Primary Management of Spinal Cord Injury

Dr. Soma Cham
Associate Professor, Anaesthesiology
Trauma Care Centre, GMC, Nagpur
Hon. Secretary, ISA Nagpur

Introduction: Spinal cord injury is the most common devastating and disabling injury after head injury. The anaesthesiologist plays a crucial role in resuscitation, intensive care and in rehabilitative surgeries in such patients. An apt primary management can go a long way to decrease the mortality and disability.

A spinal cord injury (SCI) is defined as damage to the spinal cord caused by an insult resulting in the transient or permanent loss of usual spinal motor, sensory, and autonomic function. In India, though there is no proper epidemiological study, it is estimated that the incidence is 2 per lakh population and the main mode of injury is fall from height which could be due to fall from un-protected terrace, tree, electricity pole, well, overloaded bullock carts / tractors / buses / trucks / trains / other vehicle, construction site etc. Road traffic accidents are the second most common mode of injury and are on the increase.

Notably, most injuries do not completely sever the spinal cord.1 Four main characteristic mechanisms of primary injury have been identified that include: (1) Impact plus persistent compression; (2) Impact alone with transient compression; (3) Distraction; (4) Laceration/transection .2 The most common form of primary injury is impact plus persistent compression, which typically occurs through burst fractures with bone fragments compressing the spinal cord or through fracture-dislocation injuries, causing either damage to the cord via direct cord compression or via impairment to the vascular supply.


SCI develops in two stages – initial or primary injury, and later, secondary injury. Primary injury occurs at the time of the traumatic insult. Secondary injury begins within minutes following the initial injury and can evolve over several hours. Mechanisms include vascular damage, ionic imbalance, neurotransmitter accumulation (excitotoxicity), free radical formation, calcium influx, lipid peroxidation, inflammation, ischemia, hypoxia, inflammation and apoptosis of neurons. This underlying pathological process results in further cord edema and it reaches its maximum between 4 and 6 days after the injury.3 As the injury progresses, the sub-acute phase of injury begins which involves apoptosis, demyelination of surviving axons, Wallerian degeneration, axonal dieback, matrix remodeling, and evolution of a glial scar around the injury site. Further changes occur in the chronic phase of injury including the formation of a cystic cavity, progressive axonal die-back, and maturation of the glial scar.4

Neurological Outcomes of Spinal Cord Injury

In clinical management of SCI, neurological outcomes are generally determined at 72 h after injury using ASIA scoring system. This time-point has shown to provide a more precise assessment of neurological impairments after SCI. 5 One important predictor of functional recovery is to determine whether the injury was incomplete or complete. As time passes, SCI patients experience some spontaneous recovery of motor and sensory functions. Most of the functional recovery occurs during the first 3 months and in most cases reaches a plateau by 9 months after injury. However, additional recovery may occur up to 12–18 months post-injury. Long term outcomes of SCI are closely related to the level of the injury, the severity of the primary injury and progression of secondary injury.6

The validity and reproducibility of ASIA system combined with its accuracy in prediction of patients’ outcome have made it the most accepted and reliable clinical scoring system utilized for neurological classification of SCI.6

Definitions and clinical syndromes associated with SCI that have been agreed by the International Standards for Neurological and Functional Classification of SCI (adapted from7). ASIA, American Spinal Injury Association.

ASIA impairment scale (modified from the Frankel Classification):


No sensory or motor function is preserved in the sacral segments S4–S5 (45%


Preservation of sensory but not motor function below the neurological level and includes the sacral segments S4–S5 (15%) 


Preservation of motor function below the neurological level. More than half of key muscles below the neurological level have a muscle grade of <3 (10%


Preservation of motor function below the neurological level. More than half of key muscles below the neurological level have a muscle grade of ≥3 (30%


Sensory and motor function is normal 

Neurological Classification:


This is attributable to a lesion or injury within the cervical spinal cord. There is incomplete or complete loss of motor (sensory function in the arms, the torso, pelvic organs, and the legs) 


This is attributable to a lesion or injury within the thoracic, lumbar, or sacral spinal cord. There is incomplete or complete loss of motor (sensory function of the torso, pelvic organs, and the legs). The level of injury will affect which of these are affected. Arm function is preserved 

Anterior spinal artery syndrome

The anterior spinal artery runs as a single artery anterior to the cord and supplies the anterior 2/3 of the cord. Transection therefore produces sparing of the dorsal columns, resulting in paralysis and loss of pain and temperature with preservation of proprioception, fine touch and vibration 

