TBI: Introductory Information - NeuroRehab I Flashcards

Introduction to Traumatic Brain Injury (TBI)

  • Definition of TBI: An insult or injury caused by an external force that may produce an altered or diminished state of consciousness and/or results in impairment of cognitive abilities and or physical function.

  • Prevalence and Statistics:

    • Over 1.5 million people per year visit the Emergency Room with TBI.

    • Older age is associated with a worse prognosis, including higher mortality rates and prolonged hospitalization.

    • Reported statistics often do not account for mild TBI (mTBI), unrecognized sports-related injuries, or military-related injuries.

  • Sobering Statistics:

    • Life expectancy is lowered by more than 3×3 \times compared to the general population.

    • Significant loss of income potential: 4 out of 10 individuals are not working one year post-injury.

    • 5.3 million individuals in the US live with a disability due to TBI.

    • 1 in 3 individuals face poor social integration (lifetime disability issues).

    • Financial burden is close to 50 billion50 \text{ billion} dollars annually in the US.

Mechanisms and Causes of Injury

  • Common Causes (Mechanism of Injury - MOI):

    • Falls (Especially traumatic in the elderly, even from ground level).

    • Motor Vehicle Accidents (MVA).

    • Struck by objects.

    • Assaults.

  • Primary Injury Types:

    • Direct Blow: Skull contacts another object with force (e.g., car accident hitting the windshield, strikes/punches in assaults).

    • Rapid Acceleration/Deceleration: Leads to Diffuse Axonal Injury (DAI).

    • Penetrating: Caused by Gunshot Wounds (GSW) or shrapnel.

    • Blast Wave: Common in military contexts; often results in mTBI but can be more severe.

  • Coup-Contrecoup Injury:

    • Coup Injury: Occurs when the head stops suddenly and the brain rushes forward. Damage occurs from hitting the side of the skull and rubbing against inner ridges.

    • Contrecoup Injury: Occurs when the brain bounces off the primary surface and impacts the opposing side of the skull, rubbing against inner ridges again.

Pathophysiology of TBI

  • Categorization of Injury:

    • Primary Injury: Tissue damage occurring at the exact site of the accident (e.g., skull fractures, contusions, lacerations, intracranial lesions, DAI).

    • Secondary Injury: Occurs after initial onset but is a direct result of the primary injury (e.g., increased Intracranial Pressure (ICP) leading to ischemia, hypoxia, herniation, and mass effect).

  • Metabolic and Cellular Cascade:

    • Brain edema and cell swelling.

    • Release of cytokines, chemokines, and neurotrophins causing inflammation.

    • Metabolic disarray: Increased lactate (Lactate↑\text{Lactate} ↑).

    • Excitotoxic effects: Release of Glutamate acting on NMDA-receptors.

    • Ion Flux: Influx of Sodium (Na+\text{Na}^+) and Calcium (Ca2+\text{Ca}^{2+}); efflux of Potassium (K+\text{K}^+).

    • Energy Failure: Mitochondrial dysfunction leading to decreased ATP.

    • Oxidative Stress: Generation of Reactive Oxygen Species (ROS) and Nitric Oxide species.

    • Axonal Damage: Cytoskeleton disruption and impaired axonal transport involving axonal filaments.

    • Involvement of Microglia, Macrophages, and Leucocyte infiltration from capillaries.

Acute Medical Management and Monitoring

  • Pre-Hospital Phase:

    • Emergency care is critical for establishing an effective airway.

    • Maintenance of cardiovascular support.

    • Primary goal: Save life and transport to the ER.

  • Acute Care Goals:

    • Minimize further/secondary damage (hypoxia, edema, infection, neurochemical imbalances, herniations).

    • Support cardiopulmonary system.

    • Address polytrauma complications.

  • Hyper-Oxygenation:

    • Increased O2O_2 improves mitochondrial function.

    • Hyperoxia Risks: Evidence is mixed; plasma O2O_2 is less than 1%1\% of transported O2O_2. If blood flow is reduced, increased plasma O2O_2 is ineffective. Excess O2O_2 can cause free radicals, toxicity, and pulmonary damage.

    • Hyperbaric O2O_2 is often not available for critical clients.

    • Requirement: Correct anemic state to improve oxygen delivery.

  • Hypothermia Intervention:

    • Used to reduce refractory intracranial hypertension.

    • Aimed at reducing metabolic demand, apoptosis, and edema.

    • Not widely used due to associated risks but remains under study.

  • Autoregulation of Cerebral Blood Flow (CBF):

    • Changes in vasculature diameter to maintain homeostasis.

    • Vasoconstriction Factors: Increased PaO2PaO_2, Increased ICP, or Decreased Mean Arterial Pressure (MAP).

    • Vasodilation Factors: Increased PaCO2PaCO_2, Increased Cerebral Perfusion Pressure (CPP), Increased MAP, or Hypotension.

Neuromonitoring and Surgical Management

  • Acute Monitoring:

    • ICP Monitoring: Normal range is < 20 \text{ cmH}_2\text{O}.

    • Cerebral Perfusion Pressure (CPP): Calculated as CPP=MAP−ICP\text{CPP} = \text{MAP} - \text{ICP}. Goal is \text{CPP} > 50 \text{ mmHg} to prevent hypoxia.

    • Maintenance of CPP: Maintain BP, improve venous drainage, reduce CSF pressure, mild short-term hyperventilation, avoid pressure-increasing activities (coughs, Valsalva, bucking the ventilator), and use medications (Mannitol, Barbiturates).

  • Multimodal Monitoring: Newer devices combine oximetry, blood flow, microdialysis, temperature, and continuous electrocorticography; however, these are invasive.

  • Surgical Procedures:

    • Craniotomy: A small section of the skull (bone flap) is removed to clean a hematoma and then replaced and fixed with plates.

