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Delayed extradural hematoma after mild head injury: Report of three cases
ELSEVIER
Trauma
DELAYED EXTRADURAL HEMATOMA AFTER MILD HEAD INJURY: REPORT THREE CASES
OF
Pedro Riesgo, M.D.,* Jo& Piquer, M.D., Ph.D.,* Carlos Botella, M.D., Ph.D.,t Miguel Orozco, M.D.,* Jo& Navarro, M.D.,t and Jerbnimo Cabanes, M.D., Ph.D. *Department of Neurosurgery, Hospital Universitario “La Fe, ” Valencia, and THospital Universitario de San Juan, Alicante, Spain
Riesgo P, Piquer J, Botella C, Orozco M, Navarro J, Cabanes J. Delayed extradural hematoma after mild head injury: report of three cases. Surg Neural 1997;48:226-31.
KEY
WORDS
Delayed epidural hematoma, Glasgow coma scale, head injury, computed tomography.
BACKGROUND
Extradural hematoma has been classically considered to be an acute complication of head injury whose maximum development takes place in the minutes following trauma. Delayed extradural hematoma (DEH) is defined on the basis of an exclusively radiologic criterion: epidural hematoma that is not present in the first neuroradiologic examination made after trauma but that appears in sequential neuroradiologic examinations during patient evolution. This is an infrequent complication that usually appears in hypotensive multiple trauma patients or is related to severe head injury with other intracranial lesions. CASE
DESCRIPTION
We present three cases of DEH after mild head injury (GCS > 12) without associated intracranial or traumatic systemic lesions. Therefore, those usually considered to be “protective mechanisms” responsible for delayed development of an extradural hematoma were absent in our three patients. Diagnosis was attained by means of repetition of cranial computed tomography (CT) scan after neurologic impairment was noted. Surgical evacuation of DEH was immediately performed after diagnosis. Postop-
oodkin and Zahniser reported the first case of documented delayed extradural hematoma (DEH), demonstrated by means of cerebral angiography, in 1978 [15]. Generalization of the use of computed tomography (CT) scan in the initial and evolutive radiologic assessment of head injured patients has resulted in DEH being more frequently diagnosed [1,3,5,6,8,11,12,21,23].DEHcurrentlyrep resents up to 10% of total extradural hematomas in some reported series [1,12,21]. In spite of this, to our knowledge only four cases of DEH after mild head injury (Glasgow Coma Scale score > 12) have been reported [1,5,11,19] in the literature. We present three cases of patients who developed DEH, demonstrated by means of CT scan, after sustaining mild head injury with no associated intracranial and/or systemic traumatic lesions.
G
erative outcome was favorable in two patients who suffered DEH in the supratentorial tient who presented a posterior
compartment. One pafossa DEH died 3 days
after surgery. CONCLUSIONS
Early diagnosis and immediate treatment have proved to be essential for improving the prognosis of patients affected by DEH. Hospital admission under neurologic observation is recommended for patients who have sustained mild head injury associated with those factors that are related to the development of DEH, including GCS score under 15 or the detection of a skull fracture. Normality of a CT scan does not rule out subsequent appearance of delayed traumatic lesions. 0 1997 by Elsevier Science Inc. Address reprint requests to: Pedro A. Riesgo, M.D., Miramar 46100 Burjasot, V&n&, Spain. Received August 2, 1996; accepted December 4, 1996. 009c-3019/97/$17.00 PII s0090-3019(97)00194-8
4-3” A,
CASEREPORTS CASE 1 This 17-year-old man sustained a head injury in a motor vehicle accident after which he lost consciousness for 3 minutes. He was immediately taken to the nearest local hospital, 70 kms away from our center. After ruling out associated traumatic lesions and confirming hemodynamic stability, the patient was transferred to our hospital. On arrival, 5 hours after the accident, he was conscious with a score of 15 points on the GCS, with no evidence of neurologic deficits. A plain X ray film of the skull was obtained, showing a linear skull fracture in the right frontal region. In view of this finding, a CT scan was 655 Avenue
0 1997 by Elsevier Science Inc. of the Americas, New York, NY 10010
DEH after Mild Head Injury
also performed that showed the previously diagnosed skull fracture with no associated intracranial lesions (Figure 1 APB). The patient was admitted to the hospital. Thirty hours after the accident, clinical deterioration was detected, consisting of a decrease in his level of consciousness (GCS 9). A second CT scan was done showing an extradurai hematoma underlying the right frontal skull fracture (Figure 1 C,D,E). The patient was immediately operated on. A right frontal craniotomy was performed with aspiration of a partially coagulated extradural hematoma originating from a frontal branch of the middle meningeal artery. After surgery the patient made a good recovery and was discharged from the hospital 14 days after trauma without neurologic sequelae. Two months after the
Surg Neurol 1997;48:226-31
accident the patient resumed (Glasgow Outcome Scale 1).
