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Intracranial Hemorrhage of Traumatic Origin
Intracranial Hemorrhage of Traumatic Origin '"rUNG HUI LIN, M.D.*
ALBERT W. COOK, M.D., }i'.A.C;.S.** E. JEF:FERSON BROWDER, M.D., F.A.C.S.t
upon contact trauma to the head, one to several blood vessels supplying structures within the intracranial cavity may be torn with resulting hemorrhage of variable quantities and concomitant or subsequent dysfunctions of the brain. l'he evidence accumulated in recent years tends to point toward alterations in function of the vascular system of the brain as the basic factor, or factors, in the great variety of clinical pictures resulting from craniocerebral trauma, the hemorrhagic collection serving at times only as the initiating agent for venous stasis, cerebral s\velling, and later distortion of the brain stem. Although our knowledge at present does not permit ready correlation of each hemorrhagic accumulation in the intracranial structures with the clinical manifestations, particularly in those patients with multiple lesions, certain important syndromes have been clearly delineated and effective therapeutic measures advocated. It is these gross hemorrhages \vithin the intracranial cavity, secondary to a blow to the head, which may be termed "surgical blood clots" that concern us in this communication. During the past 26 years, 46,574 patients with craniocerebral trauma
CONSEQUENT
From the Department of Neurosurgery, State University of New York Downstate Medical Center, and the Neurosurgical Service of Kings County Hospital, Brooklyn, New York.
* Assistant Instructor in Neurosurgery, State Univers1'ty of New York Downstate Medical Center, and the Neurosurgical Service of K i'rtgs County Hospital, Brooklyn, New York.
** Assistant Professor of Neurosurgery, State University of N ew York Downstate Medical Center, and the Neurosurgical Serv'ice of Kings County Hospital, Brooklyn, New York. t Professor of Neurosurgery, State [Jniversity of New York Downstate Medical Center, and the Neurosurgical Service of Kings County Hospital, Brooklyn, New York. 603
604
Tung Hui Lin, AlbertW. Cook, E. Jeiferson Browder
were admitted to the Kings County Hospital of Brooklyn. Among these were 171 patients with epidural hemorrhages requiring surgical therapy, 873 with subdural collections of surgical significance, and 153 with solitary intracerebral hematomas subjected to operation. In other words, an average of 1800 patients with craniocerebral insults were admitted to the hospital each year with an annual average of 7 + patients with epidural hematomas, 33+ with subdural hematomas and six with intracerebral hematomas. Over the years there has been considerable fluctuations in the total numbers admitted-1500 to 2700 annually. Increasing experience has been rewarding in that diagnostic acumen has been sharpened and surgical procedures have become more definitive. li'or example, from July 1956 to July 1957 there were approximately 2500 patients with craniocerebral injuries admitted to the service. Fifteen of those had epidural hemorrhage, 51 subdural and ten intracerebral hematomas. These data indicate not only the relative frequency of intracranial hemorrhage of traumatic origin, but also the surgeon's opportunity to whittle down, slowly but surely, the mortality associated with patients so injured. EPIDURAL HEMORRHAGE l~'ew clinical syndromes are as dramatic in their manifestations as that of the classical epidural hemorrhage: a blo,v to the head, transitory loss of contact with surroundings, several hours of lucidity albeit with pain in the head, then vomiting, drowsiness, hemiparesis contralateral to the lesion, coma, decerebrate rigidity and death. This sequence of events may be in general correlated with contusion and swelling of the scalp at the site of traumatic impact, linear fracture of the skull, so-called "commotio cerebri," rent in the epidural blood vessels, return of relatively normal cerebral function, hemorrhage from the ruptured blood vessel with further stripping of the dura from the skull, compression of the cerebral surface, stasis of blood flow within the transcerebral venous system, cerebral swelling implicating the diencephalon, herniation of the uncus, mesencephalic hypoxia with or without secondary hemorrhage at this level, and terminally dysfunction of the hindbrain. It is quite generally known that prompt definitive surgical therapy is mandatory before evidence of decerebration sets in if complete recovery of cerebral functions is to be attained. And it may be added somewhat parenthetically that this is not a lesion to be dealt with effectively through a socalled "subtemporal decompression" opening in the skull, a moderate sized bone flap being the preferred technical approach to the hematoma. Unfortunately, insofar as diagnosis is concerned, only about one-half of the patients with gross hemorrhage into the intracranial epidural zone run the classical clinical course just described. The remaining 50 per cent may be placed in two further categories, those harboring cerebral
Intracranial H emorrhage of Traumatic Origin
605
