Two Types of Delayed Post-Traumatic Intracerebral Hematoma

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1 Two Types of Delayed Post-Traumatic Intracerebral Hematoma Takashi TSUBOKAWA Department of Neurological Surgery, Nihon University School of Medicine, Tokyo 173 Summary The findings of repeated CT scans, clinical courses and pathological studies in 28 cases of delayed post-traumatic intracerebral hematoma were studied retrospectively to elucidate the mechanism of bleeding and to establish adequate treatment. Based on the results obtained, it became clear that there are two types of delayed hematoma. In 10 of the 28 cases, initial CT findings within 6 hours after head injury revealed cerebral contusion or hemorrhagic contusion, and spots of high density scattered in the low density zone gradually became confluent to form an irregularly shaped hematoma according to follow-up CT findings. This was termed "hematoma within a contusional area." In 15 of the 28 cases, initial CT findings within 6 hours after head injury revealed no abnormal density within the brain and the hematoma appeared suddenly 3 6 days after the injury. In eight of the 15 cases, emergency surgery was performed for the removal of epidural or subdural hematoma. This type of hematoma is termed "contusional hem atoma" and constitutes the second group. In three of the 28 cases, both types of hematoma were observed. Based on histological findings for the two types of delayed hematoma. The first group may be induced by an anoxic vasodilation mechanism (Evans et al.9)), while the second group may be derived from a different mechanism related to ishemic changes and the free radical reaction caused by the reflow phenomenon (Tsubokawa et al.14-16)1 It is important to establish correct diagnoses 1 for delayed hematomas based on differences between follow-up findings of repeated CT and an initial CT performed within 6 hours after head injury since the operative indications and operative results for the two groups are different as indicated by our 28 cases. Key words: Head injury, repeated CT, contusion, delayed hematoma Introduction Delayed intracerebral hematoma following head injury is characterized by the appearance of focal neurological signs or depression of the level of consciousness, developing days or weeks after the trauma. Prompt diagnosis and a decision concerning indication for surgery are necessary to minimize the harmful effects that the hematoma may exert on the already traumatized brain. Because delayed traumatic intracerebral hem atoma occurs in cases of severe head injury is associated with focal neurological signs and depression of the level of consciousness occurring immediately after trauma but with no typical posttraumatic apoplexy-like symp toms (Bollinger4), and has accounted for more than 50 % of traumatic intracerebral hematomas since CT was introduced in this particular field of diagnostics, computerized tomographic scanning (CT) is now the key diagnostic tool for this condition. However, even with CT it is difficult to make a correct diagnosis of a delayed post-traumatic intracere bral hematoma, to determine its exact patho genetic mechanism and to decide on the indication for surgery unless CT studies are begun early after head injury and repeated until a hematoma of demonstrable size is formed (Tsubokawa et al ))

2 We reported previously that intracerebral hematomas which, although not demonstrable in initial CT performed within 6 hours after head injury, appear in repeated CT on 1 to 5 days later can be classified into two types. One type includes those hematomas formed within a contused area which show evidence of cerebral contusion or hemorrhagic contusion in initial CT and are formed by the gradual confluence of small hemorrhagic areas. The other type consists of those contusional hema tomas which are not demonstrable, with no evidence of contusion (Lanksch et al.101), in initial CT but appear within a normal brain area later between 8 hours and 6 days after injury. The purpose of the present study was to explore the possibility that these two types of intracerebral hematomas are dissimilar with respect to the mechanism of bleeding and hence should be treated in a different way, based on CT findings, clinical courses and operative results obtained in our own series of 28 cases of delayed traumatic intracerebral hematoma, and thereby to assess the clinical value of the above classification. Subjects From among the head injury cases seen at our hospital after the introduction of CT, 28 cases in which initial CT was nerformed 6 hours after injury and diagnosis of delayed traumatic intracerebral hematoma was ultimately estab lished by operation or autopsy were selected for the study (Table 1). Results I. Development and course of the two types of hematoma In 10 of these 28 cases there was initial CT evidence of cerebral contusion or hemorrhagic contusion, and a typical finding of multiple punctiform or patchy areas of minor bleeding appearing in low density areas within 6 hours after injury. These CT findings correspond respectively to Type I and Type II cerebral contusions according to the classification of Lanksch et al. Four of the 10 cases had an extracerebral hematoma, i.e., two with subdural hemorrhage and the other two with small epidural hematomas at the fracture line. In all cases of Type I cerebral contusion showing low density only in initial CT, the lesion developed into a hemorrhagic contusion (Lanksch Type II10)) within 24 hours. By the third day of injury, these spots of bleeding gradually became confluent to form an ir regularly shaped hematoma (diameter of high density area exceeding 3 cm) which occupied part of the initial low density area (Fig. 1). These hematomas are termed hematomas Table 1 Twenty-eight cases of traumatic delayed intracerebral hematoma classified into 2 groups based on CT findings, clinical courses and pathological findings.

