Dr. waney squire shaken baby syndromee

  • 196 views
Uploaded on

 

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
    Be the first to like this
No Downloads

Views

Total Views
196
On Slideshare
0
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
0
Comments
0
Likes
0

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide

Transcript

  • 1. Shaken Baby Syndrome adult head injury in road traffic accidents. Following Guthkelch’s paper, the “shaken baby syndrome” has become widely accepted as a form of child abuse [1].IntroductionThe diagnosis “shaken baby syndrome” (SBS) has The Triad of Injuriesbeen widely accepted for over 30 years, but recent The three elements of the triad are encephalopathy,evidence from biomechanical and clinical observa- RH, and SDH.tional studies questions the validity of the syndrome. Retinal Hemorrhages (RHs)Definition RHs have been regarded as an important indicatorThe diagnosis of SBS is based on the clinical triad of inflicted injury, but many other causes of reti-of encephalopathy, retinal hemorrhage (RH), and nal bleeding are recognized in infants, for examplesubdural hemorrhage (SDH) in infants, usually under after normal birth, raised intracranial pressure, bloodsix months of age, who may die unexpectedly or dyscrasias, hemoglobinopathies, extracorporeal mem-survive with greater or lesser degrees of neurolog- brane oxygenation, cataract surgery, and accidentalical damage [1]. The term non-accidental head injury trauma [8]. Postmortem indirect ophthalmoscopy has(NAHI) has been preferred as it has no implications shown RHs to be more common after natural dis-for mechanism of injury. Other features often associ- ease and accidental injury than after inflicted injuryated include a sole carer at the time of collapse and [9]. These authors also noted that infants suspecteda clinical history that is incompatible with the sever- to have been abused were more likely to have oph-ity of the injuries. The diagnosis of inflicted injury thalmological examination in life than infants withbecomes less problematic if there is objective evi- accidental injuries or natural diseases. This bias read-dence of violence, such as bruises, fractures, or burns, ily distorts the true incidence of RH in non-accidentalbut objective evidence of trauma has not always been injury. Indeed Vinchon [10] noted in his study ofnecessary in making the diagnosis. infant head injury that “In the construct of our study Central to the assessment of these cases is whether we could not obviate the circularity bias, and the eval-the triad of findings can be regarded as diagnostic uation of the incidence of RH in child abuse remains aof abuse with any degree of certainty. This review self-fulfilling prophecy”. These authors did, however,examines the evidence base for each element of suggest that the extent and nature of retinal bleedsthe triad and the current biomechanical evidence may be more important as indicators of inflicted headregarding mechanisms of infant head injury and its injury than their existence per se [10].pathological investigation. The main hypotheses for genesis of RH are that it is the result of venous obstruction, which in turn may result from compression of the optic nerveHistory by raised intracranial or intravascular pressure, even transiently, or that the tissues of the retina are tornSDH has been associated with child abuse since the during the act of shaking. This latter hypothesis doesmid-19th century [2]. Kempe described SDH with not withstand biomechanical scrutiny [11].multiple skeletal injuries and bruises as the bat-tered child syndrome and Caffey described long bone Encephalopathyfractures and SDH [3–5], but it is Guthkelch [6]who developed the hypothesis that the whiplash–like This term may be widely interpreted to include amovements during shaking cause the characteristic range of clinical manifestations from feeding dif-bilateral thin film SDH of the syndrome. He based ficulties, vomiting, and sleepiness to seizures andhis hypothesis, that shaking causes tearing of the fulminating cerebral edema.cerebral bridging veins leading to SDH, on the biome- The specific neuropathological features of trau-chanical studies of Ommaya [7] who was researching matic brain injury are contusions and traumatic
