Peripheral Nerve Disease and Spinal Cord Injury Flashcards

1
Q

What is trigeminal neuralgia?

A

Relative uncommon cranial nerve disorder (CN V); sensory branches of the maxillary and mandibular branches are involved. Irritation leads to increased firing of the afferent or sensory fibers and causes excruciating pain in the lips, upper/lower gums, cheeks, forehead or side of the nose

  1. pain, twitching, grimacing, frequent blinking/tearing during attack; possible facial sensory loss
  2. Attacks last seconds to 2-3 minutes. Clustering can occur
  3. Attacks are triggered by light cutaneous stimulation at a trigger zone along the distribution of nerve branches (chewing, tooth brushing, hot/cold air on face, yawning, talking)
  4. Severity of pain can disrupt life, lead to phsyical/psychological dysfunction and suicide
  5. seizure meds and nerve blocks are used to treat trigeminal neuralgia
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2
Q

What are the TNIs for trigeminal neuralgia?

A
  1. Health promotion: goal is to reduce recurrent episodes in those who have trigeminal neuralgia
  2. Acute Intervention:
    1. pain relief through medication therapy
    2. caution with opioids due to risk of addiciton over time
    3. keep room at an even, moderate temp and free of drafts; private room
    4. nurse should avoid touching the patient’s face or jarring the bed
    5. Teach importance of hygiene, nutrition, and oral care
    6. lukewarm, soft washcloths with solutions that don’t require rinsing
    7. small, soft bristled toothbrush or warm mouthwash for oral care
    8. hygiene activities carried out when meds are at their peak action
    9. avoid extra conversation during acute period (alternative communication)
    10. food: high in protein and calories, easy to chew, lukewarm, offered frequently
    11. NG tube inserted on unaffected side for enteral feedings if poor po intake
  3. Ambulatory/Home
    1. plan regular follow up care
    2. teach re: dosage/side effects of medications
    3. teach to keep environmental stimuli to moderate level and to reduce stress
    4. teach re interventions (chew on unaffected side, avoid hot foods/drink)
    5. check oral cavity after meals to remove food particles, meticulous oral care
    6. regular dental visits, wear a protective eye shield
    7. protect face against temperature extremes, use an electric razor
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3
Q

What is Bell’s Palsy?

A

Disorder characterized by a disruption of the motor branches of the facial nerve (CN VII) on one side of the face in the absence of any other disease (ie stroke)

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4
Q

What are the signs and symptoms of Bell’s Palsy?

A
  1. acute peripheral facial paresis of unknown cause
  2. considered benign, with full recovery after six months in most patients, especially if treatment is started immediately
  3. looks like stroke but no other symptoms of stroke
  4. fever, tinnitus, hearing loss, loss of taste
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5
Q

What are the TNIs for Bell’s Palsy?

A
  • Corticosteroids started immediately, especially before paralysis is complete, then tapered down
  • mild analgesics may be used for pain relief, along with moist heat
  • associated with HSV, so treatement with acyclovir may be recommended
  • protect face from cold and drafts because trigeminal hyperesthesia (extreme sensitivity to pain or touch) may be present
  • maintain good nutrition, good oral hygiene
  • dark glasses, artificial tears to prevent drying of cornea, eye inspected for eye lashes
  • taping eyelids closed at night may be necessary to provide protection; report ocular pain/drainage
  • facial sling may be helpful to support affected muscles
  • when function begins to return, active facial exercises are performed several times per day
  • teach patients that most patients recover within about six weeks of the onset of symptoms
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6
Q

What is Guillian Barre Syndrome?

A

acute, progressive, ascending segmental demyelination with edema and inflammation in the peripheral nerves. Etiology is unknown, but it’s believed to be a cell-mediated immunologic reaction directed at the peripheral nerves. Demyelination occurs and transmission of nerve impulses is slowed or stopped.

The muscles innervated by the affected peripheral nerves become weak and atrophy. Parasthesias (numbness and tingling) also occur. In more severe cases, the autonomic nervous system is involved and clients can have orthostatic hypotension, hypertension, bradycardia, heart block and bowel/bladder dysfunction. The most serious complication is respiratory failure; other complications include autonomic dysfunction. Pain is also a common symptom of GBS.

Pathophysiology of GBS: autoimmune peripheral nerve demyelinization, usually triggered by a stressor of the immune system

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7
Q

What are the signs and symptoms of GBS?