Fig. 1 CT scans illustrating the time course of delayed posttraumatic intracerebral hematoma (hematoma within a contusional area). A : Initial CT 5 hours after head injury.

3 Fig. 1 CT scans illustrating the time course of delayed posttraumatic intracerebral hematoma (hematoma within a contusional area). A : Initial CT 5 hours after head injury. r subdural hemorrhage and 1-temporal contusion (Lanksch Type II) are observed. B: CT findings 3 days after head injury. An irregularly shaped intracerebral hematoma is present in the contusion observed by the initial CT. within a contusional area since they are formed from bleeding spots within a contused brain area as reflected in the findings of repeated CT scans (Tsubokawa et al.14-16)) At the time when the diameter of the hema toma exceeded 3 cm, shifting of the median structure was noted in eight of the 10 cases. In the other two cases where a hematoma appeared at the frontal tip bilaterally or in the frontal lobe, no shifting of the median structure was seen. Fifteen of the remaining cases of delayed traumatic intracerebral hematoma had no abnormalities or only showed evidence of subarachnoid or sub or epidural hematoma in CT performed within 8 hours after injury. The appearance of an intracerebral hematoma was recognized in repeated CT performed between 8 hours and 6 days after injury. This type of hematoma differed from hematomas within the contused area in that it did not show any contusion or high density spots in the brain in initial CT (Fig. 2). It was arbitrarily termed a contusional hematoma (Tsubokawa et al.14-16)) Initial CT scan findings were negative in cases of contusional hematoma within 8 hours after injury except in nine cases with concurrent subdural hematoma and two cases with con comitant epidural hematoma. In eight out of 11 case of extracerebral hematoma, evacuation was performed within 24 hours after injury and four of them underwent additional decom pressive craniectomy. Among seven cases not undergoing emer gency evacuation surgery (three with subdural hematoma and four without extracerebral hematoma), an intracerebral hematoma became demonstrable in repeated CT scans within 24 hours after injury in two cases, within 48 hours in another two cases, and 3 to 5 days after injury in the remaining three cases. Among eight cases in which an intracerebral hematoma developed after surgical removal of an extracerebral hematoma, the intracerebral hematoma was formed within 4 hours after the operation in one case, 1 to 2 days after the operation in six cases and on the 5th postopera tive day in one case. Intracerebral hematomas occurring after surgery for subdural or epidural hematomas were ipsilateral to the preceding extracerebral hematoma in six cases and con tralateral in the other two cases. There were also three cases in the present series where both a contusional hematoma and a hematoma within a contusional area were formed. In these cases, however, there was no concurrent extracerebral hematoma formation. In these two types of delayed traumatic intracerebral hematoma, impairment of con Fig. 2 CT scans illustrating the time course of delayed posttraumatic intracerebral hematoma (contusional hematoma). A: Initial CT 8 hours after head injury. There are no visible pathological findings apart from r-subdural hematoma. This hematoma was re moved by emergency surgery just after the CT. B : CT findings 4 days after emergency cra niotomy. There is no remaining r-subdural hematoma, but intracerebral hematoma is observed in the 1-front-temporal area.

sciousness ranging from confusion to a coma, anisocoria or impaired light reaction was noted in about 20% of the cases and hemiplegia was present in 30% of the cases.

