Nursing Management of DI and SIADHApril 24, 2012Lauren Walker RN, BSN, CCRN

ObjectivesDescribe the normal function of ADH in water and electrolyte regulation.

Compare and contrast the etiologies of SIADH and DI.

Describe the assessment findings of SIADH and DI.

Evaluate the management and treatment of SIADH and DI.

Evaluate the possible complications of SIADH and DI.

Brain Regulation Disorder of sodium and water balance is a common complication following neurosurgery

Neuroscience patients must be continually assessed and monitored for their response to therapy

Early detection is critical to the protection and integrity of the brain

Normal Brain RegulationTBW accounts for 60% of body weight20% ECF40% ICF

Fluid shifts can occur depending on concentrations of solutes in ICF and ECF

Na and K are principle determinants in fluid shifts

Osmolarity: amount of solute in fluid (urine, blood)

Normal Serum Osmolarity: 280-295 mOsm/L

Serum Osmo above 295 mOsm/L = water deficitConcentration is too great ORWater concentration is too little

Serum Osmo below 280 mOsm/L = water excessAmount of particles or solute is too small in proportion to the amount of water ORToo much water for the amount of solute

To maintain plasma or serum osmo within range, free water intake and excretion must balance

Antidiuretic Hormone (ADH): balances Na and water in body and controls water conservation

Changes in pressure of ECF triggers release of ADH from pituitary gland

Release is coordinated with activity of the thirst center- regulates intake

ADH binds with receptor sites of the collecting duct in kidney resulting in increased free-water resorption

ADH causes vasoconstriction

Presence of ADH- renal tubule permeability to water is increased and water is reabsorbed

Absence of ADH- renal tubule permeability to water is decreased renal excretion to fluids

Plasma osmolality = Primary regulatory mechanism for the release of ADH

Receptors in the brain are sensative to changes in osmolality

Receptors that trigger thirst mechanism are close to those that control ADH release

Serum osmo greater than 290 mOsm/L triggers thirst

ADH Feedback Loop

Syndrome of Inappropriate Antidiuretic HormoneSIADH: Persistent abnormally high (inappropriate) levels of ADH in the absence of stimuli with normal renal functionNo longer regulated by plasma osmo and volumeImbalance of fluid and electrolytes

Feedback system is impaired and posterior pituitary continues to release ADH

Renal tubules continue to reabsorb free water regardless of the serum osmolality

Excessive activity of the neurohypophyseal system r/t brain disease

At Risk Patients for SIADHPost-Operative with pituitary surgery

Acute head injury

Pulmonary infections (Pneumonia)

Psychoses

Drugs

Nervous system infections (meningitis)

Investigate the following conditions for SIADHThirst and fluid status with accurate I&OConfusionDyspneaHeadacheFatigueWeakness

Increased weight w/o edemaChange in LOCLethargyVomitingMuscle weakness and crampingMuscle twitchingSeizures

Labs to Diagnose SIADHSerum NaUrine NaUrine OsmolalitySerum OsmolalityBUN/CreatinineUrine Specific GravitySerum Potassium

Lab Results for SIADH

Serum SodiumLess than 135 mEq/LUrine SodiumGreater than 20 mEq/LUrine OsmolalityHigher than serumSerum OsmolalityLess than 275 mOsm/LBUN/CreatWNLUrine Specific GravityGreater than 1.005Adrenal/thresholdWNLSerum PotassiumLess than 3.5 mEq/L

Treatment of SIADHCorrect underlying cause

Fluid restriction 500-1000 ml/day

Severe hyponatremia:3% NS may be given

Lasix may be given (watch K level)

Nursing Management of SIADHFrequent Neuro assessmentMental status and LOC

Pulmonary assessments/s fluid overload

Cardiac assessmentDysrhythmias and BP abnormalities

Monitor for seizure activitySeizure precautions

Accurate I&O

Daily WeightsSame time each day, same scale, same clothes

Oral hygiene

Reduce stress, pain, discomfort

Correlation of Decreasing Sodium Levels and Symptoms

Serum Sodium LevelSymptoms145-135 mEq/LNormal concentration, no symptoms135-120 mEq/LGenerally no changes120-110 mEq/LHA, apathy, lethargy, weakness, disorientation, thirst, fatigue, seizures110-100 mEq/LConfusion, hostility, lethargy, N/V, abdominal cramps, muscle twitching100-95 mEq/LDelirium, convulsions, coma, hypothermia, areflexia, Cheyne-Stokes respirations, death

Diabetes InsipidusDisordered regulation of water balance due to impaired urinary concentrating ability secondary to inadequate secretion of ADH or resistance to ADH.

