This document provides an overview of head injuries, including definitions, surgical anatomy of relevant structures like the scalp, skull, meninges and brain, epidemiology, etiology, classifications, pathophysiology, clinical presentation, workup and management. It discusses different types of head injuries such as blunt and penetrating injuries, and classifications based on integrity of the dura mater, site of injury and pathology. Specific types of injuries like fractures, hematomas, and brain injuries are described in detail.

1. HEAD INJURIES
Dr Phillipo L. Chalya M.D. ;M.Med [Surg]
Surgeon specialist
Dept of Surgery
BMC

2. OUTLINE
 Definition
 Surgical Anatomy
 Epidemiology
 Etiology
 Mechanism of injury
 Classifications
 Pathophysiology
 Clinical presentation
 Workup
 Management
 Complications

3. DEFINITION
 Head injury is defined as traumatic injuries involving the cranium
and intracranial structures (i.e., brain; cranial nerves; meninges;
and other structures
 Head injury can also be defined as any alteration in mental or
physical functioning related to a blow to the head
 Maxillofacial injuries is not part of head injury

5. SURGICAL ANATOMY
 Structures to be considered in head injuries
 Scalp
 Skull
 Meninges
 Brain
 CSF

6. Scalp
 Skin
 Thick, hair bearing with many
sebaceous glands
 Connective tissue
 Fibro-fatty
 Many blood vessels
 Aponeurosis [epicranial]
 Tough structure joining occipitalis
muscle posteriorly and frontalis
anteriorly
 Loose areola tissue
 Occupies the subaponeurotic space
 Pericranium
 Periosteum covering the outer
surface of the skull

7. Skull
 22 bones in total
 Consists of:-
 8 cranial bones [cranium]
 14 facial bones
 Cranium is that part of the skull that encloses the brain
 The cranium is made up of the vault [the upper part] and the base
of the skull [lower part]
 The inner aspect of the base of the skull consists of 3 cranial
fossae:-
 Anterior cranial fossa
 Middle cranial fossa
 Posterior cranial fossa

10. Meninges
 3 layers
 Dura mater
 Arachnoid mater
 Pia mater

11. Dura mater
 Conventionally 2 layers:
 Endosteal layer (periosteum)
 Meningeal layer (true dura)
 Septa: made up of dural folds
 Divides the cranial cavity into 3 compartments
 2 upper compartments [supratentorial compartments]
 1 lower compartment [infratentorial compartment]
 Major dural folds include:-
 Falx cerebri
 Tentorium cerebelli

12. Falx cerebri
 Sickle-shaped
 Upper part is fixed and the lower
part is free
 Lies vertically in the longitudinal
fissure between the 2 cerebral
hemispheres
 Divides the supratentorial
compartment into 2 parts
 The 2 supratentorial
compartments are occupied by
the two cerebral hemispheres

14. Tentorium cerebelli
 Crescent shaped
 Lies horizontally between the occipital lobe of the cerebrum and
the cerebellum
 Posteriorly is fixed
 Anteriorly is free with an opening [tentorial notch] for passage of
the midbrain
 Has a protective function
 it prevents shuddering movements of the brain within the cranial
cavity and the folds prevent damage to nervous tissue during
sudden rotational movements

16. Arachnoid Mater
 Internal to the dura mater
 Is an avascular membrane
 Lies between the pia mater internally and the dura mater
externally
 It is separated from the pia mater by the subarachnoid cavity or
space, which is filled with cerebrospinal fluid.
 Called arachnoid because the cobweblike trabeculae crossing the
subarachnoid spase to become continuous with the pia mater

17. Pia Mater
 Vascular membrane
 Closely invests the brain
 Descends into gyri
 Extends over cranial nerves as they come out the brain – fuses
with the epineurium
 Forms Tela Choroidea of 3rd & 4th ventricles
 Fuses with ependyma to form Choroid Plexus in Lateral, 3rd & 4th
ventricles --> CSF

18. Brain
 Divided into three major areas
 Cerebrum
 Brain stem
 Cerebellum

19. Cerebrum
 The cerebrum is composed of 2 cerebral hemispheres
 The hemispheres are connected by the corpus callosum
 Consists of 4 lobes
 Parietal lobe
 Frontal lobe
 Occipital lobe
 Temporal lobe

