For thousands of years, spinal cord injury (SCI) was considered synonymous with death. Ancient Egyptian and Greek physicians described symptoms of complete SCI such as paralysis and loss of sensation. Treatment was conservative without hope of survival until the early 20th century. Developments like dedicated SCI units in the 1930s-40s demonstrated lower mortality through improved care such as bladder management. Current incidence of SCI is highest in males aged 16-30 from vehicular or fall-related accidents, though trends show a decline in accidents and a rise in fall-related injuries. Advances in treatment have increased life expectancy for SCI patients but it remains below able-bodied individuals.

2.  For thousands of years, injury to
the spinal cord was synonymous
with death, either instantly or
after a period of great suffering
 The Edwin Smith Surgical
Papyrus, written by an Egyptian
physician almost 5000 years ago,
vividly describes the symptoms of
neurologically complete injury to
the cervical spinal cord—that is,
paralysis and sensory loss in the
arms and legs, urinary
incontinence, and priapism

3.  approximately 400 bc,
Hippocrates described
paraplegia caused by injury
or disease as being
associated with paralysis,
bladder and bowel
dysfunction, and pressure
ulcers

4.  During the nineteenth century, treatment of SCI
continued to be conservative and without much
hope for survival.
 In 1805, Lord Nelson, the Admiral of the British
Fleet, received a gunshot wound to his thoracic
spine during the battle of Trafalgar, causing
paraplegia.

5.  Nelson spoke with his ship’s
surgeon, Mr. Beatty, and
described his loss of power
of motion and feeling below
the chest, and then
expressed his view that he
would have but a short time
to live. The surgeon’s reply
was, “My lord, unhappily for
our Country, nothing can
be done for you.”
 Within a few hours Lord
Nelson was dead.

6.  In 1881 the twentieth
president of the United
States, James A. Garfield,
was shot in the spine,
causing a neurologically
incomplete conus–cauda
equina lesion, but even
with such a lesion he was
dead within 3 months

7.  During the early part of the twentieth century,
there was little progress made in the management
of SCI, and most persons with SCI died within
weeks or months. Harvey Cushing observed that
during World War I, 80% of all U.S. soldiers with
SCI died within 2 weeks

8.  During the 1930s and 1940s,
management of SCI finally
started to change.
 During the late 1930s, Dr.
Donald Munro at Boston City
Hospital developed a dedicated
unit for comprehensive care of
persons with SCI, and by 1943,
he was able to demonstrate
significant drops in both
morbidity and mortality,
primarily by focusing on better
bladder management.

9.  A few years later, in Great Britain during World
War II, it was decided to congregate all casualties
with SCI in special units that were supervised by
an experienced physician.
 These units were to be sufficiently staffed by
nurses and therapists, housed in facilities with
rehabilitation workshops, and organized to provide
resettlement and aftercare services.


10.  Dr. Ludwig Guttmann
was placed in charge
of such a unit at Stoke
Mandeville, where he
introduced
comprehensive care
and interdisciplinary
rehabilitation for
persons with SCI, a
program that was
widely modeled
around the world

11.  The annual incidence of traumatic SCI requiring
hospitalization in the United States is
approximately 40 new cases per million
population.
 Almost all studies show that the incidence of SCI
is lowest for persons younger than 15 years and
highest for persons 16 to 30 years of age. After the
age of 30, there is a consistent decline in
incidence

12.  More than 80% of all SCI occurs in males, a figure
that has remained essentially constant for more
than 30 years in the United States
 Although India is the second most populous
country in the world, to date no demographic data
are available for SCI.

13.  vehicular crashes (42.1%),
 falls (26.7%),
 violence (15.1%),
 sports (7.6%).
 In recent years, there has been a gradual decline
in SCIs related to vehicular crashes and sports,
whereas those relating to falls have increased.

14.  According to the National SCI Database,
tetraplegia is more common than paraplegia
(50.5% vs. 44.1%). These are subdivided into the
following neurologic categories:
 incomplete tetraplegia (30.1%),
 complete tetraplegia (20.4%),
 complete paraplegia (25.6%), and
 Incomplete paraplegia (18.5%).
 Recent trends show an increase in incomplete
tetraplegia and a slight reduction in complete
paraplegia.