his normal
227
activities
CASE 2 This 45-year-old man suffered head injury with initial loss of consciousness (< 1 minute) after falling from a bicycle. The patient was taken to the hospital 45 minutes after the accident. At the time of initial evaluation he was conscious (G CS 14) with no neurologic deficits. His hemodynamic status remained stable. Clinical and radiologic evaluation excluded the presence of associated traumatic lesions. A cranial CT scan was done and was considered normal (Figure 2 A,B,C). The patient was admitted to our service under neurologic observation. Six hours after trauma a decline in his level of con-
228
q
Surg Neurol 1997;48:226-31
Riesgo et al
(A,B,C) Case 2: initial CT scan; @,E,F’) case 2: second CT scan (6 hours after trauma). Right temporoparietal hematoma with marked mass effect.
sciousness (GCS 7) was noted. A second CT scan was obtained showing a right temporoparietal hematoma with association of marked mass effect (Figure 2 D,E,F). The patient was operated on. A completely coagulated hematoma was evacuated through a right temporoparietal craniotomy. A vertical right temporal skull fracture that had gone unnoticed in radiologic examination was found during surgery. This fracture caused laceration of the main trunk of the middle meningeal artery leading to extradural hematoma development. Clinical outcome after surgery was satisfactory and the patient was discharged from hospital 11 days after trauma with no significant neurologic sequelae and resumed normal activities 2 months later (Glasgow Outcome Scale 1).
CASE
3
This 23-year-old man with a previous history of intravenous drug abuse, sustained head injury with initial loss of consciousness (2 minutes) after falling from a height of 3 meters. On admission to the hospital, 1 hour after the accident, he was conscious although confused (GCS 13) with no detectable focal neurologic deficits. The patient did not suffer other associated traumatic lesions and his hemodynamic status remained stable. A CT scan was obtained showing a left occipital skull fracture (Figure 3 A,B,C) with no evidence of intracranial lesions (Figure 3 D,E,F). Sixteen hours after admission a sudden decrease in his level of consciousness (GCS 8) was noted. A second CT scan was
DEH after Mild Head Injury
done, demonstrating a left posterior fossa extradural hematoma underlying the previously diagnosed skull fracture (Figure 3 G,H). The patient was immediately operated on. A partially coagulated extradural hematoma, venous in origin (laceration of the left lateral sinus wall), was evacuated through a left suboccipital craniectomy. During the immediate postoperative period the patient did not recover consciousness. Four hours after surgery bilateral areactive midriasis was noted and a further CT scan was performed but did not show any significant findings. The patient died 3 days after head injury (Glasgow Outcome Scale 5).
