Artigo Revisado por pares

Delayed Traumatic Intracerebral Hematoma: Case Report and Review of Literature

1991; King Faisal Specialist Hospital and Research Centre; Volume: 11; Issue: 1 Linguagem: Inglês

10.5144/0256-4947.1991.102

ISSN

0975-4466

Autores

Rewati Raman Sharma, Mathew J. Chandy, Santosh D. Lad,

Tópico(s)

Neurosurgical Procedures and Complications

Resumo

Case ReportsDelayed Traumatic Intracerebral Hematoma: Case Report and Review of Literature Rewati Raman Sharma, MBBS, MS Mathew Jacob Chandy, and MS, MCh Santosh D. LadMBBS, MS Rewati Raman Sharma Address reprint requests and correspondence to Dr. Sharma: Junior Specialist Neurosurgeon, Khoula Hospital, Mina Al Fahal, P.O. Box 51090, Muscat, Sultanate of Oman. From the Department of Neurosurgery, Khoula Hospital, P.O. Box 51090, Mina Al Fahal, Muscat, Sultanate of Oman Search for more papers by this author , Mathew Jacob Chandy From the Department of Neurosurgery, Khoula Hospital, P.O. Box 51090, Mina Al Fahal, Muscat, Sultanate of Oman Search for more papers by this author , and Santosh D. Lad From the Department of Neurosurgery, Khoula Hospital, P.O. Box 51090, Mina Al Fahal, Muscat, Sultanate of Oman Search for more papers by this author Published Online:1 Jan 1991https://doi.org/10.5144/0256-4947.1991.102SectionsPDF ToolsAdd to favoritesDownload citationTrack citations ShareShare onFacebookTwitterLinked InRedditEmail AboutIntroductionDelayed traumatic intracerebral hematoma is an uncommon serious complication of severe head injury that is associated with a high mortality. By definition, it arises in an area of the brain where intracerebral hematoma had been noted on a computed tomographic (CT) scan performed in the early postinjury period. The lesion was originally described a century ago by Bollinger[1]; however, Morin and Pitis[2] found only 24 cases reported in the literature before 1970. Baratham and Dennyson[3] in 1972 reported 21 cases out of 7886 cases of head injury seen during a ten-year period. It was only after the advent of CT that it was possible to confirm the de novo occurrence of hemorrhage in areas of the brain shown to be normal on an initial scan[4–7]. Currently, the reported incidence represents between 1.5 and 7% of the cases of severe head injury[8,9]. However, French and Dublin[10] could find only one case among their 1000 consecutive cases of head injury.Because delayed traumatic intracerebral hematoma frequently occurs in patients with cerebral contusion, a deteriorating neurological state in such patients may erroneously be attributed to edema around a preexisting cerebral contusion causing an increase in mass effect[6]. Thus, correct diagnosis and treatment are not infrequently delayed, with irreversible neurological damage as the outcome. The value of repeated CT scanning as part of the clinical management of severe head injury patients cannot be overemphasized.In our prospective study of 120 patients with a severe head injury (with a Glasgow Coma Scale [GCS] of 8 or below) who were seen over a one-year period, we found only one had a solitary delayed traumatic intracerebral hematoma, and this case forms the basis of our report, along with a brief review of the literature.CASE REPORTA 35-year-old Omani male was admitted with a GCS of 6 (i.e., no eye opening to pain, flexion withdrawal to pain, no verbal response to pain) following a road traffic accident. He had stable vital parameters (pulse, 90 bpm; blood pressure, 130/90 mm Hg; respiration, normal) and no focal neurological deficits. There were no injuries to the chest, abdomen, or limbs. Plain x-ray studies of the skull showed no fracture and CT scan done 16 hours after the accident showed no abnormality (Figure 1). With symptomatic management, his level of consciousness improved to a GCS of 11 (i.e., spontaneous eye opening, localizing to pain, voicing noise on pain). On the fourth postinjury day, a rapid-onset left hemiplegia developed and he became restless. However, his vital signs remained stable and an urgent CT scan (Figure 2) was performed that revealed a moderate-sized right posterior frontal intracerebral hematoma with surrounding edema, producing slight mass effect. He was treated conservatively, and this consisted of mannitol and dexamethasone therapy along with nursing care and physiotherapy. Over three weeks, his level of consciousness improved to a GCS of 15, and the left hemiplegia abated to a power grade of 4–5/5. Repeat CT scan at three weeks (Figure 3) showed considerable resolution of the right posterior frontal intracerebral hematoma and no mass effect. He was continued