[Abstract] Objective To investigate the clinical characteristics and early diagnosis and treatment of traumatic progressive epidural hematoma (TPEDH). Methods The clinical and imaging data and prognostic results of 93 TPEDH cases were retrospectively summarized and analyzed with the literature. Results Among the 93 cases in this group, 72 were male and 21 were female, with a mean age of 33±12 years; the mean time from injury to TPEDH diagnosis was 8±13 h; 41 cases were enlarged with a small amount of bleeding on the first CT scan, and 52 cases were new hematomas; 28 of them occurred after the first craniotomy for decompression. The site of hematoma was most common in the top temporal and frontotemporal areas (54%,,followed by frontal, top, top occipital and occipital areas; 83 cases were unilateral and 10 cases were bilateral in this group. The most common clinical manifestation was worsening of consciousness disorder, and the prominent manifestation was increased intracranial pressure in postoperative cases. In this group, 5 cases were treated conservatively and 88 cases were treated surgically, among which 33 cases had bone flaps removed at the same time. 83 cases had fractures present at TPEDH. The group was discharged with a GOS score of 5 in 56 cases, 4 in 20 cases, 3 in 10 cases, 2 in 3 cases, and 1 in 4 cases. Conclusion TPEDH occurs mostly within 12 h after injury, the impact site is the most common, and skull fracture is the underlying factor for its occurrence. Dynamic neurological status assessment and CT review can help early diagnosis, and timely surgical removal of TPEDH with occupancy effect can help improve the prognosis. [Keywords] Cranial trauma, progressive epidural hematoma, CT scan, prognosis Traumatic epidural hematoma (EDH) accounts for approximately 22-29% of acute intracranial hematomas, most of which can be diagnosed on the first CT scan after injury and have a good outcome with prompt and definitive treatment. However, some EDHs present progressively, and the incidence of such hematomas increases significantly, especially with the development of prehospital emergency care and the availability of imaging equipment. Failure to detect and give exact disposition in time will affect the prognosis of patients. In this paper, we retrospectively summarize 93 cases of traumatic progressive epidural hematoma (TPEDH) and discuss their clinical features and early diagnosis and management experience. DATA AND METHODS 1. Inclusion criteria and CT follow-up methods: those who came to the clinic within 12 h after craniocerebral trauma and performed the first cranial CT scan, and subsequently confirmed by a second cranial CT scan or/and surgery, had no EDH present at the site of the hematoma on the first CT scan, or saw a small amount of EDH (<15 ml on the curtain and <10 ml on the subcurtain) bleeding enlargement on the first CT scan (those with ≥25% increase in bleeding volume). Those with previous coagulation abnormalities and those taking anticoagulant medications were excluded from this retrospective statistic. Patients were given a first cranial CT scan immediately after initial vital signs, neurological status and systemic status assessment upon presentation. For those who needed emergency surgery, the first cranial CT scan was given immediately after surgery if new abnormal neurological manifestations appeared, and the cranial CT scan was routinely reviewed within 6 h after surgery for patients with stable status; for those who were initially treated conservatively, the first cranial CT scan was reviewed within 6 h after the first CT scan, and then the necessary dynamic cranial CT follow-up was given according to the clinical monitoring results. 2. General data: 72 males and 21 females in this group; age: 52-71 years old, mean age 33±12 years old; causes of injury: 69 cases of car accident, 16 cases of fall injury, 3 cases of percussion injury, 5 cases of fall on flat ground; force sites: 13 cases of frontal, 29 cases of temporal top, 17 cases of occipital top, 8 cases of occipital, 26 cases of multiple force. Glasgow coma score (GCS) at the time of consultation: 1 case with 3-5 points, 17 cases with 6-8 points, 39 cases with 9-12 points, and 36 cases with 13-14 points. Pupil examination: 4 cases with bilateral dilated pupils and loss of light radiation, 9 cases with dilated pupils and loss of light reflex on one side, 11 cases with bilateral narrow pupils and dull light reflex, and 69 cases with normal pupils. There were 11 cases of combined limb fracture and 13 cases of pulmonary contusion, and no combined shock cases in this group. 3. Initial treatment and first CT scan after injury: The group was given peripheral blood for routine blood and coagulation index examination immediately after the visit, and intravenous access was opened for those who needed it, and CT scan of the head was performed immediately after the simple fixation of the limb fracture. Injury-first CT scan time: within 1 to 3 h, mean 1±0.5 h. First CT examination results: unilateral frontotemporal subdural hematoma (SDH) with brain swelling in 18 cases, unilateral EDH in 4 cases, open temporal injury with brain contusion in 1 case, skull fracture with small localized epidural hemorrhage in 41 cases, unilateral SDH in 5 cases, skull fracture and/or SAH in 24 cases. /or SAH in 24 cases. In this group, 22 cases of SDH and EDH with occupying effect on the first CT scan and 1 case of open injury were operated craniotomically under emergency general anesthesia, with hematoma removal and decompression by debridement (21 cases unilaterally and 1 case bilaterally). The remaining 70 cases were given standardized treatment according to the guidelines for diagnosis and treatment of craniocerebral trauma after admission, and the changes of consciousness and neurological signs were closely observed, and another cranial CT scan examination was given within 6h after admission. 