Presentation on theme: "Nursing Management of DI and SIADH April 24, 2012 Lauren Walker RN, BSN, CCRN."— Presentation transcript:
Nursing Management of DI and SIADH April 24, 2012 Lauren Walker RN, BSN, CCRN
Objectives Describe 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 Regulation TBW accounts for 60% of body weight –20% ECF –40% 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: mOsm/L
Serum Osmo above 295 mOsm/L = water deficit –Concentration is too great OR –Water concentration is too little Serum Osmo below 280 mOsm/L = water excess –Amount of particles or solute is too small in proportion to the amount of water OR –Too 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 Hormone SIADH: Persistent abnormally high (inappropriate) levels of ADH in the absence of stimuli with normal renal function –No longer regulated by plasma osmo and volume –Imbalance 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 SIADH Post-Operative with pituitary surgery Acute head injury Pulmonary infections (Pneumonia) Psychoses Drugs Nervous system infections (meningitis)
Investigate the following conditions for SIADH Thirst and fluid status with accurate I&O Confusion Dyspnea Headache Fatigue Weakness Increased weight w/o edema Change in LOC Lethargy Vomiting Muscle weakness and cramping Muscle twitching Seizures
Labs to Diagnose SIADH Serum Na Urine Na Urine Osmolality Serum Osmolality BUN/Creatinine Urine Specific Gravity Serum Potassium
Lab Results for SIADH Serum SodiumLess than 135 mEq/L Urine SodiumGreater than 20 mEq/L Urine OsmolalityHigher than serum Serum OsmolalityLess than 275 mOsm/L BUN/CreatWNL Urine Specific GravityGreater than Adrenal/thresholdWNL Serum PotassiumLess than 3.5 mEq/L
Treatment of SIADH Correct underlying cause Fluid restriction ml/day Severe hyponatremia: –3% NS may be given Lasix may be given (watch K level)
Nursing Management of SIADH Frequent Neuro assessment –Mental status and LOC Pulmonary assessment –s/s fluid overload Cardiac assessment –Dysrhythmias and BP abnormalities Monitor for seizure activity –Seizure precautions Accurate I&O Daily Weights –Same time each day, same scale, same clothes Oral hygiene Reduce stress, pain, discomfort
Correlation of Decreasing Sodium Levels and Symptoms Serum Sodium LevelSymptoms mEq/LNormal concentration, no symptoms mEq/LGenerally no changes mEq/LHA, apathy, lethargy, weakness, disorientation, thirst, fatigue, seizures mEq/LConfusion, hostility, lethargy, N/V, abdominal cramps, muscle twitching mEq/LDelirium, convulsions, coma, hypothermia, areflexia, Cheyne- Stokes respirations, death
Diabetes Insipidus Disordered 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) Dipsogenic Gestational
Pathophysiology of DI Central/Neurogenic Inadequate secretion of ADH due to loss or malfunction of neurosecretory neurons that make up the posterior pituitary. Vasopressin Sensitive Nephrogenic 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 DI Head 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
Investigate the following for DI Unquenchable 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 DI Serum calcium Glucose Creatinine Potassium Urea level The following may also be indicated: –24hr urine collection to quantitative polyuria –CT/MRI rule out pituitary causes, metastases, hemorrhage, neuronal damage, cerebral tumors. –Radioimmunoassy: to measure circulating ADH concentrations
Lab Results for diagnosis of DI Lab ValueResult Serum SodiumAbove 135 mEq/L Serum OsmolalityAbove 290 mOsm/kg Urine Specific Gravity of the first morning voiding Below Urine SodiumAbove 145 mEq/L Urine OsmolalityBelow 300 mOsm/L Diagnosis of DI should be considered in any person producing large volumes of dilute urine
Water Deprivation Test After 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 <500 mOsm/kg.
Nephrogenic DI vs Neurogenic DI DDAVP Challenge Check urine osmolality 1-2hrs after 1mcg SQ DDAVP If little or no change: likely NDI or dipsogenic DI If significant increase in urine osmolality, likely CDI 5 units vasopressin IV Measure osmolality A significant increase (>50%) in urine osmolality after administration of ADH is indicative of CDI
Treatment of DI Correct 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 DI Removal of the underlying cause/offending drug DDAVP 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 DI Hourly 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 FindingSIADHDI Urine OutputLess than 200 mls x 2hrs Greater than 250 mls x 2hrs Serum SodiumBelow 135 mEq/LAbove 135 mEq/L Urine SodiumBelow mEq/LDecreased Urine OsmolalityAbove 900 mOsm/kgBelow 400 mOsm/kg Plasma OsmolalityBelow 275 mOsm/LAbove 295 mOsm/L Blood PressureNormotensionHypotension Fluid StatusNo DehydrationDehydration Neuro SymptomsConfusion, delirium, coma with low Na Seizures, coma
Complications 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 brainstem Na levels rise too fast or corrected too quickly s/s: (not necessarily immediate) –Acute paralysis –Dyschagia –Dysarthria
Most Important Nursing Intervention for DI and SIADH Frequent Labs –We have severe electrolyte abnormalities –Careful not to correct too quickly!! –Na should not rise more than 0.5mEq/L/hr and 10 mmol/L/24 hrs Frequent neuro assessment –The nurse can pick up abnormal behavior and signs and symptoms first –Note any changes from baseline
References A.D.A.M. Medical Encyclopedia. (2010). Central pontine myelinolysis. Retrieved April/18, 2012, from 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 &imgrefurl=http://legacy.owensboro.kctcs.edu/gcaplan/anat2/notes/APIINotes3%2520urinary%2520syste m.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%26tb m%3Disch&itbs=1. &imgrefurl=http://legacy.owensboro.kctcs.edu/gcaplan/anat2/notes/APIINotes3%2520urinary%2520syste m.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%26tb m%3Disch&itbs=1