Shigemori M, Ogata T, Shirahama M, Tokutomi T, Kusano N, Nakajima O
No Shinkei Geka. 1981;9(3):331-5.
A case of severe head injury associated with fulminant pulmonary edema considered as neurogenic which developed within short time after the injury was presented. A five-year-old boy who had no previous history of cardiopulmonary disease was struck on his right frontal region by car accident at 15.30 PM on July 5 of 1979. Immediately after the impact he lost his consciousness and subsequently transferred to a local hospital where bilateral dilated pupil and flaccid paralysis of the limbs were noted. On transmission of the patient to Omuta City Hospital 30 minutes after the injury, massive foamy fluid was discharged from the tracheal tube. On admission, he was comatous, with bilateral dilated and fixed pupils and flaccid paralysis of the limbs. There was no retinal bleeding. He showed ataxic respiration with severe stridor and massive discharge of foamy fluid pinkish in colour from the trachea characteristic in pulmonary edema was significant. Chest x-ray film demonstrated perihilar densities suggesting pulmonary edema. CT scan showed extremely small ventricle on both sides without manifestations of intracranial hematomas or cerebral contusion. With an intensive medical treatments including corticosteroids, alkalizing agents and alpha-blocker were administered under controlled respiration, the discharge of edema fluid was gradually decreased and the findings on blood gases were also improved. However neurological signs were aggravated and he died 8 hours after the injury. Central venous pressure was maintained at the level between 8 to 10 cm. From these clinical findings the pulmonary edema was concluded as neurogenic. Direct or indirect injury to the hypothalamic efferent pathway at the level of lower brain stem seemed to be important as the cause of neurogenic pulmonary edema in this case. The possible pathophysiology of neurogenic pulmonary edema associated with brain stem injury and intracranial hypertension was discussed with other related literature.
本文报告1例重型颅脑损伤合并暴发性肺水肿,伤后短时间内即发展为神经源性肺水肿。1979年7月5日下午3时30分,一名既往无心肺疾病史的5岁男孩在车祸中右额部受撞击。受伤后立即昏迷,随后被转至当地医院,当时发现双侧瞳孔散大,四肢弛缓性瘫痪。受伤30分钟后转至大牟田市立医院时,气管导管内有大量泡沫样液体流出。入院时,患者昏迷,双侧瞳孔散大且固定,四肢弛缓性瘫痪。无视网膜出血。患者出现共济失调性呼吸,伴有严重喘鸣,气管内大量粉红色泡沫样液体流出,这是肺水肿的典型表现。胸部X线片显示肺门周围密度增高,提示肺水肿。CT扫描显示双侧脑室极小,无颅内血肿或脑挫伤表现。在控制呼吸下给予包括皮质类固醇、碱化剂和α受体阻滞剂在内的强化治疗,水肿液的流出逐渐减少,血气结果也有所改善。然而,神经体征加重,患者于伤后8小时死亡。中心静脉压维持在8至10厘米水柱之间。根据这些临床表现,诊断为神经源性肺水肿。在本病例中,脑干下部水平的下丘脑传出通路的直接或间接损伤似乎是神经源性肺水肿的重要原因。结合其他相关文献,讨论了与脑干损伤和颅内高压相关的神经源性肺水肿的可能病理生理学。