epidural blood clots associated with multiple traumatic lesions of the cerebrum and those with epidural hemorrhage compressing the structures of the subtentorial compartment. If severe trauma of the brain is followed by enduring deep stupor to coma, then the clinician may overlook the scanty abnormal physical findings suggesting supratentorial epidural bleeding. Two of these are outstanding, namely hemiparesis or hemiplegia on the side contralateral to linear fracture of the skull demonstrated by roentgen examination and/or a dilated pupil not reactive to light on the side of the linear fracture. In addition, a worsening of the clinical picture, especially deepening of stupor and recurring transitory skeletal muscle rigidity unilaterally, indicate that all is not \vell and that more precise diagnostic procedures are in order. Cerebral arteriography may be used to advantage, especially in young adults but carries some danger of aggravating a bad situation in older patients. It is advisable to attempt a selection of the diagnostic procedure, or procedures, best suited to the possible problem presented by a particular patient, rather than to adhere to standardized formulas. In our clinic, even a suspicion of epidural hemorrhage based on sound clinical evidence is the signal for surgical intervention. The patient is positioned on the operating table in a fashion to permit biparietal burr holes to be made if desired. The line of incision of the scalp for a bone flap is marked on the side of the linear fracture, with the center of the proposed flap at the site where the fracture line crosses a major groove of the inner table of the skull. In this area a single burr hole is made to establish or disprove the notion that an epidural clot is present. If a blood clot is present, the bone flap is reflected and the mass removed. If epidural hemorrhage is not disclosed and a nick in the dura establishes that a subdural collection is not present, biparietal burr holes are made. In the absence of lesions of the surface bilaterally, a ventriculogram is carried out and further surgical maneuvers performed if this discloses a mass lesion within the intracranial cavity. In the last-mentioned group may be placed the syndrorne of the posterior fossa produced by hemorrhage from vessels of the dura overlying the cerebellum. In some the blood clot strips the dura of the adjacent inferior occipital area and with it the lateral sinus. If the formation of the clot is relatively rapid, the patient may succumb within an hour or so following injury. Those with slovver bleeding develop symptoms and abnormal physical findings in a progressive manner, thus permitting a proper clinical evaluation of the problem. Frequently, on entry to the hospital, there is disorientation and drowsiness from which partial recovery ensues. Usually, there is evidence of a blow to the occipital region and roentgen findings of a linear fracture of the skull overlying the posterior cranial fossa. After a few hours of relative lucidity, drowsiness returns and, with this, slo\ving of the respiratory rate and pulse. It is
606
Tung Hui Lin, Albert W. Cook, E. Jefferson Browder
the slow and at times sighing type of respiration occurring in a patient with edema of the scalp overlying a linear fracture of the occipital skull that strongly suggests compression of the hindbrain by a blood clot. At all events, this clinical picture calls for prompt surgical exploration of the area under suspicion and evacuation of the hematoma if present. SUBDURAL HEMATOMAS
As stated, up to July 1, 1957 there have been 873 verified examples of subdural hematoma at this hospital. At present 45 to 50 patients a year with a variety of subdural collections have been sufficient to maintain a continuing active interest in this clinical problem. At intervals during the past 15 years reports concerning the anatomicopathology and the pathophysiology of this lesion have emanated from our clinic. Especially attractive to us has been the study of the pathogenesis of the symptomatology, in particular the causative factors for the late symptoms frequently observed in patients with subdural collections. To date, observations regarding the alterations in the patency of veins following surface compression of a cerebral hemisphere by hemorrhage, the pathological changes of the white matter of the brain underlying surface hemorrhage, the electroencephalographic findings associated with these changes, the pneumoencephalographic evidence that cerebral swelling persists for days and even weeks following surgical evacuation of the surface hemorrhage, and the arteriographic visualization of the position of the cerebral cortex in relation to the persistently swollen cerebral hemisphere following removal of the subdural collection, have all been recorded in the literature. These data strongly support the notion that a cerebral subdural hemorrhage resulting from contact trauma of the head serves as the initiating factor for cerebral swelling and it is this slowly developing intracerebral swelling which is responsible for the late symptoms of subdural hematomas. In addition to these studies concerning the anatomical alterations and the pathological