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Vitamin K deficiency bleeding (VKDB) in early infancy
1The Centre for Haemostasis and Thrombosis, St. Thomas' Hospital, Westminster Bridge Road, London, UK. martin.shearer@gstt.nhs.uk
Insights
Vitamin K deficiency bleeding (VKDB) is a serious infant disorder. Parenteral vitamin K at birth is the most effective prevention, particularly for late-onset cases.
Area of Science:
- Pediatrics
- Neonatology
- Hematology
Background:
- Vitamin K deficiency bleeding (VKDB) is a rare but severe bleeding disorder in infants.
- Infants are born with low vitamin K stores, and breast milk has low concentrations, increasing risk.
- Classical VKDB occurs in the first week, while late VKDB (3-8 weeks) often involves intracranial hemorrhage due to malabsorption.
Purpose of the Study:
- To review the epidemiology, diagnosis, and prevention of Vitamin K deficiency bleeding (VKDB).
- To highlight the effectiveness of different vitamin K prophylaxis strategies.
Main Methods:
- Review of existing literature on VKDB incidence, risk factors, and prevention.
- Discussion of diagnostic methods, including PIVKA-II measurements.
- Analysis of the efficacy of oral versus parenteral vitamin K prophylaxis.
Main Results:
- Late VKDB incidence is higher in Southeast Asia compared to Europe without prophylaxis.
- Parenteral vitamin K offers the best protection against VKDB.
- Oral prophylaxis efficacy varies with dose and frequency, with some infants with undetected liver disease remaining at risk.
Conclusions:
- Vitamin K deficiency bleeding (VKDB) is largely preventable with appropriate vitamin K administration.
- Parenteral vitamin K prophylaxis is superior to oral routes for comprehensive protection.
- Targeted surveillance of high-risk infants is a potential strategy to improve prophylaxis efficacy.
Abstract:
Vitamin K deficiency bleeding (VKDB) is a rare and potentially life-threatening bleeding disorder of early infancy. Vitamin K stores are low at birth; thereafter breast-fed infants are at risk because of low concentrations in human milk. Classical VKDB occurs in the first week of life, is related to delayed or inadequate feeding and is readily prevented by small doses of vitamin K at birth. Late VKDB peaks at 3-8 weeks, typically presents with intracranial haemorrhage often due to undiagnosed cholestasis with resultant malabsorption of vitamin K. Diagnosis can be difficult but PIVKA-II measurements can provide confirmation even several days post-treatment. Without vitamin K prophylaxis, the incidence of late VKDB in Europe is 4-7 cases per 10(5) births; it is higher in SE Asia where in rural, low-income areas some 0.1% of affected infants may suffer intracranial bleeding. Late VKDB is largely preventable with parenteral vitamin K providing the best protection. The efficacy of oral prophylaxis is related to the dose and frequency of administration. Most multi-dose oral regimens provide protection for all except a small reservoir of infants with undetected hepatobiliary disease. Targeted surveillance of high-risk groups (e.g. biliary atresia) offers a novel approach to assess efficacy of prophylaxis.
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