Progressive intracerebral hemorrhage leading to brain herniation after traumatic skull fracture is not uncommon, and the authors admitted one case, which is reported below with the literature. 1. Clinical data The patient, male, 45 years old. He was admitted to the local hospital on May 14, 2008 due to a head injury caused by a falling object. The external medical history showed that the patient had a Glasgow Coma Scale (GCS) score of 13 on admission, a left top scalp contusion with subcapsular hematoma, grade 3 muscle strength of the right limb, and slightly low muscle tone, and no abnormal findings in the rest of the neurological examination. 1h post-injury cranial CT scan showed a comminuted, depressed fracture of the left parietal bone with depression depth >1cm, with localized cerebral contusion, a clearly visible circumferential pool, and a centered midline structure. The diagnosis was left parietal lobe cerebral contusion with comminuted and depressed fracture of the parietal bone. The local hospital gave an emergency craniotomy under general anesthesia. After taking an S-shaped incision and removing the top fragment of bone, a linear fracture line was seen extending to the lateral temporal floor, and an extra-dural active hemorrhage was seen. After enlarging the incision and bone window to the temporal area, electrocoagulation was performed to stop the bleeding and suspend the dura, and the scalp was sutured in layers. The patient’s consciousness did not improve significantly on the first postoperative day, and 25 h after surgery, the patient showed dilated left pupil, loss of light reflex, and right limb hemiparesis. The patient was immediately transferred to our hospital and underwent another emergency surgery under general anesthesia. The frontal horn of the right ventricle was punctured and the intracranial pressure (ICP) probe was placed, and the ICP was measured at 46 mm Hg. The original surgical incision was then extended to the temporal floor and anterior to the ear to form a base-facing frontotemporoparietal flap. After turning the flap and temporalis muscle flap, high dural tension was seen, and after opening the extraventricular drainage, the original bone window was enlarged to a size of 13 cm × 15 cm. After radiolucent dissection of the dura, cerebral tissue edema was seen to be evident, and intracerebral hematoma emerged after a small cortical incision at the parietal contusion. After removing the contusion foci and hematoma, the brain tissue tension was reduced, and the dura was repaired with autologous periosteum after dural hypotension suture, and one negative pressure drain was left in place outside the dura. After the operation, the patient was given 125 ml of 20% mannitol/8 h and the extraventricular drain was opened (the outlet was 20 cm above the external auditory foramen). 3 days later, the ICP was stabilized at 15 mmHg or less, the mannitol was stopped, and the extraventricular drain was removed after 5 days. The patient was awake on postoperative day 1, but had motor aphasia. Ten days after surgery, the right limb muscle strength recovered to grade 3 and incomplete motor aphasia was discharged from the hospital for rehabilitation. Six months after the injury, the patient’s speech function was basically restored, and the muscle strength of the right limb was restored to grade 4-5. A cranial CT scan showed a slightly enlarged left lateral ventricle with a small amount of hypointense shadow in the parietal lobe. The patient was readmitted to the hospital for skull repair. After 1.5 years of follow-up, the patient was able to take care of himself. 2.Discussion Progressive hemorrhagic brain injury after craniocerebral trauma is most common with intracerebral hematoma and subarachnoid hemorrhage, followed by epidural hematoma and subdural hematoma. Those with cerebral contusions and skull fractures on the first post-injury CT scan have the highest risk of progressive intracranial hemorrhage. In the present case, the CT scan of the head 1 h after injury showed a compound fracture with cerebral contusion at the site of impact with both comminution and depression, and the depth of fracture depression was >1 cm. After surgical removal of the fragmented bone, the postoperative local contusion focal hemorrhage progressed and was accompanied by obvious cerebral edema formation, leading to the development of ipsilateral temporal lobe hook gyrus herniation 25 h after surgery. For patients with traumatic skull fracture depression depth >1cm, the dura should be incised and explored even if no breakage of the dura is found during surgery. At the same time, the neurological status should be closely observed after surgery, and early CT review should be performed. The authors advocate that the first review should be performed at least 6h postoperatively for stable patients as well, in order to detect the progress of intracranial hemorrhage at an early stage. In this case, no abnormal coagulation was found in the laboratory tests before both operations, indicating that the formation of progressive intracerebral hemorrhage after the 1st operation was caused by the expansion of bleeding after the removal of the protective effect of the depressed skull compression by the local contusion foci, excluding the factor of systemic coagulation abnormalities. In this case, at the time of the 2nd surgery, the intracranial pressure was significantly increased and brain herniation had occurred. Because of the transfer, there was a 3-h time interval between the 2nd cranial CT scan and the 2nd surgery, and the intraoperative intracerebral hematoma was significantly more than that seen on the CT scan. In order to prevent the occurrence of intraoperative cerebral bulge, the following 2 points are worthy of attention in this case: (1) The frontal horn of the contralateral ventricle was punctured first, and the intracerebroventricular ICP monitoring probe was left in place. The ICP was measured while opening the external drainage to release part of the cerebrospinal fluid during the dural incision, which effectively reduced the ICP; (2) before incising the dura, the autologous periosteum was taken in the surgical area for backup, so that the dural hypotonic suture was completed soon after the intracranial lesion was removed, reducing the exposure time of the brain tissue. Intraoperative intracerebroventricular ICP monitoring in this case not only provided reliable data for the strategy of surgical decompression, but also allowed continuous external drainage after surgery to effectively reduce ICP and guided the application of dehydrating and diuretic drugs such as mannitol, avoiding the blindness of empirical application and reducing the risk of potential side effects of giving such drugs, and the patient also achieved a better outcome.