SYNDROM OF INAPPROPRIATE ANTIDIURETIC HORMONE

(SIADH)

Syndrome of inappropriate antiduretic hormone (SIADH) is characterized by excessive secretion

of antidiuretic hormone causing resorption of excessive amounts of free water resulting in the dilution
of the main solute of plasma, sodium. This causes water retention and extracellular fluid expansion
without edema or hypertension.

ETIOLOGY
The most frequent causes of SIADH include the secretion of ectopic ADH by malignant neoplasms;
non-neoplastic diseases of the lung; and local injury to the hypothalamus, posterior pituitary, or both.
Drugs predispose clients to the development of SIADH, along with several other factors.
 Central nervous system disorders
o Head trauma
o Stroke
o Subarachnoid hemorrhage
o Hydrocephalus
o Brain tumor
o Encephalits
o Guillain-Barré syndrome
o Meningitis
o Acute psychosis
o Acute intermittent porphyria
 Malignancies
o Bronchogenic carcinoma
o Pancreatic carcinoma
o Prostatic carcinoma
o Renal cell carcinoma
o Adenocarcinoa of colon
o Thymoma
o Osteosarcoma
o Leukemia
o Malignant lymphoma
 Pulmonary lesions
o Tuberculosis
o Bacterial pneumonia
o Aspergillosis
o Bronchiectasis
o Neoplasms
o Positive pressure ventilation
 Drugs
o Increased ADH production
 Antidepressants:
 TCAs
 MAOIs
 SSRIs
  Antineoplastics:
 Cyclophosphamide
 Vincristine
 Carbamazepine
 Methylenedioxymethamphetamine (MDMA); Ecstasy)
 Clofibrate
 Neuroleptics:
 Fluphenazine
 Trifluoperazine
 Haloperidol
 Thiotexine
 Thioridazine
o Potentiated ADH action
 Carbamazepine
 Chlorpropamide, tolbutamide
 Cyclophosphamide
 NSAIDs
 Somatostatin and analogs
 Others
o Postoperative
o Pain
o Stress
o AIDS
o Pregnancy (physiologic)
o Hypokalemia

CLINICAL MANIFESTATIONS
Clinical manifestations of SIADH correlate with signs and symptoms of hyponatremia related to the
CNS dysfunction
 Headache
 Irritability
 Confusion
 Muscle cramps
 Weakness
 Obtundation
 Seizures
 Coma
 Weight gain without edema
 Jugular venous
 Anorexia
 Nausea and vomiting
 Cerebral edema
 Neurologic dysfunction
o Decreased reaction times
o Cognitive slowing
o Ataxia resulting in frequent falls
 Polyuria and Oliguria
LABAORATORY AND DIAGNOSTIC STUDIES
 Decreased serum sodium level
 Increased urine osmolality
 Increased urine sodium
 Elevated BUN
 Water load test

MEDICAL MANAGEMENT
 Hypertonic IV fluids to correct hypernatremia
o 0.9 % saline with furosemide may be used in asymptomatic patients whose serum sodium is
less than 120 mEq/L
 Sodium restriction
o Diet must contain only 8 gms of sodium chloride (NaCl) per day
 Fluid restriction to 500-1000 ml/day
 Medications:
o Demeclocycline (300-600 mg twice daily)
 is useful for patients who cannot adhere to water restriction or need additional
therapy; it inhibits the effect of ADH on the distal tubule. Onset of action may
require 1 week, and concentration may be permanently impaired. Therapy with
demeclocycline in cirrhosis appears to increase the risk of renal failure
o Fludrocortisone
 Hyponatremia occurring as part of the cerebral salt-wasting syndrome can be
treated with fludrocortisones
o Furosemide
 Give PO and IM doses in morning to prevent nocturia. Give second dose early
afternoon
 Store tablets in a light resistant container to prevent discoloration. Don’t use yellow
injectable preparation
 Refrigerate oral furosemide solution to ensure drug stability
 Advise patient to stand slowly to prevent dizziness, to avoid alohol, and to minimize
strenuous exercise in hot weather
 Instruct patient to report ringing in ears, severe abdominal pain, or sore throat and
fever because they may indicate toxicity
o Mannitol
 Tell patient he may feel thirsty or have a dry mouth, and emphasize the importance
of drinking only the amount of fluid provided
 Instruct patient to immediately report pain in chest, back, legs, or shortness of
breath
 Caution is exercised when correcting hyponatremia. A rapid rise in sodium levels may cause central
pontine myelinolysis/myelosis (CPM).
o Monitor for the following signs:
 Acute paralysis
 para- or quadriparesis
 Dysphagia
 Dysarthria
 Diplopia
  Loss of consciousness.
o Patient may experience locked-in syndrome where all muscles are paralyzed with the
exception of eye blinking
 Avoid overcorrection of sodium by more than 10mEq/L/day to prevent CPM

NURSING MANAGEMENT
 Know which clients are at risk
 Monitor appropriate urine and serum laboratory tests
 Assess for manifestations of hyponatremia by evaluating neurologic status
 Monitor daily weights and intake and output
 Observe for changes in concurrent isorders
 Administer demeclocycline as ordered to interfere with ADH action; monitor for possible
nephrotoxicity
 Monitor for hypernatremia with fluid overcorrection
 Client and family teaching

 PATHOPHYSIOLOGY

Precipitating factors: Predisposing factors:

 CNS disorders  Stress
 Pulmonary lesions  Pain
 Malignancies Secretion of high levels  Drugs
 Pregnancy Of antidiuretic hormone  Surgery
 Hypokalemia (ADH)  AIDS

Increased water reabsorption and urine concentration

Dilution of blood
(Reduction of plasma osmolality)

Increased plasma volume Decreased serum

concentration of sodium

 Weight gain without Suppresses renin-angiotensin

edema system
 Jugular venous
distension
 Tachycardia
 Tachypnea
 Rales

Hypotonic (dilutional)
Decreased water loss hyponatremia
Increased sodium loss
 Decreased deep tendon
reflexes
 Fatigue
 Headache
 Anorexia
 Nausea
 Decreased mental
status
 Seizures
 Coma
Increase in intracellular water

 Cerebral edema
 Neurologic dysfunction