DISCUSSION Extradural hematoma has been classically considered to be an acute complication of head injury whose maximum development takes place immediately following trauma [lo]. However, there are many references in the literature to cases of extradural hematoma of subacute or chronic evolution [4,7,14]. The concept of DEH is defined on the basis of an exclusively radiologic criterion: epidural hematoma that is not present in the first neuroradiologic examination made after trauma, but that appears in sequential neuroradiologic explorations during patient evolution [ 191. Concurrent systemic traumatic lesions leading to a hypotensive state and/or intracranial traumatic lesions with associated increase of intracranial pressure (ICP) have been classically identified as “protective mechanisms” responsible for the development of DEH [ 1,5,11,12,15]. Nevertheless, the incidence of DEH in patients affected by mild head injury (GCS > 12) with no associated traumatic intracranial and/or systemic lesions is rare and has infrequently been reported in the literature [ 11. Milo et al. reported three cases of DEH and reviewed 32 cases that had been published up to 1987 [ 191. Only four of these 35 patients had sustained mild head injury according to described neurologic criteria, although GCS score has not specifically been reported in any of them. On the other hand, two of these patients, reported by Frankhauser et al. [ 1 l] and Milo et al. [ 191, suffered other traumatic intracranial lesions whose surgical treatment preceded development of DEH [ 11,191. The patient reported by Cervantes was initially hypotensive after trauma and DEH was diagnosed after the patient had undergone an exploratory laparotomy because of a hemoperitoneum [5]. Thus, only the case contributed by Borovich et al. [l] fulfills the standards that lead to diagnosis of DEH in a patient who sus-
Surg Neurol 1997;48:226-31
229
tained mild head injury with no association of other intracranial and/or systemic lesions; however, the evolution of this patient was chronic, with an interval of 11 days between head injury and diagnosis of DEH. All our patients developed an extradural hematoma underlying a skull fracture, which in one case had gone unnoticed on preoperative neuroradiologic examination. Presence of a skull fracture has been identified by several authors as a common feature of reported cases of DEH and should be considered a predisposing factor for the development of this complication [ 1,5,8,15,21,22], although as an isolated finding, it does not explain the delay in the evolution of an extradural hematoma. Moreover, none of these patients suffered associated traumatic intracranial or systemic lesions that could have acted as “protective mechanisms” leading to the delayed occurrence of the hematoma. Some authors have tried to explain the development of DEH as a consequence of the venous origin of the bleeding [ 13,191. However, this was the case in only one of our patients who suffered a posterior fossa DEH due to laceration of the left lateral sinus wall, underlying an occipital skull fracture. Neurologic impairment preceded detection of a DEH in all the cases, after an interval of 630 hours after head injury. Hospital admission under neuro logic observation permitted early suspicion of significant neurosurgical complications in all our patients. Diagnosis was attained after urgent repetition of a cranial CT scan in all the cases. Recently, Gopinath et al. [16] reported their expe rience with the application of near-infrared spectroscopy in the detection of delayed traumatic intracere bra1 hematomas. This is a promising technique of undoubted interest, although at present it has only limited value in clinical practice. In the last decade, CT scan has become the elective neuroradiologic examination for initial and also evolutive evaluation of patients with head injury. Increasing use of CT in the early diagnosis of patients whose clinical neurologic examination could be regarded as normal, will lead to an increase in frequency of diagnosis of delayed traumatic lesions [ 1,6,9,18,22,23]. Moreover, normality of an early CT scan of a patient with mild head injury does not rule out the subsequent development of DEH or other significant neurosurgical complications [ 6,9,18,23]. Surgical evacuation of DEH was performed immediately after diagnosis. Postoperative outcome was favorable in two patients who suffered DEH in the supratentorial compartment. These patients recovered without neurologic sequelae and resumed their previous activities 2 months after trauma. The
230
Surg Neurol 1997;48:226-31
Riesgo et al
Case 3: initial CT scan. Bone settings showing a left occipital skull fracture; @,E,F) case 3: initial CT scan with no evidence of intracranial lesions;(G,H) case 3: second CT scan (16 hours after trauma) demonstrating a left posterior fossa extradural hematoma. (A,B,C)
DEH after Mild Head Injury
remaining patient, who presented a posterior fossa DEH failed to improve and died 3 days after surgery in spite of early diagnosis and surgical treatment. In recent years, extradural hematoma has been considered a benign entity with low associated morbidity and mortality [%,8,17,20]. However, a posterior fossa location constitutes an unfavorable prognostic factor, probably due to early irreversible hypoxic damage to brain stem structures because of direct compression during extradural hematoma development [ 131.