changes associated with subdural collections, the various clinical pictures resulting from these lesions have concurrently received appropriate consideration. Largely as a convenience in presentation, the clinical syndromes have been placed in three groups; however, it is to be recognized that the members of one group merge with the adjoining one. In Group I may be placed those with subdural hemorrhage and minimal evidence of cerebral insult. Some authors have described these as chronic subdural hematomas since frequently few symptoms and abnormal physical features indicate their presence shortly after injury. Be that as it may, patients with this type of lesion may lead a relatively normal life for weeks, or even months, subsequent to injury and then become drowsy and within a few days comatose. In
Intracranial H ernorrhage of Trau'matic
Origir~
607
truth, the same pathophysiological mechanism may develop from any mass in the intracranial cavity, be it tumor, abscess or blood clot. It is the regional swelling consequent upon venous stasis, which when extensive enough to implicate the diencephalic-mesencephalic-hindbrain complex, produces a drowsy-to-comatose state associated with neurological deficits in accordance with the position of the lesion. So the reasons become evident why longstanding subdural collections produce symptoms and abnormal physical signs comparable to cerebral tumor and why this lesion is frequently diagnosed preoperatively as cerebral neoplasm. As in the case of all intracranial mass lesions associated with drowsiness, surgical therapy should not be delayed. In Group 11 may be placed patients with subdural hemorrhage and moderate cerebral insult. They usually enter the hospital within an hour following a blow to the head which rendered them unconscious. Multiple injuries of the trunk and extremities are not exceptional and must be evaluated in the total individual problem. Usually the clinical evidence indicates that cerebral functions are not seriously affected, although drowsiness and possibly hemiparesis may persist for several days. Gradually limited contact with surroundings is attained and after three to four days the average patient appears to be well on the way to recovery. Although out of bed and about the ward, it is obvious that intellectual blunting persists. After two or three weeks there is again drowsiness, indifference as regards excreta, possibly inequality of the pupils, stiffness of the neck and Babinski toe sign bilaterally. Other neurological deficits may be demonstrable; however, these are the ones most commonly encountered. Prompt evacuation of the subdural collection is mandatory when there is the slightest evidence of returning drowsiness. Often the hemorrhagic collection is entirely liquid and may be "washed out" through two burr holes. If a part of the surface mass consists of clotted blood, then a bone flap is reflected and complete evacuation accomplished. It is to be remembered that approximately 20 per cent occur bilaterally, consequently both sides are always surgically explored. By far the largest number of the series of 873 fall in Group 11. We have been able to study the patients with this syndrome in more detail than those falling in Group I and Group Ill. There is conclusive evidence that cerebral swelling of considerable magnitude exists in the white matter in particular, underlying a surface hemorrhagic collection. That this swelling persists for days and sometimes weeks after surgical removal of a subdural hemorrhage is incontestable. The persistence of drowsiness-to-stupor after operation is entirely consistent with the pathophysiological state resulting from the intracerebral swelling. In a few patients evacuation of a large liquid subdural collection is followed by prompt clearing of the sensorium. It would seem that, in these, intracerebral swelling was not the major factor in the drowsiness. It is
608
Tung Hui Lin, Albert W. Cook, E. Jefferson Browder
possible that the brain stem may have been rendered hypoxic by distortion produced by the large collection. Further study concerning the effect of the mass alone on conscious states is now in progress. In Group III have been placed patients with severe craniocerebral injuries and subdural hemorrhage. 1-'he pathophysiological import of the subdural hemorrhage in a patient with multiple cerebral lesions is at present impossible to estimate. Ilegardless of therapy, surgical or otherwise, the mortality is high. Certainly early evacuation of the surface hematoma and generous decompression is not the answer. Owing to the complex nature of the problem and our inability to relate certain abnormal clinical features to one of the several intracranial lesions, we have of necessity resorted to a conservative therapeutic regimen during the early hours following injury in an attempt to tide the patient over a critical period. If successful and the vital signs become somewhat stabilized, evacuation of the subdural collection on the fourth or fifth day following injury may result in additional improvement. In others, the removal of the subdural collection has little, if any, influence on the outcome, while