Outcomes (NOC)	Interventions (NIC) and Rationales
Respiratory Status	Respiratory Monitoring
• Respiratory rate _____ • Respiratory rhythm _____ • Depth of respiration _____ • Auscultated breath sounds _____ • Tidal volume _____ • Achievement of expected incentive spirometer _____ • Vital capacity _____ • Oxygen saturation _____ • Pulmonary function tests _____ Measurement Scale 1 = Severe deviation from normal range 2 = Substantial deviation from normal range 3 = Moderate deviation from normal range 4 = Mild deviation from normal range 5 = No deviation from normal range	• Monitor rate, rhythm, depth, and effort of respirations to note baseline and changes in status. • Monitor for diaphragmatic muscle fatigue (paradoxic motion) to identify need for ventilation assistance. • Determine need for suctioning by auscultating for crackles and rhonchi over major airways. • Note changes in SaO₂, SvO₂, end-tidal CO₂, and ABG values. • Monitor pulmonary function test (PFT) values, particularly vital capacity, maximal inspiratory force, and forced expiratory volume, to identify hypoventilation requiring mechanical ventilation. • Monitor patient’s ability to cough effectively to identify need for suctioning. Airway Management • Identify patient requiring actual/potential airway insertion to ensure timely intervention. • Perform endotracheal or nasotracheal suctioning to stimulate coughing and to clear respiratory secretions.

Nursing Diagnosis

Impaired skin integrity related to skull tong placement, immobility, and/or poor tissue perfusion as evidenced by open tong sites and reddened skin over bony prominences

Patient Goals

1. Demonstrates no signs of infection at skull tong sites

2. Maintains intact skin over bony prominences

Outcomes (NOC)	Interventions (NIC) and Rationales
Tissue Integrity: Skin and Mucous Membranes	Skin Surveillance
• Skin lesions _____ • Erythema _____ • Necrosis _____ • Induration_____ • Blanching _____ Measurement Scale 1 = Severe 2 = Substantial 3 = Moderate 4 = Mild 5 = None	• Monitor for sources of pressure and friction to identify areas at risk for breakdown. • Monitor for infection at open tong sites to promote early detection and treatment. Infection Control • Ensure appropriate wound care technique to prevent bacterial colonization at tong sites. Pressure Management • Monitor skin for areas of redness and breakdown so that interventions can be initiated promptly if a problem develops. • Place on an appropriate therapeutic mattress/bed to relieve pressure. • Use appropriate devices to keep heels and bony prominences off the bed. • Facilitate small shifts of body weight to relieve pressure without disrupting traction. • Monitor the patient’s nutritional status to maintain healthy skin resistant to breakdown.

Nursing Diagnosis

Constipation related to neurogenic bowel, inadequate fluid intake, diet low in roughage, and/or immobility as evidenced by lack of bowel movement for more than 2 days, decreased bowel sounds, palpable impaction, hard stool, or stool incontinence

Patient Goals

1. Establishes a bowel management program based on neurologic function and personal preference

2. Maintains a bowel movement no less than every other day

Outcomes (NOC)	Interventions (NIC) and Rationales
Bowel Elimination	Bowel Management
• Elimination pattern _____ • Control of bowel movements _____ • Stool soft and formed _____ • Ease of stool passage _____ Measurement Scale 1 = Severely compromised 2 = Substantially compromised 3 = Moderately compromised 4 = Mildly compromised 5 = Not compromised	• Monitor bowel movements, including frequency, consistency, shape, volume, and color, to establish baseline function. • Monitor bowel sounds to determine if peristalsis is present. • Instruct patient on foods high in fiber because bulk and fiber are necessary to the success of a bowel program. • Initiate a bowel training program to establish a bowel routine as quickly as possible.

Nursing Diagnosis

Impaired urinary elimination related to spinal injury and/or limited fluid intake as evidenced by urinary retention, bladder distention, involuntary emptying of bladder (after spinal shock)

Patient Goal

Establishes a bladder management program based on neurologic function, caregiver status, and lifestyle choices

Outcomes (NOC)	Interventions (NIC) and Rationales
Urinary Elimination	Urinary Retention Care
• Urinary retention _____ • Urinary incontinence _____ Measurement Scale 1 = Severe 2 = Substantial 3 = Moderate 4 = Mild 5 = None	• Monitor intake and output to evaluate fluid balance. • Monitor degree of bladder distention by palpation and percussion because loss of autonomic and reflex control of bladder and sphincter can cause urinary retention. • Insert urinary catheter to relieve urinary retention in spinal shock. • Implement intermittent catheterization in postacute phase of spinal cord injury to maintain bladder tone and avoid infection associated with long-term use of indwelling catheter. • Refer to urinary continence specialists to establish long-term bladder management program.

