SPINE SGD
SAN GABRIEL, SANIANO, SANTOS JJ, SANTOS MS, SISON, SORREDA, SOTALBO
General Data
AA is a 15 year old female from Bacoor, Cavite who came
in for consult due to bilateral lower extremity weakness
and sensory deficits
DOI: June 21, 2009
TOI: 1:30 PM
POI: road in Bacoor, Cavite
MOI: vehicular crash
History of Present Illness
June 21, 2009 (1:30 PM)
While walking towards the other side of the road, the
patient was hit by a jeepney at speed on the back
lumbar area. She was flung over the hood and again fell
in front of the still moving vehicle and was run over. The
vehicle stopped with her pinned under the rear wheel.
Bystanders lifted the jeepney and she was pulled out.
She was unconscious at this time and sustained
abrasions over her face, arms, legs and back. No gross
deformities were seen.
History of Present Illness
She was then brought to Crisostomo Medical Center, 30
minutes away from the site of the accident.
At the CMC, she regained consciousness. Her wounds
were cleaned and x-rays of her neck, chest, arms and
kegs were done. This allegedly revealed a compression
fracture of one of her lumbar vertebrae. Difficulty
breathing prompted her to be given O2 support
She was confined at CMC untill...
History of Present Illness
June 28, 2009
She was brought to the PGH ER with an admitting
impression of SCI secondary to VC. Repeat labs and xrays were done.
July 2, 2009
She was transferred to the Spine Ward and is awaiting
definitive management.
Past Medical History
Left Knee Lacerations secondary to trauma from broken
glass (2001) –required stitches, healed with no
complications
(-) Asthma
(-) TB
(-) Hypertension
(-) Diabetes
No other past surgeries or hospitalizations
Family Medical History
(+) Asthma
(-) HPN
(-) DM
(-) TB
(-) CA
(-) Stroke
(-) CVD
Personal and Social History
No vices, currently studying in Grade 5 but had to stop
schooling since the injury.
She is the 2nd of 3 children and has good relationships
with her siblings. She has good social support from both
family and friends .
Review of Systems
(+) Pain over lumbar area, VAS 5/10
(-) Headache
(-) Blurring of Vision
(-) Neck Pain/Stiffness
(-) Nausea
(-) Vomiting
(-) Chest Pain
(-) Urinary/Bowel Changes
(-) Dysuria
(-) Abdominal Pain
Physical Examination
General Survey:
Found in bed, alert, conscious, coherent and not in
cardiorespiratory distress. She speaks in sentences, can
follow commands and can converse clearly.
Physical Examination
Vital Signs:
HR 84
RR 24
BP 100/70
HEENT:
Anicteric sclerae, pink palpelbral conjunctivae, full
EOMs, pupils EBRTL, subconjunctival hemorrhages on
both eyes, (-) blurring of vision, (-) CLAD, (-) ANM, (-)
masses/tenderness, (-) facial asymmetry
Physical Examination
Chest/Lungs:
Clear breath sounds, equal chest expansion, (-)
crackles/ rales/wheezes
Heart:
Adynamic precordium, regular rate and rhythm, no
murmurs
Abdomen:
Soft, flabby abdomen with normoactive bowel
sounds, (-) bowel changes
Genitourinary:
(-) urinary changes, CVA not assessed
Physical Examination
Extremities:
Multiple abrasions over facial area, arms, legs and back.
No gross deformities on inspections. CRTs <2 secs, good
pulses for all extremities. Both legs extended, R foot in
extended plantar flexion. Manual muscle testing for UE
all 5/5. Lower extremities; left 3/5, right 0/5.
Assessment
Compression Fracture L1 Vertebra
Incomplete Spinal Cord Injury, ASIA class B, intact
sensory perception, Neurologic Level L1
DISCUSSION
Goals
Short Term
Prevent SCI complications
Wheelchair mobility
Maintain range of motion of all joints
Prevent bed sore formation
Long Term
Go back to schooling
Independent ADLs
Compression Fractures
 Force ruptures plates of vertebra & shatters the body
 Wedge shaped appearing vertebra on X-ray
 May involve injury to nerve root &/or cord
 Fragments may project into spinal canal
Shearing / Spinal Cord Compression
 traumatic necrosis of the spinal cord
 destruction of gray and white matter
 variable amount of hemorrhage, chiefly on vascular
central parts
 maximal at the level of injury and 1 or 2 segments
above and below it
Clinical Effects of SCI
1) voluntary movement in parts of the body below the
lesion immediately and permanently lost
2) all sensation from the lower (aboral) parts is
abolished
3) reflex functions in all segments of the isolated spinal
cord are suspended
Clinical Effects of SCI
2 Stages
1. Spinal Shock / Areflexia
2. Stage of Hypereflexia
Spinal Shock
• Reflex arc is not functioning
• motor function lost with atonic paralysis of bladder,
bowel, gastric atony
• muscles below level of lesion become flaccid and
hyporeflexic
• Loss of sensation below the level of the lesion
• Duration: Lasts from 24 hours to 3 months after injury.
