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 antidiuretic hormone (ADH). SIADH is the most common cause of hyponatremia in a hospitalized and more specific post-operative patient. 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. 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)

Drug

Treat the source of the problem therapy for SIADH includes: Furosemide (Lasix) for diuresis Lithium Carbonate (900-1200mg QD) to inhibit renal response to ADH Demeclocycline Hydrochloride (300 mg QID) to suppress ADH activity

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. 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) 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 - Blood products may be useful for volume expansion - 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 - Urine replacement (cc for cc) - Positive sodium balance - Fludocortisone (enhances sodium reabsorption, can cause hypokalemia)

Treatment

fluid restriction

The following chart provides further lab values to assist in differentiating between SIADH and CSWS: Clinical Manifestations to Monitor ECF volume ( the primary way to differentiate SIADH and CSWS) Hematocrit Albumin concentration BUN/creatinine Potassium Uric acid Treatment CSWS SIADH

Decreased Increased Increased Increased normal or Increased normal or Decreased normal saline

Increased normal normal Decreased normal Decreased

fluid restriction

Clinical Manifestations to Monitor SIADH ECF volume ( the primary way to differentiate SIADH and CSWS) Increased Hematocrit normal Albumin concentration normal BUN/creatinine Decreased Potassium normal Uric acid Decreased