Ch63 PPTa Neurologic Trauma – Traumatic Brain & Spinal Cord Injury Comprehensive Notes

Learning Objectives

• Describe mechanisms, clinical signs/symptoms, diagnostics, and treatments for traumatic brain and spinal cord injuries (TBI & SCI).
• Apply the nursing process to patients with TBI and SCI.
• Identify populations at risk for SCI and TBI.
• Explain neurogenic shock and autonomic dysreflexia pathophysiology and interventions.
• Maintain holistic, inter-professional plans of care addressing physiologic, psychosocial, and rehabilitative needs.

Epidemiology of Head Injury

• $2.9\,\text{ million}$ ED visits per year in the United States—majority mild TBI.
• Approx. $56,800$ deaths/year (≈ $30\%$ of all injury-related deaths).
• Highest-risk groups: children $0!–!4\,\text{yr}$ , adolescents $15!–!19\,\text{yr}$ , adults $\ge 65\,\text{yr}$ .
• Most common etiology: falls (see pie chart – $47\%$ ). Others: struck by/against $15\%$ , traffic $14\%$ , assault $9\%$ , unknown $8\%$ , other $7\%$ .
• Prevention (helmets, seat belts, fall-proofing) stressed as best approach.

Classification of Brain Injuries

• Acquired (non-traumatic): anoxia, infection, stroke, tumor, metabolic disorders.
• Traumatic: open vs closed.
• Open (penetrating) – object breaches skull/scalp (assault, gunshot, surgery).
• Closed (blunt) – acceleration/deceleration & shearing forces (MVAs, falls).

Types of Brain Injury

Acquired Brain Injury subdivided into 2 categories

·Non-Traumatic Brain Injury

·Traumatic Brain Injury

Pathophysiology of Brain Damage

Primary injury: consequence of direct contact to head/brain during the instant of initial injury

These injuries result from the mechanical force exerted on the brain and can lead to immediate neurological dysfunction.

·Contusions: Bruising of brain tissue caused by the impact of the brain against the inner skull.

·Lacerations: Tears in brain tissue or blood vessels due to severe trauma, which can lead to bleeding and inflammation.

·External Hematomas: Accumulation of blood outside the brain tissue, such as epidural hematomas, which can cause increased pressure and brain shift.

·Skull Fractures: Breaks in the skull bone that can expose the brain to infection, bleeding, and cerebrospinal fluid (CSF) leaks.

·Subdural Hematomas: Bleeding between the dura mater and the brain, often due to ruptured veins, leading to pressure on brain structures.

·Concussion: A temporary disruption of brain function caused by a sudden blow, often resulting in altered mental status, headache, and dizziness.

·Diffuse Axonal Injury (DAI): Widespread shearing and tearing of nerve fibers due to rapid acceleration or deceleration, often seen in high-impact trauma such as car accidents.

Secondary injury: damage evolves over ensuing days and hours after the initial injury.

Result of the primary injury which can result to

§Cerebral Edema: Swelling of brain tissue increases intracranial pressure (ICP), reducing blood flow and oxygen delivery.

§ Ischemia: Reduced or blocked blood supply to brain tissue, leading to hypoxia and cell death.

§Chemical Changes Associated with Trauma: Neurotransmitter imbalances, inflammatory responses, and the release of toxic substances (e.g., excitotoxicity from excessive glutamate) contribute to further neuronal damage and dysfunction.

Non-Traumatic Brain Injury caused by

·Anoxia: A lack of oxygen to the brain can lead to widespread neuronal injury and cell death, resulting in cognitive deficits, motor impairments, or even permanent brain damage.

·Infections: Conditions such as meningitis, encephalitis, or brain accesses can cause inflammation and destruction of brain tissue, leading to neurological dysfunction.

·Strokes: A cerebrovascular event can deprive specific brain regions of oxygen and nutrients, leading to localized or widespread neurological impairments.

·Tumors: Brain tumors can compress, invade, or disrupt normal brain structures, affecting cognition, motor function, and overall neurological health.

·Metabolic Disorders: Conditions like diabetes, hepatic encephalopathy, or electrolyte imbalances can alter brain chemistry and function, potentially leading to confusion, coma, or permanent damage.

