Spinal Cord Injury 1

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Spinal cord injury
Dr. R. Muthu Kumar

Definition


SCI (spinal cord injury ) defined as disruption of the normal spinal cord anatomy with neurological deficit may be traumatic or non - traumatic

Epidemiology


More common in males (80%) average age 31.4 years 10000 cases reported per year 2.25 to 2.28 lakh people in US are living with paralysis Most commonly injured regions Cervical 4 to 6 (51%) and thorocolumbar T12 to L1(34%)









Fourth leading cause of death next to IHD, cancer and CVA Annual cost in for caring these patients was 7.73 billion $



Etiology


Motor vehicle accidents (40-56%) Falls (20-25%) Recreational and sports (10-15%) Violence eg -gun shot wounds (10-15%) Other causes ( work related) [10-15%]









Frequency of SCI according to level of injury
Level of injury
Cervical spine C 4-6 Thoracic spine Thorocolumbar T 12 to L2 lumbosacral Sacral Multiple levels Associated head injury (mild) severe

Frequency in %
50-55 10-15 15 -20 10 < 10 20 40 -50 2-3

Pathophysiology


Primary SCI


Caused by mechanical forces Direct neuronal disruption, petechial hemorrhages, hematomyelia, vasospasm and ischemia





Histologically extravasations of proteins into central grey horn Cord edema leading to necrosis and scar formation



Pathophysiology


Secondary SCI


Complex cascade of events (biochemical, enzymatic and micro vascular)



Release of cytokinins and AA generates inflammatory cascade Leading to free radical formation, cellular edema and cellular apoptosis





Loss of vascular auto regulation Compounded by hypoxia, hypotension, and local cord edema causing destruction of axons



Anatomical correlates


Flexion injuries causes anterior column and vertebral injury Hyperextension mostly whiplash and posterior column Vertical compression burst # and ligamentous rupture Rotational facetal and peduncle # Combined Stable or unstable potential for further injury and failure to heal











Mechanistic classification of cervical spinal injuries

Allen and colleagues

Clinical presentation of SCI
Clinical syndromes


Key clinical features
Arm weakness in disproportion to legs Sparing vibratory and position senses Loss of fine vibration and positional senses Ipsilateral motor & touch and , contra lateral pain and temperature loss Flaccid areflexic parperesis or paraplegia

Central cord syndrome Anterior cord syndrome Posterior cord syndrome Brown -sequard syndrome Cauda equina syndrome











Conus medularis syndrome Deep tendon reflexes preserved. Areflexic bladder, bowel, legs Complete cord transection Complete loss of autonomic, sensory, and motor functions below



General measures in acute SCI patients


airway breathing circulation immobilization transportation

Careful oxygenation with attention to spine mobility Nasotracheal intubation and avoidance of neck extension Volume and vasopressors as needed Hard collars with block , sand bags and strapping Immediate transport to SCI centers < 4 hrs ASIA score









Clinical examination Radiological examination


X rays (5 views) CT and MRI

Immobilization and transportation
  

Moved by log roll technique Soft collars- 96% flexion, 73% extension & full lateral rotation Rigid collars ± (Philadelphia collar) 2 pieces- 30% flexion & extension and 45% lateral rotation

  

Easy to remove during intubation, easy to fix without lifting the head Sandbags and tapes -flexion & lateral rotation 5% , extension 35% Tong and Halo permits 4% flexion, 1% rotation and no extension So intubation is only fibroptic

Immobilization


A, Soft cervical collar B, Philadelphia-type reinforced cervical collar





C, halo brace.

Comprehensive neurological examination
    

Should be quick and efficient Assess consciousness and orientation Motor system assessment (grade 0-5) & Deep tendon reflexes Cerebellar function & cranial nerves examination in head injury Sensory system- light touch, pin prick, temperature, proprioception and vibration



Perirectal sensation , bulbo cavernous or anal cutaneous reflex {sacral sparing} favorable prognosis

Comprehensive neurological examination
Classification


Explanation
No motor or sensory function preserved in sacral segments Only sensory function is preserved below the neurological level including sacral segments Motor function preserved below the lesion & 50% and more of muscles have > grade 3 strength Motor function preserved below the lesion & less than 50% of muscles have > grade 3 strength Motor and sensory normal

Complete ASIA (A) Incomplete ASIA (B) incomplete ASIA (C) Incomplete ASIA (D)









Normal ASIA (E)

Radiological evaluation


Five views of cervical spine X ray ( visualized till C7)
    

Lateral - misses about 15 to 20% of CS # oblique Antero posterior Open mouth odontoid views Flexion & extension 93% sensitivity

