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
GUILLAIN BARRE SYNDROME - onset
Characteristics: Ranges from mild to severe
Onset: acute and rapidly progressing, potentially life threatening if respiratory muscles affected
GUILLAIN BARRE SYNDROME - diagnosis
(EMgod, it’s guillian)
Diagnosis:
Hx and clinical signs
CSF shows more proteins
EMG (tests conductivity in muscle) to confirm dx (progressive weakness of >1 limb and diminished/absent reflexes
GUILLAIN BARRE SYNDROME - nursing care - assess for what?
(gillian is ascending)
Nursing care:
Assess for ascending paralysis: ABCs
Emotional support
Nutritional support
Assess gag, corneal and swallow reflexes
Monitor BP, pulse and rhythm
80% of patients recover completely but may take months to years. 65% will have minor residual deficits
nclex
HOB
check for bladder clothes
assess pt
loosen clothes
contact dr
administer anti-htn
types of primary injuries
Cord compression, spinal cord ischemia, or traction on spinal cord
Penetrating trauma causing tearing and laceration to spinal cord
level of injury - Neurological level
(the neuro is down low)
Neurological level (lowest segment of the spinal cord) – retaining both motor and sensory function on both sides of the body
level of injury - Paraplegia
(para is all 3)
Paraplegia-damage to thoracic, lumbar or sacral spinal cord
level of injury - Tetraplegia
Tetraplegia (quadriplegia) – Cervical cord involvement leading to paralysis of all 4 extremities
level of injury - C1-3
C1-3 Fatal or require mechanical ventilation
emergency management - Acute care phase - what should O2 sat be?
Acute care phase:
Obtain hx surrounding event (from patient or EMS)
Immobilize and stabilize vertebral column
Get appropriate imaging to determine level of injury
Maintain ABCs and hemodynamic monitoring
SaO2 >90%, hypoxemia can cause worsening spinal cord deficit
Complete neuro exam
Observe for signs of progressing neurologic deficits
Full extent of damage not known until edema subsides usually in 3-7 days
** Any MVA, diving, contact sport injury or direct trauma to head or neck should be considered to have SCI until ruled out
SCI - systems complications - GI:
Bowel dysfunction (Constipation/fecal impaction)
Adequate nutrition to prevent infection, muscle atrophy, skin break down
SCI - systems complications - GU:
Bladder dysfunction (loss of bladder control): neurogenic bladder / spasticity
Frequent UTIs (Advise to drink cranberry juice and >2L water a day)
Classic signs of PE
acute dyspnea, SOB, tachycardia, pleuritic chest pain, hemoptysis
PNA
Poikilothermism
(polki is hot and cold)
(inability to regulate body temp)
spinal shock - s/sx
(arie is shocked by the hot flaccidity)
Areflexia
Loss of sensation
Absent thermoregulation
Flaccid paralysis below level of injury
neurogenic shock - s/sx
(neurogenic is shockingly slow)
*Autonomic hyper-reflexia
Loss of sympathetic drive causing massive vasodilation
Chronic low BP and orthostatic hypotension
Poor venous return→↓ preload → ↓ cardia output
Hypothermia
Bradycardia
neurogenic shock - what is the HR? you already know this - brady - but what #?
HR often <60 ppm d/t unopposed parasympathetic drive
neurogenic shock - what can cause cardiac arrest?
(neuro in vagus)
Vagal stimulation such as coughing, suctioning, turning may potentially cause cardiac arrest.
meds for neurogenic shock?
(neurogenic shock is dope)
Vasopressors
Dopamine: a positive inotrope
Treat bradycardia. Atropine if symptomatic
Treat hypothermia
autonomic hyper-reflexia - what vertebrae?
(mattias hyper at 6)
Excessive uncompensated hypertension by a noxious stimulus below T6.
Occurs with SCI above T6 (Lesions below T6 do not produce this complication)
autonomic hyperreflexia - are sympathetic and para working?
