Ct hypodensity accidpedinj_neurosurg_steinbok_poskitt


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Ct hypodensity accidpedinj_neurosurg_steinbok_poskitt

  1. 1. CLINICAL STUDIES EARLY HYPODENSITY ON COMPUTED TOMOGRAPHIC SCAN OF THE BRAIN IN AN ACCIDENTAL PEDIATRIC HEAD INJURYPaul Steinbok, M.B.B.S. OBJECTIVE: Hypodensities on computed tomographic (CT) brain scans are thought toDivision of Pediatric Neurosurgery, take at least 6 hours to become apparent after blunt head trauma. This finding, in con-Department of Surgery,BC Children’s Hospital, junction with the later evolution of the hypodensities, is used in timing the injury inand University of British Columbia, children with suspected non-accidental brain injury, in whom the history may be inac-Vancouver, Canada curate. The purpose of this study is to report the occurrence of diffuse cerebral parenchy- mal hypodensities on CT scans performed within 5 hours of a well-defined accidentalAshutosh Singhal, M.Sc., M.D. head injury.Division of Pediatric Neurosurgery,Department of Surgery, METHODS: A retrospective review was performed of five patients admitted to BritishBC Children’s Hospital, Columbia Children’s Hospital who had accidental head injury and who were identi-and University of British Columbia, fied as having diffuse cerebral hemispheric hypodensities on early CT scans.Vancouver, Canada RESULTS: We present five patients (age range, 4 mo–14 yr) with well-documented acci-Ken Poskitt, M.D.C.M. dental head injuries who demonstrated obvious and extensive CT brain scan cerebralDepartment of Radiology, hemispheric hypodensity from 60 minutes to 4.5 hours after trauma. All five patients pre-BC Children’s Hospital sented with severe head injuries and immediate, unremitting coma, and all five pro-and University of British Columbia, gressed rapidly to brain death within 48 hours.Vancouver, Canada CONCLUSION: It is unusual, but possible, to develop CT hypodensities as early asD. Douglas Cochrane, M.D. 1 hour after accidental head injury. In our small series of cerebral hemispheric hypo-Division of Pediatric Neurosurgery, density occurring less than 5 hours after trauma, all five patients had a uniformly fatalDepartment of Surgery, outcome. These observations may be important medicolegally in the assessment of theBC Children’s Hospital,and University of British Columbia, timing of head injury when the history of the trauma is not clear, as in children withVancouver, Canada suspected non-accidentally inflicted injury. It is inappropriate to generalize these find- ings to patients who are not unconscious immediately after a head injury, who regainReprint requests: consciousness after an injury before deteriorating, or who do not progress rapidly toPaul Steinbok, M.B.B.S.,Division of Pediatric Neurosurgery, brain death.Department of Surgery, KEY WORDS: Cerebral edema, Child abuse, Computed tomographic hypodensity, Head injury, Medicolegal,BC Children’s Hospital, Timing of injury4480 Oak Street, #K3–159,Vancouver, BC, Canada V6H 3V4. Neurosurgery 60:689–695, 2007 DOI: 10.1227/01.NEU.0000255398.00410.6B www.neurosurgery-online.comEmail: psteinbok@cw.bc.ca HReceived, June 7, 2006. ypodensities on computed tomo- next 3 to 5 days and then regress during theAccepted, December 8, 2006. graphic (CT) brain scans after head subsequent few days. Thus, the presence of trauma have traditionally been attrib- obvious CT scan hypodensities within 6 hours uted to cerebral ischemia. Previously pub- of a reported head injury may lead physicians lished reports have suggested that it is diffi- to call into question the timing of the injury or cult to precisely determine how much time raise the possibility of an etiology other than must elapse between the injury and the devel- the reported head injury. In young children opment of hypodensities, particularly diffuse and infants, the apparent inconsistency hypodensities (6, 20). As commented on by between the CT scan findings and the reported Dias et al. (9), and in keeping with our experi- history of the trauma may lead to a concern ence, the standard opinion is that CT scan low regarding non-accidental inflicted injury. densities do not become readily apparent until There are a number of reports in which the at least 6 hours after the injury. Typically, they occurrence of parenchymal hypodensities on become progressively more obvious during the the initial CT scan after non-accidentallyNEUROSURGERY VOLUME 60 | NUMBER 4 | APRIL 2007 | 689