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Traumatic Brain Injury

Open Brain Injury

·Assaults: Violent attacks, such as gunshot wounds or sharp object injuries, can penetrate the skull and cause direct trauma to brain tissue.

·Falls: Severe falls, especially from significant heights or onto hard surfaces, can result in skull fractures and brain exposure.

·Accidents: Motor vehicle crashes or workplace incidents can involve sharp or high-impact trauma that breaches the skull.

·Abuse: Physical abuse, including blunt force trauma, can lead to open head injuries, particularly in vulnerable populations such as children and the elderly.

·Surgery: Certain medical procedures, such as craniotomies, intentionally open the skull to address underlying neurological conditions but also carry risks of complications.

Close Internal Pressure and Shearing

·Assaults: Blunt force trauma from punches, kicks, or strikes to the head can cause rotational or linear brain movement, leading to shearing injuries.

·Falls: Sudden impacts from falls can cause the brain to shift inside the skull, leading to internal bruising, hemorrhaging, or swelling.

·Accidents: Car crashes, sports injuries, or industrial accidents can cause rapid acceleration-deceleration forces, leading to diffuse axonal injury (DAI).

·Abuse: Shaken baby syndrome is a prime example, where violent shaking leads to severe shearing forces, causing widespread brain damage.

Pathophysiology of Traumatic Brain Injury (TBI)

• Primary injury – occurs at moment of impact (contusion, laceration, skull fracture, external or subdural hematoma, concussion, diffuse axonal injury).
• Secondary injury – evolves hours/days later: cerebral edema, ischemia, electrolyte/biochemical cascade, ↑ICP → herniation → loss of cerebral blood flow.
• Classic sequence:

Trauma → edema/bleed ↑ intracranial volume.
Rigid cranium prevents expansion → ↑ICP.
Cerebral vessels compressed → ↓CBF.
Hypoxia/ischemia → further swelling.
Possible herniation → cessation of CBF → brain death.

Pathophysiology of Traumatic Brain Injury

·Brain suffers traumatic injury

·Brain swelling or bleeding increases intracranial volume

·Rigid cranium allows no room for expansion of content so intracranial pressure increases

·Pressure on blood vessels within the brain causes blood flow to the brain to slow

·Cerebral hypoxia and ischemia occur

·Intracranial pressure continues to rise. The brain may herniate

·Cerebral blood flow ceases.

Clinical Manifestations of TBI

Mild TBI

• Headache, confusion.
• Dizziness, blurred vision.
• Sleepiness/fatigue, altered sleep pattern.
• Behavior/mood change, cognitive difficulty.
• Photophobia, hyperacusis.
• Nausea/vomiting.
• LOC: seconds–minutes.

Severe TBI (accentuation of mild symptoms + red flags)

• Persistent/worsening headache.
• Slurred speech, seizures.
• Loss of coordination.
• Unilateral pupil dilation.
• Numbness/tingling in extremities.
• LOC: minutes–hours.

Scalp Wounds & Skull Fractures

• Scalp: profuse bleeding, high infection risk.
• Skull fracture – localized pain; basilar fracture signs:
• Bleeding from nose, pharynx, ear; “Battle sign” (post-auricular ecchymosis).
• CSF leak → halo sign (ring of fluid encircling blood).

Major Types of Traumatic Brain Injury

• Closed (blunt) – acceleration/deceleration.
• Open (penetrating).
• Concussion – transient neuro dysfunction; no structural lesion.
• Observe at home or admit; report: ↓LOC, awakening difficulty, confusion, severe HA, vomiting, speech/motor problems.
• Contusion – coup/contrecoup bruising ± hemorrhage; longer LOC, VS changes, focal deficits.
• Diffuse Axonal Injury (DAI) – widespread axonal shearing → immediate coma; poor prognosis.

Intracranial Hemorrhages

Epidural Hematoma (EDH)

• Arterial bleed between skull & dura.
• Brief LOC → lucid interval → rapid deterioration (↑ICP).
• Neurosurgical emergency: burr holes/craniotomy, ICP control, airway/resp support.

Subdural Hematoma (SDH)

• Venous bleed between dura & arachnoid.
• Acute: onset $24!–!48\,h$ ; subacute $48\,h!–!2\,wk$ → craniotomy/ICP control.
• Chronic: onset weeks–months, often minor forgotten trauma; fluctuating neuro signs; treat by clot evacuation.

