syndrome of inappropriate antidiuretic hormone

syndrome

[sin´drōm] a combination of symptoms resulting from a single cause or so commonly occurring together as to constitute a distinct clinical picture. For specific syndromes, see under the name, such as adrenogenital syndrome or reye's syndrome. See also disease and sickness.syndrome of crocodile tears spontaneous lacrimation occurring parallel with the normal salivation of eating. It follows facial paralysis and seems to be due to straying of the regenerating nerve fibers, some of those destined for the salivary glands going to the lacrimal glands.syndrome of inappropriate antidiuretic hormone (SIADH) a syndrome in which secretion of vasopressin (antidiuretic hormone) is not inhibited by hypotonicity of extracellular fluid and hyponatremia is produced. It occurs in conjunction with oat cell carcinoma of the lung and certain other malignant tumors and is caused by production of vasopressin by the tumor. See also hormones" >ectopic hormones.

syndrome of inappropriate antidiuretic hormone

SIADH

A syndrome of increased ADH activity in spite of reduced plasma osmolarity. Often first suggested by a relative hyponatremia, it is most commonly associated with disorders of the central nervous system, various tumors, anxiety, pain, pneumonia, and drugs.

Syndrome of Inappropriate Antidiuretic Hormone

DRG Category:	644
Mean LOS:	4.9 days
Description:	MEDICAL: Endocrine Disorders With CC

Syndrome of inappropriate antidiuretic hormone (SIADH), a disorder of the posterior pituitary gland, is a condition of excessive release of antidiuretic hormone (ADH) that results in excessive water retention and hyponatremia. SIADH occurs when ADH secretion is activated by factors other than hyperosmolarity or hypovolemia. Excess ADH secretion increases renal tubular permeability and reabsorption of water into the circulation, resulting in excess extracellular fluid volume, reduced plasma osmolality, increased glomerular filtration rates, and decreased sodium levels. Without treatment, SIADH can lead to life-threatening complications. Water intoxication accompanied by sodium deficit may lead to free water movement into cerebral cells, which can cause cerebral edema and result in coma and even death.

Causes

Several conditions contribute to SIADH. Central nervous system (CNS) responses to fear, pain, psychoses, and acute distress are known to increase the rate of ADH secretion by the posterior pituitary gland. Physiological conditions that increase intracranial pressure, such as acute CNS infections, brain trauma, anoxic brain death, cerebrovascular accident, and brain surgery, may lead to SIADH. Other conditions associated with SIADH include peripheral neuropathy, delirium tremens, and Addison’s disease and also certain medications such as analgesics, anesthetics, thiazide diuretics, and nicotine. Some tumors have been associated with ADH production, such as small cell carcinoma of the lungs, pancreatic cancer, prostate cancer, and Hodgkin’s disease. Positive pressure ventilation can also lead to SIADH in normovolemic individuals.

Genetic considerations

No clear genetic contributions to susceptibility have been defined.

Gender, ethnic/racial, and life span considerations

Both children and adults are at risk, but being a hospitalized patient over age 30 is a risk factor, as is low body weight, which may result in more women than men being affected. Women are more affected by drug-induced and exercise-induced hyponatremia than men. Typical childhood conditions that can lead to SIADH include pneumonia, meningitis, head trauma, and subarachnoid bleeding. In adults, the condition is most commonly associated with CNS disorders. The very old and very young develop symptoms with smaller decreases in serum sodium levels than adults. There are no known racial or ethnic considerations.

Global health considerations

While SIADH and hyponatremia occur around the world, no prevalence data are available.

Assessment

History

Ask if the patient has experienced alterations in urinary patterns. Question the patient about recent weight gain.

Physical examination

Signs of sodium deficit generally occur slowly. Ask if the patient has experienced recent fatigue, weakness, nausea, anorexia, or headaches. Late signs include nausea, vomiting, muscle weakness, decreased reaction time, irritability, decreased level of consciousness, seizures, and even coma. Note that the most severe, life-threatening signs of SIADH are not fluid overload and pulmonary congestion but rather the CNS effects from acute sodium deficiency. The severity of hyponatremia determines the severity of findings on physical assessment. Perform a neurological assessment to determine if the patient has experienced changes in the level of consciousness, which can range from confusion to seizure activity. Life-threatening symptoms such as seizures may indicate acute water excess, whereas nausea, muscle twitching, headache, and weight gain are more indicative of chronic water accumulation.

Psychosocial

The family and significant others may be fearful if the patient has experienced CNS changes that alter behavior and alertness. If the patient has had seizures, note that family members may have many questions. The patient’s and family’s responses to SIADH are often a reflection of their responses to these other conditions, which are important to consider in any evaluation of patient and family coping.