A
  1. Ascending weakness
  2. Ascending parasthesia
  3. hypotonia
  4. pain
  5. GBS can be mild or severe with respiratory involvement
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8
Q

What are risk factors for GBS?

A
  1. flu/illness
  2. trauma
  3. surgery
  4. immunization
  5. HIV
  6. childbirth
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9
Q

What are the diagnostic studies for GBS?

A

Nerve conduction exam; diagnosis based on clinical symptoms/history. Nursing care is aimed at managing symptoms and preventing complications. Outcomes for GBS patients:

  1. return to usual level of physical funcitoning
  2. be free from pain and discomfort
  3. maintain nutritional status
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10
Q

What are the priority TNIs for GBS patients?

A
  1. Assessment: how far up has it progressed? Is respiratory involved? Spirometry/FEV1 used to assess respiratory system. Listen to lung sounds and assess work of breathing
  2. plasmapheresis: dialysis catheter is used to remove blood, separate the “bad” component, and replace remaining blood
  3. safety: patient is at risk for injury and risk for aspiration (be prepared to intubate/trach)
  4. may require foley if no feeling in bladder (can’t tell if they have to urinate)
  5. may require months of years of rehab; can have some residual effects
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11
Q

What is reflex urinary incontinence?

A

Involuntary loss of urine at somewhat perdictable intervals when a specific bladder volume is reached. Involuntary loss of urine caused by a defect in the spinal cord between the nerve roots at or below the first cervical segment and those above the second sacral segement. Urine elimination occurs at unpredictable intervals; mictrition may be elicited by tactile stimuli (ie. stroking the inner thigh or perineum)

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12
Q

What are the TNIs for reflex urinary incontinence?

A
  1. assess neuro functioning and ability to perform bladder management tasks
  2. inspect perineal/perigential skin
  3. complete bladder log to determine pattern of urine elimination, incontinence episodes, current bladder management program
  4. determine a bladder management program in consultation with the client, family, and rehab team
  5. teach to consume adequate amounts of fluids daily (30mL/kg/day)
  6. advise that cranberry is fine but does NOT reduce the risk of UTI
  7. intermittent catheterization with modified clean/sterile technique (per hospital policy)
  8. teach client/family intermittent catheterization
  9. teach condom catheter application. must be removed daily to clean/inspect skin. new one each day
  10. teach signs and symptoms of UTI to report to MD
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13
Q

What is autonomic dysreflexia?

A

life-threatening uninhibited sympathetic response of the nervous system to a noxious stimuli after a spinal cord injury at T7 or above

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14
Q

What are the defining characteristics of autonomic dysreflexia?

A
  1. brady or tachy, HTN, diaphoresis, red patches ABOVE level of injury
  2. Facial flushing, pallor; no sweating BELOW the level of injury
  3. blurred vision, chest pain, HA, conjunctival congestion, metallic taste in the mouth, nasal congestion, chills, potential for intracerebral hemorrhage, seizures, intraocular hemorrhage due to increased HTN
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15
Q

What are the TNIs of autonomic dysreflexia?

A
  • Monitor signs and symptoms of autonomic dysreflexia, esp with high level/extensive spinal cord injuries
  • Collaborate with HCPs to ID cause of dysreflexias
  • If dysreflexia: high fowlers, remove binders/TEDs, determine noxious stimuli
  • If BP can’t be lowered within one minute, notify MD stat
  • Determine source: bladder, bowel, or skin
  • Initiate hypertensive meds as soon as ordered
  • Be careful not to increase noxious stimuli - use numbing agent/spray
  • Monitor VS q3-5 minutes during acute event; continue to monitor after the event
  • Watch for complications ie cerebral hemorrhage, seizures, MI, intraocular hemorrhage
  • Accruately document any incidences of dysreglexia esp note the precipiatating stimuli

TNIs to PREVENT DYSREFLEXIA:

  1. Ensure foley drains and bladder is not distended
  2. Ensure regular BMs and avoid fecal impactation; frequently change positions to relieve pressure and prevent pressure ulcers; wedgies/wrinkles on sheets, too

If ordered, anesthetic agent to wounds below level of injury before performing wound care. Treatment: BETA BLOCKERS IVP (is metroprolol, esmalol)

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16
Q

What are the clinical manifestations of spinal cord injury?