Intracerebral Hemorrhage (ICH)

• Bleeding within brain parenchyma from trauma or spontaneous causes.
• Management: supportive, ICP control, fluid/electrolyte balance, antihypertensives; surgical removal only if accessible.

Subarachnoid Hemorrhage (SAH)

• Blood in subarachnoid space; listed but not elaborated in transcript.

Diagnostic Evaluation for TBI

• Comprehensive physical & neuro exam.
• Imaging: skull/spine X-ray, CT (first-line), MRI, PET for function.
• Continuous GCS & multisystem monitoring.

Nursing Assessment & Collaborative Problems (TBI)

• History: mechanism, time, direction, force.
• Baseline GCS, VS, multisystem survey.
• Ongoing neuro checks: pupils, motor, sensation.
• Labs: serum/urine electrolytes, osmolality, glucose.
• Potential complications: ↓cerebral perfusion, cerebral edema/herniation, impaired oxygenation/ventilation, fluid-electrolyte imbalance, post-traumatic seizures.

Planning & Goals (TBI)

• Patent airway & adequate cerebral perfusion pressure (CPP).
• Stabilized fluids/electrolytes; adequate nutrition (early EN/TPN).
• Prevent secondary injury & infection; maintain normothermia & skin integrity.
• Promote coping, sleep, knowledge of rehab; avoid complications.

Nursing Interventions (TBI)

• Maintain airway, suction cautiously; monitor GCS & ICP parameters.
• Hemodynamic monitoring, I&O, daily weight, labs.
• Early enteral feeding; glucose control.
• Environmental safety: padded rails, mittens; avoid restraints.
• Reduce stimuli, optimize light, protect sleep–wake cycles.
• Temperature management: acetaminophen, cooling blankets—avoid shivering.
• Skin care, infection prevention (dressings, lines).
• Family education & psychosocial support; realistic short-term goals.

Medical/Surgical Management & Supportive Measures (TBI)

• Assume cervical injury until cleared; apply collar.
• Optimize oxygenation & circulation (ventilation, fluid resuscitation).
• Control bleeding & hypovolemia; treat ↑ICP (osmotics, drainage, positioning).
• Surgical evacuation (EDH, SDH, depressed skull fracture) when indicated.
• Continuous ICP monitoring; CSF drainage.
• NG tube for gastric decompression; seizure prophylaxis; pain/anxiety control.

Spinal Cord Injury (SCI) Overview

• $294,000$ Americans live with SCI-related disability.
• Etiologies: MVAs, falls, violence (GSW), sports.
• Demographics: $78\%$ male; mean age $43$ .
• Risk factors: young males, ETOH/drug use.
• Leading mortality: pneumonia, PE, sepsis.

Pathophysiology of SCI

• Primary insult: concussion, contusion, laceration, compression → often permanent.
• Secondary injury: edema, hemorrhage, ischemia, necrosis—expand lesion; critical-care focus to limit extension.
• Mechanisms: acceleration–deceleration, compression fractures, penetrating trauma.

Top 5 Causes of SCI

Vehicular accidents.
Falls (especially ≥ $65$ yr).
Violence (e.g., shootings).
Sports/diving.
Disease complications.

Functional Effects by Level

• Tetraplegia (C1–C8): all four limbs paralyzed.
• Paraplegia (T1–L4): lower limbs paralyzed.

Patient Assessment (SCI)

• Systematic head-to-toe; skin integrity; respiratory pattern, cough effort, breath sounds.
• Neuro: motor/sensory changes; monitor for spinal shock.
• Bowel/bladder: retention, distention, ileus.
• Temperature regulation; psychosocial state.

Collaborative Problems/Complications (SCI)

• Spasticity, infection/sepsis, DVT, orthostatic hypotension, autonomic dysreflexia.

Planning & Goals (SCI)

• Effective ventilation & airway clearance.
• Safe mobility/positioning; skin integrity.
• Bladder/bowel control; sexual expression.
• Adequate coping & long-term self-management.
• Prevention/recognition of complications.