Nursing Diagnosis

Risk for autonomic dysreflexia related to reflex stimulation of sympathetic nervous system after spinal shock resolves

Patient Goals

1. Experiences no episodes of dysreflexia

2. Describes causes, prevention, symptoms, and management of dysreflexia

Outcomes (NOC)	Interventions (NIC) and Rationales
Neurologic Status: Autonomic	Dysreflexia Management
• Apical heart rate _____ • Systolic blood pressure _____ • Diastolic blood pressure _____ • Bowel elimination pattern _____ • Urinary elimination pattern _____ Measurement Scale 1 = Severely compromised 2 = Substantially compromised 3 = Moderately compromised 4 = Mildly compromised 5 = Not compromised • Headaches _____ • Dysreflexia _____ Measurement Scale 1 = Severe 2 = Substantial 3 = Moderate 4 = Mild 5 = None	• Identify and minimize stimuli that may precipitate dysreflexia: bladder distention, renal calculi, infection, fecal impaction, rectal examination, suppository insertion, skin breakdown, and constrictive clothing or bed linen. • Monitor for signs and symptoms of autonomic dysreflexia: paroxysmal hypertension, bradycardia, tachycardia, diaphoresis above the level of injury, facial flushing, pallor below the level of injury, headache, nasal congestion, engorgement of temporal and neck vessels, conjunctival congestion, chills without fever, pilomotor erection, and chest pain. • Investigate and treat or remove offending cause (e.g., distended bladder, fecal impaction, skin lesions, and constricting bedclothes). • Place head of bed in upright position if hyperreflexia occurs to reduce blood pressure by allowing blood to pool in the lower extremities. • Stay with patient and monitor status every 3-5 min if hyperreflexia occurs. • Administer antihypertensive agents intravenously as ordered to reduce blood pressure. • Instruct patient and caregiver about causes, symptoms, treatment, and prevention of dysreflexia to reverse occurrence and prevent occurrence of status epilepticus, stroke, and possible death.

Nursing Diagnosis

Ineffective coping related to loss of control over bodily functions and altered lifestyle secondary to paralysis as evidenced by verbalization of inability to cope, expression of anger or other negative feelings, refusal to discuss changes in function and/or participate in social contacts

Patient Goals

1. Reports ability to cope with effects of spinal cord injury

2. Expresses feelings of grief in adapting to losses related to chronic condition

Outcomes (NOC)	Interventions (NIC) and Rationales
Coping	Coping Enhancement
• Identifies effective coping patterns _____ • Identifies ineffective coping patterns _____ • Verbalizes sense of control _____ • Verbalizes acceptance of situation _____ • Modifies lifestyle as needed _____ • Uses personal support system _____ • Uses effective coping strategies _____ • Reports decrease in negative feelings _____ Measurement Scale 1 = Never demonstrated 2 = Rarely demonstrated 3 = Sometimes demonstrated 4 = Often demonstrated 5 = Consistently demonstrated	• Appraise patient’s adjustment to changes in body image. • Appraise impact of patient’s life situation on roles and relationships. • Provide an atmosphere of acceptance. • Encourage verbalization of feelings, perceptions, and fears to aid patient in clarifying feelings. • Provide factual information concerning diagnosis, treatment, and prognosis because knowledge of expectations can help patient cope with the future. • Provide patient with realistic choices about certain aspects of care. • Support use of appropriate defense mechanisms. • Assist patient to identify positive strategies to deal with limitations and manage needed lifestyle or role changes to prevent patient from practicing ineffective behaviors such as smoking, drinking, or angry outbursts. • Encourage family involvement to enhance patient’s sense of worth and value as a person. • Assist patient to grieve and work through the losses of chronic illness and/or disability because spinal cord injury results in a real loss, which requires adjustment through grieving.

ABG, Arterial blood gas; PFT, pulmonary function test; SaO₂, arterial oxygen saturation; SvO₂, venous oxygen saturation.

^*Nursing diagnoses listed in order of priority.

eTABLE 61-1

COMPARISON OF MULTIPLE SCLEROSIS AND GUILLAIN-BARRÉ SYNDROME

Multiple Sclerosis	Guillain-Barré Syndrome
• Chronic, progressive, degenerative disorder of the CNS	• Acute, rapidly progressing, and potentially fatal form of polyneuritis
• Characterized by disseminated demyelination of nerve fibers in brain and spinal cord	• Characterized by ascending, symmetric paralysis that usually affects cranial nerves and PNS
• Results in chronic inflammation, demyelination, and gliosis in CNS	• Results in loss of myelin (a segmental demyelination) and edema and inflammation of affected nerves
• Autoimmune disease thought to be triggered by a virus	• A syndrome that is preceded by a viral infection, trauma, surgery, viral immunizations, or HIV infection
• Onset is gradual and often insidious with vague symptoms occurring intermittently over months to years	• Onset is usually 1-3 wk after URI or GI infection, but symptoms of lower extremity weakness can occur over hours to days to weeks, usually peaking at about day 14
• Chronic, progressive deterioration with remissions and exacerbations that eventually lead to permanent deterioration in neurologic function	• Self-limiting with full neurologic recovery in most cases

CNS, Central nervous system; PNS, peripheral nervous system; URI, upper respiratory tract infection.