in still others a bad situation is made worse by the operation. The mortality in Group III is approximately 80 per cent, the majority of patients dying within a few days after injury. Finally, in a discussion of cerebral subdural hematoma should be mentioned those occurring in the subdural space of the subtentorial compartment. Hemorrhage into this space is usually secondary to traumatic laceration of the cerebellar cortex and this is in turn frequently associated with moderate-to-severe craniocerebral insult. Clinically, one must be on the alert to entertain seriously the possibility of subdural hemorrhagic collection in this site. Slow irregular respirations associated with coma and relative flaccidity of the skeletal musculature are abnormal features suggesting a blood clot in this area. More often the lesion is located by making burr holes in the skull over the posterior fossa after a mass lesion of the supratentorial compartments has been unequivocally excluded. IN1"'RACEREBRAL HEMATOMAS
Hemorrhage into the cerebral substance as a consequence of craniocerebral injury is usually regarded as an index of severe cerebral insult, as is also the so-called cerebral dissolution. One of the common anatomical sites for these lesions is the frontotemporal region (posteriorinferior frontal and anterior temporal). The latter lesion consists of cerebral softening with multiple small blood clots, some coalescing, others not. The abnormal clinical features of the two lesions in this particular location are similar, as is the pathogenesis of each. In some previous communications from our clinic the two pathological states have been
Intracranial H emorrhage of Traumatic Origin
609
drawn together and the diagnostic and therapeutic measures discussed under one heading. The 153 examples recorded here as a basis for the present presentation were single blood clots sizable enough to be of "surgical significance," 20 grams or more. Pathogenetically they were of two types, coup and contrecoup. The majority were regarded as being produced by the contrecoup mechanism and about half of these were associated with a surface hematoma, mostly subdural in position. In the last 40 cases the intracerebral blood clot was in the frontal lobe in 16, temporal lobe 16, parietal lobe 5, occipital lobe 2, and one in the cerebellum. In other words, 33 of the 40 were probably the result of contrecoup damage, whereas the remaining seven were of the coup variety. If the examples of cerebral dissolution were included, the figures would run into hundreds. It is the solitary intracerebral hemorrhage usually produced by the so-called coup mechanism that affords an uncomplicated lesion for pathophysiological study and clinical correlation. Interestingly enough, these lesions not infrequently produce a train of symptomatic events and abnormal physical signs simulating somewhat epidural hemorrhage: A blow to the head, transitory loss of consciousness, reorientation, residual hemiparesis in some and after a few days to several weeks, drowsiness, headache and vomiting, choked disk and increasing hemiparesis. Pathologically there is cerebral swelling of the white matter about the blood clot, as frequently observed about a cerebral tumor. As for hematomas in other anatomical positions, it is the cerebral swelling which produces the recrudescence of symptomatology. The accepted surgical approach is accurate diagnosis, either ventriculography or angiography, followed by removal of the hematoma through an osteoplastic cranial opening and an incision in the cerebral cortex. Intracerebellar hemorrhage, similar to subdural hemorrhage of the posterior fossa, seemingly results from contusion-laceration of the cerebellar cortex. Traumatic damage of the brain of this character is almost invariably associated with evidence of severe cerebral insult. An interesting clinical feature characterized by paroxysmal "bridging" or severe opisthotonos is observed occasionally in patients with contusion-laceration of the cerebellum and/or intracerebellar hematoma. Although intracerebellar hemorrhage of traumatic origin is relatively uncommon (certainly far less common than spontaneous hemorrhage in this location), it does occur and whenever the clinical features suggest dysfunction of t.he hindbrain as previously described, the presence or absence of such a lesion must be established through a suboccipital craniectomy. SUMMARY AND CONCLUSIONS
In a series of 46,574 patients with craniocerebral injury, 2.5 per cent had intracranial hemorrhage of surgical significance. Hemorrhage in the
610
1 urtg Hui l.Jin, Albert W. CYook, E. J eiJerson Browder 1
cerebral subdural space was encountered five times as frequently as that occurring epidurally or intracerebrally. The known pathophysiological features associated with hemorrhage in these three anatomical sites have been mentioned. Although one frequently resorts to the use of the ancillary diagnostic procedures, these are not a substitute for sound, clinical evaluation. The surgical opening of the skull for the removal of an intracranial hematoma should be sufficiently large and appropriately fashioned to permit total removal of the blood clot. 200 Hicks Street Brooklyn 1, New York (Drs. Cook and Browder)