4. CT follow-up examination results and treatment methods: Among the 70 cases treated conservatively after admission, 5 cases of progressive hematoma with occupying effect were found on CT follow-up, and cranial hematoma removal and decompression were performed in these 5 cases immediately. In the above 28 patients with emergency craniotomy, 10 cases were found to have intraoperative brain swelling and CT scan was reviewed immediately after cranial closure, and 9 cases were found to have contralateral temporoparietal or occipitoparietal EDH, and 1 case had bilateral occipitoparietal EDH; the remaining 18 cases were found to have contralateral EDH, 5 cases had ipsilateral EDH, 2 cases had bilateral occipitoparietal EDH, and 1 case had bilateral parietal EDH on review CT within 6 h after surgery. In these 28 cases with TPEDH, all of them were reoperated to remove the hematoma, and 11 cases had bone flaps removed at the same time. Of the remaining 65 cases, 41 cases had enlarged epidural hemorrhage, 3 cases were treated conservatively with stable clinical manifestations, and the remaining 38 cases had a tendency of deterioration of consciousness and surgical removal of hematoma, including 11 cases with removal of bone flap. Among the 5 cases with unilateral SDH on the first CT scan, the CT follow-up revealed the disappearance of SDH and the appearance of contralateral EDH in 4 cases, and the enlargement of contralateral TPEDH and ipsilateral cerebral contusion in another case, which were also surgically removed. Of the 24 cases with simple skull fracture or/and SAH on first CT scan, PTEDH was seen on follow-up CT scan in 18 cases unilaterally and 6 cases bilaterally. The hematoma was surgically removed in 22 of these 24 cases and conservatively treated in 2 cases. The main manifestations of TPEDH at the time of diagnosis: this group was diagnosed at 3-96h (average 8±13h) after injury, except for one case at 4d and one case at 3d after injury, 88% were diagnosed within 12h after injury. The main manifestations at the time of diagnosis were: among the 28 cases of emergency surgery, 10 cases showed intraoperative brain swelling, 8 cases showed increased pressure on intracranial pressure monitoring, 3 cases showed dilated contralateral pupils after surgery, 7 cases showed no special manifestations and the diagnosis was confirmed by routine CT review after surgery; among the remaining 65 cases, 35 cases showed worsening of consciousness, 27 cases showed headache with vomiting, and 3 cases were confirmed by routine CT review. A The left temporoparietal SDH with brain swelling was seen on CT 1h after injury; B CT immediately after left frontotemporoparietal decompression. Conclusion The results of coagulation index examination after this group came to the clinic showed that platelet count, PT and PTT were within the normal range. sites of TPEDH: frontal 13 cases, frontotemporal 24 cases, top temporal 26 cases, top 11 cases, top occipital 10 cases, and occipital 9 cases. Among them, 11 cases were bilateral and 82 cases were unilateral. Of the 88 cases treated surgically, the presence of skull fracture was confirmed in 79 cases at the site of hematoma (90%), and among the 5 cases treated conservatively, skull fracture was determined on CT scan in 4 cases (80%). Intraoperatively, the source of bleeding was clearly identified in 76 cases, all of which had bleeding from the plate barrier at the fracture site, including 13 cases with combined venous sinus bleeding and 14 cases with combined arterial bleeding; hematoma volume: 20-30 ml in 42 cases, 30-50 ml in 32 cases, and >50 ml in 19 cases. In 5 cases treated conservatively, the hematoma was stable and gradually absorbed. A 1h post-injury CT left temporal parietal isointensity thin layer EDH; B 4h post-injury CT left temporal parietal TPEDH. There were 4 cases of death in this group, with a morbidity and mortality rate of 4,3%; causes of death: 2 cases of intracerebral rebleeding and 2 cases of massive cerebral infarction; 3 of these 4 cases were those with brain swelling due to contralateral EDH occurring during debulking decompression of SDH on one side, and the other case was combined with multiple foci of cerebral contusion. The length of stay of this group of patients was 10-45 d (mean 14±8 d), and the results of Glasgow Outcome Scale (GOS) scores at discharge: 5 in 56 cases, 4 in 20 cases, 3 in 10 cases, 2 in 3 cases, and 1 in 4 cases. The results of 6-month follow-up after discharge: 68 cases with a score of 5, 11 cases with a score of 4, 7 cases with a score of 3, 1 case with a score of 2, and 6 cases with a score of 1. Among them, 14 cases underwent skull repair and 2 cases underwent ventriculo-abdominal shunt due to hydrocephalus; among the 3 cases with a score of 2 at discharge, 2 cases died due to pulmonary infection. Discussion The timing of the appearance of secondary intracranial hemorrhage after craniocerebral trauma is influenced by a variety of factors and thus shows clinical diversity. Clinical studies have found that 35% to 65% of patients after craniocerebral trauma have worsening progressive clinical manifestations due to secondary cerebral ischemia, hemorrhage, and edema. Progressive hemorrhagic injury (PHI), which increases the risk of clinical deterioration by 5-fold, is a major cause of disability and death in patients with craniocerebral trauma, and TPEDH is one of the major types of PHI that, if diagnosed early and managed promptly, can significantly improve the prognosis of the injured. There are various views on the mechanism of TPEDH. Most scholars believe that the injury to the skull or/and dura at the site of impact is the underlying factor for the occurrence of TPEDH; while the intracranial