Neurological Assessment Tips

 If a patient develops any decrease in level of consciousness, the priority is to promptly identify and treat
any alterations in ABCGS (Airway, Breathing, Circulation, Glucose or Seizures) that may be causing the
deterioration.

 If the neurological change persists despite normalization of the ABCGS, a detailed neurological
assessment should be performed. The examination should attempt to determine if focal findings are
present (suggesting a structural abnormality, such as stroke, bleed, tumour, etc.) or absent (suggesting
generalized neurological depression, as seen with sedation or septic encephalopathy, etc.). Bilateral
findings may also suggest cord injury.

 Change is the most important finding in any neurological assessment and should be reported promptly to
ensure timely medical intervention if warranted. To ensure that neurological findings are communicated
effectively at change of shift, exiting nurses should perform a neurological examination with the
oncoming shift.

 Propofol may be used to sedate patients with neurological impairment to facilitate rapid awakening and
assessment. Remember that propofol does not provide analgesia, and pain can raise intracranial
pressure. In patients with catastrophic brain injury who are being sedated for raised intracranial
pressure, deep analgesia and sedation is provided to promote brain rest. Analgesia and sedation should
not be stopped for routine neurological assessment unless approved by neurosurgery.

Steps to Neurological Assessment in the Critical Care Unit:

1. Assess mental status/higher function:

A. Conscious patient:
1) Talk to patient and ask questions that avoid yes/no answers if possible.
• Evaluate orientation, attention, coherence, comprehension, memory/recall
• Screen for delirium
• Identify symptoms such as headache, nausea or visual problems
2) Determine Glasgow Coma Scale (GCS)

B. Altered patient:
1) Assess for response to:
a) Normal voice
b) Loud voice (if no response to normal voice)
c) Light touch (if no response to loud voice)
d) Central pain (if no response to light touch)
Differentiate between higher function of “awareness” (e.g., purposeful movement,
recognition of family) versus arousability (grimacing or eye opening to pain only)
2) Determine Glasgow Coma Scale (GCS)

2. Consider whether seizures could be present

Look for evidence of seizures (non-convulsive seizures should be considered in patients with an
unexplained decrease in level of consciousness, particularly in the setting of injury, stroke, tumour etc)

3. Test Cranial Nerves (see next page)

4. Assess motor function (look for asymmetry)

5. Assess sensory function (look for asymmetry)

6. Assess cerebellar function

 CRANIAL NERVES:
 The cranial nerves are arranged in pairs in descending order along the brainstem.
 There are 3 sensory (S) nerves (CN I, II and VIII), 5 motor (M) nerves (CN III, IV, VI, XI and XII)
and 4 mixed motor and sensory (MS) nerves (CN V, VII, IX and X). CN IX (accessory is actually a
spinal nerve that arises upward toward the brainstem.
 Cranial nerves control the same side of the body (ipsilateral response). For example, an
expanding lesion that compresses on the R CN III would cause a loss of the R CN III function.
This would mean that the right pupil would lose its ability to constrict to light (or become fixed and
dilated). Exception: CN IV controls contralateral funtion (moves eye downward toward the nose).
 All cranial nerves can be tested in alert patients who are able to participate in the examination.
 Only some of the cranial nerves can be tested if the patient is unconscious. Pairs of cranial nerves
can be tested by stimulating a sensory nerve and watching for an automatic motor nerve
response. Light reflex is an example; light is carried toward the brain via CN II (optic, sensory
nerve). This automatically causes reflex stimulation of both CN IIIs (oculomotor, motor), making
both pupils constrict to light.
 When brainstem herniation syndromes occur, cranial nerve function can be lost in descending
order (if the origin of the injury is above the tentorium and compression moving downward).
 CN I and II are located above the brainstem; CN III through XII are located along the brainstem.
 CN III is located at the level of the tentorium; sudden change in CN III function (decreased
reactivity, droopy eye, dilated pupil) suggests herniation through the tentorium/top of brainstem.
 Asymmetrical loss of any CN function suggests unilateral compression
 Because of their arrangement along the brainstem, most brainstem reflex tests are tests of cranial
nerve function.

