NSG210 Hinkle Ch. 63: Management of Patients with Neurologic Trauma

Source: Hinkle & Cheever, Brunner & Suddarth’s Medical-Surgical Nursing 15e, Chapter 63, pp. 2055-2086 (textbooks/HINKLE_MS_CH63.pdf, also in textbooks/exam04/). Week 11 reading (spinal cord injury); Exam 4 content (the course calendars end Exam 3 content with the October 28 OB lecture). Numbering note: the syllabus lists “Ch. 64” (16th edition); neurologic trauma is Ch. 63 in the 15th edition (see nsg210-textbook-chapter-crosswalk). ICP physiology and seizure care are in nsg210-hinkle-ch61-neurologic-dysfunction.

Learning Outcomes

1. Describe mechanisms of injury, signs and symptoms, diagnostics, and treatment for traumatic brain injury (TBI) and spinal cord injury (SCI).
2. Use the nursing process for the patient with TBI.
3. Identify the population at risk for SCI and explain the features and management of neurogenic shock.
4. Discuss the pathophysiology of autonomic dysreflexia and the nursing interventions.
5. Apply the nursing process to the patient with SCI and the patient with tetraplegia or paraplegia.

Key Terms

• Autonomic dysreflexia (hyperreflexia): life-threatening hypertensive emergency in SCI
• Complete spinal cord lesion: total loss of sensation and voluntary muscle control below the lesion
• Incomplete spinal cord lesion: some sensory or motor fibers preserved below the lesion
• Concussion: temporary loss of neurologic function with no apparent structural damage
• Contusion: bruising of the brain surface
• Neurogenic bladder: bladder dysfunction from nervous system disorder (retention or overactivity)
• Paraplegia: lower extremity paralysis with bowel and bladder dysfunction (thoracic, lumbar, sacral lesion)
• Tetraplegia (formerly quadriplegia): paralysis of arms and legs with bowel and bladder dysfunction (cervical lesion)
• Primary injury: initial damage from the traumatic event. Secondary injury: later insult to the brain after the original event
• Transection: severing of the cord, complete or incomplete
• TBI, closed (blunt): acceleration-deceleration or collision; no opening through skull and dura
• TBI, open (penetrating): object penetrates skull and brain, or blunt force opens scalp, skull, and dura

I. Head Injuries: Overview

• Head injury does not always mean brain injury. TBI = injury from external force severe enough to interfere with daily life.
• Statistics (CDC 2019): 2.9 million ED visits per year, mostly mild TBI; about 56,800 deaths (about 30 percent of injury deaths); 78 percent treated and released from the ED.
• Causes: falls 48 percent, struck by objects 15 percent, motor vehicle crashes 14 percent, assaults 10 percent.
• Highest risk ages: 0-4 years, 15-19 years, 65 and older; males higher at every age.
• Prevention (Chart 63-1): obey traffic laws, no impaired driving; seat belts; children under 12 in age/size-appropriate restraint in back seat; no riding in pickup beds; helmets; violence and suicide prevention; water safety; fall prevention in older adults; protective sports gear; firearms locked.

A. Pathophysiology

• Primary injury: direct contact at the instant of injury (contusions, lacerations, external hematomas, skull fractures, subdural hematoma, concussion, diffuse axonal injury).
• Secondary injury: evolves over hours to days from inadequate delivery of oxygen and glucose. Intracranial causes: hemorrhage, cerebral edema, intracranial hypertension, hyperemia, seizures, vasospasm. Systemic causes: hypotension, hyperthermia, hypoxia, hypercarbia, infection, electrolyte imbalance, anemia.
• Preventing secondary injury is the main focus of early management.
• Monro-Kellie hypothesis: brain, blood, CSF in a closed vault; an increase in one must be offset or ICP rises.
• Veterans: TBI prevalence 15 to 23 percent in combat roles; blast injuries cause four levels (primary overpressure, secondary shrapnel, tertiary thrown against surface, quaternary burns and crush). Treatment same as civilians.