hypertension and hypotensive state that occurs after the injury is a protective mechanism to prevent bleeding immediately after the injury. When treatment to lower intracranial pressure (including dehydration therapy to control cerebral edema, hyperventilation, barbiturate therapy, etc., and decompression surgery such as surgical craniotomy to remove hematoma) and restore blood volume to correct the hypotensive state are used, this protective effect disappears and the pre-existing source of bleeding begins to bleed to form TPEDH. in addition, post-injury cerebrospinal fluid leakage, or extraventricular drainage can also lower intracranial pressure and induce the TPEDH can also occur. It has also been suggested that abnormalities in post-injury coagulation may be associated with the development of TPEDH. In this group, 28 cases occurred after decompressive surgery, which is a predisposing factor for TPEDH; however, the post-injury coagulation index examination in this group did not show abnormal platelet count, PT and PTT, so it cannot be considered that there is a factor of coagulation abnormality in the occurrence of TPEDH. The following clinical characteristics of TPEDH can be seen from the comprehensive data of this group and the literature: 1, it mainly occurs at the traumatic impact site, with frontotemporal and temporal top being the most common (54% in this group), followed by frontal, occipital top, top and occipital areas, and this result is basically consistent with the results reported in the literature; 2, skull fracture is the basic element of TPEDH formation, and skull fracture exists at TPEDH in this group In this group, the presence of skull fracture at TPEDH accounted for 89% of the cases; while bleeding from the plate barrier at the fracture and venous bleeding from the venous sinus were the main sources of bleeding, therefore, on the first CT scan after the injury, it often showed a small amount of mixed density shadow or no bleeding; 3, the clinical manifestations were diverse but lacked characteristics, and deterioration of consciousness and the appearance of new neurological deficits were the main clinical manifestations; brain swelling during decompression surgery and postoperative intracranial pressure increased again The possibility of TPEDH is suggested by brain swelling during decompression surgery and the re-increase of intracranial pressure after surgery; while some patients can have no obvious clinical manifestation changes, and can only rely on routine imaging review for early detection; 4, decompression treatment such as cranial decompression, cerebrospinal fluid drainage, giving diuretic dehydrating agents, etc., can contribute to the formation of TPEDH, 28 cases of TPEDH in this group occurred after cranial decompression surgery; 5, mostly seen in the acute period after injury, among which the most common is within 24h. The most common is within 24 hours, and can occur in the subacute period. It is noteworthy that four cases in this group had SDH on one side on the first CT scan in the hospital, and the subsequent CT review within 5 h showed the dissipation of SDH and the formation of TPEDH on the contralateral side. In the case of Figure 3, a craniotomy based on the first CT scan would have had serious adverse consequences. Moreover, in some patients with TPEDH, there can be no obvious clinical abnormalities, so we advocate routine cranial CT review within 6 h after the first CT scan after injury, especially for those who are transferred after in-hospital examination very short time after injury and have more than 1 h time interval, to pay attention to the occurrence of progressive changes. TPEDH after decompression surgery can occur contralaterally, ipsilaterally or bilaterally, and if the patient’s status permits, the cranial CT examination should be reviewed immediately to clarify the presence of new bleeding and sites to avoid blindness of surgical exploration. If the patient’s status does not allow for moving and it is clear that a skull fracture exists at the site of impact, exploratory surgery is feasible. The prognosis of TPEDH is closely related to the ability of early diagnosis and timely management. Comparative observation of neurological status is an important method for early detection of TPEDH, and quantitative assessment of the state of consciousness is particularly important. In addition, continuous ICP monitoring after injury enables timely determination of intracranial hematoma and edema development at the time of craniocerebral injury before clinical symptoms, especially for patients requiring sedation and inotropic drug maintenance. Dynamic CT follow-up should be one of the important methods for early detection of TPEDH, and the use of CT scan follow-up in this group contributed to the early detection of TPEDH. 82% good prognosis rate (GOS ≥ 4 points) at the time of discharge of this group also circumstantiated the value of this protocol. The use of mobile CT in the future may reduce patient moving and contribute to the early diagnosis of TPEDH. EDH is usually slow to resorb, so we advocate aggressive surgical removal of the hematoma in those with occupying effects, even if the patient does not show significant neurological deficits. The main factors affecting the prognosis, in addition to early diagnosis and exact management, mainly depend on the extent and severity of the combined brain injury. Among the four cases of death in this group, two cases developed progressive intracerebral hematoma after surgery and two cases developed large cerebral infarction, which eventually led to death due to malignant intracranial hypertension. It is evident that early control of intracranial hypertension and reduction of secondary damage such as complications are still the key elements to improve the prognosis of TPEDH.