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Vitamin K deficiency bleeding (VKDB) is a rare haemostatic disorder that occurs in the first 6 months of life and is subclassified, according to age of presentation, as either early, classical or late VKDB. Late VKDB (day 8 onwards) is the most insidious form, typically presenting between 3 weeks and 8 weeks in exclusively breastfed infants as an intracranial haemorrhage (ICH). Estimations of the prevalence of ICH as the first presenting symptom of late VKDB range from 40% to 80% in different populations1 and so preventing it is a major objective of global healthcare. Vitamin K prophylaxis was first introduced in the 1940s for the treatment and prevention of bleeding in the first week of life (classical VKDB). Because the early use of menadione (vitamin K3) often provoked neonatal haemolytic anaemia and kernicterus, it was replaced in the late 1950s by synthetic phylloquinone (vitamin K1), the major dietary form of vitamin K. By 1961, the American Academy of Pediatrics had concluded that a single intramuscular dose of 0.5–1.0 mg (or oral dose of 1.0–2.0 mg) vitamin K1 was ‘probably adequate for prophylaxis’. In Europe, the 1970s saw a decline in universal vitamin K prophylaxis in favour of selective prophylaxis for infants considered at risk (eg, preterms), a trend no doubt influenced by a supportive 1978 Editorial in the Lancet. This all changed with a spate of case reports from across the world (particularly in the Far East) of what came to be defined as late VKDB …