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Chronic extradural hematoma
Chronic
Extradural
Hematoma
PAUL F. NORA, M.D. AND PAUL R. ROSENBLUTH, M.D., Chicago, Zllinois From tbe Neurosurgical Service, Cook County Hospital, Chicago, Illinois.
INCE the classic paper on middIe meningea1 appeared in the Guy’s Hospital Reports in 1885 [I], the syndrome of extradural hematoma has appeared in neuroIogic texts. The sequence of injury to the head fracturing the squamosa of the tempora1 bone with Ioss of consciousness, a Iucid interva1 foIIowed by progressiveIy deepening coma, ipsilatera diIated pupi and contraIatera1 hemipIegia has Iong been considered one of the true neurosurgica1 emergencies. However, as is so often the case, many exceptions have been reported to the cIassic sequence and in the physical findings that occur with an expanding extradura1 cIot. The inadequacy of the lucid interva1 as a diagnostic sign has been re-emphasized by Knighton [2] and Ver Brugghen [3]. Munro and MaItby [4] found no history of Iucid interva1 in more than 50 per cent of their forty-four cases. Extradural hemorrhage may coexist with Iaceration or severe contusion of the brain, which wouId prohibit a return to consciousness before the cIot became suffrcientIy Iarge to cause unconsciousness itseIf. The amount and rapidity of bIeeding wouId be factors that wouId inff uence the presence and duration of the Iucid interva1. AIcohoIic stupor coexisting with injury to the head may aIso obscure the Iucid interva1. Knighton aIso pointed out that acute subdura1 bIeeding, cerebra1 contusion with secondary edema and intracerebra1 hemorrhage couId have a period of Iucidity, and it has been feIt generaIIy that of the components of the classic syndrome, this was the Ieast reIiabIe. A fracture of the skuI1 usuaIIy is found with extradura1 hemorrhage and Munro states that “We have yet to see an extradura1 hematoms in the absence of a fracture of the bone in the immediate vicinity of the bIeeding point, provided an adequate search for the Iatter has 628 American Journal of Surgery. Volume 94. October, 191,
S hemorrhage
been made.” However, epidura1 hematoma without fracture has been reported by other authors [5,6]. The deveIopment of a uniIateraIIy diIated and fixed pupil has been noted in other types of cerebra1 Iesions that might cause herniation of the uncus, such as acute subdura1 cIot, acute traumatic edema of the tempora1 Iobe and also direct trauma to the orbit with fracture of the superior orbital fissure. However, it is generally accepted that the uniIateraIIy diIated pupi is one of the most reIiabIe signs in the diagnosis of extradura1 hematoma. Progressive contraIatera1 hemipIegia may aIso be deceptive since paralysis may be found homoIatera1 to the side of injury due to dispIacement of the opposite peduncIe against the free edge of the tentorium. The spina fluid in the cIassic syndrome of extradura1 hematoma is clear. However, the spina fIuid wiI1 reff ect the presence of bIeeding into the subarachnoid space; and if a Iaceration of the brain occurs together with extradura1 bIeeding, the fluid wiI1 be bIood-tinged. To disrupt further the stereotyped cIinica1 description were the anatomic and cIinica1 observations of Wood Jones [7] in 1912. In a paper entitIed “On the grooves upon the ossa parietaIia commonIy said to be caused by the arteria meningea media,” Wood Jones emphasized that ancient anatomists had considered the meningea1 grooves in the crania1 bones to encIose the meningea1 veins. “The practice of injecting the arteries for the purpose of dissection Ied to the arteria meningea media being regarded as practicaIIy the soIe vascuIar channeI coursing over the dura mater and Iodged within the grooves of the crania1 bones.” He took exception to the concept that these vascular impressions were soIeIy due to pulsation of the meningea1 arteries. He found that the diameter of the bony grooves was Iarger than that of the ‘foramen spinosum and the
Chronic
ExtraduraI
FIG. I. Diagram of cross section through dura and temporal complex.
