Describe spinal cord injury and its complication

SPINAL ANATOMY
• Familiarity with spinal cord anatomy helps correlate how specific traumas translate into primary
or secondary injuries.
• The bony spine (vertebral column) is comprised of 24 vertebrae, the sacrum, and connective
ligaments.
• The spinal column and cord are contained within the vertebrae and are divided in to 4 distinct
regions: cervical, thoracic, lumbar, and sacral.
• The thoracic spine is normally kyphotic and relatively fixed, whereas the cervical and lumbar
regions are normally more mobile.
• The spine is more susceptible to injury at junctions between these mobile and less mobile areas,
and therefore injuries appear more commonly at these levels.
• The diameter of the canal varies along its length, with its narrowest point in the thoracic spine.
• Thus, thoracic injuries leave less space for spinal cord oedema or impingement when the canal is
compromised.
• The spinal cord contains several neuronal tracts: sensory pathways (spinothalamic) ascending
from the periphery to the brain, and descending motor pathways (cortico-spinal) from the brain
to the periphery.
• The autonomic fibres within these tracts control various physiologic functions of the cardiac,
gastrointestinal, and other organ systems.
• The location and severity of an SCI can thus commonly be diagnosed by the specific pattern of
signs and symptoms observed.
• Blood supply to the posterior third of the spinal cord is via a pair of posterior spinal arteries,
while the ventral two thirds of the cord is supplied by a single anterior spinal artery.
• This artery is particularly sensitive to disruption by retropulsion injuries.
• Several radicular arteries from the aorta supplement the anterior spinal artery blood supply,
these are most numerous in the cervical region and least in the thoracic region.
• The artery of Adamkiewicz is the main thoraco-lumbar radicular and supplies the cord from T8
to the conus.
• The thoracic areas dependant on this single artery are therefore more vulnerable to ischaemia
when it is compromised.

The vertebral column

• The spinal canal and cord are protected by the vertebral column whose integrity depends on a
series of ligaments joining together and strengthening the vertebrae
 • The integrity and stability of the system may be functionally divided into three complexes, the
anterior longitudinal ligaments with the anterior half of the intervertebral discs, the posterior
longitudinal ligaments with the posterior half of the intervertebral discs, and the posterior
complex of the ligamentum flavum, interspinous, and supraspinous ligaments joining the
spinous and transverse processes.
• The posterior complex provides the most strength to the integrity to the vertebral column.
• If any two of these three complexes are disrupted, then the vertebral column is unstable.
• Additional strength is given to the system by the inclination of the facet joints.
• The thoracic spine is also strengthened by the ribcage.
• The commonest sites of injury occur where there is the greatest risk of conformational change
where the spine changes in curvature and construction, namely the craniocervical,
cervicothoracic, thoracolumbar, and lumbosacral junctions.

The spinal canal

• The spinal canal contains the spinal cord in a potential space filled with epidural fat and blood
vessels.
• The size of this potential space varies considerably along the length of the canal.
• It is narrowest in the mid-thoracic region and unstable injuries here easily impact onto the cord,
particularly retropulsion of bone fragments, leading to a high chance of complete cord injury
 • In contrast, the upper cervical area has more space around the cord, particularly in the region of
C1/2, and injuries at this level often do not produce associated cord injury.
• The spinal cord extends from the brainstem to L1/2 in the adult and L2/3 in the neonate.
• Below this level, the cord terminates in the conus medularis, and the cauda equina, consisting of
lumbosacral nerve roots.
• Injury at this level produces the cauda equina syndrome.

The spinal cord

• The function of the spinal cord is to allow both sensory and motor information to pass between
the body and brain.
• The two major sensory pathways are the posterior columns and the spinothalamic tracts and
the major motor pathway is the corticospinal tract

• The posterior column transmits sensory information for vibration, fine touch, and
proprioception on the ipsilateral side of the body (fibres cross over in the medulla).
• The spinothalamic tracts carry pain, temperature, and coarse touch on the contralateral side of
the body (fibres cross over to the contralateral side at 1–2 vertebral bodies above their level of
sensory innervation).
• In brief, motor fibres from the cortex descend to the contralateral side of the body via the
corticospinal tracts.
• The arterial supply of the spinal cord is via the anterior and posterior spinal arteries, branches of
the vertebral, and posterior inferior cerebellar arteries respectively.
 • Radicular arteries, including the arteries of Adamkiewicz also contribute especially in the
thoracic region.
• The anterior spinal artery is particularly vulnerable to retropulsion of bone and disc fragments
and may give increase to cord infarction in watershed areas, particularly at C6/7.
• Injury at any level may produce a variety of clinical symptoms and signs depending on the
nature of the insult to the cord and the anatomical area damaged.
• This can range from mild paraesthesia to complete motor, sensory, and autonomic paralysis.

Perform basic neurological examination

 • The ASIA score at 72 hours postinjury is currently the most sensitive predictor of a patient’s
long-term prognosis.

Complete Versus Incomplete Injuries

• Complete injuries are characterised by a loss of motor and sensory function in the anal and
perineal region, representing the lowest sacral segments (S4 and S5) of the spinal cord.
• Incomplete injuries involve some degree of preserved neurological function, and are
subsequently described by their residual functions.
Pathophysiology of spinal cord injury
 Spinal injury can be divided into three distinct phases:
i) The initial phase:
 Very short (minutes) period of intense neuronal discharge caused by direct cord stimulation.
 This leads to extreme hypertension and arrhythmias, with risk of LV failure, MI, and pulmonary
oedema.
 Steroid usage in acute spinal cord injury remains controversial.
 If used, steroids must be given within 8hr of injury, in high dosage (e.g. 30mg/kg of
methylprednisolone)
ii) Spinal shock follows rapidly
 characterized by hypotension and bradycardia due to loss of sympathetic tone.
 It is commonest after high cord lesions (above T7).
 There is associated loss of muscle tone and reflexes below the level of the lesion.
 Vagal parasympathetic tone continues unopposed, causing profound bradycardia or asystole—
especially on tracheal suction/intubation.
 This phase may last from 3d to 8wk.
 Paralytic ileus is common
iii) Reflex phase:
 as neuronal ‘rewiring’ occurs, efferent sympathetic discharge returns, along with muscle tone
and reflexes.

Damage from SCI can be divided into 2 stages: Primary and secondary
 - Primary injury is the damage from the initial mechanical trauma to the spinal cord resulting from
direct cord compression, haemorrhage, traction forces, or penetrating trauma.
- Secondary injury occurs when the primary injury results in local and spreading changes at a
cellular level over the subsequent hours, days, and weeks.
• Secondary SCI stems from a cascade of changes involving altered cellular permeability,
interruption of the microvascular blood supply (either by vasospasm or thrombosis), and an
influx of inflammatory cells, cytokines, and vasoactive peptides.
• These changes all lead to increasing cord oedema, which can expand across multiple spinal
segments, further exacerbating the initial spinal cord damage.

