TOPIC- DIABETES INSIPIDUS
PRESENTED BY
OM VERMA
ASSISTANT PROFESSOR
RELIANCE INSTITUTE OF NURSING
INTRODUTION
Diabetes incipidus is an uncommon
condition that often begins in childhood or
early adult life and affects more andles than
females. People with diabetes incipidus
pass excessive amounts of urine.
In diabetes mellitus urine contains large
amounts of glucose, where as urine in
diabetes incipidus is highly dilute and
contain no glucose.
diabetes insipidus primarily results from
deficiency of ADH. The major function of
ADH are:-
Promote water reabsorption by the kidney
and
Control the osmotic pressure of ECF.
Thus, when ADH production excessively the
kidney tubules do not reabsorb water, and
consequently the person excretes large
amount of dilute to urine.
DEFINITION
 It is a disorder of water metabolism caused
by deficiency of ADH (Vasopresin) or by
inability of the kidneys to respond to ADH.
According to AND
A disease in which the secretion of or
response to the pituitary hormone
vasopressin is impaired, resulting in the
production of very large quantities of
dilute urine, often with dehydration and
insatiable thirst.
According to lewis
ACC TO Lippincott
“ Diabetes insipidus is a disorder
of water metabolism caused by
deficiency of vasopressin, the
antidiuretic hormone (ADH)
secreted by the posterior pituitary.”
ACC to Joyce M. Black 6th edition.-
“ A deficiency of antidiruteic homone
ADH vasopressin) result in inability to
conserve water.”
ACC to Beare / Myeres 2nd edition
Diabetes insipidus is a condition
characterized by impaired renal
conservation of water resulting form a
deficiency of the ant diuretic hormone
(ADH) arginine vasopressin.
INCIDENCE:-
unknown DI idiopathic in
about 30% of all clients with
DI; tumor can be related to
25% of DI cases, head injury
accounts for 16% cranial
surgery for 20% of DI cases.
TYPES
TYPES:- There are 4 types:-
1.Central Diabetes Insipidus
2.Nephrogenic Diabtes Insipidus
3.Dispogenic Diabetes Insipidus
4.Complete Diabetes Insipidus
CENTRAL DIABETES INSIPIDUS
A defect of the pituituar gland or
hypothalamus
It is usually occurs suddenly
Central Di usually has a triphasic
In central DI, problem stems from an
interference with ADH synthesis or
release.
Multiple causes include brian tumor,
head injury, brain surgery CNS
infection.
Con….
The acute phase, with abrupt onset
of polyuria.
An interphase, where urine volume
apparently normalizes
A third phases, where central DI is
permanent. The 3rd phase is usually
apparent within 10 to 14 days
postoperatively.
II) NEPHROGENIC DIABETES
INCIPIDUS:-
Kidney tubular defect resulting in less
than use water absorption .
Problem stems form an interference
with renal responses to ADH despite
presence of adequate ADH, caused by
drug therapy ( especially lithium), renal
damage or hereditary renal disease.
III) DIAGNOSTICS DIABETES
INCIPIDUS-
problem stems from an
excessive water intake causes
by structural lesion in thirst
center or psycholigic disorder.
IV) COMPLETE DIABETES
INCIPIDUS
it occurs when there is
disruption of hypophyseal
tract and a complete
absence of ADH.
ETIOLOGY
Deficiency of Vasopressine ( ADH Deficiency):-
Due to :-
1.Abnormalities in the hypothalamus and pituitary
gland from familial or idiopathic causes ( 7 degree
Diabetes insipidus )
2.Destruction of the glands by tumor in the
hypothalamopituitary region, trauma, infectious
processes, vascular accidents or metastatic
tumors from the breast or lung ( 2 degree DI).
3.Medications such as phenytoin ( Dilantin),
alcohol, and lithium carbonate, which may
interfere with the synthesis or release of ADH in
some individuals.
