2 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

Posterior Pituitary Hypersecretion 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 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

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) dilutional low sodium (normal Na 135-145 mEq/L) low chloride (normal95-105 mEq/L) Causes - Diseases effect the hypothalmus pneumonia TB positive pressure ventilation Trauma 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. AIDs delirium tremens Ectopic ADH secreting tumor

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)

Posterior Pituitary: SIADH,DI *Affect kidney’s 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 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 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

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: 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

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 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)

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

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 (headache seizures,cerebral edema, coma,): Energy limitations (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

Posterior Pituitary hyposecretion Diabetes Insipidus Symptoms - 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. Sleep deprivation-due to interrupted by need to drink fluids & urinate Urine specific gravity low (1.001-1.005) Urine osmolality decreased (50-200 mOsm.kg) Urine less concentrated than plasma Plasma osmolality elevated (>295 mOsm/kg) Hypernatremia in blood

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.

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 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

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)

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: