ABSTRACT
BACKGROUND: Central venous catheters (CVC) are commonly required for pediatric congenital cardiac surgeries. The current standard for verification of CVC positioning following perioperative insertion is postsurgical radiography. However, incorrect positioning may induce serious complications, including pleural and pericardial effusion, arrhythmias, valvular damage, or incorrect drug release, and point of care diagnostic may prevent these serious consequences. Furthermore, pediatric patients with congenital heart disease receive various radiological procedures. Although relatively low, radiation exposure accumulates over the lifetime, potentially reaching high carcinogenic values in pediatric patients with chronic disease, and therefore needs to be limited. We hypothesized that correct CVC positioning in pediatric patients can be performed quickly and safely by point-of-care ultrasound diagnostic. METHODS: We evaluated a point-of-care ultrasound protocol, consistent with the combination of parasternal craniocaudal, parasternal transversal, suprasternal notch, and subcostal probe positions, to verify tip positioning in any of the evaluated views at initial CVC placement in pediatric patients undergoing cardiothoracic surgery for congenital heart disease. RESULTS: Using the combination of the four views, the CVC tip could be identified and positioned in 25 of 27 examinations (92.6%). Correct positioning was confirmed via chest X-ray after the surgery in all cases. CONCLUSIONS: In pediatric cardiac patients, point-of-care ultrasound diagnostic may be effective to confirm CVC positioning following initial placement and to reduce radiation exposure.
ABSTRACT
BACKGROUND AND GOAL OF THE STUDY: Pulmonary inflammation, increased vascular permeability, and pulmonary edema, occur in response to primary pulmonary infections like pneumonia but are also evident in endotoxemia or sepsis. Mechanical ventilation augments pre-existing lung injury and inflammation resulting from exposure to microbial products. The objective of this study was to test the hypothesis that low-tidal-volume prevent ventilation induced lung injury in sepsis. MATERIALS AND METHODS: 10-12-week-old male C57BL/6N-mice received an intraperitoneal (i.p.) injection with equipotent dosages of LPS, 1668-thioate, 1612-thioate, or PBS. 120 min after injection, mice were randomized to low- (LV, 7 ± 1 ml/kg) or high-tidal-volume (HV, 25 ± 1 ml/kg) ventilation. Hemodynamic and ventilatory parameters were recorded and inflammatory markers were analyzed form BAL that was generated after 90 minute ventilation. RESULTS AND DISCUSSION: Arterial blood pressures declined during mechanical ventilation in all groups. pO2 decreased in LPS injected and CO2 increased in sham, LPS, and 1612-thioate administered mice at 45 min and in 1668-thioate injected mice after 90 minute LV ventilation compared to respective HV groups. BAL protein concentrations increased in HV ventilated and 1668- or 1612-thioat pre-treated mice. BAL TNF-α protein concentrations increased in both LPS- and 1668-thioate-injected and IL-1ß protein concentrations only in LPS-injected and HV ventilated mice. Most notably, no increased protein concentrations were observed in any of the LV ventilated groups. CONCLUSION: We conclude that low-tidal-volume ventilation may be a potential strategy for the prevention of ventilator induced lung injury in a murine model of systemic TLR agonist induced lung injury.