    • Burr Holes: Used for ICP bolts or ventriculostomy.

    • Craniectomy: A section of the skull is removed for a period of time to allow the brain to swell without the pressure constraints of the skull.

Herniation Syndromes

  • Subfalcine: Cingulate gyrus pushed under the falx cerebri. Often asymptomatic unless the Anterior Cerebral Artery (ACA) is occluded.

  • Central: Downward displacement of the brainstem.

    • Mild: Can stretch Cranial Nerve VI (Abducens), causing lateral rectus palsy.

    • Severe: Can lead to uncal herniation or tonsillar herniation.

  • Tonsillar: Cerebellar tonsils through the foramen magnum; results in compression of the medulla, leading to coma and death.

  • Transtentorial (Uncal):

    • Clinical Triad: Blown pupil (CN III) usually ipsilateral; hemiplegia (compression of cerebral peduncles, usually contralateral); Coma (distortion of midbrain reticular formation).

    • Kernohan’s Phenomenon: Ipsilateral hemiplegia if there is significant compression of the medulla.

    • Can also compress the Posterior Cerebral Artery (PCA).

Clinical Presentation and Impairments

  • Common Primary Impairments:

    • Neuromuscular: Paresis, abnormal tone, motor function deficits, postural control issues.

    • Cognitive: Arousal level, attention, concentration, memory, learning, and executive function.

    • Neurobehavioral: Agitation, aggression, disinhibition, apathy, emotional lability, mental inflexibility, impulsivity, irritability.

    • Other: Communication, swallowing, dysautonomia, and seizures.

  • Common Secondary Impairments:

    • Deep Vein Thrombosis (DVT), Heterotopic Ossification (HO), pressure ulcers, pneumonia, chronic pain, contractures, decreased endurance, muscle atrophy, fracture, and peripheral nerve damage.

Rehabilitation and Pharmacology

  • Continuum of Care: Injury → Emergent Care → Acute Care (ICU/Stepdown/Floor) → Post-acute Inpatient (SNF/Rehab) → Post-acute Outpatient (Day program/Home health) → Wellness and Conditioning.

  • Early Intervention Goals:

    • Prevention: Maintain tissue extensibility (splint schedules, ROM, stretching). Education of family/nursing on positioning.

    • Upright Tolerance: Get patient Out of Bed (OOB) or Edge of Bed (EOB) daily when vitals are stable. Use stimulatory activities (avoid keeping patient supine).

    • Recovery Focus: Increase consciousness (attentional meds, coma stimulation protocols), improve neuro-cognitive skills (orientation is key), and functional mobility.

  • Medications Frequently Seen:

    • Attention: Ritalin, Ambien.

    • Tone Reduction: Botox, Phenol, Baclofen.

    • Behavioral: Geodon, Anti-depressants.

    • Neurological Pain/Seizure: Neurontin, Anti-seizure meds.

    • Intracranial Pressure: Barbiturates, Mannitol.

  • Limiting Factor: Hemodynamic stability is the biggest limiting factor in acute and critical care.

Prognosis and Outcome Measures

  • Classification of TBI Severity:

Feature

Mild

Moderate

Severe

LOC

0−30 min0-30 \text{ min}

30 \text{ min} < > 24 \text{ hr}

> 24 \text{ hr}

AOC

Brief < 24 \text{ hrs}

> 24 \text{ hr}

> 24 \text{ hr}

PTA

0−1 day0-1 \text{ day}

1 < > 7 \text{ days}

> 7 \text{ days}

GCS

13−1513-15

9−129-12

< 9

Imaging

Normal

Mixed

Mixed

  • GCS (Glasgow Coma Scale): Low motor/eye response in moderate-to-severe TBI predicts poor recovery. Typically used in the field/ED, not after the acute phase.

  • Post-Traumatic Amnesia (PTA): The length of time between injury and when the patient can remember ongoing events.

    • Severity Scores:

      • < 5 \text{ mins}: Very mild.

      • 5−60 mins5-60 \text{ mins}: Mild.

      • 1−24 hrs1-24 \text{ hrs}: Moderate.

      • 1−7 days1-7 \text{ days}: Severe.

      • 1−4 weeks1-4 \text{ weeks}: Very severe.

      • > 4 \text{ weeks}: Extremely severe.

    • Recovery Predictions:

      • < 53 \text{ days}: Likely to live without assistance.

      • < 48.5 \text{ days}: Higher FIM at discharge.

      • < 34 \text{ days}: Good overall recovery (GOS).

      • < 27 \text{ days}: Likely to be employed.

  • Galveston Orientation and Amnesia Test (GOAT):

    • 10 questions regarding person, place, time, situation, and memory.

    • Normal: 76−10076-100; Borderline: 65−7565-75; Impaired: < 66.

  • Coma Recovery Scale (CRS): 23 items with six subscales (hierarchically arranged):

    • Auditory (0−40-4), Visual (0−50-5), Motor (0−60-6), Oromotor/Verbal (0−30-3), Communication (0−20-2), Arousal (0−30-3).

  • Prognostic Factors:

    • Negative: Advanced age, coma > 1 \text{ week}, secondary injury, anoxia, DAI, minimal change in GCS/RLAS in 4 weeks, PTA > 2 \text{ weeks}.

    • Positive: Younger age, higher education, increased activity prior to injury, rapid change in skills, comprehensive care.

The Multidisciplinary Team

  • Patient and Family.

  • Physicians: Neurologist, Physiatrist, Pulmonologist, Orthopedist, Neurosurgeon.

  • Neuropsychologist.

  • Therapist Team: PT, SLP, OT, Recreation Therapist, Respiratory Therapist.

  • Nursing and Coordination: Rehab Nurse, Case Manager, Social Worker.