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