Neurologic Disorders 2

Neurologic Disorders
ASSESSMENT
A baseline neurologic assessment is needed to detect changes in neurologic function.
Neurologic assessment includes a patient history, general physical examination, and thorough
neurologic examination. An important principle underlying neurologic assessment is: maximum
stimulation for maximum response. Common manifestations of neurologic dysfunction include
motor, sensory, autonomic, and cognitive deficits. By exploring these symptoms, obtaining a
pertinent history, and performing a thorough neurologic examination, the reader will gain an
understanding of the underlying disorder and become skilled in planning care for patients with
neurologic disorders. Documentation using appropriate terminology and comparison of right to
left for asymmetrical findings is important.
DIAGNOSTIC TESTS
RADIOLOGY AND IMAGING
Structural and functional imaging techniques have evolved to facilitate the rapid diagnosis and
treatment of neurologic disorders. Brain mapping describes the process of translating the brain
into a functionally useful group of dynamic maps or patterns. The diagnosis and evaluation of
neurologic disorders is increasingly guided by functional brain mapping techniques that detect
changes in brain patterns associated with neuropathology. Structural or anatomic imaging
reveals information about the structure of the nervous system, including the brain and spinal
cord. Functional or physiologic imaging focuses on the function of the brain and biochemical
and metabolic processes in brain cells.
Definitions of Neurologic Findings

Acalculiaâ€”inability to do mathematical calculations
Agnosiaâ€”inability to recognize sensory input
Alexiaâ€”visual aphasia
Amaurosis fugaxâ€”sudden, temporary or fleeting blindness, not caused by disease of the eye
Anisocoriaâ€”inequality in size of the pupils
Apraxiaâ€”inability to perform coordinated movements
Broca's (motor) aphasiaâ€”inability to express self
Confabulationâ€”fluent, nonsensical speech
Decerebrate rigidityâ€”posture indicating lesion of the diencephalon, midbrain, or pons with jaw
clenched, neck extended, arms adducted, elbows extended, forearms pronated, wrists flexed,
knees extended, and feet plantar flexed
Decorticate rigidityâ€”posture indicating lesion within the corticospinal tracts within or very near
the cerebral hemispheres, with arms adducted, elbows and wrists flexed, legs extended and
internally rotated, and feet plantar flexed
Dyspraxiaâ€”partial loss of ability to perform coordinated movements
Dysarthriaâ€”difficulty speaking
Homonymous hemianopsiaâ€”corresponding visual field deficits in half of the visual field
bilaterally
Micrographiaâ€”change in handwriting with the script becoming smaller and more cramped
Nystagmusâ€”involuntary oscillation of the eyeball, either vertical, horizontal, or rotary
Paratoniaâ€”progressively increasing and irregular resistance to passive movements
Wernicke's (sensory) aphasiaâ€”inability to understand spoken language
Computed Tomography Scan

Description
• Computed tomography (CT) scan is a structural imaging study that uses a computer-
based X-ray to provide a cross-sectional image of the brain. A computer calculates
differences in tissue absorption of the X-ray beams. The CT produces a three-
dimensional view of structures in the brain and distinguishes between soft tissues and
water. I.V. contrast dye may be used to examine the integrity of the blood-brain barrier.
• CT is primarily used to detect tumors and inflammatory disorders. Spinal CT scan may
be used to evaluate lower back pain due to herniated intervertebral disk or other spinal
lesions.
• Advantages of CT: Widespread availability, short imaging time, excellent images of
bone, and 100% sensitivity for detection of cerebral hemorrhage. CT scans can be used
for patients with metallic implants or electronic devices where other techniques are
contraindicated.
• Disadvantages of CT: Does not provide information about function of tissues; exposes
the patient to ionizing radiation.
• Preferred procedure for detection of subarachnoid hemorrhage (SAH) and other rapidly
evolving neurologic disorders. When magnetic resonance imaging (MRI) is
contraindicated, CT is often the scan of choice.
Nursing and Patient Care Considerations
• Instruct patient to remove metal items, such as earrings, eyeglasses, and hair clips.
• Ask whether patient has an allergy to iodine or history of previous allergy to I.V. dye, to
determine if premedication is indicated for prevention of allergic reaction to the contrast
agent.
• Tell patient to expect a sensation of feeling flushed if contrast dye is injected through the
I.V. catheter.
• Inform patient that the procedure normally takes 10 to 30 minutes.
• Request that patient remain as immobile as possible during the examination.
• Tell patient to resume usual activities after the procedure.
• Encourage increased fluid intake for the rest of the day to assist in expelling the contrast
dye.
Magnetic Resonance Imaging
Description
• Conventional MRI is a noninvasive structural imaging procedure that uses powerful
magnetic field and radio frequency waves to create an image. When tissue is placed in a
strong magnetic field, hydrogen atoms in the tissue line up within the field. In MRI,
pulsating radio frequency waves are applied to the magnetic field to alter the tissue
magnetization, creating a clear image of the tissue.
• The imaging procedure of choice for most neurologic diseases (eg, detection of
demyelinating diseases, nonacute hemorrhage, and cerebral infarction).
• Closed MRI uses scanning equipment that resembles a tunnel-like chamber. Open MRI
uses more sophisticated equipment that does not involve a closed chamber. During
open MRI, the patient can comfortably see the surroundings from all views while the
scan is in progress. This is ideal for patients who are claustrophobic or anxious, children,
the elderly, and the very obese.
• Advantages of MRI: No ionizing radiation or exposure to contrast medium, sensitivity to
blood flow, imaging in several planes, and superior visualization of soft tissues. An
important advantage is its ability to distinguish water, iron, fat, and blood. Sensitive to
detection of white matter changes and valuable in detecting changes associated with
Alzheimer's disease and multiple sclerosis.
• Disadvantages of MRI: Contraindicated for patients with pacemakers, aneurysm clips, or
other implanted objects that could be dislodged by the magnetic field. Dental amalgam,
gold, and stainless steel are generally considered safe, but may distort the image. MRI
scanner has the appearance of a tunnel-like chamber, and its constricted opening
prevents its use for extremely obese people. Because of its narrow dimensions, MRI
may induce claustrophobic and anxiety reactions, so antianxiety medication may be
necessary before the procedure, or an open MRI used.
• Encourage patient to use the bathroom before the procedure because it may take from
40 to 90 minutes.
• Instruct patient to remove metal items, including eyeglasses, jewelry, hair clips, hearing
aids, dentures, and clothing with zippers, buckles, or metal buttons.
• Encourage patient to remain as still as possible during the procedure.
• Describe the tunnel-like narrow chamber of the closed MRI scanner, and inform patient it
sometimes causes feelings of anxiety or claustrophobia. Teach relaxation techniques
and sedate patient, as directed.
• Inform patient the scanner will make a dull, thumping noise throughout the procedure.
• Tell patient to resume usual activities after the procedure.
Functional MRI
Description
• Functional MRI (fMRI) is an imaging study that aids in identifying regions of brain
activated by particular stimuli and tasks. Imaging is performed during presentation of a
stimulus or performance of a specific task and during rest periods. A statistical
comparison is performed with images obtained during the stimulus/task periods
compared to those performed during the rest periods. Involves I.V. administration of
contrast material that lowers signal intensity on MRI in relation to blood flow as the
material passes through the brain.
• Advantages of fMRI: Does not use ionizing radiation, and can be applied repeatedly in
the same patient without risk. Offers potential in early detection of patients with
prodromal dementia.
• Disadvantages of fMRI: Same as MRI. The role of the fMRI in the clinical evaluation of
patients remains to be established.
• Instruct patient as for MRI. Full cooperation of the patient is vital for head motion and
task performance reasons. Global cognitive impairment, aphasia, neglect, substantial
sensory disturbances, and severe depression are usually exclusion criteria. The
performance of motor tasks during imaging should be monitored and fixed across
patients and controls over time to compare data and interpret results.
• Medications that may interfere with performance of tasks during the procedure should be
avoided, if possible, including antiepileptics, benzodiazepine, and antidepressants.
Positron-Emission Tomography Scan
Description
• A computer-based functional imaging technique that permits study of the brain's
metabolism, blood flow, and chemical processes. Positron-emission tomography (PET)
measures emissions of particles of injected radioisotopes, called positrons, and converts
them to an image of the brain.
• PET scanners are not frequently used or widely available due to their high cost ($2 to $3
million). PET requires sophisticated equipment to produce its radioisotopes, or positron
emitters.
• A glucoselike solution and mildly radioactive tracers are combined for injection or
inhalation. After injection into the arterial blood stream, or inhalation of this radioactive
compound, pairs of gamma rays are emitted into adjacent tissue during radioactive
decay. The PET scanner measures the gamma rays to determine how quickly tissues
absorb the radioactive isotopes. A computer processes the data into an image that
shows where radioactive material is located, corresponding to cellular metabolism.
• Advantages of PET: Provides information on patterns of glucose and oxygen
metabolism. Areas of decreased metabolism indicate dysfunction. Useful in early
detection of dementia, tumors, seizures, head trauma, Parkinson's disease, amyotrophic
lateral sclerosis (ALS), and multiple sclerosis.
• Disadvantages of PET: Ionizing radiation, high initial costs, limited access.
• Inform patient that this procedure requires injection or inhalation of a radioactive
substance that emits positively charged particles. Explain that the image is created when
the negative particles found in the body combine with the positive particles of the
imaging substance.
• Explain that, after injection of the radioisotope, patient will be asked to rest quietly on a
stretcher for about 45 minutes to allow the substance to circulate to the brain.
• Reassure patient that radiation exposure is minimal.
• Encourage patient to void before the test because the scan and associated procedures
may take several hours.
• Advise patient to increase fluid intake after the procedure to flush out the radioisotope,
and resume meals.
• Tell patient that it may take a few days to get results of the PET scan because it requires
processing before it is available for interpretation.
Single Photon-Emission Computed Tomography
Description
• A widely available noninvasive functional imaging technique that measures blood
perfusion in the brain, in contrast to the neuronal uptake of glucose in PET. It uses
principles similar to PET, but the radioactive tracer decays to emit only a single photon.
• It uses a rotating camera to track the single photons emitted from radioactive decay and
collects information from multiple views. Radioactive tracers reveal cerebral blood flow in
various regions of the brain.
• The radioactive tracer compounds used in single photon-emission computed
tomography (SPECT) are commercially prepared and do not require the specialized
equipment used in PET scanning. SPECT scanning does not require an I.V. line.
• Used to evaluate cerebral blood flow of patients with ischemic stroke, SAH, migraine,
dementia including Alzheimer's disease, epilepsy, and other degenerative diseases.
• Advantages of SPECT: Can perform hemodynamic, chemical, and functional imaging;
widely available.
• Disadvantages of SPECT: Ionizing radiation, provides only relative measurements.
• Inform patient that this is a noninvasive procedure that should cause minimal discomfort.
• Tell patient that results of the scan are typically available for interpretation by a specialist
immediately after the procedure.
Cerebral Angiography
Description
• Following local anesthesia, a radiopaque dye is injected through a catheter in the
brachial or femoral artery and passed through one of the major cervical blood vessels to
assess cerebral circulation. Serial X-rays are taken after contrast dye illuminates each
common carotid artery and each vertebral artery. The structure and patency of cerebral
arteries are examined.
• Advantages of cerebral angiography: Useful in detection of stenosis or occlusion,
aneurysms, and vessel displacement due to pathologic processes (eg, tumor, abscess,
hematoma).
• Disadvantages of cerebral angiography: Involves considerable exposure to radiation.
Contraindicated in patients with a stroke in evolution. Potential complications: temporary
or permanent neurologic deficit, including stroke, anaphylaxis, bleeding or hematoma at
the I.V. site, and impaired circulation in the extremity distal to the injection site, usually
the femoral artery.
• Omit the meal before the test, although clear liquids may be taken.
• Ask patient about allergies and specifically rule out presence of iodine allergy, which
requires pretest preparation. Commonly, patients with allergy to iodine also have
allergies to radiopaque contrast media that may cause severe reaction.
• Options for pretest preparation include:
○ Administration of I.V. corticosteroid 24 hours in advance of procedure and
diphenhydramine (Benadryl) 50 mg orally 1 hour before procedure or
○ Diphenhydramine 50 mg orally 1 hour before the procedure or
○ I.M. injection of corticosteroid, in the event the test is emergent, followed by
diphenhydramine 50 mg orally.
• Mark pedal peripheral pulses.
• Explain that a local anesthetic will be used to insert a catheter into the femoral artery
(brachial artery may be used) and threaded into the required cerebral vessel.
• Tell the patient to expect some discomfort when the catheter is inserted into the artery.
Additionally, the sensation of a warm, flushed feeling and metallic taste should be
expected when the dye is injected.
• Caution the patient to lie still during the procedure.
• After the angiography:
○ Maintain bed rest and do not flex extremity, as ordered, and monitor vital signs.
○ Apply an ice pack or sandbag to the I.V. site, as ordered, to prevent hematoma.
Remove the sandbag frequently to observe for bleeding, swelling, or redness.
○ Check the patient frequently for neurologic symptoms, such as motor or sensory
alterations, reduced level of consciousness (LOC), speech disturbances,
dysrhythmias, or blood pressure (BP) fluctuations.
○ Monitor for adverse reaction to contrast medium (eg, restlessness, respiratory
distress, tachycardia, facial flushing, nausea and vomiting).
○ Assess skin color, temperature, and peripheral pulses of the extremity distal to
the I.V. siteâ€”change may indicate impaired circulation due to occlusion.
Digital Subtraction Angiography
Description
• Digital subtraction angiography is a variation of cerebral angiography. First, an X-ray is
taken of the patient's skull and stored by a computer. Next, contrast material is
administered I.V., and serial X-rays are taken of the area. The computer digitally
subtracts the original image from subsequent images, producing a clear image of the
highlighted arterial vessels.
• There is less potential for bleeding than cerebral angiography because injection of dye is
I.V. rather than arterial.
• Used to evaluate extracranial circulation. Size of vessels, patency, stenosis, or
displacement can be determined.
• May be done on an outpatient basis.
• Tell patient to restrict food 4 hours before the test.
• Ask patient about allergies and specifically rule out presence of iodine allergy, which
requires pretest preparation. Commonly, patients with allergy to iodine also have
allergies to radiopaque contrast media, which may cause severe reaction. Options for
pretest preparation include:
○ Administration of I.V. corticosteroid 24 hours in advance of procedure and
diphenhydramine 50 mg orally 1 hour before procedure or
diphenhydramine 50 mg orally
• Explain that a contrast dye will be administered through an I.V. catheter, and injection of
the dye may cause a warm, flushed feeling and metallic taste.
• Instruct patient to remain absolutely motionless during the procedure.
• After the I.V. is removed, instruct patient to resume usual activities.
• Encourage increased fluids for the rest of the day to help flush out the contrast medium.
Myelography
Description
• Provides visualization of the subarachnoid space or spinal canal. A lumbar puncture is
performed to inject a contrast dye or air into the subarachnoid space. After injection of a
local anesthetic into the lumbar area, a hollow needle is inserted through which a dye or
air is injected into the subarachnoid space surrounding the spinal cord.
• The patient is secured on an X-ray table, which is tilted in various directions while spinal
films are taken to view the flow of the contrast dye.
• Observation of the subarachnoid space reveals obstructions due to bone displacement,
spinal cord compression, herniated intervertebral disks, or other lesions.
• Food and fluids may be restricted for 8 to 12 hours before the procedure.
• Administer anxiolytics, such as diazepam (Valium), before the procedure as prescribed
to promote relaxation.
• Explain that a local anesthetic will be given at the site of lumbar puncture, but that the
patient will likely experience discomfort when the lumbar puncture is performed to inject
dye into the spinal column.
• Inform patient that a headache may occur after the procedure. This is due to central
nervous system (CNS) irritation by the chemical. Back pain may be exacerbated by the
lumbar puncture and dye injection.
• Explain that patient will be strapped to a table that will tilt up or down during the
procedure while X-rays are taken.
• Before the procedure, ask patient about allergies, and specifically rule out presence of
iodine allergy, which requires pretest preparation. Commonly, patients with allergy to
iodine also have allergies to radiopaque contrast media, which may cause severe
reaction. Options for pretest preparation include:
○ I.V. corticosteroid 24 hours in advance of procedure and diphenhydramine 50 mg
orally 1 hour before or
diphenhydramine 50 mg orally
• Postprocedure care is determined by the type of contrast dye used:
○ If patient has received Metazamide (a water-based contrast medium), elevate the
head of the bed to a semi-Fowler's position (45 degrees) to reduce upward
dispersion of the medium.
 Keep patient quiet for first several hours.
 Avoid administration of phenothiazines.
○ If Pantopaque (an oil-based contrast medium) is used, instruct the patient to lie in
a prone position for 2 hours, then supine for 2 to 4 hours. If the oil was not
withdrawn, elevate the head to prevent the oil from reaching the brain.
 Encourage the patient to force fluids for rehydration and replacement of
cerebrospinal fluid (CSF).
 Observe the patient for signs and symptoms of meningeal irritation (eg,
headache, fever, stiff neck, back spasms, nausea and vomiting,
seizures).
○ If air was used, place the patient's head in a position lower than the body.
• Monitor vital signs and compare with baseline readings.
• Check patient's ability to void.
• Note and report warmth, flushing, nausea, vomiting, or itching as signs of a reaction to
iodinated contrast medium.
• Perform neurologic checks to detect headache, photophobia, stiff neck, or seizure
activity caused by meningeal irritation.
Brain Scan
Description
• A CT study that measures the brain's uptake of a radioactive isotope that is administered
I.V. Provides images of internal structures of the head, brain tissues, and CSF.
Radioactive uptake is increased at the site of damaged brain tissue, probably due to
abnormal permeability of the blood-brain barrier.
• Assists in the diagnosis of abnormalities in brain tissue and blood circulation, such as
tumors, multiple sclerosis, aneurysms, infections, trauma, or injury. Shows location and
size of cerebral lesions, but does not specify the source of the lesion (eg, abscess,
tumor, cerebral infarction).
• Withhold medications, as ordered, 24 hours before the test (eg, antihypertensives,
vasoconstrictors, vasodilators).
• Explain that, after injection of the dye, patient will be asked to change positions while the
scanner takes pictures of various views of the brain.
• Advise patient that the brain scan normally takes 30 minutes to 1 hour.
• Inform patient that the head is placed in a stabilized holder with the face uncovered. The
holder is placed in a frame that revolves around the head while pictures are taken.
• Assure patient that no discomfort will be felt during this procedure.
Magnetic Source Imaging
Description
• Magnetic source imaging (MSI) provides information about electric function of the brain
without injection of isotopes, attachment of electrodes, or other types of invasive
procedures.
• Currents in the neurons of the brain produce magnetic fields outside the body. Using
detectors placed near the head, MSI measures external magnetic fields to evaluate the
flow of electric currents within the brain.
• May be used in surgery for intractable epilepsy to locate an epileptic focus.
• Remove all metal from patient; report any metal implants.
• Change patient into clothing without metal clasps, buttons, and so forth.
• Explain that dental work may need to be demagnetized.
• Tell patient that washable markings will be pinned on his or her head as reference
points.
Cerebral Blood Flow Studies
Description
• Injection or inhalation of a radioisotope or nitrous oxide, which is absorbed by the brain.
The information is read by 16 to 32 probes placed on the head and analyzed by a
computer.
• Provides regional or overall data regarding cerebral blood flow. Normal blood flow is 50
to 55 mL flow/100 g of cerebral tissue per minute.
• Reassure patient that this is a relatively noninvasive procedure and requires cooperation
only during the inhalation or injection process.
Transcranial Doppler Studies
Description
• Noninvasive tests that measure the velocity of blood flow through cerebral arteries,
providing information about the circulation to the brain.
• A technician applies a gel to skin at temporal, transorbital, or foramen magnum areas of
the skull. A probe is applied to transmit a signal to the cerebral artery being studied.
Detected velocities are recorded.
• Explain the study will be done with patient in a reclining position.
• Inform patient the test normally takes less than 1 hour, depending on the number of
arteries that will be studied.
Intracarotid Amobarbital Procedure (Wada Test)
Description
• A technique used to assess language dominance and memory function before ablative
surgery for epilepsy.
• The patient undergoes cerebral angiography to visualize the cerebral vasculature, and a
catheter is placed into the internal carotid artery. When the catheter is positioned, a
short-acting barbiturate is injected (sodium amobarbital [Amytal]) to anesthetize the
cerebral hemisphere to mimic the proposed surgery.
• EEG and clinical symptoms are used to determine effectiveness. The patient is then
tested for language and memory. Drug effects wear off in 2 to 12 minutes.
• Prepare patient as for a cerebral angiography.
• Instruct patient to be nothing by mouth (NPO) after 8 PM the night before the test.
• Reassure patient that speech alterations will be temporary.
OTHER DIAGNOSTIC TESTS
Other diagnostic tests include lumbar puncture, which provides information about the CNS
through direct contact with the CSF; a variety of tests that measure electrical impulses in
portions of the nervous system; and neuropsychological evaluation.
Lumbar Puncture
Description
• A needle is inserted into lumbar subarachnoid space, usually between the third and
fourth lumbar vertebrae, and CSF is withdrawn for diagnostic and therapeutic purposes.
• Purposes include:
○ Obtaining CSF for examination (microbiologic, serologic, cytologic, or chemical
analysis).
○ Measuring cerebrospinal pressure and assisting in detection of obstruction of
CSF circulation.
○ Determining the presence or absence of blood in the spinal fluid.
○ Aiding in the diagnosis of viral or bacterial meningitis, subarachnoid or
intracranial hemorrhage, tumors, and brain abscesses.
○ Administering antibiotics and cancer chemotherapy intrathecally in certain cases.
○ Determining levels of tau protein and beta-amyloid in the CSF, a new test that
may be used to assist the diagnosis of Alzheimer's disease. Elevated tau and
decreased levels of beta-amyloid are associated with Alzheimer's disease.
See Procedure Guidelines 15-1.
Electroencephalography
Description
• Measures electrical activity of brain cells. Electrodes are attached to multiple sites on the
scalp to provide a recording of electrical activity that is generated in the cerebral cortex.
Electrical impulses are transmitted to an electroencephalograph,which magnifies and
records these impulses as brain waves on a strip of paper.
• Usually performed in a room designed to eliminate electrical interference; however, in
the case of a comatose patient, may be performed at bedside using a portable unit.
• Provides physiologic assessment of cerebral activity for diagnosis of epilepsy, coma,
organic brain syndrome, sleep disorders, and confirmation of brain death. Provides
information about the timing of events. Particularly helpful in the investigation of patients
with seizures.
• Restlessness and fatigue can alter brain wave patterns.
• For a baseline recording, the patient is instructed to lie still and relax with eyes closed.
After a baseline recording in a resting phase, the patient may be tested in various stress
situations (eg, asked to hyperventilate for 3 minutes, look at a flashing strobe light) to
elicit abnormal electrical patterns.
PROCEDURE GUIDELINES 15-1
Assisting the Patient Undergoing Lumbar Puncture
EQUIPMENT
• Sterile lumbar puncture set
• Skin antiseptic (avoid use of chlorhexidine)
• Sterile gloves
• Adhesive bandage
• Xylocaine 1% to 2%
PROCEDURE
Nursing Action Rationale
Preparatory phase
1 Before procedure, the patient should empty1 To enhance comfort.
. bladder and/or bowel. .
2 Give a step-by-step summary of the procedure.2 Reassures the patient and gains
. For lying position, see accompanying figure. . cooperation.
3 If patient has signs of increased intracranial3 Removal of cerebrospinal fluid (CSF) in
. pressure a computed tomography scan should be. the presence of mass effect may
done to rule out mass effect before a lumbar precipitate brain herniation.
puncture.
4Position the patient on side with a small pillow4The spine is maintained in a horizontal
. under head and a pillow between legs. Patient. position. The pillow between the legs
should be lying on a firm surface. prevents the upper leg from rolling
forward.
5 Instruct the patient to arch the lumbar segment of5 This posture offers maximal widening of
. back and draw knees up to abdomen, chin to. the interspinous spaces and affords
chest, clasping knees with hands. easier entry into the subarachnoid space.
6 Assist the patient in maintaining this position by6 Supporting the patient helps prevent
. supporting behind the knees and neck. Assist the. sudden movements, which can produce a
patient to maintain the posture throughout the traumatic (bloody) tap and thus impede
examination. correct diagnosis.
7 Alternately, for sitting position, have the patient7 In obese patients and those who have
. straddle a straight-back chair (facing the back) and. difficulty in assuming an arched side-lying
rest head against arms, which are folded on the position, this posture may allow more
back of the chair. accurate identification of the spinous
processes and interspaces.
Performance phase (By the physician or credentialed health care provider)

1 The skin is prepared with antiseptic solution1 To reduce risk of contamination; to
. (avoiding use of chlorhexidine), and the skin and. decrease pain. Chlorhexidine is
subcutaneous spaces are infiltrated with local neurotoxic and should not come in
anesthetic agent. contact with CSF.
2 A spinal needle is introduced at the L3-L42 L3-L4 interspace is below the level of the
. interspace. The needle is advanced until the. spinal cord.
â€œgiveâ€ of the ligamentum flavum is felt and
the needle enters the subarachnoid space. The
manometer is attached to the spinal needle.
3 After the needle enters the subarachnoid space,3 This maneuver prevents a false increase
. help the patient to slowly straighten up. . in intraspinal pressure. Muscle tension
and compression of the abdomen give
falsely high pressures.
4 Instruct the patient to breathe quietly (not to hold4 Hyperventilation may lower a truly
. breath or strain) and not to talk. . elevated pressure. Talking can elevate
CSF pressure.