ALBERT W. COOK, M.D., }i'.A.C;.S.** E. JEF:FERSON BROWDER, M.D., F.A.C.S.t
upon contact trauma to the head, one to several blood vessels supplying structures within the intracranial cavity may be torn with resulting hemorrhage of variable quantities and concomitant or subsequent dysfunctions of the brain. l'he evidence accumulated in recent years tends to point toward alterations in function of the vascular system of the brain as the basic factor, or factors, in the great variety of clinical pictures resulting from craniocerebral trauma, the hemorrhagic collection serving at times only as the initiating agent for venous stasis, cerebral s\velling, and later distortion of the brain stem. Although our knowledge at present does not permit ready correlation of each hemorrhagic accumulation in the intracranial structures with the clinical manifestations, particularly in those patients with multiple lesions, certain important syndromes have been clearly delineated and effective therapeutic measures advocated. It is these gross hemorrhages \vithin the intracranial cavity, secondary to a blow to the head, which may be termed "surgical blood clots" that concern us in this communication. During the past 26 years, 46,574 patients with craniocerebral trauma
CONSEQUENT
From the Department of Neurosurgery, State University of New York Downstate Medical Center, and the Neurosurgical Service of Kings County Hospital, Brooklyn, New York.
* Assistant Instructor in Neurosurgery, State Univers1'ty of New York Downstate Medical Center, and the Neurosurgical Service of K i'rtgs County Hospital, Brooklyn, New York.
** Assistant Professor of Neurosurgery, State University of N ew York Downstate Medical Center, and the Neurosurgical Serv'ice of Kings County Hospital, Brooklyn, New York. t Professor of Neurosurgery, State [Jniversity of New York Downstate Medical Center, and the Neurosurgical Service of Kings County Hospital, Brooklyn, New York. 603
604
Tung Hui Lin, AlbertW. Cook, E. Jeiferson Browder
were admitted to the Kings County Hospital of Brooklyn. Among these were 171 patients with epidural hemorrhages requiring surgical therapy, 873 with subdural collections of surgical significance, and 153 with solitary intracerebral hematomas subjected to operation. In other words, an average of 1800 patients with craniocerebral insults were admitted to the hospital each year with an annual average of 7 + patients with epidural hematomas, 33+ with subdural hematomas and six with intracerebral hematomas. Over the years there has been considerable fluctuations in the total numbers admitted-1500 to 2700 annually. Increasing experience has been rewarding in that diagnostic acumen has been sharpened and surgical procedures have become more definitive. li'or example, from July 1956 to July 1957 there were approximately 2500 patients with craniocerebral injuries admitted to the service. Fifteen of those had epidural hemorrhage, 51 subdural and ten intracerebral hematomas. These data indicate not only the relative frequency of intracranial hemorrhage of traumatic origin, but also the surgeon's opportunity to whittle down, slowly but surely, the mortality associated with patients so injured. EPIDURAL HEMORRHAGE l~'ew clinical syndromes are as dramatic in their manifestations as that of the classical epidural hemorrhage: a blo,v to the head, transitory loss of contact with surroundings, several hours of lucidity albeit with pain in the head, then vomiting, drowsiness, hemiparesis contralateral to the lesion, coma, decerebrate rigidity and death. This sequence of events may be in general correlated with contusion and swelling of the scalp at the site of traumatic impact, linear fracture of the skull, so-called "commotio cerebri," rent in the epidural blood vessels, return of relatively normal cerebral function, hemorrhage from the ruptured blood vessel with further stripping of the dura from the skull, compression of the cerebral surface, stasis of blood flow within the transcerebral venous system, cerebral swelling implicating the diencephalon, herniation of the uncus, mesencephalic hypoxia with or without secondary hemorrhage at this level, and terminally dysfunction of the hindbrain. It is quite generally known that prompt definitive surgical therapy is mandatory before evidence of decerebration sets in if complete recovery of cerebral functions is to be attained. And it may be added somewhat parenthetically that this is not a lesion to be dealt with effectively through a socalled "subtemporal decompression" opening in the skull, a moderate sized bone flap being the preferred technical approach to the hematoma. Unfortunately, insofar as diagnosis is concerned, only about one-half of the patients with gross hemorrhage into the intracranial epidural zone run the classical clinical course just described. The remaining 50 per cent may be placed in two further categories, those harboring cerebral
Intracranial H emorrhage of Traumatic Origin
605
