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Re: Intracerebral haematoma: traumatic or non-traumatic
198 Journal of Clinical Forensic Medicine detainees who have sustained a head injury and have a periorbital haematoma require hospital assessment. A periorbital haematoma may be caused by percolation of blood into the orbit from a fracture of the anterior fossa of the skull and, therefore, should be viewed as providing clinical evidence of a possible skull fracture in those with head injury, just as a mastoid haematoma (BattleÕs sign) and CSF rhinorrhoea should. Similarly, the document does not suggest that drunks who allege amnesia should be sent to hospital; rather the advice is that those with a head injury who have amnesia for the incident or subsequent events should be further assessed in hospital. Impairment of conscious level, as evidenced by periods of amnesia, may indicate underlying brain injury and is an indication for referral to hospital. The Royal College of RadiologistsÕ document ‘‘Making the best use of a Department of Clinical Radiology’’ categorises a laceration down to bone or >5 cmÕ as representing a medium risk of intracranial injuryÕ which warrants a CT scan or skull X-ray.4 This guidance has merely been reiterated in the ‘‘Advice to FMEs’’ to ensure that FMEs are alert to the need to refer patients with such injuries to hospital. Guidelines are not rigid constraints on clinical practice but a concept of good practice against which the needs of the individual patient should be measured. Adherence to the guidelines in ‘‘Advice to FMEs’’ will not ensure a successful outcome in every case, nor do they exclude other acceptable means of providing care. The ultimate judgement regarding the management of a head injured detainee must be made by the FME in the light of the clinical picture presented by the patient. It is in recognition of both the uniqueness of every clinical encounter, and the skills and talents of FMEs, that it was not felt helpful to provide a proscriptive list of those extracranial injuries that a doctor should consider to be significantÕ and we rebut the suggestion that the use of such a term renders the classification unhelpful. Doctors should be aware that the guidelines in ‘‘Advice to FMEs’’ are evidence-based and have been approved for national use within the National Health Service as well as by the Education and Research Committee of the Association of Police Surgeons. Whilst they are not a set of rigid rules, it would be advisable that the reasons for any significant depar-
4 The Royal College of Radiologists. Making the best use of a Department of Clinical Radiology. Royal College of Radiologists 2000.
ture from the guidelines should be fully documented in the detaineeÕs clinical notes at the time the relevant decision is made. Dr. GUY A. NORFOLK Chairman Education and Research Committee Associate of Police Surgeons, UK Dr. DEBORAH J. ROGERS Honorary Senior Lecturer Forensic Medicine Unit St. GeorgeÕs Hospital UK 2002 Published by Elsevier Science Ltd and APS. doi:10.1016/S1353-1131(02)00096-2, available online at http://www.idealibrary.com on
Re: Intracerebral haematoma: traumatic or non-traumatic Sir, We read with great interest the article by Yukihito Yajima and co-workers, entitled ‘‘Intracerebral haematoma: traumatic or non-traumatic’’.1 We fully agree with the authors, that the discrimination of traumatic intracerebral haematomas from non-traumatic ones can be difficult. This, obviously, is even more true in the forensic setting when the classification of the manner of death as ‘‘natural’’ or ‘‘nonnatural’’ has to be given. The case of Yajima et al. is a classical example. As far as we could gather from both the case history and the morphological findings as they appear in the paper, we would have drawn the same conclusion as the authors and have classified the lesions as traumatic ones. Nonetheless, we feel that some morphological findings in this case strongly support our view, that the nature of the lesions was indeed from the classical diffuse axonal injury type – which has been dismissed by the authors (‘‘it thus seemed that no diffuse axonal injury had occurred’’). The concept of diffuse axonal injury2 (DAI) arose some 10 years ago and is a now a well recognised entity for all those working in the field of forensic neuropathology. Usually a result of acceleration–deceleration injuries as they occur most typically in traffic accidents, DAI has been found also as a result of falls from considerable heights.3 As a consequence of shearing injuries to axons resulting in primary or secondary axonal damage, these brains show (1) haemorrhagic lesions in the midline (mostly petechial haemorrhages in the corpus callosum or as ‘‘gliding
Correspondence 199 contusions’’ in the parasagittal white matter), (2) focal haemorrhagic lesions in the dorso-lateral quadrants of the rostral brain stem, and (3) microscopical evidence of widespread damage to axons. • The Fig. 2 in the paper of Yajima et al. shows a large intracerebral haematoma obviously in the white matter lateral to the left thalamus. A further lesion not mentioned (or not recognised) by the authors lies in the left parasagittal white matter just beneath the gyrus postcentralis. This lesion seems to represent a classical ‘‘gliding contusion’’ and therefore indicates the presence of diffuse axonal injury. • The authors describe ‘‘bleeding in the corpus callosum’’ but seemingly do not recognise this as another consequence of the DAI in this case. Instead, they label these lesions as ‘‘shearing strain [acting] mainly around the left basal ganglia and corpus callosum’’, whilst ‘‘no diffuse axonal injury had occurred’’ – DAI always affects the brain as a whole; the ‘‘local’’ DAI, which the authors seem to hint at, would be too improbable from a pathophysiological point of view to exist. • The authors seemingly did not do any histological investigations in this case at all – to us, this cannot be accepted – especially in a case when deciding about the nature of an intracerebral haematoma. Although the conclusion, that the haematoma was traumatic, is most probably true, the authors simply did not do enough to exclude other possible causes. The bleeding could well have been hypertensive in nature even in the absence of left ventricular hypertrophy and arteriosclerosis – the only means to securely exclude this, would have been the histological proof, that there are no signs of hypertensive angiopathy of the intraparenchymal vessels. The presence of an intracranial aneurysm or an arteriovenous malformation cannot be excluded without doing serial microscopic sections of the brain tissue and leptomeninges surrounding the bleeding, since this lesions cannot be detected macroscopically (as the authors claim to do), especially when submerged in a great haematoma. • Histological investigations would have been mandatory to prove or to exclude the presence of DAI. The classical ‘‘axonal bulbs’’ of DAI are visible in H&E stains only after survival of at least 12–18 h4 – so this might have not been successful regarding the maximal survival time of roughly 10 h in the present case. But as has been shown,5 using an antibody to the beta-amyloid precursor protein (beta-APP), evidence of axonal damage can be seen after a survival of between 2 and 3 h.