grooves became larger, rather than smaller, as they passed away from the foramen. He made sections of the dura (Fig. I) and showed that the artery was but a smaI1, constituent of a much wider vascular channe1, the bulk of which was composed of meningea1 venous sinuses. He then demonstrated histoIogic sections from severa cases of fata extradura1 hemorrhage in which the middIe meningea1 artery was intact but the meningeal venous sinuses had ruptured. These cross sections through tempora1 bone demonstrate that the grooves contain venous sinuses and that the artery does not Iie in contact with bone. Ver Brugghen [3] re-emphasized this point in his discussion of extradura1 hemorrhage in 1937 and suggested that at the time of surgery the origin of the bIeeding couId be determined by compressing the carotid trunk in the neck. If the bleeding diminished with pressure on the common or externa1 carotid artery in the neck, it couId be assumed that the source of bIeeding was arteria1. If, however, the bleeding acceIerated with pressure on the neck, it could be deduced that the jugular vein was aIso being compressed with resuItant backbIeeding from a venous tear. It has been shown that the force of the arteria1 jet is not necessary to open the potentia1 extradura1 space since Be11 [8] was abIe to demonstrate a separation of the dura mater at the site of a bIow to the skuI1. This fact would aIIow bIood under a reIativeIy Iow pressure to extravasate into the epidura1 space and wouId explain the occasiona chronic deveIopment of an extradurai hematoma.
Hematoma
bone at the side of the meningea1 artery and venous
Hemorrhage in the extradura1 space may arise from various sources: (I) ArteriaI bIeeding from the middIe meningea1 branch of the interna maxiIIary artery. (2) Venous bIeeding from the meningea1 venous sinuses that surround and accompany the middIe meningea1 artery. (3) Venous bIeeding from Iarge dura1 sinuses, particuIarIy when a fracture Iine occurs near the vertex or inion. (4) Venous bIeeding from emissary veins perforating the outer table, dipIo& and inner tabIe and entering the dura. This becomes more pIausibIe when it is remembered that the dura deveIops embryoIogicaIIy from the inner periosteum of the caIvarium. (3) Low pressure ooze from the dipIoic marrow. This wouId be of IittIe significance in the tempora1 bone where the dipIoic space is virtuaIIy non-existent, but wouId be of greater significance over the vauIt; it has been shown [9] that intradipIoic hematoma and cysts may form from marrow bIeeding due to trauma. IsoIated cases of chronic extradura1 hemorrhage have been reported by AvoI [IO], Gurdjian [I r], Jackson and Speakman [12], and Grant [13]. In Grant’s case a period of six years eIapsed between injury and operation. The hematoma was found over the right fronta poIe. King and Chambers [a reported eight cases in which deIayed onset of symptoms were seen due to extradural hematoma. Six of their patients showed fracture Iines on x-ray, and the Iongest period between injury and surgery was eIeven days. The foIIowing additiona case was treated by the authors on the neurosurgica1 service of the Cook County HospitaI. 629
Nora CASE
and
RosenbIuth
REPORT
Maltby [4], only 3 per cent of 1,200 patients admitted during a seven-year period showed significant extradura1 hematoma. However, LeCount and ApfeIbach [14] reported that patients with 20.6 per cent of 504 autopsied fractures of the skuI1 had significant extradura1 bIeeding postmortem. Therefore, aIthough the incidence of extradura1 bIeeding in closed head injury is reIativeIy smaI1, the incidence of an extradura1 cIot among those who succumb to cIosed head injury is seven times as great, indicating that the mortaIity from this Iesion is stiI1 high and that the criteria for diagnosis requires re-evaIuation to assure more widespread recognition of a potentiaIIy reversibIe condition.