Autonomic dysreflexia
 This is characterized by massive, disordered autonomic response to stimulation below the level
of the lesion.
 It is rare in lesions lower than T7.
 Incidence increases with higher lesions.
 It may occur within 3wk of the original injury.
 The dysreflexia and its effects are thought to arise because of a loss of descending inhibitory
control on regenerating presynaptic fibres.
 Hypertension is the commonest feature but is not universal.
 Other features include headache, flushing, pallor (may be manifest above the level of the
lesion), nausea, anxiety, sweating, bradycardia, and penile erection.
 Less commonly, pupillary changes or Horner’s syndrome occur.
 Dysreflexia may be complicated by seizures, pulmonary oedema, coma, and death and should
be treated as a medical emergency.
 The stimulus required to precipitate the condition varies but is most commonly:
- Urological: bladder distension, UTI, catheter insertion
- Obstetric: labour, cervical dilation, etc.
- Bowel obstruction/faecal impaction
- Acute abdomen
- Fractures
- Rarely, minor trauma to the skin, cutaneous infection (bedsores).

Management of dysreflexia
• Discover the cause, if possible, and treat.
• If no apparent cause, examine carefully for unrevealed trauma or infection; catheterize, and
check for faecal impaction.
• If simple measures fail, consider:
- Phentolamine 2–10mg IV, repeated if necessary
- Transdermal GTN
- Clonidine (150–300 micrograms) if there is hypertension and spasticity
• β-blockers are indicated only if there is associated tachycardia—esmolol 10mg IV, repeated.

What characteristic neurological changes occur immediately and in the first three months following
transection of the spinal cord at the fourth thoracic vertebra?
What other clinical problems may develop following this type of injury?
Respiratory:
1. Loss of innervation of intercostal muscles results in failure of expansion of ribcage and,
therefore, reduced tidal volumes.
2. Inefficient seesaw breathing: the diaphragm contracts, pushes abdominal contents down and
out due to loss of abdominal wall tone and the chest wall is sucked in.
3. Breathing worse in the sitting position. Abdominal contents pull down on the diaphragm, thus
expanding expiratory intrathoracic volume, so reducing volume for expansion in inspiration. A
high proportion of minute ventilation therefore spent on ventilating dead space, resulting in V/Q
mismatch and atelectasis. The FVC is better in the horizontal or slight head-down position due to
increased diaphragmatic excursion.
4. Difficulty clearing secretions: inefficient coughing due to loss of abdominal wall tone.
Cardiovascular:
1. Neurogenic shock (may last 24 hours to several weeks): vasodilatation and bradycardia resulting
in hypotension. Sensitive to position with postural hypotension. Sensitive to fluid depletion,
especially with positive pressure ventilation.
2. Later, autonomic dysreflexia predisposes to periods of uncontrolled hypertension, risking
headache, flushing, nasal congestion, seizures, retinal haemorrhages, stroke, coma, death.
 3. Long-term, patients are at risk of ischaemic heart disease due to physical inactivity and
development of diabetes.
4. Difficulty with intravenous access due to fragile skin, reduced surface blood flow.
5. Reduced blood volume—may be as little as 60mL/kg, a 20% reduction.
6. Abnormal response to the Valsalva manoeuvre with continued drop in BP (no plateau) and no
overshoot with release.
7. Profound postural hypotension, with gradual improvement after the initial injury (never to
normal).
Endocrine:
1. Initial stress response may result in hyperglycaemia which may exacerbate secondary
neurological injury.
2. Increased risk of developing diabetes in the longer term.
Gastrointestinal:
1. Reduced gastrointestinal motility: delayed gastric emptying (aspiration risk), paralytic ileus,
constipation, pseudo-obstruction.
2. Increased risk of gall stones and their complications.
3. Prone to stress ulceration due to unopposed vagal activity.
Haematological:
1. Immobility and thrombogenicity of trauma predispose to thromboembolic disease.
2. Risk falls after three months (possibly due to muscle spasm facilitating the muscle pump of
venous return, decreased venous distensibility and femoral artery atrophy).
3. Anaemia is common.
Immune, infection:
1. Risk of nosocomial colonisation with multi-resistant organisms.
Cutaneomusculoskeletal:
2. Contractures resulting from spasticity cause pain and further reduction in function.
3. Osteoporosis results from loss of limb use.
4. Risk of pressure sores including in unusual places such as occiput.
Renal and genitourinary:
1. Nephrogenic bladder. Impaired sensory and motor function may lead to incomplete voiding
(predisposing to infection) and uncoordinated voiding (predisposing to vesico-ureteral reflux
and, thus, chronic kidney disease).
2. Intermittent or long-term catheterisation is usually required
Metabolic:
1. Poor temperature regulation: vasodilatation may predispose to cooling, whilst lack of ability to
sweat below level of injury may cause hyperthermia.
2. Poor thermoregulation due to isolation of central regulatory centres from information
pathways, inability to use muscle to generate heat, and altered peripheral blood flow.
Psychological:
1. At risk of depression, suicide, drug addiction.

List the advantages of a regional anaesthetic technique for a cystoscopy in this patient.
1. Avoids autonomic dysreflexia.
 2. Avoids the need for intubation of a patient who may have previously had a tracheostomy with
its attendant complications, e.g. tracheal stenosis.
3. Avoids deterioration in lung function associated with general anaesthesia, thus reducing the risk
of postoperative respiratory complications.
4. Avoids opioid use with associated respiratory depression.
5. Reduces the risk of aspiration associated with delayed gastric emptying.
6. Avoidance of unopposed parasympathetic response to airway instrumentation (bradycardia,
cardiac arrest).

Disadvantages
 May be technically difficult to perform.
 Spinal anaesthesia is usually possible, but epidural techniques are likely to fail in the presence of
spinal instrumentation or previous spinal surgery.
 There is difficulty in determining the success or level of blockade in complete lesions.
 Incomplete lesions are tested as usual.

Why and when may suxamethonium be contraindicated in a patient with spinal injury?
 Upregulation of nicotinic acetylcholine receptors in extrajunctional sites results in massive
potassium release with suxamethonium use.
 This effect is seen between approximately 72 hours following injury and six months.

Conduct of anaesthesia
i) Spinal shock phase
• Severe bradycardia or even asystole may complicate intubation—give atropine (300 micrograms
IV) or glycopyrronium (200 micrograms IV) prior to intubation.
• Extreme care should be taken if cervical spine injury is suspected.
• Preload with fluid (500–1000mL of crystalloid) to reduce hypotension.
• Central line insertion may be necessary to manage fluid balance and guide appropriate inotrope
therapy.

Reflex phase
• Previous anaesthetic history is vital—many procedures in these patients are multiple and
repeated.
• Pay close attention to the following:
- Is there a sensory level, and is it complete? (Risk of autonomic dysreflexia is greater in
complete lesions.)
- If complete, is the proposed surgery below the sensory level? (Is anaesthesia necessary?)
- Has there been spinal instrumentation? (Potential problems with spinal/epidural anaesthesia.)
- Is the cervical spine stable/fused/instrumented? (Potential intubation difficulty.)
- Is postural hypotension present? (Likely to be worsened by anaesthesia.)
- Is there a history of autonomic dysreflexia (paroxysmal sweating and/or headache), and, if so,
what precipitated it?
 - In cervical lesions, what degree of respiratory support is necessary?
- Are there contractures or pressure sores?