A
  1. motor and sesnory impairment/dysfunction (decreased muscle strength, sensation, no reflexes)
  2. autonomic dysfunction (lack of sympathetic tone below level of injury)
    1. bradycardia and hypotension due to decreased sympathetic tone/unopposed vagal response
    2. neurogenic bladder, bowel, skin
    3. thermoregulation difficulties
    4. respiratory involvement (breathing shallow- potential for airway problems)
    5. all clinical manifestations depend on the level of injury
17
Q

What are the spinal levels?

A

Cervial levels: 1-8 (breakfast at 8)

Thoracic levels 1-12 (lunch at 12)

Lumbar levels 1-5 (dinner at 5)

18
Q

What is the nursing management for spinal cord injuries?

A
  1. Prevention first - teach safety measures to prevent spinal cord injury
  2. Sustain life and prevent secondary cord damage:
    1. stabilize back (possible traction)
    2. cardiac monitor (bradycardia)
    3. foley if unable to feel bladder
    4. IV access
    5. SCDs to increase venous return
    6. Monitor temperature (unable to autoregulate)
    7. Prevent complications
    8. Psychological/emotional support
19
Q
A
20
Q

Trigeminal Neuraligia

A

Cranial nerve V

Sudden, usually unilateral, severe, brief, stabbing, recurrent episodes of pain in the lips, upper or lower gums, cheek, forehead or side of the nose (along the nerve branches of the trigeminal nerve). Twitching, grimacing, and frequent blinking and tearing of the eye occur. Some patients expeirence facial sensory loss. Attacks are usually brief lasting only seconds to 2-3 minutes. Attacks are usually initiated by a triggering event (chewing, teeth brushing, washing the face, yawning or even talking). Condition is considered benign but the severity of the pain and the disruption of lifestyle can result in almost physical and psychologic dysfunction or even suicide. Treatment options include: medications such as carbamazepine (Tegretol), nerve blocking, biofeedback, and/or surgical therapy

21
Q

Bell’s Palsy

A

Cranicl Nerve VII

Inflammation of the facial nerve on one side of the face in the absence of any other disease. Cause is unknown but may be related to activation of herpes simplex virus. Benign and most patients recover fully in 6 months although some patients have symptoms. Symptoms: pain around and behind the ear, fever, tinnitus, drooping of the mouth with drooling, inability to close the eyelid, unilateral loss of taste. Decreased muscle movement may alter chewing ability. May be unable to close eyelid, smile, frown, or whistle. Treatment: moist heat, gentle massage, electrical stimulation of the nerve, mild analgesics, corticosteroids, acyclovir (Zovirax) and artifical tears

22
Q

GBS

A

GBS is an acute, rapidly progressing, demylinating ascending with edema and inflammation. The etiology is unknown but it is believed to be a cell-mediated immunologic reaction directed at the peripheral nerves. Demylination occurs and transmission of nerve impulses is slowed or stopped. The muscles innervated by the affected peripheral nerves undergo denervation and atrophy.

Weakness of the lower extremities occurs. Parasthesias (numbness and tingling) is frequent. Hypotonia (reduced muscle tone) and areflexia (lack of reflexes) is common. In cases with more severe muscle involvement and respiratory paralysis autonomic disturbances are seen. These include: orthostatic hypotension, hypertension, bradycardia, heart block, and bowel/bladder dysfunction, facial flushing, and diaphoresis. Pain is also a common symptom. Respiratory failure is the most serious complication. Nursing care is aimed at managing symptoms and preventing complications until the patient recovers.

23
Q

What are outcomes for a patient with GBS?

A
  1. Will maintain adequate ventillation
  2. Will not aspirate
  3. Will be pain free or have adequate pain control
  4. Maintain an acceptable level of communication
  5. Maintain adequate nutrition
  6. Return to previous physical functioning
24
Q

Primary Injury

A

Result of disruption of axons as a result of stretch or laceration injury

25
Q

Secondary Injury

A

Ongoing, progressive damage that occurs after the initial injury (ischemic, hypoxia, microhemorrhage, edema) occurs over time, the extent of injury and prognosis for recovery are most accurately determined at least 72 hours after primary injury.

*reason for not moving patient after primary injury

26
Q

Spinal Shock

A

Decreased reflexes, loss of sensation, and flaccid paralysis below the level of the injury; 50% of patients experience; lasts days to months

27
Q

Neurogenic Shock

A

Due to the loss of vasomotor tone caused by injury and is characterized by hypotension, bradycardia, and warm, dry skin. Loss of synpathetic nervous system innervations below the level of injury causes peripheral vasodilation, venous pooling, and decreased CO. Generally associated with cervical or high thoracic injury.

