Download - Spinal Cord Injury
K.K. BansalK.K. Bansal
A comma OR a full stop ?Manjunath Kalmani:
Was a software engineer. Paralyzed from neck down. Spinal cord injury level C4 when he got injured in a car accident , in April 2002, slowly injury level became C2 complete. On ventilator 100%.
Presently in Safdarjung Hospital, New Delhi.
IntroductionINTRODUCTION: Leading cause of morbidity and mortality in youth Both physical and emotional aspects of spinal cord
injury are devastating. OCCURRENCE: Approximate 20,000 new cases of SCI are added
every year in India - Sinha DK. Manual of Patna. Model for the care of Spinal cord injury patients. Patna: SPARSH. 2000; 9-13.
60-70% of them are illiterate, poor villagers. Most sustain this injury by fall from unprotected roofs, trees or fall into uncovered wells, which infact are preventable causes
No definite treatment till date; the effect of initial trauma is irreversible.
High cost of medical treatment and supporting those permanently disabled
EpidemiologyAge Group Causes
Young
Middle aged
Old
RTAAtheletic events
Industrial accidents
Fall
Urban areas
Rural areas
Violence, e.g. Gunshot
Diving
Age and sex distribution
Singh R. et al. Traumatic Spinal Cord Injuries in Haryana: An Epidemiological Study.
Indian Journal of Community Medicine, Vol. 28, No. 4 (2003-10 - 2003-12)
Mode of injury
Singh R. et al. Traumatic Spinal Cord Injuries in Haryana: An Epidemiological Study.
Indian Journal of Community Medicine, Vol. 28, No. 4 (2003-10 - 2003-12)
Being young…
Also means… Seeking risk…
Anatomy
Designation of lesion level
Three column model of Denis
Denis F. The three-column spine and its significance in the classification of acute thoracolumbar spinal injuries. Spine 1983;8:817.
Definition : Spinal cord injury is an insult to the spinal cord resulting
in the change , either temporary or permanent, in its motor, sensory or autonomic function.
Terminology :
Tetraplegia (quadriplegia) – injury to spinal cord in the cervical region with associated loss of muscle strength in all 4 extremities.
Paraplegia – injury in the spinal cord in the thoracic, lumbar, or sacral segments with associated loss of muscle strength in both lower limbs.
Pentaplegia - involving respiratory muscle i.e. Diaphragm also
Pathophysiology of Spinal Cord Injury
Primary Injury – Anatomical- Mechanical shearing of axons and
blood vessels Physiological- so called concussion which is
uncommon and totally reversible within 2-4 wk. Secondary Injury – Microvascular and neuronal injury due to a
cascade of pathophysiological events that exacerbate primary injury(Potential target of pharmacological treatment)
Primary mechanism of SCIMechanical force Mechanism of injury
Impact + compression Burst #, # dislocation, disc rupture
Impact alone Hyperextension
Distraction Hyperflexion
Laceration, transection Burst #, laminar #, # dislocation, missile
Secondary mechanismsSystemic effects (spinal shock)
Heart rate – bradycardiaBP – hypotensionPeripheral resistance – decreasedCardiac output – decreasedCatecholamines – decreased
Local vascular damage of cord micro-circulation Mechanical disruption of capillary Haemorrhage – gray matter Loss of microcirculation – mechanical, thrombosis,
vasospasmReduction of cord blood flow – thrombosis, vasospasmLoss of autoregulation
Secondary mechanismsBiochemical changes
Excitotoxicity – glutamate Neurotransmitter accumulation – norad., dopamineArachidonic acid release Free radical productionProstaglandin production Lipid peroxidation
Electrolyte shifts Increased intracellular calcium and sodiumIncreased extracellular potassium
Oedema Decreased ATP production
PRIMARY LESIONS4 types of lesions usually found : Contusion -23%, moderate contusive forces, leave
continuity of cord, centrally located hematomyelia, becoming stable cyst
Cord maceration -32%, massive compression, severe destruction of almost all nervous tissue, pial breach, subsequent connective tissue scarring
Cord laceration -27%, open injury e.g. gun shot, torn cord parenchyma
Solid cord injury –18%, overall form of cord retained, confined to white matter esp. corticospinal tract –diffuse axonal disruption, grey matter not affected
Bunge RP, et al. Observation on pathology of human spinal cord injury. A review and classification of 22 new cases with details from a case of chronic cord compression with extensive focal demyelination.
Adv Neurol 1993; 59: 75-89.
