Leinonen Ville, Vanninen Ritva, Rauramaa Tuomas
Department of Neurosurgery, Institute of Clinical Medicine, University of Eastern Finland and Department of Neurosurgery, NeuroCenter, Kuopio University Hospital, Kuopio, Finland.
Department of Radiology, Institute of Clinical Medicine, University of Eastern Finland and Department of Radiology, Kuopio University Hospital, Kuopio, Finland.
Handb Clin Neurol. 2017;145:25-37. doi: 10.1016/B978-0-12-802395-2.00004-3.
Acutely increased intracranial pressure (ICP) is a life-threatening neurosurgical emergency. Optimal management strategy is selected according to the causative process. Typical causes are intracranial bleeds like traumatic subdural, epidural, or intracerebral hematoma (ICH); spontaneous ICH, intraventricular hemorrhage, subarachnoid hemorrhage, and hydrocephalus. When occurring without significant brain injury and treated effectively before herniation, a full recovery can be expected. In intraparenchymal injuries a full recovery is unlikely since dead cells in the central nervous system leave an "empty hole," to be replaced by cerebrospinal fluid. The clinical recovery is based on the surviving cells that are able to make new synapses. Surgery may decrease ICP by removing significant mass effect. In all conditions, when notable injury of brain parenchyma occurs, brain edema may gradually increase ICP and further worsen the clinical condition. This is seen typically in large brain infarctions when the formation of brain edema may lead to increased ICP for hours and days. Brain edema is traditionally classified as vasogenic or cytotoxic but according to current knowledge is rather a continuum, starting with cytotoxic cell swelling followed by ionic edema and then vasogenic edema. Here we review the causes of increased ICP, including mechanisms of brain edema, with clinical examples.
急性颅内压（ICP）升高是一种危及生命的神经外科急症。需根据病因选择最佳治疗策略。典型病因包括颅内出血，如创伤性硬膜下血肿、硬膜外血肿或脑内血肿（ICH）；自发性ICH、脑室内出血、蛛网膜下腔出血和脑积水。如果在无严重脑损伤的情况下发生且在脑疝形成前得到有效治疗，则有望完全康复。在脑实质损伤中，由于中枢神经系统中的死亡细胞会留下一个“空洞”，并由脑脊液填充，因此不太可能完全康复。临床康复取决于存活的能够形成新突触的细胞。手术可通过消除显著的占位效应来降低ICP。在所有情况下，当脑实质发生明显损伤时，脑水肿可能会逐渐升高ICP并进一步恶化临床状况。这在大面积脑梗死中很常见，脑水肿的形成可能会导致ICP在数小时和数天内升高。传统上，脑水肿分为血管源性或细胞毒性，但根据目前的认识，它更像是一个连续过程，始于细胞毒性细胞肿胀，接着是离子性水肿，然后是血管源性水肿。在此，我们结合临床实例回顾ICP升高的原因，包括脑水肿的机制。
