Neurologic emergencies and neurologic malignancies

Neurologic emergencies include acceleration-deceleration injury, myelitis, Reye’s syndrome, skull fracture, spinal cord injury and traumatic brain injury. Neurologic malignancies include malignant brain tumors and spinal neoplasms.

NEUROLOGIC EMERGENCIES

ACCELERATION-DECELERATION INJURY

An acceleration-deceleration injury results from a sharp hyperextension and flexion of the neck that damage muscles, ligaments, disks, and nerve tissue. It commonly results from a motor vehicle accident and is also known as whiplash. It may also occur from a fall or sports activity. While this type of injury usually has an excellent prognosis, it’s a neck injury and carries the risk of paralysis occurring as a complication. Symptoms usually subside with symptomatic treatment. One million cases of whiplash occur each year in the United States. The average age of these patients is the late 40s.

Pathophysiology

Any unexpected force that causes the head to jerk back and then forward may cause the neck bones to snap out of position, causing injury. Irritated nerves can interfere with blood flow and transmission of nerve impulses. Pinched nerves can
affect certain body part functions. Usually pain is the result of the injury, with some limitation in neck movement.

Complications

Temporomandibular joint disorder
Nerve damage

Assessment findings

Mechanism of injury identifies acceleration-deceleration action
Pain initially minimal but increases 12 to 72 hours after the accident
Dizziness
Headache
Back pain
Shoulder pain
Vision disturbances
Tinnitus
Neck muscle asymmetry
Reduced neck mobility
Gait disturbances
Rigidity or numbness in the arms
Tenderness at the exact location of the injury
Decreased active and passive range of motion

Diagnostic test results

Full cervical spine X-rays rule out cervical fracture.

Treatment

Until X-rays rule out cervical fracture, treatment focuses on protecting the cervical spine through immobilization. After cervical spine injury has been ruled out, initial treatment includes limited activity during the first 72 hours after the injury, use of a soft cervical collar, and application of ice packs. (See Using a cervical collar.) Oral analgesics provide pain relief, and oral corticosteroids help reduce inflammation and relieve chronic discomfort. To restore flexibility,
physical therapy, including mobilization exercises, is started 72 hours after the injury. It’s combined with the application of moist heat and a gradually decreased use of the soft collar.

If the patient experiences persistent ligamentous or articular pain, he may benefit from cervical traction and diathermy treatment. Surgical stabilization may be necessary with severe cervical acceleration-deceleration injury.

Nursing interventions

Maintain spinal immobilization until cervical X-rays are evaluated.
Protect the patient’s spine during all care.
Give prescribed drugs.
Apply a soft cervical collar.
Monitor pain level, administer analgesics as ordered, and evaluate response to medications.
Observe for signs and symptoms of complications.
Assess the patient’s neurologic status per facility protocol and clinical status.

Provide appropriate education to the patient before discharge. (See Teaching the patient with an acceleration-deceleration injury.)

MYELITIS AND ACUTE TRANSVERSE MYELITIS

Myelitis, or inflammation of the spinal cord, can result from several diseases. Poliomyelitis affects the cord’s gray matter and produces motor dysfunction; leukomyelitis affects only the white matter and produces sensory dysfunction.

The prognosis depends on the severity of cord damage and prevention of complications. If spinal cord necrosis occurs, the prognosis for a complete recovery is poor. Even without necrosis, residual neurologic deficits usually persist after recovery. Patients who develop spastic reflexes early in the course of the illness are more likely to recover than those who don’t.

Acute transverse myelitis has many causes. It commonly follows acute infectious diseases, such as measles or pneumonia (the inflammation occurs after the infection has subsided),
and primary infections of the spinal cord itself, such as syphilis or acute disseminated encephalomyelitis. Acute transverse myelitis may also accompany demyelinating diseases, such as acute multiple sclerosis, and inflammatory and necrotizing disorders of the spinal cord such as hematomyelia.