• In conclusion, we cannot accept the authorsÕ opinion as to the exclusion of DAI in the present case. In summary, we would consider the lesions in this case as a consequence of DAI, which could have been easily detected by meticulously analysing both the macroscopic and microscopic findings – a procedure mandatory for all those working in the field of forensic science. REFERENCES 1. Yajima Y, Hayakaw H, Mimasaka S, Nata M, Hashiyada M, Funayama M. Intracerebral haematoma: traumatic or nontraumatic. J Clin Foren Med 2001; 8: 163–165. 2. Adams JH, Doyle D, Ford I, Gennarelli TA, Graham DI, McLellan DR. Diffuse axonal injury in head injury: definitions, diagnosis and grading. Histopathology 1989; 15: 49–59. 3. Adams JH, Doyle D, Graham DI, Lawrence AE, McLellan DR. Diffuse axonal injury in head injuries caused by a fall. Lancet 1989; 2: 1420–1421. 4. Graham DI, Adams JH, Nicoll JAR, Maxwell WL, Gennarelli TA. The nature, distribution and causes of traumatic brain injury. Brain Pathol 1995; 5: 397–406. 5. Sheriff FE, Bridges LR, Sivaloganatham S. Early detection of axonal injury after human head trauma using immunocytochemistry for beta-amyloid precursor protein. Acta Neuropathol 1994; 87: 55–62.
Dr JAKOB MATSCHKE Institute of Neuropathology and Institute of Legal Medicine University Hospital of Hamburg Martinistrasse 52, D-20246 Hamburg Germany E-mail: [email protected] € SCHEL Professor KLAUS PU Institute of Legal Medicine University Hospital of Hamburg Butenfeld 39, D-22529 Hamburg Germany 2002 Elsevier Science Ltd and APS. All rights reserved. doi:10.1016/S1353-1131(02)00127-X, available online at http://www.idealibrary.com on
AuthorÕs response Sir, We thank Ds Matschke and P€ uschel for their interesting comments concerning our case published in the journal [1]. Clinically this case was thought not to be the course of DAI. However, we recognized the necessity of examining the hallmark of DAI immunohistochemically. According to his suggestions, using the b-amyloid precursor protein antibody (b-APP, SIGMA, USA) we examined the brain tissues, that is, temporal lobe, corpus callosum, basal ganglia, hip-
4 The Royal College of Radiologists. Making the best use of a Department of Clinical Radiology. Royal College of Radiologists 2000.