  • 2. 2 Shaken Baby Syndrome (a) (b)Figure 1 (a) Acute axonal injury. Bands of BAPP expression in an infarcted area of brain in acute hypoxic-ischemicinjury. (b) Axonal swellings expressing BAPP restricted to the pontine cortico-spinal tracts, considered to indicate traumaticdamageaxonal injury. Hypoxic-ischemic injury and brain injury due to the specific intracranial pathophysiologyswelling are frequently seen but are not specific for before the skull bones fuse [19].trauma. Contusions are very uncommon in infant Damage to the cervical nerve roots has beenbrain trauma in the absence of skull fractures. Identifi- documented as part of the pathology of shaking injurycation of axonal injury now depends on the immuno- [14]. It has not been established that this is the resultcytochemical demonstration of beta amyloid precur- of shaking, as cervical cord displacement resultingsor protein (BAPP). This is a very sensitive marker of from brain swelling may also cause traction on nerveinterruption of normal axonal flow but may be upreg- roots in the region. Autopsy studies in man andulated after hypoxic–ischemic injury and metabolic primates have shown that the spinal cord is displaceddisruption as well as trauma (Figure 1). Distinction during extension and flexion of the neck [20, 21]of traumatic axonal expression of BAPP from other and it remains a possibility that hyperextension and flexion could cause traction damage to nerve rootscauses is fraught with difficulty, and depends in part throughout the length of the spinal cord, but this hason its distribution [12], [13], [14]. Neuropathological not been documented in living infants.studies have shown that in babies who die followingNAHI, the underlying brain pathology is widespreadhypoxic-ischemic injury and not diffuse traumatic Subdural Hemorrhage (SDH)axonal injury as previously believed [12, 13]. In this SDH is perhaps the most important and consistentseries axonal injury was seen in a limited distribu- component of the triad. In the acutely sick infant, ittion in the lower brainstem and in only a minority is frequently the first clinical sign, identified on brainof cases. Radiological studies have confirmed these scan, to raise the question of abuse. There are nopathological observations [15]. specific imaging patterns that can distinguish inflicted This observation is important as traumatic axonal from accidental intracranial injury [22, 23].injury will lead to immediate loss of function causing Autopsy and imaging studies show that infantclinical symptoms from the time of trauma. In SDH is usually a thin bilateral film and not a thick,contrast, hypoxic-ischemic injury and ensuing brain unilateral space occupying clot as seen in traumaticswelling take variable periods of time to develop SDH in older children and adults [12, 13, 24]. Thisand a baby so damaged may not show immediate raises the question of whether the two forms have thesymptoms. Even fatal brain trauma may present with same etiology and anatomical source.a lucid interval between injury and clinical collapse[16, 17]. Lucid intervals are more frequently seen Causes of Subdural Hemorrhage. The common-in infants less than two years of age [18], reflecting est cause of SDH in infants is said to be traumathe very different responses of the infant brain to [25] although a recent study has shown a significant
  • 3. Shaken Baby Syndrome 3incidence (26%) of birth-related SDH [26]. Other intracranial damage including retinal and intracranialcauses in infants include benign enlargement of hemorrhage after falls from levels as low as 3 ft [10,the extracerebral spaces (BEECS), clotting disorders, 17, 30–33]. While most babies may suffer little fromhemorrhagic disease of the newborn, rare metabolic an apparently trivial fall, this is clearly not alwaysdiseases, vascular malformations, and neurosurgical the case.procedures [25, 27]. Birth-Related SDHTraumatic SDH Three studies, using magnetic resonance imagingProposed traumatic causes of infant SDH are inflicted (MRI), have shown a surprisingly high incidenceinjury such as shaking and/or impact and accidental of SDH after birth in asymptomatic infants. Whitbyinjuries such as falls. Impact includes blunt impact of identified SDH in the first two days of life in 9%an object on the head and that resulting from a fall [32], while SDH was seen in up to 46% of otherwiseor striking the moving head on a rigid surface. The normal neonates using higher resolution MRI scan-biomechanical aspects of these injuries are discussed ning [26, 34]. With regard to method of delivery,below. The vast majority of cases described as SBS ventouse or instrumental deliveries have been asso-have evidence of impact [28]. While the pathologist ciated with a higher incidence of intracranial injurymay be able to determine features indicative of [35, 36]. Towner [37] found an increased incidenceimpact, it is not, of course, possible to distinguish of intracranial hemorrhage after instrumental deliveryaccidental from non-accidental injuries by pathology. with ventouse or forceps and emergency caesarean section, but the incidence was lower after caesareanLow-Level Falls section before labor had begun. However, it shouldLow-level falls have the potential, albeit only rarely, be noted that all of Looney’s cases followed normalto cause SDH in infants and young children. Absolute vaginal delivery [26].height is not as important a criterion for injury as While neonates with SDH may be asymptomaticthe exact nature of the fall for a particular infant, [26, 35] they may also have signs in the neonatalin a particular circumstance [29]. The effects of period including unexplained apnoea, dusky episodes,twisting, rotation, or crushing of the structures of the hypotonia, seizures, and lethargy [38].neck are crucial in terms of outcome. Biomechanicalstudies show that falls even from low levels of Sources of SDH. Traditional belief is that in SBS3–4 ft can generate far greater forces in the head the SDH results from tearing of the superficial bridg-than shaking [11]. There are a number of case series ing veins as they cross from the brain to the duraldemonstrating that infants and children may suffer sinuses [6] (Figure 2). This has never been proved.Figure 2 Infant bridging veins may be visualized by opening the skull very carefully, but they are readily torn in normalautopsy procedures. (Picture courtesy of Dr P. Lantz)
