1. Acquired vitamin K-dependent coagulation factor deficiency in adults A normal diet provides sufficient vitamin K relative to the low physiological requirement for vitamin K. Therefore, inadequate intake does not lead to clinically significant vitamin K deficiency. Bacteria in the colon can make functional vitamin K in the absence of vitamin K. Small amounts of vitamin K in the colon can be absorbed passively when vitamin K-free foods are eaten, preventing severe vitamin K deficiency. This source of vitamin K disappears in patients who receive antibiotic therapy that kills the intestinal flora, so the common clinical condition that leads to vitamin K deficiency is often in patients who eat a very small or vitamin K-free diet while receiving antibiotic therapy, and this type of vitamin K deficiency usually occurs 1 to 3 weeks after the body’s vitamin K stores are depleted. Malabsorption syndromes often lead to vitamin K deficiency. Biliary pathologies that interfere with the absorption of fat-soluble vitamins in the ileum can cause abnormal hepatic-intestinal circulation, and primary biliary cirrhosis, bilious hepatitis, and other causes of biliousness can lead to impaired vitamin K absorption. Furthermore, intestinal malabsorption caused by chronic diarrhea or restrictive enteritis can lead to impaired vitamin K utilization. Mild vitamin K deficiency occurring in some elderly people may be due to impaired intestinal absorption. Acquired vitamin K-dependent coagulation factor deficiency in adults is not common clinically, but has been reported both domestically and internationally as a result of coumarin overdose or rat poisoning. The above are the most common causes of vitamin K-dependent coagulation factor deficiency in adults. The anticoagulant effect of second-generation coumarin-based anticoagulant rodenticides such as dallon and bromadiolone is much stronger than that of warfarin, with high lipid solubility, large distribution volume and long half-life in vivo. In adults, coumarin poisoning is often diagnosed with hemorrhagic symptoms without a clear history of poisoning, and there is a certain latency period from poisoning to hemorrhage, so it is very easy to miss and misdiagnose because it is often impossible to trace a clear history of taking the drug, and the clinical latency period after poisoning can be a few days to half a month, and the first symptoms are hematuria, deep muscle and joint hemorrhage, and even visceral and intracranial hemorrhage, which are very dangerous. 2. Bleeding due to vitamin K antagonists Drugs that inhibit the reuse of vitamin K can lead to the collection of vitamin K epoxide and the reduction of vitamin K hydroquinone. Misuse, artificial administration of warfarin and similar or anticoagulant therapy overdose can lead to vitamin K-dependent coagulation factor deficiency, prolonged PT and APTT and clinical bleeding manifestations. Although these patients do not have vitamin K deficiency, their clinical and laboratory abnormalities are consistent with the manifestations of vitamin K deficiency. The results of a controlled clinical study showed that the use of vitamin K antagonists increased the incidence of major bleeding by 0.5% per year, with intracranial bleeding increasing by 0.2% per year. Risk factors for bleeding due to vitamin K antagonist therapy include treatment dose and target INR, monitoring of the treatment course, and individual patient differences. Studies have shown that an INR > 3.0 as the target for anticoagulation therapy can increase the incidence of major bleeding by a factor of 2. Standardized monitoring of INR and patient symptoms can reduce the incidence of bleeding. 3. Treatment of vitamin K deficiency The choice of treatment for vitamin K deficiency should be based on the patient’s condition and the severity of bleeding. Unless the patient has severe internal bleeding, the application of vitamin K treatment is sufficient. Vitamin K can be administered orally or by injection, with injectable administration having a faster onset of action. The decision to administer by injection should be based on the urgency of correcting the bleeding tendency and the risk of triggering local hematoma formation. If a patient has significantly prolonged PT suggesting that intramuscular injection can induce bleeding, then intramuscular vitamin K1 should be avoided in favor of intravenous administration to ensure timely dosing. However, serious allergic reactions to intravenous vitamin K1 have been reported in the past, and this mode of administration should be closely monitored to ensure that adverse reactions are managed promptly if they occur. PT improves within 2 hours and is corrected within 12-16 hours after intravenous vitamin K administration, whereas it may take more than 24 hours for PT to be corrected after oral vitamin K administration. Severe bleeding complications, such as intracranial hemorrhage, must be corrected rapidly, and although vitamin K is fast-acting, fresh frozen plasma infusion should be given prior to administration because it contains all vitamin K-dependent coagulation factors and an adequate amount of fresh frozen plasma can both correct PT and treat bleeding tendencies. The use of blood products should be carefully considered because of the risk of transmitting viral infections. Oral vitamin K can be given to patients with vitamin K deficiency without bleeding manifestations, while vitamin K injections can be given to patients with chronic vitamin K deficiency secondary to malnutrition. 4. Reversal of long-acting time vitamin K antagonists Second-generation long-acting time anticoagulant antidepressants can lead to severe bleeding syndrome after being taken by mistake or artificially. Since the inhibition of vitamin K-dependent coagulation factor synthesis in patients can persist for months or even a year or more after initial exposure to such drugs, treatment after diagnosis remains very challenging. Fresh frozen plasma is routinely used for severe bleeding complications, but this treatment can carry the risk of blood-borne infectious diseases. Although complete or partial correction of PT is desirable, long-term prophylactic transfusion of fresh frozen plasma poses a higher risk and significantly increases the cost of treatment. Because the second-generation rat poison is fat-soluble and potent, administration of normal doses of vitamin K1 is ineffective, but daily oral administration of 100-150 mg of vitamin K1 can restore PT to normal, and over time, the dose of vitamin K1 required to correct PT can be gradually adjusted downward to physiologically necessary amounts.