Related Experiment Videos
Late form of vitamin K deficiency bleeding in Germany
A H Sutor1, N Dagres, H Niederhoff
1Universitäts-Kinderklinik Freiburg/Germany.
Insights
Vitamin K deficiency bleeding (VKDB) predominantly affects breastfed infants, often presenting with intracranial bleeding and significant mortality. Vitamin K prophylaxis is crucial for preventing this serious, albeit rare, condition.
Area of Science:
- Pediatrics
- Hematology
- Neonatology
Background:
- Vitamin K deficiency bleeding (VKDB) is a serious condition in infants.
- Evaluation of VKDB cases provides insights into disease characteristics and prevention.
Observation:
- VKDB primarily affects fully breastfed infants, with a peak incidence at four weeks of age.
- Intracranial bleeding is common (58%), leading to high mortality (19%) and neurological damage (21%).
- Cholestasis was noted in 37% of patients; sudden onset with no warning signs is typical.
Findings:
- Low Quick value with normal fibrinogen and platelet levels are key diagnostic indicators.
- Vitamin K administration rapidly normalizes the Quick value.
- Vitamin K prophylaxis significantly reduces VKDB incidence, with parenteral administration being more effective in hepatobiliary disorders.
Implications:
- VKDB is a preventable disease through timely vitamin K prophylaxis.
- Parenteral vitamin K prophylaxis is more effective than oral for certain infant populations.
- Understanding VKDB risk factors and prophylaxis efficacy is vital for infant health.
Background:
The evaluation of the disease of vitamin K deficiency bleeding (VKDB).
Method:
108 reported cases between 1980 and 1990 from Germany.
Results:
VKDB occurs preferentially (90%) in fully breastfed infants, males are affected nearly twice as often as females. The peak age is four weeks; the majority (79%) of the infants are between three and seven weeks old. 58% of the patients suffer from intracranial bleeding, which results in a total mortality rate of 19% and in neurological damage in 21%. Generally the VKDB occurred suddenly as no warning signs were noticed or they were so insignificant as not to be heeded. In at least 37% of the patients cholestasis was detected. The Quick value was pathologically low in every case. Vitamin K dependent factors were low and PIVKA was detectable, whereas vitamin K independent hemostatic parameters were normal or even elevated. The combination of low Quick value and normal fibrinogen as well as platelet level is a good diagnostic indicator which can be confirmed by administration of vitamin K, after which the Quick value will rise within 30 minutes. Vitamin K prophylaxis reduces the incidence of VKDB from 5.13 per 100,000 births to a tenth of that; single dose oral prophylaxis reduces the risk by a factor of 3.3 and a single parenteral dose by 14.3. Parenteral prophylaxis is more effective in patients with hepatobiliary disorders. Patients who suffered VKDB despite having received vitamin K prophylaxis are older at onset (without prophylaxis 32 days, with oral prophylaxis 37 days, and with parenteral prophylaxis 63 days) and have less intracranial bleeding (35%) than patients who received none (62%).
Conclusion:
Late form of VKDB is a rare but serious disease which can be prevented by VK-prophylaxis.