Is anaesthesia necessary?
 In principle, if the planned procedure would require anaesthesia in a normal patient, it will be
required for a cord-injured patient.
 Minor peripheral surgery below a complete sensory level is likely to be safe without
anaesthesia.
 Even with minor peripheral surgery, minimal stimulation may provoke muscular spasm that may
require anaesthesia to resolve.
 LA infiltration may prevent its occurrence.
 Care should be taken with high lesions (T5 and above) or patients with a history of autonomic
dysreflexia undergoing urological procedures.
 If the decision is made to proceed without anaesthesia, IV access is mandatory, and ECG, NIBP,
and pulse oximeter should be applied.
 An anaesthetist should be present on ‘standby’ for such procedures.

General anaesthesia
 Monitoring should be applied prior to induction, and BP measured before and after every
position change.
 Invasive monitoring should be performed with the same considerations as normal.
 Despite the theoretical risk of gastro-oesophageal reflux, there appears to be no increased risk
of aspiration.
 If intubation is necessary for the desired procedure, anticholinergic pre-treatment is
recommended.
 Those with cervical cord lesions are likely to require assistance with ventilation under GA.
 If IPPV is performed in tetraplegics, BP may drop precipitously.
 Fluid preloading and vasopressors (e.g. ephedrine) may be required.
 With the exception of paralysis to facilitate intubation, NMB is unlikely to be necessary, unless
troublesome muscular spasm is present.
 Care should be taken to preserve the body temperature (wrapping or forced-air warming
blankets).
 Position with respect to pressure areas.
 Fluid management may be difficult, as blood volume is usually low, and, with high cord lesions,
reflex compensation for blood loss is absent.
 Fluid preloading, coupled with aggressive replacement of blood losses with warmed fluid, is
recommended.

Post-operative care
 Tetraplegics are best nursed supine or only slightly head-up due to improved ventilatory
function in this position.
 Temperature should be monitored, and hypothermia actively treated.
 Analgesia should be provided by conventional means.
  Dysreflexia may occur and require drug treatment after removal of precipitating causes (such as
pain and urinary retention).

Obstetric anaesthesia
Effect of pregnancy on spinal cord injury
 Exaggerated postural hypotension and worsened response to caval occlusion.
 Reduced respiratory reserve, with increased risk of respiratory failure and pneumonia.
 Increased O2 demand.
 Increased anaemia due to haemodilution.
 Labour is a potent cause of autonomic dysreflexia in those with lesions above T5 (dysreflexia
may be the 1st sign of labour in such patients).

Effect of spinal injury on pregnancy

 Increased risk of infection (urinary infection and pressure sores).
 Increased risk of premature labour (increasing risk with higher level injury).
 Increased risk of thromboembolic complications.
 Labour pains will not be felt in complete lesions above T5.
 Lesion between T5 and T10—some awareness of some contractions.

Management of labour
 All cord-injured patients should be reviewed early in pregnancy, and a plan formulated for the
likely need for analgesia.
 The relative risks and difficulties of epidural catheter insertion should be predicted and
discussed with the patient.
 A plan for anaesthesia, in the event of a Caesarean section, should also be formulated and
recorded in the patient notes.
 Epidural analgesia is usually possible in those with high cord lesions without vertebral
instrumentation at the level of catheter insertion.
 Spinal anaesthesia is usually possible for an elective Caesarean section and may be achievable
with both single-shot and microcatheter techniques, irrespective of the presence of spinal
instrumentation.
 GA may proceed with the precautions

Epidural analgesia in labour

 The most effective preventive measure for autonomic dysreflexia is adequate epidural analgesia.
 Those with high lesions may have an epidural commenced prior to induction of labour.
 Hypotension is not usually a problem after adequate fluid preloading (at least 1L of crystalloid or
colloid)
 However, hypotension from any cause should be treated aggressively in those with high lesions
due to the lack of compensatory mechanisms and a tendency to progressive hypotension.
 Aortocaval compression should be avoided by careful positioning for the same reasons.
 Autonomic dysreflexia has been reported up to 48hr after delivery.
 If a successful block is achieved, it would appear prudent to leave the epidural in situ for this
time.
  Failure to establish an adequate epidural blockade may necessitate drug treatment of
autonomic dysreflexia

Initial management of Traumatic SCI

Airway/Breathing
• The need to minimise further injury by maintaining in-line neck stabilisation can hinder normal
manipulation for intubation.
• Common haemodynamic swings during induction and intubation can potentiate secondary
injuries to the spinal cord.
• Spinal cord perfusion and oxygenation is imperative, yet hypoventilation is commonly
encountered in this patient population.
• This is attributable to a variety of causes: rib fractures, traumatic brain injury, pain, pneumo- or
haemothoraces, or neurologic disruption to the muscles of ventilation.
• In addition to standard indications for intubation, patients with upper or midcervical injuries are
at increased risk of respiratory deterioration, with up to 80% requiring intubation during their
care.
• The potential for mechanical airway obstruction due to enlarging a haematoma around the
cervical spine following injury can also necessitate early endotracheal intubation.
• Therefore, vigilance, with a low threshold for early intubation, is important to protect their
airway and maintain ventilation/oxygenation.

Circulation
• Autonomic dysfunction due to disruption of spinal sympathetic fibres may lead to hypotension
and bradycardia; referred to as ‘neurogenic shock’.
• This arises from unopposed vagal parasympathetic tone and a combination of vasodilatation
with interruption in the cardio-accelerator fibres from the upper thoracic spine.
• Hypotension should be aggressively treated, as poor spinal cord perfusion can exacerbate cord
ischemia and the extent of injury.
• A target mean arterial pressure of 85 to 90 mm Hg should be maintained for the initial 5 to 7
days postinjury, facilitated by the use of invasive arterial monitoring.
• Resolution of neurogenic shock usually develops 4 to 6 weeks postinjury, but may present as
early as 4 days.
• Clinically, the return of deep tendon reflexes often heralds the resolution of susceptibility to
neurogenic shock.
• This is not to be confused with ‘spinal shock’, which isn’t really shock as such, but instead refers
to a flaccid areflexia that may occur after SCI.
• In patients with higher levels of SCI, care should also be taken when performing vagally
stimulating procedures, such as laryngoscopy and tracheal suctioning.
• If unopposed by sympathetic action, vagal stimulation from these procedures can yield severe
bradycardia or even asystole.
• Pretreatment with anticholinergics, such as glycopyrrolate or atropine, are options which should
be considered.

Other Considerations
Positioning:
• Surgery for spinal injuries can be long, are often in the prone position, and involve a variety of
customised tables and supports

Nutritional support and glycaemic control:

• Traumatic SCI is known to cause a hypermetabolic state and risks rapid nitrogen depletion.
• Good nutrition is vital to aid wound healing, weaning of mechanical ventilation, and ongoing
recovery and rehabilitation.
• Both hyper- or hypoglycaemia may worsen outcomes and should be addressed.

Pressure sore prevention:

• These are a major cause of morbidity and mortality, especially in resource-poor environments.
• Regular repositioning of the patient by appropriately trained staff is essential for preventing
pressure sores.

