Diabetes insipidus is a disorder characterized by excessive production of dilute urine due to a deficiency of antidiuretic hormone (ADH). There are three main types: central, nephrogenic, and psychogenic. Central diabetes insipidus results from inadequate ADH secretion by the pituitary gland, often due to head trauma, tumors, or infections. Nephrogenic diabetes insipidus occurs when the kidneys do not respond to ADH. Symptoms include excessive thirst, urination, and fluid loss leading to dehydration. Treatment involves fluid replacement and administration of ADH analogs like desmopressin. Nursing care focuses on monitoring fluid status, administering medications, and

1. Diabetes Insipidus
Kiyemba Bob Savio, BSN

2. Diabetes Insipidus
•Description
Diabetes insipidus is a disorder of the posterior
lobe of the pituitary gland characterized by a
deficiency of antidiuretic hormone or its action.
ADH stimulates kidney tubules to be permeable
to water, so that water is reabsorbed back into the
bloodstream,
Inadequate ADH means that large quantities
of dilute urine will be passed. As extracellular
dehydration results, hypotension and
hypovolemic shock can occur.

3. ADH secretion
•ADH is an octapeptide like oxytocin.
•In man, ADH is in the form of arginine vasopressin
(AVP).
•Neurosecretory cells in the supraoptic and
paraventricular nuclei of the hypothalamus
synthesize vasopressin and oxytocin,
•These pass down nerve fibers to be stored in, and
released from the posterior pituitary.

4. Regulation of ADH secretion.
•A plasma osmolality >290 mOsm/l
•A fall in plasma volume
•Emotional factors & stress
•Sleep
•Other stimulants include;- cholinergic stimulation,
adrenergic stimulation, angiotensin ii, prostaglandin
E, opiates, nicotine, histamine, ether and
phenobarbitone.

5. ADH secretion is inhibited by
•Alcohol
•Oropharyngeal water reflex
•B-drenergic stimulants
•Atrial natriuretic factor (ANF)
•Phenytoin

6. Clinical manifestations
•Polyuria, polydipsia & thirst
•Nocturia or nocturnal enuresis
•Hypernatremic dehydration
•Anorexia, and constipation
•Hyperthermia & lack of sweating
•Decreased cerebral perfusion,
•Seizures,
•Loss of consciousness, and
•Death.

7. Etiology
•There are 3 types diabetes insipidus, that is Central
DI, Nephrogenic DI and Psychogenic DI.
•In central DI, there is an inability to secrete an
adequate amount of ADH. This can be caused by;
head trauma,
brain tumor, or
surgical ablation or irradiation of the pituitary gland
Infections of the CNS (meningitis, encephalitis,
tuberculosis)
or tumors (e.g. metastatic disease, lymphoma of the
breast or lung).

8. Etiology cont.
• Nephrogenic DI is a rare congenital or acquired
disorder that occurs when the V2 receptors on the
kidney tubule become nonresponsive to the
action of ADH.
• Primary polydipsia, is a form of polydipsia
characterized by excessive fluid intake in the
absence of physiological stimuli to drink.
 Psychogenic DI is a form of primary polydipsia
caused by psychiatric disorders, often
schizophrenia, which is often accompanied by the
sensation of dry mouth.

9. Assessment and Diagnosis
•The fluid deprivation test is carried out by
withholding fluids for 8 to 12 hours or until 3% to
5% of the body weight is lost.
•Plasma and urine osmolality studies are
performed at the beginning and end of the test.
•The following tests are done;-
Urine output
Low urine osmolality
Urine is “insipid”
Serum osmolality
Urine osmolality
Sodium
Serum ADH

10. Diagnosis cont.
•Laboratory criteria in dx of central DI
serum sodium level greater than 145 mEq/L,
serum osmolality greater than 295 mOsm/kg H2O,
urine osmolality less than 300 mOsm/kg H2O, and
urine specific gravity less than 1.005.
•Normal references
Serum sodium concentration (135 -145 mEq/L).
Serum osmolality (275 - 295 mOsm/kg.)
Normal ADH levels (1 to 5 picogram/mL (pg/mL)).
With normal hydration the normal morning fasting
serum level is lower than 4 pg/mL.

11. Pathophysiology

12. Complications
•Hypernatremic dehydration & its neurological
sequela
•Growth retardation
•Hydronephrosis (due to excessive urine
output)

13. Medical Management
•Treatment goals include;
restoration of circulating fluid volume,
pharmacologic ADH replacement, and
treatment of the underlying condition

14. Cont.
• Medications to manage Central DI
Vasopressin (Pitressin)
Desmopressin (DDAVP)
Lypressin
• Medications to manage Nephrogenic DI
Thiazide diuretics
prostaglandin inhibitors (ibuprofen, indomethacin,
and aspirin)

15. Cont. Medical management
•Desmopressin can be given by IV or SC injection,
nasal inhalation, or oral tablet.
•The doses required to control pituitary DI
completely vary widely, depending on the patient
and the route of administration.
•However, they usually range from 1–2 g qd or bid by
injection, 10–20 g bid or tid by nasal spray, or 100–
400 g bid or tid orally.
•The onset of action is rapid, ranging from as little as
15 minutes after injection to 60 minutes after oral
administration.

16. Nursing Management
•Fluid status
•Laboratory studies
•ADH replacement
•Elimination issues
•Patient education

17. Nursing care plan
•Nursing diagnosis
Deficient fluid volume related to; inability to
secrete an adequate amount of ADH, non
responsiveness of kidney tubules V2 receptors; as
evidenced by increased output of dilute urine.
•Desired outcome
To demonstrate adequate hydration as evidenced
by palpable peripheral pulse.

18. Interventions and Rationale
•Monitoring HR and BP. These are indicators of
hydration.
•Measuring urine input and output. To easily note
fluid loss or excess.
•Educating the client on the need to drink much
water. To replace lost fluids.
• Monitoring conditions of buccal membranes, skin
turgor and measuring daily weight. These are
indicators of hydration status.
•Administering DDAVP as prescribed. To replace the
body’s ADH.

19. Nursing diagnosis
Electrolyte imbalances related to; impaired
regulatory mechanisms, renal dysfunction; as
evidenced by changes in serum electrolytes
•Outcome
Client to display serum electrolytes with in normal
limits
•Interventions and Rationale
Monitoring BP. To easily note hypertension or
hypotension

20. Cont. interventions and rationale
Evaluating LOC and muscle strength. Sodium
imbalances may cause confusion or coma.
Monitoring serum electrolytes and osmolality. To
evaluate therapy needs and effectiveness.
Increase oral or IV intake of fluids. Replacement of
total body water deficit will gradually restore
sodium and water balance

21. Other diagnoses
•Decreased cerebral perfusion related to
hypovolemia as evidenced by decreased LOC.
•Risk for impaired skin integrity related to; decreased
skin perfusion or immobility.
•Deficient knowledge about the disease condition
related to unfamiliarity about the disease and
treatment as evidenced requests for more
information.