Ichai C, Ciais J F, Grimaud D
Département d'anesthésie-réanimation, hôpital Saint-Roch, Nice, France.
Ann Fr Anesth Reanim. 1997;16(4):435-44. doi: 10.1016/s0750-7658(97)81476-1.
Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral tissue depends on the osmotic pressure gradient. When it is injured, water movements across the BBB depend on the hydrostatic pressure gradient. CBV depends essentially on cerebral blood flow (CBF), which is strongly regulated by cerebral vascular resistances. In experimental studies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoosmolarity increases cerebral water content and therefore ICP, if the BBB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. On the other hand, hypooncotic solutes do not modify ICP. The osmotic therapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An i.v. perfusion of 0.25 g.kg-1 is administered over 20 minutes when ICP increases. Hypertonic saline solutes act in the same way, however they are not more efficient than mannitol. CO2 is the strongest modulating factor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decreases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia. Hyperthermia is an aggravating factor for ICHT, whereas moderate hypothermia seems to be beneficial both for ICP and cerebral metabolism. Hyperglycaemia has no direct effect on cerebral volume, but it may aggravate ICHT by inducing cerebral lactic acidosis and cytotoxic oedemia. Therefore, infusion of glucose solutes is contra-indicated in the first 24 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.
颅内压取决于脑组织体积、脑脊液体积（CSFV）和脑血容量（CBV）。生理情况下，它们的总和是恒定的（Monro-Kelly 方程），颅内压保持稳定。当血脑屏障（BBB）完整时，脑组织体积取决于渗透压梯度。当它受损时，水通过血脑屏障的移动取决于静水压力梯度。脑血容量主要取决于脑血流量（CBF），而脑血流量受脑血管阻力的强烈调节。在实验研究中，血浆胶体渗透压降低并不会增加脑水肿和颅内高压（ICHT）。另一方面，如果血脑屏障完整，血浆低渗会增加脑含水量，进而增加颅内压。如果血脑屏障受损，低渗和低胶体渗透压都不会改变脑水肿。因此，所有低渗溶质都可能加重脑水肿，在颅内高压情况下是禁忌的。另一方面，低胶体渗透压溶质不会改变颅内压。渗透疗法是急性颅内高压最重要的治疗手段之一。甘露醇仍然是首选治疗药物。它起效非常快。当颅内压升高时，以 0.25 g·kg⁻¹ 的剂量静脉输注，在 20 分钟内完成。高渗盐溶质的作用方式相同，但它们并不比甘露醇更有效。二氧化碳是脑血流量最强的调节因子。低碳酸血症通过引起脑血管收缩，降低脑血流量和脑血容量。过度通气是降低颅内压的一种有效且快速的方法。然而，如果没有适当的监测，不能系统性地使用，因为低碳酸血症可能加重脑缺血。高热是颅内高压的一个加重因素，而适度低温似乎对颅内压和脑代谢都有益。高血糖对脑体积没有直接影响，但它可能通过诱导脑乳酸酸中毒和细胞毒性水肿而加重颅内高压。因此，在头部创伤后的最初 24 小时内禁忌输注葡萄糖溶质，在颅内高压发作期间必须密切监测和控制血糖浓度。