Sympathetic and Parasympathetic responses no longer communicating d/t damaged spinal cord
autonomic hyperreflexia - baroreceptors? (remember, it’s HYPER)
Baroreceptors in carotids and aorta responds to HTN by decreasing HR → bradycardia
autonomic hyperreflexia - symptoms above T6? is it dilated or constricted?
(hyper above makes me flushed)
Flushed face and chest, nasal congestion (vasodilation above T6)
autonomic hyperreflexia - symptoms below T6? is it dilated or constricted?
(to be hyper below 6 is cool)
Pale, cool and clammy below T6 (d/t vasoconstriction)
autonomic hyperreflexia - ACT - (HOB, bladder, clothes, pain?)
A - ACT
Immediately raise HOB to sitting position
Rapid assessment to remove noxious stimuli
Empty bladder and examine rectum for fecal mass
Check skin, loosen clothing, treat pain
autonomic hyperreflexia - medications
(Mattias needs nitro)
Medications:
Prompt reduction of BP with rapid acting agents:
Nitroglycerin paste/SL (Contra-indicated if pt on a phosphoesterase inhibitor -Sildenafil)
Nitroprusside, IV hydralazine or labetalol
trigeminal neuroglia - triggers
Usually initiated by a light touch at trigger zones along nerve branch
chewing, tooth brushing, hot/cold air blast on the face, washing face, yawning and even talking
asia - A
no motor or sensory function is preserved below sacral S4-5 (complete spinal cord injury
asia - B
sensory but not motor function is preserved below and through sacral S4-5
asia - C
motor function is preserved below neuologic level and majority of key muscles below neurologic level have a muscle grade less than 3 (ie no anitgravity movement
asia D
motor function is preserved below neuologic level and majority of key muscles below neurologic level have a muscle grade of at least 3
asia E
motor and sensory functions are normal (no cord injury)
hallmark signs of bell’s palsy
(bell’s eye)
Bell’s phenomenon (hallmark sign): inability to close eyelid
bells palsy - protect what?
Protect face from cold to prevent trigeminal hyperesthesia (extreme sensitivity to pain and touch)
guillain barre syndrome
(gillian attacks my nerves)
immune system attacks the nerves. Results in segmental loss of myelin, edema, and inflammation in the PNS
Remyelination occurs slowly and returns proximal to distal manner
Etiology: Unknown. Thought to be immune mediated in the peripheral nerves
Rare – 1 in 100,100 people
guillain barre syndrome - starts with..
(gillian in pain)
Starts with pain (most common sx), paresthesia, hypotonia of limbs, areflexia, extraoculomotor dysfunction
when does guillain barre syndrome peak?
(guillian left after 4 weeks)
peaks in 4 weeks
most serious sx of guillain barre syndrome?
(gullian can’t breathe)
Most serious sx is respiratory failure d/t weakness of thoracic muscles
guillain barre syndrome - treatment
(guillian needs plasma)
Treatment:
Mechanical ventilation – 30% of people progress to respiratory failure in acute phase
Antibiotics
Plasmapheresis or high dose IVIG+ steroids
guillain barre syndrome - is there cognitive dysfunction?
No cognitive dysfunction
guillain barre syndrome - Autonomic dysfunction
Orthostatic hypotension, HTN, bowel and bladder dysfunction
guillain barre syndrome - Abnormal vagal response:
bradycardia, heart block and asystole
Spinal shock - definition
Spinal shock – Temporary shock following acute SCI. Leads to decrease reflexes, sensation loss, absent thermoregulation, and flaccid paralysis below level of injury. Lasts days to weeks.
Neurogenic shock – definition
Neurogenic shock – Loss of vasomotor tone after SCI leading to hypotension and bradycardia. Loss of SNS innervation causes peripheral vasodilation, venous pooling and decrease CO. Assoc with cervical or high thoracic injury