5 The initial pressure reading (opening pressure) is5 With respiration, there is normally some
. obtained by measuring the level of the fluid column. fluctuation of spinal fluid in the
after it comes to rest. manometer. Normal range of spinal fluid
pressure with the patient in the lateral
recumbent position is 70 to 200 mm H2O.
Opening pressure exceeds normal range
when hydrocephalus or increased ICP is
present.
6 About 2 to 3 mL of spinal fluid is placed in each of6 Bloody spinal fluid may indicate
. three test tubes for observation, comparison, and. subarachnoid hemorrhage or a traumatic
laboratory analysis. Spinal fluid should be clear tap. If traumatic tap, blood should
and colorless. gradually clear with subsequent
specimens.
7 Closing pressure is the pressure on the7 Closing pressure should be within normal
. manometer after the CSF specimen is collected. CSF pressure range.
and/or excess CSF removed.
Follow-up phase
1 After the procedure, the patient is instructed to1 This reduces pressure on tissue surfaces
. remain flat for about 2 hours. . along the needle track to prevent CSF
leakage.
2 Ensure adequate hydration with oral or parenteral2 This facilitates replacement of CSF and
. fluids. . prevents spinal headache.
3 Monitor for spinal headache, and observe for CSF3 CSF leaks from lumbar puncture are
. leak. . characterized by intractable spinal
headache.
• For routine EEG, tranquilizers, anticonvulsants, sedatives, and stimulants should be held
for 24 to 48 hours before the study.
• Thoroughly wash and dry patient's hair to remove hair sprays, creams, or oils.
• Explain that the electrodes will be attached to patient's skull with a special paste.
• Assure patient that the electrodes will not cause shock, and encourage patient to relax
during the procedure because anxiety can affect brain wave patterns.
• Meals should be taken as usual to avoid sudden changes in blood glucose levels.
Magnetoencephalogram
Description
• A magnetoencephalogram uses a magnetometer to measure the location, depth,
orientation, and polarity of spike field strength.
• Used in determining the epileptogenic focus.
• Remove all metal.
• Demagnetize dental work.
• Assure patient that the procedure will cause no discomfort.
Evoked Potential Studies
Description
• These tests measure evoked potentials, or the brain's electrical responses to visual,
auditory, or sensory stimuli. Three types of responses are measured: visual,
somatosensory, and auditory.
○ Visual evoked potentials are produced by asking the patient to look at rapidly
reversing checkerboard patterns. These assist in evaluating multiple sclerosis
and traumatic injury. EEG electrodes are placed over the occiput and record the
transmission time from the retina to the occiput.
○ Somatosensory evoked potentials are generated by stimulating a peripheral
sensory nerve and are useful in diagnosing peripheral nerve disease. These
measure transmission time up the spinal cord to the sensory cortex.
○ Auditory evoked potentials are produced by applying sound, such as clicks, to
help locate auditory lesions and evaluate integrity of the brain stem. The
transmission time up the brain stem into the cortex is measured.

• Explain that the electrodes will be attached to patient's scalp to measure the electrical
activity of the nervous system. Placement of the electrodes will depend on the type of
evoked potentials being measured.
• Ask patient to remove all jewelry.
• Assure patient that the procedure is not painful and does not cause any electric shock.
• Inform patient that the test normally takes 45 to 60 minutes.
Needle Electromyography
Description
• In combination with nerve conduction studies, needle electromyography (EMG) is the
gold standard method for assessing the neurophysiologic characteristics of
neuromuscular diseases. Because it is invasive and painful, its use is limited when
activity from several muscles needs to be monitored simultaneously. It is the recording of
a muscle's electrical impulses at rest and during contraction. A needle is attached to an
electrode and inserted into a muscle. A mild electric charge is delivered to stimulate the
muscle at rest and during voluntary contraction. The response of the muscle is
measured on an oscilloscope screen.
• Useful in distinguishing lower motor neuron disorders from muscle disorders (eg, ALS
from muscular dystrophy).
• Nerve conduction time, another diagnostic test, is often measured simultaneously.
• Explain that this test measures the electrical activity of muscles.
• Advise the patient to avoid caffeine and tobacco products for three hours before the test,
as these substances can affect test results.
• Inform the patient that the procedure normally takes at least 1 hour.
• Tell the patient a needle will be inserted through the skin into selected muscles, and to
expect some degree of discomfort when the needle is inserted.
• Inform the patient that, after the test, a mild analgesic or warm compresses may be
needed to relieve muscle soreness.
• Inform the patient to observe the needle insertion sites for bleeding, hematoma, redness,
or other signs of infection and to notify the health care provider if any of these are
observed.
Tensilon Test
Description
• A pharmacologic challenge study that assists in the diagnosis of myasthenia gravis. The
patient is administered an I.V. injection of Tensilon (edrophonium), a short-acting
anticholinesterase, which improves muscle strength by increasing muscle response to
nerve impulses. After the injection of Tensilon, the patient is asked to perform repetitive
muscle movements (eg, open and close eyes, cross and uncross legs) to evaluate the
muscle response.
• If the patient has myasthenia gravis, muscle strength should improve as soon as the
Tensilon is injected. EMG may supplement Tensilon test findings to confirm this disease.
• Contraindicated in patients with breathing difficulties and apneic conditions, hypotension,
bradycardia, or obstruction of the urinary or intestinal tract.
• Check patient's history for use of medications that may affect muscle function,
anticholinesterase therapy, medication hypersensitivities, and respiratory disease.
Withhold medications as ordered.
• Explain that this test helps to determine the cause of muscle weakness.
• Inform patient that the test normally takes 15 to 30 minutes.
• Do not describe the exact response that is expected because this may influence test
results.
• Explain that, after administration of an I.V. medication, the patient will be instructed to
make specific repetitive muscle movements. Explain that the test may be repeated
several times to ensure accuracy.
• Assure patient that a nurse or other health care provider will be available at all times
because the medication can have some adverse effects. Explain that any adverse
effects should disappear quickly.
• Observe patient closely during the test to monitor for adverse reactions to Tensilon.
• Keep resuscitation equipment nearby, in case of respiratory distress.
Nerve Conduction Studies (Electroneurography)
Description
• A peripheral nerve is stimulated electrically through the skin and underlying tissues. A
recording electrode detects the response from the stimulated nerve. The time between
the stimulation of the nerve and the response is measured on an oscilloscope, and
speed of conduction along the nerve is calculated.
• Used to determine peripheral nerve disease or injury by measuring nerve conduction
velocity. In peripheral nerve injuries and disease, nerve conduction time is delayed.
• Explain that surface-stimulating electrodes with special paste are applied and taped to
the nerve site (leg, arm, or face).
• Advise patient that an electric current is passed through the electrode and that a mild
sensation or slight discomfort maybe experienced while the current is applied.
Neuropsychological Testing
Description
• A series of tests that evaluate effects of neurologic disorders on cognitive functioning
and behavior.
• A neuropsychologist selects appropriate tests to determine the extent and type of
functional deficits.
• Paper and pencil tests, puzzles, word and recall games are commonly used. Testing
may assess the following:
○ Intelligence, attention span, memory, judgment
○ Motor, speech, and sensory function
○ Affect, coping, and adaptation
○ Language quality, abstraction, distractibility
○ Ability to sequence learned behaviors
○ Used in diagnosis of organic brain dysfunction and dementia
○ Valuable in determining vocational rehabilitation training needs
• Assure patient that these tests are not intended to evaluate mental illness.
• Explain that testing evaluates the ability to remember, calculate numbers, and perform
abstract reasoning.
• Patient should be well rested because testing is mentally tiring and lengthy. A complete
examination is a 4- to 6 hour process, depending on patient's ability to concentrate.
• Anticipate fatigue and frustration after the examination.
Stereotaxis
Description
• In conjunction with CT scan monitoring, stereotactic biopsy of brain lesions is performed
when deep lesions are inaccessible to surgical resection, or when preoperative
neurologic symptoms are absent and risks of craniotomy outweigh benefits.
• Allows precise targeting of deep brain lesions for biopsy or surgery. Minimizes tissue
trauma to surrounding cerebral areas. Can also be used for aspiration of intracranial
hematomas, abscesses, and cystic lesion.
• Explain to patient that, although the stereotactic surgery penetrates the skull, it does not
penetrate the brain.
• Tell patient that a CT scan will help pinpoint the exact surgical site and that the position
of the electrode or microinstrument will be checked by X-ray or CT scan before the
procedure begins.
• Keep patient NPO before the procedure.
• Administer analgesics for headaches as ordered.
Polysomnography
Description
• Polysomnography is a noninvasive, all-night sleep study that measures character of
sleep, simultaneously monitoring EEG, cardiac and respiratory function, and movements
during sleep. It is used to confirm fragmented sleep patterns in narcolepsy and sleep-
related epilepsy.
• Testing is time-consuming and labor-intensive. Procedures typically include multiple
physiologic measures such as EEG, EMG, electrocardiogram (ECG), heart rate,
respiratory effort, air flow, and oxygen saturation.
• Explain that the electrodes placed on the scalp, chest, extremities, and face will be
uncomfortable but do not deliver electrical current.
• Reassure patient that a technician will be in the next room.
• Advise patient to wear comfortable nightwear.
Multisleep Latency Test
Description
• Multisleep latency test (MSLT) is a sleep study performed during the day. It is the most
widely objective assessment of daytime sleepiness and is commonly used to confirm a
diagnosis of narcolepsy.
• Testing consists of four â€œnappingâ€ periods of 20 to 35 minutes, during which time
the patient lies down on a bed in a darkened room and is allowed to fall asleep. The
multiple short sleep periods during the MSLT increase the observation of rapid-eye-
movement (REM) periods.

• Explain the time and duration of the naps.
• Reassure patient that he or she will be free to move about between naps.
• Tell patient to wear comfortable clothing and to bring reading or other materials for use
between naps.
GENERAL PROCEDURES AND TREATMENT MODALITIES
NURSING MANAGEMENT OF THE PATIENT WITH AN ALTERED STATE OF
CONSCIOUSNESS
Unconsciousness is a condition in which there is a depression of cerebral function ranging from
stupor to coma. Coma results from impairment in both the arousal and the awareness of
consciousness. The arousal of consciousness is mediated by the reticular activating substance
(RAS) in the brain stem. The awareness component of consciousness is mediated by the
cortical activity within the cerebral hemispheres.
Both arousal and awareness are assessed when using the Glasgow Coma Scale (GCS) as a
measure of LOC (see Table 15-1).
TABLE 15-1 Glasgow Coma Scale
PARAMETER FINDING SCORE
Eye opening Spontaneously 4
To speech 3
To pain 2
Do not open 1
Best verbal response Oriented 5
Confused 4
Inappropriate speech 3
Incomprehensible sounds 2
No verbalization 1
Best motor response Obeys command 6
Localizes pain 5
Withdraws from pain 4
Abnormal flexion 3
Abnormal extension 2
No motor response 1
Interpretation: Best score = 15; worst score = 3; 7 or less generally indicates coma; changes
from baseline are most important.
When using the GCS, coma may be defined as no eye opening on stimulation, absence of
comprehensible speech, and failure to obey commands. The GCS is designed to provide a
rapid assessment of LOC and does not provide a means to monitor or localize neurologic
dysfunction. Facility generated neurologic assessment tools may be used in combination with
the GCS to assess, monitor, and trend neurologic function.
An altered state of consciousness may be caused by many factors, including hypoxemia,
trauma, vascular disorders, neoplasms, degenerative, and infectious disorders as well as a
variety of metabolic disorders and structural neurologic lesions. Diagnostic evaluation and
management depend on the underlying cause, overall intracranial dynamics, age, comorbidities,
and general state of health.
Nursing Assessment
• Assess eye opening (level of responsiveness):
Eye opening = arousal
Tracking = awareness
• Assess neurologic function using the GCS. The GCS addresses eye opening, verbal
responses, and motor responses, rating the response based on the stimuli used
(spontaneous response, response to verbal stimuli, and response to painful stimuli).
Painful stimuli include applying pressure against the nail bed, trapezius/axillary pinch, or
sternal rub. Use the least amount of stimuli for the best response.
• Assess cognitive function:
○ Orientation
 Person, place, and time
 Where are you, why are you here
 General informationâ€”national and local current events
○ Speechâ€”aphasia
 Motor aphasia (Broca's)â€”inability to express self
 Sensory aphasia (Wernicke's)â€”inability to understand the spoken
language
 Global aphasiaâ€”inability to speak or understand spoken language
 Confabulationâ€”fluent, nonsensical speech
 Preservationâ€”continuation of thought process with inability to change
train of thought without direction or repetition
• Assess motor functionâ€”voluntary versus reflexive movement:
○ Voluntary movement
 Normal complex movementâ€”strength and symmetry in the upper
extremities (UE), pronator drift proximally and grip strength distally; in the
lower extremities (LE), leg lifts proximally and dorsi/plantar flexion distally
 Localizationâ€”ability to determine location of stimuli; patient localizes
area of painful stimuli
 Withdrawalâ€”abduction of the upper extremity; moving away from the
stimuli
○ Reflexive movement :
 Abnormal flexor posturing (decorticate)â€”dysfunction of corticospinal
tracts above the brainstem. Abnormal flexion of the UE with adduction of
the UE, internal rotation of the upper extremity, wrist and extension,
internal rotation and plantar flexion of the LE.
 Abnormal extension posturing (decerebrate)â€”dysfunction with
vestibulospinal tract and the RAS of the upper brain stem. Abnormal
extension, hyperpronation, and adduction of the UE and wrist flexion;
abnormal extension and internal rotation of the LE with plantar flexion of
the feet and toes.
 Mixed posturingâ€”varied extensor and flexor tone in UE.
 Flaccidâ€”medullary compression with complete loss of motor tone.
• Test cranial nerve (CN) reflexes to assess for brain stem dysfunction:
○ Assess pupil size, symmetry, and reaction to light.
○ Assess extraocular movements (CN 3, 4, 6) and reflex eye movements elicited
by head turning (oculocephalic response). This should not be performed on
patients with suspected cervical spine injury, patients in a cervical collar, or
patients known to have cervical spine injuries unless it is part of the brain death
exam.
○ The oculovestibular (caloric) response (CN 3, 4, 6, 8) is tested by medical staff
when the patient is comatose and the oculocephalic response is absent, as a
determination of brain death.
○ Assess CN 5, 7 together to evaluate facial pain, blink, eye closure, and grimace.
○ Assess CN 9, 10, 12 to evaluate gag, swallowing reflex, tongue protrusion, and
patient's ability to handle own secretions.
• Assess respiratory rate and pattern (normal, Kussmaul, Cheyne-Stokes, apneic).
• Assess deep tendon reflexes; evaluate tone for spasticity, rigidity, and paratonia
(abnormal resistance increasing throughout flexion and extension, indicating frontal lobe
dysfunction).
• Examine head for signs of trauma, and mouth, nose, and ears for evidence of edema,
blood, and CSF (may indicate basilar skull fracture).
• Monitor any change in neurologic status over time, and report changes to health care
provider as indicated.
NURSING ALERT
A critical indicator of neurologic function is the LOC and a change in GCS of two or more points
may be significant. If patient demonstrates deterioration, as evidenced by a change in
neurologic checks, notify the health care provider without delay, and reevaluate the neurologic
status more often than required by orders, based on nursing judgment.
Nursing Diagnoses
• Decreased Intracranial Adaptive Capacity
• Ineffective Airway Clearance related to upper airway obstruction by tongue and soft
tissues; inability to clear respiratory secretions
• Risk for Imbalanced Fluid Volume related to inability to ingest fluids, dehydration from
osmotic therapy (when used to reduce intracranial pressure)
• Impaired Oral Mucous Membranes related to mouth breathing, absence of pharyngeal
reflex, inability to ingest fluid
• Risk for Impaired Skin Integrity related to immobility or restlessness
• Impaired Tissue Integrity of cornea related to diminished/absent corneal reflex
• Hyperthermia related to infectious process; damage to hypothalamic center
• Impaired Urinary Elimination related to unconscious state
• Bowel Incontinence related to unconscious state
Nursing Interventions
Minimizing Secondary Brain Injury
• Monitor for change in neurologic status, decreased LOC, onset of cranial nerve deficits.
• Identify emerging trends in neurologic function, and communicate findings to medical
staff.
• Monitor response to pharmacologic therapy including drug levels, as indicated.
• Monitor laboratory data, CSF cultures, and Gram's stain, if applicable, and communicate
findings to medical staff.
• Assess neurologic drains/dressings for patency, security, and characteristics for
drainage.
• Institute measures to minimize risk for increased intracranial pressure (ICP), cerebral
edema, seizures, or neurovascular compromise.
• Adjust care to reduce risk of increasing intracranial pressure (ICP): body positioning in a
neutral position (head aligned with shoulders) without flexing head, reduce hip flexion,
distribute care throughout 24-hour period sufficiently for ICP to return to baseline.
• Monitor temperature status. Maintain normothermia.
Maintaining an Effective Airway
• Position patient to prevent tongue from obstructing the airway, encourage drainage of
respiratory secretions, and promote adequate exchange of oxygen and carbon dioxide.
• Keep the airway free from secretions with suctioning. In the absence of cough and
swallowing reflexes, secretions rapidly accumulate in the posterior pharynx and upper
trachea and can lead to respiratory complications (eg, aspiration).
○ Insert oral airway if tongue is paralyzed or is obstructing the airway. An
obstructed airway increases ICP. This is considered a short-term measure.
○ Prepare for insertion of cuffed endotracheal tube to protect the airway from
aspiration and to allow efficient removal of tracheobronchial secretions.
○ For technique of tracheal suctioning.
○ Use oxygen therapy as prescribed to deliver oxygenated blood to the CNS.
○ Pretreat before suctioning with sedative, opioid, or endotracheal lidocaine, if
indicated.
Attaining and Maintaining Fluid and Electrolyte Balance
• Monitor prescribed I.V. fluids carefully, maintaining euvolemia, minimizing large volumes
of â€œfree water,â€ which may aggravate cerebral edema.
• Maintain hydration and enhance nutritional status with use of enteral or parenteral fluids.
• Measure urine output and specific gravity.
• Evaluate pulses (radial, carotid, apical, and pedal); measure BP; these parameters are a
measure of circulatory adequacy/inadequacy.
• Maintain circulation; support the BP and treat life-threatening cardiac dysrhythmias.
Maintaining Healthy Oral Mucous Membranes
• Remove dentures. Inspect patient's mouth for dryness, inflammation, and the presence
of crusting.
• Provide mouth care by brushing teeth and cleansing the mouth with appropriate solution
every 2 to 4 hours to prevent parotitis (inflammation of parotid gland).
• Apply lip emollient to maintain hydration and prevent dryness.
Maintaining Skin Integrity
• Keep the skin clean, dry, well-lubricated, and free from pressure because comatose
patients are susceptible to the formation of pressure ulcers.
• Turn the patient from side to side on a regular schedule to relieve pressure areas and
help clear lungs by mobilizing secretions; turning also provides kinesthetic (sensation of
movement), proprioceptive (awareness of position), and vestibular (equilibrium)
stimulation.
• Reposition carefully after turning to prevent ischemia and shearing over pressure areas.
• Position extremities in functional position, and monitor skin underneath splints/orthoses
to prevent skin breakdown and pressure neuropathies.
• Perform range-of-motion (ROM) exercises of extremities at least four times daily;
contracture deformities develop early in unconscious patients.
Maintaining Corneal Integrity
• Protect the eyes from corneal irritation as the cornea functions as a shield. If the eyes
remain open for long periods, corneal drying, irritation, and ulceration are likely to result.
○ Make sure the patient's eye is not rubbing against bedding if blinking and corneal
reflexes are absent.
○ Inspect the condition of the eyes with a flashlight.
○ Remove contact lenses, if worn.
○ Irrigate eyes with sterile saline or prescribed solution to remove discharge and
debris.
○ Instill prescribed ophthalmic ointment in each eye to prevent glazing and corneal
ulceration.
○ Apply eye patches, when indicated, ensuring that eyes remain closed under
patch.
• Prepare for temporary tarsorrhaphy (suturing of eyelids in closed position) if unconscious
state is prolonged.
Reducing Fever
• Look for possible sites of infections (respiratory, CNS, urinary tract, wound) when fever
is present in an unconscious patient.
• Monitor temperature frequently or continuously.
• Control persistent elevations of temperature. Fever increases metabolic demands of the
brain, decreases circulation and oxygenation, and results in cerebral deterioration.
○ Monitor core temperature continuously and treat hyperthermia promptly.
Hyperthermia increases the brain's metabolic rate and increases the risk of
secondary injury. A body core temperature is 4 to 5 degrees lower than brain
temperature.
○ Maintain a cool ambient temperature. Anticipate potential for overcooling and
make environmental adjustments accordingly (eg, operating room environment).
○ Minimize excess covering on bed.
○ Administer prescribed antipyretics.
○ Use cool-water sponging and an electric fan blowing over the patient to increase
surface cooling for hyperthermia resistant to antipyretics.
○ Use a hypothermia blanket for hyperthermia to maintain normothermia. Avoid
rapid overcooling.
Promoting Urinary Elimination

• Insert an indwelling urethral catheter for short-term management.
• Use intermittent bladder catheterization for distention as soon as possible to minimize
risk of infection. Palpate over the patient's bladder at intervals or use a bladder scan to
detect urine retention and an overdistended bladder.
• Monitor for fever and cloudy urine.
• Initiate a bladder-training program as soon as consciousness is regained.
Promoting Bowel Function
• Observe for constipation due to immobility and lack of dietary fiber. Stool softener or
laxative, scheduled or as needed, may be prescribed to promote bowel elimination.
• Monitor for diarrhea resulting from infection, antibiotics, enteric feedings, hyperosmolar
fluids, and fecal impaction.
○ Perform a rectal examination if fecal impaction is suspected.
○ Use fecal collection bags, and provide meticulous skin care if patient has fecal
incontinence.
• Auscultate for bowel sounds; palpate lower abdomen for distention.
Family Education and Support
• Develop a supportive and trusting relationship with the family or significant other.
• Provide information and frequent updates on the patient's condition and progress.
• Involve them in routine care, and teach procedures that they can perform at home.
• Demonstrate and teach methods of sensory stimulation to be used frequently.
○ Use physical touch and reassuring voice.
○ Talk to patient in a meaningful way even when the patient does not seem to
respond. Assume patient is able to hear even if unresponsive.
○ Orient the patient periodically to person, time, and place.
• Demonstrate and teach methods frequently used to manage restlessness/agitation.
○ Eliminate distractions.
○ Reduce environmental stimuli (turn off television and radio, close door).
○ Use one-to-one communication.
○ Talk slowly and simplify information without talking down to the person.
• Teach the family to recognize and report unusual restlessness, which could indicate
cerebral hypoxia, metabolic imbalance, or pain.
• Enlist the help of the social worker, home health agency, or other resources to assist
family with such issues as financial concerns, need for additional follow-up care
(rehabilitation, long-term care facility), need for medical equipment in home, and/or
respite care.
Evaluation: Expected Outcomes
• Neurologic status remains at baseline or improved
• Maintains clear airway; coughs up secretions
• Absence of signs of dehydration
• Intact, pink mucous membranes
• No skin breakdown or erythema
• Absence of trauma to cornea
• Core temperature within normal limits
• Absence of urinary tract infection (UTI); maintenance of normal bladder emptying
• Bowel movement on regular basis in response to bowel regimen
NURSING MANAGEMENT OF THE PATIENT WITH INCREASED INTRACRANIAL
PRESSURE
ICP is the pressure exerted by the contents inside the cranial vaultâ€”the brain tissue (gray and
white matter), CSF, and the blood volume. Increased ICP is defined as CSF pressure greater
than 15 mm Hg.
Pathophysiology and Etiology
• ICP is comprised of the following components and volume ratio: brain tissue, 80%; CSF,
10%; blood volume, 10%. The Monro-Kellie doctrine states that the pressure relationship
of these elements constantly adjusts to achieve an acceptable steady state or
equilibrium between the components of the intracranial system.
• The brain contents must be kept in equilibrium, and the ratio between volume and
pressure must remain constant. Any increase in the volume of one component must be
accompanied by a reciprocal decrease in one of the other components. When this
volume-pressure relationship becomes unbalanced, ICP increases.
• The brain attempts to compensate for rises in ICP by:
○ Displacement/shunting of CSF from the intracranial compartment to the lumbar
subarachnoid space (SAS). Normally, about 500 mL of CSF are produced and
absorbed in 24 hours. About 125 to 150 mL circulate throughout the ventricular
system and the SAS in the following ratio: 25 mL in the ventricles, 90 mL in the
lumbar SAS, and 35 mL in the cisterns and surrounding SAS.
○ Increased CSF absorption.
○ Decreased cerebral blood volume by displacement of cerebral venous blood into
the venous sinuses. Compensatory measures are finite. Increased ICP will
ultimately occur if the volume of the intracranial mass exceeds the volume
compensated.
• Intracranial compliance is â€œtightnessâ€ of the brain. Compliance is the relationship
between intracranial volume and ICP. It is a nonlinear relationship; as ICP increases,
compliance decreases. With functional compensatory mechanisms, an increase in
volume causes a small, transient increase in ICP. As compliance decreases, small
increases in volume result in moderate increases in pressure. When compensatory
mechanisms are exhausted, very slight increases in volume will produce large increases
in pressure. The patient's response to changes in ICP will depend on where the patient
is on the volume-pressure curve.
• Factors that influence the ability of the body to achieve this steady state include:
○ Systemic BP.
○ Ventilation and oxygenation.
○ Metabolic rate and oxygen consumption (fever, shivering, physical activity).
○ Regional cerebral vasospasm.
○ Oxygen saturation and hematocrit.
• Inability to maintain a steady state, results in increased ICP. Traumatic brain injury,
cerebral edema, abscess and infection, lesions, intracranial surgery, and radiation
therapy can be potential etiologies of increased ICP.
