spinal cord injury Flashcards
SPINAL CORD INJURY
Trauma or damage to the spinal cord
Highest risk: Young males 16-30 due to life style activities
Common causes:
MVA
Falls
Diving in shallow waters
Sports injuries, violent injuries
Non-traumatic causes:
Tumors, congenital defects, post thoracic aneurysm repair (TEVAR)
PRIMARY INJURY
Initial stage of physical disruption to spinal cord
SECONDARY INJURY
Ongoing, progressive damage after primary injury
Vascular changes d/t hemorrhage, vasospasm, thrombosis
Loss of autoregulation, breakdown of BBB, inflammation and eventual scar tissue
Irreversible nerve damage and permanent neurological deficit
SCI: 3 CLASSIFICATIONS
MECHANISM OF INJURY
How was the spinal cord injured?
LEVEL OF INJURY
At what level was the spinal cord injured?
The higher the level, the more deficits
DEGREE OF INJURY
Partial or complete injury to the spinal cord
SCI- Level of injury
Level where the vertebral damage occurred
SCI- Degree of Injury (just 2)
Complete – loss of sensory and motor function below level of injury
Incomplete – Mix loss of sensory and motor function below level of injury
ASSESSING SCI: ASIA SCALE - ON TEST
ASIA: American Spinal Injury Assoc Impairment scale is the gold standard assessment tool used in the classification of SCI
Combines assessment of motor and sensory function to determine level and completeness of injury
Also used for recording changes in status and setting rehab goals
SCI: EMERGENCY MANAGEMENT - immediate - what should SBP be?
Immediate post injury:
Maintain ABCs
Stabilize cervical spine (not recommended in patient with penetrating trauma)
Treat systemic and neurogenic shock (keep SBP >90)
MANAGEMENT OF SCI - meds - think BP
Pharmacotherapy:
Methylprednisolone (steroid) no longer FDA approved for SCI d/t no evidence of benefits (may result in more harm)
Vasopressors during acute phase to maintain SBP >90 and MAP 85-90
Lovenox/Heparin SQ for DVT prophylaxis unless contraindicated
Early realignment of unstable spine fracture/dislocation with craniocervical traction
Surgical intervention indicated for cord compression, compound fracture and penetrating wound
SCI: SYSTEMS COMPLICATIONS - Pulmonary - frequently trached when it’s at what vertebrae?
(3 not a good number)
Pulmonary : Frequently trach if injury above C3 injury
PE
SCI: COMPLICATIONS
Integumentary
Pressure injuries from immobility
MSK
Contractures and spasticity
Psychological
Grieve and depression
Chronic pain
Thermoregulation: Poikilothermism (inability to regulate body temp)
Loss of SNS prevents peripheral temp sensation from reaching hypothalamus. Also decreased shiver and sweat ability to regulate body temp. Keep room warm.
Cardiovascular
CAD: increased risk
DVT (How would you assess a para/tetra for DVT?)
May lead to pulmonary embolus (PE) and heart failure
Assess thigh and calf for pain, redness, and diameter daily
Use low molecular weight heparin
Use TED hose or SCDs
Spinal shock- how long does it last?
(temporarily in shock)
Associated with motor and sensory loss below level of SCI
Temporary shock lasting days to weeks
Neurogenic shock - what part of the spine?
Assoc with cervical or high thoracic injury (injury above T6)
NEUROGENIC SHOCK: INTERVENTION - where to keep bp?
Stabilize spine, spine precaution, log roll
Treat shock: Keep SBP >90 to maintain perfusion to spine
IV fluids
SCI: AUTONOMIC HYPER-REFLEXIA (DYSREFLEXIA) - is it an emergency?
An exaggerated sympathetic response by the automatic nervous system
Acute neurological emergency
AUTONOMIC HYPERREFLEXIA: TRIGGERS
(B hyper)
The 3 Bs
Bladder (Distended bladder most common trigger, UTI)
Bowel (stool impaction)
Breakdown of skin (Pressure injury, infected skin)
Tight clothing
Chills
Pain
AUTONOMIC HYPER-REFLEXIA: symptoms (HR?)