15. Mathur N1, jain S1, kumar N1, srivastava A1, purohit N1, patni A1. Spinal cord
injury: scenario in an indian state. Spinal cord. 2015 may;53(5):349-52.
Doi: 10.1038/sc.2014.153. Epub 2014 sep 16.

17.  The average length of stay for patients with SCI
has declined dramatically over the years,
according to the National SCI Database. This is
true for both acute and rehabilitation
hospitalizations, from 25 acute days in 1974 to 12
days in 2008, and from 115 rehabilitation days to
37 days.

18.  Life expectancy for persons with SCI has increased
steadily for many decades but still remains below
that of able bodied individuals. The mortality rate
is highest during the first postinjury year, at 6.3%,
but declines significantly thereafter.

19.  Diseases of the
respiratory system,
especially pneumonia,
are the leading cause of
death both during the
first post injury year and
during subsequent
years. The second most
common cause of death,
“other heart disease,” is
thought to reflect deaths
that are apparently
caused by heart attacks
in younger persons
without apparent
underlying heart or
vascular disease and
cardiac dysrhythmia

20.  The Primary injury

21.  The secondary injury cascade is a term that
refers to a series of biochemical processes that
occur after an SCI, and that tend to cause further
neuronal damage beyond the mechanical damage
caused at the moment of impact. Ischemia of the
gray matter at the site of injury occurs almost
immediately after SCI. This ischemia appears to
result from vasoconstriction of blood vessels
supplying the cord, and is mediated by the rapid
release of various vasoactive substances such as
serotonin, thromboxanes, platelet-activating
factor, peptidoleukotrienes, and opioid peptides
after SCI

22.  Ischemia is followed by the development of edema
at the site of injury.
 At a cellular level, there is a marked rise in
intraneuronal calcium concentrations.
Intracellular calcium facilitates the activation of
phospholipases A2 and C, which leads ultimately
to the production of free radicals and free fatty
acid metabolites, which cause damage to local
cell membranes

23.  Microhemorrhages appear in the central gray
matter at the site of impact. Iron in this
hemorrhaged blood catalyzes the peroxidation of
lipids, leading to further tissue damage as well
as catalyzing the further production of oxygen free
radicals

24.  Initially, neutrophils migrate to the site of injury,
where they can contribute to cellular injury by
producing lysosomal enzymes and oxygen
radicals. These are followed by macrophages that
phagocytose cell debris

25.  There is no universally accepted definition of
spinal stability. White and Panjabi467 defined
clinical instability as “the loss of the ability of the
spine under physiologic loads to maintain
relationships between vertebrae in such a way
that there is not initial damage or subsequent
irritation to the spinal cord or nerve roots and, in
addition, there is no development of
incapacitating deformity or pain due to
structural changes.”

26.  The anterior column
is composed of the
anterior longitudinal
ligament, the anterior
two thirds of the
vertebral body, and
the anterior two
thirds of the annulus
fibrosis or disk.

27.  The middle column is
composed of the
posterior one third of
the vertebral body, the
posterior one third of
the annulus fibrosis,
and the posterior
longitudinal ligament.

28.  The posterior column
is composed of the
pedicles, facet joints,
laminae, supraspinous
ligament, interspinous
ligament, facet joint
capsule, and
ligamentum flavum

29.  When the integrity of the middle and either the
anterior or the posterior column is affected, the
spine is likely to be unstable

30. Flexion Injuries Compression
Fractures
Mechanism: cervical flexion with
axial loading
• C5 is the most common
compression fracture of the
cervical spine.
• Force ruptures the plates of
the vertebra, and shatters the
body. Wedge-shaped
appearing vertebra on x-ray
• May involve injury to the nerve
root and/or cord itself.
• Fragments may project into
spinal canal.