Nephrogenic Diabetes Insipidus:-
Owing to an inherited defect, the
kidney tubules cannot reabsorb water,
this condition also may 2 degree
potassium depletion or Phelonephritis
Other- Idiopathic DI,
RISK FACTOR;-
# Head injury
# Neurosurgery
# Hypothalamic tumors
# Pituitary tumor
# Brain infection or inflammation
# Drugs that inhibits vasopressin
release, ethanol , glucocorticoids ,
adrenergic agents, phenytoin ,
narcotic
antagonists lithium
PATHOPHYSIOLOGY
Due to etiological factors such as abnormalities in the
hypothalamus and pituitary gland, destruction of the
gland by tumor in the hypothalamus region and
medication
Phynytonin alcohol which may interfere with the ADH
released
ADH deficiency occurs
Impairment of water reabsorption
Kidney tubules do not reabsorbs water
Inappropriate dilute urine or excretes large
amount of dilute urine.
Then lead to Diabetes Incipidus
( Polyuria, Polydipsia)
CLINICAL MANIFESTATION
Integumentary:- Dry, cold skin, dry mucous
membranes.
Cardiovascular:- Tachycardia,
Genitourinary:- Polyuria – a few liters to 18 lt
per day, clear urine; urinary frequency,
nocturia
Gastrointestinal – weight loss, polydipsia
Neurologic- Mentation changes as electrolyte
imbalances and hypotension worsen.
Other- A triad of clinical sympotoms,
excessive thrist, polydipsia, and polyuria
Polyuria- Urine is diluted serum
osmolality is increased appearance of
urine like that of water, daily output of
5 -25 liters.
Polydipsia- usually normalizes
hydration but dehydration may occur
as a results of fluid restriction,
anesthesia or trauma. 4-40 liters of
fluid daily. Often preference for cold
drinks.
DIAGNOSTIC EVALUATION ;-
Fluid/water deprivation test:-
Objective:- to restrict water intake
and observe changes in urine
volume and concentration .
Hypertonic saline test:-
Objective:- to stimulate release of ADH
Intervention – Administer normal water load to client
followed by infusion of hypertonic saline to detected
ADH release. A serene decreased is sigh of ADH
release.
Measure urinary output hourly positive results.
Urine test –after polyuria(urine output
greater than 200ml/hr.)and specific
gravity less than 1000.
Chest x ray
Serum sodium-increased secondary to
hypovolemia and dehydrations.
Serum osmolality- 290 mOsm/ kg H20.
CT scan and MRI
Con…….
 History collection
 Physical Examination
 Water deprivation test
 Hyper-tonic Saline test
 Urine output
 Serum Na+ level
 Plasma and Serum Osmolality
MANAGEMENT
MEDICAL MANAGEMENT
Administration of ADH or its derivative:
a) Vasopressin (Pitressin)
- IM, Effective for 24 to72hrs.
Dose- 5 units IM, inj 20, 5 units/ml
Ac tion – Promotes reabsorption of water by action on renal tubular
epithelium, causes vasoconstriction.
Side effect t – Drowsiness, head ache, nail irritation, tremors,
sweating, nausea, rhinitis, icreases B.P.
Nsg Consideration
Intake pulse, B/P
Weight dailya
Check for edema in extremis
b)Lypressin (Diapid nasal
Spray)
- Absorbed through nasal
mucosa
- Duration of action 4 to 6
hrs
- may cause chronic nasal
irritation.
CONT….
c) Desmo-pressin acetate.
- Vasopressin deratives administered into the nose
through a
soft, flexible nasal.
- Duration of action 12 to 24 hrs
-For patient who have some residual hypothalamic
ADH.
d) Chloropropamide:
- Potenciate action of reducing polyuria.
e) Hydro – Chlorothiacin:
- Reduce the urine volume
- Dose 20 – 75 mg /kg/day
Carbamazepin ( Tegretol)
Dose- 200 – 400 mg/day.