Brown-Séquard syndrome

This is caused by lateral cord damage. It may occur because of osteophyte impaction on half of the cord producing sensorimotor damage at the level of the injury. There is ipsilateral loss of motor function, fine touch, proprioception and vibration and contralateral loss of pain and temperature below this level 

Cauda equina syndrome

Bladder and bowel dysfunction associated with upper motor neurone symptoms and signs in the legs caused by injury to the lumbosacral nerve roots 

Central cord syndrome

Results from bleeding, infarction or oedema to the central grey matter of the spinal cord. This is most common in the cervical region where it presents as upper motor neurone signs in the legs and mixed upper and lower motor signs in the arms with loss of pain and temperature sensation in the arms. Sacral nerve fibres are positioned laterally in the cord and the patient may demonstrate sacral sparing of sensation. This indicates incomplete cord damage & therefore offers a theoretical chance of some recovery of the cord 

Posterior cord syndrome

Produces loss of vibration and proprioception. This is associated with damage to the posterior spinal artery and is very rare 

Management: The anaesthesiologists plays the most important role be it initial airway management, resuscitation in the Emergency Unit / Intensive care Unit or in the Operation Room for spine surgeries or other surgeries in a patient with SCI.

Initial management: The basic principles of BLS, CAB (Circulation, Airway & Breathing) should be followed. SCI in polytrauma is common (30%) and needs to be considered. Spinal immobilization is indicated if a patient has sustained an injury with a mechanism compatible with spinal damage. Any patient with spinal pain or tenderness, neurologic deficit, depressed level of consciousness, drug or alcohol intoxication, or a painful distracting injury should be immobilized at the scene and transferred to hospital with a cervical collar for neck immobilization, lateral supports and straps, and spinal hardboard.

Airway Management: Airway management of the patient with known or suspected traumatic SCI can be categorized either as an emergent management of respiratory failure or airway protection as part of Advanced Trauma Life Support (ATLS) algorithm, to maintain oxygenation and prevent hypoxia (leading to secondary SCI) or the perioperative management of the patient with known cervical injury for his/her spinal or other associated injuries.

Cervical SCI occurs in up to 10% of head injured patients. Techniques to minimize cervical movement should be employed during emergent management of the airway in such patients & in patients with high thoracic while considerations should be given to other potential injuries. Associated facial or head injuries, retropharyngeal hematoma, edema, presence of cervical collar, makes airway management difficult. Care should also be taken with mask ventilation, as it may cause significant cervical spine movement. The use of oral and nasophayngeal airway with the neck in neutral position and the absolute minimum of jaw thrust and chin lift should be used to maintain the patient’s airway during mask ventilation.

MILS (Manual in-line stabilization): The goal of MILS is to apply sufficient opposite forces to the head and neck to limit the movement during airway intervention. MILS is recommended by current ATLS guidelines as a standard for airway intervention in patients with known or suspected cervical injury. An assistant grasps the mastoid process with finger tips with the occiput in the palms of the hands, standing at the head of the table beside the intuiting anaesthetist or alternatively may stand at beside the patient, facing the intubating anaesthetist, holding the mastoid with his palms and occiput with finger tips. The assistant should apply enough forces to counter the force of laryngoscopy to keep the head and neck in the neutral position without applying traction. Too much traction should be avoided as there may be a risk of excess spinal distraction.3,8

MILS reduces cervical movement better than a rigid collar during laryngoscopy. Also, an improved view is obtained at laryngoscopy with MILS compared to a hard collar, owing to better mouth opening. However, it worsens the view of the glottis compared to conventional uncomplicated visualization and prolongs intubation time and increases the chance of failed intubation. The application of cricoid pressure as a part of RSI (Rapid Sequence Intubation) and also to improve the success of intubation with MILS may cause increased distraction, angulation and translation in cervical spine injury leading to worsening of the neurological deficit.8 Applying cricoid pressure with the posterior part of the hard collar still in place (with MILS) with the assistant’s second hand supporting the posterior part of the hard collar may further decrease cervical movement as this does not necessitate removing the whole collar. The hard collar and head blocks should be replaced after intubation.9 Direct laryngoscopy with MILS is the most common used technique in for emergency intubation in patients with cervical SCI (recommended by ATLS and familiarity of procedure) and, will cause movement of cervical spine, though the degree of movement is unknown.

Awake intubation can be preferred in co-operative patients. It has the advantage of maintenance of head and neck in neutral position, maintenance of spontaneous breathing in a difficult airway, enables a neurological exam to be performed after intubation and positioning for surgery; however, it requires a cooperative patient. Coughing and gagging may aggravate the injury to the spine. Presence of blood, vomitus or secretions may make awake intubation difficult.  Awake intubation may warrant sedation for smooth intubation, which can lead to hypoxia and hypercarbia causing haemodynamic instability especially in cervical SCI.