4 sciousness ranging from confusion to a coma, anisocoria or impaired light reaction was noted in about 20% of the cases and hemiplegia was present in 30% of the cases. However, no gross alterations of neurological symptoms were seen to occur coincidentally with the development of delayed intracerebral hema toma, nor were these instances in which late apoplectic symptoms according to Bollinger manifested themselves at the time of hematoma formation. When a worsening of the preexisting disturbance of consciousness occurs or no symptomatic improvement is noted after sur gical removal of an extracerebral hematoma, development of delayed intracerebral hema toma can be suspected. As mentioned previously, a hematoma within a contused area and a contusional hematoma coexisted in three out of the total 28 cases. However, these cases did not present any specific symptoms. II. Methods of treatment of the two types of hematoma and therapeutic results Among the 10 cases of hematoma within a contused area, two received conservative treat ment only, while the other eight cases under went surgical removal of the hematoma as soon as the diagnosis was established. During the operation, the brain surface was found to be damaged and markedly swollen. The hematoma was present either as a mass or protruding into adjacent edematous or necrotized brain tissue. Two patients died postoperatively, another two had sequelae necessitating assistance in their daily activities and the remaining four returned to their premorbid life. Of the two patients treated nonsurgically, one had a disability necessitating assistance in daily life and the other successfully returned to a normal life (Table 2). Of the 15 cases of contusional hematoma, two presented brain stem symptoms immedia tely after sustaining injury, while in another there was confusion at the time of hospitaliza tion and a hematoma later developed in the right frontal lobe in the absence of impairment of consciousness. In a fourth case, a hematoma was formed in the occipital lobe 2 days after the operation for an epidural hematoma in the occipital region, but there was later im provement of consciousness with no shifting of the median structure. These four cases were treated nonoperatively, while the remain ing 11 cases underwent evacuation of the hematoma as soon as it was discovered. Of the four nonsurgically treated patients, the two with brainstem symptoms immediately after injury had a fatal outcome, while the other two who showed improvement of im paired consciousness with no shifting of the median structure in CT in spite of the develop ment of an intracerebral hematoma, were successfully rehabilitated. Among the 11 patients undergoing surgery, three died postoperatively, two others con tinued to have some degree of disability and the remaining six returend to their premorbid life (Table 2). During surgery no appreciable damage was noted on the brain surface. The hematoma formed a mass and adjacent brain tissues were Table 2 Operative results for traumatic delayed intracerebral hematoma

5 affected mainly by edematous changes with no evidence of contusion. III. Histological findings for both types of hematoma Four cases of contusional hematoma and two cases of hematoma within a contusional area were examined for histological features of the hematoma per se and its surrounding brain tissues. The hematomas within a contusional area contained coagulated blood only with no cerebral vessels and nervous tissue. The sur rounding brain tissues were edematous and necrotic, the blood vessels were dilated and at times obstructed, hemorrhagic spots were seen in the perivascular areas and petechiae were often noted even in fairly distant areas (Fig. 3). In the contusional hematomas the reactions of the surrounding brain tissues were essentially the same as in the former type apart from the fact that the necrotic areas in the adjacent tissues were thin and dilatation of small vessels was seen within a limited zone (Fig. 4). Within the hematomas, however, blood vessels, which were thrombosed and infiltrated by lymphoid cells, developed (Fig. 4). Discussion A study of repeated CT, operative and his tological findings in 28 cases of delayed intra cerebral hematoma (in which the initial CT was performed within 6 hours after injury) showed that these hematomas could be rea sonably divided into two distinct types. One was the hitherto hypothesized delayed type of intracerebral hematoma, i.e., hematoma within a contusion which is formed by the confluence of small bleeding spots occurring in the contused area. The other was contusional hematoma which develops from a hemorrhage in an area appearing as normal density in CT as reported previously by Tsubokawa et al.14-16) and Diazet et al.8). Those intracerebral hematomas which, as claimed by Evans & Scheinker,9) develop from hemorrhages caused by anoxia and vasoparalysis occurring in a contused area of the brain correspond to hematomas within a contusional area. This has been considered to represent the main mechanism of formation of delayed intracerebral hematomas (Evans et al.,9) Lanksch et al.,") Weigel et al., 17) Ariga et al.') and Tsubokawa et al.14-16)) If Fig. 3 Histological findings for hematoma within a contusional area. The sur rounding brain tissue is edematous and necrotic, while blood vessels are dilated with small perivascular bleeding.

6 Fig. 4 Histological findings for contusional hematoma. The findings in the brain tissue surrounding the hematoma are essentially the same as for a hematoma within a contusional area, except that the border line of the contusional hema toma is clearer than that in the other type of hematoma. One specific finding, however, is the presence of thrombosed blood vessels with lymphoid cell infiltra tion in the hematoma. the CT findings of contusion obtained by Lanksch are true, this would mean that no contusion has occurred at the time of injury in cases of contusional hematoma. However, histological findings indicate that there is obstruction of small vessels with a distinct tendency for hemorrhages to occur in areas peripheral to the contused area, suggesting that the hematoma is apparently unrelated to the lesion of the contusion both spatially and temporally. Moreover, contusional hematomas tend to occur following surgery for epidural or subdural hematomas. These facts strongly suggest that local traumatic ischemia with subsequent displacement of brain tissue and changes in intracranial pressure as well as an increase in cerebral blood flow following surgical removal of coexisting extracerebral hematomas, are involved in the pathogenetic mechanism of contusional hematomas. It seems justified therefore to conclude that small cerebral vessels become thrombosed as a result of injury and the resultant alterations in intracranial pressure give rise to an abrupt increase in blood flow in the ischemic brain area before low density becomes demonstrable by CT, thus causing hemorrhages in areas surrounding the ischemic lesion. It is postulated, therefore, that at least two different mecha nisms exist for the development of delayed intracerebral hematomas. Both types of intracerebral hematoma are associated with slight disturbances of con sciousness and tend to show gradual improve ment. In cases without shifting of the median structure, conservative treatment proved to be effective, while those with a deteriorated level of consciousness and shifting of the median structure required surgical treatment. In this respect, no substantial differences were observed between the two types of hematoma. The success rate for rehabilitation following opera tive treatment was higher in contusional hematomas than in hematomas within a con

