Head injuries are a major cause of death and disability worldwide. Road traffic accidents are the most common cause of head injuries in India. The brain is encased within the rigid skull, so any increase in intracranial volume from bleeding or swelling can rapidly increase intracranial pressure. The document discusses the epidemiology, anatomy, physiology and classification of head injuries as well as guidelines for management including medical therapies to reduce intracranial pressure and criteria for surgical intervention for specific injuries like epidural hematomas.

1. Dr.Sumit S. Hadgaonkar
Moderator : Dr.Th. Gojen

2. Epidemology
Head injury
 Number One Killer in Trauma
 25% of all trauma deaths
 50% of all deaths from MVC
 200,000 people every year in
the world live with the
disability caused by these
injuries

3. Indian Head Injury Foundation
 India – highest rate of head injuries in the world
 Yearly 1,00,000 lives lost with 1 million suffering from
severe head injury
 1 out off 6 trauma victim dies in India ; in USA the
figure is 1 out off 200
 RTA (road traffic accidents) most common cause
followed by falls and assault
 Motorcylist and pedesticians most common victims of
RTAs

4.  In the year 2050
India will have the highest number of automobiles on
the planet , overtaking USA

5. Etiology
 Road traffic accidents (RTA) – most common cause
 Falls
 Sports injury
 Assault
 Gun shot wounds to head

6. Basic Anatomy
 Scalp
 Skull
 Meninges
 Dura Mater
 Arachnoid
 Pia Mater
 Brain Tissue
 CSF and Blood

7. Skull

8. Dura-
mater

9. Venous
sinuses

10. Arachnoid
mater

11. Pia-
mater

12. CSF

13. Grey
matter

14. White
matter

15. Ventricles

16. Intracranial Volume
 80%
Brain Matter
 10%
Blood
 10%
CSF

17. Dictates that “the total volume of
the intracranial contents MUST
remain constant”
The MONROE KELLIE doctrine

18. Brain Physiology
 Brain Metabolism :
1.Brain oxygen consumption (CMRO2, cerebral
metabolic rate for oxygen) – 3.5 ml per 100 g per min
2.90% of energy from blood glucose
 Cerebral blood flow (CBF) :
CBF is 55 ml per 100g per min
autoregulated over mean arterial pressure range of 50 -
150 mm of Hg

19. Intracranial Pressure
 The pressure of the brain contents within the skull is
intracranial pressure (ICP)
 The pressure of the blood flowing through the brain is
referred to as the cerebral perfusion pressure (CPP)
 The pressure of the blood in the body is the mean arterial
pressure (MAP)
 Cerebral Perfusion Pressure (CPP) can be determined by
the following formula:
CPP = MAP - ICP

20. Normal state- ICP normal

21. Compensated state- ICP normal

22. Uncompensated state- ICP Elevated

23. Volume-Pressure Curve

24.  Primary Brain Injury :
-occurs at the time of impact
- mechanical damage which is irreversible
- causes permanent mechanical cellular disruption
and microvascular injury.
-includes 1) cerebral contusions
2) diffuse axonal injuries (DAI)
3) cerebral lacerations
PATHOPHYSIOLOGY

25. Secondary Brain Injury
 occurs at some time after the moment of impact
 often preventable
 Prevention of secondary brain injury results in
improved neurological outcome after head injury
 may make the difference between independent
survival and dependent survival/death.

26. Brain suffers from traumatic
injury
Brain swelling or bleeding
increases intracranial volume
Rigid cranium allows no room for
expansion of contents so ICP
increases
Pressure on blood vessels within
the brain causes blood flow to the
brain slowly
Cerebral hypoxia and ischemia
occurs
Intracranial pressure continues
to rise. Brain may herniate
Cerebral blood flow decreases

28. CLASSIFICATION
morphology
severity
mechanism

29. MECHANISM
 BLUNT INJURY
 High Velocity
 Low Velocity
 PENETRATING INJURY
 Gunshot
 Sharp instruments

30. Morphology
 Scalp injury
 Skull fractures : a) vault fracture
b) base of skull fracture
 Intracranial injury : a) focal lesions
– extradural hematoma
- subdural hematoma
- subarachnoid hematoma
- intracranial hematoma
b)diffuse lesions
-contusions (multiple)
- DAI