B. Scalp Injury

• Bleeds profusely (vessels constrict poorly). Abrasion, contusion, laceration, subgaleal hematoma. Large avulsion is a true emergency.
• Irrigate before suturing (portal of entry for intracranial infection). Subgaleal hematomas usually reabsorb.

C. Skull Fractures

• Types: linear (simple), comminuted (splintered), depressed (bone pushed into brain). Location: frontal, temporal, basal. Open (dura torn) vs closed.
• Persistent localized pain suggests fracture.
• Basal skull fracture signs: bleeding from nose, pharynx, or ears; blood under conjunctiva; Battle sign (ecchymosis over mastoid); CSF otorrhea and CSF rhinorrhea. CSF leak risks meningitis.
• Diagnosis: CT; MRI for associated brain injury.
• Management: nondepressed fractures observed, no surgery. Depressed fractures usually need surgery (elevation and debridement) within 24 hours.
• Older adults: worse outcomes; about 81 percent of TBIs in those 65 and older are from falls; risk for hematoma from brain atrophy, dura more adherent, slower reactions, anticoagulant and aspirin use. Report more physical symptoms (fatigue, balance, noise sensitivity).

II. Brain Injury

• The brain cannot store oxygen or glucose; irreversible damage occurs if blood supply is interrupted even a few minutes.
• Focal injuries: contusions, hematomas. Diffuse injuries: concussion, diffuse axonal injury.

A. Contusion

• Bruising from acceleration-deceleration; usually frontal and temporal lobes.
• Loss of consciousness, stupor, confusion. Hemorrhage and edema peak about 18 to 36 hours; temporal lobe contusions most likely to raise ICP and herniate.

B. Intracranial Hemorrhage (hematomas)

• Symptoms often delayed until hematoma distorts brain and raises ICP. A rapidly developing small hematoma can be fatal; a slow larger one may be compensated.

Epidural hematoma (EDH):

• Blood between skull and dura; usually from skull fracture tearing the middle meningeal artery (arterial, rapid). 2.7 to 4 percent of head injuries.
• Classic pattern: brief loss of consciousness, then lucid interval (awake, conversant), then restlessness, agitation, confusion, coma; sudden herniation signs (dilated fixed pupil, paralysis of an extremity). Most common herniation: uncal (midbrain pressure).
• Extreme emergency: burr holes or craniotomy to remove clot and control bleeding; drain placed.

Subdural hematoma (SDH):

• Blood between dura and brain; usually venous (bridging veins). Trauma most common; also coagulopathy, aneurysm.
• Acute SDH: usually from a fall; LOC changes, pupillary signs, hemiparesis. Coma, rising BP, falling HR, slowing respirations = rapidly expanding mass. Immediate craniotomy. High mortality.
• Chronic SDH: older adults (brain atrophy), seemingly minor injury; symptoms 3 weeks to months later, injury may be forgotten; may mimic stroke. Clot becomes “motor oil” in a few weeks. Fluctuating severe headache, alternating focal signs, personality change, mental deterioration, focal seizures. Treatment: evacuation via burr holes or craniotomy; reverse anticoagulation.

Intracerebral hemorrhage:

• Bleeding into brain parenchyma; trauma over a small area (bullets, stabs) or hypertension, aneurysm, vascular anomaly, tumor, bleeding disorders, anticoagulants.
• Insidious onset: neurologic deficits, then headache. Supportive care, ICP control, fluids, electrolytes, antihypertensives; surgery if accessible.

C. Concussion

• Temporary loss of neurologic function, no structural damage; about 80 percent of TBIs (“mild TBI”).
• Frontal lobe: bizarre irrational behavior. Temporal lobe: temporary amnesia, disorientation.
• Duration of mental status abnormalities indicates grade. Discharged once back to baseline.
• Red flags to report: decreased LOC, worsening headache, dizziness, seizures, abnormal pupil response, vomiting, irritability, slurred speech, numbness or weakness of arms or legs.
• Repeat injuries common. Chronic traumatic encephalopathy (CTE) from repeated concussions (football, boxing): resembles Alzheimer (personality change, memory impairment, speech and gait disturbance), temporal lobe atrophy.