epidural blood clots associated with multiple traumatic lesions of the cerebrum and those with epidural hemorrhage compressing the structures of the subtentorial compartment. If severe trauma of the brain is followed by enduring deep stupor to coma, then the clinician may overlook the scanty abnormal physical findings suggesting supratentorial epidural bleeding. Two of these are outstanding, namely hemiparesis or hemiplegia on the side contralateral to linear fracture of the skull demonstrated by roentgen examination and/or a dilated pupil not reactive to light on the side of the linear fracture. In addition, a worsening of the clinical picture, especially deepening of stupor and recurring transitory skeletal muscle rigidity unilaterally, indicate that all is not \vell and that more precise diagnostic procedures are in order. Cerebral arteriography may be used to advantage, especially in young adults but carries some danger of aggravating a bad situation in older patients. It is advisable to attempt a selection of the diagnostic procedure, or procedures, best suited to the possible problem presented by a particular patient, rather than to adhere to standardized formulas. In our clinic, even a suspicion of epidural hemorrhage based on sound clinical evidence is the signal for surgical intervention. The patient is positioned on the operating table in a fashion to permit biparietal burr holes to be made if desired. The line of incision of the scalp for a bone flap is marked on the side of the linear fracture, with the center of the proposed flap at the site where the fracture line crosses a major groove of the inner table of the skull. In this area a single burr hole is made to establish or disprove the notion that an epidural clot is present. If a blood clot is present, the bone flap is reflected and the mass removed. If epidural hemorrhage is not disclosed and a nick in the dura establishes that a subdural collection is not present, biparietal burr holes are made. In the absence of lesions of the surface bilaterally, a ventriculogram is carried out and further surgical maneuvers performed if this discloses a mass lesion within the intracranial cavity. In the last-mentioned group may be placed the syndrorne of the posterior fossa produced by hemorrhage from vessels of the dura overlying the cerebellum. In some the blood clot strips the dura of the adjacent inferior occipital area and with it the lateral sinus. If the formation of the clot is relatively rapid, the patient may succumb within an hour or so following injury. Those with slovver bleeding develop symptoms and abnormal physical findings in a progressive manner, thus permitting a proper clinical evaluation of the problem. Frequently, on entry to the hospital, there is disorientation and drowsiness from which partial recovery ensues. Usually, there is evidence of a blow to the occipital region and roentgen findings of a linear fracture of the skull overlying the posterior cranial fossa. After a few hours of relative lucidity, drowsiness returns and, with this, slo\ving of the respiratory rate and pulse. It is
606
Tung Hui Lin, Albert W. Cook, E. Jefferson Browder
the slow and at times sighing type of respiration occurring in a patient with edema of the scalp overlying a linear fracture of the occipital skull that strongly suggests compression of the hindbrain by a blood clot. At all events, this clinical picture calls for prompt surgical exploration of the area under suspicion and evacuation of the hematoma if present. SUBDURAL HEMATOMAS
As stated, up to July 1, 1957 there have been 873 verified examples of subdural hematoma at this hospital. At present 45 to 50 patients a year with a variety of subdural collections have been sufficient to maintain a continuing active interest in this clinical problem. At intervals during the past 15 years reports concerning the anatomicopathology and the pathophysiology of this lesion have emanated from our clinic. Especially attractive to us has been the study of the pathogenesis of the symptomatology, in particular the causative factors for the late symptoms frequently observed in patients with subdural collections. To date, observations regarding the alterations in the patency of veins following surface compression of a cerebral hemisphere by hemorrhage, the pathological changes of the white matter of the brain underlying surface hemorrhage, the electroencephalographic findings associated with these changes, the pneumoencephalographic evidence that cerebral swelling persists for days and even weeks following surgical evacuation of the surface hemorrhage, and the arteriographic visualization of the position of the cerebral cortex in relation to the persistently swollen cerebral hemisphere following removal of the subdural collection, have all been recorded in the literature. These data strongly support the notion that a cerebral subdural hemorrhage resulting from contact trauma of the head serves as the initiating factor for cerebral swelling and it is this slowly developing intracerebral swelling which is responsible for the late symptoms of subdural hematomas. In addition to these studies concerning the anatomical alterations and the pathological changes associated with subdural collections, the various clinical pictures resulting from these lesions have concurrently received appropriate consideration. Largely as a convenience in presentation, the clinical syndromes have been placed in three groups; however, it is to be recognized that the members of one group merge with the adjoining one. In Group I may be placed those with subdural hemorrhage and minimal evidence of cerebral insult. Some authors have described these as chronic subdural hematomas since frequently few symptoms and abnormal physical features indicate their presence shortly after injury. Be that as it may, patients with this type of lesion may lead a relatively normal life for weeks, or even months, subsequent to injury and then become drowsy and within a few days comatose. In