  • 4. 4 Shaken Baby SyndromeIndeed it is very difficult to find documented evidence alternative sites of origin exist, the dura itself andof torn bridging veins at surgery or at autopsy. Cush- the old subdural membranes (Figure 4).ing, who operated on neonates with SDH and sub-sequently performed the autopsies wrote “In two of Dural Hemorrhagethe cases I have examined I have satisfied myself that The dura is composed of two leaflets, the periostealsuch ruptures were present. A positive statement, how- and the meningeal dura, separated by a thin vascularever, cannot be given even for these cases, since the channel, which widens to form the large dural sinusesdissection and exposure, difficult enough under any [44]. There are particularly extensive venous sinusescircumstances, owing to the delicacy of the vessels is in the posterior falx, [45] a frequent site of high signalthe more so when they are obscured by extravasated on brain scans in asphyxiated infants. Bleeding intoblood” [39]. More recently Maxeiner [40] addressed the falx is well recognized in asphyxiated infantsthe problem by injecting radio-opaque dye into the [46]. It has long been acknowledged that opticveins at autopsy to assess their integrity after remov- nerve sheath hemorrhage arises from the dura [47]ing the top of the head in one piece, hard-boiled egg and more recently the dura was proposed as the source of intracranial SDH in infants [48] (Figure 5).style. This approach is not widely used as it destroys Careful microscopic examination of the dura confirmsmuch of the brain and injection pressures need to be that intradural bleeding is common in asphyxiatedcarefully monitored if the veins are not to be ruptured infants, particularly in the dural folds of the falx andartifactually. tentorium close to the large venous sinuses [49]. In Volpe [41] said that SDH was by no means some cases intradural bleeding leaks out on to thealways traumatic and suggested that in neonates subdural surface leading to macroscopically evidentwithout tentorial tears the bleeding may arise from subdural haematoma [50].the tributary veins of the dural sinuses. Autopsystudies from the older literature show bridging vein Healing Subdural Membranesrupture is uncommon, Craig described 62 neonatal Healing of SDH is by formation of a thin, vascu-SDH, of which only 3 had torn bridging veins, lar membrane consisting of fibroblasts, macrophages,all of those with overriding sutures [42]. Larroche which often contain altered blood products, and widedescribed 700 autopsies 18% with SDH. [43] She thin-walled capillaries with a potential to rebleednoted an association with hypoxic-ischemic injury [51] (Figure 6). It is uncommon in infants to see a(Figure 3). She did not identify torn veins. double layered membrane around a localized mass If SDH does not arise from torn bridging veins, of resolving clot, as seen in the elderly, probablywhat other sources may there be? Two obvious because the infant SDH usually forms as a thin filmFigure 3 Fresh subdural blood seen after birth asphyxia. (Picture courtesy of Dr I. Scheimberg)
  • 5. Shaken Baby Syndrome 5 Arachnoid Superior sagittal sinus Intradural fluid channel granulation Lateral lacuna of sagittal sinus Dura Inner dural plexus Subarachnoid space Cortical draining vein Arachnoid barrier membrane FalxFigure 4 Diagram representing a coronal slice through the brain and dura indicating the intradural sinuses and theirrelationship to cortical surface veins, arachnoid granulations, and intradural fluid channels (a) (b)Figure 5 (a) The dura is thickened and congested and there is patchy subarachnoid and subdural blood. Autopsy 44 hafter collapse following choking episode. (Courtesy of Dr I. Sheimberg.) (b) H & E stained section of falx showing it tobe destroyed by massive acute bleedingrather than as a mass lesion. Contrast injection is and be influenced by the method of treatment ofrequired to identify the membranes radiologically the acute hematoma. Surgical evacuation or tap-[52]. In some cases, acute SDH leads to accumu- ping may prevent later reaccumulation of fluid [53,lation of fluid in the subdural space. The reasons 54]. The period of time for redevelopment of sub-for this are unknown. Fluid collections may result dural fluid collections may be long, between 15from immaturity of the arachnoid granulations and and 111 days [55]. It is likely that an importantimpaired cerebrospinal fluid (CSF) absorption [22], contribution to chronic subdural fluid accumulation is
