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 Na

Urine Na

Urine Osmolality

Serum Osmolality

BUN/Creatinine

Urine Specific Gravity

Serum 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)

Dipsogenic

Gestational

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.