Surg Neurol 1997;48:226-31
7. 8.
9.
10.
SUMMARY Early diagnosis and treatment of DEH have proved to be essential for improving outcome of affected patients. Hospital admission under neurologic observation should be mandatory for those patients who have sustained mild head injury with associated risk factors for the development of DEH, including detection of a skull fracture and/or GCS score under 15. Normality of an early CT scan does not rule out further development of delayed traumatic lesions.
A second CT examination should be carried out as soon as any impairment in the neurologic situation of the patient is noted.
11. 12. 13. 14. 15.
16.
We wish to thank Mr. Mike Harrison for his editorial counseling, and also Miss Marta Riesgo and Mrs. Mercedes Santhis for their help in the preparation of this manuscript.
17.
REFERENCES
18.
1. Borovich B, Braun J, Guilburd JN, Zaaroor M, Michich M, Levy L, Lemberger A, Grushkiewicz I, Feinsod M, Schachter I. Delayed onset of traumatic extradural hematoma. J Neurosurg 1985;63:30-4. 2. Bricolo AP, Pasut LM. Extradural hematoma: toward zero mortality. A prospective study. Neurosurgery 1984;14:8-12. 3. Bucci MN, Philips TW, McGillicuddy JE. Delayed epidural hemorrhage in hypotensive multiple trauma patients. Neurosurgery 1986;19:65-8. 4. Bullock R, Van Dellen JR. Chronic extradural hematoma. Surg Neurol 1982;18:300-2. 5. Cervantes LA. Concurrent delayed temporal and posterior fossa epidural hematomas. Case report. J Neurosurg 1983;59:351-3. 6. Ciquini-Junior O., Dos-Santos AL, Manreza LA, Plese JP, Marino-Junior R. Traumatic extradural hematoma in childhood and normal early computerized tomog-
19. 20.
21. 22. 23.
23 1
raphy: report of 2 cases. Arq Neuropsiquiatr 1992;50: 361-4 (abstr). Clavel M, Onzain I, Gutierrez F. Chronic epidural haematomas. Acta Neurochir (Wien) 1982;66:71-81. Cordobes F, Lobato RD, Rivas JJ, Muiioz MJ, Chillon D, Portillo J, Lamas E. Observations on 82 patients with extradural hematoma. Comparison of results before and after the advent of computerized tomography. J Neurosurg 1981;54:179-86. Dacey RG, Alves WM, Rime1 RW, Winn R, Jane JA. Neurosurgical complications after apparently minor head injury. Assessment of risk in a series of 610 patients. J Neurosurg 1986;65:203-10. Ford LE, McLaurin RL. Mechanisms of extradural hematomas. J Neurosurg 1963;20:760-9. Frankhauser H, Kiener M. Delayed development of extradural hematomas. Acta Neurochir (Wien) 1982; 60:29-35. Frankhauser H, Uske A, de Tribolet N. Les hematomes epiduraux retard&. A propos d’une serie de 8 cas. Neurochirurgie 1983;29:255-60. Garza-Mercado R. Extradural hematoma of the posterior cranial fossa. Report of seven cases with survival. J Neurosurg 1983;59:664-72. Giner R, Beltran A, Vila M, Garcia-Herreros 1. Hematomas extradurales de evolution benigna. Rev Esp Oto-Neuro-Oftalm 1975;33:115-21. Goodkin R, Zahniser J. Sequential angiographic studies demonstrating delayed development of an acute epidural hematoma. Case report. J Neurosurg 1978; 48~479-82. Gopinath SP, Robertson CS, Contant CF, Narayan RK, Grossman RG, Chance B. Early detection of delayed traumatic intracranial hematomas using nearinfrared spectroscopy. J Neurosurg 1995;83:438-44. Kuday C, Uzan M, Hanci M. Statistical analysis of the factors affecting the outcome of extradural hematomas: 115 cases. Acta Neurochir (Wien) 1994;131: 203-6. Lobato RD, Sarabia R, Rivas