4110-MS II Neuro Guided Reading
Read chapter 60, pp 1403-1427 to answer the following questions on neurological nursing
care.
1. What is the difference between primary and secondary injuries in spinal cord injuries
(SCI)?
Primary injury results from direct physical trauma to the spinal cord due to blunt
or penetrating trauma. Trauma can cause spinal cord compression by bone
displacement, interruption of blood supply, or distraction from pulling.
Secondary injury refers to the ongoing, progressive damage that occurs after the
primary injury. Secondary injury causes further permanent damage. It begins a few
minutes after injury and lasts for months. hese events result in edema, ischemia,
and inflammation. They result in cell death, disruption of the blood-brain barrier,
and demyelination. This can extend the level of deficit and worsen long-term
outcome
2. In a secondary injury, what effect does the vasoactive substances serotonin,
norepinephrine and dopamine have on the spinal cord blood flow?
An increase in vasoactive substances, including norepinephrine, serotonin, and
dopamine, occur. High levels of these substances cause vasospasms and hypoxia
with subsequent necrosis. Unfortunately, the spinal cord has minimal ability to
adapt to vasospasm.
3. What is a glial scar? What is the impact of a glial scar?
The inflammatory response at the site of the initial injury focuses on clearing up the
initial cellular debris without damaging normal tissue. This results in a central nonneural core of connective tissue that we refer to as a glial scar (Fig. 60.2).
The glial scar creates a physical barrier. It restricts the cells in the spinal cord from
migration and regeneration. This leads to irreversible nerve damage and permanent
neurologic deficit.
4. What is the term for the temporary (can last for weeks) state of decreased/absent
reflexes, sensation and paralysis that can mask the permanent effects of an SCI?
Spinal shock may occur shortly after acute SCI. It is characterized by loss of deep
tendon and sphincter reflexes, loss of sensation, and flaccid paralysis below the
level of injury. This syndrome lasts days to weeks. It often masks postinjury
neurologic function. 3
5. Describe neurogenic shock. What changes in vital signs characterize neurogenic
shock?
Neurogenic (vasogenic) shock can occur in cervical
or high thoracic injury (T6 or higher). It occurs from unopposed parasympathetic
response due to loss of sympathetic nervous system (SNS) innervation.
It causes peripheral vasodilation, venous pooling, and decreased cardiac output.
Manifestations include significant hypotension (< 90 mmHg), bradycardia,
and temperature dysregulation.
6. How does an injury at C3 or above impact the respiratory system?
Cervical injuries above C3 present special problems because of the total loss of
respiratory muscle function. These patients have respiratory arrest within
minutes of injury if not intubated.
Patients with high cervical injury (C3-5) have respiratory insufficiency due to loss
of phrenic nerve innervation to the diaphragm and decreases in chest and
abdominal wall strength. 8 Patients with complete SCI
above C5 should be intubated at once.
7. How does an upper thoracic or lower cervical injury increase the risk of pulmonary
dysfunction and infection?
Associated traumatic injuries, such as lung contusions, can further compromise
pulmonary function. Fluid overload can cause pulmonary edema. Neurogenic
pulmonary edema may occur due to a dramatic increase in SNS activity at the
time
of injury
8. In order to cause tetraplegia (quadriplegia), a SCI is typically located in what skeletal
region? What regions result in paraplegia?
Injury from C1 to T1 can cause paralysis of all 4 extremities, resulting in
tetraplegia (formerly called quadriplegia). The degree of impairment in the arms
after cervical injury depends on the level of injury. The lower the level, the more
function is retained in the arms.
Paraplegia (paralysis and loss of sensation in the legs) can occur in SCI below
the level of T2. 2 Fig. 60.4 shows affected structures and functions at different
levels of cord injury.
9. What level of injury causes possible dysfunction of the sympathetic nervous system?
What effect does this have on heart rate and blood pressure?
Any cord injury above T6 leads to dysfunction of the SNS.
The result may be bradycardia, peripheral vasodilation, and hypotension
(neurogenic shock).
Peripheral vasodilation causes relative hypovolemia because of the increase in
the capacity of the dilated veins. It reduces venous return of blood to the heart.
Cardiac output then decreases, leading to hypotension.
10. What are common problems as a result of neurogenic bladder? What is the greater
concern, retention or incontinence? Does this pose a risk in the acute period following
an SCI (spinal shock)?
Neurogenic bladder describes any type of bladder dysfunction related to abnormal
or absent bladder innervation.
After SCI, the ability for the bladder muscles and the micturition center in the brain
to transmit information is impaired. Both the detrusor muscle (bladder wall) and
sphincter muscle (a valve around the top of the urethra) may be overactive due to
the lack of brain control.
