Nursing Management of DI and SIADH April 24

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: 280 -295 m. Osm/L

• Serum Osmo above 295 m. Osm/L = water deficit – Concentration is too great OR – Water concentration is too little • Serum Osmo below 280 m. Osm/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 m. Osm/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 • Psychoses • Drugs • Acute head injury • Pulmonary infections (Pneumonia) • 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 Osmolality Serum Osmolality BUN/Creatinine Urine Specific Gravity Serum Potassium

Lab Results for SIADH Serum Sodium Less than 135 m. Eq/L Urine Sodium Greater than 20 m. Eq/L Urine Osmolality Higher than serum Serum Osmolality Less than 275 m. Osm/L BUN/Creat WNL Urine Specific Gravity Greater than 1. 005 Adrenal/threshold WNL Serum Potassium Less than 3. 5 m. Eq/L

Treatment of SIADH • Correct 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 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 Level Symptoms 145 -135 m. Eq/L Normal concentration, no symptoms 135 -120 m. Eq/L Generally no changes 120 -110 m. Eq/L HA, apathy, lethargy, weakness, disorientation, thirst, fatigue, seizures 110 -100 m. Eq/L Confusion, hostility, lethargy, N/V, abdominal cramps, muscle twitching 100 -95 m. Eq/L Delirium, 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 • Nephrogenic • Dispogneic Inadequate secretion of Inadequate response Suppression of ADH by the kidneys to ADH due to loss or ADH. secondary a defect malfunction of or damage to the neurosecretory A disorder of renal neurons that make up tubular function thirst mechanism the posterior pituitary. resulting in the located in the inability to respond hypothalamus to ADH in resulting in increased Vasopressin Sensitive absorption of water. fluid intake or psychogenic causes Vasopressin Resistant

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 • Idiopathic • Post-operative (hypophysectomy, pituitary tumor) • ICH • Brain Tumors • Hypoxia • CNS Infection (meningitis, abcess) • Medications (Dilantin, clonidine, alcohol) • Increased ICP • Damage to hypothalamus or posterior pituitary • Stroke

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: – 24 hr 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 Value Result Serum Sodium Above 135 m. Eq/L Serum Osmolality Above 290 m. Osm/kg Urine Specific Gravity of the first morning voiding Below 1. 005 Urine Sodium Above 145 m. Eq/L Urine Osmolality Below 300 m. Osm/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 (q 2 h) monitoring of plasma and urine osmolality follows. • The test is generally terminated when plasma osmolality is >295 m. Osm/kg or the patient loses ≥ 3. 5% of initial body weight. • DI is confirmed if the plasma osmolality is >295 m. Osm/kg and the urine osmolality is <500 m. Osm/kg.

Nephrogenic DI vs Neurogenic DI • DDAVP Challenge ² Check urine osmolality 1 -2 hrs after 1 mcg SQ DDAVP • If little or no change: likely NDI or dipsogenic DI • If significant increase in urine osmolality, likely CDI • 5 units vasopressin IV ² Measure osmolality ² 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 Finding SIADH DI Urine Output Less than 200 mls x Greater than 250 mls 2 hrs x 2 hrs Serum Sodium Below 135 m. Eq/L Above 135 m. Eq/L Urine Sodium Below 25 -30 m. Eq/L Decreased Urine Osmolality Above 900 m. Osm/kg Below 400 m. Osm/kg Plasma Osmolality Below 275 m. Osm/L Above 295 m. Osm/L Blood Pressure Normotension Hypotension Fluid Status No Dehydration Neuro Symptoms Confusion, delirium, Seizures, coma with low Na

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. 5 m. Eq/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 http: //www. ncbi. nlm. nih. gov/pubmedhealth/PMH 0001779/. Barker, E. (Ed. ). (2008). Neuroscience nursing, A spectrum of care (3 rd 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/anat 2/notes/Image 43. gif &imgrefurl=http: //legacy. owensboro. kctcs. edu/gcaplan/anat 2/notes/APIINotes 3%2520 urinary%2520 syste m. htm&usg=__Xj. NUn. NDfvc. RKXEREA 8 DAxd 1 t 5 w=&h=440&w=392&sz=17&hl=en&start=3&sig 2=DGkmr. Cq 21 f 5 a. XMs. TSMj. Em. A&zoom=1&tbnid =7 gqzst. Tr. Zlnu. CM: &tbnh=127&tbnw=113&ei=Hxa. PT--Fu. Xb 0 QGtp 8 GODw&prev=/search%3 Fq%3 Dadh%2 Bfeedback%2 Bloop%26 hl%3 Den%26 gbv%3 D 2%26 tb m%3 Disch&itbs=1.