head injuries

Introduction to Trauma: Head Injuries

Introduction to Traumatic Brain Injuries

  • Traumatic brain injuries (TBIs) are a significant contributor to death and disability in seriously injured patients.

Lesson Objectives

By the end of this lesson, you will be able to:

  • Define traumatic brain injury.
  • State the components of cerebral perfusion pressure (CPP).
  • List several types of primary brain injury.
  • List the causes of secondary brain injury.
  • Describe the signs of increased intracranial pressure (ICP) leading to cerebral herniation.
  • Explain the assessment and management of traumatic brain injuries.

Case Study

Incident Details

  • Dispatch: Head-on road traffic incident (RTI).
  • Driver: Restrained driver.

Scene Size-Up

  • Scene is safe; Personal Protective Equipment (PPE) utilized.
  • One patient involved.
  • Major damage noted to the front of the vehicle.
  • Police and Civil Defense present at the scene.

General Impression

  • Civil Defense has extricated the patient to the ground.
  • Patient only responds to painful stimuli.
  • Patient’s face is covered in blood.
  • Check for potential cervical spine (C-spine) injury.

Primary Survey

Observations

  • A: Profuse bleeding from a head laceration (management required).
  • B: Sonorous respirations noted (management required).
  • C: Rapid, deep, equal chest rise (assessment for management).
  • D: Rapid, bounding radial pulse with cool skin (initial management considerations).
  • E: Eyes do not open, groaning to pain, withdrawing from pain, pupils equal and reactive to light (PERRL).
  • F: Seatbelt sign across thorax.

Discussion Points

  • Why is hemorrhage control prioritized?
  • Discuss the possible reasons for the patient’s level of consciousness.
  • Identify life-threatening conditions associated with head injuries.

Neurologic Assessment

Components of the Neurologic Exam

The complete neurologic exam includes six components:

  • Mental status (Glasgow Coma Scale - GCS).
  • Cranial nerves (specific applicable cranial nerves only).
  • Motor function.
  • Sensory function.
  • Coordination.
  • Reflexes.
  • Typically, only the first four are evaluated in the prehospital setting.

Blood Glucose Evaluation

  • Check blood glucose level to rule out hypoglycemia before assessment.

Glasgow Coma Scale (GCS)

  • GCS should be scored after correcting factors affecting altered mental status.
  • Must be scored during each reassessment and recorded with vital signs.

Assessing CNS Function

Function Symmetry

  • Assess symmetry in function as asymmetry is abnormal until proven otherwise.
  • Ask patients if observed asymmetry is normal for them.

Cranial Nerves

  • There are 12 pairs of cranial nerves.
  • Not all cranial nerves are evaluated in the prehospital setting.
  • Key cranial nerves for evaluating eye dysfunction: CN II (Optic), CN III (Oculomotor), CN IV (Trochlear), CN VI (Abducens).

Specific Cranial Nerves & Functions

  • Olfactory Nerve (I): Sensory - Smell.
  • Optic Nerve (II): Sensory - Vision.
  • Oculomotor Nerve (III): Motor - Most eye movements.
  • Trochlear Nerve (IV): Motor - Moves eye to look at the nose.
  • Trigeminal Nerve (V): Both - Face sensation, mastication.
  • Abducens Nerve (VI): Motor - Abducts the eye.
  • Facial Nerve (VII): Both - Facial expression, taste.
  • Vestibulocochlear Nerve (VIII): Sensory - Hearing and balance.
  • Glossopharyngeal Nerve (IX): Both - Taste, gag reflex.
  • Vagus Nerve (X): Both - Gag reflex, parasympathetic innervation.
  • Accessory Nerve (XI): Motor - Shoulder shrug.
  • Hypoglossal Nerve (XII): Motor - Swallowing, speech.

Pupillary Assessment

  • Pupils should normally be equal, round, and 3 to 5 mm.
  • Anisocoria (unequal pupils) may suggest CNS disease or traumatic injury; a difference of > 1 mm is abnormal.
  • Light reflex should constrict both pupils (tests CNs II and III).

Extraocular Movement (EOM)

  • Fully assess the range of motion of eyes.
  • Inability to move one or both eyes indicates a neurologic deficit (Cranial Nerves III, IV, VI).
  • Paralysis of lateral gaze may indicate rising ICP in TBI; upward gaze paralysis may suggest orbital fractures.

