SIADH vs. Cerebral Salt Wasting Syndrome - 5 Nursing CEs

Author: Kristi Hudson RN MSN CCRN

Written: July 4, 2005

Updated: September 25, 2009

Course Objectives:

Upon completion of this course the student will be able to:

• Differentiate between SIADH vs. Cerebral Salt Wasting Syndrome (CSWS)
• Define SIADH
• Define Cerebral Salt Wasting Syndrome
• List 2 causes for each syndrome
• Explain necessary lab tests to diagnosis both SIADH and CSWS
• Describe the signs and symptoms of each syndrome
• List 2 treatment options for SIADH
• List 2 treatment options of Cerebral Salt Wasting Syndrome
• Describe the use of 3% Sodium Chloride IV infusion for CSWS

Defining SIADH:

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) can be defined as a dilutional hyponatremic state that is caused by an excessive release of anti-diuretic hormone (ADH). SIADH is the most common cause of hyponatremia in a hospitalized and more specific post-operative patient.

Defining Anti-Diuretic hormone (ADH):

ADH is a hormone stored in the posterior pituitary gland in the brain. It is the primary regulator of body water. ADH acts on the kidneys to increase total body water. Ordinarily it is a physiological response to a drop in plasma volume or an increase in serum osmolality that causes the release of ADH.

Pathophysiology of SIADH:

In SIADH, there is a persistent production of ADH despite body fluid hypotonicity and an expanded effective circulating volume so that the negative feedback mechanism that normally controls ADH fails, and ADH continues to be released.

Causes of SIADH:

SIADH tends to occur in three disease groups; CNS disorders, carcinomas and pulmonary disorders. Other and more specific causes of SIADH include:

• Oat cell lung cancer
• Encephalitis
• Stroke
• Head trauma
• Psychosis
• Damage to the hypothalamus or pituitary gland during surgery
• Fluid and electrolyte imbalances
• Pancreatic cancer
• Prostate cancer
• Hodgkin’s disease
• Hypothyroidism
• Adrenal insufficiency
• Osmotic diuretics
• Central nervous system disorders
• Pulmonary disorders
• Thymomas
• Myxedema
• The acute phase of meningitis in children
• Guillain-Barre’ syndrome
• Cerebral abscess
• The following drugs can also cause SIADH:
  • Analgesics
  • Antidepressants
  • Antineoplastics
  • Barbiturates
  • Carbamamzepine
  • Clofibrate
  • Diuretics
  • Neuroleptics
  • Oral hypoglycemics
  • Antibiotics

Other conditions that may cause temporary SIADH include:

• Fever
• Pain
• Positive-pressure breathing on the ventilator

Risk factors are related to the causes and include:

• Weight gain
• Loss of appetite
• Nausea
• Muscle weakness
• Muscle spasm/cramps
• Restlessness/Fatigue
• Abnormal mental status (altered LOC, convulsions, coma)

Signs and Symptoms of SIADH:

Patients with SIADH are usually euvolemic and hypertensive. This patient population often displays symptoms of peripheral and pulmonary edema, dry mucous membranes, reduced skin turgor and are “absent” of orthostatic hypotension. Neurologic complications occur as a result of the brains adaption to changes in osmolality. Acute brain cell edema is can cause a critical condition. Neurologic signs to look for in patients with SIADH include:

• Drowsiness
• Seizures
• Coma

Diagnosis of SIADH:

In addition to a complete medical history and physical, confirmatory labs must be drawn, these include:

Rule out of renal, adrenal or other endocrine disease

• Hyponatremia (serum sodium <135 mEq/L)
• Hypotonicity (plasma osmolality <280 mOsm/kg)
• Inappropriately concentrated urine (>100 mOsm/kg water)
• Elevated urine sodium concentration (>20 mEq/L), except during sodium restriction
• High urine osmolality (higher then serum)
• Normal BUN and creatinine

Treatment Options for SIADH:

Treatment depends on the severity and the underlying cause of the problem. The principles of treatment for SIADH include:

• Fluid Restriction (usually 500cc to 1 Liter of fluid per day)
• Treat the source of the problem

Drug therapy for SIADH includes:

• Furosemide (Lasix) for diuresis
• Demeclocycline Hydrochloride (300 mg QID) to suppress ADH activity
• Lithium Carbonate (900-1200mg QD) to inhibit renal response to ADH

Nursing Care and Management:

• Strict monitoring of Intake and Output (monitor close for signs of fluid overload)
• Daily weight
• Urine and serum sodium and osmolality
• Urine specific gravity
• BUN levels
• Monitor for S/S of fluid and electrolyte imbalance
• Monitor for sodium depletion
• Monitor for lethargy, confusion, weakness, cramping, headache, seizures, coma

Defining Cerebral Salt Wasting Syndrome:

CSWS is defined as “true” hyponatremia which occurs when there is a primary loss of sodium into the urine without an increase in total systemic volume. It is related to acute or chronic damage of the central nervous system.

Pathophysiology: The exact mechanism that causes CSWS is unclear, but one hypothesis states that it is due to an exaggerated renal pressure-natriuresis that occurs from increased sympathetic nervous system activity.

Causes of CSWS:

Humeral mechanisms such as an increase in circulating atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are thought to be contributing factors to the development of CSWS. Brain insult from the following disease processes are thought to also increase the risk of developing CSWS:

• Sub-Arachnoid Hemorrhage
• Intracerebral Hemorrhage/Stroke
• Cerebral Neoplasm/Intracranial Surgery
• Increased Intracranial Pressure
• Tuberculous Meningitis

Signs and Symptoms of CSWS:

Physical signs of CSWS include those associated with severe hyponatremia or intravascular depletion. These can include:

• Hypovolemia (low CVP)
• Absence of Weight gain
• Orthostatic tachycardia/hypotension
• Increased capillary refill time/increased skin turgor
• Dry mucous membranes
• Sunken anterior fontanel (in infants)

Lab Studies:

• Patients with untreated CSWS are hyponatremic
• Serum uric acid concentrations are normal in CSWS
• Urine flow rate is often high in CSWS
• Urine sodium excretion is high in CSWS
• Net sodium balance (intake minus output is negative in CSWS)

Differentiating the Diagnosis of CSWS and SIADH:

Identical acute cerebral insults may cause either SIADH or CSW. The clinical manifestation of both conditions can be virtually identical. The only true discriminative feature is that extracellular volume is “expanded” in SIADH and is “low” in CSWS.  The following chart provides further lab values to assist in differentiating between SIADH and CSWS:

Treatment of CSWS:

Making the distinction between CSW and SIADH is of particular importance with regard to therapy. The following treatment regiment is recommended for treatment of patients who are suffering from CSWS:

• Treat the underlying neurological process
• Volume replacement (to maintain a positive salt balance)
• IV Hydration with  0.9%  NaCl infusion
• IV Hydration with hypertonic 3% NaCl infusion
• Colloids may effective to absorb third-space fluid
• Blood products may be useful for volume expansion
• Urine replacement (cc for cc)
• Positive sodium balance
• Fludocortisone (enhances sodium reabsorption, can cause hypokalemia)

Nursing Care and Management of CSWS:

Monitor for clinical dehydration: (For patients with invasive hemodynamic monitoring, a low pulmonary capillary wedge pressure (<8 mm Hg) or low CVP (< 6 mm Hg) implies volume deficit).

 Other clinical interventions include:

• Vital signs
• Fluid intake and output
• Labs (serum sodium, urine sodium, serum/urine osmolality)
• BUN and creatinine
• Titration of 0.9% and 3% Sodium Chloride infusion per hospital protocol
• Administration of salt tablets

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