Rigid indirect videolaryngoscopy with MILS has become an alternative to conventional direct laryngoscopy.  Intubation can be accomplished without direct visualization of glottis and without the need of cervical spine movement. Wherever feasible, videolaryngoscopy should be the method of intubation.

 Awake intubation using a flexible fiberoptic or flexible videoscope is best option causing little motion of the cervical spine and an awake patient, however, it is time consumable and has a high failure rate in in-experienced hands. Inadequate local anaesthesia can cause coughing and presence of blood, vomitus or secretions can obscure visualization of laryngeal structures and glottis.

Supraglottic airway (SGA) devices cause cervical movement and exert pressure on the cervical spine during insertion, inflation and removal. Moreover, considering full stomach, SGA should not be used as primary airway device. But, it can be always used as a part of difficult airway algorithm when needed. In the “can’t intubate, can’t ventilate” scenario, early consideration should be given to the surgical airway or cricothyroidotomy.  These techniques may still produce critical movement of the cervical spine, but this should not prevent their use for life-saving procedures.10

No technique is shown to be superior to others than to prevent neurological deterioration during managing patients with unstable cervical spine. The clinical scenario, patient factors, availability of instruments & expertise of the anaesthesiologist should determine the airway plan.

Breathing: The effect on breathing is dependent on the site of injury. Cord injury above T1 removes intercostal function and respiration will be entirely diaphragmatic. Lesions involving the phrenic nerves (C3–5) will impair diaphragmatic function and if the damage is above C3 the patient will be permanently ventilator dependant unless there is partial recovery of the cord.

Level of injury and effect on respiratory function:11

Level of injury

Nerve denervation

VC (% of normal)

Effect on cough

Need for ventilation

Above C3

Loss of phrenic nerves. Total diaphragmatic paralysis if bilateral C3 injury 



Immediate and long-term ventilation 

Between C3–C5

Partial phrenic nerve denervation/ weakness/ paralysis of diaphragm 


Weak/ ineffective

Ventilation required in 80% within 48 h. Older patients may need long-term ventilation. Role of non-invasive ventilation in weaning 

Above T8

Loss of inspiratory intercostal muscles/abdominal muscles 


Normal to weak cough

Short-term ventilation sometimes required because of impaired sputum clearance. If respiratory co-morbidities, may occasionally still need long-term support 

Below T8

Loss of abdominal muscles & lower expiratory intercostals forced cough may be weak especially in older patients 


Normal to weak cough

Short-term ventilation occasionally required because of weak cough and impaired sputum clearance 

Vital capacity (VC) is increased in the supine position as abdominal wall paralysis permits greater displacement of abdominal contents during caudad diaphragmatic excursion. Patients will benefit from being recovered in the supine position. Lung volumes are altered and patients with cervical SCI exhibit a restrictive ventilatory deficit with reduced forced vital capacity and forced expiratory volume in 1 s values. Expiratory reserve volume, total lung capacity, and functional residual capacity are also reduced and correlate with the level and completeness of the lesion.12 Cervical lesions also result in reduced lung and chest wall compliance because of intercostal muscle spasticity and blunted responses to hypercapnia & there is an increased risk of sleep apnoea.

Sympathectomy in injuries above T6 result in bronchospasm, increased pulmonary secretions, ineffective cough leading to mucus plugging, obstruction, pneumonia, increased work of breathing & ventilation failure. Associated direct trauma can cause flail chest, rib fractures, diaphragmatic rupture, pulmonary contusions, lacerations, haemothorax which can complicate the respiratory system further.

Ventilatory support:

Around a fifth of patients with cervical SCI patients require a tracheostomy. This is commonly necessary for prolonged mechanical ventilation resulting from respiratory muscle fatigue, impaired secretion clearance, and respiratory complications such as pneumonia and atelectasis.

Cardiovascular system management:

Hypotension: Traumatic SCI is frequently complicated by systemic hypotension and reduced spinal cord perfusion pressure (SCPP). Systemic hypotension most commonly results either from hemorrhage due to associated traumatic injuries (chest, intra-abdominal, retroperitoneal, pelvic or long bone fractures) or neurogenic shock, or a combination of both.13

Neurogenic shock refers to the hypotension and inadequate tissue perfusion as a result of vasodilatation and loss of central supraspinal sympathetic control. It is more common after cervical SCI due to involvement of cardiac sympathetics (T2–5) resulting in a decrease in systemic vascular resistance, decreased inotropism and is usually associated with bradycardia from unopposed vagal tone.14

