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REVIEW ARTICLE
Year : 2008  |  Volume : 52  |  Issue : 1  |  Page : 13 Table of Contents     

Anaesthetic and Intensive Care Management of Traumatic Cervical Spine Injury


Professor of Neuroanaesthesia, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore 560 029., India

Date of Acceptance07-Jan-2007
Date of Web Publication19-Mar-2010

Correspondence Address:
G S Umamaheswara Rao
Professor of Neuroanaesthesia, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, 560020.
India
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Source of Support: None, Conflict of Interest: None


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Trauma to the cervical spine may have devastating consequences. Timely interventions are essential to prevent avoidable neurological deterioration. In the initial stabilization of patients with acute cervical spine injuries, physiological disturbances, especially those involving cardiac and respiratory function require careful attention. Early surgery, which facilitates rapid mobi­lization of the patient, is fraught with important management considerations in the intraopoerative period and the subsequent critical care. Airway management poses a crucial challenge at this stage. Those patients who survive the injury with quadriplegia or quadriparesis may present themselves for incidental surgical procedures. Chronic systemic manifestations in these patients require attention in providing anaesthesia and postoperative care at this stage. The current review provides an insight into the physiological disturbances and the management issues in both acute and chronic phases of traumatic cervical spine injury.

Keywords: Quadriplegia, Trauma, Cervical spine, Anaesthesia, Intensive care


How to cite this article:
Umamaheswara Rao G S. Anaesthetic and Intensive Care Management of Traumatic Cervical Spine Injury. Indian J Anaesth 2008;52:13

How to cite this URL:
Umamaheswara Rao G S. Anaesthetic and Intensive Care Management of Traumatic Cervical Spine Injury. Indian J Anaesth [serial online] 2008 [cited 2019 Nov 18];52:13. Available from: http://www.ijaweb.org/text.asp?2008/52/1/13/60593


   Introduction Top


Cervical spinal injuries occur in 2-5% of blunt trauma. In 7-14% of cases, these lesions are unstable. In a study of 34,069 patients of blunt trauma [1] , 818 pa­tients sustained 1193 fractures and 231 subluxations of cervical spine. Twenty four percent of them had a fracture at C-2. Dislocations occurred most commonly at C­5/6 and C-6/7 levels. The incidence of missed or de­layed diagnosis of cervical spine lesions was 1-5%. Sec­ondary neurological damage occurs in 10-30% of pa­tients with a missed diagnosis of cervical spine fractures [2] .

The outcome of these injuries depends not only on the primary injury that occurs at the time of accident but also on the meticulousness of management during im­mediate resuscitation, in the perioperative period and the intensive care unit. Attention to the associated multisys­tem sequelae forms the essence of the perioperative and critical care management of these patients. With a significant increase in survival in recent years, there is a possibility of some of the patients of chronic spinal injury presenting for elective surgery. Urological procedures and procedures for treatment of pressure sores are com­mon. Other incidental procedures include abdominal sur­gery, fixation of fractures and electroconvulsive therapy for depression.


   Systemic changes in quadriplegic patients Top



   Respiratory function Top


The degree of respiratory dysfunction caused by respiratory muscle paralysis depends on the level of the spinal lesion. Voluntary respiratory control is possible with lesions below C4 level, albeit, with a vital capacity which is 20-25% of the normal. Injuries above this level neces­sitate mechanical ventilation. Cervical spinal injuries at C6 or below spare diaphragmatic involvement, but may affect intercostal muscles to a varying extent. Involve­ment of the intercostal muscles leads to paradoxical in­ward movement of the upper chest during inspiration. Inadequate expansion of the chest during inspiration and instability of the thoracic cage during expiration lead to poor cough, facilitating retention of secretions. Pulmo­nary infection, pulmonary oedema and pulmonary em­bolism may further impair alveolar ventilation.

With regard to the pulmonary function testing, stud­ies have shown that: (a) forced vital capacity (FVC), forced expiratory volume during the first second (FEV1.0) and inspiratory capacity (IC) increase with descending spinal cord injury (SCI) level up to T10 and (b) former smokers demonstrate significantly lower spiro­metric values compared to nonsmokers [3] .