on physiotherapy for six weeks, with good improvement.Figure 1. CT scan 16 hours after the accident, showing no abnormality.Download FigureFigure 2. CT scan on fourth postinjury day, showing a right posterior frontal intracerebral hematoma with little mass effect.Download FigureFigure 3. CT scan three weeks following the accident, showing resolving right posterior frontal intracerebral hematoma.Download FigureDISCUSSIONOf the various types of traumatic intracranial hematoma, the appearance of the intracerebral type is most likely to be delayed – the so-called delayed traumatic apoplexy of Bollinger[11]. Delayed traumatic intracerebral hematoma is a serious complication with a high mortality of from 30 to 72% reported for various series[2,3,12–15]. Delayed diagnosis and treatment is a common cause of this high mortality[3], although the severity of the initial impact and secondary insults are also contributory[15].The etiology of delayed traumatic intracerebral hematoma has been the subject of considerable speculation. Focal brain injury is thought to result in decreased vascular resistance, allowing an increased head of arterial pressure and increased blood flow to be transmitted to an already traumatized capillary–vascular bed, with resultant hemorrhage into the cerebral parenchyma[2,7,13,16]. Compression of the brain caused by a hematoma or edema can produce ischemia, necrosis, and secondary hemorrhage[12]. Mechanical distortion producing ischemia and infarction may cause delayed traumatic intracerebral hematoma[17]. Severe head trauma can also result in coagulopathies which in turn cause cerebral hemorrhage[18,19]. Recent data indicate that delayed traumatic intracerebral hematomas frequently occur in patients with disseminated intravascular clotting and fibrinolysis[18,19]. Baratham and Dennyson[3] attempted to correlate the development of delayed intracerebral hemorrhage with hypoxic or hypercarbic episodes. The local loss of autoregulation from focal trauma coupled with increased blood flow from hypoxia and hypercarbia or stagnation from elevated venous pressure could enhance diapedesis, and therefore the gradual development of a hematoma.Baratham and Dennyson[3] stated that delayed traumatic intracerebral hematomas tend to arise in elderly patients in the seventh or eighth decades of life, with a deterioration in consciousness after a lucid interval lasting hours to days. However, our patient was a young Omani male (35 years old) who was unconscious on admission with a GCS of 6, when delayed traumatic intracerebral hematoma developed on the fourth postinjury day. His state of consciousness had already improved to a GCS of 11, when there was rapid onset of left hemiplegia. Delayed traumatic intracerebral hematoma may develop within 24 hours of injury[4,10]. The clinical signs are frequently insidious. In an clinical setting, a deteriorating state of consciousness, a newly developed third nerve palsy, or a rise in intracranial pressure may be secondary to delayed traumatic intracerebral hematoma, progressive edema around a cerebral contusion, or a cerebrovascular episode[6,18]. The real advantage of the CT scan lies with its ability to show that portions of a parenchymatous lesion are hematoma, contusion, and edema. Gentleman et al[14] contended that a patient whose admission CT scan is normal will not sustain delayed traumatic intracerebral hematoma. However, the first CT scan seen in our patient was entirely normal, signifying its rarity and underlining the fact that a normal CT scan at admission does not rule out the possible delayed development of an intracerebral hematoma. A delayed traumatic intracerebral hematoma should be suspected in any patient with severe head injury who shows clinical signs of deterioration with or without a lucid interval.Surgical treatment is required for cases of delayed traumatic hematomas, but depends on the amount of mass effect, the location of the mass, and whether there is a discrete hematoma. Clinical and not radiological indications must predominate in the decision to perform surgical intervention[10,20]. Many lesions can be monitored by repeat CT scans without an operation. However, prompt craniotomy, when necessary, for removal of a large delayed traumatic intracerebral hematoma can yield gratifying results[21]. Our patient was treated conservatively and responded well to this approach.Repeat CT scans in patients with severe head injuries help monitor the possible formation of a delayed traumatic intracerebral hematoma, and allow for proper management before irreversible brain damage occurs.Normal initial CT scans in the immediate post-injury period do not rule out the possible later development of an intracerebral hematoma. A high index of suspicion must be maintained to allow for its early recognition and management.ARTICLE REFERENCES:1. Bollinger O. Uber traumatische Spat-Apoplexie. Ein Beitrag zur lehrevander Hirnerschutterung. In: Internationale Beitrage zur Wissen-Schaftlichen Medizin Festschrift Rudolph Virchow. Berlin: Hirschwald, 1891; 2:457–70. Google Scholar2. Morin MA, Pitis FW. "Delayed apoplexy following head injury (“Traumotische Spat-Apoplexie”)" . J Neurosurg. 