Causes of vitamin K deficiency
- Vitamin K deficiency can result from lack of vitamin K in the diet. In adults, low dietary intake alone is seldom reason for severe vitamin K deficiency but may become common in association with the use of broad-spectrum antibiotics.
- From disorders that impair fat absorption and that thus reduce the absorption of vitamin K.
- Disease or surgical interventions that affect the ability of the intestinal tract to absorb vitamin K, either through anatomic alterations or by changing the content of bile salts and pancreatic juices in the proximal small bowel, can result in significant reduction of vitamin K levels.
- Chronic liver diseases such as primary biliary cirrhosis also deplete vitamin K stores.
- Taking large amounts of mineral oil may reduce the absorption of vitamin K.
- Inherited deficiency of the functional activity of the enzymes involved in vitamin K metabolism result in bleeding disorders.
- Vitamin K deficiency in the newborn can be present for various reasons-
- Maternal medications that interfere with vitamin K stores or function (eg, carbamazepine, phenytoin, barbiturates, some cephalosporins, rifampin, isoniazid, warfarin or warfarin like drugs) can result in vitamin K deficiency bleeding in the infant.
- Transplacental transfer of vitamin K is very limited during pregnancy,
- The storage of vitamin K in neonatal liver is also limited.
- Breast milk is a poor source of vitamin K.
- The other causes for late onset of vitamin K deficiency in infants include-
- Cystic fibrosis
- Celiac disease
- Short bowel syndrome
- Chronic exposure to broad spectrum antimicrobials
Newborn infants are at risk of developing vitamin K deficiency, and this coagulation abnormality leads to serious bleeding. This makes the newborn infant uniquely vulnerable to hemorrhagic disorders unless exogenous vitamin K is given for prevention of bleeding immediately after birth.
Once the infantile gut is colonized with bacterial flora, the microbial production of vitamin K, results in a lower risk of infantile vitamin K deficiency bleeding. A gut-related microbial source of vitamin K is particularly important if dietary phylloquinone is restricted.
The most common sites of hemorrhage or bleeding are the umbilicus, mucus membrane, the GI tract, circumcision, and venipuncture sites. Hematomas frequently occur at the sites of trauma (ie, large cephalohematomas, scalp bruising related to instrumentation used at delivery, and, rarely, intracranial hemorrhage). Neonatal mortality and long-term neurologic morbidity are severe consequences of vitamin K deficiency bleeding.
Breast milk is a poor source of vitamin K (breast milk levels are 1-4 μ g/L). The recommended dietary intake of vitamin K is 1 μ g/kg/d. Exclusively breastfed infants have intestinal colonization with lactobacilli that do not synthesize vitamin K; thus, reduced production of menaquinones increases the neonatal risk of developing a hemorrhagic disorder if not supplemented with vitamin K. Formula-fed infants have higher fecal concentrations of vitamin K1 because of dietary intake and significant quantities of fecal menaquinones, reflecting the gut’s microflora.
Preterm infants who are receiving total parenteral nutrition (TPN) are not at risk because they are receiving vitamin K via the multivitamin additive to the TPN. Special consideration is needed for very low birth weight infants whose intestinal tract bacterial flora is altered because of multiple courses of broad-spectrum antimicrobials. Once preterm infants are weaned off of TPN, they may develop vitamin K deficiency if they are exclusively fed breast milk.
The routine intramuscular administration of vitamin K immediately after birth has made vitamin K deficiency bleeding an uncommon occurrence.
- The main symptom is bleeding (hemorrhage)—into the skin (causing bruises), from the nose, from a wound, in the stomach, or in the intestine.
- Sometimes bleeding in the stomach causes vomiting with blood.
- Blood may be seen in the urine or stool. In newborns, life-threatening bleeding within or around the brain may occur.
- Having a liver disorder increases the risk of bleeding because proteins that help blood clot (clotting factors) are made in the liver.
- Vitamin K deficiency may also weaken bones.
- Most newborn infants are healthy upon examination, even if early onset bleeding is present; however, intracranial hemorrhage can occur during the delivery process and can lead to severe complications.
- Internal hemorrhage of organs other than the brain may be difficult to detect; however, if they are suspected, careful physical monitoring and serial imaging after birth are indicated.
- Soft tissue hemorrhages may be there.
- A Prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen levels, and a platelet count should be included in the initial workup for vitamin K deficiency bleeding (VKDB) in a newborn.
- A prolonged PT is usually the first laboratory test result to be abnormal in vitamin K deficiency bleeding due to reduction in Prothrombin, FVII, FIX, and FX levels.
- A direct blood measurement of vitamin K is not useful because levels normally are low in newborns.
- Infants with vitamin K deficiency bleeding typically have a prolonged PT with platelet counts and fibrinogen levels within the normal range for newborns.
- Thrombocytopenia or a prolonged aPTT should prompt workup for other causes of bleeding during the neonatal period.
- The diagnosis of vitamin K deficiency bleeding is confirmed if administration of vitamin K halts the bleeding and reduces the PT value.
- MRI exposes the neonate to no radiation and is becoming the preferred way to study the brain because tissue damage can be better defined.
- A full coagulopathy work-up and hematology consultation are required if clinical and laboratory findings are suggestive of non–vitamin K deficiency bleeding.
- A work-up that includes functional tests and imaging are mandatory if liver disease is suspected.
- Hereditary defects in the coagulation system must always be considered among the differential diagnoses.
A vitamin K injection in the muscle is recommended for all newborns to reduce the risk of bleeding within the brain after delivery. Otherwise, vitamin K is usually taken by mouth or given by injection under the skin. If a drug is the cause, the dose of the drug is adjusted or extra vitamin K is given. For patients with chronic malabsorption, 1–2 mg/d of vitamin K should be given orally, or 1–2 mg/week can be taken parenterally. Patients with liver disease may have an elevated prothrombin time because of liver cell destruction as well as vitamin K deficiency. If an elevated prothrombin time does not improve on vitamin K therapy, it can be deduced that it is not the result of vitamin K deficiency.
People who have vitamin K deficiency and a severe liver disorder may also need blood transfusions to replenish the clotting factors. A damaged liver may be unable to synthesize clotting factors even after vitamin K injections are given.
The reversal of excessive anticoagulant therapy with warfarin or warfarin-like drugs can be achieved by minimal doses of vitamin K (1 mg orally or by intravenous injection) for asymptomatic patients. This strategy can diminish the risk of bleeding while maintaining therapeutic anticoagulation for an underlying prothrombotic state.
Toxicity from dietary phylloquinone and menaquinones has not been described. High doses of vitamin K can impair the actions of oral anticoagulants.
- Intramuscular (IM) vitamin K prophylaxis at birth is the standard of care.
- Commercial infant formulas contain supplemental vitamin K.
- These measures have served to make vitamin K deficiency bleeding a rarity. However, parental refusal of prophylaxis and an increasing frequency of breastfeeding may cause a resurgence of vitamin K deficiency bleeding in developed countries.
- In the absence of intracranial hemorrhage, the prognosis for vitamin K deficiency bleeding in an otherwise healthy infant is excellent.
- Prognosis after intracranial hemorrhage depends on the extent and location of the hemorrhage.
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