• Increased ICP constitutes an emergency and requires prompt treatment. ICP can be
monitored by means of an intraventricular catheter, a subarachnoid screw or bolt, or an
epidural pressure-recording device.
• Alterations or compromise in cerebral blood flow can be measured noninvasively by a
Transcranial Doppler (TCD). Increased velocities indicate vasospasm, diminished
velocities indicate low blood flow, and absent velocities are consistent with no flow, or
brain death.
Nursing Assessment
Change in LOC
Caused by increased cerebral pressure. Assess for:
• Change in LOC (awareness): drowsiness, lethargy
• Early behavioral changes: restlessness, irritability, contusion, and apathy
• Falling score on the GCS (see page 475)
○ Change in orientation: disorientation to time, place, or person
○ Difficulty or inability to follow commands
○ Difficulty or inability in verbalization or in responsiveness to auditory stimuli
○ Change in response to painful stimuli (eg, purposeful to inappropriate or absent
responses)
○ Posturing (abnormal flexion or extension)
Changes in Vital Signs
Caused by pressure on brain stem. Assess for:
• Rising BP or widening pulse pressure (the difference between systolic and diastolic BP).
This may be followed by hypotension and labile vitals signs, indicating further brain stem
compromise.
• Pulse changes with bradycardia changing to tachycardia as ICP rises.
• Respiratory irregularities: tachypnea (early sign of increased ICP); slowing of rate with
lengthening periods of apnea; Cheyne-Stokes (rhythmic pattern of increasing and
decreasing depth of respirations with periods of apnea) or Kussmaul (paroxysms of
difficult breathing) breathing; central neurogenic hyperventilation (prolonged, deep
breathing); apneuistic (sustained inspiratory effort) breathing; and ataxic (incoordinated
and spasmodic) breathing.
• Hyperthermia followed by hypothermia.
NURSING ALERT
Respiratory irregularities may not be apparent if patient is mechanically ventilated.
Pupillary Changes
• Caused by increased pressure on optic and oculomotor nerves.
• Inspect the pupils with a flashlight to evaluate size, configuration, and reaction to light.
• Compare both eyes for similarities or differences, particularly pupillary changes related
to location and progression of brain stem herniation.
○ Midbrain involvementâ€”fixed and dilated
○ Pontine involvementâ€”pinpoint pupils
○ Uncal herniation
 Unilaterally dilating pupil ipsilateral to lesion.
 Anisocoria (unequal) with sluggish light reaction in dilated pupil.
 If treatment is delayed or unsuccessful, contralateral pupil becomes
dilated and fixed to light.
 When herniation of brainstem occurs, both pupils assume midposition
and remain fixed to light.
○ Central transtentorial herniation
 Pupils are small bilaterally (1 to 3 mm).
 Reaction to light is brisk but with small range of constriction.
 Treatment is delayed or unsuccessful; small pupils dilate moderately (3 to
5 mm) to fix irregularly at midposition.
 When herniation of brainstem occurs, both pupils dilate widely and remain
fixed to light.
○ Perform fundoscopic examination to inspect the retina and optic nerve for
hemorrhage and papilledema.
Extraocular Movements
• Evaluate gaze to determine if it is conjugate (paired, working together) or dysconjugate
(eye deviates or movement is asymmetrical).
• Evaluate movement of eyes.
○ Inability to abduct or adduct: deviation of one or both eyes.
○ Alteration in vision (eg, blurred vision, diplopia, field cut)
○ Spontaneous roving, random eye movements
○ Nystagmus on horizontal/vertical gaze
• Oculocephalic reflex (doll's eyes): brisk turning of the head left, right, up, or down with
observation of eye movements in response to the stimulus. Tests brain stem pathways
between cranial nerves III, IV, VI, and VIII. This should not be performed on patients with
suspected cervical spine injury, patients in a cervical collar, or patients with known
cervical spine injuries unless part of the brain death exam.
• Oculovestibular reflex (ice water calorics): 30 to 60 mL of ice water instilled into the ear
with the head of the bed elevated to 30 degrees. Tests brain stem pathways between
cranial nerves III, IV, VI, and VIII. Response preserved longer than the doll's eyes
maneuver. Performed by physician as part of brain death examination.
Other Changes
Be alert for:
• Headache increasing in intensity and aggravated by movement and straining
• Vomiting recurrent with little or no nausea; especially in early morning; may be projectile
• Papilledema from optic nerve compression
• Subtle changes, such as restlessness, headache, forced breathing, purposeless
movements, and mental cloudiness
• Motor and sensory dysfunctions (proximal muscle weakness, presence of pronator drift)
• Contralateral hemiparesis progressing to complete hemiplegia
• Speech impairment (expressive, receptive, or global aphasia) when dominant
hemisphere involved
• Seizure activity: focal or generalized
• Decreased brain stem reflexes (cranial nerve deficits; eg, corneal, gag, and swallow)
• Pathologic reflexes: Babinski, grasp, chewing, sucking.
Nursing Diagnosis
• Decreased Intracranial Adaptive Capacity
Decreasing Intracranial Pressure
NURSING ALERT
Increased ICP is a true life-threatening medical emergency that requires immediate recognition
and prompt therapeutic intervention.
• Establish and maintain airway, breathing, and circulation.
• Promote normal PCO2. Hyperventilation is not recommended for prophylactic treatment
of increased ICP as cerebral circulation is reduced by 50% the first 24 hours after injury.
Hyperventilation causes cerebral vasoconstriction and decreases cerebral blood volume
and results in decreased ICP; this can potentiate secondary injury to the brain.
Hyperventilation should be used only after all other treatment options have been
exhausted or in an acute crisis.
• Avoid hypoxia. Decreased PO2 (less than 60) also causes cerebral vasodilation, thus
increasing ICP.
• Maintain adequate cerebral perfusion pressure (CPP). CPP is determined by subtracting
the ICP from the mean arterial pressure (MAP): CPP = MAP â€“ ICP
• Administer mannitol (Osmitrol), an osmotic diuretic, if ordered. Osmotic diuretics act by
establishing an osmotic gradient across the blood-brain barrier that depletes the
intracellular and extracellular fluid volume within the brain and throughout the body. The
mannitol will be ineffective if the blood-brain barrier is not intact.
• Administer hypertonic saline, as ordered. It creates an osmotic gradient that pulls extra
fluid from the brain with an intact blood-brain barrier, lowers ICP, improves cerebral blow
flow, and delivers oxygen. Use of hypertonic saline/dextran is currently under
investigation.
• Insert an indwelling urinary catheter for management of diuresis.
• Administer corticosteroids, such as dexamethasone (Decadron), as ordered, to reduce
edema surrounding brain tumor, if present. Corticosteroids are used to reduce
inflammation and decrease vasogenic (extracellular) cerebral edema. Corticosteroids
are useful in the treatment of vasogenic edema associated with brain tumors but are not
recommended in the treatment of cytoxic (intracellular) cerebral edema related to
trauma.
• Maintain balanced fluids and electrolytes. Diabetes insipidus (DI) results from the
absence of antidiuretic hormone (ADH); this is reflected by increased urine output with
elevation of serum osmolarity and sodium. The syndrome of inappropriate antidiuretic
hormone (SIADH) results from the secretion of ADH in the absence of changes in serum
osmolality. This is reflected by decreased urine output with decreased serum sodium
and increased free water. Either extreme may occur with ICP.
• Monitor effects of neuromuscular paralyzing agents, such as pancuronium (Pavulon),
anesthetic agents, such as propofol (Diprivan), and sedatives, such as midazolam
(Versed) or lorazepam (Ativan), which may be given along with mechanical ventilation to
prevent sudden changes in ICP due to coughing, straining, or â€œfightingâ€ the
ventilator. Neuromuscular paralyzing agents, such as pancuronium (Pavulon) or
vecuronium (Norcuron), or high-dose barbiturates, may be used in cases that are difficult
to manage.
○ High-dose barbiturates induce a comatose state and suppress brain metabolism,
which, in turn, reduces cerebral blood flow and ICP (not recommended unless all
other treatments failed).
○ Be alert to the high level of nursing support required. All responses to
environmental and noxious stimuli (suctioning, turning) are abolished as well as
all protective reflexes.
○ Cough or gag reflex will be absent and the patient will be unable to protect the
airway, increasing susceptibility to pneumonia.
○ Monitor ICP, arterial pressure, and serum barbiturate levels as indicated. Perform
continuous EEG monitoring to document burst suppression (suppression of
cortical activity) and ensure adequate dosing of barbiturates, if used.
○ Monitor temperature because barbiturate coma causes hypothermia.
• Treat fever aggressively because fever increases cerebral blood flow and cerebral blood
volume; acute increases in ICP occur with fever spikes. Cerebral temperature is 4 to 5
degrees higher then body core temperature; therefore, small increases in body core
temperature can create drastic increases in the core temperature of the brain. Also,
infection is a common complication of ICP.
• Avoid positions or activities that may increase ICP. Keep head in alignment with
shoulders; neck flexion or rotation increases ICP by impeding venous return. Keep head
of bed elevated 30 degrees to reduce jugular venous pressure and decrease ICP.
○ Minimize suctioning, keep procedure less than 15 seconds, and, if ordered, instill
lidocaine via endotracheal (ET) tube before suctioning. Coughing and suctioning
are associated with increased intrathoracic pressure, which is associated with
ICP spikes. Lidocaine 5 to 10 ml injected into ET tube before suctioning dampens
the cough response.
○ Minimize other stimuli, such as alarms, television, radio, and bedside
conversations, that may precipitously increase ICP (stimuli are patient
dependent).
• Avoid hyperglycemia. Treat with sliding scale insulin or insulin drip as ordered.
• Initiate treatment modalities as ordered for sustained increased ICP (above 20 mm Hg
persisting 15 minutes or more or if there is a significant shift in pressure).
• Avoid taking pressure readings immediately after a procedure. Allow patient to rest for
approximately 5 minutes.
• Record ICP readings every hour, and correlate with significant clinical events or
treatments (suctioning, turning).

• ICP and vital signs stable; alert and responsive
INTRACRANIAL MONITORING
Intracranial monitoring, including ICP monitoring, is a technology that helps the nurse assess,
plan, intervene, and evaluate patient responses to care. ICP monitoring is most widely used.
See Figure 15-1..
FIGURE 15-1 Intracranial pressure monitoring system. (A) intraventricular; (B) subarachnoid;
(C) subdural; (D) parenchymal; (E) epidural.
• Intraventricular catheter inserted into lateral ventricle using a drill or burr hole opening;
connected to fluid-filled transducer, which converts mechanical pressure to electrical
impulses and waveform; allows ventricular drainage.
• Subarachnoid (bolt) hollow screw inserted into SAS beneath skull and dura through drill
hole; also connected to pressure transducer system.
• Epidural sensor inserted beneath skull but not through dura, so does not measure
pressure directly; fiber-optic cable is connected directly to monitor.
• Parenchymal device is inserted directly into brain tissue.
ICP Waveforms
• ICP fluctuates, creating three distinct waveforms.
• Plateau or A waves are characterized by rapid increases and decreases of pressure with
recurring elevations of 15 to 50 mm Hg or higher and may last 2 to 15 minutes.
○ A waves are clinically significant.
○ May be accompanied by transient symptoms of headache, nausea, and
decreased consciousness.
• B waves are of shorter duration and smaller amplitude than A waves and are not
clinically significant unless these occur frequently; then these may precede A waves.
• C waves are small, rhythmic oscillations that are not clinically significant but fluctuate
with changes in BP.
Other Monitoring Systems
• LICOX Monitoring Systemâ€”placed in the brain tissue through a burr hole and monitors
brain tissue partial pressure of oxygen (PbtO2), cerebral temperature, and indirect ICP.
Continual monitoring of the cerebral temperature and oxygenation levels provides direct
information on the acute changes in the intracranial tissue that can potentiate secondary
brain injury.
• Microdialysisâ€”catheter is placed into the brain tissue through a burr hole for monitoring
of cerebral oxygen, glucose, lactate, lactate-pyruvate, glutamate, and glycerol. The
catheter is connected to a 2.5-ml syringe and into a microinfusion pump. The pump is
perfused with Ringer's solution. Samples are obtained periodically for analysis.
• Jugular venous oximetryâ€”A fiber-optic oximetric catheter is placed into the jugular bulb
of the internal jugular vein for measurement of jugular venous oxygen saturation (SjvO2).
SjvO2 is helpful in evaluating arterial saturation, cerebral metabolic rate for oxygen, and
cerebral blood flow. The normal range is between 54% and 75%. A low SjvO2 is
suggestive of increased brain extraction of oxygen related to systemic arterial hypoxia,
decreased cerebral blood flow from hypotension or vasospasm, or an elevated ICP with
a low CPP.
• Transcranial cerebral oxygen saturationâ€”indirect measurement of cerebral
oxygenation using the INVOS 4100 system. Near-infrared light emitting diode and two
photodiode electrodes are applied bilaterally on the forehead by self-adhesive skin
patches to measure returning scattered light intensities. Near-infrared light entering the
cerebral cortex is absorbed or scattered, some of which is passed back through the
surface near the entry point, and oxygen saturation is measured by computer analysis
and converted to digital format. The normal range is between 54% and 75%.
• Note the pattern of waveforms and any sustained elevation of pressure above 15 mm
Hg.
• Avoid overstimulation of the patient.
○ Note the stimuli that cause increased pressure, such as bathing, suctioning,
repositioning, or visitors. Adjust care as indicated.
○ Premedicate as indicated.
○ Provide rest periods between periods of care.
○ Limit visitors as status indicates.
○ Limit unnecessary conversation at patient's bedside.
○ Eliminate external environmental stimuli. Close doors, turn off suction equipment
when not in use, limit television or radio as status indicates.
• Watch for developing or increasing frequency of plateau waves. Report these, and begin
measures to lower increased ICP as described on page 481.
PROCEDURE GUIDELINES 15-2
Intracranial Monitoring/Licox Monitoring System/Microdialysis System
EQUIPMENT
• Sterile gloves, mask, and surgical cap
• Monitoring system (intraventricular, subarachnoid, epidural)
• I.V. pole or standard on which to mount the system
• I.V. solutions as ordered
• I.V. high-pressure tubing
• Burr hole tray for insertion or as needed
• Topical anesthetic
• Vital sign records
PROCEDURE
Nursing Action Rationale
Preparatory phase
1.Explain the need for extensive, continuous assessment 1 Explanations will decrease anxiety,
and appropriate nursing intervention to the family and . allow patient and family a sense of
patient, if possible. control, and encourage compliance
with procedure.
2.Gather and assemble equipment. Flush lines with 2 Availability of equipment will
ordered solution according to manufacturer's . enhance success of procedure.
directions.
3.Calibrate equipment according to directions. 3 Accurate interpretation of intracranial
. pressure (ICP) values, wave
patterns, cerebral temperature, and
brain tissue partial pressure of
oxygen (PbtO2) will depend on
appropriate baseline function.
4.Perform neurologic assessment. 4 Patient baseline must be established
. to determine changes and guide
therapy.
5.Administer light sedation or analgesia if patient is 5 Procedure is invasive, and injury
agitated. . may result with excessive patient
movement.
Performance phase
1.Establish head of bed at 30 degrees. 1 Head elevation is a conventional
. nursing intervention used to control
elevated ICP and avoid
complications in patients with
neurotrauma.
a. Head elevation facilitates venous
drainage, decreasing intracranial
volume, and prevents collapse of
the ventricles if ventricular
placement.
b. However, elevating the head of
the bed may decrease cerebral
perfusion pressure, creating
ischemia.
2.Don mask and surgical cap. 2 Reduces risk of transmission of
. airborne bacteria.
3.Shave and cleanse the operative site. 3 Removes bacteria from the site,
. reducing the risk of infection.
4.Establish the sterile field. 4 A sterile field reduces the risk of
. infection.
5.Assist with burr hole and placement of intracranial 5 Direct monitoring of ICP allows for
monitoring system. . early detection of decompensation
and management of complications.
6.Connect monitoring catheter to transducer/monitoring 6 Allows for conduction of intracranial
equipment according to directions. . and cerebral perfusion pressures
(CPP) to the interpretive component
of the system.
7.Observe numeric readings and wave patterns. Adjust 7 Changes in baseline readings
characteristics to obtain optimal visual reading. . indicate alterations in ICP or
problems with the mechanics of the
monitoring system.
8.Cover the catheter insertion site with a sterile dressing. 8 The skull and meninges have been
Observe for possible cerebrospinal fluid (CSF) . penetrated, leaving the patient at
drainage depending on the placement of the catheter. risk for infection.
9.Adjust alarm system according to ordered parameters. 9 Alarms should be on at all times to
. alert the nurse away from the
bedside of ongoing adverse
changes.
(A) Normal waveform; (B) A waves (plateau waves), B waves, and C waves.
Follow-up phase
1.Frequently assess the patient and the system to 1 Manipulation of the system may
ascertain neurologic status, assessing ICP and CPP, . inadvertently close the system,
and patency of the system. leaving the patient without benefit of
monitoring.
2.Irrigate the system using sterile technique according to 2 Irrigation helps maintain the patency
policy or as needed to maintain patency. . of the system.
3.Report dampened waveforms, and have 1 ml of normal 3 The tip of the catheter may have
saline (without preservatives) available for irrigation if . migrated against the ventricular wall
indicated. or cerebral tissue depending on
location, or ventricular collapse may
be imminent. Irrigation is done by
the health care provider in this case.
4.Assess head dressing for CSF drainage. Change 4 Because of its high glucose content,
dressing according to facility policy. . CSF is an excellent medium for
bacterial growth.
5.Adjust the height of the transducer of the system to the 5 Position of the transducer in relation
level of the patient's ventricles (inner canthus of eye . to the ventricles will influence the
and tip of ear) with every position change for accurate accuracy of the readings because of
readings and per orders. fluid gradient pressures.
NURSING MANAGEMENT OF THE PATIENT UNDERGOING INTRACRANIAL SURGERY

Craniotomy is the surgical opening of the skull to gain access to intracranial structures to
remove a tumor, relieve increased intracranial pressure (ICP), evacuate a blood clot, stop
hemorrhage, or remove epileptogenic tissue. Surgical approach is based on location of lesion
and may be supratentorial (above the tentorium or dural covering that divides the cerebrum from
cerebellum) or infratentorial (below the tentorium, including the brain stem). Craniotomy may be
performed by means of burr holes (made with a drill or hand tools) or by making a bony flap.
Craniectomy is excision of a portion of the skull. Cranioplasty is repair of a cranial defect by
means of a plastic or metal plate. Transsphenoidal surgery is an approach that gains access to
the pituitary gland through the nasal cavity and sphenoidal sinus.
Preoperative Management
• Diagnostic findings, surgical procedure, and expectations are reviewed with the patient.
• Presurgical shampoo with an antimicrobial agent may be ordered. Shave and prep are
performed in the operating room.
• Depending on primary diagnosis, corticosteroids may be ordered preoperatively to
reduce cerebral edema.
• Depending on the type and location of lesion, anticonvulsants may be ordered to reduce
risk of seizures.
• The patient is prepared for the use of intraoperative antibiotics to reduce risk of infection,
and urinary catheterization to assess urinary volume during operative period.
• If cerebral edema develops, intraoperative or postoperative osmotic diuretic (mannitol
[Osmitrol]) or corticosteroids may be ordered for its treatment.
• Neurologic assessment is performed to evaluate and record the patient's neurologic
baseline and vital signs for postoperative comparison.
• Family and patient are made aware of the immediate postoperative care and where the
physician will contact the family after surgery.
• Supportive care is given as needed for neurologic deficits.
Postoperative Management
• Respiratory status is assessed by monitoring rate, depth, and pattern of respirations. A
patent airway is maintained.
• Vital signs and neurologic status are monitored, using GCS; findings are documented.
• Arterial and central venous pressure (CVP) are monitored, possibly with a pulmonary
Swan-Ganz catheter for accurate assessment of hemodynamic status.
• Pharmacologic agents may be prescribed to control increased ICP.
• Incisional and headache pain may be controlled with mild analgesic (codeine and
acetaminophen) or low dose opioids (morphine sulfate or fentanyl/Duragesic), as
prescribed. Monitor response to medications.
• Position head of bed at 15 to 30 degrees, or per clinical status of patient, to promote
venous drainage. Determining appropriate position of head of bed is patient-dependent
and should be adjusted based on observed changes in the patient's clinical response
and ICP to positioning. A decrease in CPP is observed with raising the head of the bed
to lower ICP.
• Turn side-to-side every 2 hours; positioning restrictions will be ordered by the physician.
• CT scan of the brain is performed if patient's status deteriorates.
• Oral fluids are provided after swallow reflex and bowel sounds have returned. Intake and
output are monitored. Speech therapy may be ordered for bedside swallow study or
radiographic swallow study.
• Signs of infection are monitored by checking craniotomy site, ventricular drainage,
nuchal rigidity, or presence of CSF (fluid collection at surgical site).
• Periorbital edema is controlled by such measures as elevation of head of bed and cold
compresses. Removal of surgical dressing and increase in activity will assist in the
resolution of periorbital edema.
Potential Complications
• Intracranial hemorrhage/hematoma
• Cerebral edema
• Infections (eg, postoperative meningitis, pulmonary, wound)
• Seizures
• Cranial nerve dysfunction
• Decreased CPP causing cerebral ischemia
Nursing Diagnoses
• Ineffective Tissue Perfusion (cerebral) related to increased ICP
• Risk for Aspiration related to decreased swallow reflex and postoperative positioning
• Risk for Infection related to invasive procedure
• Acute Pain related to physiologic changes produced due to invasive procedure
• Constipation related to use of opioid medication and immobility
Maintaining ICP Within Normal Range
• Closely monitor LOC, vital signs, pupillary response, and ICP, if indicated. Notify health
care provider if ICP greater than 20 mm Hg or CCP less than 70 mm Hg.
• Teach patient to avoid activities that can raise ICP, such as excessive flexion or rotation
of the head and Valsalva maneuver (coughing, straining with defecation).
• Administer medications as prescribed to reduce ICP.
• Eliminate noxious tactile stimuli, such as suctioning, prolonged physical assessment,
turning, and providing ROM exercises (based on patient response).
Preventing Aspiration
• Offer fluids only when patient is alert and swallow reflex has returned.
• Have suction equipment available at bedside. Suction only if indicated. Pretreat with
sedation or endotracheal lidocaine to prevent elevation of ICP.
• Elevate head of bed to maximum of order, or per clinical status, and patient comfort.
Preventing Nosocomial Infections
• Use sterile technique for dressing changes, catheter care, and ventricular drain
management.
• Be aware of patients at higher risk of infectionâ€”those undergoing lengthy operations,
those with ventricular drains left in longer than 72 hours, and those with operations of the
third ventricle.
• Assess surgical site for redness, tenderness, and drainage.
• Watch for leakage of CSF, which increases the danger of meningitis.
○ Watch for sudden discharge of fluid from wound; a large leak usually requires
surgical repair.
○ Warn against coughing, sneezing, or nose blowing, which may aggravate CSF
leakage.
○ Assess for moderate elevation of temperature and neck rigidity.
○ Note patency of ventricular catheter system.
• Institute measures to prevent respiratory or UTI postoperatively.
Relieving Pain
• Medicate patient as prescribed and according to assessment findings.
• Elevate head of bed per protocol to relieve headache.
• Provide distractive measures for pain management.
• Darken room if patient is photophobic.
Avoiding Constipation
• Encourage fluids when patient is able to manage liquids.
• Ambulate as soon as possible.
• Change to nonopioid agents for pain control as soon as possible.
• Avoid Valsalva-like maneuvers.
• Use stool softeners and laxatives, as ordered.
Family Education and Support
• Keep patient and family aware of progress and plans to transfer to step-down unit,
general nursing unit, subacute care, or rehabilitation facility.
• Encourage frequent visiting and interaction of family for stimulation of patient as care
allows.
• Begin discharge planning early, and obtain referral for home care nursing, social work,
physical and occupational therapy as needed.
• Decreased ICP and CPP maintained greater than 70 mm Hg
• Gag reflex present; breath sounds clear
• Afebrile without signs of infection
• Verbalization of decreased pain
• Passed soft stool
CRANIAL NERVE DISORDERS
BELL'S PALSY
Idiopathic Bell's palsy is an acute peripheral facial paralysis of the infratemporal portion of the
seventh cranial nerve (facial) unilaterally. It is typically a self-limiting process that usually
improves in 3 to 6 months.
• Cause is unknown. Possible etiologies include sensory ganglionitis of the CNS with
secondary muscle palsy, caused by inflammation, vascular ischemia, and autoimmune
demyelination.
• Most patients experience a viral prodrome (eg, upper respiratory infection 1 to 3 weeks
before onset of symptoms).
• The common cold sore virus, herpes simplex, and other herpes viruses are usually
present before symptom onset.
• Can affect anyone at any age; however, it disproportionately affects pregnant women
and those who have diabetes or influenza.
• Incidence of recurrence is less than 10%, especially among diabetics.
• Generally self-limiting. With or without treatment, most patients improve significantly
within 2 weeks, and about 80% recover completely within 3 months. In rare cases, the
symptoms may never completely resolve.
Clinical Manifestations
• Paralysis of ipsilateral side of face from vertex of scalp to chin; facial muscles weak
throughout forehead, cheek, and chin; can affect speech, distort face
• Involvement of all branches of facial nerve: facial weakness, diminished taste from
anterior two-thirds of tongue, decreased blink reflex, decreased lacrimation, inability to
close eye, painful eye sensations; photophobia, drooling
• Hyperacusis on the affected side
• Distorted body image due to change in facial appearance
Diagnostic Evaluation
• History to determine previous illness, onset of paralysis
• Physical examination for evaluation of seventh cranial nerve function and corneal
sensation
• Exclusion of lesions that mimic Bell's palsy, such as tumor, infection, trauma, or stroke
• Electrophysiologic testing, specifically action potentials and EMGs and nerve conduction
velocities, to evaluate nerve function.
