There is near‐global consensus that all newborns be given parenteral vitamin K₁ (VK₁) at birth as prophylaxis against VK deficiency bleeding (VKDB). Breastmilk has a low VK content and cases of late VKDB are reported in exclusively breastmilk‐fed preterm infants despite VK prophylaxis at birth. To assess the prevalence of functional VK insufficiency in preterm infants based on elevated under‐γ‐carboxylated (Glu) species of Gla proteins, factor II (PIVKA‐II), and osteocalcin (GluOC), synthesized by liver and bone, respectively. Prospective, multicenter, observational study in preterm infants born <33 weeks' gestation. Blood samples and dietary history were collected before hospital discharge, and after discharge at 2–3 months’ corrected age. Outcome measures were serum VK₁, PIVKA‐II, and %GluOC (GluOC as a percentage of the sum of GluOC plus GlaOC) compared between exclusively breastmilk‐fed and formula/mixed‐fed infants after discharge. After discharge, breastmilk‐fed babies had significantly lower serum VK₁ (0.15 vs. 1.81 μg/L), higher PIVKA‐II (0.10 vs. 0.02 AU/ml) and higher %GluOC (63.6% vs. 8.1%) than those receiving a formula/mixed‐feed diet. Pre‐discharge (based on elevated PIVKA‐II), only one (2%) of 45 breastmilk‐fed infants was VK insufficient. After discharge, eight (67%) of 12 exclusively breastmilk‐fed babies were VK insufficient versus only one (4%) of 25 formula/mixed‐fed babies. Preterm infants who remain exclusively or predominantly human breastmilk‐fed after neonatal unit discharge are at high risk of developing subclinical VK deficiency in early infancy. Routine postdischarge VK₁ supplementation of breastfed infants to provide intakes comparable to those from formula milks should prevent this deficiency.

Difenacoum is a long-acting superwarfarin-type anticoagulant that exerts its effect through inhibiting vitamin K 2,3-epoxide reductase. Inhibition of this enzyme leads to reduced bioavailability of the metabolically active form of vitamin K resulting in decreased production of vitamin K-dependent proteins including coagulation factors II, VII, IX and X. A 45-year-old woman with psychiatric illness presented with haematuria. Laboratory test results indicated she had been exposed to a vitamin K antagonist which was subsequently identified as difenacoum. She was initially treated with phytomenadione, red cell suspension and octaplex. She was discharged on 30 mg phytomenadione daily but monitoring of vitamin K markers indicated that compliance was poor, and 152 days post-admission she presented with haemoptysis. Difenacoum and other superwarfarin rodenticides are freely available for purchase by the public. Cases such as this continue to raise issues about their availability and regulation.

All newborns need extra phylloquinone (vitamin K₁; K₁) to prevent vitamin K deficiency bleeding (VKDB). In preterm babies, the main sources are prophylactic K₁ given at birth and parenteral and/or enteral feeding thereafter. Preterm babies are at risk of late-onset VKDB if ongoing K₁ supplementation is inadequate. For extremely preterm infants fed an exclusive human milk diet, the low K₁ content of human milk may predispose them to vitamin K deficiency. Human milk fortification with either bovine milk-derived fortifier or human milk-based fortifier (HMF) made from pooled donor milk is a widely used strategy to improve the micronutrient and growth status of preterm infants. However, the K₁ content of HMF is markedly lower than that of bovine-based preparations. We present an unusual case of late-onset VKDB in an extremely preterm infant who received an exclusive human milk diet and HMF and quantify total K₁ intake prior to the bleeding.

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