Abstract: To analyze the risk factors for death in patients with intracranial venous sinus thrombosis treated with anticoagulation. Methods: The clinical data of 164 patients with intracranial venous sinus thrombosis treated with standard dose heparin anticoagulation were retrospectively analyzed, and the risk factors for in-hospital death were analyzed by logistic regression. The results showed that 23 (14%) of the 164 patients died, and the results of the univariate analysis showed that 8 associated factors, including seizures and increased intracranial pressure, were related to the patients’ death. . 75), and inadequate anticoagulation therapy (P = 0. 026, OR = 5. 77) were independent risk factors for death. Conclusion Delayed intracranial circulation time, combined intracranial hemorrhage, combined diabetes mellitus, and inadequate anticoagulation therapy are risk factors for death in patients with intracranial venous sinus thrombosis. Aggressive treatment such as endovascular thrombolytic therapy may help to improve the prognosis of such patients. Intracranial venous sinus thrombosis accounts for 1% of strokes], and anticoagulation is the first-line therapy for it. Studies have shown that heparin anticoagulation is safe and effective and does not increase the incidence of intracranial hemorrhage, but also reduces the mortality and disability rates of intracranial venous sinus thrombosis; however, the mortality and disability rates are still as high as 6% to 10% in patients treated with anticoagulation. In recent years, the incidence of intracranial venous sinus thrombosis has been increasing in China. 164 patients with intracranial venous sinus thrombosis were admitted from January 2001 to October 2012, all of whom were treated with standard heparin anticoagulation therapy, and 23 of them died. The risk factors for death are now analyzed. 1. Clinical data 1.1. Basic data 164 patients with intracranial venous sinus thrombosis treated with standard heparin anticoagulation, including 88 males and 76 females; age 30-65 years. All cases were diagnosed by cerebral angiography, and cranial CT examination was performed before and after treatment to compare the changes of intracranial hemorrhage site and hemorrhage volume, and detailed records of gender, age, height, body mass, clinical manifestations, treatment, combined underlying diseases (diabetes, hypertension, stroke), smoking, drinking habits and other auxiliary examinations were recorded. All 164 cases in this group were treated with anticoagulation therapy by subcutaneous injection of low molecular heparin 5,000 U per umbilical area once/12 h or regular heparin 1.25-25,000 U continuously pumped intravenously once/24 h. Coagulation function was monitored regularly to maintain APTT at 80-90 s. A course of treatment was given for 7-10 days. All cases were treated with phenytoin sodium antiepileptic therapy, midazolam sedation and fentanyl pain relief. Patients with increased intracranial pressure were treated with mannitol dehydration and cranial pressure reduction. 1.3. 23 patients died 2 to 16 days after admission, including 18 males and 5 females, aged 27 to 60 years, average 51 years. Characteristic clinical manifestations: 6 cases of headache, 6 cases of cognitive impairment, 3 cases of apathy, 9 cases of xerostomia, 14 cases of coma, 4 cases of tetraplegia, 4 cases of hemiplegia, 16 cases of epilepsy, and 4 cases of optic papilledema. Cerebral angiography showed that the intracranial circulation time was 14 s in 4 cases, >20 s in 17 cases, and undetected in 2 cases. CT examination showed intracranial hemorrhage in 17 cases, and during heparin treatment, 14 cases had enlarged intracranial hemorrhage, including 6 cases with new intracranial hematoma. 15 cases had worsened after heparin reduction treatment. The duration of coma and mucosal stiffness after admission: 17 patients with ≤6 d, 3 patients with 9 d, 2 patients with 14 d, and 1 patient with 19 d. There were 14 cases of combined diabetes mellitus, 5 cases of stroke, 9 cases of heart disease and 6 cases of hypertension. 2.1 The risk factors and variable types associated with death are shown in Table 1. 2.2 Statistical methods Logistic regression analysis was used to select the risk factors associated with death for analysis, and the variables and value types of the selected risk factors are shown in Table 1. P < 0. 1 was considered statistically significant. The screened factors were subjected to multifactorial logistic regression analysis, and P values, OR values, and 95% CIs were calculated to derive independent risk factors for death in patients with intracranial venous sinus thrombosis. The results of the single-factor analysis are shown in Table 2; the results of the multi-factor analysis are shown in Table 3. The results of the multi-factor logistic regression showed that delayed intracranial circulation time, intracranial hemorrhage, combined diabetes mellitus, and inadequate anticoagulation were independent risk factors for patient death, and the regression equation was: ln(P /(1-P)) = -3.018+ 2.147X5+2/384: 151X14 + 2. 