Wacks I, Oster J R, Roth D, Norenberg M, Gardner L B, Perez G O, Burke G, Milgrom M
Clearwater Community Hospital, Florida.
Clin Nephrol. 1992 Jan;37(1):19-22.
We describe a woman whose fatal post-liver transplantation cerebral edema was unexpected and of unusual pathogenesis. Her severe cerebral edema is of considerable pathophysiologic interest: 1) it developed in the setting of marked anasarca and persistent hypernatremia, and 2) although hepatic function was poor, it was not considered sufficiently deranged to induce cerebral edema. Furthermore, there was no histologic evidence of hepatic rejection or antemortem hepatic necrosis. We postulate that an impairment of the blood brain barrier in association with a degree of hepatic dysfunction insufficient by itself to cause cerebral edema permitted the brain interstitial fluid volume to increase pari passu with ECF expansion. Cytotoxic cerebral edema and vascular engorgement may also have contributed to a life-threatening increase in intracranial pressure.
我们描述了一名女性，她在肝移植后发生了致命性脑水肿，这一情况出乎意料且发病机制异常。她严重的脑水肿具有相当大的病理生理学研究价值：1）它在明显全身性水肿和持续性高钠血症的情况下发生；2）尽管肝功能不佳，但并不认为其紊乱程度足以引发脑水肿。此外，没有肝排斥反应或生前肝坏死的组织学证据。我们推测，血脑屏障受损，加之肝功能不全本身程度不足以导致脑水肿，使得脑间质液体积随细胞外液扩张而相应增加。细胞毒性脑水肿和血管充血也可能导致了威胁生命的颅内压升高。
