Disorders of the Posterior Pituitary Diabetes Insipidus

Syndrome of Inappropriate Antidiuretic Hormone (SAIDH)

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

SIADH
Posterior Pituitary Hypersecretion

SIADH - Syndrome of Inappropriate

Hormone Secretion
ADH (anti-diuretic hormone) is a hormone made in the pituitary gland. ADH does what the name says it stops urination - diuresis

Slowing or stopping urine production leads to fluid retention.

That in turn causes a dilution of body sodium

SIADH - Syndrome of Inappropriate

Hormone Secretion
Depending on the rapidity & the extent of the sodium drop, a battery of S/S appear.

Lethargy, weakness, & foggy thinking are common. Personality changes can happen.
Low sodium levels often make pt nauseated If the situation is not corrected, seizures, coma, & even death can follow.

Syndrome of Inappropriate Antidiuretic Hormone Secretion - SIADH

Results from many

SIADH occurs
when there is too much vasopression (ADH) with inappropriate water retention and decreased blood Na levels

different conditions and drugs

May be produced by
certain tumors such as lung cancer or may result from chronic lung diseases. Medicines associated with SIADH include common meds as antidepressants, antianxiety agents, antipsychotic agents, seizure meds, and desmopressin (DDAVP)

Syndrome of Inappropriate Antidiuretic Hormone Secretion - SIADH Results from

Inability to produce & secrete dilute urine Water retention Increased extra cellular fluid volume Hyponatremia Diseases that affect the hypothalamus

Dx of SIADH
The following criteria should be fulfilled before a diagnosis of SIADH can be made: persistent excretion of concentrated urine with no reason for ADH release normal renal and adrenal function

no edema or hypovolaemia should be present

the urine osmolarity should be greater than the serum osmolarity

Physical Assessment of SIADH

Initially, S/S are R/T retention of water. Most common complaints GI disturbances-loss of appetite, N,V Nurse Weighs pt & documents any recent weight gain Checks pt extremities for presence of edema Pt with SIADH have free water, not salt, that is retained & edema is not usually present due to intracellular free water

Assessment-Clinical Manifestations of SIADH

Water retention, hyponatremia, & resulting fluid shifts have an effect on CNS function, especially when serum sodium level drops. Normal serum Na 135-145. S/S occur when serum Na level drops below 125, and especially below 115 Clinical S/S Lethargy, headaches, hostility, uncooperativeness, disorientation Early sign -Change in LOC Neurological S/S can progress from lethargy and headaches to decreased responsiveness, seizures, and coma. Nurse assess deep tendon reflexes, which are often < or sluggish V/S changes-tachycardia associated with increased fluid volume & hypothermia associated with CNS disturbance

Normal Lab Values

serum osmolality (285-295 mOsm/kg)

sodium (Na 135-145 mEq/L)

chloride (95-105 mEq/L)

Urine osmolality -24 hr specimen 500-800 mOsm/kg H20

-Random specimen: 50-1200 mOsm/kg/H20

Osmolality is measures in milliosmoles per kilogram of water (mOsm/kg). The major determinants of plasma osmolality are Na, glucose, & urea

Urine specific gravity 1.003-1.030 1.002-1.035 High=dehydration Low=diabetes insipidus

concerntrated urine > than 50-100 mOsm/kg with normal vascular volume and normal renal function

Lab Assessment in SIADH

Extracellular fluid volume expansion affects electrolyte levels in the serum and the urine

Elevated urine sodium levels and specific gravity reflect an

increased concentration of the urine
Serum sodium levels are decreased, often as low as 110 mEq/L (normal serum sodium 135-145 mEq/L) due to extracellular volume expansion and increased Na excretion

Fluid retention causes changes in both plasma and urine osmolality

Plasma osmolality is decreased, and the urine is hyperosmolar in relation to the plasma

Osmolality
Urine osmolality -24 hr specimen 500-800 mOsm/kg H20
Random specimen: 50-1200 mOsm/kg/H20

Osmolality is measures in milliosmoles per kilogram of water (mOsm/kg). The major determinants of plasma osmolality are Na, glucose, & urea. The Kidneys are mainly responsible for maintaining the concentration of body fluids within this range of osmolality. When the plasma osmolality becomes abnormal, changes in the level of antidiuretic hormones (ADH) cause the kidneys to conserve or increase the excretion of water to return the osmolality to normal

