DI AND SIADH
Pat Hock RN
PICU Nurse Educator
Lucile Packard Children’s
Hospital
DI and SIADH
Disturbances of Water Balance
• 60% to 80% of the human body is
composed of water.
• Water content varies with age, gender,
skeletal muscle mass and fat content.
• Osmolality is one of several factors
regulating fluid balance between the
intracellular and extracellular fluid
compartments.
ADH: AntiDiuretic Hormone
• Formed in the supraoptic and paraventricular
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nuclei of the hypothalamus.
Transported to the posterior lobe of the Pituitary
Gland and stored.
ADH is released: in response to an increase in
intravascular osmotic pressure, hypovolemia,
decrease in pulse pressure. And in response to
fear, pain, anxiety.
Function of ADH
• ADH increases the permeability of the
renal distal tubule and collecting ducts to
water.
• Less free water is excreted in urine
• Urine volume is decreased
• Concentration of urine is increased
Diabetes Insipidus
• DI is a clinical condition due to a deficit of
ADH or due to the kidney’s resistance to
the effects of ADH.
• DI may be central (neurogenic) or
nephrogenic.
• DI may be a transient or a permanent
condition.
Etiologies of DI
• CNS disorders that damage or create pressure in the
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area of the hypothalamus, pituitary stalk, or posterior
pituitary gland
Head Injuries
CNS infections
Intraventricular Hemorrhage
Neurosurgical Procedures: common postoperatively with
resection of craniopharyngiomas, pituitary gland tumors,
or suprasellar tumors.
Associated with certain drugs: Ethanol, phenytoin,
halothane, opiate antagonists, lithium
Signs and Symptoms of DI
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POLYURIA- first sign
Low Urine osmolality (less than 100-200 mOsm/L)
Urine specific gravity <1.010
Hypernatremia (serum sodium greater than 145 mEq/L)
Serum hyperosmolar (greater than 300 mOsm/L)
Thirst, polydipsia
Irritability or mental status changes
Dehydration
Shock
Clinical Management of DI
• Goal is to prevent circulatory failure and
hyperosmolar encephalopathy.
• Replace volume deficit and ongoing losses
• Replace ADH
• Close monitoring of serum and urine
lytes/osmolality
Fluid Replacement
• Correct Hypernatremia slowly
• Bolus with NS if hypotensive
• Volume deficit replaced over 24 to 48
hours
• Replace ongoing urine losses
Vasopressin
• Available IV, subcutaneous, and intranasal
forms
• DDAVP given intranasally
• Pitressin IV
• Therapeutic effect: increase in specific
gravity and decrease in urine output
within 1 hour of dose.
Nursing Management
• Close monitoring of intake and output
• Frequent hemodynamic monitoring
• Frequent Neuro assessments
• Serial labs: urine specific gravity and
osmolality, Serum sodium and osmolality
Complications
• Cardiac collapse
• Shock
• Cerebral Edema
• Herniation
• Death
• Electrolyte imbalances
• Water intoxication and fluid overload
Syndrome of Inappropriate
AntiDiuretic Hormone
• SIADH is a clinical condition involving and
excess of ADH secretion.
• The patient is hyponatremic with a low serum
osmolality, which normally would inhibit ADH
secretion.
Etiology of SIADH
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Head Trauma
Cerebral Tumors
Meningitis
Cerebral Hemorrhage
Pulmonary Diseases
Chronically ill or malnourished children
Spinal surgery
BMT or Stem Cell Transplants
Medications
Positive pressure ventilation
Signs and Symptoms of SIADH
• Low urine output in absence of
hypovolemia
• Hyponatremia (serum sodium<135mEq/L)
• Low Serum osmolality (<285 mOsm/L)
• High urine specific gravity (>1.020)
• Nausea and vomiting
• Mental status changes
Clinical Management
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Normalize serum sodium over 24 to 48 hours
Normalize serum osmolality
Correct excess extravascular fluid volume
Prevent neurological sequelae
Restrict fluids
3% NaCl
Loop diuretics
Nursing Management
• Close monitoring of intake and output
• Maintain fluid Restriction
• Frequent Hemodynamic monitoring
• Frequent Neuro assessments
• Serial labs: serum electrolytes, serum
osmolality, specific gravity
Complications
• Seizures
• Cerebral edema
• Cerebral hemorrhage
• Pulmonary edema
• Muscle cramps or weakness
Triphasic response post
Neurosurgery
• Transient DI 12-48 hours postop
• SIADH after transient DI phase lasting up
to 10 days postop
• Permanent DI
Case Scenario #1
A 3 month old is admitted to the PICU for
shock with a 2 day history of fever and
irritability. Blood and CSF cultures are
positive for Streptococcus pneumoniae.
He has had decreasing urine output over
the last 24 hours (< 0.5 ml/kg/hr)
? Assessment
? Labs might be ordered
Labs
Serum
Na 126 mEq/L
Cl 98 mEq/L
K 3.7 mEq/L
CO2 25mEq/L
Urine sp gr 1.025
se osmo 260mOsmo/L
Bun 4mg/dl
Cr 0.4 mg/dl
glucose 129 mg/dl
? Abnormal findings
? Etiology
? Treatment
Abnormalities
• Hyponatremia
• Oliguria
• Concentrated urine
• Low serum osmolality
SIADH
Treatment:
Fluid Restriction
Case Study #2
A 5 year old (15kg) boy is admitted to the PICU
with a history of MVA 2 days ago. He sustained
an isolated head injury with an intraventricular
hemorrhage and multiple cerebral contusions.
Three hours ago he had an episode of severe
intracranial hypertension (ICP 90mmHg, MAP 50
mmHg) requiring volume and an epi drip for
hypotension. Over the last 2 hours his uo has
increased to 130-150 ml/hr (~8ml/kg/hr.)
? Assessment
? Labs might be ordered
Labs
Serum:
Na 155mEq/L
Cl 114 mEq/L
K 4.2 mEq/L
CO2 22 mEq/L
Urine sp gr 1.005
BUN 13 mg/dl
Cr 0.6 mg/dl
glu 86 mg/dl
se osmo 320 mOsmo/L
?Abnormal Findings
? Etiology
? Treatment
Abnormalities
• Hypernatremia
• Polyuria
• Dilute urine
• High serum osmolality
DI
Treatment:
Acute: Vasopressin infusion
Chronic: DDAVP
Monitor for Hyponatremia
References
• Curley, Critical Care Nursing of Infants and
Children. Saunders
• Hazinski. Manuel of Pediatric Critical Care.
Mosby
• Kliegman. Nelson’s Textbook of Pediatrics.
Saunders
• Slota. AACN’s Core Curriculum for Pediatric
Critical Care. Saunders