Neuroradiology
Delayed Intracranial Hematoma in Patients with Severe Head Injury 1 Maurice H. Lipper, M.B., Ch.B., D.M.R.D., F.F. Rad(D), Pulla R. S. Kishore, M.D., Alexander K. Girevendulis, M.D., J. Douglas Miller, Ph.D., M.D., and Donald P. Becker, M.D.
Serial computed tomography was performed on 119 consecutive patients suffering from severe head injury. The development of delayed intracranial hematomas, both intra- and extraaxial, was evaluated by comparing the initial scan with subsequent studies. Ten delayed intracerebral hematomas and nine delayed extracerebral collections were encountered. The occurrence of delayed intracerebral hemorrhage is more frequent than previously reported and is associated with a poor outcome. INDEX TERMS: Brain, hemorrhage. Head, computed tomography, 1[0].1211 • Head, injuries • (Head, intracranial effect of trauma, 1[0].430). (Head, subdural hematoma, 1[0].433) • (Head, traumatic brain hematoma, 1[0].434) Radiology 133:645-649, December 1979
severe head injury, i.e., those whose neurological deficit made them unable to obey even a simple command or speak recognizable words, were studied. Intracranial pressure was monitored during the first 72 hours by an intraventricular catheter or subarachnoid screw. Seven patients were excluded from the study either because they died or were taken to the operating room before CT could be performed. CT was performed on 119 patients on admission, on Days 3, 5, 14, 90, and one year following trauma as per the protocol. Eighty patients underwent 14-day scans, 72 had 90-day scans, and 42 had one-year studies. Forty-two deaths occurred in this series (33 %). CT findings were correlated with clinical outcome which was graded according to the scale of Jennett and Bond, namely: good recovery, moderate disability, severe disability, permanent vegetative state or death (6). A diagnosis of delayed intracerebral hematoma was made if no lesion or a negligible one (smaller than 1 em) was present on the
intracranial hematomas following head injury are generally considered to be uncommon. Reports in the literature have been based on analysis of findings in patients with varying degrees of head injury and CT studies made at varying time intervals following head trauma (1,2,4,8, 10). We have undertaken a prospective study to evaluate the development of delayed intra- and extracerebral hematoma in 119 consecutive patients suffering from head injury of clearly defined severity using serial computed tomography, and have found these lesions to be more common than previously believed.
D
ELA YEO
PATIENTS AND METHODS
One hundred and twenty-six consecutive patients were admitted to a head injury program in which they were managed according to a standardized protocol between April 1976 and April 1978. Only patients suffering from TABLE I:
Patient No.
DELAYEO INTRACEREBRAL HEMATOMAS
Initial CT
Prior Surgery
State of Delayed Hematoma
Time of Appearance Surgery After Injury Required
Clinical Outcome
1 2 3
Normal L temporal contusion Intraventricular hematoma, R frontal contusion
Thalamic Multiple, L hemispheric L temporal
2 days 2 days 2 days
4
L epidural hematoma, L temporal hematoma
R temporal
1 day
5 6
L subdural hematoma R subdural hematoma
+ +
R temporal L parietal
1 day 2 days
+
7
R subdural hematoma, R temporooccipital contusion L subdural hematoma, L temporal contusion L epidural hematoma L epidural hematoma, R suodural hematoma
+
L frontal, L temporal
24 days
+
Death Death Moderate disability Moderate disability Death Moderate disability Death
+ + +
L frontal L occipital R frontoparietal, L temporal
1 day 1 day 1 day
+ + +
Death Good recovery Good recovery
8 9 10
+
1 From the Departments of Radiology (Section of Neuroradiology), and Neurosurgery, Medical College of Virginia, Richmond, Va. 23298. Received Jan. 11, 1979; accepted and revision requested June 1; revision received July 24. Presented in part at the Sixty-fourth Scientific Assembly and Annual Meeting of the Radiological Society of North America, Chicago, 111., Nov. 26-Dec. 1. 1978. Supported by NIH Grant 1P01NS12587. ds
645
646
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LIpPER AND OTHERS
initial scan and parenchymal high-density lesions developed on subsequent studies. These were correlated with the initial lesion, the performance of prior surgery and clinical outcome. The occurrence of delayed extraaxial collections and their time of appearance were noted and the same correlations made as for the intracerebral hematomas. RESULTS Delayed Intracerebral Hematomas {TABLE
n