  2. 2. STEINBOK ET AL.inflicted injury has been mentioned (8–10, 15). Because the diag- vehicle collision in one case, and a bicycle accident (without anosis of inflicted shaking injury is associated with inaccuracies helmet) in one case.in the history, it may be argued that the timing of the trauma in None of the patients was documented to have a cardiorespi-such reports may be unreliable. There are well-documented ratory arrest or any period of hypoxia or hypotension duringreports of brain “swelling” within 6 hours of accidental head initial transfer or during the trauma resuscitation before thetrauma, but no reports of early parenchymal CT scan hypoden- initial CT scan. None of the patients was identified to havesities in documented accidental injuries in children or adults. radiographic or clinical evidence of spine or spinal cord injury. We present this case series to demonstrate that diffuse and In one of three patients in whom funduscopy was documented,obvious CT scan parenchymal hypodensities occur within 5 retinal hemorrhages, consistent with non-accidental trauma,hours of well-documented accidental pediatric head injury and were identified (Table 1). This patient was one of three in thisto discuss the prognostic and medicolegal implications of these series investigated by our child protection team. On the basis offindings. corroborating eyewitness accounts, it was concluded that the injury was genuinely the result of a fall as described by the PATIENTS AND METHODS family. In another patient, there were bilateral retinal infarcts, which are not typical of non-accidental injury. In the third British Columbia’s Children’s Hospital is a tertiary referral patient, funduscopy was normal.center for pediatric head trauma, with a catchment area includ- All five initial CT scans demonstrated diffuse, obvious, cere-ing approximately 4.2 million residents of British Columbia, bral hemisphere hypodensity, and, in some scans, there wereCanada. This is a retrospective review of a series of children hypodensities in more-central structures, such as the basal gan-treated at British Columbia’s Children’s Hospital and identified glia and/or the brainstem (Table 2). All five patients had tento-as having early CT scan hypodensities after accidental head rial and/or interhemispheric acute subdural blood. In twoinjury. The medical records of these patients were reviewed to patients, there were acute convexity subdural hematomas, bothreconfirm the timing and accidental nature of the injury. All of which were of mixed density; a right frontoparietal convex-information in the medical record, including ambulance ity hematoma, 7 mm in maximal thickness, and a right frontalreports, emergency department reports, medical and nurses hematoma, 7 mm in maximal thickness. All five initial CT scansnotes, as well as any social worker notes and discharge sum- showed evidence of brain swelling with basal cistern efface-maries were reviewed. The time of injury was estimated from ment, and four of the five scans showed complete obliterationthese records and only patients with well-corroborated trauma of the basal cisterns. Only one of five patients had a cranial frac-histories were included in this review. The timing and find- ture. The distributions of the hypodensities on the initial CTings on the CT scans performed after the trauma were ascer- scan are presented in Table 2. Representative early CT scantained with the assistance of a pediatric neuroradiologist (KP). images of each patient are shown in Figure 1.The clinical course of the patients and the results of any addi- In Patients 2 and 4 (Table 1), carotid Doppler ultrasound per-tional radiological investigations were also determined. The formed 18 and 8 hours, respectively, after injury demonstratedstudy was approved by the Ethics Committee of the University reversed diastolic flow. In Patient 3, an intracranial pressureof British Columbia and the Research Review Committee of monitor was inserted, which demonstrated pressures of greaterBritish Columbia’s Children’s Hospital. than 65 mmHg. In Patient 4, xenon-CT and magnetic resonance angiography at approximately 6.5 hours after injury confirmed RESULTS the absence of cerebral blood flow (CBF). A diffusion-weighted magnetic resonance imaging scan performed at the same time Five patients were identified with well-documented acciden- as the magnetic resonance angiography showed markedtal head trauma and early posttraumatic hypodensities; all restriction of diffusion in the cerebral hemispheres. In Patient 5,were noted on CT scans performed less than 5 hours after the a craniotomy was performed to evacuate a 1-cm-thick cerebralinjury. In three of the five patients, the possibility of non- convexity acute subdural hematoma, and postoperativeaccidental inflicted injury had been raised because of the CT intracranial pressure monitoring demonstrated