Jafari Neda, Gesner Lyle, Koziol Joseph M, Rotoli Giorgio, Hubschmann Otakar R
Department of Neurosurgery, Saint Barnabas Medical Center, Livingston, New Jersey, USA.
Department of Radiology, Saint Barnabas Medical Center, Livingston, New Jersey, USA.
World Neurosurg. 2017 Nov;107:376-381. doi: 10.1016/j.wneu.2017.07.108. Epub 2017 Jul 25.
The origin of chronic subdural hematomas (CSDH) and the pathophysiology of its enlargement remain unknown. The chemical fluid composition of CSDH, the contribution of cerebrospinal fluid (CSF) to its enlargement, and the relationship to its appearance on computed tomography (CT) also are not entirely clear.
In this prospective study, 58 samples in 41 patients treated surgically for CSDH were analyzed. CSDHs were evaluated for the presence of CSF via β-2 transferrin and substances related to cell breakdown and hemolysis. These were compared with normal value of those substances in the serum and the CT appearances of the CSDH.
In this study, 24% of the samples contained β-2 transferrin, which was statistically significant. Total protein, lactate dehydrogenase, total bilirubin, and red blood cells also were statistically different when compared with their normal serum concentration, indicating an active process of rebleeding and hemolysis rather than plasma ultrafiltration; however, their concentrations did not correlate with specific CT scan appearance. The absence of CSF in CSDH in 76% of cases did not support the theory that most CSDHs originate from subdural hygromas. The presence of hemolysis and cell breakdown, byproducts supports the hypothesis that the primary enlargement of CSDH develops through neomembrane and neovascular formation, rebleeding, and inhibition of the blood coagulation process. Our study did not test for serum transudation as a component of the enlargement of CSDH.
Our study confirms that the origin and enlargement of CSDH is multifactorial, but the contribution of individual factors and condition under which it occurs still remains unclear. CT scan findings do not correlate with the chemical composition or the presence of CSF in the CSDH.
慢性硬膜下血肿（CSDH）的起源及其扩大的病理生理学仍不清楚。CSDH的化学液体成分、脑脊液（CSF）对其扩大的作用以及与计算机断层扫描（CT）表现的关系也不完全清楚。
在这项前瞻性研究中，分析了41例接受CSDH手术治疗患者的58个样本。通过β-2转铁蛋白以及与细胞分解和溶血相关的物质评估CSDH中CSF的存在情况。将这些与血清中这些物质的正常值以及CSDH的CT表现进行比较。
在本研究中，24%的样本含有β-2转铁蛋白，具有统计学意义。与正常血清浓度相比，总蛋白、乳酸脱氢酶、总胆红素和红细胞也有统计学差异，表明存在再出血和溶血的活跃过程而非血浆超滤；然而，它们的浓度与特定的CT扫描表现无关。76%的CSDH病例中不存在CSF，这并不支持大多数CSDH起源于硬膜下积液的理论。溶血和细胞分解副产物的存在支持了CSDH原发性扩大是通过新膜和新血管形成、再出血以及凝血过程受抑制而发生的假说。我们的研究未检测血清渗出作为CSDH扩大的一个组成部分。
我们的研究证实CSDH的起源和扩大是多因素的，但各个因素的作用以及其发生的条件仍不清楚。CT扫描结果与CSDH的化学成分或CSF的存在无关。