22. Brain stem
 Three major divisions
 Midbrain
 Pons
 Medulla
 10 of the 12 pairs of cranial nerves arise from the brainstem
(ipsilateral signs)
 Cortical pathways pass through the brainstem and decussate
(cross) in the medulla (contralateral signs)

23. Cerebellum
 This is the largest part of the hind brain

24. EPIDEMIOLOGY
 Incidence
 Morbidity/mortality
 Age
 Sex
 Race

25.  Head injury continues to be an enormous public health
problem, even with modern medicine in the 21st century
 It is one of the most common cause of admissions to the A&E
department worldwide
Incidence

26. Morbidity /mortality
 Head injury are the major cause of morbidity and mortality
among trauma admissions

27. Age
 Head injuries occur in all age groups, with a peak incidence
between the ages of 16 and 25 years and a second peak in the
elderly who have a high incidence of chronic subdural
haematomas
 Head injuries are a leading cause of trauma related deaths in
patients young than 45 years

28. sex
 Males are more affected than females
 The male to female ratio is 2:1 [M:F= 2:1] worldwide

29. AETIOLOGY
 Road traffic accidents
 Fall injuries
 Assault injuries
 Sport injuries
 Penetrating injuries e.g. bullets, knives, screwdrivers, arrows,
nails etc

30. MECHANISM OF INJURY
 Blunt head injury
 Penetrating head injury

31. Blunt head injury
 Direct trauma to the head
 Occurs in 2 ways: a moving head strikes a fixed object or a
moving object strikes an immobile head scalp injury,→
fractures of the skull, contused brain etc
 Deceleration head injuries
 These are injuries resulting from rapid deceleration of the
head causing the brain to move within the cranial cavity and to
come into contact with bony protuberances within the skull→
brain contusions, lacerations etc

32. Penetrating head injury
 The severity of penetrating injury is directly proportional to the
K.E. of the moving object
 K.E. = 1/2mv2,
where m= mass, v= velocity
 Classified into 2 types according to the velocity which is the main
determinant in the equation
 High velocity injury
 Bullets
 Low velocity injury
 Knifes, arrows, screwdrivers etc

33. CLASSIFICATION
 According to mechanism of injury
 According to the integrity of the dura mater
 According to the site of injury
 According to the pathology
 According to severity

34. According to mechanism
of injury
 Blunt head injury [Non-missile injuries]
 Penetrating head injury [Missile injuries]

35. Blunt head injury
 Occurs as a result of blunt force trauma or non-missile injury
to the head →injury to the scalp, skull and other intracranial
structures
 Can also occur as a result of rapid deceleration and
acceleration causing the brain to move within the cranial cavity
and come into contact with bony prominences within the skull→
contusion, laceration and shearing strains within the brain
substances

36. Penetrating head injury
 A penetrating head injury occurs when a sharp object pierces
the skull and breaches the dura mater

37. According to the integrity of
the dura mater
 Open head injury
 Closed head injury

38. Open head injury
 Is one in which there is a wound which extends through the
scalp, the skull and the dura mater, that is to say the brain is
exposed
 In open head injury the dura mater is not intact
 There is grave danger of infection

39. Closed head injury
 In the closed type of head injury the brain is not exposed to
outside world, that is any or all , of the scalp, skull bone and
dura mater are intact
 In closed head injury the dura mater is intact and the risk of
infection is low
 Today we are talking of “ BRAIN INJURIES INSIDE THE CLOSED
BOX”

40. According to the site of
injury
 Scalp injury
 Skull injury
 Meningeal injury
 Brain injury
 Intracranial vascular injury
 Cranial nerves injury

41. Scalp injury
 Scalp lacerations
 Scalp cut wounds
 Scalp hematoma
 Subcutaneous
 Subaponerotic
 Subpericranial

42. Skull injury
 Fracture of the vault [vault skull fracture]
 Fracture of the base of the skull [basilar fracture]

43. Fracture of the vault
 According to whether the fracture is exposed to the outside world
 Simple [closed] fracture: The fracture is not exposed the outside
 Compound [open] fracture : The fracture is exposed to the outside
 According to the type of fracture
 Liner fracture
 Depressed fracture
 Comminuted fracture

44. Fracture of the base of the
skull
 Fracture of the anterior cranial fossa
 Fracture of the middle cranial fossa
 Fracture of the posterior cranial fossa

