Syndrome of inappropriate antidiuretic
hormone secretion (SIADH) occurs when
there’s a continuous, inappropriate action
or excessive secretion of antidiuretic hor–
mone (ADH), specifically the hormone
arginine vasopressin (AVP), which is pro–
duced in the hypothalamus and secreted
by the posterior pituitary gland. AVP
controls the conservation and release of
water in the body. SIADH occurs even in
the presence of an increased or normal
plasma volume and results in hypo–
osmolality and hyponatremia (blood se–
rum sodium levels less than 135 mEq/L).
In SIADH, hyponatremia isn’t the result
of a sodium deficiency; rather, it’s caused
by an excess of water.
Causes
SIADH is often thought of as a manifes–
tation of another disease or condition, as
a symptom rather than a cause. SIADH is
associated with diseases/conditions that
affect the osmoreceptors of the hypothal–
amus, which detect changes in osmotic
pressure. These osmoreceptors cause an
afferent neurologic signal to be sent to
the hypothalamus, which then triggers re–
lease of ADH from the posterior pituitary
gland to regulate blood concentration
(see Understanding SIADH).
According to the Mayo Clinic, causes
of SIADH include medications, such as
hydrochlorothiazide, methotrexate, cip–
rofloxacin, cisplatin, haloperidol, and
amphetamines; central nervous system
disturbances; cancers/tumors; lung dis–
eases; surgical procedures, such as for
traumatic brain injury and exploratory
laparotomy; HIV/AIDS; and congestive
heart failure (CHF).
SIADH in children occurs due to water
imbalance caused by medication admin–
istration, such as chemotherapy; brain
tumors; or fluid imbalances.
Complications
SIADH is the leading cause of hypona–
tremia in hospitals, with approximately
one-third of all hyponatremia cases being
directly attributed to it.
Complications of SIADH are related
to the magnitude and rate of hyponatre–
mia development. Onset can be acute,
develop in less than 48 hours, and lead
to potentially life-threatening complica–
tions. However, if hyponatremia is chron–
ic and has developed slowly over many
days or weeks, complications are often
subtle and can be easily overlooked.
Whether acute or chronic, hyponatremia
is a serious electrolyte imbalance that
studies show leads to increased morbid–
ity and mortality both inside the hospital
and out.
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patho puzzlerCopyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
Mild complications generally associ–
ated with chronic SIADH and a serum
sodium level of greater than 125 mEq/L
include:
• headaches
• depression
• memory problems
• muscle cramps
• tremors
• anorexia
• weight gain
• decreased urine output.
Severe complications of SIADH are
more often associated with an acute onset
of hyponatremia and a serum sodium level
of less than 120 mEq/L. These complica–
tions are more advanced and related to
systemic water intoxication. Neurologic
complications develop because of osmoti–
cally induced cerebral edema. Monitoring
for cardiac and pulmonary complications
is essential because vascular congestion
Understanding SIADH
Source: Nurse’s 5-Minute Clinical Consult: Diseases. Philadelphia: PA: Lippincott
Williams & Wilkins; 2006.
CEREBRAL EDEMA
Intracellular
fluid shift
Increased renal tubule permeability
Excessive ADH secretion
Elevated
glomerular
filtration rate
Dilutional
hyponatremia
Increased
sodium
excretion
HYPONATREMIA
Reduced
plasma
osmolality
Increased water retention and expanded extracellular fluid volume
Diminished
aldosterone
secretion
Decreased sodium
reabsorption in
proximal tubule
stresses both the heart and lungs. In severe
SIADH, complications can include:
• hallucinations
• seizures
• cerebral edema, leading to brain
herniation
• noncardiogenic pulmonary edema
• CHF
• coma
• death.
Diagnosis
The diagnosis of SIADH can be challeng–
ing because there’s no single definitive
test for it. Often, SIADH will be first
suspected due to abnormally low serum
sodium levels discovered during routine
blood chemistry for another condition.
Note that patients with serum sodium
levels below 120 mEq/L are at a high
risk for seizures. Although hyponatre–
mia can be found in nearly all patients
with SIADH, a low serum sodium level
isn’t sufficient to act as a positive test for
SIADH. The primary reason for this is be–
cause other common conditions can lead
to hyponatremia, such as gastrointestinal
illness (with corresponding vomiting and
diarrhea) and adrenal insufficiency.
Uric acid levels can be used as a gen–
eral indicator. SIADH will often cause
uric acid levels to be low. This presents
in around 70% of SIADH cases, whereas
patients with salt depletion present in
around 40% of cases.
A reliable way to test whether a patient
meets the basic criteria to be considered for
SIADH is to perform these three checks:
1. Is the patient hyponatremic (serum
sodium level less than 135 mEq/L)?
2. Does the patient present with hypo–
osmolality (less than 280 mOsm/kg)?
3. Is urine osmolality high?
If these three conditions are met, then
the distal nephrons are being acted on by
AVP. Although this is helpful, it doesn’t
indicate if AVP is being secreted inappro–
priately, as may be the case with patients
with cirrhosis or CHF.
