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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
Contents- 
• Introduction 
• Initial assessment 
• Rapid initial assessment 
• Types of brain injuries 
• Neurological complications in Maxillofacial 
trauma. 
• References
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.
• 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.
• 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.
Initial assessment and treatment 
It includes 
1. Airway maintenance 
2. Breathing - Mechanical ventilation 
3. Circulatory stabilization 
4. Assessment of Disability / Definitive care 
5. Exposure
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 
C 
R 
A 
N 
I 
A 
L
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.
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.
Pupillary findings 
• Unilaterally dilated -Light response(Sluggish or fixed) - 
Occulomotor nerve compression 
• 
• Bilaterally dilated -Light response (Sluggish or fixed) – 
Bilateral Occulomotor nerve palsy 
• Unilaterally dilated – Light response(cross reactive)- Optic 
nerve injury. 
• Bilaterally constricted –Light response (difficult to 
determine )- Metabolic encephalopathy or pontic lesion. 
• Unilaterally constricted – Light response (preserved ) 
Carotid sheath injury.
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.
• Paresis of Upward gaze – 
• This can occur with hemorrhage causing 
compression of the midbrain tectum. 
• Common manifestations- Lack of light reflex & 
convergence.
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 .
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
• 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.
Neurological complications in 
Maxillofacial trauma
Intracranial lesions - 
Traumatic brain injury is divided into two distinctive 
components 
1. Primary brain injury – 
2. Secondary brain injury -
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
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.
Types of primary brain injury 
• Cerebral Concussion 
• Cerebral Contusion 
• Epidural Hematoma 
• Subdural hematoma
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. 
.
Cause -
• 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
Cerebral Contusion 
• Incidence - 20–30% of all head 
injuries 
Cause - 
Cerebral contusion can be 
caused by multiple 
microhemorrhages into brain 
tissue following injury.
• 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.
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.
• 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.
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.
• Signs and symptoms – 
• Irritability 
• Seizures 
• Pain 
• Numbness 
• Headache 
• Dizziness 
• Disorientation 
• Amnesia 
• Weakness 
• Nausea 
• vomiting
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.
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.
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.
Glasgow Coma Scale
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
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.
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.
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.
• 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.
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.
• 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.
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.
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
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.
• General signs are – 
1. Deterioration in the level of consciousness 
2. Restlessness 
3. Vomiting 
4. Hypertension 
5. Headache & photophobia 
6. Papilloedema.
• 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.
• If diagnosed , then steps can be taken to avoid 
serious problems of midbrain distortion & 
haemorrhage, cerebral compression, infarction, 
particularly of temporal and occipital lobes.
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.
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
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.
• 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.
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.
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.
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
• 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.
• 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.
• 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.
• 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.
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 .
• 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.
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.
• 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.
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
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.
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.
Nasal fractures
Neurological complication - 
• CSF rhinorrhoea may be present if the 
fractures of the NOE complex involve the base 
of the skull and a dural breach.
Zygomatico-maxillary complex 
fractures (ZMC)
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.
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.
Maxillary fractures
Neurological complication - 
• Infraorbital paraesthesia. 
• Tenderness at the fronto-zygomatic sutures . 
• CSF rhinorrhoea due to dural tear and fracture 
of the anterior cranial fossa
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.
Frontal bone fractures
Neurological complication - 
• CSF rhinorrhoea may be present when 
involved with nasal fractures and NOE.
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.
Mandibular fractures
• 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.
• 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.
•Thank you

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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
  • 2. Contents- • Introduction • Initial assessment • Rapid initial assessment • Types of brain injuries • Neurological complications in Maxillofacial trauma. • References
  • 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 C R A N I A L
  • 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.
  • 11. Pupillary findings • Unilaterally dilated -Light response(Sluggish or fixed) - Occulomotor nerve compression • • Bilaterally dilated -Light response (Sluggish or fixed) – Bilateral Occulomotor nerve palsy • Unilaterally dilated – Light response(cross reactive)- Optic nerve injury. • Bilaterally constricted –Light response (difficult to determine )- Metabolic encephalopathy or pontic lesion. • Unilaterally constricted – Light response (preserved ) Carotid sheath injury.
  • 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.
  • 17. Neurological complications in Maxillofacial trauma
  • 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.
  • 21. Types of primary brain injury • Cerebral Concussion • Cerebral Contusion • Epidural Hematoma • Subdural hematoma
  • 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.
  • 32.
  • 33. • Signs and symptoms – • Irritability • Seizures • Pain • Numbness • Headache • Dizziness • Disorientation • Amnesia • Weakness • Nausea • vomiting
  • 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.
  • 78. Neurological complication - • CSF rhinorrhoea may be present when involved with nasal fractures and NOE.
  • 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.

Editor's Notes

  1. Axial view of ct showing Large left sided fronto-parietal subdural hematoma with associated midline shift. Appearance is Crescent shaped.
  2. 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
  3. Anosmia- no sense of smell