FIGURE 25.1 Differential diagnosis between cerebral salt wasting (CSW) and syndrome of inappropriate secretion of antidiuretic hormone (SIADH).
Some patients with aSAH become extremely polyuric, and this tends to occur at the peak of cerebral vasospasm. In these situations it is all too common that we get stuck in a vicious circle of giving more crystalloid fluids to compensate for the unrelenting fluid and sodium loss. One must scale back fluid administration to avoid complications such as pulmonary edema or renal medullary washout.
Mineralocorticoids are useful to prevent or ameliorate excessive urinary excretion and hyponatremia in patients with aSAH. Only early initiation (within 72 hours of aneurysm rupture) has been formally tested and proven effective. In placebo-controlled studies, fludrocortisone was associated with fewer side effects than hydrocortisone (which may cause hyperglycemia due to its glucocorticoid activity), but neither medication increased the risk of congestive heart failure. In our practice, we start fludrocortisone (0.2 mg twice daily) early in most patients with aSAH (higher doses of fludrocortisone may be needed in refractory cases).
Hypotonic intravenous fluids (Table 25.1) should be avoided in patients with aSAH, not only because hyponatremia is so frequent but also because these patients are at increased risk of intracranial hypertension. In alert patients tolerating an oral diet, the tonicity and sodium concentration of ingested fluids should also be regulated. These patients usually get thirsty as they become polyuric, and abundant ingestion of water may exacerbate the hyponatremia. In these cases, we have patients drink fluids enriched with high concentrations of sodium (attempting to treat hyponatremia with sodium tablets or salty foods is inefficient).
Intravenous fluid | Sodium content (mmol per liter) |
5% dextrose* | 0 |
0.45% sodium chloride* | 77 |
Ringer’s Lactate* | 130 |
0.9% sodium chloride† | 154 |
1.5% sodium chloride† | 256 |
3% sodium chloride†** | 513 |