other possible causes of hyponatremia including congestive heart failure and cirrhosis. Both of these disorders can be associated with an elevated total body sodium content and normal or increased extracellular fluid volume; however, effective plasma volume is reduced which restricts the delivery of sodium and water to the diluting segments of the nephron. As a result, sodium-retaining mechanisms are activated as ADH release increases. As time passes, a net gain of water relative to sodium leads to dilutional hyponatremia (Abrams et al., 1995).

Since hyponatremia is a hallmark sign of adrenal insufficiency, patients with suspected SIADH should have serum and urinary cortisol levels. These levels would be decreased with Addison's disease but normal in SIADH. A thyroid profile would rule out hypothyroidism as a possible cause of hyponatremia.

The three main criteria for the clinical diagnosis of this syndrome are: (a) hyponatremia and hypoosmolality, (b) urine osmolality greater than 11 mOsm/kg of water, and (c) urine sodium concentration greater than 20 mEq/24 hours (Poe & Taylor, 1989). See Table 3 for additional laboratory values.

Table 3. Laboratory Values in SIADH
Serum              Normal                    SIADH

Osmolality         275 to 295 mOsm/kg H20    <275 mOsm/kg
Sodium             135 to 145 mEq/L          Decreased, <135 mEqL
BUN                5 to 25 mg/dL             Normal or decreased
Creatinine         f.6 to 0.9 mg/dL          Normal or decreased
                   m0.8 to 1.2 mg/dL
Calcium            8.5 to 10.5 mg/dL         Dilutional hypocalcemia
Potassium          3.5 to 5.5 mg/dL          Dilutional hypokalemia
Cortisol                                     Normal
Thyroid profile                              Normal
Uric acid                                    Low


Osmolality         400 to 1200 mOsm/kg H20   >1200 mOsm/kg H20
Specific gravity   1.025 to 1.032            >1.032
Cortisol                                     Normal

(*) Water Load Test (Patterson & Noroiam, 1989; Poe & Taylor, 1989)

    >80% of water load excreted        <40% to 80% of water load
     in 5 hours                         exerted
    Urine osmolality reaches low       No diuresis occurs
     of >100 mOsm/kg during 2nd        Urine osmolality remains >
     or 3rd hour                        the plasma osmolality
    Urine specific gravity

(*) This test begins with the patient testing overnight. The serum sodium must be 125 mEg/L or higher prior to starting. The patients is kept lying down for the test's duration because the upright position can decrease glomerular filtration and impair water excretion. An hour before the test begins, the patient is given 200 cc of water by mouth to replace overnight insensible losses. Begin the test by administering the test load of water (25 cc/kg of body weight). The patient is asked to drink the test load within 30 minutes. Urine volumes and osmolalities are obtained and recorded with each void for the next 4 to 5 hours.


Definitive treatment is directed at eliminating the underlying cause of the disorder whenever possible. Surgical resection, radiotherapy, and chemotherapy may successfully alleviate malignancy-induced SIADH. Medications that stimulate ADH release should be avoided or discontinued when possible (Poe & Taylor, 1989). Interventions aimed at relieving pain and/or reducing stress can help diminish stimulation of the limbic system.

The degree of water overload dictates the therapeutic regimen. Water excess (or the amount of water to be removed in order to achieve the desired sodium concentration) can be calculated using the formula shown in Figure 1.

Figure 1. Calculating Water Excess

Water Excess = TBW - TBW (Observed Serum Sodium/Desired Serum Sodium)

TBW (total body water) = (0.5 L/kg) (weight in kg)

(Tang & Lau, 1995)

Patients who present with mild to moderate hyponatremia (serum sodium levels between 125 to 134 mEq/l) will require fluid restriction of 800 to 1,000 ml/day. For those with severe hyponatremia, 500 ml/day is necessary (Abrams et al., 1995; Batcheller, 1994; Lindaman, 1992; Poe & Taylor, 1989). When fluid restriction is ordered, fluid intake via any route is tallied as intake, and meticulous monitoring of daily weights and intake/output records is necessary. Most patients prefer receiving 50% of the allotted fluids during the day shift, 30% during the evening shift, and the remainder during the nighttime hours (Poe & Taylor, 1989). Medications should be scheduled with meals to provide for maximum flexibility in fluid intake. Oral mucous membranes can be kept moist by providing frequent mouth care (for example, oral rinses without swallowing) and having the patient suck on hard candy. Tap water and saline enemas should be avoided as the fluid may be absorbed from the intestines. Nasogastric and other enteral tubes should be irrigated with normal saline solution rather than water (Batcheller, 1994).