A forty-seven year oId typesetter was struck on the head by an assaiIant on January 15, 1956. He was immediateIy rendered unconscious but soon regained consciousness and was removed to the House of Correction by the poIice because of absence of identification. He was sent to the Cook County HospitaI Admitting Room five days Iater. During this five-day period IittIe record of his course had been made except for the fact that he was able to feed himseIf. A fracture of the skuI1 had been noted on x-ray. Physical examination on admission reveaIed an aphasic, dehydrated white male. The bIood pressure was 140/60, pulse 80 and respirations 20. BiIateraI mastoid ecchymoses were present. The pupiIs were equa1 and the fundi normaI. There was a right hemiparesis including the face, but the pIantar reffexes were normaI. Lateral x-rays of the skull reveaIed extensive Iinear fractures of the Ieft parieta1 and tempora1 bones. Anteroposterior fiIms were not satisfactory. The patient was thought to have suffered a cerebra1 Iaceration and was treated ConservativeIy. He continued to have diffIcuIty with speech .and weakness on the right side persisted. When the anteroposterior x-rays of the skuI1 were repeated, an 8 mm. deviation of the pineal caIcification from Ieft to right was seen. Because of the pinea shift, surgery seemed indicated. Twenty-one days had eIapsed since injury. The preoperative diagnosis was subdura1 hematoma. A smaI1, Ieft scaIp Aap was turned over the centra1 portion of the fracture and the bone was found to be markedIy thinned. Craniectomy was performed and an organized extradura1 hematoma measuring IOO cc. was evacuated. There was no epidura1 bIeeding after evacuation of the cIot. The dura was sutured to the pericranium and opened. The subdura1 space contained no cIot. The cortex showed minima1 areas of contusion. The neuroIogic status rapidIy returned to norma and the patient was discharged from the hospital two weeks Iater with the onIy neuroIogic residuum, continuing awkwardness of the right hand in fine movement. Postoperative x-rays of the skuI1 reveaIed the pinea gIand to be again in the midIine.
CONCLUSION
It is evident from this and other reported clinica experience that the cIassic picture of the extradura1 hemorrhage may not appear in its compIete form and that any or a11 of the component features may be aItered. It is suggested that the rapidity and progression of symptoms and the clinical signs wiI1 depend on the amount, site and rapidity of bIeeding in the extradural space. In this type of injury to the head, x-ray is of considerabIe vaIue to demonstrate fracture Iines adjacent to venous sinuses or across the meningea1 grooves, and in chronic extradura1 bIeeding it may indicate deviation of the pinea gland. EpiduraI hematoma, even in its chronic form, can only be treated by surgical intervention. REFERENCES I. JACOBSON, W. H. A. On middIe meningea1 hemor-
rhage. Guy’s Hosp. Rep., 43: 147-308, 1885. 2. KNIGHTON, R. S. The interva1 syndrome. Bull. Los Angeles Neural. Sot., 19: 72-86, 1954. 3. VER BRUGGHEN, A. Extradural hemorrhage. Am. J. Surg.9 37: 275-290, 1937. 4. MUNRO, D. and MALTBY, G. L. ExtraduraI hemorrhage. Ann. Surg., I 13: 192-203, 1941. 5. MCKENZIE, K. G. ExtraduraI hemorrhage. Brit. J. Surg., 26: 34G365, 1938. 6. KING, A. B. and CHAMBERS,A. W. DeIayed onset of symptoms due to extradurat hematomas. Surgery, 31: 839-844, 1952. 7. WOOD JONES, F. H. On the grooves upon the ossa parietalia commonIy said to be caused by the arteria meningea media. J. Anat. +Y Pbysiol., 46: 228, 1912. 8. BELL, C. SurgicaI observations,’ pp. 446-447. London, 1816. Longman, Herst, Rees, Arnie TV Brown.
COMMENTS
In a series of cIosed head injuries reported from the Boston City HospitaI by Munro and
630
.
Chronic
Extradural
9. ROSENBLUTH,P.R.,LUEDEKS, H.W.and MOYER, J. L. Traumatic dipIoic hematomas of the skuII. u. S. Armed Forces M. J., 4: 378-382, 1953. 10. AVOL, M. Chronic extradura1 hematoma. Bull. Los Angeles Neurol. Sot., 19: 64-69, 1954. I I. GURDJIAN, E. S. Intracranial hemorrhage. Am. J. Surg., 40: 596_6ro, 1938. I 2. JACKSOU, I.J. and SPEAKMAN, T. J. Chronic extra-
631
Hematoma dural hematoma. J. Neurosurg., 7: 444-447,
1950.
I 3. GRANT, W. T. Chronic extradural hematoma in the anterior crania1 fossa. Bull. Los Angeles Neural. Sot., 9: 156-162, 1944. 14. LIZCOUNT, E. R. and APFELBACH, C. W. Pathological anatomy of traumatic fractures of the cranial bones and concomitant brain injuries. J. A. M. A., 74: 501-508, 1920.