an intracranialscan findings and the child protection team had investigated pressure of greater than 40 mmHg.the circumstances of the injury. In all cases, there was incontro- Autopsies were performed in two patients (Patients 2 andvertible evidence that the injury was a bona fide accident. The 4). In both patients, there was marked cerebral edema withdemographic data, mechanism of injury, initial Glasgow Coma uncal and tonsillar herniation. In Patient 2, there was a thinScale (GCS) score, pupillary reaction at initial assessment, CT subdural hematoma, with an associated contusion and lacera-scan findings, and outcome are summarized in Table 1. All five tion of the right cerebral hemisphere, diffuse subarachnoidpatients had severe blunt head injuries and were immediately blood, and diffuse hypoxic-ischemic changes, with no definiteunconscious, with a GCS score of less than 8. The age range histopathological evidence of acceleration/deceleration brainwas 4 months to 14 years; four of the five patients were injury. No abnormalities were noted in the brainstem. Inyounger than 2 years of age at the time of injury. There were Patient 4, there were thin diffuse subdural hemorrhages overtwo girls and three boys. The mechanism of injury was a fall in the cerebral hemispheres and neuroaxonal spheroids at the cer-three cases, one of which was from a moving vehicle, a motor vicomedullary junction, but not in the remainder of the brain,690 | VOLUME 60 | NUMBER 4 | APRIL 2007 www.neurosurgery-online.com
  3. 3. COMPUTED TOMOGRAPHIC SCAN HYPODENSITIES AFTER HEAD INJURY TABLE 1. Patient summarya Patient no. Age/sex Mechanism GCS Pupils Funduscopy CT scan Outcome 1 4 mo/F MVC 3 2 fixed Not performed 3.5 hr: SAH, IVH, tentorial Ͻ24 hr: brain death ASDH, PH 2 7 mo/M Fall down stairs 3 1 fixed Bilateral retinal and 2 hr: falx, tentorial and con- Ͻ24 hr: brain death preretinal hemorrhages vexity ASDH, mild IVH, PH 3 14 yr/M Bike accident 4 2 fixed Not performed 4.5 hr: DAI, mild falx ASDH, Ͻ36 hr: brain death mild SAH, mild IVH, PH 4 12 mo/F Fall from fast 5 2 fixed Bilateral retinal infarcts 3.5 hr: mild SAH, mild falx Ͻ24 hr: brain death moving hay wagon and tentorial ASDH, PH 5 2 yr/M Fall from stool 4 2 fixed Normal 1 hr: tentorial and convexity 48 hr: death ASDH, PHa GCS, Glasgow coma scale; CT, computed tomographic; MVC, motor vehicle collision; SAH, subarachnoid hemorrhage; IVH, intraventricular hemorrhage; ASDH, subduralhematoma; PH, parenchymal hypodensities; DAI, diffuse axonal injury.and extensive bilateral retinal hemorrhages. The vertebral andcarotid arteries were normal. TABLE 2. Distribution of low densities on initial computed tomographic scana DISCUSSION Patient Bilateral Lentiform Brain- Cere- cerebral Thalamus Caudate no. nucleus stem bellum The patients reported in this study all experienced acciden- hemispherestal severe traumatic brain injuries, characterized on CT scans 1 ϩ ϩwithin 5 hours by severe diffuse brain swelling and parenchy- 2 ϩ ϩmal hypodensities and resulting in rapid brain death. The 3 ϩ ϩ ϩ ϩmechanisms of injury varied from a relatively mild type of 4 ϩ ϩ ϩ ϩtrauma, a fall from a stool, to a high-energy impact, a motor 5 ϩ ϩ ϩvehicle collision. There was nothing special regarding the a ϩ, hypodensity was present in that anatomical location.mechanism of injury in any of the patients that would havesuggested the rapid progression to death that occurred there-after. The patients in this study did not necessarily experience hypodensity of the gray matter, but the authors did not com-severe diffuse axonal injury because neither of the two autop- ment specifically regarding hypodensities.sied brains showed evidence of acceleration and deceleration Early CT scan hypodensities after head injury have beeninjury in the cerebral hemispheres. demonstrated previously in non-accidental injuries (8–10, 15). It is well documented that diffuse brain swelling can be iden- However, only Dias et al. (9) tried to time the first CT scantified on CT scans performed within hours of a severe trau- after the injury; in their report, parenchymal CT scan hypo-matic brain injury in both children and adults (1, 5, 12, 18). densities were noted on scans performed an average of 3.2However, the establishment of early and extensive hypo- hours after the “suspected” time of the injury. The authors trieddensities in association with the brain swelling after well- to pinpoint the time of the injury but, in some cases, had to datedocumented accidental pediatric head injury, as noted in the the injury to the time of “an apneic spell, seizure, abrupt coma,cases presented in this series, is, to our knowledge, a novel or other significant and