Diabetes Insipidus

by : Irwan Subekti,SKep,Ners

Posterior Pituitary
Posterior pituitary hormones are actually produced in the hyopthalamus and only stored in the posterior pituitary Posterior pituitary hormones Antidiuretic hormone (ADH) Oxytocin The hormones secreted by the posterior pituitary are Antidiuretic hormone (ADH) (Also call vasopressin) and oxytocin. ADH contributes to fluid balance by Controlling renal reabsorption of free water It also has potent vasoconstrictive properties.

Posterior Pituitary
Antidiuretic hormone (ADH) (Also called vasopressin)
Disorders/diseases resulting from dysfunction

Excess: Syndrome of
Inappropriate ADH secretion (SIADH)

Deficiency:
Diabetes Insipidus

Pathophysiology of Diabetes Insipidus

Injury to hypothalamus pituitary gland
Free water excreted in urine Extracellular dehydration
Hypotension Hypovolemic shock

or

Hypernatremia Decreased cerebral perfusion

DI: Pathogenesis
Inability to concentrate urine Central
ADH deficiency from hypothalamoneurohypophyseal damage or atrophy, ADH mutations Renal inability to respond to ADH secondary to disturbance of corticomedullary osmotic gradient, defect of ADH-cAMP system, or osmotic diuresis.

Nephrogenic

Psychogenic polydipsia

physiologic ADH inhibition

Posterior Pituitary hyposecretion Diabetes Insipidus Symptoms Urine specific gravity Thrist & polyuria 5 low (1.001-1.005) 20L/day SG < 1005 Urine osmolality Urine osmol < 100 mmol/L decreased (50-200 Se osmol > 295 mmol/kg mOsm.kg) Nocturia Urine less Weakness => weight loss, hypotension, concentrated than tachycardia, constipation, plasma shock. Plasma osmolality Sleep deprivation-due to elevated (>295 interrupted by need to mOsm/kg) drink fluids & urinate

Diabetes Insipidus : Etilogy

Familial or idiopathic Head injury Neuorsurgery Damage to the hypothalamic areas that produce ADH
Cause Lesion of hypothalmus interferes with ADH synthesis/transport/re lease brain tumour pituitary/cranial surgery head trauma CNS infection vascular disease.

Diabetes Insipidus Etilogy

Drug Related Ethanol & Phenytoin (Classification: Antiarrhythmic,
Anticonvulsant):

Inhibit ADH secretion Lithium (Classification: Antimanic) & Demeclocycline(Classification:anti-infective-Tetracycline): Inhibit ADH action in kidney

4 Types of Diabetes Insipidus

1) Neurogenic -also known as
central hypothalamic pituitary neurohypophyseal Caused by a deficiency of the Antidiuretic hormone, vasopressin

3) Gestagenic-also known as
Gestestional Caused by a deficiency of the antidiuretic hormone, vasopressin, that occurs only during pregnancy

2) Nephrogenic-also known
as Vasopressin - resistant Caused by insensitivity of the kidneys to the effect of the antidiuretic hormone, vasopressin

4) Dipsogenic, a form of primary polydipsis

Caused by
Abnormal thirst and the Excessive intake of water or other liquids

 Diagnosis D.I.
History and examination Water deprivation test
Vasopressin challenge test 24 hours urine

Diagnosis & Rx
Diabetes Insipidus
Treatment Intravenous fluids Hypertonic saline IVExtracellular solution to pull fluid from outside the cell to inside the cell Vasopressin SC/IM/IV, nasal prep Long term DDAVP (Desmopression) nasal prep. (analog ADH)

High sodium in
blood MRI of pituitary, hypothalmus and skull to see damaged areas

Diagnosis - Fluid Deprivation Test

(To identify cause of polyuria) Baseline VS, then check hourly-allows RN to
detect changes, esp postural hypotensin & tachycardia

Deprive pt of fluid-Observe for compliance with

fluid restriction

Hourly- urinary output, specific gravity, & osmololity Urine test results determine whether testing can proceed.
Testing can proceed if urinary osmolality stabilized for 3 samples and 3% wt loss is noted

Dx- Vasopressin challenge

Order for 5 Units of aqueous vasopressin sc Continue hourly urinary measurements Vasopressin triggers and ongoing assessment detects Changes in urinary specific gravity and osmolality Specific gravity & osmolality decrease with primary and secondary diabetes insipidus No response is seen with nephrogenic diabetes insipidue

Diabetes insipidus treatment

Vasopressin (Pitressin) : is ADH Classification: Hormone (antidiuretic) Uses: Treatment of central diabetes insipidus sue to deficient antidiuretic hormone. Route/Dose: IM, sc, nasal spray Nsg Implications: replace fluid: saline and glucose monitor I & O check specific gravity observe electrolytes Monitor adverse reactions-abdominal cramps, angina, MI

Diabetes insipidus treatment

Desmopressin (DDAVP) Classification: Hormone (andiuretic) Indication: Management of primary nocturnal eneuresis unresponsive to other treatment modalities po, sc, IV, Intranasal Action: An anologue of naturally occuring vasopressin (antiuretic hormone). Primary action is enhanced reabsorption of water in the kidneys Therapeutic Effects: Prevention of nocturnal enuresis. Maintenace of appropriate body water content in diabetes insipidus. Nsg Implication: Monitor urine & plasma osmolality & urine volume frequently. Assess pt for symptoms of dehydration (excessive thirst, dry skin & mucous membranes, tachycardia, poor skin turgor) Weigh pt daily & assess for edema