Action- Unknown. Appears to decreased plysynaptic
responses and block posttetanic potentiating .
Side effect _ Dizziness, fatitgue paralysis, HTN, CHF,
worsening seiaures.
Treatment of Nephrogenic Causes:- if the diabetes 1 is
renal is origin, the previously describe are ineffecitce.
Thiazide diuretic, mild salt depletion and porstaglanldin
inhibitors ( ibuporfern, indomethacin, aspirin) are used.
SURGICAL MANAGEMENT
1.) Hypophysectomy:-
- Removal of pituitary gland may be performed
for the
treatment of primary tumor of the pituitary
gland.
COMPLICATION
 Electrolyte imbalance
 Hypotension
 Hypovolemia – extracellular fluid volume deficit ( ECFVD)
commonly called dehydration, is a decreae in intravascular and
interstitial fluids
 Shock A reduction in the circulation blood volume due to
external loss of body bluids or to loss from the blood in to the
tissues, as in shock.
 Death
HEALTH EDUCATION :-
1.Instruct the patient to administer demopresin by nasal
insufflations or by mouth.
2.Advice the patient about possible drug adverse effect for
eg- head aching
3.Tell him/her to report any weight gain.
4.Advice the patients to wear a medical identifying
bracelet and to carry his medication with him at all time
5.Give written instruction on vaspressin administration.
Have a patient demonstrate infemction techniques.
6.Weight daily to maonitoring fluid retention /fluid loss.
Consider dimination coffe and tea from diet may have an
exaggeratied diuretic effect.
7.Ecourage for follow up.
NURSING DIAGNOSIS
 Risk for fluid volume deficit r/t disease process.
 Imbalanced Nutrition Less than Body
Requirements related to insufficiency of insulin,
decreased oral input.
 Fluid Volume Deficit related to osmotic diuresis.
 Risk for Infection related to hyperglycemia.
Diabetic insipidus

Diabetic insipidus

  • 3.
    TOPIC- DIABETES INSIPIDUS PRESENTEDBY OM VERMA ASSISTANT PROFESSOR RELIANCE INSTITUTE OF NURSING
  • 5.
    INTRODUTION Diabetes incipidus isan uncommon condition that often begins in childhood or early adult life and affects more andles than females. People with diabetes incipidus pass excessive amounts of urine. In diabetes mellitus urine contains large amounts of glucose, where as urine in diabetes incipidus is highly dilute and contain no glucose.
  • 6.
    diabetes insipidus primarilyresults from deficiency of ADH. The major function of ADH are:- Promote water reabsorption by the kidney and Control the osmotic pressure of ECF. Thus, when ADH production excessively the kidney tubules do not reabsorb water, and consequently the person excretes large amount of dilute to urine.
  • 7.
    DEFINITION  It isa disorder of water metabolism caused by deficiency of ADH (Vasopresin) or by inability of the kidneys to respond to ADH. According to AND
  • 8.
    A disease inwhich the secretion of or response to the pituitary hormone vasopressin is impaired, resulting in the production of very large quantities of dilute urine, often with dehydration and insatiable thirst. According to lewis
  • 9.
    ACC TO Lippincott “Diabetes insipidus is a disorder of water metabolism caused by deficiency of vasopressin, the antidiuretic hormone (ADH) secreted by the posterior pituitary.”
  • 10.
    ACC to JoyceM. Black 6th edition.- “ A deficiency of antidiruteic homone ADH vasopressin) result in inability to conserve water.” ACC to Beare / Myeres 2nd edition Diabetes insipidus is a condition characterized by impaired renal conservation of water resulting form a deficiency of the ant diuretic hormone (ADH) arginine vasopressin.
  • 11.
    INCIDENCE:- unknown DI idiopathicin about 30% of all clients with DI; tumor can be related to 25% of DI cases, head injury accounts for 16% cranial surgery for 20% of DI cases.
