Pediatric ICU, Apollo Children's Hospital, Chennai, India.
The University of British Columbia, The Child and Family Research Institute, and BC Children's Hospital, Vancouver, BC, Canada.
Pediatr Crit Care Med. 2021 Aug 1;22(8):e448-e458. doi: 10.1097/PCC.0000000000002714.
Fluid boluses are commonly administered to improve the cardiac output and tissue oxygen delivery in pediatric septic shock. The objective of this study is to evaluate the effect of an early fluid bolus administered to children with septic shock on the cardiac index and mean arterial pressure, as well as on the hemodynamic response and its relationship with outcome.
DESIGN, SETTING, PATIENTS, AND INTERVENTIONS: We prospectively collected hemodynamic data from children with septic shock presenting to the emergency department or the PICU who received a fluid bolus (10 mL/kg of Ringers Lactate over 30 min). A clinically significant response in cardiac index-responder and mean arterial pressure-responder was both defined as an increase of greater than or equal to 10% 10 minutes after fluid bolus.
Forty-two children with septic shock, 1 month to 16 years old, median Pediatric Risk of Mortality-III of 13 (interquartile range, 9-19), of whom 66% were hypotensive and received fluid bolus within the first hour of shock recognition. Cardiac index- and mean arterial pressure-responsiveness rates were 31% and 38%, respectively. We failed to identify any association between cardiac index and mean arterial pressure changes (r = 0.203; p = 0.196). Cardiac function was similar in mean arterial pressure- and cardiac index-responders and nonresponders. Mean arterial pressure-responders increased systolic, diastolic, and perfusion pressures (mean arterial pressure - central venous pressure) after fluid bolus due to higher indexed systemic vascular resistance and arterial elastance index. Mean arterial pressure-nonresponders required greater vasoactive-inotrope support and had higher mortality.
The hemodynamic response to fluid bolus in pediatric septic shock was variable and unpredictable. We failed to find a relationship between mean arterial pressure and cardiac index changes. The adverse effects of fluid bolus extended beyond fluid overload and, in some cases, was associated with reduced mean arterial pressure, perfusion pressures and higher vasoactive support. Mean arterial pressure-nonresponders had increased mortality. The response to the initial fluid bolus may be helpful to understand each patient's individualized physiologic response and guide continued hemodynamic management.
在小儿感染性休克中，常给予液体冲击以改善心输出量和组织氧输送。本研究的目的是评估早期给予感染性休克患儿液体冲击对心指数和平均动脉压的影响，以及对血流动力学反应及其与结局的关系。
设计、地点、患者和干预措施：我们前瞻性地收集了急诊科或 PICU 中出现感染性休克并接受液体冲击（10mL/kg 林格乳酸盐水在 30 分钟内输注）的患儿的血流动力学数据。心指数反应者和平均动脉压反应者的临床显著反应均定义为液体冲击后 10 分钟心指数增加≥10%或平均动脉压增加≥10mmHg。
42 例年龄 1 个月至 16 岁的感染性休克患儿，儿科死亡率风险Ⅲ期中位数为 13（四分位距 9-19），其中 66%存在低血压，在休克识别后 1 小时内接受液体冲击。心指数和平均动脉压反应率分别为 31%和 38%。我们未能发现心指数和平均动脉压变化之间存在任何关联（r=0.203；p=0.196）。在平均动脉压和心指数反应者和无反应者中，心功能相似。由于更高的指数全身血管阻力和动脉弹性指数，平均动脉压反应者在液体冲击后增加了收缩压、舒张压和灌注压（平均动脉压-中心静脉压）。由于需要更多的血管活性-正性肌力支持，平均动脉压无反应者的死亡率更高。
在小儿感染性休克中，液体冲击的血流动力学反应是可变的和不可预测的。我们未能发现平均动脉压和心指数变化之间存在关系。液体冲击的不良影响不仅限于液体超负荷，在某些情况下，还与平均动脉压降低、灌注压降低和更高的血管活性支持相关。平均动脉压无反应者的死亡率更高。对初始液体冲击的反应可能有助于了解每个患者的个体化生理反应，并指导进一步的血流动力学管理。