immediate event,” which might notobservation in the literature. represent the precise timing of the actual injury itself. In the The radiological diagnosis of diffuse brain swelling after cases reported herein, the injuries were accidental and the timetrauma has typically been based on the findings of obliterated of injury was precisely documented.or compressed basal cisterns, with or without small lateral and The CT scan hypodensities in our cases were diffuse, severe,third ventricles, in the absence of significant midline shift (Ͻ3–6 and very obvious. The hypodensities affected primarily themm, depending on the study) or significant intracranial focal cerebral hemispheres (Table 2), which were uniformly hypo-mass lesion (1, 12). In one study by Willman et al. (18), “poor dense, and the findings were similar to the cases described bygray-white differentiation” was also included as one of the CT Han et al. (11) as having the so-called “reversal sign.” Han et al.scan criteria of brain swelling. None of the studies included used the term reversal sign to indicate diffuse cerebral edemacomments regarding the presence of hypodensities on the CT on CT scan, with decreased density of the cortical gray andscans in the patients with a diagnosis of early diffuse brain white matter, and relatively increased density of the thalami,swelling. It can be argued that the presence of poor gray-white brainstem, and cerebellum. In their study, there were eight chil-differentiation, as in the study by Willman et al. (18), implies dren with the reversal sign present at the time of the first CTNEUROSURGERY VOLUME 60 | NUMBER 4 | APRIL 2007 | 691
  4. 4. STEINBOK ET AL. to the occurrence of the reversal sign in the list of parenchymal A B abnormalities among the 15 patients with well-defined times of the initial CT scan relative to the injury. However, they note in their discussion that “among infants with the reversal sign, 50% were evident on the initial scans performed an average of 3.5 hours after the injury was reported.” The findings in our patients with accidental head injury support the contention of Dias et al. (9) with respect to the abused child, namely that hypodensities may not take 6 to 48 hours to develop. In our series, there was no doubt regarding the accidental nature or the timing of the trauma and all patients had extensive cerebral hemisphere hypodensity, similar to the reversal sign, between 1 and 5 hours after the head injury. C D The pathophysiology of the parenchymal hypodensities noted in the children in this series is not clear. These CT scan findings indicate the presence of cerebral edema, as was iden- tified in the two patients who had autopsies. However, the pathophysiology of such extensive edema within hours of the trauma is not clear. In the series by Han et al. (11) of children with reversal sign, when trauma was the etiology, child abuse was the most common cause. The authors opined that in this group of children with abuse, the posttraumatic reversal sign may have been the result of repeated trauma to the brain, resulting in repeated “edema induced hypoperfusion of the brain, in turn resulting in stress induced hyperglycemic cere- bral patterns of anoxic injury.” However, in our series, repeated E traumatic brain injury cannot be implicated.FIGURE 1. A, Patient 1, CT scan Acute posttraumatic diffuse brain swelling without cerebralobtained 3.5 hours after injury in a hypodensities has been attributed to cerebral vascular engorge-motor vehicle collision. B, Patient 2, ment secondary to hyperemia, on the basis of the initial reportCT scan obtained 2 hours after a fall of Bruce et al. (7) on so-called “malignant brain swelling” indown stairs. C, Patient 3, CT scan children. Studies that are more recent, with CT scan dynamicobtained 4.5 hours after a fall off a scanning (19) and CT scan xenon assessment of CBF within afast-moving bicycle. D, Patient 4, CT few hours of head injury, have indicated that, in the most severescan obtained 3.5 hours after a fall offof a fast-moving wagon during a hay brain injuries, decreased CBF, sometimes to ischemic levels,ride. E, Patient 5, CT scan obtained 1 rather than cerebral hyperemia may be present (4, 5, 14). Onhour after a fall from a stool. serial CBF measurements, the decreased CBF may be replaced by cerebral hyperemia after 24 hours (4, 5, 14); thus, if CBF is not measured within hours of the injury, the period of decreased CBF may be missed. It may, therefore, be that the reduced CBF,scan after admission; of these, two had an accidental head which can occur early after trauma, is enough to cause ischemiainjury and three were thought to have experienced child abuse. and