1970; 33:542–7. Google Scholar3. Baratham G, Dennyson WG. "Delayed traumatic intracerebral hemorrhage" . J Neurol Neurosurg Psychiatr. 1972: 35:696–706. Google Scholar4. Brown FD, Mullan S, Duda EE. "Delayed traumatic intracerebral hematomas: report of three cases" . J Neurosurg. 1978; 48:1019–22. Google Scholar5. Brunetti J, Zingesser L, Dunn J, Rovit RL. "Delayed intracerebral hemorrhage as demonstrated by CT scanning" . Neuroradiology. 1979; 18:43–6. Google Scholar6. Cooper PR (ed). Post-traumatic intracranial mass lesions. In: Head Injury; ed 2. Baltimore: Williams & Wilkins, 1987;239–84. Google Scholar7. Lipper MH, Kishore PRS, Girevendulis AK, et al.. "Delayed intracranial hematoma in patients with severe head injury" . Radiology. 1979; 133:645–9. Google Scholar8. Kaufman HH, Moake JH, Olson JD, et al.. "Delayed and recurrent intracranial hematomas related to disseminated intravascular clotting and fibrinolysis in head injury" . Neurosurgery. 1980; 7:445–50. Google Scholar9. Ninchoji T, Uemura K, Shimayama I, et al.. "Traumatic intracerebral haematomas of delayed onset" . Acta Neurochir. 1984; 71:69–90. Google Scholar10. French BN, Dublin AB. "The value of computerized tomography in the management of 1000 consecutive head injuries" . Surg Neurol. 1977; 7:171–83. Google Scholar11. Adams JH. Head injury. In: Adams JH, Corsallis JAN, Dunchen LW, eds. Greenfield's Neuropathology. ed 4. London: Edward Arnold. 1984:85–124. Google Scholar12. Clifton GL, Grossman RG, Makela ME, et al.. "Neurological course and correlated computerized tomography findings after severe closed head injury" . J Neurosurg. 1980; 52:611–24. Google Scholar13. Diaz FG, Yock DH, Larson D, Rockswald GL. "Early diagnosis of delayed post traumatic intracerebral hematomas" . J Neurosurg. 1979; 50:217–23. Google Scholar14. Gentleman D, Nath F, Macpherson P. "Diagnosis and management of delayed traumatic intracerebral haematomas" . Br J Neurosurg. 1989; 3:367–72. Google Scholar15. Gudemann SK, Kishore PRS, Miller JD, et al.. "The genesis and significance of delayed traumatic intracerebral hematoma" . Neurosurgery. 1979; 5:309–13. Google Scholar16. Jamieson KG. "Delayed traumatic intracerebral hemorrhage (traumatische spat Apoplexie)" . Aust NZ J Surg. 1954; 23:300–7. Google Scholar17. Macpherson P, Graham DI. "Correlation between angiographic findings and the ischaemia of head injury" . J Neurol Neurosurg Psychiatr. 1978; 41:122–7. Google Scholar18. Miner ME. Delayed and recurrent intracranial hematomas and post-traumatic coagulopathies. In: Wilkins RH, Rengachary SS, eds. Neurosurgery, Vol 2. New York: McGraw-Hill, 1985;1666–9. Google Scholar19. Pretorius ME, Kaufman HH. "Rapid onset of delayed traumatic intracerebral haematoma with diffuse intravascular coagulation and fibrinolysis" . Acta Neurochir (Wien). 1982; 65:103–9. Google Scholar20. Roberson FC, Kishore PRS, Miller JD, et al.. "The value of serial computerized tomography in the management of severe head injury" . Surg Neurol. 1979; 12:161–7. Google Scholar21. Becker DP, Miller JD, Ward JD, et al.. "The outcome from severe head injury with early diagnosis and intensive management" . J Neurosurg. 1977; 47:491–502. Google Scholar Previous article Next article FiguresReferencesRelatedDetailsCited byIbrahim A and Al-Majid H (1992) Delayed Intracerebral Hematoma, Annals of Saudi Medicine, 12:4, (412-413), Online publication date: 1-Jul-1992.Haddad F (1992) Delayed Traumatic Intracerebral Hematoma: Case Report and Review of Literature, Annals of Saudi Medicine, 12:4, (412-412), Online publication date: 1-Jul-1992. Volume 11, Issue 1January 1991 Metrics History Accepted12 May 1990Published online1 January 1991 ACKNOWLEDGMENTWe thank members of the Department of Surgery and Medicine, Armed Forces Hospital, Muscat, who referred this case and Mrs. Anita Rastogi for excellent secretarial assistance in the preparation of this manuscript.InformationCopyright © 1991, Annals of Saudi MedicinePDF download

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