Nursing Management: Peripheral Nerve and Spinal Cord Problems



Nursing Management


Peripheral Nerve and Spinal Cord Problems


Teresa E. Hills





Reviewed by Jean Burt, RN, MSN, Instructor, Wilbur Wright College, Chicago, Illinois; and Fernande E. Deno, RN, MSN, CNE, Instructor, Anoka Ramsey Community College, Coon Rapids, Minnesota.




image eNursing Care Plan 61-1   Patient With a Spinal Cord Injury




Patient Goals







Patient Goals







Patient Goals







Patient Goal


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





Patient Goals

















Outcomes (NOC) Interventions (NIC) and Rationales
Neurologic Status: Autonomic Dysreflexia Management





• 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.



image




Patient Goals

















Outcomes (NOC) Interventions (NIC) and Rationales
Coping Coping Enhancement




• 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.



image


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



*Nursing diagnoses listed in order of priority.




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).



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.



Clinical Manifestations


The classic feature of trigeminal neuralgia is an abrupt onset of paroxysms of excruciating pain described as a burning, knifelike, or lightning-like shock in the lips, upper or lower gums, cheek, forehead, or side of the nose. Intense pain, twitching, grimacing, and frequent blinking and tearing of the eye occur during the acute attack (giving rise to the term tic). Some patients may also experience facial sensory loss. The attacks are usually brief, lasting only seconds to 2 or 3 minutes, and are generally unilateral.


Recurrences, which are unpredictable, may occur several times a day, or weeks or months apart. After the refractory (pain-free) period, a phenomenon known as clustering can occur. Clustering is characterized by a cycle of pain and refractoriness that continues for hours.


The painful episodes are usually initiated by a triggering mechanism of light touch at a specific point (trigger zone) along the distribution of the nerve branches. Precipitating stimuli include chewing, tooth brushing, feeling a hot or cold blast of air on the face, washing the face, yawning, or even talking. As a result, the patient may eat improperly, neglect hygienic practices, wear a cloth over the face, and withdraw from interaction with other individuals. The patient may sleep excessively as a means of coping with the pain.


Although this condition is considered benign, the severity of the pain and the disruption of lifestyle can result in almost total physical and psychologic dysfunction or even suicide.




Collaborative Care


Once the diagnosis is made, the goal of treatment is relief of pain either medically or surgically (Tables 61-1 and 61-2).





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.




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).



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




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).



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.57



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.57


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.




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.57



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.1012


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




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.




*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.



Etiology and Pathophysiology


SCIs are usually a result of trauma. The most common causes are motor vehicle collisions (42%), falls (27%), violence (15%), sports injuries (7%), and other miscellaneous causes (8%).15



Types of Injury.

The extent of the neurologic damage caused by an SCI results from primary injury (actual physical disruption of axons) and secondary injury (ischemia, hypoxia, hemorrhage, and edema).


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Nov 17, 2016 | Posted by in NURSING | Comments Off on Nursing Management: Peripheral Nerve and Spinal Cord Problems

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