Motor Function Assessment

  • Assess by having the patient:
    • Move hands and arms.
    • Follow a two-part command.
  • For lower extremities, instruct the patient to:
    • Wiggle their toes.
    • Push and pull feet against resistance.

Sensory Function Assessment

  • For conscious patients, evaluate sensation by testing light touch perception in both extremities.
  • For unconscious patients, use deep pain response tests like trapezius squeeze or nailbed compression.

Types of Head Injuries

Open Scalp Injuries

  • Highly vascular; minor lacerations can cause significant bleeding.
  • Indicate potential skull fractures and TBIs.

Closed Scalp Injuries

  • Result from blunt trauma.
  • May lead to hematoma formation; must consider underlying brain injury.
  • Cold packs can help reduce bleeding.

Skull Fractures

  • Composed of thick fused bones that protect the brain.
  • Can result from impacted forces, causing brain injury.
  • Maintain airway, breathing, circulation; assess for TBIs and C-spine injuries.

Types of Skull Fractures

  • Linear Skull Fracture: Thin fracture line across the bone with no obvious deformity on X-ray.
  • Depressed Skull Fracture: Multiple cracks from impact; fragment pushed into the skull.
  • Closed Skull Fracture: Scalp intact.
  • Open Skull Fracture: Open injury to scalp present. Do not remove any impaled objects in the skull.

Basilar Skull Fracture

  • Fracture at the base of the skull.
  • Clear or bloody fluid from ears, nose, or mouth suggests cerebrospinal fluid (CSF) leakage.

Clinical Signs of Basilar Skull Fracture

  • “Raccoon eyes” (periorbital ecchymosis).
  • “Battle’s sign” (postauricular ecchymosis).

Traumatic Brain Injury (TBI)

  • Moderate and severe TBIs can result in prolonged rehabilitation and long-term disability.
  • TBIs account for nearly half of all trauma-related deaths, especially in multisystem trauma patients.

Signs and Symptoms of TBI

  • Altered mental status.
  • Weakness.
  • Altered respiratory rate or pattern.
  • Bradycardia.
  • Hypertension.
  • Impaired speech.
  • Unusual behavior.
  • Unequal pupils.
  • Nausea and vomiting.
  • Seizures.
  • Posturing.
  • Trismus (jaw clenching).

Specific Types of TBIs

Concussion

  • Caused by blunt force trauma to the brain without identifiable structural damage on imaging.
  • Post-concussive syndrome includes symptoms like headaches, memory problems, and balance issues.

Cerebral Contusion

  • Bruising of the brain leading to loss of consciousness or confusion.
  • Risk of edema in the brain.
  • Coup-contrecoup mechanism might appear in severe cases.

Cerebral Laceration

  • Tearing of brain tissue from penetrating or blunt injury.
  • Can result in severe brain tissue damage and intracranial hemorrhage, leading to increased ICP.
  • Symptoms depend on the location of the laceration and size of hemorrhage.

Diffuse Axonal Injury (DAI)

  • Widespread nerve axon damage usually from rotational forces.
  • Symptoms: diffuse cerebral edema, loss of consciousness, increased ICP.
  • Up to 90% of DAI patients may remain in a persistent vegetative state.

Penetrating Head Injury

  • Injuries from gunshot wounds, stab wounds, or other projectiles.

Intracranial Hematomas

Types of Intracranial Hematomas

  • Epidural Hematoma: Occurs above the dura mater.
  • Subdural Hematoma: Located beneath the dura mater.
  • Subarachnoid Hemorrhage: Blood collects in the subarachnoid space.

Epidural Hematoma

  • Characterized by:
    • Loss of consciousness post-event, rapid return to consciousness (lucid interval), and then subsequent loss of consciousness.
    • Symptoms include headaches, dilated pupils, and seizures.

Subdural Hematoma

  • Symptoms may take hours to weeks to develop:
    • Includes altered consciousness, pupil dilation, weakness, and seizures.
  • Higher risk in elderly populations due to brain atrophy.

Subarachnoid Hemorrhage

  • The most prevalent post-traumatic intracranial bleed.
  • Symptoms: severe headache (possibly the worst headache of the patient’s life), nausea, vomiting, and changes in level of consciousness (LOC).

