炎症指标对创伤性脑损伤后阵发性交感神经亢进的预测价值：单中心回顾性病例对照研究

引用本文

史汉童, 陈文, 郭彦谷, 桑贤正, 张丹枫, 侯立军. 炎症指标对创伤性脑损伤后阵发性交感神经亢进的预测价值：单中心回顾性病例对照研究[J]. 海军军医大学学报, 2025, 46(3): 330-335

SHI Hantong, CHEN Wen, GUO Yangu, SANG Xianzheng, ZHANG Danfeng, HOU Lijun. Predictive value of inflammatory markers for paroxysmal sympathetic hyperactivity after traumatic brain injury: a single-center retrospective case-control study[J]. Academic Journal of Naval Medical University, 2025, 46(3): 330-335 (in Chinese with English abstract)

炎症指标对创伤性脑损伤后阵发性交感神经亢进的预测价值：单中心回顾性病例对照研究

史汉童, 陈文, 郭彦谷, 桑贤正, 张丹枫, 侯立军

海军军医大学(第二军医大学)第二附属医院神经外科, 上海 200003

收稿日期: 2024-08-30 接受日期: 2024-10-30

基金项目: 国家自然科学基金（82271396），上海市医学领先专业重点学科基金（21Y21900400）.

作者简介: 史汉童，硕士，住院医师.E-mail: shihantong_2021@qq.com.

通信作者(Corresponding author): 侯立军, Tel: 021-81885671, E-mail: ljhou668@163.com.

摘要: 目的探索炎症指标对创伤性脑损伤（TBI）后发生阵发性交感神经亢进（PSH）的预测价值。方法回顾性分析海军军医大学（第二军医大学）第二附属医院2016年12月至2020年11月收治的84例TBI患者的病例资料，根据患者在住院期间是否发生过PSH分为PSH组（n＝41）与非PSH组（n＝43）。收集并比较两组患者的一般资料和实验室检查结果。采用Kendall相关分析法分析炎症指标与TBI后PSH发生的相关性，采用ROC曲线分析炎症指标对PSH发生的预测价值。结果两组患者的年龄、性别、入院格拉斯哥昏迷量表评分等基线资料差异均无统计学意义（均P＞0.05）。与非PSH组患者相比，PSH组患者的白细胞计数、中性粒细胞计数、中性粒细胞/淋巴细胞比值（NLR）、血小板/淋巴细胞比值（PLR）、全身免疫炎症指数（SII）均升高（均P＜0.05）。NLR、SII和中性粒细胞计数均与PSH呈正相关（r＝0.360、0.308、0.289，均P＜0.01），对应ROC的AUC值分别是0.752、0.716和0.702。结论炎症指标NLR、SII及中性粒细胞对TBI后PSH的发生具有预测价值。

关键词: 创伤性脑损伤阵发性交感神经亢奋中性粒细胞中性粒细胞/淋巴细胞比值全身免疫炎症指数

Predictive value of inflammatory markers for paroxysmal sympathetic hyperactivity after traumatic brain injury: a single-center retrospective case-control study

SHI Hantong, CHEN Wen, GUO Yangu, SANG Xianzheng, ZHANG Danfeng, HOU Lijun

Department of Neurosurgery, The Second Affiliated Hospital of Naval Medical University (Second Military Medical University), Shanghai 200003, China

Supported by National Natural Science Foundation of China (82271396) and Key Discipline Fund of Shanghai Medical Leading Subject (21Y21900400).