Delayed intracerebral hematomas developed in 12 patients. In two patients the lesions occurred in the immediate vicinity of surgical decompression and were not considered to be spontaneous delayed hematomas; they were therefore excluded from this study. Of the ten patients with intracerebral hematomas, six had undergone surgical decompression for their original lesions but four had had no previous surgery (Figs. 1, 2). All of these lesions were detected during the first 48 hours following injury , that is. between the scans performed on Days 1 and 3; the exception was a delayed hematoma in one patient that developed 24 days after surgery. Of the ten patients only two made a good recovery , three suffered moderate disability and five died. This is a much poorer outcome than for the group as a whole. Six of the ten patients required further
December 1979
surgery for decompression of the hematomas . Various initial CT findings were followed by delayed intracerebral hematomas in various sites. Of the four nonsurgical patients, one had a normal initial CT scan, one had a small contusion ipsilateral to the hematoma site , another suffered a contralateral contusion and the remaining patient had a combined extraaxial collection and intracerebral hematoma contralaterally. Of the six patients treated surgically, four had acute extracerebral hematomas prior to the occurrence of contralateral intracerebral lesions. One patient treated for an epidural hematoma suffered a delayed ipsilateral intracerebral hematoma . Bilateral intracerebral hematomas developed in the remaining patient who had bilateral extraaxiallesions. Delayed Extracerebral Collections {TABLE
In
Extraaxial collections developed in nine patients . All were of low density and should therefore be classified as chronic hematomas or hygromas (11, 12). These fell into two distinct groups , being either bifrontal or unilateral in location . Five bifrontal collections were seen, all of which developed before the 14th day postinjury. Two of the initial scans showed no abnormalities, two showed intracerebral hematomas and one showed an epidural hematoma. One patient in this group had undergone surgery for an epidural
a,b
Fig. 1. a. (left) Initial CT scans of a 40-year-old man following head trauma showing a small temporal lobe tip contusion (arrow) . b. (right) Study performed on Day 3 without intervening surgery. An intraventricular catheter was inserted via a frontal burrhole for intracranial pressure monitoring contralaterally. Multiple, large hem ispher ic intracerebral hematomas are evident on the ipsilateral side.
TABLE II:
Patient No.
Initial CT
1 2 3 4 5
Normal L temporal hematoma Normal R temporal contusion R epidural hematoma L subdural hematoma R occipitoparietal edema R temporofrontal hematoma L frontoparietal fracture
6 7
8 9
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Neuroradiology
DELAYED EXTRACEREBRAL COLLECTIONS
Prior Surgery
+ + +
hematoma. In only one of these patients was surgical decompression thought to be indicated . A small quantity of bloodstained fluid was obtained at surgery and there was no evidence of raised intracranial pressure. None of these collections was large (Fig. 3). Clin ical outcome was poor in this group with only one patient making a good recovery. Four unilateral collections were noted, one occurring 14 days after injury (Fig. 4), another at 90 days; the remaining two were discovered one year following the original trauma . Only the CT scans of the patient whose lesion was discovered after 90 days showed peripheral enhancement suggesting membrane formation. Preceding
Site of Delayed Hematoma
Time of Appearance After Injury
Bifrontal Bifrontal Bifrontal Bifrontal Bifrontal R frontoparietal R frontoparietal R frontal R frontoparietal
14 days 5 days 14 days 5 days 7 days 14 days 90 days 1 year 1 year
Surgery Required
Clinical Outcome
+
Death Death Moderate disability Death Good recovery Death Moderate disability Moderate disability Moderate disability
+ +
these lesions were a subdural hematoma, an intracerebral hematoma, multifocal edema and a frontoparietal fracture. In two patients repeat surgery was performed for drainage of the collections. Of this group one patient died and the remaining three suffered moderate disability. DISCUSSION
Baratham and Dennyson found 21 cases of delayed intracerebral hematoma out of 7,866 head injuries of all grades (1). This study was performed before the advent of CT, however, and the incidence of this phenomenon was probably underestimated . Brown et al. described three 2a ,b
Fig. 2. a. (left) Admission CT scans of a 31-year-old man demonstrating a subdural hematoma with a small temporal lobe contusion (arrows) . b. (right) CT scans 24 hours later , following surgical decompression, showing a delayed frontal intracerebral hematoma on the contralateral side. An intraventricular catheter was used to monitor intracranial pressure.