infarction in some patients. This could, in turn, lead to rap-In these patients with an acute reversal sign, the time of the idly apparent low densities and swelling on CT scans.scan relative to the time of the injury was not reported. In the One of the concerns with the proposition that the hypoden-study by Dias et al. (9), in which a concerted attempt was made sities in our cases were caused by ischemia is that the timeto time the CT scan abnormalities in infants after non-acciden- course of such extensive low densities, as noted in our patients,tal head injury, there were 15 patients out of a total of 33 in is not in keeping with the CT scan findings observed afterwhom the authors thought that the time of the alleged abuse known ischemic events. For example, CT scan hypodensitiescould be pinpointed. Six of these 15 patients had parenchymal are usually not observed for the first 12 hours after neonatalhypodensities on a CT scan performed an average of 3.2 hours asphyxial injures (3) and become more obvious and extensiveafter injury. The extent of the hypodensities in these six patients during a 72-hour time course (13). Similarly, in typical cere-was not reported but they were not extensive enough to be brovascular accidents in adults, CT scan hypodensities are dif-categorized as showing the reversal sign because those authors ficult to identify until at least 6 hours (16). Indeed, for entry intoindicated the presence of the reversal sign as a separate cate- one multicenter trial for stroke, CT scan evidence of thegory. In their results, Dias et al. (9) noted that six patients exhib- ischemic event within 6 hours of a clinical middle cerebralited the reversal sign on CT scans but they make no reference artery territory stroke included loss of density contrast of the692 | VOLUME 60 | NUMBER 4 | APRIL 2007 www.neurosurgery-online.com
  5. 5. COMPUTED TOMOGRAPHIC SCAN HYPODENSITIES AFTER HEAD INJURYlentiform nucleus and/or the insular ribbon and hemispheric accidentally inflicted injury was queried and the child protec-sulcus effacement (2) but not hypodensity. tion team was asked to investigate because the CT scan find- In support of the hypothesis that ischemia may be the cause ings of severe low density changes were thought to be incom-of the early hypodensities observed in our patients, there is patible with the time of the injury as indicated in the historyevidence that, in the most severe ischemic situations, CT scan taken at the time of arrival to the hospital. The case series ofhypodensities may be present earlier than in typical cases. Our children with non-accidentally inflicted head injury reported bypatients, all of whom died, certainly qualify for being in that Dias et al. (9) and this case series of children with accidentalmost severely affected group. In the study of hypoxic ischemic head injury indicate that the traditional expectation regardingterm neonates by Lupton et al. (13), the most severely involved the timing of onset of CT scan brain hypodensities after headchildren had patchy CT scan hypodensities on the first day of trauma may not always be correct. We think the usual expectedlife, although the specific time in hours was not reported. In evolution of low densities on CT scan is still what one wouldaddition, they had evidence of intracranial hypertension and observe in the vast majority of patients and that the five caseswent on to die or have poor outcomes. Furthermore, CT scan reported with early diffuse hypodensities are unusual. Hence,hypodensities have been described within 5 hours of proven a question regarding possible child abuse in some of our casesmiddle cerebral artery occlusions, and extensive hypodensities was, and still would be, appropriate. However, the knowledgeassociated with local brain swelling in the middle cerebral that obvious and diffuse intracerebral low densities on CT scanartery distribution predicted a fatal outcome (17). In two of can occur, albeit rarely, as early as 1 hour after a documentedour five patients, absent CBF was demonstrated, and it may be accidental head injury may have allayed some of the concernsthat extensive low densities on CT scan can occur rapidly, even regarding the possibility of non-accidental injury in these chil-as early as 1 hour after trauma, in special and unusual situa- dren. Furthermore, in cases of suspected non-accidental fataltions in which there is total ischemia with no blood flow into head injury in which the time of the head injury is not clear, thethe brain. If so, these findings may predict inevitable brain possibility of very early appearance of diffuse low densities ondeath, as occurred in all of the patients reported in