VITAMIN K

DEFICIENCY
HEMATOLOGY ONCOLOGY DIVISION
Introduction

The vitamin K :
K1: phytonadione or phylloquinone
(Aquamephyton): is a natural
derivative from fish or plants
K2: menaquinone: fat-soluble form
made by intestinal bacteria
K3: menadione: the synthetic
water-soluble form tends to have a
greater degree of toxicity
 The recommended dietary allowance (RDA) for
vitamin K:

adult males: 80 mcg

adult females: 65 mcg

children 7 to 10 years: 30 mcg

infants: 10 mcg

pregnant and lactating women 65 mcg

 Source

Leafy vegetables (spinach,

kale,collards, brocoli)
Pork
Liver
Vegetable oils (soybean oil,olive oil,
cottonseed oil, canola oil)
Intestinal flora
Synthesized by bacteria
 Epidemiology

In adults, Vitamin K deficiency is

uncommon
In infants, Vitamin K deficiency without
bleeding may occur in as many as 50%
of infants younger than 5 days old
The classic haemorrhagic disease
:occurs in 0.25-1.7% of infants
The prevalence of late haemorrhagic
disease 20 per 100,000 live births with
no prior prophylaxis with Vitamin K
Risk Factors
Excessive anticoagulation with Coumarins, eg
Warfarin
Liver disease: e.g. cirrhosis, malignancy,
amyloidosis and Gauchers disease decrease the
synthesis of Vitamin K-dependent factors
Malabsorption: coeliac disease, tropical sprue,
Crohns disease, ulcerative colitis, Ascaris
infection, short bowel syndrome due to multiple
abdominal surgeries, bacterial overgrowth, and
chronic pancreatitis
Biliary tract disease: common duct obstruction
due to stones and strictures, primary biliasy
cirrhosis, cholangiocarcinoma, and chronic
cholestasis. Leads to a decrease in fat absorption
and so a deficiency of fat-soluble vitamins
Risk Factors
Dietary deficiency occurs in people with
malnutrition, including people with alcoholism,
as well as patients undergoing long-term
parenteral nutrition without Vitamin K
supplements.
Drugs: Cholestyramine, cefamandole,
salicylates, rifampin,isoniazid and barbiturates
are some of the common drugs that are
associated with Vitamin K deficiency.
Diseases with endogenously produced
coagulation inhibitors (e.g. lupus anticoagulant
and antithrombins) and paraproteinaemias such
as myeloma, may cause vitamin K deficiency.
Miscellaneous causes include massive
transfusion, DIC,polycythaemia vera, nephrotic
syndrome, cystic fibrosis and leukaemia
Vitamin K
Function
Involved in the formation of:
Prothrombin (factor II)
Coagulation factors VII, IX, X

Factors dependent on Vitamin K

Protein C, S (anticoagulants)
Protein Z
Bone matrix proteins
 The deficiency syndrome is
traditionally known as haemorrhagic
disease of the newborn or more
recently, to give a better definition of
the cause, vitamin K deficiency
bleeding (VKDB)
Classification of vitamin K deficiency
bleeding of the newborn
Syndrome Time of presentation Common bleeding
sites

Early VKDB 0-24 hours Cephalohaematoma,

intracranial,
intrathoracic, intra-
abdominal

Classic VKDB 1-7 days Gastrointestinal,

skin, nasal,
circumcision
Late VKDB 1-12 weeks Intracranial, skin,
gastrointestinal
 Early hemorrhagic disease of the
newborn :
The placenta transmits lipids and vitamin K
relatively poorly
The neonatal liver is immature with respect
to prothrombin synthesis
Breast milk is low in vitamin K, containing
about 2.5 g/L (cow's milk contains 5000
g/L)
The neonatal gut is sterile during the first
few days of life
 Late hemorrhagic disease of the
newborn
Breastfeeding
Malabsorption
Liver disorder
Diagnosis

Lab findings
PT/PTT usually prolonged
Fibrinogen, platelet, bleeding time,
thrombin time normal
Vitamin K levels not usually helpful
Most sensitive indicator
des--carboxyprothrombin (DCP)
PIVKA (Plasma Induced in Vitamin
K Abscence or Antagonism)
Management

Therapy depends on the severity of

the bleeding and the underlying cause

In life-threatening bleeds, Fresh

Frozen Plasma should be administered
prior to Vitamin K

Vitamin K is available as
phytomenadione (vitamin K) and as
the synthetic water-soluble analogue
menadiol sodium diphosphate
Management

Intravenous injections should be

given slowly as fast intravenous
injection can cause bronchospasm
and peripheral vascular collapse

Intramuscular injections may lead to

severe haematoma formation at the
injection site if clotting is impaired
Prognosis

Patients have a very good prognosis

if the Vitamin K deficiency is
recognized early and treated
appropriately

Morbidity correlates with severity of

Vitamin K deficiency, but severe
bleeding can be fatal
Prevention

Dosages for IM and Oral Vitamin K

The recommended route of
administration is intramuscular, being
given at birth, and that this should be
as a single IM injection:
Term babies 0.5-1mg IM soon after birth
Preterm 0.5mg IM soon after birth

Parents should be advised that with

intramuscular injection, the risk of
haemorrhagic disease of the newborn
is extremely low.
Prevention

If parents do not consent to IM but

consent to oral vitamin K, this needs
to be given in 3 separate doses
according to the following regime:
2mg oral soon after birth
2mg oral at 3-7 days
2mg oral at 6 weeks