31. • Mechanism: flexion-rotation injury
• Vertebral body < 50% displaced on x-
ray
• Unstable if the posterior ligament is
disrupted.
• Narrowing of the spinal canal and
neural foramen
• C5–C6 most common level
• Also note that flexion and rotation
injuries may disrupt the
intervertebral disc, facet joints, and
interspinous ligaments with little or
no fracture of the vertebrae.
• If spinal cord injury results, it is more
likely to be an incomplete injury

32. • Mechanism: flexion injury
• Vertebral body > 50%
displaced on x-ray, causing
significant narrowing of the
spinal canal
• Unstable with disruption of
the PLL
• Most common level is C5–C6
because of increased
movement in this area.
• Injury more likely to be
neurologically complete

33. • Can be caused by
acceleration-deceleration
injuries,
• Soft tissue injury may not be
seen on radiologic studies.
• Hyperextension injury of the
C-spine in the elderly may
result in a central cord
syndrome.
• C4–C5 is the most commonly
affected level.

35. • NT-SCI includes etiologies, such as spinal stenosis
with myelopathy, spinal cord compression from a
neoplasm, multiple sclerosis (MS), transverse
myelitis, infection (viral, bacterial, fungal,
parasitic), vascular ischemia, radiation
myelopathy, motor neuron diseases,
syringomyelia, vitamin B12 deficiency, and
others.
• Spinal stenosis and spinal cord tumors are the
most common causes of NT-SCI presenting for
inpatient rehabilitation in the United States.

36. Spinal cord tumors
– Can be primary or metastatic, intradural, or
extradural. The majority of spinal cord tumors are
metastatic in origin, and 95% of these are
extradural.
– Approximately 70% of spinal metastasis occurs in
the thoracic spine, with clinical presentation of
pain, typically worse at night, and when the
patient is in the supine position.
– The most common sources of secondary tumors are
the lung, breast, and prostate. The most common
primary tumors are ependymoma and
astrocytomas

37. • Jefferson Fracture (C1 Burst
Fracture)
– Burst fracture of the C1 ring.
Usually a stable fracture with
no neurological findings
– Mechanism: axial loading
causing fractures of anterior
and posterior parts of the
atlas (ie, football spearing)
– Treatment: rigid orthosis (ie,
Halo vest) if it is a stable
fracture. If it is unstable, will
require surgery.

38. Hangman Fracture (C2 Burst
Fracture)
Usually bilateral from an
abrupt deceleration injury
(eg, MVC with head hitting
windshield)
– Most often stable with only
transient neurological
findings
– Treatment: external orthoisis
(halo is first line treatment).
Unstable fracture will require
surgery.

39. Odontoid (Dens) Fracture
– Type I: fracture through the tip
of dens. No treatment usually
required.
– Type II (most common): fracture
through the base of odontoid
at junction with the C2
vertebra. Usually treated with
a Halo vest, but surgery may
be required if unstable.
– Type III: fracture extends from
base of odontoid into the body
of the C2 vertebra proper.
Usually treated with a Halo
vest

40. • Chance Fracture
Transverse fracture of thoracic or
lumbar spine from posterior – to
anterior through the spinous process,
pedicles, and vertebral body
– Usually affects T12, L1, L2 levels
– Previously was most commonly seen in
patients wearing lap seat belts. Now
typically due to falls/crush injury
with acute hyperflexion of the thorax.
– Tend to be stable fractures and are
seldom associated with n neurological
compromise unless a significant
amount of translation occurs

41. Vertebral Body Compression
Fracture (Anterior Wedge
Fracture)
– Most commonly caused by
axial compression with or
without flexion: vertebrae
body height is reduced—
may cause thoracic
kyphosis (Dowager hump)
– Spontaneous vertebral
compression fractures are
stable injuries—ligaments
remain intact.

42. The International Standards for Neurological
Classification of Spinal Cord Injury (ISNCSCI)
provides a procedure for classifying an SCI.
A complete injury is defined within the ISNCSCI as
an injury in which there is the lack of any sensory
or motor function in the lowest sacral segment;
this includes sensation deep within the anus,
sensation at the anal mucocutaneous junction, or
a voluntary contraction of the external anal
sphincter.
An incomplete injury is defined as an injury in
which there is at least partial sensory or motor
function in the lowest sacral segment

43. The sensory portion of the neurologic examination
includes the testing of a key point for absent,
impaired, or normal sensation in each of the 28
dermatomes on each side of the body for both light
touch and pinprick.
The motor portion of theneurologic examination
includes the testing of a key muscle function for
strength on a 6-point scale for each of 10
myotomes on each side of the body), as well as
testing for contraction of the external anal
sphincter

46.  C 5
 C6
 C7
 C8
 T1
• L 2
• L3
• L4
• L5
• S1

48. “Will I walk again?” “Will I regain use of my
hands?” “Will I regain control of my bowel and
bladder?”

