Presentation is loading. Please wait.

Presentation is loading. Please wait.

Nursing Management of DI and SIADH April 24, 2012

Similar presentations

Presentation on theme: "Nursing Management of DI and SIADH April 24, 2012"— Presentation transcript:

1 Nursing Management of DI and SIADH April 24, 2012
Lauren Walker RN, BSN, CCRN

2 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.

3 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

4 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

5 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

6 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

7 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

8 ADH Feedback Loop

9 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

10 At Risk Patients for SIADH
Post-Operative with pituitary surgery Acute head injury Pulmonary infections (Pneumonia) Psychoses Drugs Nervous system infections (meningitis)

11 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

12 Urine Specific Gravity
Labs to Diagnose SIADH Serum Na Urine Na Urine Osmolality Serum Osmolality BUN/Creatinine Urine Specific Gravity Serum Potassium

13 Urine Specific Gravity
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 Serum Potassium Less than 3.5 mEq/L

14 Treatment of SIADH Correct underlying cause
Fluid restriction ml/day Severe hyponatremia: 3% NS may be given Lasix may be given (watch K level)

15 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

16 Correlation of Decreasing Sodium Levels and Symptoms
Serum Sodium Level Symptoms mEq/L Normal concentration, no symptoms mEq/L Generally no changes mEq/L HA, apathy, lethargy, weakness, disorientation, thirst, fatigue, seizures mEq/L Confusion, hostility, lethargy, N/V, abdominal cramps, muscle twitching mEq/L Delirium, convulsions, coma, hypothermia, areflexia, Cheyne-Stokes respirations, death

17 Central/Neurogenic (CDI)
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

18 Vasopressin Sensitive Vasopressin Resistant
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

19 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

20 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 Drug toxicity Lithium is the most common cause of nephrogenic DI in adults Ampho B, Colchicine, Gentamicin, Lithium, Loop Diuretics, Methoxyflurane, Foscarnet, Demeclocycline

21 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

22 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 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, hypoplasia MRI 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

23 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

24 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. 

25 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

26 Correct the underlying cause and maintain adequate fluid replacement.
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

27 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.

28 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.

29 SIADH vs DI Lab Values Finding SIADH DI Urine Output
Less than 200 mls x 2hrs Greater than 250 mls x 2hrs Serum Sodium Below 135 mEq/L Above 135 mEq/L Urine Sodium Below 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

30 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

31 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

32 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

Download ppt "Nursing Management of DI and SIADH April 24, 2012"

Similar presentations

Ads by Google