45. Fracture of the anterior cranial fossa
 The patient will present with:-
 Nasal bleeding (epistaxis), traumatic CSF rhinorrhoea or escape
of brain mater through the nose
 Periorbital ecchymosis (racoon eyes), subconjuctival h’ge
extending beyond the conjuctival reflections intraorbital h’ge
 Anosmia if both olfactory nerves are damaged
 Injuries to 3rd
, 4th
, 1st
division of 5th
and 6th
at the sphenoidal fissure
 3rd
palsy produces dilated a pupil in a conscious patient

46. Fracture of the middle cranial fossa
 This presents with:-
 Bleeding from the ears [hemotympanum] or mouth
 CSF otorrhoea
 CSF Rhinorrhoea via the eustachian tube
 Oscular disruption
 7th
and 8th
cranial nerve palsies →facial palsy and deafness
respectively

47. Fracture of the posterior cranial fossa
 Extravasation of blood may be seen in the suboccipal region
producing a swelling at the back
 Post auricular [posterior to the mastoid process] ecchymosis
[Battle’s sign]
 Injury to the 9th
, 10th
and 11st at the jugular foramen

48. Meningeal injury
 This occurs commonly as a result of fracture of the skull
 The type of fracture of the skull which causes laceration of
the dura mater is the depressed compound fracture

49. Brain injury
 Primary brain injury
 That is damage which occurs at the time of injury
 Secondary brain injury
 That is damage which occurs as a consequence of primary
brain damage

50. Primary brain injury
 Cerebral concussion
 Cerebral contusion
 Cerebral laceration
 Diffuse axonal injury

51. Cerebral concussion
 Temporary physiological loss of function without any organic
structural damage
 The patient becomes unconscious for a short period ,
followed by complete and perfect recovery
 Develops immediately after injury
 It may be accompanied by autonomic abnormalities e.g.
bradycardia, hypotension & sweating
 Prolonged LOC means something easy than pure concussion

52. Cerebral contusion
 Bruising of the brain
 Characterized by rupture of white fibres of the brain causing
peticheal h,ge in the cerebral parenchyma
 Usually produces neurological deficits that persist for > 24
hrs
 Contusions may resolve together with the accompanying
deficits or the may persist
 Blood-brain barrier defects and cerebral edema are common
and these lesions enlarge or coalesce with time

53. Cerebral laceration
 In this condition the brain surface is torn with effusion of blood
into CSF→SAH [subarachnoid h’ge]
 This occurs when there is a significant force to the skull
→laceration of the brain as a result of rapid movement and
shearing of brain tissue
 The pia mater and arachnoid may be torn →ICH [intra-cerebral
h’ge]
 Focal neurological deficits are common
 Clinically presents as cerebral contusion

54. Diffuse axonal injury
 This type of brain damage occurs as a result of mechanical
shearing following deceleration, causing disruption and tearing of
axons, especially at the grey/white matter interfaces

55. Secondary brain injury
 Intracranial hematoma
 Cerebral edema
 Brain herniation
 Cerebral ischaemia
 Infection
 Epilepsy

56. Intracranial vascular injuries
 Epidural / extradural hematoma
 Subdural haematoma
 Subarachnoid haematoma
 Intracerebral hematoma

57. Epidural / extradural
hematoma
 This is haematoma between the
inner table of the skull and the dura
mater
 Occurs as a result of injury to the
middle meningeal artery
 If untreated →midline shift, brain
herniation, midbrain compression
 Commonly presents with “lucid
interval”

58. Subdural haematoma
 Haematoma between the dura and the
arachnoid mater
 More common
 Occurs as result of tearing of bridging
veins crossing the subdural space
from the cortex to the dura
 Can also occur as a result of cortical
laceration or bleeding from the dural
venous sinuses
 Described as acute or chronic
depending on the age

59. Subarachnoid haematoma
 Haematoma in the space between the arachnoid space and the pia
mater [subarachnoid space]
 Occurs when a vessel ruptures into the subarachnoid layer or in
case of cerebral lacerations
 There is extravasations of blood under pressure into the CSF
space, ventricles or into the brain itself
 The patient presents with severe headache of sudden onset,
nausea and vomiting

60. Intracerebral hematoma
 This is haematoma formed within the brain parenchyma
 They are due to areas of contusion coalescing into a contusional
haematoma
 They appear as hyperdense lesions on the CT scan with
associated mass effect and midline shift

