Vitamin K Deficieny, Bleeding in the Newborn
Vaginal Bleeding in the Newborn, Vit K deficiency, GI Bleeding
 

• Home birth is associated with many clinical problems, including vitamin K deficiency.
• IM 0.5 to 1.0 mg vitamin K1 (phytonadione) is a routine part of neonatal care in the United States and helps to prevent hemorrhagic disease of the newborn.
• Vitamin K is required to activate the procoagulant factors 2, 7, 9, and 10 as well as proteins C and S, all of which are synthesized in the liver.

All of the following factors contribute to vitamin K deficiency, low levels of vitamin K-dependent factors, and when severe enough, clinical hemorrhagic disease of the newborn:

• Neonatal hepatic immaturity impairs the synthesis of these factors and limits the effectiveness of vitamin K.
• Inefficient transplacental transfer of vitamin K also may be a contributing factor.
• Delayed colonization of the gut by bacteria (which become an endogenous source of vitamin K) is another factor that occurs with delayed feeding, breastfeeding, vomiting,  severe diarrhea, and the use of antibiotics (including those that are present in human milk).

Presentation

• Classic vitamin K deficiency presents in the first week of life (except first 24 hrs) with
  • epistaxis, purpura
  • large cephalohematomas, intracranial hemorrhage
  • melena, GI, GU bleeding
  • bleeding from the umbilical stump, injection sites, and after circumcision.
  • Bleeding occurs most commonly from the second to seventh days of life in healthy, solely breastfed, and often term infants who have not received prophylactic vitamin K.
  • It occurs rarely in formula-fed infants because of the supplemental vitamin K in those products.
  • When prophylactic vitamin K is not administered, the frequency of clinical bleeding averages 1.5%.
  • much more common than the early or late forms of the disease.
• Early vitamin K deficiency
  • severe bleeding within the first 24 hours of life
  • linked to maternal use of medications (most often anticonvulsants (phenobarb, phenytoin), coumadin, also anti-Tb meds) that interfere with vitamin K stores or function.
• Late vitamin K deficiency (2 to 8 weeks of age) is linked to a compromised supply of vitamin K or malabsorption, as seen with
  • exclusive breast feeding without vit K ppx
  • diarrhea
  • cystic fibrosis of the pancreas
  • hepatitis
  • biliary atresia
  • celiac disease
  • may cause: CNS and other life-threatening bleeding

Labs

• In vitamin K deficiency:
  • prolonged PT, PTT are prolonged
  • decreased vitamin K-dependent factors (factors II, VII, IX, and X and proteins C and S) a
  • normal non-vitamin K- dependent factors (factors V, VIII, and fibrinogen)
  • platelet counts are normal.
• Immunoassays, however, will reveal normal antigenic levels of the vitamin K-dependent factors. 

DDX

• Bleeding in the neonate has many other etiologies
• If thrombocytopenia accompanies a prolonged PT and PTT, disseminated intravascular coagulation is likely.
• Factor VIII and IX deficiency hemophilia will cause prolongation of the PTT but not the PT. Both of these disorders  are X-linked recessive and, thus, rarely occur in females.
• Liver disease can be the most confusing aspect of the differential diagnosis. It prolongs the PT and PTT and decreases vitamin K-dependent factors, but factor V and fibrinogen also are decreased. Hepatic function is abnormal in contrast to the normal-for-age function seen in vitamin K deficiency.
• Disorders such as necrotizing enterocolitis and rectal fissures can result in gastrointestinal bleeding in the absence of coagulopathy. However, rectal fissures do not cause melena, and necrotizing enterocolitis rarely occurs in healthy term infants.

Management

• Prophylactic vitamin K is used widely to prevent hemorrhagic disease of the newborn.
• There had been some debate over the necessity of prophylaxis because of the relative rarity of clinically evident hemorrhage and questions of toxicity. However, discontinuation of prophylaxis resulted in a recurrence of hemorrhagic disease of the newborn.
• Current consensus is that prophylaxis should be continued (1 mg Vit K IM)
• The initial dose of vitamin K1 usually is administered in a parenteral dose of 1 mg or an oral dose of 2 mg.
• Subsequent doses have been recommended for infants who are breastfed or who have a malabsorptive disorder.
• In underdeveloped countries, an alternative is administration of oral vitamin K, which is considerably less expensive  to breastfed infants.
• Treatment of clinical hemorrhagic disease of the newborn necessitates frequent doses of subcutaneous or intravenous vitamin K1 (NOT IM); intramuscular administration should be avoided. May also give FFP.
• Improvement will occur within 24 hours with vitamin K1 alone, but plasma should be used to treat infants who are experiencing serious bleeding.

References:
Andrew M. Developmental hemostasis: relevance to newborns and infants.
In: Nathan DG, Orkin SH, Oski FA, Ginsburg D, eds. Nathan and Oski's
Hematology of Infancy and Childhood. 5th ed. Philadelphia, Pa: WB
Saunders Co; 1998:114-158
Grosset ABM, Rodgers GM. Acquired coagulation disorders. In: Lee GR,
Foerster J, Lukens J, Paraskevas F, Greer JP, Rodgers GM, eds.
Wintrobe's Clinical Hematology. 10th ed. Baltimore, Md: Williams &
Wilkins; 1999:1733-1737