您好, 访客   登录/注册

中青年患者轻度颅脑损伤后形成慢性硬膜下血肿的危险因素

来源:用户上传      作者:

  摘要:目的  探討中青年患者轻度颅脑损伤后形成慢性硬膜下血肿的危险因素。方法  回顾性分析2018年1月~2019年5月安徽省立医院收治的轻度颅脑损伤患者236例,根据年龄分为青年组(18~44岁)116例和中年组(45~60岁)120例,另根据头颅CT复查结果将两个年龄组患者进一步分成CSDH患者和无CSDH患者,分析年龄组中CSDH患者和无CSDH患者各临床指标与慢性硬膜下血肿形成的关系,并采用Logistic回归分析不同年龄组创伤后CSDH形成的因素,采用ROC曲线分析脑实质距颅骨最大距离(Dm)预测CSDH形成的准确性。结果  青年组CSDH患者与无CSDH患者的Dm、蛛网膜囊肿、颅骨骨折及急性硬膜外血肿占比比较,差异有统计学意义(P<0.05);中年组CSDH患者与无CSDH患者的Dm、蛛网膜囊肿、颅骨骨折及急性硬膜外血肿、高血压、糖尿病、抗凝/抗血小板治疗占比、吸烟饮酒量比较,差异有统计学意义(P<0.05)。多因素Logistic回归分析显示,Dm、颅骨骨折及蛛网膜囊肿是青年患者创伤后CSDH形成的独立危险因素;Dm、颅骨骨折、高血压及抗凝/抗血小板治疗是中年患者创伤后CSDH形成的独立危险因素。ROC曲线分析显示,青年组曲线下面积为0.780,最佳截断值为3.5 mm,预测CSDH形成敏感度为58.33%,特异性为86.96%;中年组ROC曲线下面积为0.855,最佳截断值为2.6 mm,预测CSDH形成敏感度为90.00%,特异性为80.00%。结论  青年患者创伤后形成慢性硬膜下血肿的独立危险因素是脑实质与颅骨间的最大距离、颅骨骨折及蛛网膜囊肿;中年患者独立危险因素是脑实质与颅骨间的最大距离、颅骨骨折、抗凝/抗血小板治疗及高血压。同时青年患者硬膜外血肿,中年患者硬膜外血肿、蛛网膜囊肿、糖尿病、饮酒及吸烟亦与创伤后慢性硬膜下血肿的形成有相关性,有以上临床特征者应加强临床随访。
  关键词:颅脑损伤;慢性硬膜下血肿;危险因素
  中图分类号:R651.1                               文献标识码:A                                   DOI:10.3969/j.issn.1006-1959.2020.09.019
  文章编号:1006-1959(2020)09-0062-05
  Risk Factors for the Formation of Chronic Subdural Hematoma in Young
  and Middle-aged Patients with Mild Head Injury
  YIN Sheng,WANG Yang,DONG Yong-fei,BAO De-jun,WEI Xiang-pin
  (Department of Neurosurgery,Provincial Hospital Affiliated to Anhui Medical University,Hefei 230036,Anhui,China)
  Abstract:Objective  To explore the risk factors of chronic subdural hematoma in young and middle-aged patients after mild head injury.Methods A retrospective analysis of 236 patients with mild craniocerebral injury admitted to Anhui Provincial Hospital from January 2018 to May 2019 was divided into youth group (18 to 44 years old) 116 cases and 120 patients in the middle-aged group (45 to 60 years old) ,which were further divided into CSDH patients and patients without CSDH according to the results of head CT review.The relationship between the clinical indicators and the formation of SCDH in the two age  groups were analyzed.The logistical regression was used to further evaluate the statistically significant indicators in different age  groups, and the ROC curve was used to analyze the accuracy of predicting the formation of CSDH by the maximum distance(Dm) of the brain