Extradural
Hematoma
PAUL F. NORA, M.D. AND PAUL R. ROSENBLUTH, M.D., Chicago, Zllinois From tbe Neurosurgical Service, Cook County Hospital, Chicago, Illinois.
INCE the classic paper on middIe meningea1 appeared in the Guy’s Hospital Reports in 1885 [I], the syndrome of extradural hematoma has appeared in neuroIogic texts. The sequence of injury to the head fracturing the squamosa of the tempora1 bone with Ioss of consciousness, a Iucid interva1 foIIowed by progressiveIy deepening coma, ipsilatera diIated pupi and contraIatera1 hemipIegia has Iong been considered one of the true neurosurgica1 emergencies. However, as is so often the case, many exceptions have been reported to the cIassic sequence and in the physical findings that occur with an expanding extradura1 cIot. The inadequacy of the lucid interva1 as a diagnostic sign has been re-emphasized by Knighton [2] and Ver Brugghen [3]. Munro and MaItby [4] found no history of Iucid interva1 in more than 50 per cent of their forty-four cases. Extradural hemorrhage may coexist with Iaceration or severe contusion of the brain, which wouId prohibit a return to consciousness before the cIot became suffrcientIy Iarge to cause unconsciousness itseIf. The amount and rapidity of bIeeding wouId be factors that wouId inff uence the presence and duration of the Iucid interva1. AIcohoIic stupor coexisting with injury to the head may aIso obscure the Iucid interva1. Knighton aIso pointed out that acute subdura1 bIeeding, cerebra1 contusion with secondary edema and intracerebra1 hemorrhage couId have a period of Iucidity, and it has been feIt generaIIy that of the components of the classic syndrome, this was the Ieast reIiabIe. A fracture of the skuI1 usuaIIy is found with extradura1 hemorrhage and Munro states that “We have yet to see an extradura1 hematoms in the absence of a fracture of the bone in the immediate vicinity of the bIeeding point, provided an adequate search for the Iatter has 628 American Journal of Surgery. Volume 94. October, 191,
S hemorrhage
been made.” However, epidura1 hematoma without fracture has been reported by other authors [5,6]. The deveIopment of a uniIateraIIy diIated and fixed pupil has been noted in other types of cerebra1 Iesions that might cause herniation of the uncus, such as acute subdura1 cIot, acute traumatic edema of the tempora1 Iobe and also direct trauma to the orbit with fracture of the superior orbital fissure. However, it is generally accepted that the uniIateraIIy diIated pupi is one of the most reIiabIe signs in the diagnosis of extradura1 hematoma. Progressive contraIatera1 hemipIegia may aIso be deceptive since paralysis may be found homoIatera1 to the side of injury due to dispIacement of the opposite peduncIe against the free edge of the tentorium. The spina fluid in the cIassic syndrome of extradura1 hematoma is clear. However, the spina fIuid wiI1 reff ect the presence of bIeeding into the subarachnoid space; and if a Iaceration of the brain occurs together with extradura1 bIeeding, the fluid wiI1 be bIood-tinged. To disrupt further the stereotyped cIinica1 description were the anatomic and cIinica1 observations of Wood Jones [7] in 1912. In a paper entitIed “On the grooves upon the ossa parietaIia commonIy said to be caused by the arteria meningea media,” Wood Jones emphasized that ancient anatomists had considered the meningea1 grooves in the crania1 bones to encIose the meningea1 veins. “The practice of injecting the arteries for the purpose of dissection Ied to the arteria meningea media being regarded as practicaIIy the soIe vascuIar channeI coursing over the dura mater and Iodged within the grooves of the crania1 bones.” He took exception to the concept that these vascular impressions were soIeIy due to pulsation of the meningea1 arteries. He found that the diameter of the bony grooves was Iarger than that of the ‘foramen spinosum and the
Chronic
ExtraduraI
FIG. I. Diagram of cross section through dura and temporal complex.
