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460 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

TABLE 17.3, Continued

Item Level I Level II Level III
Anaesthetics, Insufficient data Manage pain and agitation None advised
analgesics High-dose barbiturate may be used in
and sedatives haemodyamically stable patients refractory
to other ICP treatments.
Propofol for the control of ICP. High dose
propofol can produce significant morbidity.
Nutrition Insufficient data Full caloric replacement by day 7 post injury None advised
Antiseizure Insufficient data Phenytoin or valproate is not recommended None advised
prophylaxis for preventing late post traumatic seizures.
Anticonvulsants are indicated to decrease the
incidence of early post traumatic seizures.
Hyperventilation Insufficient data Prophylactic hyperventilation (PaCO 2 Use hyperventilation for temporary
<25 mmHg) is not recommended. reduction of elevated ICP.
Hyperventilation should be avoided during
the first 24 hrs after injury when CBF is
often critically reduced.
If hyperventilation used; SjO 2 or PbrO 2
measures recommended to monitor
oxygen delivery
Steroids Not None advised None advised
recommended

level of injury, he/she is considered to be sensory- and decreased cutaneous sensation of pain, temperature
motor-incomplete. There are four incomplete SCI syn- and touch on the same side of the spinal cord at the
dromes as follows: level of the lesion. Below the level of the lesion on
the same side, there is complete motor paralysis. On
● Anterior cord syndrome: Injury to the motor and the patient’s opposite side, below the level of the
sensory pathways in the anterior parts of the spine; lesion, there is loss of pain, temperature and touch,
thus patients are able to feel crude sensation, but because the spinothalamic tracts cross soon after
movement and detailed sensation are lost in the pos- entering the cord.
terior part of the spinal cord. Clinically, the patient
usually has complete motor paralysis below the level
of injury (corticospinal tracts) and loss of pain, tem- Pathophysiology
perature, and touch sensation (spinothalamic tracts), SCIs can be separated into two categories: primary inju-
with preservation of light touch, proprioception and ries and secondary injuries. Primary injuries are the
position sense. The prognosis for anterior cord syn- result of the initial insult or trauma, and are usually per-
drome is the worst of all the incomplete syndrome manent. The force of the primary insult produces its
prognoses. initial damage in the central grey matter of the cord.
● Posterior cord syndrome: This is usually the result of Secondary injuries are usually the result of a contusion
a hyperextension injury at the cervical level and is or tear injury, in which the nerve fibres begin to swell
not commonly seen. Position sense, light touch and disintegrate. Secondary neural injury mechanisms
and vibratory sense are lost below the level of the include ischaemia, hypoxia and oedema. Ischaemia, the
injury. most prominent post-SCI event, may occur up to 2 hours
● Central cord syndrome: Injury to the centre of the post-injury and is intensified by the loss of autoregula-
cervical spinal cord, producing weakness, paralysis tion of the spinal cord microcirculation. This will
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and sensory deficits in the arms but not the legs. decrease blood flow, which is then dependent on the
Hyperextension of the cervical spine is often the systemic arterial pressure in the presence of hypotension
mechanism of injury, and the damage is greatest to or vasogenic spinal shock. Oedema develops at the
the cervical tracts supplying the arms. Clinically, the injured site and spreads into adjacent areas. Hypoxia
patient may present with paralysed arms but with no may occur as a result of inadequate airway maintenance
deficit in the legs or bladder. and ventilation. Immune cells, which normally do not
● Brown-Séquard syndrome: This involves injury to the enter the spinal cord, engulf the area after a spinal cord
left or right side of the spinal cord. Movements are injury and release regulatory chemicals, some of which
lost below the level of injury on the injured side, are harmful to the spinal cord. Highly reactive oxidising
but pain and temperature sensation are lost on the agents (free radicals) are produced, which damage the
opposite side of injury. The clinical presentation is cell membrane and disrupt the sodium–potassium
one in which the patient has either increased or pump.