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CLINICAL JOURNAL OF ONCOLOGY NURSING • VOLUME 7, NUMBER 4 • SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION IN MALIGNANCY 425

Syndrome of Inappropriate AntidiureticHormone Secretion in Malignancy: Reviewand Implications for Nursing Management

Lori A. Langfeldt, RN, BSN, OCN ®, and Mary E. Cooley, PhD, CRNP, CS

Submitted February 2003. Accepted for pub-lication March 3, 2003.

Digital Object Identifier: 10.1188/03.CJON.425-430

Hyponatremia is a common fluid and electrolyte distur-bance in adults with cancer. Although a number of etiolo-gies are associated with hyponatremia, the syndrome ofinappropriate antidiuretic hormone (SIADH) secretion isone of the most common underlying causes. Early symp-toms often associated with SIADH are subtle but, if leftuntreated, may progress to life-threatening seizures,coma, and death. Because oncology nurses have frequentand ongoing contact with patients, they are in an idealposition to recognize patients who are at increased risk forSIADH and those who present with early symptoms. Be-ginning signs and symptoms are mild and can be mistak-enly attributed to other causes. This article reviews thepathophysiology of SIADH, associated risk factors, signsand symptoms, diagnosis, treatment, and nursing care.

Key Words: inappropriate ADH syndrome; hyponatre-mia; carcinoma, small cell

H yponatremia is a com-mon fluid and electro-lyte disturbance in

adults with cancer. Hyponatre-mia has many causes, includingthe primary tumor, metastasis,diagnostic procedures, andtherapeutic interventions, or itcan result as a secondary com-plication (Berghmans, 1996;McDonald & Dubrose, 1993).Although the syndrome of inap-propriate antidiuretic hormone(SIADH) secretion is a rareparaneoplastic syndrome (oc-curring in 1%–2% of adults withcancer), it is a common under-lying etiology for hyponatremia(Poe & Taylor, 1989). In fact,several studies have identifiedthat SIADH is among the mostcommon reasons for hyponatre-mia and accounts for up to one-third of cases (Anderson, Chung,Kluge, & Schrier, 1985; Berghmans,Paesmans, & Body, 2000; Miller, Hecker,Friedlander, & Carter, 1996). Therefore, on-cology nurses must be knowledgeable aboutthis syndrome. This article provides a reviewof the pathophysiology, risk factors, signsand symptoms, diagnosis, treatment, and ap-propriate nursing management of patientswith SIADH.

PathophysiologySodium and water balance is tightly regu-

lated in narrow physiologic ranges. Fourmechanisms are involved in the regulation ofsodium and water (Terpstra & Terpstra,2000). The first mechanism is the secretionand regulation of antidiuretic hormone(ADH) from the hypothalamus-neurohypo-

physeal system. ADH is produced in specialneurosecretory cells in the supraoptic andparaventricular nuclei of the posterior hypo-thalamus (Keenan, 1999; Terpstra & Terp-stra). ADH is stored and released by the pos-terior pituitary gland (Batcheller, 1994). Theproduction and release of ADH is regulatedby receptors located in the kidneys, heart, andbrain. Normally, ADH is secreted in responseto increased serum osmolality and decreasedplasma volume (Finley, 1998a). The releaseof ADH is inhibited by low plasma volumeor an increased circulating blood volume.When serum osmolality reaches 295 mOsm/kg, arginine vasopressin (AVP), the biologicactive form of ADH, is released (Haapoja,2000; Metheny, 1982; Terpstra & Terpstra).

The second mechanism of action occursin the kidneys (Terpstra & Terpstra, 2000).

ADH acts on the V2 receptors,

which are located in the collect-ing ducts (Robertson, 2001). Theensuing reaction from the ADHand V

2 complex causes water

channels to be inserted into theapical cell membrane, makingthe cell permeable to water(Haapoja, 2000; Robertson).This promotes water reabsorp-tion and decreases urine output(Haapoja; Poe & Taylor, 1989).

