Presentation on theme: "Nursing Management of DI and SIADH April 24, 2012"— Presentation transcript:
1Nursing Management of DI and SIADH April 24, 2012 Lauren Walker RN, BSN, CCRN
2ObjectivesDescribe 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.
3Brain RegulationDisorder of sodium and water balance is a common complication following neurosurgeryNeuroscience patients must be continually assessed and monitored for their response to therapyEarly detection is critical to the protection and integrity of the brain
4Normal Brain Regulation TBW accounts for 60% of body weight20% ECF40% ICFFluid shifts can occur depending on concentrations of solutes in ICF and ECFNa and K are principle determinants in fluid shiftsOsmolarity: amount of solute in fluid (urine, blood)Normal Serum Osmolarity: mOsm/L
5Serum Osmo above 295 mOsm/L = water deficit Concentration is too great ORWater concentration is too littleSerum 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 soluteTo maintain plasma or serum osmo within range, free water intake and excretion must balance
6Antidiuretic Hormone (ADH): balances Na and water in body and controls water conservation Changes in pressure of ECF triggers release of ADH from pituitary glandRelease is coordinated with activity of the thirst center- regulates intakeADH binds with receptor sites of the collecting duct in kidney resulting in increased free-water resorptionADH causes vasoconstrictionPresence of ADH- renal tubule permeability to water is increased and water is reabsorbedAbsence of ADH- renal tubule permeability to water is decreased – renal excretion to fluids
7Plasma osmolality = Primary regulatory mechanism for the release of ADH Receptors in the brain are sensative to changes in osmolalityReceptors that trigger thirst mechanism are close to those that control ADH releaseSerum osmo greater than 290 mOsm/L triggers thirst
9Syndrome of Inappropriate Antidiuretic Hormone SIADH: 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 electrolytesFeedback system is impaired and posterior pituitary continues to release ADHRenal tubules continue to reabsorb free water regardless of the serum osmolalityExcessive activity of the neurohypophyseal system r/t brain disease
10At Risk Patients for SIADH Post-Operative with pituitary surgeryAcute head injuryPulmonary infections (Pneumonia)PsychosesDrugsNervous system infections (meningitis)
11Investigate the following conditions for SIADH Thirst and fluid status with accurate I&OConfusionDyspneaHeadacheFatigueWeaknessIncreased weight w/o edemaChange in LOCLethargyVomitingMuscle weakness and crampingMuscle twitchingSeizures
12Urine Specific Gravity Labs to Diagnose SIADHSerum NaUrine NaUrine OsmolalitySerum OsmolalityBUN/CreatinineUrine Specific GravitySerum Potassium
13Urine Specific Gravity Lab Results for SIADHSerum SodiumLess than 135 mEq/LUrine SodiumGreater than 20 mEq/LUrine OsmolalityHigher than serumSerum OsmolalityLess than 275 mOsm/LBUN/CreatWNLUrine Specific GravityGreater than 1.005Adrenal/thresholdSerum PotassiumLess than 3.5 mEq/L
14Treatment of SIADH Correct underlying cause Fluid restriction ml/daySevere hyponatremia:3% NS may be givenLasix may be given (watch K level)
15Nursing Management of SIADH Frequent Neuro assessmentMental status and LOCPulmonary assessments/s fluid overloadCardiac assessmentDysrhythmias and BP abnormalitiesMonitor for seizure activitySeizure precautionsAccurate I&ODaily WeightsSame time each day, same scale, same clothesOral hygieneReduce stress, pain, discomfort
16Correlation of Decreasing Sodium Levels and Symptoms Serum Sodium LevelSymptomsmEq/LNormal concentration, no symptomsmEq/LGenerally no changesmEq/LHA, apathy, lethargy, weakness, disorientation, thirst, fatigue, seizuresmEq/LConfusion, hostility, lethargy, N/V, abdominal cramps, muscle twitchingmEq/LDelirium, convulsions, coma, hypothermia, areflexia, Cheyne-Stokes respirations, death
17Central/Neurogenic (CDI) 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
18Vasopressin Sensitive Vasopressin Resistant Pathophysiology of DICentral/NeurogenicInadequate secretion ofADH due to loss or malfunction of neurosecretory neurons that make up the posterior pituitary.Vasopressin SensitiveNephrogenicInadequate 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 ResistantDispogneicSuppression of ADH secondary a defect or damage to the thirst mechanism located in the hypothalamus resulting in increased fluid intake or psychogenic causes
