2. Diabetes insipidus
Diabetes insipidus is a disorder of the
posterior pituitary gland
Inability of the kidneys to concentrate urine.
Two forms
Central (neurogenic) and nephrogenic diabetes
insipidus.
Central diabetes insipidus results from
inadequate production of vasopressin
(antidiuretic hormone)
Nephrogenic diabetes insipidus results from
ineffective action of vasopressin in the kidneys
3. Antidiuretic hormone facilitates concentration
of the urine by stimulating reabsorption of
water from the distal tubule of the kidney.
When ADH is inadequate, the tubules do not
resorb, leading to polyuria (passage of a
large volume of urine in a given period).
Therefore, the body is unable to conserve
water, resulting in severe dehydration.
4. Causes
The cause of 20% to 50% of cases of central diabetes
insipidus is unknown and is classified as being
idiopathic.
Known causes of central diabetes insipidus include
brain tumors, brain trauma, central nervous system
infection, and neurosurgery
Genetic nephrogenic diabetes insipidus is not as
common as the acquired type, but its presentation is
more severe.
Acquired nephrogenic diabetes insipidus may be
caused by
drug toxicity, an adverse drug reaction, or illnesses that
impair the ability of the kidneys to concentrate urine
5. Clinical features
Polyuria and polydipsia (excessive thirst)
are the cardinal signs of diabetes insipidus.
Enuresis is common in children.
Polydipsia is the body’s attempt to preserve
fluid balance.
Additional manifestations observed in children
with diabetes insipidus include hypernatremia,
dilute urine, and dehydration
6.
7. In infants, symptoms may include irritability,
lethargy, vomiting, poor feeding, failure to thrive,
and constipation
In all forms of diabetes insipidus, the urine cannot
be concentrated no matter how dehydrated the
child becomes. A dehydration episode usually
leads to the diagnosis.
Serum sodium concentration and osmolality
increase rapidly to pathologic levels.
Often an unconscious child is admitted to the
emergency department with dehydration and
hypernatremia
8. Diagnosis
Initial testing involves serum electrolyte
concentrations and a urinalysis including specific
gravity and osmolality.
Serum osmolality is increased (greater than 300
mOsm/kg), and urine osmolality is decreased (less
than 300 mOsm/kg).
Urine specific gravity is decreased (less than 1.005),
and serum sodium is elevated (greater than 145
mEq/L).
A CT scan or MRI may be ordered to visualize the
pituitary gland to detect a tumor.
A fluid deprivation test evaluates the level of ADH and
helps to confirm the diagnosis
9. Assessment
Increased excretion of large qualities (5-10 L per day) of hypotonic
urine
Extreme thirst
Altered LOC, orthostatic hypotension
Poor skin turgor, dry mucus membrane
Vital signs
TEM, RR, HR INCREASED
BP DECREASED
ICP INCREASED
CVP decreases
Urine osmolality decreases to 200 mOsm/kg
Serum osmolality increases to 300 mOsm/kg
Increased serum Na >147mEq/L
Plasma ADH is decreased
10. Multidisciplinary management
Water deprivation test
Measure the lab values every hourly
Prohibit fluid intake
Assess for negative results
Urine specific gravity > 1.020
Urine osmolality >800 mOsm/kg
Assess for positive results
>= 5% body weight loss
Urine specific gravity not to increase for three
consecutive hourly measurements
11. Multidisciplinary management
Vasopressin test
Administer vasopressin subcutaneously
Urine specimen collected every 3o mts for 2
hours and evaluated for quantity and osmolality.
(increased)
Rehydration therapy with hypotonic solutions to
replace fluid and wt loss
Rapid dehydration .. Later based on urine output
Administer exogenous vasopressin
Administer thiazide diuretics,Low sodium and low
protein diet in case of nephrogenic DI