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