49. Only 2% to 3% of persons initially classified as
having an AIS of A convert to AIS D by 1 year
Overall, between 30% and 80% of persons with
motor complete tetraplegia recover a single
motor level, meaning gaining functional motor
strength at that level, within 1 year of injury
A muscle with grade 1 or 2 strength at 1 week
has a 70% to 80% chance of reaching grade
3 by 1 year.

50. Maynard et al reported that 87% of persons with
motor incomplete tetraplegia initially were
walking by 1 year, whereas 47% of persons
with sensory incomplete, but motor complete,
tetraplegia were walking by 1 year.

51.  Persons with preservation of pinprick sensation
near the anus have a greater than 70% chance
of regaining ambulatory ability, while persons
who have spared light touch sensation only in
the same region are unlikely to regain
ambulatory ability

52. Among persons with complete paraplegia, about 75%
retain the same NLI at 1 year that they had at 1
month postinjury, 20% gain a single level, and 7%
gain two neurologic levels.
Persons with T1–T8 complete paraplegia do not
recover lower limb voluntary movement. However,
15% of persons with complete paraplegia between
T9 and T11, and 55% of persons with paraplegia at
T12 and below, recover some lower limb function

53. Persons with incomplete paraplegia have the
best prognosis for ambulation among all the
groups of persons with traumatic SCI.
80% of individuals with incomplete paraplegia
regain functional hip flexion and knee extension
within 1 year of injury, making both indoor and
community-based ambulation possible

54.  1. accident site management
 2. primary care
 3. care at tertiary care hospital

55.  Airway
 Breathing
 Circulation

66. We suggest that MRI be performed in adult patients with
acute SCI prior to surgical intervention, when feasible, to
facilitate improved clinical decision-making. (Grade: Weak
Recommendation; Very Low Evidence
We suggest that MRI should be performed in adult patients in
the acute period following SCI, before or after surgical
intervention,
to improve prediction of neurologic outcome. (Grade: Weak
Recommendation; Low Evidence)

67.  Plain films
› Lateral, A/P, odontoid; C-T-L
spines
› May be used for rapid
identification of gross deformity
 CT Scan
› Comprehensive, cervical through
sacral
› Demonstrates degree of
compression and cord canal
impingement
 MRI Scan
› Demonstrates ligamentous, spinal
cord injury

68.  Occiput to T1 need to be cleared
 ER, Neurosurgery or Orthopedics physician
 If the patient
› Is awake and oriented
› Has no distracting injuries
› Has no drugs on board
› Has no neck pain
› Is neurologically intact
then the c-spine can be cleared clinically, without any
need for XRays
 CT and/or MRI is necessary if the patient is
comatose or has neck pain
 Subluxation >3.5mm is usually unstable

69.  Gardner-Wells tongs
 Provides temporary stability of the cervical spine
› Contraindicated in unstable hyperextension injuries
 Weight depends on the level (usually 5lb/level,
start with 3lb/level, do not exceed 10lb/level)
 Cervical collar can be removed while patient is in
traction
 Pin care: clean q shift with appropriate solution,
then apply povidone-iodine ointment
 Take XRays at regular intervals and after every
move from bed

71.  Indications
› Decompression of the neural elements (spinal
cord/nerves)
› Stabilization of the bony elements (spine)
 Timing
› Emergent
 Incomplete lesions with progressive neurologic
deficit
› Elective
 Complete lesions (3-7 days post injury)
 Central cord syndrome (2-3 weeks post injury)

73. McQuillan, K., Von Rueden, K., Hartsock, R., Flynn, M.,
& Whalen, E. (eds.). (2002). Trauma Nursing: From
Resuscitation Through Rehabilitation. Philadelphia: W.
B. Saunders Company. Reprinted with permission.