JJ, Cordobes F, Castro S, Mmioz MJ, Cabrera A, Barcena A, Lamas E. Normal computerized tomography scans in severe head injury. J Neurosurg 1986;65:784-9. Milo R, Razon N, Schiffer J. Delayed epidural hematoma. A review. Acta Neurochir (Wien) 1987;84:13-23. Paterniti S, Fiore P, Macri E, Marra G, Cambria M, Falcone F, Cambria S. Extradural hematoma: report of 37 consecutive cases with survival. Acta Neurochir (Wien) 1994;131:207-10. Piepmeier JM, Wagner FC Jr. Delayed post-traumatic extracerebral hematomas. J Trauma 1982;22:455-60. Rappaport ZH, Shaked 1, Tadmor R. Delayed epidural hematoma demonstrated by computed tomography. Case report. Neurosurgery 1982;10:487-9. Smith HK, Miller JD. The danger of an ultra-early computed tomographic scan in a patient with an evolving acute epidural hematoma. Neurosurgery 1991;29:258-60.
Trauma
DELAYED EXTRADURAL HEMATOMA AFTER MILD HEAD INJURY: REPORT THREE CASES
OF
Pedro Riesgo, M.D.,* Jo& Piquer, M.D., Ph.D.,* Carlos Botella, M.D., Ph.D.,t Miguel Orozco, M.D.,* Jo& Navarro, M.D.,t and Jerbnimo Cabanes, M.D., Ph.D. *Department of Neurosurgery, Hospital Universitario “La Fe, ” Valencia, and THospital Universitario de San Juan, Alicante, Spain
Riesgo P, Piquer J, Botella C, Orozco M, Navarro J, Cabanes J. Delayed extradural hematoma after mild head injury: report of three cases. Surg Neural 1997;48:226-31.
KEY
WORDS
Delayed epidural hematoma, Glasgow coma scale, head injury, computed tomography.
BACKGROUND
Extradural hematoma has been classically considered to be an acute complication of head injury whose maximum development takes place in the minutes following trauma. Delayed extradural hematoma (DEH) is defined on the basis of an exclusively radiologic criterion: epidural hematoma that is not present in the first neuroradiologic examination made after trauma but that appears in sequential neuroradiologic examinations during patient evolution. This is an infrequent complication that usually appears in hypotensive multiple trauma patients or is related to severe head injury with other intracranial lesions. CASE
DESCRIPTION
We present three cases of DEH after mild head injury (GCS > 12) without associated intracranial or traumatic systemic lesions. Therefore, those usually considered to be “protective mechanisms” responsible for delayed development of an extradural hematoma were absent in our three patients. Diagnosis was attained by means of repetition of cranial computed tomography (CT) scan after neurologic impairment was noted. Surgical evacuation of DEH was immediately performed after diagnosis. Postop-
oodkin and Zahniser reported the first case of documented delayed extradural hematoma (DEH), demonstrated by means of cerebral angiography, in 1978 [15]. Generalization of the use of computed tomography (CT) scan in the initial and evolutive radiologic assessment of head injured patients has resulted in DEH being more frequently diagnosed [1,3,5,6,8,11,12,21,23].DEHcurrentlyrep resents up to 10% of total extradural hematomas in some reported series [1,12,21]. In spite of this, to our knowledge only four cases of DEH after mild head injury (Glasgow Coma Scale score > 12) have been reported [1,5,11,19] in the literature. We present three cases of patients who developed DEH, demonstrated by means of CT scan, after sustaining mild head injury with no associated intracranial and/or systemic traumatic lesions.