The third mechanism of actionoccurs in the cardiovascular sys-tem. The body is able to senseshifts in the circulating blood vol-ume and blood pressure by thestretch receptors in the left atriumand baroceptors in the aortic archand carotid sinus (Terpstra &Terpstra, 2000). These receptorsrelease atrial natriuretic peptide(ANP) in response to increasedatrial pressure (Smeltzer & Bare,

2002). ANP acts on the distal tubule and col-lecting ducts to decrease water and sodiumchloride reabsorption (Guyton & Hall, 1996).

The fourth mechanism is the stimulationof the limbic system. ADH production is in-creased by limbic stimulation (Terpstra &Terpstra, 2000). The limbic system is an in-terconnected complex of basal brain function,and its control center is the hypothalamus(Guyton & Hall, 1996). One major functionof the limbic system is to control behavior,but it also controls many internal functions,including osmolality of body fluids (Guyton& Hall). Stimulation of the limbic system, by

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426 JULY/AUGUST 2003 • VOLUME 7, NUMBER 4 • CLINICAL JOURNAL OF ONCOLOGY NURSING

factors such as stress, pain, nausea, or sur-gery, causes an increased production of ADH(Poe & Taylor, 1989; Terpstra & Terpstra).

When the production and release of ADHcontinues despite hypotonicity, SIADH oc-curs. The kidneys continue to reabsorb wa-ter with a proportionate decrease in serumsodium levels. Three mechanisms most of-ten are responsible for SIADH: inappropri-ate secretion of ADH from the supraoptic-hypophyseal system, ectopic production ofADH, and enhanced action of ADH in therenal distal tubules (Otto, 1997).

The inappropriate secretion of ADHfrom the supraoptic-hypophyseal systemoccurs most often in patients who have cen-tral nervous system disorders or those whohave had shock, pain, stress, or recent sur-gery. These conditions increase intratho-racic pressure or decrease venous return tothe heart, thereby stimulating ADH secre-tion. Malignant cells can secrete ADH orADH-like substances, creating ectopicsources for production of ADH. Patientswith malignancies or pulmonary infectionsmay develop SIADH by this mechanism.Finally, many medications cause SIADHby enhanced action of ADH in the renal dis-tal tubules or increased release of ADH(Chan, 1997). The most common medica-tions that have been associated withSIADH are narcotics, tranquilizers, barbi-turates, general anesthetics, thiazide diuret-ics, hypoglycemic agents, antidepressants,and certain chemotherapy agents.

Risk FactorsPatients with cancer often have multiple

factors that put them at risk for SIADH (Otto,1997). Figure 1 provides a list of conditionsand medications that are associated with anincreased risk of SIADH. The most commonrisk factors associated with SIADH are theprimary diagnosis, medications, concomitantdiseases, advanced age, or a combination offactors. The most common diagnosis associ-ated with SIADH is a malignancy. Abouttwo-thirds of patients who are diagnosed withSIADH have an underlying malignancy(Otto), and small cell lung cancer accountsfor approximately 80% of all cases of SIADH(Haapoja, 2000; Keenan, 1999). One percentof patients with non-small cell lung cancerand 3% of patients with head and neck can-cer experience SIADH (Ferlito, Rinaldo, &Devaney, 1997; Strewler, 1998). Other ma-lignancies that can cause SIADH are pancre-atic, prostate, duodenal, or colon carcinoma;Hodgkin’s and non-Hodgkin’s lymphoma;thymoma; and primary brain tumors (Otto;Poe & Taylor, 1989; Terpstra & Terpstra,2000). SIADH also can be caused by pulmo-

nary infections or central nervous system dis-orders (Haapoja).

Patients with AIDS also are at risk forSIADH. Hyponatremia is seen in 40%–60%of hospitalized patients with AIDS. The twomost common causes of hyponatremia inpatients with AIDS are SIADH and volumedepletion (Akalin, Chandrakantan, Keane,& Hamburger, 2001). Factors that put thesepatients at high risk for SIADH are second-ary malignancies, opportunistic infections(e.g., tuberculosis, pneumocystis cariniipneumonia), and medications such as pyra-zinamide or ethambutol used to treat tuber-culosis (Akalin et al.).