Diet can also be manipulated to correct water overload in SIADH. Since the urine osmolality is relatively fixed, the urine output is primarily dependent upon the rate of solute excretion. Consequently, patients with a high urine osmolality will excrete the same osmotic load in a smaller volume of urine (they retain more water) when compared to those with a lower urine osmolality (they retain less water). More stringent water restriction would then be required in patients with higher urine osmolalities. Enhancing solute output by providing a high-sodium, high-protein diet may increase urine excretion (Tang & Lau, 1995). Patients can be encouraged to choose fluids high in sodium content such as milk, orange juice, tomato juice, and beef or chicken broth (Poe & Taylor, 1989). Serum electrolyte levels should be monitored at least daily initially.

If fluid restriction and dietary alterations are not successful and the serum sodium level is greater than 120 mEq/L with few or no symptoms, the urine can be made more dilute if necessary by prescribing a loop diuretic, demeclocyline, or lithium (Batcheller, 1994; Bryce, 1994; Patterson & Noroian, 1989; Tang & Lau, 1995). Loop diuretics such as furosemide are chosen over thiazide diuretics when treating SIADH because of their differing modes of action. Thiazides do not affect free-water reabsorption but act mainly at the cortical diluting site, increasing urinary excretion of sodium, chloride, and potassium, and thus worsening hyponatremia. On the other hand, furosemide inhibits free-water reabsorption, and this effect also lasts longer than the increase in sodium, potassium, and chloride excretion. It is possible that furosemide may also interfere with the action of ADH on the collecting tubule (Decaux, Waterlot, Genette, & Mockel, 1981). When potent diuretics are used, careful attention must be given to preventing the depletion of important electrolytes (Poe & Taylor, 1989).

Both demeclocyline and lithium directly impair the response to ADH at the nephron's collecting tubule which results in a more dilute urine and an increase in serum sodium (Batcheller, 1994; Bryce, 1994; Cherill, Stote, Birge, & Singer, 1975; Tang & Lau, 1995; White & Fetner, 1975). Demeclocyline, a tetracycline derivative antibiotic, is useful for patients who are unable to tolerate fluid restriction and if symptomatic hyponatremia threatens (Poe & Taylor, 1989). It is thought to be better tolerated than lithium carbonate which has a more toxic potential and is no longer a preferred drug for treating SIADH. Demeclocyline dosing ranges from 900 to 1,200 mg orally daily. This drug has a delayed onset of action (several days) and is therefore not recommended for acute management of SIADH. Monitoring of renal function is necessary because nephrotoxity is a possible untoward effect (Batcheller, 1994; Poe & Taylor, 1989; Tang & Lau, 1995). Demeclocyline (a) should be taken 1 to 2 hours before or after a meal, (b) should not be taken with aluminum, magnesium, iron, or calcium products which delay its absorption, and (c) may cause photosensitivity-type reactions or superinfections (Patterson & Noroian, 1989). In addition to these two drugs, there is limited data to suggest that phenytoin inhibits ADH secretion but its effectiveness remains questionable (Tanay, Yust, Peresecenschi, Abramov, & Aviram, 1979; Tang & Lau, 1995).

For patients with neurologic symptoms of severe hyponatremia, intravenous hypertonic sodium chloride replacement may be necessary until symptoms begin to clear and the serum sodium level reaches about 120 to 125 mEq/L. A hypertonic solution is used because, in some cases, normal saline (0.9%) may actually worsen hyponatremia. Normal saline has an osmolality of 308 mOsm/L. The patient who has a urine osmolality [is greater than] 308 mOsm/L will excrete the solute given as normal saline in less volume than it was infused. The remaining volume is retained as free water, further diluting the blood volume (Davis & Minaker, 1994). The hypertonic solution must be administered via infusion pump, and the patient is watched closely for manifestations of hypernatremia. The amount of sodium in mEq required to raise the sodium level to 120 mEq/L is calculated by using the formula shown in Figure 2.

Figure 2. Sodium Level Calculation

mEq Sodium Required = (0.5 L/kg) (weight in kg) (120 - actual sodium)

(Tang & Lau, 1995)

Most researchers agree that severe hyponatremia can be treated promptly, rapidly, and safely by raising the serum sodium level at a rate of 1.0 to 2.0 mEq/L/hour with intravenous therapy (Abrams et al., 1995; Ayus, Olivero, & Frommer, 1982; Davis & Minaker, 1994; Tang & Lau, 1995). This can usually be accomplished by administering 200 to 300 ml of 3% sodium chloride solution over 4 to 6 hours. Patients with extremely low serum sodium levels (less than 105 mEq/L) and severe neurologic sequelae such as seizures or coma may benefit from the simultaneous use of a loop diuretic such as furosemide to promote diuresis (Abrams et al., 1995; Poe & Taylor, 1989). The 3% saline solution only temporarily raises the serum sodium as it will continue to be rapidly excreted from the kidneys. Furosemide facilitates the normalization of serum sodium by decreasing its excretion (Germon, 1987).