74.  Atlanto-occipital
dissociation
› Complete injury; death
 Atlanto-axial dislocation
› Complete injury; death
 Jumped, Jump-locked
facets
› Require reduction; may
impinge on cord; unstable
due to ligamentous injury

75.  Facet fractures
› High incidence of
cord injury in
cervical spine
 Odontoid (dens)
fractures
› Rarely cord injury

76. Compression
fractures
Burst
fracture
Chance
fracture

77.  Spinal Cord Injury without
Radiographic Abnormality
› Most frequently children
› Dislocation occurs with spontaneous
relocation
› Cord injury evident
› Radiographs negative

78.  Airway
› C1-4 injuries require definitive airway
› Injuries below C4 may also require airway due
to
 Work of breathing
 Weak thoracic musculature
 Breathing
› Adequacy of respirations
 SpO2
 Tidal volume
 Effort
 Pattern

79.  Circulation
› Neurogenic shock
 Injuries above T6
 Hypotension
 Bradycardia –treat symptomatic
only
 Warm and dry
 Poikilothermic – keep warm
› Fluid resuscitation
› Identify and control any source
of bleeding
› Supplement with vasopressors

80. Injury to T6 and above
Loss of sympathetic innervation Increase in venous
capacitance
Bradycardia Decrease in venous
return
Hypotension
Decreased cardiac output
Decreased tissue perfusion

81.  Urine output
› Urinary retention
 Atonic bladder
› Foley
 Initially avoid
intermittent
catheterization
 High urine output
from resuscitation
fluids

82.  Deficit
› Spinal shock
 Flaccid paralysis
 Absence of cutaneous and/or
proprioceptive sensation
 Loss of autonomic function
 Cessation of all reflex activity below the
site of injury
› Identify level of injury

83.  Pain
› Frequent physical and
verbal contact
› Explain all procedures to
patient
› Patient-family contact as
soon as possible
› Appropriate short-acting
pain medication and
sedatives

84.  Communication
› Blink board
› Adapted call bell system
› Avoid clicking, provide a
better option
› Speech and occupational
therapy
› Prism glasses
› Setting limits/boundaries
for behavior

85.  Special Treatment
› Hypothermia
 Recommends 33oC intravascular cooling
 Rapid application, Monitor closely
 Anecdotal papers
› High dose methylprednisolone
 No longer considered standard of care

86.  Rotational bed therapy
› Maintain alignment and traction
› Prevent respiratory complications of
immobility

87.  Surgical
› Determined by
 Degree of deficit, location of injury,
instability, cord impingement
 Anterior vs. posterior decompression/ both
› Emergent
 Reserved for neurologic deterioration when
evidence of cord compression is present

90. PMR
specialist
Physiotherap
ist
Occupational
therapist
Medical
social
worker
orthotist
Clinical
psycologist
Vocational
counselor
Rehab
Nurse

109.  Pulmonary complications
 Pulmonary complications, including
atelectasis, pneumonia, respiratory
failure, pleural complications, and
pulmonary embolism (PE), are the
leading causes of death for
persons with SCI in all years after
SCI. They accounted for 37% of
all deaths during the first year
after SCI, and 21% of the deaths
beyond the first year

110.  Atelectasis is the most
common respiratory
complication in people
with SCI and can
predispose to
pneumonia, pleural
effusion, and
empyema

111.  Secretion clearance
 CPAP
 Mechanical insufflator-exsufflator
 Bronchodilators

112.  DVT
 Persons with SCI are prone to stasis of the venous
circulation, hypercoagulability of the blood, and intimal
vascular injuries. These risk factors for development of
deep vein thrombosis (DVT) are known as Virchow’s triad.
 Stasis is a direct result of the loss of the muscle-
pumping action of the lower limbs and peripheral
vasodilatation. Hypercoagulability is caused by release of
procoagulant factors after injury, whereas intimal injury
can occur from trauma.