Abstract: Objective To explore the value of inflammatory markers in predicting paroxysmal sympathetic hyperactivity (PSH) after traumatic brain injury (TBI). Methods A total of 84 TBI patients who were admitted to The Second Affiliated Hospital of Naval Medical University (Second Military Medical University) from Dec. 2016 to Nov. 2020 were retrospectively analyzed. They were classified into PSH group (n＝41) and non-PSH group (n＝43) according to whether PSH occurred during hospitalization. The baseline data and laboratory results of the 2 groups were collected and compared. Kendall correlation analysis was used to analyze the correlation between inflammatory markers and the occurrence of PSH after TBI, and receiver operating characteristic (ROC) curve was used to analyze the predictive value of inflammatory markers to PSH. Results There were no significant differences in baseline data, including age, gender, or Glasgow coma scale score, between the 2 groups (all P > 0.05). Compared with patients in the non-PSH group, the neutrophil to lymphocyte ratio (NLR), platelet to lymphocyte ratio (PLR), systemic immune-inflammation index (SII), neutrophils and leukocytes in the PSH group were significantly increased (all P < 0.05). NLR, SII and neutrophil were positively correlated with PSH (r＝0.360, 0.308, 0.289; all P < 0.01), with the corresponding ROC area under curve values being 0.752, 0.716 and 0.702, respectively. Conclusion NLR, SII and neutrophils have a value in predicting the occurrence of PSH after TBI.

Key words: traumatic brain injuries paroxysmal sympathetic hyperactivity neutrophils neutrophil to lymphocyte ratio systemic immune-inflammation index

创伤性脑损伤（traumatic brain injury，TBI）是指因外力直接或间接作用于头部, 导致脑组织结构受损而引起的暂时性或永久性脑功能障碍性疾病^[1-2]，在中低收入国家，它是致死、致残的主要原因之一^[3]。中国的TBI患者数量比世界上大多数国家多，使得TBI成为中国一个主要的公共卫生问题^[4]。TBI的治疗过程中多伴有各种并发症^[5]，其中炎症与阵发性交感神经亢进（paroxysmal sympathetic hyperactivity，PSH）作为TBI后的重要并发症，与TBI的预后相关^[6-7]。炎症反应作为TBI病理过程的重要环节之一，对脑组织损伤程度具有提示意义^[8]。而PSH是指表现为阵发性、短暂性的多种交感神经兴奋症状，包括心动过速、高血压、呼吸急促、体温升高、出汗增多和肌肉张力增高等症状，常见于重型颅脑损伤患者^[9]。PSH的发生与脑损伤严重程度呈正相关，脑损伤程度越重，PSH发生的可能性越高，伴发PSH的TBI患者常常预后不良^[10]。但是炎症与PSH之间是否存在相关性仍有待进一步研究。本课题组前期研究发现下丘脑室旁核区中性粒细胞胞外诱捕网（neutrophil extracellular trap，NET）的形成可能参与了TBI后PSH的发生，提示TBI后中枢神经系统的神经炎症和氧化应激损伤与PSH的发生密切相关^[11]。一项单中心临床研究发现，炎症与PSH的发生在时间上存在重叠，在症状上也有部分相似，均有体温升高、心动过速、呼吸急促等症状^[7]。这提示外周炎症可能与PSH发生有关，但具体机制仍需要进一步探索。基于以上观点，笔者推测TBI后PSH的发生与炎症反应相关，外周血炎症标志物水平对于TBI后PSH的发生可能具有预测价值。因此，本研究探讨了炎症指标与TBI后PSH发生的相关性及其预测价值，并探索了PSH对TBI患者住院时间及短期预后的影响。

1 资料和方法 1.1 研究对象

回顾性分析2016年12月至2020年11月海军军医大学（第二军医大学）第二附属医院神经外科收治的84例TBI患者的病例资料。本研究已通过海军军医大学（第二军医大学）第二附属医院伦理委员会审核批准。

纳入标准：（1）有头部创伤史；（2）经CT或MRI检查确诊为TBI，且根据格拉斯哥昏迷量表（Glasgow coma scale，GCS）评分进行脑损伤严重程度评估（GCS评分13~15分为轻度脑损伤，9~12分为中度脑损伤，3~8分为重度脑损伤）；（3）符合PSH诊断标准（见1.2节）。排除标准：（1）确诊恶性肿瘤或恶性肿瘤待排除者；（2）严重肝肾功能异常者；（3）免疫功能异常者；（4）因既往病史遗留严重神经系统功能障碍者；（5）精神分裂症及其他精神心理疾病患者；（6）动脉瘤、脑血管畸形及烟雾病患者。