Venous Thromboembolism (VTE) prophylaxis:

• Patients will be immobile and hypercoagulable post injury, with a high risk of deep vein
thrombosis or pulmonary embolus.
• Mechanical thromboprophylaxis should be used as soon as possible and (when deemed safe by
the surgical team), pharmacologic thromboprophylaxis (such as heparin or enoxaparin) should
be utilised.

Gastric prophylaxis:
• Stress ulceration is common in trauma patients.
• Prophylaxis with a proton pump inhibitor (such as pantoprazole) should be considered.

Bladder and bowel dysfunction:

• These are common due to autonomic dysfunction.
• Urinary catheterisation should be initiated, with laxatives prescribed to minimise constipation.

Thermoregulation:
• Vasodilation below the spinal cord lesion predisposes to hypothermia, while a compromised
ability to sweat impairs heat dissipation, hence monitoring and maintenance of body
temperature is vital.

ONGOING CARE
• Patients with SCI require ongoing treatment and rehabilitation.
• After acute management, transfer to specialised SCI centre for continued management and
rehabilitation is commonly necessitated.
• These patients often re-present to hospital for further interventions, many of which may require
anaesthesia.
• Autonomic dysreflexia is a physiologic derangement commonly found in injuries above the T6
level.
 • This is an inappropriate autonomic response to stimuli below the level of injury, resulting in
episodes of malignant hypertension, characterised by headache, flushing, pallor, and sweating
above the level of the lesion.
• Autonomic dysreflexia can be triggered by even minor stimuli, such as bladder distention,
constipation, or pressure sores.
• It is important to appropriately manage this condition as a matter of urgency.
• Removing the stimulus will often improve the situation, as will sitting the patient up if possible.
• Pharmacological agents, such as sublingual glyceryl trinitrate (GTN) or a short acting vasodilator
may be beneficial for acute management.
• In areas where access to ongoing support and rehabilitation is limited, survival rates have
improved, but mortality is still high, particularly amongst populations in lower- to middle-
income countries.
• The most common complications in management encountered amongst patients after SCIs
include urinary tract infections, pressure sores, pneumonia, and associated sepsis.
• Simple steps, such as access to wheelchairs, catheters, and repositioning to reduce pressure
sores is invaluable; however the associated cost and availability of these resources can be a
limiting factor.

Initial management of acute spinal cord injury 2013

Pathophysiology
Primary injury
• Initial damage results from direct cord compression, haemorrhage, and traction forces.
• The commonest mechanism in trauma is subluxation of the vertebral elements causing a pincer
like direct damage to the cord.
• This can cause complete cord transection in extreme cases.
• Hyperextension injuries are common in the elderly.
• This can cause compression of the cord between the ligamentum flavum and anterior
osteophytes.
• Retropulsion of bone or disc fragments, particularly in burst fractures, can cause either damage
to the cord via direct cord compression or via impairment to the vascular supply, the anterior
spinal artery being particularly vulnerable.
• Penetrating injury can also cause direct compression and vascular injury.
• An associated fracture may or not be present and is dependent on site of injury.
• Pickett and colleagues reported an associated spinal fracture present in only 56% of patients
with cervical SCI, compared with 100% in those with thoracic SCI, and 85% with lumbar SCI.

Secondary injury
• Within minutes after injury, secondary damage begins.
• Haemorrhage in the central grey matter occurs and axons and neuronal cell membranes become
damaged.
• These events lead to spinal cord oedema and subsequent spinal cord ischaemia.
• Loss of autoregulation with high thoracic lesions contributes to neurogenic shock.
• Untreated the resultant decrease in systemic arterial pressure may lead to further cord
hypoperfusion and spreading penumbra of damage.
 • Cord ischaemia extends bi-directionally, along the site of injury within hours and secondary SCI
continues.
• Within the first 72 h, this may manifest as an ascending SCI level, which may lead to clinical
deterioration.
• Systemic effects, local vasomotor changes, the release of free radicals, intracellular electrolyte
shifts, neurotransmitters, cord oedema, disruption of cell metabolism, and cell death are all
thought to play their part in secondary injury most of which have no specialist treatment but
have resulted in the search for drug suppression of inflammation to limit secondary injury.
• Prevention of secondary cord damage may make a dramatic difference to the quality of life of a
SCI patient.
• A tetraplegic with damage at C4, may present with diaphragmatic breathing but not have
respiratory failure.
• If the cord damage extends only one level higher, phrenic nerve (C3–5) innervation will be lost,
with resultant respiratory failure, and need for ventilation.
• If permanent, this patient will require long-term ventilation.

Neurogenic shock
• Neurogenic shock is the interruption of autonomic pathways leading to hypotension and
bradycardia (and hypothermia).
• It is common in injuries involving cardiac sympathetics (T2–5) resulting in a decrease in systemic
vascular resistance, decreased inotropism, and increased unopposed resting vagal tone.

Spinal shock
• 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).

Classification of injury
• A SCI affects the functioning of the spinal cord at the level of injury.
• There are a number of associated definitions and clinical syndromes
 • It is important to discriminate between complete and incomplete injury.
• Up to 80% of patients with incomplete paraplegia will stand by 12 months, 50% will walk out of
hospital within 12 months, and patients may show neurological improvement up to 2 years after
injury.

Initial management of the SCI

• The immediate resuscitation phase follows the basic principles of ‘ABC’.
• SCI in polytrauma is common (30%) and needs to be considered.
• One-third of patients with acute SCI may also have associated major injuries or other spinal
fractures and injuries to the head, chest, abdomen, pelvis, lower limb, and upper limb all need
to be excluded.
• Some may be life threatening and will require urgent attention; preserving spinal alignment at
all times is imperative.

Extraction and transport

• 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
with a hard collar.
• They should be transferred to hospital with surrounding head blocks on a spinal board.
• Patients must be ‘log rolled’ off the board, ideally within 30 min after arrival in hospital.
• The spinal board is a transport device only and its prolonged use is associated with pressure
sores.
• SCI patients should continue to have spinal immobilization according to specialist advice and be
‘log rolled’ for transfer at all times until spinal fixation.
Airway
• Patients should be well oxygenated at all times to prevent secondary cord damage and a low
threshold for intubation is required.
• Patients with high cervical lesions around C3–5 (diaphragmatic innervation) are especially at risk
of deterioration, with vital capacities <30% of predicted and 80% of all cervical cord injuries
require ventilation at some point, most within the first 48 h.
• Patients with SCI are also at increased risk of regurgitation and pulmonary aspiration of gastric
contents because of paralytic ileus and loss of gastroesophageal sphincter tone.
• In the acute setting, a rapid sequence induction (RSI) should be used.
• Before induction the patient’s hard collar and head blocks should be removed and manual in
line cervical spine stabilization (MILS) should be initiated by a second operator.
• Cervical spine movement should be minimized during laryngoscopy, especially flexion, which is
thought to be more dangerous to the cord than extension.
• 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.
• Associated maxillofacial trauma, blood or vomit in the upper airway, airway oedema secondary
to direct trauma, or access problems such as cervical immobilization devices including halo
traction can all make intubation difficult.
• Difficult airway equipment including a fibre-optic bronchoscope should be immediately available
and awake fibre-optic intubation (AFI) may also be considered.
• The spine must be immobilized if AFI is undertaken.
• No individual airway technique is superior, it is more important to avoid hypoxia and use
familiar methods.
• Despite direct and indirect intubation techniques and cricoid pressure all being associated with
spinal movement, this movement is unlikely to result in neurological injury providing reasonable
care is taken.
• It must be remembered that after 72 h post-injury succinylcholine should be avoided as it may
precipitate life threatening hyperkalaemia.
• Acute denervation causes acetylcholine receptors to spread beyond motor end plate of the
neuromuscular junction, increasing receptor exposure to succinylcholine, an effect that wears
off at ~6 months.
• Gastric emptying remains reduced so a modified RSI (or AFI if airway or access limited) may be
considered in the weeks after initial injury.