Radiological evaluation


15 -20 % have to be evaluated with CT and MRI to rule out whiplash and ligamentous injury

  

SCIWORET- without radiological evidence SCIWBA- without bony injury (children) Widening of paravertibral space indicates unstable spine and airway problems

Radiological evaluation
  

  

1-anterior vertebral border 2-posterior margins 3-jn between lamina and spinous processes 4-Tips of spinous process 2 & 3 ± borders of spinal canal Lardotic alignment on 4 anatomical lines

Airway management
    

Urgency of airway intervention Associated facial, neck and soft tissue injuries Basilar skull fractures Awake or unconscious patient Skill of the operator

Airway management
   

Intubation worsens C ±spine injuries polytrauma are considered to have C spine injury unless proved Jaw thrust causes 5mm widening of disc space (aprahamain et al) Single handed Cricoid pressure causes 9 mm posterior displacement (Gabbot A .D et al )

 

No evidence to prove the efficiency of posterior support I-LMA and LMA causes posterior displacement @ C2-3
Wood P.R et al

Airway management
     

MILS reduces neck movement during intubation Axial traction causes subluxation and distortion Laryngoscopy (curved/straight) 3-4 mm widening @ C5-6 Maximal extension @ C1-2 & occipito-attlantal joint Bullard and glide-scope reduces movement @C2-5 <50% Blind nasal intubation -2 to 5mm subluxation @ C5-6
Hastings R.H et al

Blind nasal intubation
Advantages Minimal head movement Disadvantages Trauma to nasal passage and infections Can be done in spontaneously Longer time breathing Contraindicated in basal skull # and facial injury Needs expertise

Awake fibroptic
Advantages Least neck movement Patient need not be anesthetized and breathing spontaneous Disadvantages Need expertise only in non emergency Airway free of blood and aspirate only in non emergent situations Patient should be cooperative

Summary of airway control


There is no evidence that any particular airway management technique is either safe or dangerous in a patient with an unstable cervical Several retrospective studies have failed to demonstrate a higher incidence of neurologic injury in patients with cervical instability after trauma associated with intubation





The method for definitive airway control should be based primarily on the operator¶s skill and experience rather than on the fear of inflicting cervical cord damage
Cotrell and Young

Medical management of SCI


Cardiovascular system


Intense SNS activity immediately after injury Can cause MI, pulmonary edema, raised ICP Spinal shock ± 4 phases Hypo reflexive / flaccid paralysis / loss of DTR- 24 hrs Denervation super sensitivity ± return of initial reflexes Initial hyper reflexia after a week ± axonal growth Final hyper reflexia after a month of phase 3 ± soma growth





1. 2. 3. 4.

Cardiovascular system


Spinal shock ( neurogenic shock)- phase 1


Loss of SNS more with lesions above T6 Hypotension, vasodilatation, ventricular dysfunction and dysrhythmias Unopposed vagal tone with loss of T2 ±T5 fibers Reflex bradycardia and asystole during airway manipulation Relative tachycardia indicates hypovolumia











Treatment
  

Isotonic fluids and vasopressors to maintain cord perfusion PA catheter / CVP guided volume loading to prevent PE Atropine and even TPI for severe bradycardia

Autonomic dysreflexia (ADR)
      

Occurs in 85% with SCI > T6 usually 1-3 weeks after injury Uninterrupted sympathetic over discharge in response to stimuli Increase in BP > 250/>150 ( 20mmhg > baseline) Bradycardia , throbbing occipital or bi-frontal headache sweating, pallor, flushing above the lesion Spasticity and muscle rigidity below the lesion Triggering factor occur usually below the level of lesion ( bladder, bowel, uterus, rectal, lower limb)

Autonomic dysreflexia (ADR)


Treatment ( medical emergency)


Remove the trigger Upright position Close monitoring of BP and HR Nefidepine, nitrates, SNP, ganglion blockers Urinary retention & fecal impaction should be relieved Manipulations done under anesthesia Can lead to seizures, MI, ICH if not treated aggressively













Respiratory system
    

monitored close as most common cause of morbidity and mortality Respiratory rate, O2 saturation, vital capacity recorded CXR obtained; ABG for CO2 levels C 1-3 level injury patient in apneic and intubation instantaneously Intubation criteria
    

VC < 15 ml/kg ( PaCO2 >50 mmhg) RR > 35 breaths /min Fall in SpO2 (PaO2 < 60mmhg) Negative inspiratory force < 20 cmH2O Pulmonary edema, aspiration