648
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H.
LIpPER AND OTHERS
patients with delayed intracerebral hematoma following closed head injury; hematomas developed in two of these patients 24 hours after a normal CT scan (2). The remaining case was diagnosed seven days after initial CT and might well have been detected earlier if an intervening study had been performed. French and Dublin described only one patient with a delayed temporal intracerebral hematoma out of a total of 1,000 consecutive patients with head injuries (4). This occurred six hours after injury . MerinodeViliasante and Taveras (8) described two patients with delayed lesions in their series of 100; one lesion was seen two days after the traumatic episode and the second was discovered on a CT scan taken 12 days later. A study was performed on the latter patient three days posttrauma which showed extensive and generalized edema. This is the only previously reported and proved case of a delayed hematoma developing after Day 3 with an intervening normal CT scan . A review of these series shows that 25 out of the 27 patients with delayed hematomas had undergone surgery before development of the lesions. It must be noted that the studies mentioned above were
3a,b
December 1979
not restricted to comatose patients but were made on patients with various grades of head trauma. Also. in those studies in which CT was performed. examinations were carried out at varying time intervals for specific reasons. In contrast, we investigated only patients who had suffered severe head trauma; serial scans were obtained at fixed time intervals following injury in all cases and our incidence of ten delayed hematomas out of 119 (8.4 % ) is higher. Furthermore, our results indicate that delayed intracerebral hematomas develop more frequently in patients who do not undergo surgery than previously suspected (4 out of 10). All of the hematomas, except one which occurred on Day 24, were noted to develop within 48 hours of the trauma and it would therefore appear that a CT scan on the third day postinjury is critical for discovery of these lesions. A suggested mechanism for development of a delayed intracerebral hematoma is a local failure of the mechanisms that regulate cerebral blood flow due to the contusional injury (1). Relaxation of cerebrovascular resistance permits transmission of intraarterial pressure to the capillary bed and encourages diapedesis and hematoma formation. An addedetiological factor in patients who have undergone surgical decompression for preexisting
4a,b
Fig. 3. a. (top) Admission CT scans showing no obvious lesion. Air , which has been inserted through a twist drill ventriculostomy, is present in the frontal horns. b. (bottom) Scans on day 14 show shallow , low-density . bifrontal extracerebral collections with ventricular enlargement.
Fig. 4. a. (top) Initial study demonstrating subdural and posterotemporal intracerebral hematomas (arrows). b. (bottom) CT scans on day 14 following craniotomy and temporal lobectomy. A large frontoparietal , low-density , extraaxial collection with no ventricular shift is evident on the contralateral side.
