Management Issues in Patients

with Acute and Chronic Spinal

Cord Injuries

Andy Jagoda, MD
Professor of Emergency Medicine
Residency Program Director
Mount Sinai School of Medicine
 Objectives
Review the anatomy of the spinal cord
Review the pathophysiology of SCI
Review clinical presentations of SCI
Provide an overview of diagnostic and
therapeutic interventions that may be
helpful in managing SCI both acutely and
over time

Andy Jagoda, MD, FACEP

 Case Study: Spinal Cord Injury
16 yo male
Tramboline for his birthday
Brought EMS; 2 IVs, backboard, C-collar
Nasal intubation in the field
VS: P 128; BP 90/55
Alert
No spontaneous movement or reflexes

Andy Jagoda, MD, FACEP

X-Ray
 Case Study: Questions
How would this spinal cord injury be
classified?
Does methylprednisolone play a role?
What new treatments are on the horizon?
What complications occur subacutely
and over time in patients with SCI

Andy Jagoda, MD, FACEP

 Spinal Cord Injury: Epidemiology
12,000 new cases in the US/year
Majority from MVAs (36%)
Violence (30%), falls (20%), sports (7%)
Peak incidence: ages 15 - 35
Rehab/medical care:
First year: $225,000
Average lifetime: $30,000 / year
DeVivo. Causes and costs of SCI. Spinal Cord 1997; 35:809-813

Andy Jagoda, MD, FACEP

 Anatomy of the Spinal Cord
Corticospinal tracts: motor from the
cerebral cortex
Cross in the lower medulla
Spinothalamic tracts: pain and
temperature
Cross 1 or 2 levels above entry
Posterior column: proprioception and
vibration

Andy Jagoda, MD, FACEP

Picture
 SCI: Subtypes
Complete: complete transection of motor
and sensory tracts
Incomplete:
Central Cord Syndrome
Anterior Cord Syndrome
Posterior Cord Syndrome
Brown Sequard Syndrome

Andy Jagoda, MD, FACEP

 Anatomy: Vascular Supply
Single anterior artery perfuses anterior
and central cord
Paired posterior from vertebral arteries
(except in the cervical cord)
Radicular arteries from aorta
Varying degrees of contribution
Great radicular artery of Adamkiewicz T-
10 to L-2 (Major source of blood flow to
50% of anterior cord in 50% of patients)

Andy Jagoda, MD, FACEP

Picture
 Neurologic Examination
Document all findings
Level of consciousness
Motor strength
Sensation to light touch and pinprick
Position sense
Diaphragm, abdominal, and sphincter
function
DTRs, plantar reflexes, sacral reflexes
Sacral sparing (perineal sensation,
sphincter tone)
Andy Jagoda, MD, FACEP
Picture
Picture
Picture
Upper Versus Lower Motor Neuron Weakness
UMN often symmetric
LMN often single muscle group (with
atrophy)
UMN increased (after spinal shock)
LMN decreased DTR
UMN muscle tone increased
LMN muscle tone decreased
UMN no fasciculations
LMN fasciculations

Andy Jagoda, MD, FACEP

 ASIA Impairment Scale
A: Complete
B: Incomplete: Sensory, but no motor
function below neurological level
C: Incomplete: Motor function
preserved below level; muscle grade < 3
D: Incomplete: Motor function
preserved below level: muscle grade > 3
E: Normal
Andy Jagoda, MD, FACEP
Spinal Shock Versus Neurogenic Shock
Spinal shock is loss of motor and sensory
after trauma
Neurogenic shock involves the sympathetic
chain and is associated with autonomic
instability
Best timing of exam for prognosis is
undetermined: Probably 72 hours post insult
though some studies use 30 days

Andy Jagoda, MD, FACEP

 Complete Cord
No sensation
Flaccid paralysis
Initially areflexia
Hyperreflexia, spasticity, positive planter
reflex (days to months)
<5% chance of functional recovery if no
improvement within 24 hours

Andy Jagoda, MD, FACEP

 Central Cord Syndrome
Hyperextension injuries, tumor,
syringomylia
MUD
Paresis or plegia of arms > legs
Posterior column spared
Sensation UE > LE; sacral
sparing
Perforating branches of the
anterior spinal artery at greatest
risk for vascular insult
Good prognosis
Andy Jagoda, MD, FACEP
 Anterior Cervical Cord Syndrome
Typically after hyperflexion
Motor loss
Pain and temperature loss
Dorsal column preserved
Autonomic dysfunction
Sacral sparing
50% Recovery

