Traumatic Brain Injuries
Traumatic Injuries to the Brain
Causes of TBI
80% of traumatic brain injuries (TBI) relate to:
Motor Vehicle Crashes
Falls
Struck by or against an object
Assault and self-harm
Mechanisms of Injury
Coup-Contre Coup: Injury at impact site and opposite side due to brain's motion.
Deceleration: Head stops quickly, brain collides with skull.
Rotation: Head is twisted.
Penetration Injury: Object breaches skull and brain tissue.
Primary Brain Injuries
Laceration: Tear in brain tissue.
Fracture: Skull break, risk of hematoma.
Concussion: Temporary loss of consciousness or brain dysfunction.
Contusion: Brain bruise from impact.
Diffuse Axonal Injury: Widespread axon damage from acceleration/deceleration.
Hematomas (Blood Collections)
Epidural Hematoma:
Blood between dura mater and skull.
Often arterial, requires surgical evacuation.
Symptoms: headache (HA), decreased level of consciousness (LOC), seizures, vomiting, hemiparesis, pupillary dilation.
Subdural Hematoma:
Bleeding between dura and arachnoid layers.
Common in elderly and alcoholics (history of falls/medications).
Treatment: burr holes or craniotomy.
Intracerebral Hematoma:
Bleeding within brain tissue (e.g., penetrating trauma).
Requires surgical intervention and ICP monitoring.
Initial Management of Severe Brain Injury
Priority Actions:
Immediate neurological assessment.
Airway management (CRITICAL).
Address hypotension (text{MAP} < 65 \text{ mm Hg}) immediately.
For Severe Brain Injury (GCS 8):
Endotracheal intubation (to control and adequate ).
Fluid resuscitation, sedation, pharmacologic paralysis.
Emergency surgeries if herniation/deterioration evident.
Hyperventilation and mannitol () for specific conditions.
Glasgow Coma Scale (GCS)
Components: Eye opening, verbal response, motor response.
If GCS < 8: Immediate intubation.
Motor Function: Assess reactions to commands/pain: local, withdraw, decorticate, decerebrate, flaccid.
Decorticate Posturing: Arms flexed towards body (damage to thalamus/cerebral hemispheres).
Decerebrate Posturing: Arms extended away from body (damage to midbrain/pons) - WORSE PROGNOSIS.
Cranial Nerve & Brainstem Assessment
Nerve II (Optic) & III (Oculomotor): Pupil constriction, reaction to light, accommodation.
Nerve V (Trigeminal): Corneal reflex.
Nerve VII (Facial): Facial symmetry.
Nerve IX (Glossopharyngeal) & X (Vagus): Gag reflex, airway protection.
"Blown Pupils": Dilated, non-reactive pupils - sign of oculomotor damage or brainstem herniation.
Oculocephalic (Doll's Eyes): Eyes do not move with head turning = severe brainstem dysfunction.
Oculovestibular (Ice Water Test): Lack of eye movement with ice water in ear = loss of brainstem activity.
Respiratory Assessment (Impact of Brain Injury)
Cerebral Damage: Cheyne-Stokes respiration.
Pons Damage: Gasping, hyperventilation, or apnea.
Medulla Damage: Uncoordinated deep/shallow breathing with irregular pauses.
Imaging and Diagnostics
CT Scan: Detects contusions, fractures, acute bleeds, lesions.
MRI: Better for soft tissue and multi-planar visualization.
Electroencephalography (EEG): Diagnoses seizure disorders, brain death.
Lumbar Puncture: Detects blood in CSF, relieves ICP.
Secondary Brain Injury (Worsening Factors)
Causes: Increased ICP (often from cerebral edema), hypo/hyperglycemia, hypotension (MAP < 65 \text{ mm Hg}), hypoxia, infection.
Intracranial Pressure (ICP) & Cerebral Perfusion
Key Components of ICP: 3-10% cerebral blood, 8-12% CSF, 80% brain parenchyma (water).
Cerebral Perfusion Pressure (CPP): Must be (CPP = MAP - ICP).
Increased ICP
Causes: Cerebral edema, tumors, infections, ischemic/hypoxic injuries, brain herniation.
Clinical Manifestations: Restlessness, headache, nausea, drowsiness, pupillary changes (irregular shape, blown pupils).
Monitoring ICP
Factors that Increase ICP: Hypoxia, hypercapnia, pain, seizures, fever, straining, increased stimulation.
Normal ICP: ; intervention required for levels >20 \text{ mm Hg}.
Monitoring Setup: Invasive catheter into ventricles, leveled at foramen of Monro.
Risks: Infection, hemorrhage.
Nursing Considerations for ICP Monitoring
CSF Drainage: Check hourly, rebalance every 2-4 hours.
Positioning: Head of bed (HOB) at 30 degrees to promote drainage, ensure HOB is stable.
Management of Elevated ICP
Strategies:
Drain CSF.
Osmotic Therapy: Hypertonic saline (>3\% requires central line) and mannitol (monitor for dehydration).
Respiratory Support: Prevent VAP, monitor arterial blood gases (ABGs).
Sedation Protocol: Continuous sedation/analgesia, use sedation scales, schedule sedation vacations.
Neuromuscular Blockade (NMB): Assess with train-of-four every 4 hours.
Pharmacological Interventions for ICP
Sedatives & NMBs, antiseizure medications, mannitol, hypertonic saline.
Paroxysmal Sympathetic Hyperactivity (Sympathetic Storming)
Clinical Manifestations: Diaphoresis, agitation, restlessness, abnormal posturing, hyperventilation, transient tachycardia/fever.
Triggers: Suctioning, elevated temperatures, turning, alarm sounds.
Management: Minimize sensory stimuli, hyper-oxygenate during suctioning, limit visitation, manage temperature.
Immediate and Long-Term Effects of Brain Injury
Cognitive: Memory, attention, executive function deficits, reduced processing speed.
Physical: Motor impairments, fatigue, headaches, sleep disturbances.
Emotional/Behavioral: Personality changes, emotional dysregulation, social withdrawal.