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DELA YED INTRACRANIAL HEMATOMA
lesions is relief of the tamponade effect, permitting hemorrhage into an already traumatized area. The outcome in these patients is poor, especially if bilateral high density lesions are present, a fact supported by the study of Sweet et et. (13). We encountered five deaths in our series, with three patients showing moderate disability and only two making a good recovery. The death rate for this group was thus 50 % as compared with an overall 33 % death rate in the whole series. The nine patients who had delayed extraaxial collections fell into two different groups, bifrontal or unilateral, and this suggests different etiologies. Although the exact mechanism is unclear, the probable etiology of bifrontal collections is CSF effusion due to diffuse brain injury and arachnoidal tears. This is supported by the fact that all bifrontal collections occurred within the first 14 days and that outcome was poor in these patients also-three deaths, one moderate residual disability, and only one good recovery. The last patient underwent a burr-hole craniotomy but only a negligible amount of fluid was obtained with no evidence of raised intracranial pressure; thus, it is doubtful whether repeat surgery accounted for the good result. Because we believe that diffuse brain injury leads to these collections, we feel that surgical intervention is impractical. Of the four patients with unilateral extraaxial collections, two collections occurred contralateral to the site of injury and followed surgical decompression. This suggests that surgical relief of tamponade played an important role in causing these collections. Collections developed in the remaining two patients on the same side as the injury which suggests a combined etiology. Unilateral lesions developed later than bifrontal ones. Two patients underwent repeat surgery for drainage, one 90 days and the other one year after trauma, but with no improvement in clinical status. French and Dublin discuss ten patients in whom lucent extracerebral collections developed as delayed sequelae of head injury (4). Two patients improved markedly after drainage of the hygromas, but the authors state that this degree of improvement appears to be the exception rather than the rule. Despite our findings that surgical treatment did not improve our patients clinically, we feel that one should continue to look for these lesions on repeat examinations with the hope that surgical intervention may result in improved clinical status. Forbes et el. found that almost 40 % of 148 subdural collections were of low attenuation and were most commonly seen after surgery (5). They feel that suspected collections not seen on at least two sections and not having prominent secondary signs should be viewed with caution and at their institution these patients were not commonly treated by operation. The two patients in our series who had further surgery showed ventricular compression and displacement. Other authors have described the occurrence of delayed, low-density extracerebral collections (3, 7, 9). Doubt exists, however, as to whether these are subdural hygromas, i.e., subdural collections of cerebrospinal fluid, or chronic subdural hematomas in which liquefaction of the
649
Neuroradiology
hematoma with resultant low density has occurred. Scotti et el. found that the surgical diagnosis of subdural hygromas is not always easy but should be made when the fluid is clear and no membrane formation is found (11). One of our patients had a right frontoparietal collection discovered 90 days after trauma; a peripheral rim of enhancement was evident on the CT scans and this was the only patient who could possibly be considered to have a chronic subdural hematoma. CONCLUSIONS
1. Delayed intracerebral hematomas following severe craniocerebral trauma in the absence of surgery are more common than previously thought. They may be due to a local failure of cerebral blood flow regulation. 2. Postsurgical intracerebral hematomas may be due to the reason just mentioned, to surgery itself or to surgical relief of a tamponade effect. 3. All delayed intracerebral hematomas except one were detected within 48 hours f'ollowing head injury and were associated with a poor outcome. 4. Most delayed extracerebral collections in our series were seen within two weeks following trauma. These were thought to be due to effusion as a result of diffuse brain injury, collection of fluid at another site after surgical relief of tamponade or reaccumulation of fluid at the site of a surgically removed hematoma. Maurice H. Lipper, M.B., Ch.B. Department of Radiology Medical College of Virginia, Box 615 Richmond, VA 23298