parenchyma from the skull.Results  The proportions of Dm, arachnoid cyst, skull fracture and acute epidural hematoma in CSDH patients and those without CSDH were statistically significant(P<0.05); The difference in Dm, arachnoid cyst, skull fracture and acute epidural hematoma, hypertension, diabetes, anticoagulation/antiplatelet therapy, smoking and alcohol consumption between CSDH patients and patients without CSDH in the middle-aged group was statistically significant(P<0.05).Multivariate Logistic regression analysis showed that Dm, skull fractures and arachnoid cysts were independent risk factors for the formation of post-traumatic CSDH in young patients; Middle-aged patients independent risk factors for the formation of post-trauma CSDH included Dm, skull fracture, hypertension and anticoagulation/antiplate therapy.ROC curve analysis showed that the area under the curve of the youth group was 0.780, and the best cut-off value was 3.5 mm. The sensitivity of CSDH formation was 58.33% and the specificity was 86.96%.The area under the ROC curve of the middle-aged group was 0.855, and the optimal cutoff value was 2.6 mm. The sensitivity of CSDH formation was predicted to be 90.00%, and the specificity was 80.00%.Conclusion  The independent risk factors for chronic subdural hematoma after trauma in young patients are the maximum distance between brain parenchyma and skull, skull fracture and arachnoid cyst; the independent risk factors for middle-aged patients are the maximum distance between brain parenchyma and skull, skull fracture, anticoagulant/antiplatelet therapy and hypertension. At the same time, young patients with epidural hematoma, middle-aged patients with epidural hematoma, arachnoid cyst, diabetes, drinking and smoking are also associated with the formation of chronic subdural hematoma after trauma. Those with above clinical features should strengthen clinical follow-up.   Key words:Head injury;Chronic subdural hematoma;Risk factors
  外伤性颅脑损伤(traumatic brain injury,TBI)是神经外科主要急重症之一,其中轻型占据大部分,因其临床症状轻微,甚至无明显症状[1],常被忽视,尤其是中青年人。輕度颅脑损伤是神经外科常见疾病之一,也是慢性硬膜下血肿(chronic subdural hematoma,CSDH)的重要诱因,大多数CSDH患者有外伤病史[2],多数患者病程进展缓慢,早期常无明显症状,或仅有轻微头痛,未能及时就诊,逐渐进展可出现记忆减退、偏瘫、意识障碍甚至脑疝[2]。本文旨在探讨中青年患者轻度颅脑损伤后形成CSDH的危险因素,为临床诊疗提供依据,现报道如下。