After surgery, patients are at increased riskfor SIADH. One factor associated with thisincreased risk is that fluids often are replacedwith hypotonic IV solutions such as 5% dex-trose in water, which dilutes plasma electro-lyte concentrations and predisposes patientsto hyponatremia (Smeltzer & Bare, 2002).Another factor is that patients on mechanicalventilation and/or positive pressure breathingdevices have a decrease in ANP production,which stimulates the release of ADH (Me-theny, 1982; Otto, 1997). Similarly, pain,stress, shock, trauma, general anesthesia, andopioid medications stimulate ADH release,leading to SIADH (Chan, 1997; Haapoja,2000; Otto). All of these factors combined putpostoperative patients at risk for SIADH.

Increased age is another risk factor forSIADH (Miller et al., 1996). Older patientsare at greater risk for SIADH from any dis-ease state when compared with younger pa-tients because of normal physiologic changesassociated with aging, such as elevated ADHand atrial natriuretic hormone levels and anincreased responsiveness to osmotic stimula-tion (Miller, 2001). Moreover, fluid and elec-trolyte balance and sodium regulation is notas effective when treating the elderly. This isbecause of decreased total body fluids andglomerular filtration rate as well as impairedrenal diluting capacity and sodium conserva-tion (Miller). Multiple medications also putolder patients at risk for SIADH (Terpstra &Terpstra, 2000). The typical patient in a nurs-ing home receives about seven medications,and many of these medications are associatedwith SIADH (Terpstra & Terpstra).

Medications can cause SIADH eitherthrough stimulation of ADH release from thecentral nervous system or an enhanced ADHeffect in the kidneys (Keenan, 1999). Che-motherapeutic and biotherapy agents that areimplicated in SIADH are cisplatin, cyclo-phosphamide, ifosfamide, interferon alpha orgamma, and vinca alkaloids (Chan, 1997;Kirch, Gachot, Germann, Blot, & Nitenberg,1997; Miaskowski, 1997). Case studies ofvinorelbine and docetaxel causing SIADH

have been reported (Garrett & Simpson,1998; Langer-Nitsche, Luck, & Heilmann,2000). Other medications that can causeSIADH are narcotics, tranquilizers, barbitu-rates, general anesthetics, thiazide diuretics,hypoglycemic agents, and antidepressants.An in-depth discussion of medications thatcause SIADH is beyond the scope of this ar-ticle, and readers are referred to another, morecomprehensive source (Chan).

Signs and SymptomsThe key presenting sign of SIADH is hy-

ponatremia associated with serum hypo-osmolality and continued urinary sodium loss(Haapoja, 2000; Miller, 2001; Sorenson,Anderson, & Hansen, 1995). Early symptomsassociated with SIADH often are subtle but,if left untreated, may progress to life-threat-ening seizures, coma, and death (Haapoja;Heater, 1999). Because oncology nurses havefrequent and ongoing contact with patients,they are in an ideal position to recognize pa-tients who are at increased risk for SIADHand those who present with early symptoms.

Early signs and symptoms are mild andcan be attributed mistakenly to other causes.Therefore, nurses must maintain a high in-dex for suspicion in patients who are at po-tential risk for SIADH. Early signs andsymptoms associated with mild to moderatehyponatremia are nausea, anorexia, thirst,weight gain, oliguria, weakness, fatigue, andmuscle cramps, all of which usually becomeapparent when serum sodium falls to the115–120 mEq/l range. Neurologic signs mayinclude headache and mild altered mentalstatus (Keenan, 1999; Poe & Taylor, 1989).

Nurses must recognize that the severity ofthe symptoms of SIADH depends not onlyon sodium level but, more importantly, onhow rapidly the syndrome develops. Symp-toms develop because of water retention lead-ing to water intoxication (Keenan, 1999). Assodium levels decrease, progressive symp-toms include mental status changes such aslethargy, irritability, disorientation, andmental confusion. Late, severe symptomsare seizures and coma as a result of cerebraledema (Haapoja, 2000). Death can occur inadults if serum sodium decreases below110–115 mEq/l or below 128 mEq/l in chil-dren unless the decrease is correctedpromptly (Poe & Taylor, 1989).