D. Diffuse Axonal Injury (DAI)

• Widespread shearing and rotational forces damaging axons in hemispheres, corpus callosum, brain stem.
• No lucid interval, immediate coma, decorticate and decerebrate posturing, global cerebral edema. Poorer prognosis than focal lesions.

E. Medical Management of TBI

• Assume cervical spine injury in any head injury until ruled out: backboard, head and neck aligned, cervical collar until x-rays clear.
• All therapy aims to preserve brain homeostasis and prevent secondary injury: stabilize cardiovascular and respiratory function, control hemorrhage and hypovolemia, maintain optimal blood gases. Brain Trauma Foundation guidelines.
• ICP: monitor; surgery for clot evacuation, depressed fractures, scalp lacerations. Oxygenation, HOB elevation, normal blood volume.
• Supportive: ventilation (comatose patients intubated), seizure prevention, fluids and electrolytes, nutrition, pain and anxiety.
• Sedation: benzodiazepines (lorazepam, midazolam) do not affect cerebral blood flow or ICP but can prolong sedation. Propofol is the sedative of choice: ultrashort-acting, titratable, half-life under 1 hour, allows accurate neuro assessment.
• NG tube: reduced gastric motility and reverse peristalsis make regurgitation and aspiration common in the first hours.
• Brain death: three cardinal signs are coma, absent brain stem reflexes, and apnea. Adjunct tests: cerebral blood flow studies, EEG, transcranial Doppler, brain stem auditory evoked potentials. Support family; potential organ donation; the injury, not removal of support or organs, causes death.

III. Nursing Process: Traumatic Brain Injury

A. Assessment

• History: when, what caused it, direction and force; loss of consciousness, duration, arousable. Unconsciousness or amnesia indicates significant brain damage.
• Glasgow Coma Scale (Chart 63-4): eye opening (spontaneous 4, to voice 3, to pain 2, none 1); verbal (oriented 5, confused 4, inappropriate words 3, incomprehensible sounds 2, none 1); motor (obeys 6, localizes 5, withdraws 4, flexion 3, extension 2, none 1). Range 3 (deep coma) to 15. GCS 3 to 8 = severe head injury.
• Concept Mastery Alert: GCS (change in LOC) is the most sensitive indicator of neurologic deterioration and often the earliest sign of acute change in ICP.
• Table 63-1 multisystem assessment: neurogenic pulmonary edema from sympathetic discharge; arrhythmias; DVT and PE risk; DI, SIADH, electrolyte imbalance, hyperosmolar states; paralytic ileus; nutrition consult within 24-48 h; skin breakdown; family support.

B. Nursing Diagnoses

• Impaired airway clearance and gas exchange; risk for ineffective tissue perfusion (ICP, CPP, seizures); hypovolemia; impaired nutrition; risk for injury; risk for impaired thermoregulation; risk for impaired skin integrity; difficulty coping; impaired sleep; risk for impaired family coping; lack of knowledge.
• Complications: decreased cerebral perfusion, cerebral edema and herniation, impaired oxygenation and ventilation, fluid/electrolyte/nutrition imbalance, posttraumatic seizures.

C. Interventions

Maintaining the airway (top priority):

• Brain is extremely sensitive to hypoxia; CO2 retention causes vasodilation and raised ICP.
• Position to drain secretions, HOB about 30 degrees; effective suctioning (coughing and straining raise ICP); guard against aspiration; monitor ABGs; watch for ARDS and pneumonia; oral hygiene to prevent ventilator-associated pneumonia.

