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DIABETIC INSPIDUS

INTRODUCTION

The word diabetes is derived from the Greek verb diabainein , which means to stand with legs apart (as inurination) or to go through. Insipidus comes from a Latin word meaning without taste. Body has a complex systemfor balancing the volume and composition of body fluids. Kidneys remove extra body fluids from the bloodstream.This fluid waste is stored in the bladder as urine.If the fluid regulation system is working properly, the kidneysmake less urine to conserve fluid when the body is losing water. The hypothalamus makes antidiuretichormone (ADH), which directs the kidneys to make less urine.

In order to keep the volume and composition of body fluids balanced, the rate of fluid intake is governed by thirst,and the rate of excretion is governed by the production of antidiuretic hormone (ADH), also called vasopressin.This hormone is made in the hypothalamus, a small gland located in the base of the brain. ADH is stored in thenearby pituitary gland and released from it into the bloodstream when necessary. When ADH reaches the kidneys,it directs the kidneys to concentrate the urine by returning excess water to the bloodstream and therefore make lessurine.

DEFINITION

Diabetes insipidus (DI) is a metabolic disorder that occurs when the body can't secrete or utilize antidiuretichormone (ADH). Sometimes diabetes insipidus is referred to as "water" diabetes.

Diabetes Insipidus (DI) is a disorder in which there is an abnormal increase in urine output, fluid intake and oftenthirst. It causes symptoms such as urinary frequency, nocturia (frequent awakening at night to urinate) or enuresis(involuntary urination during sleep or "bedwetting"). Urine output is increased because it is not concentratednormally. Consequently, instead of being a yellow color, the urine is pale, colorless or watery in appearance andthe measured concentration (osmolality or specific gravity) is low.

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EPIDEMILOGY

Tumors, infiltrative lesions, malformations, and neurosurgical procedures are the most common causes of centraldiabetes insipidus. Of the genetic etiologies, the overall incidence in the general population is estimated to be 3cases per 100,000 population (0.003%). The male-to-female ratio is 60:40. X-linked nephrogenic diabetes insipidusis very rare, although it exceeds the recessive variety by a ratio of 9:1. The mutation for males is 4 cases per million population.

MORTALITY/ MORBIDITY

D ehydration results from an inability to reabsorb free water at a site distal to electrolyte reabsorption. Any patientunable to continuously replace water loss is vulnerable to dehydration, especially in warm weather when insensiblewater loss through perspiration and respiration substantially increases risk. Electrolyte abnormalities are caused bythe loss of urinary free water, which produces hyperosmolar dehydration, leading to hypernatremia,hyperchloremia, and prerenal azotemia. Diminished blood volume increases blood viscosity and the risk of sludging and thrombosis.

Failure to thrive occurs because of the patient's constant thirst conferring a sense of fullness that offsets the senseof hunger. The affected individual eats less than necessary for normal growth. Seizures are a consequence of theelectrolyte abnormalities introduced in the CNS by severe hypernatremia and hyperosmolar dehydration. Mentalretardation results from the damage to the CNS caused by severe hyperosmolarity, seizures, and potential hypoxia,all of which are thought to account for the frequent occurrence of mental retardation. Death can occur from ahypovolemic shock or a hypernatremic seizure.

SEX

Central diabetes insipidus secondary to hypothalamic-pituitary lesions occurs at random and should, therefore, beevenly distributed between the sexes. Autosomal dominant and autosomal recessive central diabetes insipidusoccur equally in both sexes. Nephrogenic diabetes insipidus caused by an X-linked mutation affects only males.Autosomal dominant and autosomal recessive forms of nephrogenic diabetes insipidus equally affect both sexes.

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AGE

Diabetes insipidus occurs in people of a wide age range. Children who present with autosomal recessive centraldiabetes insipidus are generally younger than 1 year. Children who present with autosomal dominant centraldiabetes insipidus are often older than 1 year. Nephrogenic diabetes insipidus forms (including X-linked,autosomal dominant, and autosomal recessive forms) develop in early infancy, often in neonates younger than 1week.