Respiratory system


Most frequent respiratory complications
   

Atelectasis Pneumonia Pulmonary edema Respiratory failure



Treatment & prevention
    

Aggressive pulmonary toileting IPPV Intrapulmonary percussion Cough stimulation Postural drainage



Early tracheostomy

Genitourinary system
  

Acute SCI causes atonic bladder , intermittent catheterization Ach like oxybutin or propantheline added to lower the pressure Complications
   

UTI Pyelonephritis Nephrolithiasis Renal failure



Chronic bacteruria leads to urosepsis prevented by
  

Good hydration Chronic low dose antibiotic Intravesical instillation



Surgical options

Gastrointestinal system
    

GERD , delayed gastric emptying, Increased transit time , severe constipation Abdominal distension & hemorrhoids Ileus ( complete lesions) Treatment
    

Adequate diet and fluid intake Fibre diet and stool softener Contact irritants and prokinetic agents Ryles tube Hypo Cl- metabolic alkalosis due to gastric suctioning

DVT prophylaxis
  

Incidence of 60% even with prophylaxis Included as a part of therapeutic regimen from admission Combination is better than either alone


Low dose UF heparin or LMWH if no contraindication Sequential compression devices ( SCD) Gradient elastic stockings





 

Continued for 3 months and during rehabilitation INR of 2 -3 to be maintained

Temperature & pressure sore control
       

Loss of thermoregulatory ability below the level of lesion Injury > T6 become poikilothermic (temp of surroundings) Arrhythmias common Delayed awakening during anesthesia Temperature monitoring and warming efforts needed Skin care and treatment of pressure sores is vital Prevention is better Surgical modalities of treatment

Neuro protective strategies
  

Spine immobilisation Surgical decompression Physiological therapy


Avoid hyperthermia, hypotension, hyperglycemia



Pharmacological therapy
   

NASCIS- II inj MP 30 mg/kg for 15 min followed by 5.4 mg/kg /hr for 23 hrs Treatment started within 8 hrs of injury had significant improvement NASCIS ±III ; 24 hr regimen for patients < 3 hrs of injury Continued for 48 hrs for patients presenting 3 -8 hrs



Use of high dose steroids remain controversial

Anesthesia for SCI patients

Preoperative evaluation
   

Multiple medical complications Airway evaluation Neurologic evaluation Counseling about awake intubation and wake up test

Investigations
      

Complete blood count Renal function LFT Electrolytes ECG ,CXR ABG PFT if needed

Premedication
   

Minimal sedation Anti-sialogogue Prokinetic for gastric emptying DVT prophylaxis if not contrandicated

Intraoperative monitoring
      

Invasive arterial BP in shock patients NIBP CVP or PA catheter for monitoring volume status SpO2, ECG, ETCO2, temperature SSEP ICP monitoring if head injury is associated Urinary catheter

Induction agent
     

Induced after securing the airway in lesion < C6 Nerve block preferred over sedation for awake intubation Sometimes positioned before anesthesia or paralysis Flexometallic armored tube fixed and secured Ketamine is the drug of choice in spinal shock Avoid scoline if injury < 24 hrs ( hyperkalemia)

Positioning
      

Head and neck in neutral position Adequate padding at pressure points ( eyes, nose, extremities) Avoid excessive neck extension and flexion Avoid sudden change of position Pressure points changed every 15 minutes under anesthesia Abdomen free of compression Prevent peripheral nerve injuries , blindness, pressure necrosis

Positioning
    

A, Kneeling prone B, Wilson Frame Pad C, Georgia prone; D, Relton - Hall frame E, Seated prone.

Fluid management
    

Preoperative deficit and intra-operative loss replaced Cardiopulmonary status of high cervical lesion High propensity for pulmonary edema with < T6 Avoid glucose containing solutions( RBS <150mg%) Crystalloid VS colloid debatable

Temperature management
   

Warm blankets and warm enviroment Humidification of gases Warm fluids Avoid hyperthermia

Postoperative care
 Extubation
       

Cautious in deciding in high cervical and thoracic injuries Patients with preoperative pulmonary impairment Metabolic derangement and persistent muscle weakness Excessive facial or pharyngeal edema in prolong surgery Cuff leak test to confirm reduction of edema Ability to generate cough Minimal secretion and stable cardiac function Absence of pulmonary infection

Postoperative care


Analgesia
       

Intermittent iv or im opioid Continuous infusion of low dose opioids PCA ; epidural and intravenous with opioid PCEA with opioid +LA or only LA Intercostal nerve block Paravertibral blocks Wound infiltration Non-opioid analgesics

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