Monitoring neurologic function:

• ICU: cardiac monitor, pulse oximetry, arterial line, end-tidal CO2, temperature. Neurologic flow sheet.
• Vital signs: Cushing reflex (bradycardia, rising systolic BP, widening pulse pressure) indicates increasing ICP. Then rapid respirations, falling BP, slower pulse = ominous. Rapid fluctuation of VS also ominous.
• Temperature kept below 38 C (100.4 F). Concept Mastery Alert: rapid rise in temperature is unfavorable (raises brain metabolic demand, may signal brain stem damage).
• Tachycardia and hypotension may mean bleeding elsewhere in the body.
• Motor: hand grips, push against hands with feet; central painful stimulus (pinch pectoralis major) rather than peripheral, which may give reflex movement. Abnormal (extension, no response) = poorer prognosis.
• Pupils: unilateral dilated, poorly responsive pupil = developing hematoma pressing CN III. Both fixed and dilated = upper brain stem damage, poor prognosis.
• Residual deficits: anosmia, eye movement abnormalities, aphasia, memory deficits, posttraumatic seizures, impulsiveness, emotional lability, aggression.

Fluid and electrolyte balance:

• Serial blood and urine electrolytes and osmolality; hyponatremia common (SIADH); hypernatremia possible; daily weights if hypothalamic involvement (DI risk); urine tested for acetone.

Nutrition:

• Hypermetabolic and catabolic; increased protein demand. Early nutrition improves outcomes; enteral preferred. If CSF rhinorrhea or suspected skull base fracture, use an oral (not nasal) feeding tube. HOB elevated to prevent aspiration.

Preventing injury:

• Emerging from coma: lethargy, then agitation. Restlessness may be from hypoxia, fever, pain, or full bladder (or a sign of regaining consciousness).
• Check oxygenation and bladder; check dressings and casts for constriction.
• Padded side rails, hand mitts; restraints used judiciously (straining raises ICP); enclosed or floor-level beds.
• Avoid opioids to control restlessness (depress respiration, constrict pupils, alter responsiveness).
• Quiet room, limit visitors, speak calmly, frequent orientation; adequate lighting to prevent visual hallucinations; protect sleep-wake cycles; lubricate skin; external (condom) catheter or intermittent catheterization instead of indwelling.

Thermoregulation:

• Fever from hypothalamic damage, hemorrhage, or infection. Temperature every 2 to 4 hours; acetaminophen and cooling devices; avoid shivering (raises ICP). Culture if infection suspected.

Skin integrity:

• Assess skin every 8 hours; turn every 2 hours; skin care every 4 hours; out of bed to chair three times a day when able.

Coping and cognition:

• Memory deficits, distractibility, impulsivity, egocentricity, slowed thinking. Neuropsychologist and cognitive rehabilitation.
• Rancho Los Amigos Scale (Table 63-2):
  • Levels I-III (no response, generalized, localized): provide stimulation (olfactory, visual, auditory, tactile, movement); explain what you are doing.
  • Level IV (confused, agitated; lasts 2-4 weeks): decrease agitation, calm soft voice, quiet controlled environment, remove agitating devices; no functional goals yet.
  • Levels V-VI (confused inappropriate, confused appropriate): provide structure; supervision, repetition and cues, consistent posted schedule, reorient.
  • Levels VII-X (automatic appropriate through purposeful appropriate): integration into community; reduce structure, adapt home-living skills, monitor for depression.

Sleep: cluster care to allow longer rest; reduce noise and light.

Family coping: accurate honest information, short-term goals, counseling, support groups, Brain Injury Association of America; support around brain death and organ donation decisions.

D. Monitoring and Managing Complications

• Decreased CPP: adequate CPP is greater than 50 mm Hg (TBI section). Treat systemic hypotension with IV fluids or vasopressors.
• Cerebral edema: most common cause of increased ICP after head injury; peaks about 48 to 72 hours after injury.
• Chart 63-5, controlling ICP in severe brain injury: elevate HOB as prescribed; head and neck neutral; prevent Valsalva (stool softeners); normothermia; oxygen to keep PaO2 greater than 90 mm Hg; normal saline for fluid balance; avoid noxious stimuli (excess suctioning); sedation for agitation; maintain CPP 60 to 70 mm Hg.
• Fluid/electrolytes: hyponatremia (SIADH), hypokalemia, hyperglycemia. Keep blood glucose 80 to 160 mg/dL. Caloric expenditure increases 120 to 140 percent.
• Posttraumatic seizures: immediate (within 24 hours), early (1 to 7 days), late (more than 7 days). Prophylactic anticonvulsants supported for immediate and early seizures, not late. Anticonvulsants may impair cognition.
• Other complications: infections (pneumonia, UTI, sepsis, wound infection, osteomyelitis, meningitis, ventriculitis, brain abscess), heterotopic ossification.