  1资料与方法
  1.1一般资料  回顾性分析2018年1月~2019年5月安徽省立医院神经外科因有头颅CT有阳性表现的轻度颅脑外伤入院的中青年患者236例。按年龄分成青年患者组(18~44岁)116例,男性83例,女性33例;中年患者组(45~60岁)120例,男性86例,女性34例。纳入标准为:①年龄18~60岁;②入院GCS评分13~15分,为轻度颅脑损伤[3];③相关病历资料完备(部分患者致伤不明也纳入其中)。排除标准:①住院治疗过程中颅脑损伤程度加重,进展为中、重度;②在随访期间再次受到颅脑损伤;③患者失访。
  1.2方法  收集患者临床资料,包括年龄、性别、致伤原因及机制、基础疾病包括高血压、糖尿病、脑梗等,抗凝/抗血小板治疗史,既往脑部手术史,吸烟及饮酒史、CT阳性表现包括颅骨骨折、急性硬膜外血肿、急性硬膜下血肿、创伤性硬膜下积液、脑内血肿、蛛网膜下腔出血、蛛网膜囊肿及脑实质距颅骨最大距离(Dm,图1)。随访3个月,复查头颅CT资料,根据是否有CSDH形成将两个年龄组患者进一步分成CSDH患者和无CSDH患者。
  1.3统计学方法  采用SPSS 24.0统计软件进行数据分析,计量资料以(x±s)表示,采用t检验或Fisher精确检验;计数资料以[n(%)]表示,采用?字2检验或Fisher精确检验。采用多因素Logistic回归分析创伤后CSDH形成的因素。采用GraphPad Prism 5.0软件作ROC曲线。以P<0.05为差异有统计学意义。
  2结果
  2.1不同年龄组中有无CSDH临床特征比较  青年组中CSDH患者24例,中年组中CSDH患者20例。青年患者中CSDH与无CSDH患者的Dm、蛛网膜囊肿、颅骨骨折及急性硬膜外血肿占比比较,差异有统计学意义(P<0.05);中年组中CSDH与无CSDH患者的Dm、蛛网膜囊肿、颅骨骨折及急性硬膜外血肿、高血压、糖尿病、抗凝/抗血小板治疗占比、吸烟饮酒量比较,差异有统计学意义(P<0.05),见表1。
  2.2不同年龄组创伤后CSDH形成的多因素分析  Dm、颅骨骨折及蛛网膜囊肿是青年患者创伤后CSDH形成的独立危险因素(P<0.05);Dm、颅骨骨折、高血压及抗凝/抗血小板治疗是中年患者创伤后CSDH形成的独立危险因素(P<0.05),见表2。
  2.3 Dm预测CSDH形成的准确性分析  为进一步揭示Dm与CSDH关系,ROC曲线分析显示,青年组曲线下面积为0.780,最佳截断值为3.5 mm,预测CSDH形成敏感度为58.33%,特异性为86.96%。中年组ROC曲线下面积为0.855,最佳截断值为2.6 mm,预测CSDH形成敏感度为90.00%,特异性为80.00%,见图2。
  3讨论
  CSDH形成的机制目前尚未完全阐明,早期认为外伤后从脑实质引流到硬脑膜静脉窦的桥静脉撕裂出血,血肿逐渐积聚形成CSDH[4],但此理论不能很好地解释血肿缓慢进展的过程。有研究提出[5],硬脑膜内面的硬脑膜边界细胞(dural border cells)损伤,启动了炎症反应,促使硬脑膜边界细胞增生,形成包裹血肿的包膜,其壁层上有着丰富的不成熟的毛细血管,易反复渗血。CSDH形成的本质是血肿积聚的趋势超过了吸收[5],在此过程中有众多因素参与。有研究表明[6-8],脑萎缩、创伤性硬膜下积液、抗凝/抗血小板治疗、高血压、糖尿病、脑梗、脑部手术史、饮酒等是老年人创伤后CSDH形成的重要影响因素。目前有关CSDH危险因素的研究人群大多为老年人,而关于中青年创伤后CSDH形成的危险因素研究较少,但中青年作为颅脑外伤的重要人群,了解其创伤后CSDH形成的危险因素,有助于早期发现CSDH,早期干预治疗,对于改善中青年患者预后具有重要意义。
  本研究结果显示,青年组中CSDH与无CSDH患者的年龄、性别、受伤原因、受伤机制、急性硬膜下血肿、创伤性硬膜下积液、蛛网膜下腔出血、脑内出血、高血压、糖尿病、脑梗、抽烟、饮酒比较,差异无统计学意义(P>0.05);青年患者中CSDH与无CSDH患者的Dm、蛛网膜囊肿、颅骨骨折及急性硬膜外血肿占比比较,差异有统计学意义(P<0.05)。中年组中CSDH与无CSDH患者的年龄、性别、受伤原因、受伤机制、急性硬膜下血肿、创伤性硬膜下积液、蛛网膜下腔出血、脑内出血、脑梗、脑外伤术后、脑积水比较,差异无统计学意义(P>0.05);中年组中CSDH与无CSDH患者的Dm、蛛网膜囊肿、颅骨骨折及急性硬膜外血肿、高血压、糖尿病、抗凝/抗血小板治疗占比、吸烟饮酒量比较,差异有统计学意义(P<0.05)。多因素Logistic回归分析显示,Dm是青、中年创伤后CSDH形成的独立危险因素(P<0.05)。硬膜下腔隙的存在是CSDH基础之一[9],其大小以脑实质距颅骨的最大距离来量化。Dm作为青、中年患者创伤后CSDH形成的独立危险因素,同时其数值3.5、 2.6 mm可作为预测青、中年患者创伤后CSDH形成的一个较准确指标。硬膜下腔隙成因最常见的为脑萎缩,脑萎缩与年龄增长相关,在50岁以上的人群中,大脑的质量可减少近200 g,导致脑外容积增加多达11%[10]。在有充足的硬膜下空间的患者中,大脑在颅腔内活动度大,轻微的损伤即可使边界细胞层分离,桥静脉拉紧撕裂。