Four Types of DI:Central/Neurogenic (CDI)Nephrogenic (NDI)DipsogenicGestational

Pathophysiology of DICentral/Neurogenic

Inadequate secretion ofADH due to loss or malfunction of neurosecretory neurons that make up the posterior pituitary.

Vasopressin SensitiveNephrogenic

Inadequate response by the kidneys to ADH.A disorder of renal tubular function resulting in the inability to respond to ADH in absorption of water.

Vasopressin Resistant Dispogneic

Suppression of ADH secondary a defect or damage to the thirst mechanism located in the hypothalamus resulting in increased fluid intake or psychogenic causes

Diabetes Insipidus (DI) Clinical Signs!Dehydration! Excessive loss of water from body tissue and imbalance of essential electrolytes (Ns, K, Cl)

Polydipsia (excessive thirst)

Polyuria (excessive amount of urine)

Low specific gravity (1.001 to 1.005)

Serum hyperosmolality and hypernatremia

Causes of DIHead Trauma

Post-operative (hypophysectomy, pituitary tumor)

Brain Tumors

CNS Infection (meningitis, abcess)

Increased ICP

Idiopathic

ICH

Stroke

Hypoxia

Medications (Dilantin, clonidine, alcohol)

Damage to hypothalamus or posterior pituitary

*Drug toxicityLithium is the most common cause of nephrogenic DI in adultsAmpho B, Colchicine, Gentamicin, Lithium, Loop Diuretics, Methoxyflurane, Foscarnet, Demeclocycline

Investigate the following for DIUnquenchable thirst

Polydipsia

Polyuria

(hourly urine output > 200 mls)

Unexplained weight loss

Urinary frequency

Nocturia

Dry skin/poor skin turgor

Tachycardia and hypotension

Inability to respond to the increased thirst stimulus and compensate for the excessive polyuria

Hypernatremia that becomes severe and is manifested by- confusion, irritability, stupor, coma and neuromuscular hyperactivity progressing to seizures.

Elderly

Unconscious/intubated

Labs and Diagnostics for DISerum calciumGlucoseCreatininePotassiumUrea level

The following may also be indicated:24hr urine collection to quantitative polyuria

CT/MRIrule out pituitary causes, metastases, hemorrhage, neuronal damage, cerebral tumors.

Radioimmunoassy: to measure circulating ADH concentrations

*CT/MRI- if acute DI results from ICP or visualize the anterior and posterior pituitary glands and stalks and to demonstrate the presence of a suprastellar mass, cyst, hypoplasiaMRI or CT scan of the brain to rule out pituitary causes, metastases, hemorrhage, neuronal damage, cerebral tumors.

MRI of the brain if CDI is confirmed

Lab Results for diagnosis of DIDiagnosis of DI should be considered in any person producing large volumes of dilute urine

Lab ValueResultSerum SodiumAbove 135 mEq/L

Serum OsmolalityAbove 290 mOsm/kgUrine Specific Gravity of the first morning voidingBelow 1.005

Urine SodiumAbove 145 mEq/L

Urine OsmolalityBelow 300 mOsm/L

Water Deprivation TestAfter baseline measurement of: weight, ADH, plasma sodium, and urine/plasma osmolality, the patient is deprived of fluids under strict medical supervision

Frequent (q2h) monitoring of plasma and urine osmolality follows.

The test is generally terminated when plasma osmolality is >295 mOsm/kg or the patient loses 3.5% of initial body weight.

DI is confirmed if the plasma osmolality is >295 mOsm/kg and the urine osmolality is

Nephrogenic DI vs Neurogenic DIDDAVP Challenge

Check urine osmolality 1-2hrs after 1mcg SQ DDAVPIf little or no change: likely NDI or dipsogenic DIIf significant increase in urine osmolality, likely CDI

5 units vasopressin IV

Measure osmolalityA significant increase (>50%) in urine osmolality after administration of ADH is indicative of CDI

Treatment of DICorrect the underlying cause and maintain adequate fluid replacement.

DI Therapy varies with the degree and type of DI present or suspected.