CN I (S)
CN II (S)
CN III (M)
CN IV (M)
CN V1(S)
CN VI (M)
CN V2 (S)
CN V3 (MS)
CN V (MS)
CN VII (MS)
CN VIII (S)
CN IX (MS)
CN X (MS)
CN XII (M)
CN XI (M)
CN Name Main Function Testing in ICU
(assess symmetry)
I Olfactory (S) • Sense of smell • Block one nare and test ability to smell
equally from each nare (cloves, coffee)
(may be injured with anterior basal skull #) • Dysfunction causes food to lose its taste

II Optic (S) • Sense of sight • Recognition of objects or people.

Each of the 4 quadrants of vision in each eye • Eye chart, reading
(visual fields) take a unique pathway between • If alert, ability to see objects in all 8 fields.
the retina and brain. One or more visual • Light reflex tests CN II and III
fields can be lost due to damage to the retina, • Remember to test with glasses on
a branch of the optic nerve or the occipital
lobe (visual cortex).

III Oculomotor (M) • Pupil constriction • Light reflex

• Eyelid opening • Eye opening against resistance
• Eye movement (all directions except • Ability to follow an object upward,
those of CN IV and VI; CN III, IV and horizontally toward nose, straight
VI tested together for eye movement) down and downward/laterally
IV Trochlear (M) • Contralateral downward and nasal • Ability to look down toward nose.
rotation of eye. • The only CN that arises posteriorly
• Arises posteriorly. Crosses behind and controls contralateral function
brainstem and emerges anteriorly. • Compression usually occurs after it
R CN IV is between L CN III and V. crosses causing ipsilateral findings.
V Trigeminal (SM) • Primary Sensory: feeling to face in • Sensory: assess each region with
three branches: V1(forehead, cornea, tissue (light touch) and pin (pain).
nose), V2 (cheeks), V3 (jaw) Assess for symmetry.
• Motor: Chewing or mastication (V3) • Motor: ability to lift cheeks
• Corneal reflex tests V1 branch of CN
V (sensation) and CN VII (blink)
VI Abducens (M) • Horizontal and lateral movement of • Ability to follow an object in the
the eye horizontal/temporal gaze

VII Facial (M/S) • Primarily Motor: face movement, • Face symmetry for eye closure
eyelid closure, lacrimation, salivation against resistance, face movement
• Sensation/taste to front 2/3 tongue (smile, nasolabial fold, show teeth)
• Loss of forehead wrinkle on paralyzed
side suggests CN VII dysfunction
versus stroke
VIII Auditory or • Hearing and balance (cochlear) • Response to voice, tuning fork
vestibulocochlear • Vestibular system sends information • Balance during mobilization
(S) about head movement to pons; makes • Detailed testing by audiology post ICU
CN III/VI move eyes together for discharge
horizontal movement • Included in Doll’s eyes/Cold Calorics
IX Glossopharyngeal • Sensation to back of tongue/tonsils • CN IX and X collectively tested by
(MS) • Parotid secretion touching each side of the back of the
• Stylopharyngeus muscle throat and observing for gag
X Vagal (MS) • Contraction larynx/pharynx • Barro/chemo receptors important for
• Parasympathetic function all organs BP regulation
except adrenal glands • Cough reflex during suctioning
• Sensation pharynx, taste
XI Accessory/ • Shoulder shrug • Ability to shrug or turn cheek against
spinal (M) • Head rotation resistance

XII Hypoglossal (M) • Tongue movement • Ability to move tongue side to side
Cranial Nerve Testing: Awake Patient