Overcorrection of hyponatremia must be avoided. For that reason, restoring the serum sodium level to 120 to 125 mEq/L is the initial goal. Most major symptoms will dissipate at this point. The remaining deficit should then be gradually replaced over the next several days at a rate no faster than 5 to 7 mEq/ 24 hours. Too rapid correction of the sodium deficit could result in central pontine myelinolysis especially in severely malnourished patients and those with a history of alcoholism (Abrams et al., 1995; Ayus et al., 1982; Davis & Minaker, 1994).

Nursing Care

Ongoing assessment of the patient with SIADH is essential. To assist with monitoring of hydration status, a Foley catheter can be inserted and is helpful for those patients with an altered level of consciousness who are incontinent. It ensures accuracy of output data and facilitates ease of specimen collection (Bartter & Schwartz, 1967). The risk of infection posed by the Foley catheter must be weighed against its clinical benefit. Initially, an hourly assessment of intake and output data as well as urine specific gravity may be necessary. Daily weights obtained on the same scale, at the same time of day, with the patient wearing the same amount of clothing are recorded and reviewed for gains or losses. Other components of the fluid status assessment would include auscultation of the lungs to detect overhydration and monitoring of skin turgor (Poe & Taylor, 1989).

Frequent assessment of neurologic status and neuromuscular function helps detect subtle signs and symptoms of deterioration or improvement. When working with elderly patients in particular, it is important to obtain information about the patient's previous level of functioning and awareness. Family members, close friends, or previous caregivers can help provide this baseline data for comparison. Safety precautions such as low beds, gym pads on the floor, or a sitter would be necessary if confusion and disorientation occur or seizures are likely.

Finally, patient education is an important aspect of care. Basic information about SIADH, what causes it, and its signs and symptoms are included in the teaching plan. Provide a quick guide which lists fluid amounts in cc's for commonly used containers such as milk cartons or coffee cups, and then, when possible, have the patient record intake at the bedside him or herself. Urinals or appropriate collection receptacles for measuring urine output should be provided if there is no indwelling Foley catheter. The importance of accuracy when recording intake and output is stressed along with adherence to the prescribed fluid restriction. Patients should learn how to obtain accurate daily weights and are asked to report acute gains or losses of more than 1 kilogram (2.2 pounds). Indications and side effects of the medications used to treat SIADH should be discussed, and the patient's ability to self-administer prescribed drugs assessed (Patterson & Noroian, 1989).


SIADH can have a number of precipitating factors ranging from disease states to various medications. It can have an insidious onset but the sequelae can be life threatening. Nurses who encounter geriatric patients in particular need to have a high degree of suspicion for this disorder and be able to recognize signs and symptoms so that early intervention occurs.

Choose one correct answer for each question. CE Questions
1. The reason older persons are at greater risk to
develop hyponatremia is that:

a. They perspire more freely.
b. They tend to consume less sodium.
c. Their kidneys regulate sodium less effectively.
d. They replace table salt with potassium-based

2. Antidiuretic hormone (ADH) is produced in the
-- and stored in the --.

a. Hypothalamus, pituitary
b. Pituitary, hypothalamus
c. Nephrons, glomerulus
d. Glomerulus, nephrons

3. The most frequent cause of SIADH is:

a. Cancer, especially lung cancers.
b. Diuretic use.
c. Mechanical ventilation.
d. Vomiting.

4. SIADH occurs due to which of the following

a. A decrease in ADH production.
b. An increase in ADH production.
c. A decrease in renal sodium excretion.
d. An increase in renal sodium excretion.

5. Signs and symptoms of SIADH include

a. Urine output.
b. Blood pressure.
c. Bowel sounds.
d. Cognition.

6. Which of the following laboratory values are consistent
with SIADH?

a. Urine-specific gravity [is less than] 1.032
b. Urine osmolality [is less than] 1200 mOsm/kg H20
c. Serum sodium [is less than] 135 mEq/L
d. Serum osmolality [is greater than] 275 mOsm/kg

7. Included in the three main criteria for clinical
diagnosis of SIADH is/are:

a. Hyponatremia and hypo-osmolality.
b. Hypernatremia and hyperomolality.
c. Urine osmolality [is less than] 11 mOsm/kg H20.
d. Urine sodium concentration [is less than] 20 mEq/24hrs.

