1. Pediatric Head Trauma Presented by Jennifer L. Ross, M.D.
Glenn D. Sandberg, M.D.
Neuropathologist
Harris County Institute of Forensic Sciences
Presented by Jennifer L. Ross, M.D.
Neuropathology Fellow
The Methodist Hospital

2. Objectives Review the epidemiology of pediatric head trauma
Provide an introduction to major subtypes of head injuries observed in pediatric head trauma
Show examples of typical head injuries
Discuss challenges specific to the investigation of fatal, non-accidental pediatric head trauma

3. Pediatric Head Trauma
80% of all significant head injury under the age of 2 years is due to abuse
75-80% of child abuse fatalities are due to head injury
Majority are infants <1 year
Percentage of deaths due to head trauma decreases with age as abdominal trauma becomes more prevalent

4. Sequelae of Head Injury
7-30% of children with abusive head injuries die
30-50% live, but have significant cognitive or neurological deficits
Mental retardation, learning disabilities, seizures, and blindness
30% recover

5. Types of Head Injuries Focal injuries Diffuse injuries
Epidural hematomas
Subdural hematomas
Subarachnoid hemorrhages
Contusions
Parenchymal hemorrhages
Diffuse injuries
Axonal
Traumatic
Concussion
Vascular

7. Epidural Hematoma Bleeding between skull and dura
Occurs in approximately 2% of head injury
5-15% of fatal head injuries
Almost always associated with skull fracture
Usually thin squamous portion of temporal bone
May occur in children without fracture
Laceration of arteries or veins
Middle meningeal artery-up to 50%
Middle meningeal veins-30%
Second mass effect: Cerebral swelling, edema, contusion, & disturbed CSF absorption
Intradural lesion 4-5 x more likely than epidural
Classical lucid interval sequence, brief unconsciousness after injury followed by conscious lucid interval then coma occurs in 13-43% of EDH-in reality might be no more frequent in EDH than SDH
Torn middle meningeal veins 30%, diploic veins (10%dural sinuses and bone fragments account for 40% of EDH

8. Epidural Hematoma Clinical Classical lucid interval sequence Features:
Brief period of unconsciousness after injury
Conscious, lucid interval of variable duration
Coma
Occurs in 13-43% of EDH
Might be no more frequent in EDH than SDH
Second mass effect: Cerebral swelling, edema, contusion, & disturbed CSF absorption
Intradural lesion 4-5 x more likely than epidural

9. EPIDURAL HEMATOMA Trauma ‑> fracture & concussion
Tearing/stripping of dura away from inner table
Laceration of meningeal vessels
Blood between naked bone and dura
NORMAL arterial pressure continues to dissect

10. Epidural Hematoma Blood cannot cross suture lines
Often causes significant mass effect
Acutely can tolerate up to 40 mL
Rarely survive if > 150 mL
Second mass effect: Cerebral swelling, edema, contusion, & disturbed CSF absorption
Intradural lesion 4-5 x more likely than epidural

11. Subdural Hematoma Accumulation of blood between dura and brain
Blood free to diffuse throughout subdural space
Evident in ~95% of abusive head trauma
May be small (<5 ml), bilateral and non-compressive
May be associated with skull fracture
May be present in open or closed head injury
Association with skull fracture 69.7% in an forensic series
8.1% in surgical series

12. Subdural Hematoma Commonly occur in Falls Assaults MVA: 24%
Child abuse
Sports
72%
Association with skull fracture 69.7% in an forensic series
8.1% in surgical series

13. Subdural Hematoma Result of torn bridging veins
Some are secondary to ruptured cortical arteries
Sudden, rapidly applied angular acceleration/deceleration of the moveable head
High strain stretches and snaps bridging veins
Span between cerebral hemispheres and superior sagittal sinus
Subdural portions have a thin, irregular collagenous wall
Subarachnoid portions are covered by arachnoid trabeculae
Subacute: 2 weeks
Chronic: > 2 weeks

14. Subdural Hematoma
Characteristically form over the frontoparietal regions
Bilateral
Adults: 18.5%
Children: 76.7%
Posterior fossa
Rare: <1 %
Particularly rare in a neonate
Fracture to occiput present in 20-80%
Spinal cord
Rare; usually not compressive

15. Subdural Hematoma Gross: Loosely adherent dark red blood: 3-5 days.
Well-formed outer membrane: 1 week.
Well-formed inner membrane: 3-4 weeks.

16. Table for dating SDH

17. Table 2 for dating SDH

18. Subdural Hematoma Associated findings
25% who undergo removal of acute subdural have underlying cerebral edema
>80% of these patients die
Ischemia
May be due to local compression of the microcirculation or effects of vasoactive substances released from the SDH
Excitotoxic neuronal injury
table 19.7 pg 1199

19. Subarachnoid Hemorrhage
Trauma most frequent cause
Associated with contusions and lacerations
Fatal traumatic SAH should be suspected in
Ear injuries
Parotid region injuries
Upper neck injuries

20. Contusion Overlying dura usually remains intact
“Bruise” of cerebral cortex
Focal type of brain injury occurring at the moment of impact
Caused primarily by the surface of the brain striking the skull or being impacted by it
Overlying dura usually remains intact
Injury patterns differ whether head is stationary or in motion at moment of impact
Freely mobile head motionless at impact
Coup injury
Freely mobile head accelerated in a fall prior to impact
Contrecoup injury

21. Contusion Do not occur in infancy Contusional tears
Tears at cortex-white matter junction
Occur before 6 months of age
Especially in frontal and temporal lobes
Not usually hemorrhagic