113.  Management
 Low molecular wight heparin
 Warfarine
 IVC filters
 DVT prevention pumps
 ROM ex.

114.  Persons who have SCI, both paraplegia and
tetraplegia, often lead sedentary lives, resulting
in poor physical fitness and an increased risk
for untoward cardiovascular events. Persons with
SCI, both those with paraplegia and tetraplegia,
have a high prevalence of asymptomatic
coronary artery disease as detected by
thallium stress testing

115. Daily exercise
Lifestyle modification
Dietary modification

116.  The autonomic nervous system is under
supraspinal control, and therefore its function is
disturbed by SCI. The autonomic nervous
system normally controls visceral functions
and maintains internal homeostasis through
its nerve supply to smooth muscles, cardiac
muscle, and glands

118.  After SCI, autonomic reflex function is generally
retained, but in those with high-level SCI, this is
without supraspinal control.

119. Immediately after SCI, there is a complete loss of
sympathetic tone, resulting in neurogenic (“spinal”)
shock with hypotension, bradycardia, and
hypothermia.
The hypotension occurs as a result of systemic loss of
vascular resistance, accumulation of blood within the
venous system, reduced venous return to the heart,
and decreased cardiac output

120.  Over the course of time, the sympathetic reflex
activity returns, with normalization of blood
pressure. Supraspinal control continues to
be absent in those individuals with high-level
and neurologically complete SCI, however, and
they continue to be prone to orthostatic
hypotension.

121.  SCI leads to disruption of the descending spinal
cardiovascular pathways, resulting in
sympathetic hypoactivity and unopposed
prevalence of the intact vagal parasympathetic
control.18 Sympathetic hypoactivity results in
low resting blood pressure, loss of regular
adaptability of blood pressure, and disturbed
reflex control

122.  Orthostatic hypotension is defined by The
Consensus Committee of the American
Autonomic Society and the American Academy of
Neurology (1996) as a decrease in systolic blood
pressure of 20 mmHg or more, or in diastolic
blood pressure of 10 mmHg or more, upon the
assumption of an upright posture from a supine
position, regardless of whether symptoms occur.

124.  Management of orthostatic hypotension includes
application of elastic stockings and
abdominal binders, adequate hydration,
gradually progressive daily head-up tilt, and
at times, administration of salt tablets,
midodrine, or fludrocortisone

125.  AD is a syndrome that affects persons with SCI
at the T6 level or above, which is above the
major splanchnic outflow. It is caused by a
noxious stimulus below the injury level, which
elicits a sudden reflex sympathetic activity,
uninhibited by supraspinal centers, resulting
in profound vasoconstriction and other
autonomic responses

126. The symptoms of AD are somewhat variable but include
a pounding headache; systolic and diastolic
hypertension; profuse sweating and cutaneous
vasodilatation with flushing of the face, neck,
and shoulders; nasal congestion; pupillary
dilatation; and bradycardia. The hypertension can
be profound and result in cerebral hemorrhage and
even death

127. Strong Sensory stimulus (noxious/non noxious)
Exaggerated Sympathetic response
Vasoconstriction below level of injury (splanchnic and peripheral vessels)
Baroreceptors response to hypertension
Parasympathetic response through vagus nerve
Bradycardia, vasodilatation above level of injury
Absen transmission of inhibitory signals due to spinal cord injury

128.  Recognition of symptoms and identification of the
precipitating stimulus are paramount. The patient
should be sat up, constrictive clothing and garments
should be loosened, the blood pressure monitored
every 2 to 5 minutes, and evacuation of the bladder
done promptly to ensure continuous drainage of
urine. If symptoms are not relieved by these
measures, fecal impaction should be suspected and,
if present, resolved.

129.  Local anesthetic agents should be used during
any manipulations of the urinary tract or rectum.
If hypertension is present, fast-acting
antihypertensive agents shouldbe administered,
usually nitroglycerin or nifedipine.
 After resolution of the AD episode, the person’s
symptoms and blood pressure should be
monitored for at least 2 hours.

130.  Bladder management
 Bowel management
 Pressure ulcer management
 Sexual rehabilitation
 Vocational rehabilitation
…….To be discussed in other
presentations!

131.  Spinal cord injury person can live normal life
with proper rehab management.
 Interdisciplinary integrated team approach for
complete rehab of Spinal cord injury person is
must. Physical Medicine and Rehabilitation
specialists trained in Rehabilitation of SCI are
key person for this !