Newborn Resuscitation Skills in Health Care Providers at a Zambian Tertiary Center, and Comparison to World Health Organization Standards.

BACKGROUND: Birth asphyxia is a leading cause of early neonatal death. In 2013, 32% of neonatal deaths in Zambia were attributable to birth asphyxia and trauma. Basic, timely interventions are key to improving outcomes. However, data from the World Health Organization suggest that resuscitation is often not initiated, or is conducted suboptimally. Currently, there are little data on the quality of newborn resuscitation in the context of a tertiary center in a lower-middle income country. We aimed to measure the competencies of clinical practitioners responsible for newborn resuscitation. METHODS: This observational study was conducted over 5 months in Zambia. Health care professionals were recruited from anesthesia, pediatrics, and midwifery. Newborn skills and knowledge were examined using the following: (1) multiple-choice questions; (2) a ventilation skills test; and (3) 2 low-medium fidelity simulation scenarios. Participant demographics including previous resuscitation training and a self-efficacy rating score were noted. The primary outcome examined performance scores in a simulated scenario, which assessed the care of a newborn that failed to respond to basic interventions. Secondary outcome measures included apnea times after delivery and performance in the other assessments. RESULTS: Seventy-eight participants were enrolled into the study (13 physician anesthesiology residents, 13 pediatric residents, and 52 midwives). A significant difference in interprofessional performance was observed when examining checklist scores for the unresponsive newborn simulated scenario (P = .006). The median (quartiles) checklist score (out of 18) was 14.0 (13.0-14.75) for the anesthesiologists, 11.0 (8.5-12.3) for the pediatricians, and 10.8 (8.3-13.9) for the midwives. A score of 14 or more was required to pass the scenario. There was no significant difference in performance between participants with and without previous newborn resuscitation training (P = .246). The median (quartiles) apnea time after delivery was significantly different between all groups (P = .01) with anesthetic and pediatric residents performing similarly, 61 (37-97) and 63 (42.5-97.5) seconds, respectively. The midwifery participants displayed a significantly longer apnea time, 93.5 (66.3-129) seconds. Self-efficacy rating scores displayed no correlation between confidence level and the primary outcome, Spearman coefficient 0.06 (P = .55). CONCLUSIONS: Newborn resuscitation skills among health care professionals are varied. Midwives lead the majority of deliveries with anesthesiologists and pediatricians only being present at operative or high-risk births. It is therefore common that midwifery practitioners will initiate resuscitation. Despite this, midwives perform poorly when compared to anesthesia and pediatric residents. To address this discrepancy, a multidisciplinary, simulation-based newborn resuscitation program should be considered with continual clinical reenforcement of best practice.

The yellow fluorescent protein (YFP-H) mouse reveals neuroprotection as a novel mechanism underlying chondroitinase ABC-mediated repair after spinal cord injury.

Chondroitinase ABC (ChABC) represents a promising therapeutic strategy for the treatment of spinal cord injury due to its potent effects on restoring function to spinal-injured adult mammals. However, there is limited mechanistic insight as to the underlying effects of ChABC treatment, where the effects are mediated, and which signaling pathways are involved in ChABC-mediated repair. Here we use a transgenic (YFP-H) mouse to demonstrate that cortical layer V projection neurons undergo severe atrophy 4 weeks after thoracic dorsal column injury and that ChABC is neuroprotective for these neurons after ICV infusion. ChABC also prevented cell atrophy after localized delivery to the spinal cord, suggesting a possible retrograde neuroprotective effect mediated at the injury site. Furthermore, neuroprotection of corticospinal cell somata coincided with increased axonal sprouting in the spinal cord. In addition, Western blot analysis of a number of kinases important in survival and growth signaling revealed a significant increase in phosphorylated ERK1 at the spinal injury site after in vivo ChABC treatment, indicating that activated ERK may play a role in downstream repair processes after ChABC treatment. Total forms of PKC and AKT were also elevated, indicating that modification of the glial scar by ChABC promotes long-lasting signaling changes at the lesion site. Thus, using the YFP-H mouse as a novel tool to study degenerative changes and repair after spinal cord injury we demonstrate, for the first time, that ChABC treatment regulates multiple signaling cascades at the injury site and exerts protective effects on axotomized corticospinal projection neurons.

Therapeutic time window for the application of chondroitinase ABC after spinal cord injury.

Rats with a crush in the dorsal funiculi of the C4 segment of the spinal cord were treated with chondroitinase ABC delivered to the lateral ventricle, receiving 6 intraventricular injections on alternate days. In order to investigate the time window of efficacy of chondroitinase, treatment was begun at the time of injury or after a 2, 4 or 7 days delay. Behavioural testing over 6 weeks showed that acutely treated animals showed improved skilled forelimb reaching compared to penicillinase controls. Forelimb contact placing recovered in treated animals but not controls, and gait analysis showed recovery towards normal forelimb stride length in treated animals but not controls. Chondroitinase-treated animals showed greater axon regeneration than controls. The treatment effect on contact placing, stride length and axon regeneration was not dependent on the timing of the start of treatment, but in skilled paw reaching acutely treated animals recovered better function. The area of chondroitinase ABC digestion visualized by stub antibody staining included widespread digestion around the lateral ventricles and partial digestion of cervical spinal cord white matter, but not grey matter.