This chapter discusses peripheral nerve and spinal cord problems, including cranial nerve disorders, polyneuropathies, spinal cord injuries, and spinal cord tumors. A focus of this chapter is the nursing management of the many problems encountered by the patient with a spinal cord injury.

Cranial Nerve Disorders

Cranial nerve disorders are commonly classified as peripheral neuropathies. The 12 pairs of cranial nerves are considered the peripheral nerves of the brain. The disorders usually involve the motor or sensory (or both) branches of a single nerve (mononeuropathies). Causes of cranial nerve problems include tumors, trauma, infections, inflammatory processes, and idiopathic (unknown) causes. Two cranial nerve disorders discussed in this chapter are trigeminal neuralgia and Bell’s palsy.

Trigeminal Neuralgia

Trigeminal neuralgia (tic douloureux) is sudden, usually unilateral, severe, brief, stabbing, recurrent episodes of pain in the distribution of the trigeminal nerve. It is diagnosed in approximately 150,000 Americans each year and is the most commonly diagnosed neuralgic condition. It is seen approximately twice as often in women as in men. The majority of cases (more than 90%) are diagnosed in individuals over age 40.¹

Etiology and Pathophysiology

The trigeminal nerve is the fifth cranial nerve (CN V) and has both motor and sensory branches. In trigeminal neuralgia the sensory or afferent branches, primarily the maxillary and mandibular branches, are involved (Fig. 61-1).

FIG. 61-1 A, Trigeminal (fifth cranial) nerve and its three main divisions: ophthalmic, maxillary, and mandibular nerves. B, Cutaneous innervation of the head.

The etiology and pathophysiology of trigeminal neuralgia is not fully understood.² One theory is that blood vessels, especially the superior cerebellar artery, become compressed, resulting in chronic irritation of the trigeminal nerve at the root entry zone. This irritation leads to increased firing of the afferent or sensory fibers. Risk factors are multiple sclerosis and hypertension. Other factors that may cause neuralgia include herpesvirus infection, infection of the teeth and jaw, and a brainstem infarct.

TABLE 61-2

SURGICAL THERAPY FOR TRIGEMINAL NEURALGIA

Procedure	Description	Effect
Peripheral
Glycerol rhizotomy (injection into one or more branches of the trigeminal nerve)	Chemical ablation	Total pain relief with sparing of touch and corneal reflex.
Intracranial
Percutaneous radiofrequency rhizotomy	Destruction of sensory fibers by low-voltage current	Total pain relief, sparing of touch and corneal reflex (increased risk for sensory changes).
Microvascular decompression	Lifting of artery pressing on nerve root in posterior fossa with wedge of sponge, leading to removal of pressure at nerve-root entry zone, or removing the involved vessel	Pain relief without loss of sensation.
Gamma knife radiosurgery	Technique that uses high doses of radiation focused on the trigeminal nerve root using stereotactic localization	Pain relief 1 day–4 mo posttreatment. Noninvasive with no loss of sensation.

Drug Therapy.

Antiseizure drug therapy may reduce pain by stabilizing the neuronal membrane and blocking nerve firing.² These first-line drugs include carbamazepine (Tegretol), oxcarbazepine (Trileptal), topiramate (Topamax), clonazepam (Klonopin), phenytoin (Dilantin), lamotrigine (Lamictal), and divalproex (Depakote). Gabapentin (Neurontin) or baclofen (Lioresal) can be used in combination with any of the antiseizure drugs if a single agent is not effective. Tricyclic antidepressants such as amitriptyline (Elavil) or nortriptyline (Pamelor, Aventyl) can be used to treat constant burning, or aching pain.² Analgesics or opioids are usually not effective in controlling pain.

Conservative Therapy.

Nerve blocking with local anesthetics is another treatment option. Relief of pain is temporary, lasting from 6 to 18 months. This treatment is usually tolerated well by older adults.

Some patients use complementary and alternative therapies, usually in combination with drug treatment. These techniques include acupuncture, biofeedback, vitamin therapy, nutritional therapy, and electrical stimulation of the nerves.

Surgical Therapy.

If a conservative approach including drug therapy is not effective, surgical therapy is available (see Table 61-2). Glycerol rhizotomy is a percutaneous procedure that consists of an injection of glycerol through the foramen ovale into the trigeminal cistern (Fig. 61-2).

FIG. 61-2 A, Patient with trigeminal neuralgia having needle placed. B, Physician injecting glycerol.

