Hi. This is Dr. Amit T. Suryawanshi. Oral & Maxillofacial surgeon from Pune, India. I am here on slideshare.com to share some of my own presentations presented at various levels in the field of OMFS. Hope this would somehow be helpful to you making your presentations. All the best.
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Neurological complications in omfs trauma by Dr. Amit T. Suryawanshi, Oral Surgeon, Pune
1. Neurological complications in
Maxillofacial trauma
Dr. Amit T. Suryawanshi
Oral and Maxillofacial Surgeon
Pune, India
Contact details :
Email ID - amitsuryawanshi999@gmail.com
Mobile No - 9405622455
3. Introduction
• Trauma is the leading cause of death and in more
than 75% of cases, head injury accounts for a
notable portion of the morbidity.
• Despite recent medical advancements, physical
and functional morbidity frequently follows
traumatic brain injury (TBI) even in seemingly
minor trauma.
4. • Fall, sport activities, motor vehicle accidents and
assaults are the major causes of maxillofacial
injuries which are commonly associated with
cervical spine and intracranial injury.
5. • The principles of management of trauma are
directed at stabilizing patient’s medical
condition and providing safe reconstruction to
maximize both functional and aesthetic
rehabilitation.
6. Initial assessment and treatment
It includes
1. Airway maintenance
2. Breathing - Mechanical ventilation
3. Circulatory stabilization
4. Assessment of Disability / Definitive care
5. Exposure
7. Rapid Initial Assessment
• Consciousness
• Respiration and vital signs
• Associated trauma
• Neck
Cervical spine injury -Cervical spine must be
immobilized
Carotid injury
• Eyes – Pupils , movements , reflexes
• Airway – Gag reflex
• Limbs –Motor examination, reflexes, sensation
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8. Cervical spine injury-
• Incidence – 2% in maxillofacial trauma
• One must assume that every head injury has an
associated cervical spine injury until proven otherwise.
• Clinical features –
1. Patient particularly complains of neck pain
2. Paralysis or weakness of limbs depending on
extent of injury.
3. If it is severe , there is loss of respiratory drive and
death.
9.
10. Management -
• Patients with unrestrained cervical spine must
be immobilized in a carefully placed hard
cervical collar until cervical spine radiographs
or CT obtained and examined.
12. Extraoccular muscles
Examination of the movements of the extraoccular
muscles may reveal various nerve palsies
• Unilateral lateral gaze palsy-
It can occur due to damage to the Abducens nerve
by direct trauma to the clivus region or lateral
orbital wall fracture.
13. • Paresis of Upward gaze –
• This can occur with hemorrhage causing
compression of the midbrain tectum.
• Common manifestations- Lack of light reflex &
convergence.
14. Complete opthalmoplegia –
• It is the inability to move all the extraoccular
muscles, resulting in damage to occulomotor
nerve, trochlear nerve, abducens nerve which
is often accompanied by proptosis, ptosis, a
fixed and dilated pupil, and loss of sensation
of the forehead .
15. Motor examination
• Tone, strength and reflexes must be assessed.
Tone & strength assessment –
1. Increased tone –due to compression of
contralateral cerebral peduncle
2. Flaccid tone –implies either brainstem
infarction or spinal cord transection
16. • Deep tendon reflexes –
• Hyperreflexia – Usually occurs with compression
lesions in contralateral cerebral peduncle.
Extensor plantar reflex (positive babinski’s sign)
• Areflexia –Occurs in spinal cord trauma or
transection.
18. Intracranial lesions -
Traumatic brain injury is divided into two distinctive
components
1. Primary brain injury –
2. Secondary brain injury -
19. Primary brain injury –
Primary brain injury occurs immediately
upon impact and results from rapid
acceleration or the shearing and rotational
effects of a blow to the head. This can lead to
irreversible damage as a result of direct
mechanical cell disruption.
It is divided into
1. Focal injury
2. Diffuse injury
20. Focal injury - Focal injury is associated with blows
to the head that produce cerebral contusion
and hematoma.
Diffuse injury – It includes concussion which is
temporary loss of consciousness with no
permanent organic brain damage and diffuse
axonal injury secondary to shearing of axons.
22. Concussion
• Incidence –6 % of all head injuries
• A concussion is a mild brain injury in which
consciousness is preserved but there is a
noticeable degree of temporary neurologic
dysfunction.
.