Intracranial H ernorrhage of Trau'matic
Origir~
607
truth, the same pathophysiological mechanism may develop from any mass in the intracranial cavity, be it tumor, abscess or blood clot. It is the regional swelling consequent upon venous stasis, which when extensive enough to implicate the diencephalic-mesencephalic-hindbrain complex, produces a drowsy-to-comatose state associated with neurological deficits in accordance with the position of the lesion. So the reasons become evident why longstanding subdural collections produce symptoms and abnormal physical signs comparable to cerebral tumor and why this lesion is frequently diagnosed preoperatively as cerebral neoplasm. As in the case of all intracranial mass lesions associated with drowsiness, surgical therapy should not be delayed. In Group 11 may be placed patients with subdural hemorrhage and moderate cerebral insult. They usually enter the hospital within an hour following a blow to the head which rendered them unconscious. Multiple injuries of the trunk and extremities are not exceptional and must be evaluated in the total individual problem. Usually the clinical evidence indicates that cerebral functions are not seriously affected, although drowsiness and possibly hemiparesis may persist for several days. Gradually limited contact with surroundings is attained and after three to four days the average patient appears to be well on the way to recovery. Although out of bed and about the ward, it is obvious that intellectual blunting persists. After two or three weeks there is again drowsiness, indifference as regards excreta, possibly inequality of the pupils, stiffness of the neck and Babinski toe sign bilaterally. Other neurological deficits may be demonstrable; however, these are the ones most commonly encountered. Prompt evacuation of the subdural collection is mandatory when there is the slightest evidence of returning drowsiness. Often the hemorrhagic collection is entirely liquid and may be "washed out" through two burr holes. If a part of the surface mass consists of clotted blood, then a bone flap is reflected and complete evacuation accomplished. It is to be remembered that approximately 20 per cent occur bilaterally, consequently both sides are always surgically explored. By far the largest number of the series of 873 fall in Group 11. We have been able to study the patients with this syndrome in more detail than those falling in Group I and Group Ill. There is conclusive evidence that cerebral swelling of considerable magnitude exists in the white matter in particular, underlying a surface hemorrhagic collection. That this swelling persists for days and sometimes weeks after surgical removal of a subdural hemorrhage is incontestable. The persistence of drowsiness-to-stupor after operation is entirely consistent with the pathophysiological state resulting from the intracerebral swelling. In a few patients evacuation of a large liquid subdural collection is followed by prompt clearing of the sensorium. It would seem that, in these, intracerebral swelling was not the major factor in the drowsiness. It is
608
Tung Hui Lin, Albert W. Cook, E. Jefferson Browder
possible that the brain stem may have been rendered hypoxic by distortion produced by the large collection. Further study concerning the effect of the mass alone on conscious states is now in progress. In Group III have been placed patients with severe craniocerebral injuries and subdural hemorrhage. 1-'he pathophysiological import of the subdural hemorrhage in a patient with multiple cerebral lesions is at present impossible to estimate. Ilegardless of therapy, surgical or otherwise, the mortality is high. Certainly early evacuation of the surface hematoma and generous decompression is not the answer. Owing to the complex nature of the problem and our inability to relate certain abnormal clinical features to one of the several intracranial lesions, we have of necessity resorted to a conservative therapeutic regimen during the early hours following injury in an attempt to tide the patient over a critical period. If successful and the vital signs become somewhat stabilized, evacuation of the subdural collection on the fourth or fifth day following injury may result in additional improvement. In others, the removal of the subdural collection has little, if any, influence on the outcome, while in still others a bad situation is made worse by the operation. The mortality