1. Assess sense of smell (CN I [Olfactory]):

 Block each nare individually and test ability to smell a strong aroma such as cloves or coffee.
Assess for symmetrical sensation (omitted in most critical care assessments)
2. Evaluate ability to see (CN II [Optic]):
 If patient wears glasses, test with glasses on.
 Assess ability to identify objects or the number of digits held up by examiner. If unable to speak,
have them mimic actions or number of digits. Does patient recognize family members?
 Observe response to visual stimulation from either side of bed; occipital lobe stroke causes loss of
vision to the opposite visual field of one or both eyes (e.g., a left occipital lobe stroke can cause
blindness to the right visual field of the right and/or left eye).
 Assess ability to read
 While looking ahead, ask patient to indicate when he/she can see a pen that is wiggled into each of
the 8 visual fields shown. Deficits require follow-up for proper visual field assessment.
3. Light Reflex (CN II [Optic] and CN III [Oculomotor]):
 Conduct 4 point assessment: a) direct light response in L eye; 1 3 5 7
b) direct light response in R eye; c) consensual response in L eye; .
and d) consensual response in R eye. Record pupil size when exposed 2 4 6 8
to ambient room light. Hold both lids open to determine size/symmetry.
4. Eye Opening (CN III [Oculomotor]):
Visual fields of each eye
 Ask patient to open eyes wide; observe for upward movement of lids.
 Look at the white portion of each eye. Ptosis (eyelid droop) may be present if there is less white
showing on the affected side.
5. Eye Movement (EOM) (CN III [Oculomotor], IV [Trochlear] and VI [Abducens]):
 Hold a pen in front of the patient. Stand at least a couple of feet away.
 Ask patient to follow the pen as you SLOWLY move it horizontally, vertically and diagonally, in both
directions. Follow eye movements into extreme vertical and horizontal positions.
 Eye movements should be conjugate (together). Dysconjugate gaze causes diplopia and may be
due to CN III, IV or VI dysfunction, disorders of one of the muscles involved in eye movement or
during recovering from coma (not awake enough).
 Observe for nystagmus (extra eye movements). Nystagmus can be normal in the extreme
horizontal gaze but never in vertical gaze.
5. Facial Sensation (CN V [Trigeminal]; test 3 branches [V1, V2 and V3] independently):
 Sensory: Preferably with patient’s eyes closed, touch each side of the forehead (V1), cheek (V2)
and jaw (V3) with a whisp of tissue (light touch). Repeat with a blunt needle (pin).
 Ask patient to identify when they perceive the stimulus; assess for symmetry.
 Motor (V3): Place two fingers on each of the patient’s cheeks and ask him/her to raise them.
6. Facial Movement (CN VII [Facial]):
 Have patient smile, show teeth and wrinkle forehead. Observe nasal labial fold and symmetry.
 Ask patient to close eyelids tightly; assess ability to keep eyes closed against resistance. CN VII
protects the eye (eyelid closure/lacrimation). CN VII produces saliva/sensation to anterior tongue.
7. Hearing (CN VIII [Auditory]):
 Arise in pons. Critical care screening includes response to voice or loud noises. Comprehensive
testing following critical care discharge by audiologist.
 Tinnitus, vertigo and nausea with upright positioning, or impaired horizontal eye movement may
indicate CN VIII or pons disorders.
8. Gag Reflex (CN IX [Glossopharyngeal] and X [Vagus]).
 Touch back of throat (on each side) and assess for gag. Assess for cough during suctioning.
9. Assess Shoulder Shrug and Face Turning (CN XI [Accessory]).
 Ask patient to raise both shoulders and hold up against resistance; observe symmetry.
 Have patient turn head side-to-side. Repeat while you apply resistance to cheek.
10. Assess Tongue Movement (CN XII [Glossopharyngeal]).
 Ask patient to stick out tongue and move it side to side, can test against resistance.
 Neurological Assessment Tips

Brainstem Testing: Unconscious Patient:

Light reflex (CN II [Optic], III [Oculomotor]):

 Light impulse is carried to CN III via CN II.
 Light shone into either eye causes bilateral CN III stimulation (pupils constrict). Both pupils
constrict to light that is shone into either eye (direct and consensual response).
 If the pupil reacts to light from either direction, it is probably not a CN III problem.
 Record pupil size and symmetry when both lids are open in response to ambient room light.

Corneal reflex (V1 branch of CN V [Trigeminal] and CN VII [Facial]):

 Touching the cornea causes blink response. The sensation is detected by the first branch of
CN V (V1 branch), which stimulates CN VII bilaterally to cause both eyes to blink.
 Be careful to “sneak in from the side” when touching the cornea (with a whisp of tissue). If the
patient blinks because they see you, you have tested CN II and VII. If they blink because they
hear you, you have tested CN VIII (Acoustic) and VII.
 Blinking of only one eye suggests weakness on the side of the face where the blink is absent.

