Head and Neck Trauma Surgery

1. HEAD & NECK
TRAUMA

2. Head Trauma
• Accounts for 13 – ½ of trauma deaths .
• Good outcomes are possible without CT scan and
neurosurgeons.
• Aim to avoid further injury to the brain.
• Hypoxia & Hypotension double mortality.
• Trauma is the leading cause of death in children and young
adults; however, the incidence of death and disability from
trauma has been slowly decreasing.

4. Glasgow Coma Scale Score.
- The initial assessment of the trauma patient includes the primary
survey, resuscitation, secondary survey, and definitive care.
- GCS ( ranges from 3 to 15).
- Tracheal intubation or severe facial or eye swelling can impede
verbal and eye responses.

6. Scalp injury
• Blunt or penetrating trauma to the head.
• Direct pressure initially controls the bleeding, allowing close
inspection of the injury.
• simple laceration  copiously irrigated and closed primarily.
• Short laceration  a single-layer, percutaneous suture closure
will suffice.
• Long laceration or has multiple arms  the patient may need
debridement and closure in the operating room.
• Careful reapproximation of the galea will provide a more
secure closure and better hemostasis.

7. Example of small scalp laceration

8. Example of long laceration

9. Skull fractures
• The fracture may be characterized by skull X-rays or head CT.
• Closed (intact skin) Or opencompound fractures.
• Fracture Line :
- Linear ( single)
- stellate ( multiple radiating from a point )
- Comminuted ( creating fragments of bone)
• Indications for craniotomy include depression greater than the
cranial thickness, intracranial hematoma, and frontal sinus
involvement.

12. • Depressed skull fractures may result from a focal injury of
significant force.
• The inner cortex of the bone fragments often has multiple sharp
edges that can lacerate Dura, brain, and vessels.
• Craniotomy is required to elevate the fracture, repair Dural
disruption, and obtain hemostasis in these cases.

13. laceration of cortical vessels by the edge of the fractured bone.

14. • Fractures of the skull base are common in head-injured
patients, and they indicate significant impact. They are generally
apparent on routine head CT, but should be evaluated with
dedicated fine-slice coronal-section CT scan to document and
delineate the extent of the fracture and involved structures.
• Skull base fractures requiring intervention include those with an
associated cranial nerve deficit or CSF leak.
• Extravasation of blood results in ecchymosis behind the ear,
known as “ Battle’s sign”.
• fracture of the anterior skull base can result in anosmia (loss of
smell from damage to the olfactory nerve), CSF drainage from
the nose (rhinorrhea), or periorbital ecchymoses, known as
“raccoon eyes”.

18. Management of head and neck tissue
lacerations principles :
• In the acute settings, patients should be managed with
the head-of-bed elevation to decrease tissue edema.

19. • Most lacerations without significant tissue loss can be
closed primarily, which is preferred where possible.
• Head and neck soft tissues have the benefit of a robust
blood supply. Thus, nearly devitalized soft tissues often
survive, such that any tissue debridement should be very
conservative.

20. • Closure of trapdoor lacerations requires conservative
undermining of surrounding tissue and good approximation of
subdermal levels prior to epidermal closure. A pressure dressing
is also applied. These measures are employed to avoid a
pincushion deformity .

22. • Systemic antibiotics are reserved for through-and-through
mucosal lacerations, contaminated wounds, bite injuries, and
when delayed closure is performed (>72 hours) , The chosen
antibiotic should cover S. aureus. After skin injuries.
• the patient is instructed to avoid sunlight, because this can
cause pigmentary abnormalities in the abrasion or scar line,
which matures over a 6- to 12-month period.

23. Injury to the Eyelid
• Requires identification of the orbicularis oculi, which is
closed in a separate layer.
• Gray line must be carefully approximated to avoid lid
notching or height mismatch.
• Injuries involving one-fourth the width of the eyelid may be
closed primarily; otherwise, flap or grafting procedures may
be required

26. Injury to the Auricle
• With laceration of the auricle, key structures such as the helical
rim and antihelix must be carefully aligned. These injuries must
be repaired so that the cartilage is covered.
• The principles of auricular repair are predicated on the fact that
the cartilage has no intrinsic blood supply and is thus
susceptible to ischemic necrosis following trauma.
• The suture should be passed through the perichondrium, while
placement through the cartilage itself should be avoided.
• A pressure dressing is frequently advocated after closure of an
ear laceration.