TYPE S AND CAU SE S OF DIABETE S IN SIPIDU S

1) Neurogenic Diabetes Insipidus2) Nephrogenic Diabetes Insipidus3) Dipsogenic Diabetes Insipidus4) Gestational Diabetes Insipidus

Neurogenic or Central Diabetes Insipidus This type of diabetes insipidus is due to the inability of hypothalamus to produce vasopressin or pituitary glandreleasing vasopressin. Either way, it affects the kidneys ability to reabsorb necessary amounts of water back into

blood resulting in excessive water loss from the body. The causes of neurogenic diabetes insipidus are:

y It is usually associated with some form of damage to pitutary gland.y Head injuries, surgeries, brain tumors and in rare cases diseases such as sarcoidosis, are responsible for the

occurrence of diabetes insipidus.y This form of diabetes insipidus, in some cases, is hereditary.

Nephrogenic Diabetes Insipidus This type of diabetes insipidus results from the kidneys inability to respond to vasopressin. The kidney goes on

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trying to purge the body of as much water as person drink because there is no regulatory means to stop it. Thecauses of nephrogenic diabetes insipidus are:

y Most of the cases of nephrogenic diabetes insipidus are due to some previous diseases that cause damage or changes in kidney function.

y In other cases, it is due to medications that include lithium. Lithium is known to interfere with the kidneysfunction when vasopressin is released to retain water to maintain liquid levels in the body.

y In rare cases, nephrogenic diabetes insipidus is known to be caused by genetic defects.

Gestational Diabetes Insipidus This type of diabetes insipidus occurs during third trimester of pregnancy. During this time, an enzyme calledvasopressinase is released which causes a decrease in vasopressin resulting in excess liquid discharge.

y The reason for this type of diabetes is usually pregnancy related diseases such as acute fatty liver, or preeclampsia.

Dipsogenic Diabetes Insipidus Dipsogenic diabetes insipidus occurs due to disruption in thirst mechanism and resulting in abnormal or excessivethirst. Large amount of water intake also suppresses the production of vasopressin by hypothalamus.

Causes of DIAmong some of the major causes are the following:

(1) Neurogenic . acquired: brain tumors; head trauma; granulomatous diseases;Autoimmune; idiopathicinherited: autosomal dominant or recessive mutation in the vasopressin

gene; X-linked recessive mutation in an unknown gene(2) Nephrogenic : acquired: hypokalemia; hypercalcemia; lithium

inherited: X-linked recessive mutation in vasopressin receptor;autosomal recessive or dominant mutation in water channel

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(3) P olydipsic acquired: idiopathic (most); chronic meningitis; granulomatous diseases;multiple sclerosis or other diffuse pathology of brain;

psychiatric illness

(4) Gestagenic : acquired: pregnancy

PATHOPHY SIOLOGY OF DIABETE S IN SIPIDU S

Head Injury Tumour Pressure Surgical Ablation

Destruction of paraventricular or supraoptic nuclei

Decreased ADH secretion

Kidneys tubules fails to reabsorb Plasma Hyperosmolarity

Increased urination of dilute urine Stimulate thirst center NocturiaDecreased specific gravityDecreased B.P.Water dehydration Polydipsia

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CLINICAL MANIFE STATION S OF DIABETE S IN SIPIDU S

1)Universal Symptoms of Diabetes Insipidus

Increased thirstIncreased drinkingIncreased urination

2 )V ariable Symptoms of Diabetes Insipidus

Bed-wettingGetting up at night to urinateUrine is dilutedDisrupt sleepChildren with diabetes insipidus may be irritable or listless and may have fever, vomiting , or diarrhea

An irritable infant with a dripping wet diaper, along with detectable signs of dehydration (eg, dry mucousmembranes, diminished skin turgor, decreased tearing, tachycardia).In severely dehydrated patients, the pulse may be thready and rapid. Hypotension may be present because of

hypovolemic shock.Mobile fecaliths may be palpable in the abdomen.

LABORATORY FINDING S 1)Urine Specific Gravity - The urine specific gravity of the first morning urine is helpful in assessing renal abilityto concentrate urine. Dilute urine with a relatively high serum sodium and osmolarity effectively establishes thediagnosis.

The serum sodium may be as high as 170 mEq/L, while the serum osmolarity is greater than 300 mOsm/kg.Patients with prerenal azotemia present with severe dehydration.

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2 ) W ater deprivation test- which can be used both to confirm the diagnosis and to distinguish between centraldiabetes insipidus (CDI) and nephrogenic diabetes insipidus (NDI) by response to a vasopressin analogue.

