Mary Case, MD Professor of Pathology St. Louis University USA MO Juvenile Justice Association Conference Lake Ozark, MO

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1 Mary Case, MD Professor of Pathology St. Louis University USA 2015 MO Juvenile Justice Association Conference Lake Ozark, MO

2 I have nothing to disclose

3 75 80% of child abuse deaths are due to head trauma 80% of all significant head injuries < 2 years due to inflicted injury Majority of victims - < 1 year old Same injury occurs also in older children as old as 5 or 6 years

4 Not all abusive head injury is fatal About 7-30% die 30-50% - significant cognitive or neurological deficits 30% may recover Deficits - mental retardation or slowness, learning disorders, seizures, blindness, irritability

5 4 years post injury

6

7 infant brain 7 years after injury

8 Anatomical and developmental differences of children under age 4 to 5 years Brain and skull are in process of maturing Mechanisms and thresholds of injury differ from those affecting older ages

9 Skull - thin and pliable Large heavy head Undeveloped neck muscles Softness of brain - high water content and paucity of myelin Flatness of skull base Large shallow SA space

10 Impact to young brain - more apt to produce inertial injury rather than contusion Impact force - easily transferred thru thin pliant skull and shallow SA space Lack of myelin and small axon size - predisposes to shear

11 Large heavy head on weak neck- greater movement of head and brain on acceleration- deceleration forces Flatter skull base - brain more vulnerable to inertial motion in response to acceleration - deceleration

12 Static force loaded > 200 msec crushing head injuries - rare Dynamic force loaded < 200 msec great majority of injuries at all ages Caused by impulsive loading causing head to move either by direct impact or by action to body which causes head to move

13 Impulsive loading imparts inertial movement of the brain within the cranial cavity Differential movement between skull/dura and brain/arachnoid tears bridging veins ASDH/SAH and causes axonal shearing Impact loading produces both contact and inertial injuries

14 After a violent shaking - child may be thrown down Scalp is very elastic - may not reflect impact Brain pathology is identical in either shaking or impact Impact - scalp bruises, subgaleal hemorrhage, skull fracture

15 Subgaleal hemorrhage

16 Inertial movement of brain/arachnoid separating from dura/skull SDH - results from tearing of bridging veins SDH - over convexities, especially posterior, and interhemispheric, basilar May be uni- or bilateral If fracture - need not be at site of fx

17 Infant with fractures and subgaleal hemorrhages SDH

18 Subdural hemorrhage

19

20 SDH - evident in ~95% of abusive head trauma May be very small < 5 ml may be too small to image on CT Need not be space occupying mass although it maybe May continue to increase in size during time of survival

21

22 Accompanies SDH Inertial movement between dura/skull and brain/arachnoid Usually parasagittal over convexities 95% of cases of abusive head trauma

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25 RHs may occur in many disorders sepsis, meningitis, genetic disease, newborn, bleeding disorders RHs are few in number, do not involve all layers of retina, confined to the posterior pole, may have other unique features

26 80% of cases of inflicted head trauma Although they may be few and only posterior, usually are very numerous, in multiple layers of retina, and extend to the periphery at the ora serrata Optic nerve sheath hemorrhage is frequent

27

28 hemorrhages in retina

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32 Optic nerve sheath hemorrhage - hemorrhage in the perineural area Not specific for trauma May be observed in increased ICP from other causes

33 Retinal hemorrhages Optic nerve sheath hemorrhages

34 Diffuse injury encephalopathy causing severe brain disorder SDH, SAH, RH - markers for traumatic diffuse axonal injury (tdai) tdai - tears of axonal processes Areas of predilection - corpus callosum, subcortical white, periventricular areas, dorsolateral quadrants of rostral brainstem

35 Axonal tears - may be seen microscopically after hours by H&E or silver stains or 2 hours by B- APP stain H&E - retraction bulbs - very difficult to see because of small size of axons in children

36 Retraction bulbs

37 Immunohistochemical process Β- amyloid precursor protein membrane spanning glycoprotein normally present in axons Β- APP accumulates at points of axonal damage Β- APP is a marker for damaged axons

38 BAPP expression in hypoxic pattern VAI

39 BAPP expression in traumatic pattern dtai

40 Often not possible to identify DAI by demonstrating axonal tears Markers of inertial brain injury - SDH, SAH, RH

41 When SDH/SAH is found at autopsy - brain needs to be closely examined to exclude possibility of bleeding from other causes - berry aneurysm or AVM Distribution of hemorrhage in natural causes in not likely to resemble that of trauma

42 Pathologist needs to be present to visualize each step Remove periosteum over any blood on skull Remove brain with spinal cord attached Remove eyes from anterior cranial fossae

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48 Abusive head injuries are very common in young children Due to special anatomical and developmental features in young children, head injuries are different from later ages in terms of thresholds and mechanisms.

49 Special anatomical and developmental features make them particularly vulnerable to inertial brain injury. These injuries result from inertial brain motion from either impact or shaking or combination. Pathology of brain injury is dtai with SDH, SAH, and RH.

50 tdai may be difficult to demonstrate. SDH and SAH are markers of tdai. Timing issues in cases in which tdai is mechanism - these cases have immediate onset of change in level of consciousness.

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