24. • Signs and symptoms –
• Headache, confusion, disorientation, dizziness,
vomiting, nausea, lack of motor coordination
difficulty in balancing, blurred vision, double
vision, tinnitus, difficulty with reasoning,
concentrating and performing daily activities.
• A slightly greater injury causes confusion with both
retrograde and anterograde amnesia
25. Cerebral Contusion
• Incidence - 20–30% of all head
injuries
Cause -
Cerebral contusion can be
caused by multiple
microhemorrhages into brain
tissue following injury.
26.
27. • Signs and symptoms –
Headache, confusion, dizziness, loss of
consciousness; nausea and vomiting; seizures;
Hemiparesis, aphasia and difficulty with
coordination, movement, vision, speech,
hearing and thinking.
28. Epidural hematoma
Causes –
It occurs due to haemorrhage between inner
table of skull and dura mater.
• It is caused by fracture across grooves of
frontal, temporal and occipital bone.
Hematoma rapidly increases in size and
compresses cerebral cortex.
29.
30. • Signs and symptoms–
1. Unconsciousness for a brief period
2. LUCID INTERVAL after regaining
consciousness .
3. After lucid interval gradual deterioration of
consciousness that progresses to coma and
death if hematoma is not evacuated.
31. Subdural hematoma
• More common than epidural hematoma( 30%)
• Caused due to tear of veins bridging cerebral
cortex to venous sinuses or intracerebral
hematoma extends into subdural space.
• Patient’s outcome depends upon injury
caused by force of impact rather than
pressure of the bleed.
34. Secondary brain injury
• It occurs after the initial trauma. Damage to
neurons is caused by systemic physiologic
response to initial injury. It may be within
minutes, hours, or days after initial injury.
It can lead to further damage and permanent
dysfunction.
• Hypotension and hypoxia following injury are
major causes of secondary brain injury.
35. Intra-cranial complications
• Facial bones absorb much of the impact of
trauma associated with frontal violence, the
majority of patients with severe facial injuries
should be considered as having sustained
concomitant head injuries, with or without
fractures of the base of the skull.
• Morbidity and mortality due to complications
such as intracranial haemorrhage and
infection are high.
36. General consideration of diagnosis and
care
• Many potential fatal complications can occur at
any time during first 2 weeks following injury or
even later, so high standard experienced nursing
care and medical supervision is important.
• It is important to remember that the level of
consciousness or responsiveness is the most
useful indicator of any change for better or worse
in patient’s condition.
38. Early complications
These are early complications of head injury occurs
within few hours or so
1. Unconsciousness
2. Cerebrospinal fluid leaks
3. Meningism
4. Skull fractures
39. Unconsciousness
• Unconscious patient may be admitted
(Witnesses should be questioned)
1. Unconscious, having previously been
conscious since the injury -
There may have been lucid interval followed
by acute rise in intracranial pressure leading to
unconsciousness.
40. 2. Never have been conscious since the injury –
Here, patients are more likely to have cerebral
contusions, but it does not preclude the
development of other intracranial complications.
41. Cerebrospinal fluid leaks
• Fractures of the facial skeleton frequently
involve the floor of anterior cranial fossa,
usually in the region of posterior wall of
frontal sinus or cribriform plate.
• These injuries are associated with a
communication between the meninges and
nose or paranasal sinuses leading to cause csf
rhinorrhoea or otorrhoea from an associated
dural laceration.
42. • In early hours following injury, leakage will be
blood stained but later persists as a clear
watery discharge from the nostrils, ears or
associated laceratons.
• Patient in reclined position is more like to have
flow down the posterior pharyngeal wall.
43. Meningism
• Sometimes signs of meningism are present
shortly after injury, although they may take
several hours to develop, and are usually due
to traumatic subarachnoid haemorrhage.
• Photophobia, headache, neck stiffness and
positive kernig’s sign should be sought in
initial examination.
44. • These findings alone are not indications for
performing lumbar puncture unless there is risk
brain stem compression
• Bacterial meningitis may be suspected from the
development of pyrexia and changes in blood
picture. Use of antibiotics or sulphonamides are
advised rather than early diagnostic lumbar
puncture.
45. Skull fractures
• Although it is not necessarily important for
neurosurgeon to treat all skull fractures, it is
desirable that they are diagnosed early so that
complications may be anticipated and
definitive treatment is planned.