22. Contusion Gliding Head is in motion at the time of impact
Hematoma confined to the parasagittal white matter of the frontal lobes
Each hemisphere is firmly tethered to dura by arachnoid granulations
Subcortical white matter glides more than cortex
Deep basal ganglia hematomas and DAI often present
Forces sufficient to cause both axonal and vascular damage

23. Contusion
Fracture
Occur at site of fracture, related to displaced bone against cortex, may not be at site of impact

24. Contusion Patients usually make good recovery Remote contusion
In absence of DAI
Remote contusion
Common incidental finding at autopsy
Cavitary lesion
Destruction involving full thickness of cortex
Hemosiderin deposition
Rarely contrecoup injuries in occipital region
As they are focal

25. Diffuse Primary Head Injuries
Diffuse injuries
Concussion
Diffuse axonal injury

26. Concussion Temporary, reversible neurological deficit caused by trauma
Velocity r necessary
Consciousness can be retained in crush injury of fixed head
Results in immediate temporary loss of consciousness
Both retrograde and post-traumatic amnesia always accompanies concussion
Length of amnesia is indicative of severity of concussion

27. Diffuse Axonal Injury
First recognized as an essential component of post-traumatic dementia in 1956 by Strich
Caused by inertial forces
Angular or rotational acceleration
Produced by long acceleration loading
Common in MVA
Falls have shorter acceleration loading
Injury attributed to shear and tensile strains
Occurs at moment of injury
Do not experience lucid interval in severe cases
Most common cause of coma and severe disability in absence of intracranial hemorrhage

28. Diffuse Axonal Injury Occurred in:
34% of all fatal head injuries
53% of deaths that occurred after at least 12 hour survival
For equivalent levels of angular acceleration
Lateral most severe
Sagittal best tolerated
Horizontal intermediate

29. Diffuse Axonal Injury Low incidence of: Increased incidence of:
Surface contusions
Skull fracture
Intracranial hemorrhages
Increased ICP
Increased incidence of:
Gliding contusions
Deep intracerebral hematomas

30. Diffuse Axonal Injury Location Corpus callosum
Cerebral lobar white matter
Dorsolateral quadrant of rostral brainstem adjacent to the superior cerebellar peduncles
“Shearing injury triad”
Only seen microscopically

31. DAI-Gross

33. Diffuse Axonal Injury Primary axotomy Secondary axotomy Rare
Calcium hypothesis
Physical stretch of axon
Disrupts axons ability to regulate ions
Influx of Ca2+ , K +,& Cl –
Activation of neutral proteases
Disruption of axonal cytoarchitecture
Mechanical disruption
Neurofilament subunits disrupted
Axonal transport impaired

34. Axonal Spheroids H&E BAPP Need at least 18-24 hour survival

35. DAI-H&E

36. Retinal Hemorrhages 80% of inflicted head trauma Multifocal
Involve multiple retinal layers
Extend to the ora serrata
Optic nerve sheath hemorrhage is frequent

37. Causes of Retinal Hemorrhages
Severe head injuries (not limited to abuse)
Birth trauma - 30% are resolved by 1 month
Bleeding disorders
Sepsis
Vasculopathies
Sudden changes in intracranial pressure
Terson’s syndrome
CPR – Rarely
Purtscher’s retinopathy-head or chest trauma

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42. Pediatric Head Trauma “Lucid interval” concept
Vast majority of children who sustain fatal head trauma show an immediate decrease in consciousness (i.e. no lucid interval)
An infant or young child who has sustained an ultimately fatal head injury is not likely to act normally
Has important implications in criminal investigation of cases of fatal inflicted blunt head trauma

43. Shaken Baby Syndrome (SBS)
Caffey, 1972
Retinal, subdural, and/or subarachnoid hemorrhages caused by violent shaking
Whiplash action of head associated with weak neck muscles resulting in acceleration-deceleration injuries
Immature, partial membranous skull
Relatively large subarachnoid space
Soft, immature brain

44. Shaken Baby Syndrome (SBS)
Controversies
SBS injuries (retinal, subdural, subarachnoid hemorrhage) can also be seen in impact head injury
Impact site may not be recognized by treating physicians
Even if no impact site is identified at autopsy, the possibility of impact against a broad, superficially soft surface cannot be excluded
In addition, the specificity of retinal hemorrhages for abuse has been questioned
Conflicting research models

45. Shaken Baby Syndrome (SBS)
Diagnosis of SBS should not be made when evidence of direct impact is present
Most cases of fatal head injury have evidence of direct impact (facial or scalp contusions, skull fractures)
Even without identifiable impact site, impact cannot be ruled out
Therefore, SBS is rarely listed as a cause of death

46. Infant Death Investigation
Age, date of birth, birth weight, race, sex
Normal delivery vs C-section; any complications
Last known alive - by whom, date, time
Found dead - by whom, date, time
Place of death - crib, bed, floor
Position of infant when found - supine, prone
Resuscitation - method and by whom
Recent injuries/illnesses and medical history
Change in behavior or appearance; last time child was behaving “normally”
Prior infant deaths in the family

47. Investigative Challenges
Caregivers are often perpetrators
Reliable witness accounts are often lacking
Confessions may be unreliable
Determining mechanism of injury from autopsy findings alone may be impossible
Estimating age of injuries may be critical, but is unreliable and further complicated by medical treatment and hospital survival

48. Investigation – Red Flags
Reported history is inconsistent with physical findings
Injuries that occur during the course of normal daily activities (including playing and short falls) do not usually result in fatal injuries
Delay in seeking treatment
Prior history of child abuse in household