虽然脑萎缩在老年人中更为明显,但有研究表明[6],在低于65岁患者中,脑萎缩与CSDH的相关性甚至更为显著。创伤性硬膜下积液亦是硬膜下腔增大的常见原因之一。有研究显示[11],积液演变成CSDH的比率在11.6%~58%[12],但这种演变多发生在10岁以下儿童或60岁以上老人。而本研究结果显示,中、青年组中CSDH与无CSDH患者的硬膜下积液比较,差异无统计学意义(P>0.05),可能是因为中、青年患者因脑组织相对饱满,硬膜下积液一般不多,因此对CSDH影响较小。   此外,本研究结果显示,存在颅骨骨折是青、中年创伤后CSDH形成的独立危险因素(P<0.05)。对于此因素,目前尚未发现有相关研究者进行探讨,推测可能是外力使颅骨形变移位的过程中,硬脑膜边界细胞及桥静脉损伤的可能性更大,从而形成CSDH,但具体机制还需进一步研究验证。急性硬膜外血肿也是影响青、中年患者CSDH形成的危险因素,可能与硬膜外血肿多因外伤致颅骨骨折撕裂脑膜中动脉或静脉出血所致有关[22]。蛛网膜囊肿是一种先天性发育异常病变,年轻人多见[13],被认为是年轻患者特有的CSDH危险因素。外伤后硬脑膜与蛛网膜囊肿之间的桥静脉或其上横行的静脉撕裂是CSDH形成的基础;同时,蛛网膜撕裂,脑脊液流入硬膜下腔,可促进边界细胞增生,包膜形成[14,15]。本研究中蛛网膜囊肿是青年患者创伤后CSDH的独立危险因素,同时在中年患者中,蛛网膜囊肿亦与创伤后CSDH形成相关。研究表明,蛛网膜囊肿在普通人群发病率为0.3%~2.6%[14],蛛网膜囊肿患者继发CSDH的发生率约4.6%[15],蛛网膜囊肿合并CSDH在临床中是相当少见的病例。因此,目前大多数对于蛛网膜囊肿相关的CSDH研究,均为病案报道[14],其作为CSDH形成的危险因素的证据并不充分。本研究中高血压是中年患者创伤后CSDH形成的独立危险因素。血脑屏障可隨年龄增大逐渐受到损害,此时高血压可导致更高的颅内压,Johnston IH等[16]研究表明,颅内压升高可导致脑内静脉内压力的升高。因而高血压患者中桥静脉压力较高,受伤时更易撕裂出血。同时,更高的血压使得血肿壁毛细血管静水压更高,增加了其反复出血的可能性和出血量[17]。而高血压在青年患者中较少见,且年纪较轻,血脑屏障完整,其对青年患者影响小。
  近年来CSDH发病率增高部分归因于抗凝、抗血小板治疗在老年人的广泛应用[18]。一般认为,不同药物虽然影响凝血过程的机制不同,但均阻碍了颅内小血管渗血的凝血过程,促进了血肿的扩大[8,18]。本研究结果显示,抗凝/抗血小板治疗是中年患者CSDH的独立危险因素。临床中,服用抗凝或抗血小板药物者一般为缺血性心脏病、脑血管疾病、静脉血栓形成、心脏换瓣术后等患者,这些疾病一般多见于年纪较大人群中,青年人少见。本研究青年组患者无抗凝/抗血小板药物服药史,因而此指标对青年患者无影响。本研究中糖尿病、饮酒及吸烟量不是中年患者CSDH的独立危险因素,但亦对中年患者创伤后CSDH形成有统计学意义。高血糖可造成血肿包膜上的毛细血管退变[8,17],长期饮酒及吸烟均对大脑有损害作用,可加速脑萎缩[19-21],但需长期作用才能体现效果,对青年人影响较小。
  综上所述,轻度颅脑损伤后,在青年患者中若存在颅骨骨折、急性硬膜外血肿、蛛网膜囊肿、脑实质与颅骨间距离较大,尤其是大于3.5 mm,出院后仍需警惕慢性硬膜下血肿的形成;而在中年患者中,除颅骨骨折、急性硬膜外血肿、蛛网膜囊肿、脑实质与颅骨间距离(大于2.6 mm)之外,还需关注高血压、糖尿病、抗凝治疗史、吸烟饮酒史及入院时的APTT、PT,患者如有不适应及时就诊,复查头颅CT。
  参考文献:
  [1]Skandsen T,Nilsen TL,Einarsen C,et al.Incidence of Mild Traumatic Brain Injury:A Prospective Hospital, Emergency Room and General Practitioner-Based Study[J].Front Neurol,2019(10):638.
  [2]Kitya D,Punchak M,Abdelgadir J,et al.Causes,clinical presentation,management,and outcomes of chronic subdural hematoma at Mbarara Regional Referral Hospital[J].Neurosurg Focus,2018,45(4):7.
  [3]Teasdale G,Jennett B.Assessment of coma and impaired consciousness.A practical scale[J].Lancet,1974,2(7872):81-84.
  [4]Ahn JH,Jun HS,Kim JH,et al.Analysis of Risk Factor for the Development of Chronic Subdural Hematoma in Patients with Traumatic Subdural Hygroma[J].J Korean Neurosurg Soc,2016,59(6):622-627.
