Oral anticoagulant and antiplatelet drugs have been widely used for the prevention of cardiovascular disease, but in recent years, reports of cerebral hemorrhage associated with OAD have gradually increased, and the drugs involved are heparin, warfarin, reserpine, aspirin, and clopidogrel [1-2]. It has been reported that 10-16.6% of patients with spontaneous cerebral hemorrhage are associated with OAD [2-3]. It has been pointed out that OAD has become the main cause of SICH after hypertension and amyloid cerebrovascular disease [4]. Seven cases of OAD-ICH were admitted to our department from October 2009 to August 2012 and are summarized as follows. 1. clinical data 1.1 General data As shown in Table 1, among the 7 patients, 4 were male and 3 were female; age was 49-77 years old, with an average of 68.86 years. The onset of disease ranged from 1 hour to 7 days from the time of consultation, with an average of 44.6 h. Two cases received oral warfarin, one case received oral aspirin, and four cases received dual antiplatelet therapy (clopidogrel + aspirin). The duration of medication ranged from 2 months to 10 years, with a mean of 35.29 months. 1 case had a history of minor head trauma; the remaining 6 cases had a course similar to that of SICH. 2 of the 7 cases had a history of hypertension; 3 had a history of cerebral infarction; and 1 had a history of diabetes mellitus. 1.2 Laboratory tests Routine blood tests and coagulation functions, including international normalized ratio, prothrombin time, activated partial thromboplastin time, prothrombin time, fibrinogen (FIB), platelet count, etc., were routinely checked at the time of hospitalization. In this group, there was 1 case of INR over standard and 6 cases of normal. 4 cases of TT over standard and 3 cases of FIB abnormal. 3 patients had normal PT, APTT, TT and FIB. 6 cases had normal platelet count and 1 case was slightly low. 1.3 Imaging All patients underwent cranial CT examination. 1 case underwent cranial MRI and MRA. 2 cases of hemorrhage in the basal ganglia, 1 of which broke into the ventricular system. One case of cerebellar hemisphere hemorrhage. One case of acute subdural hematoma in the frontotemporal roof bilaterally. Multiple subcortical intracerebral hematomas in 2 cases. Extensive cerebral contusion with intracerebral hematoma in 1 case. Two cases with multiple lacunar infarcts. One case with old infarct foci in the contralateral basal ganglia region. 1 case with cerebral white matter degeneration. Two cases on oral warfarin were given intravenous vitamin K. One case with INR exceeding the standard was given intermittent transfusion of fresh frozen plasma and intraoperative prothrombin complex; the other case with normal INR, PT and APTT was not treated with FFP or PCC. Of the 4 cases on dual antiplatelet therapy, 2 cases received intraoperative infusion of FFP and platelets and postoperative intermittent infusion of FFP; the other 2 cases were not given special treatment. Three cases were treated surgically and four cases were treated non-surgically; two cases had microscopic clearance of the hematoma and the other case had ventriculoscopic clearance of the hematoma (Figure 1), and both cases were decompressed with bone flaps. After the disease stabilized in 10-14 days, OAD was resumed and all were changed to low-dose aspirin (50-100 mg/day) and INR was monitored regularly. 2. Results The Glasgow prognostic score (GOS) at the 6th month after the onset of the disease was 2 in 3 cases, 3 and 4 in 1 case each, and 5 in 2 cases, and there were no deaths. bilateral occipital infarcts were seen in all 3 operated cases in the early postoperative period. 3, Discussion Warfarin belongs to the coumarins class and is the most commonly used oral anticoagulant in clinical practice, producing anticoagulation by blocking vitamin K reduction, which causes coagulation factors II, VII, IX, and X containing glutamate residues to remain in a precursor phase without anticoagulant biological activity [7]. The metabolism of warfarin is subject to genetic polymorphisms and is influenced by many drugs, foods, and disease states, making individual differences in both clinical efficacy and adverse effects [7]. The dose of warfarin is mainly adjusted clinically by monitoring the INR to ensure its efficacy and safety. The currently accepted anticoagulation standard for warfarin is INR 2.0-3.0, but due to racial and geographical differences, bleeding and coagulation functions also vary greatly, and it is generally believed that Asian patients have lower coagulation functions than European and American patients, are more prone to bleeding, and are recommended to apply low-intensity anticoagulation therapy. Some studies have shown that the amount of warfarin required to bring the INR to 2.0 in our patients is relatively small, but some patients are at risk of bleeding even if the INR is <2.0 [8]. In our six patients, the INR was between 0.8 and 1.5 at the time of bleeding. It is clear that there is no absolute "safe" INR range. The mechanism of WICH is unclear and may be related to oral anticoagulant-mediated vascular injury or inhibition of the vascular repair process [2]. However, WICH occurs in approximately 39.3% of patients whose INR does not exceed the target range [2]. It has been reported that judging the anticoagulation effect by INR is inaccurate because INR assay is mainly sensitive to coagulation factors VII and X and prothrombin complexes, while it is weakly sensitive to the reduced level of factor IX. Therefore, even if the INR is controlled within the normal range, there is still a risk of rebleeding [9]. Continued bleeding after SICH is a continuous process of continued slow bleeding from the ruptured vessel after acute bleeding and is one of the main causes of early exacerbation and death in SICH. The prolonged duration of continued bleeding is an important feature of OAD-ICH. It is now generally accepted that continued bleeding in SICH occurs mostly within 6 h of onset, with a few occurring between 6 and 24 h. Continued bleeding almost never occurs after 24 h [8]. The principles of treatment of OAD-ICH are similar to those of other SICHs, only slightly complicated by the fact that they involve the correction of coagulation. OAD should be discontinued immediately after onset. those taking oral warfarin should be given intravenous vitamin K and/or intermittent FFP infusion, and if surgery is required, we recommend preparation of PCC regardless of normal INR, PT, and APTT, since intraoperative coagulation status of the patient cannot be predicted based on preoperative INR, PT, and APTT. patients on antiplatelet therapy should be given platelet transfusion. In conclusion, OAD-ICH can occur in patients with normal INR, long duration of bleeding and poor prognosis. We suggest that the following should be emphasized during the application of OAD: ① Close observation and dynamic imaging monitoring should also be performed after minor craniocerebral injury to detect the appearance or progression of bleeding or contusion foci in a timely manner; ② For patients with little bleeding, the time frame for imaging monitoring should be extended and the frequency of imaging should be increased to strive for timely detection of increased bleeding so as not to miss the timing of surgery; ③ For national patients, especially those of advanced age, careful control of anticoagulation intensity, and strengthen monitoring and advocacy work.