Chapter 6
Review the key anatomic features of the head (face) and neck
Describe injury patterns Describe the evaluation of the patient with
suspected head (face)/neck injury Review epidemiology and pathology
associated with traumatic brain injury (TBI) Understand the initial evaluation and
management of a patient with a TBI
Soft Tissues◦ Includes parotid glands
Bones◦ Facial and cervical spine
Neck blood vessels◦ Carotid and vertebral arteries◦ Jugular and other veins
Trachea
Esophagus
Globes and surrounding ducts
Soft tissue or bony injuries may immediately threaten the airway◦ Uncontrolled bleeding can change “stable” to “unstable”
very quickly◦ Standard maneuvers may be less successful in setting of
fractures, etc.
Associated brain or spine injuries may cause airway loss as well◦ All blunt face/neck trauma must be considered at risk for
C-spine injury◦ Neurologic injuries may worsen with time as well
Securing the airway remains critical
Tracheal injuries may cause significant air leak◦ Pneumomediastinum◦ Pneumothorax, even tension pneumothorax
Surgical repair is required◦ If unavailable, manage with secure airway and chest
tubes if necessary◦ Minimize airway pressure on ventilator
Pneumothorax and Pneumomediastinum
Tracheal Injury
May result in significant bleeding
Separated into anterior and posterior sources
Intubation for airway control prior to packing may be needed
Posterior Packing
Anterior Packing Epistat Balloon
Difficult to access from neck incision, may need sternotomy/thoracotomy
Initial management with angio/CT angio, bronchoscopy, esophagoscopy◦ Basically need to evaluate all vascular and aerodigestive
structures potentially in harm’s way
As with most trauma, “stable or unstable” guides the initial management◦ Active bleeding, expanding hematomas, or hemodynamic
instability need to be addressed first in the OR and then with staged work up if indicated
Only zone that is easily accessed from a neck incision
Still requires investigation of vascular and aerodigestive structures
In a STABLE patient, can be investigated with CT and endoscopy potentially
Again, unstable patients or those with active bleeding issues need to be addressed in the operating room!
Similar to Zone I, potentially difficult to access surgically and so angiography or CT needed, with possible endoscopy◦ These tend to be vascular injuries at the skull base that
are very difficult to control surgically
Again, instability should prompt rapid damage control in OR, followed by additional work up if needed
Hemorrhage is the first concern
Stroke is the second concern (up to 25% of ICA injuries)
Revascularization may be required ICA/ECA Injury with Reconstruction
More frequent that was believed in the past◦ Roughly 1-1.5% of blunt admissions
Workup with CT Angio or conventional angiography
Treatment based on grade◦ Low grade lesions no intervention or ASA◦ Higher grade lesions need anticoagulation or possibly
stenting, with recent interest in aggressive antiplatelet agents
Complications related to increased stroke risk
Frequent injuries, but rarely have to be addressed immediately from a surgical standpoint
The primary question should be one of airway protection◦ The anatomic disruption or bleeding may cause loss of
airway◦ The situation may deteriorate as swelling progresses in
the upper airway
Remember that the globes may be injured by fractures and a good exam, including visual acuity, is mandatory
Clinical exam is very useful – pain, bruising, crepitance, movement
Malocclusion often occurs with mandible fractures
Check a cranial nerve exam!
