This document summarizes vitamin K deficiency (VKD). It describes vitamin K's role in blood clotting factor synthesis and the various forms of vitamin K. Risk factors for VKD include poor maternal intake, breastfeeding, and malabsorption issues. Clinical manifestations range from mild bruising to life-threatening bleeding. VKD is diagnosed through prolonged clotting times that normalize with vitamin K administration. Treatment involves parenteral vitamin K with plasma transfusion for severe bleeding. Prevention centers on newborn vitamin K injections and supplementation in high-risk groups.

2. Vitamin
Deficiency
DR.MUJEEBULLAH MAHBOOB
PED-MED RESIDENT AT FMIC
19/10/2015

3. Contents of the presentation
 Overview of vitamin k
 Physiological functions of vitamin k
 Vitamin K deficiency
 Clinical findings of VKD
 Laboratory findings
 Diagnosis and Dx
 Treatment of VKD
 Prevention of VKD
 Conclusion

4. Overview of
 Vitamin k is a fat soluble vitamin necessary for the
synthesis(activation) of clotting factors :
a. Clotting factor II(prothrombin)
b. Clotting factor VII(proconvertin)
c. Clotting factor IX(thromboplastin)
d. Clotting factor X(Stuart factor)
So sometimes it is also called
“clotting vitamin”

5. Overview of…
 Biochemically the term vitamin k refers to all those
compounds that have the common naphthoquinone
ring structure bellow:

6. Overview of…
 Based on the alkyl-(R) group vitamin k may be
classified as:
 vitamin K1 (Phllyoquinone) --- R-phytyl
 vitamin K2 (menaquinone)--- R-prenyl
 vitamin K3 (menadione)—no side chain

7. Vitamin K1 (Phylloquinone)
 One of the natural forms of vitamin k found in plant
sources (Green leafy vegetables such as cabbage,
spinach, cauliflower are highly rich in vitamin k)
 Animal sources (liver) are intermediate and cereals low
in having vitamin k.
 Vitamin k1 is used to fortify foods and as a medication
an the united states.

9. Vitamin K2 (menaquinone)
 Menaquinone is produced by intestinal bacteria and
also present in animal origin foods like:
 Meat especially liver
 Cheese
 Menaquinone is used pharmacologically in some
countries.

10. Synthetic forms of vitamin K
 Vitamin k also has two synthetic forms known as:
 Menadiol or Menadione
 Menadiol diacetate
 These two synthetic forms are converted to
menaquinone in the liver.
 Both synthetic forms are water soluble and are for
treatment of VKD.

12. Absorption and
metabolism
 Water soluble vitamin absorb directly into portal
blood.
 Fat soluble vitamins
Absorbed from intestine via lymph
(requires bile salts for absorption)
Temporarily stored in liver
Metabolized by side chain cleavage
(glucuronide conjugation )
Metabolites are excreted in bile &
urine

13. Physiologic Functions
 Vitamin k is a necessary factor for blood coagulation
because it plays role is as a cofactor in the synthesis of
clotting factors II, VII, IX, X.
 It is necessary for Synthesis of anti-coagulation
Proteins C,S,.
 Also necessary for formation of protein Z.

14. Mechanism of Action

15. Vitamin k deficiency, Etiology
At Birth or first
24hours of life
1-14 days of life 2-12 weeks of life Beyond infancy
a) Maternal
intake of
medications
like: anti-
TB(rifimpine,I
NH), Anti-
convulsants(ph
enobarbital,
phenytoin),
vitamin k
antagonists(wa
rfarin), some
cephalosporin'
s.
a) Poor transport
across the
placenta
b) No intestinal
synthesis of
vit-k2
c) Inadequate
intake
d) No post-natal
prophylaxis
e) Breast-fed
newborns
(delayed
feeding)
a) Breast-feeding
b) Malabsorption
Syn (C.F,
Biliary
obstruction)
c) Chronic use of
broad-
spectrum Abx
d) Diarrhea,
Hepatitis
a) Fat-
malabsorption
b) Prolonged use
of broad-
spectrum Abx.
c) TPN without
vit-k
supplementati
on.
d) Lack of oral
intake.

16. Vitamin k deficiency…
 Fat malabsorption can cause vitamin k deficiency at
any, these syndromes include:
 Cholestatic liver diseases (biliary atresia, alpha-1
antitrypsin deficiency.
 Pancreatic diseases
 Intestinal disorders (celiac sprue, IBD, short-Bowel Syn)
 C.F if liver diseases and pancreatic insufficiency was
present.

17. Vitamin k deficiency…
 Prolonged diarrhea can cause vitamin k deficiency
especially in breast-fed infants.
 Its enough for a patient to receive at least for 10 days a
broad-spectrum anti-biotic to cause vitamin k
deficiency in that patient. (kaplan Med)

18. Clinical Manifestations of VKD
 VKD causes a systemic bleeding disorder in newborn
infants, the Vitamin k-deficiency bleeding (VKDB)
of the newborn.
 Mild vitamin k deficiency can affect long-term bone
and vascular health.

20. Clinical Manifestations of VKD
 Intracranial bleeding can cause convulsion,
permanent sequelae or death.
 In some cases of VKD the presence of the underlying
cause can be suggested in the form of Jaundice or
Failure to thrive.
 Older child with VKD can present with bruising,
mucocutaneous bleeding or a more serious bleeding.