  • 6. 6 Shaken Baby Syndrome (a) (b) (c)Figure 6 (a) Dural surface showing a very thin yellow-brown membrane, which has partly lifted during removal of thebrain. Head injury four weeks prior to death. (b) H & E stained section of acute bleed overlying a chronic membrane, whichconsists of some six layers of fibroblasts between which are macrophages and new capillaries (three days after collapsewith acute SDH) (c) Same section stained with CD34 to show endothelial cells. Note capillaries growing into the fresh clotrepeated rebleeding and oozing from a chronic sub- Distribution. In the first few days after bleeding,dural membrane [56, 57]. subdural blood sediments under the influence of There is little information regarding the potential gravity and undergoes secondary redistribution to thefor birth-related SDH to evolve into chronic fluid most dependent part, the posterior falx and tentoriumcollections. Whitby followed nine cases with a repeat [59]. Radiological studies show that subdural bloodscan at one month; none had developed a chronic tracks down around the spinal cord [60] and, if thecollection [35]. Rooks followed 18 cases for up to 3 spine of babies with intracranial SDH is examined atmonths, one developed a further subdural bleed [34]. autopsy, blood is regularly seen in the subdural spaceHowever these studies could not identify membranes and around sacral nerve roots in the most dependentas contrast was not used. Chronic membranes have parts of the dural sac (Figure 7).been seen at autopsy in up to 31% of infants dyingunexpectedly without previous clinical evidence ofchronic SDH [58]. In view of the potential for acute Differential Diagnosis of SBSaccidental SDH to evolve into a chronic collectionseveral months later [55], it would appear likely that The most common causes of the triad are impact,the same pattern would follow birth-related SDH. At birth-related SDH, BEECS, coagulopathies, apnoea,this time, we simply have insufficient information. asphyxia and choking, acute life-threatening events
  • 7. Shaken Baby Syndrome 7 (a) (b)Figure 7 (a) A collection of fresh subdural blood at the dorsal aspect of the sacral spinal cord. Baby died within hoursof inflicted abdominal injury with acute and chronic subdural hemorrhage. (b) Microscope section showing an ellipticalcollection of fresh blood dorsal to the spinal cord. The blood is within a chronic subdural membrane indicated by the ironpigment, stained here by Perl’s stain. Baby died three weeks after traumatic subdural hemorrhage(ALTEs), osteogenesis imperfecta, osteopenia of Biomechanicsprematurity, and metabolic diseases [14, 28, 61,62, 63]. Biomechanics is the application of principles of physics to biological systems and has been the main- stay of research into motor vehicle safety for sixChoking/Asphyxia decades. It was just such research into noncontact head injury from rear-end shunts that stimulatedIn a considerable number of cases, vomiting and/or Guthkelch to formulate his hypothesis for SBS inreflux are described at the time of collapse, and 1971 [6]. Ommaya [7] had caused concussion, SDH,in some there is a history of feeding difficulties, and white matter shearing injury (diffuse axonalgastroesophageal reflux, and choking or apnoeic injury) in primates by whiplash. Guthkelch suggestedepisodes [14, 62]. SBS is commonly diagnosed in the that the rotational forces of shaking would causefirst three months of life, the age of peak incidence of tearing of bridging veins and bilateral subdural bleed-sudden infant death syndrome. Inhalation of feed or ing, although Ommaya himself warned that “It isvomit may play a part in sudden infant death [64] and improbable that the high speed and severity of theawake apnoea is associated with gastroesophageal single whiplash produced in our animal model couldreflux [65]. The physiological response to aspiration be achieved by a single manual shake or even a shortmay be dramatic; foreign material on the larynx series of manual shaking of an infant in one episode”.causes laryngospasm, which is associated with startle, More recent studies using “crash test dummies”cessation of respiration, hypoxaemia, bradycardia, indicate that impact generates far more force thanand a doubling of blood flow to the brain [66]. shaking (Figure 9) and that impact is required toThese circumstances, with or even without vigorous produce SDH [68]. Cory and Jones [69] generatedresuscitation, may cause reperfusion injury and a pre- forces that exceeded the injury threshold for concus-existing healing subdural membrane may bleed. The sion, but not for SDH or axonal injury. Their adultdura itself may become hemorrhagic and ooze blood shaker volunteers fatigued after 10 seconds. Whileinto the subdural space (Figure 8). As long ago as they concluded that “It cannot be categorically stated,1905, Cushing suggested that coughing, choking, and from a biomechanical perspective, that pure shak-venous congestion may explain some forms of infant ing cannot cause fatal head injuries in an infant”,SDH [39], a hypothesis recently revived by Geddes, they noted that in their experiments there were chin[48, 67]. and occipital contacts at the extremes of the shaking