8. Which of the following medications works in the
treatment of SIADH by impairing the response of
the nephron to ADH?

a. Hydrochlorothiazide
b. Furosemide
c. Demeclocycline
d. Adriamycin

9. Diet therapy intended to promote urine excretion
in patients with SIADH includes providing a

a. Low sodium, low protein
b. Low sodium, high protein
c. High sodium, low protein
d. High sodium, high protein

10. Assessment of an elderly client who has SIADH
is more difficult if which of the following is not

a. Usual daily fluid intake.
b. Previous neurological and neuromuscular
c. Family history of SIADH.
d. Previously prescribed dietary sodium restrictions.


Abrams, W.B., Beers, M.H., & Berkow, R. (Eds.) (1995). The Merck manual of geriatrics (pp. 16-25). Whitehouse Station, NJ: Merck Research Laboratories.

Ayus, J.C., Olivero, J.J., & Frommer, J.P. (1982). Rapid correction of severe hyponatremia with intravenous hypertonic saline solution. The American Journal of Medicine, 72, 42-48.

Bartter, F.G., & Schwartz, W.B. (1967). The syndrome of inappropriate secretion of antidiuretic hormone. American Journal of Medicine, 42, 790-806.

Batcheller, J. (1994). Syndrome of inappropriate antidiuretic hormone secretion. Nursing Clinics of North America, 6(4), 687-691.

Brunner, L.S., & Suddarth, D.S. (1988). Textbook of medical surgical nursing (6th ed.) (pp. 297-298). Philadelphia: JB Lippincott Co.

Bryce, J. (1994). SIADH: Recognizing and treating syndrome of inappropriate antidiuretic hormone secretion. Nursing, 3, 33.

Cherill, D., Stote, R., Birge, J., & Singer, I. (1975). Demeclocycline treatment in the syndrome of inappropriate antidiuretic hormone secretion. Annals of Internal Medicine, 83, 654-656.

Davis, K.M., & Minaker, K.L. (1994). Disorders of fluid balance: Dehydration and hyponatremia. In W.R. Hazzard, E.L. Bierman, J.P. Blass, W.H. Ettinger, & J. Halter, J. (Eds.), Principles of geriatric medicine and gerontology (3rd ed.) (pp. 1183-1190). New York: McGraw-Hill, Inc.

Decaux, G., Waterlot, Y., Genette, F., & Mockel, J. (1981). Treatment of the syndrome of inappropriate secretion of antidiuretic hormone with furosemide. Medical Intelligence, 304(6), 329-330.

Germon, K. (1987). Fluid and electrolyte problems associated with diabetes insipidus and syndrome of inappropriate antidiuretic hormone. Nursing Clinics of North America, 22(4), 785796.

Isley, W.L. (1990). Serum sodium concentration abnormalities. Critical Care Nurse Quarter/y, 13(3), 82-88.

Larsen, P.D., & Martin, J. (1994). Renal system changes in the elderly. AORN Journal, 60(2), 298-301.

Lindaman, C. (1992). SIADH: Is your patient at risk? Nursing, 6, 60-63.

Patterson, L.M., & Noroian E.L. (1989). Diabetes insipidus versus syndrome of inappropriate antidiuretic hormone. Dimensions of Critical Care Nursing, 8(4), 226-234.

Poe, C.M., & Taylor L.M. (1989). Syndrome of inappropriate antidiuretic hormone: Assessment and nursing implications. Oncology Nurse Forum, 16(3), 373-381.

Tanay, A., Yust, I., Peresecenschi, G., Abramov, A.L., & Aviram, A. (1979). Long-term treatment of the syndrome of inappropriate antidiuretic hormone secretion with phenytoin. Annals of Internal Medicine, 90, 50-52.

Tang, I., & Lau, A. (1995). Fluid and electrolyte disorders. In L.V. Young & M.A. Koda Kimble (Eds.), Applied therapeutics: The clinical use of drugs (pp.1-27). Vancouver, WA: Applied Therapeutics, Inc.

White, M.G., & Fetner, C.D. (1975). Treatment of the syndrome of inappropriate secretion of antidiuretic hormone with lithium carbonate. New England Journal of Medicine, 292(8), 390-392.

Additional Readings

Bluff, D., & Oji, N. (1995). SIADH in a patient receiving sertraline (letter). Annals of Internal Medicine, 123, 811.

Manocha, A.A. (1991). Imipramine-induced syndrome of inappropriate antidiuretic hormone secretion (letter). Southern Medical Journal, 84, 1507-1509.

Terry L. Terpstra, MSN, RN, CS, A/GNP, is an Advanced Practice Nurse/Medicine, Battle Creek VA Medical Center, Battle Creek, MI.

Tammy L. Terpstra, MSN, RN, CS, A/GNP is an Advanced Practice Nurse/Extended Care, Battle Creek VA Medical Center, Battle Creek, MI.
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Author:Terpstra, Terry L.; Terpstra, Tammy L.
Publication:MedSurg Nursing
Geographic Code:1USA
Date:Apr 1, 2000
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