Wirtz Mathijs R, Moekotte Jiri, Balvers Kirsten, Admiraal Marjolein M, Pittet Jean-Francois, Colombo Joe, Wagener Brant M, Goslings J Carel, Juffermans Nicole
Department of Intensive Care Medicine, Onze Lieve Vrouwe Gasthuis and Amsterdam University Medical Centers, Amsterdam, The Netherlands.
Laboratory of Experimental Intensive Care and Anesthesiology of the Amsterdam University Medical Center, Amsterdam, The Netherlands.
Intensive Care Med Exp. 2020 Nov 25;8(1):69. doi: 10.1186/s40635-020-00359-3.
Nosocomial infection contributes to adverse outcome after brain injury. This study investigates whether autonomic nervous system activity is associated with a decreased host immune response in patients following stroke or traumatic brain injury (TBI).
A prospective study was performed in adult patients with TBI or stroke who were admitted to the Intensive Care Unit of our tertiary university hospital between 2013 and 2016. Heart rate variability (HRV) was recorded daily and assessed for autonomic nervous system activity. Outcomes were nosocomial infections and immunosuppression, which was assessed ex vivo using whole blood stimulations with plasma of patients with infections, matched non-infected patients and healthy controls.
Out of 64 brain injured patients, 23 (36%) developed an infection during their hospital stay. The ability of brain injured patients to generate a host response to the bacterial endotoxin lipopolysaccharides (LPS) was diminished compared to healthy controls (p < 0.001). Patients who developed an infection yielded significantly lower TNF-α values (86 vs 192 pg/mL, p = 0.030) and a trend towards higher IL-10 values (122 vs 84 pg/mL, p = 0.071) following ex vivo whole blood stimulations when compared to patients not developing an infection. This decreased host immune response was associated with altered admission HRV values. Brain injured patients who developed an infection showed increased normalized high-frequency power compared to patients not developing an infection (0.54 vs 0.36, p = 0.033), whereas normalized low-frequency power was lower in infected patients (0.46 vs 0.64, p = 0.033).
Brain injured patients developing a nosocomial infection show parasympathetic predominance in the acute phase following brain injury, reflected by alterations in HRV, which parallels a decreased ability to generate an immune response to stimulation with LPS.
医院感染会导致脑损伤后出现不良后果。本研究调查自主神经系统活动是否与中风或创伤性脑损伤(TBI)患者宿主免疫反应降低有关。
对2013年至2016年间入住我校三级大学医院重症监护病房的成年TBI或中风患者进行了一项前瞻性研究。每天记录心率变异性(HRV),并评估自主神经系统活动。结果指标为医院感染和免疫抑制,通过用感染患者、匹配的未感染患者和健康对照者的血浆对全血进行体外刺激来评估免疫抑制情况。
64例脑损伤患者中,23例(36%)在住院期间发生感染。与健康对照相比,脑损伤患者对细菌内毒素脂多糖(LPS)产生宿主反应的能力降低(p<0.001)。与未发生感染的患者相比,发生感染的患者在体外全血刺激后产生的TNF-α值显著更低(86对192 pg/mL,p = 0.030),且IL-10值有升高趋势(122对84 pg/mL,p = 0.071)。这种宿主免疫反应降低与入院时HRV值的改变有关。发生感染的脑损伤患者与未发生感染的患者相比,标准化高频功率增加(0.54对0.36,p = 0.033),而感染患者的标准化低频功率更低(0.46对0.64,p = 0.033)。
发生医院感染的脑损伤患者在脑损伤后的急性期表现为副交感神经占优势,这通过HRV的改变得以体现,同时这与对LPS刺激产生免疫反应的能力降低相平行。