Nursing Management of SIADH

August 24, 2017

Pria WRG, Ns., M.Kep., EMT-B
Objectives

Describe the normal function of ADH in water and

electrolyte regulation.

Describe the etiologies of SIADH.

Describe the assessment findings of SIADH.

Evaluate the management and treatment of SIADH.

Evaluate the possible complications of SIADH.

Brain Regulation

Disorder of sodium and water balance

is a common complication following
neurosurgery

Neuroscience patients must be

continually assessed and monitored for
their response to therapy

Early detection is critical to the

protection and integrity of the brain
Normal Brain Regulation
TBW accounts for 60% of body weight
20% ECF
40% ICF

Fluid shifts can occur depending on

concentrations of solutes in ICF and ECF

Na and K are principle determinants in fluid

shifts

Osmolarity: amount of solute in fluid (urine,

blood)

Normal Serum Osmolarity: 280-295 mOsm/L

 Serum Osmo above 295 mOsm/L = water
deficit
Concentration is too great OR
Water concentration is too little

Serum Osmo below 280 mOsm/L = water

excess
Amount of particles or solute is too small in
proportion to the amount of water OR
Too much water for the amount of solute

To maintain plasma or serum osmo within range,

free water intake and excretion must balance
 Antidiuretic Hormone (ADH): balances Na and water in body and
controls water conservation

Changes in pressure of ECF triggers release of ADH from pituitary

gland

Release is coordinated with activity of the thirst center- regulates

intake

ADH binds with receptor sites of the collecting duct in kidney resulting
in increased free-water resorption

ADH causes vasoconstriction

Presence of ADH- renal tubule permeability to water is increased and

water is reabsorbed

Absence of ADH- renal tubule permeability to water is decreased

renal excretion to fluids
 Plasma osmolality = Primary regulatory
mechanism for the release of ADH

Receptors in the brain are sensative to

changes in osmolality

Receptors that trigger thirst mechanism are

close to those that control ADH release

Serum osmo greater than 290 mOsm/L

triggers thirst
ADH Feedback Loop
Syndrome of Inappropriate Antidiuretic
Hormone
SIADH: Persistent abnormally high (inappropriate)
levels of ADH in the absence of stimuli with normal
renal function
No longer regulated by plasma osmo and volume
Imbalance of fluid and electrolytes

Feedback system is impaired and posterior pituitary

continues to release ADH

Renal tubules continue to reabsorb free water

regardless of the serum osmolality

Excessive activity of the neurohypophyseal system

r/t brain disease
At Risk Patients for SIADH

Post-Operative with Psychoses

pituitary surgery
Drugs
Acute head injury
Nervous system
Pulmonary infections
infections (meningitis)
(Pneumonia)
Investigate the following conditions for
SIADH

Thirst and fluid Increased weight

status with accurate w/o edema
I&O Change in LOC
Confusion Lethargy
Dyspnea Vomiting
Headache Muscle weakness
Fatigue and cramping
Weakness Muscle twitching
Seizures
Labs to Diagnose SIADH

Serum Na
Urine Na
Urine Osmolality
Serum Osmolality
BUN/Creatinine
Urine Specific Gravity
Serum Potassium
Lab Results for SIADH

Serum Sodium Less than 135 mEq/L

Urine Sodium Greater than 20 mEq/L
Urine Osmolality Higher than serum
Serum Osmolality Less than 275 mOsm/L
BUN/Creat WNL
Urine Specific Gravity Greater than 1.005
Adrenal/threshold WNL
Serum Potassium Less than 3.5 mEq/L
Treatment of SIADH

Correct underlying cause

Fluid restriction 500-1000 ml/day

Severe hyponatremia:
3% NS may be given

Lasix may be given (watch K level)

Nursing Management of SIADH
Frequent Neuro assessment
Mental status and LOC

Pulmonary assessment
s/s fluid overload

Cardiac assessment
Dysrhythmias and BP abnormalities

Monitor for seizure activity

Seizure precautions

Accurate I&O

Daily Weights
Same time each day, same scale, same clothes

Oral hygiene

Reduce stress, pain, discomfort

Correlation of Decreasing Sodium
Levels and Symptoms
Serum Sodium Level Symptoms

145-135 mEq/L Normal concentration, no

symptoms
135-120 mEq/L Generally no changes

120-110 mEq/L Apathy, lethargy, weakness,

disorientation, thirst, fatigue,
seizures
110-100 mEq/L Confusion, hostility, lethargy,
N/V, abdominal cramps, muscle
twitching
100-95 mEq/L Delirium, convulsions, coma,
hypothermia, areflexia, Cheyne-
Stokes respirations, death
Complications to treatments of SIADH

Cerebral Edema!

Central Pontine Myelinolysis: brain cell

dysfunction caused by destruction of the
myelin sheath covering nerve cells in
brainstem
Na levels rise too fast or corrected too
quickly

s/s: (not necessarily immediate)

Acute paralysis
Dyschagia
Dysarthria
Most Important Nursing Intervention for
SIADH

Frequent Labs
We have severe electrolyte abnormalities
Careful not to correct too quickly!!
Na should not rise more than 0.5mEq/L/hr
and 10 mmol/L/24 hrs

Frequent neuro assessment

The nurse can pick up abnormal behavior
and signs and symptoms first
Note any changes from baseline
References

A.D.A.M. Medical Encyclopedia. (2010). Central pontine

myelinolysis. Retrieved April/18, 2012, from
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001779/.
Barker, E. (Ed.). (2008). Neuroscience nursing, A spectrum of care
(3rd ed.). St Louis, MO.: Mosby Elsevier.
Darling, J. (2012). In Walker L. (Ed.), Essentials to know, diabetes
insipidus.
Marino, P. (2009). The little ICU book. Philadelphia: Lippincott
Williams & Wilkins.
Urinary system" physiology & urine formation. (2010). Retrieved
April/17, 2012, from
http://www.google.com/imgres?imgurl=http://legacy.owensboro.kctcs.edu/gcaplan/anat2/notes/Image43.gif
&imgrefurl=http://legacy.owensboro.kctcs.edu/gcaplan/anat2/notes/APIINotes3%2520urinary%2520syste
m.htm&usg=__XjNUnNDfvcRKXEREA-
8DAxd1t5w=&h=440&w=392&sz=17&hl=en&start=3&sig2=DGkmrCq21f5aXMsTSMjEmA&zoom=1&tbnid
=7gqzstTrZlnuCM:&tbnh=127&tbnw=113&ei=HxaPT---
FuXb0QGtp8GODw&prev=/search%3Fq%3Dadh%2Bfeedback%2Bloop%26hl%3Den%26gbv%3D2%26tb
m%3Disch&itbs=1.