  [5]Edlmann E,Giorgi-Coll S,Whitfield PC,et al.Pathophysiology of chronic subdural haematoma:inflammation,angiogenesis and implications for pharmacotherapy[J].Journal of neuroinflammation,2017,14(1):108.
  [6]Yang AI,Balser DS,Mikheev A,et al.Cerebral atrophy is associated with development of chronic subdural haematoma[J].Brain Inj,2012,26(13-14):1731-1736.
  [7]Sim YW,Min KS,Lee MS,et al.Recent changes in risk factors of chronic subdural hematoma[J].J Korean Neurosurg Soc,2012,52(3):234-239.   [8]Kostic A,Kehayov I,Stojanovic N,et al.Spontaneous chronic subdural hematoma in elderly people-Arterial hypertension and other risk factors[J].J Chin Med Assoc,2018,81(9):781-786.
  [9]Lee KS.Chronic Subdural Hematoma in the Aged,Trauma or Degeneration[J].J Korean Neurosurg Soc,2016,59(1):1-5.
  [10]Oh JS,Shim JJ,Yoon SM,et al.Influence of Gender on Occurrence of Chronic Subdural Hematoma;Is It an Effect of Cranial Asymmetry[J].Korean J Neurotrauma,2014,10(2):82-85.
  [11]刘玉光,朱树干,江玉泉,等.外伤性硬膜下积液演变的慢性硬膜下血肿[J].中华外科杂志,2002(5):43-45.
  [12]赵卫海,吕超,邢泽刚,等.老年外伤性硬膜下积液演变为慢性硬膜下血肿的临床治疗分析41例[J].中国社区医师,2017,33(27):70-71.
  [13]王科大,赵继宗,李京生,等.蛛网膜囊肿合并慢性硬膜下血肿临床分析[J].中华医学杂志,2011,91(7):460-463.
  [14]Wu X,Li G,Zhao J,et al.Arachnoid Cyst–Associated Chronic Subdural Hematoma:Report of 14 Cases and a Systematic Literature Review[J].World Neurosurgery,2018(109):118-130.
  [15]匡柏成,程坤,刘宗霖,等.蛛网膜囊肿合并慢性硬膜下血肿1例并文献复习[J].中国临床神经外科杂志,2019,24(5):306-308.
  [16]Johnston IH,Rowan JO.Raised intracranial pressure and cerebral blood flow.3.Venous outflow tract pressures and vascular resistances in experimental intracranial hypertension[J].Journal of Neurology,Neurosurgery,and Psychiatry,1974,37(4):392-402.
  [17]Han SB,Choi SW,Song SH,et al.Prediction of Chronic Subdural Hematoma in Minor Head Trauma Patients[J].Korean J Neurotrauma,2014,10(2):106-111.
  [18]Aspegren OP,Astrand R,Lundgren MI,et al.Anticoagulation therapy a risk factor for the development of chronic subdural hematoma[J].Clin Neurol Neurosurg,2013,115(7):981-984.
  [19]Weis S,Buttner A.Alcohol-related diseases[J].Handbook of clinical neurology,2017(145):175-180.
  [20]Garcia-Valdecasas-Campelo E,Gonzalez-Reimers E,Santolaria-Fernandez F,et al.Brain atrophy in alcoholics:relationship with alcohol intake;liver disease;nutritional status,and inflammation[J].Alcohol and Alcoholism(Oxford, Oxfordshire),2007,42(6):533-538.
  [21]Duriez Q,Crivello F,Mazoyer B.Sex-related and tissue-specific effects of tobacco smoking on brain atrophy:assessment in a large longitudinal cohort of healthy elderly[J].Frontiers in Aging Neuroscience,2014(6):299.
  [22]王忠誠.王忠诚神经外科学[M].第2版.武汉:湖北科学技术出版社,2015:404-406.
  收稿日期:2020-03-09;修回日期:2020-03-25
  编辑/杜帆
  基金项目:合肥市借转补项目(编号:YW201512010001)
  作者简介:尹胜(1994.7-),男,安徽宿松县人,硕士研究生,主要从事颅脑创伤的研究
  通讯作者:魏祥品(1964.11-),男,安徽霍邱县人,本科,主任医师,主要从事颅脑创伤与神经重症、癫痫的诊疗工作
转载注明来源:https://www.xzbu.com/1/view-15236497.htm