477X15, P < 0. 001. Inadequate coagulation therapy was an independent risk factor for patient death, with the regression equation: ln (P / (1-P)) = -3.018+2.147X5+ 2/384: 151X14 + 2. 477X15, P < 0. 001. 3. Discussion Intracranial venous sinus thrombosis is a rare type of stroke with complex and varied clinical manifestations and a high incidence in young and middle-aged populations. The clinical manifestations of stroke and increased intracranial pressure in patients with frequent headache or lack of stroke risk factors, cranial MRI showing venous sinus lesions, and magnetic resonance venography (MRV) suggesting loss of venous sinus blood flow are important diagnostic evidence. In recent years, with the popularization of MRI, the diagnosis rate of this disease has increased. Anticoagulation is an important treatment for intracranial venous sinus thrombosis. However, due to the rapid progression of intracranial venous sinus thrombosis, the prognosis of patients with anticoagulation therapy is still poor in 6-10% of patients. Factors associated with poor prognosis of intracranial venous sinus thrombosis have been studied, but the findings are inconsistent due to the small sample size. In this study, delayed intracranial circulation time, intracranial hemorrhage, diabetes mellitus, and inadequate anticoagulation therapy were found to be independent risk factors for patient death. In cerebral angiography, the clearance of cerebral circulating contrast agent reflects the functional status of cerebral hemodynamics in patients. Delayed intracranial circulation suggests that patients have severe intracranial venous reflux disorders and extensive intracranial venous thrombosis. It has been suggested that intracranial circulation time exceeding 20 s indicates poor prognosis. In the present study, the mean intracranial circulation time was 21.2 s in 23 deceased cases and 13.3 s in surviving cases, and the majority (83%) of the deceased cases had delayed intracranial circulation time, which is consistent with the literature. Heparin anticoagulation can reestablish intracranial venous circulation to some extent, but some studies have shown that even earlier heparin anticoagulation in patients with prolonged intracranial circulation time does not prevent irreversible brain damage and does not significantly improve patient prognosis. A recent study on thrombolytic therapy for intracranial venous sinus thrombosis showed that thrombolytic therapy for patients with severe intracranial venous sinus thrombosis significantly improved the prognosis of patients. This suggests the need for more aggressive therapy in conjunction with anticoagulation in those with delayed intracranial circulation. Many studies have shown that heparin anticoagulation for intracranial venous sinus thrombosis is safe and effective and does not increase the risk of intracranial hemorrhage in patients [9]. However, in many cases with intracranial hemorrhage at the onset, we believe that heparin anticoagulation is also appropriate in such patients because the APTT can return to normal levels within 1 h if surgical intervention is required during the treatment. In this study, the presence of intracranial hemorrhage was found to be an independent factor influencing death. Intracranial hemorrhage was present in 17 of the 23 patients who died in this group. During heparin therapy, intracranial hemorrhage was enlarged in 14 cases compared with the previous one, and new intracranial hematoma was present in 6 of them, indicating that the enlarged intracranial hematoma was a sign of deterioration of the patient's condition. The relationship between heparin therapy and intracranial hematoma enlargement is controversial, but some studies have shown that thrombolytic therapy carries a greater risk of poor prognosis than anticoagulation in those with pre-treatment intracranial hematoma. Fuentes et al. concluded that interruption of heparin anticoagulation therapy is the most common cause of deterioration in patients with intracranial venous sinus thrombosis. In the present study, 15 patients who died had improved significantly after heparin anticoagulation but died after heparin reduction or interruption of therapy, confirming these findings. This study also found a significantly increased risk of death in patients with intracranial venous sinus thrombosis combined with diabetes mellitus, suggesting that diabetes mellitus may play a potential role in the development and progression of intracranial venous sinus thrombosis. The results of this study suggest that patients with delayed intracranial circulation time, intracranial hemorrhage, interruption of anticoagulation therapy and combined diabetes mellitus are at significantly increased risk of death, and future studies should further clarify how high-risk factors impact on patient death, so that safe and effective individualized treatment plans can be developed for different patients to improve their prognosis.