Percutaneous radiofrequency rhizotomy is an outpatient procedure consisting of placing a needle into the trigeminal rootlets that are adjacent to the pons and destroying the area by means of a radiofrequency current. This can result in facial numbness (although some degree of sensation may be retained), corneal anesthesia, and trigeminal motor weakness.³

Microvascular decompression of the trigeminal nerve is another commonly used procedure for neuralgia. It is done by first performing a small craniotomy behind the ear (suboccipital craniotomy). The next step involves displacing and repositioning the blood vessels that appear to be compressing the nerve at the root entry zone where it exits the pons. This procedure relieves pain without residual sensory loss, but it is potentially dangerous.³

Gamma knife radiosurgery is another surgical treatment that is used to treat trigeminal neuralgia. Radiosurgery (see Chapter 57) using a gamma knife provides precise radiation of the proximal trigeminal nerve identified on high-resolution imaging.

Nursing Management Trigeminal Neuralgia

Patients with trigeminal neuralgia are primarily treated on an outpatient basis. Assessment of the attacks, including the triggering factors, characteristics, frequency, and pain management techniques, helps you plan for patient care. The nursing assessment should include the patient’s nutritional status, hygiene (especially oral), and behavior (including withdrawal). Evaluate the degree of pain and its effects on the patient’s lifestyle, drug use, emotional state, and suicidal tendencies.

Monitor the patient’s response to drug therapy and note any side effects. Alternative pain relief measures, such as acupuncture and biofeedback, should be explored for the patient who is not a surgical candidate and whose pain is not controlled by other measures. Environmental management is essential during an acute period to decrease triggering stimuli. The room should be kept at an even, moderate temperature and free of drafts. Many patients prefer to carry out their own care, fearing that someone else will inadvertently injure them.

Teach the patient about the importance of nutrition, hygiene, and oral care and convey understanding if previous oral neglect is apparent. A small, soft-bristled toothbrush or a warm mouthwash assists in promoting oral care. Hygiene activities are best carried out when analgesia is at its peak.

Food should be high in protein and calories and easy to chew. It should be served lukewarm and offered frequently. When oral intake is sharply reduced and the patient’s nutritional status is compromised, a nasogastric tube can be inserted on the unaffected side for enteral feedings.

Appropriate teaching related to surgical procedures depends on the type of procedure planned (e.g., percutaneous). Patients need to know that they will be awake during local procedures so that they can cooperate when corneal and ciliary reflexes and facial sensations are checked. After the procedure the patient’s pain is compared with the preoperative level. The corneal reflex, extraocular muscles, hearing, sensation, and facial nerve function are evaluated frequently (see Chapter 56). If the corneal reflex is impaired, take special care to protect the eyes. This includes the use of artificial tears or eye shields.

If intracranial surgery is performed, general postoperative nursing care after a craniotomy is appropriate. (Nursing care related to craniotomy is discussed in Chapter 57 on p. 1379.)

After a percutaneous radiofrequency procedure, apply an ice pack to the jaw on the operative side for 3 to 5 hours. To avoid injuring the mouth, the patient should not chew on the operative side until sensation has returned.

Plan for regular follow-up care, and instruct the patient on the dosage and side effects of medications. Although relief of pain may be complete, encourage the patient to keep environmental stimuli to a moderate level and to use stress management techniques. Long-term management after surgical intervention depends on the residual effects of the procedure. If anesthesia is present or the corneal reflex is altered, teach the patient to (1) chew on the unaffected side; (2) avoid hot foods or beverages, which can burn the mucous membranes; (3) check the oral cavity after meals to remove food particles; (4) practice meticulous oral hygiene and continue with semiannual dental visits; (5) protect the face against extremes of temperature; (6) use an electric razor; (7) wear a protective eye shield or avoid rubbing eyes; and (8) examine eye regularly for symptoms of infection or irritation.

Bell’s Palsy

Bell’s palsy (peripheral facial paralysis, acute benign cranial polyneuritis) is a disorder characterized by inflammation of the facial nerve (CN VII) on one side of the face in the absence of any other disease such as a stroke. Bell’s palsy is an acute, peripheral facial paresis of unknown cause. Each year approximately 40,000 Americans are diagnosed with Bell’s palsy. It can affect any age-group. Despite its good prognosis, Bell’s palsy leaves more than 8000 people a year in the United States with permanent, potentially disfiguring facial weakness.⁴

Etiology and Pathophysiology

Although the exact etiology is not known, it is believed that a viral infection such as viral meningitis or activation of herpes simplex virus 1 (HSV1) may trigger Bell’s palsy. The viral infection causes inflammation, edema, ischemia, and eventual demyelination of the nerve, creating pain and alterations in motor and sensory function. Bell’s palsy has also been associated with influenza or a flu-like illness, headaches, chronic middle ear infection, hypertension, diabetes, sarcoidosis, tumors, Lyme disease, and trauma such as skull fracture or facial injury.⁴

Bell’s palsy is considered benign, with full recovery in 3 to 6 months, especially if treatment is begun immediately. A small group of patients have long-term facial paralysis.⁴

Clinical Manifestations and Diagnostic Studies

The onset of Bell’s palsy is often accompanied by an outbreak of herpes vesicles in or around the ear. Patients may complain of pain around and behind the ear. Additional manifestations may include fever, tinnitus, and hearing deficit. Paralysis of the motor branches of the facial nerve typically results in flaccidity of the affected side of the face, with drooping of the mouth accompanied by drooling (Fig. 61-3).

