scalp hematoma, skull fractures, Extradural hematoma, subdural Hematoma, subaraichnoid hematoma, coup and cont re coup injury, cereberal concussion, cereberal laceration, heat hematoma

1. Forensic Aspect of

2.  Defined as a morbid state, resulting from gross or subtle structural changes in the
scalp, skull or the content of skull produced by mechanical forces applied externally.
 Depending on involvement of Dura mater it can be
categorized into:
 Open head injury
 Closed head injury

6.  Anatomically it can be categorized into:
1. Scalp injury
2. Skull injury
3. Injury to meninges
4. Brain injuries
5. Facial injuries

7. Scalp injury
It is composed of 5 layers:
1. Skin
2. Connective tissue
3. Galea aponeurotica
4. Loose areolar tissue
5. Pericranium

9.  Abrasions : brush abrasions are less common
 Contusion: black eye, spectacle hematoma
 Lacerations: split Lacerations ( incised looking lacerated wound)
 Incised wounds: clean cut margins, hair bulbs are cleanly cut
 MLI: infected wounds of scalp and may cause thrombophlebitis of emissary vein.

12.  Local violence to extra ocular structures.
 Blow to skull
 Facture of orbital plate

13.  Local violence
 Blow on skull
 # of orbital plate

14.  May be the result of direct or indirect violence
 Direct : compression injury- RTA, forceps delivery, fall from height, repeated blows-
boxing, moving object strikes head- bullet
 Indirect : injury to other body parts e.g. fall on buttocks or feet, or blow to chin
 In all Medicolegal autopsies the dura should be stripped thoroughly from the vault and
the base so that presence of fractures can be excluded

15.  Puppe was the first to point out that it is possible to
determine the sequence of injuries in skull fractures
caused by blows to the head because ….
 The second fracture ends at the point where a break
in cohesion is already present.

17. Fissured fractures/ Linear #
 May involve outer table or inner table or both
 Cannot be detected by X- ray
 May cause traumatic epilepsy
 Coup # - when head is stationary
 Contre coup #- when as a result of blow head moves and strikes a stationary object
 Follow path of least resistance like sinuses, orbital roof, squama

18.  May correspond in shape and size to causative weapon
 Late effect is post traumatic epilepsy
 Comminuted/crushed fracture
 Bone is broken into 2 or more pieces
 Often complication of depressed fracture
 Pond/indented fracture
 Occur in children
 It resembles a dent on a ping-pong ball
 Inner table is intact
 Fissured # may be seen around the periphery of dent

23.  Elevated fracture
 One end of the segment is elevated
 Gutter fracture
 When part of a thickness of skull is removed, e.g. in glancing bullet
wound
 Penetrating fracture
 Clean cut opening due to a penetrating weapon such as dagger or bullet

25.  A comminuted fracture is a break or splinter of the
bone into more than two fragments.
 Fractures of this degree occur after high-impact
trauma such as in vehicular accidents

29.  Fracture of anterior cranial fossa:
 Usually d/t direct impact
 May be due to contre coup injury
 Present as escape of blood and CSF from nose and/or as black eye (spectacle
haematoma/ raccoon eyes)

30.  Fracture of middle cranial fossa:
 Usually d/t direct impact behind the ear or crush injury of head
 Present as escape of blood and CSF from ear if petrous part of temporal bone is #
 Mastoid haemorrage from # of middle cranial fossa present as retroauricular bruise (
Battle’s sign)

32.  Commonly due to direct impact
 Present as escape of blood in the nape of neck
 Ring Fracture
 Fissured fracture about 3.5 cm outside the foramen
magnum involving middle ear sideways and roof of
nose anteriorly .
 May result from : fall on feet, twisting of neck, blow on
vertex or chin
 Hinge/ motor cyclist Fracture
 Base of skull is divided into two halves each moving independently of each
other

34.  Time since injury - in fissured fracture
 Edges stick to each other- 1 week
 Calcification of inner table and rounding of fractured edges- 2 weeks
 Formation of band of osseous tissue- 4 weeks
 Time since injury - in comminuted fracture
 No new bone formation
 Gap is filled by fibrous tissue – 1-3 months

35.  Injury to brain substance occur d/t
 Movement (gliding and rotational strains) pull constituent particles of brain apart
 Relative movement of brain within the skull
 Movement is arrested by rigid structures like falx cerebri , tentorium cerebelli
 Distortion of skull