Such toxic agents as carbon monoxide, lead, and arsenic can cause a type of myelitis in which acute inflammation (followed by hemorrhage and possible necrosis) destroys the entire circumference (myelin, axis cylinders, and neurons) of the spinal cord. Other forms of myelitis may result from poliovirus, herpes zoster, herpesvirus B, or rabies virus; disorders that cause meningeal inflammation, such as syphilis, abscesses, tuberculosis, and other suppurative conditions; smallpox or polio vaccination; parasitic and fungal infections; and chronic adhesive arachnoiditis.

Peak incidence occurs from ages 10 to 19 and then again from ages 30 to 39. About 33,000 Americans have some type of disability from this disorder, with approximately 1,400 new cases diagnosed each year.

Pathophysiology

Myelitis is an inflammation of the spinal cord. Only the cord’s gray matter may be affected, producing motor dysfunction, or the white matter may be affected, producing sensory dysfunction. These types of myelitis can attack any level of the spinal cord, causing partial destruction or scattered lesions. Acute transverse myelitis, which affects the entire thickness of the spinal cord, produces motor and sensory dysfunction. It’s rapid in onset and is the most devastating form of myelitis.

Complications

Shock
Motor impairment
Sensory impairment

Assessment findings

Sensory or motor dysfunction, depending on the site of damage to the spinal cord
Rapid onset with motor and sensory dysfunctions below the level of spinal cord damage appearing in 1 to 2 days
Flaccid paralysis of the legs (sometimes beginning in just one leg) with loss of sensory and sphincter functions; may follow pain in the legs or trunk
Absent reflexes in early stages but possibly reappearing in later stages
Extent of damage dependent on level of the spinal cord affected; transverse myelitis seldom involving the arms; with severe spinal cord damage, shock possible (hypotension and hypothermia)

Diagnostic test results

Neurologic examination confirms paraplegia or neurologic deficit below the level of the spinal cord lesion and absent (or, in later stages) hyperactive reflexes.
Cerebrospinal fluid may be normal or show increased lymphocytes or elevated protein levels.
Magnetic resonance imaging rules out spinal cord tumor.
Culture specimens identify the cause of any underlying infection.

Treatment

No definitive treatment exists for acute transverse myelitis. Rather, the condition requires appropriate treatment of the underlying infection. Steroid therapy is a possible treatment modality; however, more research is needed to determine its benefits.

Nursing interventions

Monitor vital signs. Watch carefully for signs of spinal shock (hypotension and excessive sweating).

DISCHARGE TEACHING

TEACHING THE PATIENT WITH MYELITIS

Before discharge, be sure to cover with the patient and his family:

the disorder and its implications
medication administration, dosage, and possible adverse effects, and when to notify the physician
when to report changes in mental status, level of consciousness, or motor ability
types of therapy that may be beneficial, such as physical therapy, occupational therapy, or counseling
the importance of maintaining adequate nutrition
bowel and bladder training
exercises to maintain or improve muscle tone and function
signs and symptoms of complications
the importance of follow-up care
the benefit of utilizing available community support groups such as the local chapter of the Transverse Myelitis Association.

Assist with range-of-motion exercises and proper body alignment.
Reposition the patient every 2 hours, assess his skin condition, and provide appropriate skin care.
Monitor intake and output.
Initiate rehabilitation immediately. Assist the patient with physical therapy, bowel and bladder training, and lifestyle changes that his condition requires.
Provide appropriate education to the patient and his family before discharge. (See Teaching the patient with myelitis.)

NEUROLOGIC MALIGNANCIES

BRAIN TUMOR, MALIGNANT

A malignant brain tumor is an abnormal growth of cancerous cells within the intracranial space. The tumor may affect brain tissue, the meninges, the pituitary gland, and blood vessels. In
adults, the most common tumor types are gliomas and meningiomas, which usually occur above the covering of the cerebellum, or supratentorial tumors. In children, the most common tumor types are astrocytomas, medulloblastomas, ependymomas, and brain stem gliomas. The exact cause unknown, but risk factors include preexisting cancer, radiation or chemical exposure, and head trauma.

