Editorial Comment: Salting the Brain to Improve CBF in SAH Patients
Hypertonic saline solutions (HSs) have been used in various concentrations in patients with intracranial pathologies to treat cerebral edema and elevated intracranial pressure (ICP).1 Since the first animal experiments by Weed and McKibben2 in 1919, many data have been published on the use of HSs in both animal models and human patients with hemorrhagic shock with and without elevated ICP and with isolated intracranial processes. All these studies have shown that HS effectively reduces ICP and cerebral edema with subsequent enhancement of cerebral perfusion pressure. Another beneficial effect of HS is an increase in intravascular volume and therefore maintenance of adequate cardiac output and blood pressure. Several possible mechanisms of action of HS have been reported: reduction in brain water by creation of an osmotic effect to draw water from the brain to the intravascular space; improvement of cerebral blood flow (CBF), presumably by exertion of a dehydrating effect of cerebrovascular endothelium and erythrocytes; restoration of normal membrane resting potential; and reduction in adhesion of polymorphonuclear cells to cerebral microvasculature with attenuation of pial vessel dilatation. Taken together, all these effects may reduce cerebral ischemia and improve cerebral oxygen delivery.
Subarachnoid hemorrhage (SAH) is a devastating condition that carries high morbidity and mortality. A major cause of poor outcome after SAH is the development of cerebral vasospasm with subsequent infarction. Because of the CBF-enhancing properties noted in animal models and its maintenance of adequate intravascular volume, HS may be a good candidate for fluid resuscitation in SAH patients. Despite this evidence, there is a scarcity of studies in this area. In a case series of patients with cerebral vasospasm after SAH, administration of an HS achieved a positive fluid balance and short-term clinical improvement without adverse effects.3 However, CBF was not measured. In this issue of Stroke, Tseng et al4 present an interesting report on the effect of HS on CBF in poor-grade patients with SAH. Although its sample size is small, this attempt represents the first human study investigating this topic. The authors have convincingly found that HS exerts an early CBF-augmenting effect in this patient population. Such a phenomenon was independent of ICP or cerebral perfusion pressure and was present up to 7.5 hours after HS administration. These findings are certainly preliminary but raise the possibility that HS may be useful in situations in which CBF is diminished after SAH. A likely scenario would be in the presence of cerebral vasospasm. Patients can be resuscitated aggressively with HS to achieve hypervolemia and hyperdynamia with the possible added advantage of improved CBF for several hours. This may allow clinicians extra time until a more definitive treatment, ie, cerebral angioplasty, is carried out. Alternatively, HS administration may lead to sustained clinical improvement, thus avoiding further invasive treatments. Until such evidence becomes available, I agree with the authors that further studies are needed to elucidate the effects of HS on cerebral metabolism and long-term clinical outcome in these patients. This is even more pressing and important when we consider that cerebral vasospasm after SAH is associated with a 30% mortality rate.5