Page 484 - ACCCN's Critical Care Nursing

Neurological Alterations and Management 461

Free-radical production and lipid peroxidation lead to hypercapnia occur, both of which promote neuronal and
vasoconstriction, increased endothelial permeability and glial acidosis, oedema and neuroexcitation.
increased platelet activation. A secondary chain of events
produces ischaemia, hypoxia, oedema and haemorrhagic
lesions, which in turn result in the destruction of myelin Nursing Practice
and axons. Autoregulation of spinal cord blood flow may Spinal cord injury should be suspected in patients with
be impaired in patients with severe lesions or substantial neck pain, sensory and motor deficits, unconsciousness,
oedema formation. These secondary reactions, believed intoxication, spondylitis or rheumatoid arthritis, head
to be the principal causes of spinal cord degeneration at injury and facial fractures. If spinal cord injury is
the level of injury, are now thought to be reversible 4–6 suspected or cannot be excluded, the patient must be
hours after injury. Therefore, if the cord has not suffered placed on a spine board with the head and neck immo-
irreparable damage, early intervention is needed to bilised in a neutral position using a rigid collar to reduce
prevent partial damage from developing into total and the risk of neurological deterioration from repeated
permanent damage. 80 mechanical insults. Spinal injury patients are susceptible
to pressure insults, so time must be considered when
Spinal shock occurs with physiological or anatomical
transection or near-transection of the spinal cord; it occurs hard surfaces are used for immobilisation. Total neck
immediately or within several hours of a spinal cord immobilisation should not interfere with maintenance of
injury and is caused by the sudden cessation of impulses the airway, and inadequate respiratory function must be
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from the higher brain centres. It is characterised by the avoided.
loss of motor, sensory, reflex and autonomic function
below the level of the injury, with resultant flaccid paral- Resuscitation
ysis. Loss of bowel and bladder function also occurs. In Initial treatment aims for decompression of the spinal
addition, the body’s ability to control temperature (poi- cord and reversal of neurogenic shock and respiratory
kilothermia) is lost and the patient’s temperature tends failure. Spinal shock is associated with decreases in sys-
to equilibrate with that of the external environment. temic vascular resistance, arterial hypotension, venous
Neurogenic spinal shock occurs as a result of mid- to pooling, severe bradycardia and decreased myocardial
upper-level cervical injuries and is the result of sympa- contractility. Consequently, treatment of neurogenic
thetic vascular denervation and peripheral vasodilation. shock includes fluid replacement using crystalloid or
The loss of spinal cord vasculature autoregulation occurs, colloid solutions to maintain arterial blood pressure, cir-
causing the blood flow to the spinal cord to be depen- culatory volume, renal function and tissue oxygenation.
dent on the systemic blood pressure. Signs and symptoms Infusion of free water must be avoided, as this decreases
include hypotension, severe bradycardia, and loss of the plasma osmolarity and promotes spinal cord oedema.
ability to sweat below the level of injury. The same Atropine may be administered to reverse bradycardia and
clinical findings pertaining to disruption of the sympa- increase cardiac output. Administration of vasopressors
thetic transmissions in spinal shock occur in neurogenic (e.g. noradrenaline) prior to correction of the intravascu-
shock. 78 lar volume status may increase systemic vascular resis-
tance (left ventricular afterload) and further impair
Systemic effects of spinal cord injury myocardial contractility. Therefore, volume replacement
The traumatic insult causing the spinal cord injury is is the first step, and administration of vasopressors the
associated with an immediate stimulation of central second step in the treatment of arterial hypotension and
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and peripheral sympathetic tone. Initially, the elevated low cardiac output after acute cervical spinal cord injury.
sympathetic activity raises systemic arterial blood pres- The major early cause of death in patients with acute
sure and induces cardiac arrhythmias. At the stage of cervical SCI is respiratory failure. Tracheal intubation may
spinal shock with loss of neuronal conduction, the sym- be indicated in unconscious patients, during shock, in
pathetic excitation is closely followed by decreases in patients with other major associated injuries, and during
systemic vascular resistance, arterial hypotension and cardiovascular and respiratory distress. It is also indicated
venous pooling. Lesions above the level of T5 addition- in conscious patients presenting with the following
ally present with severe bradycardia and cardiac dysfunc- criteria: maximum expiratory force below +20 cmH 2 O,
tion. The decreases in cardiac output combined with maximum inspiratory force below −20 cmH 2 O, vital
systemic hypotension further aggravate spinal cord isch- capacity below 1000 mL, and presence of atelectasis, con-
aemia in tissues with defective autoregulation. tusion and infiltrate. 81
Spinal cord injury may produce respiratory failure. The
extent of respiratory complications is related to the level Investigations and alignment
of the injured segments. Injuries above the level of C4–C5 Following the initial assessment of the patient, detailed
produce complete paralysis of the diaphragm, with diagnostic radiography defines the bone damage and
substantial decreases in tidal volume and consecutive compression of the spinal cord. First, lateral, ante-
hypoxia. With lesions below C6, the function of the dia- roposterior, odontoid and possibly oblique cervical
phragm is maintained and there is incomplete respiratory spine radiographs are obtained. If there is no evidence
failure due to paralysed intercostal and abdominal of injury, flexion and/or extension views may be con-
musculature. As a consequence, arterial hypoxia and sidered. If any of these radiographs suggest cervical spine