Risk Assessment & Emergency

Management of Spinal trauma

PREVIEW
 Introduction
 Anatomy
 MOI – Risk assessment
 SCI –
 Spinal injury
 Pathophysiology
 Management – Inv. & Treatment
Definition of SCI
 Injury of spinal cord ranging from mild
flexion-extension injuries to whiplash
injuries, to complete transection of
cord.

Whiplash—ligamentous injury of cervical

spine.
Spine
Incidence
 Male :female =4:1
 C4-6; T11-112 More common as it is
most mobile
 Cervico- thoracic and thoraco-lumbar
 RTA (45%) FALLS 20% SPORTS (15%)
VIOLENCE 15%
 Causes
 RTA-High Speed MV
Collisions
 Falls Greater than 3x
pt.’s body height
 Violent situations near
the spine
 Stabbing

 Gun shots

 Sports Injuries
 SPINAL CORD INJURY
 Causes:-

Falls Car accidents

Stab wounds

Gun shot
Infections
Wounds

Diving into shallow water Tumors Congenital

anomalies
Non traumatic causes
 Cervical spondylosis with myelopathy
 Myelitis
 Osteoporosis
 Syringiomyelia
 Tumors-infiltration and compression
 Vascular diseases
Classification of SCI
 Mechanism
 Level of injury- anatomical level
 Degree of injury-severity of injury
 classification of Spinal Injuries
 Mechanisms and Associated Injuries
 Hyperextension- chin hits an object, head thrown back

 Pure flexion-compression of vertebrae, fall from height

 Hyperflexion- head bent forward

 Rotational – motor vehicle crash, forced sudden jarring action

 Compression- falls directly on the head, sacrum or feet
 Distraction-stretching of SC without disruption
 Penetrating-rod penetration etc
 (Specific Injuries)
 Cord Injuries
 Concussion - temporary or transient disruption of cord
function
 Contusion - Bruising of the cord with associated tissue
damage, swelling and vascular leaking
 Compression - Pressure on cord secondary to vertebrae
displacement, disk herniation and/or associated
swelling
 (Specific Injuries)

 Cord Injuries cont.

 Laceration - Direct damage to cord with associated bleeding,
swelling and potential disruption of cord
 Hemorrhage - Often associated with a contusion, laceration or
stretching injury that disrupts blood flow, applies pressure
secondary to blood accumulation, and/or irritation due to blood
crossing blood-brain barrier.
 Transection - Partial or complete severing of cord
Types of injuries

A higher level of injury

results in more loss of
feeling and movement
than a lower level of
injury.
 (Specific Injuries)

 Spinal Shock
 Temporary insult affecting body below level of the
injury
 Flaccidity and decreased sensation
 Loss of bladder and/or bowel control
 Loss of temperature control
 Often transient if no significant damage to cord
 (Specific Injuries)

 Neurogenic Shock
 Injury disrupts brain’s control over body
 lack of sympathetic tone
 Arterial and vein dilation causing relative hypovolemia
 Decreased cardiac output
 Decrease release of epinephrine
 Decreased BP
 Decreased HR
 Decreased Vasoconstriction
 Spinal Cord Injury
pathophysiology
Primary injury
 Initial insult to cord