To perform the test, follow these steps:

* Obtain a baseline plasma osmolality level and weigh the patient. Then begin withholding his fluids.

* Every hour, measure his urine output, osmolality, and specific gravity and monitor his overall condition, such asmental status and vital signs, for signs and symptoms of dehydration.

* Weigh your patient if signs and symptoms of dehydration worsen. If he loses 2 kg (4.4 pounds) or more or develops hypotension, tachycardia, or lethargy, discontinue the test and notify his physician.

* When two consecutive urine osmolality levels vary by less than 30 mOsm/kg H sub 2 O, measure your patient's plasma osmolality level. Then administer five units of aqueous vasopressin (exogenous ADH). One hour later,again measure his urine osmolality and compare the results with the baseline value.

If the patient has neurogenic DI, his urine osmolality will increase after vasopressin administration; if he has

nephrogenic DI, he won't respond to vasopressin.3) Serum potassium and calcium concentrations- are important to exclude the possibility of polyuria secondaryto hypokalemia or hypercalcemia, both of which interfere with renal concentrating mechanisms.

IMAGING FINDING

Cranial MRI can be used to exclude pituitary cysts, hypoplasia, and destruction secondary to mass lesions. Often,the bright spot that is thought to represent vasopressin-secreting neurons in the posterior pituitary is absent incentral diabetes insipidus.

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MEDICAL TREATMENTI ) D rugs

F or central diabetes insipidus (CDI), the treatment of choice is desmopressin (a synthetic vasopressin analogue). R oute- It is available in parenteral, intranasal, and oral dosage forms. The doses widely vary depending on the preparation used, so take care to correctly calculate the dose.

Other umedications include chlorpropamide and thiazide diuretics . Nephrogenic diabetes insipidus (NDI) cannot be effectively treated with desmopressin because the receptor sitesare defective and the kidney is prevented from responding. Thiazide diuretics, amiloride, and indomethacin or aspirin are useful when coupled with a low-solute diet.

1)Pituitary hormones

Desmopressin Acetate (DDA VP )

A synthetic analogue (1-[3-mercaptopropionic acid]-8-D-arginine vasopressin monoacetate trihydrate) of pituitaryADH. Increases cellular permeability of collecting ducts, resulting in reabsorption of water by kidneys.

Dosage must be individualized. Drug is supplied as parenteral (4 mcg/mL), nasal (100 mcg/mL rhinal tube), andPO (0.1- and 0.2-mg tab) preparations.

VasopressinHas vasopressor and ADH activity. Increases water reabsorption at distal renal tubular epithelium (ADH effect)

and promotes smooth muscle contraction throughout vascular bed of renal tubular epithelium (vasopressor effects).However vasoconstriction also increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, andintrahepatic vessels.

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Use only the aqueous preparation, which has a short half-life. Vasopressin tannate in oil, which has a longer action,should not be used.

2 ) Diuretic agents

Thiazide diuretics impair sodium chloride reabsorption in the distal tubule, reducing the loss of free water to thecollecting system and increasing urine concentration. Reduction in urine volume derives from a concomitant actionon the proximal tubule, which causes enhanced reabsorption of isoosmotic sodium chloride from the glomerular filtrate.

Hydrochlorothiazide

Thiazide diuretic,Combination of decreased free water delivery to distal tubule and increased sodium chloridereabsorption in proximal tubule underlies the efficacy in DI therapy.

Amiloride (Midamor )

Potassium-sparing diuretic. Has a potassium-sparing effect, so risk of hypokalemia is decreased in combination

with hydrochlorothiazide. In addition, the 2 agents are synergistic with respect to antidiuresis.

3)Nonsteroidal anti-inflammatory agents

These agents act synergistically with thiazides to diminish urine volume, although precise mechanism is unknown.

Indomethacin (Indocin )

Nonsteroidal prostaglandin inhibitor with antipyretic properties.

4 )Sulfonylurea compounds

These compounds are an alternative therapy to desmopressin and can be used in combination with thiazidediuretics. Sulfonylurea compounds have the reported property of causing a syndrome identical to inappropriateADH secretion.

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Chlorpropamide (Diabinese )

Promotes renal response to ADH. In CDI, ADH secretion is absent, although ADH receptor sites remain present inthe kidney. Thus, interaction of the receptors with sulfonylurea compounds can produce a physiologic antidiuresis.