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.
• Any patient with cervical cord injury or those demonstrating signs of high cord injury with
inability to cough or diaphragmatic breathing should be monitored acutely in a critical care
setting as they may deteriorate neurologically especially in the first 72 h postinjury and again
early intubation should be considered.
• It is important to remember that in the acute phase high cord-injured patients will have better
respiratory function lying flat as the diaphragm has a greater excursion in inspiration as it is
pushed into the chest by abdominal contents, whereas if sitting up the diaphragm is pulled
down by abdominal contents impeding further excursion in inspiration.
• Patients should, therefore, not sit up for the first few days after injury and thereafter only
gradually as intercostal paralysis develops and the chest no longer collapses in during inspiration
preserving the smaller tidal volumes produced by diaphragmatic descent.
• It is important that early assessment of respiratory function, vital capacity, pulmonary
recruitment, and passive limb movements by an experienced spinal injury physiotherapist is
carried out.

Cardiovascular
• In the minutes after cord injury a massive release in catecholamines occurs, particularly after
high cervical injury producing dramatic hypertension and tachycardia.
• Following this phase, paralysis of sympathetic tone leads to hypotension.
• This is attributable to a combination of vasodilatation, decreased inotropism, and bradycardia (if
above T5 and cardiac sympathetics are involved).
• Bradycardia occurs because of unopposed vagal tone and intermittent atropine or
glycopyrrolate may be required, especially before vagally stimulating procedures such as
laryngoscopy or tracheal suctioning as the incidence of asystole in severe cervical injury may be
as high as 20%.
• Classically, the patient presents with hypotension and bradycardia, but they may be warm and
vasodilated.
• Systolic arterial pressure will often settle at 80–90 mm Hg but this is unpredictable.
• Hypotension may be fluid resistant and most patients with high cord injury require vasopressor
support.
• Overtransfusion of fluid may lead to pulmonary oedema as capillary integrity of the pulmonary
circulation may be impaired as a result of the catecholamine surge.
 • Invasive pressure monitoring should be used for cord injuries associated with neurogenic shock,
i.e. above T4.
• The neurogenic shock phase lasts from 24 h to several weeks.
• Early catheterization is essential not only to act as a marker of renal perfusion but also to avoid
bladder overdistension that may precipitate bradycardia.
• Consider supra pubic catheterization if priapism is present.

Neurological imaging and examination

Examination
• Signs that may indicate spinal injury (especially in the patient with the depressed level of
consciousness) include:
† Diaphragmatic breathing,
† Hypotension without obvious cause,
† Bradycardia,
† Priapism,
† Flaccid areflexia (e.g. in legs but tone in arms), and
† Loss of pain response below a level.
• A thorough evaluation should be undertaken as soon as possible and should include assessment
of motor function, sensation, respiratory function, reflexes, and anal tone on log rolling (sacral
sparing).
• It should also document whether the injury is complete or incomplete and whether a clinical
syndrome is suspected.
• A standardized form has been produced by The American Spinal Injury Association (ASIA) to
assist in this assessment

Imaging
• Plain X-rays have largely been superseded by computerized tomography (CT) and magnetic
resonance imaging (MRI).
• Early total body CT is crucial in excluding other life threatening injuries in trauma patients with a
cord injury to exclude occult haemorrhage as usual physiological response to shock is impaired.
• Therefore, neurogenic shock may mask other injuries such as ruptured spleen/fractured pelvis,
etc. and the patient may also be unable to describe pain below the level of injury.
• Spinal reformatting of CT images will aid immediate assessment of vertebral column, assist in
spinal clearance, and give some information on cord integrity
 • Early MRI has a role in investigating cord integrity and guiding early surgery (e.g. epidural
haematoma identification).
• It is a balance of risk vs benefit in this unstable group, ventilated patients, and those on
vasopressors or inotropes should be carefully monitored by experienced personnel if MRI is
undertaken.

Neuroprotection strategies in SCI

• There are no magic bullets in protecting the cord, but avoidance of hypoxia, hypotension, and
hypercarbia are crucial in the days after injury.
• Some specific areas of investigation include:

Vasopressor support
• Early vasopressor support has been advocated to ensure adequate spinal cord perfusion
pressure and reduce secondary cord injury.
• There is weak evidence from historical cohort studies that a mean arterial pressure of >85 mm
Hg for 5–7 days may be associated with a better functional outcome, but given potential
complications of prolonged inotropic support it seems pragmatic to also target arterial pressure
to age of the patient and presence of co-morbidities such as hypertension, ischaemic heart
disease, renal insufficiency, etc.
 • Given fluid resistant arterial pressure in some patients and predisposition to pulmonary oedema
it has been recommended that if >2000ml of fluid is required acutely, further fluid should be
target based with invasive monitoring and inotropes started.
• There is little evidence for choice of inotrope, although vasoconstriction appears logical as first
line.

Therapeutic hypothermia
• A number of animal studies showing a potential benefit in functional recovery have been
reviewed; however, human studies are limited and at present cooling is not recommended.

Steroids
• The high-profile NASCIS II study recommended use of steroids demonstrating a small reduction
in the level of injury in those treated early with high dose methylpredisolone, and this has
recently been ratified in a review.
• However, concerns over the mortality and rates of sepsis in the steroid group have led to them
not being recommended by the British Association of Spinal Cord Injury Specialists and are not
routinely used in the UK or in the USA.

Surgery
• Stabilization, open or closed reduction, and surgical decompression must be considered to
relieve direct pressure on the cord and prevent secondary injury.
• Urgent stabilization should be considered in patients with any deterioration in neurology.
• Early surgical decompression has been shown to reduce length of stay and days of mechanical
ventilation but not injury level.

Other considerations
Thromboprophylaxis
• Fatal pulmonary embolus occurs in 3% of SCI patients and rates of deep vein thrombosis and
non-fatal PE are 90 and 10%, respectively.
• These patients are at high risk both because of immobility and increased thrombogenicity
secondary to trauma.
• 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.
• If anticoagulant use is contraindicated early insertion of an IVC filter may be considered.

Gut protection
• Unopposed vagal activity increases gastric acid and therefore rates of peptic ulceration.
• A routine use of prophylactic H2 antagonists or proton-pump inhibitors for 6 weeks significantly
reduces duodenal ulceration from an incidence of ~20 to <5%.