Diagnosis and TreatmentThe diagnosis of SIADH is based on find-

ings of hyponatremia, decreased serum osmo-larity, euvolemia (hypotonic hyponatremia),high urine specific gravity, urine sodium lessthan 20 mEq/l, urine osmolality greater than


1,400, normal or decreased blood urea nitro-gen (BUN) and creatinine, hypouricemia, andnormal renal, adrenal, and thyroid function(Terpstra & Terpstra, 2000) (see Table 1).Other potential causes of hyponatremia (e.g.,congestive heart failure, cirrhosis, adrenal in-sufficiency, Addison’s disease, and hypothy-roidism) must be evaluated and ruled out dur-ing the diagnostic workup.

A water-loading test may be performedto establish the diagnosis of SIADH. Pa-tients are instructed to drink 20 cc water perkg of body weight over 15–20 minutes, andurine is collected hourly for five hours andtested for specific gravity and osmolality.In the case of SIADH, the specific gravityis normal or increased and less than 80% ofthe water is excreted (Finley, 1998b). Be-fore beginning the test, the sodium levelmust be greater that 125 mEq/l and patientsshould be asymptomatic (Otto, 1997). Awater test rarely is needed to make a defini-tive diagnosis of SIADH (Arnold, Patchell,Lowy, & Foon, 2001; Otto).

Once the diagnosis of SIADH is estab-lished, the primary treatment is to identify andtreat the underlying cause. If a disease is caus-ing the SIADH, treatment for the underlying

disease must be initiated as quickly as pos-sible, whether it is a malignancy, pulmonaryinfection, or condition of the central nervoussystem. If a medication is the suspected rea-son for SIADH, the medication should be dis-continued and the patient should be moni-tored for resolution of SIADH.

Mild hyponatremia (serum sodium levelsof 125–134 mEq/l) is treated with fluid re-striction of 800–1,000 ml per day (Haapoja,2000). Serum sodium levels and symptomsgenerally improve over three to five days(Haapoja). In severe hyponatremia (less than115 mEq/l) accompanied by seizures orcoma, patients are treated in an intensive careunit (Haapoja). A fluid restriction of 500 mlper day is initiated. IV fluid administration of3%–5% saline at a rate of 1–2 ml/kg is ad-ministered over two to three hours, and IVfurosemide is given at a dose of 1 mg per kgof body weight (Finley, 1998b; Haapoja). Theadministration of furosemide inhibits freewater reabsorption and also may interferewith the action of ADH in the kidneys(Terpstra & Terpstra, 2000). Serum sodiumlevels are taken every one to two hours toguide the initial stages of therapy. Serum so-dium levels can be raised safely at a rate of

1–2 mEq/l per hour (Terpstra & Terpstra).Hypertonic solutions are discontinued whenthe serum sodium level is from 120–125mEq/l and neurologic symptoms subside(Haapoja).

An important consideration when initi-ating treatment for SIADH is whether thehyponatremia developed acutely overhours to days (less than 24–36 hours) or ifit developed insidiously and lasts more than48 hours (Hojer, 1994; Keenan, 1999).Slow sodium correction (0.5 mmol/l perone hour) in patients with chronic hy-ponatremia and rapid correction (1–2mmol/l per one hour) to a moderatelyhyponatremic level in those with acute de-velopment are recommended (Chan, 1997).In cases where the rate of development can-not be determined, rapid correction with so-dium chloride and furosemide for three tofour hours followed by slow correctiontherapy is suggested for patients with sei-zures or those in coma (Hojer).

