In order to explore the cause of the rapid

In order to explore the cause of the rapid change in the consciousness of our patient, the literature with regard to vertex EDH and sagittal sinus injury was reviewed. Injury to the sagittal sinus and vertex EDH may change the intracranial pressure. It is believed that cerebrospinal fluid drains through the arachnoid granulations into the dural venous blood of the sagittal sinus. Vertex EDH may compress the sagittal sinus and compromise cerebral venous drainage, so the protein phosphatase of cerebrospinal fluid is impaired, which may be related to the presence of venous blood hypertension. Hydrocephalus and restricted blood supply then occur. Thus, patients may present features of increased intracranial pressure. If intracranial hypertension develops, it can induce uncal herniation and reflex bradycardia, which may then result in sudden death. Due to the impairment of venous drainage and diminished cerebrospinal fluid resorption, vertex EDH caused by injury to the sagittal sinus requires aggressive surgical treatment, even with a relatively small hematoma. Vertex EDH is easily misdiagnosed, even when a brain CT is performed immediately. Conventional axial plane CT is likely to miss the vertex EDH, and the presence of a small vertex EDH is commonly misdiagnosed as a bone artifact. Magnetic resonance imaging (MRI) venography is suggested when the vital signs of the patient are relatively stable. MRI venography is more sensitive and there is less chance of a misdiagnosis occurring, in terms of detecting obstruction of the superior sagittal sinus, than with conventional axial plane CT. Most cases of head injury with EDH are complicated, however, due to a critical condition and deteriorating consciousness. A time-consuming MRI venography may prevent these patients from obtaining a definitive diagnosis. Follow-up MRI venography is appropriate after surgery. If the patient’s vital signs are relatively stable and small vertex EDHs are difficult to diagnose in routine CT, MRI can be an excellent tool to solve this problem in patients with trauma to the skull vertex. The other challenging event in the operation our patient underwent was how to deal with profuse sinus bleeding. Massive hemorrhaging will disturb the operative exposure. The literature on venous sinus injury in the past 30 years was reviewed. Small holes or tears of the venous sinus can be managed with Surgicel or Gelfoam and gentle pressure. Temporary control of hemostasis is easily obtained by packing pledgets of hemostatic materials. Direct closure of tears can be performed if it does not result in sinus stenosis. For larger ruptures, patch repair using a vein graft, pericranium or the fascia lata is required, with two hemi-running sutures. If the hemorrhage is out of control, ligation can be performed in non-critical areas (in the first quarter of the superior sagittal sinus). A temporary sinus–sinus shunt may be necessary to properly repair the sinus tear without compromising sinus blood flow. Massive red cell transfusions are required in such cases. There are some respectable technical aspects, as follows, that may greatly facilitate proper management. Before elevation of the bone fragments, preparations for rapid hemorrhage and air embolism should be in place and an assistant should be ready to maneuver the operating table at a moment’s notice. Continuous generous irrigation over the sinus during elevation of the bone fragments reduces the chance of embolism. Wet swabs should be at hand to immediately cover the sinus. The semi-sitting (lounging) position allows a good venous return without increased intracranial pressure. The operative exposure should be as extensive as possible. The skin flap and craniotomy should extend across the midline to permit visualization of both sides of the sinus. The bridging veins, especially in the rolandic outflow area, should be preserved. To facilitate venous sinus patency after surgery, blood pressure, volume and viscosity must be carefully monitored.