Classical vitamin K deficiency
bleeding in newborn with mother on antitubercular drugs
Bhat M1, More V2
1Dr. Minakshi Bhat, Assistant
professor, department of
pediatrics Terna Medical College ,Nerul, 2Dr.Vaishali More, Fellow Nephrology, Ex professor
department of pediatrics Terna
Medical College, Nerul, Navimumbai, Maharashtra, India
Address for
correspondence: Dr. Minakshi Bhat,
Email: minakshi_libra@yahoo.in
Abstract
Early vitamin K deficiency bleeding in neonate born to a mother on
antitubercular drugs is a known entity .We report a case of a full
term, small for gestation age baby born per vaginally to a mother on
antitubercular drugs. The baby developed classical vitamin K deficiency
bleeding in the form of intracranial bleed on third day of life inspite
of receiving vitamin K at birth.
Key words:
New born, haemorrhagic disease, vitamin K, Antitubercular drugs
Manuscript received:
15th April 2016, Reviewed:
26th April 2016
Author Corrected; 11th
May 2016, Accepted for
Publication: 24th May 2016
Introduction
Vitamin K deficiency bleeding (VKDB ) in infancy is an acquired
coagulopathy secondary to reduction of vitamin K (VK)-dependent
coagulation factors below hemostatic levels [1]. The clinical forms of
hemorrhagic disease due to Vitamin K (VK) deficiency are classified
into early, classic and late on the basis of age of onset and etiology.
Early VKDB (onset less than 24 hours of age) is almost exclusively due
to placental transfer of maternal drugs like anticonvulsants,
antitubercular drugs and VK antagonists which inhibit vitamin K (VK)
activity in the baby. Classical VKDB (onset between 2 to 7 days) occurs
primarily in exclusively breast fed infants due to delayed or
inadequate feeding and who have received no or inadequate neonatal VK
prophylaxis. Late hemorrhagic disease (onset between 8days to 12 weeks)
occurs in exclusively breast fed infants who have not received VK
prophylaxis at birth or have suffered from chronic diarrhea or
cholestatic liver disease [2]. We report a case where a neonate born to
a mother on antitubercular drugs developed classical VKDB in spite of
receiving Vitamin K prophylaxs.
Case
Report
A full term, small for gestation, male baby with birth weight 2.2 kg
was born to a second gravida mother per vaginally. The baby did not
require any resuscitation, received vitamin K prophylaxis and was
exclusively breast fed. The baby was admitted in neonatal intensive
care unit at the age of 56 hours with complains of refusal to feed and
irregular breathing .On examination baby had severe pallor, cyanosis,
tachycardia, shallow respiration, prolonged capillary refill time and
feeble peripheral pulses. He had a bulging and tense anterior
fontenalle of size 3x3 cm. He also had a haematoma on the left thigh at
the site where vitamin K injection was given and was bleeding from all
pricking sites. His central nervous system (CNS) examination showed
hypertonia and dilated but weakly reacting pupils. His investigations
revealed haemoglobin of 7 gm/dl, normocytic normochromic anemia, wbc
count 20,000/cumm, platelet count 2,20,000, prolonged prothrombin
time(PT) 120 seconds, partial thromboplastin time 100sec and normal
liver function tests (LFTS). Ultrasongraphy of skull showed large
intraparenchymal and intraventricular bleed. Initial septic workup was
normal. The baby was resuscitated, put on mechanical ventilator. He
received parentral vitamin K, fresh frozen plasma and pack cell
transfusion, but died on eighth day of hospitalization due to
ventilator associated pneumonia and coagulase negative staphylococcus
sepsis. Maternal history revealed intake of isoniazid and rifampicin by
mother since 5 months of gestation with normal LFTS. Based upon the
age, clinical presentation, abnormal PT and maternal history a
diagnosis of classical VKDB was made.
Discussion
Antenatal use of antitubercular drugs usually leads to early VKDB where
as classical VKDB occurs in exclusively breastfed babies due to delayed
or inadequate feeding. Vk prophylaxis at birth helps in preventing
classical VKDB [1,3,4]. Our case had atypical features. Firstly, the
baby born to a mother on antitubercular drugs had bleeding on the third
day of life and hence the presentation was in classical form. Secondly
classical VKDB commonly presents with bleeding from umbilicus,
circumcision site and gastrointestinal tract, but our case had
intracranial bleed which is a rare manifestation of classical VKDB.
Late HDN commonly presents with intracranial bleed as is suggested by
various studies and case reports [5,6,7]. Thirdly, our case developed
VKDB inspite of receiving prophylactic vitamin K at birth .Now the
question arises , is there any way by which this could have been
prevented ? It has been proved in various studies that early VKDB can
be prevented by prophylactic use of vitamin K antenatally in mother on
antiepileptics [4,8,9,10]. But whether similar prophylaxis will also
help in preventing VKDB in neonates with mother on antitubercular
drugs, more studies need to be done in this regard.
Conclusion
VKDB in neonate born to a mother on antitubercular drugs can occur
inspite of VK prophylaxis at birth and present in classical form also.
Hence the role of antenatal vitamin K prophylaxis in such mothers need
to be studied.
Funding:
Nil, Conflict of
interest: Nil
Permission from IRB:
Yes
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How to cite this article?
Bhat M, More V. Classical vitamin K deficiency bleeding in newborn with
mother on antitubercular drugs. Int J Pediatr
Res.2016;3(5):356-357.doi:10.17511/ijpr.2016.5.14.