21. LAB Findings of VKD
Abnormal findings Normal findings
Prothrombin time(PT)
Partial thromboplastin time(PTT)
Decreased levels of:
II, VII, IX, X
BT, fibrinogen, platelets, factor5 and 8,

22. LAB Findings of VKD…
 Factor VII has the shortest half-life and is the first
to be affected by VKD.
 In case of Mild VKD the PT is normal but there are
elevated levels of uncarboxylated proteins known
as the Proteins induced by vitamin k absence
(PIVKA).
 Measurement of PIVKA- II can detect mild VKD.
 Measuring of blood vit-k is less useful because of
significant variations based on dietary intake and blood
levels do not always reflect tissue stores of vitamin K.

23. Diagnosis of VKD
 Dx of VKD is established by the presence of prolonged
PT that corrects rapidly after administration of vitamin
K, which stops active bleeding.

24. Differential diagnosis of VKD
 Other possible causes of bleeding and prolonged PT
include:
 DIC
 Liver failure
 Hereditary deficiency of clotting factors.
 Vitamin C deficiency.

25. Differential diagnosis of VKD…
 In DIC mostly due to Sepsis there is consumption of
coagulation factors and Lab investigations shows
thrombocytopenia, low fibrinogen and elevated D-
dimers.
 DIC is characterized by asphyxia, hypoxia, acidosis,
shock and hemangiomas and infection.
 Treatment is to correct the primary clinical problem
such as infection and interrupt consumption of
clotting factors and their replacement.

26. Differential diagnosis of VKD…
 In case of severe liver disorders like cirrhosis the
production of clotting factors is decreased and
administration of vitamin k is not effective (PT may
not correct with vitamin k).
 Children with hereditary disorders have deficiency of
specific factors.

28. Anticoagulants effects on vit-K
 Warfarin and cumarin derivatives inhibit the action of
vitamin k by preventing its recycling to an active form
after it functions as a cofactor for gamma-glutamyl
carboxylase.
 Bleeding can occur with over dosage of warfarin and
ingestion of rodent poison (rat poison) that contains a
coumarin derivate
 High doses of salisylate also inhibit regeneration of
vitamin k and can cause prolongation of PT and
clinical bleeding.

29. Anticoagulants effects on vit-K..
 Warfarin prevents coagulation only in vivo and cannot
prevent coagulation of blood in vitro.
 When warfarin is given to patient 2-3days are required
to see its full anti-coagulant activity and so to prevent
formation of thrombosis in these 3days we must
heparinize the patient ,behind this there are two
issues:
 Warfarin only acts in the liver to inhibit synthesis of the
next generation of the clotting factors, so to run out the
already formed active clotting factors from blood we
must heparinize the patient.

30. Treatment of VKD
 Acute VKDB is treated with 1mg/kg of parenteral
vitamin k(0.5-1.0mg/kg) in newborns.
 After administration of vitamin k
PT should decrease within 6hours and normalize
within 24hours.
 Older children with acute bleeding should receive
2.5-10mg vitamin k IM or IV.
 In addition to vitamin k a Patient with severe and life-
threatening bleeding should receive infusion of fresh-
frozen plasma to correct the coagulapathy rapidly.

31. Treatment of VKD…
 In case of malabsorption chronic administration of
high doses of oral vitamin k(2.5mg twice/wk to
5mg/day) along with bile salts is required.
 To reserve warfarin effects 25-50mg IV vitamin k1
(phytonadione which acts rapidly) is given.
 If severe bleeding occurs 10mg IM followed by 5mg
4hourly is given with this bleeding stops in 6-12hrs
but PT became normal in 24 hrs.

32. Prevention of VKD
 IM Administration of 1mg vitamin k soon after birth
prevents early VKDB.
 Discontinuing the offending medication before
delivery can prevent VKDB if this was not possible
administration of 5-10mg IM vitamin k 4-12 hrs before
delivery to mother may be helpful, in addition the
neonate should receive IM injection of vitamin k
immediately after birth and in severe cases use fresh-
frozen plasma.
 In malabsorption chronic supplementation of vitamin
k and periodic measurement of PT is necessary.

33. Toxicity and adverse effects of
vitamin k
 Fat-soluble vitamin has very low order of toxicity.
 Water-soluble, synthetic vitamin k3 causes:
 Vomiting
 Porphyrinuria
 Albuminuria
 Hemolytic anemia
 Hemoglubinuria
 hyperbilirubinemia

34. Toxicity and adverse effects of
vitamin k
 Rapid IV injection of emulsified vit K causes:
 Flushing
 Breathlessness
 Chest constriction
 Fall in B.P
 Anaphylactic reaction
 Hematomas at the site of IM injection.
 Association between parenteral use of vitamin k at
birth and later development of malignancy is not
confirmed.

35. Vitamin K is also used for
 Anticoagulant drug overdose
 Reduces excessive menstrual blood flow
 Protection against osteoporosis
 Prolonged treatment with broad-spectrum ABx
antibiotics especially in ICU patients.
 Obstructive jaundice, liver cirrhosis, viral hepatitis.
 Prolonged high doses salisylate therapy .

36. Conclusion
 Vitamin k is the mainstay for prevention of and
treatment of vitamin k deficiency bleeding(VKDB).
 Severe bleeding may warrant the use of fresh-frozen
plasma.
 Subcutaneous administration of vitamin k is preferred
over IM route in symptomatic infants.

37. References
 NELSON TEXTBOOK OF PEDIATRICS 20E
medilibros.com_2.pdf
 Current pediatrics Diagnosis and Treatment 18th
edition
 GHAI Essential Pediatrics, 8th edition
 KAPLAN medical pediatrics lecture notes 2008-2009
 www.Medscape.com
 https://www.google.com.af/
 www.slideshare.net/
 https://studentconsult.inkling.com/

40.  Prepared By:
 Dr.mujeebullah Mahboob
 1St year resident of Ped-Med
 FMIC
 Afghanistan, Kabul
 19/10/2015
 01:15pm
 W_mahboob@yahoo.com
 0798984142