Sever pounding headache
Hypertension
Profuse diaphoresis: commonly on the forehead. Cannot sweat below lesion
Nausea
Bradycardia
AUTONOMIC HYPERREFLEXIA: NURSING MANAGEMENT - PDA
P – PREVENT
Monitor UOP, bladder scan, straight cath, bowel regimen
D - DETECT
A - ACT
NCLEX REVIEW QUESTION
A patient with SCI suddenly experiences an episode of autonomic hyperreflexia. Number the list in order of highest to lowest priority
Contact the doctor
Raise the head of bed
Check for bladder distention
Loosen tight clothing on the client
Administer anti-hypertensive
Document the occurrence, treatment and response
PERIPHERAL NEUROPATHIES & CRANIAL NERVE DISORDERS - how many nerves are involved?
Can affect the sensory or motor segment of the nerve or both
Often involves a single nerve
Trigeminal neuralgia: aka tic douleureux
Bell’s palsy: aka peripheral facial paralysis
Guillain-Barre Syndrome
TRIGEMINAL NEURALGIA (TN)
Also known as tic douloureux
Affects the sensory/afferent branches of CN V (innervates forehead, opthmalic, maxilla, and mandible areas)
Pathophysiology
Not well understood
Thought to be due to constant compression on the nerve root by the abnormal loop of the superior cerebellar artery → demyelination of the nerve
TRIGEMINAL NEURALGIA - Symptoms: is it 1 side, or both sides? How long does pain last?
Symptoms:
Sudden onset of unilateral severe brief stabbing episodes of pain in the distribution of the CNV
Pain, burning in the lips, upper/lower gums, cheeks, forehead or side of the nose
Pain lasts secs to 2-3 minutes
Facial twitching (hence “ tic”), grimacing, constant blinking and tearing of the eye
TRIGEMINAL NEURALGIA: TREATMENTS - what med?
(tri tegretol)
Aimed at treating pain:
Anti-seizure meds, especially Tegretol (1st line therapy to decrease nerve firing)
Nerve blocking: last 6-18 months i.e. Botox
Surgery:
Rhizotomy (severing of nerve roots)
Microvascular decompression: repositioning of the blood vessels
Gamma knife radiosurgery (permanently disrupting pain nerves to the brain by causing a lesion)
BELL’S PALSY - is it one side, or both?
Acute peripheral unilateral facial paresis involving inflammation of the CN VII (facial nerve)
Not related to a stroke
Benign cranial neuropathy with good prognosis
Full recovery in 3-9 months
1/3 with residual deficits: facial weakness, involuntary movement and persistent tearing of affected eye
Etiology:
Unknown
May be related to overactivated HSV or HZV causing inflammation, edema and eventual demyelination, pain, sensory and motor changes
Inflammation leads to nerve compression → facial paralysis
Other viruses: adenovirus, CMV, Epstein Barr, influenza, mumps and rubella
BELL’S PALSY: MANIFESTATIONS - how fast does it start?
Sudden onset of unilateral facial weakness within hours
Pain behind the ear, fever, tinnitus, numbness of face, tongue, ear, headache, hearing deficit
Paralysis to one side of the face with drooping of the mouth and eyebrow; drooling
Inability to smile, frown or whistle
Common to lose taste sensation to one side
Excessive tearing
BELL’S PALSY
Diagnosis of exclusion, no specific test
Treatment:
Moist heat to herpes lesions, gentle massage, exercise
Electric stimulation of nerve to help muscle tone
Corticosteroid before onset of full paralysis for best result
Antiviral: acyclovir
Education
Encourage optimism as the condition is usually temporary
Artificial tears to keep cornea moist
GUILLAIN BARRE SYNDROME - is it 1 side, or both? Most common virus that causes it?
(gillian has CMV?)
Aka: Post infectious polyneuropathy
Autoimmune process that occurs a few days or weeks after a viral or bacterial infection (i.e. URI or GI infection; CMV most common virus)
Acute ascending, rapidly progressing symmetrical paralysis