19Diabetes 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
20Causes of DI Head Trauma Post-operative (hypophysectomy, pituitary tumor)Brain TumorsCNS Infection (meningitis, abcess)Increased ICPIdiopathicICHStrokeHypoxiaMedications (Dilantin, clonidine, alcohol)Damage to hypothalamus or posterior pituitaryDrug toxicityLithium is the most common cause of nephrogenic DI in adultsAmpho B, Colchicine, Gentamicin, Lithium, Loop Diuretics, Methoxyflurane, Foscarnet, Demeclocycline
21Investigate the following for DI Unquenchable thirstPolydipsiaPolyuria(hourly urine output > 200 mls)Unexplained weight lossUrinary frequencyNocturiaDry skin/poor skin turgorTachycardia and hypotensionInability to respond to the increased thirst stimulus and compensate for the excessive polyuriaHypernatremia that becomes severe and is manifested by- confusion, irritability, stupor, coma and neuromuscular hyperactivity progressing to seizures.ElderlyUnconscious/intubated
22Labs and Diagnostics for DI Serum calciumGlucoseCreatininePotassiumUrea levelThe following may also be indicated:24hr urine collection to quantitative polyuriaCT/MRIrule out pituitary causes, metastases, hemorrhage, neuronal damage, cerebral tumors.Radioimmunoassy: to measure circulating ADH concentrationsCT/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
23Lab Results for diagnosis of DI Lab ValueResultSerum SodiumAbove 135 mEq/LSerum OsmolalityAbove 290 mOsm/kgUrine Specific Gravity of the first morning voidingBelow 1.005Urine SodiumAbove 145 mEq/LUrine OsmolalityBelow 300 mOsm/LDiagnosis of DI should be considered in any person producing large volumes of dilute urine
24Water Deprivation Test After baseline measurement of: weight, ADH, plasma sodium, and urine/plasma osmolality, the patient is deprived of fluids under strict medical supervisionFrequent (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 <500 mOsm/kg.
25Nephrogenic DI vs Neurogenic DI DDAVP ChallengeCheck urine osmolality 1-2hrs after 1mcg SQ DDAVPIf little or no change: likely NDI or dipsogenic DIIf significant increase in urine osmolality, likely CDI5 units vasopressin IVMeasure osmolalityA significant increase (>50%) in urine osmolality after administration of ADH is indicative of CDI
26Correct the underlying cause and maintain adequate fluid replacement. 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 replacementFree water restrictionAfter assessing fluid status and serum sodium level, treat both dehydration and hypernatremiaFor chronic neurogenic DI- require hormonal replacement therapy: DDAVP (nasal vasopressin)Consultation with an endocrinologist is strongly recommended
27Treatment for Nephrogenic DI Removal of the underlying cause/offending drugDDAVP usually ineffectiveThiazide diuretic (HCTZ) is first line treatmentAdequate hydrationLow-sodium diet + thiazide diuretics to induce mild sodium depletion.Indomethacin may also be useful to reduce urine volume.
28Nursing Management of DI Hourly Neuro ChecksFrequent Vital SignsEvaluate for s/s of hypovolemic shockStrict I&ORehydrate for symptoms of extreme thirstMeasure and record weight using the same scales at the same time and with the patient wearing the same clothingAssess mucous membranes and skin turgor and monitor for symptoms of dehydrationProvide restSafety measures to prevent injury secondary to dizziness and fatigueAlert the health care team of problems of urinary frequency and extreme thirst that interferes with sleep and activities.
29SIADH vs DI Lab Values Finding SIADH DI Urine Output Less than 200 mls x 2hrsGreater than 250 mls x 2hrsSerum SodiumBelow 135 mEq/LAbove 135 mEq/LUrine SodiumBelow 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
30Complications to treatments of DI and SIADH Cerebral Edema!Central Pontine Myelinolysis: brain cell dysfunction caused by destruction of the myelin sheath covering nerve cells in brainstemNa levels rise too fast or corrected too quicklys/s: (not necessarily immediate)Acute paralysisDyschagiaDysarthria
31Most Important Nursing Intervention for DI and SIADH Frequent 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 hrsFrequent neuro assessmentThe nurse can pick up abnormal behavior and signs and symptoms firstNote any changes from baseline
32ReferencesA.D.A.M. Medical Encyclopedia. (2010). Central pontine myelinolysis. Retrieved April/18, 2012, fromBarker, 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