Management
• Corticosteroid therapy initiated early to decrease inflammation (eg, prednisone 1
mg/kg/day for 10 to 14 days, followed by a tapering dose). Acyclovir combined with
prednisone is possibly effective in improving facial function.
• Eye care to maintain lubrication and moisture if unable to close. May need to be patched
during sleep.
• Physical therapy, electrical stimulation to maintain muscle tone.
• Biofeedback (controversial).
• Surgery to anastomose facial nerve to other cranial nerve (CN VII to XI or CN VII to XII;
controversial due to natural history); surgical closure of eyelid to protect cornea
(tarsorrhaphy).
• Nonsteroidal anti-inflammatory drugs (NSAIDs) and analgesics to relieve pain.
Complications
• Corneal ulceration
• Impairment of vision
• Body image disturbance related to facial nerve paralysis
NURSING ALERT
Keratitis (inflammation of the cornea), ulceration, and vision loss are major threats to a patient
with Bell's palsy. Protect the cornea if eye does not close.
Nursing Assessment
• Test motor components of facial nerve (VII) by assessing patient's smile, ability to
whistle, purse lips, wrinkle forehead, and close eyes. Observe for facial asymmetry.
• Observe patient's ability to handle secretions, food, fluids; observe for drooling.
• Assess patient's ability to blink and speak clearly.
• Assess effect of altered appearance on body image.
Nursing Diagnoses
• Impaired Tissue Integrity related to loss of protective eye closure
• Chronic Pain related to physiologic alterations of disorder
• Disturbed Body Image related to facial nerve paralysis
Protecting Corneal Integrity
• Administer or teach patient to administer artificial tears and ophthalmic ointment as
prescribed.
• Patch eye to keep shut at night as directed.
• Inspect eye for redness or discharge.
• Advise patient to report eye pain immediately.
Relieving Pain
• Administer or teach patient to administer corticosteroids to reduce inflammation and
nonopioid analgesics to relieve pain.
• Teach patient to apply moist heat to face.
• Perform or teach patient to perform facial massage to alleviate feelings of stiffness.
Enhancing Body Image
• Encourage patient to express feelings related to body image disturbance.
• Assist patient to use mirror as means to obtain feedback about actual versus perceived
appearance and identify factors that impede or enhance.
Patient Education and Health Maintenance
• Instruct the patient to wear wraparound sunglasses to decrease normal evaporation from
the eye from sun and wind, to avoid eye irritants, and to increase environmental
humidity.
• Instruct the patient in use of ophthalmic drops and ointment, proper methods of lid
closure, and patching of the eye.
• Demonstrate facial exercises (eg, raise eyebrows, squeeze eyes shut, purse lips) and
stress their importance to prevent muscle atrophy.
• For further information, refer to National Organization for Rare Disorders,
http://www.rarediseases.org, or Bells Palsy Research Foundation,
http://www.bellspalsyresearch.com.
• Cornea without redness, pain, or discharge
• Reports adequate pain control
• Verbalizes adjustment to body image disturbance
TRIGEMINAL NEURALGIA (TIC DOULOUREUX)
Trigeminal neuralgia (tic douloureux) is an intensely painful neurologic condition that affects one
or more branches of the fifth cranial (trigeminal) nerve. Patients experience sudden paroxysms
of â€œlancinatingâ€ or electric shocklike facial pain (see Figure 15-2) localized to one or more
branches of the nerve. The pain is often precipitated by trigger points that â€œfireâ€ when the
patient talks, shaves, eats, touches the face, brushes the teeth, or is exposed to cold wind.
FIGURE 15-2 The main divisions of the trigeminal nerve are the ophthalmic, maxillary, and
mandibular. Sensory root fibers arise in the gasserian ganglion.
• Unknown cause, but degenerative or viral origin suspected.
• Any of the three trigeminal nerve branches can be affected:
○ V1: ophthalmic branch; pain involves the eye and forehead
○ V2: maxillary branch; pain involves the cheek, upper teeth, upper gums, and nose
○ V3: mandibular branch; pain involves the lower jaw, side of tongue, lower teeth,
lower gum, extends to ear
• Compression from artery adjacent to the nerve strips myelin from nerve when it pulsates.
Loss of myelin acts like an uninsulated wire that â€œfiresâ€ abnormally in response to
stimuli.
GERONTOLOGIC ALERT
Trigeminal neuralgia is commonly seen in the elderly population. Pain typically appears to be
localized to one or more teeth. Patients may seek dental care for pain relief, resulting in one or
more tooth extractions without alleviation of pain.
• Sudden, severe episodes of intense facial pain localized to one or more of the branches
of the nerve, lasting less than 30 to 60 seconds and ending abruptly.
• Pain may occur spontaneously or be precipitated by activation of trigger points, such as
touching the face, talking, chewing, yawning, and brushing the teeth, that place pressure
on the terminal end of the branch affected.
• Pain is always unilateral and does not cross the midline. Bilateral pain is sometimes
seen in patients with multiple sclerosis (MS) and should result in high index of suspicion
for this condition.
• Some patients experience numbness, particularly around the mouth.
• History of characteristic symptoms and pattern
• Neurologic examination
• CT scan, MRI, skull X-rays to rule out structural lesions, such as tumor, arteriovenous
malformation, MS, or other disorders
• Important to rule out atypical facial pain, vasomotor or postherpetic neuralgia, and dental
pain
• Initial response to pharmacologic treatment in the majority of cases
Management
Pharmacologic
• Use of carbamazepine (Tegretol) is first and most effective medication used to treat
condition. Other drugs, such as imipramine (Tofranil), phenytoin (Dilantin), baclofen
(Lioresal), divalproex (Depakote), or gabapentin (Neurontin), may be added or
substituted over time.
• Although pain generally responds to pharmacologic intervention, it gradually becomes
refractory over time or patients suffer undesirable adverse effects.
Surgical
Operative procedure selected is one that will provide the greatest chance of long-term pain relief
with the fewest complications.
• Alcohol, phenol block, or glycerol injection for pain may last several months after
injection.
• Percutaneous radiofrequency trigeminal gangliolysis low-voltage stimulation of nerve by
electrode inserted through foramen ovale; sensory function destroyed but attempt to
preserve motor function; may cause decreased corneal sensation if V1 affected;
paresthesias, jaw weakness, undesirable, painful numbness (anesthesia dolorosa). Pain
may recur as nerve regenerates, necessitating repeat procedure.
• Rhizotomy (transection of nerve root at gasserian ganglion) causes complete loss of
sensation; other complications include burning, stinging, discomfort in and around eye,
herpetic lesions of face, keratitis, and corneal ulceration. Pain may recur as nerve
regenerates.
• Percutaneous balloon microcompression to selectively injure myelinated fibers that
mediate light touch and trigger pain in all three sensory branches of the nerve. Relieves
pain in ophthalmic branch while sparing corneal sensation.
• Microvascular decompression of trigeminal nerve. Most effective form of therapy, with
75% to 80% of patients pain-free without need for medication long-term after procedure.
Treatment of choice for younger patients who are good anesthesia risk, do not want
facial numbness, and are willing to accept craniotomy.
Complications
• Anorexia and weight loss
• Dehydration
• Anxiety/fear
• Depression/social isolation/suicidal ideations in extreme cases
Nursing Assessment
• Take history of the pain, including duration, severity, and aggravating factors.
• Assess nutritional status and hydration.
• Assess for anxiety and depression, including problems with sleep, social interaction,
coping ability/skills.
Nursing Diagnoses
• Chronic Pain related to physiologic changes of the disorder
• Imbalanced Nutrition: Less Than Body Requirements related to fear of eating
• Powerlessness related to lack of control over painful episodes
Relieving Pain
• To minimize painful episodes, review with patient potential trigger factors, and develop
individualized methods of coping with identified triggers.
• Encourage patient to take medication regularly, including â€œrescueâ€ medication for
breakthrough periods.
• Help patient maintain a method of communication without causing pain from talking.
Maintaining Adequate Nutrition
• To maximize nutritional intake, instruct patient to take foods and fluids at room
temperature and to chew on the unaffected side.
• Have the patient consult with the dietitian for appropriate meal texture and composition.
• Encourage small, frequent meals to avoid fatigue and pain.
• Advise about use of nutritional supplements if indicated.
Increasing Control
• Support patient through treatment trials.
• Teach relaxation exercises, such as relaxation breathing, progressive muscle relaxation,
and guided imagery to relieve tension.
• Encourage participation in support groups (eg, Trigeminal Neuralgia Association), and
facilitate therapeutic relationship with health care provider.
• Educate the surgical patient regarding self-care after denervation procedures.
• Instruct patient to look at eye in mirror for redness and foreign bodies, three to four times
per day if corneal sensation is impaired.
• Instruct patient to instill eyedrops every 4 hours for loss of corneal sensation.
• Instruct patient to avoid drinking hot liquids through a straw.
• Instruct patient to chew on unaffected side to avoid biting tongue, lips, and inside of
mouth.
• Instruct patient who wears dentures that jaw muscle will regenerate over time; avoid
having dentures refitted.
• Instruct patient to maintain regular dental checkups because pain will not be felt with
caries.
• Ask patient if face is numb, and instruct patient to report any change in sensation.
• Refer patient to the Trigeminal Neuralgia Association for education and support network,
http://www.tna-support.org, or National Institute of Neurologic Disorders and Stroke,
http://www.ninds.nih.gov.
• Verbalizes reduced pain
• Maintains weight
• Verbalizes decreased anxiety and depression
CEREBROVASCULAR DISEASE
CEREBROVASCULAR INSUFFICIENCY
Cerebrovascular insufficiency is an interruption or inadequate blood flow to a focal area of the
brain resulting in transient or permanent neurologic dysfunction. Transient ischemic attack (TIA)
lasts less than 24 hours. Ischemic stroke is similar to myocardial infarction, in that the
pathogenesis is loss of blood supply to the tissue, which can result in irreversible damage if
blood flow is not restored quickly.
• Cerebrovascular insufficiency is caused by atherosclerotic plaque or thrombosis,
increased PCO2, decreased PO2, decreased blood viscosity, hyperthermia/hypothermia,
increased ICP.
• Carotid arteries, vertebral arteries, major intracranial vessels, or microcirculation may be
affected.
• Cardiac causes of emboli include atrial fibrillation, mitral valve prolapse, infectious
endocarditis, and prosthetic heart valve.
• Event may be classified as TIAâ€”transient episode of cerebral dysfunction with
associated clinical manifestations lasting usually minutes to an hour, possibly up to 24
hours.
• Symptoms persisting longer than 24 hours are classified as stroke (also known as brain
attack).
Risk Factors for Stroke

Medical Conditions
• Hypertension (30% to 40% risk reduction with treatment): goal BP is lower than 140/90;
if renal insufficiency or heart failure, less than 130/85; if diabetic, less than 130/80
• Cardiac disordersâ€”congenital heart disease, valvular conditions, endocarditis
• Atrial fibrillation (risk reduction is 68% with oral anticoagulant therapy; 21% with aspirin
therapy for nonvalvular causes)
• Diabetes mellitus (44% risk reduction in hypertensive diabetics with controlled BP)
• Hyperlipidemia (20% to 30% risk reduction with those with known coronary heart
disease [CHD] on statin therapy): goal LDL is less than 160 mg/dL if one or no risk
factor; less than 130 if two or fewer risk factors or 10-year CHD risk is less than 20%;
less than 100 if two or fewer risk factors and 10-year CHD risk greater than 20%
• Carotid stenosis
• Prior history of TIA or stroke
• Elevated homocysteine level in blood
Behaviors
• Cigarette smoking (50% risk reduction in 1 year; return to baseline in 5 years)
• Alcohol abuse
• Physical inactivity
• Cocaine use (hemorrhagic stroke)
Nonmodifiable factors
• Increasing ageâ€”risk doubles for each decade over age 50
• Genderâ€”men are at greater risk than women
• Heredityâ€”increased risk with family history of stroke
• Ethnic backgroundâ€”Blacks and Hispanics at higher risk than Whites
Other
There have been reports in the literature of increased risk due to childbirth, hormone
replacement therapy or contraceptive use, chiropractic manipulation, migraine headaches, and
positioning for shampoos in the beauty shop.
NURSING ALERT
Increased stroke risk has been noted in women who smoke and take oral contraceptives and
have a history of migraines.
Clinical Manifestations of Transient Ischemic Attacks
• History of intermittent neurologic deficit, sudden in onset, with maximal deficit within 5
minutes and lasting less than 24 hours.
• Carotid system involvement: amaurosis fugax, homonymous hemianopsia, unilateral
weakness, unilateral numbness or paresthesias, aphasia, dysarthria.
• Vertebrobasilar system involvement: vertigo, homonymous hemianopsia, diplopia,
weakness that is bilateral or alternates sides, dysarthria, dysphagia, ataxia, perioral
numbness.
• Carotid bruit.
• History of headaches of duration of days before ischemia.
• Cerebral angiography, digital subtraction angiography, CT angiography, MRA, Doppler
ultrasoundâ€”all provide information about carotid and intracranial circulation.
• Partial prothrombin time (PTT) or International Normalized Ratio (INR) if anticoagulation
is considered. Blood levels are monitored to document therapeutic ranges and
determine dosing. PTT is utilized for heparin therapy and INR is utilized for oral warfarin
(Coumadin) therapy.
• Diffusion-weighted MRI may be done to rule out stroke.
• Transesophageal echocardiography to rule out emboli from heart.
Management
• Platelet aggregation inhibitors, such as aspirin, ticlopidine (Ticlid), dipyridamole/aspirin
200/25 (Aggrenox), and clopidogrel (Plavix), to reduce risk of stroke.
• Surgical or endovascular intervention to increase blood flow to brainâ€”carotid
endarterectomy, extracranial/intracranial anastomosis, transarterial stenting, or
angioplasty.
• Reduction of other risk factors to prevent stroke, such as control of hypertension,
diabetes, and hyperlipidemia, and smoking cessation.
• Treatment of arrhythmias.
• Treatment of isolated systolic hypertension.
• Anticoagulation agents for patients who continue to have symptoms despite antiplatelet
therapy and those with major source of cardiac emboli.
Complications
• Complete ischemic stroke
• Hemorrhagic conversion of ischemic stroke
• Cerebral edema
Nursing Assessment
• Obtain history of possible TIA; hypertensive and diabetic control; hyperlipidemia;
cardiovascular disease, such as atrial fibrillation; smoking.
• Perform physical examination, including neurologic, cardiac, and circulatory systems; be
sure to listen for carotid bruit.
• Assess patient for history of headache and, if positive, for duration of headache.
Nursing Diagnoses
• IneffectiveTissue Perfusion (cerebral) related to underlying arteriosclerosis
• Risk for Injury related to surgical procedure
• Readiness for Enhanced Knowledge of risk factors and therapeutic lifestyle changes
Improving Cerebral Perfusion
• Teach patient signs and symptoms of TIA and need to notify health care provider
immediately.
• Administer or teach self-administration of anticoagulants, antiplatelet agents,
antihypertensives, and other medication, monitoring for adverse effects and therapeutic
effect.
• Prepare patient for surgical or endovascular intervention as indicated (see page 484).
Providing Care and Preventing Complications After Surgical Procedure
For postoperative extracranial-intracranial care, also see Nursing Management of the Patient
Undergoing Intracranial Surgery, page 484.
• After surgery, closely monitor vital signs and administer medication as prescribed to
avoid hypotension (which can cause cerebral ischemia) or hypertension (which may
precipitate cerebral hemorrhage).
• Perform frequent neurologic checks, including pupil size, equality, and reaction; handgrip
and plantar flexion strength; sensation; mental status; and speech. Notify the health care
provider of any deficits immediately.
• Observe operative area closely for swelling. Mild swelling is expected, but if hematoma
formation is suspected, prepare patient for immediate surgery.
• Medicate for pain and avoid agitation or sudden changes in position, which could affect
BP.
• Elevate head of bed when vital signs are stable.
• Following carotid endarterectomy:
○ Monitor for hoarseness, impaired gag reflex, or difficulty swallowing and facial
weakness, which indicate cranial nerve injury.
○ Keep head in neutral position to relieve stress on surgical site; monitor drainage.
○ Keep tracheostomy tube at bedside and assess for stridor; hematoma formation
can cause airway obstruction.
• Following extracranial-intracranial anastomosis, avoid pressure over the anastomosis of
the superior temporal artery (extracranial) and the middle cerebral artery (intracranial) to
prevent rupture or ischemia of the site. If the patient wears glasses, remove the eyeglass
arm on the operative side to avoid this possible pressure point.
• Following transcranial stenting, administer medications as directed.
○ Heparinâ€”bolus given intraprocedure then continuous I.V. drip postprocedure to
maintain PTT within ordered range; monitor PTT every 6 hours.
○ Clopidogrel (Plavix) before procedure, as ordered. Can be given as a loading
dose of 150 mg the evening before procedure, 300 mg loading dose before
procedure, 75 mg 48 hours before procedure or 75 mg daily 1 week before
procedure. Dosing is physician-dependent.
○ Daily dosing of 75 mg clopidogrel for 30 to 90 days, as directed.
○ Aspirin 81 mg daily as directed.
NURSING ALERT
In the advent of an acute neurologic deficit, the heparin drip should be stopped until an acute
intracerebral bleed has been ruled out.
DRUG ALERT
Loading dose of clopidogrel, intraprocedure heparin bolus, postprocedure heparin drip, and
postprocedure clopidogrel daily dosing minimizes the risk of thromboembolic complications
following transarterial carotid stenting while increasing the risk of hemorrhagic complications.
Close monitoring of neurologic status and PTT is warranted. Inform health care provider of any
changes in neurologic status, PTT levels out of ordered range, and signs of bleeding.
Encouraging Lifestyle Changes to Reduce Risk
• Help patient begin to formulate a plan for smoking cessation (see page 31).
• Teach patient and family members the basics of the food pyramid, how to read labels,
and how to follow a low-fat, and particularly a lowâ€“saturated fat diet (see page 31).
• Obtain a referral to a nutritionist for help with weight management and low-fat, low-
sodium diet as indicated.
• Encourage daily activity for 30 minutes if possible. Obtain physical therapy referral for
endurance training and monitoring as indicated.
• Encourage patient receiving long-term oral anticoagulants to comply with follow-up
monitoring of INR and to report any signs of bleeding.
• Encourage patients receiving antiplatelets agents to report any signs of bleeding.
• Encourage the use of electric razors and toothbrushes to prevent bleeding.
• Reinforce with patient and family importance of accessing the medical system, by calling
911, when symptoms first occur.
• Refer to National Institute of Neurologic Disorders and Stroke, http://www.ninds.nih.gov,
for additional information and support.
• Alert without neurologic deficits
• Respirations unlabored, vital signs stable, no swelling of neck; reports relief of pain
• Expresses readiness to quit smoking and adhere to a low-fat diet menu
CEREBROVASCULAR ACCIDENT (STROKE, BRAIN ATTACK)
Stroke, cerebrovascular accident (CVA), or brain attack is the onset and persistence of
neurologic dysfunction lasting longer than 24 hours and resulting from disruption of blood supply
to the brain and indicates infarction rather than ischemia. Strokes are classified as ischemic
(more than 70% of strokes) or hemorrhagic (associated with greater morbidity and mortality).
About 14% of strokes in the United States are of cardiac origin. About 60% of hemorrhagic
strokes are the result of hypertension. Stroke is the leading cause of long-term disability and the
third leading cause of death in the United States, with an annual incidence of 700,000.
Ischemic Stroke
• Partial or complete occlusion of a cerebral blood flow to an area of the brain due to:
○ Thrombus (most common)â€”due to arteriosclerotic plaque in a cerebral artery,
usually at bifurcation of larger arteries; occurs over several days.
○ Embolusâ€”a moving clot of cardiac origin (frequently due to atrial fibrillation) or
from a carotid artery that travels quickly to the brain and lodges in a small artery;
occurs suddenly with immediate maximum deficits.
• Area of brain affected is related to the vascular territory that was occluded. Subtle
decrease in blood flow may allow brain cells to maintain minimal function, but as blood
flow decreases focal areas of ischemia occur, followed by infarction to the vascular
territory. See Figure 15-3 for cerebral circulation.
FIGURE 15-3 The Circle of Willis as seen at the base of a brain removed from the skull.
• An area of injury includes edema, tissue breakdown, and small arterial vessel damage.
The small arterial vessel damage poses a risk of hemorrhage. The larger the area of
infarction, the greater the risk of hemorrhagic conversion.
• Ischemic strokes are not activity dependent; may occur at rest.
Hemorrhagic
• Leakage of blood from a blood vessel and hemorrhage into brain tissue, causing edema,
compression of brain tissue, and spasm of adjacent blood vessels.
• May occur outside the dura (extradural), beneath the dura mater (subdural), in the
subarachnoid space (SAS or subarachnoid), or within the brain substance
(intracerebral).
• Causal mechanisms include:
○ Increased pressure due to hypertension.
○ Head trauma causing dissection or rupture or vessel.
○ Deterioration of vessel wall from chronic hypertension, diabetes mellitus, or
cocaine use.
○ Congenital weakening of blood vessel wall with aneurysm or arteriovenous
malformation (AVM).
• The intracranial hemorrhage becomes a space-occupying lesion within the skull, further
compromising brain function.
○ The mass effect causes pressure on brain tissue.
○ The hemorrhage irritates local brain tissue leading to surrounding focal edema.
○ SAH or hemorrhage into a ventricle can block normal CSF flow, leading to
hydrocephalus.
• Hemorrhage commonly occurs suddenly while a person is active.
NURSING ALERT
Early detection of warning signs promotes early diagnosis and intervention aimed at lessening
stroke mortality and morbidity.
=Clinical manifestations vary depending on the vessel affected and the cerebral territories it
perfuses. Symptoms are usually multiple. Headache may be a sign of impending cerebral
hemorrhage or infarction; however, it is not always present.
=Common clinical manifestations related to vascular territory (see Table 15-2, page 492).
TABLE 15-2 Stroke Deficits Related to Vascular Territory
CEREBRAL
ARTERY BRAIN AREA INVOLVED SIGNS AND SYMPTOMS*
Anterior Infarction of the medial Paralysis of contralateral foot or leg; impaired
cerebral aspect of one frontal lobe if gait; paresis of contralateral arm;
lesion is distal to contralateral sensory loss over toes, foot,
communicating artery; and leg; problems making decisions or
bilateral frontal infarction if performing acts voluntarily; lack of
flow in other anterior cerebral spontaneity, easily distracted; slowness of
artery is inadequate thought; aphasia depends on the hemisphere
involved; urinary incontinence; cognitive and
affective disorders
Middle Massive infarction of most of Contralateral hemiplegia (face and arm);
cerebral lateral hemisphere and contralateral sensory impairment; aphasia;
deeper structures of the homonymous hemiplegia; altered
frontal, parietal, and temporal consciousness (confusion to coma); inability
lobes; internal capsule; basal to turn eyes toward paralyzed side; denial of
ganglia paralyzed side or limb (hemiattention);
possible acalculia, alexia (visual aphasia),
finger agnosia and left-right confusion;
vasomotor paresis and instability
Posterior Occipital lobe; anterior and Homonymous hemianopia and other visual
cerebral medial portion of temporal defects, such as color blindness, loss of
lobe central vision, and visual hallucinations;
memory deficits; perseveration (repeated
performance of same verbal or motor
response)
Thalamus involvement Loss of all sensory modalities; spontaneous
pain; intentional tremor; mild hemiparesis;
aphasia
Cerebral peduncle Oculomotor nerve palsy with contralateral
involvement hemiplegia
Basilar and Cerebellum and brain stem Visual disturbance such as diplopia,
vertebral dystaxia, vertigo, dysphagia, dysphonia
* Dependent on hemisphere involved and adequacy of collaterals.
○ Numbness (paresthesia), weakness (paresis), or loss of motor ability (plegia) on
one side of the body.
○ Difficulty in swallowing (dysphagia).
○ Aphasia (expressive, receptive, global).
○ Visual difficulties of inattention or neglect (lack of acknowledgment of one side of
the sensory field), loss of half of a visual field (hemianopsia), double vision,
photophobia.
○ Altered cognitive abilities and psychological affect.
○ Self-care deficits.
• Carotid ultrasoundâ€”to detect carotid stenosis.
• CT scanâ€”to determine cause and location of stroke.
• MRA or CT angiogramâ€”noninvasive evaluation of cerebrovascular structures.
• Cerebral angiographyâ€”to determine extent of cerebrovascular insufficiency and to
evaluate for structural abnormalities.
• PET, MRI with diffusion-weighted imagesâ€”to localize ischemic damage.
• TCDâ€”noninvasive method used to evaluate cerebral perfusion. Useful in the bedside
evaluation and to provide a means for ongoing monitoring of cerebral blood flow to
document changes and trends.
Management
Acute Treatment
• Support of vital functionsâ€”maintain airway, breathing, oxygenation, circulation.
• Reperfusion and hemodilution with colloids and volume expanders (albumin).
• Thrombolytic therapy (see Box 15-2, page 493, for inclusion and exclusion criteria for
tPA therapy)â€”recombinant tissue plasminogen (tPA) given I.V. 0.9 mg/kg within 3
hours of onset of symptoms; transarterially within 6 hours of onset of symptoms.
○ Advantages of transarterial therapy
 Higher concentration delivered to clot
 Allows gentle mechanical disruption of clot
 Provides precise imaging of pathology and evaluation of collateral
circulation
 Defines extent of injury and recanalization
○ Additional transarterial treatment options
 Abciximab (Repro)â€”antiplatelet agent delivered intra-arterially
 Verapamilâ€”Potent vasodilator injected into intracranial vessel to treat
acute spasm.