G
erative outcome was favorable in two patients who suffered DEH in the supratentorial tient who presented a posterior
compartment. One pafossa DEH died 3 days
after surgery. CONCLUSIONS
Early diagnosis and immediate treatment have proved to be essential for improving the prognosis of patients affected by DEH. Hospital admission under neurologic observation is recommended for patients who have sustained mild head injury associated with those factors that are related to the development of DEH, including GCS score under 15 or the detection of a skull fracture. Normality of a CT scan does not rule out subsequent appearance of delayed traumatic lesions. 0 1997 by Elsevier Science Inc. Address reprint requests to: Pedro A. Riesgo, M.D., Miramar 46100 Burjasot, V&n&, Spain. Received August 2, 1996; accepted December 4, 1996. 009c-3019/97/$17.00 PII s0090-3019(97)00194-8
4-3” A,
CASEREPORTS CASE 1 This 17-year-old man sustained a head injury in a motor vehicle accident after which he lost consciousness for 3 minutes. He was immediately taken to the nearest local hospital, 70 kms away from our center. After ruling out associated traumatic lesions and confirming hemodynamic stability, the patient was transferred to our hospital. On arrival, 5 hours after the accident, he was conscious with a score of 15 points on the GCS, with no evidence of neurologic deficits. A plain X ray film of the skull was obtained, showing a linear skull fracture in the right frontal region. In view of this finding, a CT scan was 655 Avenue
0 1997 by Elsevier Science Inc. of the Americas, New York, NY 10010
DEH after Mild Head Injury
also performed that showed the previously diagnosed skull fracture with no associated intracranial lesions (Figure 1 APB). The patient was admitted to the hospital. Thirty hours after the accident, clinical deterioration was detected, consisting of a decrease in his level of consciousness (GCS 9). A second CT scan was done showing an extradurai hematoma underlying the right frontal skull fracture (Figure 1 C,D,E). The patient was immediately operated on. A right frontal craniotomy was performed with aspiration of a partially coagulated extradural hematoma originating from a frontal branch of the middle meningeal artery. After surgery the patient made a good recovery and was discharged from the hospital 14 days after trauma without neurologic sequelae. Two months after the
Surg Neurol 1997;48:226-31
accident the patient resumed (Glasgow Outcome Scale 1).
his normal
227
activities
CASE 2 This 45-year-old man suffered head injury with initial loss of consciousness (< 1 minute) after falling from a bicycle. The patient was taken to the hospital 45 minutes after the accident. At the time of initial evaluation he was conscious (G CS 14) with no neurologic deficits. His hemodynamic status remained stable. Clinical and radiologic evaluation excluded the presence of associated traumatic lesions. A cranial CT scan was done and was considered normal (Figure 2 A,B,C). The patient was admitted to our service under neurologic observation. Six hours after trauma a decline in his level of con-
228
q
Surg Neurol 1997;48:226-31
Riesgo et al
(A,B,C) Case 2: initial CT scan; @,E,F’) case 2: second CT scan (6 hours after trauma). Right temporoparietal hematoma with marked mass effect.
sciousness (GCS 7) was noted. A second CT scan was obtained showing a right temporoparietal hematoma with association of marked mass effect (Figure 2 D,E,F). The patient was operated on. A completely coagulated hematoma was evacuated through a right temporoparietal craniotomy. A vertical right temporal skull fracture that had gone unnoticed in radiologic examination was found during surgery. This fracture caused laceration of the main trunk of the middle meningeal artery leading to extradural hematoma development. Clinical outcome after surgery was satisfactory and the patient was discharged from hospital 11 days after trauma with no significant neurologic sequelae and resumed normal activities 2 months later (Glasgow Outcome Scale 1).