Overaggressive correction of hyponatre-mia must be avoided because it can lead tocentral pontine myelinolysis, a condition thatcauses a breakdown of the blood-brain bar-rier mainly in the pons and thalamus

Diagnosis

Malignancy

Bladder carcinomaCarcinoid tumorCentral nervous system

tumors• Primary• Metastatic• Ewing carcinomaGastrointestinal cancer• Colon• Duodenum• Esophagus• PancreasGynecologic cancer• Ovary• CervixHead and neck cancerHematologic cancer• Acute myelogenous leukemia• Chronic lymphocytic leuke-

mia• LymphomaLung cancer• Small cell• Non-small cellMesotheliomaProstate cancerThymomaThymic neuroblastoma

Nonmalignancy

Acute intermittent porphyriaAIDSCentral nervous system disorders• Cerebral vascular accident• Cerebral hemorrhage• Cerebral abscess• EncephalitisGuillain-Barre syndromeLupus erythematosusPulmonary disorders• Infections• Status asthmaticus• Chronic obstructive

pulmonary disease

Medications

Chemotherapy

CisplatinCyclophosphamideIfosfamideInterferon—alpha or

gammaMelphalan (high dose)Vinca alkaloids

Other

AngiotensinConverting enzyme

inhibitorsAcetaminophenBarbituratesChlorpropamideDopaminergic drugsGeneral anestheticIsoproterenolMorphineOpioidsOxytocinNonsteroidal anti-inflammatory

drugsSomatostatinSelective serotonin reuptake

inhibitorsThiadize diureticsTricyclic antidepressants

Other

History of smokingIdiopathic syndrome of inap-

propriate antidiuretic hor-mone secretion in the elderly

Current nicotine usePainPositive pressure respiratorsPostoperative time periodStressTrauma

FIGURE 1. RISK FACTORS IN SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE SECRETION

Note. Based on information from Akalin et al., 2001; Chan, 1997; Finley, 1998b; Garrett & Simpson, 1998; Haapoja, 2000; Hirshberg & Ben-Yehuda, 1997;Keenan, 1999; Kirch et al., 1997; Langer-Nitsche et al., 2000; Miaskowski, 1997; Miller, 2001; Otto, 1997; Poe & Taylor, 1989; Robertson, 2001.


(Haapoja, 2000). Symptoms associated withthis condition occur because of shrinkage ofthe central nervous system neurons resultingin progressive muscle weakness, dysarthria,dysphagia, cerebral edema, and seizures thattypically occur two to six days after the hy-ponatremia is corrected (Keenan, 1999; Poe& Taylor, 1989). Nurses must recognize thatthis neurologic disorder can lead to perma-nent brain damage or death (Miller, 2001).

Fluid restriction is the mainstay of man-agement of chronic SIADH (Keenan, 1999).The amount of fluid restriction prescribed isrelated to the severity of the hyponatremiasuch that as the severity of the hyponatremiaincreases, the fluid intake restriction also in-creases. Many patients have difficulty com-plying with this over a long period of time;therefore, pharmacologic agents are used toeffectively treat SIADH in the ambulatoryoncology setting. Pharmacologic interventionis added in the form of demeclocycline,lithium, or urea. Demeclocycline and lithiumblock the action of ADH in the collecting tu-bule (Poe & Taylor, 1989; Robertson, 2001).Patients do not need to adhere to a fluid re-striction while on these medications.Demeclocycline, a tetracycline derivative, isgiven at doses of 600–1,200 mg orally on adaily basis (Keenan). This medication istaken one to two hours before or after mealsand should not be taken with aluminum, mag-nesium, iron, or calcium products becausethey delay absorption of the medication (Poe& Taylor). Because demeclocycline cancause renal dysfunction, serum BUN andcreatinine are monitored on a regular basis.Other potential side effects associated withthis medication are nausea, vomiting, diar-rhea, and photosensitivity. Demeclocycline is

preferred over lithium because it is better tol-erated and may be more effective (Terpstra& Terpstra, 2000). Occasionally, urea is usedas an osmotic diuretic (Haapoja, 2000). Theusual dose for urea is 30–60 mg per day(Finley, 1998b). Gastrointestinal upset is apotential side effect associated with urea(Finley, 1998b).

