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Table 1.Summary of 12 Patients with Brain Death and Deep Coma: Clinical Findings Patients No. Age/Sex Underlying Cause Study No. Brain Stem Reflex EEG Clinical Diagnosis 01 40/M Trauma 01 ECS Brain death 02 35/M Trauma 02 ECS Brain death 03 17/M Trauma 03 ECS Brain death 04 18/F Trauma 04 N.A Brain death 05 43/M Hypoxia 05 ECS Brain death 06 44/M Aneurysm rupture 06 ECS Brain death 07 49/F Hypoxia 07 Burst suppression C o m a 08 57/M Basilar artery occlusion 08 Artifact Brain death 09 17/F Trauma 09 + Burst suppression Coma 10 45/M Hypoxia 10 + N.A C o m a 11 38/M Hypoxia 11 Diffuse slowing C o m a 12 ECS Brain death 12 53/F Trauma 13 + N.A Coma 14 + N.A C o m a 15 N.A Brain death EEG : Electroencephalography, ECS : Electrocerebral silence, N.A: not available, : absence, + : presence 3 9 6
Table 2. Summary of 12 Patients with Brain Death and Deep Coma: CT Angiographic Findings Patients No. Study No. c-ica s-ica VBA Proximal Distal STA Skull Diagnosis No. ACA/MCA/PCA Branches 01 2 01 + Brain death 02 2 02 + + + Multiple fractures Brain death 03 2 03 +(Lt) +(Lt) + 1 + Trepanation(Lt) Brain death 04 2 04 + + + Brain death 05 2 05 + + Brain death 06 2 06 + Brain death 07 2 07 + + + + + + C o m a 08 2 08 + + + + + C o m a 09 2 09 + + + + + + C o m a 10 2 10 + + + + + + C o m a 11 2 11 + + + + + + C o m a 12 + + Brain death 12 3 13 +(Lt) +(Lt) + + + + Trepanation(Rt) Coma 14 +(Lt) +(Lt) + + + + Trepanation(Rt) Coma 15 +(Lt) +(Lt) + + Trepanation(Rt) Brain death c-ica : cavernous portion of internal carotid artery, s-ica : supraclinoid portion of internal carotid artery, VBA : vertebral / basilar artery, ACA : anterior cerebral artery, MCA : middle cerebral artery, PCA : posterior cerebral artery, STA : superficial temporal artery, : faint opacification in thin and elongated artery, 1 preserved flow only in skull defect area, 2 repeated study 7 days after the first CT angiography, 3 repeated studies 2 and 5 days after the first CT angiography. A B C Fig. 1. Patient 3. Brain death caused by trauma in a 17-year-old man. A. Axial source image with 1 mm thickness shows faint opacification of the left internal carotid artery (arrow), whereas the right internal carotid artery is not visible. B. Axial source image cranial to A shows opacification of the left distal middle cerebral artery branches in the area of large skull defect (arrow) and anterior cerebral artery (arrowhead). Note normal opacification in the superficial temporal arteries (long arrows). C. CT angiogram with maximum-intensity-projection shows faint opacification in the left internal carotid artery, both middle cerebral artery, both posterior cerebral arteries, and distal branches in left temporal lobe. 3 9 7
A B Fig. 2. Patient 11. Brain death caused by hypoxic brain damage in a 38-yearold man. A. CT angiogram with shaded-surface-display at the day of admission shows preserved cerebral flow. The patient was diagnosed as deep coma because of slow wave on EEG. B. 5Follow-up CT angiogram obtained 7 days after admission shows complete circulatory arrest. The distal branches of the external carotid arteries (superficial temporal arteries) are still opacified (arrows). Note lack of opacification of the both internal carotid arteries (arrowheads). The EEG examination at the same day revealed electrocerebral silence. A B Fig. 3. Patient 12. Brain death caused by trauma in a 53-year-old woman. A, B. Axial source image at the level of circle of Willis (A) and CT angiogram with shaded-surface-display (B) at the day of admission show opacification in the thin and elongated anterior cerebral arteries, middle cerebral arteries, and posterior cerebral arteries. Note a large skull defect in the right temporal bone after osteoclastic trepanation. EEG examination was impossible due to extensive brain herniation. But, some brain stem reflexes were preserved. C, D. Axial source image at the same level with A (C) and CT angiogram (D) 5 days after admission show marked progression of intracerebral circulatory arrest. The left internal carotid artery (arrow), left middle cerebral artery (arrowhead), and basilar artery (long arrow) are thin and elongated. The clinical examination at the same day demonstrated complete loss of brain stem reflexes. C D 3 9 8