 Clot retrieval
 Balloon angioplasty to treat acute spasm
○ Disadvantages of transarterial therapy
 Risk of hemorrhage related to catheter manipulation
 Delay in thrombolytic therapy due to access delays
 Limited facility based accessibility
• Management of increased ICP (see page 478).
• Maintain BP within prescribed parameters. Limit hypertensive fluctuations and keep
systolic BP (SBP) less than 200 mm Hg to reduce vessel wall stressors to prevent
rebleed in hemorrhagic stroke or potentiate hemorrhagic conversion of ischemic stroke,
while promoting adequate cerebral perfusion to prevent further ischemia.
○ Management of systemic hypertension with nitroprusside (Nipride) or alternative
I.V. antihypertensive agents
○ Vasopressor agents to maintain SBP within prescribed range
• Diuretic treatment to reduce cerebral edema, which peaks 3 to 5 days after infarction
may be used, although this is controversial.
• Calcium channel blockers, nimodipine (Nimotop), to reduce BP, promote vasodilatation,
and prevent cerebral vasospasm.
Subsequent Treatment
• Anticoagulation after hemorrhage is ruled out.
• Antiplatelet agents such as ticlopidine (Ticlid), Dipyridamole/aspirin 200/25 (Aggrenox),
and clopidogrel (Plavix), or aspirin.
• Antispasmodic agents for spastic paralysis.
• A rehabilitation program, including physical therapy, occupational therapy, speech
therapy (as soon as stable), and counseling as needed.
• Treatment of poststroke depression with antidepressants such as selective serotonin
reuptake inhibitors.
Complications
• Aspiration pneumonia
• Dysphagia in 25% to 50% of patients after stroke
• Spasticity, contractures
• Deep vein thrombosis, pulmonary embolism
• Brain stem herniation
• Poststroke depression
Nursing Assessment
• Maintain neurologic flow sheet (the Modified Rankin scale or NIH Stroke Scale may be
used).
• Assess for voluntary or involuntary movements, tone of muscles, presence of deep
tendon reflexes (reflex return signals end of flaccid period and return of muscle tone).
• Also assess mental status, cranial nerve function, sensation/proprioception.
• Monitor bowel and bladder function/control.
• Monitor effectiveness of anticoagulation therapy.
• Frequently assess level of function and psychosocial response to condition.
• Assess for skin breakdown, contractures, and other complications of immobility.
DRUG ALERT
Oral anticoagulants are adjusted to maintain an INR at 2 to 3 to prevent stroke and the
associated complication of intracranial and subdural hemorrhage. Report INRs that are elevated
to reduce the risk of bleeding or decreased levels to adjust therapy to be more effective.
Nursing Diagnoses
• Risk for Injury related to neurologic deficits
• Impaired Physical Mobility related to motor deficits
• Disturbed Thought Processes related to brain injury
• Impaired Verbal Communication related to brain injury
• Self-Care Deficit: Bathing, Dressing, Toileting related to hemiparesis/paralysis
• Imbalanced Nutrition: Less Than Body Requirements related to impaired self-feeding,
chewing, swallowing
• Impaired Urinary Elimination related to motor/sensory deficits
• Disabled Family Coping related to catastrophic illness, cognitive and behavioral
sequelae of stroke, and caregiving burden
NURSING ALERT
Use of clinical pathways maximizes stroke patient outcomes. Case management models of care
foster interdisciplinary utilization, timeliness of referrals, patient education, patient satisfaction,
and efficient use of health care resources. The specific role of the nurse in stroke recovery
integrates therapeutic aspects of coordinating, maintaining, and training.
Preventing Falls and Other Injuries
• Maintain bed rest during acute phase (24 to 48 hours after onset of stroke) with head of
bed slightly elevated and side rails in place.
• Administer oxygen as ordered during acute phase to maximize cerebral oxygenation.
• Frequently assess respiratory status, vital signs, heart rate and rhythm, and urine output
to maintain and support vital functions.
• When patient becomes more alert after acute phase, maintain frequent vigilance and
interactions aimed at orienting, assessing, and meeting the needs of the patient.
• Try to allay confusion and agitation with calm reassurance and presence.
• Assess patient for risk for fall status.
Preventing Complications of Immobility
Interventions to improve functional recovery require active participation of the patient and
repetitive training. Functional demand and intensive training are believed to trigger CNS
reorganizationâ€”responsible for late functional recovery after stroke.
BOX 15-2 Inclusion and Exclusion Criteria for tPA Therapy
INCLUSION
• Onset of symptoms
○ Within 3 hours IV tPA
○ Within 6 hours IA tPA
• Ischemic stroke with measurable deficits using the NIH stroke scale (see Table 15-4,
page 526)
• No hemorrhage noted on CT scan of brain
• Clearly defined time of symptom onset
EXCLUSION
• Head CT demonstrates early signs of infarction or hemorrhage
• Uncontrolled hypertensive nonresponsive to I.V. or oral agent (systolic > 185 or diastolic
> 110 mm Hg)
• Glucose level > 400 mg/dL
• Coagulopathy
• Heparin within past 48 hours
○ Patient on warfarin
○ Elevated PTT or PT
○ Platelet count < 100,000
• History of previous intracranial hemorrhage, head trauma, or stroke within last 3 months
• GI or genitourinary tract hemorrhage in the past 3 weeks
• History of major surgery in the past 2 weeks
• Maintain functional position of all extremities.
○ Apply a trochanter roll from the crest of the ilium to the midthigh to prevent
external rotation of the hip.
○ Place a pillow in the axilla of the affected side when there is limited external
rotation to keep arm away from chest and prevent adduction of the affected
shoulder.
○ Place the affected upper extremity slightly flexed on pillow supports with each
joint positioned higher than the preceding one to prevent edema and resultant
fibrosis; alternate elbow extension.
○ Place the hand in slight supination with fingers slightly flexion.
○ Avoid excessive pressure on ball of foot after spasticity develops.
○ Do not allow top bedding to pull affected foot into plantar flexion; may use tennis
shoes in bed.
○ Place the patient in a prone position for 15 to 30 minutes daily, and avoid sitting
up in chair for long periods to prevent knee and hip flexion contractures.
○ Encourage neutral positioning of affected limbs to promote relaxation and to limit
abnormal increases in muscular tone to enhance functional recovery (reflex-
inhibiting positioning).
○ â€œForced useâ€ is an experimental treatment designed to overcome nonuse
of the hemiparetic upper extremity in regaining functional use of the affected arm
with selected chronic hemiparetic patients.
○ â€œConstraint-induced movement therapyâ€ restricts the contralateral upper
extremity in effort to force use of the affected arm.
• Apply splints and braces as indicated to support flaccid extremities or on spastic
extremities to decrease stretch stimulation and reduce spasticity.
○ Volar splint to support functional position of wrist
○ Sling to prevent shoulder subluxation of flaccid arm
○ High-top sneaker for ankle and foot support
• Exercise the affected extremities passively through ROM four to five times daily to
maintain joint mobility and enhance circulation; encourage active ROM exercise as able .
• Teach patient to use unaffected extremity to move affected one.
• Assist with ambulation as needed with help of physical therapy as indicated.
○ Check for orthostatic hypotension when dangling and standing.
○ Graduate the patient from a reclining position to head elevated, and dangle legs
at the bedside before transferring out of bed or ambulating; assess sitting
balance in bed.
○ Assess the patient for excessive exertion.
○ Have patient wear walking shoes or tennis shoes.
○ Assess standing balance, and have patient practice standing.
○ Help patient begin ambulating as soon as standing balance is achieved; ensure
safety with a patient waist belt.
○ Provide rest periods as patient will tire easily.
Optimizing Cognitive Abilities
• Be aware of the patient's cognitive alterations, and adjust interaction and environment
accordingly.
• Participate in cognitive retraining programâ€”reality orientation, visual imagery, cueing
proceduresâ€”as outlined by rehabilitation nurse or therapist.
• In patients with increased awareness, use pictures of family members, clock, calendar;
post schedule of daily activities where patient can see it.
• Focus on patient's strengths, and give positive feedback.
• Be aware that depression is common and therapy should include psychotherapy and
pharmacological agents.
Facilitating Communication
• Speak slowly, using visual cues and gestures; be consistent, and repeat as necessary.
• Speak directly to the patient while facing him.
• Give plenty of time for response, and reinforce attempts as well as correct responses.
• Minimize distractions.
• Use alternative methods of communication other than verbal, such as written words,
gestures, or pictures.
Fostering Independence
• Teach patient to use nonaffected side for activities of daily living (ADLs) but not to
neglect affected side.
• Adjust the environment (eg, call light, tray) to side of awareness if spatial neglect or
visual field cuts are present; approach patient from uninvolved side.
• Teach the patient to scan environment if visual deficits are present.
• Encourage family to provide clothing a size larger than patient wears, with front closures,
Velcro, and stretch fabric; teach patient to dress while sitting to maintain balance.
• Make sure personal care items, urinal, and commode are nearby and that patient
obtains assistance with transfers and other activities as needed.
• Be aware that ADLs require anticipatory (automatic coordination of multiple muscle
groups in anticipation of a specific movement) and reactive (adjustment of posture to
stimuli) postural adjustments.
• Be aware that patients usually have clear goals in relation to functional abilities, against
which all success and forward progress will be measured; help them set realistic short-
and long-term goals.
Promoting Adequate Oral Intake
• Initiate referral for a speech therapist for individuals with compromised LOC, dyspraxic
speech, or speech difficulties, to evaluate swallowing function at bedside or
radiographically to demonstrate safe and functional swallowing mechanisms before
initiation of oral diet.
• Help patient relearn swallowing sequence using compensatory techniques.
○ Place ice on tongue and encourage sucking.
○ Progress to ice pops and soft foods.
○ Make sure mechanical soft or pureed diet is provided, based on ability to chew.
• Encourage small, frequent meals, and allow plenty of time to chew and swallow. Dietary
consults can be helpful for selection of food preferences.
• Remind patient to chew on unaffected side.
• Encourage patient to drink small sips from a straw with chin tucked to the chest,
strengthening effort to swallow while chin is tucked down.
• Inspect mouth for food collection and pocketing before entry of each new bolus of food.
• Inspect oral buccosa for injury from biting tongue or cheek.
• Encourage frequent oral hygiene.
• Teach the family how to assist the patient with meals to facilitate chewing and
swallowing.
○ Reduce environmental distractions to improve patient concentration.
○ Provide oral care before eating to improve aesthetics and afterward to remove
food debris.
○ Position the patient so he is sitting with 90 degrees of flexion at the hips and 45
degrees of flexion at the neck. Use pillows to achieve correct position.
○ Maintain position for 30 to 45 minutes after meals to prevent regurgitation and
aspiration.
Attaining Bladder Control
• Insert indwelling bladder catheterization during acute stage for accurate fluid
management; remove as soon as status stabilizes.
• Establish regular voiding scheduleâ€”every 2 to 3 hours, correlated with fluid
intakeâ€”when bladder tone returns. If patient is unable to void, intermittent
catheterization can be used to empty bladder and prevent overstretching of bladder. The
bladder scan device is useful in monitoring bladder capacity and identifying individuals at
risk.
• Assist with standing or sitting to void (especially males).
Strengthening Family Coping
• Encourage the family to maintain outside interests.
• Teach stress management techniques, such as relaxation exercises, use of community
and faith-based support networks.
• Encourage participation in support group for family respite program for caregivers, or
other available resources in area.
• Involve as many family and friends in care as possible.
• Provide information about stroke and expected outcome.
• Teach family that stroke survivors do show depression in the first 3 months of recovery.
Community and Home Care Considerations
• Hemiplegic complications resulting from stroke commonly include â€œfrozenâ€
shoulder; adduction and internal rotation of arm with flexion of elbow, wrist, and fingers;
external rotation of the hip with flexion of the knee and plantar flexion of the ankle.
• Perform ROM exercises, and instruct the patient and family on these as well as proper
positioning.
• Reinforce that these muscle and ligament deformities resulting from stroke can be
prevented with daily stretching and strengthening exercises.
• Depression after stroke is a major problem because it can increase the morbidity.
Monitor for signs of depression, such as difficulty sleeping, frequent crying, anorexia,
feelings of guilt or sadness.
• Notify health care provider for possible medication therapy.
• Continue to support family who may be caring for a hemiplegic or aphasic person at
home or in long-term care for a long time. Six months after stroke, around 9% to 21% of
survivors are severely disabled, fully dependent, and live in institutions.
• Teach the patient and family to adapt home environment for safety and ease of use.
• Instruct the patient of the need for rest periods throughout day.
• Reassure the family that it is common for poststroke patients to experience emotional
lability and depression; treatment can be given.
• Encourage consistency in the environment without distraction.
• Assist family to obtain self-help aids for the patient.
• Instruct the family in management of aphasia (see Box 15 3).
• Educate those at risk for stroke about lifestyle modifications and medication therapy that
can lower risk (see page 490).
• Refer the patient/family for more information and support to such agencies as The
National Stroke Association, at http://www.stroke.org.
BOX 15-3 Aphasia
Aphasia is an acquired disorder of communication resulting from brain damage due to stroke,
head injury, brain tumors, or brain cysts. It may involve impairment of the ability to speak, to
understand speech of others, to read, write, calculate, and understand gestures. Most aphasic
individuals have difficulty with expression and comprehension to varying degrees. Fatigue has
adverse effect on speech.
To enhance your communication with the aphasic patient, keep the environment simple and
relaxed, minimize distractions, and use multiple sensory channels.
Refer the family to:
American Speech-Language-Hearing Association
10801 Rockville Pike
Rockville, MD 20852
301-897-5700
http://www.asha.org
APHASIA SYNDROMES
• Fluent aphasia: Patient retains verbal fluency but may have difficulty in understanding
speech.
• Wernicke's aphasia, receptive aphasia: Able to speak but lacks clear content,
information, and direction; difficulty with comprehension.
• Broca's aphasia, expressive aphasia: Partial or complete inability to initiate speech, form
words, and word find.
• Anomic or amnesiac aphasia: Speech is almost normal, but marred by word-finding
difficulty.
• Conduction aphasia: Comprehension of language is good but has difficulty repeating
spoken material.
• Nonfluent aphasia: Speech is sparse and produced slowly and with effort and poor
articulation; usually has a relative preservation of auditory comprehension.
• Global aphasia: severe disruption of all aspects of communication (verbal speech,
written, reading, understanding).
NURSING INTERVENTIONS
• Speak at your normal rate and volume: The patient is not hard of hearing.
• Allow plenty of time to answer.
• Do not ask questions that require complex answers.
• Rote phrases can be spontaneous.
• Provide pad and pen if the patient prefers and is able to write.
• Avoid forcing speech.
• Watch the patient for clues and gestures if his speech is jargon; make neutral
statements.
• Allow plenty of time for response.
• Ask for minimal word response.
• Encourage patient to speak slowly.
• Expect frustration and anger at inability to communicate.
• Keep environment simple.
• Use gestures as well as language.
• Allow patient to manipulate objects for additional sensory input.
• No falls, vital signs stable
• Maintains body alignment, no contractures
• Oriented to person, place, and time
• Communicates appropriately
• Brushing teeth, putting on shirt and pants independently
• Feeds self two-thirds of meal
• Voids on commode at 2-hour intervals
• Family seeks help and assistance from others
RUPTURE OF INTRACRANIAL ANEURYSM
An intracranial aneurysm is an abnormal localized dilatation of the wall of a cerebral artery due
to congenital absence of the muscle layer of the vessel. Constant blood flow against the
weakened area results in growth of the aneurysm and thinning of the vessel wall. Aneurysms
usually occur at a bifurcation of an artery or major branches of the circle of Willis. They may be
of congenital, traumatic, arteriosclerotic, or infectious origin. Most are saccular and
asymptomatic until rupture; other types are fusiform and berry (see Figure 15-4). When
aneurysms rupture, sudden bleeding occurs in the SAS between the arachnoid and the pia,
causing SAH, which produces symptoms related to meningeal irritation. Hemorrhage can
extend into the ventricular system, causing obstruction of CSF flow (hydrocephalus), or into the
brain tissue (intracerebral bleed), causing further neurologic compromise. Depending on the
extent of SAH, cerebral vasospasm (arterial vasoconstriction) can occur, producing decreased
cerebral blood flow, ischemia, and potential infarction. Vasospasm is believed to be related to
the circulating blood and/or its breakdown products in the CSF, which cause irritation to the
cerebral arteries and can cause vasoconstriction or spasm. Vasospasm commonly occurs 4 to
12 days after SAH. Studies show surgery and endovascular treatment are more effective if done
before vasospasm occurs.
FIGURE 15-4 Saccular, fusiform, and berry aneurysms. (A), saccular aneurysm; (B), berry
aneurysm; (C), fusiform aneurysm.
Grading of Aneurysms
Used to determine prognosis and timing of surgical or endovascular intervention.
Hunt-Hess Scale
0 Unruptured; asymptomatic discovery
I Asymptomatic or minimal headache with slight nuchal rigidity
II Moderate to severe headache, nuchal rigidity; no neurologic deficit other than cranial nerve
deficit
III Drowsiness, confusion, or mild focal deficit (eg, hemiparesis), or combination of these findings
IVStupor, moderate to severe deficit, possibly early decerebrate rigidity and vegetative
disturbances
V Deep coma, decerebrate rigidity, moribund appearance
• Cause unknown or related to congenital abnormality, atherosclerosis, intracranial AVM,
hypertensive vascular disease, infection, or head trauma.
• May become symptomatic due to pressure of enlarging aneurysm on nearby cranial
nerves or brain tissue.
• Rupture and hemorrhage into SAS may cause increased ICP and ischemia.
• Vasospasm may occur 4 to 12 days after rupture, causing ischemia and infarction.
• Rebleeding may occur due to lysis of clot with greatest risk for rebleeding in the first 4 to
14 days after initial bleed.
• Sudden onset of severe headache, often accompanied by nausea, vomiting, but no
neurologic deficits; leaking of aneurysm or AVM may cause a warning bleed.
• Sudden, severe headache (commonly described as the â€œworst headache of my
lifeâ€), meningeal signs (nuchal rigidity, photophobia, irritability) and neurologic
dysfunction (related to vascular territory) are commonly related to SAH secondary to
ruptured intracranial aneurysm, which can be catastrophic.
• Neurologic deficit related to vascular territory (see page 492); progressive CN III, IV, VI
deficits due to mass effect.
• History and physical examination.
• CT scanâ€”to determine presence of blood in SAS, rule out other lesions, and evaluate
mass effect.
• Lumbar puncture (if no mass effect on CT): grossly bloody CSF with more than 25,000
red blood cells (RBCs), CSF will not clear with subsequent taps as a traumatic tap
would.
• MRI and MRA or CT angiogramâ€”noninvasive evaluation of cerebral vascular
structures. Can be useful in the workup of suspected aneurysms (individuals with
persistent headaches or unexplained neurologic deficits such as cranial nerve palsies).
• Cerebral angiogramâ€”gold standard test; provides definitive evaluation of aneurysm
etiology, presence, location, and configuration. Will also reveal presence of vasospasm,
extent of vasospasm, and collateral circulation.
• TCDâ€”noninvasive method to evaluate cerebral perfusion. Useful in the bedside
evaluation and to provide a means for ongoing monitoring of cerebral blood flow to
document changes and trends.
Management
Unruptured
• Evaluation of diagnostic studies is key to determine need for intervention, scheduling of
elective surgical clipping or endovascular embolization, if indicated.
• Normalize BP if hypertensive.
• Smoking cessation.
After Rupture
• Intracranial aneurysm precautions to minimize the risk of rebleeding and control
BPâ€”bed rest with head elevated, decreased environmental stimuli, avoidance of
Valsalva maneuver and neck flexion, no caffeine, provide physical care as condition
indicates.
• Management of systemic hypertension with nitroprusside (Nipride) or alternative I.V.
antihypertensive agent, and close monitoring to prevent precipitous drop in BP,
aggravating ischemia.
• Prevention of vasospasm with calcium channel blockers such as nimodipine (Nimotop),
plasma expanders, and hypervolemia to increase cerebral perfusion.
○ Nimodipine has cerebral specificity to block the influx of calcium at the
intracellular space. It is the only drug approved by the Food and Drug
Administration (FDA) for treatment of vasospasm.
○ Nimodipine is administered at a dose of 60 mg orally q4h for SBP greater than
140 mm Hg and 30 mg orally q4h for SBP 120 to 140 mm Hg, or per physician
orders (for 21 consecutive days from the time of SAH).
○ For optimal effect, the nimodipine should be started within 96 hours of SAH.
• Triple H therapyâ€”Promotion of cerebral blood flow aimed at medically treating
vasospasm.
○ Hypertensionâ€”use of vasopressors, colloids, albumin and, possibly,
fludrocortisone (Florinef) to maintain goal SBP. Goal is based on physician
preference and clinical status of the patient; for a treated aneurysm the goal is
usually systolic 160 to 180; for untreated aneurysm the goal is 120 to 140.
○ Hypervolemiaâ€”maintain CVP greater than 8 to 12 cm H2O or pulmonary wedge
pressure 12 to 18 mm Hg through fluid/colloid boluses; closely monitor 24-hour
fluid status and replace urine output.
○ Hemodilutionâ€”decreases viscosity and increases flow velocity through I.V.
fluids; maintain hematocrit 30% to 32%.
○ Risks of Triple H therapy are pulmonary edema and dilutional hyponatremia.
• Management of acute hydrocephalus related to intraventricular hemorrhage by
placement of ventriculostomy or external ventricular drain (see Nursing Management of
the Patient Undergoing Intracranial Surgery, page 484).
○ Adjustment of drain to promote drainage of CSF.
○ Intraventricular tPA-clot lysis to promote CSF drainage. (Controversial and
presently under investigation.)
○ Surgical placement of ventricular-peritoneal (VP) shunt may be necessary.
• Prophylactic seizure management is controversial. If ordered, phenytoin (Dilantin),
fosphenytoin (Cerebyx), and phenobarbital (Luminal) are the preferred medications.
Duration of drug therapy is variable.
Surgical Intervention
• Clipping or ligation of aneurysm, evacuation of clot via craniotomy
• Strengthening the wall by wrapping if inaccessible to clipping, ligation, or coiling
• Surgical treatment of hydrocephalus with VP shunt
• Factors favoring early surgery
○ Stable medical condition
○ Hunt-Hess grade less than or equal to 3
○ Under 72 hours from initial bleed
Endovascular Intervention
• Transarterial embolization
○ Superselective angiography with placement of micro-catheter into the aneurysm
for evaluation of the aneurysm.
○ Obliteration of the aneurysm
 Guglielmi detachable coils (GDC). Coils fill the aneurysm and are
detached using electronic heating. Multiple coils are placed until the
aneurysm is obliterated.
 Balloon occlusionâ€”entrapment of aneurysm using detachable balloons
 GDC coils with micro-stentâ€”The micro-stent is used to form a bridge
across the neck of the aneurysm allowing for placement of coils
• Balloon angioplastyâ€”dilation of vessel by expansion of a transarterial balloon to treat
vasospasm
NURSING ALERT
Heparin is used intraprocedure and postprocedure, as per physician order, to minimize risk of
thromboembolic events. Risks include thromboembolic complications and rupture of aneurysm
with extension of SAH.
Complications
• Aneurysm rebleedâ€”risk is 4% on day 1, then 1.5% per day on days 2 to 13, 20% within
14 days, and 50% within 6 months; highest risk within first 6 hours.
• Hydrocephalusâ€”obstructive requiring ventriculostomy; nonobstructive long-term may
require shunt.
• Cerebral vasospasm causing arterial constriction 4 to 12 days after SAH, producing
ischemia and potential infarction.
• Seizures; permanent neurologic deficit.
• Hyponatremia or hypernatremia related to alterations in ADH secretion or imbalance in
fluid status.
• Abnormal catecholamine release.
○ Cardiovascular changes ranging from atrial fibrillation, bradycardia, and T-wave
abnormalities to ventricular dysfunction and myocardial injury in severe cases.
○ Neurogenic pulmonary edema
• Neurologic deterioration and death.
Nursing Assessment
• Perform and document neurologic assessment with vital signs and as patient condition
warrants.
• Monitor for changes in or decreasing LOC, cranial nerve dysfunction, pupillary
abnormality, and motor deficit, which signify increased ICP or expanding lesion.
• Assess for increasing headache, which could signal rebleeding.
• Monitor for focal neurologic deficits, which may indicate vasospasm.
Nursing Diagnoses
• Risk for Injury related to potential rebleeding, vasospasm, hydrocephalus, and seizures
• Ineffective Tissue Perfusion (cerebral) related to disease process and vasospasm
• Acute Pain secondary to cerebral hemorrhage, meningeal irritation, surgical procedure
• Anxiety of patient/family related to treatment, intracranial surgery or endovascular
treatment, and uncertainty of patient outcome
Modifying Activity to Prevent Complications
• Institute aneurysm/SAH precautions to reduce environmental stimuli, limit stress, and
decrease the risk of rebleed and/or increased ICP. Degree of precautions is variable
depending on the patient's clinical status and response to environmental stimuli.
○ Maintain complete bed rest with head elevated 30 degrees to reduce cerebral
edema.
○ Maintain quiet environment with low lighting, noise control, and limit activity to
prevent photophobia, agitation, and pain.
○ Restrict visitors to only immediate family or significant other who has been
counseled to ensure quiet environment.
○ Encourage the awake patient to avoid activities that increase BP or ICP:
straining, sneezing, acute flexion/rotation of the neck, cigarette smoking; assist
patient with position changes.
○ Avoid Valsalva maneuver, which may increase ICP, by administering stool
softeners to prevent straining; avoiding rectal temperatures, enemas, and
suppositories; and teaching the awake patient to exhale through mouth during
defecation.
