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Intracranial hemorrhage (ICH) can be a devastating complication of extracorporeal life support (ECLS); however, studies on the timing of ICH detection by head ultrasound (HUS) are from 2 decades ago, suggesting ICH is diagnosed by day 5 of ECLS. Given advancements in imaging and critical care, our aim was to evaluate if the timing of ICH diagnosis in infants on ECLS support has changed. Patients6 months old undergoing ECLS 2011-2020 at a tertiary care children's hospital were included. Primary outcome was timing of ICH diagnosis on HUS. Seventy-four infants underwent ECLS for cardiac (54%) or pulmonary (46%) indications. Venoarterial ECLS was most common (88%). Median ECLS duration was 6 days (range 1-26). Sixteen patients were diagnosed with ICH (21.6%), at a median of 2 days postcannulation (range 1-4). Nearly all were4 weeks old at cannulation (93.8%). In conclusion, one-fifth of infants developed ICH diagnosed by HUS while on ECLS, all within the first 4 days of ECLS, consistent with previous literature. Despite advances in critical care and imaging technology, the temporality of ICH diagnosis in infants on ECLS is unchanged.

BACKGROUND: Pediatric patients immobilized for certain procedures, such as extracorporeal membrane oxygenation (ECMO), are at high risk for developing hospital-acquired pressure injuries (HAPIs). PURPOSE: To evaluate the rate of HAPI occurrence in ECMO patients before and after implementation of prevention interventions. METHODS: Patients younger than 18 years of age who were placed on ECMO from January 2012 through March 2020 were identified, and patient data, including the development of a stage 3, 4, or unstageable pressure injuries, were abstracted. From August 2018 through December 2018, HAPI prevention interventions were implemented, which included targeted HAPI prevention and ECMO provider education, fluidized positioner provider education, and the addition of 2 wound care interventions for ECMO patients. RESULTS: Of the 120 ECMO patients identified, 5 (4.2%) developed a HAPI. All patients developed HAPI in the occipital region, and 1 patient developed an additional HAPI on their back. The median age of patients with HAPI was 1 month (interquartile range [IQR], 0.3–6.8 months). The median duration from ECMO cannulation to identification of HAPI was 9.5 days (IQR, 4.8–32.3 days). The median total run time was 4.9 days (IQR, 2.5-7.6 days): 8.5 days for patients who did develop a HAPI and 4.8 days for those who did not develop a HAPI (P = .02). The overall HAPI rate dropped from 4.8% of ECMO patients before quality improvement interventions to 0% of ECMO patients after quality improvement interventions. CONCLUSIONS: The development of stage 3, 4, or unstageable HAPIs in pediatric ECMO patients was low (4.2%) over the period studied (January 2012 through March 2020). As of the time of this writing, no HAPIs occurred after implementation of provider education in 2018.

The COVID-19 pandemic has created multiple, complex and intense demands on hospitals, including the need for surge planning in the many locations outside epicenters such as northern Italy or New York City. We here describe such surge planning in an Academic Health Center that encompasses a children's hospital. Interprofessional teams from every aspect of inpatient care and hospital operations worked to prepare for a COVID-19 surge. In so doing, they successfully innovated ways to integrate pediatric and adult care and maximize bed capacity. The success of this intense collaborative effort offers an opportunity for ongoing teamwork to enhance efficient, effective, and high-quality patient care.

Extracorporeal Life Support (ECLS) is rarely used in pediatric trauma patients due to bleeding risk, and the use of ECLS following angioembolization of traumatic hemorrhage has never been reported in a child. We report a case of a 10-year-old boy run over by a parade float resulting in severe thoracic, abdominal, and pelvic trauma, with hemorrhage from pelvic fractures requiring massive transfusion. Due to ongoing blood product requirements and contrast extravasation near the symphysis pubis, angioembolization of the internal iliac arteries was performed. Extreme hypoxemia persisted despite maximal ventilator support due to pulmonary contusions and aspiration pneumonitis. Six hours after angioembolization, venovenous ECLS was initiated. Following an initial heparin bolus, ECLS was run without anticoagulation for 12 h, but development of circuit clot required resumption of low-dose heparin. After four days, his respiratory status improved substantially and ECLS was discontinued. There were no hemorrhagic complications. The patient was discharged home in good health following inpatient rehabilitation. In this case, ECLS was successfully used in the treatment of post-traumatic respiratory failure 6 h following angioembolization of pelvic hemorrhage in a pediatric trauma patient. Further research is needed to determine the safest interval between hemorrhage control and ECLS in severely injured children.

