1Pediatric Intensive Care Unit, Apollo Children's Hospital, Chennai, Tamil Nadu, India. 2Pediatric Intensive Care Unit, Manipal Hospital, Bangalore, Karnataka, India. 3Emergency Department and Intensive Care Unit, British Columbia Children's Hospital and the University of British Columbia, Vancouver, BC, Canada. 4Pediatric Intensive Care Unit, SRM Institute of Medical Sciences, Chennai, Tamil Nadu, India.
Pediatr Crit Care Med. 2014 Jan;15(1):e17-26. doi: 10.1097/PCC.0b013e3182a5589c.
To evaluate the cardiovascular aberrations using multimodal monitoring in fluid refractory pediatric septic shock and describe the clinical characteristics of septic myocardial dysfunction.
Prospective observational study of patients with unresolved septic shock after infusion of 40 mL/kg fluid in the first hour.
Two tertiary care referral Indian PICUs.
Patients aged 1 month to 16 years who had fluid refractory septic shock.
Changes in therapy were based on findings of clinical assessment, bedside echocardiography, and invasive blood pressure monitoring within 6 hours of recognition of septic shock.
Over a 4-year period, 48 patients remained in septic shock despite at least 40 mL/kg fluid infusion. On clinical examination, 21 patients had cold shock and 27 had warm shock. Forty-one patients (85.5%) had vasodilatory shock on invasive blood pressure; these included 14 patients who initially presented with cold shock. The commonest echocardiography findings were impaired left ± right ventricular function in 19 patients (39.6%) and hypovolemia in 16 patients (33%). Three patients who had normal myocardial function on day 1 developed secondary septic myocardial dysfunction on day 3. Echocardio graphy, along with invasive arterial pressure monitoring, allowed fluid, inotropy, and pressors to be titrated more precisely in 87.5% of patients. Shock resolved in 46 of 48 patients (96%) and 44 patients (91.6%) survived to discharge.
Bedside echocardiography provided crucial information leading to the recognition of septic myocardial dysfunction and uncorrected hypovolemia that was not apparent on clinical assessment. With invasive blood pressure monitoring, echocardiography affords a simple noninvasive tool to determine the cause of low cardiac output and the physiological basis for adjustment of therapy in patients who remain in shock despite 40 mL/kg fluid.
通过多模态监测评估液体难治性小儿感染性休克患者的心血管异常，并描述感染性心肌功能障碍的临床特征。
对第 1 小时内输入 40ml/kg 液体后仍未缓解的感染性休克患者进行前瞻性观察性研究。
印度两家三级转诊 PICUs。
年龄在 1 个月至 16 岁之间、存在液体难治性感染性休克的患者。
在识别感染性休克后 6 小时内，根据临床评估、床边超声心动图和有创血压监测的结果来改变治疗方法。
在 4 年期间，尽管至少输入了 40ml/kg 的液体，但仍有 48 名患者持续处于感染性休克状态。在临床检查中，21 名患者有冷休克，27 名患者有暖休克。41 名患者（85.5%）在有创血压上有血管扩张性休克，其中包括 14 名最初表现为冷休克的患者。最常见的超声心动图表现是 19 名患者（39.6%）左心室和右心室功能受损和 16 名患者（33%）存在低血容量。3 名在第 1 天心肌功能正常的患者在第 3 天出现继发性感染性心肌功能障碍。超声心动图加上有创动脉压监测，使 87.5%的患者能够更精确地滴定液体、正性肌力药和升压药。48 名患者中的 46 名（96%）休克得到缓解，44 名患者（91.6%）存活至出院。
床边超声心动图提供了关键信息，导致识别出感染性心肌功能障碍和临床评估上不明显的未纠正低血容量。有创血压监测结合超声心动图，为确定低心输出量的原因以及在尽管输入 40ml/kg 液体后仍处于休克状态的患者中调整治疗的生理基础提供了一种简单的非侵入性工具。