E. Home and Transitional Care

• Home care checklist (Chart 63-6): medications, safe self-care and feeding techniques, behavior monitoring, safe home, report neurologic changes and complications.
• Rehabilitation begins at admission; improvement may continue 3 or more years after injury.

IV. Spinal Cord Injury

A. Epidemiology

• About 294,000 living with SCI in the US; about 17,810 new cases per year. Causes: motor vehicle crashes, falls, violence (gunshot), sports.
• 78 percent male; average age 43. Risk factors: younger age, male, alcohol and drug use.
• Leading causes of death: pneumonia, PE, sepsis.
• Most frequent injury: incomplete tetraplegia, then complete paraplegia, complete tetraplegia, incomplete paraplegia.

B. Pathophysiology

• Ranges from transient concussion to contusion, laceration, compression, and complete transection.
• Most often involved vertebrae: C5-C7, T12, L1 (greatest mobility).
• Primary injury usually permanent; secondary injury from edema and hemorrhage. Early treatment is essential to prevent partial damage becoming total.

C. Clinical Manifestations

• Depend on type and level. Complete lesion: loss of sensory and voluntary motor communication (paraplegia or tetraplegia). Incomplete: some fibers preserved.
• Cord syndromes (Chart 63-7):
  • Central cord: upper extremities affected more than lower (motor and sensory); bowel and bladder variable. Cervical hyperextension injuries.
  • Anterior cord: loss of pain, temperature, and motor below lesion; light touch, position, vibration intact. Disc herniation, hyperflexion, anterior spinal artery injury.
  • Brown-Sequard (lateral): ipsilateral paralysis and loss of touch, pressure, vibration; contralateral loss of pain and temperature. Hemisection, often knife or missile injury.
• ASIA classification (Fig. 63-4): neurologic level = lowest level with intact sensory and motor function. ASIA Impairment Scale: A complete (no S4-5 function); B sensory incomplete; C motor incomplete (less than half of key muscles below level grade 3 or more); D motor incomplete (half or more grade 3 or more); E normal.
• Below the level: paralysis, loss of bowel and bladder control (retention, distention), loss of sweating and vasomotor tone, marked hypotension from loss of peripheral vascular resistance.
• Acute back or neck pain may radiate; absence of pain does not rule out spinal injury.
• Respiratory muscles: diaphragm C4 (phrenic nerve), intercostals T1-T6, abdominals T6-T12. Injuries at C4 or above often need ventilator support. Injuries at T12 and above affect respiratory function.
• Table 63-3 functional abilities by level (highlights): C1-C3 ventilator dependent, sip-n-puff or voice-controlled wheelchair; C4 may breathe off ventilator for short periods, dependent; C5 eats with adaptive sling, electric wheelchair; C6 wrist extension, independent or minimal assist, independent transfers; C7-C8 independent, manual wheelchair; T1 and below full hand control, independent; T11-L5 short distance to full ambulation with assistance; S2-S4 control perineal muscles for bowel, bladder, sexual function.

D. Assessment and Diagnostics

• Detailed neuro exam; lateral cervical spine x-rays and CT first; MRI for ligamentous injury; myelogram if MRI contraindicated.
• Look for concomitant head and chest injuries.
• Continuous ECG: bradycardia and asystole common in acute SCI.

E. Emergency Management

• Any MVC, diving or contact sports injury, fall, or direct head/neck trauma: assume SCI until ruled out.
• Immobilize on spinal board, head and neck neutral (prevents incomplete injury becoming complete). One person controls the head (hands on both sides at ear level). At least four people to slide onto board; head blocks.
• No twisting; patient not allowed to sit up; keep on transfer board in ED and x-ray. Transport to a regional spinal injury or trauma center.
• Later: rotating specialty bed or cervical collar; if no specialty bed, cervical collar and firm mattress.