REFERENCES 1. Baratham G, Dennyson WG: Delayed traumatic intracerebral hemorrhage. J Neurol Neurosurg Psychiatry 35:698-706, Oct 1972 2. Brown FD, Mullan S, DueJa EE: Delayedtraumatic intracerebral hematomas. Report of 3 cases. J Neurosurg 48:1019-1022, Jun 1978 3. Davis, KR, Taveras JM, Roberson GH, et al: Computed tomography in head injury. Sernin RoentgenoI12:53-62, Jan 1977 4. French BN, Dublin AB: The value of computerized tomography in the management of 1000 consecutive head injuries. Surg Neurol 7:171-183, Apr 1977 5. Forbes GS, Sheedy PF II, Piepgras DG, et al: Computed tomography in the evaluation of subdural hematomas. Radiology 126: 143-148, Jan 1978 6. Jennett B, Bond M: Assessment of outcome after severe brain damage: A practical scale. Lancet 1:480-484, 1975 7. Koo AH, laRoque RL: Evaluationof head trauma by computed tomography. Radiology 123:345-350, May 1977 8. Merino-de Villasante J, Taveras JM: Computerized tomography (CT) in acute head trauma. AJR 126:765-778, Apr 1976 9. New PFJ, Scott WR: Computed Tomography of the Brain and Orbit. Baltimore, Williams & Wilkins, 1975, p 486 10. Paxton R, Ambrose J: The EMI scanner. A brief review of the first 650 patients. Br J RadioI47:530-565, Sept 1974 11. Scotti G, Terbrugge K, Melancon D, et al: Evaluation of the age of subdural hematomas by computerized tomography. J Neurosurg 47:311-315, Sep 1977 12. SvendsenP: Computer tomography of traumatic extracerebral lesions. Br J Radiol 49:1004-1012, Dec 1976 13. Sweet RC, Miller JD, Lipper MH, et al: Significance of bilateral abnormalities on the CT scan in patients with severe head injury. Neurosurgery 3:16-21, Jul-Aug 1978
Delayed Intracranial Hematoma in Patients with Severe Head Injury 1 Maurice H. Lipper, M.B., Ch.B., D.M.R.D., F.F. Rad(D), Pulla R. S. Kishore, M.D., Alexander K. Girevendulis, M.D., J. Douglas Miller, Ph.D., M.D., and Donald P. Becker, M.D.
Serial computed tomography was performed on 119 consecutive patients suffering from severe head injury. The development of delayed intracranial hematomas, both intra- and extraaxial, was evaluated by comparing the initial scan with subsequent studies. Ten delayed intracerebral hematomas and nine delayed extracerebral collections were encountered. The occurrence of delayed intracerebral hemorrhage is more frequent than previously reported and is associated with a poor outcome. INDEX TERMS: Brain, hemorrhage. Head, computed tomography, 1[0].1211 • Head, injuries • (Head, intracranial effect of trauma, 1[0].430). (Head, subdural hematoma, 1[0].433) • (Head, traumatic brain hematoma, 1[0].434) Radiology 133:645-649, December 1979
severe head injury, i.e., those whose neurological deficit made them unable to obey even a simple command or speak recognizable words, were studied. Intracranial pressure was monitored during the first 72 hours by an intraventricular catheter or subarachnoid screw. Seven patients were excluded from the study either because they died or were taken to the operating room before CT could be performed. CT was performed on 119 patients on admission, on Days 3, 5, 14, 90, and one year following trauma as per the protocol. Eighty patients underwent 14-day scans, 72 had 90-day scans, and 42 had one-year studies. Forty-two deaths occurred in this series (33 %). CT findings were correlated with clinical outcome which was graded according to the scale of Jennett and Bond, namely: good recovery, moderate disability, severe disability, permanent vegetative state or death (6). A diagnosis of delayed intracerebral hematoma was made if no lesion or a negligible one (smaller than 1 em) was present on the
intracranial hematomas following head injury are generally considered to be uncommon. Reports in the literature have been based on analysis of findings in patients with varying degrees of head injury and CT studies made at varying time intervals following head trauma (1,2,4,8, 10). We have undertaken a prospective study to evaluate the development of delayed intra- and extracerebral hematoma in 119 consecutive patients suffering from head injury of clearly defined severity using serial computed tomography, and have found these lesions to be more common than previously believed.
D
ELA YEO
PATIENTS AND METHODS
One hundred and twenty-six consecutive patients were admitted to a head injury program in which they were managed according to a standardized protocol between April 1976 and April 1978. Only patients suffering from TABLE I:
Patient No.
