Vitamin K deficiency

Vitamin K is an essential fat-soluble vitamin for the human body and plays an important role in the coagulation process. Vitamin K deficiency can occur at any age and is most common in infants. The incidence of vitamin K deficiency varies in different regions. The incidence of asymptomatic vitamin K deficiency in children under 5 years old can be as high as 50%. Overt bleeding symptoms can occur in 0.25% to 1.7% of infants. In breastfed infants after birth, if prophylactic vitamin K supplementation is not given, the incidence of late hemorrhagic disease is 20 per 100,000. When infants have vitamin K deficiency, it can lead to hemorrhagic disease of the newborn. The main causes of vitamin K deficiency include: (1) low levels of vitamin K transferred to the fetus through the placenta; (2) low levels of vitamin K in breast milk; (3) small amounts of vitamin K synthesized by intestinal bacteria in infants can cause vitamin K deficiency; (4) immature hepatic prothrombin synthesis function in infants. The main clinical manifestations of vitamin K deficiency are: skin ecchymosis, petechiae, hematoma, and oozing from surgical or puncture sites. Infants may also have other physical defects, such as developmental abnormalities of the face, nose, bones, and fingers. The treatment of vitamin K deficiency depends on the severity of bleeding and the underlying disease state. If patients with vitamin K deficiency are identified early and treated appropriately, the prognosis is good. To date, there have been no reports of death due to vitamin K deficiency. However, if vitamin K deficiency is not controlled, severe bleeding may occur. The incidence of bleeding is related to the severity of vitamin K deficiency. The most effective treatment is exogenous vitamin K supplementation. It should be noted that hematoma may occur at the injection site. For life-threatening bleeding, fresh frozen plasma should be given first, followed by vitamin K. In adults, vitamin K1 can be administered subcutaneously or intramuscularly. If vitamin K deficiency cannot be corrected after vitamin K supplementation, the possibility of liver disease or disseminated intravascular coagulation should be considered. If there is concern about hematoma formation from intramuscular or subcutaneous injection, vitamin K can also be given orally, at a dose of 5 to 20 mg depending on the severity of the deficiency. Absorption of the oral formulation requires bile salts in the ileum and is therefore less stable. The oral formulation is suitable for asymptomatic vitamin K deficiency. Vitamin K3, a synthetic water-soluble compound, is used to treat vitamin K deficiency associated with dyspepsia and malabsorption syndromes; however, because high doses may induce hemolysis, it is not suitable for newborns. In emergency situations, 10-20 mg of vitamin K1 can be dissolved in 5% glucose or 0.9% normal saline for intravenous infusion. During the infusion, the patient's condition needs to be closely monitored. Cardiopulmonary arrest and/or shock are occasionally seen. Intravenous administration of vitamin K1 can correct vitamin K deficiency within 12 to 24 hours.