ture from the guidelines should be fully documented in the detaineeÕs clinical notes at the time the relevant decision is made. Dr. GUY A. NORFOLK Chairman Education and Research Committee Associate of Police Surgeons, UK Dr. DEBORAH J. ROGERS Honorary Senior Lecturer Forensic Medicine Unit St. GeorgeÕs Hospital UK 2002 Published by Elsevier Science Ltd and APS. doi:10.1016/S1353-1131(02)00096-2, available online at http://www.idealibrary.com on
Re: Intracerebral haematoma: traumatic or non-traumatic Sir, We read with great interest the article by Yukihito Yajima and co-workers, entitled ‘‘Intracerebral haematoma: traumatic or non-traumatic’’.1 We fully agree with the authors, that the discrimination of traumatic intracerebral haematomas from non-traumatic ones can be difficult. This, obviously, is even more true in the forensic setting when the classification of the manner of death as ‘‘natural’’ or ‘‘nonnatural’’ has to be given. The case of Yajima et al. is a classical example. As far as we could gather from both the case history and the morphological findings as they appear in the paper, we would have drawn the same conclusion as the authors and have classified the lesions as traumatic ones. Nonetheless, we feel that some morphological findings in this case strongly support our view, that the nature of the lesions was indeed from the classical diffuse axonal injury type – which has been dismissed by the authors (‘‘it thus seemed that no diffuse axonal injury had occurred’’). The concept of diffuse axonal injury2 (DAI) arose some 10 years ago and is a now a well recognised entity for all those working in the field of forensic neuropathology. Usually a result of acceleration–deceleration injuries as they occur most typically in traffic accidents, DAI has been found also as a result of falls from considerable heights.3 As a consequence of shearing injuries to axons resulting in primary or secondary axonal damage, these brains show (1) haemorrhagic lesions in the midline (mostly petechial haemorrhages in the corpus callosum or as ‘‘gliding
Correspondence 199 contusions’’ in the parasagittal white matter), (2) focal haemorrhagic lesions in the dorso-lateral quadrants of the rostral brain stem, and (3) microscopical evidence of widespread damage to axons. • The Fig. 2 in the paper of Yajima et al. shows a large intracerebral haematoma obviously in the white matter lateral to the left thalamus. A further lesion not mentioned (or not recognised) by the authors lies in the left parasagittal white matter just beneath the gyrus postcentralis. This lesion seems to represent a classical ‘‘gliding contusion’’ and therefore indicates the presence of diffuse axonal injury. • The authors describe ‘‘bleeding in the corpus callosum’’ but seemingly do not recognise this as another consequence of the DAI in this case. Instead, they label these lesions as ‘‘shearing strain [acting] mainly around the left basal ganglia and corpus callosum’’, whilst ‘‘no diffuse axonal injury had occurred’’ – DAI always affects the brain as a whole; the ‘‘local’’ DAI, which the authors seem to hint at, would be too improbable from a pathophysiological point of view to exist. • The authors seemingly did not do any histological investigations in this case at all – to us, this cannot be accepted – especially in a case when deciding about the nature of an intracerebral haematoma. Although the conclusion, that the haematoma was traumatic, is most probably true, the authors simply did not do enough to exclude other possible causes. The bleeding could well have been hypertensive in nature even in the absence of left ventricular hypertrophy and arteriosclerosis – the only means to securely exclude this, would have been the histological proof, that there are no signs of hypertensive angiopathy of the intraparenchymal vessels. The presence of an intracranial aneurysm or an arteriovenous malformation cannot be excluded without doing serial microscopic sections of the brain tissue and leptomeninges surrounding the bleeding, since this lesions cannot be detected macroscopically (as the authors claim to do), especially when submerged in a great haematoma. • Histological investigations would have been mandatory to prove or to exclude the presence of DAI. The classical ‘‘axonal bulbs’’ of DAI are visible in H&E stains only after survival of at least 12–18 h4 – so this might have not been successful regarding the maximal survival time of roughly 10 h in the present case. But as has been shown,5 using an antibody to the beta-amyloid precursor protein (beta-APP), evidence of axonal damage can be seen after a survival of between 2 and 3 h.
• In conclusion, we cannot accept the authorsÕ opinion as to the exclusion of DAI in the present case. In summary, we would consider the lesions in this case as a consequence of DAI, which could have been easily detected by meticulously analysing both the macroscopic and microscopic findings – a procedure mandatory for all those working in the field of forensic science. REFERENCES 1. Yajima Y, Hayakaw H, Mimasaka S, Nata M, Hashiyada M, Funayama M. Intracerebral haematoma: traumatic or nontraumatic. J Clin Foren Med 2001; 8: 163–165. 2. Adams JH, Doyle D, Ford I, Gennarelli TA, Graham DI, McLellan DR. Diffuse axonal injury in head injury: definitions, diagnosis and grading. Histopathology 1989; 15: 49–59. 3. Adams JH, Doyle D, Graham DI, Lawrence AE, McLellan DR. Diffuse axonal injury in head injuries caused by a fall. Lancet 1989; 2: 1420–1421. 4. Graham DI, Adams JH, Nicoll JAR, Maxwell WL, Gennarelli TA. The nature, distribution and causes of traumatic brain injury. Brain Pathol 1995; 5: 397–406. 5. Sheriff FE, Bridges LR, Sivaloganatham S. Early detection of axonal injury after human head trauma using immunocytochemistry for beta-amyloid precursor protein. Acta Neuropathol 1994; 87: 55–62.
Dr JAKOB MATSCHKE Institute of Neuropathology and Institute of Legal Medicine University Hospital of Hamburg Martinistrasse 52, D-20246 Hamburg Germany E-mail: [email protected] € SCHEL Professor KLAUS PU Institute of Legal Medicine University Hospital of Hamburg Butenfeld 39, D-22529 Hamburg Germany 2002 Elsevier Science Ltd and APS. All rights reserved. doi:10.1016/S1353-1131(02)00127-X, available online at http://www.idealibrary.com on
AuthorÕs response Sir, We thank Ds Matschke and P€ uschel for their interesting comments concerning our case published in the journal [1]. Clinically this case was thought not to be the course of DAI. However, we recognized the necessity of examining the hallmark of DAI immunohistochemically. According to his suggestions, using the b-amyloid precursor protein antibody (b-APP, SIGMA, USA) we examined the brain tissues, that is, temporal lobe, corpus callosum, basal ganglia, hip-