After controlling for arm position, 47% of PICCs placed in the upper limb migrated at 24 hours postinsertion with 32.6% migrating toward the heart. We recommend a follow-up X-ray at 24 hours postinsertion for all catheters placed in the upper limb.
We used the isolated-perfused rat lung model to study the influence of pulmonary ventilation and surfactant instillation on the development of postreperfusion lung microvascular injury. We hypothesized that the state of lung inflation during ischemia contributes to the development of the injury during reperfusion. Pulmonary microvascular injury was assessed by continuously monitoring the wet lung weight and measuring the vessel wall (125)I-labeled albumin ((125)I-albumin) permeability-surface area product (PS). Sprague-Dawley rats (n = 24) were divided into one control group and five experimental groups (n = 4 rats per group). Control lungs were continuously ventilated with 20% O(2) and perfused for 120 min. All lung preparations were ventilated with 20% O(2) before the ischemia period and during the reperfusion period. The various groups differed only in the ventilatory gas mixtures used during the flow cessation: group I, ventilated with 20% O(2); group II, ventilated with 100% N(2); group III, lungs remained collapsed and unventilated; group IV, same as group III but pretreated with surfactant (4 ml/kg) instilled into the airway; and group V, same as group III but saline (4 ml/kg) was instilled into the airway. Control lungs remained isogravimetric with baseline (125)I-albumin PS value of 4.9 +/- 0.3 x 10(-3) ml x min(-1) x g wet lung wt(-1). Lung wet weight in group III increased by 1.45 +/- 0.35 g and albumin PS increased to 17.7 +/- 2.3 x 10(-3), indicating development of vascular injury during the reperfusion period. Lung wet weight and albumin PS did not increase in groups I and II, indicating that ventilation by either 20% O(2) or 100% N(2) prevented vascular injury. Pretreatment of collapsed lungs with surfactant before cessation of flow also prevented the vascular injury, whereas pretreatment with saline vehicle had no effect. These results indicate that the state of lung inflation during ischemia (irrespective of gas mixture used) and supplementation of surfactant prevent reperfusion-induced lung microvascular injury.
Nosocomial infections are the most common complications encountered in the neonatal intensive care unit (NICU). They are associated with high mortality and prolonged duration of hospitalization in the survivors, contributing to an increased cost of health care. In this article, we review the literature on the value of routine endotracheal aspirate cultures for the prediction of neonatal sepsis and provide guidelines to prevent nosocomial infections. Upon reviewing the literature it appears that the practice of routine cultures of endotracheal aspirate and cultures obtained from multiple body sites is an expensive proposition with low yield. The sensitivity of this test is at best 50% and all studies report a very low positive predictive value. The specificity of this test is 80%, hence its role is mainly limited to identifying infants who are at low risk for sepsis. As we do not have any reliable test for early diagnosis of neonatal sepsis and also to identify infants at high risk for sepsis, our main emphasis should be towards preventing nosocomial infections. Guidelines for reducing nosocomial infections are described.
Escherichia coli as a causative agent for neonatal sepsis is well established. However, there is paucity of reports in the medical literature of E. coli sepsis following scalp electrode placement. We report a preterm infant who developed scalp abscess and E. coli sepsis following a scalp electrode. We recommend a careful examination of babies with a history of fetal electrode monitoring as this could be a nidus for local and generalised infection.
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