CASE
3
This 23-year-old man with a previous history of intravenous drug abuse, sustained head injury with initial loss of consciousness (2 minutes) after falling from a height of 3 meters. On admission to the hospital, 1 hour after the accident, he was conscious although confused (GCS 13) with no detectable focal neurologic deficits. The patient did not suffer other associated traumatic lesions and his hemodynamic status remained stable. A CT scan was obtained showing a left occipital skull fracture (Figure 3 A,B,C) with no evidence of intracranial lesions (Figure 3 D,E,F). Sixteen hours after admission a sudden decrease in his level of consciousness (GCS 8) was noted. A second CT scan was
DEH after Mild Head Injury
done, demonstrating a left posterior fossa extradural hematoma underlying the previously diagnosed skull fracture (Figure 3 G,H). The patient was immediately operated on. A partially coagulated extradural hematoma, venous in origin (laceration of the left lateral sinus wall), was evacuated through a left suboccipital craniectomy. During the immediate postoperative period the patient did not recover consciousness. Four hours after surgery bilateral areactive midriasis was noted and a further CT scan was performed but did not show any significant findings. The patient died 3 days after head injury (Glasgow Outcome Scale 5).
DISCUSSION Extradural hematoma has been classically considered to be an acute complication of head injury whose maximum development takes place immediately following trauma [lo]. However, there are many references in the literature to cases of extradural hematoma of subacute or chronic evolution [4,7,14]. The concept of DEH is defined on the basis of an exclusively radiologic criterion: epidural hematoma that is not present in the first neuroradiologic examination made after trauma, but that appears in sequential neuroradiologic explorations during patient evolution [ 191. Concurrent systemic traumatic lesions leading to a hypotensive state and/or intracranial traumatic lesions with associated increase of intracranial pressure (ICP) have been classically identified as “protective mechanisms” responsible for the development of DEH [ 1,5,11,12,15]. Nevertheless, the incidence of DEH in patients affected by mild head injury (GCS > 12) with no associated traumatic intracranial and/or systemic lesions is rare and has infrequently been reported in the literature [ 11. Milo et al. reported three cases of DEH and reviewed 32 cases that had been published up to 1987 [ 191. Only four of these 35 patients had sustained mild head injury according to described neurologic criteria, although GCS score has not specifically been reported in any of them. On the other hand, two of these patients, reported by Frankhauser et al. [ 1 l] and Milo et al. [ 191, suffered other traumatic intracranial lesions whose surgical treatment preceded development of DEH [ 11,191. The patient reported by Cervantes was initially hypotensive after trauma and DEH was diagnosed after the patient had undergone an exploratory laparotomy because of a hemoperitoneum [5]. Thus, only the case contributed by Borovich et al. [l] fulfills the standards that lead to diagnosis of DEH in a patient who sus-
Surg Neurol 1997;48:226-31
229
tained mild head injury with no association of other intracranial and/or systemic lesions; however, the evolution of this patient was chronic, with an interval of 11 days between head injury and diagnosis of DEH. All our patients developed an extradural hematoma underlying a skull fracture, which in one case had gone unnoticed on preoperative neuroradiologic examination. Presence of a skull fracture has been identified by several authors as a common feature of reported cases of DEH and should be considered a predisposing factor for the development of this complication [ 1,5,8,15,21,22], although as an isolated finding, it does not explain the delay in the evolution of an extradural hematoma. Moreover, none of these patients suffered associated traumatic intracranial or systemic lesions that could have acted as “protective mechanisms” leading to the delayed occurrence of the hematoma. Some authors have tried to explain the development of DEH as a consequence of the venous origin of the bleeding [ 13,191. However, this was the case in only one of our patients who suffered a posterior fossa DEH due to laceration of the left lateral sinus wall, underlying an occipital skull fracture. Neurologic impairment preceded detection of a DEH in all the cases, after an interval of 630 hours after head injury. Hospital admission under neuro logic observation permitted early suspicion of significant neurosurgical complications in all our patients. Diagnosis was attained after urgent repetition of a cranial CT scan in all the cases. Recently, Gopinath et al. [16] reported their expe rience with the application of near-infrared spectroscopy in the detection of delayed traumatic intracere bra1 hematomas. This is a promising technique of undoubted interest, although at present it has only limited value in clinical practice. In the last decade, CT scan has become the elective neuroradiologic examination for initial and also evolutive evaluation of patients with head injury. Increasing use of CT in the early diagnosis of patients whose clinical neurologic examination could be regarded as normal, will lead to an increase in frequency of diagnosis of delayed traumatic lesions [ 1,6,9,18,22,23]. Moreover, normality of an early CT scan of a patient with mild head injury does not rule out the subsequent development of DEH or other significant neurosurgical complications [ 6,9,18,23]. Surgical evacuation of DEH was performed immediately after diagnosis. Postoperative outcome was favorable in two patients who suffered DEH in the supratentorial compartment. These patients recovered without neurologic sequelae and resumed their previous activities 2 months after trauma. The
230
Surg Neurol 1997;48:226-31
Riesgo et al
Case 3: initial CT scan. Bone settings showing a left occipital skull fracture; @,E,F) case 3: initial CT scan with no evidence of intracranial lesions;(G,H) case 3: second CT scan (16 hours after trauma) demonstrating a left posterior fossa extradural hematoma. (A,B,C)
DEH after Mild Head Injury
remaining patient, who presented a posterior fossa DEH failed to improve and died 3 days after surgery in spite of early diagnosis and surgical treatment. In recent years, extradural hematoma has been considered a benign entity with low associated morbidity and mortality [%,8,17,20]. However, a posterior fossa location constitutes an unfavorable prognostic factor, probably due to early irreversible hypoxic damage to brain stem structures because of direct compression during extradural hematoma development [ 131.
Surg Neurol 1997;48:226-31
7. 8.
9.
10.
SUMMARY Early diagnosis and treatment of DEH have proved to be essential for improving outcome of affected patients. Hospital admission under neurologic observation should be mandatory for those patients who have sustained mild head injury with associated risk factors for the development of DEH, including detection of a skull fracture and/or GCS score under 15. Normality of an early CT scan does not rule out further development of delayed traumatic lesions.
A second CT examination should be carried out as soon as any impairment in the neurologic situation of the patient is noted.
11. 12. 13. 14. 15.
16.
We wish to thank Mr. Mike Harrison for his editorial counseling, and also Miss Marta Riesgo and Mrs. Mercedes Santhis for their help in the preparation of this manuscript.
17.
REFERENCES
18.
1. Borovich B, Braun J, Guilburd JN, Zaaroor M, Michich M, Levy L, Lemberger A, Grushkiewicz I, Feinsod M, Schachter I. Delayed onset of traumatic extradural hematoma. J Neurosurg 1985;63:30-4. 2. Bricolo AP, Pasut LM. Extradural hematoma: toward zero mortality. A prospective study. Neurosurgery 1984;14:8-12. 3. Bucci MN, Philips TW, McGillicuddy JE. Delayed epidural hemorrhage in hypotensive multiple trauma patients. Neurosurgery 1986;19:65-8. 4. Bullock R, Van Dellen JR. Chronic extradural hematoma. Surg Neurol 1982;18:300-2. 5. Cervantes LA. Concurrent delayed temporal and posterior fossa epidural hematomas. Case report. J Neurosurg 1983;59:351-3. 6. Ciquini-Junior O., Dos-Santos AL, Manreza LA, Plese JP, Marino-Junior R. Traumatic extradural hematoma in childhood and normal early computerized tomog-
19. 20.
21. 22. 23.
23 1
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