Several new agents have demonstratedpromising results in early clinical trials. Onegroup of agents selectively targets AVP re-ceptors in the kidneys (Haapoja, 2000). Thepeptide antagonists that are not specific tothe V2 receptors are available only in paren-teral form and become less effective withchronic use (Haapoja). Peptide V2 receptorantagonists also have limited clinical use-fulness because of marked species differ-ences, poor oral bioavailability, and shortbiologic half-life (Verbalis, 1998, 2002).The nonpeptide V2 receptor antagonists areanother potent group of drugs that selec-tively block the action of ADH in the col-lecting ducts and are available in both an IVand oral form (Keenan, 1999; Serradeil-LeGal et al., 2002). V2 receptor antagonistsblock the antidiuretic effects of AVP by pre-venting the insertion of the AVP water chan-nels into the luminal membrane of the col-lecting ducts. (Serradeil-Le Gal et al.). Twosuch receptor antagonists that are beingtested are SR121463 and OPC-31260 (Saitoet al., 1997; Serradeil-Le Gal et al.). Saito etal. reported that in human subjects, a singleIV dose of OPC-31260 significantly in-creased sodium levels during a four-hour ob-servation period. YM-087 (conivaptin) is aV1A and V2

vasopressing receptor antagonistthat is being tested in clinical trials (Ser-radeil-Le Gal et al.; Udelson et al., 2001). In

human subjects, conivaptin produced in-creased urine output and significantly re-duced urine osmololity as well as demon-strated a favorable change in hemodynamics(Udelson et al.). The CenterWatch ClinicalTrial Listing Service Web site lists clinicaltrial sites for conivaptin, and more informa-tion can be accessed at www.centerwatch.org/patient/studies/stu20175.htm.

Nursing ManagementFirst and foremost, oncology nurses must

have a high index of suspicion in patientswho have multiple risk factors for SIADHbecause the symptoms often are nonspecific.Knowledge about the early signs and symp-toms associated with SIADH and carefulnursing assessment also are critical for earlyidentification of the syndrome. Nursing as-sessment consists of conducting a thoroughhistory and physical examination and re-viewing the appropriate laboratory values.

Oncology nurses should focus assessmenton detecting subtle signs of hyponatremia,which may mimic side effects of chemo-therapy, dehydration, and neurologic disor-ders. Assessment of hydration status focuseson checking the skin turgor, condition ofmucus membranes, intake and output, anddaily weights. In assessing patients who areat high risk for SIADH, nurses must moni-tor patients for fluid overload. Specific signsto watch for are fluid intake more than urineoutput as well as weight gain (Metheny,1982). Laboratory values also provide infor-mation about hydration status and aid in thediagnosis of SIADH. Laboratory valuesmust be reviewed, paying close attention tothe electrolytes, BUN, creatinine, serum os-molality, urine osmolarity, and specificgravity. Table 1 provides a description of thelaboratory abnormalities that commonly areseen in SIADH. Assessment of neurologicstatus focuses on early assessment ofchanges in the level of consciousness. Earlysigns and symptoms include headache andmild altered mental status. These symptomsmay become progressively worse and in-clude lethargy, irritability, disorientation,mental confusion, seizures, or coma.

Nurses are responsible for the safetyneeds of patients with neurologic manifes-tations of their disease. Seizure precautionsare initiated when serum sodium levels fallbelow 125 mEq/l (Finley, 1998b). Nursinginterventions include assessing patients formental status changes and any associatedmuscle weakness and assisting patients withactivities of daily living and ambulation(Metheny, 1982; Otto, 1997; Terpstra &Terpstra, 2000). Other safety measures in-clude keeping the immediate area well lit