Malignant brain tumors are slightly more common in males than in females and have an overall incidence of 4.5 per 100,000 people. They can occur at any age. In adults, incidence is highest between ages 40 and 60. Most tumors in children occur before age 1 or between ages 2 and 12.

Pathophysiology

Tumors are classified based on histology or grade of cell malignancy. Central nervous system changes are caused by cancer cells invading and destroying tissues and by compression of the brain, cranial nerves, and cerebral vessels; cerebral edema; and increased intracranial pressure (ICP).

Complications

Radiation encephalopathy
Cerebral edema
Seizures
Neurologic deficits
Hydrocephalus
Brain herniation

LIFE-THREATENING COMPLICATIONS FROM INCREASED ICP

Coma
Respiratory or cardiac arrest
Brain herniation

Assessment findings

Headache
Nausea and vomiting
Signs and symptoms of increased ICP
- Vision disturbances
- Weakness, paralysis
- Aphasia, dysphagia
- Ataxia, incoordination
- Seizures (see Brain tumors: Site-specific signs and symptoms, pages 346 and 347, and Assessment findings in malignant brain tumors, pages 348 to 353)

Diagnostic test results

Skull X-rays confirm tumor.
Brain scan confirms tumor.
Computed tomography scan confirms tumor.
Magnetic resonance imaging evaluates tumor location, size, and vascularity and cerebral edema.
Cerebral angiography confirms tumor.
Positron emission tomography confirms tumor.
Tissue biopsy confirms the type of tumor.
Lumbar puncture may show increased cerebrospinal fluid (CSF) pressure, which reflects ICP, increased protein levels, decreased glucose levels and, occasionally, tumor cells in CSF.

Treatment

Specific treatments vary with the tumor’s histologic type, radiosensitivity, and location. Such treatments may include surgery, radiation therapy, chemotherapy, and decompression of increased ICP (with diuretics, corticosteroids, or possibly, ventriculoatrial or ventriculoperitoneal shunting of the CSF).

Treatment of a glioma usually consists of resection by craniotomy. Radiation therapy and chemotherapy follow resection. The combination of carmustine (BiCNU), lomustine
(CeeNU), or procarbazine (Matulane) with radiation therapy is more effective than radiation alone.

