Rarely does a very low birthweight infant escape at least 10 ml/kg of colloid in the first few hours of life. Most units do not give volume routinely on admission, in the same way that most units don’t prescribe routine antibiotics, yet almost every very preterm baby gets both, as routinely as vitamin K or a photograph for the mother. In the case of antibiotics there is usually some feature of the history or examination that can be invoked to suggest a risk of infection, even if the mother had an elective caesarean section. In the case of colloid there is always a slight metabolic acidosis, or a lowish temperature on arrival from labour ward, or a casual tweak of the big toe by a passing consultant which, of course, provides conclusive proof of hypovolaemia.

A few hours later the baby is warmer and pinker, peripheral perfusion is improved (the ritual toe tweak evokes a satisfied hmm rather than a tut-tut), the base deficit is less, so the colloid must have worked. But is this necessarily cause and effect? These improvements may well have occurred without specific treatment.

The clinical instinct to improve peripheral perfusion and blood pressure fairly quickly after birth is not purely cosmetic in very preterm infants who are at major risk of both haemorrhagic and ischaemic cerebral lesions. Both intraventricular haemorrhage (IVH) and periventricular leucomalacia have been attributed to hypotension and cerebral hypoperfusion,1 but does routine volume expansion prevent these complications of prematurity?

In 1985 Beverley et al 2 randomised 80 infants who were <1500 g birthweight or <32 weeks of gestation, or both, to a regimen of 10 ml/kg fresh frozen plasma (FFP) on admission and again 24 hours later, or to a control group who were to be given “small volumes” of purified …