grooves became larger, rather than smaller, as they passed away from the foramen. He made sections of the dura (Fig. I) and showed that the artery was but a smaI1, constituent of a much wider vascular channe1, the bulk of which was composed of meningea1 venous sinuses. He then demonstrated histoIogic sections from severa cases of fata extradura1 hemorrhage in which the middIe meningea1 artery was intact but the meningeal venous sinuses had ruptured. These cross sections through tempora1 bone demonstrate that the grooves contain venous sinuses and that the artery does not Iie in contact with bone. Ver Brugghen [3] re-emphasized this point in his discussion of extradura1 hemorrhage in 1937 and suggested that at the time of surgery the origin of the bIeeding couId be determined by compressing the carotid trunk in the neck. If the bleeding diminished with pressure on the common or externa1 carotid artery in the neck, it couId be assumed that the source of bIeeding was arteria1. If, however, the bleeding acceIerated with pressure on the neck, it could be deduced that the jugular vein was aIso being compressed with resuItant backbIeeding from a venous tear. It has been shown that the force of the arteria1 jet is not necessary to open the potentia1 extradura1 space since Be11 [8] was abIe to demonstrate a separation of the dura mater at the site of a bIow to the skuI1. This fact would aIIow bIood under a reIativeIy Iow pressure to extravasate into the epidura1 space and wouId explain the occasiona chronic deveIopment of an extradurai hematoma.
Hematoma
bone at the side of the meningea1 artery and venous
Hemorrhage in the extradura1 space may arise from various sources: (I) ArteriaI bIeeding from the middIe meningea1 branch of the interna maxiIIary artery. (2) Venous bIeeding from the meningea1 venous sinuses that surround and accompany the middIe meningea1 artery. (3) Venous bIeeding from Iarge dura1 sinuses, particuIarIy when a fracture Iine occurs near the vertex or inion. (4) Venous bIeeding from emissary veins perforating the outer table, dipIo& and inner tabIe and entering the dura. This becomes more pIausibIe when it is remembered that the dura deveIops embryoIogicaIIy from the inner periosteum of the caIvarium. (3) Low pressure ooze from the dipIoic marrow. This wouId be of IittIe significance in the tempora1 bone where the dipIoic space is virtuaIIy non-existent, but wouId be of greater significance over the vauIt; it has been shown [9] that intradipIoic hematoma and cysts may form from marrow bIeeding due to trauma. IsoIated cases of chronic extradura1 hemorrhage have been reported by AvoI [IO], Gurdjian [I r], Jackson and Speakman [12], and Grant [13]. In Grant’s case a period of six years eIapsed between injury and operation. The hematoma was found over the right fronta poIe. King and Chambers [a reported eight cases in which deIayed onset of symptoms were seen due to extradural hematoma. Six of their patients showed fracture Iines on x-ray, and the Iongest period between injury and surgery was eIeven days. The foIIowing additiona case was treated by the authors on the neurosurgica1 service of the Cook County HospitaI. 629
Nora CASE
and
RosenbIuth
REPORT
Maltby [4], only 3 per cent of 1,200 patients admitted during a seven-year period showed significant extradura1 hematoma. However, LeCount and ApfeIbach [14] reported that patients with 20.6 per cent of 504 autopsied fractures of the skuI1 had significant extradura1 bIeeding postmortem. Therefore, aIthough the incidence of extradura1 bIeeding in closed head injury is reIativeIy smaI1, the incidence of an extradura1 cIot among those who succumb to cIosed head injury is seven times as great, indicating that the mortaIity from this Iesion is stiI1 high and that the criteria for diagnosis requires re-evaIuation to assure more widespread recognition of a potentiaIIy reversibIe condition.