FIG. 61-3 Facial characteristics of Bell’s palsy. A, At rest the face may look almost normal, but the patient is not able to wrinkle her forehead on the affected side and the right corner of the mouth droops. B, When she is asked to close her eyes and show her teeth, the differences between the affected and unaffected sides become more obvious.

An inability to close the eyelid, with an upward movement of the eyeball when closure is attempted, is also evident. Other manifestations include a widened palpebral fissure (the opening between the eyelids); flattening of the nasolabial fold; and inability to smile, frown, or whistle. Unilateral loss of taste is common. Decreased muscle movement may alter chewing ability. Although some patients experience a loss of tearing, many patients complain of excessive tearing. The muscle weakness causes the lower lid to turn out, allowing overflow of normal tear production. Pain may be present behind the ear on the affected side, especially before the onset of paralysis.

Complications include psychologic withdrawal because of changes in appearance, malnutrition, dehydration, mucous membrane trauma, corneal abrasions, muscle stretching, and facial spasms and contractures.

The diagnosis of Bell’s palsy is one of exclusion. There is no definitive test. The diagnosis and prognosis are indicated by observing the typical pattern of onset and signs and testing percutaneous nerve excitability by electromyography (EMG).

Collaborative Care

Methods of treatment for Bell’s palsy include moist heat, gentle massage, and electrical stimulation of the nerve and prescribed exercises. Stimulation may maintain muscle tone and prevent atrophy. Care is primarily focused on relief of symptoms, prevention of complications, and protection of the eye on the affected side.

Corticosteroids (prednisone) are started immediately, with best results if corticosteroids are initiated before paralysis is complete. When the patient improves to the point that the corticosteroids are no longer necessary, the drug should be tapered over a 2-week period. Because HSV is implicated in approximately 70% of cases of Bell’s palsy, treatment with acyclovir (Zovirax), alone or in conjunction with prednisone, may be used. Additional antiviral agents, including valacyclovir (Valtrex) and famciclovir (Famvir), have also been used in the management of Bell’s palsy.

Nursing Management Bell’s Palsy

The patient with Bell’s palsy is treated on an outpatient basis. Mild analgesics can relieve pain. Hot wet packs can reduce the discomfort of herpetic lesions, aid circulation, and relieve pain. Tell the patient to protect the face from cold and drafts because trigeminal hyperesthesia (extreme sensitivity to pain or touch) may occur. Maintenance of good nutrition is important. Teach the patient to chew on the unaffected side of the mouth to avoid trapping food and to enjoy the taste of food. Thorough oral hygiene must be carried out after each meal to prevent parotitis, caries, and periodontal disease from accumulated residual food.

The patient may wear dark glasses for protective and cosmetic reasons. Artificial tears (methylcellulose) should be instilled frequently during the day to prevent drying of the cornea. Ointment and an impermeable eye shield can be used at night to retain moisture. In some patients, taping the lids closed at night may be necessary to provide protection. Instruct the patient to report ocular pain, drainage, or discharge.

A facial sling may be helpful to support affected muscles, improve lip alignment, and facilitate eating. The facial sling is usually made and fitted by a physical or occupational therapist. When function begins to return, active facial muscle exercises are performed several times a day.

The change in physical appearance as a result of Bell’s palsy can be devastating. Reassure the patient that a stroke did not occur and that chances for a full recovery are good. Enlisting support from family and friends is important. Tell the patient that most patients recover within about 6 weeks of the onset of symptoms.

Polyneuropathies

Guillain-Barré Syndrome

Guillain-Barré syndrome (Landry-Guillain-Barré-Strohl syndrome, postinfectious polyneuropathy, ascending polyneuropathic paralysis) is an acute, rapidly progressing, and potentially fatal form of polyneuritis. It is characterized by ascending, symmetric paralysis that usually affects cranial nerves and the peripheral nervous system. The syndrome is rare, affecting an estimated 3000 to 6000 Americans each year. It affects males and females equally.5,6

Etiology and Pathophysiology

The etiology of this disorder is unknown. Both cellular and humoral immune mechanisms play a role in the immune reaction directed at the nerves. The result is a loss of myelin (a segmental demyelination) and edema and inflammation of the affected nerves. As demyelination occurs, the transmission of nerve impulses is stopped or slowed down. The muscles innervated by the damaged peripheral nerves undergo denervation and atrophy. In the recovery phase, remyelination occurs slowly, and neurologic function returns in a proximal-to-distal pattern.⁶ Guillain-Barré syndrome is similar in presentation to multiple sclerosis (MS), and therefore a full diagnostic workup should be performed to rule out MS (see Chapter 59).