Andy Jagoda, MD, FACEP

 Anterior Cord: Spinal Cord Infarction
Anterior more common than posterior
Most common in the thoracic area
Acute paralysis below the lesion
Dissociated sensory loss
Loss of pain and temperature: posterior column
function remains
Loss of sphincter function
Urinary retention
Brown-Sequard may occur
Andy Jagoda, MD, FACEP
 Brown - Sequard
Usually after penetrating trauma
Tumor
Ipsilateral motor paralysis
Ipsilateral loss of light touch and
propioception (anesthesia) below the level of
the lesion
Ipsilateral hyperanesthesia
Contralateral loss of pain and temperature
found one or two segments below the lesion
Andy Jagoda, MD, FACEP
 Cauda Equina / Conus Medularis
Conus Medullaris: S3-5
Saddle anesthesia, sphincter loss
Intact LE motor and sensory
Cauda equina
Spinal cord ends at L2
Injury to lumbosacral roots
Variable sensorimotor deficits and bowel
and bladder function

Andy Jagoda, MD, FACEP

 SCI: Pathophysiology

Early NECROTIC cellular death at focus of

traumatic injury
Extension of cellular injury continues long
after trauma; ?as a result of APOPTOSIS

Andy Jagoda, MD, FACEP

Morphology of Cell Death
 Evidence for Apoptosis in Humans:
Spinal Cord Injury
Spinal cords from 15 patients examined: 3 hr -
2 mo following traumatic SCI.
Apoptotic cells found at the edges of the
lesion epicenter and in adjacent white matter,
particularly in the ascending tracts.
Apoptosis prominent in 14/15 samples when
compared to 5 controls.
Apoptotic cells present around periphery of
zone of injury as well as in areas of Wallerian
degeneration.
Emery E: Nat Med 1999;5:943 Andy Jagoda, MD, FACEP
 Traumatic SCI: Management
ABCs: Treat / prevent hypoxia and
hypotension
Stabilize the spine to prevent additional
mechanical injury
R/O other serious injuries
Careful neurological examination: level of
neurological impairment
Imaging
Neuroprotective pharmacotherapy?
Early rehabilitation Andy Jagoda, MD, FACEP
 National Acute Spinal Cord
Injury Study: NASCIS
NASCIS I: no benefit of MP (dose too low?)
NASCIS II:
487 pts randomized: MP, naloxone or placebo
30 mg/kg bolus then 5.4mg/kg/hr for 23 hours
Negative results in primary analysis
Positive results only in subgroup analysis; those
patients treated within 8 hr; only 62 receiving MP; 67
placebo
Benefit had no clinical relevance
Steroid Rx: 2.6x inc pneumonia; length in ICU days
NASCIS III: Compared tirilazad mesylate, MP for 24
hours and 48 hours: No placebo; no functional
benefit Andy Jagoda, MD, FACEP
Guidelines for the Management of Acute Cervical
Spine and SCI. Neurosurg 2002;50 (suppl) :1-200

Evidence based practice guideline

22 chapters
Chapter on pharmacologic therapy most
controversial
17 pages of editorial commentary in the
preface

Andy Jagoda, MD, FACEP

 IX. Pharmacological Therapy after Acute
Cervical Spinal Cord Injury
Recommendations: Corticosteroids
Standards: None
Guidelines: None
Options: Treatment with methylprednisolone for either 24 or
48 hours is recommended as an option in the treatment of
patients with acute spinal cord injury within 12 hours of injury.
B) GM-1 Ganglioside
Standards: None
Guidelines: None
Options: Treatment of acute spinal cord injury patients with
GM-1 ganglioside is an option for treatment without clear
evidence of clinical benefit or harm.
Andy Jagoda, MD, FACEP
Apoptosis: Therapeutic Strategies
Caspase inhibition
Bcl-2 administration or up-regulation
Mitochondrial protectants, e.g.,
Cyclosporin A
Combination of anti-excitotoxic and anti-
apoptotic strategies

