Miller Jimmy D, Nader Remi
Division of Neurosurgery, Greenwood Leflore Hospital, Greenwood, Mississippi;
J Neurosurg. 2014 Jun;120(6):1378-84. doi: 10.3171/2013.10.JNS13272. Epub 2013 Dec 6.
Most acute subdural hematomas (ASDHs) develop after rupture of a bridging vein or veins. The anatomy of the bridging vein predisposes to its tearing within the border cell layer of the dura mater. Thus, the subdural hematoma actually forms within the dura. The hematoma grows by continued bleeding into the border cell layer. However, the venous pressure would not be expected to cause a large hematoma. Therefore, some type of mechanism must account for the hematoma's expansion. Cerebral venous pressure (CVP) has been demonstrated in animal models to be slightly higher than intracranial pressure (ICP), and CVP tracks the ICP as pressure variations occur. The elevation of CVP as the ICP increases is thought to result from an increase in outflow resistance of the terminal portion of the bridging veins. This probably results from a Starling resistor model or, less likely, from a muscular sphincter. A hypothesis is derived to explain the mechanism of ASDH enlargement. Tearing of one or more bridging veins causes these vessels to bleed into the dural border cell layer. Subsequent ICP elevation from the ASDH, cerebral swelling, or other cause results in elevation of the CVP by increased outflow resistance in the intact bridging veins. The increased ICP causes further bleeding into the hematoma cavity via the torn bridging veins. Thus, the ASDH enlarges via a positive feedback mechanism. Enlargement of an ASDH would cease as blood within the hematoma cavity coagulates. This would stop the dissection of the dural border cell layer, and pressure within the hematoma cavity would equalize with that in the torn bridging vein or veins.
大多数急性硬膜下血肿（ASDHs）是在桥静脉破裂后形成的。桥静脉的解剖结构使其易于在硬脑膜的边界细胞层内撕裂。因此，硬膜下血肿实际上是在硬脑膜内形成的。血肿通过持续出血进入边界细胞层而增大。然而，静脉压力预计不会导致大的血肿。因此，必须有某种机制来解释血肿的扩大。在动物模型中已证明脑静脉压（CVP）略高于颅内压（ICP），并且随着压力变化，CVP会跟踪ICP。随着ICP升高，CVP升高被认为是由于桥静脉末端流出阻力增加所致。这可能是由斯塔林电阻模型引起的，或者不太可能是由肌肉括约肌引起的。由此得出一个假设来解释ASDH扩大的机制。一条或多条桥静脉的撕裂导致这些血管向硬脑膜边界细胞层出血。随后，由于ASDH、脑肿胀或其他原因导致的ICP升高，通过完整桥静脉流出阻力的增加导致CVP升高。升高的ICP通过撕裂的桥静脉导致进一步出血进入血肿腔。因此，ASDH通过正反馈机制扩大。随着血肿腔内的血液凝固，ASDH的扩大将停止。这将阻止硬脑膜边界细胞层的剥离，并且血肿腔内的压力将与撕裂的一条或多条桥静脉内的压力相等。