  • 8. 8 Shaken Baby Syndrome (a) (b)Figure 8 (a) Cortical vein thrombosis. Infant died 10 days after collapse following two choking episodes. Several surfaceveins are thrombosed (arrows). (b) Section of thrombosed vein shows a network of new capillaries growing into theperiphery of the thrombus (CD31) Peak head acceleration (g) 125 100 From adult male’s arms 76.2 cm Inflicted slamming style impacts onto 75 surfaces noted 50.8 cm Bed – mattress Leather sofa 50 25.4 cm 25 Free fall impacts onto carpeted stairs (fall heights noted) 0Figure 9 Comparative forces generated by dropping or shaking and slamming a dummy representing a six-month-oldinfant (C Van Ee, personal communication 2007)motion that could have caused impact. These authors It is likely that the forces required to cause intracra-expressed their concerns regarding the difficulties in nial injury will also damage the weak infant neckextrapolating to human infants the findings in both [71]. In road traffic accidents, infants who suffer sin-dummy and animal models. Biomechanical studies gle severe hyperextension forces have cervical frac-have shown that falls and impact to the head pro- tures, dislocations, spinal cord injury, and torn nerveduce significant rotational forces when the impacting roots, not SDH [72–74].forces are not aligned through the center of gravityof the head, due to hinging of the head on the Investigation of Shaken Baby Syndromeneck. Shaking is not necessary to cause rotationalacceleration. SBS or NAHI is most likely to occur in an infant Neck injuries may be underreported in babies dying suddenly under the age of six months. Autopsydying after severe abuse [70]. In Ommaya’s study, should be performed with careful consideration of11 of 19 primates had neck injuries; these were adult this diagnosis and appropriate steps taken to supportanimals with mature neck structure and musculature. or exclude it. The records of pregnancy and delivery
  • 9. Shaken Baby Syndrome 9must be carefully studied to look for any evidence of evidence of intradural bleeding and rupture ontocomplications that could mimic NAHI. These include the subdural surface. This may be the source ofpregnancy disorders such as oligohydramnios, fetal significant subdural blood.hypokinesia, and prematurity, which lead to osteope- The brain must be fixed for detailed histologicalnia and predispose to fractures. The birth history and examination.method of delivery are important as SDH may arise In all of these cases, the time between collapseat this time while being entirely asymptomatic in and death may play a significant part in the finalthe neonatal period. Head circumference charts are pathology. A baby who has collapsed and becomesimportant; head circumference measurements taken at apnoeic with subsequent cardiopulmonary rescusci-birth and in the subsequent weeks may reflect abnor- tation (CPR) and ventilation will be shocked andmal head growth, which can indicate an accumulating suffer multiorgan failure with altered clotting, losssubdural fluid collection and a propensity to rebleed. of integrity of vessels and membranes, oozing of The clinical history may give clues to other prob- blood into intracranial compartments, including thelems in the early weeks of life. Vomiting, feeding subarachnoid and subdural spaces, and developmentproblems, and apnoeic episodes and ALTEs may of the “respirator brain”.indicate difficulties with coordination of breathing, Review of the brain imaging in life is essentialsucking and swallowing, and vulnerability to chok- in assessing, as far as possible, just how muching. Any event that threatens life may also potentially hemorrhage occurred at the time of collapse and howend it. much may be the result of subsequent secondary The history of the baby’s terminal collapse must changes. It is recognized that SDH may continue toalso be carefully examined. Parents may describe bleed after initial onset [75] especially if a baby isevents that reveal a cause for collapse. In any other very sick. Finding a large clot at autopsy may suggestfield of medicine, the clinical history is regarded as traumatic rupture of a large vessel, but comparisonthe cornerstone of diagnosis and it should not be with early brain scans may indicate that the bleed wasdisregarded without serious critical evaluation. only minor at the outset, indicating a slower oozing The autopsy can reveal evidence of trauma such process with different implications for causation. Itas deep bruises and fractures not seen in clinical is becoming increasingly obvious that not all