Andy Jagoda, MD, FACEP

 Spinal Cord Injury: The Future?
Development of neuroprotectant agents
Nerve grafts/neural transplants
Gene therapy
Stimulating adult neurons to grow
axons again; changing the environment
encountered by regenerating axons

Andy Jagoda, MD, FACEP

X-Ray
X-Ray
Picture
 Morbidity
Acute rehabilitation phase
Pressure ulcerations in 25%; most
commonly over the sacrum
Atelectasis / pneumonia in 13%
DVT in 10%
Autonomic dysreflexia in 8%
UTI

Chen. Medical complications during acute rehabilitation. Arch Phys

Med Rehab 1999; 80:1397 Andy Jagoda, MD, FACEP
 Mortality
Mortality is highest in the first year after
injury
Persons sustaining paraplegia at age 20
have an average subsequent life
expectancy of 44 years vs 57 years for the
general population
Leading cause of death are pneumonia, PE,
followed by heart disease and sepsis
Renal failure is no longer a leading cause of
death
Andy Jagoda, MD, FACEP
 Neurologic Recovery
Majority of complete injuries
remain complete
Initial sparing of sacral pin
sensation suggests a favorable
prognosis for eventual ambulation
Appearance of hemorrhage within
the cord suggests unfavorable
recovery
Marino. Neurologic recovery after traumatic SCI. Arch Phys
Med Rehab 1999; 80:1391 Andy Jagoda, MD, FACEP
 One Year Prognosis after SCI
A: Complete
One Year follow-up

Admission ASIA
B: Incomplete: Sensory, but no motor
function below neurological level
C: Incomplete: Motor function
preserved below level;
muscle grade <3
D: Incomplete: Motor function
preserved below level: muscle
grade >3
E: Normal
Neurologic decline is unusual and suggests underlying process, eg,
skeletal instability, cystic degeneration, etc. Andy Jagoda, MD, FACEP
 Thromboembolic Disease
Increased risk due to venous stasis and
hypercoagulability
Highest risk in patients with cancer; flaccid
paralysis
Risk of death from PE in the first year following
SCI is > 200 x that of the general population
51 / 243: 8 deaths
Prophylactic strategies
Pneumonic compression devices
Unfractionated heparin
Caval filters in patients with high cord lesions
Green. SCI risk for PE (SPIRATE study). Am J Phys
Med Rehab 2003;82:950 Andy Jagoda, MD, FACEP
 Autonomic Dysfunction
High thoracic (above T6) and cervical
lesions
Loss of supraspinal control of sympathetic
activity with dysregulation of function
Sympathetic outflow to splanchnic beds
Acute SCI
Low sympathetic activity
Subacute and chronic SCI
High sympathetic activity
Andy Jagoda, MD, FACEP
Picture
 Autonomic Dysfunction
Resting blood pressure is low
Bradycardia with suctioning or stimulation
Usually resolves after first weeks
Orthosatic changes cause weakness,
lightheadedness, fainting
Management:
Gradual mobilization
Liberal sodium intake
Compression stockings
Abdominal binding
Fludrocortisone acetate .1 mg po qd for volume
expansion Andy Jagoda, MD, FACEP
 Autonomic Hyperreflexia
Generally in lesions above T7
Does not occur acutely
Unmoderated sympathetic response to noxious
stimuli below the level of the lesion, e.g. bladder
distention or fecal impaction
Severe headache; Hypertension
Headache may be due to intracranial arterial dilatation to
compensate for hypertension
Management: Place in sitting position (to
decrease intracranial pressure), check for inciting
stimulus, minimize all noxious stimuli
Andy Jagoda, MD, FACEP
Autonomic Hyperreflexia: BP Management

No scientific evidence to guide intervention

Nifedipine / nitrate historically used
Medline reports no adverse effects in these
patients treated with nifedipine
Avoid nitrates if patient is using sildenafil
(Viagra)
Consider alpha blocking agent (terazosin)
Admit to observation unit or hospital
Andy Jagoda, MD, FACEP
 Autonomic dysreflexia: One more way EMS can
positively affect patient survival. JEMS 2003; 28:46-51

Bladder catherization and digital bowel

emptying are not everyday EMS skills. They
are, however, skills within the range of EMS
abilities. Providers should contact their
medical directors or training supervisors to
obtain the training necessary to carry out
both techniques.