28. • Auricular hematomas should be drained promptly, with
placement of a bolster as a pressure dressing.

29. Facial Bone Fractures
• Facial bone fractures most commonly involve the mandible.
• Fractures are described as either favorable or unfavorable,
depending on whether or not the masticatory musculature
tends to pull the fracture into reduction or distraction.

30. Unfavorable fracture - Distraction

31. Favorable fracture- Reduction

32. • Classical management of mandible fractures dictated closed
reduction and a 4- to 6-week period of Intermaxillary fixation
(IMF) with arch bars applied via circumdental wiring.
• Comminuted, displaced, or unfavorable fractures underwent
open reduction and wire fixation in addition to IMF.

33. • Selected fractures, such as those of the body, benefit from
dynamic compression plating, which applies pressure toward the
fracture line. With rigid fixation, IMF is required to establish
occlusion, and may not be necessary for a full 6 postoperative
weeks. This is preferable because IMF is associated with
gingival and dental disease, as well as with significant weight
loss and malnutrition, during the fixation period.

34. Mid-Face Fractures
• Midface fractures are classically described in three patterns:
Le Fort I, II, and III.
• Classical signs of midface fractures in general include
subconjunctival hemorrhage; malocclusion; midface numbness
or hypesthesia (maxillary division of the trigeminal nerve); facial
ecchymoses/ hematoma; ocular signs/symptoms; and mobility of
the maxillary complex.

35. • Three vertical buttresses support the midface:
nasofrontalmaxillary,
frontozygomaticomaxillary,
pterygomaxillary.

36. • Le Fort I fractures :
occur transversely across the alveolus, above the level of the
teeth apices. In a pure Le Fort I fracture, the palatal vault is mobile
while the nasal pyramid and orbital rims are stable.

37. • Le Fort II fracture :
extends through the nasofrontal buttress, medial wall of the orbit,
across the infraorbital rim, and through the zygomaticomaxillary
articulation. The nasal dorsum, palate, and medial part of the
infraorbital rim are mobile.

39. • The Le Fort III fracture “craniofacial disjunction” :
The frontozygomaticomaxillary, frontomaxillary, and frontonasal
suture lines are disrupted. The entire face is mobile from the
cranium.

40. Temporal Bone Fracture
• Temporal bone fractures occur in approximately one fifth of skull
fractures.
• Unfortunately, the incidence of temporal bone fracture from
gunshot wounds to the head is rising.
• Fractures are divided into two patterns, longitudinal and
transverse, based on the clinical picture and CT imaging

41. • longitudinal fractures :
constitute 80% and are associated with lateral skull trauma. Signs
and symptoms include conductive hearing loss, ossicular injury,
bloody otorrhea, and labyrinthine concussion.
The facial nerve is injured in approximately 20% of cases.

42. • transverse Fractures :
constitute only 20% of temporal bone fractures and occurs
secondary to frontooccipital trauma, These injuries frequently
involve the otic capsule to cause sensorineural hearing loss and
loss of vestibular function.
The facial nerve is injured in 50% of cases.

44. • The most significant consideration in the management of
temporal bone injuries is the status of the facial nerve.
• Delayed or partial paralysis is almost always resolves with
conservative management .
• Immediate paralysis that doesn’t recover within 1 week should
be considered for nerve decompression.
• The Electroneurography findings of >90% degeneration more
than 72 hours after the onset of complete paralysis is considered
an indication for surgery.

45. • It is of paramount importance to protect the eye in patients
with facial nerve paralysis of any etiology, because absence
of an intact blink reflex will predispose to corneal drying and
abrasion. This requires the placement of artificial tears
throughout the day with lubricant ointment, eye taping,
and/or a humidity chamber at night.