SDHexamination. The examination of the intracranial arises from traumatic rupture of blood vessels.contents is paramount. The scalp and skull requirecareful examination for evidence of bruising and Acknowledgmentfractures. Suture separation due to raised intracranialpressure and wormian bones can be mistaken for I would like to thank Dr Irene Scheimberg and Dr Pat Lantzfractures. When the cranium is opened, the presence for providing pictures and Dr Chris Van Ee for valuableof any intracranial bleeding must be noted. Unclotted discussion and for preparing Figure 8.blood may escape from the subdural space as theskull is opened and be mistaken for bleeding from the Referencesdural sinuses. It is important to note the volume andnature of blood and the presence of xanthochromia, [1] American Academy of Pediatrics Committee on childindicating older bleeding. As the cranium is opened, abuse and neglect: shaken baby syndrome: inflictedthe bridging veins should be visualized and their cerebral trauma. (1993). Pediatrics 92(6), 872–875. [2] Tardieu, A. (1860). Etude medico-legale sur les sevicesintegrity assessed. If there is a question of bridging et mauvais traitements exerces sur des enfants.vein rupture, histological examination may assist in [3] Kempe, C.H., Silverman, F.N., Steele, B.F., Droege-establishing this. The dural sinuses and draining veins mueller, W. & Silver, H.K. (1962). The battered-childshould be examined for evidence of thrombosis. syndrome. JAMA 181, 17–24. The dura must be carefully examined for evidence [4] Caffey, J. (1972). On the theory and practice of shakingof older bleeding. A chronic subdural membrane may infants. Its potential residual effects of permanent brain damage and mental retardation. American Journal ofbe thin and patchy and represented only by patches Diseases of Children 124(2), 161–169.of light brown discoloration. Multiple samples should [5] Caffey, J. (1974). The whiplash shaken infant syndrome:be taken from the dura, including the falx and manual shaking by the extremities with whiplash-tentorium, for histological examination to look for induced intracranial and intraocular bleedings, linked
  • 10. 10 Shaken Baby Syndrome with residual permanent brain damage and mental retar- [22] Vinchon, M., Noizet, O., Defoort-Dhellemmes, S., Soto- dation. Pediatrics 54(4), 396–403. Ares, G. & Dhellemmes, P. (2002). Infantile subdural[6] Guthkelch, A.N. (1971). Infantile subdural haematoma hematomas due to traffic accidents. Pediatric Neuro- and its relationship to whiplash injuries. British Medical surgery 37(5), 245–253. Journal 2(759), 430–431. [23] Ewing-Cobbs, L., Prasad, M., Kramer, L., Louis, P.T.,[7] Ommaya, A.K., Faas, F. & Yarnell, P. (1968). Whiplash Baumgartner, J., Fletcher, J.M. & Alpert, B. (2000). injury and brain damage: an experimental study. JAMA Acute neuroradiologic findings in young children with 204(4), 285–289. inflicted or noninflicted traumatic brain injury. Child’s[8] Tongue, A.C. (2007). The ophthalmologist’s role in diag- Nervous System 16(1), 25–33. nosing child abuse. Ophthalmology 98(7), 1009–1010. [24] Duhaime, A.C., Christian, C.W., Rorke, L.B. & Zim-[9] Lantz, P.E. & Stanton, C.A. (2006). Postmortem detec- merman, R.A. (1998). Nonaccidental head injury in tion and evaluation of retinal hemorrhages. American infants–the “shaken-baby syndrome”. New England Academy of Forensic Science 271. Journal of Medicine 338(25), 1822–1829.[10] Vinchon, M., Defoort-Dhellemmes, S., Desurmont, M. [25] Kemp, A.M. (2002). Investigating subdural haemorrhage & Dhellemmes, P. (2005). Accidental and nonaccidental in infants. Archives of Disease in Childhood 86(2), head injuries in infants: a prospective study. Journal of 98–102. Neurosurgery 102(4 Suppl), 380–384. [26] Looney, C.B., Smith, J.K., Merck, L.H., Wolfe, H.M.,[11] Ommaya, A.K., Goldsmith, W. & Thibault, L. (2002). Chescheir, N.C., Hamer, R.M. & Gilmore, J.H. (2007). Biomechanics and neuropathology of adult and paedi- Intracranial hemorrhage in asymptomatic neonates: atric head injury. British Journal of Neurosurgery 16(3), prevalence on MR images and relationship to obstetric 220–242. and neonatal risk factors. Radiology 242(2), 535–541.[12] Geddes, J.F., Hackshaw, A.K., Vowles, G.H., Nickols, [27] Hymel, K.P., Jenny, C. & Block, R.W. (2002). Intracra- C.D. & Whitwell, H.L. (2001). Neuropathology of nial hemorrhage and rebleeding in suspected victims of inflicted head injury in children. I. Patterns of brain abusive head trauma: addressing the forensic controver- damage. Brain 124(Pt 7), 1290–1298. sies. Child Maltreatment 7(4), 329–348.[13] Geddes, J.F., Vowles, G.H., Hackshaw, A.K., Nickols, [28] Leestma, J.E. (2005). Case analysis of brain-injured C.D., Scott, I.S. & Whitwell, H.L. (2001). Neuropathol- admittedly shaken infants: 54 cases, 1969–2001. Amer- ogy of inflicted head injury in children. II. Microscopic ican Journal of Forensic Medicine and Pathology 26(3), brain injury in infants. Brain 124(Pt 7), 1299–1306. 199–212.