Andy Jagoda, MD, FACEP

 Neuropathic Spinal Pain
Occurs at or below the level of injury
Reported in 6 50% of patients
Results from: changes in neuronal function,
increased spontaneous activity and / or
reduced thresholds of response
Descriptors: temperature, electric
Evaluation must look for other causes of pain,
e.g. unstable spine, cystic myelopathy, other
new condition e.g. renal stone
Treatment: physical therapy, anticonvulsants,
antidepressants, ???
Andy Jagoda, MD, FACEP
 Neurogenic Bladder Dysfunction
Initial bladder flaccidity; reflexes return
with suprasacral injury
Acute management with indwelling catheter
Reflexes may be unable to cause efficient
voiding due to tendency of reflex
sphincter activity to directly oppose
reflex detrusor contraction (detrusor
sphincter dyssynergy)
Management must avoid high storage
pressures (>40 cm H2O) to avoid renal
damage Andy Jagoda, MD, FACEP
SCI and bladder recovery. Arch Phys Med Rehab 996;77:1133
Retrospective review; 19 consecutive patients
18-68 / C4 T12
Correlation of perianal sensation and position
sense with bladder function at one year
Presence of perianal pinprick sensation and toe
position sense are positive predictors
Patients without initial position sense or the
great toes will likely not regain volitional voiding
Patients without initial perianal pinprick
sensation will not regain volitional voiding
Andy Jagoda, MD, FACEP
 Neurogenic Bladder Dysfunction
Clean intermittent catheterizatons
Needs good hand function or skilled attendants
Limit fluid intake; performed q 4-6 hours
Reflex bladder contractions can cause high storage
pressures and incontinence
Oxybutynin 5 mg po tid / Tolterodine 2 mg po bid
Reflex voiding in a condom catheter
Problems including urinary retention or high
intravesical voiding pressure due to DSD (can be
decreased with alpha blocking agents e.g. terazosin,
sphincter defeating surgery, or urethral stent)
Electrical stimulation
Andy Jagoda, MD, FACEP
Neurogenic Bladder Dysfunction
In the past, renal disease was a
frequent cause of death in SCI
patients
Urinary tract complications continue
to be a cause of morbidity
Infection: 20% annual incidence
Calculi
Hydronephrosis

Andy Jagoda, MD, FACEP

 Neurogenic Bowel Dysfunction
Upper motor neuron dysfunction causes
constipaton with slow colonic transit and
stool retention due to spasticity
Reflexes allowing defecation may remain
intact
Cauda equina causes lower motor neuron
dysfunction causing constipation with
slow colonic transport and incontinence
due to a flaccid sphincter
Andy Jagoda, MD, FACEP
 Neurogenic Bowel Dysfunction
Diarrhea
Impaction
Complications of medications e.g., C.
Difficile from antibiotics
Constipation
Manual disimpaction
Stimulants

Andy Jagoda, MD, FACEP

 Hypertrophic Bone Formation
Formation of new bone in soft tissue
planes surrounding a joint
Most commonly involves the hips
Presentation: Lower extremity
swelling, loss of hip ROM, fever
Must be distinguished from other
problems, e.g., DVT
Treatment: ROM exercises, NSAIDs,
irradiation, etidronate
Andy Jagoda, MD, FACEP
Picture
 Pressure Ulceration
Pressure to soft tissue above
capillary pressure results in
breakdown
Evaluation includes assessment of
ulcers depth
Treatment: wet / dry dressing;
topical antibiotics; debridement
Myocutaneous flap

Andy Jagoda, MD, FACEP

 Spasticity
Increase in upper motor neuron injury after
upper motor neuron injury
Spasticity causes: Resistance to passive
motion, exaggerated DTRs, clonus,
involuntary contraction of muscle groups
Advantages of spasticity: assist mobility,
imporves circulation, decrease risk of DVT
and osteoporosis
Disadvantages: may interfere with
positioning, mobility, and spasms may be
painful Andy Jagoda, MD, FACEP
 Spasticity
Prevention and treatment of noxious
stimuli
Muscle stretching and joint ROM
Botulinum toxin: blocks presynaptic
release of Ach at the NMJ
Effect lasts about 3 months (collateral
sprouting of axon)

