The choice of treatment for vitamin K deficiency should be based on the patient’s condition and the severity of the bleeding. Unless the patient has severe internal bleeding, the application of vitamin K therapy 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 the patient has a 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. PT improves within 2 hours and is corrected within 12 to 16 hours after intravenous administration of vitamin K, whereas it may take more than 24 hours for PT to be corrected after oral vitamin K. 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 before 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 may be given to patients with vitamin K deficiency without bleeding manifestations, while vitamin K injections may be given to patients with chronic vitamin K deficiency secondary to malnutrition. Second-generation long-acting anticoagulant rodenticides can lead to severe bleeding syndromes when taken by mistake or artificially. Treatment after diagnosis remains challenging because the inhibition of vitamin K-dependent coagulation factor synthesis in patients persists for months or even a year after initial exposure to these drugs, even if they are not exposed again. 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 second-generation rat poison is fat-soluble and potent, giving normal doses of vitamin K1 is ineffective, but daily oral administration of 100-150 mg of vitamin K1 can normalize PT, and over time, the dose of vitamin K1 needed to correct PT can be gradually adjusted downward to physiologically necessary amounts. In conclusion, the disease can be cured by identifying the cause and standardizing treatment as much as possible.