Dosage must be individualized. Available only in tab form.

II )Further Inpatient Care

Subsequent admissions are determined by the need for intravenous rehydration, especially during intercurrent GI

illnesses.III )Further Outpatient Care

Regular follow-up visits with an endocrinologist (for central diabetes insipidus [CDI]) or a nephrologist (for nephrogenic diabetes insipidus [NDI]) are necessary for dosage adjustment.

When indomethacin is used in long-term therapy, carefully observe renal function for any signs of toxicity.

IV) Inpatient & Outpatient Medications In addition to the medications already listed, aqueous vasopressin (Pitressin) and desmopressin (DDAVP)

preparations are available for intravenous use in emergency circumstances.

SURGICAL CARE

y Postoperatively, administer the usual dose of desmopressin to patients with diabetes insipidus and administer (hypotonic) IV fluids to match urine output.

y After pituitary surgery, patients should undergo continuous monitoring of fluid intake, urine output, and specificgravities, along with daily measurements of serum electrolytes. [14] In patients who develop diabetes insipidus,administer parenteral desmopressin every 12-24 hours, along with adequate fluid to match losses. F ollow thespecific gravity of the urine and administer the next dose of desmopressin when the specific gravity has fallen to

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less than 1.008-1.005 with an increase in urine output. When the patient can tolerate oral intake, thirst can becomean adequate guide.

NUR SING MANAGEMENT

Nursing Diagnosis-

1) F luid Volume Deficit related to excessive urination secondary to diabetes insipidus.

2) Alteration in patterns of urinary elimination related to polyuria

3) Potential for fluid imbalance related to ADH deficiency

4) Parents Anxiety and Loss of Control, Ineffective Coping related to hospital environment, procedures,illness , pain,past experiences, new diagnosis

5) Potential for knowledge deficit related to disease,administration of medications, sign and symptoms of dehydration and prevention of dehydration

6) Inability to manage care at home related to knowledge deficit of parents

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NURSING CARE PLAN

ASSESSMENT NURSINGDIAGNOSIS PLANNING

NURSINGINTERVENTION RATIONALE

EVALUATION /OUTCOME

Subjective Cues:>Patient states, Iamvery thirsty.

Objective Cues:

> excessive thirst

> dry oral mucousmembranes

> increased heartrate (HR= 140)

> decreased BP(BP= 80/57)

> increased bodytemperature(T= 38)

> severe polyuria(>7L/day)

> urine specificgravity= 1.001

> decreased skinturgor

F luid VolumeDeficitrelated toexcessiveurinationsecondary todiabetesinsipidus

(A state in whichan individual isat risk of experiencing

vascular,cellular,or intracellular dehydration dueto active or regulatory lossesof body water inexcess of needsor replacementcapability.)

Within 8 hours, patient willmaintainadequate fluidvolumeas evidenced by:

> vital signswithin Nrange for age

> urine output of 50-80ml/hr

> urine specificgravity between1.004 and 1.030

> moist mucousmembranes

> good skinturgor

> patientverbalizingthat thirst is nolonger excessive.

Independent:Monitored vital signs;noted changes in bodytemperature.

Observed for posturalBP changes;encouraged gradual

position changes.

Palpated peripheral

pulses, assessedcapillary refill, mucousmembranes, and skinturgor; observed for changes in mentalstatus.

Monitored I/O qh;obtained daily weightsand compared with 24-hr I/O.

Encouraged increase in

> Increased HR along withdecreased BP and elevatedtemperature,is present inconditions with fluid volumedeficit.Increased bodytemperature also increases fluidloss by increasing metabolism.

> Patients with may experiencevarying degrees of posturalhypotension depending ondegree of fluid volume deficit.

> Excessive fluid loss through

regulatory mechanisms failuremay result in severedehydration, cuirculatorycollapse,and shock. Decreasedcerebral perfusion may result inchanges in mentation.

> F luid replacement needs are based on correction of currentdeficits and ongoing losses.Decreased urinary output mayrequire aggressive fluidreplacement. A sudden weightincrease may indicate third-spacing.

> Relieves thirst and aids in

Goal met. Patientmaintainedadequatefluid volume asevidenced by N

vitalsigns, adequateurinary output withnormal specificgravity, moistmucousmembranes, goodskinturgor, and

patientsverbalization thatthirst is notexcessive.

