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| REVIEW ARTICLE |
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| Year : 2008 | Volume
: 52
| Issue : 1 | Page : 13 |
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Anaesthetic and Intensive Care Management of Traumatic Cervical Spine Injury
GS Umamaheswara Rao
Professor of Neuroanaesthesia, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore 560 029., India
| Date of Acceptance | 07-Jan-2007 |
| Date of Web Publication | 19-Mar-2010 |
Correspondence Address:
G S Umamaheswara Rao
Professor of Neuroanaesthesia, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, 560020.
India
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 2013 May 18];52:13. Available from: http://www.ijaweb.org/text.asp?2008/52/1/13/60593 |
 Introduction | |  |
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 | | |
| Respiratory function | | |
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 | | |
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 | | |
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 | | |
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 | | |
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 | | |
Anaesthetic concerns in patients with spinal injuries at various time points are as follows:
Acute phase (0-48 h)
- Spinal shock with hypotension, bradycardia and poor response to any stimulus
- Relative or absolute hypovolemia requiring a careful combination of volume replacement and inotropic support under central venous pressure monitoring
- Full stomach necessitating "Crash-induction" with Sellicks' manoeuvre for intubation
- 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)
- Persistent spinal shock in some patients
- Risk of hyperkalemia from succinyl choline
- Risk of hypercalcemia
Intermediate phase (1-12 wks)
- Spinal shock resolved
- Autonomic hyper-reflexia
- Risk of hyperkalemia from succinyl choline
- Risk of hypercalcemia
Chronic phase (> 3 months)
- Risk of hyperkalemia from succinyl choline up to 812 months post injury
- Autonomic hyper-reflexia
- Hypercalcemia
- Contractures
- Osteoporosis
| Preanaesthetic evaluation | | |
| Neurological assessment | | |
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 | | |
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 | | |
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 | | |
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 | | |
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 | | |
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 | | |
Depending on the needs of the individual surgery, and the condition of the patient, there are three options of anaesthesia:
- Standby, local anaesthesia and sedation
- General anaesthesia
- Regional anaesthesia
| Standby, local anaesthesia and sedation | | |
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 | | |
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 | | |
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.
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[Figure 1]
[Table 1], [Table 2], [Table 3], [Table 4]
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