Diagnostic highlights

Test	Normal Result	Abnormality With Condition	Explanation
Urine osmolality (osmolality refers to a solution’s concentration of solute particles per kilogram of solvent)	200–1,200 mOsm/L	> 100 mOsm/L	Excretion of inappropriately concentrated urine and hyponatremia caused by overproduction of ADH
Blood osmolality	275–285 mOsm/L	< 275 mOsm/L	Water loss in urine and hypernatremia leads to hemoconcentration; levels above 320 mOsm/L are considered “panic levels” and require immediate intervention
Serum sodium	136–145 mEq/L	< 120 mEq/L	Sodium loss in the urine leads to hyponatremia and hemodilution
Urine sodium	< 20 mEq/L	> 20 mEq/L	Sodium loss in the urine

Other Tests: Blood urea nitrogen, urine specific gravity, serum electrolytes, plasma cortisol, computed tomography of head, radioimmunoassay of ADH

Primary nursing diagnosis

Diagnosis

Fluid volume excess related to retention of free water

Outcomes

Fluid balance; Hydration; Circulation status; Cardiac pump effectiveness

Interventions

Fluid monitoring; Fluid/electrolyte management; Circulatory care; Vital signs monitoring; Medication management

Planning and implementation

Collaborative

Restoration of normal electrolyte and fluid balance and normal body fluid concentration are the treatment goals. Treatment involves correction of the underlying cause and correction of hyponatremia. If the patient’s life is not in danger from airway compromise or severe hyponatremia, the physician often restricts fluids initially to 600 to 800 mL per 24 hours or less. With fluid restriction, the hormone aldosterone is released by the adrenal gland and the patient begins to conserve sodium in the kidneys. As serum sodium increases, SIADH gradually corrects itself. The patient needs assistance to plan fluid intake, and a dietary consultation is also required for consistency in fluid management.

If fluid restriction is unsuccessful, the physician may prescribe an intravenous (IV) infusion of a 3% to 4.5% saline solution. Use caution in administering these hypertonic solutions and always place them on an infusion control device to regulate the infusion rate precisely. Monitor the patient carefully because sodium and water retention may result, leading to pulmonary congestion and shortness of breath.

Diuretics to remove excess fluid volume may be used in patients with cardiac symptoms.

Pharmacologic highlights

Medication or Drug Class	Dosage	Description	Rationale
Vasopressin receptor antagonists	Varies with drug	Conivaptan; tolvaptan	Block vasopressin receptors; used for hypervolemic and euvolemic (normal volume) hyponatremia when serum sodium level < 125 mEq/L, when hyponatremia is symptomatic, and when there has been inadequate response to fluid restriction
Diuretics	Varies with drug	Thiazide diuretics; loop diuretics (furosemide)	Remove excess fluid volume (may be used in patients with cardiac symptoms)
Demeclocycline (Declomycin)	600–1,200 mg/day in two or three divided doses PO	Antibiotic: Tetracycline derivative	Blocks action of ADH at distal and collecting tubules of the kidney

Other Drugs: Blood urea nitrogen, urine-specific gravity, urine sodium, radioimmunoassay of ADH

Independent

If the patient is at risk for airway compromise because of low serum sodium levels or seizure activity, maintaining a patent airway is the primary nursing concern. Insert an oral or nasal airway if the patient is able to maintain her or his own breathing or prepare the patient for endotracheal intubation if it is needed. If the patient is able to maintain airway and breathing, consider positioning the patient so that the head of the bed is either flat or elevated no more than 10 degrees. This position enhances venous return and increases left atria filling pressure, which, in turn, reduce the release of ADH.

Explore with the patient methods to maintain the fluid restriction. If thirst and a dry mouth cause discomfort, try alternatives such as hard candy (if the patient is awake and alert) or chewing gum. Allocate some of the restricted fluids for ice chips to be used throughout the day at the patient’s discretion. Work with the patient to determine the amount of fluid to be sent on each tray so that fluid intake is spread equitably throughout the day. If the patient is receiving fluids in IV piggyback medications, consider those volumes as part of the 24-hour intake. Work with the pharmacy to concentrate all medications in the lowest volume that is safe for the patient.

Promote range-of-motion exercises for patients who are bedridden and turn and reposition them every 2 hours to limit the complications of immobility. Maintain side rails in the up position to prevent injury if the patient has a decreased mental status. Initiate seizure precautions to ensure the patient’s safety.

Evidence-Based Practice and Health Policy

Lim, Y.J., Park, E.K., Koh, H.C., & Lee, Y.H. (2010). Syndrome of inappropriate secretion of antidiuretic hormone as a leading cause of hyponatremia in children who underwent chemotherapy or stem cell transplantation. Pediatric Blood & Cancer, 54(5), 734–737.

In a study among 63 children who were treated with chemotherapy or stem cell transplantation, SIADH was the leading cause of hyponatremia, occurring in 40.2% of patients.
Hyponatremia was observed in 63.5% of patients, and 92.7% of the hyponatremic episodes developed while patients were receiving hypotonic fluids with sodium chloride concentrations between 30 and 150 mEq/L.
SIADH was more common among the children who were treated with stem cell transplantation than among children who were treated with chemotherapy (66.6% versus 31%; p = 0.02).

Documentation guidelines

Physical findings: Status of airway, assessment of CNS, fluid volume status (presence of edema, skin turgor, intake and output), serum sodium level
Response to fluid restriction, diuretics, and other medications
Presence of complications: Changes in lung or cardiac sounds; changes in level of consciousness; seizures

Discharge and home healthcare guidelines

Be sure the patient and significant others understand the medication regimen, including the dosage, route, action, adverse effects, and need for follow-up laboratory tests (ADH level, serum sodium and potassium, blood urea nitrogen and creatinine, urine and serum osmolality). Instruct the patient to report changes in voiding patterns, level of consciousness, presence of edema, symptoms of hyponatremia, reduced neurological functioning, nausea and vomiting, and muscle cramping. If the patient is going home on fluid restriction, be sure to discuss methods of limiting fluid intake and encourage the patient to weigh himself or herself daily to monitor for fluid retention.