31. MORPHOLOGY
 SCALP INJURY
Cephal Hematoma
Subgaleal Hematoma
Scalp laceration

32.  SKULL FRACTURES
 Vault : linear/stellate
depressed/non depressed
open/closed

33. Basilar skull fractures
 Usually diagnosed on CT imaging or on clinical
evidences
 Clinical signs include Battle sign ,Raccoon Eyes and
CSF leak.
 May or may not be associated with seventh and eighth
cranial nerve injury

34. Battle sign
Raccoon eyes
CSF rhinorrhea

35. INTRACRANIAL LESIONS
Epidural hematoma
 Collection of blood & clot b/n dura mater and bones of
the skull
 Source Middle Meningeal Artery
Dural Venous Sinuses
 C/F Brief loss of consciousness, headache,
drowsiness, dizziness ,nausea, vomitting
 Rapid clinical deterioration

36.  Classical presentation seen only in 1/3 rd cases
 On CT scan lentiform hyper dense lesion between
skull and brain
 Associated with mass effect on underlying brain with
or without midline shift.
 Overall mortality rate 18% in all cases but only 2% in
isolated EDH

38. Acute subdural Hematoma
 Accumulates in space between dura and arachnoid
 Disruption of cortical vessels or brain laceration
produces hematoma
 A/w significant primary injury- patients present with
impaired conscious level from the time of injury
 CT scan –hyperdense concave lesion spreading across
brain
midline shift disproportionate to size of lesion
 Mortality rate as high as 40% in some series

40. Subarachnoid Hemorrhage
 Trauma is most common cause followed by Aneurysms
 Rarely aneurysmal hemorrhage immediately precedes
trauma.
 Most can be managed conservatively

41. Chronic subdural Hemorrhage
 Usually occurs in elderly on anti coagulant or anti
platelet agents
 h/o minor head injury in weeks or months prior to
presentation
 Small bridging veins tear and cause small clinically
silent ASDH ,when hematoma breaks down and
increases in size mass effect is produced
 c/f- headache, cognitive impairment, focal
neurological deficit and seizures.
 CT scan – acute blood (0-10 days) = hyperdense
- sub acute blood (10-14 days) = isodense
- chronic blood (>2 weeks) =hypodense

42. Acute on chronic SDH
 Chronic SDH will more recent hemorrhage in
dependant (posterior) areas.
 Treatment is Burr hole evacuation rather than
craniotomy

43. Cerebral contusions
 Coup and counter coup injuries
 Most commonly affecting inf frontal fossa and
temporal lobes
 CT appears heterogeneous with mixed areas of high
and low density
 Rarely require immediate surgery
 Observation for 48-72 hrs

45. Concussion
 Temporary & brief interruption of neurological function
after minor head injury
 Due to shearing / stretching of white matter fibres at the
time of impact or temporary neuronal dysfunction
 C/o headache, confusion, amnesia
 CT/MRI cannot detect
 3 grades (Colorado Grading)
grade I- symptoms for 15 mins no LOC , only confusion
grade II-symptoms for > 15 mins ,no LOC, amnesia
gradeIII- LOC present
 Medical opinion should be sought in Grade II and III

46. DAI
 Diffuse Axonal Injury
 Disruption of axons in white matter and brainstem
 Injury occurs immediately and is irreversible
 Seen after MVC or shaken baby syndrome
 Usually have persistent sequlae e.g. cognitive
impairment, spasticity etc.
 90% pts with severe DAI will be vegetative
 CT usually normal
 MRI with multiple, diffuse abnormalities
 Hemorrhagic spots classically seen over corpus
callosum, dorsolateral midbrain.