○ Avoid caffeinated beverages and extremes of temperatures.
○ Provide physical care, such as bathing and feeding, as needed.
• Medicate patient as ordered during periods of extreme agitation.
• Institute seizure precautions by providing padded side rails, suction equipment, and oral
airway at the bedside.
warrants; to include LOC, cranial nerve function, pupillary function, and motor function.
• Assess for signs of increased ICP, including bradycardia and widening pulse pressure,
changes in respiratory pattern (Cheyne-Stokes pattern, apneustic, ataxic).
• Implement nursing interventions to minimize ICP and cerebral swelling (eg, elevate head
of bed 30 degrees, maintain proper head and neck alignment to avoid jugular vein
compression, avoid prolonged suctioning procedures, keep procedure less than 15
seconds, collaborate with physicians to use lidocaine before suctioning if intubated).
• Monitor arterial blood gas (ABG) values for hypoxia and hypercapnia, which aggravate
ICP.
• Monitor ventriculostomy, if present, for patency, amount and character of drainage, and
correct height level every 4 hours.
○ Obtain daily CSF sample for routine cultures, white blood cell (WBC) count,
chloride, and protein.
○ Monitor results and report abnormal values.
○ Administer prophylactic antibiotics as ordered.
• Recognize need for maintenance of BP parameters based on status of treated vs.
untreated aneurysm: (ie, treated: SBP 160 to180; untreated: SBP 120 to 140).
• Evaluate effectiveness of antihypertensive or vasopressor therapy.
• Perform ongoing physical assessment including respiratory, cardiac, GI, genitourinary
(GU) function to detect potential complications.
• Maintain safety factors based on neurologic deficits (eg, prevent sensory overload,
physical injury related to vision, hearing, body awareness deficits).
Maintaining Cerebral Perfusion
• Frequently monitor neurologic status based on condition, including LOC, pupillary
reaction, motor and sensory function, cranial nerve function, speech, presence of
headache.
• Administer hypervolemia/hypertensive therapy with colloid, crystalloid, and
pharmacologic agents, as ordered, to increase cerebral perfusion.
• Monitor fluid and electrolytes; monitor hematocrit and hemoglobin throughout
hydrotherapy.
• Evaluate adequacy of hypervolemic therapy regimen by assessment of BP,
hemodynamic monitoring, neurologic status, and input and output status at least every
hour, or as status indicates, while in the intensive care unit (ICU).
• Assess for subjective neurologic complaints specific to decreased perfusion (eg,
diplopia, headache, blurred vision), and recognize peak time for vasospasm occurrence
is 4 to 12 days after bleed.
• Assess for signs and symptoms of vasospasm: insidious onset of confusion,
disorientation, and decreased LOC, or focal deficit associated with vascular territory
associated with aneurysm bleed.
• Document findings and report changes; subtle change in LOC, such as drowsiness and
speech slurring, or onset of pronator drift (inability to maintain unsupported position of
outstretched pronated forearm), may be first sign of deterioration.
Reducing Pain
• Assess level of pain and pain relief; report any increase in headache.
• Administer analgesics as prescribed; if opioid is being given with sedative, monitor for
CNS depression, decreased respirations, decreased BP.
• Encourage distraction and relaxation techniques that will promote calming effect.
• Explain to patient/significant other limited use of opioids secondary to need to assess
patient's LOC at all times.
• Encourage elevated head of bed to minimize cerebral swelling.
• Provide cool compresses to head.
• Provide quiet, dark environment.
• Assess patient for experiences of unrelieved or increased pain, assess for any changes
in neurologic signs, nuchal rigidity, photophobia, and/or changes in vision, which could
signal hemorrhage, hydrocephalus, or meningeal irritation.
Reducing Anxiety
• Provide ongoing assessment of psychosocial issues (sexuality, anxiety, fear,
depression, frustration, emotional lability).
• Be attuned to verbal and nonverbal cues from the patient/family that signal problems
with coping.
• Inform the patient regarding all treatment modalities.
• Encourage discussion of risks/benefits with the surgeon/interventional neuroradiologist.
• Use reassurance and therapeutic conversation to relieve fear and anxiety.
• Provide support to the patient/family in dealing with the stress and uncertainty of
hospitalization.
• Consult Social Services for assistance with patient/family support and long-term care
decisions as needed.
• Prepare patient and family for surgery (see Nursing Management of the Patient
Undergoing Intracranial Surgery, page 484) or endovascular treatment.
• Assess level of knowledge and ability of patient/significant other to retain information.
• Assess ongoing home care needs.
• Assess need for nursing home placement or rehab center, and obtain social service
referral to help with planning.
• Provide teaching to family and caregivers, and act as liaison between health care team
and family.
• Teach patient and family how to deal with permanent neurologic deficits, and make sure
that they obtain needed supplies and services.
• Instruct patient/family on purpose and frequency of neurologic radiologic procedures.
• Explain what an aneurysm is, signs/symptoms of rupture, and possible threats of
rupture.
• Educate the patient to the risk of rebleed, which is highest within first 2 weeks of rupture,
but may remain for rest of life if not definitively treated.
• Educate the patient to activities to avoid to prevent sudden increased pressure, such as
heavy lifting and straining.
• Encourage lifelong medical follow-up and immediate attention if severe headache
develops.
• Instruct patient/family on need for and use of invasive monitoring and drainage systems.
• Reinforce the need for head of bed not to be adjusted.
• Explain aneurysm precautions and rationale.
• Provide educational material for procedures.
• Set mutual goals for discharge, and communicate discharge preparations with other
disciplines (registered nurse, physician, physical therapist, discharge coordinator).
• Explain medications to patient/significant other and potential adverse effects. Explain
importance of continued nimodipine therapy and correct usage.
• Have patient verbalize discharge instructions regarding wound care, activity restrictions,
medications, and reportable signs/symptoms.
• No signs of rebleeding, increased ICP, decreased cerebral perfusion, or seizures; quiet
environment maintained; vital signs stable; neurologic parameters stable
• SBP goals maintained
• Verbalizes decreased pain or control of pain to an intensity that is acceptable
• Patient and family able to state reason for surgery/endovascular intervention, possible
risks; openly discuss fears and uncertainties
RUPTURE OF INTRACRANIAL ARTERIOVENOUS MALFORMATION
An AVM is a system of dilated arteries and veins with dysplasic vessels. The normal capillary
beds are absent and the arterial blood flows directly into the draining veins (fistula). AVMs are
congenital lesions that can enlarge over the patient's life span; these lesions are often
asymptomatic until rupture. The lifetime risk of bleed in an unruptured AVM is 2% to 4% per
year throughout the patient's life span, depending on size and structural configuration of the
lesion.
• AVMs generally contain a nidus (central core) and â€œredâ€ engorged veins
(oxygenated veins) and have been described as a tangled mass of discolored vessels
that have the appearance of a cluster of grapes.
• The artery to venous connection, or fistula, creates increased pressure within the venous
system, resulting in vascular dilatation, congestion, and hypoperfusion.
• AVMs are generally low-pressure abnormalities at birth and can progress to a high flow,
high-pressure abnormality in adulthood.
• Parenchymal AVMs can be located in the pia matter, subcortical tissue, paraventricular
region, or a combination of these regions.
• Approximately 50% of patients with AVMs present with hemorrhage. Other signs of AVM
rupture include seizures and signs of mass effect.
• Intracerebral bleeding in a ruptured AVM tends to be superficial; cerebral vasospasm
rarely occurs.
The Spetzler-Martin grading system is used as a prognostic indicator as well as a tool to
define risks associated with treating AVMs. Grading scale of 1 to 5: 1 = lowest risk, 5 =
greatest risk for treatment. (See Table 15-3.)
TABLE 15-3 Spetzler-Martin Grading System
POINTS
Size of nidus
Small 1
Medium 2
Large 3
Eloquence of brain tissue
No 0
Yes 1
Deep vascular component
No 0
Yes 1
Grading scale of 1 to 5: 1 = lowest risk, 5 = greatest risk for
treatment.
• Sudden onset of severe headache, often accompanied by nausea and vomiting, but
without neurologic deficits, may be early signs of a ruptured AVM.
• Progressively worsening headache, as well as new onset of seizure activity due to
spontaneous superficial intracerebral hemorrhage, are commonly related to a ruptured
AVM.
• May present with loss of consciousness and severe deficits if massive bleed. Focal signs
or deficits are dependent on the location of the bleed and compression of adjacent brain
structures (visual disturbances, cranial nerve deficits, hemiparesis, and so forth).
• History and physical examination.
• CT scanâ€”to determine presence of blood, rule out other lesions; increased density if
blood present, may also show increased ICP or mass effect.
• MRI and MRA or CT angiogramâ€”Noninvasive evaluation of cerebral vascular
structures. Useful in the diagnosis of AVM, but does not define vascular changes and
flow patterns.
• Cerebral angiogramâ€”Gold standard test and the only diagnostic tool that provides
definitive evaluation of AVM presence, location, and vascular structure. Will also
evaluate flow patterns, pressure gradients, collateral circulation, identify intranidal
aneurysms, and feeding vessels.
Management
Unruptured
• Aimed at diagnostic evaluation of AVM to determine appropriate interventionâ€”surgical,
endovascular, radiosurgery, or a combination.
• Surgical resectionâ€”dependent on location, eloquence of brain tissue, and size.
• Endovascular management with N-butyl cyanoacrylate liquid polymer, polyvinyl alcohol
particles, detachable coils, balloon occlusion.
○ Staged embolization is generally performed on larger AVMs to gradually reduce
flow patterns.
○ Initial embolization is aimed at protecting area at risk for rupture, reducing the
nidus, or controlling the area at highest risk for bleeding.
○ Can be used as primary treatment modality or as an adjunct to surgical resection
and radiosurgery.
• Radiosurgery (gamma knife/linear accelerator)â€”lesions less than or equla to 2.5 to 3
cm in size. Radiation creates vessel wall injury, initiating clot formation that leads to
eventual blockage of vessel (this takes 1 to 3 years to occur). During this time, the AVM
remains at risk for rupture.
• Seizure managementâ€”defined by risk of seizure related to location or seizures as
presenting symptoms.
• Normalize BP if hypertensive.
• Smoking cessation.
After Rupture
• Maintenance and close monitoring of SBP within prescribed limits to prevent rebleed
from hypertension and ischemia from decreased cerebral perfusion.
○ Management of systemic hypertension with nitroprusside (Nipride) or alternative
I.V. antihypertensive agents.
○ Vasopressor agents to maintain SBP within prescribed range
• Antiepileptic drugs (AEDs) for seizures as presenting symptomâ€”phenytoin (Dilantin),
fosphenytoin (Cerebyx), and phenobarbital (Luminal); duration based on physician
preference, and location and extent of bleed.
• Follow up cerebral angiography confirms elimination of AVM.
Complications
• Bleed or rebleed
• Hydrocephalus; obstructive initially requiring ventriculostomy, nonobstructive long-term,
may require shunt
• Seizures
• Permanent deficit or deterioration and death
Nursing Assessment
warrants.
• Monitor for changes in or decreasing LOC, cranial nerve function, pupillary function, and
motor function, including drift (inability to maintain unsupported position).
• Assess for increasing headache or focal neurologic deficits, which could signal
rebleeding.
• Assess vital signs and pupillary changes frequently for development of increased ICP.
Nursing Diagnoses
• Risk for Injury related to potential rebleeding, hydrocephalus, and seizures
• Ineffective Tissue Perfusion (cerebral) related to disease process
• Acute Pain secondary to cerebral hemorrhage, meningeal irritation, surgical procedure
• Anxiety of patient/family related to treatment, intracranial surgery or endovascular
treatment, and uncertainty of patient outcome
Modifying Activity to Prevent Complications
• Medicate patient as ordered during periods of extreme agitation.
• Institute seizure precautions by providing padded side rails, suction equipment, and oral
airway at the bedside.
warrants; to include LOC, cranial nerve function, pupillary function, and motor function
with pronator drift.
• Assess for signs of increased ICP, including bradycardia and widening pulse pressure,
changes in respiratory pattern (Cheyne-Stokes pattern, apneustic, ataxic).
• Implement nursing interventions to minimize ICP and cerebral swelling (eg, elevate head
of bed 30 degrees, maintain proper head and neck alignment to avoid jugular vein
compression, avoid prolonged suctioning procedures, keep procedure less than 15
seconds, collaborate with physicians to use lidocaine presuctioning if intubated).
• Monitor ABG values for hypoxia and hypercapnia, which aggravate ICP.
• Monitor ventriculostomy, if present, to manage acute hydrocephalus, for patency,
amount and character of drainage, and correct height level every 4 hours.
○ Obtain daily CSF sample for routine cultures, WBC count, chloride, and protein.
○ Monitor results and report abnormal values.
○ Administer prophylactic antibiotics as ordered.
• Recognize need for maintenance of BP parameters
• Evaluate effectiveness of antihypertensive or vasopressor therapy.
• Perform ongoing physical assessment including respiratory, cardiac, GI, GU function to
detect potential complications.
• Maintain safety factors for neurologic deficits (eg, prevent sensory overload, physical
injury related to vision, hearing, body awareness deficits).
Maintaining Cerebral Perfusion
• Frequently monitor neurologic status based on condition, including LOC, pupillary
reaction, motor and sensory function, cranial nerve function, speech, presence of
headache.
• Administer vasopressive therapy, as ordered, to increase cerebral perfusion.
• Monitor fluid and electrolytes; monitor hematocrit and hemoglobin.
• Evaluate adequacy of therapy regimen by assessment of BP, hemodynamic monitoring,
neurologic status, and input and output status at least every hour, or as status indicates,
while in the ICU.
• Assess for subjective neurologic complaints specific to decreased perfusion (eg,
diplopia, headache, blurred vision).
• Assess for signs and symptoms of rebleed: insidious onset of confusion, disorientation,
and decreased LOC, or focal deficit associated with area of bleed.
• Document findings and report changes; subtle change in LOC, such as drowsiness and
speech slurring, or onset of pronator drift, may be first sign of deterioration.
Reducing Pain
• Assess level of pain and pain relief; report any increase in headache.
• Administer analgesics as prescribed; if opioid being given with sedative, monitor for CNS
depression, decreased respirations, decreased BP.
• Encourage distraction and relaxation techniques that will promote calming effect.
• Explain to patient/significant other limited use of opioids secondary to need to assess
patient's LOC at all times.
• Encourage elevated head of bed to minimize cerebral swelling.
• Provide cool compresses to head.
• Assess patient for experiences of unrelieved or increased pain; assess for any changes
in neurologic signs which could signal hemorrhage, hydrocephalus, or meningeal
irritation.
Reducing Anxiety
• Provide ongoing assessment of psychosocial issues (sexuality, anxiety, fear,
depression, frustration, emotional lability).
• Be attuned to verbal and nonverbal cues from the patient/family that signal problems
with coping.
• Inform the patient regarding all treatment modalities.
• Encourage discussion of risks/benefits with the surgeon/interventional neuroradiologist.
• Use reassurance and therapeutic conversation to relieve fear and anxiety.
• Provide support to the patient/family in dealing with the stress and uncertainty of
hospitalization.
• Consult Social Services for assistance with patient/family support and long-term care
decisions as needed.
• Prepare patient and family for surgery (see Nursing Management of the Patient
Undergoing Intracranial Surgery, page 484) or endovascular treatment.
• Assess level of knowledge and ability of patient/significant other to retain information.
• Assess ongoing home care needs.
• Assess need for nursing home placement or rehabilitation center, and obtain social
service referral to help with planning.
• Provide teaching to family and caregivers, and act as liaison between health care team
and family.
• Teach patient and family how to deal with permanent neurologic deficits, and make sure
that they obtain needed supplies and services.
• Instruct patient/family on purpose and frequency of neurologic radiologic procedures.
• Explain what an AVM is, signs/symptoms of rupture, and possible threats of rupture.
• Educate the patient to the risk of rebleed, which is 50% within 6 months if untreated, and
remains for rest of life if not definitively treated.
• Encourage lifelong medical follow-up and immediate attention if severe headache
develops.
• Explain the need for follow up angiograms to verify complete eradication of AVM or to
define extent of eradication to facilitate treatment planning.
• Provide educational material for procedures.
• Set mutual goals for discharge, and communicate discharge preparations with other
disciplines (registered nurse, physician, physical therapist, discharge coordinator).
• Explain medications to patient/significant other and potential adverse effects.
• Have patient verbalize discharge instructions regarding wound care, activity restrictions,
medications, and reportable signs/symptoms.
• No signs of rebleeding, IICP, decreased cerebral perfusion, or seizures; vital signs
stable; neurologic parameters stable
• Verbalizes decreased pain or control of pain to an intensity that is acceptable
• Patient and family able to state reason for surgery/endovascular intervention, possible
risks
• Decrease in anxiety sufficient to allow the completion of necessary procedures and to
promote recovery
INFECTIOUS DISORDERS
MENINGITIS
Meningitis is an inflammation of the pia mater and arachnoid membranes that surround the
brain and the spinal cord. The SAS between these two meninges contains CSF that may reflect
the signs and symptoms of meningitis.
• In the United States, the incidence of acute, bacterial meningitis is approximately 3
cases per 100,000 per year. The organisms causing these infections seem to vary
depending on the age and immune status of the patient. The mortality is 5% for children,
but children who recover may have long-term neurologic problems (eg, hearing deficit).
These organisms may have epidemic potential.
• Viral meningitis is the most common form and is usually self-limiting; management is
supportive. It is usually caused by a nonpolio enterovirus (90%). It targets children and
the elderly. This organism is spread by the fecal-oral route and through sewage.
• Bacterial meningitis may cause damage to the CNS from the inflammatory process
rather than the pathogen. Bacterial meningitis is usually more serious than viral
meningitis. It is typically caused by Streptococcus pneumoniae (pneumococcal
meningitis), a gram-positive diplococci, and Neisseria meningitidis (meningococcal
meningitis), a gram-negative diplococci.
○ With a mortality of 30%, S. pneumonia is the leading cause of bacterial
meningitis in children younger than age 5; it is spread by droplet.
○ Most bacteria that cause meningitis begin by colonizing the nasopharynx, then
invade the circulation and CSF, causing an inflammatory response mediated by
cytokines.
○ Bacterial meningitis can result in brain damage due to chemicals released by
bacteria that kill or damage neurons, purulent exudates that may result in
vasculitis and vasospasm, and increased ICP that causes cerebral edema.
• Fungal meningitis, particularly Cryptococcus neoformans, affects immunosuppressed
patients (eg, human immunodeficiency virus [HIV]â€“positive) through soil contaminated
with excrement from pigeons and chickens. Cryptococcal antigen, or culture, is found in
the CSF, but meningeal signs may be minimal. In HIV-positive patients, tuberculous
meningitis, tuberculomas, and atypical mycobacterial infections of the brain may be
noted.
• Parasitic meningitis is usually cause by flukes, worms, or amoeba.
• Hospital-acquired postcraniotomy meningitis, caused predominantly by gram-negative
bacilli, can result in mortalities of 30%; multiple craniotomy operations place the patient
at even higher risk. It develops approximately 7 to 8 days postoperatively.
• Neoplastic meningitis affects approximately 3% to 8% of patients who have systemic
cancers. The mean survival time is approximately 5 to 8 months. In neoplastic
meningitis, malignant cells infiltrate the leptomeninges as a complication of breast
cancer, lung cancer, malignant melanoma, non-Hodgkin's lymphoma, and acute
leukemia.
• Meningitis is the primary intracranial complication of acute and chronic sinusitis
(sphenoid sinusitis most common). S. pneumonia and Staphylococcus aureus are the
most common organisms.
• Listeria monocytogenes, a gram-positive bacilli, may cause meningitis through
contaminated hot dogs, cold meats, and unpasteurized dairy products.
• The incidence of Haemophilus influenzae meningitis has decreased due to the
haemophilus b conjugate vaccine.
• Classic symptoms are fever, headache, and nuchal rigidity.
• Altered mental status; confusion in older patients.
• Petechial (appears like â€œrugâ€ burn) or purpuric rash from coagulopathy, especially
with N. meningitidis.
• Photophobia.
• Nuchal rigidity, neck tenderness, or a bulging the anterior fontanelle in infants.
• Children may exhibit behavioral changes, arching of the back and neck, a blank stare,
refusal to feed, and seizures. Viral meningitis can cause a red, maculopapular rash in
children.
• Positive Brudzinski's and Kernig's signs (see Figure 15-5).
FIGURE 15-5 Signs of meningeal irritation include nuchal rigidity and positive
Brudzinski's and Kernig's signs. (A) To elicit Brudzinski's sign, place the patient supine
and flex the head upward. Resulting flexion of both hips, knees, and ankles with neck
flexion indicates meningeal irritation. (B) To test for Kernig's sign, once again place the
patient supine. Keeping the bottom leg straight, flex the other hip and knee to form a 90-
degree angle. Slowly extend the upper leg. This places a stretch on the meninges,
resulting in pain and spasm of the hamstring muscle. Resistance to further extension
can be felt.
• Neonates may exhibit poor feeding, altered breathing patterns, or listlessness.
• Onset may be over several hours or several days depending on the infectious agent, the
patient's age, immune status, comorbidities, and other variables.
• Complete blood count (CBC) with differential is indicated to detect an elevated leukocyte
count in bacterial and viral meningitis, with a greater percentage of polymorphonuclear
leukocytes (90%) in bacterial and (less than 50%) in viral meningitis (normal 0% to
15%).
• Blood cultures are obtained to indicate the organism.
• CSF evaluation for pressure, leukocytes, protein, glucoseâ€”CSF normally has five or
fewer lymphocytes or mononuclear cells/mm3.
○ In acute bacterial meningitis, the CSF may indicate elevated pressure, elevated
leukocytes (several thousand), elevated protein, elevated glucose. A culture and
smear will identify the organism. WBC differential should be done by a stained
smear of sediment.
○ In viral encephalitis, the CSF may indicate normal/moderately elevated pressure,
few/elevated leukocytes (fewer than 1,000), normal or slightly elevated protein,
normal glucose.
• MRI/CT scan with and without contrast rules out other disorders. A CT scan with
contrast must be done to detect abscesses.
• Low CD4+ counts indicate immunosuppression in HIV-positive patients and other
patients with immunosuppressive disorders.
• Latex agglutination may be positive for antigens in meningitis.
• In patients with acquired immunodeficiency syndrome (AIDS), MRI is used to detect
meningeal irritation, evidence of a sinus infection, or brain abscess.
Management
• The assessment and management of meningitis should be approached through a team
effort with nursing, infectious diseases specialists, neurology, internal medicine, and
otolaryngology specialists, and laboratory and diagnostic staff.
• Most patients are given I.V. antibiotics until the laboratory findings determine the type of
meningitis (eg, viral, bacterial). However, cultures should be taken before initiating
antibiotics.
• To manage inflammation, dexamethasone (Decadron) or another corticosteroid is given
I.V.
○ This may result in GI bleeding and mask clinical responses to treatments (eg,
resolved fever).
○ This steroid should be used before or with the first dose of antibiotics (I.V. 0.6
mg/kg/day in four divided doses for the first 4 days of antibiotics), and should be
confined to patients older than age 6 weeks.
○ Plasmapheresis may be used experimentally to remove cytokines in some cases.
• Temozolomide (Temodar), a second-generation alkylating agent, is effective against
many cancers that result in neoplastic meningitis. External beam radiation may be used
in conjunction with chemotherapy (eg, intrathecal thiotepa or methotrexate).
• Cochlear implantation rehabilitation due to deafness caused by meningitis should be
considered. Realistic goals must be set, as the patient may develop only environmental
sound awareness and still have to deal with learning disabilities.
• If meningitis is suspected after neurosurgical procedures, potential I.V. line bacteremia,
CSF leak, or immunosuppression, therapy is also indicated for S. aureus and gram-
negative bacilli.
• Antifungal agents, such as amphotericin B (Fungizone) and the triazoles, fluconazole
(Diflucan) and itraconazole (Sporanox), are indicated for cryptococcal meningitis.
Relapse is common if the patient does not have chronic suppressive therapy with
fluconazole or another antifungal agent.
• Empiric antituberculosis drugs must be initiated if infection by Mycobacterium
tuberculosis is suspected.
NURSING ALERT
Be aware that bacterial resistance to antibiotics has been increasing, making meningitis very
difficult to treat in some instances.
Complications
• Bacterial meningitis, particularly in children, may result in deafness, learning difficulties,
spasticity, paresis, or cranial nerve disorders.
• Increased ICP in AIDS patients with cryptococcal meningitis has resulted in severe
visual losses.
• Seizures occur in 20% to 30% of patients.
• Increased ICP may result in cerebral edema, decreased perfusion, and tissue damage.
• Severe brain edema may result in herniation or compression of the brain stem.
• Purpura may be associated with disseminated intravascular coagulation.
Nursing Assessment
• Obtain a history of recent infections such as upper respiratory infection, and exposure to
causative agents.
• Assess neurologic status and vital signs.
• Evaluate for signs of meningeal irritation.
• Assess sensorineural hearing loss (vision and hearing), cranial nerve damage (eg, facial
nerve palsy), and diminished cognitive function.
Nursing Diagnoses
• Hyperthermia related to the infectious process and cerebral edema
• Risk for Imbalanced Fluid Volume related to fever and decreased intake
• Ineffective Tissue Perfusion (cerebral) related to infectious process and cerebral edema
• Acute Pain related to meningeal irritation
• Impaired Physical Mobility related to prolonged bed rest
Reducing Fever
• Administer antimicrobial agents on time to maintain optimal blood levels.
• Monitor temperature frequently or continuously, and administer antipyretics as ordered.
• Institute other cooling measures, such as a hypothermia blanket, as indicated.