The syndrome is often preceded by immune system stimulation from a viral infection, trauma, surgery, or viral immunizations. Campylobacter jejuni gastroenteritis is thought to precede Guillain-Barré syndrome in approximately 30% of cases.5–7

Clinical Manifestations and Complications

Guillain-Barré syndrome is a heterogeneous condition with manifestations ranging from mild to severe. Weakness of the lower extremities (evolving more or less symmetrically) occurs over hours to days to weeks, usually peaking about the fourteenth day. Paresthesia (numbness and tingling) is common, with paralysis usually following in the extremities. Hypotonia (reduced muscle tone) and areflexia (lack of reflexes) are common manifestations.5–7

In Guillain-Barré syndrome, autonomic nervous system dysfunction results, with manifestations of orthostatic hypotension, hypertension, and abnormal vagal responses (bradycardia, heart block, asystole). Other autonomic dysfunctions include bowel and bladder dysfunction, facial flushing, and diaphoresis. Patients may also have syndrome of inappropriate antidiuretic hormone (SIADH) secretion.⁸ (SIADH is discussed in Chapter 50.) Cranial nerve involvement is manifested as facial weakness, extraocular eye movement difficulties, dysphagia, and paresthesia of the face.

Pain is a common symptom in the patient with Guillain-Barré syndrome. The pain can be paresthesias, muscular aches and cramps, and hyperesthesias. Pain appears to be worse at night. Opioids may be indicated for those experiencing severe pain. Pain may lead to a decrease in appetite and may interfere with sleep.

The most serious complication is respiratory failure, which occurs as the paralysis progresses to the nerves that innervate the thoracic area. Constant monitoring of the respiratory system by checking respiratory rate and depth provides information about the need for immediate intervention, including intubation and mechanical ventilation. Respiratory or urinary tract infections (UTIs) may occur. Immobility from the paralysis can cause problems such as paralytic ileus, muscle atrophy, deep vein thrombosis, pulmonary emboli, skin breakdown, orthostatic hypotension, and nutritional deficiencies.

Diagnostic Studies

Diagnosis is based primarily on the patient’s history and clinical signs. Cerebrospinal fluid (CSF) is normal or has a low protein content initially, but after 7 to 10 days it shows an elevated protein level (normal protein is 15 to 45 mg/dL [0.15 to 0.45 g/L]) with a normal cell count. Results of EMG and nerve conduction studies are markedly abnormal (reduced nerve conduction velocity) in the affected extremities. A brain MRI can be done to rule out MS.

Nursing and Collaborative Management Guillain-Barré Syndrome

Management of Guillain-Barré syndrome is aimed at supportive care, particularly ventilatory support, during the acute phase. Plasmapheresis is used in the first 2 weeks. (Plasmapheresis is discussed in Chapter 14.) IV administration of high-dose immunoglobulin (Sandoglobulin) has been as effective as plasma exchange and is more readily available.

Beyond 3 weeks after disease onset, plasmapheresis and immunoglobulin therapies have little value. Corticosteroids appear to have little effect on the prognosis or duration of the disease.

Assessment of the patient is the most important aspect of nursing care during the acute phase. During the routine assessment, monitor the ascending paralysis; assess respiratory function; monitor arterial blood gases (ABGs); and assess the gag, corneal, and swallowing reflexes. Reflexes are usually decreased or absent.

Monitor blood pressure (BP) and cardiac rate and rhythm during the acute phase because dysrhythmias may occur. Autonomic dysfunction is common and usually takes the form of bradycardia and dysrhythmias. Orthostatic hypotension secondary to muscle atony may occur in severe cases. Vasopressor agents and volume expanders may be needed to treat the low BP. However, the presence of SIADH may require fluid restriction.

The objective of therapy is to support body systems until the patient recovers. Respiratory failure and infection are serious threats. Monitoring the vital capacity and ABGs is essential. If the vital capacity drops to less than 800 mL or the ABGs deteriorate, endotracheal intubation or tracheostomy may be done so that the patient can be mechanically ventilated (see Chapter 68). If fever develops, obtain sputum cultures to identify the pathogen. Appropriate antibiotic therapy is then initiated.

Nutritional needs must be met in spite of possible problems associated with delayed gastric emptying, paralytic ileus, and potential for aspiration if the gag reflex is lost. In addition to testing for the gag reflex, note drooling and other difficulties with secretions that may indicate an inadequate gag reflex. Initially, enteral or parenteral nutrition may be used to ensure adequate caloric intake. Because of delayed gastric emptying, assess residual volumes of the feedings at regular intervals or before feedings (see Chapter 40).