• Accordingly radiological examination should
be made for cervical spine injuries which may
limit manipulation of the head.
46. Intermediate complications
• Intermediate complications may occur at any
time up to several days or even later .These are
1. Increasing intracranial pressure
2. Meningitis
3. Persistent or recurrent CSF leaks
4. Intracranial air
47. Increasing intracranial pressure
• This very serious complication may occur at
any time up to several days , or even later ,
following head injury.
• Causes –
contusion, oedema , extradural, subdural or
intracerebral haemorrhage or combination of
these.
48. • General signs are –
1. Deterioration in the level of consciousness
2. Restlessness
3. Vomiting
4. Hypertension
5. Headache & photophobia
6. Papilloedema.
49. • Examination of pupils is of vital importance
• A dilating pupil which becomes less responsive to
light in the eye(direct) or opposite eye in the
presence of deterioration in the level of
responsiveness is the classical sign of developing
ipsilateral intracranial hematoma.
• Developing motor weakness on one side may
indicate contralateral hematoma in the region of
motor cortex. There may be developing aphasia.
50. • If diagnosed , then steps can be taken to avoid
serious problems of midbrain distortion &
haemorrhage, cerebral compression, infarction,
particularly of temporal and occipital lobes.
51. Meningitis
• Although this is relatively uncommon
complication of maxillofacial injuries.
• All cases where there is Le Fort –II or III or
naso –ethmoidal fracture , should be given
prophylactic penicillin and sulphonamides IM,
along with adequate fluid intake.
• The diagnosis of bacterial meningitis requiring
intrathecal treatment is the only indication for
lumbar puncture following head injury.
52. Persistent or recurrent CSF leaks
• In patients with maxillary fracture, the average
duration of CSF rhinorrhoea is 4-5 days with or
without reduction of fracture.
• Most neurosrgeons agree that CSF rhinorrhoea
lasts for 14 days after reduction and
immobilisation of facial fractures.
Diagnostic method –
1. Tc cisternogram
2. CT scan for the site of leak
53. Intracranial air
• The finding of intracranial air is usually
associated with a cerebrospinal fluid leak at
some age following injury.
• Subdural or subarachnoid collections of air are
often seen on the radiographs taken within
the 1st day or so but are usually absorbed
instantaneously.
54. • The development of aerocoel may coincide
with recurrence of CSF rhinorrhoea indicating
a breakdown of healing dural fistula
Symptoms – Headache, nausea, personality
disturbance, hemiparesis
• Most significant danger of aerocoel is infection
with the development of cerebral abcess.
55. Late complications
• Late complications of head injury pass
unnoticed at the time of injury but occurs
within few weeks. These are
1. Cranial nerve damage.
2. Epilepsy.
3. Accident or compensation neurosis.
56. Cranial nerve damage
• Damage to cranial nerves may pass unnoticed at
the time of injury. It is important that any
sensory or motor neurological deficit is
documented soon after injury, in order that the
impairment may be properly ascribed either to
the injury or to the subsequent events for both
prognosis and medicolegal purpose.
57. Trigeminal nerve
• Sensory disturbances in the distribution of
terminal branches of trigeminal nerve are
common after facial injuries, and are due to
stretching, compression or division of nerves.
Examples –
Inferior alveolar nerve in mandibular fractures
and infraorbital nerve in maxillary and
zygomatic fractures
58. • When nerve is contused but intact
(Neurapraxia), the sensory disturbances
referred to usually respond to reduction and
immobilization of fractures. Recovery takes
places within days or weeks.
• When nerve has been divided(neurotmesis),
loss of function is absolute and may never
recover.
59. • However, assuming the divided nerve has
been resutured or its bony canal re-aligned,
adequate time should be allowed for wallerian
degeneration and regeneration to take place
Example – In angle of mandible, it will take 12-
18 moths.
60. • During follow-ups, if there is no improvement
in reduced sensation,
paraethesia(altered sensation) and
increased sensation(hyperaesthesia), it is
often important to explore the nerve close to
the site of injury in an attempt to decompress
it, particularly in the region of infraorbital
foramen or mental foramen.
61. • Because, in these sites it is sometimes
possible to either refracture and reposition
the fragment or to enlarge the foramen.
• Rarely, injury to sensory nerve leads to
intactable neuralgic pain, termed as causalgia.
Treatment includes, carbamazepine , alcohol
injections or division of nerve.
