Page 579 - ACCCN's Critical Care Nursing

556 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

PREVENTATIVE CARE NURSING PRACTICE AND COLLABORATIVE
Individuals with known allergies are taught avoidance of MANAGEMENT
allergens, and the use of emergency kits with adrenaline The extent of injury, whether complete (no sensory or
for IM injection. 120,124 Desensitisation therapy may reduce motor function) or incomplete (some sensory or motor
severity of symptoms. function), determines clinical medical management. Pri-
ority focuses on airway, breathing and circulation.
NEUROGENIC/SPINAL SHOCK After neck and torso stabilisation, a patient is placed in a

Neurogenic shock is a form of distributive shock caused position that supports spinal precautions (neutral neck
by loss of vasomotor (sympathetic) tone from disruption positioning) with the spinal boards removed within 20
to or inhibition of neural output. Characteristics include minutes if possible. Caution for spinal instability remains
SBP <90–100 mmHg and a HR <80 bpm without other despite medical imaging clearance, due to the potential
obvious causes. 128 Note that the HR is within otherwise for spinal ligament damage. The patient is positioned
accepted normal limits. Most often it is described as a supine, with their legs in alignment with the torso. Eleva-
triad of hypotension, bradycardia and hypothermia. The tion of the head may cause pooling of blood in the lower
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primary cause is a spinal cord injury above T6, secondary limbs, exacerbating hypotension, and makes the patient
to disruption of sympathetic outflow from T1–L2 and to sensitive to sudden position changes.
unopposed vagal tone, leading to decreased vascular Loss of sympathetic outflow requires close cardiac and
resistance and associated vascular dilation. 129 It may also haemodynamic monitoring for bradycardia and hypoten-
develop after anaesthesia, particularly spinal, cerebral sion. Symptomatic bradycardia is treated and may require
medullary ischaemia or when there is spinal cord com- cardiac pacing if unresponsive to atropine. Therapies
plete or partial injury above the midthoracic region (tho- include fluid resuscitation with the addition of inotropes
racic outflow tract). if necessary to improve vasomotor tone to increase
Spinal shock is a subclass of neurogenic shock, with a preload and maintain a MAP >80–85 mmHg 129 to restore
transient physiological (rather than anatomical) reflex spinal cord perfusion and to prevent secondary neuronal
131
depression of cord function below the level of injury and hypoperfusion. A higher (supranormal) MAP may be
associated loss of sensorimotor functions. Incidence has targeted to improve recovery and prevent secondary inju-
131
been reported at 14% of patients presenting to the ED ries. Volume expansion with colloids and crystalloids
within 2 hours of injury and predominantly affects or blood products will vary depending on patient situa-
patients with cervical damage. 128 Spinal shock can also tion, however subgroup analysis in the SAFE trial indi-
occur with a spinal cord laceration or contusion, and is cated that colloids and hypotonic solutions may not be
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associated with varying degrees of motor and sensory the best options.
deficit (see also Chapters 17 and 23). Trauma is fre- Respiratory function is closely monitored to prevent or
quently the reason for primary injury and simultaneous minimise atelectasis, pneumonia and secretion reten-
131
injuries may also be responsible for haemodynamic com- tion. The level of injury is indicative of the potential for
promise. 128 Haemorrhagic shock in combination with respiratory muscle weakness (see Table 20.11). The dia-
neurogenic shock has a poor outcome. phragm is innervated by the phrenic nerve (originating at
C3–C5); any injury above C3 leads to complete respira-
CLINICAL MANIFESTATIONS tory muscle paralysis and patients will require ventilatory
131
support. Incomplete injuries between C3 and C5 may
Inhibited sympathetic outflow results in dominance of
the parasympathetic nervous system, with a reduction in also require ventilation initially but subsequently recover
systemic vascular resistance and lowered blood pressure. some respiratory function.
Preload to the right heart is reduced, which lowers stroke Hypothermia may be present, resulting from dilated
volume and subsequent cardiac output/index. The usual peripheral blood vessels allowing radiant loss of heat. A
response to reduction in cardiac output (a raised heart patient is monitored for core temperature changes, and
rate) does not occur due to the parasympathetic nervous external warming devices may be required.
system and blockage of sympathetic compensatory
responses, and the patient may be bradycardic and hypo-
tensive, 129 with their skin warm and dry.
TABLE 20.11 Respiratory muscle innervation by
In spinal shock there may be an initial rise in blood pres- cord level
sure due to release of catecholamines, followed by hypo-
tension. 129 Flaccid paralysis, including that of the bladder Cord level innervation Accessory muscle
and bowel, is observed and sustained priapism may
develop. Symptoms may last hours to days, until the C3–C5 (mostly C4) Diaphragm
reflex arcs below the level of injury begin to regain func- C6 Serratus anterior
tion. This is a result of damage to the spinal cord, and Latissimus dorsi
results in pale, cold skin above the site of injury, and Pectoralis
warm, pink skin below the site of injury. Anhidrosis T1–11 Intercostals
(absence of sweating) may be present. Heart rate may be
slow, requiring intervention. T6–L1 Abdominals