This document provides an overview of diabetes insipidus (DI), including defining the condition as a deficiency of antidiuretic hormone resulting in excessive thirst and urine production. It discusses the objectives of teaching about DI, risk factors, types of DI, clinical manifestations involving polyuria and polydipsia, pathophysiology of increased serum osmolality, assessment, management involving vasopressin replacement and fluid conservation, nursing management, monitoring, self-care, and references research studies on DI.

1. DIABETES INSIPIDUS
PRESENTED BY
MONIKA
M.Sc NURSING
NINE, PGIMER, Chandigarh

2. OBJECTIVES
At the end of the teaching students will be able to:
Introduce the topic diabetes insipidus
Define the diabetes insipidus
Enlist the risk factors of diabetes insipidus
Describe the etiology and types of diabetes insipidus
Discuss the clinical manifestations of diabetes insipidus
Explain the pathophysiology of diabetes insipidus
Discuss the management of diabetes insipidus
Research article r/t diabetes insipidus

3. INTRODUCTION:
• Diabetes insipidus is an uncommon disease process
with a low prevalence of 1 in 250000. In clinical
practice, congenital forms of diabetes
insipidus constitute less than 10% of patient cases. DI
is relatively rare. Males and females are affected
equally.

4. DEFINITION:
• Diabetes insipidus is a disorder of the posterior lobe of
the pituitary gland that is characterized by a deficiency
of antidiuretic hormone (ADH)/(vasopressin).
Excessive thirst (polydipsia) and large volumes of
dilute urine characterize the disorder.

5. • Deficiency of vasopressin/ADH release results in a
clinical condition called diabetes insipidus. This
condition results from unresponsiveness of renal distal
convoluted tubules to ADH, it is called nephrogenic
diabetes insipidus and if cause lie in the
cranium(head), it is called cranial diabetes insipidus.

7. RISK FACTORS:
• Surgery, infection, or trauma to the hypothalamus
• Kidney disease
• Chronic hypercalcemia or chronic hypokalemia (nephrogenic DI)
• Neurosurgery, skull fracture
• Pregnancy (gestational DI)
• Tumors
• Vascular lesions
• Anorexia nervosa
• Medications, such as lithium

8. ETIOLOGY & TYPES:
• It starts in childhood or early middle life. The cause
may lie in hypothalamus or pituitary or in the kidneys.
It may be due to a congenital or an acquired defect.
20% to 50% cases are idiopathic.

9. TYPES ETIOLOGY
1. Central (neurogenic) DI  This is results from an interference with ADH
synthesis, transport, or release.
 Eg. Brain tumor, head injury, brain surgery,
CNS infection
1. Nephrogenic DI  This results from inadequate renal response to
ADH despite presence of adequate ADH
 Eg. Drug therapy specially lithium, renal
damage, hereditary renal disease.
1. Primary DI  This is results from excessive water intake
 Eg. Structural lesion in thirst center,
psychologic disorder.

11. CLINICAL MENIFESTATIONS:
• Polyuria (excretion of large quantities of urine 2 to 20L/day with
very law specific gravity 1.001 to 1.005 and osmolality of less
than 100 mOsm/kg).
• Polydipsia (patient experience intense thirst and drink lot of water
and cold or hot drink to compensate water loss)
• If diabetes insipidus is inherited, the primary symptoms may
begin at birth; in adults, onset may be insidious or abrupt.

12. Common symptoms include:
• Nocturia
• Severe thirst
• Frequent urination where
excessive diluted urine is excreted
• Bed-wetting
• Inconsolable crying in children
• Trouble sleeping
• Delayed growth
• Dizziness
• Weakness and fatigue
• Fever
• Weight loss
• Vomiting
• Diarrhea

13. Pathophysiology

14. Increased serum
osmolality
(hypernatremia)
Excessive
urine output
Decreased intravascular fluid volume
Decreased water reabsorption in renal tubules
Due to the decreased antidiuretic hormone

15. ASSESSMENT AND DIAGNOSTIC
FINDINGs
History is obtained
Physical examination
laboratory tests are performed:
• Including urine and plasma osmolality and urine specific
gravity. A water deprivation test is performed to confirm a
suspected case of central DI.
• Urinalysis shows colorless urine with low osmolality (less
than 200 mOsm/kg) and low specific gravity (usually 1.005
or less).

17. • Sodium level (serum) is greater than 145 mEq/L.
• Osmolality (serum) is increased (greater than 287 mOsm/kg).
• Serum vasopressin level is decreased.
• A 24-hour urine test shows decreased specific gravity and
increased volume.
• Blood urea nitrogen level test results and creatinine level
(serum) are elevated.
• Antidiuretic hormone (serum) test shows absent or below-
normal levels.

18. • Fluid deprivation test: Fluids are withheld for 8 to 12 hours
until 3% to 5% of the body weight is lost.
• Other diagnostic procedures include concurrent
measurements of plasma levels of ADH and plasma and urine
osmolality as well as a trial of desmopressin (synthetic
vasopressin) therapy and intravenous (IV) infusion of
hypertonic saline solution.
Imaging
• Magnetic resonance imaging of the brain rules out a tumor or another
abnormality

19. COMPLICATIONS:
• Without medical treatment, the potential diabetes insipidus
complications include:
• Chronic dehydration
• Tachycardia
• Decreased temperature
• Hypotension
• Weight loss
• Fatigue
• Headaches
• Kidney damage
• Brain damage

20. MANAGEMENT

21. Medical Management:
The objectives of therapy are:-
• To replace ADH (which is usually a long-term therapeutic
program)
• To ensure adequate fluid replacement.
• To identify and correct the underlying intracranial pathology.
• Nephrogenic causes require different management
approaches.