48. Brain Herniation

49. APPROACH TO A PATIENT WITH HEAD
INJURY
 History
 Initial Assessment
 Primary Survey
 Secondary Survey

50. History

51.  This is early triage mostly done by paramedics
 Core of ATLS system and constitutes ABCDE of trauma
care
PRIMARY SURVEY

52.  Airway maintenance with cervical spine protection

53. Intubation with Cervical inline stabilization
 Breathing and ventilation : Intubation precautions
Pre-medicate with Lidocaine, 1mg/kg IV 2 minutes
prior to attempt
 Laryngoscopy produces an ICP Spike

54. Circulation
 Maintain MAP >90mmhg- adequate
 Hematocrit >30%

55.  Isolated intracranial injuries do not cause hypotension
 LOOK FOR THE CAUSE OF HYPOTENSION

56.  Pupillary size and reaction
 GCS (Glasgow Coma Scale)
 Motor function
 Injury level
Disability

57. Assessment Findings
 Constricted?
 narcotics?
 Sluggish/dilated?
 mid brain ICP
 Unilateral dilation?
 pressure on CNIII
 Fixed and Dilated?
 herniation

58. SECONDARY SURVEY
 AMPLE history
 Examination of Head to toe
 Glasgow Coma Scale
 Detailed Neurological Examination

59. SYMPTOMS & SIGNS OF INCREASED ICP
 Diminishing level of consciousness
 Headache, vomiting, seizures
 Cushing’s Triad –
 bradycardia
 hypertension
 abnormal respiration
 Pupillary changes
 Papilloedema

63. Severity of Head Injury

64. MANAGEMENT OF
MILD HEAD INJURY (GCS14 -15)
 History
 General Examination
 Limited Neurologic Examination
 C-spine and other X-rays as indicated
 CT scan??
 Discharge with advice

65.  Patient can be discharged if following criteria are met
before discharge
1.GCS must be 15/15
2.no focal neurological deficit
3.accompanied by responsible adult
4.verbal and written advice given

67.  Aim is prevention of secondary brain injury
 Achieved by avoidance of hypoxia and hypotension
 CT scan after complete stabilization of patient.
 Early neurosurgery consult if intracranial hematoma
seen
 Measures to reduce ICP (reverse Trendelenburg) i.e.
head up position by 20-30 degrees ?
 ICP monitoring
 Mannitol during transport.
MANAGEMENT OF MODERATE HEAD
INJURY(GCS 9-12)

68. MANAGEMENT OF SEVERE HEAD INJURY(3 -
8 )
 Primary Survey and Resuscitation
 Secondary Survey and ‘AMPLE’ history
 Admit to facility – neurosurgical care
 Neurologic Re-evaluation
 Eye opening
 Motor response
 Verbal response
 Pupillary reaction

69.  CT scan only after hemodynamic stabilization
 Medical therapy for raised ICP
 Immediate neurosurgeon opinion
 If needed surgical management

70. MEDICAL THERAPIES FOR HEAD INJURY
 Head end elevation – 30 deg
 Intravenous fluids:
 Maintain normovolemia
 Hypotonic/glucose containing fluids
should not be used
 Serum sodium levels monitored daily

71. Mannitol
 0.25-1g/kg
 Osmotic agent- dec ICP, maintains CBF,CPP and brain
metabolism
 Dec ICP within 6 hrs.
 Expands volume, O2 carrying capacity.
 Diuretic effect- net intravascular volume is reduced.

72. Furosemide
 To reduce ICT in conjunction with mannitol
 Dose 0.3 to 0.5 mg/kg
 Never use in Hypovolemia

73.  Hypertonic Saline
 Improves CPP and brain tissue O2 levels
 Decreased ICP by 35% (8-10 mm HG)
 CPP increased by 14%
 MAP remained stable
 Greatest benefit in those with higher ICP and lower CPP
 Repeated doses were not associated with rebound,
hypovolemia or HTN
 30 mL of 23.4% over 15 minutes

74. HYPERVENTILATION
 No role as prophylaxis in 24 hrs.
 Reducing PaCO2 cerebral vasoconstriction
 Maintain PaCo2 25 – 35 mmhg
 Last resort for reducing ICP
 TEMPORARY MEASURE ONLY.

75. Barbiturates
 Effective in reducing ICP – refactory to other measures
 Not used in presence of hypotension/hypovolemia

76. Anticonvulsants
 Phenytoin-
Loading dose - 18 – 20 mg/kg
Maintenance dose - 100 mg q 8 hrly

77. Surgical Management of Specific
Head injuries
 Various guideline followed
 Guidelines For Surgical Management of Traumatic
Brain Injury
 Published in 2001
 All new reports and literature regularly updated
through Neurosurgical Evidence Based Medicine
Centre ,University Of Washington.