Nutrition/glycaemic control
 • Despite normal bowel sounds and increased gastric acid secretion, 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, further impairing respiration.
• However, early enteral feeding decreases mortality in polytrauma patients and it is usual
practice to feed all intubated patients within 24 h.
• Glycaemic control is essential to avoid both hypo- and hyperglycaemia.

Pressure areas
• Pressure sores are devastating for cord-injured patients leading to prolonged immobilization or
severe sepsis.
• These usually develop in 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.

Perioperative management for patients with a chronic spinal cord injury 2015
• Leading causes of death are attributed to the cardiovascular, genitourinary, and respiratory
systems.
Pathophysiology
Cardiovascular system
Autonomic dysreflexia
• ADR is the most important and relevant complication of CSCI for the anaesthetist.
• It is a clinical emergency characterized by a massive disordered autonomic response to certain
stimuli below the level of the lesion, such as bladder and bowel distension.
• The clinical manifestations include:
- an increase in blood pressure of at least 20%,
- headache,
- flushing,
- sweating,
- chills,
- nasal congestion,
- piloerection,
- pallor.
• Severe hypertension can lead to raised intracranial pressure resulting in seizures and intracranial
haemorrhage, and cardiac complications including myocardial ischaemia, arrhythmias, and
pulmonary oedema.
• Factors affecting the development of ADR include level of the spinal injury, duration of injury,
and whether the injury is complete or incomplete.
• The incidence of ADR is between 50% and 70% in patients with lesions above T6 and increases in
frequency with higher level lesions and complete lesions.
• There are reports of ADR with lesions as low as T10; however, symptoms are less severe in
patients with lower lesions.
• Although it is most commonly observed in the chronic stage of CSI (a year after injury), early
episodes can occur within weeks of injury, and 10% of patients with lesions above T6 experience
ADR within first year of injury.
• The pathophysiology of ADR is thought to be a result of a disorganized sympathetic response to
stimuli below the level of the lesion

• Normal regulation of sympathetic output from the spinal cord is modulated by input from higher
centres.
• Interruption within the spinal cord results in loss of this higher input.
• Spinal circuits below the lesion are established and result in exaggerated responses.
• Activation of the autonomic nervous system below the level of the lesion results in a profound
sympathetic response up to the level of injury.
• If the level is above T6, the splanchnic circulation becomes involved resulting in splanchnic
vasoconstriction, and hence, a greater severity of symptoms.
• Compensatory mechanisms aiming to reduce the hypertension, via parasympathetic activity, are
activated up to the level of the lesion.
• This results in the characteristic symptoms of bradycardia and vasodilation above the lesion.
• Stimuli arise from caudal roots below the level of the lesion, with ∼80% of patients being
because of bladder distension.
 • Other triggers include bowel distension, acute abdominal pathology, urinary tract infections,
skeletal fractures, pressure ulcers, activation of pain fibres, sexual activity, and uterine
contractions.
• The management of ADR is illustrated in Figure 2.

Arrhythmias
• Patients with high cervical lesions often have vagal hypersensitivity leading to bradyarrhythmias.
• This is usually temporary, mostly resolving within 5 weeks from injury, although occasionally it
persists necessitating a pacemaker.

Cardiovascular disease
• Patients are at risk of cardiovascular disease because of a lack of physical activity, reduced
muscle mass, and the development of metabolic syndromes including diabetes.
• The risk of cardiovascular disease increases with age, and also with higher and more severe
spinal cord lesions.
• Some 40% of deaths in patients with CSCI are attributable to cardiovascular disease.
Temperature regulation
• Thermoregulation is often impaired, especially if the lesion is high.
• There is a reduced sensory input to higher thermoregulatory centres, reduced sympathetic
control of vascular tone, and reduction in sweating below the level of the injury.

Thromboembolism
• The risk of venous thromboembolism in the first 3 months after an acute SCI is ∼85% if left
untreated, necessitating prophylactic anticoagulation.
• After this period, the risk decreases and prophylaxis is not routinely required
• This reduction in risk from 3 months may be secondary to the effect of lower limb spasms on
muscle pump action along with femoral artery atrophy and reductions in venous distensibility.
• However, in the perioperative period, the risk is again increased and standard
thromboprophylaxis is recommended according to local hospital policy, with low-molecular-
weight heparin and antithrombotic stockings, or mechanical devices as appropriate for the
procedure.

Other cardiovascular changes

• Blood volume is reduced, and anaemia is present in ∼50% of patients.
• Patients are prone to postural hypotension because of a combination of reduced plasma
volume, pooling of blood in the lower limbs, and an altered baroreceptor reflex.
• I.V. access is often difficult because of atrophic, hyperaesthetic skin with reduced cutaneous
blood flow.

Respiratory system
Respiratory mechanics
• Respiratory mechanics are altered after SCI, with the degree of ventilatory dysfunction
dependent on the level and completeness of the lesion.
• Complete injury renders ventilatory muscles below the injury completely non-functional.
• Incomplete lesions may allow for variable muscle function.

Effect of the level of the lesion

• Lesions above C3: complete dependence on mechanical ventilation because of phrenic nerve
denervation causing complete diaphragmatic paralysis.
• Lesions between C3 and C5: variable dependence on ventilatory support because of variable
effect on diaphragmatic and accessory muscle function.
• Lesions between C6 and C8: they may require intermittent non-invasive ventilatory support.
Intact diaphragmatic function and accessory neck muscles enable adequate inspiratory effort.
-However, intercostals and abdominal wall muscles remain paralysed.
-Exhalation occurs via passive recoil of the chest wall, and cough is impaired.
-There is an increased risk of pneumonia because of poor mobilization of lung secretions.
• Thoracic injuries: little respiratory compromise; the main problems are attributable to an
inefficient cough.
• Vital capacity 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.
• 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, possibly because of increased neck circumference
associated with a higher incidence of obesity and accessory muscle hypertrophy.

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.
• Occasionally, they are needed for airway protection in patients of high cervical lesions involving
cranial nerves.
• Most are uncuffed tubes for use with domiciliary ventilators.
• These allow greater tolerance of leaks, compared with conventional ventilators, facilitating
communication.

Musculoskeletal system
Spasticity and contractures
• Spasticity occurs as a result of hyper-excitable spinal reflexes causing exaggeration of the stretch
reflex arc.
• Spasms can be a cause of severe morbidity and can be provoked by minor stimuli.
• Contractures are also common and can complicate optimal surgical positioning
• The most common oral treatment for spasticity is the GABA-B agonist baclofen, with an
occasional use of benzodiazipines; both of which may cause sedation.
• Increasingly, intrathecal baclofen delivered via indwelling infusion pumps are used and vigilance
to the position of the diathermy plate must be paid in these instances.

Osteoporosis
• Decreased bone density is common in CSCI patients with ∼60% of patients having osteoporosis
at 15 yr after their injury and 34% have had at least one fracture.
• This must be considered in patient handling and positioning.