TBI Pathophysiology

  • The skull does not expand, and swelling or blood accumulation within the skull can lead to increased ICP.

Intracranial Pressure (ICP)

  • ICP is the pressure exerted against the inside of the skull by brain contents.
  • Intracranial volume is fixed; any increase in the volume of any of its constituents may raise ICP.

Monro-Kellie Doctrine

  • States that the sum of the volumes of brain, blood, and cerebrospinal fluid (CSF) must remain constant.
    • As one volume increases, the others must compensate.

Herniation Syndromes

  • As ICP rises, brain tissue may herniate due to lack of compensatory ability, leading to compressive injuries.

Types of Herniations

  • Cingulate Herniation: Most common, leads to abnormal posturing/coma.
  • Central Herniation: Causes brain stem tears and possible death.
  • Uncal Herniation: Pressure on CN III; signs include pupils and motor weakness issues.
  • Tonsillar Herniation: Cerebellar tonsils compress medulla and cervical spinal cord, leading to severe risks.

Signs of Herniation

  • Cushing’s triad: Increased blood pressure, bradycardia, irregular respirations.
  • Changes in pupils, altered reactions to stimuli.

Factors Worsening Cerebral Edema and Ischemia

  • Include hypoperfusion, hypoxia, hypo/hypercapnia, hypo/hyperglycemia.

Primary vs. Secondary Brain Injury

Primary Brain Injury

  • Occurs at impact; irreversible damage.

Secondary Brain Injury

  • Develops post-impact; potentially reversible with intervention, caused by:
    • Systemic causes: e.g., hypotension, hypoxia.
    • Intrinsic causes: e.g., increased ICP, edema, hematomas.

Brain Perfusion

  • Adequate cerebral blood flow (CBF) is essential and is maintained through cerebral perfusion pressure (CPP).
  • Formula: CPP = MAP - ICP
    • Normal ICP: 10-15 mmHg.
    • Normal Mean Arterial Pressure (MAP): 70-110 mmHg.

Complications of Increased ICP

  • A vicious cycle can ensue; brain vasodilation leads to increased blood volume and further raises ICP.

Pathophysiology of Increased ICP

  • Causes of increased ICP include hypercarbia leading to vasodilation, thus elevating ICP.
  • Managing hypotension is crucial as it directly impacts cerebral perfusion.

Clinical Effects of Increased ICP

  • Symptoms include:
    • Altered LOC due to pressure on the brainstem and reticular activating system (RAS).
    • Projectile vomiting from hypothalamus involvement.
    • Changes in vital signs due to compensation against rising ICP.
    • Changes in pupil reactions and signs of abnormal posturing.

Management Strategies

Management of Increased ICP

  • Prevention strategies must include:
    • Avoiding systemic injuries: hypotension and hypoxia.
    • Early detection of symptoms of increasing ICP (e.g., altered LOC).
    • Utilize GCS and AVPU systems for monitoring.

Warning Signs for Increased ICP

  • Declines in GCS score by 2 or more.
  • Sluggish/nonreactive pupils.
  • Development of abnormal motor response or posturing.

XABCDE Approach

  • Maintain airway integrity while ensuring C-spine safety.
  • Maintain oxygen saturation above 95%.
  • Prevent causes of secondary brain injury, and manage blood CO2 levels for optimal ICP.
  • Adjust ventilation rates based on patient age and needs.

Controlled Hyperventilation

  • Used to reduce ICP by lowering blood CO2, but it carries risks of decreased cerebral blood flow.

Additional Management Considerations

  • Ensure fluid resuscitation to maintain blood pressure.
  • Regular monitoring of vitals and neurological assessments for TBI patients.
  • Early patient transportation to appropriate facilities is critical with minimal on-scene time.

References

  • American College of Surgeons (2020). Prehospital Trauma Life Support, 9th Edition, Jones & Bartlett Learning.
  • Campbell J (2020). International Trauma Life Support for Emergency Care Providers, 9th Edition, Pearson.
  • Pollak A (2018). Nancy Caroline’s Emergency Care in the Streets, 8th Edition, Jones & Bartlett Learning.
  • Tintinalli J (2011). Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th Edition, McGraw Hill.