Body position markedly affects the alveolar venti­lation in a quadriplegic patient. Supine position improves ventilation compared to head-up position [3] . In supine po­sition, descent of the diaphragm during inspiration pushes the abdominal contents downward and the flaccid ab­dominal wall forward. At the end of inspiration, elastic recoil of the abdominal wall along with an upward move­ment of the abdominal contents moves the diaphragm cephalad decreasing the end-expiratory volume of the lungs and allowing for greater descent of the diaphragm during the subsequent inspiration.

Pulmonary oedema and pulmonary embolism may also affect the respiratory function. Pulmonary oedema occurs as result of over-enthusiastic fluid administration to correct spinal shock, in the presence of myocardial depression that is common after spinal cord injury. Pul­monary embolism occurs in 15% of the cervical cord injuries. Most often, it occurs in acute rather than chronic phase.

Patients with lower cervical injury may be able to breathe spontaneously, but involvement of trunk and ab­dominal muscles limits their ability to produce effective cough. A direct relationship has been demonstrated be­tween level of motor deficit and peak expiratory flow during coughing [4] . Airway hyper-responsiveness has been reported in tetraplegic patients, which has been attrib­uted to the unopposed parasympathetic activity.

In patients with spinal injury, both FEV1 and FVC improve with time, secondary to decreased cord oedema, strengthening of accessory muscles of respiration and recovery from spinal shock. Apart from the cord injury, other factors such as associated chest and tracheal inju­ries, gastric atony and dilation, pre-existing lung disease, sedatives / narcotics, atelectasis and pneumonia could affect ventilation in paraplegics during the first few weeks after injury.

Airway considerations and mechanical ventilation

Patients with cervical and upper thoracic injuries may require tracheal intubation and mechanical ventila­tion. Close observation should be maintained in these patients for any indications for endotracheal intubation and mechanical ventilation [Table 1].

The technique of intubation and the choice of an­aesthetic for intubation in these patients depend on a number of variables: the level the lesion, its association with the injuries of the skull base, the cooperation of the patient, the nature of equipment and the expertise avail­able. Orotracheal intubation under thiopentone and suxamethonium combination is recommended in most centers. If this technique is used, hyperkalemic response to suxamethonium should be anticipated from 48 h on­wards. The response is maximal between 4 weeks and 5 months. Provided the patient does not have injuries of the skull base, awake nasotracheal intubation under regional anaesthesia seems to be a good alternative. Un­conscious patients with unstable lesions and cardiovas­cular disturbances may be better managed by fibreoptic intubation, which is least disturbing physiologically. But considerable expertise is required to achieve this in an emergency situation. In a study of 150 patients with spi­nal cord injury [5] 85 patients were intubated under gen­eral anaesthesia and the rest under regional anaesthe­sia. Seventy one percent of all the patients were intu­bated orally and the rest nasally. The results of the study indicated no significant difference in the neurological outcome between the two groups.

Alternatives to endotracheal intubation in case of difficult airway include cricothyroidotomy and percuta­neous or conventional tracheostomy. A recent surgery on the cervical spine through anterior approach is a limi­tation for these procedures. Apart from technical diffi­culties in performing the procedure, proximity of the tra­cheostomy to the operative site may favour infection of the surgical wound.