(1) have no reflex detrusor contractions (flaccid, hypotonic), which can result in
bladder stretching from overdistention; (2) have hyperactive reflex detrusor
contractions (spastic), seen in SCI above T12, leading to incontinence; or (3) lack
coordination between detrusor contraction and urethral relaxation (dyssynergia),
resulting in reflux of urine into the kidneys. Reflux into the kidneys can lead to
stone formation, hydronephrosis, pyelonephritis, and renal failure
11. Why is a patient at a high risk of stress ulcers post SCI? What is the main
complication related to gastric ulcers and how will this risk be detected?
Gastric emptying may be delayed, especially in patients with higher level SCI.
Excessive release of hydrochloric acid (HCl) in the stomach may cause stress
ulcers
12. What is poikilothermism? How does this impact nursing care? Who is at a higher risk
of not being able to control their body temperature?
Poikilothermia is the inability to maintain a constant core temperature, with the
patient assuming the temperature of the environment. It occurs in SCI because
interruption of the SNS prevents peripheral temperature sensations from reaching
the hypothalamus.
13. What is the preferred study to diagnose location, degree and compromise of SCI?
CT scan is the preferred imaging study to diagnose the location and degree of
injury and the degree of spinal canal compromise.
Cervical x-rays are done when CT scan is not readily available. However, it is
hard to see C7 and T1 on a cervical x-ray, decreasing the ability to fully evaluate a
cervical spine injury.
14. What are the four post injury goals of prehospital care post SCI?
Goals immediately after injury include maintaining a patent airway, adequate
ventilation/breathing, and adequate circulating blood volume (ABCs) and
preventing extension of spinal cord damage (secondary injury). Table 60.3
outlines emergency management of the patient with SCI.
15. What type of surgery might be done to stabilize the spine if two or more vertebrae
have been injured?
Fixation involves attaching metal screws, plates, or other devices to the bones of
the spine to help keep them aligned. This procedure is usually done when 2 or more
vertebrae are injured. Small pieces of bone may be attached to the injured bones to
help them fuse into 1 solid piece.
16. Why is low molecular weight heparin (enoxaparin) used post SCI? Why would
vasopressors be used in the acute phase post injury?
VTE prophylaxis with low-molecular-weight heparin (LMWH) (e.g.,
enoxaparin [Lovenox]) or fixed, low-dose heparin should start within 72 hours
after injury, unless contraindicated. Contraindications include internal or external
bleeding and recent surgery. For those with abnormal kidney function, heparin is
best as LMWH is mainly excreted via the kidneys
Vasopressor agents (e.g., phenylephrine, norepinephrine) are used in the acute
phase of injury as adjuvants to treatment. They maintain the MAP to improve
perfusion to the spinal cord.
*note the book’s explanation of lack of clear evidence on use of methylprednisolone
for acute SCI.
17. What are Crutchfield or Gardner-Wells tongs (or halo ring). What action should you
take if the tongs become dislodged?
Crutchfield (Fig. 60.6) or Gardner-Wells tongs or halo
(halo ring) can provide this type of traction. A rope extends from the center of
the device over a pulley to weights attached at the end. Traction must be
maintained at all times. Possible displacement of the skull pins is a disadvantage of
tongs. If pin displacement occurs, hold the patient’s head in a neutral position and
get help. Immobilize the head while the HCP reinserts the tongs.
18. How and why are assisted coughing exercises performed?
Clearing secretions is vital in reducing the risk for lung complications and
possible respiratory failure. 16 Perform tracheal suctioning if crackles or coarse
breath sounds are present.
Chest physiotherapy and assisted (augmented) coughing can help. Perform assisted
coughing either manually, by placing the heels of both hands just below the xiphoid
process and exert firm upward pressure to the area timed with the patient’s efforts
to cough (see Fig. 67.6), or mechanically with an insufflation-exsufflation device.
Encourage the use of incentive spirometry.
19. What physiological mechanisms result in bradycardia in some clients with SCI? What
anticholinergic drug can be used if the patient has symptomatic bradycardia?
Heart rate is slowed, often to less than 60 beats/min, because of unopposed vagal
response. Any increase in vagal stimulation, as occurs with turning or suctioning,
can cause cardiac arrest.
20. What diet should be given for clients with SCI?
Due to severe catabolism, a high-protein, high-calorie diet is needed for energy and
tissue repair.
21. Once a patient post SCI is stabilized, what type of catheterization is typically used to
decrease risk of CAUTI? How much urine stored in the bladder places the patient at
risk for bladder distention?
The best way to prevent CAUTI is regular and complete bladder drainage. Once the
patient is stabilized, assess the best means of managing long-term urinary function.
Clean intermittent catheterization (CIC) is the preferred method for emptying
the bladder. CAUTI and CIC are discussed in Chapter 45. CIC should be done 4 to
6 times daily to prevent bacterial overgrowth from urinary stasis. Keep urine
residuals under 500 mL to prevent bladder distention.