22. Pharmacologic Therapy: Vasopressin replacement
• Desmopressin (DDAVP), administered intranasally, one or
two administrations daily to control symptoms.
• Lypressin (Diapid), absorbed through nasal mucosa into
blood; duration may be short for patients with severe disease
• Intramuscular administration of ADH (vasopressin tannate in
oil) every 24 to 96 hours to reduce urinary volume (shake
vigorously or warm; administer in the evening; rotate
injection sites to prevent lipodystrophy).

23. Fluid conservation:
• Clofibrate (Atromid-S), a hypolipidemic agent, has been
found to have an antidiuretic effect on patients who have
some residual hypothalamic vasopressin.
• Chlorpropamide (Diabinese) and thiazide diuretics are also
used in mild forms of the disease because they potentiate the
action of vasopressin.
• Thiazide diuretics, mild salt depletion, and prostaglandin
inhibitors (ibuprofen [Advil, Motrin], indomethacin
[Indocin], and aspirin) are used to treat the nephrogenic form
of diabetes insipidus.

24. Nursing Management
1) Anxiety
2) Coping Impairment
3) Decreased Cardiac Tissue Perfusion
Risk
4) Electrolyte Imbalance Risk
5) Fatigue
6) Hypovolemia
7) Impaired Comfort
8) Injury Risk
9) Knowledge Deficiency

25. Special consideration:
• maintenance of fluid and electrolyte balance, and patient education.
• Encourage adequate fluid intake. Ensure that the patient has free access
to water.
• Baseline vital signs and weight are important to accurately document and
monitor throughout therapy
• Assess hemodynamic status, as indicated. Auscultate heart and lung
sounds for changes.
• Check skin turgor for evidence of overall hydration status.
• Strict (hourly) intake and output monitoring are essential to correct fluid
losses and to titrate IV fluid replacement.

26. • Assess for signs and symptoms of fluid overload if the patient is receiving IV
fluid therapy.
• Instruct patient and family members about follow-up care and emergency
measures.
• Provide specific verbal and written instructions, including the actions and
adverse effects of all medications; demonstrate correct medication
administration and observe return demonstrations.
• Advise patient to wear a medical identification bracelet and to carry medication
information about this disorder at all times.

27. Monitoring
• Intake and output; 24-hour urine output volume
• Vital signs
• Daily weight
• Urine specific gravity and osmolality
• Serum electrolytes levels, especially sodium level
• Blood urea nitrogen level
• Signs and symptoms of hypovolemic shock
• Changes in mental or neurologic status
• Cardiac rate and rhythm
• Thirst

28. Self-care
• Adequate water intake to avoid dehydration.
• Reduce salt intake.
• Avoid medications that increase urine output, after consultation with
your doctor.
• Avoid activities that cause dehydration.
• Advice low-sodium, low protein diet (nephrogenic DI)

29. RESEARCH STUDIES
• Koundal H; Dhandapani M (September 2021)
Effectiveness of dietary diabetes insipidus bundle on the
severity of postoperative fluid imbalance in pituitary
region tumours: A randomized controlled trial
conclution of this is probably the first ever report of dietary DI
bundle among operated pituitary patients, which seem to
flatten the DI trend with significant benefits in polyuria,
hypernatraemia, vasopressin requirement and hospital stay.

30. Conclusion
• Diabetes insipidus prevalence is very low. This is the disorder
of the posterior lobe of pituitary gland that is characterized by
deficiency of ADH. Patient have symptom of polydipsia,
polyuria that may due to neurogenic or nephrogenic cause.
Which is diagnose by laboratory urinalysis or electrolyte test.
If is not treated patient may develop complications like
tachycardia, hypotension chronic dehydration, kidney
damage etc. it is treated with vasopressin replacement,
adequate fluid replacement or either different management
approaches according to the cause of disease.

31. Summary

32. Assignment
1. Write an assignment on NANDA nursing
diagnosis of diabetes insipidus patient.

33. REFERENCE LIST:
• Chugh SN, ”textbook of Medical-Surgical-Nursing”,edition-first,
published by Avichal publishing company2013, p.596-602.
• Sudddarth ‘s & brunner, “A Textbook of Medical-Surgical-Nursing”,
Edition eleventh, published by lippncott Williams & Wilkins,2008 pp
1147-1149.
• Basavanthappa BT. “Medical Surgical Nursing (2volumes)”. 3st
Edition. Jaypee Publisher ,2015. Pp 1128, 1053-1058
• Dewit,Stromberg,dallred, “Medical-Surgical-Nursing concepts and
practice”, edition 3rd , published by Elsevier, pp.1432-1434.
• http://advisor.lww.com.elibpgimer.remotexs.in/lna/document.do?bid=4
&did=913853

34. • http://ovidsp.dc2.ovid.com.elibpgimer.remotexs.in/ovid-
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• http://ovidsp.dc2.ovid.com.elibpgimer.remotexs.in/ovid-
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• http://ovidsp.dc2.ovid.com.elibpgimer.remotexs.in/ovid-
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