7 tusional area. It thus became clear that there are two types of delayed intracerebral hematomas which are similar concerning indication for surgery but differ in the treatment measures required for necrosis or edema of the surround ing brain tissue as well as in the results and outcome of operative treatment. The present study stresses the importance of a 1-week repeated CT follow-up subsequent to initial CT performed within 6 hours after injury for the discovery of delayed intracerebral hema tomas, and also the necessity of differentiating between contusional hematomas and hema tomas within a contusional area by repeated CT and thereby formulating an appropriate therapeutic plan. References 1) Ariga, T., Masuzawa, H., Mizutani, H., Mii, K., Eguchi, T. and Sano, K.: Evolution of traumatic intracerebral hematoma. Neurol Med Chir (Tokyo) 19: , ) Austarheim, K.: Delayed traumatic intra cerebral hemorrhage (Bollinger's Spät-Ap plexie). Report of one case with onecropsy. Acta Pathol Microbiol Scand 38: , ) Baratham, G. and Dennyson, W. G.: Delayed traumatic intracerebral hemorrhage. J Neurol Neurosurg Psychiatry 35: , ) Bollinger, O.: Uber traumatische Spät-Apo plexie; ein Betitrag aus Lehre von der Hirnerschutterung. Festschr. Rud. Virchow 70, Lebensjahr Berlin, 2: , ) Brown, F. D., Mullan, S. and Duda, E. E.: Delayed traumatic intracerebral hematoma. J Neurosurg 48: , ) Courville, C. B. and Blomquist, O. A.: Traumatic intracerebral hemorrhage with particular reference to its pathogenesis and its relation to delayed traumatic apoplexy. Arch Surg 41: 1-28, ) Courville, C. B.: Intracerebral hematoma, its Psychiat Rockswold, delayed II. gic Cranial Verlag, head and traumatic Goto, Classification intracerebral , ) ) Univ 5: pathology Morin, Tsubokawa, 62, Post-traumatic deficit. trauma. J Moriyasu, Spat-Apoplexie ). T., Med Ed. M. N.Y., results. computerized Computerized 77: posttraumatic ) International F.: Shinozaki, course. A. intracerebral and Frowein, Surg 21: Neurol , Lanksch, CT T., G. hematoma Am p hemorrhage. and W., of Moriyasu studies tomography Med 318, , follow-up Meese, of Koide, traumatic J Neurol N.: pathogenesis. L.: Pitts, J the Roentgenol petechial ) Neurosurg Chir brain control ) New H. Springer tomography. W. Conference following Early Levinthal, F. Diaz, with ) and R. Y., hematoma. 7: (Tokyo) F. W.: and Ad. J classification intracerebral G., Tsubokawa, , (CT) Stern, Nakamura, T., Yock, Moriyasu, stable of diagnosis head 126: Verlag, and Delayed Yamada, W. D. 33: Arch Kazner, J., Neurosurg., E.: H., Tomizawa, 19: Traumatic traumatic Larson, The , , of Springer trauma. massive D. neurol Neurol hematoma. Nihon , acute J ) Neurotraumatolog apoplexy findings ) and Cairo, N.: Neurosurg N., E.: ) 3: Merino-De following of S. 50: Weigel, by CT-scanning Villasante, , head Tsubokawa, K., J ) repeated related Ostertag, and T., injury C. Sidican, with Evans, Taveras, (&ldquo B. J. S. operati and P. M.: E., and Yam Mun clin Sch J. I.

MR imaging as predictor of delayed posttraumatic cerebral hemorrhage

J Neurosurg 69:203-209, 1988 MR imaging as predictor of delayed posttraumatic cerebral hemorrhage TOKUTARO TANAKA, M.D., TSUNEO SAKAI, M.D., KENICHI UEMURA, M.D., ATSUSHI TERAMURA, M.D., ICHIRO FUJISHIMA,