Malocclusion a common hint on exam
50% will break multiple places
Can be managed with soft diet/liquids and pain control in short term
Operative repair ultimately required
Panorex
Open fractures may require broad spectrum antibiotic coverage◦ This isn’t agreed upon, but if a sinus is violated
then initial coverage is reasonable
Remember that if enough trauma occurred to fracture bones, the nearby structures are also at risk◦ At least 20% of facial fractures will have a TBI◦ About 2% will have a C-spine fracture
Evaluation requires a careful exam, including visual acuity
Open globes are as emergent as threatened limbs, and need antibiotic coverage like open fractures
Remember that open globes need an altitude restriction for MEDEVAC
Layering of blood in the inferior anterior chamber
Usually managed with rest, elevation of HOB, and correction of clotting factors
5% will require surgical evacuation Hyphema
Minor injury
Resolves spontaneously, though may take weeks
Avoid anticoagulant or antiplatelet drugs
Lubricant eye drops as needed
Subconjunctival hemorrhage
Airway control remains the primary concern
Control of hemorrhage may require packing, angiography, or operation
Facial fracture repair may be delayed if necessary once wounds are closed
Tracheal and esophageal injuries require more urgent repair
Globe injuries should be considered with facial fractures, and known injuries treated with the same urgency as threatened limbs
EYE OPENING (E) Spontaneous 4To Speech 3To Pain 2None 1
BEST MOTOR Obeys Commands 6RESPONSE (M) Localizes Pain 5
Normal Flexion (Withdraws) 4Abnormal Flexion (Decorticate) 3Extension (Decerebrate) 2None 1
VERBAL RESPONSE (V) Oriented 5Confused Conversation 4Inappropriate Words 3Incomprehensible Sounds 2None 1
Mild: GCS 14 – 15 Moderate: GCS 9 – 13 Severe: GCS 3 - 8
#1 Cause of Traumatic Death◦ 500,000 CHI per year◦ Upon ER Arrival:
Dead: 14% Mild Injury: 80% Moderate – Severe Injury: 10% each
◦ Overall Mortality Mild: 0% Moderate: 7 – 10% Severe: 30%
CHI: Disability within each group◦ Mild: 10%◦ Moderate: 50 – 67%◦ Severe: > 95%
Penetrating GSW to Head◦ Vegetative or Severely Disabled: 10%◦ Moderate Disability: 20%◦ Good Outcome: 20%◦ The Others: Dead
Anatomy Types of Injury
Pia Mater Arachnoid Layer Dura Mater
Most common traumatic lesion
In 20-40% of severely head-injured
Located in space between dura and arachnoid layers
Venous bleed Concave Shape
Located in space between dura and inner table
Arterial bleed Classic presentation Convex shape
Most common in subfrontal and temporal regions
Bruised tissue with violation of BBB
Axonal structural failure due to mechanical forces along axons
Culmination in physical separation of axon into proximal and distal segments
Number of axonal disruptions = Amount of deficit
Initial Evaluation Emergent Surgical Management Initial Management
First Priority: Airway, Breathing, Circulation
Disability◦ Pupillary Exam◦ Calculate GCS
Resuscitation◦ Standard Techniques◦ DO NOT postpone treating
hypotension◦ Preferred Crystalloid: Hypertonic
Saline or Isotonic Saline◦ Blood
Secondary Survey◦ Assess for other injuries◦ Complete neurological assessment
Radiologic Evaluation◦ Hemodynamically stable◦ CT Scan of Head: Gold Standard
Significant mass effect Displacement of > 5mm off midline Penetrating injuries may need simple
debridement
Significant reductions in mortality & morbidity by using intensive management protocols:◦ Early intubation◦ Rapid transportation to appropriate trauma care
facility◦ Prompt resuscitation◦ Early CT scanning◦ Immediate evacuation of intracranial mass
lesions TCDB Mortality: 50% vs 36% (using these
protocols)
Sedation◦ No studies have proven sedation to influence TBI
outcome Neuromuscular Blockade – Results in:
◦ Longer ICU Course◦ Increased pneumonia rate◦ Trend towards increased sepsis◦ No improvement in outcome
Blood Pressure◦ Single episode of hypotension (SBP < 90 mm Hg)
Increased morbidity Doubled mortality Hypotension is an INDEPENDENT predictor of
outcome
Cerebral Perfusion Pressure◦ CPP = MAP – ICP◦ Very low following TBI; may be near ischemic
threshold◦ Critical threshold is 60 mm Hg
Significant decline in outcome for those with persistent CPP < 60 mm Hg
◦ CPP < 50 mm Hg associated with: Critical reductions in PbO2
Increased morbidity and mortality
Oxygenation◦ Hypoxemia: PaO2 < 60 mm Hg◦ Results in:
Increased mortality: 14% vs 50% Worse outcome
Mannitol◦ Studies support use of mannitol for ICP
management
Hyperventilation◦ Introduction
Cerebral blood flow in first day after injury is half that of normal individuals
Severe hyperventilation results in cerebral ischemia Hyperventilation is known to decrease ICP and lower
CBF◦ Aggressive Hyperventilation (PaCO2 < 30 mm
Hg) Reduces CBF, reduces ICP, possible loss of
autoregulation Outcomes at 3 and 6 months are better without
prophylactic hyperventilation
Hyperventilation (continued)◦ Guidance
STANDARD: In absence of increased ICP, chronic prolonged hyperventilation (pCO2 < 35 mm Hg) therapy should be avoided after severe TBI
Guideline: Use of prophylactic hyperventilation during first 24 hours after severe TBI should be avoided because it can compromise CBF during a time when CBF is already low
At Risk Patients ICP Data and Patient Management Guidelines
Mild and Moderate Head Injury◦ Low risk for ICH◦ Less than 3% (Mild) and 10 – 20% (Moderate) will
deteriorate into coma◦ Routing ICP monitoring is not recommended
Severe Head Injury◦ ICH Incidence
Abnormal CT: 53 – 63% Normal CT: 10 – 15% Normal CT + 2 of 3 adverse features: Similar to abnormal CT
◦ Normal CT Strategy Up to 1/3 may develop new pathology within a few days from
injury Follow-up scanning for those without ICP monitoring
All Therapies are Double-Edged Swords◦ Hyperventilation
Reduces ICP Causes cerebral vasoconstriction and ischemia
◦ Mannitol Reduces ICP Cumulative doses can exacerbate brain edema
◦ Sedation, analgesia, and paralysis Reduce ICP Impossible to interpret clinical exam
Severe TBI (after resuscitation) and Abnormal CT
Severe TBI (after resuscitation) and Normal CT + 2 of 3:◦ Age over 40 years◦ Unilateral or bilateral posturing◦ SBP < 90 mm Hg
Not routinely in Mild or Moderate TBI ICP management initiated at upper
threshold of 20 – 25 mm Hg
Definitions◦ Early post-traumatic seizure: Within 7 days of injury◦ Late post-traumatic seizure: 7 days after injury
Incidence◦ Penetrating head trauma: 50%◦ Following head injury (up to 3 years)
Early: 4 – 25% Late: 9 – 42%
Guideline◦ Prophylactic use of phenytoin, carbamazepine
phenobarbital, or valproate is NOT recommended for preventing LATE post-traumatic seizures
Early Maneuvers◦ Control of body temperature◦ Seizure prophylaxis◦ Elevation of HOB◦ Avoidance of jugular venous outflow obstruction◦ Volume resuscitation to CPP > 60 mm Hg◦ Ventilation to low end of eucapnia (pCO2 = 35
mm Hg)◦ IVC drainage of CSF
Further Maneuvers◦ Ventilate to pCO2 = 30 – 35 mm Hg◦ Mannitol◦ Hypertonic Saline
Alternative to mannitol Given as 30-ml bolus (7.5% NaCl)
Second Tier Therapy◦ High Dose Barbiturate Therapy◦ Decompressive Craniectomy◦ Hypertensive Therapy
Age Intracranial Diagnosis (CT) Pupillary Reactivity Post-resuscitation GCS Presence or absence of hypotension
ONLY HYPOTENSION is amenable to
medical manipulation
TBI is the #1 cause of traumatic death Initial Evaluation and Management
consists of:◦ ABCs◦ Use of INTENSIVE TBI management protocol
(including ICP management pathways) ICP lowering therapies are double-edged
swords Hypotension is the ONLY TBI prognostic
factor that is amenable to medical manipulation