ASSESSMENT FINDINGS IN MALIGNANT BRAIN TUMORS

TUMOR AND CHARACTERISTICS	ASSESSMENT FINDINGS
*GLIOBLASTOMA MULTIFORME (SPONGIOBLASTOMA MULTIFORME)*
Most common; accounts for 60% of all gliomas Peak incidence between ages 50 and 60; more common in males than in females Unencapsulated, highly malignant; grows rapidly and infiltrates the brain extensively; may become enormous before diagnosed Usually occurs in cerebral hemispheres, especially frontal and temporal lobes (rarely in brain stem and cerebellum) Occupies more than one lobe of affected hemisphere; may spread to opposite hemisphere by corpus callosum or metastasize into cerebrospinal fluid (CSF), producing tumors in distant parts of the central nervous system (CNS)	*GENERAL* Increased intracranial pressure (ICP) (nausea, vomiting, headache, papilledema) Mental and behavioral changes; speech and sensory disturbances Altered vital signs (increased systolic pressure, widened pulse pressure, respiratory changes) In children, irritability and projectile vomiting *LOCALIZING* Midline: headache (bifrontal or bioccipital) that’s worse in morning; intensified by coughing, straining, or sudden head movements Temporal lobe: psychomotor seizures Central region: focal seizures Optic and oculomotor nerves: vision deficits Frontal lobe: abnormal reflexes and motor responses
*ASTROCYTOMA*
Second most common malignant glioma, accounting for 10% of all gliomas Occurs at any age; incidence higher in males than in females Usually occurs in central and subcortical white matter; may originate in any part of CNS Cerebellar astrocytomas usually confined to one hemisphere	*GENERAL* Headache and mental activity changes Decreased motor strength and coordination Seizures and scanning speech Altered vital signs *LOCALIZING* Third ventricle: changes in mental activity and level of consciousness, nausea, pupillary dilation and sluggish light reflex; paresis or ataxia in later stages of disease Brain stem and pons: ipsilateral trigeminal, abducens, and facial nerve palsies in early stages; cerebellar ataxia, tremors, and other cranial nerve deficits as disease progresses Third or fourth ventricle or aqueduct of Sylvius: secondary hydrocephalus Thalamus or hypothalamus: various endocrine, metabolic, autonomic, and behavioral changes
*OLIGODENDROGLIOMA*
Third most common glioma; accounts for less than 5% of all gliomas Occurs in middle adult years; more common in females than in males Slow growing	*GENERAL* Mental and behavioral changes Decreased visual acuity and other vision disturbances Increased ICP *LOCALIZING* Temporal lobe: hallucinations and psychomotor seizures Central region: seizures (confined to one muscle group or unilateral) Midbrain or third ventricle: pyramidal tract symptoms (dizziness, ataxia, paresthesia of face) Brain stem and cerebrum: nystagmus, hearing loss, dizziness, ataxia, paresthesia of face, cranial nerve palsies, hemiparesis, suboccipital tenderness, loss of balance
*EPENDYMOMA*
Rare glioma Most common in children and young adults Usually located in fourth and lateral ventricles	*GENERAL* Increased ICP and obstructive hydrocephalus, depending on tumor size Other assessment findings similar to those of oligodendroglioma
*MEDULLOBLASTOMA*
Rare glioma Most common in children and young adults Incidence highest in children ages 4 to 6 Affects males more than females Frequently metastasizes by way of CSF	*GENERAL* Increased ICP *LOCALIZING* Brain and cerebrum: papilledema, nystagmus, hearing loss, perception of flashing lights, dizziness, ataxia, paresthesia of face, cranial nerve palsies (V, VI, VII, IX, X, primarily sensory), hemiparesis, suboccipital tenderness; compression of supratentorial area produces other general and focal symptoms
*MENINGIOMA*
Most common nongliomatous brain tumor, constituting 15% of primary brain tumors Usually occurs in people in their 50s; rare in children; more common in females than in males (ratio 3:2) Arises from the meninges Common locations: parasagittal area, sphenoidal ridge, anterior part of base of skull, cerebellopontine angle, and spinal canal Benign, well-circumscribed, highly vascular tumor that compresses underlying brain tissue by invading overlying skull	*GENERAL* Headache Seizures (in two-thirds of patients) Vomiting Changes in mental activity Other assessment findings similar to those of schwannomas *LOCALIZING* Skull changes (bony bulge) over tumor Sphenoidal ridge, indenting optic nerve: unilateral Vision changes and papilledema Prefrontal parasagittal: personality and behavioral changes Motor cortex: contralateral motor changes Anterior fossa compressing both optic nerves and frontal lobes: headaches and bilateral vision loss Pressure on cranial nerves, causing varying symptoms
*SCHWANNOMA (ACOUSTIC NEUROMA, NEURILEMOMA, CEREBELLOPONTINE ANGLE TUMOR)*
Accounts for about 10% of all intracranial tumors Onset of symptoms between ages 30 and 60; higher incidence in females than in males Affects the craniospinal nerve sheath, usually cranial nerve VIII; also, V and VII, and to a lesser extent, VI and X on the same side as tumor Benign, but usually classified as malignant because of its growth patterns; slow-growing; may be present for years before symptoms occur	*GENERAL* Unilateral hearing loss with or without tinnitus Stiff neck and suboccipital discomfort Secondary hydrocephalus Ataxia and uncoordinated movements of one or both arms due to pressure on brain stem and cerebellum *LOCALIZING* V: early signs including facial hypoesthesia and paresthesia on the side of hearing loss; unilateral loss of corneal reflex VI: diplopia VII: paresis progressing to paralysis (Bell’s palsy) X: weakness of palate, tongue, and nerve muscles on same side as tumor

For low-grade cystic cerebellar astrocytomas, surgical resection permits long-term survival. For other astrocytomas, treatment consists of repeated surgery, radiation therapy, and shunting of fluid from obstructed CSF pathways. Radiation therapy works best in radiosensitive astrocytomas; some astrocytomas are radioresistant.