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of intracranial pressure. Acta Neurol 1964;4 :1-57 3. Nau R, Prange HW, Klingelhofer J, et al. Results of four technical investigations in fifty clinically brain dead patients. Intensive Care M e d 1992;18:82-88 4. Napel S, Marks MP, Rubin GD, et al. CT angiography with spiral CT and maximum intensity projection. R a d i o l o g y 1992 ; 185 : 607-610 5. Schwartz RB. Neuroradiological applications of spiral CT. S e m i n 6.,,. C T :. 1995;33:183-188 7. Greitz T, Gordon E, Kolmodin G, Widen L. Aortocranial and 1. Link J, Schaefer M, Lang M. Concepts and diagnosis of brain death. Forensic Sci Int 1994 ; 16 : 195-203 2. Heiskanen O. Cerebral circulatory arrest caused by acute increase Ultrasound CT MR 1 9 9 2 ; 1 3 : 2 4 6-2 5 5 carotid angiography in determination of brain death. N e u r o r a d i o l o g y 1973;5:13-19 8. Kricheff II, Pinto RS, George AE, Braunstein P, Korein J. Angiographic findings in brain death. Ann N Y Acad Sci 1978 ; 315 : 168-183 9. Ducrocq X, Braun M, Debouverie M, Junges C, Hummer M, Vespignani H. Brain death and transcranial Doppler: experience in 130 cases of brain dead patients. J Neurol Sci 1998;160:41-46 10. Ducrocq X, Hassler W, Moritake K, et al. Consensus opinion on diagnosis of cerebral circulatory arrest using Doppler-sonography: Task Force Group on cerebral death of the Neurosonology Research Group of the World Federation of Neurology. J Neurol Sci 1998 ; 159:145-150 11. Bonrtti MG, Ciritella P, Valle G, Perrone E. 99mTc HMPAO brain perfusion SPECT in brain death. N e u r o r a d i o l o g y 1995 ; 37 : 365-369 12. Facco E, Zucchetta P, Munari M, et al. 99mTc-HMPAO SPECT in the diagnosis of brain death. Intensive Care Med 1998;24:911-917 1 3. Flowers WM Jr, Patel BR. Radionuclide angiography as a confirmatory test for brain death: a review of 229 studies in 219 patients. South Med J 1997;90:1091-1096 14. Kiyoshi I, Takehide O, Toshibumi K, Genzo S, Motonobu K, and Yasuko S. Brain Death: MR and MR angiography. AJNR Am J Neuroradiol 1996;17: 731-735 1 5. Alvarez LA, Lipton RB, Hirschfeld A, Salamon O, Lantos G. Brain death determination by angiography in the setting of a skull defect. Arch Neurol 1988;45:225-227 1 6. Dupas B, Gayet-Delacroix M, Villers D, Antonioli D, Veccherini MF, Soulillou,JP. Diagnosis of brain death using two-phase spiral CT. AJNR Am J Neuroradiol 1 9 9 8 ; 1 9 : 6 4 1-6 4 7 4 0 0
Evaluation of Brain Death by CT Angiogra p hy : Initial Experience 1 Sung Hwan Kim, M.D., Dae Young Yoon, M.D., Joo Eun Shim, M.D., Chul Soon Choi, M.D., Sang Hoon Bae, M.D., Hong Ki Song, M.D. 2, Hyung Chul Kim, M.D. 2 1 Department of Radiology, Hallym University College of Medicine 2 Department of Neurology, Hallym University College of Medicine Purpose : The angiographic demonstration of absent cerebral blood flow is presently considered to be the most reliable method of confirming brain death. The purpose of this study is to determine whether CT angiography (CTA) with spiral CT can rapidly and specifically establish a diagnosis of brain death. Materials and Methods : A total of fifteen CT angiograms (brain death, n=9;severe coma, n=6 within 24 hours of the study) were obtained prospectively in 12 patients with an established clinical diagnosis; Two patients underwent repeated CTA. Twenty seconds after beginning the injection of contrast media (100 ml at a rate of 3 ml/sec), CT scanning (30second continuous exposure and 60mm length) was performed with a table speed of 2 mm/sec and a section thickness of 2 mm. For each case, the presence or absence of opacification of internal carotid arteries (ICA), vertebral and basilar arteries (VBA), anterior cerebral arteries (ACA), middle cerebral arteries (MCA), posterior cerebral arteries (PCA), distal branches of cerebral arteries, and superficial temporal arteries (STA) was ascertained. Results : Except in one clinically brain-dead patient, whose EEG was difficult to interpret due to excessive artifacts, the distal branches of cerebral arteries did not opacify. STA, on the other hand, was always visible on both sides. In all brain-dead patients but three, the ICA and proximal ACA, MCA, or PCA escaped visualization. In the remaining three cases with large skull defect or skull fracture, however, CT angiography showed faint opacification of the ICA and proximal segments of cerebral arteries. Cerebral arterial flow was preserved in all six patients in whom there was no clinical evidence of brain death. Conclusion : CTA may be used as a confirmatory test for the determination of brain death. Index words : Brain death Computed tomography (CT), angiography Address reprint requests to : Dae Young Yoon, M.D., Department of Radiology, Hallym University College of Medicine #445, Gil-dong, Kangdong-gu, Seoul, 134-701 Korea. Tel. 82-2-2224-2308 Fax. 82-2-488-7370 4 0 1
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