Respiratory care and mechanical ventilation :A spontaneously breathing patient with cervical cord in­jury essentially has an acute restrictive lung disease. Further loss of lung volume and reduction of functional residual capacity can occur as a result of atelectasis, retention of secretions and pulmonary infection. The use of continuous positive airway pressure CPAP may avert deterioration of the pulmonary function to some extent. If immediate intubation is not necessary, aggressive chest physiotherapy is required to maintain pulmonary func­tion. Incentive spirometry, aerosol therapy, percussion and vibration chest physiotherapy, frequent change of position, humidification of the inspired gases and avoid­ance of anticholinergics are some of the measures to prevent deterioration of the pulmonary function. Blind nasotracheal suctioning may be required to remove re­tained secretions. Care should be taken to prevent life­threatening arrhythmias during these manoeuvres. Bor­derline hypoxia exaggerates the occurrence of such arrhythmias. Therefore, the patient should be adequately oxygenated before attempting suction. During physio­therapy, abdominal push and use of abdominal corset can assist the cough mechanism. In spite of all the phys­iotherapeutic measures if the pulmonary function dete­riorates, endotracheal intubation should not be delayed for emotional reasons. Most patients who show substan­tial improvement in respiratory function are ready for weaning in 2-3 weeks time. The weaning process has to be gradual with progressive loading of the respiratory muscles. Rapid weaning with acute loading of the respi­ratory muscles may not be tolerated well. The risk of aspiration in the immediate post-extubation period should be kept in mind. If the patient requires mechanical ven­tilation even at 4-6 weeks, home-ventilation and diaphrag­matic pacing may be explored.


   Cardiovascular function Top


In experimental animals, arterial hypertension, in­creased pulmonary capillary wedge pressure (PCWP), lowered myocardial contractility, raised ICP and brain oedema were noticed transiently following spinal cord injury [6] . Such a response is not documented in clinical setting. Most often, the patients are hypotensive due to spinal shock when they reach the postoperative ward following early surgery. They may also have bradycar­dia. The degree of hypotension and bradycardia are a function of the level of the injury and the extent of the injury suffered by the spinal cord. In injuries above mid­thoracic level, loss of sympathetic tone forms the basis of hypotension and bradycardia. Tracheal suctioning and change of body position may precipitate bradycardia and supraventricular arrhythmias. These episodes may be treated with vagolytic agents and increased ventilation and oxygenation. These patients may also be at exag­gerated risk of hypotension during positive pressure ven­tilation due to loss of baroreflexes. Hyperventilation may aggravate the myocardial depression that is associated with high spinal injuries. Treatment of hypotension in these patients should comprise of a judicious combination of intravascular volume replacement, inotropes and vaso­pressors. Attempts at restoration of normal blood pressure by excessive volume replacement and/or periph­eral vasoconstrictors could precipitate pulmonary oedema [4] . ST and T wave changes on electrocardiography that mimic myocardial ischemia may be seen in some patients. Vagal stimulation through procedures such as tracheal suction might precipitate bradycardia and asys­tole. The integrity of the sino-aortic baroreceptors, as well as efferent parasympathetic function may be com­promised in otherwise apparently healthy individuals with chronic spinal injuries. Profound hypotension may be caused by positional changes and blood loss.


   Autonomic hyper-reflexia Top


Autonomic hyper-reflexia occurs in 85% of patients with spinal cord lesions above T5. It is seen in about 20% of patients with thoracic lesions. Afferent impulses originating from bowel, bladder, manipulations of urinary tract, child birth or surgical stimulation are transmitted through pelvic, pudendal and hypogastric nerves to the isolated spinal cord and cause massive sympathetic re­sponse from adrenal medulla and sympathetic nervous system which is no longer under the central hypotha­lamic control. Vasoconstriction occurs below the level of the lesion causing hypertension. Baroreceptor reflexes produce bradycardia, heart block, ventricular arrhythmias and even cardiac arrest. Compensatory vasodilation above the level of injury results in headache, flushing and nasal congestion. Some of the serious consequences of autonomic hyperreflexia include retinal, cerebral or subarachnoid haemorrhage. Noradrenaline plays an im­portant role in autonomic hyper-reflexia. Though the lev­els of noradrenaline are lower than the normal levels, the response is much higher suggesting that the patients with spinal cord injury have a higher sensitivity to cat­echolamines. Manipulation of pressure sores, toenails and even sunburn has been reported to trigger autonomic hyperreflexia. Management of autonomic hyperreflexia begins with the removal of the precipitating stimulus. Blocked urinary catheter or impacted faecal matter must be attended to. Positioning the patient upright may pro­duce a desirable fall in blood pressure. Clonidine is help­ful if autonomic hyperreflexia is combined with spasticity. A wide range of vasoactive drugs including direct vasodilators, beta adrenergic blocking agents, beta adr­energic blocking agents in combination with calcium chan­nel blocking agents and ganglion blocking drugs have been used to abort episodes of autonomic hyperreflexia. Sedation or topical anaesthesia does not alter the re­sponse. Deep general anaesthesia and spinal or epidural anaesthesia seem to be effective in preventing its oc­currence intraoperatively and postoperatively.