Observe for Water Intoxication with all agents

ADH excess = water intoxication water is reabsorbed, so assess for
increased blood volume, fluid retention concentrated urine, low urine output dilutional hyponatremia (same Na, more H20)
muscle cramps and weakness anorexia, n/v, irritable, confused, disorient, seizure

Diabetes Insipidus

Fluid Volume Deficit R/T inability to conserve water

Thirst, dry mucous membranes Decreased skin turgor Hypotension, tachycardia Hemoconcentration, plasma hyperosmolality, hypernatremia Increased urine output Dilute urine-monitor specific gravity

Nursing Issues
Fluid and electrolyte imbalance:

R/T >diuresis, monitor urine and plasma osmolarity monitor specific gravity (usually will be low with >diuresis) monitor urine volume (usually will be high 5-10L in 24 hr) Therapy successful when urine output and specific gravity begin to return to normal monitor s/s dehydration weight pt daily & assess for edema Fluid volume deficit Nurse will monitor for hypotension, constipation, shock

Sleeping problems:
thirst

R/T nocturia & increased

Education:

Assessment and Diagnosis

Clinical manifestations
Urine output may be >300 ml/hr

Laboratory studies
Serum sodium >145 mEq/L Serum osmolality >295 mOsm/kg H2O Urine osmolality <300 mOsm/kg H2O

Medical Management
Immediate management
Restoration of circulation fluid volume Pharmacologic ADH replacement
Medications to manage central DI
Vasopressin (Pitressin) DDAVP (Desmopressin)
Thiazide diuretics

Medications to manage nephrogenic DI

Diagnose and treat cause of DI

Nursing Management
Nursing priorities in the care of the patient with DI are directed toward:
Administering fluids and medications. Evaluating response to therapy. Maintaining surveillance for complications. Providing patient and family education.

Nursing Diagnosis Deficient Fluid Volume

Common Related Factors Defining Characteristics

Compromised endocrine regulatory mechanism Neurohypophyseal dysfunction Hypopituitarism Hypophysectomy Nephrogenic DI

Polyuria Output exceeds intake Polydipsia (increased thirst) Sudden weight loss Urine specific gravity less than 1.005 Urine osmolality less than 300 mOsm/L Hypernatremia (sodium greater than 145 mEq/L) Altered mental status Requests for cold or ice water NOC Outcomes Fluid Balance; Electrolyte and Acid-Base Balance NIC Interventions Fluid Monitoring; Fluid Management; Electrolyte Management

Common Expected Outcome Patient experiences normal fluid volume as evidenced by absence of thirst, normal serum sodium level, and stable weight.

Actions/Interventions

Ongoing assessment

Rationale With DI, the patient voids large urine volumes independent of the fluid intake. Urine output ranges from 2 to 3 L/day with renal DI to greater than 10 L/day with central DI.

Monitor intake and output. Report urine volume greater than 200 mL for each of 2 consecutive hours or 500 mL in a 2-hour period. Monitor for increased thirst (polydipsia).

If the patient is conscious and the thirst center is intact, thirst can be a reliable indicator of fluid balance. Polyuria and polydipsia strongly suggest DI. Also, the DI patient prefers ice water.

Weigh daily. Monitor urine specific gravity. Monitor serum and urine osmolality. Monitor urine and serum sodium levels. Monitor serum potassium. Monitor for signs of hypovolemic shock (e.g., tachycardia, tachypnea, hypotension).

Weight loss occurs with excessive fluid loss. This may be 1.005 or less. Urine osmolality will be decreased and serum osmolality will increase. The patient with DI has decreased urine sodium levels and hypernatremia. Hypokalemia may result from the increase in urinary output of potassium. Frequent assessment can detect changes early for rapid intervention. Polyuria causes decreased circulatory blood volume.

Therapeutic Interventions
Actions/Interventions Allow the patient to drink water at will. Rationale Patients with intact thirst mechanisms may maintain fluid balance by drinking huge quantities of water to compensate for the amount they urinate. Patients prefer cold or ice water. Provide easily accessible fluid source, keeping adequate fluids at bedside. Administer intravenous (IV) fluids: 5% dextrose in water or 0.45% sodium chloride This encourages fluid intake. IV fluids are indicated if the patient cannot take in sufficient fluids orally. Hypotonic IV fluids provide free water and help lower serum sodium levels gradually. Isotonic fluids may be indicated for the patient who has sustained significant fluid loss and is hemodynamically unstable. Once circulatory volume has been restored, hypotonic IV fluids can be given.

0.9% sodium chloride

Administer medication as prescribed.

Aqueous vasopressin is usually used for DI of short duration (e.g., postoperative neurosurgery or head trauma). Pitressin tannate (vasopressin) in oil (the longer-acting vasopressin) is used for longer-term DI. Patients with milder forms of DI may use chlorpropamide (Diabinese), clofibrate (Atromid), or carbamazepine (Tegretol) to stimulate release of ADH from the posterior pituitary and enhance its action on the renal tubules. Hydrochlorothiazide (HydroDIURIL) may also be used for nephrogenic DI.

If vasopressin is given, monitor for water intoxication or rebound hyponatremia.

Overmedication can result in volume excess.