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Spinal cord injury
An injury to the spinal cord, vertebral column, supporting soft tissue, or intervertebral disks caused by trauma
Pathophysiology of SCI
Ranges from transient concussion (which is fully recoverable) to contusion, laceration, and compression of the spinal cord tissue to complete severing of the spinal cord
Renders patient paralyzed below the level of injury
Vertebra C5-C7, T12, and L1 are the most susceptible to injury due to a greater range of motion
Primary injuries = result of initial insult or trauma; permanent damage
Secondary injuries = result from hypoxemia, edema, or hemorrhage which damages the tissue
Risk factors of SCI
Younger age
Male gender
Alcohol and illicit drug use
clinical manifestations of SCI
Complete spinal cord lesion = loss of sensory and voluntary motor communication; paraplegia or tetraplegia
Incomplete spinal cord lesion = sensory and motor communication is preserved below the lesion
s/s of SCI
Total or partial paralysis
Loss of bowel and bladder control
Loss of sweating
Reduction in BP with loss of peripheral vascular resistance
Acute back or neck pain
Respiratory dysfunction (depending on level of injury)
Associated priorities of SCI
Immobilization in the extended position until proper assessment and treatment is performed
Incomplete injury may become complete if pt continues to move after trauma event
Neurological assessment
X-ray
CT scan
MRI scan for further workup
Monitor respirations/pattern
Vitals
Usual treatment of SCI
Respiratory therapy
Pacing
High dose IV corticosteroids
Methylprednisolone
Immobilization
Stabilization of vertebral column
Reduction of dislocations
Skeletal traction (cervical injuries)
Surgical intervention (thoracic and lumbar injuries)
Nursing considerations of SCI
Spinal shock
Neurogenic shock
VTE
DVT
PE
Pressure injuries
Monitor respirations and breathing pattern
Lung sounds and cough
Monitor for changes in motor or sensory function; report immediately
Assess for spinal shock
Monitor for bladder retention or distention, gastric dilation, and ileus
Temperature; potential hyperthermia
Characteristics of central cord syndrome
Motor deficits
In the upper extremities compared to the lower extremities
Sensory loss more pronounced in upper extremities
bowel/bladder dysfunction
Cause of central cord syndrome
Injury
Edema
Hyperextension injuries
Characteristics of anterior cord syndrome
Loss of pain (below the level of lesion)
Loss of temperature function (below the level of lesion)
Loss of motor function (below the level of lesion)
Light touch, position, and vibration sensation remain intact
Cause of anterior cord syndrome
Acute disc herniation
Hyperflexion injuries associated with fracture or dislocation of vertebra
Injury to anterior spinal artery
Characteristics of lateral cord syndrome
Ipsilateral paralysis or paresis is noted
Ipsilateral loss of touch, pressure, and vibration
Contralateral loss of pain and temperature
Cause of lateral cord syndrome
Lesion is caused by a vertical transection
Result of knife or missile injury, fracture/dislocation, or acute ruptured disk
Skeletal traction
Used to reduce cervical fractures and align the cervical spine
Traction is applied to via weights
As the traction increases, the spaces between the intervertebral disks widen, allowing the disks to slip back into place
Reduction in traction occurs after proper alignment is restored
Spinal shock
Sudden depression of reflex activity below the level of injury caused by muscles being paralyzed and flaccid
s/s of spinal shock
Decreased BP
Bradycardia
Bowel distention
Paralytic ileus
Considerations of spinal shock
Maintain MAP of at least 85 mm Hg
NG tube
Neurogenic shock
Result of the loss of autonomic NS function below level of injury
Vital organs are affected
s/s of neurogenic shock
Decrease BP, HR, and cardiac output
Venous pooling
Respiratory complications
Decreases vital capacity
Retention of secretions
Increased PaCO2
Decreased O2
Pulmonary edema
Autonomic hyperreflexia
Acute life threatening emergency that occurs as a result of exaggerated autonomic responses to stimuli after spinal shock has been resolved
Pathophysiology of autonomic dysreflexia
Exaggerated autonomic responses to stimuli
Triggers:
Distended bladder
Distention or contraction of visceral organs
Bowel
Stimulation of the skin
Risk factors of autonomic dysreflexia
SCI
Spinal shock
Clinical manifestations of autonomic dysreflexia
Paroxysmal HTN