Schonwald et al reported 11 episodes of autonomic hyperreflexia in 219 surgical procedures in 97 patients with spinal cord injury (80% with lesions above T5) [7] . Two episodes occurred in 9 procedures conducted un­der N2O-narcotic anaesthesia. Tetracaine spinal anaesthesia (97 procedures) and general anaesthesia with halothane (37 procedures) or enflurane (12 procedures) were not associated with autonomic hyperreflexia. One instance each was documented under local anaesthesia, intravenous sedation and lidocaine spinal anaesthesia and two during 'standby' procedures. Four episodes occurred in the recovery room. Two of the episodes occurred in patients with lesions below T5.


   Deep vein thrombosis Top


Deep venous thrombosis (DVT) occurs in the majority of all patients with complete spinal cord injury. Most centres administer heparin initially followed by warfarin on a long term basis to prevent DVT. Labora­tory studies must be carried out to optimise coagulation function prior to surgery in these patients.

Haematological changes : Blood volume is often reduced in chronic spinal injury patients. Pooling of blood in lower limbs leads to oedema. Normocytic hypochro­mic anaemia is common in these patients. Anaemia is most often secondary to some chronic infection, decubi­tus ulcers and urinary tract infection. Circulating renin levels are high resulting in increased release of angio­tensin II and aldosterone with consequent salt and wa­ter retention.

Changes in muscle : Proliferation of acetylcho­line receptors occurs over the entire muscle membrane surface. Depolarising muscle relaxants cause massive efflux of potassium due to the simultaneous depolarisation of the entire muscle surface. Use of succinyl choline may be restricted to 24-48 h after injury. Serum potas­sium increases are maximum between 1 month and 5 months. The problem may persist up to one year in some patients [8] . Pretreatment with nondepolariser relaxants may not prevent hyperkalemic response to succinyl cho­line effectively unless they are used in full paralysing doses. In paretic patients assessment of neuromuscular blockade seems to be more reliable on proximal muscles than on distal muscles. When neuro-muscular blockade was monitored in trapezius and abductor digiti minimi, greater sensitivity has been noticed in trapezius [9] .

Spasticity develops after the phase of spinal shock subsides generally in about 3-4 months. Spasms can be provoked by minor stimuli and can be violent and pain­ful. Spasticity helps to improve venous return and pre­vents muscle wasting and osteoporosis. Baclofen, ben­zodiazepines and dantrolene have been used to treat the spasms when they prove troublesome to the patient.

Temperature control : Sympathetic paralysis may cause vasodilation and heat loss below the level of the lesion. It may also affect the sweating mechanism. The patients may behave poikilothermic. Some recent evi­dence suggests that reflex sweating response to heat stimulus is present even in quadriplegic patients; this re­sponse seems to be mediated by isolated spinal cord re­flexes [10] .

Immune function : In a study evaluating the natu­ral killer cell cytotoxicity (NKCC) and the bactericidal function of circulating neutrophils in quadriplegics, paraple­gics with lesions below T10 and normal controls, signifi­cant difference was demonstrated in the immune func­tion of patients with spinal cord injury and that of the normal controls [11].

Metabolism : Basal metabolic rate (BMR) is sig­nificantly decreased in patients with spinal cord injury. The low metabolic rates reduce the energy needs. Lower metabolic CO2 production implies need for lower minute volumes to maintain normocapnia in spinal injury patients receiving mechanical ventilation [12] .