TABLE 1. LABORATORY VALUES: NORMAL LIMITS AND ALTERATIONS SEEN WITH SYNDROME OF

INAPPROPRIATE ANTIDIURETIC HORMONE (SIADH) SECRETION

LABORATORY TEST

Serum sodiumSerum osmolalityUrine sodiumUrine osmolality

Typical rangeExtreme range

Urine specific gravityWater load test

NORMAL VALUES

135–145 mEq/l275–295 mOsm/kg50–220 mEq/l400–1,200 mOsm/kg500–800 mOsm/kg*50–1,400 mOsm/kg*1.025–1.032> 80% of water load excreted in five hoursUrine osmolality reaches low of > 100

mOsm/kg during second or third hourUrine specific gravity decreased

VALUES IN SIADH

< 135 mEq/l< 275 mOsm/kg> 220 mEq/l> 1,200 mOsm/kg

––

> 1.032< 40%–80% of water load exertedNo diuresis occursUrine osmolality remains greater

than the plasma osmolality

Note. From “Syndrome of Inappropriate Antidiuretic Hormone Secretion: Recognition and Manage-ment,” by T.L. Terpstra and T.L. Terpstra, 2000, Medsurg Nursing, 9, p. 65. Copyright 2000 byJannetti Publications, Inc. Adapted with permission.* Values have been updated based on information from Smeltzer & Bare, 2002.


and free from clutter, using side rails atnight, and keeping clocks and calendarswithin sight to help keep patients oriented.

Patient and family education is anotherimportant component of nursing care (Poe& Taylor, 1989). Patients and their caregiv-ers should have knowledge about the under-lying cause of the SIADH, the signs andsymptoms of hyponatremia that must be re-ported to the healthcare team, and the treat-ment plan (Poe & Taylor). The symptomsthat should be reported to the healthcareteam include increased thirst, weight gainwithout edema, decreased urine output, nau-sea, anorexia, weakness, headache, or men-tal status change such as irritability or con-fusion. Caregivers should be taught what todo if a seizure occurs at home. Patients andtheir significant others should know emer-gency numbers and how to access medicalhelp after clinic hours. Written informationshould be provided to reinforce verbal in-structions (see Figure 2). A printed self-careguide for SIADH can be downloaded atwww.CancerSourceRN.com under “PatientEducation” (Jones, 1999).

Thorough knowledge about the treat-ment plan is essential. Nurses must instructpatients about home medications andshould include the following in the instruc-tions: purpose, dose, appropriate time totake the medication, and potential side ef-fects. If a patient is discharged on fluid re-striction, the patient and caregiver shouldreceive instructions on the reason for fluidrestriction and a plan for scheduling intakeof fluids. Specific nursing interventions forpatients who are on fluid restriction includeteaching patients and their families the ra-tionale for fluid restriction and institutinginterventions that promote comfort (Poe &Taylor, 1989). Nurses should help patientsdivide fluid throughout the day, based ontheir preferences, and encourage patients todrink fluids that are high in sodium, suchas orange juice, tomato juice, milk, or beefand chicken broth (Poe & Taylor). If nocontraindications exist, nurses should teachpatients to take their medications withmeals (Otto, 1997). Nursing interventionsneed to promote comfort and minimize ir-ritating effects of fluid restriction such asoffering mouth care every two to four hoursand avoiding mouthwash and oral productsthat dry the mucous membranes (e.g.,mouthwashes that contain alcohol, lemonglycerin swabs, tobacco) (Otto). Specificinterventions for decreasing the discomfortassociated with a dry mouth are rinsing themouth out frequently and using sugarlessgum, sugarless candy, mouth moisturizers,or artificial saliva products (Finley, 1998b;Otto).

ConclusionOncology nurses play a key role in the

successful management of SIADH. Nursesshould be aware of which patients are at risk,early signs and symptoms of SIADH, andappropriate medical and nursing manage-ment for SIADH. Early recognition ofSIADH in patients who are at high risk iscritical to allow for initiation of appropriatetreatment interventions and the preventionof neurologic complications (Keenan, 1999;Poe & Taylor, 1989). Treatment includeseliminating the underlying cause and man-aging the hyponatremia. Assessment of theeffectiveness of interventions continues onongoing bases. Patient and family educationis an integral part of nursing management,so nurses must recognize that patient andfamily learning needs must be reevaluatedduring clinic visits.