Posterior Pituitary hypersecretion - SIADH

Symptoms - fluid retention low serum osmolality (normal285-295 mOsm/kg)

Causes Diseases effect the hypothalmus

dilutional low sodium (normal Na 135-145 mEq/L)

low chloride (normal95-105 mEq/L)

pneumonia TB positive pressure ventilation Trauma

AIDs delirium tremens Ectopic ADH secreting tumor

concerntrated urine
(> than 50-100 mOsm/kg) with normal vascular volume and normal renal function

muscle cramps & weakness

cerebral edema, lethargy, anorexia, headache, seizures, coma.

SIADH - Diagnostic Tests

Blood & Urine tests Must have low serum sodium

These tests indicate

excess of body water relative to the amount of body sodium. In other words, ADH is inappropriately holding onto too much water. Important to eliminate other causes of a low sodium level, such as hypothyroidism or adrenal insufficiency, before settling on a dx of SIADH Rx- removing the offending drug or tumor, & treat the

low plasma osmolality level Inappropriated concentrated urine (increased urine osmolality level)

Posterior Pituitary: SIADH,DI

*Affect kidneys ability to concentrate urine*

Measured by urine specific gravity Measures number and size of particles

Normal: 1.003 - 1.030 High = dehydration Low = Diabetic Insipidus 1.001-1.005 Concentrated urine: SIADH Dilute urine: DI

Posterior pituitary: SIADH

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

SIADH and Hyponatremia

Hyponatremia- a lower than normal concentration of sodium in
the blood

Caused by inadequate excretion of water of by excessive water

in the circulating bloodstream In a severe case the pt may experience water intoxication, with confusion and lethargy, leading to muscle excitability, convulsions, and coma.

Treatment: Fluid and electrolyte balance may be restored by IV

infusion of a balanced solution or a fluid restricted diet.

SIADH Diagnosis & Treatment

Diagnosis measure urine volume and osmolality Treatment If Na<125 Restrict fluids 800 - 1000 ml/day. Daily weigh Monitor 3% - 5% Saline solution IV

Na < 134mmol/L se osmol >280mmol/kg SG>1005 low BUN, creatinine, Hb, Hct.

Lasix if Na<105 (cardiac symptoms)

SIADH
Diagnostic Study
Hyponatremia Decreased plasma osmolality Urine sodium and urine osmolality elevated Elevated ADH levels++++++ Normal renal, adrenal, & thyroid functions

Nursing Assessment
Headache,Personality change, Confusion,Irrritability, Dysarthria(difficult, poorly articulated speech), Lethargy,Impaired memory Restless, weakness, fatigue, gait disturbances Weight gain+++++

SIADH Treatment
Water Restriction is the cornerstone of treatment
Decreased water intake allows serum sodium level to rise normally.
The maximum amount of water that pt with SIADH are allowed to drink is just slightly more that the amount of urine they produce Pt must have regular serum sodium measurements to ensure that the water restriction has been effective

Dehydration- The most concerning potential side effect from

treatment is dehydration.

SIADH treatment
Restrict fluid intake (800-1000 cc/day) Daily weight Strict I & O Monitor urine specific gravity 0.9 NS infusion(to raise the serum Na level if water
intoxication is severe)

Monitor for hyponatremia Lasix may be admin to block circulatory overload Drugs-demeclocyclin HCL & lithium-may be admin to
block renal response to ADH, intereferes with action of ADH

Drugs - Phenytoin - inhibits ADH release Surgery & Chemo -to remove or destroy neoplasms that may
be the underlying cause of this syndrome

SIADH treatment
Demeclocycline (Declomycin) Lithium Used for:
Excess secretion of ADH or SIADH

Action:
Inhibits ADH action in kidney Blocks renal response to ADH, interferes with action of ADH

Therapeutic outcome:
Decreased urine specific gravity

Analysis - Nursing Diagnosis - SIADH

1. Fluid Volume Excess R/T compromised regulatory mechanism, excess ADH 2. High Risk for Injury R/T an altered level of consciousness, confusion, & the possibility of seizures 3. Altered Nutrition: Less than Body Requirements R/T an inability to ingest or digest food or absorb nutrients because of biologic factors (ex-anorexia, N/V) 4. Altered Thought Processes R/T physiologic changes within the central nervous system