1.2 PSH的诊断标准

患者存在下列8种症状中的任意4种即可诊断为PSH：（1）心动过速；（2）高血压；（3）呼吸急促；（4）意识水平降低；（5）肌肉强直；（6）高热；（7）发汗；（8）瞳孔扩张。以上症状和体征均不能通过严重感染、脑疝或其他原因解释^[12]。

1.3 研究方法

收集患者的一般资料，包括年龄、性别、高血压病史、入院GCS评分、入院症状（喷射性呕吐、四肢抽搐、意识障碍）、合并损伤（胸部损伤、四肢骨折、颈部损伤）、损伤模式（高处坠落、车祸）、入院颅脑CT检查结果（局灶性损伤、弥漫性损伤）、是否进行颅脑手术（包括术式）、是否进行气管切开术，以及ICU停留天数。收集患者入院3 d内的空腹外周静脉血检测结果，包括血钾、血钠、血糖、白细胞计数、中性粒细胞计数、淋巴细胞计数、血小板计数、CRP等。计算患者的外周血炎症指标：中性粒细胞/淋巴细胞比值（neutrophil to lymphocyte ratio，NLR）、血小板/淋巴细胞比值（platelet to lymphocyte ratio，PLR）、全身免疫炎症指数（systemic immune-inflammation index，SII）。文献报道脑出血后血糖/淋巴细胞比值（glucose to lymphocyte ratio，GLR）及血糖/血钾比值（glucose to potassium ratio，GPR）显著升高^[13-14]，因此除炎症指标外，本研究还将GLR、GPR纳入统计分析。

1.4 统计学处理

应用SPSS 26.0软件对收集到的临床资料进行统计学分析。呈正态分布的计量资料以x±s表示并采用独立样本t检验进行组间比较，呈偏态分布的计量资料以中位数（下四分位数，上四分位数）表示并采用Mann-Whitney U检验进行组间比较。计数资料以例数和百分数表示，采用χ²检验进行组间比较。检验水准（α）为0.05。采用Kendall相关分析法分析炎症指标与PSH发生的相关性及各炎症指标之间的相关性，采用ROC曲线分析炎症指标对TBI后PSH发生的预测价值。

2 结果 2.1 基线资料比较

共纳入84例TBI患者，年龄为14~81岁，男73例、女11例。根据患者住院期间是否发生过PSH分为PSH组及非PSH组，其中PSH组41例、非PSH组43例。两组患者年龄、性别、入院GCS评分、高血压病史、入院症状（喷射性呕吐、四肢抽搐、意识障碍）、合并损伤（胸部损伤、四肢骨折、颈部损伤）、损伤模式（高处坠落、车祸）、入院颅脑CT检查结果（局灶性损伤、弥漫性损伤）、是否进行颅脑手术及术式、是否进行气管切开术和ICU停留天数差异均无统计学意义（均P＞0.05）。见表 1。

表 1 PSH组与非PSH组TBI患者基线资料比较 Tab 1 Comparison of baseline data of TBI patients between PSH and non-PSH groups