Doll’s Eyes or Oculocephalic reflex (CN III [Oculomotor], VI [Abducens] and VIII [Acoustic]
and pons)
 Normally, when the head is turned, the vestibular apparatus (CN VIII) is activated, causing the
eyes to move in the opposite direction. CN VIII communicates in the pons to activated both
CN III and VI to produce horizontal eye movement.
 Doll’s eyes CONTRAINDICATED IF C-SPINE UNCLEARED or vertebral vessel disease.
 Vertical eye movement is located at top of brainstem (CN III) and frontal eye fields. This loop
ensures that both CN III look upward together.

Cold Caloric or Oculovestibular reflex (CN III [Oculomotor], VI [Abducens] and VIII
[Auditory] and pons)
 If done in an awake patient, will cause vertigo, nausea and nystagmus (involuntary and erratic
eye movement)
 Integrity of eardrum should be assessed first, HOB elevated to 30 degrees
 Cold water instilled into ear of an awake person causes nystagmus with the fast beating
toward the opposite side. Warm water causes fast beating toward same side (COWS: Cold
Opposite Warm Same). Lack of nystagmus on one side in awake person suggests CN VIII
disorder.
 Cold water instilled into the ear of an unconscious patient will cause eyes to deviate slowly
toward irrigated ear. Eyes will remain in this position until the irrigation stops, and then quickly
return to mid position.
 Observe for 1 minute after completion of test, wait 5 minutes before testing other ear
 Delayed or absent movement indicates abnormality; fixed position in brain death.

Gag Reflex (CN IX [Glossopharyngeal] and X [Vagus]):

 Test one side at a time

Coughing and Breathing (CN X and Medulla):

 Assess for cough reflex during suctioning.
 Elevated PCO2 must be confirmed before apnea can be verified.

Pupillary Dilation
• Sympathetic control of the pupil is located in the pons; pons damage is associated with
pinpoint non-reactive pupils (loss of sympathetic dilation) and loss of horizontal eye
movement.
 Motor Assessment

Motor Assessment:
 Observe patients for symmetry of movements. Observe response to command and spontaneous/localizing
movements. Apply central pain if no response to verbal command.
 If the patient is able to obey commands, describe motor response using the 0-5/5 Motor Scoring Scale.
 The single best test to identify a mild upper motor neuron weakness in a patient who is able to obey
commands is the pronator drift test. Have the patient hold their arms forward, 90 degrees to his/her body
(modify position as tolerated). Have the hands positioned palms up with eyes closed (if possible). Mild
weakness is noted if the palm rotates toward the floor. This is more sensitive than waiting for the arm to drift
downward. Shoulder injuries may make this difficult to perform.
 Asymmetrical weakness may indicate that the weakness is due to a lesion in a specific area of the brain
(focal finding)
 When motor weakness is identified, the area of weakness should be evaluated to determine whether is
cause is likely due to a problem in the upper (brain or cord) or lower (peripheral) motor nerve pathway.
 Summary: When motor weakness is identified, look for focal findings (asymmetrical findings). When focal
findings are present, evaluate weakness for signs of upper or lower motor neuron problems. Symmetrical
weakness due to a brain lesion is uncommon and usually metabolic in nature, however, spinal cord injury
can cause symmetrical (or asymmetrical) weakness.
 Document a clear description of the method of stimulation and specific patient response. A detailed
description provides more information than the GCS/graphic entries alone.

Upper versus Lower Motor Neuron Weakness

The upper motor neuron (UMN) pathway begins in the motor strip of the contralateral cerebral hemisphere,
terminating in the spinal cord. Following impulse transmission to the end of the UMN pathway, the impulse
synapses with the lower motor neuron (LMN) of the spinal nerve to activate the muscle.

Motor weakness can occur as a result of UMN pathway damage (such as stroke or cord injury), or LMN injury
(e.g., injury to the brachial plexus or disc protrusion into a spinal nerve). Increased tone and deep tendon
reflexes (2+ is normal, 3+ or 4+ is increased) are characteristics of an UMN cause for weakness. Upgoing toe
following Babinski testing in conjunction with lower extremity weakness suggests an UMN cause for the
weakness. Clonus may also be present (>5 sustained involuntary contractions following muscle stretching).

