The Surprising Truth About Vitamin K Nobody Tells You

Video transcript :-

Vitamin K is an essential fat soluble vitamin that plays a critical role in the production of coagulation factors, including factor 2, 7, 9, and 10.
It is also essential for the production of proteins C and S, which are anti-coagulant proteins.
Vitamin K is also required for the carboxylation of glutamic acid residues of osteocalcin, a calcium binding protein the bone.
Major sources of vitamin K include leafy greens such as kale, Swiss chard, collard greens, and spinach.
Beef liver.
Chicken.
Beans.
And oils such as olive oil, soybean oil, and canola oil.
Additionally, vitamin K is also produced by the gut bacteria.
Vitamin K deficiency can affect individuals of all ages, but is much more common in newborns.
In neonates, vitamin K deficiency can occur due to several factors.
Including reduced transmission of vitamin K across the placenta, liver prematurity, lack of vitamin K in breast milk, and the sterile gut in neonates, which cuts off the fraction of vitamin K that comes from the gut bacteria.
Therefore, vitamin K is given prophylactically to the neonate during birth.
Parental refusal of vitamin K prophylaxis may result in various bleeding manifestations.
Additionally, neonatal cholestatic disease can also lead to vitamin K deficiency.
In adults, vitamin K deficiency can be caused by various factors, including chronic illnesses, abdominal surgery, malabsorption syndromes, alcoholism, long term parenteral nutrition, cholestatic disease, infective diarrhea, liver disease, cystic fibrosis, inflammatory bowel disease, massive blood transfusion, disseminated intravascular coagulation, chronic kidney disease, and certain medications.
Including antibiotics such as cephalosporins, warfarin, salicylates, anticonvulsants, and sulfa drugs.
The clinical manifestations of vitamin K deficiency are only seen if the patients’ prothrombin time is low.
Bleeding is the predominant symptom, especially following minor trauma.
Common bleeding manifestations include epistaxis, hematoma formation, gastro-intestinal bleeding, heavy menstrual bleeding, hematuria, gum bleeding, and oozing from venipuncture sites.
Examination may reveal ecchymosis and petechiae.
Additional findings in infants may include birth defects such as underdevelopment of the face, nose, bones, and fingers.
In infants, vitamin K deficiency can be complicated with hemorrhagic disease of the newborn, which manifests as intracerebral hemorrhage and retroperitoneal bleeding.
In adults, osteoporosis may occur due to reduced gamma carboxylation of osteocalcin.
In vitamin K deficiency, prothrombin time is typically high, but the activated partial thromboplastin time is normal.
However in severe disease, both PT and APTT can be prolonged.
A delayed INR, typically more than 3.5, with a normal fibrinogen and platelet count is highly suggestive of vitamin K deficiency.
Confirmation of vitamin K deficiency requires the measurement of specific vitamin K dependent coagulation factors in blood.
Medical therapy of vitamin K deficiency depends on the severity of the disease.
In adults, vitamin K should be administered subcutaneously or intramuscularly.
If the prothrombin time does not normalize following vitamin K supplementation, presence of liver disease or disseminated intravascular coagulation should be excluded.
Oral vitamin K administration should be considered when there is a risk of hematoma formation with intramuscular route.
Oral vitamin K is also used to treat asymptomatic vitamin K deficiency.
Finally, in life-threatening bleeds, fresh frozen plasma should be administered prior to vitamin K.

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