1. 2 Disorders of the Posterior Pituitary Diabetes Insipidus Syndrome of Inappropriate Antidiuretic Hormone (SAIDH)

2. 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.

3. Posterior Pituitary
Antidiuretic hormone (ADH) (Also called vasopressin)
Disorders/diseases resulting from dysfunction
Excess: Syndrome of Inappropriate ADH secretion (SIADH)
Deficiency: Diabetes Insipidus

4. Posterior Pituitary Hypersecretion
SIADH
Posterior Pituitary Hypersecretion

5. 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

6. 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.

7. Syndrome of Inappropriate Antidiuretic Hormone Secretion - SIADH
Results from many 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)
SIADH occurs when there is too much vasopression (ADH) with inappropriate water retention and decreased blood Na levels

8. 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

9. 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

10. 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

11. 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 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

12. Normal Lab Values serum osmolality (285-295 mOsm/kg)
sodium (Na mEq/L)
chloride ( mEq/L)
Urine osmolality -
-24 hr specimen
mOsm/kg H20
-Random specimen: 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
High=dehydration
Low=diabetes insipidus
concerntrated urine > than mOsm/kg with normal vascular volume and normal renal function

13. 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 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

14. 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

15. Posterior Pituitary hypersecretion - SIADH
Symptoms - fluid retention
low serum osmolality (normal mOsm/kg)
dilutional low sodium (normal Na mEq/L)
low chloride (normal mEq/L)
Causes -
Diseases effect the hypothalmus
pneumonia TB
positive pressure ventilation
Trauma
concerntrated urine (> than mOsm/kg) with normal vascular volume and normal renal function
muscle cramps & weakness
cerebral edema, lethargy, anorexia, headache, seizures, coma.
AIDs
delirium tremens
Ectopic ADH secreting tumor

16. SIADH - Diagnostic Tests
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 underlying condition.
Blood & Urine tests
Must have
low serum sodium
low plasma osmolality level
Inappropriated concentrated urine (increased urine osmolality level)

17. Posterior Pituitary: SIADH,DI
*Affect kidney’s ability to concentrate urine*
Measured by urine specific gravity
Measures number and size of particles
Normal:
High = dehydration
Low = Diabetic Insipidus
Concentrated urine: SIADH
Dilute urine: DI

18. 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

19. 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.

20. SIADH Diagnosis & Treatment
measure urine volume
and
osmolality
Treatment
If Na<125
Restrict fluids ml/day.
Daily weigh Monitor % - 5% Saline solution IV
Na < 134mmol/L
se osmol >280mmol/kg
SG>1005
low BUN, creatinine, Hb, Hct.
Lasix if Na< (cardiac symptoms)

21. SIADH Nursing Assessment Diagnostic Study Hyponatremia
Headache,Personality change, Confusion,Irrritability, Dysarthria(difficult, poorly articulated speech), Lethargy,Impaired memory
Restless, weakness, fatigue, gait disturbances
Weight gain+++++
Diagnostic Study
Hyponatremia
Decreased plasma osmolality
Urine sodium and urine osmolality elevated
Elevated ADH levels++++++
Normal renal, adrenal, & thyroid functions

22. 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.

23. 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

24. SIADH treatment Demeclocycline (Declomycin) Lithium Used for: Action:
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

25. 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

26. Planning & Implementation
Planning: Pt Goals
The primary goal is that the pt’s 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)

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

28. 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

29. Nursing issues Monitoring fluid balance(s/s fluid retention):
Cardiac problems (water reabsorbed so >bld volume):
Neurological problems (headache seizures,cerebral edema, coma,):
Energy limitations (muscle cramps, weakness):
Allied health problems (anorexia):
Risk for injury: (confusion, muscle tremors, etc.)

30. 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

31. Diabetes Insipidus
Posterior Pituitary

32. 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

33. 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 ( )
polyuria (>urine output), polydipsia (>thirst)
fluid deficit
weight loss, turgor,dehydration, hypotension, constipation, shock

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

35. 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/release
brain tumour
pituitary/cranial surgery
head trauma
CNS infection
vascular disease.

36. 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

37. 4 Types of Diabetes Insipidus
3) Gestagenic-also known as
Gestestional
Caused by a deficiency of the antidiuretic hormone, vasopressin, that occurs only during pregnancy
4) Dipsogenic, a form of primary polydipsis
Caused by
Abnormal thirst and the
Excessive intake of water or other liquids
1) Neurogenic -also known as
central
hypothalamic
pituitary
neurohypophyseal
Caused by a deficiency of the Antidiuretic hormone, vasopressin
2) Nephrogenic-also known as
Vasopressin - resistant
Caused by insensitivity of the kidneys to the effect of the antidiuretic hormone, vasopressin

38. Diagnosis & Rx Diabetes Insipidus
Diagnosis D.I.
History and examination
Water deprivation test (see next slide)
Vasopressin challenge test (see next slide)
24 hours urine
High sodium in blood
MRI of pituitary, hypothalmus and skull to see damaged areas
Diagnosis & Rx Diabetes Insipidus
Treatment
Intravenous fluids Hypertonic saline IV-Extracellular 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)

39. 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

40. 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

41. 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

42. 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

43. 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

44. 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

45. 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: