Nursing Management of DI and SIADH
April 24, 2012
Lauren Walker RN, BSN, CCRN
Objectives
• Describe the normal function of ADH in water and
electrolyte regulation.
• Compare and contrast the etiologies of SIADH and
DI.
• Describe the assessment findings of SIADH and DI.
• Evaluate the management and treatment of SIADH
and DI.
• Evaluate the possible complications of SIADH and
DI.
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
pituitary surgery
• Psychoses
• Drugs
• Acute head injury
• Pulmonary
infections
(Pneumonia)
• Nervous system
infections
(meningitis)
Investigate the following conditions for
SIADH
• Thirst and fluid
status with accurate
I&O
• Confusion
• Dyspnea
• Headache
• Fatigue
• Weakness
• Increased weight
w/o edema
• Change in LOC
• Lethargy
• Vomiting
• Muscle weakness
and cramping
• 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
HA, 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, CheyneStokes respirations, death
Diabetes Insipidus
Disordered regulation of water balance
due to impaired urinary concentrating
ability secondary to inadequate
secretion of ADH or resistance to ADH.
Four Types of DI:
Central/Neurogenic (CDI)
Nephrogenic (NDI)
Dipsogenic
Gestational
Pathophysiology of DI
• Central/Neurogenic
• Nephrogenic
Inadequate secretion of Inadequate response
by the kidneys to
ADH due to loss or
ADH.
malfunction of
neurosecretory
A disorder of renal
neurons that make
tubular function
up the posterior
resulting in the
pituitary.
inability to respond
to ADH in
absorption of
Vasopressin Sensitive
water.
Vasopressin
Resistant
• Dispogneic
Suppression of ADH
secondary a defect
or damage to the
thirst mechanism
located in the
hypothalamus
resulting in increased
fluid intake or
psychogenic causes
Diabetes Insipidus (DI) Clinical Signs!
• Dehydration! Excessive loss of water from
body tissue and imbalance of essential
electrolytes (Ns, K, Cl)
• Polydipsia (excessive thirst)
• Polyuria (excessive amount of urine)
• Low specific gravity (1.001 to 1.005)
• Serum hyperosmolality and hypernatremia
Causes of DI
• Head Trauma
• Idiopathic
• Post-operative
(hypophysectomy,
pituitary tumor)
• ICH
• Brain Tumors
• Hypoxia
• CNS Infection
(meningitis, abcess)
• Medications (Dilantin,
clonidine, alcohol)
• Increased ICP
• Damage to
hypothalamus or
posterior pituitary
• Stroke
Investigate the following for DI
• Unquenchable thirst
• Polydipsia
• Polyuria
(hourly urine output > 200 mls)
• Unexplained weight loss
• Urinary frequency
• Nocturia
• Dry skin/poor skin turgor
• Tachycardia and
hypotension
• Inability to respond to the
increased thirst stimulus and
compensate for the
excessive polyuria
• Hypernatremia that
becomes severe and is
manifested by- confusion,
irritability, stupor, coma and
neuromuscular hyperactivity
progressing to seizures.
• Elderly
• Unconscious/intubated
Labs and Diagnostics for DI
Serum calcium
Glucose
Creatinine
Potassium
Urea level
• The following may also be indicated:
– 24hr urine collection to quantitative polyuria
– CT/MRI
• rule out pituitary causes, metastases, hemorrhage, neuronal
damage, cerebral tumors.
– Radioimmunoassy: to measure circulating ADH
concentrations
Lab Results for diagnosis of DI
Lab Value
Result
Serum Sodium
Above 135 mEq/L
Serum Osmolality
Above 290 mOsm/kg
Urine Specific Gravity of the
first morning voiding
Below 1.005
Urine Sodium
Above 145 mEq/L
Urine Osmolality
Below 300 mOsm/L
Diagnosis of DI should be considered in any person
producing large volumes of dilute urine
Water Deprivation Test
• After baseline measurement of: weight, ADH, plasma
sodium, and urine/plasma osmolality, the patient is deprived
of fluids under strict medical supervision
• Frequent (q2h) monitoring of plasma and urine osmolality
follows.
• The test is generally terminated when plasma osmolality is
>295 mOsm/kg or the patient loses ≥3.5% of initial body
weight.
• DI is confirmed if the plasma osmolality is >295 mOsm/kg
and the urine osmolality is <500 mOsm/kg.
Nephrogenic DI vs Neurogenic DI
• DDAVP Challenge
 Check urine osmolality 1-2hrs after 1mcg SQ DDAVP
• If little or no change: likely NDI or dipsogenic DI
• If significant increase in urine osmolality, likely CDI
• 5 units vasopressin IV
 Measure osmolality
 A significant increase (>50%) in urine osmolality after
administration of ADH is indicative of CDI
Treatment of DI
Correct the underlying cause and maintain adequate fluid
replacement.
• DI Therapy varies with the degree and type of DI present or
suspected.
• IVF may be necessary to correct hypernatremia; avoid rapid
replacement
• Free water restriction
• After assessing fluid status and serum sodium level, treat both
dehydration and hypernatremia
• For chronic neurogenic DI- require hormonal replacement
therapy: DDAVP (nasal vasopressin)
• Consultation with an endocrinologist is strongly recommended
Treatment for Nephrogenic DI
Removal of the underlying cause/offending drug
• DDAVP usually ineffective
• Thiazide diuretic (HCTZ) is first line treatment
• Adequate hydration
• Low-sodium diet + thiazide diuretics to induce mild
sodium depletion.
• Indomethacin may also be useful to reduce urine
volume.
Nursing Management of DI
•
Hourly Neuro Checks
•
Frequent Vital Signs
•
Evaluate for s/s of hypovolemic shock
•
Strict I&O
•
Rehydrate for symptoms of extreme thirst
•
Measure and record weight using the same scales at the same time and with
the patient wearing the same clothing
•
Assess mucous membranes and skin turgor and monitor for symptoms of
dehydration
•
Provide rest
•
Safety measures to prevent injury secondary to dizziness and fatigue
•
Alert the health care team of problems of urinary frequency and extreme thirst
that interferes with sleep and activities.
SIADH vs DI Lab Values
Finding
SIADH
DI
Urine Output
Less than 200 mls x
2hrs
Greater than 250 mls
x 2hrs
Serum Sodium
Below 135 mEq/L
Above 135 mEq/L
Urine Sodium
Below 25-30 mEq/L
Decreased
Urine Osmolality
Above 900 mOsm/kg Below 400 mOsm/kg
Plasma Osmolality
Below 275 mOsm/L
Above 295 mOsm/L
Blood Pressure
Normotension
Hypotension
Fluid Status
No Dehydration
Dehydration
Neuro Symptoms
Confusion, delirium,
coma with low Na
Seizures, coma
Complications to treatments of DI and
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
DI and 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
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