F. Medical Management (Acute)

• Goals: prevent secondary injury, watch for progressive deficits, prevent complications.
• High-dose methylprednisolone in first 24-48 hours is controversial; no longer standard of care.
• Oxygen to keep PaO2 high (hypoxemia worsens cord deficit). If intubating, avoid neck flexion or extension.
• High cervical injury: phrenic nerve lost; diaphragmatic pacing.
• Fracture reduction and traction: skeletal tongs or halo device; weights hang free; neck neutral; reduction confirmed by x-ray and neuro exam.
• Halo: ring fixed to skull with four pins, attached to vest; allows early ambulation.
• Thoracic and lumbar injuries: usually surgery then fitted brace.
• Surgery indications: cord compression, fragmented or unstable vertebral body, penetrating wound to cord, bony fragments in canal, deteriorating neuro status. Early stabilization may improve outcome.
• Quality and Safety Alert: vital functions must be supported until spinal and neurogenic shock abate; recovery can take up to 4 months.

G. Acute Complications

Spinal shock:

• Sudden depression of reflex activity (areflexia) below injury: flaccid paralysis, no sensation, absent reflexes; BP may drop, bradycardia.
• Keep MAP 85 mm Hg or higher in the hyperacute phase.
• Bladder and bowel reflexes affected: paralytic ileus usually occurs in first 2 to 3 days and resolves in 3 to 7 days; NG decompression.

Neurogenic shock:

• Loss of autonomic (sympathetic) function below the lesion: hypotension, bradycardia, decreased cardiac output, venous pooling, peripheral vasodilation.
• No sweating in paralyzed areas: watch for abrupt onset of fever.
• Cervical and upper thoracic injuries: decreased vital capacity, retained secretions, rising PaCO2, falling O2, respiratory failure, pulmonary edema.

Venous thromboembolism:

• High risk for DVT and PE (immobility, flaccidity, decreased vasomotor tone). Fatal PE in up to 2 percent in first 3 months.
• PE signs: pleuritic chest pain, anxiety, dyspnea, increased PaCO2, decreased PaO2.
• Prevention: anticoagulation started within 72 hours and continued at least 3 months (LMWH or low-dose unfractionated heparin, then possibly warfarin); anti-embolism stockings, SCDs, ROM, hydration; vena cava filter in some; measure thigh and calf circumferences daily; avoid knee flexion pressure.
• Quality and Safety Alert: never massage calves or thighs of an immobile patient.

Other: respiratory failure, pneumonia, autonomic dysreflexia, pressure injuries, infection (urinary, respiratory, pin sites).

V. Nursing Process: Acute SCI

A. Assessment

• Breathing pattern, cough strength, lung sounds (diaphragm and abdominal paralysis impair coughing).
• Serial motor and sensory exams on a flow sheet: spread fingers, squeeze hand, move toes; sensation by light pinch or touch from shoulders down both sides with patient’s eyes closed. Report any decrease in function immediately.
• Edema may be indistinguishable from transection early.
• Spinal shock: bladder distention (palpate lower abdomen), gastric dilation, paralytic ileus.
• Temperature: poikilothermia (body temperature depends on surroundings; cannot sweat).

B. Diagnoses and Complications

• Impaired breathing and airway clearance; impaired mobility; risk for injury; risk for impaired skin integrity; urinary retention; constipation; acute pain; autonomic dysreflexia.
• Complications: VTE, orthostatic hypotension.

C. Interventions

Breathing and airway:

• Watch for impending respiratory failure: vital capacity, SpO2, ABGs.
• Suction with caution: vagal stimulation can cause bradycardia and cardiac arrest.
• Assisted coughing (like abdominal thrusts) and chest physiotherapy; breathing exercises; humidification and hydration. Assisted coughing may beat suctioning (suction clears right mainstem; atelectasis and pneumonia most often left lower lobe).
• Ascending cord edema in the acute phase can cause sudden respiratory difficulty.

