Fang Xiaoyi, Xie Jinzhi, Zhang Airun, Li Guanming, Yang Silan, Huang Xiaoling, Guo Jizhong, Lin Niyang
Department of Neonatology, the Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen 518107, Guangdong, China.
Department of Neonatology, the First Affiliated Hospital, Shantou University Medical College, Shantou 515000, Guangdong, China. Corresponding author: Guo Jizhong, Email:
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2025 Jan;37(1):29-35. doi: 10.3760/cma.j.cn121430-20240312-00213.
To observe the characteristics of changes in non-invasive hemodynamic parameters in neonates with septic shock so as to provide clinical reference for diagnosis and treatment.
A observational study was conducted. The neonates with sepsis complicated with septic shock or not admitted to neonatal intensive care unit (NICU) of the First Affiliated Hospital of Shantou University Medical College were enrolled as the study subjects, who were divided into preterm infant (< 37 weeks) and full-term infant (≥ 37 weeks) according to the gestational age. Healthy full-term infants and hemodynamically stable preterm infants transferring to NICU after birth were enrolled as controls. Electronic cardiometry (EC) was used to measure hemodynamic parameters, including heart rate (HR), mean arterial pressure (MAP), stroke volume (SV), stroke volume index (SVI), cardiac output (CO), cardiac index (CI), systemic vascular resistance (SVR) and systemic vascular resistance index (SVRI), before treatment in the septic shock group, at the time of diagnosis of sepsis in the sepsis without shock group, and before the discharge from the obstetric department or on the day of transferring to NICU in the control group.
Finally, 113 neonates with complete data and parental consent for non-invasive hemodynamic monitoring were enrolled, including 32 cases in the septic shock group, 25 cases in the sepsis without shock group and 56 cases in the control group. In the septic shock group, there were 17 cases at the compensated stage and 15 cases at the decompensated stage. There were 21 full-term infants (20 cured or improved and 1 died) and 11 premature infants (7 cured or improved and 4 died), with the mortality of 15.62% (5/32). There were 18 full-term infants and 7 premature infants in the sepsis without shock group and all cured or improved without death. The control group included 28 full-term infants and 28 premature infants transferring to NICU after birth. Non-invasive hemodynamic parameter analysis showed that SV, SVI, CO and CI of full-term infants in the septic shock group were significantly lower than those in the sepsis without shock group and control group [SV (mL): 3.52±0.99 vs. 5.79±1.32, 5.22±1.02, SVI (mL/m): 16.80 (15.05, 19.65) vs. 27.00 (22.00, 32.00), 27.00 (23.00, 29.75), CO (L/min): 0.52±0.17 vs. 0.80±0.14, 0.72±0.12, CI (mL×s×m): 40.00 (36.67, 49.18) vs. 62.51 (56.34, 70.85), 60.01 (53.34, 69.68), all P < 0.05], while SVR and SVRI were significantly higher than those in the sepsis without shock group and control group [SVR (kPa×s×L): 773.46±291.96 vs. 524.17±84.76, 549.38±72.36, SVRI (kPa×s×L×m): 149.27±51.76 vs. 108.12±12.66, 107.81±11.87, all P < 0.05]. MAP, SV, SVI, CO and CI of preterm infants in the septic shock group were significantly lower than those in the control group [MAP (mmHg, 1 mmHg ≈ 0.133 kPa): 38.55±10.48 vs. 47.46±2.85, SV (mL): 2.45 (1.36, 3.58) vs. 3.96 (3.56, 4.49), SVI (mL/m): 17.60 (14.20, 25.00) vs. 25.50 (24.00, 29.00), CO (L/min): 0.32 (0.24, 0.63) vs. 0.56 (0.49, 0.63), CI (mL×s×m): 40.01 (33.34, 53.34) vs. 61.68 (56.68, 63.35), all P < 0.05], while SVR and SVRI were similar to the control group [SVR (kPa×s×L): 1 082.88±689.39 vs. 656.63±118.83, SVRI (kPa×s×L×m): 126.00±61.50 vs. 102.37±11.68, both P > 0.05]. Further analysis showed that SV, SVI and CI of neonates at the compensation stage in the septic shock group were significantly lower than those in the control group [SV (mL): 3.60±1.29 vs. 4.73±1.15, SVI (mL/m): 19.20±8.33 vs. 26.34±3.91, CI (mL×s×m): 46.51±20.34 vs. 61.01±7.67, all P < 0.05], while MAP, SVR and SVRI were significantly higher than those in the control group [MAP (mmHg): 52.06±8.61 vs. 48.54±3.21, SVR (kPa×s×L): 874.95±318.70 vs. 603.01±111.49, SVRI (kPa×s×L×m): 165.07±54.90 vs. 105.09±11.99, all P < 0.05]; MAP, SV, SVI, CO and CI of neonates at the decompensated stage in the septic shock group were significantly lower than those in the control group [MAP (mmHg): 35.13±6.08 vs. 48.54±3.21, SV (mL): 2.89±1.17 vs. 4.73±1.15, SVI (mL/m): 18.50±4.99 vs. 26.34±3.91, CO (L/min): 0.41±0.19 vs. 0.65±0.15, CI (mL×s×m): 43.34±14.17 vs. 61.01±7.67, all P < 0.05], while SVR and SVRI were similar to the control group [SVR (kPa×s×L): 885.49±628.04 vs. 603.01±111.49, SVRI (kPa×s×L×m): 114.29±43.54 vs. 105.09±11.99, both P > 0.05].