IVF may be necessary to correct hypernatremia; avoid rapid replacement

Free water restriction

After assessing fluid status and serum sodium level, treat both dehydration and hypernatremia

For chronic neurogenic DI- require hormonal replacement therapy: DDAVP (nasal vasopressin)

Consultation with an endocrinologist is strongly recommended

Treatment for Nephrogenic DIRemoval of the underlying cause/offending drugDDAVP usually ineffective

Thiazide diuretic (HCTZ) is first line treatment

Adequate hydration

Low-sodium diet + thiazide diuretics to induce mild sodium depletion.

Indomethacin may also be useful to reduce urine volume.

Nursing Management of DIHourly Neuro Checks

Frequent Vital Signs

Evaluate for s/s of hypovolemic shock

Strict I&O

Rehydrate for symptoms of extreme thirst

Measure and record weight using the same scales at the same time and with the patient wearing the same clothing

Assess mucous membranes and skin turgor and monitor for symptoms of dehydration

Provide rest

Safety measures to prevent injury secondary to dizziness and fatigue

Alert the health care team of problems of urinary frequency and extreme thirst that interferes with sleep and activities.

SIADH vs DI Lab Values

FindingSIADHDIUrine OutputLess than 200 mls x 2hrsGreater than 250 mls x 2hrsSerum SodiumBelow 135 mEq/LAbove 135 mEq/LUrine SodiumBelow 25-30 mEq/LDecreasedUrine OsmolalityAbove 900 mOsm/kgBelow 400 mOsm/kgPlasma OsmolalityBelow 275 mOsm/LAbove 295 mOsm/LBlood PressureNormotensionHypotensionFluid StatusNo DehydrationDehydrationNeuro SymptomsConfusion, delirium, coma with low NaSeizures, coma

Complications to treatments of DI and SIADHCerebral Edema!

Central Pontine Myelinolysis: brain cell dysfunction caused by destruction of the myelin sheath covering nerve cells in brainstem Na levels rise too fast or corrected too quickly

s/s: (not necessarily immediate)Acute paralysisDyschagiaDysarthria

Most Important Nursing Intervention for DI and SIADHFrequent LabsWe have severe electrolyte abnormalitiesCareful not to correct too quickly!!Na should not rise more than 0.5mEq/L/hr and 10 mmol/L/24 hrs

Frequent neuro assessmentThe nurse can pick up abnormal behavior and signs and symptoms firstNote any changes from baseline

ReferencesA.D.A.M. Medical Encyclopedia. (2010). Central pontine myelinolysis. Retrieved April/18, 2012, from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001779/. Barker, E. (Ed.). (2008). Neuroscience nursing, A spectrum of care (3rd ed.). St Louis, MO.: Mosby Elsevier. Darling, J. (2012). In Walker L. (Ed.), Essentials to know, diabetes insipidus.Marino, P. (2009). The little ICU book. Philadelphia: Lippincott Williams & Wilkins. Urinary system" physiology & urine formation. (2010). Retrieved April/17, 2012, from http://www.google.com/imgres?imgurl=http://legacy.owensboro.kctcs.edu/gcaplan/anat2/notes/Image43.gif&imgrefurl=http://legacy.owensboro.kctcs.edu/gcaplan/anat2/notes/APIINotes3%2520urinary%2520system.htm&usg=__XjNUnNDfvcRKXEREA-8DAxd1t5w=&h=440&w=392&sz=17&hl=en&start=3&sig2=DGkmrCq21f5aXMsTSMjEmA&zoom=1&tbnid=7gqzstTrZlnuCM:&tbnh=127&tbnw=113&ei=HxaPT---FuXb0QGtp8GODw&prev=/search%3Fq%3Dadh%2Bfeedback%2Bloop%26hl%3Den%26gbv%3D2%26tbm%3Disch&itbs=1.

*Drug toxicityLithium is the most common cause of nephrogenic DI in adultsAmpho B, Colchicine, Gentamicin, Lithium, Loop Diuretics, Methoxyflurane, Foscarnet, Demeclocycline*CT/MRI- if acute DI results from ICP or visualize the anterior and posterior pituitary glands and stalks and to demonstrate the presence of a suprastellar mass, cyst, hypoplasiaMRI or CT scan of the brain to rule out pituitary causes, metastases, hemorrhage, neuronal damage, cerebral tumors.

MRI of the brain if CDI is confirmed