in Group III is approximately 80 per cent, the majority of patients dying within a few days after injury. Finally, in a discussion of cerebral subdural hematoma should be mentioned those occurring in the subdural space of the subtentorial compartment. Hemorrhage into this space is usually secondary to traumatic laceration of the cerebellar cortex and this is in turn frequently associated with moderate-to-severe craniocerebral insult. Clinically, one must be on the alert to entertain seriously the possibility of subdural hemorrhagic collection in this site. Slow irregular respirations associated with coma and relative flaccidity of the skeletal musculature are abnormal features suggesting a blood clot in this area. More often the lesion is located by making burr holes in the skull over the posterior fossa after a mass lesion of the supratentorial compartments has been unequivocally excluded. IN1"'RACEREBRAL HEMATOMAS
Hemorrhage into the cerebral substance as a consequence of craniocerebral injury is usually regarded as an index of severe cerebral insult, as is also the so-called cerebral dissolution. One of the common anatomical sites for these lesions is the frontotemporal region (posteriorinferior frontal and anterior temporal). The latter lesion consists of cerebral softening with multiple small blood clots, some coalescing, others not. The abnormal clinical features of the two lesions in this particular location are similar, as is the pathogenesis of each. In some previous communications from our clinic the two pathological states have been
Intracranial H emorrhage of Traumatic Origin
609
drawn together and the diagnostic and therapeutic measures discussed under one heading. The 153 examples recorded here as a basis for the present presentation were single blood clots sizable enough to be of "surgical significance," 20 grams or more. Pathogenetically they were of two types, coup and contrecoup. The majority were regarded as being produced by the contrecoup mechanism and about half of these were associated with a surface hematoma, mostly subdural in position. In the last 40 cases the intracerebral blood clot was in the frontal lobe in 16, temporal lobe 16, parietal lobe 5, occipital lobe 2, and one in the cerebellum. In other words, 33 of the 40 were probably the result of contrecoup damage, whereas the remaining seven were of the coup variety. If the examples of cerebral dissolution were included, the figures would run into hundreds. It is the solitary intracerebral hemorrhage usually produced by the so-called coup mechanism that affords an uncomplicated lesion for pathophysiological study and clinical correlation. Interestingly enough, these lesions not infrequently produce a train of symptomatic events and abnormal physical signs simulating somewhat epidural hemorrhage: A blow to the head, transitory loss of consciousness, reorientation, residual hemiparesis in some and after a few days to several weeks, drowsiness, headache and vomiting, choked disk and increasing hemiparesis. Pathologically there is cerebral swelling of the white matter about the blood clot, as frequently observed about a cerebral tumor. As for hematomas in other anatomical positions, it is the cerebral swelling which produces the recrudescence of symptomatology. The accepted surgical approach is accurate diagnosis, either ventriculography or angiography, followed by removal of the hematoma through an osteoplastic cranial opening and an incision in the cerebral cortex. Intracerebellar hemorrhage, similar to subdural hemorrhage of the posterior fossa, seemingly results from contusion-laceration of the cerebellar cortex. Traumatic damage of the brain of this character is almost invariably associated with evidence of severe cerebral insult. An interesting clinical feature characterized by paroxysmal "bridging" or severe opisthotonos is observed occasionally in patients with contusion-laceration of the cerebellum and/or intracerebellar hematoma. Although intracerebellar hemorrhage of traumatic origin is relatively uncommon (certainly far less common than spontaneous hemorrhage in this location), it does occur and whenever the clinical features suggest dysfunction of t.he hindbrain as previously described, the presence or absence of such a lesion must be established through a suboccipital craniectomy. SUMMARY AND CONCLUSIONS
In a series of 46,574 patients with craniocerebral injury, 2.5 per cent had intracranial hemorrhage of surgical significance. Hemorrhage in the
610
1 urtg Hui l.Jin, Albert W. CYook, E. J eiJerson Browder 1
cerebral subdural space was encountered five times as frequently as that occurring epidurally or intracerebrally. The known pathophysiological features associated with hemorrhage in these three anatomical sites have been mentioned. Although one frequently resorts to the use of the ancillary diagnostic procedures, these are not a substitute for sound, clinical evaluation. The surgical opening of the skull for the removal of an intracranial hematoma should be sufficiently large and appropriately fashioned to permit total removal of the blood clot. 200 Hicks Street Brooklyn 1, New York (Drs. Cook and Browder)