Prostaglandin E1 is used to maintain ductal patency in critical congenital heart disease (CHD). The standard starting dose of prostaglandin E1 is 0.05 µg/kg/minute. Lower doses are frequently used, but the efficacy and safety of a low-dose regimen of prostaglandin E1 has not been established.

We investigated neonates with critical CHD who were started on prostaglandin E1 at 0.01 µg/kg/minute. We reviewed 154 consecutive patients who were separated into three anatomical groups: obstruction to systemic circulation, obstruction to pulmonary circulation, and inadequate mixing (d-transposition of the great arteries). Treatment failure rates and two commonly reported side effects, respiratory depression and seizure, were studied.

A total of 26 patients (17%) required a dose increase in prostaglandin E1. Patients with pulmonary obstruction were more likely to require higher doses than patients with systemic obstruction (15/49, 31% versus 9/88, 10%, p = 0.003). Twenty-eight per cent of patients developed respiratory depression and 8% of patients needed mechanical ventilation. Prematurity (<37 week gestation) was the primary risk factor for respiratory depression. No patient required dose escalation or tracheal intubation while on transport. No patient had a seizure attributed to prostaglandin E1.

Prostaglandin E1 at an initial and maintenance dose of 0.01 µg/kg/minute was sufficient to maintain ductal patency in 83% of our cohort. The incidence of respiratory depression requiring mechanical ventilation was low and was mostly seen in premature infants. Starting low-dose prostaglandin E1 at 0.01 µg/kg/minute is a safe and effective therapy for critical CHD.

To explore the prevalence and severity of external auditory exostoses in a population of experienced breath-hold divers, and to compare these to the same parameters within surfing and self-contained underwater breathing apparatus diving populations.

A stepwise, multiple regression analysis of cross-sectional data examining the relative contributions of sea surface temperature, latitude of exposure and years of exposure to the prevalence and severity of stenosis due to external auditory exostoses. A chi-square analysis of the prevalence and severity of external auditory exostosis stenosis in the breath-hold divers was compared with previously published data for surfers and self-contained underwater breathing apparatus divers.

Seventy-six male and thirty-five female breath-hold divers attending an international ‘freedive’ competition completed a questionnaire describing aquatic sports habits, geography of participation and symptomatology. Those completing the questionnaire (111/154 attendees) were examined otoscopically for evidence of external auditory exostoses. Images were digitally recorded, scored and graded.

Exostoses were evident in 87.7 per cent of the 204 ears scored and graded for severity of stenosis due to external auditory exostoses. The prevalence of exostoses was no different from that found in previous studies of surfers and self-contained underwater breathing apparatus divers (p = 0.101). However, the pattern of affliction was more similar to that found in surfers. The severity of exostoses was significantly less than that found in surfing populations (p ≤ 0.001 to 0.007), but greater than that found in self-contained underwater breathing apparatus diving populations (p ≤ 0.001). Sea surface temperature at the location of open-water exposure was the most significant predictor of the prevalence and severity of external auditory exostoses in breath-hold divers (p = 0.019).

The prevalence and severity patterns of stenosis due to external auditory exostoses in breath-hold divers are more similar to previously published results for surfing populations than to previously published results for self-contained underwater breathing apparatus diving populations. In breath-hold divers, sea surface temperature is the strongest predictor of severity of stenosis due to external auditory exostoses.

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.