Spinal Shock

• Immediate transient loss of motor, sensory, reflex, autonomic function below lesion.
• Flaccid paralysis, areflexia.
• Duration: < $48$ h to weeks; monitor for reflex return.

Neurogenic Shock

• Injury above T6; loss of sympathetic tone.
• ↓BP, ↓HR, ↓CO; peripheral vasodilation → venous pooling; anhidrosis below lesion.

Autonomic Dysreflexia (AD) / Hyperreflexia

Pathophysiology

• Occurs after spinal shock resolves (may be years post-injury).
• Noxious stimulus below lesion (e.g., full bladder) → massive sympathetic discharge → widespread vasoconstriction below injury → severe HTN.
• Baroreceptors trigger vagal response → bradycardia & vasodilation above lesion, but descending inhibitory impulses blocked at lesion ⇒ unchecked HTN.
• Risks: lesions above T6.

Common Triggers

• Bladder distension/kinked catheter (most common), UTI, stones.
• Bowel impaction, hemorrhoids, digital stimulation.
• Skin: pressure ulcer, tight clothing, burns, ingrown toenail.
• Sexual activity, labor, menstruation, abdominal pain.

Clinical Manifestations

• Sudden severe pounding HA.
• Rapid ↑BP (≥ $20!–!30\,\text{mmHg}$ above baseline).
• Bradycardia (≈ $\le 60\,\text{bpm}$ ).
• Flushing/diaphoresis above injury; pallor below.
• Nasal congestion, nausea, blurred vision, dilated pupils, pilo-erection, restlessness.

Emergency Nursing Management

• Sit patient upright (↓ICP/HTN).
• Rapid assessment & removal of stimulus:
• Check catheter for kinks; empty bladder or re-catheterize.
• Check for fecal impaction—apply anesthetic lubricant & remove.
• Inspect skin, clothing, devices.
• Monitor BP q2–3 min; call provider if unresolved.
• Pharmacologic: IV hydralazine or other ganglionic blocker for persistent HTN.
• Document & teach patient/family; flag chart for AD risk.

Nursing Interventions (SCI)

Respiratory

• Vigilant monitoring for failure; ABG, pulse-ox, suction (with caution), assisted cough, humidification.

Mobility & Alignment

• Neutral spine; log-roll if cleared; specialized beds (RotoRest®, RotoProne®), cervical collar, halo fixation.
• PROM ≥4×/day; gradual upright positioning; monitor BP for orthostatic drops.

Skin & Sensory

• Frequent repositioning; pressure-relief surfaces; inspect under braces/vests; pin site care for traction/halo.
• Environmental modifications for visual/auditory deficits.

Elimination & Nutrition

• Intermittent/indwelling catheter management; monitor residuals.
• NG tube for gastric decompression; initiate high-calorie/high-protein/high-fiber diet; bowel program with softeners.

Psychosocial & Education

• Support coping, goal-setting, counseling, support groups.
• Educate on AD prevention, skin care, DVT avoidance (no calf/thigh massage), long-term self-management.

Equipment Used in SCI Care

• Cervical collars (e.g., Vista®), halo vest systems (bars, pins, vest) for C-T stabilization.
• Rotational & prone therapy beds to prevent complications & aid pulmonary toilets.

Sample NCLEX-Style Review Points (From Lecture Questions)

• Contusion ≠ concussion; concussion = temporary neuro loss without structural damage (Q#1 – FALSE if statement said contusion equals that).
• Clear rhinorrhea (CSF) indicates basilar skull fracture – TRUE (Q#2).
• Avoid massaging calves/thighs to prevent DVT embolization – TRUE (Q#3).
• Autonomic dysreflexia inappropriate action: lower patient flat (Q#4 & Q#8 answer B).
• AD priority: sit patient up first, then search for cause; do NOT call HCP before action (Q#5 answer B or D depending on sequence; lecture emphasized sitting first).
• Earliest sign of ↑ICP: agitation & confusion (Q#6 answer C).
• Bilateral dilated nonreactive pupils suggest brainstem herniation (Q#7 answer B).

These bullet-point notes consolidate every major and minor detail from the transcript, explain pathophysiologic processes, outline nursing care using the nursing process, integrate numerical data, and connect real-world implications, providing a comprehensive standalone study guide.