Flaccid paralysis with decreased deep tendon reflexes (0-1+) suggests a LMN cause. Fasciculations may be
present. Note that during the early spinal shock phase of an acute spinal cord injury, the temporary loss of
reflexes can produce a paralysis similar to that of a LMN injury.

While UMN causes for hemiplegia are far more common in CCTC than LMN lesions, LMN injury can also be
seen in critical care. Examples include:

 Brachial plexus injury: the brachial plexus is a network of motor nerves from the cervical spine, that join
together to form a plexus (group of nerves) that pass below the collar bone. These nerves, which include
C5-8 and T1 are collectively responsible for all arm and hand movement. Flaccid paralysis of the arm with
decreased upper extremity deep tendon reflexes, particularly in conjunction with a shoulder injury, may
indicate brachial plexus injury. This is an example of a LMN cause for the arm weakness.
 Cranial nerves are LMNs. Injury to CN VII causes facial paralysis (motor weakness) on the same side. This
includes an inability to close the eyelid or wrinkle the forehead on the affected side. Examples of CN VII
injuries are Bell’s Palsy and injury due to middle fossa basal skull fracture (with CN VII impingement).
 Contralateral facial weakness following stroke or brain injury (inability to stimulate the contralateral CN VII)
is an example of an UMN cause for facial weakness. Forehead wrinkle and at least weak eyelid closure is
generally preserved in UMN facial weakness. The preservation of the forehead wrinkle occurs because
stimulation of the forehead wrinkle response from either side of the brain automatically stimulates the upper
branches of CN VII bilaterally.
 Any spinal cord injury that causes disc protrusion onto the spinal nerve can cause LMN weakness.
LMN weakness is associated with decreased reflexes.
 Deep Tendon Reflexes

 Motor weakness associated with increased tone and deep tendon reflexes (3 or 4+), upgoing great toe,
and/or with clonus suggests an UMN cause for the weakness.
 Motor weakness associated with flaccid paralysis and decreased deep tendon reflexes (< 2+) suggests a
LMN cause for the weakness.

Biceps Brachii Tendon

C5, C6

Triceps Tendon
C7, C6
Plantar Reflex (Babinski)

Brachioradialis Tendon
C6, C5

Clonus: Oscillations between flexion

and extension
Quadriceps Tendon (knee jerk)
L4, L3, L2

Achilles Tendon (ankle jerk)

S1
 Spinal Cord Function

Information between the brain and spinal cord are carried via one of several tracts. Each tract
has a unique channel and crossing point. Consequently, incomplete spinal cord injuries can
produce a variety of motor and sensory deficits, depending upon the location of the lesion.

Motor Pathways (Corticospinal Tract): Pain/Temperature (Spinothalamic)

Upper motor neuron

Brain Stem
Figure 1

Spinal cord

Step 3:
Sensory pathway Figure 2
Sensory
information
Upper motor neuron continues to
brain for
Lower motor neuron interpretation
Lower motor
neuron

Motor pathways originate in the motor strip of the cerebral cortex, descending
to cross at the brainstem before traveling down the contralateral cord Spinal
(Figure 1). At the end of the upper motor neuron pathway, the impulse Step 1:
Reflex Noxious
activates the lower motor nerve that causes the muscle activity.
The right side of the brain makes the left side of the body work. stimulus
enters
dorsal spine
Figure 2 above shows the pathway for pain and temperature interpretation
(Spinothalamic). Painful stimuli enter the sensory nerve root in the dorsal horn
of the spinal cord (back of cord). This impulse crosses to the opposite side of
the cord, ascending to the contralateral parietal lobe for interpretation.
Step 2: Sensory to
Both motor and pain pathways are oriented toward the anterio-lateral cord, motor reflex arch
and are vulnerable to compromised anterior spinal artery flow. A common stimulates motor nerve
cervical cord injury is a flexion injury at C5-6. This can cause anterior spinal (muscle jerk)
artery occlusion and incomplete spinal cord injury with a loss of motor and Figure 3
pain function.

