This product is carefully used in patients with thrombocytopenia and platelet deficiency, severe liver and kidney dysfunction, uncontrolled hypertension, hypertensive or diabetic retinopathy. Recent surgical patients should also be cautious when using large doses of heparin sodium.

　　Platelet counts and regular monitoring are recommended prior to initiation of dheparin therapy, especially during the first week of treatment.

　　Special attention should be paid to rapidly developing thrombocytopenia and severe thrombocytopenia (<100000/ mul) that has been shown to be positive for antiplatelet antibodies or to have unknown results in vitro studies related to the use of this product or other low molecular weight heparin and/or heparin. Platelet counts should be performed before the use of this product for the treatment of acute venous thrombosis and should be reviewed regularly. Treatment should be discontinued when such thrombocytopenia occurs. Only after in vitro studies have shown that heparin does not induce platelet aggregation can treatment be restarted. Platelet counts should be performed at least twice a week after the start of treatment, especially during the first three weeks of treatment. Important: type II thrombocytopenia induced by heparin should not be confused with early postoperative thrombocytopenia.

　　This product has only moderate prolongation of clotting time (such as plasma clotting time (APTT) or thrombin time). Determination of anti-xa activity is recommended for laboratory monitoring. Increasing the dose to prolong APTT may lead to overdose and bleeding. In general, patients on long-term hemodialysis need very few times to adjust the dose of this product, and therefore very few times to detect the concentration of anti-xa. Patients undergoing acute hemodialysis have shorter treatment intervals and should be fully monitored for alpha-xa concentrations.

　　Patients with unstable coronary artery disease, such as unstable angina and non-q-wave myocardial infarction, can be treated with thrombolysis if they have a transmural myocardial infarction. Discontinuation of this product for thrombolysis is not necessary, but may increase the risk of bleeding.

　　The use of LMWH prior to spinal or epidural puncture or anaesthesia has rarely been reported with varying degrees of nerve injury due to spinal hematoma, including prolonged or permanent paralysis. The risk of this adverse event is increased when an epidural catheter is used postoperatively or when combined with a drug that affects clotting, such as a non-steroidal anti-inflammatory drug. When dheparin sodium injection is used in combination with spinal or epidural anesthesia, to reduce the risk of bleeding, it is best to insert or remove the catheter before dheparin sodium injection has had its anticoagulant effect. When dheparin sodium injection is used to prevent deep vein thrombosis, the catheter should be inserted or removed 12 hours after the last dose or 24 hours after the last dose if the patient is at increased risk of bleeding. Contraindicated in patients undergoing acute deep venous thrombosis with local epidural or spinal anesthesia or puncture. Dheparin sodium injection should be administered at least 4 hours after catheter removal. When doctors decide to use anticoagulants before spinal or epidural puncture or anesthesia, they need to be especially careful and monitored frequently, and to be on the lookout for any signs or symptoms of neurological dysfunction, such as back pain, sensory or motor disturbances (numbness or weakness in the lower extremities, bladder dysfunction). Nurses should receive special training on how to recognize symptoms of neurological dysfunction in a timely manner, and patients should be required to inform their doctors of symptoms of neurological dysfunction. If signs or symptoms of an intra-spinal hematoma are suspected, emergency diagnosis or treatment, including bone marrow decompression, is required.