To the Editor:

As a PA practicing in neurosurgery, I read with interest the article on intracranial aneurysms and subarachnoid hemorrhage (“Coil or clip? Current trends in the treatment of intracranial aneurysms,” published in February 2009). The author, however, makes a rather substantial error in defining the acronym SIADH as symptoms of inappropriate diuretic hormone.

According to the Handbook of Neurosurgery, 5th ed, which is regarded as an authoritative text on the management of neurosurgery patients, SIADH is an acronym for syndrome of inappropriate antidiuretic hormone secretion (Mark S. Greenburg; New York, NY: Thieme Medical Publishers; 2000:17).

Diagnosis of SIADH is, according to Greenburg, based on three diagnostic criteria: hyponatremia, inappropriately concentrated urine, and no evidence of renal or adrenal dysfunction. The patient will actually have a low serum osmolality (<280 mOsm/L), a low serum sodium (usually <134mEq/L), high urine sodium (as correctly stated by the author), normal BUN and creatinine, and normal adrenal function, with no signs of hypothyroidism or overhydration. Treatment of SIADH varies, depending on whether the disease is acute or chronic.

Patients with acute SIADH, if caused by anemia, usually respond to transfusion. If disease is mild and asymptomatic, fluid restriction may be employed. If severe or symptomatic, hypertonic saline or, if necessary, furosemide are effective.

For patients with chronic SIADH, long-term fluid restriction, furosemide, phenytoin, and demeclocycline are all useful.

Ronald McCall, DFAAPA, MPAS, PA-C
Springfield, Missouri

Author's response:

I would like to acknowledge the errors discovered by Mr. McCalls' fastidious reading of my article. First, SIADH is properly known as syndrome of inappropriate diuretic hormone.

Second, I meant to say that serum osmolality is high or normal in cerebral salt wasting syndrome, whereas serum osmolality is low in SIADH (as indicated in Table 1).

I hope this did not distract from my main point: clinicians should not assume that hyponatemia in a patient with cerebral insult is always caused by SIADH. For a more thorough discussion of this topic, I direct readers to Dr Mark Harrigan's excellent article, “Cerebral salt wasting syndrome: a review” (Neurosurgery. 1996;38[1]:152-160).

Thank you Mr. McCall for your careful inspection!

Robert F. Brach, PA-C