Spinal Reflex
The spinal reflex arch provides a rapid and protective motor response to noxious stimuli
(Figure 3). A noxious stimulus enters the sensory nerve via the dorsal root (Step 1). Sensory
information is immediately transmitted to the lower motor nerve at the same cord level (Step 2). This
sensory to motor communication is called the reflex arch, and triggers the muscle activity or jerk. The
sensory information continues to travel up the cord via the spinothalamic tract for interpretation of the
sensation by the brain (Step 3). Consequently, when you get a paper cut, you jerk your hand back first
and recognize the painful message after you have your protective motor response has already taken
place. As long as the spinal cord is intact, pain is perceived immediately after the muscle jerks.
In the setting of spinal cord injury, the jerk remains intact below the level of the lesion, but the
pain is not perceived. Preservation of this spinal reflex also occurs in brain death. It is
temporarily lost during the early spinal shock phase of an acute spinal cord injury.
 Spinal Cord Function

Pathways for light touch (Figure 5) are carried up both the spinothalamic tract and the
posterior columns (up the back of the cord, Figure 4). Proprioception (position sense) is also
carried up the posterior columns. Many spinal cord injuries are incomplete with preservation of
some function in one or more pathways.

Proprioception (Posterior Columns) Light touch (Posterior Columns

and Spinothalamic Pathway)

Brain Stem
Figure 4

Figure 5

Proprioception-Stereognosis

Posterior Columns

Spinothalamic

Incomplete Spinal Cord Syndromes

Central Cord Syndrome:

A central cord syndrome occurs when the worst cord damage is in the centre of the cord.
Because lower extremity motor pathways are located more laterally and upper extremity motor
pathways are closer to the centre of the cord, upper extremity deficits are usually worse than
lower extremity deficits in a central cord syndrome (patient can walk but not move their arms).
Bladder dysfunction is usually present, while vibration and proprioception may be spared.
There is variable sensory loss below the injury. Cervical level central cord injuries are often
caused by extreme hyperextension of the neck (hitting chin on the pavement and extending
head backward).

Brown-Sequard Syndrome:
This type of injury involves damage to one half of the cord, and may be due to penetrating
trauma or unilateral cord compression from tumour or hematoma. Because pain and motor
function for a given limb travel via opposite sides of the cord (Figure 1 and 2), Brown-Sequard
Syndrome is characterized by a loss of motor function below the level of the injury on the side
of the lesion, with preservation of pain and temperature. On the side opposite the lesion, pain
and temperature is lost but motor function is preserved below the injury.

Anterior Cord Injury:

This type of injury is often due to disruption of the anterior spinal artery, causing the worst cord
damage toward the front of the cord. Motor function and pain sensation are often the most
impaired, while preservation of the posterior columns may be present (light touch, vibration
and proprioception). Bladder dysfunction is usually present. This type of cord damage may be
due to injuries that cause flexion of the neck (chin to chest).
 Spinal Cord Injury

Spinal Shock
Following acute spinal cord injury, all reflexes above the level of injury are typically lost for a
period of hours to days or weeks. During this period known as spinal cord shock, the patient
typically has flaccid paralysis with a loss of deep tendon reflexes and bladder and bowel tone.
Anal sphincter reflex is one of the first reflexes to return after the spinal shock phase ends.
Reflex contraction of the anal sphincter (motor) following sensory stimulation suggests
resolution of the spinal shock phase. A gentle tug on the Foley catheter can provide the
sensory stimulus (bulbocavernosus reflex) that should automatically trigger anal sphincter
contraction.

The end of the spinal shock period is significant for the following reasons. One hopes that any
paralysis or sensory deficit immediately following an acute injury will be at least partially due
to swelling and spinal cord shock. When the shock period ends, continued absence of
sensation during a rectal exam and/or inability to voluntarily “squeeze” the anal sphincter is a
bad sign.

During spinal shock, the loss of the bladder and anal sphincter reflex is associated with
incontinence. Because relaxation to void or defecate is a voluntary function, the end of the
spinal shock phase is usually associated with urinary and fecal retention. Early and
aggressive bowel routine is important to facilitate future ADLs. Conversion to intermittent
catheterization should begin as soon as it is no longer necessary to measure hourly urine
output for other reasons and diuretic use is not required. Over distension of the bladder
should be avoided (500 ml per catheterization optimal); over distension can lead to overflow
incontinence and ureteral reflux.

