Acute subdural hematoma: is the blood itself toxic?

Recently developed rodent models of acute subdural hematoma have shown an associated large area of infarction underlying the clot. Excitotoxic processes have been postulated to play an important role in the extensive cell death seen with these models. However, whether increased pressure, vasoactive effects, or toxicity of the blood itself is responsible for initiating or sustaining these processes remains unclear. To study the effect of blood itself, an opaque layer of autologous clot was placed on the widely exposed parietal cortex of 15 Long-Evans rats and left in place for 72 h. In control animals the cortical surface was exposed but no blood was placed and contact with blood products was carefully limited. These animals were compared to a group in whom blood was injected into the closed subdural space. Histologic analysis showed that the majority of the cortex in both control and experimental animals in the open cranial model group appeared normal. Scattered small, discrete hemorrhagic lesions on the cortical surface of both control and experimental animals were seen, which had the appearance of focal mechanical trauma or vessel avulsion. There was no significant difference in average volume of lesions between experimental and control animals (9.1 versus 9.7 mm3, p = 0.85). No areas of infarction or selective neuronal loss were seen. In comparison, animals in which blood was injected into the subdural space had significantly larger lesions underlying clot, averaging 133.6 mm3 in volume (p < 0.0003). Blood in prolonged contact with the cortical surface in the absence of increased pressure, ischemia, or other insult is insufficient to cause underlying infarction like that seen when a similar volume of blood is injected into the closed subdural space.