Characteristic	PSH group N＝41	Non-PSH group N＝43	Statistic	P value
Age/year, x±s	50.37±15.91	52.49±15.05	t＝－0.628	0.531
Gender, n (%)			χ²＝2.350	0.125
Male	38 (92.68)	35 (81.40)
Female	3 (7.32)	8 (18.60)
GCS score at admission, M (Q_L, Q_U)	6.0 (4.0, 9.5)	6.0 (5.0, 10.0)	Z＝－0.370	0.711
Hypertension, n (%)	9 (21.95)	7 (16.28)	χ²＝0.202	0.653
Symptom at admission, n (%)
Vomiting	26 (63.42)	27 (62.79)	χ²＝0.004	0.953
Spasm	20 (48.78)	24 (55.81)	χ²＝0.416	0.519
Consciousness dysfunction	37 (90.24)	40 (93.02)	χ²＝0.212	0.645
Combined injury, n (%)
Thoracic injury	12 (29.27)	12 (27.91)	χ²＝0.019	0.890
Limb fracture	5 (12.20)	5 (11.63)	χ²＝0.006	0.936
Neck injury	2 (4.88)	2 (4.65)	χ²＝0.002	0.961
Damage mode, n (%)
Falling accident	12 (29.27)	11 (25.58)	χ²＝0.143	0.705
Traffic accident	27 (65.85)	30 (69.77)	χ²＝0.147	0.701
Result of CT examination, n (%)
Focal injury	15 (36.59)	19 (44.19)	χ²＝0.503	0.478
Diffuse injury	26 (63.42)	23 (53.49)	χ²＝0.851	0.356
ICU stay/d, x±s	25.00±18.53	24.40±14.82	t＝0.166	0.869
Craniocerebral operation, n (%)	24 (58.54)	21 (48.84)	χ²＝0.794	0.373
Removal of intracerebral hematoma	10 (24.39)	8 (18.60)	χ²＝0.417	0.518
Removal of subdural hematoma	5 (12.20)	6 (13.95)	χ²＝0.057	0.811
Removal of epidural hematoma	0	2 (4.65)
Ventricle puncture drainage	11 (26.83)	7 (16.28)	χ²＝1.388	0.239
Tracheotomy, n (%)	21 (51.22)	20 (46.51)	χ²＝0.186	0.666
In the PSH group, 2 patients underwent intracerebral hematoma removal+subdural hematoma removal (these 2 cases were included in the analysis of intracerebral hemorrhage) and 2 patients underwent intracerebral hematoma removal+ventricle puncture drainage (due to the prognostic significance of hematoma in ventricle, it was analyzed separately). In the non-PSH group, 1 patient underwent intracerebral hematoma removal+epidural hematoma removal, and 1 patient underwent subdural hematoma removal+epidural hematoma removal. Due to the small number of patients who underwent the 2 combined operations, no separate comparison was made between the 2 groups. In addition, there were no cases of epidural hematoma removal in the PSH group, so statistical analysis of epidural hematoma removal was not conducted. PSH: Paroxysmal sympathetic hyperactivity; TBI: Traumatic brain injury; GCS: Glasgow coma scale; CT: Computed tomography; ICU: Intensive care unit; M (Q_L, Q_U): Median (lower quartile, upper quartile).

表 1 PSH组与非PSH组TBI患者基线资料比较 Tab 1 Comparison of baseline data of TBI patients between PSH and non-PSH groups

2.2 两组TBI患者实验室指标比较

与非PSH组TBI患者相比，PSH组TBI患者的白细胞计数、中性粒细胞计数、NLR、PLR、SII均升高（均P＜0.05），淋巴细胞计数降低（P＝0.050），而CPR、红细胞计数、血小板计数、血糖、血钠、血钾、乳酸、GPR、GLR、INR、总胆红素、总蛋白、白蛋白及白蛋白/球蛋白比值、血尿素和血肌酐差异均无统计学意义（均P＞0.05）。见表 2。

表 2 PSH组与非PSH组TBI患者实验室指标比较 Tab 2 Comparison of laboratory indicators of TBI patients between PSH and non-PSH groups