78. Depressed skull Freacture
 Indications of operative treatment
1.gross wound contamination
2.significant intracranial hematoma
3.gross cosmetic deformity
4.frontal sinus involvement
5.dural penetration
6.depression > 1cm
7.wound infection
8.pneumocephalus
 Elevation and debridement – method of choice

79. Fracture Skull Base
 With CSF leaks
no acute surgery required for CSF leak
for first 72 hrs observation (elevation of head)
if leak persists
temporary CSF diversion (lumbar drainage or
ventriculostomy)
Still leak persists surgery to be done
 Exploration of floor of frontal fossa with closure of
dural defect

80. EDH
 Absolute indications of surgery (regardless of GCS)
1. > 30 ml vol of hematoma
2. > 15 ml thickness of blood clot
3. midline shift >5 mm
4. anisocoria ( > 1mm)
 If GCS <8 = immediate surgery
 If GCS > 8 = as soon as possible
 If size less than above but GCS <8 = surgery
 If size less than above but GCS >8 =nonoperative
management can be done
 Mean time of EDH for reexpansion is 8 hrs -36 hrs.

81. SDH
 Absolute indication of surgery
1. > 10 mm thickness of blot clot
2.Midline shift > 5mm
 If size less than above but GCS <8 along with
1. GCS decreased by 2 from time of injury to
admission
2. Pt. with asymmetric or fixed dilated pupils
3.ICP >20 mm of Hg
 If size less than above and GCS >8 = non operative
treatment.
 If planned surgery should be within first 4 hrs
 Craniotomy with duraplasty with or without bone flap
removal

82. Posterior Fossa Lesions
 No monitoring possible because of location
 Guidelines for evacuation
1. > 3cm clot on CT scan
2. any size of clot with ASDH or EDH

83. Penetrating Brain Injury
 Meningitis and abscess most common complications
followed by Seizures
 If grossly contaminated wound then craniotomy and
debridement required
 Small clean wounds with no scalp devitalization can be
managed conservatively
 If open sinus suspected repair should be done
 If dural injury suspected repair should be done.

84. Burr hole
 Pentrator
 Burr hole bit
 Bone rongeur
 Scalpel

85. Procedure
A burr hole is placed on
the side of the dilating
pupil.
In the absence of a CT
scan, the burr hole is
placed 2 finger widths
anterior to the tragus of
the ear and 3 finger widths
above the tragus of the ear.

86. A vertical incision is made approximately 3
cm long, centered over the entry point all
the way down to the temporalis muscle
dividing the fibers of the muscle vertically.
The periosteum is then cut in the same
manner.

87. The outer table of the skull is drilled with the
penetrator

88. If there continues to be excessive bleeding
through the hole, packing the wound should
be tried with Gel foam or by cutting off a piece
of temporalis muscle and stuffing it into the
hole.

89. Decompressive Craniectomy
 Controversial
 Used in patients without focal lesion and raised ICP
who are refractory to maximum medical management
 The operation involves removing a large section of
skull and opening the dura, allowing the swollen brain
to expand underneath the scalp
 The bone flap is stored and can be replaced 3–6
months later when the patient has made a good
neurological recovery and the brain swelling has
resolved

91. Long term sequelae of Head Injury
 Neurorehabilitation
 Neuropsychology – after minor head injuries such as
headache, dizziness, impaired short term memory,
concentration etc.
 Seizures –prophylactic anticonvulsants cant prevent long
term seizures
 Delayed CSF leak –CT cisternography or CT isotope studies
can be done

92.  Seizure Disorder
 2% Early post-traumatic incidence
 Increased to 30% in children, alcoholics and with
intracranial hematoma
 Prophylactic antiepileptics reduce early occurrence
 Use not supported by the literature
 Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - Cognitive/Memory dysfunction

93.  Concussion
 Up to 80% may have symptoms at 3 months
 15% may have symptoms at 1 year
 Persistence of these symptoms is termed Postconcussive
Syndrome
 85-90% recover after 1 year
 Risk factors:
- Female - Litigation - Low socioeconomic status

94. Outcome

95. Pheneas Gage – most popular
patient in Neurosurgery

96. THANK YOU