Infections : Infections are the common cause of morbidity and mortality in patients with spinal cord in­jury. Pneumonia and urosepsis are the common forms of infections in these patients. When present, they must be adequately treated before surgery. Presence of pressure ulcers on the back may limit the use of regional techniques such as spinal and epidural anaesthesia.

Consequences of immobilisation : Prolonged immobilisation leads to altered Ca ++ metabolism, some of the consequences of which are: (a) calcification of muscles (b) joint immobility (c) osteoporosis (d) hyper­calcemia (e) nephrocalcinosis with renal failure (f) pathological fractures.

Concomitant head injury : Occult head injury as revealed by neuropsychologic evaluation is present in 36% of patients with spinal cord injury [13] .Attention must be paid to the possibility of worsening the intracranial dynamics if surgery is undertaken within first few days after spinal injury.

Response to anaesthetics : With high spinal cord injury, relative hypovolemia and decreased sympathetic outflow make the patients susceptible to the hypoten­sive effects of anaesthetic agents. Therefore, slow in­duction is mandatory.


   Definitive therapies in spinal cord injuries Top


Wide ranging trials with anaesthetic agents, cal­cium channel blockers, naloxone, local hypothermia, hy­perventilation etc. have been carried out, but till today, steroids seem to be the only agents which have offered some demonstrable clinical benefit.

The role of steroids : Steroids have been under experimental investigation for a number of years. The second National Acute Spinal Cord Injury Study (NASCIS-II ) [14] compared naloxone (5.4 mg.kg -1 IV fol­lowed by 4.0 mg.kg -1 .h -1 for 23 h) with methyl predniso­lone (30 mg.kg -1 IV followed by 5.4 mg.kg -1 .h -1 for 23 h). Both at 6 months and 1 year, the motor function was sig­nificantly better when methyl prednisolone was adminis­tered within 8 h after injury. Though neurological exami­nation revealed improvement in methyl prednisolone­treated group, the improvement was not functionally sig­nificant. In the NASCIS-III trial, additional benefit was conferred by prolonging the administration of steroid up to 48 h in patients presenting between 3 and 8 h.


   Anaesthetic management Top


Anaesthetic concerns in patients with spinal inju­ries at various time points are as follows:

Acute phase (0-48 h)

  1. Spinal shock with hypotension, bradycardia and poor response to any stimulus
  2. Relative or absolute hypovolemia requiring a care­ful combination of volume replacement and inotro­pic support under central venous pressure monitor­ing
  3. Full stomach necessitating "Crash-induction" with Sellicks' manoeuvre for intubation
  4. Other concomitant injuries, especially those involv­ing long bones, abdomen and thorax


Semi-acute phase (48 h to a variable period rang­ing from 1 to 12 weeks)

  1. Persistent spinal shock in some patients
  2. Risk of hyperkalemia from succinyl choline
  3. Risk of hypercalcemia


Intermediate phase (1-12 wks)

  1. Spinal shock resolved
  2. Autonomic hyper-reflexia
  3. Risk of hyperkalemia from succinyl choline
  4. Risk of hypercalcemia


Chronic phase (> 3 months)

  1. Risk of hyperkalemia from succinyl choline up to 8­12 months post injury
  2. Autonomic hyper-reflexia
  3. Hypercalcemia
  4. Contractures
  5. Osteoporosis



   Preanaesthetic evaluation Top



   Neurological assessment Top


A standardised neurological assessment of patients with spinal injuries, as proposed by the American Spinal Injury Association (ASIA), consists of: (a) Muscle test­ing (b) Sensory testing and (c) Assessment of complete­ness of injury. For muscle testing, 10 groups of muscles are examined, 5 in the upper limbs and 5 in the lower limbs. Each muscle group is graded on a 6 point scale of 0-5. In total, there are 100 points [Table 2]. For sensory testing 28 dermatomes are identified on each side. Each dermatome is graded on a scale of 0-2. Testing is done for light touch and pin prick. A total of 112 points are possible for each one of these sensations. Complete­ness of injury is assessed on the basis of ASIA impair­ment scale [Table 3].