Indicator	PSH group n＝41	Non-PSH group n＝43	Statistic	P value
CRP/(mg·L^－1), M (Q_L, Q_U)	25.68 (22.13, 59.43)	35.73 (14.4, 55.13)	Z＝－0.139	0.890
Leukocyte/(L^－1, ×10⁹), M (Q_L, Q_U)	13.10 (10.85, 16.90)	10.80 (7.20, 13.60)	Z＝－3.003	0.003
Erythrocyte/(L^－1, ×10¹²), M (Q_L, Q_U)	3.40 (3.01, 3.98)	3.25 (2.92, 3.86)	Z＝－0.913	0.361
Platelet/(L^－1, ×10⁹), M (Q_L, Q_U)	204.0 (139.5, 255.0)	177.0 (118.0, 245.0)	Z＝－0.913	0.364
Neutrophil/(L^－1, ×10⁹), x±s	12.25±3.97	9.12±3.96	t＝3.615	0.001
Lymphocyte/(L^－1, ×10⁹), M (Q_L, Q_U)	0.77 (0.61, 1.02)	0.95 (0.72, 1.17)	Z＝－0.908	0.050
Glucose/(mmol·L^－1), M (Q_L, Q_U)	6.7 (5.4, 8.9)	6.6 (5.4, 8.0)	Z＝－0.470	0.638
Sodium/(mmol·L^－1), M (Q_L, Q_U)	140 (135, 144)	140 (137, 143)	Z＝－0.045	0.964
Potassium/(mmol·L^－1), M (Q_L, Q_U)	3.98 (3.66, 4.42)	4.00 (3.62, 4.45)	Z＝－0.076	0.939
Lactic acid/(mmol·L^－1), M (Q_L, Q_U)	31.00 (28.15, 38.55)	29.80 (25.80, 34.70)	Z＝－1.428	0.153
NLR, M (Q_L, Q_U)	12.76 (10.93, 21.54)	9.28 (6.47, 12.76)	Z＝－3.983	＜0.001
PLR, M (Q_L, Q_U)	222.08 (166.33, 372.50)	166.67 (103.61, 285.00)	Z＝－2.121	0.034
SII/(L^－1, ×10⁹), M (Q_L, Q_U)	2 996.67 (1 906.75, 4 116.45)	1 657.45 (928.62, 2 996.67)	Z＝－3.401	0.001
GPR, M (Q_L, Q_U)	1.68 (1.32, 2.33)	1.56 (1.33, 2.10)	Z＝－0.398	0.690
GLR, M (Q_L, Q_U)	8.53 (6.02, 13.58)	6.97 (5.21, 10.00)	Z＝－1.718	0.086
INR, x±s	1.19±0.15	1.17±0.13	t＝0.437	0.664
Total bilirubin/(μmol·L^－1), x±s	25.21±10.33	21.23±9.79	t＝1.813	0.073
Total protein/(g·L^－1), x±s	59.01±9.44	56.50±10.24	t＝1.168	0.246
Albumin/(g·L^－1), x±s	32.63±6.91	30.72±7.68	t＝1.198	0.234
Albumin to globulin ratio, M (Q_L, Q_U)	1.19 (1.00, 1.41)	1.15 (0.97, 1.38)	Z＝－0.868	0.385
Serum urea/(mmol·L^－1), M (Q_L, Q_U)	5.30 (4.30, 6.45)	5.20 (3.60, 6.20)	Z＝－1.034	0.301
Serum creatinine/(μmol·L^－1), M (Q_L, Q_U)	58.00 (49.50, 71.50)	56.00 (45.00, 71.00)	Z＝－0.627	0.531
PSH: Paroxysmal sympathetic hyperactivity; TBI: Traumatic brain injury; CRP: C reactive protein; NLR: Neutrophil to lymphocyte ratio; PLR: Platelet to lymphocyte ratio; SII: Systemic immune-inflammation index; GPR: Glucose to potassium ratio; GLR: Glucose to lymphocyte ratio; INR: International normalized ratio; M (Q_L, Q_U): Median (lower quartile, upper quartile).

表 2 PSH组与非PSH组TBI患者实验室指标比较 Tab 2 Comparison of laboratory indicators of TBI patients between PSH and non-PSH groups

2.3 炎症指标与TBI后PSH发生的相关性

Kendall相关分析结果显示，NLR、SII、中性粒细胞计数、白细胞计数、PLR均与PSH呈正相关（r＝0.360、0.308、0.289、0.273、0.192，P＜0.01或P＜0.05）。在这些与PSH相关的炎症指标中，NLR与SII、中性粒细胞计数、白细胞计数及PLR均呈正相关（r＝0.482、0.448、0.394、0.278，均P＜0.01），PLR与SII和NLR呈正相关（r＝0.699、0.278，均P＜0.01）。见表 3。

表 3 炎症指标与TBI后PSH发生之间及各炎症指标之间的Kendall相关性分析 Tab 3 Kendall correlation analyses between inflammatory markers and PSH after TBI and between inflammatory markers