Throughout the course of the illness, provide support and encouragement to the patient, caregiver, and family. Although 85% to 95% of patients almost completely recover, it is generally a slow process that takes months or years. About 30% of those with Guillain-Barré have some residual weakness.5–7

Botulism

Botulism is rare but the most serious type of food poisoning. It is caused by gastrointestinal (GI) absorption of the neurotoxin produced by Clostridium botulinum. This organism is found in the soil, and the spores are difficult to destroy. It can grow in any food contaminated with the spores. Improper home canning of foods is often the cause.⁹ It is thought that the neurotoxin destroys or inhibits the neurotransmission of acetylcholine at the myoneural junction, resulting in disturbed muscle innervation.

Neurologic manifestations can develop rapidly or evolve over several days. They include a descending paralysis with muscle incoordination and weakness, difficulty swallowing, seizures, and respiratory muscle weakness that can rapidly deteriorate to respiratory and/or cardiac arrest.

The clinical manifestations, prevention, and treatment are presented in Table 42-24. Patient and caregiving teaching related to food poisoning are presented in Table 42-25. Nursing care during the acute illness is similar to that for Guillain-Barré syndrome. Supportive nursing interventions include rest, activities to maintain respiratory function, adequate nutrition, and prevention of loss of muscle mass.

Tetanus

Tetanus (lockjaw) is a severe infection of the nervous system affecting spinal and cranial nerves. It results from the effects of a potent neurotoxin released by the anaerobic bacillus Clostridium tetani. The spores of the bacillus are present in soil, garden mold, and manure. C. tetani enters the body through a wound that provides an appropriate low-oxygen environment for the organisms to mature and produce toxin. Examples of possible wounds include IV drug use injection sites, human and animal bites, burns, frostbite, open fractures, and gunshot wounds.10,11

Initial manifestations of tetanus include stiffness in the jaw (trismus) and neck and signs of infection (e.g., fever). As the disease progresses, the neck muscles, back, abdomen, and extremities become progressively rigid. In severe forms, continuous tonic seizures may occur with opisthotonos (extreme arching of the back and retraction of the head). Laryngeal and respiratory spasms cause apnea and anoxia. The slightest noise, jarring motion, or bright light can set off a seizure. These seizures are agonizingly painful. Mortality rate is almost 100% in the severe form.¹¹

Tetanus prevention and immunizations, which are the most important factors influencing the incidence of this disease, are summarized in Table 69-6. Adults should receive a tetanus and diphtheria toxoid booster every 10 years. Teach the patient that immediate, thorough cleansing of all wounds with soap and water is important to prevent tetanus. If an open wound occurs and the patient has not been immunized within 5 years, the health care provider should be contacted so that a tetanus booster can be given.

The management of tetanus includes administration of a tetanus toxoid, diphtheria toxoid, and pertussis (Tdap) booster and tetanus immune globulin (TIG) in different sites before the onset of symptoms to neutralize circulating toxins (see Table 69-6). A much larger dose of TIG is administered to patients with clinical manifestations of tetanus.^10–12

Control of spasms is essential and is managed by sedation and skeletal muscle relaxation, usually with diazepam (Valium), barbiturates, and, in severe cases, neuromuscular blocking agents such as vecuronium (Norcuron) that act to paralyze skeletal muscles. Opioid analgesics such as morphine or fentanyl are also indicated for pain management. A 10- to 14-day course of penicillin, metronidazole, tetracycline, or doxycycline is recommended to inhibit further growth of C. tetani.¹¹

Because of laryngospasm and the potential need for neuromuscular blocking drugs, a tracheostomy is usually performed early and the patient is maintained on mechanical ventilation. Sedative agents and opioid analgesics are given concomitantly to all patients who are pharmacologically paralyzed. Any recognized wound should be debrided or an abscess drained. Antibiotics may be given to prevent secondary infections.

Neurosyphilis

Neurosyphilis is caused by Treponema pallidum, the bacteria that cause syphilis. It usually occurs about 10 to 20 years after a person is first infected with syphilis. Not everyone who has syphilis will develop this complication. It is the result of untreated or inadequately treated syphilis (see Chapter 53). The organism can invade the central nervous system within a few months of the original infection. Untreated neurosyphilis, although not contagious, can be fatal.

Late neurosyphilis results from degenerative changes in the spinal cord (tabes dorsalis) and brainstem (general paresis). Tabes dorsalis (progressive locomotor ataxia) is characterized by vague, sharp pains in the legs; ataxia; “slapping” gait; loss of proprioception and deep tendon reflexes; and zones of hyperesthesia. Charcot’s joints, which are characterized by enlargement, bone destruction, and hypermobility, also occur as a result of joint effusion and edema. Other manifestations of neurosyphilis include seizures, vision and hearing problems, and cognitive impairment.¹³

Management includes treatment with penicillin, symptomatic care, and protection from physical injury.¹³ The prognosis after treatment depends on how severe the neurosyphilis is before treatment. The neurologic deficits may remain or progress after treatment.