Maintaining Fluid Balance
• Prevent I.V. fluid overload, which may worsen cerebral edema.
• Monitor intake and output closely.
• Monitor CVP frequently.
Enhancing Cerebral Perfusion
• Assess LOC, vital signs, and neurologic parameters frequently. Observe for signs and
symptoms of ICP (eg, decreased LOC, dilated pupils, widening pulse pressure).
• Maintain a quiet, calm environment to prevent agitation, which may cause an increased
ICP.
• Prepare patient for a lumbar puncture for CSF evaluation, and repeat spinal tap, if
indicated. Lumbar puncture typically precedes neuroimaging (see page 471).
• Notify the health care provider of signs of deterioration: increasing temperature,
decreasing LOC, seizure activity, or altered respirations.
Reducing Pain
• Administer analgesics as ordered; monitor for response and adverse reactions. Avoid
opioids, which may mask a decreasing LOC.
• Darken the room if photophobia is present.
• Assist with position of comfort for neck stiffness, and turn patient slowly and carefully
with head and neck in alignment.
• Elevate the head of the bed to decrease ICP and reduce pain.
Promoting Return to Optimal Level of Functioning
• Implement rehabilitation interventions after admission (eg, turning, positioning).
• Progress from passive to active exercises based on the patient's neurologic status.
DRUG ALERT
Note and report any missed doses of antibiotics, osmotic diuretics, and steroids; administer as-
necessary doses as soon as possible to avert deleterious consequences due to missed doses.
• Prevent bacterial meningitis by eliminating colonization and infection with the offending
organism.
○ Administer vaccines against H. influenzae type B for children; N. meningitidis
serogroups A, C, Y, and W135 for patients at high risk (especially college
students, those without spleens, immunodeficient); and S. pneumoniae for
patients with chronic illnesses and the elderly.
○ Administer vaccines for travelers to countries with a high incidence of
meningococcal disease and household contacts of someone who has had
meningitis.
○ Chemoprophylaxis for meningococcal disease, most commonly with rifampin,
may be necessary for health care workers, household contacts in the community,
day care centers, and other highly susceptible populations.
• If maintenance antifungal prophylaxis is initiated for patients with low CD4+ counts, as
seen in some patients with AIDS, the patient must understand the importance of long-
term pharmacologic therapy.
• Advise close contacts of the patient with meningitis that prophylactic treatment may be
indicated; they should check with their health care providers or the local public health
department.
• Encourage the patient to follow medication regimen as directed to fully eradicate the
infectious agent.
• Encourage follow-up and prompt attention to infections in future.
• Afebrile
• Adequate urine output; CVP in normal range
• Alert LOC; normal vital signs
• Pain controlled
• Optimal level of functioning after resolution
ENCEPHALITIS
Encephalitis is an inflammation of cerebral tissue, typically accompanied by meningeal
inflammation. Meningoencephalitis is most commonly caused by a viral infection. Like
meningitis, encephalitis can be infectious or noninfectious and acute, subacute, or chronic.
• In primary encephalitis, the brain or spinal cord is the predominate foci of the toxin or
pathogen. Secondary encephalitis is a less serious form of encephalitis; it is caused by
an infection that is spread from another part of the body.
• Acute viral encephalitis, accounting for the vast majority of cases, is caused by a direct
infection of the gray matter containing neural cells. It results in perivascular inflammation
and neuronal destruction. It is more common in children, and is most commonly caused
by the herpes simplex virus and, to a lesser degree, by the arboviruses.
• Brainstem encephalitis targets the basal ganglia or cranial nerves.
• Postischemic inflammatory encephalitis occurs due to brain inflammation following a
CVA. In patients with cerebral ischemia, inflammation can result in secondary brain
injury, and microvascular occlusion can be caused by activated leukocytes or a
microvascular thrombus. This edema can result in increased ICP and compromised
cerebral perfusion.
• West Nile Virus (WNV) is an arthropod virus (arbovirus). The mosquito is the primary
vector and birds are the primary hosts. Mortality can be as high as 30%.
• Herpes simplex encephalitis may result from reactivation of the virus that has been
dormant in the cranial and other ganglia, or to reinfection. Direct spread to the brain by
the olfactory or trigeminal nerve is suspected with herpes simplex virus type 1, which is
responsible for almost all cases of herpes simplex encephalitis in children and adults.
Mortality is as high as 75%. Herpes simplex type 2 is more common in neonates who
are born to mothers with this infection during pregnancy.
• Postinfectious encephalomyelitis follows a viral or bacterial infectious process, but
organisms do not directly affect the neural tissue in the white matter; however,
perivascular inflammation and demyelination do occur in the cerebral tissue.
○ The incidence of postinfectious encephalomyelitis has decreased considerably
with immunization against measles, mumps, and rubella and the infrequent
administration of vaccines due to the eradication of smallpox. It is rare in infancy.
○ The most common cause is respiratory or GI infection 1 to 3 weeks before the
acute onset of encephalomyelitis symptoms.
○ May be caused by specific species of mosquitoes and ticks (arthropods), which
may be seasonal and geographic hosts (eg, California encephalitis, St. Louis
equine encephalitis).
• Cytomegalovirus encephalitis should be considered in patients who have advanced HIV
infection, have evidence of the cytomegalovirus in other sites, and have progressive
neurologic deterioration.
• Toxoplasma encephalitis is also common in patients with AIDS.
• Signs and symptoms may develop hours or weeks after exposure.
• Classic symptoms include fever, headache, and brain aberration (eg, disorientation,
neurologic deficits, seizures).
• Increased ICP may result in alteration in consciousness, nausea, and vomiting.
• Motor weakness, such as hemiparesis, may be detected.
• Increased deep tendon reflexes and extensor plantar response are noted.
• Bizarre behavior and personality changes may present at onset.
• Hypothalamic-pituitary involvement may result in hypothermia, diabetes insipidus,
SIADH (see page 480).
• Neurologic symptoms may include superior quadrant visual field defects, aphasia,
dysphagia, ataxia, and paresthesias.
• The patient with brainstem encephalitis may present with nystagmus, decreased
extraocular movements, hearing loss, dysphagia, dysarthria, respiratory abnormalities,
and motor involvement.
• Limbic encephalitis may cause mood and personality changes that progress to severe
memory loss and delirium.
• In WNV, about two-thirds of symptomatic patients have encephalitis with signs and
symptoms of fever, vomiting, headache, nuchal rigidity, decreased LOC, cranial nerve
dysfunction, and an erythematous rash. Seizures are uncommon.
• Lumbar puncture, with evaluation of CSF, is performed to detect leukocytosis, increased
mononuclear cell pleocytosis, increased proteins, and normal or slightly lowered
glucose.
• Polymerase chain reaction analysis of the virus' deoxyribonucleic acid (DNA), and the
detection of intrathecally produced viral antibodies, are essential in diagnosing the
specific virus (eg, herpes simplex virus, cytomegalovirus). Arbovirus-specific
immunoglobulin (IgM) in CSF and a fourfold change in specific IgG antibody are
diagnostic for arboviral encephalitis.
• EEG may demonstrate slow brain wave complexes in encephalitis.
• Gadolinium-enhanced MRI differentiates postinfectious encephalomyelitis from acute
viral encephalitis.
○ Enhanced multifocal white matter lesions are seen in encephalomyelitis, which
may remain for months after clinical recovery.
○ Herpes simplex virus encephalitis typically causes medial-temporal and orbital-
frontal lobe inflammation and necrosis; low-density abnormalities may be present
in the temporal lobes. An MRI is preferred compared to a CT scan.
○ Cytomegalovirus, seen in patients who have advanced HIV disease, may have
enhanced periventricular areas.
• Brain tissue biopsy indicates presence of infectious organisms.
• WNV can have pleocytosis, and may be seen on an MRI with enhancement of the
meninges and periventricular areas. The assay, WNV ELISA, can be done from blood or
CSF; a cell culture can also be diagnostic.
Management
• Differentiate acute viral encephalitis from noninfectious diseases such as sarcoidosis,
vasculitis, systemic lupus erythematosus, and others.
• In patients who are immunosuppressed, such as HIV-positive patients, differentiate
acute viral encephalitis from cytomegalovirus encephalitis, toxoplasmic encephalitis, and
fungal infections.
○ Patients with cytomegalovirus may be treated with ganciclovir (Cytovene) and
foscarnet (Foscavir), commonly used to treat cytomegalovirus retinitis in HIV-
positive patients.
○ Pyrimethamine (Daraprim) and sulfadoxine (Fansidar) are commonly used to
treat Toxoplasma encephalitis.
○ When encephalomyelitis develops, supportive care is indicated because there is
no known treatment; corticosteroids may be used.
• I.V. acyclovir over 10 to 21 days is indicated for herpes simplex virus. Mothers who have
genital herpes simplex may be treated with acyclovir during the third trimester to avoid
shedding the virus to their babies.
• Anticonvulsants manage seizures.
DRUG ALERT
Acyclovir, indicated for acute viral encephalitis caused by herpes simplex type 1, inhibits
replication of the virus DNA. Acyclovir should be infused over 1 hour because crystalluria and
renal failure may result if administration is too rapid.
Complications
• Sequelae of the herpes simplex virus may cause temporal lobe swelling, which can
result in compression of the brain stem. This virus may also cause aphasia, major motor
and sensory deficits, and Korsakoff's psychosis (amnestic syndrome).
• Relapse of encephalitis may be seen after initial improvement and completion of antiviral
therapy.
• Mortality and morbidity depend on the infectious agent, host status, and other
considerations.
Nursing Assessment
• Obtain patient history of recent infection, animal exposure, tick or mosquito bite, recent
travel, exposure to ill contacts.
• Before delivery, women should be questioned regarding a history of congenital herpes
simplex virus and examined for evidence of this virus; a cesarean delivery should be
explored with the physician.
• Strict standard precautions should be adhered to in order to contain drainage from
herpetic lesions.
• Vesicular lesions or rashes on neonates should be reported immediately because these
could indicate active herpes simplex infection.
• Perform a complete clinical assessment.
Nursing Diagnoses
• Risk for Injury related to seizures and cerebral edema
• Ineffective Tissue Perfusion (cerebral) related to disease process
• Hyperthermia related to infectious process
• Disturbed Thought Processes due to personality changes
• Risk of Infection related to transmittal
Preventi ng Injury
• Maintain quiet environment and provide care gently, avoiding overactivity and agitation,
which may cause increased ICP.
• Maintain seizure precautions with side rails padded, airway, and suction equipment at
bedside.
• Administer medications as ordered; monitor response and adverse reactions.
Promoting Cerebral Perfusion
• Monitor neurologic status closely. Observe for subtle changes, such as behavior or
personality changes, weakness, or cranial nerve involvement. Notify health care
provider.
• In arbovirus encephalitis, restrict fluids to passively dehydrate the brain.
• Reorient patient frequently.
• Provide supportive care if coma develops; may last several weeks.
• Encourage significant others to interact with patient, and participate in the patient's
rehabilitation, even while the patient is in a coma.
Relieving Fever
• Monitor temperature and vital signs frequently.
• Administer antipyretics and other cooling measures as indicated.
• Monitor fluid intake and output, and provide fluid replacement through I.V. lines as
needed. Be alert to signs of other coexisting infections, such as UTI or pneumonia, and
notify health care provider so cultures can be obtained and treatment started.
Managing Aberrations in Thought Processes

• Orient to person, place, time.
• Maintain memory book, and provide cues to perform required activities.
Avoiding Infectious Disease Transmission
• Maintain strict standard precautions.
• Initiate and maintain isolation per your facility's policy.
• Promote vaccination of patient, family, and significant others for measles, mumps, and
rubella.
• Pregnant women who have a history of genital herpes simplex, or their partners, should
inform their physician of this history.
• Contacts of rabies-infected patients should be offered rabies prophylaxis.

• Explain the effects of the disease process and the rationale for care.
• Reassure significant others based on patient's prognosis.
• Encourage follow-up for evaluation of deficits and rehabilitation progress.
• Educate others about the signs and symptoms of encephalitis if epidemic is suspected.
• To prevent WNV, advise the use of repellants when outdoors and removal of standing
water that acts as a breeding ground for mosquitoes.
• No seizures or signs of increased ICP
• Alert with no neurologic deficits
• Afebrile
• Oriented, memory intact
• No transmission of infection
BRAIN AND SPINAL ABSCESSES
A brain abscess is a free or encapsulated collection of infectious material of brain parenchyma,
between the dura and the arachnoid linings (subdural abscess) or between the dura and the
skull (epidural abscess). Spinal abscesses typically occur in the epidural region.
• Intracranial subdural abscesses, usually due to a streptococcus organism, are caused
by purulent drainage between the dura and arachnoid. It can result from pus from the
meninges, middle ear or mastoid, sinuses, septicemia, or skull fracture. It occurs most
frequently in children and young adults.
• Intracranial epidural abscesses, typically involving an infection of the cranium, commonly
occur due to chronic mastoiditis or sinusitis, head trauma, or craniotomy. Abscesses
may be related to a subdural empyema (collection of purulent drainage originating from
nasal sinuses, meninges, middle ear, or skull osteomyelitis), meningitis, or
intraparenchymal abscess.
• Spinal epidural abscesses occur in the spinal canal external to the dura. Epidural
penetration may seed through the blood and occur from infected adjacent tissue (eg,
infected pressure ulcer), from another infected site (eg, skin), or contamination from
spinal surgery or spinal instrumentation (eg, lumbar puncture). S. aureus is a frequent
causative agent and the midthoracic vertebrae are most commonly affected.
• Intermedullary abscesses are more common in the pediatric population, and are
associated with lumbosacral dermal sinuses. Approximately 20% to 30% are
â€œcrypticâ€ abscesses with no apparent source of infectious seeding.
• In the initial inoculation period, organisms invade the brain parenchyma resulting in local
inflammation and edema. The resulting cerebritis develops into a necrotic lesion and
then becomes encapsulated.
• Fungal brain abscesses are commonly seen in HIV-positive patients and other
populations that are immunosuppressed. Diffuse microabscesses may occur with
infections caused by Candida species.
• M. tuberculosis may cause abscesses of pus containing acid-fast bacilli (AFB)
surrounded by a dense capsule. These abscesses are also found in patients who are
HIV-positive or have other immunosuppressive diseases.
• Headache is poorly localized with a dull ache.
• Increased ICP may result in nausea, vomiting, decreased LOC.
• Fever is found in less than 50% of cases.
• Neurologic findings such as hemisensory and paresis deficits, aphasia, ataxia may be
present.
• Seizures are frequently present.
• Dental abscess, sinusitis, and otitis media may be present.
• Signs and symptoms of a cerebral subdural empyema include severe headache, fever,
nuchal rigidity, and Kernig's sign (see page 503).
• Patients with intracranial epidural abscess commonly present with fever, lethargy, and
severe headache.
• Spinal epidural abscesses may be evidenced by severe back pain, fever, headache,
lower extremity weakness or paralysis, nuchal rigidity, Kernig's sign, and local
tenderness.
• CT scan, MRI with contrast locate the sites of abscess, and follow evolution and
resolution of the suppurative process.
○ In the inflammatory stage of cerebritis, imaging reveals a high signal intensity
centrally (inflammation) and peripherally (edema). When an abscess develops,
the capsule becomes isointense.
○ There may be decreased ring enhancement with patients who are
immunosuppressed, which may be due to a lack of inflammatory response.
○ Microabscesses may not be detected by the CT scan or MRI.
○ MRI with gadolinium enhancement should be considered to detect spinal epidural
abscesses.
• Blood cultures are obtained to identify the organism, positive Gram's stain, leukocytosis,
and elevated erythrocyte sedimentation rate (ESR).
• Cultures are obtained from the suspected source of infection, using stereotaxic needle
aspiration or brain surgery, to identify the organism and sensitivity to antimicrobials.
• A metastatic brain abscess may be differentiated from a metastatic tumor by CT scan or
MRI. Abscesses have hypodense centers with a smooth surrounding capsule, whereas
tumors may have irregular borders and diffuse enhancement.
• EEG detects seizure disorders.
• Findings in cerebral subdural empyema include increased WBC and increased pressure
of the CSF.
• In intracranial epidural abscesses, CT or MRI scans are useful; MRIs are usually more
sensitive. Findings from the CSF may not be definitive. To avoid transtentorial
herniation, lumbar puncture is not indicated until large cranial masses are ruled out.
• Diagnostic findings in spinal epidural abscesses may include increased WBC and ESR.
The CSF may be cloudy. Myelography is typically abnormal.
Management
• With cerebral subdural empyema or intracranial epidural abscesses, management
consists of trephining (drilling through skull to evacuate purulent material), systemic
antibiotics, and treatment of cerebral edema.
• Spinal epidural abscesses may be managed with a laminectomy and surgical drainage,
with antibiotics before and after the procedure. The abscess site is thoroughly irrigated
with antibiotic solution and aerobic and anaerobic cultures are taken.
• Closed stereotaxic needle biopsy, under CT guidance, may be used for drainage
evacuation instead of craniotomy.
• Radical surgical dÃ©bridement, especially with fungal infections, may be indicated with
antimicrobial therapy.
• Initiation of empiric antimicrobial therapy is based on Gram's stain and the suspected
site of origin.Because brain abscesses are frequently caused by multiple organisms,
antimicrobial therapy is directed toward the most common etiologic agents: streptococci,
anaerobic bacteria (eg, Bacteroides species).
○ S. aureus may be suspected if surgical procedures have been performed.
○ Gram-negative bacteria (eg, Clostridium species) should be suspected if a
cranial wound has been contaminated with soil.
○ A 6- to 8-week course of parenteral antibiotics is typical, followed by a 2- to 3-
month course of oral antimicrobial therapy.
○ Penicillin G, metronidazole, and third-generation cephalosporins are common
therapeutic agents.
• Antifungal therapy, such as amphotericin B, is initiated for candidiasis and other fungal
infections.
• Antituberculosis pharmacotherapy, such as rifampin, isoniazid, and pyrazinamide,
should be used to treat abscesses containing AFB.
• Adjunctive therapy includes corticosteroids and osmotic diuretics to reduce cerebral
edema, and anticonvulsants to manage seizures.
Complications
• The brain abscess can rupture into the ventricular space, causing a sudden increase in
the severity of the patient's headache. This complication is often fatal.
• Papilledema may occur in less than 25% of cases, indicating intracranial hypertension.
• Lumbar puncture may be dangerous due to the possibility of brain stem herniation.
Lumbar puncture is also contraindicated if there is a spinal epidural abscess because
pus may be transferred into the subarachnoid space. Cervical puncture should be
considered in such patients.
• Permanent neurologic deficits, such as seizure disorders, visual defects, hemiparesis,
and cranial nerve palsies, may be present.
• There is greater mortality if the patient has symptoms of short duration, has severe
mental status changes, and has rapid progression of neurologic impairment.
• Delayed treatment of a spinal epidural abscess may result in transaction syndrome, in
which flaccid paraplegia with sensory loss occurs at the level of the abscess.
• In chronic otitis media, intracranial and intratemporal complications frequently result from
progressive bony erosion, which may expose the dura, labyrinth, and facial nerves.
Nursing Assessment
• Obtain history of previous infection, immunosuppression, headache, and related
symptoms.
• Perform neurologic assessment, including cranial nerve evaluation, motor, and cognitive
status.
Nursing Diagnoses
• Acute Pain related to cerebral mass
• Disturbed Thought Processes related to disease process
• Risk for Injury related to neurologic deficits
• Anxiety related to surgery, prognosis, and relapse
Relieving Pain
• Administer pain medications as ordered.
• Provide comfort measures, such as quiet environment, positioning with head slightly
elevated, and assistance with hygiene needs.
• Provide passive relaxation techniques, such as soft music and backrubs.
Promoting Thought Processes
• Frequently monitor vital signs, LOC, orientation, and seizure activity.
• Report changes, which can signal increased ICP, to health care provider.
• Administer medications as ordered, noting response and adverse reactions.
• Prepare patient for repeated diagnostic tests to evaluate response to therapy and
surgery.
Minimizing Neurologic Deficits
• Maintain a safe environment with side rails up, call light within reach, and frequent
observation.
• Evaluate other cranial nerve function, and report changes.
• Refer to occupational therapy, speech therapist, or other rehabilitation specialist to
provide adjunct to nursing rehabilitation.
Reducing Anxiety
• Prepare patient and family for surgery when indicated. Encourage discussion with
surgeon to understand risks, benefits of the procedure.
• Explain postoperative progression and nursing care (see page 484).
• Patient follow-up is essential for sinusitis, otitis media, respiratory infections, and other
infectious processes that may result in a brain abscess.
• Continue with rehabilitation to regain or compensate for neurologic deficits.
• Continue with pharmacologic regimen in community setting.
• Observe for recurrence of brain and spinal abscesses.
• Maintain wellness with vaccinations, immunizations, and overall health.
• Reinforce need for dental procedure prophylaxis to avoid dental abscesses.
• Instruct in need for immediate assessment of head wounds.
• Oriented to person, place, and time; follows simple commands
• No injury related to neurologic deficits
• Reduced anxiety regarding disease process and procedures
DEGENERATIVE DISORDERS
PARKINSON'S DISEASE
Parkinson's disease is a chronic, progressive neurologic disease affecting the brain centers
responsible for control and regulation of movement. It is characterized by tremor, bradykinesia,
rigidity, and postural abnormalities. Parkinson's can complicate the diagnosis, clinical course,
and recovery from other illness. Approximately 1% of the total U.S. population older than age 60
is affected by idiopathic Parkinson's disease, and it less commonly affects people of younger
ages. It is the second most common neurodegenerative disease.
• A deficiency of dopamine, due to degenerative changes in the substantia nigra of the
brain, is thought to be responsible for the symptoms of Parkinson's disease.
• Underlying etiology may be related to a virus; genetic susceptibility; toxicity from
pesticides, herbicides, methyl-phenyl-tetrahydropyridine, or welding fumes; repeated
head injuries, or other unknown cause.
• The clinical diagnosis of Parkinson's disease may be difficult because elderly patients
may have other causes of rigidity, bradykinesia, and tremor.
• Bradykinesia (slowness of movement), loss of spontaneous movement and delay in
initiating movements
• Resting (â€œpill-rollingâ€) tremor of 4 to 5 Hz. The tremor may be worse on one side
of the body affecting the limbs and sometimes involves the head, neck, face, and jaw.
• Rigidity in performance of all movements. Rigidity is always present but increases during
movement. May lead to sensations of pain, especially in the arms and shoulders.
• Poor balance when moving abruptly or suddenly changing body position. May lead to
falls.
• Autonomic disordersâ€”sleeplessness, salivation, sweating, orthostatic hypotension,
dizziness.
• Depression, dementia.
• Masklike facies secondary to rigidity.
• Gait difficulties characterized by a decreased or nonexistent arm swing; short, shuffling
steps (festination); difficulty in negotiating turns; and sudden freezing spells (inability to
take the next step).
• Verbal fluency may be impaired.
• Finger tapping responses are slowed.
• Micrographia (change in handwriting, with the script becoming smaller)
• Problems with speech, breathing, swallowing, and sexual function.
• Observation of clinical symptoms; may do imaging studies to rule out other disorders.
• Physical examination of upper extremity elbow flexion/extension reveals rigidity on
extension.
• Sensorimotor assessment of grip reveals abnormally high grip forces and longer than
normal to complete object lift, particularly with lighter loads.
• Favorable response to a single dose of levodopa helps confirm the diagnosis.
Management
Pharmacologic
• Anticholinergics, including trihexyphenidyl (Artane), benztropine (Cogentin), NS
procyclidine (Kemadrin) to reduce transmission of cholinergic pathways, which are
thought to be overactive when dopamine is deficient. These medications are most
effective in controlling tremor, but are known to cause confusion and hallucinations.
• Amantadine (Symmetrel), originally an antiflu medication, blocks the reuptake of
dopamine or increases the release of dopamine by neurons in the brain, thereby
increasing the supply of dopamine in the synapses. Widely used as an early
monotherapy, its effect may be augmented by drug-free days.
• Levodopa, a dopamine precursor, combined with carbidopa, a decarboxylase inhibitor,
to inhibit destruction of L-dopa in the bloodstream, making more available to the brain.
• The combination of levodopa-carbidopa (Sinemet) usually is used. The addition of
carbidopa prevents levodopa from being metabolized in the gut, liver, and other tissues,
and allows more to get to the brain. Therefore, a smaller dose of levodopa is needed to
treat symptoms, and the unpleasant adverse effects are greatly reduced.
• Bromocriptine (Parlodel), pergolide (Permax), pramipexole (Mirapex), and ropinirole
(Requip) are dopaminergic agonists that activate dopamine receptors in the brain. Can
be taken alone or in combination with Sinemet.
• Use of the monoamine oxidase inhibitor selegiline or deprenyl (Eldepryl) boosts the
effect of Sinemet when levodopa becomes less effective.
• Tolcapone (Tasmar) and entacapone (Comtan) are in a new drug class (COMT
inhibitors) for adjunct treatment.
They prolong the duration of symptom relief by blocking the action of an enzyme that
breaks down levodopa before it reaches the brain. Must be taken with levodopa.
GERONTOLOGIC ALERT
Elderly patients may have reduced tolerance to anti-Parkinson's drugs and may require smaller
doses. Watch for and report psychiatric reactions, such as anxiety, confusion, and
hallucinations; cardiac effects, such as dizziness, orthostatic hypotension, and pulse irregularity;
and blepharospasm (twitching of the eyelid), an early sign of toxicity. Other adverse effects may
include dry mouth, nausea, drowsiness, and insomnia.
Surgery
• New surgical treatments for Parkinson's disease and essential tremor are promising.
• Medial pallidotomy (electrode destroys cells in the globus pallidus) often improves
longstanding symptoms such as dyskinesia, akinesia, rigidity, tremor, and for patients
who have developed dyskinetic movements in reaction to their medications.