Treatment of oligodendrogliomas and ependymomas include surgical resection and radiation therapy. Medulloblastomas call for surgical resection and, possibly, intrathecal infusion of methotrexate (Rheumatrex) or another antineoplastic drug. Meningiomas require surgical resection, including the dura mater and bone.

For schwannomas, microsurgical technique allows complete resection of the tumor and preservation of the facial
nerve. Although schwannomas are moderately radioresistant, treatment still calls for postoperative radiation therapy.

Chemotherapy for malignant brain tumors includes the nitrosoureas that help break down the blood-brain barrier and allow other chemotherapeutic drugs to go through as well. Intrathecal and intra-arterial administration of drugs maximizes drug action.

Palliative measures for gliomas, astrocytomas, oligodendrogliomas, and ependymomas include dexamethasone (Decadron) for cerebral edema; osmotic diuretics, such as urea and mannitol, to reduce brain swelling; analgesics to control pain; and antacids and histamine-2 receptor antagonists for stress ulcers. These tumors and schwannomas may also require anticonvulsants, such as phenytoin (Dilantin) to prevent seizures.

DISCHARGE TEACHING

TEACHING THE PATIENT WITH A MALIGNANT BRAIN TUMOR

Before discharge, be sure to cover with the patient and his family:

the disorder and its implications
medication administration, dosage, and possible adverse effects, and when to notify the physician
the importance of good nutrition
signs of infection or bleeding that may result from chemotherapy
adverse effects of chemotherapy and other treatments and actions that may alleviate them
physical and cognitive limitations that may occur
seizure precautions
early signs of tumor recurrence
wound care
types of therapy that would be beneficial, such as physical therapy, speech therapy, and occupational therapy
signs and symptoms of complications, espically increased intracranial pressure and infection
information regarding end-of-life care, such as advance directives and hospice
the importance of follow-up care
the benefit of available community support groups such as the local chapter of the National Brain Tumor Foundation.

Nursing interventions

Maintain a patent airway.
Document the occurrence, nature, and duration of seizure activity.
Take steps to protect the patient’s safety.
Give prescribed drugs and note any adverse reactions.
Monitor for changes in the patient’s neurologic status and observe for signs of increased ICP.
Monitor vital signs and pulse oximetry. Note changes in respiratory status and temperature.
After supratentorial craniotomy, elevate the head of the bed about 30 degrees.
After infratentorial craniotomy, keep the patient flat for 48 hours.
Monitor ICP and cerebral perfusion pressures, and provide measures to maintain adequate readings.
Monitor head dressings and provide wound care.
As appropriate, instruct the patient to avoid Valsalva’s maneuver and isometric muscle contractions when moving or sitting up in bed.
Consult with occupational, speech, and physical therapists.
Provide emotional support to the patient and his family. Encourage them to talk about their concerns. Listen carefully and answer their questions honestly and completely.
Provide appropraite education to the patient and his family before discharge. (See Teaching the patient with a malignant brain tumor.)

REYE’S SYNDROME

Reye’s syndrome is an acute childhood illness that causes fatty infiltration of the liver with concurrent hyperammonemia, encephalopathy, and increased intracranial pressure (ICP). Reye’s syndrome affects children from infancy to adolescence and occurs equally in boys and girls. It affects whites older than age 1 more often than it does blacks.

Reye’s syndrome almost always follows within 1 to 3 days of an acute viral infection, such as an upper respiratory tract infection, type B influenza, or varicella (chickenpox).

Only gold members can continue reading. Log In or Register to continue