2.4 炎症指标对TBI后PSH发生的预测价值

通过分析PSH组与非PSH组TBI患者炎症指标参数，绘制ROC曲线（图 1）。对比AUC值发现，NLR（AUC值＝0.752，95% CI 0.651~0.854，灵敏度为0.976，特异度为0.372）、SII（AUC值＝0.716，95% CI 0.607~0.824，灵敏度为0.854，特异度为0.488）及中性粒细胞计数（AUC值＝0.702，95% CI 0.592~0.813，灵敏度为0.976，特异度为0.326）对TBI后PSH的发生具有预测价值，而白细胞计数及PLR对TBI后PSH的发生不具有预测价值（AUC值均＜0.7）。

图 1 炎症指标对TBI后PSH发生的预测价值 Fig 1 Predictive value of inflammatory markers for PSH after TBI TBI: Traumatic brain injury; PSH: Paroxysmal sympathetic hyperactivity; NLR: Neutrophil to lymphocyte ratio; SII: Systemic immune-inflammation index; PLR: Platelet to lymphocyte ratio.

3 讨论

TBI表现为多种形式，可从轻微的意识改变到持续的昏迷状态甚至死亡^[15]。TBI的病理过程可以分为原发性损伤和继发性损伤^[16]。原发性损伤多为外力作用于头部引起脑组织结构破坏所致。继发性损伤则是由于炎症活动、脑水肿、血脑屏障破坏、脑组织缺血缺氧、炎症细胞浸润及包括趋化因子和IL在内的许多免疫介质大量释放所致^[17-18]。其治疗方式也多种多样，轻度TBI患者经过保守治疗多可缓解；而重度TBI患者因脑损伤严重、脑组织肿胀或血肿压迫，需手术治疗，常规术式有去骨瓣减压术、血肿清除术等^[19]。脑出血是TBI病理过程中的重要环节，临床实践及相关研究提示，脑出血后炎症反应与脑损伤程度相关并对脑出血患者预后有预测价值^[20]。炎症作为TBI的主要早期并发症之一，也是TBI治疗的主要靶点^[21]。PSH作为一种获得性交感神经功能异常升高的表现，在TBI患者中较为常见^[22]。其发生机制复杂，可能涉及交感神经兴奋-抑制失衡、内分泌激素紊乱与神经炎症等多种因素。本研究结果提示多项炎症指标与PSH的发生密切相关。ROC曲线分析结果也提示多项炎症指标对于TBI后PSH的发生具有预测价值。在众多炎症指标中，NLR的预测价值最高（AUC值＝0.752）且识别作用较强，其灵敏度为0.976，有望成为TBI患者的监测指标之一，进一步提高对PSH的早期识别率，有助于PSH的早期诊断和预防。NLR与中性粒细胞是反映机体炎症状态和免疫功能的重要指标，TBI后中性粒细胞在损伤部位迅速聚集，释放TNF-α、IL-6等炎症因子并作用于神经系统，导致神经元损伤、突触功能障碍，进而引发交感神经系统过度激活^[23]。此外，本研究中PSH组TBI患者的淋巴细胞计数降低，淋巴细胞数量的相对减少可能会削弱机体的免疫调节能力^[24]。

本研究通过回顾分析既往病例探讨了炎症与PSH的相关性及炎症指标对TBI后PSH发生的预测价值，为临床治疗TBI及预防PSH发生提供了新思路。本研究也存在不足之处：（1）由于回顾性研究的局限性，部分临床信息如手术时长、治疗费用、术后其他并发症等因素未纳入研究。（2）本研究未对TBI患者的炎症指标进行动态监测，未明确炎症指标升高与PSH发生的时间顺序，有待进一步。（3）本研究所纳入的样本量相对较小，仅为单中心回顾性研究，可能存在偏倚，所得结论未必适用于所有TBI患者。针对上述不足，期望后期开展相关针对性的前瞻性临床研究，纳入患者伤后至就医的时长、手术时长及麻醉后苏醒时间等参数以进一步探索TBI后PSH发生的可能危险因素；对炎症指标进行动态监测，明确炎症及PSH发生的时间间隔；通过多中心临床试验进一步验证炎症与TBI后PSH发生的关系，并尝试以抗炎治疗为核心、辅以对症治疗的PSH综合治疗策略。

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海军军医大学学报 2025, Vol. 46 Issue (3): 330-335	PDF