A checklist of other points for preanaesthetic as­sessment of spinal cord injury patients is given in [Table 4].


   Anaesthesia for surgical procedures Top


Securing the airway is the most crucial step during the anaesthetic management of a patient cervical spine injury.


   Assessment of cervical spinal stability prior to airway maneuvers Top


Despite liberal use of cervical spine x-rays in trauma, the majority of them are normal. In order to avoid unwanted radiographs, five clinical criteria have been used to clear cervical spine in conscious trauma pa­tients (3). These criteria are: a) no posterior midline cer­vical spine tenderness, (b) no intoxication, (c) alert pa­tient, (d) no focal neurological deficits and (e) no painful distracting injuries. The overall sensitivity of these crite­ria for identification of any type of cervical spine injury is 97.6% and 99% for significant injury. The criteria, however, have a low specificity. Conscious patients who do not satisfy the above criteria must be investigated cervical radiography. In patients with altered mental status, there is no consensus on the criteria for cervical spine clearance. It is a common practice to rule out in­jury to cervical spine by a lateral radiograph. The North American Emergency X-Ray Usage (NEXUS) database however has shown that screening radiography using three cervical views (anteroposterior, lateral and odon­toid views) can identify only 61% of the injuries [16] . Com­puted tomography with 3 mm slices using helical scan­ning and multiplanar reconstruction has been shown to have a much higher sensitivity of 97-100%. Spinal cord injury may occur without any radiological abnormality in 2.8-3.8% of all spinal injuries [16],[17]. MRI is the investiga­tion of choice to detect this condition.


   Effect of basic airway maneuvers on cervical spine mobility Top


Chin lift and jaw thrust in an adult cadaver model of C5-6 ligamentous injury caused a greater than 5 mm in­crease in the disc space [18] . A Philadelphia collar did not prevent this widening. Anterior neck pressure to facilitate nasotracheal intubation causes a posterior subluxation of more than 5 mm. Head tilt, and insertion of an oropharyn­geal or nasopharyngeal airway are not associated with any significant displacement of the spinal segments. Cri­coid pressure applied during emergency intubation has been generally believed to displace the spine. But a recent ca­daver study using a lateral cervical spine x-ray showed negligible spine movement with cricoid pressure along with manual inline stabilisation [19] .


   Effect of spinal immobilisation on techniques of airway management Top


Immobilisation of neck with collars, straps and sand bags restricted the mouth opening and caused a poor laryngoscopic view (grade 3 and 4) in 64% of the pa­tients [20] . Visualisation improved with manual inline trac­tion but was still poorer compared to the view in the optimal intubating positioning. Manual inline stabilization decreases, but does not completely eliminate cervical spine movement during laryngoscopy [21] .


   Techniques of securing airway in patients with cervical spine injury Top


Direct laryngoscopic intubation : Direct laryn­goscopic orotracheal intubation with manual inline neck stabilization is the most commonly recommended tech­nique for securing airway in a patient with cervical spine injury. During normal direct laryngoscopy and oral intu­bation, significant extension occurs between occipital bone and C1 and also between C-1 and C-2 [22],[23] . Manual inline neck stabilization reduces this head extension by 50% in anaesthetized patients [24] . However, in a cadaver study of injuries at C4, this type of stabilisation did not reduce the movement, suggesting the limitation of this manoeuver in preventing movement of the spine in pa­tients with cervical spine injury [22] . Axial traction on spine should be avoided during laryngoscopy and intubation as this could increase the spinal cord injury. Gum elastic bougie is an important adjunct to avoid displacement of the fractured spine during direct laryngoscopic intuba­tion [25] .