22. What are the typical two components of a bowel program for a patient with
neurogenic bowel?
This involves inserting a rectal stimulant (suppository or small-volume enema)
daily at a regular time, followed by gentle digital stimulation or manual evacuation
until evacuation is complete.
23. What medications are used to prevent stress ulcers?
Histamine (H2 )-receptor blockers (e.g., ranitidine) or proton pump inhibitors
(e.g., pantoprazole, omeprazole) given prophylactically decreases the secretion of
HCl acid and prevents ulcers.
24. Can a patient with a SCI have pain? What medications might be appropriate?
Musculoskeletal nociceptive pain can develop from injuries to bones, muscles,
and ligaments.
The pain is worse with movement or palpation. Antiinflammatory
drugs, such as ibuprofen (Motrin), may help with pain. Opioids may be used to
manage nociceptive pain
25. Once spinal shock has resolved and the reflexes have returned, what complication
could arise in clients with T6 or above injuries when the sympathetic nervous system
responds to sensory stimulation? What affect does this complication have on the
body?
Once spinal cord shock is resolved, return of reflexes may complicate
rehabilitation. Lacking control from the higher brain centers, reflexes are often
hyperactive and have exaggerated responses. Penile erection can occur from a
variety of stimuli, causing embarrassment and discomfort. Spasms ranging from
mild twitches to convulsive movements below the level of injury may occur
26. What immediate interventions should be taken during an episode of autonomic
dysreflexia (hyperreflexia) What S/S might indicate an episode?
Autonomic dysreflexia (AD) is a massive, uncompensated cardiovascular reaction
mediated by the SNS. It involves stimulation of sensory receptors below the level
of the SCI. The intact SNS below the level of injury responds to the stimulation
with a reflex arteriolar vasoconstriction that increases BP. The parasympathetic
nervous system is unable to directly counteract these responses via the injured
spinal cord.
27. What is the first line treatment for impotence in men post SCI?
Treatment for erectile dysfunction includes drugs, vacuum devices, and surgical
procedures. Phosphodiesterase inhibitors (e.g., sildenafil [Viagra]) have become
the first-line treatment in men with SCI between T6 and L5. Sexual stimulation
is needed to get an erection after taking the medication. Penile injection of
vasoactive substances (papaverine, alprostadil, or a combination) is another
medical treatment.
28. What cranial nerve (CN) is affected in trigeminal neuralgia? Is it the motor or sensory
function that is affected? Answer the same questions about Bell’s palsy.
Trigeminal neuralgia (TN) (tic douloureux) is characterized by sudden, usually
unilateral, severe, brief, stabbing, recurrent episodes of pain in the distribution of
the trigeminal nerve. The fifth cranial nerve (CN V).
29. What strategies can be employed by the nurse to decrease the number of trigeminal
neuralgia attacks?
• Drug therapy
• Antiseizure drugs (e.g., carbamazepine, oxcarbazepine [Trileptal],
gabapentin [Neurontin])
• Tricyclic antidepressants (e.g., amitriptyline)
• Local nerve block
• Surgical therapy (Table 60.15)
30. What modifications might be made to a patient for oral care and nutrition who has
trigeminal neuralgia?
31. Why are heat packs sometimes used for Bell’s Palsy?
Moist heat can reduce discomfort and aid circulation
32. Describe the characteristic paralysis that occurs in Guillan Barre Syndrome (GBS)?
The main features of GBS include acute, ascending, rapidly progressive,
symmetric weakness of the limbs. The first symptoms are weakness, paresthesia
(numbness and tingling), and hypotonia (reduced muscle tone) of the limbs.
Reflexes in the affected limbs are weak or absent. Maximal weakness is reached in
4 weeks.
33. What affects are typically seen due to the autonomic nervous system dysfunction that
occurs with GBS?
Autonomic nervous system dysfunction occurs with AIDP and AMSAN,
causing orthostatic hypotension, hypertension, and abnormal vagal responses
(bradycardia, heart block, asystole). Other autonomic dysfunction effects include
bowel and bladder dysfunction, facial flushing, and diaphoresis. Cranial nerve
involvement manifests as facial weakness and paresthesia, extraocular eye
movement problems, and dysphagia.
34. What can cause the life-threatening complications related to the respiratory system in
GBS?
The most serious complication of GBS is respiratory failure. It occurs if the
paralysis progresses to nerves that innervate the thoracic area. Frequently assess
the respiratory system by checking respiratory rate and depth to determine the
need for immediate intervention, including intubation and mechanical ventilation.
35. In its severest form, tetanus can cause what life-threatening complication? What can
trigger these complications?
In severe forms, continuous tonic seizures may occur with
opisthotonos (extreme arching of the back and retraction of the head)
Patients are given immediate treatment with tetanus immune globulin (TIG)