nursing management of di and siadh
TRANSCRIPT
Nursing Management of DI and SIADHApril 24, 2012Lauren 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 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 NaUrine Na
Urine OsmolalitySerum OsmolalityBUN/Creatinine
Urine Specific GravitySerum Potassium
Lab Results for SIADH
Serum Sodium Less than 135 mEq/L
Urine Sodium Greater than 20 mEq/L
Urine Osmolality Higher than serum
Serum Osmolality Less than 275 mOsm/L
BUN/Creat WNL
Urine Specific Gravity Greater than 1.005
Adrenal/threshold WNL
Serum Potassium Less than 3.5 mEq/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 mEq/L Normal concentration, no symptoms
135-120 mEq/L Generally no changes
120-110 mEq/L HA, apathy, lethargy, weakness, disorientation, thirst, fatigue, seizures
110-100 mEq/L Confusion, hostility, lethargy, N/V, abdominal cramps, muscle twitching
100-95 mEq/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)DipsogenicGestational
Pathophysiology of DI
• Central/Neurogenic
Inadequate secretion ofADH 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 calciumGlucose
CreatininePotassiumUrea 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 Value Result
Serum Sodium Above 135 mEq/L
Serum Osmolality Above 290 mOsm/kg
Urine Specific Gravity of the first morning voiding
Below 1.005
Urine Sodium Above 145 mEq/L
Urine Osmolality Below 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 ChallengeCheck 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 IVMeasure osmolalityA 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 DIUrine Output Less than 200 mls x
2hrsGreater than 250 mls x 2hrs
Serum Sodium Below 135 mEq/L Above 135 mEq/L
Urine Sodium Below 25-30 mEq/L Decreased
Urine Osmolality Above 900 mOsm/kg Below 400 mOsm/kg
Plasma Osmolality Below 275 mOsm/L Above 295 mOsm/L
Blood Pressure Normotension Hypotension
Fluid Status No Dehydration Dehydration
Neuro Symptoms Confusion, 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 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.