Influence of the type of laryngoscope on cervical movement: The cervical spine movement caused by McIntosh curved blade or Miller's straight blade are not significantly different during direct laryngoscpic intuba­tion [26] . In a comparison of McIntosh and McCoy laryngoscopes, McCoy laryngoscope improved visual­ization of the larynx by at least one grade in 49% of cases [27] . In another study, Miller and McIntosh blades were compared with Bullard laryngoscope [28] . Head ex­tension and neck movements were less and laryngeal visualization better with Bullard laryngoscope. However, there were problems associated with Bullard laryngo­scope, which included prolonged time for intubation, fog­ging, and occasional inability to pass the tracheal tube through the glottis. Angulated video intubating laryngo­scope significantly improved the laryngeal view com­pared with direct laryngoscopy with cricoid pressure [29] .

Awake intubation : Awake intubation is consid­ered safe in a patient with spinal injury as the normal muscle tone provides protection and the neurological sta­tus of the patient can be monitored. The various options available for awake intubation are awake oral or nasal intubation and awake fibreoptic intubation. Despite the safety claimed for awake intubation, a number of limita­tions of these techniques must be appreciated. Awake intubation is slower compared to rapid sequence intuba­tion. Cooperation from the patient is very essential for the success of the procedure. Considerable expertise of the operator is required to accomplish awake intubation. Blind nasal intubation is complicated by epistaxis, laryn­gospasm and oesophageal intubation.

In cadavers with a C-5/6 instability, blind nasal in­tubation caused least cervical spine movements [30] . With C-1/2 instability both oral and nasal intubations produced similar cervical spine movement [31] . In cadavers with C­3 injury, awake fibreoptic technique produced no move­ment of unstable segments as assessed by video fluo­roscopy [32] .

Laryngeal mask airway (LMA) : Intubating LMA has been used successfully for blind intubation in patients undergoing cervical spine surgery [33] . It has also been used in conjunction with rapid sequence intubation and also for awake oral intubation with fibreoptic bronchoscope [34] . Both standard LMA and intubating LMA have been shown to cause a temporary pressure of 250 cm H2O against the posterior pharyngeal wall during insertion. The pressure is sufficient to cause up to 2 mm of displacement of C3 [35] . The cervical spine movement that occurs during insertion of LMA and intubation through LMA is less than that pro­duced during direct laryngoscopy [36] .

Surgical airway : Cricothyroidotomy, which is at­tempted when non-surgical techniques of securing air­way have failed may be associated with movement of cervical spine. In a cadaver model of C-5/6 transection, cricothyriodotomy resulted in 1-2 mm anteroposterior displacement and 1 mm axial compression of the spinal cord [37].

Plan for airway management in a patient with cervical spine injury

Emphasis during the airway care of a patient with cervical spinal injury is not on the specific technique of management, but on operator-experience and case-spe­cific management. No single technique of airway management has been shown to be superior to others. Bag- mask ventilation, introduction of oral or nasal airway, chin lift, jaw thrust and oral or nasal intubation may be re­quired based on the needs of the individual patients. There is no evidence for an association between the technique of intubation and neurological deterioration when manual inline stabilization is ensured. Therefore, the fear of in­flicting cord damage should not prevent securing the air­way with the technique that the operator is conversant with.

A practical approach for airway management in a patient with suspected cervical spine injury is shown in [Figure 1].


   Anaesthetic techniques Top


Depending on the needs of the individual surgery, and the condition of the patient, there are three options of anaesthesia:

  1. Standby, local anaesthesia and sedation
  2. General anaesthesia
  3. Regional anaesthesia



   Standby, local anaesthesia and sedation Top


Absence of sensations below the level of the le­sion enables many surgical procedures to be carried out without any form of anaesthesia subject to absence of risk factors for autonomic hyperreflexia (high level le­sions, previous h/o autonomic hyperreflexia, urological procedures) and absence of frequent troublesome spasms and the patient is willing. Local anaesthetic infiltration may be required in cases of incomplete lesions. Adrena­line should be avoided in local anaesthetic solutions as these patients are sensitive to catecholamines. Sedation with bezodiazepines might decrease the risk of spasms. Presence of an anaesthetist, standard monitoring and an intravenous access are mandatory even during 'standby' procedures.