DELAYEO INTRACEREBRAL HEMATOMAS
Initial CT
Prior Surgery
State of Delayed Hematoma
Time of Appearance Surgery After Injury Required
Clinical Outcome
1 2 3
Normal L temporal contusion Intraventricular hematoma, R frontal contusion
Thalamic Multiple, L hemispheric L temporal
2 days 2 days 2 days
4
L epidural hematoma, L temporal hematoma
R temporal
1 day
5 6
L subdural hematoma R subdural hematoma
+ +
R temporal L parietal
1 day 2 days
+
7
R subdural hematoma, R temporooccipital contusion L subdural hematoma, L temporal contusion L epidural hematoma L epidural hematoma, R suodural hematoma
+
L frontal, L temporal
24 days
+
Death Death Moderate disability Moderate disability Death Moderate disability Death
+ + +
L frontal L occipital R frontoparietal, L temporal
1 day 1 day 1 day
+ + +
Death Good recovery Good recovery
8 9 10
+
1 From the Departments of Radiology (Section of Neuroradiology), and Neurosurgery, Medical College of Virginia, Richmond, Va. 23298. Received Jan. 11, 1979; accepted and revision requested June 1; revision received July 24. Presented in part at the Sixty-fourth Scientific Assembly and Annual Meeting of the Radiological Society of North America, Chicago, 111., Nov. 26-Dec. 1. 1978. Supported by NIH Grant 1P01NS12587. ds
645
646
MAURICE
H.
LIpPER AND OTHERS
initial scan and parenchymal high-density lesions developed on subsequent studies. These were correlated with the initial lesion, the performance of prior surgery and clinical outcome. The occurrence of delayed extraaxial collections and their time of appearance were noted and the same correlations made as for the intracerebral hematomas. RESULTS Delayed Intracerebral Hematomas {TABLE
n
Delayed intracerebral hematomas developed in 12 patients. In two patients the lesions occurred in the immediate vicinity of surgical decompression and were not considered to be spontaneous delayed hematomas; they were therefore excluded from this study. Of the ten patients with intracerebral hematomas, six had undergone surgical decompression for their original lesions but four had had no previous surgery (Figs. 1, 2). All of these lesions were detected during the first 48 hours following injury , that is. between the scans performed on Days 1 and 3; the exception was a delayed hematoma in one patient that developed 24 days after surgery. Of the ten patients only two made a good recovery , three suffered moderate disability and five died. This is a much poorer outcome than for the group as a whole. Six of the ten patients required further
December 1979
surgery for decompression of the hematomas . Various initial CT findings were followed by delayed intracerebral hematomas in various sites. Of the four nonsurgical patients, one had a normal initial CT scan, one had a small contusion ipsilateral to the hematoma site , another suffered a contralateral contusion and the remaining patient had a combined extraaxial collection and intracerebral hematoma contralaterally. Of the six patients treated surgically, four had acute extracerebral hematomas prior to the occurrence of contralateral intracerebral lesions. One patient treated for an epidural hematoma suffered a delayed ipsilateral intracerebral hematoma . Bilateral intracerebral hematomas developed in the remaining patient who had bilateral extraaxiallesions. Delayed Extracerebral Collections {TABLE
In
Extraaxial collections developed in nine patients . All were of low density and should therefore be classified as chronic hematomas or hygromas (11, 12). These fell into two distinct groups , being either bifrontal or unilateral in location . Five bifrontal collections were seen, all of which developed before the 14th day postinjury. Two of the initial scans showed no abnormalities, two showed intracerebral hematomas and one showed an epidural hematoma. One patient in this group had undergone surgery for an epidural
a,b
Fig. 1. a. (left) Initial CT scans of a 40-year-old man following head trauma showing a small temporal lobe tip contusion (arrow) . b. (right) Study performed on Day 3 without intervening surgery. An intraventricular catheter was inserted via a frontal burrhole for intracranial pressure monitoring contralaterally. Multiple, large hem ispher ic intracerebral hematomas are evident on the ipsilateral side.
TABLE II:
Patient No.