Average is 3 weeks.
Stage of Hypereflexia
• As spine recovers from shock, reflex arc functions
w/out inhibitory or regulatory impulses from the
brain, creating local spasticity & clonus
• Reflexes become stronger
• Pattern of higher flexion is noted
• Dorsiflexion of the big toe (Babinski sign)
• Bladder starts to contract irregularly
Complete Lesion
Complete Injury (Waters 1991)
Absence of sensory and motor function in the lowest
sacral segment
Zone of Partial Preservation (only used with complete
lesions): dermatomes & myotomes caudal to
neurological level of injury that remain partially
innervated
Incomplete Lesion
Partial preservation of sensory and/or motor functions
below the neurological level, which
With Sacral Sparing —voluntary anal sphincter
contraction or sensory function
Due to preservation of the periphery of the SC
 Sacral sparing indicates possibility of SC recovery
PROBLEMS IN SPINAL CORD INJURY
Orthostatic Hypotension
Sudden drop in systolic blood pressure (BP) of at least
20 mm Hg or diastolic BP by at least 10 mm Hg within 3
minutes of standing upright or 60 degrees on a tilt table
lightheadedness, dizziness, ringing of the ears, fatigue,
tachycardia, and sometimes syncope
Occurs more frequently in persons with cervical level or
neurologically complete injuries
When bedrest is prolonged, the degree of orthostasis
tends to be more severe
Intensifies after eating, exposure to hot environments,
defecation, and rapid bladder emptying
Orthostatic Hypotension
exact mechanism is unknown, but theories include
increased
sensitivity
of
baroreceptors
and
catecholamine receptors in the vessel walls,
development of spasticity, improved autoregulation of
cerebral vascular perfusion, and adaptations of the
renin-angiotensin system
Autonomic Dysreflexia
A composite of symptoms, most notably a sudden rise
in BP, seen in those with SCI due to autonomic
dysfunction
Usually restricted to those with injuries at or above T6
Most common source of noxious stimulus is from the
bladder, either from overdistension or infection,
followed by fecal impaction
Hypercalcemia
Occurs when bone resorption is increased in
association with an impaired fractional excretion of
calcium by the kidney
Risk factors: multiple fractures, age under 18 because
of high rate of bone turnover, male gender, high level
lesion, complete neurological injury, prolonged
immobilization, and dehydration
Hypercalcemia
Symptoms: acute onset of nausea, vomiting, anorexia,
lethargy, polydipsia, polyuria, or dehydration
Tx: intravenous fluid (normal saline at 100 to 150
cc/hour), as tolerated to increase calcium excretion
Other meds:calcitonin, etidronate, glucocorticoids ,
pamidronate
Heterotrophic Ossification
Formation of lamellar bone within the soft tissue
surrounding a joint
Clinical limitation of the range of motion (ROM), joint
may also appear warm and swollen
In severe cases, adjacent neurovascular structures may
be compromised leading to distal extremity swelling and
nerve entrapment
Heterotrophic Ossification
Treatments: passive- and active-assisted ROM with
gentle stretching after the acute inflammatory period is
over (1 to 2 weeks), nonsteroidal antiinflammatory drugs
(NSAIDs) (e.g., indomethacin), bisphosphonates,
radiation therapy, and surgical excision
Thromboembolic Disorders
Development of DVT is low in the first 72 hours, and
occurs most frequently during the first 2 weeks
(approximately 80% of cases) following injury
PE is the 3rd leading cause of death in all SCI px in the
first-year post injury
Clinical signs: unilateral edema, low-grade fever, and
pain in a patient with an incomplete injury
Pressure Ulcers
 Risk factors: level and severity of the injury, gender,
ethnicity, marital status, employment status,
educational achievement, tobacco and alcohol use,
nutritional status, and possibly depression
 Having a previous ulcer is a risk factor as well.
 The longer the time a person has been injured the
greater the risk of developing an ulcer.