Profuse diaphoresis above injury
bradycardia
s/s of autonomic dysreflexia
Severe pounding headache
Nausea
Nasal congestion
Associated priorities of autonomic dysreflexia
Remove the triggering stimulus
Immediately place in sitting position to lower BP
Empty bladder
Examine for fecal mass and remove
Skin assessment for pressure or broken skin
Usual treatment of autonomic dysreflexia
Antihypertensives
Slow IV
Low back pain
Caused by musculoskeletal problems such as
Acute lumbosacral strain
Insatiable lumbosacral ligaments
Weak muscles
Unequal leg length
Intervetebral disc problems
Pathophysiology of low back pain
The spinal column has rigid units = vertebrae and flexible units = intervetebral discs, held together by joints, ligaments, and muscles
Spinal curves absorb vertical shocks from movement
Abdominal and thoracic muscles are important in lifting and minimize stress on the spinal units
Intervertebral discs change with age
Fibrocartilage becomes dense and irregularly shaped with time; disc degeneration
Low lumbar discs, L4 and L5-S1, are subject tot he greatest mechanical stress and degeneration
Cauda equina syndrome
compression of a bundle of spinal nerves from the lower spinal cord
Results from the compression of the cauda equina, a bundle of spinal nerves from the lower portion of the spinal cord
Requires immediate attention before nerve damage occurs
Risk factors of low back pain
Depression
Smoking
Alcohol abuse
Obesity
Stress
Clinical manifestations of low back pain
Acute back pain (lasting <3 months)
Chronic back pain (lasting 3< without improvement)
Fatigue
Pain radiating down the leg
Radiculopathy = pain from a diseased spinal nerve root
Sciatica = pain from inflamed sciatic nerve
Affected gait, spinal mobility, reflexes, leg length, motor strength, and sensory perception
Cauda equina
Associated priorities of low back pain
Focused history and physical exam
Gait evaluation
Neurologic testing
X-ray, CT scan, MRI, etc.
Assess posture, position changes, and gait
Usual treatment of low back pain
Analgesics, rest, and avoidance of strain
Activity modification
NSAIDs and short term muscle relaxants
Opioids (1-2 weeks)
Thermal applications
Spinal manipulation (chiropractor)
Cognitive behavioral therapy
Exercise regiments
Spinal manipulation
PT
Acupuncture
Massage
Avoid stress to back
Nursing considerations of low back pain
Positioning
Location, severity, duration, characteristics, radiation (radiculopathy), leg weakness
How the pain occurred and has been managed by the patient
Work and recreational activities
Spinal curvature, back and limb symmetry
Palpate paraspinal muscles
Movement ability and effects on ADLs
DTRs, sensation, and muscle strength
s/s of cauda equina
Sever or progressive neurologic deficit
Recent bowel or bladder dysfunction
Saddle anesthesia
Paresthesias in the but and inner thighs
Osteomyelitis
An infection of the bone that results in inflammation, necrosis, and formation of new bone
Can be
Hematogenous (bloodborne spread)
Contagious-focus (contamination from surgery, fracture, or trauma)
With vascular insufficiency
Pathophysiology of Osteomyelitis
Infections caused by staph aureus, MRSA, streptococci, enterococci, or pseudomonas
Initial response is inflammation, increased vascularity, and edema; after 2-3 days, thrombosis of local blood vessel occurs causing ischemia with bone necrosis
Infection spreads to tissues and joints, and may cause a bone abscess
Abscess contains dead bone tissue and cannot heal, but instead new bone growth forms around the dead bone tissue
Chronic infection of the bone tissue = chronic osteomyelitis
Risk factors of Osteomyelitis
Old age
Poor nourishment
Obesity
Impaired immune function
Chronic illness
Long term corticosteroid therapy
Clinical manifestations of Osteomyelitis
Sudden onset of sepsis manifestations
Chills
High fever
Rapid pulse
General malaise
Infected area becomes painful, swollen, and extremely tender
Constant, pulsating pain that intensifies with movement
Pus
Associated priorities of Osteomyelitis
Early x-ray
MRI
Blood studies
Bone biopsies
Ability to adhere to prescribed therapeutic regimen— antibiotic therapy
Signs and symptoms of infection, localized pain, edema, erythema, fever, drainage
Usual treatment of Osteomyelitis
IV antibiotics
Prophylactic antibiotics
Surgical debridement
All dead, infected bone, tissue, and cartilage must be removed for permenant healing
Nursing considerations of Osteomyelitis
Disposable medical tools (to minimize possibility of infection)