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> weakness> irritability

fluid intake andconsumption of foodshigh in fluid content.

Turned patient q2hand provided supportfor body prominences.

Provided skin and

mouth care, massagedskin, and appliedemollients asnecessary.

Monitored IV flowrates regularly;observed for markedelevations in BP,restlessness, moistcough, dyspnea,

basilar crackles, andfrothy sputum.

Provided healthteachings on the needfor lifelong hormonalreplacement.

body fluid replacement.

> Patients with fluid volumedeficit are more at risk for skin

breakdown.

> Regular skin and mouth care

relieves dryness and discomfort.Light massage promotescirculation. Use of emolientsand mild soaps promotes goodhygiene and comfort withoutexcessive drying of the skin.

> Patients on IV fluid therapymay be at risk for cardiopulmonary compromise.

> Lifelong fluid replacement tocontrol polyuria and polydipsiais necessary for patients withDiabetes Insipidus.

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Nursing Interventions for a patient with DI are related to fluid deficit caused by DI or treatment-induced water retention-

* Manage your patient's fluid replacement by providing oral liquids or administering intravenous fluids, as prescribed. Assess his intake and output every hour, and look for signs of dehydration. Measure urine specificgravity every 2 hours.

* Assess his vital signs every 2 hours. Tachycardia, hypotension, and orthostatic hypotension signal hypovolemia;hypertension may indicate water intoxication.

* Monitor for hypernatremia and hyperosmolality by assessing serum electrolyte levels and plasma osmolality, as prescribed.

* Monitor for changes in behavior, mood, anxiety level, and level of consciousness, which may indicate alteredcerebral function. Provide uninterrupted rest periods.

* Administer exogenous ADH, as prescribed, and monitor for decreased urine output, hyponatremia, increased blood pressure, tremors, or headache. If these signs and symptoms of systemic water retention develop, notify the physician--she may need to reduce your patient's dosage.

* Weigh your patient daily. A weight gain or loss of 1.4 kg (3 pounds) or more over 2 to 3 days indicates fluidaccumulation or loss.

* Teach your patient about DI, his medication, and the need for follow-up care. Review the signs and symptoms of water intoxication, which may signal the return of ADH function or the need for a reduction in his medicationdosage.

PRE VENTION

Reduce or eliminate activities resulting in increased insensible fluid losses.

Avoid creating barriers to drinking water.

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DIET

Provide affected infants a breast milk diet to decrease solute load. Protein should comprise 6% of caloric intake,and sodium should be reduced to 0.7 mEq/kg/d.

Provide young children 8% of their caloric intake as protein to enable normal growth. Sodium intake must bemaintained at 0.7 mEq/kg/d.

COMPLICATION S

Complications include the following:

y Growth failurey Nocturia and enuresisy Hypernatremic dehydrationy Seizuresy

Mental retardation

PROGNO SIS

Long-term survival in cases of central diabetes insipidus depends on the precipitating cause. In primary centraldiabetes insipidus, the prognosis is excellent with early recognition and appropriate DDAVP therapy.

The earlier onset of nephrogenic diabetes insipidus and the reduced ability to treat this variety of the diseaserenders the child more prone to attention deficits, hyperactivity, learning disorders, and psychomotor delay.

As long as water remains available at all times to replace the massive losses, long-term survival is not in question.

PATIENT EDUCATION

Parents must replace water in infants and young children who cannot express thirst or access fluids withoutassistance.

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GI illnesses that cause decreased intake, increased stool losses, or both must receive early and serious attention to prevent life-threatening electrolyte and fluid balance abnormalities.

Symptoms of diabetes insipidus include uncontrollable thirst, a yearning for ice water, increased urine volume of diluted urine reaching 2.5 liters a day in mild diabetes insipidus to 15 liters a day in severe conditions and if a lot of fluids were ingested. The average urine volume output for a healthy adult person is 1.5 to 2.5 liters a day.

Another symptom of diabetes insipidus is nocturia, or the need to arise from bed in the evening just to urinate,and bed wetting. Children who have diabetes insipidus have the following signs and symptoms like crying thatcannot be consoled, abnormally wet diapers, fever, nausea and diarrhea, and dry skin with the extremeties that arecold.

Activities resulting in increased insensible water loss should be moderated in the presence of massive urinarywater loss to prevent dehydration.

Heat exposure should be minimized, especially when participating in sports.