Mobility:

• Maintain alignment; do not turn unless provider says it is safe (unless on rotating bed).
• Splints for footdrop (remove and reapply every 2 hours); trochanter rolls from iliac crest to midthigh.
• Lesions above midthoracic level: poor tolerance of position changes (hypotension); monitor BP.
• Passive ROM at least four, ideally five, times daily.
• Cervical fracture without deficit: traction then rigid immobilization 6 to 8 weeks.

Sensory/perceptual: stimulate intact senses; prism glasses to see from supine; hearing aids; emotional support.

Skin:

• Pressure injuries can begin within hours. Move off backboard as soon as possible. Collar pressure points (chin, shoulders, occiput).
• Reposition at least every 2 hours; inspect skin each turn; mild soap, blot dry, lubricate.

Urinary elimination:

• Bladder atonic immediately: retention. Indwelling catheter initially; discontinue promptly (CAUTI risk).
• Then intermittent catheterization to prevent overdistention and UTI; teach family.
• Record intake, voiding pattern, residuals. Condom catheters for males with reflex or total incontinence.

Bowel:

• Paralytic ileus early: NG tube. Bowel activity usually returns within the first week.
• Bowel program: stool softeners, stimulant, bulk, and rectal laxatives plus rectal stimulation.

Traction, tongs, halo vest:

• Headache or discomfort for several days after pin insertion.
• Pin sites cleaned at least daily; watch for redness, drainage, pain, loosening.
• If a pin detaches: one person stabilizes head in neutral, another notifies provider. Torque screwdriver at bedside.
• Inspect skin under vest; open sides to wash torso; liner must not get wet; no powder inside vest; change liner periodically. Chart 63-8 home teaching.

Autonomic dysreflexia:

• Acute life-threatening emergency; occurs only after spinal shock resolves; lesions above T6 (sympathetic visceral outflow level).
• Signs: severe pounding headache, paroxysmal hypertension, profuse diaphoresis above the lesion (forehead), nausea, nasal congestion, bradycardia.
• Risks: retinal hemorrhage, hemorrhagic stroke, MI, seizures.
• Triggers: distended bladder (most common); bowel distention or impaction; skin stimulation (tactile, pain, thermal, pressure injury).
• Actions, in order:
  1. Sit the patient up immediately to lower BP.
  2. Rapid assessment for the cause.
  3. Empty bladder immediately via catheter; if indwelling catheter not patent, irrigate or replace.
  4. Check rectum for fecal mass; insert topical anesthetic 10 to 15 minutes before removing.
  5. Check skin for pressure, irritation, or breaks; remove other stimuli (tight objects, cold drafts).
  6. If not relieved, give antihypertensives slowly IV.
  7. Label the record clearly; teach prevention; patients with lesions above T6 can have episodes years later.

VTE and orthostatic hypotension:

• BP unstable and low for first 2 weeks.
• Orthostatic hypotension common with lesions above T7.
• Monitor VS before and during position changes; optimize fluids, vasopressors; anti-embolism stockings; abdominal binder; slow progression; tilt table.

D. Pregnancy and SCI

• Pregnancy not contraindicated; fertility relatively unaffected. Risks: autonomic dysreflexia, pyelonephritis, respiratory insufficiency, thrombophlebitis, PE, unattended delivery. Preconception counseling.

VI. Long-Term Care: Tetraplegia and Paraplegia

• Lifelong risks: disuse syndrome, autonomic dysreflexia, bladder and kidney infections, spasticity, depression, pressure injuries (about 10 percent; sepsis, osteomyelitis, fistulas), heterotopic ossification (hips, knees, shoulders, elbows).
• Grief stages: shock, disbelief, denial, anger, depression, acceptance. Denial may be protective early.
• Diagnoses: impaired mobility, risk for disuse, risk for impaired skin integrity, urinary retention, constipation, impaired sexual functioning, difficulty coping, lack of knowledge. Complications: spasticity, infection and sepsis.