   General anaesthesia Top


Sedative premedication is generally avoided. Oral premedication may have inadequate effect because of delayed gastric emptying. Some centres use antihypertensives such as nifedipine for premedication to prevent autonomic hyperreflexia.

Reduced distribution volume renders spinal cord injured patients sensitive to intravenous induction agents, a problem that is compounded by the absence of sympa­thetic reflexes. Thiopentone, propofol and all available inhalational anaesthetics have been used for general anaesthesia. Nondepolariser muscle relaxants are used to facilitate intubation. Repeat doses are rarely required. Suxamethonium is generally avoided between day 3 and 9 months. Preloading the patient with about 500-1000 ml of crystalloid might decrease the incidence of hypoten­sion at induction. Atropine must be kept handy to treat any episodes of bradycardia.

General anaesthesia with an inhalational agent and spontaneous respiration is appropriate for short proce­dures. Controlled ventilation has the advantage of main­taining adequate gas exchange. Impaired baroreflexes may cause hypotension during IPPV.

Quadriplegic patients poorly tolerate acute positional changes. Therefore, positioning must be done gradually. All pressure points must be adequately protected. Heat loss must be prevented by using heated humidifiers and forced air warming devices. Autonomic dysreflexia, muscular spasms and penile erection complicating uro­logical surgery may be effectively treated by deepening the anaesthesia.


   Regional anaesthesia Top


Spinal anaesthesia has been used for urological surgery in chronic spinal injuries. Reliable suppression of autonomic dysreflexia is the argument in favour of spinal anaesthesia. Technical difficulties may be encoun­tered due to kyphoscoliosis, previous surgery and muscle spasms. Hyperbaric bupivacaine (0.5%) in a dose of 1.5­2.0 ml has been successfully used. Difficulties may be encountered in defining the level of the block unless the block has spread to above the level of the spinal lesion. Level of block may also be determined by observing the level at which the spastic paralysis becomes flaccid af­ter administration of spinal anaesthesia. Many centres are hesitant to use spinal anaesthesia despite lack of evidence suggesting worsening of neurological outcome with spinal anaesthesia [19] . Epidural anaesthesia is less satisfactory than spinal anaesthesia because of distor­tion of the epidural space and missed segments. Epidu­ral pethidine and fentanyl have been used to control au­tonomic hyperreflexia.

 
   References Top

1.Goldberg W, Mueller C, Panacek E, et al. Distribution and patterns of blunt traumatic cervical spine injury. Ann Emerg Med 2001; 38:17-21  Back to cited text no. 1      
2.Reid DC, Henderson R, Saboe L, et al. Etiology and clinical course of missed spine fractures. J Trauma 1987;27:980-986  Back to cited text no. 2      
3.Baydur A, Adkins RH, Milic-Emili J. Lung mechanics in indi­viduals with spinal cord injury: effects of injury level and pos­ture. J Appl Physiol 2001; 90:405-411  Back to cited text no. 3      
4.Wang AY, Jaeger RJ, Yarkony GM, et al. Cough in spinal cord injured patients; the relationship between motor level and peak expiratory flow. Spinal Cord 1997; 35:299-302  Back to cited text no. 4      
5.Linn WS, Spungen AM, Gong H Jr, et al. Forced vital capacity in two large out patient populations with chronic spinal cord injury. Spinal Cord 2001;39:263-268  Back to cited text no. 5      
6.Almenoff PL, Spungen AM, Lesser M, et al. Pulmonary func­tion survey in spinal cord injury: influence of smoking and level and completeness of injury. Lung 1995;173:297-306  Back to cited text no. 6      
7.Schonlwald G, Fish KJ, Perkash l. Cardiovascular complica­tions during anaesthesia in chronic spinal cord injured patients. Anesthesiology 1981; 55:550-558  Back to cited text no. 7      
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37.Gerling MC, Davis DP, Hamilton RS, et al. Effect of surgical cricothyrotomy on the unstable cervical spine in a cadaver model of intubation. J Emerg Med 2001; 20:1-5.  Back to cited text no. 37  [PUBMED]  [FULLTEXT]  


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