[14] Shannon, P., Smith, C.R., Deck, J., Ang, L.C., Ho, M. & [29] Monson, K., Sparrey, C., Cheng, L., Van Ec, C. & Becker, L. (1998). Axonal injury and the neuropathology Manley, G. (2007). Head Exposure Levels in Pediatric of shaken baby syndrome. Acta Neuropathologica 95(6), Falls (P48), National Neuro Trauma Society Meeting, 625–631. Kansas City, USA.[15] Stoodley, N. (2002). Non-accidental head injury in [30] Kim, K., Wang, M., Griffith, P., Summers, S. & Levy, M. children: gathering the evidence. Lancet 360(9329), (2000). Analysis of pediatric head injury from falls. 271–272. Neurosurgical Focus 8(1), e3.[16] Denton, S. & Mileusnic, D. (2003). Delayed sudden [31] Greenes, D.S. & Schutzman, S.A. (1998). Occult death in an infant following an accidental fall: a case intracranial injury in infants. Annals of Emergency report with review of the literature. American Journal of Medicine 32(6), 680–686. Forensic Medicine and Pathology 24(4), 371–376. [32] Schloff, S., Mullaney, P.B., Armstrong, D.C., Siman-[17] Plunkett, J. (2001). Fatal pediatric head injuries caused tirakis, E., Humphreys, R.P., Myseros, J.S., Buncic, by short-distance falls. American Journal of Forensic J.R. & Levin, A.V. (2002). Retinal findings in children Medicine and Pathology 22(1), 1–12. with intracranial hemorrhage. Ophthalmology 109(8),[18] Arbogast, K.B., Margulies, S.S. & Christian, C.W. 1472–1476. (2005). Initial neurologic presentation in young children [33] Aly-Hamdy, N., Childs, A.M., Ferrie, C.D. & Liv- sustaining inflicted and unintentional fatal head injuries. ingston, J.H., BPNA (2001). Subdural haemorrhage with Pediatrics 116(1), 180–184. bilateral retinal haemorrhage following accidental house-[19] Talbert, D.G. (2006). The ‘Sutured Skull’ and intracra- hold trauma. Developmental Medicine and Child Neurol- nial bleeding in infants. Medical Hypotheses 66(4), ogy 43(Suppl. 90), 24. 691–694. [34] Rooks, V.J., Eaton, J.P., Ruess, L., Petermann, G.W.,[20] Reid, J.D. (1960). Effects of flexion-extension move- Keck-Wherley, J. & Pedersen, R.C. (2008). Prevalence ments of the head and spine upon the spinal cord and and evolution of intracranial hemorrhage in asymp- nerve roots 1. Journal of Neurology, Neurosurgery, and tomatic term infants. American Journal of Neuroradi- Psychiatry 23, 214–221. ology 29(6), 1082–1089.[21] Smith, C.G. (1956). Changes in length and position of [35] Whitby, E.H., Griffiths, P.D., Rutter, S., Smith, M.F., the segments of the spinal cord with changes in posture Sprigg, A., Ohadike, P., Davies, N.P., Rigby, A.S. & in the monkey 1. Radiology 66(2), 259–266. Paley, M.N. (2004). Frequency and natural history of
  • 11. Shaken Baby Syndrome 11 subdural haemorrhages in babies and relation to obstetric [51] Friede, R.L. (1989). Subdural haematomas, hygro- factors. Lancet 363(9412), 846–851. mas and effusions, in Developmental Neuropathology,[36] Pollina, J., Dias, M.S., Li, V., Kachurek, D. & R. Friede, ed, Springer-Verlag, Gottingen, p. 198–208. Arbesman, M. (2001). Cranial birth injuries in term new- [52] Bruce, D.A. & Zimmerman, R.A. (1989). Shaken impact born infants. Pediatric Neurosurgery 35(3), 113–119. syndrome. Pediatric Annals 18(8), 482–489, 492.[37] Towner, D., Castro, M.A., Eby-Wilkens, E. & Gilbert, [53] Aoki, N. & Masuzawa, H. (1984). Infantile acute sub- W.M. (1999). Effect of mode of delivery in nulliparous dural hematoma. Clinical analysis of 26 cases. Journal women on neonatal intracranial injury. New England of Neurosurgery 61(2), 273–280. Journal of Medicine 341(23), 1709–1714. [54] Loh, J.K., Lin, C.L., Kwan, A.L. & Howng, S.L.[38] Chamnanvanakij, S., Rollins, N. & Perlman, J.M. (2002). Acute subdural hematoma in infancy. Surgical (2002). Subdural hematoma in term infants. Pediatric Neurology 58(3–4), 218–224. Neurology 26(4), 301–304. [55] Hwang, S.K. & Kim, S.L. (2000). Infantile head injury,[39] Cushing, H. & Goodrich, J.T. (2000). Reprint of “Con- with special reference to the development of chronic cerning Surgical Intervention for the Intracranial Hem- subdural hematoma. Child’s Nervous System 16(9), orrhages of the New-born” by Harvey Cushing, M.D. 590–594. 1905. Child’s Nervous System 16(8), 484–492. [56] Ito, H., Yamamoto, S., Komai, T. & Mizukoshi, H.[40] Maxeiner, H. (2001). Demonstration and interpretation (1976). Role of local hyperfibrinolysis in the etiology of bridging vein ruptures in cases of infantile subdural of chronic subdural hematoma. Journal of Neurosurgery bleedings. Journal of Forensic Sciences 46(1), 85–93. 45(1), 26–31.[41] Volpe, J.J. (1995). Intracerebellar haemorrhage, in Neu- [57] Markwalder, T.M. (1981). Chronic subdural hematomas: rology of the Newborn, WB Saunders, p. 384–389. a review. Journal of Neurosurgery 54(5), 637–645.[42] Craig, W. (1938). Intra cranial haemorrhage in the [58] Rogers, C.B., Itabashi, H.H., Tomiyasu, U. & Heuser, newborn - a study of diagnosis and differential diagnosis E.T. (1998). Subdural neomembranes and sudden infant based on pathological and clinical findings in 126 cases. death syndrome. Journal of Forensic Sciences 43(2), Archives of Disease in Childhood 13, 89–124. 