Multimodal Monitoring for Hemodynamic Categorization and Management of Pediatric Septic Shock

Authors:
  • GAGnanam Aram
    Gnanam Aram
  • MAMhd Kashif Ali
    Mhd Kashif Ali
  • RNRajeshwari Natraj
    Rajeshwari Natraj
  • SSSharad Shresti
    Sharad Shresti
  • IJIndira Jayakumar
    Indira Jayakumar
  • DGDeepika Gandhi
    Deepika Gandhi
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Abstract
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.

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