MECHANISM OF SCI
Flexion Injury Vertical Compression Injury
Flexion-rotation Injury Hyperextension injury
Intercostal Muscles
T1-11
Risk Associated with Level of Injury
Diaphragm
C3-5
Accessory Muscles C1-7
Abdominal Muscles Abdominal Muscles T6-12T6-12
CLASSIFICATION OF INJURY: either quadriplegia or paraplegia with
Complete Lesions- no sensory or motor function below the lesion
Incomplete Lesions- preservation of some sensory or motor function below lesion. May present as one of the following
Complete injury- worst prognosisIncomplete injury- With no motor function- poor recovery
With some motor function- good recovery
Other factors responsible- age, sex, rectal tone, reflexes, medical & surgical treatment, neurological status and initial strength of muscles.
CLINICAL MANIFESTATIONS: DIRECTSPINAL SHOCK –common to all ptsPain in the neck or backMotor / sensory impairmentsImpaired temperature controlRespiratory impairmentSpasticityBowel & Bladder dysfunction Sexual dysfunction
INDIRECTPressure soresContracturesDeep vein thrombosis (DVT)PainOsteoporosis & Renal calculi
SPINAL SHOCKIt is a state of transient physiological reflex depression
of cord function below the level of injury with associated loss of all sensorimotor and autonomic functions.
Spinal shock manifested by triad of hypotension, bradycardia, and hypothermia
Neurogenic shock is due to combination of
1.Decresed sympathetic tone
2.Unopposed cardiac vagotonia
3.Possible secondary changes in heart
Kiss ZHT, et al. Neurogenic shock. In Geller ER (ed). Shock and Resuscitation. New York: Mc Graw Hill, 1993, pp 421-440
Syndromes assoc. with SCICentral cord syndrome
Often associated with a cervical region injury leading to weakness greater in the upper limbs than in lower limbs with sacral sensory sparing
Seen after hyperextension injury
Anterior cord syndrome
Often associated with lesions causing variable loss of motor function and senstivity to pain and temperature, while proprioception is preserved.
Seen in hyperflexion injury
Poor prognosis
Brown-sequard syndrome
Hemisection lesion of the cord, causing a ipsilateral proprioceptive and motor loss with contralateral loss of senstivity to pain and temperature
Seen after penetrating injury
Better prognosis
Conus medullaris syndrome –assoc. with injury leading toto the sacral cord and lumbar nerve roots areflexic bladder, bowel, and lower limbs, while the sacral segments occasionally may show preserved reflexes( bulbocavernous and micturition reflexes)
Cauda equina syndrome is due to the injury to lumbosacral nerve roots below L3 vertebrae leading to areflexic bladder, bowel and lower limb.
Posterior cord syndrome –damage in post. column leading to preservation of motor function and loss of sensory function below injury level.
MANAGEMENT Goals :1. Preservation of life –by primary
management as A B C2. Preservation of function –by protecting the
spine by external support e.g collar,spine-board,sand bags,traction etc.
3. Restoration of the function –by decompression, fusion/fixation and finally by rehablitation.
At the site of accident Assume every pt of trauma has SCI
until radiography of entire length proves otherwise
↓ Until then the head & neck must be
stabilized with rigid collar of appropriate size with sandbags on each side with forehead tape on spinal board
↓ Spine immobilisation and log rollinglog rolling ↓ Transfer to hospital
At emergencyAirway – clear airway , avoid excessive
suction( as it may stimulate vagal reflex-aggravate pre-existing bradycardia & precipitate cardiac arrest), tracheostomy if needed.
Avoid hyperextension of the neck, which will prevent worsening of canal stenosis as well as exacerbating motion of fractured segments or dislocations.
Breathing – oxygen support ,ventilator
Circulation – maintain B.P >110/70 (establishment of adequate intravenous line). General support of patient’s cardiovascular function is important to optimize spinal cord perfusion and prevent ischemic secondary injury.
The use of vasopressors, such as dopamine and neosynephrine, is useful in reversing the effects of neurogenic shock.
Spine immobilisation and positioning Avoid spinal rotaion
during resuscitation and transfer.
If pt comes within 8 hrs of injury—start steroid infusion (methylprednisolone)
Complete history & neurological examination –rule out any other ass. Injury and see for local bruising, tenderness and deformity of spine
Shift to radiology
High Dose Methylprednisolone (MP) Therapy for Acute Spinal Cord Injury
MP acts through microvascular and neuroprotective effects
Inhibition of post-traumatic lipid peroxidation appears to be the principal neuroprotective mechanism
Glucocorticoid receptor-mediated anti-inflammatory effects play only a minor role in comparison to lipid antioxidant effects
Early treatment is required since lipid peroxidation
develops rapidly and is irreversible
Indication and duration of treatmentFor acute non-penetrating SCI (<3 hours
after injury), MP should be given for 24 hours
For acute non-penetrating SCI (after 3 hours, within 8 hours), MP should be given for 48 hrs
For acute non-penetrating SCI (>8 hours after injury), MP should not be used.