36.  Coup injury:
▪ Which occurs immediately subjacent to the area of impact
▪ Immediate effects are contusions and hemorrhage
 Contre coup injury :
▪ Which is on the contra lateral side of the area of impact.
▪ Can occur only when head is free to move
▪ Most frequently occur in temporal poles, frontal poles, orbital surfaces of frontal lobes
 Intermediate coup contusion:
▪ Mimic spontaneous intra cerebral hemorrhage in deep cerebral parenchyma e.g. brain stem

40.  Classified according to the main effect of
trauma as:
 Acceleration/ deceleration injury
(a) Diffuse neuronal injury
(b) Diffuse axonal injury
(c) Subdural haematoma

41.  Impact injury of brain
(a) Cerebral concussion
(b) Cerebral contusion
(c) Cerebral laceration
(d) Cerebral edema
(e) Cerebral hemorrhage
(f) Intracranial hemorrhage

42.  D/t sudden acceleration/deceleration
 By diffuse neuronal damage in brain stem
 Conduction defects at synaptic junction and intracellular
disturbances , e.g Concussion

43.  Damage of axons and blood vessels
 Stretching of axons with consequent disruption and loss of
function depending on strain
 M/E: wide spread white matter damage in the form of
ruptured axons and spheroids( circular or elongated
granular bodies containing cell organelles)
 Dilatation of axons
 Long standing duration: microglial reaction, myelin
degeneration, micro cavites, enlargement of ventricular
system d/t loss of white matter
 e.g. punch drunk syndrome

48.  Caused by diffuse neuronal damage brain stem with little or
no anatomical disturbance
 More severe in deceleration injury.
 No naked eye lesion on autopsy
 On histology microscopic hemorrhage may be found.
 There is sudden loss of consciousness with tendency for
spontaneous recovery

49.  In less severe cases pt regains consciousness with
signs of cerebral irritation
 Recovery is often followed by retrograde
amnesia, which may extend from fortnight to
month or more
 Post traumatic automatism may follow
 Can be confused with acute alcohol intoxication

50. Drunk Concussed
1. Face flushed, warm Pale, clammy
2. Pulse Fast, bounding Slow, feeble
3. Pupils Sluggish Brisk
4. Breathing Sighs Shallow
5. Memory confused Retrograde amnesia
6. Behaviour abusive quiet, curled up

51.  Extravasations of blood from traumatically ruptured blood
vessel into brain substance
 Generally involve crest of gyri but may extend as wedge shaped
lesion
 Cerebral hemorhage by small punctate or streak like hemohages
and mass focal destruction of tissue with or without oedema

52.  They enlarge with time, esp in persons with HTN, liver cirrhosis or
bleeding disorder.
 After absorption of contusion golden brown area of gliosis (blood
cyst) is left.
 Clinical manifestations vary with site and size of contused area.
 Brain contusions in infants differ from adults, they appear as mild
haemorrhagic tears in sub cortical white matter.

53.  Can be caused by penetrating wound as well as by closed head
inj with high degree of shear strain
 These are accompanied by rupture of pia mater
 Usually surrounded by group of contusions
 Subarachnoid Hg commonly accompanies the lesion because
of rupture of pia mater.

55.  Healing may be in form of adhesions b/w brain and
dura mater , which may result in post traumatic
epilepsy
 Healing of laceration in cerebral ventricle may be in
form of large glial cysts k/a Porencephalic cysts, can
be differentiated from blood cysts by presence of
blood pigments

56.  Most common cause of raised intracranial pressure
 m/b related to diffuse neuronal injury and concussion
 Autopsy findings: dura is stretched, brain bulges
through incision, gyri are pale and flattened, sulci are
obliterated, cut surface appears pale, ventricles are
greatly reduced in size, herniation of hippocampal gyri,
secondary brain stem Hg and coning of intracellular
tonsil

59.  Epidural haemorrhage
 Subdural haemorrhage
 Subarachnoid haemorrhage
 Intracerebral haemorrhage

63.  Bleeding b/w dura and skull
 Invariably traumatic
 Associated with skull # except in infants
 m/b acute or subacute
 Classical clinical course: loss of conciousness followed
by lucid interval and then deep coma d/t ↑ ICP
 Undergo rapid resolution without anatomic sequelae

64.  D/T Rupture Of Middle Meningial Artery
▪ Pt looses consciousness
▪ Unless the clot is surgically removed pt rapidly dies d/t displacement of
brainstem
▪ Usual cause of death is respiratory failure d/t brain stem compression
 Sub acute – when # tears Dural sinuses middle Meningial vein
or diploic vein
▪ Symptoms are slower in onset
 MLI: prognosis is good with proper treatment, patient m/b
discharged during lucid interval,
▪ condition may resemble drunkenness,
▪ m/b confused with heat artifact on autopsy.

