Department of Neurosurgery, Faculty of Medicine, Amasya University, Amasya, Turkey.
Department of Neurosurgery, Faculty of Medicine, Ataturk University, Erzurum, Turkey.
World Neurosurg. 2018 Jul;115:e476-e481. doi: 10.1016/j.wneu.2018.04.075. Epub 2018 Apr 20.
Subarachnoid hemorrhage (SAH) may be a cause of neurogenic pulmonary edema (NPE). It is well known that lymphatic fluid draining by thoracic duct to lungs consists of many dangerous metabolites, degraded tissue particles, and microbiologic pathogens. However, not enough studies have investigated whether NPE causes septicemia or not. In this study, we retrospectively examined our experimental materials to determine whether there is a meaningful relationship between NPE and cerebral abscess formation.
Forty-two rabbits were divided into 3 groups: Control (n = 5), SHAM (n = 7), and SAH (n = 30) with severe neurogenic lung edema detected in rabbits. The SHAM and SAH groups received 1 mL saline and 1 mL autologous arterial blood into the Sylvian cisterna, respectively. Weight, heartbeat, respiration rate, and blood pressure were recorded by routinely using monitoring devices. All multilevel lungs and brain tissue microsections were examined by stereologic and Cavalier methods. For statistical analysis, NPE criteria and the numbers of abscess or abscess resembling cores in the brains were estimated in all groups and compared. The Mann Whitney-U test was used to analyze the results statistically.
All rabbits were around 4 years old; body weight was between 3.94 and 4.5 kg; normal heart rhythm rate was found between 251 ± 39/minutes and 281 ± 30/minutes; and respiration rate was between 24 ± 5/minutes and 36 ± 7/minutes. Histopathologic examinations showed that abscess formations frequently spread in middle cerebral arterial territories of all animals in the NPE-detected rabbits. While average abscess numbers were estimated as 3 ± 1 in 7 animals (n = 7; P < 0.005) in severe NPE-detected rabbits, only 1 ± 1 abscess core was detected in a less severe NPE that developed in 3 (n = 3; P < 0.05) animals. The vasospasm index values of pulmonary arteries (PAs) of all animals were 1.233 ± 0.065 in the control group; 1.567 ± 0.0430 in the SHAM group, and 2.890 ± 0.0453 in the SAH group (P < 0.05).
This experimental study showed that NPE is a relatively common pathology following experimental SAH in rabbits. The NPE is frequently complicated with brain abscess as shown in this study. The pathophysiologic mechanism was concluded, as NPE may be responsible for cerebral abscess development via bacteria/cytotoxic particles conveyed by thoracic duct to lungs and transferred from the ruptured alveoli-capillary membrane to the brain by way of systemic circulation.
蛛网膜下腔出血（SAH）可能是神经源性肺水肿（NPE）的一个原因。众所周知，通过胸导管引流到肺部的淋巴液中含有许多危险的代谢物、降解的组织颗粒和微生物病原体。然而，还没有足够的研究来调查 NPE 是否会引起败血症。在这项研究中，我们回顾了我们的实验材料，以确定 NPE 是否与脑脓肿形成之间存在有意义的关系。
42 只兔子被分为 3 组：对照组（n=5）、假手术组（n=7）和 SAH 组（n=30），在兔子中检测到严重的神经源性肺水肿。假手术组和 SAH 组分别向侧脑池内注入 1 毫升生理盐水和 1 毫升自体动脉血。通过常规使用监测设备记录体重、心跳、呼吸频率和血压。使用立体学和 Cavalier 方法对所有多层肺组织和脑组织切片进行检查。为了进行统计分析，在所有组中估计了 NPE 标准和脑脓肿或类似脓肿核心的数量，并进行了比较。使用 Mann Whitney-U 检验对结果进行统计学分析。
所有兔子年龄均在 4 岁左右；体重在 3.94 至 4.5 千克之间；正常的心律率在 251±39/分钟至 281±30/分钟之间；呼吸频率在 24±5/分钟至 36±7/分钟之间。组织病理学检查显示，在所有 NPE 检测到的兔子中，脓肿形成经常在大脑中动脉区域扩散。在严重 NPE 检测到的 7 只动物中（n=7；P<0.005），平均脓肿数量估计为 3±1，而在 3 只动物中（n=3；P<0.05）仅检测到一个较轻的 NPE 发展中的 1±1 个脓肿核心。所有动物的肺动脉（PA）的血管痉挛指数值在对照组中为 1.233±0.065；在假手术组中为 1.567±0.0430，在 SAH 组中为 2.890±0.0453（P<0.05）。
这项实验研究表明，NPE 是兔蛛网膜下腔出血后一种相对常见的病理。正如本研究所示，NPE 常伴有脑脓肿。结论为，NPE 可能通过胸导管向肺部输送细菌/细胞毒性颗粒，并通过全身循环从破裂的肺泡-毛细血管膜转移到大脑，从而导致脑脓肿的发展。
