Transporting babies with known heart disease; who, what and where?

Short abstract

Perspective on the paper by Browning Carmo et al (see page 117)

Intravenous prostaglandin therapy is well established for maintaining or re‐opening the arterial duct in newborns with duct dependent congenital heart disease. An important side effect of prostaglandin therapy is its tendency to cause apnoea. Hence elective intubation and ventilation is usually considered for infants who are transferred between hospitals soon after starting such an infusion.1 The article from Dr Browning Carmo et al2(see page xxx) provides an excellent justification for transporting such infants on intravenous prostaglandin without routine mechanical ventilation. However, although the authors do comment that this may also be suitable for infants with known duct dependent heart disease (ie diagnosed antenatally), they have not highlighted how many, if any, of their own study group fall within this category.

These patients are a challenging group and represent the worst end of the spectrum of congenital heart disease.3,4 Complex single ventricle lesions and severely obstructed systemic or pulmonary circulations are overrepresented compared to the spectrum of postnatally diagnosed problems. Despite this, their parents have usually already committed to active treatment by continuing the pregnancy, and hence parental investment and expectations are often high. The theoretical advantage of diagnosing duct dependent lesions antenatally is that prostaglandin therapy can be instituted from birth to maintain ductal patency and avoid the scenario of postnatal collapse associated with ductal closure. As yet it has not been possible to prove benefit from this in terms of survival figures,5,6,7,8 but it is clear that maintenance of ductal patency requires a much lower dose of prostaglandin than is required to reopen the duct in a collapsed infant. Thus such infants are usually started on around 3–5 ng/kg/min of Prostin in the delivery room or after prompt transfer to the neonatal unit, and the risks of apnoea should be low.

The parents of these infants have generally faced difficult information and choices early on in the pregnancy. They are also usually well informed about the likely cardiac condition of their child by the time of birth. With prompt institution of Prostin therapy it is frequently possible to give these parents much needed ‘quality time' with their long awaited newborn (however delivered) whilst transfer is arranged. Monitoring of peripheral oxygen saturation and the occasional capillary blood gas for acid‐base status can be achieved without major disruption. The parents can rejoin their baby at the cardiac centre as soon as possible after transfer, having had at least some time together to fortify themselves against what is to come.

Very few paediatric cardiac centres in the UK have on‐site obstetric services, and even then, most are in a separate building from the cardiac unit. Many tertiary obstetric units do not have cardiac centres in the same city. Thus if infants with antenatally diagnosed heart abnormalities are born near their home, most will require post‐natal transfer. The practice of routine intubation and ventilation for transfer of these very well looking babies seems unnecessarily intrusive.

But who should transport a well, self ventilating neonate? Are scarce neonatal or cardiac transport resources better reserved for the critically ill? This certainly seems to be an issue in the UK from time to time, leading to requests for such babies to be delivered ‘in house' at the cardiac centre. ‘In house' delivery is generally regarded to be good practice for babies with transposition of the great arteries, as restriction of mixing at the level of the atrial septum may cause severe desaturation after birth despite adequate ductal patency.5 Although at present the majority of such infants are not detected antenatally and have to take their chance, those who are should be delivered where balloon septostomy is promptly available if required. A small number of infants with other severe conditions (such as arrhythmias and hydrops fetalis) may also need ‘in house' delivery negotiated on an individual basis. This can lead to conflicts for space and time at ‘cardiac' obstetric units.

Imposition of ‘planned' delivery at a site distant from the parental home also imposes other problems. Anxiety levels over transport times are raised even for primiparous mothers, and there is always the potential for rapid delivery ‘en route'. There is an increased need for operative delivery from labour induced before term and elective caesarean delivery may be undertaken to avoid ‘uncertainty'. All these carry their risks to both mother and fetus, and also impose additional costs on the delivery units associated with the cardiac centre. These seem unnecessary when it is clearly possible to transport such infants post‐natally in a safe manner, as demonstrated even across the much larger distances involved in Australian transfers2 compared to those in Britain.

Despite centralisation of paediatric intensive care facilities and the establishment of specialised transport teams,9 only one stand‐alone paediatric transport team has yet received dedicated funding in the UK. Funding for neonatal transport teams has only been available for the last 2 years. A transport team for these babies requires a practitioner competent to intubate if necessary, and an understanding of the physiological consequences of mechanical ventilation of such infants is therefore still required. Such babies should be delivered within an obstetric unit with Level 2 neonatal capability in order to safely assess and stabilise them prior to transfer. The question of whether the cardiac unit or the local neonatal team should then transfer the babies remains open.