Encourage adequate hydration, vitamins, and protein
Relieving pain
Immobilization
Elevation
Handle with great care and gentleness
Administer prescribed analgesics
Improving physical mobility
Activity is restricted
Gentle ROM to joints above and below the affected part
Participation in ADLs within limitations
Contusion
soft tissue injury produced by blunt force
Pain, swelling, and discoloration: ecchymosis
Strain
Pulled muscle injury to the musculotendinous unit
Pain, edema, muscle spasm, ecchymosis, and loss of function are on a continuum graded first, second, and third degree
Sprain
injury to ligaments and supporting muscle fiber around a joint
Pain (may increase with motion), edema, tenderness; severity graded according to ligament damage and joint stability
Dislocation
articular surfaces of the joint are not in contact
A traumatic dislocation is an emergency with pain change in contour, axis, and length of the limb and loss of mobility
Subluxation
partial or incomplete dislocation
Does not cause as much deformity as a complete dislocation
RICE
Rest
Ice
Compression
Elevation
Fracture
A complete or incomplete disruption in the continuity of bone structure and is defined according to its type and extent
Occur when a bone is subjected to stress greater than it can absorb
Pathophysiology of Fractures
May be caused by direct blows, crushing forces, sudden twisting motions, and extreme muscle contractions
Clinical manifestations of Fractures
Adjacent structures may have soft tissue edema, hemorrhage into the muscles and joints, joint dislocations, ruptured tendons, severed nerves, and damaged blood vessels
Continuous pain that increases in severity
Numbness immediately after
Loss of function
Displacement, angulation, or rotation
Shortening
Crepitus
Localized edema and echymosis
Associated priorities of Fractures
Immobilization of body part
X-ray
Adequate splinting
Bandaging affected to unaffected extremity or chest
Sling
Assessment of perfusion and nerve function
Cover wound with sterile dressing (open fracture)
Usual treatment of Fractures
Reduction = restoration of bone fragments to anatomic realignment and positioning with realignment
Closed uses manipulation and manual traction
Open uses surgery and internal fixation devices
Immobilization until union occurs
IV antibiotics and debridement (open)
Nursing considerations of Fractures
Maintaining and restoring function
Position changes
Pain relief
Isometric exercise
Reassurment
Factors affecting fracture healing
Age >40 years
Avascular necrosis
Bone loss
Cigarette smoking
Comorbidities (e.g., diabetes, rheumatoid arthritis)
Corticosteroids, nonsteroidal anti-inflammatory drugs
Extensive local trauma
Inadequate immobilization
Infection
Local malignancy
Malalignment of the fracture fragments
Space or tissue between bone fragments
Weight bearing prior to approval
Early complications of fractures
Shock
Fat embolism
Acute compartment syndrome
DVT; PE
Infection
Late complications of fractures
Union
Malunion
Nonunion
AVN of bone
Types of fractures
Closed
Open
Type I
Type II
Type III
Intra-articular
Closed fracture
Simple fracture
Fracture that does not break the skin
Open fracture
Compound or complex fracture
Fracture that breaks the skin or mucous membranes around it
Type I = clean wound less than 1cm ina simple fracture pattern
Type II = larger wound with minimal soft tissue damage; no flaps or avulsions
Type III = most severe, highly contaminated, and has extensive soft tissue damage
Vascular injury or traumatic amputation
Intra-articular
Extends into the joint surface of a bone
Casts
Ridgid external immobilizing device that is molded to the contours of the body; must fir the shap of the injured limb to provide the best support
Cast application
Before application
General health assessment
Emotional status
Presenting signs and symptoms and condition of the area (prior to doing immobilzation)
Monitoring of neurovascular status and for potential complications
Treat lacerations and abrasions before cast, brace, splint
Provide information about the purpose of treatment
Prepare patient for application by explaining procedure
prepare them for what they might feel while being splinted or casted.
With the cast- It may feel weird because it is warm as you put it on and gets warmer as it dried. Then it gets hard, this may make them feel claustrophobic
The 5 P’s of casts
Assessing for neurovascular changes using “5 Ps”
Pain
Pallor
Pulselessness
Paresthesia
Paralysis
Monitoring and treating pain