Cerebral Salt Wasting

By | 2022-02-03T17:29:26-05:00 January 28th, 2008|0 Comments

Patients with brain hemorrhages caused by injuries, infections, tumors, or stroke risk a serious decline in serum sodium that can cause unconsciousness, seizure, and stroke if not caught early enough.

This form of hyponatremia is called cerebral salt wasting (CSW), and 30% of patients with bleeding in the area between the brain and the membranes that cover the brain — subarachnoid hemorrhage — develop the problem, according to author M.R. Harrigan in the “Neurological Medicine Pocketbook.” Especially so for those with aneurysms of the anterior communicating artery, the small blood vessel that bridges the two larger anterior cerebral arteries. This is one of the most common sites of aneurysm in the brain.

Tampa General Hospital’s neurosciences ICU has seen a few cases of CSW following subarachnoid hemorrhage. The patients had large urinary outputs per hour and serum sodiums were dangerously low, in the 120s. Salt tabs were initiated and, in some cases, 3% saline IVs were started. Every six hours, the patients had serum and urine sodiums, and serum and urine osmolalities to make certain that the serum sodium levels were increasing. Serum sodiums are generally kept between 150mEq/L and 160mEq/L.

The 3% saline is discontinued when serum sodium levels reach 160mEq/L
or when serum osmolalities reach 320mOsm/kg.

The patients with low serum sodiums were tachycardic and volume depleted. They had increased urinary outputs, decreased weights or no weight gain, increased BUN and creatinines, and dry mucous membranes.

All patients resolved their CSW with normal sodium levels. Salt tabs or 3% saline were discontinued. The patients moved out of the neurosciences ICU.

Identifying the condition

Symptoms CSW include weakness, lethargy, confusion and seizures.

The peak time for onset is in the first week of vasospasm, the exaggerated, persistent contraction of the walls of a blood vessel occuring from the third to the 10th day after a subarachnoid hemorrhage. Without perfusion to these areas of the brain, there is an increased chance of infarction. Hypoosmolality, a state of excess of water, can lead to further cerebral edema, which can worsen the effects of strokes caused
by vasospasms.

CSW is renal loss of sodium along with a depletion of extracellular fluid volume. Some scientists, including E. Braunwald in “Harrison’s Principles of Internal Medicine,” theorize that the amino acid brain natriuretic peptide (BNP) becomes elevated following subarachnoid hemorrhage and vasospasm. BNP dilates blood vessels, causing sodium and fluid excretion, which reduces circulating levels of blood-pressure-regulating hormones aldosterone and renin. BNP is stored in the hypothalamus, so if the hypothalamus is injured, CSW could develop.

It also has been suggested that the body releases BNP as a protective measure against increased intracranial pressure, or as a result of stress from surgery or a stay in the ICU.

Sodium losses could worsen volume depletion in patients with CSW, increasing the risk for ischemia and stroke.

Caution — diagnosis pitfall!

Sodium deficiency also may be due to syndrome of inappropriate secretion of antidiuretic hormone (SIADH), which warrants very different treatment, so correct diagnosis is essential.

In CSW, the patient is hyponatremic, serum uric acid is normal or reduced, BUN and creatinine are increased, urinary output is high and very dilute, urine sodium is >40mEq/L, urine osmolality is high, the patient is hypovolemic with a low CVP, and has no weight gain. Low blood pressure, elevated hematocrit, and decreased skin turgor also are signs that CSW is present.

In SIADH, the patient is also hyponatremic, but uric acid is decreased, BUN and creatinine are decreased, urine is concentrated, there is weight gain due to fluid retention, low serum osmolality, and hematocrit is normal. Management is fluid restriction, which would worsen CSW. Drug therapy may also be used, such as furosemide, demeclocycline hydrochloride (an ADH suppressant), or lithium carbonate (a renal antagonist to ADH).

Management of the condition

Management of CSW is to control intracranial pressure, hydrocephalus, and seizures, and to replace volume. According to Kristi Hudson, RN, MSN, CCRN, director of education for Dynamic Nursing Education, an IV solution of 0.9% saline is initiated, with blood products for anemia and colloids for volume expansion. Salt tablets by mouth or 3% IV saline may be given to increase sodium levels.

Correcting the sodium level is always done slowly so as not to cause the neurological disorder central pontine myelinolysis, which is potentially fatal nerve damage caused by the destruction of the myelin sheath covering nerve cells in the brainstem. Fludrocortisone promotes sodium reabsorption by acting on the renal tubules. Close monitoring of intake and output, central venous pressure, and wedge pressure as used in a Swan Ganz catheter are necessitated.

CSW is self-limited, which means that it will resolve within three to four weeks. Usually there are no lasting effects.

Christie Soper, RN, BA, CCRN, CNRN, works in the Tampa (Fla.) General Hospital in the neurosciences ICU.

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