Initial CT
1 2 3 4 5
Normal L temporal hematoma Normal R temporal contusion R epidural hematoma L subdural hematoma R occipitoparietal edema R temporofrontal hematoma L frontoparietal fracture
6 7
8 9
647
DELAYEO INTRACRANIAL HEMATOMA
Vol. 133
Neuroradiology
DELAYED EXTRACEREBRAL COLLECTIONS
Prior Surgery
+ + +
hematoma. In only one of these patients was surgical decompression thought to be indicated . A small quantity of bloodstained fluid was obtained at surgery and there was no evidence of raised intracranial pressure. None of these collections was large (Fig. 3). Clin ical outcome was poor in this group with only one patient making a good recovery. Four unilateral collections were noted, one occurring 14 days after injury (Fig. 4), another at 90 days; the remaining two were discovered one year following the original trauma . Only the CT scans of the patient whose lesion was discovered after 90 days showed peripheral enhancement suggesting membrane formation. Preceding
Site of Delayed Hematoma
Time of Appearance After Injury
Bifrontal Bifrontal Bifrontal Bifrontal Bifrontal R frontoparietal R frontoparietal R frontal R frontoparietal
14 days 5 days 14 days 5 days 7 days 14 days 90 days 1 year 1 year
Surgery Required
Clinical Outcome
+
Death Death Moderate disability Death Good recovery Death Moderate disability Moderate disability Moderate disability
+ +
these lesions were a subdural hematoma, an intracerebral hematoma, multifocal edema and a frontoparietal fracture. In two patients repeat surgery was performed for drainage of the collections. Of this group one patient died and the remaining three suffered moderate disability. DISCUSSION
Baratham and Dennyson found 21 cases of delayed intracerebral hematoma out of 7,866 head injuries of all grades (1). This study was performed before the advent of CT, however, and the incidence of this phenomenon was probably underestimated . Brown et al. described three 2a ,b
Fig. 2. a. (left) Admission CT scans of a 31-year-old man demonstrating a subdural hematoma with a small temporal lobe contusion (arrows) . b. (right) CT scans 24 hours later , following surgical decompression, showing a delayed frontal intracerebral hematoma on the contralateral side. An intraventricular catheter was used to monitor intracranial pressure.
648
MAURICE
H.
LIpPER AND OTHERS
patients with delayed intracerebral hematoma following closed head injury; hematomas developed in two of these patients 24 hours after a normal CT scan (2). The remaining case was diagnosed seven days after initial CT and might well have been detected earlier if an intervening study had been performed. French and Dublin described only one patient with a delayed temporal intracerebral hematoma out of a total of 1,000 consecutive patients with head injuries (4). This occurred six hours after injury . MerinodeViliasante and Taveras (8) described two patients with delayed lesions in their series of 100; one lesion was seen two days after the traumatic episode and the second was discovered on a CT scan taken 12 days later. A study was performed on the latter patient three days posttrauma which showed extensive and generalized edema. This is the only previously reported and proved case of a delayed hematoma developing after Day 3 with an intervening normal CT scan . A review of these series shows that 25 out of the 27 patients with delayed hematomas had undergone surgery before development of the lesions. It must be noted that the studies mentioned above were
3a,b
December 1979
not restricted to comatose patients but were made on patients with various grades of head trauma. Also. in those studies in which CT was performed. examinations were carried out at varying time intervals for specific reasons. In contrast, we investigated only patients who had suffered severe head trauma; serial scans were obtained at fixed time intervals following injury in all cases and our incidence of ten delayed hematomas out of 119 (8.4 % ) is higher. Furthermore, our results indicate that delayed intracerebral hematomas develop more frequently in patients who do not undergo surgery than previously suspected (4 out of 10). All of the hematomas, except one which occurred on Day 24, were noted to develop within 48 hours of the trauma and it would therefore appear that a CT scan on the third day postinjury is critical for discovery of these lesions. A suggested mechanism for development of a delayed intracerebral hematoma is a local failure of the mechanisms that regulate cerebral blood flow due to the contusional injury (1). Relaxation of cerebrovascular resistance permits transmission of intraarterial pressure to the capillary bed and encourages diapedesis and hematoma formation. An addedetiological factor in patients who have undergone surgical decompression for preexisting
4a,b
Fig. 3. a. (top) Admission CT scans showing no obvious lesion. Air , which has been inserted through a twist drill ventriculostomy, is present in the frontal horns. b. (bottom) Scans on day 14 show shallow , low-density . bifrontal extracerebral collections with ventricular enlargement.