62. Facial nerve
• Motor disturbances are less common than
sensory disturbances in maxillofacial trauma
and usually result from the damage to the
facial nerve which may occur at any point in
its course.
• Example- Lower motor neuron facial palsy in
zygomatic bone fracture .
63. • Most frequently, damage is the result of a
laceration.
Example – Fracture of neck of condyle of
mandible resulting into lower motor
neuron facial palsy.
Early administration of corticosteroids or
surgical decompression improves the prognosis
of these injuries.
64. Auriculotemporal nerve
• Damage to auriculotemporal nerve in the region
of mandibular condyle can produce phenomenon
of gustatory sweating of the skin in the temporal
region, known as von Frey’s syndrome.
• The syndrome is probably caused by the
inappropriate regeneration of autonomic nerve
fibers along the distribution of the sensory part
of the nerve, with vasodilation and sweating.
In troublesome, nerve may be avulsed.
65. • Anosmia is a frequent sequel to high- level
maxillary fractures in which the olfactory nerves
may be severed at the level of cribriform plates.
• Anosmia may be associated with the oedema
around the fracture site in the base of the skull
but recovery can be anticipated.
• Positional vertigo may result form damage to the
vestibular apparatus, in which nystagmus and
distress are elicited by sudden lowering of
rotated head to 30 degree below the horizontal
plane.
66. Epilepsy
• Incidence – 5 % of all head injuries within 1st week.
while its 1% for late epilepsy (after a week)
• Risk of epilepsy is more in those where there has
been a dural laceration, intracranial hematoma, or
post-traumatic amnesia of more than 24 hrs
duration.
• Treatment –
• Phenobarbitone 30mg BD
67. Accident or compensation neurosis
• Many patients will experience protracted
symptoms of headaches, visual disturbances,
loss of concentration & irritability following
head injury.
• These symptoms frequently persists and don’t
improve with the passage of time.
68. Maxillofacial injuries
• Nasal fractures
Isolated nasal fractures are the most
commonly seen fractures in facial trauma.
However, nasal injuries may be associated
with severe mid-facial trauma involving the
naso-orbito-ethmoidal (NOE) complex, the
frontal sinuses and the orbito-zygomatic
complex.
70. Neurological complication -
• CSF rhinorrhoea may be present if the
fractures of the NOE complex involve the base
of the skull and a dural breach.
72. Neurological complication -
• Diplopia secondary to extraocular muscle
dysfunction.
• Paraesthesia of the infraorbital nerve
distribution (cheek, lateral nose, upper lip,
upper anterior teeth and gingiva)
• Tenderness and diastasis at the fronto-zygomatic
suture.
• Lower motor neuron facial palsy.
73. Retrobulbar haemorrhage
• The development of proptosis of the globe,
reduced or lost vision and severe orbital pain, are
features of retrobulbar haemorrhage. This is an
emergency with the potential for permanent
blindness and requires urgent surgical
intervention.
75. Neurological complication -
• Infraorbital paraesthesia.
• Tenderness at the fronto-zygomatic sutures .
• CSF rhinorrhoea due to dural tear and fracture
of the anterior cranial fossa
76. Frontal bone fractures
• Fractures of the frontal bone may occur:
In association with extensive facial injuries or
in isolation, as a result of direct blunt trauma
to the forehead in an MVA, sporting collision
or assault.
79. Mandibular fractures
• Mandibular fractures occur in all age groups.
Fractures of the condyle and subcondylar
regions, are the most common due to trauma
to the chin from falls.
81. • Paraesthesia in distribution of inferior alveolar
nerve (lower lip and chin)
• Frey’s syndrome in case of damage to
auriculotemporal nerve in fracture of neck of
condyle.
82. • References :
1. Text book of Oral and Maxillofacial trauma, third
edition- Fonseca
2. Text book of oral and maxillofacial surgery
Petersons
3. Maxillofacial injuries .Row & williams vol. 1& 2
4. ACS Committee on Trauma. Student Course Manual
8th ed. American College of Surgeons Chicago,
Illinois, 2009.
Axial view of ct showing Large left sided fronto-parietal subdural hematoma with associated midline shift. Appearance is Crescent shaped.
The Glasgow Coma Scale is a neurological scale that aims to give a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment.
Best possible score is 15 , worst possible score is 3
15- normal
13-14 – mild head injury
8-12- moderate head injury
<8 – severe head injury
1-2 years