Andy Jagoda, MD, FACEP

 Spasticity: Medications
Baclofen: GABA-B analog. Centrally acting.
5 mg po bid / increased up to 200 mg / day
Can be given intrathecally
Diazepam: GABA-A agonist
Tizanidine: Centrally acting muscle relaxant
Clonidine: Centrally acting alpha-2 agent
activates inhibitory neuron which reduces
sympathetic outflow which decrease
vasomotor tone and heart rate
Andy Jagoda, MD, FACEP
 Conclusions
Management of acute SCI is based on preventing
additional injury and providing supportive care
Role of methylprednisolone in SCI is questionable
Acute SCI above T7 has low sympathetic activity;
chronic SCI has high sympathetic activity
Pneumonia, PE, and sepsis are the most common
causes of death on patients with chronic SCI
Autonomic dysregulation, hypertrophic bone
formation, neurogenic bladder, and spasticity underlie
reasons for patients with chronic SCI to come to the
ED
Management of autonomic dysregulation focuses on
Andy Jagoda, MD, FACEP
Upper versus Lower Motor Neuron Weakness
Mylopathy = Spinal cord process
UMN findings (spasticity, weakness, atrophy,
sensory findings, bowel and bladder
complaints
Radiculopathy = Nerve root process
LMN findings (paresthesias, fasciculations,
weakness, decreased DTR)
Patient may have a radiculopathy with
mylopathy below the lesions
Andy Jagoda, MD, FACEP
 Traumatic Spinal Cord Injury:
Neuronal and Glial Apoptosis
Immediately following SCI in rat, typical post-
traumatic necrosis is seen.
Apoptotic cells are seen from 6 hr-3 wk;
especially in spinal white matter.
After SCI in monkeys, apoptotic cells were
found within remote degenerating fiber tracts.
Both secondary degeneration at the site of
SCI and the chronic demyelination of distant
tracts appear due to apoptosis.
Andy Jagoda, MD, FACEP
 Necrotic Cellular Death
Depletion of intracellular ATP
Swelling of cells; early protein denaturation
Disruption of organelles
Rupture of plasma membrane
Release of cytoplasmic contents into
surrounding tissue
Passive process; not ATP dependent
Andy Jagoda, MD, FACEP
 Apoptosis: Cellular Death
ATP Dependent Process
Condensation of nuclear chromatin into
sharply delineated granular masses
Margination of granular masses against
nuclear membrane, with progressive
condensation of nuclear contents
Nucleus breaks up (karyorhexis)
Dense nuclear remnants are seen
Andy Jagoda, MD, FACEP
 Apoptosis: Cellular Death (Cont)
Cell shrinkage, cytoplasmic condensation
Cell outline convoluted, forms extensions.
Extensions separate (budding); plasma
membrane seals.
Apoptotic bodies rapidly taken up by
macrophages without inflammation.
Organelles such as mitochondria preserved,
destroyed secondarily
Andy Jagoda, MD, FACEP
 Anatomy of the Spinal Column
Anterior segment
Posterior segment
Ligaments
Ligamenta flava: paired elastic
structures joining the lamina
Stretch when the spine is flexed and
buckle when it is hyperextended

Andy Jagoda, MD, FACEP

 SCI: Methylprednisolone: NASCI II
162 pts. Received MP; 171 placebo
30 mg/kg; 5.4 mg/kg/hr for 23 hr
Motor/Sensory scores at 6 wk/6 mo
Benefit for MP when administered w/in 8 hr
Motor: MP improved 16/70 compared to 11.2/70
placebo (p=0.03)
Sensation to pinprick: MP improved 11.4/87
compared to 6.6/87 placebo (p=0.02)
MP improved complete and incomplete
Andy Jagoda, MD, FACEP
 Neuro Exam: ASIA/NASCIS
Motor: Function tested bilaterally in 14
muscle segments (0 = no contraction
through 5 = normal function); scores
range 0 - 70.
Sensory: Response to pinprick and light
touch scored bilaterally from C-2
through S-5 for 29 spinal cord segments
(0 = absent through 3 = normal); scores
range 0 - 87
Andy Jagoda, MD, FACEP