Background Delivery of non‐invasive ventilation commonly occurs in the pediatric intensive care unit (PICU). With the advent of high‐flow nasal cannula (HFNC), patients with respiratory distress may be rescued on the ward without a PICU admission. We evaluated our ward HFNC algorithm to determine its safety profile and independent predictors for non‐responders, defined as requiring subsequent PICU admission. Methods A retrospective chart review of patients <17 years of age admitted with respiratory distress between 2016 and 2017 was carried out. Pediatric Early Warning System (PEWS) respiratory score was used to assess the clinical response of patients requiring HFNC. Variables associated with non‐responders were evaluated, and their PICU admission was studied for escalation of care and criticality. Results Patients with comorbidities (P = 0.02) were more likely to require HFNC. Of the 18 patients initiated on HFNC, 44% (n = 8) remained on the ward. Non‐responders (n = 10; 56%) had higher (2.7 vs 1.8; P = 0.03) and worsening (−0.1 vs 0.3; P = 0.05) PEWS respiratory scores 90 min after HFNC initiation. Eighty percent (n = 8) of non‐responders required escalation to continuous positive airway pressure or bilevel positive airway pressure in the PICU. For both HFNC responders and non‐responders, there were no requirements for intubation, evidence of air leak or difference in days of respiratory support. Conclusions High and worsening PEWS scores 90 min after HFNC initiation may indicate non‐response when coupled with a standardized ward HFNC algorithm for respiratory distress. Further improvements may be seen with an earlier initiation of HFNC in the emergency department and more aggressive flow escalation on the ward.
Mechanical ventilation strategies in pediatric acute respiratory distress syndrome (pARDS) continue to advance. Optimizing positive end expiratory pressure (PEEP) and ventilation to recruitable lung can be difficult to clinically achieve. This is in part, due to disease evolution, unpredictable changes in lung compliance, and the inability to assess regional tidal volumes in real time at the bedside. Here we report the utilization of thoracic electrical impedance tomography to guide daily PEEP settings and recruitment maneuvers in a child with pARDS.
Pediatric ARDS continues to be a management challenge in the ICU with prolonged hospitalizations and high mortality. Thromboembolic pulmonary embolism and in situ pulmonary artery thrombosis might represent underappreciated thrombotic processes for a subset of these patients. Although well described in the adult literature, descriptions of pulmonary thromboses with pediatric ARDS are limited to case reports. However, many risk factors for pulmonary thromboses are present in children with ARDS (eg, coagulopathy, endothelial injury, central venous catheters, concomitant inflammatory diseases), suggesting a much higher incidence is plausible. Based on an interpretation of animal, pediatric, and adult data, we propose a diagnostic algorithm to facilitate a timely and accurate diagnosis. Observing an alveolar dead space fraction > 0.25, or either a 50% increase in physiologic dead space/tidal volume or a central venous saturation < 60% over 24 h, triggers the algorithm. Together with targeted heparin treatment and right ventricular afterload reduction, clinical outcomes might improve if this particular patient subgroup can be identified early. While anticoagulation is recommended in adults with confirmed pulmonary embolism and low early mortality risk, data for children are limited.
Titrating ventilator settings to minimize pulmonary arterial pressures and optimize both ventilation and oxygen delivery can be challenging following cardiac arrest. Erroneous ventilator adjustments can lead to unnecessary strain on the right ventricle that may be particularly vulnerable during the acute recovery. We report a child with fulminant myocarditis who was mechanically ventilated using thoracic electrical impedance tomography to optimize regional lung inflation and possibly curtail right ventricular afterload following cardiac arrest.
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