375–376.[43] Larroche, J.-C. (1977). Lesions of haemorrhagic type, [59] Vinchon, M., Noule, N., Tchofo, P.J., Soto-Ares, G., mainly venous, in Developmental Pathology of the Fourier, C. & Dhellemmes, P. (2004). Imaging of head Neonate, Excerpta Medica, Amsterdam, p. 355–398. injuries in infants: temporal correlates and forensic[44] Haines, D.E., Harkey, H.L. & al Mefty, O. (1993). The implications for the diagnosis of child abuse. Journal “subdural” space: a new look at an outdated concept. of Neurosurgery 101(1 Suppl), 44–52. Neurosurgery 32(1), 111–120. [60] Yamaguchi, S., Hida, K., Akino, M., Yano, S. &[45] Tubbs, R.S., Louis, R.G., Acakpo-Satchivi, L. & Salter, Iwasaki, Y. (2003). Spinal subdural hematoma: a sequela E.G. (2007). Anatomy of the falcine venous plexus. of a ruptured intracranial aneurysm? Surgical Neurology Journal of Neurosurgery 107, 155–157.[46] Friede, R.L. (1989). Hemorrhages in Asphyxiated 59(5), 408–412. Premature Infants, in Developmental Neuropathology, [61] McNeely, P.D., Atkinson, J.D., Saigal, G., O’Gorman, R. Friede, ed, Springer-Verlag, Gottingen, p. 44–58. A.M. & Farmer, J.P. (2006). Subdural hematomas in[47] Walsh, F.B. & Hedges, T.R. Jr. (1951). Optic nerve infants with benign enlargement of the subarachnoid sheath hemorrhage. American Journal of Ophthalmology spaces are not pathognomonic for child abuse. AJNR. 34(4), 509–527. American Journal of Neuroradiology 27(8), 1725–1728.[48] Geddes, J.F., Tasker, R.C., Hackshaw, A.K., Nick- [62] Hylton, C. & Goldberg, M.F. (2004). Images in clinical ols, C.D., Adams, G.G., Whitwell, H.L. & Scheim- medicine. Circumpapillary retinal ridge in the shaken- berg, I. (2003). Dural haemorrhage in non-traumatic baby syndrome. New England Journal of Medicine infant deaths: does it explain the bleeding in ‘shaken 351(2), 170. baby syndrome’? Neuropathology and Applied Neurobi- [63] Paterson, C.R. (2003). Clinical Review Radiological fea- ology 29(1), 14–22. tures of the brittle bone diseases. Journal of Diagnostic[49] Smith, C., Bell, J.E., Keeling, J.W. & Risden, R.A. Radiography and Imaging 5(1), 39–45. (2003). Dural haemorrhage in nontraumatic infant [64] Thach, B.T. (2000). Sudden infant death syndrome: deaths: does it explain the bleeding in ‘shaken can gastroesophageal reflux cause sudden infant baby syndrome’? Geddes JE et al. A response. death? American Journal of Medicine 108(Suppl 4a), Neuropathology and Applied Neurobiologyeuropathol 144S–148S. Appl Neurobiol 29(4), 411–412. [65] Spitzer, A.R., Boyle, J.T., Tuchman, D.N. & Fox, W.W.[50] Cohen, M.C. & Scheimberg, I. (2008). Evidence of (1984). Awake apnea associated with gastroesophageal occurrence of intradural and subdural hemorrhage in the reflux: a specific clinical syndrome. Journal of Pediatrics perinatal and neonatal period in the context of hypoxic 104(2), 200–205. ischemic encephalopathy. An observational study from [66] Miller, M.J. & Kiatchoosakun, P. (2004). Relationship two referral institutions in the United Kingdom, Pedi- between respiratory control and feeding in the develop- atric Developmental Pathology Nov 13, 1. ing infant. Seminars in Neonatology 9(3), 221–227.
  • 12. 12 Shaken Baby Syndrome[67] Geddes, J.F. & Talbert, D.G. (2006). Paroxysmal cough- in children involved in frontal collisions, Presented at ing, subdural and retinal bleeding: a computer modelling the Society of Automotive Engineers World Congress and approach. Neuropathology and Applied Neurobiology Exhibition, April 2007, Detroit, MI. Session: Biome- 32(6), 625–634. chanics (Part 1 of 3).[68] Prange, M.T., Coats, B., Duhaime, A.C. & Margulies, [74] Winter, S.C., Quaghebeur, G. & Richards, P.G. (2003). S.S. (2003). Anthropomorphic simulations of falls, Unusual cervical spine injury in a 1 year old. Injury shakes, and inflicted impacts in infants. Journal of Neu- 34(4), 316–319. rosurgery 99(1), 143–150. [75] Case, M.E., Graham, M.A., Handy, T.C., Jentzen, J.M.[69] Cory, C.Z. & Jones, B.M. (2003). Can shaking alone & Monteleone, J.A. (2001). Position paper on fatal cause fatal brain injury? A biomechanical assessment of abusive head injuries in infants and young children. the Duhaime shaken baby syndrome model. Medicine American Journal of Forensic Medicine and Pathology Science and the Law 43(4), 317–333. 22(2), 112–122.[70] Duhaime, A.C. & McNamara, D. (2007). Child abuse injuries: new data challenge beliefs. Pediatric News 41(3), 32. Related Articles[71] Prange, M. & Myers, B. (2003). Pathobiology and biomechanics of inflicted childhood neurotrauma Autopsy response, in Inflicted Childhood Neurotrauma, R. Reece & C. Nicholson, eds, AAP Monograph, p. 237–243. Battered Child Syndrome[72] Johnston, R.A. (2004). Paediatric spinal injuries. Injury 35(2), 105–106. WANEY SQUIER[73] Prange, M.T., Newberry, W., Moore, T., Peterson, D., Smyth, B. & Corrigan, C. (2007). Inertial neck injuries