61. Cranial nerve injuries
 Head injury may be associated with the injuries to deferent
cranial nerves
 The 3rd
cranial nerve is the most important as it is involved
even by cerebral compression besides direct injury
 The different cranial nerves are injured in fracture of
different parts of the base of the skull

62. According to the
pathology
 Focal head injury
 Diffuse head injury

63. Focal head injury
 In this type, the injury is localized to only part of the head
 Focal injuries include scalp injury, skull fracture, and surface
contusions and are generally be caused by direct impact

64. Diffuse head injury
 Diffuse injuries include diffuse axonal injury, hypoxic-
ischemic damage, meningitis, and vascular injury
 They are usually caused by acceleration-deceleration forces

65. According to severity
 Classified according to Glasgow Coma Score [GCS]
 Classified into:-
 Mild head injury [GCS of 13-15]
 Moderate head injury [GCS of 9-12]
 Severe head injury [ GCS of 3-8 ]

66. PATHOPHYSIOLOGY
 Requires understanding of the following crucial concepts:-
 The concept of Monro-Kellie doctrine
 The concept of Cerebral Perfusion Pressure [CPP]
 The concept of increased ICP

67. Monro-Kellie doctrine
 The skull is a rigid structure (once the sutures have fused)
 3 components within that have a balance
 80% brain
 10% blood
 10% CSF
 If any one of these components increases [or if there is a SOL]
another component must decrease to maintain the balance (ICP)
 If this does not happen then there will be an increase in ICP
 This observations were first reported by Monro [1783] and
confirmed by Kellie 40 years later→ becoming known as the
Monro-Kellie docrine

68. Cerebral Perfusion
Pressure [CPP]
 CPP is defined as the difference between the mean arterial
pressure (MAP) and the ICP [ i.e. CPP = MAP – ICP]
 CPP is the net pressure required to deliver blood to the brain
 Cerebral blood flow (CBF) is constant in the range of MAPs of 50-
150 mm Hg
 This is due to autoregulation by the arterioles
 As ICP increases, in order to maintain a constant CPP there has to
be a compensatory rise in the MAP
 A hypertensive response is therefore elicited which classically is
associated with bradycardia
 This is termed as the Cushing reflex after the eminent American
neurosurgeon

69. Increased ICP
 May result from primary or secondary brain injury
 Normal ICP in adult is 0-15 mmHg, in children is 0-10 mmHg
 This causes:-
 Cerebral herniation
 Cerebral edema
 Cerebral ischaemia

70. Brain herniation
 Several types of herniation exist, as follows:
 Transtentorial herniation
 Subfalcine herniation
 Central herniation
 Cerebellar herniation
 Upward cerebellar herniation
 Tonsillar herniation

71. Transtentorial herniation
 Occurs when the medial aspect of the temporal lobe
(uncus) migrates across the free edge of the tentorium
 This causes pressure on the third cranial nerve,
interrupting parasympathetic input to the eye and
resulting in a dilated pupil
 This unilateral dilated pupil is the classic sign of
transtentorial herniation and usually (80%) occurs
ipsilateral to the side of the transtentorial herniation
 In addition to pressure on the third cranial nerve,
transtentorial herniation compresses the brainstem

72. Subfalcine herniation
 Occurs when the cingulate gyrus on the medial aspect of
the frontal lobe is displaced across the midline under the
free edge of the falx
 This may compromise the blood flow through the anterior
cerebral artery complexes, which are located on the
medial side of each frontal lobe
 Subfalcine herniation does not cause the same brainstem
effects as those caused by transtentorial herniation

73. Central herniation
 Central herniation occurs when a diffuse increase in ICP occurs
 Each of the cerebral hemispheres is displaced through the
tentorium, resulting in significant pressure on the upper
brainstem

74. Cerebellar herniation
 2 types:-
 Upward cerebellar herniation
 Downward cerebellar herniation [tonsillar]

75. Upward cerebellar herniation
 Occurs when either a large mass or increased pressure in
the posterior fossa is present and the cerebellum is
displaced in an upward direction through the tentorial
opening
 This also causes significant upper brainstem compression

76. Tonsillar herniation
 Occurs when increased pressure develops in the posterior
fossa
 In this form of herniation, the cerebellar tonsils are displaced
in a downward direction through the foramen magnum,
causing compression on the lower brainstem and upper
cervical spinal cord as they pass through the foramen
magnum