Pressure Ulcers
The most common location in persons with SCI within
the first 2 years is the sacrum, followed by the ischium,
heel, and trochanter.
After 2 years, the ischial tuberosities are the most
common site of development
Musculoskeletal Pain
In persons with SCI upper extremities are used for
weight-bearing activities
Shoulder pain is the most commonly reported painful
joint after SCI
chronic impingement syndrome
rotator cuff pathology
Musculoskeletal Pain
If pain develops acutely, then referred pain should be
excluded
Pain associated with neurological changes (i.e.,
weakness, sensory loss or reflex changes) may be due to
peripheral nerve entrapment, radiculopathy, or a
posttraumatic syrinx.
Neuropathic Pain
May be treated with Gabapentin
Opioids are also gaining acceptance as a therapeutic
option in nonmalignant pain syndromes and are rated by
SCI patients as one of the more effective treatments
Posttraumatic Syringomyelia
 most common cause of progressive myelopathy after
an SCI
 may develop at any time, from 2 months to decades
postinjury
 Presents as neulogical decline or as elongated cavity
in MRI
 The most common presenting symptom is pain,
usually located at the site of the original injury or may
radiate to the neck or upper limbs
Posttraumatic Syringomyelia
Pain is described as aching or burning, often worse with
coughing, sneezing, straining, and in the sitting rather
than in the supine position
Earliest sign is an ascending loss of deep tendon
reflexes
MRI with gadolinium is the gold standard in dx
MANAGEMENT
Workup
Arterial blood gas measurements
• to evaluate adequacy of oxygenation and ventilation
Lactate levels
•to monitor perfusion status
Hemoglobin and/or hematocrit levels
•to detect or monitor sources of blood loss
Urinalysis
•to detect associated genitourinary injury
Imaging
Standard Radiographs
•Not as effective as a CT scan but can be obtained faster.
It is sometimes sufficient to assess spinal injury
particularly in emergent cases
•3 standard views
a) Anteroposterior
b) Lateral
c) Odontoid (cervical spine)
Imaging
CT Scan
•More sensitive, better visualization
•For delineating bony abnormalities or fractures
•Radiography with CT scanning has a negative predictive
value between 99-100%
MRI
•best for suspected spinal cord lesions, ligamentous
injuries, or other soft tissue injuries or pathology
•for evaluation of nonosseous lesions
•can visualize soft tissue changes secondary to injury
Treatment
Prehospital Care of Suspected Spinal Injuries
1. assure patient safety and prevent further injury
2. stabilize and immobilize the spine on the basis of
mechanism of injury, pain in the vertebral column or
neurologic symptoms
3. use a cervical collar or backboard for transport
Treatment
Emergency Department Care
1. assessment and treatment of airway, respiration and
circulation
2. assessment of associated injuries or covert/overt
bleeding
3. some patients may require intubation
Treatment
4. treatment of neurogenic shock
a) fluid replacement with isotonic solution
b) systolic BP of no less than 90-100 mmHg to maintain spinal
cord perfusion
c) heart rate of 60-100 bpm with normal sinus rhythm
d) atropine treatment of hemodynamically significant
bradycardia
e) urine output of 30mL/h; inotropic support with dopamine
for patients with decreased urinary output despite
adequate fluid resuscitation
f) prevent hypothermia
Treatment
5. Neurologic assessment with imaging
6. Nasogastric tube placement since ileus is common in
SCI patients
7. Prevention of pressure sores
Steroid therapy is no longer advocated in the
management of SCI
Surgical Management
May require a team approach from different surgical
fields depending on mechanism of injury, location,
severity and other associated conditions
1. Trauma Surgeon
•Since the majority of spinal cord injuries are traumatic
in nature
2. General Surgeon
•Patients can present with more than one injury
requiring surgical intervention
Surgical Management
Rigid External Orthotic Devices
•Stabilize the spine and decrease range of motion
•Include cervical collars and halo vests
Goals of Surgical Intervention
1. Decompression of spinal cord or nerve roots
2. Stabilization of injuries judged too unstable to heal
with external orthotics only (surgical stabilization)
Surgical Management
3. Orthopedic Surgeon
For repair of affected skeletal structures and removal of
bone fragments in the case of fracture trauma to the
spine
4. Neurosurgeon
Assessment of affected neurologic structures and
appropriate repositioning, repair, anastomosis or other
procedures involving the CNS or spinal cord
Each surgical team is composed of specific members
based on the patient’s condition and type of injury.
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