this article. the CT scan has to be considered in the estimation of the tim-The outcomes of our patients are consistent with those reported ing of the severe head injury.by Han et al. (11), who noted that four out of eight children(five had head trauma) with acute reversal sign on CT scans CONCLUSIONSdied; the other four children had poor outcomes. The occurrence of acute obvious diffuse cerebral hypodensity We have presented five children with documented and well-is rare among head-injured patients, and, on the basis of the lack corroborated accidental head injuries in whom CT scans per-of reports in the literature, this is probably a rare phenomenon. formed between 1 and 5 hours after injury showed diffuse andIt is difficult to understand why these five patients developed obvious cerebral hemispheric hypodensity. These findings callthis problem. The mechanism of injury, which included a fall into question the commonly held opinion that such extensivedown stairs and a fall from a stool, was less severe than in many parenchymal hypodensities take at least 6 hours to appear afterother head-injured patients. Nonetheless, all patients clearly head trauma. This may be of medicolegal importance in discus-experienced a severe brain injury with immediate coma and a sions regarding the timing of head injuries in children. It ispoor GCS score and went on to die rapidly. It was somewhat important to recognize that, in our series, diffuse early hypo-unexpected that, in the two autopsied patients, despite the densities on CT scan were associated with a severe traumaticapparent clinical severity of the brain injury, neither showed brain injury, immediate unconsciousness that never resolved,histopathological evidence of diffuse axonal injury and one had and rapid brain death in all patients. It is inappropriate to gen-findings of axonal injury limited to the cervicomedullary junc- eralize the findings of this case series to patients who are nottion. It would be interesting to elucidate the factors that may unconscious immediately after a head injury, who regain con-have precipitated the disastrous outcome in these children. sciousness after an injury before deteriorating, or who do not The findings in this study of extensive CT scan intracerebral progress rapidly to brain death.hypodensities within 5 hours of a well-documented head injuryare of medicolegal significance, particularly in the pediatric REFERENCESpopulation. Our experience and that of others, such as Diaset al. (9), are that, generally, CT scan intracerebral low densities 1. Aldrich EF, Eisenberg HM, Saydjari C, Luerssen TG, Foulkes MA, Jane JA,take at least 6 hours (some think 24 h) to become apparent after Marshall LF, Marmarou A, Young HF: Diffuse brain swelling in severely head-injured children. A report from the NIH Traumatic Coma Data Bank. Ja traumatic brain injury. The low densities are expected to Neurosurg 76:450–454, 1992.become progressively more obvious during the next 3 to 5 days 2. Anonymous: Thrombolytic therapy with streptokinase in acute ischemicand then regress during the subsequent few days. The time stroke. The Multicenter Acute Stroke Trial—Europe Study Group. N Engl Jcourse of evolution of such changes on CT scans may be used Med 335:145–150, 1996.as one of the criteria in determining the approximate time of a 3. Barkovich AJ, Sargent SK: Profound asphyxia in the premature infant: Imaging findings. AJNR Am J Neuroradiol 16:1837–1846, 1995.head injury when the provided history is thought to be inaccu- 4. Bouma GJ, Muizelaar JP, Choi SC, Newlon PG, Young HF: Cerebral circula-rate, as might be the case in non-accidentally inflicted injuries. tion and metabolism after severe traumatic brain injury: The elusive role ofIndeed, in three of the five cases presented in this series, non- ischemia. J Neurosurg 75:685–693, 1991.NEUROSURGERY VOLUME 60 | NUMBER 4 | APRIL 2007 | 693
  6. 6. STEINBOK ET AL. 5. Bouma GJ, Muizelaar JP, Stringer WA, Choi SC, Fatouros P, Young HF: Ultra- versally poor prognosis, and, in this series, all of the patients died. early evaluation of regional cerebral blood flow in severely head-injured This is of value to the pediatric neurosurgeon, who must make a deci- patients using xenon-enhanced computerized tomography. J Neurosurg sion early on as to whether or not to perform aggressive measures 77:360–368, 1992. such as intracranial pressure monitoring or hemicraniectomy. 