Spätform der Vitamin K-Mangelblutung. Bericht über 57 Fälle

Sutor, A. H.; Pollmann, H.; Kries, Rüdiger von; Brückmann, C; Jörres, H.; Künzer, W

doi:10.1007/978-3-642-73589-9_47

Cited by 4 publications

(8 citation statements)

References 4 publications

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“…Correspondingly, except for one infant with classical haemorrhagic disease of the newborn,23 most case reports of failures of vitamin K prophylaxis concern late disease.' 24 Epidemiologically, intramuscular vitamin K prophylaxis appears to have a lower incidence of failure.8 In a recent survey in the British Isles, 27 cases of haemorrhagic disease of the newborn were recorded.8 Seven of them occurred in spite of oral vitamin K prophylaxis at birth. No failures were recorded after intramuscular administration, although there was uncertainty about intramuscular vitamin K in one case.…”

Section: Discussionmentioning

confidence: 99%

Effects of oral and intramuscular vitamin K prophylaxis on vitamin K1, PIVKA-II, and clotting factors in breast fed infants.

Cornelissen

Kollée

Abreu

et al. 1992

Archives of Disease in Childhood

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A randomised clinical trial was conducted to establish the effects of oral and intramuscular administration of vitamin K at birth on plasma concentrations ofvitamin K1, proteins induced by vitamin K absence (PIVKA-II), and clotting factors. Two groups of about 165 healthy breast fed infants who received at random 1 mg vitamin K1 orally or intramuscularly after birth were studied at 2 weeks and 1 and 3 months of age. Although vitamin K1 concentrations were statistically significantly higher in the intramuscular group, blood coagulability, activities of factors VII and X and PIVKA-II concentrations did not reveal any difference between the two groups. At 2 weeks of age vitamin K, concentrations were raised compared with reported unsupplemented concentrations and no PIVKA-II was detectable. At 3 months vitamin K1 concentrations were back at unsupplemented values and PIVKA-II was detectable in 11.5% of infants. Therefore, a repeated oral prophylaxis will be necessary to completely prevent (biochemical) vitamin K deficiency beyond the age of 1 month.

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Section: Discussionmentioning

confidence: 99%

Effects of oral and intramuscular vitamin K prophylaxis on vitamin K1, PIVKA-II, and clotting factors in breast fed infants.

Cornelissen

Kollée

Abreu

et al. 1992

Archives of Disease in Childhood

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“…28 The lower incidence of 30 to 60% in newer reports might be explained by changing policies of VK prophylaxis. Similarly, mortality declined from 23 to 6% between 1980 and 1990, 6,25 with overall mortality for the period at 19%. 12 This reflects the effect of an increase in prophylaxis with vitamin K, as does the low mortality in countries with almost 100% acceptance of prophylaxis, such as 6% in Sweden, 5 7% in Britain, 11 and 14% in Switzerland.…”

Section: Age At Onsetmentioning

confidence: 96%

“…11,12 At risk are breastfed infants, and boys are affected twice as often as girls. 12 A cluster of VKDB in the warmer months of the year was found in Germany, 12,25 in Great Britain, 11 and in Japan, where in addition a higher incidence was observed in the warmer Japanese islands in the South. 26,27 In early reports the incidence of intracranial bleeding in infants with VKDB was as high as 65 to 100%.…”

Section: Age At Onsetmentioning

confidence: 98%

“…4 Warning signs of VKDB are inconspicuous and rare in the idiopathic forms. 25 They are more common and evident in the secondary forms of VKDB: In a study by Auerswald and Sutor 29 all 10 patients with α 1 -antitrypsin deficiency had warning signs, in some cases weeks before the onset of serious hemorrhage (jaundice in the neonatal period, symptoms of minor bleeding from the second week on, failure to thrive, vomiting). Unfortunately these signs could only be recognized retrospectively after intra cranial bleeding had occurred.…”

Section: Age At Onsetmentioning

confidence: 99%

“…VKDB has also been re ported as the first sign of an underlying disorder, such as biliary atresia, cytomegaly, mucoviscidosis, and vi ral infection. 4,5,11,12,25 Vitamin K Deficiency Bleeding After Infancy. After infancy, VKDB is rare and almost always of second ary origin, that is, due to absorption problems or medica tions.…”

Section: Age At Onsetmentioning

confidence: 99%

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Vitamin K Deficiency Bleeding in Infants and Children

Sutor¹

1995

Semin Thromb Hemost

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The historical term "hemorrhagic disease of the newborn," which is used as a synonym for vitamin K deficiency bleeding (VKDB) in infancy, preferably should be abandoned, since neonatal bleeding is often not due to vitamin K (VK) deficiency and VKDB may occur after the neonatal period. VKDB is a form of bleeding that is caused by reduced activity of VK-dependent coagulation factors (II, VII, IX, X), has normal or even increased activity of VK-independent coagulation factors, and responds to VK. Acarboxy proteins are present. In a bleeding infant a prolonged one-stage prothrombin time (a decreased Quick value, which means prothrombin time expressed as percent of normal) in association with a normal (or increased) fibrinogen level and platelet count is almost diagnostic of VKDB. The diagnosis is proven, if administration of VK is followed by a shortening of the prothrombin time (after only 30 minutes) or cessation of bleeding. Classification is by age of onset as early, classic, and late form of VKDB. Rare cases of VKDB occur also after week 15; therefore the upper age limit should be 6 months and not 3 months. In idiopathic VKDB the cause (ther than breast-feeding) is unknown. In secondary VKDB additional factors can be demonstrated, such as poor intake or absorption of VK and increased consumption of VK. Most often cholestasis is present. Postnatal VK provides effective protection from the classic and late form of VKDB. The classic form can be prevented equally well by a single oral dose of 1 mg VK after birth as by parenteral VK. Parenteral prophylaxis appears to be more effective in preventing the late form, especially in patients with hepatobiliary disease. The protection achieved by single oral prophylaxis can be improved by repeated oral administration. In addition to reducing the incidence of VKDB, VK prophylaxis also reduced the proportion of intracranial hemorrhages and increases the age at onset of bleeding, parenteral prophylaxis being more effective than single oral prophylaxis in this respect. Because of the potential risks (cancer?) associated with extremely high levels of VK (20,000-fold the normal value for healthy newborns) and the possibility of injection injury, parenteral VK has been questioned as the first choice of prophylaxis for normal neonates. These disadvantages do not apply to oral prophylaxis. The major disadvantage of oral prophylaxis, namely, its lesser reliability in terms of intake and absorption, could be largely overcome by repeated administration. Although VK prophylaxis seems to be necessary only for breast-fed infants, breast-feeding should be promoted. As VK is involved not only in coagulation but also in carboxylation with multiple effects, care should be taken to avoid any excessive deviation from the physiologic conditions, that prevail in the fully breast-fed healthy mature infant, with low VK levels in the postnatal period. Repeated (daily or weekly) oral doses of VK are closer to physiologic conditions than single parenteral bolus doses, which expose neonates to excessiv...

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