Extrajunctional acetylcholine receptors

• Denervated muscle results in an increase of extrajunctional acetylcholine receptors, spreading
from motor end-plate of affected muscle fibres to cover the whole muscle membrane.
• On administration of a depolarizing neuromuscular blocking agent, depolarization will occur
across the whole muscle.
• This can result in large increases in serum potassium concentrations and potentially cause
serious cardiac disturbances and cardiac arrest.
 • The duration of this effect is difficult to determine, although it is generally agreed that
succinylcholine is safe to use after a period of 6 months from injury.

Spinal fixation
• Spinal fixation in the form of surgical fusion and bracing may have been carried out to obtain
stability.
• Lumbar metal work may prohibit the use of spinal or epidural anaesthesia, while fixed necks
may make airway management and intubation difficult.

Pressure ulcers
• Pressure ulcers are common and result from tissue damage because of unrelieved pressure,
typically occurring over bony prominences.
• Poor nutrition, muscle atrophy, and altered blood flow to the dermis contribute.
• Pressure ulcers may precipitate ADR, and be a source for local and systemic infection.

Neurological system
Chronic pain
• Around 65% of CSCI patients have chronic pain.
• Pain may be both nociceptive and neuropathic in nature, with nociceptive pain arising for
musculoskeletal structures and viscera, and neuropathic pain from spinal cord and nerve
damage.
• It is important to identify painful stimuli and take this into consideration when cannulating or
positioning patients.
• It can be a source of discomfort, but also could trigger ADR.

Psychological complications
• Psychological complications of post SCI include depression, suicide, and drug addiction.

Gastrointestinal system
• Gastric emptying is delayed in patients, particularly with high level injuries.
• The most common gastrointestinal disturbances are constipation, distension, abdominal pain,
and rectal bleeding.
• Bowel distension is a potent trigger for ADR.
• There is a high incidence of gallstones, with patients at an increased risk of developing advanced
biliary complications.

Genitourinary system
• Commonly there is impaired sensory and motor innervation to the bladder resulting in a
neurogenic bladder.
• Sequelae of this include reduction in bladder capacity, incomplete emptying, chronic retention,
and frequent urinary tract infections.
• Urinary tract infections are the most frequent source of septicaemia in SCI patients, which
carries a significant mortality.
 • Detrusor sphincter dyssynergia can also occur where the bladder contracts against a closed
sphincter leading to elevated bladder pressures and vesico-ureteral reflux.
• This can cause renal impairment and nephrolithiasis.
• Most patients therefore require bladder intervention, either in the form of indwelling catheters,
usually suprapubic, or intermittent catheterization.

Other
• The prevalence of nosocomial bacterial colonization is high amongst CSCI patients and common
organisms include Methicillin-resistant Staphylococcus aureus (MRSA), Multi-resistant
Acinetobacter Baumanii, Escherichia coli, and Pseudomonas aeruginosa.
• The patient status must be checked before operation, with appropriate consideration to the
order of the list, protective equipment, patient isolation, and antibiotic prophylaxis.

Anaesthesia and surgery

Common operations in CSCI
• A patient survey in 2005 indicated that while most patients prefer to visit an SCI centre for all
medical conditions, local hospitals are still managing both acute and elective complications
because of acute presentations and also geographical distance to the SCI centre.

Emergency surgery
• Emergency presentations of acute conditions below the level of the lesion are often missed
initially because of atypical presentations.
• These patients are at risk of developing ADR and have an increased morbidity and mortality.

General.
• These include peptic ulcer perforations, intestinal obstruction, complications of acute
cholecystitis, and appendicitis.
• Delay in diagnosis is common resulting in increased morbidity by the time of surgery.

Musculoskeletal.
• Osteopenia, contractures, spasticity, and falls all increase the risk of limb fractures requiring
emergency orthopaedic procedures.
• Pressure sores may be the source of sepsis or osteomyelitis and require intervention.

Elective surgery.
Urological.
• Recurrent urinary tract infections and long-term catheterization increase the risk of bladder
cancer.
• Cystoscopy is a common procedure as is insertion of suprapubic catheters and botox injections
for the management of neuropathic bladders.

General.
 • Patients may require a defunctioning colostomy to prevent infection from perineal and sacral
pressure sores and allow healing or for the management of neuropathic bowel and chronic
constipation.

Spinal surgery.
• In the acute phase, patients often require reduction, decompression, and stabilization of
fractures.
• Occasionally, metalwork will need to be revised or removed.
• It is common for patients with longstanding SCI to develop scoliosis, which requires correction.

Intrathecal baclofen pumps.

• Baclofen pumps are used in patients which severe spasticity requiring large doses of anti-
spasmodic medications precipitating unwanted side-effects.
• The operation includes insertion of a lumbar or low thoracic catheter, tunnelled to the
connecting pump that is inserted in the lower abdominal wall.

Preoperative assessment and investigations

• History and examination—key points
Level of and completeness of the injury.
• High and incomplete injuries are more likely to experience ADR.
• The time since the injury may influence choice of drugs used, such as succinylcholine.

Autonomic dysreflexia.
• The focus should include identification of susceptible patients, establishing a history of previous
episodes including known triggers, frequency, and severity.
• A review of previous anaesthetic charts will reveal prior anaesthetic techniques and any
episodes of ADR under anaesthesia.
• Potential triggers for ADR should be sought and treated before operation including checking for
catheter blockages, ensuring bowels have been emptied and vigilance for skin ulceration.

Muscle spasms and contractures.

 • Spasms and contractures can make patient positioning and surgery difficult.
• Spasms can be spontaneous or in response to cutaneous stimuli.

Ventilation.
• A history of prior ventilatory problems including sleep apnoea, recent pneumonia, or intensive
care admissions should be noted.
• If patients use non-invasive ventilation (NIV), their usual device and mask must be available in
the perioperative period and in recovery.
• If the patient has a tracheostomy, the size, whether it is cuffed, fenestrated, or has a speaking
valve should be noted.
• Uncuffed tracheal tubes should be changed to cuffed tubes before operation to allow adequate
ventilation under anaesthesia.

Airway assessment.
• Previous cervical spine surgery/fixation should be noted and a difficult airway predicted.
• Previous tracheostomies may cause tracheal stenosis.

Pressure areas.
• Any pressure sores should be noted and appropriate dressing and protection applied before
operation.

Anaesthetic management
• There are three options for providing anaesthesia

• No anaesthesia with an anaesthetist on standby, regional anaesthesia, and general anaesthesia.

• Consideration must be given to patient preference, the level and the completeness of the lesion
relative to the operative site, previous anaesthetic management, the presence of ADR, and
spasticity.
• In all instances, access to emergency drugs for the management of ADR should be immediately
available.

No anaesthesia, anaesthetist on standby

 • Patients having operations below the level of the lesion may not require an anaesthetic.
• Agreeable patients must give full consent and will require an anaesthetist on standby in case
ADR occurs.
• Patients must be fully monitored and counselled regarding the symptoms of ADR with advice to
report any such symptoms immediately.
• Caution must be used when using sedation, as it may mask ability to recognize ADR and cause
ventilatory depression.

