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, intraabdominal

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