Fig. 4. a. (top) Initial study demonstrating subdural and posterotemporal intracerebral hematomas (arrows). b. (bottom) CT scans on day 14 following craniotomy and temporal lobectomy. A large frontoparietal , low-density , extraaxial collection with no ventricular shift is evident on the contralateral side.
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DELA YED INTRACRANIAL HEMATOMA
lesions is relief of the tamponade effect, permitting hemorrhage into an already traumatized area. The outcome in these patients is poor, especially if bilateral high density lesions are present, a fact supported by the study of Sweet et et. (13). We encountered five deaths in our series, with three patients showing moderate disability and only two making a good recovery. The death rate for this group was thus 50 % as compared with an overall 33 % death rate in the whole series. The nine patients who had delayed extraaxial collections fell into two different groups, bifrontal or unilateral, and this suggests different etiologies. Although the exact mechanism is unclear, the probable etiology of bifrontal collections is CSF effusion due to diffuse brain injury and arachnoidal tears. This is supported by the fact that all bifrontal collections occurred within the first 14 days and that outcome was poor in these patients also-three deaths, one moderate residual disability, and only one good recovery. The last patient underwent a burr-hole craniotomy but only a negligible amount of fluid was obtained with no evidence of raised intracranial pressure; thus, it is doubtful whether repeat surgery accounted for the good result. Because we believe that diffuse brain injury leads to these collections, we feel that surgical intervention is impractical. Of the four patients with unilateral extraaxial collections, two collections occurred contralateral to the site of injury and followed surgical decompression. This suggests that surgical relief of tamponade played an important role in causing these collections. Collections developed in the remaining two patients on the same side as the injury which suggests a combined etiology. Unilateral lesions developed later than bifrontal ones. Two patients underwent repeat surgery for drainage, one 90 days and the other one year after trauma, but with no improvement in clinical status. French and Dublin discuss ten patients in whom lucent extracerebral collections developed as delayed sequelae of head injury (4). Two patients improved markedly after drainage of the hygromas, but the authors state that this degree of improvement appears to be the exception rather than the rule. Despite our findings that surgical treatment did not improve our patients clinically, we feel that one should continue to look for these lesions on repeat examinations with the hope that surgical intervention may result in improved clinical status. Forbes et el. found that almost 40 % of 148 subdural collections were of low attenuation and were most commonly seen after surgery (5). They feel that suspected collections not seen on at least two sections and not having prominent secondary signs should be viewed with caution and at their institution these patients were not commonly treated by operation. The two patients in our series who had further surgery showed ventricular compression and displacement. Other authors have described the occurrence of delayed, low-density extracerebral collections (3, 7, 9). Doubt exists, however, as to whether these are subdural hygromas, i.e., subdural collections of cerebrospinal fluid, or chronic subdural hematomas in which liquefaction of the
649
Neuroradiology
hematoma with resultant low density has occurred. Scotti et el. found that the surgical diagnosis of subdural hygromas is not always easy but should be made when the fluid is clear and no membrane formation is found (11). One of our patients had a right frontoparietal collection discovered 90 days after trauma; a peripheral rim of enhancement was evident on the CT scans and this was the only patient who could possibly be considered to have a chronic subdural hematoma. CONCLUSIONS
1. Delayed intracerebral hematomas following severe craniocerebral trauma in the absence of surgery are more common than previously thought. They may be due to a local failure of cerebral blood flow regulation. 2. Postsurgical intracerebral hematomas may be due to the reason just mentioned, to surgery itself or to surgical relief of a tamponade effect. 3. All delayed intracerebral hematomas except one were detected within 48 hours f'ollowing head injury and were associated with a poor outcome. 4. Most delayed extracerebral collections in our series were seen within two weeks following trauma. These were thought to be due to effusion as a result of diffuse brain injury, collection of fluid at another site after surgical relief of tamponade or reaccumulation of fluid at the site of a surgically removed hematoma. Maurice H. Lipper, M.B., Ch.B. Department of Radiology Medical College of Virginia, Box 615 Richmond, VA 23298
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