77. Cerebral edema
 Vasogenic cerebral edema
 Cytotoxic cerebral edema
 Interstitial cerebral edema

78. Vasogenic cerebral edema
 Refers to the influx of fluid and solutes into the brain tissue
through an incompetent or damaged blood-brain-barrier (BBB)
 This is the most common type of brain edema and results from
increased permeability of the capillary endothelial cells
 Breakdown of the BBB allows movement of proteins from the
intravascular space through the capillary wall into the
extracellular space→ influx of fluid and solutes

79. Cytotoxic cerebral edema
 In this type of edema the BBB remains intact
 This edema is due to the derangement in cellular metabolism
resulting in inadequate functioning of the sodium and potassium
pump in the glial cell membrane
 As a result there is cellular retention of sodium and water
→swelling of the glia, neurons and endothelial cells
 Cytotoxic edema affects predominantly the grey mater

80. Interstitial cerebral edema
 This is seen in hydrocephalus when the outflow of CSF is
obstructed and intraventricular pressure increases
 The result is movement of sodium and water across the
ventricular wall into the paraventricular space

81. Cerebral ischaemia
 ICP results in CPP and therefore CBF [CPP= MAP-ICP]→
cerebral ischaemia
 This is common after severe head injury and is caused by a
combination of either hypoxia and impaired cerebral
perfusion
 The brain is unable to autoregulate its blood supply with a
decrease in blood pressure

82. CLINICAL
PRESANTATION
 History
 Physical Examination

83. History [cont’d]
 Taken from an eye witness if the patient is unconscious or
from the patient
 Include;-
 Mechanism and full details of injury
 For example:
 Fall: Height, surface, posture of fall, point of contact
 Motor vehicle collision: Speed, place in car, restraint, point of
impact
 etc

84. History [cont’d]
 Time of accident
 Level of consciousness / unconscious?
 Time of onset of unconsciousness
 Duration of unconsciousness
 Lucid interval
 Amnesia [loss of memory]–
 Retrograde Traumatic Amnesia
 Post-traumatic amnesia

85. History [cont’d]
 Current symptoms
 Headache, vomiting, bleeding from ENT, LOC, fits, other associated
injuries
 Pre-morbid illness
 Diabetes mellitus
 Renal diseases
 Hypertension
 Previous history of fits
 History of medications and Allergies
 Habit of taking alcohol or opium

86. Physical Examination
 Head
 Scalp lacerations or haematoma
 Fractures: depressed, base of skull (“raccoon eyes”, “Battles
sign”
 CSF leak, blood in the ear canal or behind the tympanic
membrane, bleeding from nose or mouth etc
 Face
 Fractures
 intra-oral injuries

87. Physical Examination
[cont’d]
 Neck
 Neck rigidity
 Immobilization is required until stability is assured
 Trunk
 Evidence of chest injuries
 Evidence of abdominal injuries
 MSS [limbs, pelvis and spines]
 Closed or open wounds, fractures
 Neurological
 Level of consciousness (GCS), pupilary size and reaction to light
Focal signs, brainstem reflexes, motor function

88. WORKUP
 Laboratory investigations
 Imaging investigations
 Other investigations

89. Laboratory investigations
 Haemogram
 Serum sugar
 Serum electrolytes
 RFT
 Grouping & cross-matching
 Coagulation profile

90. Imaging investigations
 Skull x-rays
 CT Scan brain/skull
 MRI [Magnetic Resonance Imaging]
 Cervical x-rays

91. Skull x-rays
 2 views
 AP-views
 Lateral views
 Can revealed
 Fracture of the skull
 Other bony abnormalities
 If CT scan is easily available Skull x-ray can be avoided
as with CT scan all the relevant information obtained in
skull x-ray can be obtained with bone windows of CT scan

92. CT Scan brain/skull
 Investigation of choice
 Can reveal
 Bony injury
 Haematomas
 Evidence of cerebral edema
 Mass effect [midline shift]
 It is necessary for operative planning

93. CT Scan brain/skull [cont’d]
 Indications
 Moderate to severe head injury
 Deteriorating levels of consciousness
 Depressed fractures
 Focal neurological deficits
 Evidence of basilar fracture
 Penetrating head trauma
 Persistent severe headache and vomiting
 Seizures