6. Brown JK, Minns RA: Non-accidental head injury, with particular reference to None of these children had spinal cord injury nor did they have whiplash shaking injury and medico-legal aspects. Dev Med Child Neurol 35:849–869, 1993. documented hypoxic or hypotensive episodes. Because these have been 7. Bruce DA, Alavi A, Bilaniuk L, Dolinskas C, Obrist W, Uzzell B: Diffuse cere- two of the more commonly proposed mechanisims of the “black brain” bral swelling following head injuries in children: The syndrome of “malig- on computed tomographic (CT) scan, the pathophysiology of this phe- nant brain edema.” J Neurosurg 54:170–178, 1981. nomenon remains a mystery. 8. Cohen RA, Kaufman RA, Myers PA, Towbin RB: Cranial computed tomogra- Leslie N. Sutton phy in the abused child with head injury. AJR Am J Roentgenol 146:97–102, Philadelphia, Pennsylvania 1986. 9. Dias MS, Backstrom J, Falk M, Li V: Serial radiography in the infant shaken impact syndrome. Pediatr Neurosurg 29:77–85, 1998. 1. Duhaime AC, Christian CW, Rorke LB, Zimmerman RA: Nonaccidental head10. Giangiacomo J, Khan JA, Levine C, Thompson VM: Sequential cranial com- injury in infants—The “shaken-baby syndrome.” N Engl J Med 338:1822–1929, puted tomography in infants with retinal hemorrhages. 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Willman KY, Bank DE, Senac M, Chadwick DL: Restricting the time of injury interrupt the cascade of events that eventually lead to neurological in fatal inflicted head injuries. Child Abuse Negl 21:929–940, 1997. decline. This study also underlines the likely future need for early and19. Yoshino E, Yamaki T, Higuchi T, Horikawa Y, Hirakawa K: Acute brain edema aggressive intervention to attenuate the postinjury pathophysiological in fatal head injury: Analysis by dynamic CT scanning. J Neurosurg events and the individual response of these patients. 63:830–839, 1985.20. Zimmerman RA, Bilaniuk LT: Pediatric head trauma. Neuroimaging Clin N P. David Adelson Am 4:349–366, 1994. Pittsburgh, Pennsylvania COMMENTS T his article highlights the early changes on CT scans that may occur after severe head trauma and appropriately points out that suchT his report describes five children who were found to have diffuse hemispheric low density within 5 hours of well documented acci-dental blunt head trauma. In the past, it has been more or less assumed changes may occur earlier than has been touted by timing pundits. The authors make an important point that the low attenuation changes cannot be used to establish that the onset of the damage had to occurthat this finding was diagnostic of child abuse and that it took 6 to 24 6 to 12 hours before the changes but that they may occur within 1 to 2hours to develop, although loss of the gray-white junction could be hours. Diffusion imaging and diffusion tensor magnetic resonanceseen earlier. imaging have established these facts. Now, in severe trauma cases, the This report is significant in several regards. The fact that all of these same has been established for CT scans.children had clear blunt trauma rather than shaking lends further sup-port to the hypothesis of impact being required to develop this clinico- Marvin Nelsonradiographic picture, as proposed by Duhaime (1). It is important that Pediatric Neuroradiologistthe finding of diffuse hemispheric low density is not diagnostic of Los Angeles, Californianonaccidental trauma, and this finding alone does not demand thisdiagnosis. The recognition that retinal hemorrhages are also not neces-sarily diagnostic of child abuse makes this diagnosis difficult at times.A thorough investigation of the circumstances of a childhood injury is T his study documents early hypodensity in accidental head injury in five children on CT scans obtained within 5 hours of the injury. The children were very young (< 2 yr of age), had evidence of veryneeded before accusations are made. Finally, this finding carries a uni- poor clinical grade (Glascow Coma Scale score, 3–5), and severely694 | VOLUME 60 | NUMBER 4 | APRIL 2007 www.neurosurgery-online.com
  7. 7. COMPUTED TOMOGRAPHIC SCAN HYPODENSITIES AFTER HEAD INJURYincreased intracranial pressure, and all died. The finding of “black” edema would be unusual. Early low density has also been reported incerebral hemispheres on CT scans is always an ominous sign and, as nonaccidental injury in which the timing issues are much harder tothe authors discuss, probably represents irreversible global cerebral document. When this issue was raised in this series, the patients wereischemia. Distinguishing this radiological finding from that seen after appropriately investigated by the child protection team.nonaccidental injury can be difficult. Two of the children were reportedto have fallen down stairs (and had retinal hemorrhages) or from a James M. Drakestool, both instances in which a rapidly fatal outcome with extensive Toronto, CanadaNEUROSURGERY VOLUME 60 | NUMBER 4 | APRIL 2007 | 695