VKDB
VKDB
VKDB
Bleeding
Aswini A/P Nalla Mutthu Krishna
Gandi
012013050215
INTRODUCTION
Vitamin K deficiency can cause severe
haemorrhage in the newborn.
The term haemorrhagic disease of the
newborn (HDN) was coined by Charles
Townsend in 1894 to describe an acquired
bleeding disorder in the newborn due to
vitamin K deficiency.
Nowadays, the term HDN is replaced by
vitamin K deficiency bleeding (VKDB), as
neonatal bleeding is often not due to
vitamin K deficiency and VKDB often
occurs after the 4-week neonatal period.
Vitamin K
The following 3 forms of vitamin K are
known:
K 1: Phylloquinone is predominantly
found in green leafy vegetables,
vegetable oils, and dairy products.
Vitamin K given to neonates as a
prophylactic agent is an aqueous,
colloidal solution of vitamin K 1.
K 2: Menaquinone is synthesized by
gut flora.
CLASSIFICATION OF VKDB
Classification Age
1 to 12
Late VKDB
months
EPIDEMIOLOGY
The frequency of vitamin K deficiency
bleeding in varies with the use of vitamin K
prophylaxis, the efficacy of prophylaxis
programs, frequency of breastfeeding, and the
vitamin K content of locally available
formulas.
Late vitamin K deficiency bleeding has fallen
from 4.4-7.2 cases per 100,000 births to 1.4-
6.4 cases per 100,000 births in reports from
Asia and Europe after regimens for
prophylaxis were instituted.
THANK YOU
ETIOLOGY AND
PATHOPHYSILOG
Y
AZAHARI B.MOHD SHARI
EARLY-ONSET VKDB
Cephalhematoma
Ventouse delivery.
Intracranial bleeding
Usually associated with maternal medication that block
action of vitamin K
Examples: Anti-tubercular, Anti-convulsant, Anti-Coagulant
Intrathoracic bleeding
Gastrointestinal bleeding.
Exclusive breastfeeding
Fat malabsorbtion
Biliary atresia
PATHOPHYSIOLOGY
Newborn infants at risk of Vit. K deficiency
1. Immature liver does not efficiently utilize Vit. K
Classical VKDB
1. Gastrointestinal tract
2. Umbilicus
3. Skin
4. Nose
5. Circumcision site
CLINICAL FEATURES
COMMON BLEEDING SITE
Late-onset VKDB
1. Intra-cranial
2. Gastrointestinal tract
3. Skin
DIFFERENTIAL DIAGNOSIS
Differential diagnosis Description
Disseminated intravascular Usually occur secondary to sepsis
coagulation (DIC) Prolonged PT, PTT,
thrombocytopenia
Elevated D-dimers level
Decreasing plasma fibrinogen
Liver failure Prolonged PT & PTT
Normal platelets count
Increased level of liver enzyme &
bilirubin level
Haemophilia Prolonged PTT
Normal PT and platelets count
Family history of haemophilia
Factor VIII & IX inhibitor screen
DIFFERENTIAL DIAGNOSIS
Differential diagnosis Description
Immune Thrombocytopenia Purpura Thrombocytopenia
Thrombotic Thrombocytopenia Normal PT and PTT
Purpura
Von Willebrands disease Normal PT, PTT and platelets count
Family history of bleeding diathesis
VWF maybe be low or increased
Plasma factor VIII is reduced
Other rare congenital clotting factor Factors V and X deficiency will
deficiencies have prolonged PT and PTT
Factors V, VII, X, XI, XII, XIII Factors XI, XII, XIII will have
prolonged PTT and normal PT
Factors VII deficiency will have
prolonged PT and normal PTT
INVESTIGATION
i. Coagulation profile
Prothrombin time (PT)
International normalised ratio (INR)
and
https://www.aap.org/en-us/Pages/Defau
lt.aspx
https://www.cdc.gov/ncbddd/vitamink/fa
cts.html
http://emedicine.medscape.com/article
/974489-treatment#showall
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HASHIMAH MOHD
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012012100319
FOLLOW-UP VISIT: (Needed if the
patient present with the same signs and
FOLLOW-UP PLAN
symptoms after treatment)