 Local deformation

 Energy
transformation
 Spinal Cord Injury
pathophysiology
Secondary injury

 Biochemical cascade

 Cellular processes

Most acute therapies aim to

limit secondary injury
cascade
Pathophysiology

 Due to Etiological factors

 Microscopic bleeding of grey matter
 Edema develops and spreads
 Arachidonic acid and its metabolites released
( prostoglandins, thrombaxane, leukotrienes)
 Cord edema peaks 2-3 days subsides after 7 days-
temporary loss of function
 SCI- biochemical changes, initial insult and
hemodynamic instability
Patho continued…
 Fragmentation of axonal covering, loss of myelia
 phagocytes scavenge debris
 Chemotactic and inflammatory mediators extend tissue
necrosis.
 Macrophages engulf SC tissue and cause central cavity,
(9days after injury)
 oligodendral cells are lost
 Rapid loss of axonal conduction from ion changes-
increase in intracellular K and influx of Ca
 Free radicals are produced, controlled by antioxidant
enzymes
 If antioxidants are overwelhmed by free radicals damage
SC tissue
 Physiologic response
 Changes extend beyond SC
 SNS- decreased GI perfusion
 Spasticity-
 Reflux emptying of bladder & bowel.(lower
part of the cord starts to work automatically)
 Autonomic dysreflexia- severe headache,
flushing, piloerction, blurred vision( pupils
dilate) bradycardia, hypertension.
SCI types
1. Complete
• Quadriplegia
• Paraplegia
2. Incomplete
• Anterior cord syndrome
• Central cord syndrome
• Brown sequard syndrome
• Conus medularis
• Cauda equina
S/S
 Respiratory-resp insuficiency,
hypoventilation, atelectasis, pneumonia,
pulmonary edema,
 CVS- bradycardia, hypotension,
hypovolemia, hypoxemia
 Genito-urinary-retention, infection,
 GI- paralytic ileus, stress ulcer,
sphincter tone is decreased,
 Skin- pressure ulcer, ineffective thermo
regulation- decreased ability to sweat/
shiver
 PVS- DVT
 Metabolic- loss of weight
Evaluation of Spine Trauma
 ABC’s
 History
 Palpation
 Neuro exam
 GCS
 Motor
 Sensory
 Reflexes and tone
Immobilisation
 Cervical spine
1. In line immobilisation
2. Semi rigid cervical collar
3. Straps & sand bags
 Thoraco-lumbar spine
1. Spinal board
2. Log rolling
Step 2: Neurological Examination
 Detailed and Systematic
 Motor
 Sensory
 Reflexes
D
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 SPINAL CORD INJURY
 Diagnostic test findings:-
 Spinal X-rays :- Vertebral
fracture.
 CT scan :- spinal cord
edema, vertebral fracture,
spinal cord compression.
 MRI :- spinal cord edema,
vertebral fracture, spinal
cord compression.
 SPINAL CORD INJURY
 Management: Requires a multidisciplinary
approach because of multiple systems
involvement .
Immediately After Trauma (less than 1 hour)
Immobilization with rigid cervical collar, sandbags &
rigid spine board to transport from the field to acute
care facility.
Methylpredinisolone IV given with in 8 hours of
injury to decrease the extent of injury.
Contraindicated –pregnancy,hypersensitivity
 Acute Phase (1 to 24 hours)
Management
 Maintenance of pulmonary & cardiovascular stability.
 Intubation & mechanical ventilation, if needed.
 Vasopressor to maintain adequate perfusion.
 Medical stabilization before spinal stabilization &
decompression.
 Spinal cord immobilization by traction to reduce cervical
spine injuries,& kinetic turning bed such as Rotorest to
immobilize patients with thoracic & lumbar injuries.
 Management of neurogenic bladder- insert foley’s
catheter to drain bladder & monitor kidney perfusion.
 Pressure ulcer prevention- by using pressure reduction
mattress & turning the patient every 2 hourly.
 Sub acute Phase Management
(With in 1 week)
 Stabilize vertebral column & ligamentous injuries by
using traction & surgical intervention.
 GM-1 ganglioside sodium salt- IV (it stimulates the
growth of nerve cells& regenerate the nerve cells),
begun with in 72 hours after injury, & continued for 18 to
32 days.
 H2- receptor blockers to prevent gastric irritation &
hemorrhage.
 Early mobilization & passive exercise as soon as patient is
surgically & medically stable.
 Hyper alimentation.
 Small doses of heparin to reduce risk of thrombophebitis
& pulmonary emboli within 72hrs of SCI, unless there is
active bleeding, head injury or coagulopathy.
 Neurogenic bowel programme.
Chronic Phase Management
(Beyond 1 week)
Anticoagulants-
 continued until discharge with incomplete

injuries.
 For 8 weeks with uncomplicated motor injury.

 And for 12 weeks for complete motor injury &

other complications.
Management of complications include:-
 For infections – antibiotics

 For respiratory compromise – mechanical

ventilation.
 Pressure ulcer treatment.
Chronic Phase Management
(Beyond 1 week)
 Management of spasticity with oral or
Intrathecal antispasmodics.
 Management of central neuropathic pain with

anticonvulsants; minor sedatives.