94. Magnetic Resonance Imaging
[MRI]
 Has no role in acute management of patients with head injury
 Can be used in case of diffuse axonal injury and in follow-up
prognostication
 Able to detect small lesions in vital areas of brain not seen by
CT scan
 Preserved for later detail evaluation after acute problem has
been addressed

95. Cervical spine x-ray
 2 views
 AP view
 Lateral view
 Done to exclude associated cervical spine injuries
 CERVICAL SPINAL COLLAR should be kept on until a fracture
or dislocation of the cervical spine has been ruled out

96. Other investigations
 Carotid angiography
 Electro-encephalography
 Echo-encephalography

97. Carotid angiography
 Plays an important role to demonstrate the site of the lesion
 Not performed in acute conditions
 Can indicate:-
 Subdural haematoma
 Displacement of the cortical vessels away from the inner table of the
skull
 Epidural haematoma
 Displacement of middle cerebral artery inward
 Displacement of anterior cerebral artery across the midline
 Intracerebral haematoma
 Displacement of the middle cerebral artery upwards

98. Electro-encephalography
 This investigation will show areas of suppressed
activity of the cortex due to injury or pressure by h’ge

99. Echo-encephalography
 This will indicate the presence of haematoma by indicating
a shift of the midline structure
 It is not of much help in subdural haematoma as half of
the cases are bilateral with no midline shift

100. MANAGEMENT
 Criteria for admission
 The management of head injury follow Advanced Trauma
Life Support [ATLS] guideline
 6 phases
 Primary survey phase
 Resuscitation phase
 Secondary survey phase
 Tertiary survey phase
 Supportive care phase
 Definitive care phase

101. Criteria for admission
 Moderate to severe head injury
 No CT scan available or abnormal CT Head
 All penetrating head injuries
 History of loss of consciousness
 Deteriorating Level of Consciousness
 Moderate to severe Headache
 Significant Alcohol or drug intoxication
 Skull Fracture
 Cerebrospinal Fluid leakage (Otorrhea or Rhinorrhea)
 Significant associated injuries
 No reliable companion at home or displaced home
 Amnesia

102. Primary survey phase
 Aimed at identifying the immediately life threatening
conditions
 Elements of primary survey phase:-
 Airway with cervical spine control
 Breathing and ventilation
 Circulation with control of hemorrhage
 Dysfunction of the CNS
 Exposure in a controlled environment

103. Resuscitation phase
 Done simultaneously with primary survey phase
 Needs multidisciplinary approach
 Aimed at treating the immediately life threatening
conditions
 Establish a patent airway and immobilization of cervical
spine
 Ensure breathing and adequate ventilatory support
 Restore circulatory volume and h’ge control
 Brief neurological evaluation
 Fully expose [undress] the patient

104. Airway with cervical spine
control
 A clear patent and functional airway should be
established
 This can be achieved by:-
 Use of airways
 Proper position of the patient
 Endotracheal intubation
 Ambubags
 Tracheostomy

105. Breathing and ventilation
 Make sure the patient is breathing properly
 Achieved by:-
 use of oxygen masks
 Mechanical ventilators

106. Circulation with control of
hemorrhage
 Patients with head trauma may be associated with massive
blood loss leading to hemorrhagic shock
 A functional i.v. fluid should be established to restore blood
volume and prevent irreversible shock
 During the shock state use crystalloid fluid
 Glucose containing solutions should be avoided; euvolaemia
should be maintained
 BT should be given in case of hemorrhagic shock

107. Dysfunction of the CNS
 Brief neurological evaluation should be done
 This involves brief assessment of the following:-
 Level of consciousness using GCS
 Pupilary size and reaction to light
 Motor function
 Sensory function
 Reflexes

108. Exposure in a controlled
environment
 The patient should be fully exposed to be able to exclude
missed injuries

109. Secondary survey phase
 This include:-
 History
 Physical examination
 Investigations as above

110. Tertiary survey phase
 A routine head-to-toe examination of a patient should
take place within 24 hours of the injury to document any
missed injuries and re-evaluate existing injuries and
their treatment

111. Supportive care phase
 Position:
 In a recovery position
 Elevate the head by 15-30
o
[take care of cervical fracture]
 2 hourly turning to avoid pressure sores
 Urethral catheterization to empty the bladder in order to:-
 Avoid renal complications
 Enable good record of his output to be kept
 To ensure the bed is dry
 NGT should be inserted in all patients with severe head injury
except patient with nasal bleeding and rhinorrhoea
 To empty the stomach and for feeding