A forty-seven year oId typesetter was struck on the head by an assaiIant on January 15, 1956. He was immediateIy rendered unconscious but soon regained consciousness and was removed to the House of Correction by the poIice because of absence of identification. He was sent to the Cook County HospitaI Admitting Room five days Iater. During this five-day period IittIe record of his course had been made except for the fact that he was able to feed himseIf. A fracture of the skuI1 had been noted on x-ray. Physical examination on admission reveaIed an aphasic, dehydrated white male. The bIood pressure was 140/60, pulse 80 and respirations 20. BiIateraI mastoid ecchymoses were present. The pupiIs were equa1 and the fundi normaI. There was a right hemiparesis including the face, but the pIantar reffexes were normaI. Lateral x-rays of the skull reveaIed extensive Iinear fractures of the Ieft parieta1 and tempora1 bones. Anteroposterior fiIms were not satisfactory. The patient was thought to have suffered a cerebra1 Iaceration and was treated ConservativeIy. He continued to have diffIcuIty with speech .and weakness on the right side persisted. When the anteroposterior x-rays of the skuI1 were repeated, an 8 mm. deviation of the pineal caIcification from Ieft to right was seen. Because of the pinea shift, surgery seemed indicated. Twenty-one days had eIapsed since injury. The preoperative diagnosis was subdura1 hematoma. A smaI1, Ieft scaIp Aap was turned over the centra1 portion of the fracture and the bone was found to be markedIy thinned. Craniectomy was performed and an organized extradura1 hematoma measuring IOO cc. was evacuated. There was no epidura1 bIeeding after evacuation of the cIot. The dura was sutured to the pericranium and opened. The subdura1 space contained no cIot. The cortex showed minima1 areas of contusion. The neuroIogic status rapidIy returned to norma and the patient was discharged from the hospital two weeks Iater with the onIy neuroIogic residuum, continuing awkwardness of the right hand in fine movement. Postoperative x-rays of the skuI1 reveaIed the pinea gIand to be again in the midIine.
CONCLUSION
It is evident from this and other reported clinica experience that the cIassic picture of the extradura1 hemorrhage may not appear in its compIete form and that any or a11 of the component features may be aItered. It is suggested that the rapidity and progression of symptoms and the clinical signs wiI1 depend on the amount, site and rapidity of bIeeding in the extradural space. In this type of injury to the head, x-ray is of considerabIe vaIue to demonstrate fracture Iines adjacent to venous sinuses or across the meningea1 grooves, and in chronic extradura1 bIeeding it may indicate deviation of the pinea gland. EpiduraI hematoma, even in its chronic form, can only be treated by surgical intervention. REFERENCES I. JACOBSON, W. H. A. On middIe meningea1 hemor-
rhage. Guy’s Hosp. Rep., 43: 147-308, 1885. 2. KNIGHTON, R. S. The interva1 syndrome. Bull. Los Angeles Neural. Sot., 19: 72-86, 1954. 3. VER BRUGGHEN, A. Extradural hemorrhage. Am. J. Surg.9 37: 275-290, 1937. 4. MUNRO, D. and MALTBY, G. L. ExtraduraI hemorrhage. Ann. Surg., I 13: 192-203, 1941. 5. MCKENZIE, K. G. ExtraduraI hemorrhage. Brit. J. Surg., 26: 34G365, 1938. 6. KING, A. B. and CHAMBERS,A. W. DeIayed onset of symptoms due to extradurat hematomas. Surgery, 31: 839-844, 1952. 7. WOOD JONES, F. H. On the grooves upon the ossa parietalia commonIy said to be caused by the arteria meningea media. J. Anat. +Y Pbysiol., 46: 228, 1912. 8. BELL, C. SurgicaI observations,’ pp. 446-447. London, 1816. Longman, Herst, Rees, Arnie TV Brown.
COMMENTS
In a series of cIosed head injuries reported from the Boston City HospitaI by Munro and
630
.
Chronic
Extradural
9. ROSENBLUTH,P.R.,LUEDEKS, H.W.and MOYER, J. L. Traumatic dipIoic hematomas of the skuII. u. S. Armed Forces M. J., 4: 378-382, 1953. 10. AVOL, M. Chronic extradura1 hematoma. Bull. Los Angeles Neurol. Sot., 19: 64-69, 1954. I I. GURDJIAN, E. S. Intracranial hemorrhage. Am. J. Surg., 40: 596_6ro, 1938. I 2. JACKSOU, I.J. and SPEAKMAN, T. J. Chronic extra-
631
Hematoma dural hematoma. J. Neurosurg., 7: 444-447,
1950.
I 3. GRANT, W. T. Chronic extradural hematoma in the anterior crania1 fossa. Bull. Los Angeles Neural. Sot., 9: 156-162, 1944. 14. LIZCOUNT, E. R. and APFELBACH, C. W. Pathological anatomy of traumatic fractures of the cranial bones and concomitant brain injuries. J. A. M. A., 74: 501-508, 1920.