Author Contact: Lori A. Langfeldt, RN,BSN, OCN®, can be reached at [email protected].

ReferencesAkalin, E., Chandrakantan, A., Keane, J., & Ham-

burger, R.J. (2001). Normouricemia in the syn-drome of inappropriate antidiuretic hormonesecretion. American Journal of Kidney Dis-eases, 37, 1–3.

Anderson, R.J., Chung, H.M., Kluge, R., &Schrier, R.W. (1985). Hyponatremia: A pro-spective analysis of its epidemiology and thepathogenic role of vasopressin. Annals of Inter-nal Medicine, 102, 164–168.

Arnold, S.M., Patchell, R., Lowy, A.M., & Foon,K.A. (2001). Paraneoplastic syndromes. InV.T. DeVita, Jr., S. Hellman, & S.A. Rosen-berg (Eds.), Cancer: Principles and practice ofoncology (6th ed., pp. 2514–2515). Philadel-phia: Lippincott Williams and Wilkins.

Syndrome of Inappropriate Antidiuretic Hormone (SIADH) Secretion(Hyponatremia, Low Sodium Level)

SIADHSIADH can be caused by many different things, but cancer is the most common reason. Cancer cellscan give off antidiuretic hormone (ADH). In the kidneys, ADH causes water to be taken back into thebody. This causes the sodium (salt) levels in your blood to drop.Signs of SIADH• Loss of appetite• Difficulty thinking or concentrating• General tiredness• General weakness• Headaches• Muscle cramps• Increased thirst• Weight gain without swelling in feet, legs, or elsewhere• Low urine output• Feeling irritable• ConfusionThings you should do1. Weigh yourself daily.2. Limit the amount of fluids you drink.

• You can have ____ cups of fluid each day.• Try drinking orange juice, tomato juice, or beef and chicken broth.

3. If your mouth is dry, try brushing your teeth with a mild toothpaste and rinsing your mouth severaltimes a day. Avoid using mouthwashes that contain alcohol or lemon glycerin swabs. Try usingsugarless gum or candy.

4. _________________ has been ordered to treat your SIADH.• Take ____ tablets ____ times a day.• Take your medication with/without food. (Circle one answer.)• Do not stop your medication without first talking to your doctor or nurse.

5. Smoking and tobacco products make your mouth dry or may make your SIADH worse. Ask yourdoctor or nurse for help to stop smoking.

Call your doctor or nurse for• Any of the previous signs of SIADH or if the symptoms get worse, especially weight gain, low urine

output, increased thirst, or personality changes• Uncontrolled painIf your caregiver observes you having seizures or has difficulty waking you, he or she should call 911or take you to the emergency room.Clinic telephone number:After clinic hours, call:

FIGURE 2. PATIENT EDUCATION SHEET


Batcheller, J. (1994). Syndrome of inappropriateantidiuretic hormone secretion. Critical CareNursing Clinics of North America, 6, 687–692.

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Chan, T.Y. (1997). Drug-induced syndrome ofinappropriate antidiuretic hormone secretion:Causes, diagnosis and management. Drugs andAging, 11, 27–44.

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Rapid RecapSyndrome of Inappropriate Antidiuretic Hormone Secretion in Malignancy:Review and Implications for Nursing Management• Syndrome of inappropriate antidiuretic hormone (SIADH) is a rare, paraneoplastic syndrome occurring in 1%–2% of

patients with cancer.• SIADH is caused by abnormal or sustained production of antidiuretic hormone that results in water retention and dilu-

tional hyponatremia.• Patients with cancer can be at risk for SIADH because of their diagnosis (small cell lung cancer is the most common

cause of SIADH), comorbidities, medications, or age.• Early signs and symptoms of SIADH mimic common side effects of chemotherapy, such as nausea, anorexia, muscle

cramps, weakness, and fatigue.• Progressive symptoms include lethargy, irritability, disorientation, and mental confusion.• The primary treatment of SIADH is to treat the underlying cause and restrict fluids.

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