65.  Vascular injury where head rapidly decelerates because of
impact to a firm unyielding surface, Common in falls and
assaults
 Bleeding b/w under surface of Dura and outer surface of
arachnoid mater
 Commonly d/t rupture of bridging veins but m/b d/t
 Tearing of cortical artery
 Injury to Dural sinuses
 Secondary to disease processes e.g. Neoplasms,
 Ruptured cerebral aneurysms
 And not necessarily associated with skull # or brain injury.

66.  Classified as:
▪ Acute (within 24 hrs),
▪ Sub acute( 24 hrs to7 d) and
▪ Chronic

68.  Acute subdural hematoma is d/t rupture of large bridging veins
or a cortical artery.
 Onset of symptom is usually rapid and may become life
threatening when about 50 ml of blood accumulates.
 High mortality is d/t associated brain damage.
 Sub acute subdural hematoma is d/t bleeding from smaller
bridging veins

69.  Chronic subdural hematoma is result of torn perforating Dural
veins especially in elderly
 Hematoma is often secondary to slight trauma and there may not
be any neurologic effects except slight confusion, forgetfulness
and emotional disorder
 Chronic subdural hematoma consist of blood encased by outer
membrane underlying the Dura and an inner membrane that
separates the blood from arachnoids and k/a blood cysts

70.  MLI: changes in Dura-
▪ Capillary dilatation(24 hrs) →
▪ Proliferation of fibroblast on under surface of dura(2-3
days) →
▪ Thin layer of fibrin on under surface of dura(4-5 days) →
▪ Red cell decomposition (5-10) →
▪ True inner membrane (2-4 wk) →
▪ Mature connective tissue with haemosiderin &
haematoidin laden macrophages (1-3 months)

72.  Causes
 Natural Causes:
 Berry aneurysm,
 Arteriosclerotic vessels in older person with high BP ,
 Leaking intra cerebral hemorhage,
 Like leukemia, angioma etc
 Collection of blood is usually in base of brain

73.  Traumatic Causes:
 Cerebral contusion or laceration,
 Asphyxia by strangulation, # of upper cerebral vertebrae,
 Prolonged hyperextension of neck e.g. in bronchoscopy,
 Blow to face or neck it is d/t laceration of vital arteries e.g.
Vertebral , carotid, basilar

74.  Can be post traumatic or spontaneous
 Mainly d/t damage to cerebral vessels ,when close to
surface maybe d/t laceration
 Deep seated hemorrhage in the cerebrum, cerebellum
and brain stem may occur in association with other
brain injury.

75.  Factors to be considered are:
▪ Age of victim,
▪ Site and extent of hemorrhage,
▪ Associated vascular diseases,
▪ Cardiac hypertrophy,
▪ Kidney diseases,

76. post traumatic apoplexy
Cause head injuriy HTN, aneurysm, artsc
Age young past middle age
Onset variable sudden
Position head in motion any
Mechanism coup contre coup rupture d/t ds
Location white matter ganglionic region
Concussion +nt -nt
Coma variable none

77.  The court required a treatment plan that
must include
1. Patient's express preferences even while incompetent
2. Religious convictions of the incompetent person (as it
affects treatment)
3. Impact on the head injured person's family
4. Probability of side effects from the proposed medical
treatment
5. Prognosis without the proposed treatment
6. Prognosis with the proposed treatment

78. ▪ Dying declaration
▪ Concussion /Transient unconsciousness
▪ Lucid interval
▪ Compression 0r loss of consciousness
▪ Focal lesions e clinical neuro-deficiencies
▪ Interventions - Medical/Surgical/both
▪ Recovery (Total/Partial)

79. ▪ No recovery (Prolonged coma/Cerebral death/Brain
death/Clinical death)
▪ Incomplete recovery (Disability/Varying degrees/Partial
temporary/partial permanent)
▪ Completely bed ridden
▪ Loss of life
▪ Loss of earning
▪ Inability to do routine work

80. ▪ Disability assessment
▪ Compensation problems
▪ Accident claims
▪ Industrial claims/occupational claims
▪ Tort cases
▪ Criminal cases e simple injury
▪ Grievous injury
▪ Dangerous injury

81. thanks