A. Interventions

• Mobility: strengthen arms, shoulders, chest, abdomen, neck; triceps and latissimus dorsi for crutch walking; push-ups, sit-ups, weights, squeezing rubber balls. Early standing reduces osteoporosis and renal calculi. Braces and crutches for short distances (high energy cost); motorized wheelchairs.
• Weight: high obesity risk (decreased lean mass, increased BMI); nutrition counseling.
• Disuse syndrome: ROM at least four times a day; stretch Achilles tendon (footdrop); alignment.
• Skin: never stay in one position longer than 2 hours; inspect morning and night with mirrors; turn every 2 hours in bed; wheelchair push-ups, lean side to side, tilt forward; prescribed cushion. Diet high in protein, vitamins, calories, and fluids; avoid obesity.
• Bladder: reflex or nonreflex bladder; fluid intake about 2.5 L daily; empty frequently; perineal hygiene; cotton underwear changed daily; remove condom catheter nightly and clean and dry penis. UTI signs: cloudy, foul-smelling urine, hematuria, fever, chills.
• Bowel: reflex conditioning. Digital stimulation (lubricated gloved finger 2.5 to 3.7 cm, 1 to 1.5 in, circular motion) if lesion above sacral segments with reflex activity; NOT if sacral lesion (relaxed anus) or anal sphincter spasticity. Usually every 48 hours, after a meal. Fluids and fiber; watch for impaction (frequent loose stools) and hemorrhoids.
• Sexuality: counseling; penile prosthesis or ED drugs (sildenafil, vardenafil, tadalafil); oral contraceptives may raise VTE risk.
• Coping: avoid overly sympathetic attitude that fosters dependence; do not do for patients what they can do with a little effort.

B. Complications

Spasticity:

• Increased tone in weak muscle; onset weeks to 6 months after injury; same muscles flaccid during spinal shock become spastic; peaks about 2 years then regresses. Some spasticity can help weak patients.
• Treatment: botulinum toxin injections; baclofen (oral or intrathecal); diazepam, dantrolene, tizanidine; clonidine (oral or transdermal). All can cause drowsiness, weakness, vertigo. Passive ROM, frequent turning.

Infection and sepsis:

• Major cause of complications and death (urinary, respiratory, pressure injuries).
• Prevent: skin integrity, regular complete bladder emptying, avoid incontinence; avoid sick contacts; cough and deep breathe; yearly influenza vaccine; stop smoking; high-protein diet; aseptic catheter technique; hydration.

C. Home Care (Chart 63-9)

• Skin: inspect bony prominences morning and evening; weight lifts in wheelchair; protective boots.
• Bladder: clean intermittent self-catheterization; recognize UTI and catheter blockage.
• Bowel: positioning (on toilet with knees higher than hips, or left side with knees flexed and HOB 30-45 degrees); digital stimulation, warm liquids, suppositories.
• Transportation, vocational rehabilitation, recreation, lifelong follow-up and health screening.

High-Yield Numbers

Priority Nursing Actions and Red Flags

• Change in LOC (GCS) is the earliest sign of deterioration after TBI.
• Lucid interval followed by rapid decline: epidural hematoma, extreme emergency.
• Unilateral dilated, sluggish pupil: expanding hematoma pressing CN III.
• Cushing reflex (bradycardia, rising systolic BP, widening pulse pressure): rising ICP.
• Tachycardia and hypotension in head injury: look for bleeding elsewhere.
• Clear drainage from nose or ears or Battle sign: basal skull fracture; use oral, not nasal, feeding tubes.
• Any head injury: assume cervical spine injury; keep neck neutral, collar on.
• Avoid opioids for restlessness after TBI; check for hypoxia, pain, full bladder first.
• SCI patient: report any loss of motor or sensory function immediately; ascending edema can cause respiratory failure.
• Suctioning in SCI can trigger bradycardia and cardiac arrest.
• Autonomic dysreflexia: sit up first, then find and remove the trigger (bladder first).
• Never massage legs of an immobile patient.
• Halo pin detaches: one person stabilizes head in neutral, another calls provider.

Medications

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