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Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.Some of the tests for SIADH fall into
the category of positive test by negative
finding. An example of this is when the
patient’s clinical assessment offers find–
ings that don’t support decreased effec–
tive intravascular volume, yet the patient
presents with hyponatremia. One simple
way to begin to isolate what’s happening
and why is to put the patient on a sodium
restriction. Patients who have SIADH will
continue to excrete sodium in their urine
that’s less than maximally dilute, regard–
less of dietary restrictions.
Unfortunately, imaging still doesn’t
have a lot to offer in the way of diagnostic
tools. It’s more typically used to confirm
the existence of underlying conditions
that may cause the release of AVP, such
as CHF, or identify conditions caused by
hyponatremia secondary to SIADH, such
as hydrocephalus.
Treatments
Supportive care for SIADH is determined
by a multitude of factors. Treatment is
based on:
• patient health and tolerance to therapy
or medications
• determination as chronic (unknown du–
ration) or acute (less than 48 hours)
• degree of hyponatremia (mild, moder–
ate, or severe)
• presentation as symptomatic or
asymptomatic
• lab values for urine osmolality and cre–
atinine clearance.
Because SIADH may be the result of an
underlying cause, initial treatment may
include either addressing the primary
medical condition or adjusting or discon–
tinuing current medications in the event
of a drug-induced condition. Otherwise,
hyponatremia is corrected by reduc–
ing fluid retention and avoiding further
buildup by limiting fluid intake.
Fluid intake may be restricted to 500
to 1,500 mL/day. Calculations must con–
sider all intake, including oral, I.V., and
metabolic production in comparison to
Signs and symptoms
• Weight gain
• Anorexia
• Tachycardia
• Dyspnea
• Headache
sheet
cheat
• Fatigue
• Weakness
• Change in LOC
• Lethargy
• Vomiting
• Muscle weakness and cramping
• Muscle twitching
• Seizures
• Decreased urination
water loss through urine, stool, skin,
and respiration. A rise in serum sodium
concentration is expected. However, this
nonpharmacologic approach can be dif–
ficult for patients to adhere to. Taking a
daily weight measurement is important,
as is rigorous measurements of intake and
output.
Pharmacologic approaches include 3%
sodium chloride solution, loop diuretics,
urea, demeclocycline, lithium, conivaptan,
and tolvaptan. Sodium chloride solution
administration must be closely moni–
tored due to the possibility of pulmonary
edema. The loop diuretic furosemide may
be administered with 3% sodium chloride
solution to avoid edema or as a stand-alone
treatment. Note that the effectiveness of
lithium can be unreliable and may result
in renal toxicity. Adverse reactions of
conivaptan include hypotension, elevated
blood urea nitrogen, increased thirst, and
infusion-site reactions. Adverse reactions
of tolvaptan may include increased thirst,
dry mouth, and urinary frequency, along
with reports of constipation, nausea, diz–
ziness, weakness, hyperglycemia, and
urinary tract infection.
Continuous venovenous hemofiltra–
tion and sustained low-efficiency daily
dialysis are invasive procedures used in
the case of exceptional, cardiac-related
emergencies.
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Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.patho puzzler
Management of SIADH is focused
on treating symptoms related to hypo–
natremia, whether mild, moderate, or
advanced. Correction rates are monitored
closely regardless of treatment due to
the risk of central pontine myelinolysis
(CPM)—the dysfunction of brain cells
caused by the destruction of the myelin
sheath of nerve cells in the central por–
tion of the brainstem. This adverse reac–
tion can occur in relation to a rapid rise
in serum sodium levels and can lead to
decreased level of consciousness (LOC),
dysphagia, mutism, quadriparesis, and
death.
The key to avoiding CPM is careful
and appropriate correction of the patient’s
hyponatremia based on the degree of
sodium deficiency, whether the patient is
symptomatic, and whether the hypona–
tremia is acute or chronic in nature, with
frequent lab testing of serum sodium
levels. In addition to lab testing, frequent
monitoring of the patient’s neurologic sta–
tus must be performed to identify changes
as early as possible. Total sodium correc–
tion must not exceed 10 mEq in a 24-hour
period, with some authors recommending
an even more conservative rate of 8 mEq in
a 24-hour period.
Accuracy and vigilance
SIADH needs to be accurately diag–
nosed and then controlled and moni–
tored appropriately. As always, safety is
paramount. Your vigilance is crucial for
patients with this
diagnosis. ■
key points
Nursing considerations REFERENCES
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At Northern Arizona VA Medical Center in Prescott, Ariz., Jean
Brennan is a Geriatrics and Extended Care Clinical Nurse Educator,
Sabra Carpenter is an LPN, Jessica Florence is an RN, Jennifer
Hemphill is a Nurse Manager, Ramona Hicks is a Charge RN, Kim
Rooper is a Nursing Officer of the Day, Jason Sewell is an RN, and
Kimber Wagner-Hines is a Charge RN.
The authors have disclosed no financial relationships related to this
article.
DOI-10.1097/01.NME.0000534117.45270.21
24 Nursing made Incredibly Easy! July/August 2018 www.NursingMadeIncrediblyEasy.com