Chapter 6. Review the key anatomic features of the head (face) and neck Describe injury patterns ...

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