A significant gap exists between people awaiting an organ transplant and organ donors. The purpose of this study was to determine what percent of successful donors come from the emergency department (ED), whether there are any missed donors, and to identify factors associated with successful and missed donation.

This systematic review used electronic searches of EMBASE, MEDLINE, and CINAHL according to PRISMA guidelines on July 7, 2017. We included primary literature in adults describing successful and missed organ donation. Two authors independently screened articles, and discrepancies were resolved through consensus. Quality was assessed using the STROBE checklist.

This systematic review identified 1,058 articles, and 25 articles were included. For neurologic determination of death, ED patients comprised 4%–50% of successful donors and 3.6%–8.9% of successful donors for donation after circulatory determination of death. ED death reviews revealed up to 84% of missed neurologic determination of death, and 46.2% of missed circulatory determination of death donors who died in the ED are missed due to a failure to refer for consideration of organ donation. Clinical heterogeneity precluded pooling of the data to conduct a meta-analysis.

The ED is a source of actual and missed donors. Potential donors are often missed due to incorrect assumptions regarding eligibility criteria and failure of the healthcare team to refer for consideration of donation. ED healthcare professionals should be aware of organ donation referral protocols at their institution to ensure that no organ donors are missed.

A majority of transplanted organs come from donors after brain death (BD). Renal grafts from these donors have higher delayed graft function and lower long-term survival rates compared to living donors. We designed a novel porcine BD model to better delineate the incompletely understood inflammatory response to BD, hypothesizing that adhesion molecule pathways would be upregulated in BD.

Animals were anesthetized and instrumented with monitors and a balloon catheter, then randomized to control and BD groups. BD was induced by inflating the balloon catheter and animals were maintained for 6 hours. RNA was extracted from kidneys, and gene expression pattern was determined.

In total, 902 gene pairs were differently expressed between groups. Eleven selected pathways were upregulated after BD, including cell adhesion molecules.

These results should be confirmed in human organ donors. Treatment strategies should target involved pathways and lessen the negative effects of BD on transplantable organs.

Diagnosis of brain death usually requires the absence of spontaneous respiratory movements during the apnoea test and an arterial carbon dioxide partial pressure above 60 mmHg. On the other hand, although capnography (end-tidal CO2) is currently monitored in intensive care unit patients, it has not been evaluated during the apnoea test in brain-dead patients. Therefore, the aim of this prospective study was first to investigate the usefulness of capnography monitoring, and secondly to evaluate the variation of the carbon dioxide partial pressure–end-tidal CO2 gradient during the apnoea test in clinically brain-dead patients.

After local Ethics Committee approval, 60 clinically brain-dead patients were investigated. End-tidal CO2 was continuously recorded before, during and after the apnoea test. Arterial blood gases were sampled immediately before and after the apnoea test for calculation of the carbon dioxide partial pressure–end-tidal CO2 gradient.

The apnoea test was clinically positive in 58 patients, whereas end-tidal CO2 was equal to 0 during the apnoea. During the 20-min apnoea test, carbon dioxide partial pressure increased from 40 ± 7 to 97 ± 19 mmHg (P < 0.001) with a rate of 2.8 ± 0.9 mmHg min−1, end-tidal CO2 increased from 31 ± 6 to 68 ± 17 mmHg (P < 0.001) and carbon dioxide partial pressure–end-tidal CO2 gradient increased from 9 ± 4 to 29 ± 10 mmHg (P < 0.001). In two patients, the apnoea test was clinically negative because of the occurrence of spontaneous respiratory movements, whereas capnography showed contemporaneously significant increases in end-tidal CO2.

End-tidal CO2 should be systematically monitored and recorded, at least for medico-legal considerations, during the apnoea test in brain-dead patients. The high variability in the carbon dioxide partial pressure–end-tidal CO2 gradient increase precludes any extrapolation of the carbon dioxide partial pressure from the end-tidal CO2 at the end of the apnoea test.