112. Supportive care phase
[cont’d]
 Monitor:
 Levels of consciousness
 Pupillary size and reaction to light
 Vital signs
 Input-output chart
 Motor and sensory functions
 Nutrition support
 Patients who started on nutrition earlier have better out
come than when it is started later

113. Supportive care phase
[cont’d
 Hyperthermia
 Temperature of 32-34
o
C is maintained for at least 48 hours
and is to be started within 8 hours of traumatic brain injury
 Has been shown to decrease the rate of cerebral
metabolism, decreasing cerebral blood flow and
intracranial pressure
 Use of this technique is limited, as it increases risk of
infection, cardiac arrhythmia, and coagulopathy

114. Supportive care phase
[cont’d
 Hyperventilation
 Controlled hyperventilation →↓PaCO2
→

115. Supportive care phase
[cont’d
 Correction of contributory factors - Correction of factors
increasing ICP e.g.
 Hypercarbia
 Hypoxia
 Hyperthermia
 Acidosis
 Hypotension
 Hypovolaemia

116. Definitive care phase
 Medical treatment
 Surgical management

117. Medical treatment
 Osmotherapy
 Corticosteroids
 Anticonvulsants
 Barbiturates
 Antibiotics
 Analgesics

118. Osmotherapy
 Intended to draw water out of the brain by an osmotic
gradient and to decrease blood viscosity
 These changes decrease ICP and increase CBF
 Include
 Mannitol
 Diuretics [loop] –e.g. Frusemide

119. Mannitol
 Potent osmotic agent
 ↓ICP by 2 mechanisms:-
 Drawing water from the brain by osmotic gradient→ ↓cerebral
edema
 ↓viscosity of blood →↑CPP and CBF
 Used when the BBB is intact otherwise if the BBB is disrupted as
in cerebral contusion, Mannitol can leach out into the brain and
potentiate the mass effect
 It becomes ineffective when brain osmolarity becomes iso-
osmolar with that of the serum→so it is of short-term use
 Dose: 1 g/kg 4-6 hourly

120. Diuretics [loop]
 E.g. Frusemide
 Potent osmotic agent
 Reduces ICP by reducing cerebral edema and CSF production
 It may act synergistically with mannitol

121. Corticosteroids
 Commonly used corticosteroids e.g. Dexamethasone
 ↓ICP primarily in vasogenic edema
 Less effective in cytotoxic edema

122. Anticonvulsants
 Includes:-
 Diazepam
 Phenobarbitone
 Phenytoin
 E.g.
 These agents may help treat or prevent early seizures in
head injury

123. Barbiturates
 E.g. thiopentone
 ↓ICP by reducing cerebral metabolism
 Has been shown to decrease the rate of cerebral metabolism,
decreasing cerebral blood flow and intracranial pressure
 Help to ↓ICP that is refractory to other conventional
measures

124. Antibiotics
 Prophylactic antibiotics is important in preventing meningitis
and other intracranial infections

125. Analgesics
 Avoid stronger sedatives especially morphine because they
interfere with the assessment of consciousness and depress
respiration
 Moderate restless is useful, because it is good physiotherapy
for his lung and prevent pressure sores

126. Surgical management
 Aim
 Indications
 Type of surgery performed
 Site for burr holes
 Types of scalp incisions for craniotomies

127. Aim of surgical treatment
 To relieve cerebral compression
 To reduce ICP
 To elevate depressed skull pressure
 Treatment of open or penetrating head injuries

128. Indications
 Deterioration in patient’s levels of consciousness
 Development of focal neurological deficits e.g. hemiplegia
 Pupilary unilateral dilation
 A rise BP associated with bradycardia
 Depressed skull fracture
 Open head injuries

129. Types of surgery performed
 Decompressive craniotomy
 Elevation of depressed fracture
 Surgical toilet

130. Site for burr holes
 Parietal burr hole
 Temporal burr hole
 Frontal burr hole

131. Types of scalp incisions
 Question mark flap
 Bicoronal flap
 Linear incision
 Square-sided flap

132. CoMpliCATioNs
 Focal neurological deficits
 CSF fistula
 Pneumocephalus
 Intracranial infections
 Posttraumatic Hydrocephalus
 Posttraumatic seizures
 Intracranial vascular injuries
 Posttraumatic epilepsy
 Carotico-cavernous sinus fistula
 Brain death