  • 12.
  • 13.
    TYPES:- There are4 types:- 1.Central Diabetes Insipidus 2.Nephrogenic Diabtes Insipidus 3.Dispogenic Diabetes Insipidus 4.Complete Diabetes Insipidus
  • 14.
    CENTRAL DIABETES INSIPIDUS Adefect of the pituituar gland or hypothalamus It is usually occurs suddenly Central Di usually has a triphasic In central DI, problem stems from an interference with ADH synthesis or release. Multiple causes include brian tumor, head injury, brain surgery CNS infection.
  • 15.
    Con…. The acute phase,with abrupt onset of polyuria. An interphase, where urine volume apparently normalizes A third phases, where central DI is permanent. The 3rd phase is usually apparent within 10 to 14 days postoperatively.
  • 16.
    II) NEPHROGENIC DIABETES INCIPIDUS:- Kidneytubular defect resulting in less than use water absorption . Problem stems form an interference with renal responses to ADH despite presence of adequate ADH, caused by drug therapy ( especially lithium), renal damage or hereditary renal disease.
  • 17.
    III) DIAGNOSTICS DIABETES INCIPIDUS- problemstems from an excessive water intake causes by structural lesion in thirst center or psycholigic disorder.
  • 18.
    IV) COMPLETE DIABETES INCIPIDUS itoccurs when there is disruption of hypophyseal tract and a complete absence of ADH.
  • 19.
  • 20.
    Deficiency of Vasopressine( ADH Deficiency):- Due to :- 1.Abnormalities in the hypothalamus and pituitary gland from familial or idiopathic causes ( 7 degree Diabetes insipidus ) 2.Destruction of the glands by tumor in the hypothalamopituitary region, trauma, infectious processes, vascular accidents or metastatic tumors from the breast or lung ( 2 degree DI). 3.Medications such as phenytoin ( Dilantin), alcohol, and lithium carbonate, which may interfere with the synthesis or release of ADH in some individuals.
  • 21.
    Nephrogenic Diabetes Insipidus:- Owingto an inherited defect, the kidney tubules cannot reabsorb water, this condition also may 2 degree potassium depletion or Phelonephritis Other- Idiopathic DI,
  • 22.
    RISK FACTOR;- # Headinjury # Neurosurgery # Hypothalamic tumors # Pituitary tumor # Brain infection or inflammation # Drugs that inhibits vasopressin release, ethanol , glucocorticoids , adrenergic agents, phenytoin , narcotic antagonists lithium
  • 23.
  • 24.
    Due to etiologicalfactors such as abnormalities in the hypothalamus and pituitary gland, destruction of the gland by tumor in the hypothalamus region and medication Phynytonin alcohol which may interfere with the ADH released ADH deficiency occurs Impairment of water reabsorption
  • 25.
    Kidney tubules donot reabsorbs water Inappropriate dilute urine or excretes large amount of dilute urine. Then lead to Diabetes Incipidus ( Polyuria, Polydipsia)
  • 26.
    CLINICAL MANIFESTATION Integumentary:- Dry,cold skin, dry mucous membranes. Cardiovascular:- Tachycardia, Genitourinary:- Polyuria – a few liters to 18 lt per day, clear urine; urinary frequency, nocturia Gastrointestinal – weight loss, polydipsia Neurologic- Mentation changes as electrolyte imbalances and hypotension worsen. Other- A triad of clinical sympotoms, excessive thrist, polydipsia, and polyuria
  • 27.
    Polyuria- Urine isdiluted serum osmolality is increased appearance of urine like that of water, daily output of 5 -25 liters. Polydipsia- usually normalizes hydration but dehydration may occur as a results of fluid restriction, anesthesia or trauma. 4-40 liters of fluid daily. Often preference for cold drinks.
  • 29.