Regional anaesthesia
• Spinal anaesthesia is safe in patients with CSCI and is an effective way of abolishing ADR and
spasms.
• Spinal anaesthesia is becoming a widely accepted technique in patients with pre-existing spinal
cord pathology and is routinely used in Stoke Mandeville Hospital, with a low dose (1.5–2ml)
hyperbaric bupivacaine 0.5%, for most procedures.
• Spinals can be challenging to site because of poor positioning as a result of spasms and
contractures, the presence of spinal metal work, and bony deformities.
• The effectiveness and the level of the block are difficult to ascertain.
• The loss of the Babinski reflex and a change in tone from spasticity to flaccid paralysis indicate
an established block; although the height of the block remains difficult to assess.
• The anaesthetist must be vigilant for the signs and symptoms of a total spinal block.
• Epidural anaesthesia has been demonstrated to be effective in reducing ADR in labouring
women; however, it is less reliable for general and urological surgical procedures.
• For patients with incomplete lesions or chronic pain having long and painful general surgical
procedures, epidural anaesthesia may be helpful in reducing the incidence and severity of ADR
in the postoperative period.
• Upper limb surgery may be amenable to brachial plexus block, and this should be done under
ultrasound guidance as nerve stimulators may be unreliable in the presence of cervical injuries.
• Consideration should be given to the approach of the block.
• Supraclavicular and interscalene blocks carry a higher risk of pneumothorax and phrenic nerve
paralysis.
• These will have greater implications in CSCI patients who may already have impaired respiratory
function.

General anaesthesia
Premedication.
• Sedatives should be avoided as they may reduce respiratory drive.
• Premedication aimed at reducing the risk of ADR is occasionally used, such as nifedipine,
although premedication with anticholinergics has not been shown to be of benefit.
• Fasting times should be strictly adhered to as patients may have delayed gastric emptying.

Induction.
• Patients generally require lower doses of induction agents to achieve anaesthesia.
• This may in part be because of altered pharmacokinetics resulting from a reduced blood volume
and muscle mass.
 • The sympathetic response to hypotension is often absent, and thus myocardial and CNS
hypoperfusion may ensue, requiring treatment with vasopressors.
• We routinely use propofol for induction; however, there is no evidence that any particular
induction agent is superior for CSCI patients.
• Routine monitoring must be established before the induction of anaesthesia.

Airway.
• If tracheal intubation is required, precautions must be taken to ensure safe neck positioning and
a difficult airway should be anticipated in patients with fixed cervical injuries.
• There should be a low threshold for awake fibreoptic intubation.
• A non-depolarizing neuromuscular blocking agent can be safely used to facilitate intubation,
although caution must be taken when using succinylcholine.
• It is safe to use in injuries older than 6 months, but should be reserved for those patients
requiring a rapid sequence induction.
• In patients with a tracheostomy, the tube should be changed to a cuffed tube before induction.

Maintenance.
• Anaesthesia can be maintained with either a volatile anaesthetic agent or via total i.v.
anaesthesia.
• An adequate depth should be established to reduce the likelihood of ADR and prevent spasms.
• The addition of remifentanil and nitrous oxide has been demonstrated to reduce the amount of
volatile agent required to prevent ADR, and the use of monitoring to assess the depth of
anaesthesia such as bispectral index may be useful.
• Spontaneous ventilation is mostly adequate for short procedures, although in patients with
cervical lesions, hypoventilation may ensue and result in hypercapnia and hypoxia.
• Intermittent positive pressure ventilation should be used for longer procedures; however,
caution should be given to cardiovascular instability as a result of high pressures.
• Opiates should be used sparingly if at all, because of their effect on postoperative ventilation.
• Major surgery involving large fluid shifts may necessitate arterial blood pressure monitoring and
cardiac output monitoring.
• This may however be difficult to interpret because of altered responses to blood loss; monitors
capable of measuring stroke volume provide useful information.

Positioning and thermoregulation.

• Special attention must be paid to pressure areas and limbs should be secured and padded to
prevent injury from spasms.
• Urinary catheters should be clearly visible and accessible.
• Warming should begin in the anaesthetic room and continue into the recovery period.

Emergence and recovery.

• Before extubation, patients should be fully antagonized if neuromuscular blockers were used,
and the tidal volume and ventilatory frequency should be adequate.
• Patients may require a period of NIV if surgery was prolonged, or they routinely use domiciliary
NIV.
 • Patients with cervical injuries are best recovered in the supine position to aid ventilation.
• Pressure areas should be checked in recovery and temperature should be maintained as
necessary.
• Routine monitoring including regular blood pressure measurement should be continued until
patients have been fully recovered as ADR can occur well into the recovery period.

The obstetric patient with SCI

• Pregnancy in patients with SCI is associated with the following problems:
- ADR
- Urological problems including sepsis and pyelonephritis
- Thromboembolism
- Pressure sores and ulcers
- Respiratory compromise because of the effects of the gravid uterus
- Pre-term delivery
- Higher rate of Caesarean section
• The anaesthetist should be aware when considering regional block that patients with SCI have a
lower blood volume and usually have a degree of anaemia, which can be exacerbated by the
physiological changes in pregnancy.
• Thus, these patients can present their own challenges to the anaesthetic team on labour ward.
• We would recommend that these patients should be assessed in an obstetric anaesthetic clinic.
• The level of the lesion and associated pathophysiology should be documented.
• Particular attention should be paid to the following.

Respiratory function
• As mentioned previously, those patients with higher lesions may have underlying impairment in
respiratory function.
• There is potential for the gravid uterus to impair respiratory function as pregnancy progresses,
necessitating an increase in respiratory support.
• In high spinal lesions, vital capacity should regularly be assessed.

Previous spinal surgery

• Previous surgery at the level one would like to site regional anaesthesia may pose a challenge.
• We recommend obtaining further information about previous surgery, including any relevant X
rays.
• In our experience, epidural insertion should be avoided in the areas where there has been spinal
fusion, because of the high failure rate, increase in dural punctures, and potential, uneven,
patchy distribution of block.
• It is usually possible to site a single shot spinal at the level of surgery should it be required.
• Previous cervical surgery, especially fusion may make the airway particularly difficult.
• If intubation is likely to be difficult because of limited neck mobility, it is advisable to discuss in
detail with the obstetricians.
• It is preferable to avoid the need for an emergency general anaesthetic.

Autonomic dysreflexia
 • A history of ADR and frequency should be documented and a plan for the management of
labour should be devised.

Management on labour ward

• Analgesic options depend on the level of the lesion.
• With lesions below T10, it is likely that contraction pain will be felt.
• If the lesion is high, then contractions may precipitate ADR, indeed this may be the first sign of
the onset of labour.
• It is the experience in our unit that the early establishment of epidural analgesia is very effective
at managing ADR associated with labour.
• It is recognized that epidural placement may be difficult in these patients.
• If regional analgesia is ineffective at managing ADR symptoms, then antihypertensive agents
such as nifedipine, hydralazine, or verapamil can be considered.
• It has been reported that there may be a role for magnesium sulphate in this situation but
ultimately delivery under general anaesthesia should be considered.
• It is the practice in our unit that epidural catheters remain in situ post-delivery, because the
contracted uterus can still provoke ADR in susceptible patients.
• It is important to recognize that these patients still have the potential of developing
preeclampsia during their pregnancy and this diagnosis should always be considered when
hypertension is present.