46. Closed head injury
• most common type of TBI and a significant cause of morbidity
and mortality.
• primary injury  defined as the immediate injury to neurons
from transmission of the force of impact
• secondary injury  Subsequent neuronal damage due to the
sequelae of trauma .( hypotension , hypoxia , thrombosis )
• Types : Concushion / contusion / intracranial hematoma /
EDH / SDH / aortic dissection ,,,,,,

47. Initial Assessment
* The first three elements of the ABCDs of resuscitation
Airway / Breathing /Circulation - must be assessed and stabilized.
Hypoxia and hypotension are known to worsen outcome in TBI .
* Patients who cannot follow commands require intubation for
airway protection and ventilatory control.
* Assessment of “D” for Disability, is undertaken next.
* Motor activity, speech, and eye opening can be assessed in a
few seconds and a GCS score assigned.

48. Medical Managmement
* phenytoin - decrease the incidence of posttraumatic seizures.
(a 17-mg/kg phenytoin loading dose, followed by 1 week of
therapeutic maintenance phenytoin, typically 300 to 400 mg/d)
• Blood glucose levels -closely monitored.
(controlled with sliding scale insulin).
• Fevers - antipyretics.
• Peptic ulcers /Cushing’s ulcers - Ulcer prophylaxis

49. Classification
• Severe head injury - GCS score is 3 to 8.
• Moderate head injury - GCS score is 9 to 12.
• Mild head injury - GCS score is 13 to 15.
• TBI patients who are Asymptomatic, who have only headache,
dizziness, or scalp lacerations, and who did not lose
consciousness, have a low risk for intracranial injury and may be
discharged home without a head CT scan.
• Symptomatic Patients with a history of altered consciousness,
amnesia, progressive headache, skull or facial fracture, vomiting,
or seizure have a moderate risk for intracranial injury and should
undergo a prompt head CT.

50. Types of Closed Head injuries.
• Concussion :
Defined as temporary neuronal dysfunction following
nonpenetrating head trauma.
The head CT is normal, and deficits resolve over minutes to
hours.
• Symptoms - Transient loss of consciousness , alteration of
mental status , amnesia of the event.
• Consciousness grading :
Head trauma patients with confusion  grade 1
patients with amnesia  grade 2
patients who lose consciousness  grade 3.

52. • Contusion :
• A contusion is a bruise of the brain, and occurs when the force
from trauma is sufficient to cause breakdown of small vessels
and extravasation of blood into the brain.
• occipital, and temporal poles are most often involved.
• Edema may develop around a contusion, causing mass effect.
• Contusions also may occur in brain tissue opposite the site of
impact. This is known as a contre-coup injury. These contusions
result from deceleration of the brain against the skull.

54. • Diffuse Axonal Injury –
Diffuse axonal injury is caused by Damage to axons throughout
the brain, due to rotational acceleration and then deceleration.
Axons may be completely disrupted and then retract, forming
axon balls.

55. • Penetrating Injury :
The two main subtypes:
1- missile (e.g., due to bullets or fragmentation devices)
2-nonmissile (e.g., due to knives or ice picks).
• skull X-rays and CT scans are useful in assessing the nature of the
injury.
• Cerebral angiography must be considered if the object passes near a
major artery or Dural venous sinus.
• Operative exploration is necessary to remove any object extending
out of the cranium, as well as for debridement, irrigation, hemostasis,
and definitive closure.
• Small objects contained within brain parenchyma are often left in place
to avoid iatrogenic secondary brain injury.
• Antibiotics are given to decrease the chances of meningitis or abscess
formation.

56. Gun Shot – missile penetrating injury

57. Non missile penetrating head injury

58. • Traumatic Intracranial Hematoma:
• 1- Epidural Hematoma:
EDH is the accumulation of blood between the skull and the Dura.
EDH usually results from arterial disruption, especially of the
middle meningeal artery.
• three-stage clinical presentation initially
( unconscious  “lucid interval” lethargic and herniates)
• Open craniectomy  evacuation of the congealed clot and
hemostasis generally is indicated for EDH.
* Conservatively managed if : clot volume <30 cm3, maximum
thickness <1.5 cm, GCS score >8.

59. • EDH Head CT - blood clot is bright, biconvex in shape
(lentiform), and has a well-defined border that usually respects
cranial suture lines.