Spinal shock is the loss of reflexes below the level of SCI resulting in the clinical signs of flaccid areflexia and is usually combined with hypotension of neurogenic shock. There is a gradual return of reflex activity when the reflex arcs below redevelop, often resulting in spasticity, and autonomic hyperreflexia. This is a complex process and a recent four-phase classification to spinal shock has been postulated: areflexia (Days 0–1), initial reflex return (Days 1–3), early hyperreflexia (Days 4–28), and late hyperreflexia (1–12 months).15

American Association of Neurological Surgeons (AANS) published recommendations for the hemodynamic goals for a SCI patient. These include maintaining MAP to 85–90 mmHg and avoiding SBP less than 90 mmHg (Class 3 evidence) for over 5–7 days. Injuries at cervical and upper thoracic levels down to T6 warrant an agent with inotropic, chronotropic as well as vasoconstrictive properties. Agents such as dopamine, norepinephrine, or epinephrine fulfil these requirements with their α1- and β1-agonist properties.11 Phenylephrine preferentially works as an α1-receptor agonist with minimal β1 effects. It can be used to counteract the peripheral vasodilation associated with lower thoracic and lumbar cord injuries. Caution is warranted with its use due to the potential for developing reflex bradycardia. Dobutamine exerts its effect prominently as an inotropic agent and its use in SCI is limited because of its effect on vasodilation and possible reflex bradycardia.16  

Arrythmias: Bradyarrythmias (Persistent bradycardia, Heart blocks) may be seen in high cervical (C1 through C5) lesions in the first 2 weeks after traumatic SCI and requires the use of anticholinergic agents or application of pacemakers. These parameters should be maintained throughout the perioperative period and will require judicious use of intravenous fluids, vasopressors and inotropes. This is usually temporary, mostly resolving within 5 weeks from injury.

Neuroprotection:  Avoiding hypoxia, hypotension and hypercarbia should be the goals. High-dose methylprednisolone steroid therapy (bolus 30mg/kg over 15 minutes, with maintenance infusion of 5.4 mg/kg per hour infused for 23 hours) is the recommended pharmacologic therapy shown to have modest efficacy when administered within eight hours of injury. Benefit can be achieved by extending the maintenance dose from 24 to 48 hours, if start of treatment is delayed to between three and eight hours after injury.19

Thromboprophylaxis:  A high risk of pulmonary embolism exists because of immobility and increased thrombogenicity secondary to trauma. Fatal pulmonary embolus occurs in 3% of SCI patients and rates of deep vein thrombosis and non-fatal PE are 90 and 10%, respectively. The use of anticoagulants should be restricted in the first 48–72 h because of risk of bleeding around the cord and intermittent calf compression devices or graduated compression stockings should be used instead. Standard prophylactic low molecular weight heparin should be started after 72 h.9 IVC filters should be considered if pharmacological thromboprophylaxis is contraindicated.

Acid & ulcer prophylaxis: Unopposed vagal activity increases gastric acid and therefore rates of peptic ulceration. Unopposed vagal activity may also lead to a gastroparesis. Feeding patients with high cord lesions may lead to nausea, vomiting, risk of aspiration, and abdominal distension, and also further impairing respiration. Gastro-duodenal haemorrhage may occur as a result of Curling’s ulcer due to sympathetic stress and Cushing’s ulcer due to raised ICP as in TBI (above mid-thoracic SCI). A routine use of prophylactic H2 antagonists or proton-pump inhibitors for at least 6 weeks is advocated. Early enteral feeding decreases mortality in polytrauma patients.

Other considerations:

Pressure sores are devastating for cord-injured patients leading to prolonged immobilization or severe sepsis. These usually develop quickly within the first few days after admission to hospital and are a result of immobility, poor perfusion of the skin, hypoxia, and leaving patients on spinal boards. Appropriate mattresses and good nursing care are essential to reduce pressure sores and early spinal fixation will allow earlier mobilization.

Hypothermia: Sympathectomy and vasodilatation of skeletal muscle beds will cause heat loss below the level of injury. Neurogenic shock patients will have warm extremities and with central hypothermia. Core body temperature monitoring & adequate warming is necessary. In concurrent TBI hyperthermia due to overwarming should be avoided.

Electrolyte imbalance as hyponatraemia is common due to disruption of the renal sympathetic pathways leading to dysregulation of the renin angiostensin system. There may be impaired glucose tolerance due to steroid administration and traumatic stress response adding to pre-existing diabetes mellitus.8

Conclusion: The role of an anaesthetist, intensivist in the primary management of SCI is very important in such patients. Good Quality treatment & timely intervention can not only decrease mortality but morbidity. Quick overview, rigorous management with proper use of available facilities contribute to the efforts.


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