Planning & Implementation

Planning: Pt Goals The primary goal is that the pts fluid balance will be restored Interventions to treat SIADH (Pt Care Plan) consists of Restriction water intake Using diuretics to promote the excretion of water Administering drugs that interfere with the action of ADH Replacing lost sodium Fluid Restriction Any excessive free water intake will further dilute the serum sodium concentration Strict I&O, daily weights, guides the determination of the degree of fluid restriction necessary. A wt gain of 2 pounds (or 1 Kg) or more per day or a gradual increase during several days is cause for concern. A 1 Kg weight increase is equivalent to 1000ml fluid retention (1Kg = 1 L)

Planning & Implementation

Drug Therapy Diuretics are sometimes used to treat pt with SIADH, to rid the body of excessive fluid, especially if CHF IV saline is given cautiously because it results from fluid overload may contribute to the fluid overload already present & precipitate an episode of CHF. If diuretics are used, be aware of potential effect of electrolyte losses; If the pt needs routine IV fluids, the MD sodium loss can be orders a solution in saline (5% dextrose potentiated, which further in saline) rather than a solution in water. contributes to the clinical picture of SIADH

Hypertonic saline (3% NaCl) may be used to treat SIADH Helps correct serum sodium level Raises Na osmolality in the blood Removes excess intracellular fluid Cells shrink in hypertonic solution

Planning & Implementation

High Risk for Injury Promote safety Monitor pt neuro status Subtle Changes, such as muscle twitching before neuro S/S progress to seizures or coma. Check LOC to time, place, & person because disorientation may be present. Confusion is another neuro sign. Nurse reduces environmental stimuli & explain interventions in simple terms. Flow sheets contain ongoing info about LOC, motor & sensory neuro assessment, & pertinent lab data helpful in detecting trends.

Decreased LOC and seizures are complications of the low serum sodium level R/T SIADH

Nursing issues
Monitoring fluid balance(s/s fluid retention):

Cardiac problems

(water reabsorbed so >bld volume):

Neurological problems coma,): Energy limitations

(headache seizures,cerebral edema,

(muscle cramps, weakness):

Allied health problems

(anorexia):

Risk for injury: (confusion, muscle tremors, etc.)

Nursing issues
Fluid Volume Excess R/T inability to excrete water Hyponatremia with plasma hypo-osmolality Weight gain

Potential for Injury Institute seizure precautions and safety measures Reorient confused pt
Prevent complications of immobility Recognize decreased gastric motility due to hyponatremia, combined with fluid restriction and decreased mobility - >constipation

Diabetes Insipidus
Posterior Pituitary

Diabetes Insipidus
Uncommon syndrome of posterior pituitary hypofunction S/S
Increased thirst - polydipsia Increased urination - polyruia

Results from
ADH (Vasopression) deficiency, which prevents the kidneys from reabsorbing water Inability to conserve water

Posterior pituitary : DI
Diabetes insipidus: to pass through

Decreased ADH = diuresis

Water is lost, so assess for: Kidneys produce large amts of dilute urine (5L-10L in 24hrs) low urine specific gravity (1.001-1.005) polyuria (>urine output), polydipsia (>thirst) fluid deficit
weight loss, turgor,dehydration, hypotension, constipation, shock

 Symptoms -

Posterior Pituitary hyposecretion Diabetes Insipidus

Urine specific gravity low (1.001-1.005) Urine osmolality decreased (50-200 mOsm.kg) Urine less concentrated than plasma

Thrist & polyuria 5 - 20L/day

SG < 1005 Urine osmol < 100 mmol/L

Se osmol > 295 mmol/kg Nocturia Weakness => weight loss, hypotension, tachycardia, constipation, shock.

Plasma osmolality elevated (>295 mOsm/kg)

Hypernatremia in blood

Sleep deprivation-due to interrupted by need to drink fluids & urinate

Diabetes Insipidus Etilogy

Familial or idiopathic
Head injury Neuorsurgery
Cause Lesion of hypothalmus interferes with ADH synthesis/transport/relea se
brain tumour pituitary/cranial surgery head trauma CNS infection vascular disease.

Damage to the hypothalamic areas that produce ADH

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 (see next slide)

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)

Vasopressin challenge test (see next slide) 24 hours urine

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: R/T nocturia & increased thirst Education: