Out-of-hospital cardiac arrests terminated without full resuscitation attempts: Characteristics and regional variability.

BACKGROUND: Out-of-hospital cardiac arrest (OHCA) investigations may elect to exclude cases with resuscitation terminated for reasons other than a full resuscitative attempt. We sought to examine characteristics of these cases and regional variability in classification. METHODS: Using the North American Resuscitation Outcomes Consortium Epistry, we included adult emergency medical services (EMS)-treated cases, examining the rationale ("futility", do-not resuscitate [DNR] order, "verbal directive", or "obvious death") and timing of resuscitation termination, and the timing of ROSC among hospital-discharge survivors. We tested regional variability in EMS patient arrival-to-termination intervals with one-way ANOVA. RESULTS: Of 63,554 included cases, 27,232 were declared dead in the prehospital setting: (1) 23,009 (36%) for futility (after a median of 24 minutes [IQR 19-31] of professional resuscitation); (2) 1622 (2.6%) for a DNR order (at 6.3 minutes [IQR 3.0-11]); (3) 1018 (1.6%) for a verbal directive (at 12 minutes [IQR 7.0-17]); and, (4) 1583 (2.5%) for obvious death (at 5.4 minutes [IQR 3.0-9.0]). The EMS patient arrival-to-ROSC interval among hospital-discharge survivors was 7.7 (3.8-13) minutes. Among regions, 0.20-12% and 0.20-5.3% were terminated to due to obvious death or verbal directives, respectively. There were significant regional differences in the EMS patient arrival-to-termination interval for futility (p < 0.010) and obvious death (p < 0.010). CONCLUSION: There is significant variation in the rationale and interval until termination of resuscitation between regions. Cases terminated due to obvious death or DNR orders/verbal directives are often treated with similar durations of resuscitation as survivors. These data highlight a considerable risk of bias in between-region comparisons or observational analyses.

Morphological maladaptations in sympathetic preganglionic neurons following an experimental high-thoracic spinal cord injury.

Spinal cord injury (SCI) disrupts the supraspinal vasomotor pathways to sympathetic preganglionic neurons (SPNs) leading to impaired blood pressure (BP) control that often results in episodes of autonomic dysreflexia and orthostatic hypotension. The physiological cardiovascular consequences of SCI are largely attributed to the plastic changes in spinal SPNs induced by their partial deafferentation. While multiple studies have investigated the morphological changes in SPNs following SCI with contrasting reports. Here we investigated the morphological changes in SPNs rostral and caudal to a high thoracic (T3) SCI at 1-, 4- and 8-weeks post injury. SPNs were identified using Nicotinamide adenine dinucleotide hydrogen phosphate-diaphorase (NADPH- diaphorase) staining and were quantified for soma size and various dendritic measurements. We show that rostral to the lesion, soma size was increased at 1 week along with increased dendritic arbor. The total dendritic length was also increased at chronic stage (8 weeks post SCI). Caudal to the lesion, the soma size or dendritic lengths did not change with SCI. However, dendritic branching was enhanced within a week post SCI and remained elevated throughout the chronic stages. These findings demonstrate that SPNs undergo significant structural changes form sub-acute to chronic stages post-SCI that likely determines their functional consequences. These changes are discussed in context of physiological cardiovascular outcomes post-SCI.