An aggressive bowel routine that ensures a minimum of q 2 day bowel evacuation should be
instituted immediately, even before the spinal shock phase ends. Diarrhea may be present
during early training. The goal for bowel function is to have a soft stool q 2 days with
evacuation aided by digital stimulation, suppository and fleet if required.

Neurogenic Shock
Neurogenic shock usually mirrors the spinal shock phase (loss of spinal reflexes). It is
characterized by vasodilation, hypotension and bradycardia, due to disruption of autonomic
fibres below the level of the injury. Neurogenic shock usually improves or resolves with time,
however, it may remain an ongoing problem for individuals with complete and high cervical
cord injuries. Turning, head of bed elevation and suctioning can precipitate bradycardia and
hypotension. Cardiac arrest can also occur. Gradual and careful position changes and the
use of TED stockings/abdominal binders to prevent positional hypotension, can help.
Preoxygenation with 100% oxygen and abrupt termination of suctioning with return to
mechanical ventilation will usually resolve bradycardias induced by suctioning. Atropine
should be available at the bedside. Temporary pacemakers are occasionally required, less
frequently, patients may need permanent cardiac pacing.

Other causes for shock (e.g., sepsis, myocardial infarction, hypovolemia may be masked by
the loss of sympathetic response.
 Spinal Cord Injury

Autonomic Dysreflexia
Following resolution of the spinal shock phase with return of spinal cord reflexes, patients with
spinal cord injury are at risk for the development of autonomic dysreflexia. The higher the
cord injury, the great the potential. Virtually all quadriplegics and most individuals with injuries
at or above T6 can experience this problem. Thus, patients with chronic spinal cord injury or
those with acute spinal cord injury and prolonged critical care admission should be monitored
for and taught to recognize signs of autonomic dysreflexia.

Autonomic dysreflexia is a life-threatening event that is triggered by a noxious stimulus.

Sensory input causes a release of catecholamines, with vasoconstriction and hypertension.
The rise in blood pressure stimulates carotid and aortic receptors, causing inhibitory
messages to be sent down the cord. Because inhibitory messages can only transcend as far
as the level of the injury, vasoconstriction (and hypertension) continues below the cord injury.
Vasodilation above the lesion causes facial flushing, profuse sweating, bounding headache,
nasal congestion and on occasion, Horner’s syndrome. The higher the injury, the greater the
hypertension. Vagal stimulation (which exits above the lesion) causes reflex slowing of the
heart. Signs and symptoms of autonomic dysreflexia include:

 Hypertension (may only be 20-30 mmHg above baseline)

 Vasoconstriction below lesion
 Vasodilation with flushing above lesion and bounding headache
 Profuse sweating above lesion
 Bradycardia
 Goose bumps above and sometimes below lesion
 Visual disturbance; spots may be visible by patient in visual fields
 Horner’s Syndrome: constriction of the pupil, mild eyelid droopiness, loss of sweating on
one side of face.

The most common trigger for autonomic dysreflexia is a full bowel or bladder. Inadequate
bowel routine, delayed intermittent catheterization or urinary tract infection are important and
common causes. Any painful situation, including procedures or physical therapy, can cause
this syndrome. Pregnancy, especially during labour and delivery in a patient with spinal cord
injury can precipitate autonomic dysreflexia.

The treatment priority is to remove the cause of the autonomic dyreflexia (e.g., bladder
catheterization, fecal disimpaction). Sitting the patient up can cause orthostatic lowering of the
blood pressure. If antihypertensives are needed, use rapid onset agents with a short duration
of action. Nitrates can be used, but are contraindicated if patients are receiving sildenafil or
other medications for erectile dysfunction. Calcium channel blockers such as nifedipine can
be useful; labetolol should be used with caution as it may worsen bradycardia.

Brenda Morgan
Clinical Nurse Specialist
Critical Care Trauma Centre
London Health Sciences Centre
Last Revision: April 23, 2014