28
Q

Paraplegia

A

Loss of motor function in both lower extremities (partial or complete). Depends on level of spinal injury

29
Q

Tetraplegia

A

All extremities loss of motor function and sensation. Usually with some degree of respiratory dysfunction

30
Q

Neurogenic Bladder

A

abnormal/absent bladder innervation

31
Q

Neurogenic Bowel

A

bowel/defecation dysfunction due to disruption of innervation to bowel, rectum and anus. Requires “bowel program”

32
Q

Neurogenic Skin

A

Lack of innervation below level of injury. Prevention of skin break down is a priority. Skin should be inspected bid

33
Q

Autonomic Dysreflexia

A

Massive uncompensated cardiovascular reaction mediated by sympathetic nervous system. It occurs in response to visceral stimulation in SC lesions above T7. Symptoms are HTN, HA, blurred vision, diaphoresis above lesion with piloerection

34
Q

Reflex Urinary Incontinence

A

Involuntary loss of urine at somewhat predictabble intervals when a specific bladder volume is reached or when elicited by tactile stimulation such as stroking of inner aspect of thigh or perineum. Seen with paralyzing spinal disorders affecting spinal segments C1 to S2

Defining Characterisitcs:

  1. Absent/diminished sensation or urge to void
  2. Incomplete emptying of bladder
  3. May be associated with autonomic dysreflexia

Nursing Interventions:

  1. Develop bladder regimen program in conjunction with patient and family, which might include spotaneous voiding, intermittent self-cath., reflex voiding with condom cath containment or indwelling cath
  2. Ensure adequate fluid intake
  3. Protect skin integrity
  4. Protect dignity
35
Q

Nursing diagnosis: Autonomic Dysreflexia

A

At risk for life threatening uninhibited response of sympathetic nervous system; post-spinal shock; in an individual with spinal cord injury or lesions at T6/7 or above

Defining Characteristics:

  1. Bradycardia
  2. HTN
  3. HA
  4. Blurred vision
  5. Pale below level of injury
  6. Chest pain
  7. Chilling
  8. conjuctival congestion
  9. diaphoresis above injury
  10. parasthesia
  11. paroxysmal HTN
  12. pilomotor reflex
  13. tachycardia
  14. red splotches on skin above injury

Related Factors:

  1. bladder distention
  2. bowel distention
  3. skin irritation

Nursing Interventions:

  1. Monitor for symptoms and identify cause
    1. remove tight clothes - assess skin, look for points of pressure
    2. Assess skin- points of pressure
    3. assess bladder fx
    4. assess bowel fx, check for impaction after using topic anesthetic
  2. If signs are present, put patient in high fowler’s
  3. If BP cannot be decreased within 1 minute, notify provider STAT
  4. Initiate HTN therapy ASAP and monitor for dysrhythmias
  5. Do NOT increase noxious sensory stimuli- monitor VS q3-5 mins during acute event; continue monitoring VS after event resolved
  6. Monitor for complications of dysreflexia (signs of cerebral hemorrhage, seizures, MI, intraocular hemorrhage)
  7. Record incidence of dysreflexia noting the precipitating stimuli
  8. Notify members of the health care team
  9. Teach recognition interventions to prevent dysreflexia and earliest symptoms of dysreflexia to patient/caregivers
  10. Actions to be taken if they occur
  11. For patients at home instruct to call 911
36
Q

What are the priority assessments for GBS?

A
  1. respiratory fx - vital capacity, RR, SpO2, work of breathing, lung sounds and ABGs as ordered, be prepared for intubation
  2. Gag and swallowing reflex to determine aspiration risk
  3. Autonomic dysreflexia - bradycarida, dysrhythmias, orthostatic hypotension, secondary muscle atony
  4. Urinary rentention - intermittent VS indwelling, bladder scanner
  5. Constipation
  6. Skin integrity
  7. Injury risk due to weakness
37
Q

What are the priority nursing interventions for GBS?

A
  1. Nutritional support - assistance, raise HOB flex head forward or tube feeding, monitor weight, serum albumin, calorie counts, delayed gastric emptying may be a problem, maintain fluid
  2. Communication
  3. Pain management
  4. Provide ROM
  5. Psychosocial/emotional support - complete recovery can be anticipated but slow process takes months to years
38
Q

What is the medical management of GBS?

A
  1. Plasmapheresis - used in the 1st 2 weeks, maintain integrity of central access, explain procedure
  2. High dose immunoglobulin, patient must be well hydrated and have adequate renal function