Full-term infant with septic shock exhibit a low cardiac output, high vascular resistance hemodynamic pattern, while preterm infant with septic shock show low cardiac output and normal vascular resistance. At the compensated stage the hemodynamic change is low output and high resistance type, while at the decompensated stage it is low output and normal resistance type. Non-invasive hemodynamic monitoring can assist in the identification of neonatal septic shock and provide basis for clinical diagnosis and treatment.
观察新生儿脓毒性休克无创血流动力学参数变化特点，为临床诊治提供参考。
采用观察性研究。选取汕头大学医学院第一附属医院新生儿重症监护病房（NICU）收治的合并或未合并脓毒性休克的脓毒症新生儿作为研究对象，根据胎龄分为早产儿（<37周）和足月儿（≥37周）。选取健康足月儿及出生后转入NICU血流动力学稳定的早产儿作为对照。采用电子心动描记法（EC）测量脓毒性休克组治疗前、无休克脓毒症组脓毒症诊断时、对照组产科出院前或转入NICU当天的血流动力学参数，包括心率（HR）、平均动脉压（MAP）、每搏量（SV）、每搏量指数（SVI）、心输出量（CO）、心脏指数（CI）、体循环血管阻力（SVR）和体循环血管阻力指数（SVRI）。
最终纳入113例有完整数据且父母同意进行无创血流动力学监测的新生儿，其中脓毒性休克组32例，无休克脓毒症组25例，对照组56例。脓毒性休克组中，代偿期17例，失代偿期15例。足月儿21例（20例治愈或好转，1例死亡），早产儿11例（7例治愈或好转，4例死亡），死亡率为15.62%（5/32）。无休克脓毒症组足月儿18例，早产儿7例，均治愈或好转，无死亡。对照组包括出生后转入NICU的足月儿28例和早产儿28例。无创血流动力学参数分析显示，脓毒性休克组足月儿的SV、SVI、CO和CI显著低于无休克脓毒症组和对照组[SV（mL）：3.52±0.99 vs. 5.79±1.32，5.22±１.02；SVI（mL/m）：16.80（15.05，19.65）vs. 27.00（22.00，32.00），27.00（23.00，29.75）；CO（L/min）：0.52±０.17 vs. 0.80±０.14，0.72±０.12；CI（mL×s×m）：40.00（36.67，49.18）vs. 62.51（５6.３4，70.85），60.01（53.34，69.68），均P<0.05]，而SVR和SVRI显著高于无休克脓毒症组和对照组[SVR（kPa×s×L）：773.46±291.96 vs. 524.17±84.76，549.38±72.36；SVRI（kPa×s×L×m）：149.27±51.76 vs. 108.12±12.66，107.81±11.87，均P<0.05]。脓毒性休克组早产儿的MAP、SV、SVI、CO和CI显著低于对照组[MAP（mmHg，1 mmHg≈0.133 kPa）：38.55±10.48 vs. 47.46±2.85；SV（mL）：2.45（1.36，3.58）vs. 3.96（3.56，4.49）；SVI（mL/m）：17.60（14.20，25.00）vs. 25.50（24.00，29.00）；CO（L/min）：0.32（0.24，0.63）vs. 0.56（0.49，0.63）；CI（mL×s×m）：40.01（33.34，53.34）vs. 61.68（56.68，6３.35），均P<0.05]，而SVR和SVRI与对照组相似[SVR（kPa×s×L）：1 082.88±689.39 vs. 656.63±118.83；SVRI（kPa×s×L×m）：126.00±61.50 vs. 102.37±11.68，均P>0.05]。进一步分析显示，脓毒性休克组代偿期新生儿的SV、SVI和CI显著低于对照组[SV（mL）：3.60±1.29 vs. 4.73±1.15；SVI（mL/m）：19.20±8.33 vs. 26.34±3.91；CI（mL×s×m）：46.51±20.34 vs. 61.01±7.67，均P<0.05]，而MAP、SVR和SVRI显著高于对照组[MAP（mmHg）：52.06±8.61 vs. 48.54±3.21；SVR（kPa×s×L）：874.95±318.70 vs. 603.01±111.49；SVRI（kPa×s×L×m）：165.07±54.90 vs. 105.09±11.99，均P<0.05]；脓毒性休克组失代偿期新生儿的MAP、SV、SVI、CO和CI显著低于对照组[MAP（mmHg）：35.13±6.08 vs. 48.54±3.21；SV（mL）：2.89±1.17 vs. 4.73±1.15；SVI（mL/m）：18.50±4.99 vs. 26.34±3.91；CO（L/min）：0.41±0.19 vs. 0.65±0.15；CI（mL×s×m）：43.34±14.17 vs. 61.01±7.67，均P<0.05]，而SVR和SVRI与对照组相似[SVR（kPa×s×L）：885.49±628.04 vs. 603.01±111.49；SVRI（kPa×s×L×m）：114.29±４3.54 vs. 105.09±11.99，均P>0.05]。
足月儿脓毒性休克呈现心输出量低、血管阻力高的血流动力学模式，早产儿脓毒性休克则表现为心输出量低、血管阻力正常。代偿期血流动力学改变为低输出高阻力型，失代偿期为低输出正常阻力型。无创血流动力学监测有助于新生儿脓毒性休克的识别，为临床诊断和治疗提供依据。
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