    DIAGNOSTIC EVALUATION ;- Fluid/waterdeprivation test:- Objective:- to restrict water intake and observe changes in urine volume and concentration .
  • 30.
    Hypertonic saline test:- Objective:-to stimulate release of ADH Intervention – Administer normal water load to client followed by infusion of hypertonic saline to detected ADH release. A serene decreased is sigh of ADH release. Measure urinary output hourly positive results.
  • 31.
    Urine test –afterpolyuria(urine output greater than 200ml/hr.)and specific gravity less than 1000. Chest x ray Serum sodium-increased secondary to hypovolemia and dehydrations. Serum osmolality- 290 mOsm/ kg H20. CT scan and MRI
  • 32.
    Con…….  History collection Physical Examination  Water deprivation test  Hyper-tonic Saline test  Urine output  Serum Na+ level  Plasma and Serum Osmolality
  • 33.
  • 34.
    MEDICAL MANAGEMENT Administration ofADH or its derivative: a) Vasopressin (Pitressin) - IM, Effective for 24 to72hrs. Dose- 5 units IM, inj 20, 5 units/ml Ac tion – Promotes reabsorption of water by action on renal tubular epithelium, causes vasoconstriction. Side effect t – Drowsiness, head ache, nail irritation, tremors, sweating, nausea, rhinitis, icreases B.P. Nsg Consideration Intake pulse, B/P Weight dailya Check for edema in extremis
  • 35.
    b)Lypressin (Diapid nasal Spray) -Absorbed through nasal mucosa - Duration of action 4 to 6 hrs - may cause chronic nasal irritation.
  • 36.
    CONT…. c) Desmo-pressin acetate. -Vasopressin deratives administered into the nose through a soft, flexible nasal. - Duration of action 12 to 24 hrs -For patient who have some residual hypothalamic ADH. d) Chloropropamide: - Potenciate action of reducing polyuria. e) Hydro – Chlorothiacin: - Reduce the urine volume - Dose 20 – 75 mg /kg/day
  • 37.
    Carbamazepin ( Tegretol) Dose-200 – 400 mg/day. Action- Unknown. Appears to decreased plysynaptic responses and block posttetanic potentiating . Side effect _ Dizziness, fatitgue paralysis, HTN, CHF, worsening seiaures. Treatment of Nephrogenic Causes:- if the diabetes 1 is renal is origin, the previously describe are ineffecitce. Thiazide diuretic, mild salt depletion and porstaglanldin inhibitors ( ibuporfern, indomethacin, aspirin) are used.
  • 38.
    SURGICAL MANAGEMENT 1.) Hypophysectomy:- -Removal of pituitary gland may be performed for the treatment of primary tumor of the pituitary gland.
  • 39.
    COMPLICATION  Electrolyte imbalance Hypotension  Hypovolemia – extracellular fluid volume deficit ( ECFVD) commonly called dehydration, is a decreae in intravascular and interstitial fluids  Shock A reduction in the circulation blood volume due to external loss of body bluids or to loss from the blood in to the tissues, as in shock.  Death
  • 40.
    HEALTH EDUCATION :- 1.Instructthe patient to administer demopresin by nasal insufflations or by mouth. 2.Advice the patient about possible drug adverse effect for eg- head aching 3.Tell him/her to report any weight gain. 4.Advice the patients to wear a medical identifying bracelet and to carry his medication with him at all time 5.Give written instruction on vaspressin administration. Have a patient demonstrate infemction techniques. 6.Weight daily to maonitoring fluid retention /fluid loss. Consider dimination coffe and tea from diet may have an exaggeratied diuretic effect. 7.Ecourage for follow up.
  • 41.
    NURSING DIAGNOSIS  Riskfor fluid volume deficit r/t disease process.  Imbalanced Nutrition Less than Body Requirements related to insufficiency of insulin, decreased oral input.  Fluid Volume Deficit related to osmotic diuresis.  Risk for Infection related to hyperglycemia.