Ethical/Legal Dilemmas

Right to Refuse Treatment

Situation

R.D., a 25-yr-old man, suffered a spinal cord injury (SCI) to C7-8 following a motorcycle accident. He was diagnosed with anterior cord syndrome and has motor paralysis, which may prevent him from riding motorcycles again. He has become extremely depressed and no longer wishes to live. Because of his emotional state, R.D. is now refusing to eat. Can he be forced to receive enteral nutrition (tube feeding)?

Ethical/Legal Points for Consideration

• Withholding treatment in a newly injured but otherwise healthy young adult may present an ethical dilemma for some nurses. They may consider it assisted suicide and believe that it violates an ethical principle.

• A competent adult has the right to consent to or refuse medical treatment under the right to privacy, the Fourteenth Amendment of the Constitution, and case law.*

• Case law has also supported the concept that forced treatment constitutes battery (unlawful use of force on somebody). Furthermore, a mentally competent, physically incapacitated adult can refuse feeding by nasogastric tube and compel the health facility to follow the patient’s wishes.†

• To be competent to participate in informed consent or refusal, an adult must be able to understand the information provided about the procedure or treatment, consider choices between alternatives available, and make a choice based on his values and preferences. Depression may not be a determinant in competency to make informed treatment choices.

• If, after adequate treatment for pain, depression, or other medical conditions, the patient persists in his refusal, his wishes must be respected.

• Refusal to eat or drink has never been upheld as illegal, and the alternative—forced eating and drinking—is clearly a violation of patient rights and the criminal act of battery.

Discussion Questions

1. What are your feelings about requests to withhold treatment in a young person with a newly acquired disability?

2. What resources are available to help R.D., his family, and the staff work through this emotionally charged and ethically complex situation?

^*Cruzan v. Director, Missouri Department of Health, 497 U.S. 261, 1990. Retrieved from http://supreme.justia.com/cases/federal/us/497/261.

^†Bouvia v. Superior Court, 1986. Retrieved from http://law.justia.com/cases/california/calapp3d/179/1127.html.

Spinal Cord Problems

Spinal Cord Injury

Spinal cord injury (SCI) is caused by trauma or damage to the spinal cord. It can result in either a temporary or permanent alteration in the function of the spinal cord. About 12,000 Americans suffer SCIs each year. About 260,000 persons in the United States are living with SCI.14,15 With improved treatment strategies, even the very young patient with an SCI can anticipate a long life. The potential for disruption of individual growth and development, altered family dynamics, economic loss in terms of employment, and the high cost of rehabilitation and long-term health care make SCI a major problem.

Young adult men between ages 16 and 30 years have the greatest risk for SCI. Eighty-one percent of people with SCI are male. There has also been an increase in the number of older adults with SCIs. This trend toward older age at time of injury is reflected in the overall increase in mean age of people with SCI from 28 years in the 1970s to 40 years at this time.¹⁵

Although many people with SCIs can care for themselves independently, those with the highest level of injury may require round-the-clock care at home or in a long-term care facility. Almost 90% of patients with SCI are discharged from the hospital to home or another noninstitutional residence. The remaining 10% are discharged to nursing homes, chronic care facilities, or group homes.

The spinal cord is wrapped in tough layers of dura and is rarely torn or transected by direct trauma. SCI can be due to cord compression by bone displacement, interruption of blood supply to the cord, or traction resulting from pulling on the cord. Penetrating trauma, such as gunshot and stab wounds, can result in tearing and transection. The initial mechanical disruption of axons as a result of stretch or laceration is referred to as the primary injury.

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Nov 17, 2016 | Posted by admin in NURSING | Comments Off

Diagnostic	Collaborative Therapy
• History and physical examination (including neurologic examination) • CT scan • MRI	• Drug therapy • Antiseizure drugs (e.g., carbamazepine [Tegretol], oxcarbazepine [Trileptal]) • gabapentin (Neurontin) • Tricyclic antidepressants (e.g., amitriptyline [Elavil]) • Local nerve block • Surgical therapy (see Table 61-2)

Polyneuropathies

Guillain-Barré Syndrome

Nurse Key

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Nursing Management: Peripheral Nerve and Spinal Cord Problems

Nursing Management

Peripheral Nerve and Spinal Cord Problems

Cranial Nerve Disorders

Trigeminal Neuralgia

Etiology and Pathophysiology

Clinical Manifestations

Diagnostic Studies

Collaborative Care

Drug Therapy.

Conservative Therapy.

Surgical Therapy.

Nursing Management Trigeminal Neuralgia

Bell’s Palsy

Etiology and Pathophysiology

Clinical Manifestations and Diagnostic Studies

Collaborative Care

Nursing Management Bell’s Palsy

Etiology and Pathophysiology

Clinical Manifestations and Complications

Diagnostic Studies

Nursing and Collaborative Management Guillain-Barré Syndrome

Botulism

Tetanus

Neurosyphilis

Spinal Cord Problems

Spinal Cord Injury

Etiology and Pathophysiology

Types of Injury.

Primary Injury.

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