Rehabilitation includes:-
 Medical & psychosocial support.

 Physical therapy.

 Urologic evaluation.

 Occupational therapy.
Nursing Interventions
 Maintain the patient’s diet, encourage fluids.
 Administer IV fluids, & oxygen.
 Provide suction & turning;encourage coughing & deep
breathing.
 Assess neurologic & respiratory status.
 Keep the patient flat.
 Maintain body alignment.
 Initiate bowel & bladder retraining.
 Provide sexual counseling
 Assess for spinal shock.
 Apply antiembolism stockings
 Complications of SCI
• Spinal shock (neurogenic shock)– lasting a few
hours to a few weeks noted by loss of all reflex,
sensory, & autonomic activity below the level of the
lesion.
• S/S:- flaccid paralysis,hypotension, bradycardia, loss of
activity below the level of injury & paralytic ileus
• Rx:- Assessment for above symptoms, provide
supportive measures & monitor for return of reflexes.
• Respiratory arrest, pneumonia,
atelectasis;mechanical ventilation often required with
cervical injury.
 Complications of SCI

• Cardiac Arrest may result from initial trauma,

worsening of initial injury from edema,
concomitant injuries, & other illnesses.
• Thromboembolic complications – in 15% of
patients.
• Infections – respiratory, urinary, pressure sores.

• Autonomic dysreflexia:-
dysreflexia A life threatening syndrome- A
cluster of manifestations that result when multiple spinal
cord autonomic responses discharge simultaneously.
Complications of SCI
• Neurogenic bladder:-
bladder bladder storage
pressure >35 to 40 cm may result in
renal deterioration.
• Paralytic ileus:-
ileus common in sub acute &
acute stage.
• Heterotropic ossification:-
ossification bony
overgrowth that occurs below the level
of injury any time after SCI.
• Syringomyelia:-
Syringomyelia cystic formation in
spinal cord may occur any time after SCI
Complications of SCI
• Depression:-
Depression occurs in 25% of men &
47% of women with SCI.
• Pressure ulcers:-
ulcers may occur in up to
35% of persons with SCI.
• Spasticity may result in contractures.
• Amenorrhea occurs in 60% of women
with SCI, usually temporary.
• Neuropathic pain occurs in 34% to 94%
of patients with SCI
 Collaborative care
 Immobilization & skeletal traction
 Single breath count chart (cervical spine injury)
 Maintenance of HR & BP(atropine, dopamine)
 Prednisone for cord edema
 NG tube and suction
 O2
 IV fluids
 Catheterization
 DVT prophylaxis
 Bowel and bladder training
 Skin care
Surgery
 Spinal de-stabilization
 C1-C2: sagittal instability
Rehab and home care
 Physiotherapy-ROM, mobility training,
muscle strengenthening
 Occupational therapy
 Bowel and bladder training
 Autonomic dysreflexia
 Prevention of peptic ulcer
 Recreational therapy
 Patient and family education
Autonomic Dysreflexia
 A life threatening syndrome- A cluster of
manifestations that result when multiple spinal
cord autonomic responses discharge
simultaneously.
 Occurs with injuries and lesions above T6 and in
cervical lesions
 Caused by uncontrolled sympathetic nervous
system stimulation from noxious stimulus
 Common causes: distended bladder, constipation
 Is a neurological emergency – will result in a
hypertensive stroke if not treated
Autonomic Dysreflexia
Signs and Symptoms
Sudden, severe, throbbing headache
Severe hypertension
Bradycardia
Flushing above level of injury, pale below injury
Stuffy nose
Sweating
Blurred vision and dilated pupils
Nausea
Feeling of apprehension
Autonomic Dysreflexia
Signs and Symptoms
Sudden, severe, throbbing headache
Severe hypertension
Bradycardia
Flushing above level of injury, pale below injury
Stuffy nose
Sweating
Blurred vision and dilated pupils
Nausea
Feeling of apprehension
Immediate Nursing Care for Autonomic
Dysreflexia
 Raise HOB to high Fowler’s position
 Frequent vital signs
 Palpate bladder; check Foley for kinks
 Assess for fecal impaction
 Loosen tight clothing
 Ensure comfortable environmental
temperature
 Prepare for administration of vasodilators
 Calming affect
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