Introduction: Pediatric patients are immobilized for certain procedures such as extracorporeal membrane oxygenation (ECMO). These procedures place the patient at high risk for developing hospital acquired pressure injuries (HAPI). The purpose of this quality improvement initiative was to implement HAPI prevention interventions and provider education and to evaluate the rate of HAPI occurrence in ECMO patients before and after implementation. We hypothesized that the number of ECMO patients who developed a HAPI would decrease. Methods: All …

Pregnancy-associated increases in uterine artery (UA) blood flow are due, in part, to vasoactive and growth-related changes that enlarge UA diameter. Although active and passive mechanical factors can contribute to this enlargement, their role is less well understood. We hypothesized that pregnancy increased UA distensibility and/or decreased myogenic tone. Given the fetal growth restriction and lower UA flow seen under chronic hypoxia, we further hypothesized that chronic hypoxia opposed these normal active and passive mechanical changes. UA were isolated from 12 nonpregnant and 12 pregnant (0.7 gestation) guinea pigs housed under normoxia or chronic hypoxia (3,960 m) and studied by pressure myography. Pregnancy increased UA diameter similarly under normoxia and hypoxia. Although chronic hypoxia raised resting tone in UA from nonpregnant guinea pigs to ∼20% and tone was greater in preconstricted pregnant chronically hypoxic vs. normoxic UA (both P < 0.01), there was an absence of myogenic response (i.e., an increase in tone with rising pressure) in all groups. Pregnancy increased UA distensibility 1.5-fold but did not change stiffness or the stress-strain relationship. Compared with vessels from normoxic pregnant animals, hypoxic pregnancy raised UA distensibility fourfold, decreased stiffness (rate constant b = 3.80 ± 1.06 vs. 8.92 ± 1.25, respectively, P < 0.01), lowered elastin by 50%, and shifted the stress-strain relationship upward such that four times as much strain was present at a given stress. We concluded that increased distensibility and low myogenic tone contribute to enlarging UA diameter and raising UA blood flow during pregnancy. Chronic hypoxia exaggerates the rise in distensibility and alters the stress-strain relationship in ways that may provoke vascular injury.

We tested the hypotheses that pregnancy increases the uterine artery (UA) vasodilator response to flow and that this increase is impaired under conditions of chronic hypoxia (30 days, simulated elevation 3,960 m). UA were isolated from 24 normoxic or chronically hypoxic midpregnant guinea pigs and studied with the use of pressure myography. Normoxic pregnancy increased UA flow vasodilator response and protected against a rise in wall shear stress (WSS). Chronic hypoxia opposed these effects, prompting vasoconstriction at high flow and increasing WSS above levels seen in normoxic pregnant UA. The nitric oxide synthase inhibitor N G-nitro-l-arginine (l-NNA) eliminated the pregnancy-associated increase in flow vasodilation in normoxic UA, suggesting that increased nitric oxide production was responsible. The considerable residual vasodilation after nitric oxide synthase and cyclooxygenase inhibition implicated endothelial-derived hyperpolarizing factor (EDHF) as an additional contributor to flow vasodilation.l-NNA increased flow vasodilation in UA from chronically hypoxic animals, suggesting that chronic hypoxia may have lowered EDHF or elevated peroxynitrite production. In conclusion, flow is an important physiological vasodilator for the acute and more chronic UA dimensional changes required to increase uteroplacental blood flow during normal pregnancy. Chronic hypoxia may be a mechanism that opposes the pregnancy-associated rise in UA flow vasodilation, thereby increasing the incidence of preeclampsia and intrauterine growth restriction at a high altitude.