60. • Acute Subdural Hematoma :
• SDH usually results from venous bleeding, typically from tearing
of a bridging vein running from the cerebral cortex to the dural
sinuses. The bridging veins are subject to stretching and tearing
during acceleration/deceleration of the head, because the brain
shifts in relation to the Dura, which firmly adheres to the skull.
• Open craniotomy  evacuation of acute SDH is indicated for
any of the following: thickness >1 cm, midline shift >5 mm, or
GCS drop by two or more points from the time of injury to
hospitalization.
• Nonoperatively managed hematomas may stabilize and
eventually reabsorb, or evolve into chronic SDH.

61. • On head CT scan, the clot is bright or mixed-density, crescent-
shaped (lunate), may have a less distinct border, and does not
cross the midline due to the presence of the falx.

62. • Chronic Subdural Hematoma –
Chronic SDH is a collection of blood breakdown products that is at
least 2 to 3 weeks old.
* Alcoholics, the elderly, and patients on anticoagulation are at
higher risk for developing chronic SDH.
* A chronic SDH >1 cm or any symptomatic SDH should be
surgically drained.
• A simple burr hole can effectively drain most chronic SDHs.
The procedure is converted to open craniotomy if the SDH is too
congealed for irrigation drainage, the complex of membranes
prevents effective drainage, or persistent hemorrhage occurs that
cannot be reached with bipolar cautery through the burr hole.

63. • A true chronic SDH will be nearly as dark as CSF on CT. Traces
of white are often seen due to small, recurrent hemorrhages into
the collection. These small bleeds may expand the collection
enough to make it symptomatic. This phenomenon is referred to
as an acute-on-chronic SDH

64. Craniotomy SDH Evacution Burr Hole SDH Evacuation

65. • Intraparenchymal Hemorrhage :
- Isolated hematomas within the brain parenchyma are most
often associated with hypertensive hemorrhage or
arteriovenous malformations (AVMs).
-Mass effect from developing hematomas may present as a
delayed neurologic deficit.
• Indications for craniotomy include: any clot volume >50 cm3
or a clot volume >20 cm3 with referable neurologic
deterioration (GCS 6–8) and associated midline shift >5 mm
or basal cistern compression.

67. • Vascular Injury :
- Trauma to the head or neck may cause damage to the carotid or
vertebrobasilar systems.
- Dissection refers to violation of the vessel wall intima. Blood at
arterial pressures can then open a plane between the intima and
media, within the media, or between the media and adventitia.
Producing what is called “ false lumen”.
- Expansion of the hematoma within the vessel wall can lead to
narrowing of the true vessel lumen and reduction or cessation of
distal blood flow. Slow-flowing or stagnant blood within the false
lumen exposed to thrombogenic vessel wall elements may
thrombose. Pieces of thrombus may then detach and cause distal
embolic arterial occlusion.
- Angiographic abnormalities include stenosis of the true lumen, or
“string-sign,” visible intimal flaps, and the appearance of contrast in
the false lumen. Four-vessel cerebral angiography should be
performed when suspicion of dissection exists.

68. Angiography - “String sign” stenotic focus

69. • Patients with documented arterial dissection have been
anticoagulated with heparin and then warfarin to prevent
thromboembolic stroke. Trauma patients often have concomitant
absolute or relative contraindications to anticoagulation,
complicating management.!!!!
• Consider surgical or interventional techniques for persisting
embolic disease and for vertebral dissections presenting with
SAH.
• Surgical options include vessel ligation and bypass grafting.
Interventional radiology techniques include stenting and vessel
occlusion

70. • Brain Death.
Brain death occurs when there is an absence of signs of brain
stem function or motor response to deep central pain in the
absence of pharmacologic or systemic medical conditions that
could impair brain function.
• neurologist,neurosurgeon, generally performs the clinical
brain death examination. Two examinations consistent with
brain death 12 hours apart, or one examination consistent
with brain death followed by a consistent confirmatory study
generally is sufficient to declare brain death (see below).
• The patient must be normotensive, euthermic, and
oxygenating well.

71. Brain death

72. *Documentation of no brain stem function requires the
following:
• nonreactive pupils
• lack of corneal blink
• oculocephalic (doll’s eyes) reflex
• oculovestibular (cold calorics) reflexe
• loss of drive to breathe (apnea test)