For acute penetrating SCI, MP is not recommended
Recommended Dosage and Administration for Acute Spinal Cord Injury
STEP ONE: Initial bolus:30 mg/kg of body weightgiven over 15 mins. (45
mins pause)
STEP TWO: 23-hour infusion:5.4 mg/kg/hour of body
weight
Investigations
X-ray spine – AP and lateral views of suspected injured areas of spine.
X-ray chestX-ray abdomen/ultrasonographyC.T is done only when MRI is not available.MRI is mainstay of further treatment
Definitive management
Occipital condyle fractures
I. Hard cervical collar or cervicothoracic brace for 6-8 wks.
II. Halo vest for 12 wks.
III. Posterior occipital to C2 arthrodesis or Bohlman wire technique and posterior occipital cervical fusion wit atlanto-occipital reconstruction plate.
Hard cervical collar Cervicothoracic brace
Halo vest
Atlanto-occipital dislocationsI. Cervical traction + decompression +
halo vest
Internal fixationII. Cervical traction
is contraindicated
III. Same as I
Atlas fractures (C1)A. Cervical
orthotic device for 8-12 wks
B. Same as AC. Halo vest D. Collar
immobilization
Axis fractures (C2)I. Cervical collarII. Halo vest for
12 wks. In case of unstable #, posterior C1-C2 fusion with atlanto axial wiring or transarticular screw fixation.
III. Halo vest for 12 wks
Traumatic spondylolisthesisI. Cervical collarII. Reduction + halo vestIII. Same as II
Subaxial Fractures Compression # - cervical collar Burst # - operative fixation or halo vestTeardrop # - halo vest or anterior
decompression and plating + a posterior procedure
Unilateral facet dislocation – closed reduction with cervical traction + halo vest or open reduction followed by fixation.
Bilateral facet dislocation – same as aboveHyperextension injuries – surgical stabilizationClay Shoveler’s # - cervical collar
SCIWORASpinal cord injury without radiographic
abnormality Most common in 1 – 16 yrs.24 hours of steroids given although no hard
data exists Treatment: Bedrest, C-Collar until normal
flex/ext, halo vest for 1-3wks, discontinue if flex/ext X-rays normal at 3 months
No sport participation for 3 monthss
Compression #Universal
segmental fixation system or Harrington distraction rod system
Thoracolumbar orthosis for 3 mths
Surgical stabilization
Occipito-Cervico-Thoracic Spinal Fixation System
Burst #Universal segmental
fixation system or Harrington distraction rod system
Thoracolumbar orthosis for 3 mths
Anterior decompression and fusion
Laminectomy
Seat belt type injuries Osseous injuries – bracing devicesLigamentous injuries – posterior fusion and
compressive instrumentation
Fracture dislocations Posterior
fixation and fusion and decompression (if needed)
Bed rest for 6-10 wks
PreventionPrevention education -
SchoolsUniversity sports centreDriving schools
Collaboration work – with state deptt.with law enforsement agencies
Epidemiological studiesTechnical maintainanceSafety equipments (driving,work,sports)
Complications and mx Respiratory -regular chest physiotherapy,
regular monitoring of SPO2, vital capacity, Arterial blood gases(ABG)----Tracheostomy & Ventilatory support ,if required .
Urological – bladder drainage facilitated by intermittent or indwelling catheterization and avoid UTI
GIT- SCI is accompanied by paralytic ileus-so IVF for first 48 hrs and avoid acute peptic ulceration by giving antacids.
Skin & Pressure areas- turn the pt every 2 hrly to prevent pressure sores and nursing care requires use of pillows to separate limbs, maintain alignment of spine and prevent contractures.
Cx spine--- neck rolls---maintain Cx lordosis D/L spine--- pillow----maintain lumber
lordosis Foot drop---vertical pillow—prevent
equinous contracture Thrombo- Embolism- regular limb
physiotherapy,stockings and heparin therapy. Joints & Limbs —joints movement prevent
stiffness & contractures. Use splints to keep tetraplegic pt in functional position
Mulitidisciplinary approach to neurological rehabilitationMedical personnelRehabilitation nursePhysiotherapistOccupational therapistSpeech and language
therapistSocial workersDieticiansClinical psychologists
THANK YOU