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A perspective on the paper by Schulte et al (see page 31)
Despite the many advances of newborn intensive care over the past 20 years, periventricular haemorrhage (PVH) remains a significant cause of morbidity and mortality for the preterm infant. About 15% of infants with birth weight less than 1500 g develop PVH,1 and its presence significantly increases the risk of neurodevelopmental impairment.
New insights have been gained into the pathophysiology of PVH. The germinal matrix, a fragile network of blood vessels lining the ventricular system, is prone to bleeding in the preterm infant. The beagle puppy model of PVH has provided insight into our current understanding of the pathogenetic role of ischaemia and reperfusion.2 In the human preterm infant, depression of cerebral blood flow, associated with initial reduction in myocardial performance and presence of a patent ductus arteriosus, provides an environment in which ischaemia and reperfusion are likely, and PVH occurs more commonly under these circumstances.3
The absence of one unifying aetiological pathway to PVH has left those who practice neonatal medicine without a specific therapeutic strategy that has the capacity to decrease the incidence of PVH. Many therapeutic agents have been investigated over the past 30 years, in the hope of developing such a strategy.
One such agent is etamsylate (diethylammonium 1,4-dihydroxy-3-benzenesulphonate). This non-steroidal drug was shown to be effective in reducing blood loss from menorrhagia4 and after trans-urethral resection of the prostate.5 The benefits of etamsylate in reduction …
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