• Chronic deep brain stimulation of the thalamus decreases tremor and uncontrollable
movements unresponsive to medication. Electrodes are implanted in the thalamus or
globus pallidus and connected to a pacemaker-like device, which the patient can switch
on or off as symptoms dictate.
• Brain tissue transplants are still in the experimental stages but have produced
encouraging results using fetal tissue and genetically engineered and animal cells that
can be made to produce dopamine. Stem cell research is also taking place.
Complications
• Dementia
• Aspiration
• Injury from falls
Nursing Assessment
• Obtain history of symptoms and their effect on functioning. Mobility, feeding,
communication, and self-care difficulties will have many nursing implications (see Figure
15 6).
FIGURE 15-6 Appearance of female with Parkinson's disease.

• Assess cranial nerves, cerebellar function (coordination), motor function.
• Observe gait and performance of activities.
• Assess speech for clarity and pace.
• Assess for signs of depression.
• Assess family dynamics, support systems, and access to social services.
Nursing Diagnoses
• Impaired Physical Mobility related to bradykinesia, rigidity, and tremor
• Imbalanced Nutrition: Less Than Body Requirements related to motor difficulties with
feeding, chewing, and swallowing
• Impaired Verbal Communication related to decreased speech volume and facial muscle
involvement.
• Constipation related to diminished motor function, inactivity, and medications
• Ineffective Coping related to physical limitations and loss of independence
Improving Mobility
• Encourage the patient to participate in daily exercise, such as walking, riding a stationary
bike, swimming, or gardening.
• Advise the patient to do stretching and postural exercises as outlined by physical
therapist.
• Encourage the patient to take warm baths and receive massages to help relax muscles.
• Instruct the patient to take frequent rest periods to overcome fatigue and frustration.
• Teach postural exercises and walking techniques to offset shuffling gait and tendency to
lean forward.
○ Instruct patient to use a broad-based gait.
○ Have patient make a conscious effort to swing arms, raise the feet while walking,
use a heel-toe gait, and increase the width of stride.
○ Tell patient to practice walking to marching music or sound of ticking metronome
to provide sensory reinforcement.
Optimizing Nutritional Status
• Teach patient to think through the sequence of swallowingâ€”close lips with teeth
together; lift tongue up with food on it; then move tongue back and swallow while tilting
head forward.
• Instruct patient to chew deliberately and slowly, using both sides of mouth.
• Tell patient to make conscious effort to control accumulation of saliva by holding head
upright and swallowing periodically.
• Have patient use secure, stabilized dishes and eating utensils.
• Suggest smaller meals and additional snacks.
• Monitor weight.
Maximizing Communication Ability
• Encourage compliance with medication regimen.
• Suggest referral to speech therapist.
• Teach patient facial exercises and breathing methods to obtain appropriate
pronunciation, volume, and intonation.
○ Take a deep breath before speaking to increase the volume of sound and
number of words spoken with each breath.
○ Exaggerate pronunciation and speak in short sentences; read aloud in front of a
mirror or into a tape recorder to monitor progress.
○ Exercise facial muscles by smiling, frowning, grimacing, and puckering.
Preventing Constipation
• Encourage foods with moderate fiber contentâ€”whole grains, fruits, and vegetables.
• Increase water intake.
• Obtain a raised toilet seat to encourage normal position.
• Encourage patient to follow regular bowel regimen.
Strengthening Coping Ability
• Help the patient establish realistic goals and outline ways to achieve goals.
• Provide emotional support and encouragement.
• Encourage use of all resources, such as therapists, primary care provider, social worker,
and social support network.
• Encourage open communication, discussion of feelings, and exchange of information
about Parkinson's disease.
• Have patient take an active role in activity planning and evaluation of treatment plan.
• Observe for changes in depression to determine if the patient is responding to
antidepressants.
• Recommend interdisciplinary home health care program. Requires skilled assessment of
needs of patient, professional nursing and therapeutic services, patient and family
education, and case management to optimize patient outcomes.
• Encourage use of soothing music to reduce pain and depression.
• Assess safety in environment to reduce risk of falls.
• Utilize physical therapy services to encourage safe ambulation and reduce fear of falls.
• Encourage use of social services, respite care and health visitors, mental health
counselors, and support groups to prevent caregiver strain.
• Use occupational therapy aids to ensure mobility and safety, such as grab rails in the tub
or shower, raised toilet seat, hand rails on both sides of the stairway, rope secured to
foot of bed to achieve sitting position, and straight-backed wooden chairs with armrests.
• Instruct the patient to avoid sedatives, unless specifically prescribed, which have
additive effect with other medications, and to avoid vitamin B preparations, and vitamin-
fortified foods, which can reverse effects of medication.
• Instruct the patient in medication regimen and adverse reactions, such as orthostatic
hypotension, dry mouth, dystonia, muscle twitching, urine retention, impaired glucose
tolerance, anemia, and elevated liver function tests.
• Encourage follow-up and monitoring for diabetes, glaucoma, hepatotoxicity, and anemia
while undergoing drug therapy.
• Teach patient ambulation cues to avoid â€œfreezingâ€ in place and possibly avoid falls
by doing one of the following:
○ Raise head, raise toes, then rock from one foot to another while bending knees
slightly.
○ Raise arms in a sudden short motion.
○ Take a small step backward, then start forward.
○ Step sideways, then start forward.
• Instruct the family not to pull patient during episodes of â€œfreezing,â€ which
increases the problem and may cause falling.
• Refer the patient/family for more information and support to such agencies as:
○ National Parkinson's Foundation, http://www.parkinson.org
○ National Institute of Neurologic Disorders and Stroke, http://www.ninds.nih.gov.
• Attends physical therapy sessions, does facial exercises 10 minutes twice per day
• Eats three small meals and two snacks, no weight loss
• Enunciation clear, speaking in four to five words per breath
• Passes soft stool every day
• Asks questions about Parkinson's, obtains help from family and/or friends
MULTIPLE SCLEROSIS
MS is a chronic, frequently progressive neurologic disease of the CNS of unknown etiology and
uncertain trajectory. MS is characterized by the occurrence of small patches of demyelination of
the white matter of the optic nerve, brain, and spinal cord. MS is characterized by exacerbations
and remissions of symptoms over the course of the illness. MS is the most common CNS
disease among young adults and the third leading cause of disability in the United States. It is
estimated that 400,000 Americans have this disorder of the brain and spinal cord, causing
disruption of electrical messages from the brain to the peripheral nervous system.
• Demyelination refers to the destruction of the myelin, the fatty and protein material that
covers certain nerve fibers in the brain and spinal cord (see Figure 15-7).
FIGURE 15-7 Myelin destruction of the nerve cell axon in multiple sclerosis.
• Demyelination results in disordered transmission of nerve impulses.
• Inflammatory changes lead to scarring of the affected nerve fibers.
• Cause unknown but possibly related to autoimmune dysfunction, genetic susceptibility,
or an infectious process.
• More prevalent in the northern latitudes and among Caucasians.
Classification
The National Multiple Sclerosis Advisory Committee recognizes four clinical forms of MS:
• Relapsing remitting (RR)â€”clearly defined acute attacks evolve over days to weeks.
Partial recovery of function occurs over weeks to months. Average frequency of attacks
is once every 2 years and neurologic stability remains between attacks without disease
progression. (At the time of onset, 90% of cases of MS are diagnosed as RR.)
• Secondary progressive (SP)â€”always begins as RR but clinical course changes with
declining attack rate, with a steady deterioration in neurologic function unrelated to the
original attack. (Fifty percent of those with RR will progress to SP within 10 years; 90%
will progress within 25 years.)
• Primary progressive (PP)â€”characterized by steady progression of disability from onset
without exacerbations and remissions. More prevalent among males and older
individuals. Worst prognosis for neurologic disability. (Ten percent of cases of MS are
diagnosed as PP.)
• Progressive relapsing (PR)â€”the same as PP except that patients experience acute
exacerbations along with a steadily progressive course. (Rarest form)
Lesions can occur anywhere within the white matter of the CNS. Symptoms reflect the location
of the area of demyelination.
• Fatigue and weakness.
• Abnormal reflexesâ€”absent or exaggerated.
• Vision disturbancesâ€”impaired and double vision, nystagmus.
• Motor dysfunctionâ€”weakness, tremor, incoordination.
• Sensory disturbancesâ€”paresthesias, impaired deep sensation, impaired vibratory and
position sense.
• Impaired speechâ€”slurring, scanning (dysarthria).
• Urinary dysfunctionâ€”hesitancy, frequency, urgency, retention, incontinence; upper UTI.
Urinary dysfunction affects about 90% of patients with MS and may exacerbate relapse
of MS.
• Neurobehavioral syndromesâ€”depression, cognitive impairment, emotional lability.
• Symptoms of MS are often unpredictable, varying from person to person and from time
to time in the same person.
• Establishing a definitive diagnosis is often difficult, with much uncertainty concerning
prognosis once the diagnosis is made.
• Serial brain MRI studies have proved to be useful for diagnosing and monitoring patients
with MSâ€”show small plaques scattered throughout white matter of CNS.
• Magnetic resonance spectroscopy is now being studied to monitor specific
pathophysiology of evolving MS plaques.
• Electrophoresis study of CSF shows abnormal IgG antibody.
• Visual, auditory, and somatosensory evoked potentialsâ€”slowed conduction is evidence
of demyelination.
Management
MS treatment is dynamic and rapidly evolving, covering two main areas: direct treatment of MS,
and treatment of the effects or symptoms resulting from MS. Treatment is aimed at relieving
symptoms and helping the patient function. However, a therapeutic relationship between the
patient and nurse creates a critical and strong bond that is essential across the long trajectory of
the illness.
Current Disease-Modifying Drugs
• Corticosteroids or adrenocorticotropic hormone are used to decrease inflammation,
shorten duration of relapse or exacerbation.
• Immunosuppressive agents may stabilize the course.
• Interferon beta-1a (Rebif, Avonex) and interferon beta-1b (Betaseron) are being used for
treatment of rapidly progressing symptoms in some patients.
• Copolymer-1, a mixture of synthetic polypeptides composed of four amino acids, has
been effective in reducing relapse rates and disability in patients with relapsing-remitting
MS.
• Glatiramer (Copaxone), an immunomodulator, is used in relapsing-remitting disease.
• Mitoxantrone (Novantrone), a chemotherapeutic agent used for the treatment of
secondary (chronic) progressive, progressive relapsing, or worsening relapsing-remitting
multiple sclerosis to reduce neurologic disability and frequency of clinical relapses.
Treating Exacerbations
• A true exacerbation of MS is caused by an area of inflammation in the CNS.
• The treatment most commonly used to control exacerbations is I.V., high-dose
corticosteroids. Solu-Medrol (ethylprednisolone) is one of the most commonly used
corticosteroids in MS.
• Plasmapheresis (plasma exchange) is only considered for the 10% who do not respond
well to standard corticosteroid treatment.
Chronic Symptom Management
• Treatment of spasticity with agents, such as baclofen (Lioresal), dantrolene (Dantrium),
diazepam (Valium); physical therapy; nerve blocks and surgical intervention
• Control of fatigue with amantadine (Symmetrel) and lifestyle changes
• Treatment of depression with antidepressant drugs and counseling
• Bladder management with anticholinergics, intermittent catheterization for drainage,
prophylactic antibiotics
• Bowel management with stool softeners, bulk laxative, suppositories
• Multidisciplinary rehabilitation management with physical therapy, occupational therapy,
speech therapy, cognitive therapy, vocational rehabilitation, and complementary and
alternative medicine as indicated to restore or maintain functions essential to daily living
in individuals who have lost these capacities through the disease process
• Control dystonia with carbamazepine (Tegretol)
• Management of pain syndromes with carbamazepine (Tegretol), phenytoin (Dilantin),
perphenazine/amitriptyline (Triavil), and nonpharmacologic modalities
Complications
• Respiratory dysfunction
• Infections: bladder, respiratory, sepsis
• Complications from immobility
• Speech, voice, and language disorders such as dysarthria
Nursing Assessment
• Observe motor strength, coordination, and gait.
• Perform cranial nerve assessment.
• Evaluate elimination function.
• Explore coping, effect on activity and sexual function, emotional adjustment.
• Assess patient and family coping, support systems, available resources.
Nursing Diagnoses
• Impaired Physical Mobility related to muscle weakness, spasticity, and incoordination
• Fatigue related to disease process and stress of coping
• Disturbed Sensory Perception (tactile, kinesthetic, visual) related to disease process
• Impaired Urinary Elimination related to the disease process.
• Interrupted Family Processes related to inability to fulfill expected roles
• Sexual Dysfunction related to disease process
Promoting Motor Function
• Perform muscle stretching and strengthening exercises daily, or teach patient or family
to perform, using a stretch-hold-relax routine to minimize spasticity and prevent
contractures.
• Apply ice packs before stretching to reduce spasticity.
• Tell patient to avoid muscle fatigue by stopping activity just short of fatigue and taking
frequent rest periods.
• Encourage ambulation and activity, and teach patient how to use such devices as
braces, canes, and walkers when necessary.
• Inform the patient to avoid sudden changes in position, which may cause falls due to
loss of position sense, and to walk with a wide-based gait.
• Encourage frequent change in position while immobilized to prevent contractures;
sleeping prone will minimize flexor spasm of hips and knees.
Minimizing Fatigue
• Help patient and family understand that fatigue is an integral part of multiple sclerosis.
• Plan ahead, and prioritize activities. Take brief rest periods throughout the day.
• Avoid overheating, overexertion, and infection.
• Encourage energy conservation techniques, such as sitting to perform activity, limiting
trips up and down stairs, pulling, or pushing rather than lifting.
• Help patient develop healthy lifestyle with balanced diet, rest, exercise, and relaxation.
Optimizing Sensory Function

• Suggest use of an eye patch or frosted lens (alternate eyes) for patients with double
vision.
• Encourage ophthalmologic consultation to maximize vision.
• Provide a safe environment for patient with any sensory alteration.
○ Orient patient to the environment, and keep arrangement of furniture and
personal articles constant.
○ Make sure floor is free from obstacles, loose rugs, or slippery areas.
○ Teach the use of all senses to maintain awareness of environment.
Maintaining Urinary Elimination
• Ensure adequate fluid intake to help prevent infection and stone formation.
• Assess for urine retention, and catheterize for residual urine as indicated.
• Teach patient to report signs of UTI immediately.
• Set up bladder training program to reduce incontinence.
○ Encourage fluids every 2 hours.
○ Follow regular schedule of voiding, every 1 to 2 hours, lengthening as tolerated.
○ Restrict fluid volume and salty foods 1 to 2 hours before bedtime.
• See pages 184 to 186 for more information on urine retention and incontinence.
Normalizing Family Processes
• Encourage verbalization of feelings of each family member.
• Encourage counseling and use of church or community resources.
• Suggest dividing up household duties and child-care responsibilities to prevent strain on
one person.
• Explore adaptation of some roles so patient can still function in family unit.
• Expand treatment efforts to include the whole family.
• Support mothers with MS who often face fatigue and episodic exacerbations during their
child-rearing years.
Promoting Sexual Function
• Encourage open communication between partners.
• Discuss birth control options, if appropriate.
• Suggest sexual activity when patient is most rested.
• Suggest consultation with sexual therapist to help obtain greater sexual satisfaction.
• The nurse case manager functions as care provider, facilitator, advocate, educator,
counselor, and innovator aimed at intervening in a wide variety of settings to improve
patient function and mobility.
• Teach the patient and family to use their own judgment, knowledge, and ingenuity to
control MS symptoms.
• Teach patient and family how to conduct periodic self-assessment of daily functioning,
so home care team can continue to make modifications in treatment plan.
• Encourage the patient to maintain previous activities, although at a lowered level of
intensity.
• Teach the patient to respect fatigue and avoid physical overexertion and emotional
stress; remind patient that activity tolerance may vary from day to day.
• Advise the patient to avoid exposure to heat and cold or infectious agents.
• Encourage a nutritious diet that is high in fiber to promote health and good bowel
elimination.
• Advise the patient that some medications may accentuate weakness such as some
antibiotics, muscle relaxants, antiarrhythmics and antihypertensives, antipsychotics, oral
contraceptives, and antihistamines; check with health care provider or pharmacist before
taking any new medications.
• Teach the patient receiving interferon beta-1a (Rebif, Avonex) and interferon beta-1b
(Betaseron) to expect adverse effects of flulike symptoms, fever, asthenia, chills,
myalgias, sweating, and local reaction at the injection site.
Liver function test elevation and neutropenia may also occur. Adverse effects may
persist for up to 6 months of treatment before subsiding.
• Instruct the patient receiving interferon beta-1a and interferon beta-1b in self-injection
technique.
• Try to include children in the education of MS and the relationship of fatigue and
functional status.
National Multiple Sclerosis Society, http://www.nmss.org.
• Performs exercises correctly without spasm
• Rests at intervals, tolerating activity well
• Moves about in environment without injury
• Voids every 2 hours with no incontinent episodes
• Family sharing care, discussing feelings
• Reports satisfaction with sexual activity
AMYOTROPHIC LATERAL SCLEROSIS
ALS, also known as Lou Gehrig disease, is an incapacitating, fatal neuromuscular disease that
affects as many as 20,000 Americans, with 5,000 new cases occurring in the United States
each year. ALS results in progressive muscle weakness and progressive wasting and paralysis
of the muscles. It is accompanied by other lower motor neuron signs, such as atrophy or
fasciculations. Approximately 80% of cases begin between ages 40 and 70. The life expectancy
of an ALS patient averages 2 to 5 years.
• Degeneration of upper motor neurons (nerves leading from the brain to medulla or spinal
cord) and lower motor neurons (nerves leading from the spinal cord to the muscles of
the body).
• Results in progressive loss of voluntary muscle contraction and functional capacity,
involving the legs, feet, arms and hands, and those that control swallowing and
breathing.
• Cause is unknown. Usually affects men in the fifth or sixth decade of life.
• Progressive weakness and wasting of muscles of arms, trunk, and legs
• Fasciculations and signs of spasticity
• Progressive difficulty swallowing (drooling, regurgitation of liquids through nose),
speaking (nasal and unintelligible), and, ultimately, breathing
• Cranial nerve deficits (bulbar symptoms) are present in 20% of cases (prevalence
increases with age), along with dysarthria, voice deterioration, and dysphagia (Patients
with bulbar presentation have poorer prognosis; these symptoms also have a profound
impact on quality of life due to nutritional risk factors, aspiration, and respiratory
complications.)
• Electromyography to evaluate denervation and muscle atrophy
• Nerve conduction study to evaluate nerve pathways
• Pulmonary function tests to evaluate respiratory function
• Barium swallow to evaluate ability to achieve various phases of swallow
• MRI, CT to rule out other disorders
• Laboratory tests: creatine kinase, heavy metal screen, thyroid function tests, CSF
evaluation to rule out other causes of muscle weakness
Management
• There is no cure for ALS; nor is there a proven therapy that will prevent or reverse the
course of the disorder.
• Riluzole (Rilutek), the first drug that has been shown to prolong the survival of ALS
patients, was recently approved by the FDA, but its effects are limited.
• Most treatment is palliative and symptomatic.
• Baclofen (Lioresal) to control spasticity.
• Diazepam (Valium) to control fasciculations.
• Antidepressants, sleep medications.
• Feeding gastrostomy.
• Mechanical ventilation eventually becomes necessary.
Complications
• Respiratory failure
• Aspiration pneumonia
• Cardiopulmonary arrest
• Locked-in syndromeâ€”fully conscious but unable to respond in any way
Nursing Assessment
• Evaluate respiratory function: rate, depth, tidal volume.
• Perform cranial nerve assessment, particularly gag reflex and swallowing.
• Assess voluntary motor function and strength.
Nursing Diagnoses
• Ineffective Breathing Pattern related to respiratory muscle weakness
• Impaired Physical Mobility related to disease process
• Imbalanced Nutrition: Less Than Body Requirements related to inability to swallow
• Fatigue related to denervation of muscles
• Social Isolation related to fatigability and decreased communication skills
• Risk for Infection related to inability to clear airway
Maintaining Respiration
• Monitor vital capacity frequently. Document pattern, and report any decrease below
patient's baseline.
• Position patient upright, suction upper airway, and perform chest physical therapy to
enhance respiratory function.
• Encourage use of incentive spirometer to exercise respiratory muscles.
• Assess for signs of hypoxia, such as tachypnea, hypopnea, restlessness, poor sleep,
and excessive fatigue.
• Obtain ABG values as ordered.
• Establish the wishes of the patient in terms of life-support measures; obtain copy of
advance directive for chart, if applicable.
• Assist with intubation, tracheostomy, and mechanical ventilation when indicated .
• Provide suctioning and routine care of a patient with artificial airway and mechanical
ventilation.
Optimizing Mobility
• Encourage the patient to continue usual activities as long as possible, but modify
exertion to avoid fatigue.
• Encourage physical therapy exercises to strengthen unaffected muscles, and perform
ROM exercises to prevent contractures.
• Encourage energy-conservation techniques.
• Obtain assistive devices as needed to help patient maintain independence, such as
special feeding devices, remote controls, and a motorized wheelchair.
Meeting Nutritional Requirements
• Provide high-calorie, small, frequent feedings.
• Provide meals that are of a texture the patient can handle; semisolid food is usually
easiest to swallow.
○ Avoid easily aspirated, pureed, and mucus-producing foods (eg, milk).
○ Try warm or cold foods that stimulate temperature receptors in mouth and may
help in swallowing.
○ Do not wash down solids with fluidsâ€”may cause choking and aspiration.
• Allow patient to make own food selection.
• Provide assistive devices for self-feeding when possible.
• Make mealtime a pleasant experience in a bright room, with quiet company so the
patient may concentrate on eating and avoid undue embarrassment.
• Examine oral cavity for food debris before and after meals, and assess swallowing
function and buildup of saliva.
• Encourage rest periods before meals to alleviate muscle fatigue.
• Place patient upright for meals with neck flexed to partially protect the airway.
• Instruct patient to take a breath before swallowing, hold breath to swallow, exhale or
cough after swallow, and swallow again.
• Tell patient to avoid talking while eating.
• Prepare patient for gastrostomy or other alternate feeding methods when appropriate.
Minimizing Fatigue
• Encourage activity alternating with frequent naps.
• Encourage patient to accomplish most important activities early in day.
• Consult with occupational therapist about energy-conservation techniques in performing
ADLs.
Maintaining Social Interaction
• Use mechanical speech aids or communication board.
• Use an environmental control board.
• Eye movements/blinks may be the last voluntary movement; develop a code system to
serve as a communication method.
• Because standard call lights cannot be activated by the severely debilitated ALS patient,
provide adaptive call light (environmental control unit) and/or some type of constant
monitoring and surveillance to meet patient's needs.
• Allow patient to select which social activities are meaningful.
• Refer to counselor or psychologist for coping with communication barriers and
inevitability of losses.
Preventing Aspiration and Infection
• Consult with speech therapist for techniques and devices to assist swallowing.
• Discourage bed rest to prevent pulmonary stasis.
• Perform chest physiotherapy as tolerated.
• Monitor for fever and tachycardia, and obtain sputum, urine, and other cultures as
indicated.
• Teach caregivers how to perform suctioning, tracheostomy care, and ventilator care in
the home as indicated. Clean technique will be used rather than sterile.
• Teach caregivers how to perform gastrostomy feedings and care of tube.
• Assess for adequate supplies for care and ability of caregivers to carry out procedures.
• Encourage cleanliness in home environment and avoidance of contact with anyone with
respiratory infection. Give influenza and pneumonia vaccines as indicated.
• Stress the importance of maintaining physical exercise.
• Review with the patient and family proper eating mechanics to avoid fatigue and
aspiration.
• Inform the patient of right to make decisions regarding an Advance Directive if he
decides against artificial ventilation.
• Encourage the family to seek support and respite care.
• Remind the family that the patient with ALS maintains full alertness, sensory function,
and intelligence. Encourage them to maintain interaction, socialization, and stimulation,
and to seek out technology such as mind-activated computer-driven communication
devices.
Amyotrophic Lateral Sclerosis Association, http://www.alsa.org.
• Respirations 28, shallow, unlabored at rest
• Does active ROM exercises for 15 minutes twice per day; uses assistive utensils to feed
self
• Tolerates small, frequent feedings without aspiration
• Naps twice per day for 1 to 2 hours
• Communicates needs effectively to staff and family
• No signs of respiratory or urinary infection
NEUROMUSCULAR DISORDERS
GUILLAIN-BARRÃ‰ SYNDROME (POLYRADICULONEURITIS)
Guillain-BarrÃ© syndrome (GBS) is an acute, rapidly progressing, ascending inflammatory
demyelinating polyneuropathy of the peripheral sensory and motor nerves and nerve roots. GBS
is most often, but not always, characterized by muscular weakness and distal sensory loss or
dysesthesias. GBS is the most frequently acquired demyelinating neuropathy. It affects one in
100,000 people and must be identified quickly to initiate treatment and decrease life-threatening
complications. Usually GBS occurs a few days or weeks following symptoms of a respiratory or
GI viral infection. Occasionally, surgery or vaccinations will trigger the syndrome. The disorder
can develop over the course of hours, days, or weeks. Maximum weakness usually occurs
within the first 2 weeks after symptoms appear, and by the third week of the illness 90% of all
patients are at their weakest. About 30% of those with GBS have residual weakness after 3
years and the recurrence rate is approximately 3%.
Mortality results form respiratory failure, autonomic disturbances, sepsis, and complications of
immobility and occurs at a rate of about 5% despite intensive medical care.
• Believed to be an autoimmune disorder that causes acute neuromuscular paralysis due
to destruction of the myelin sheath surrounding peripheral nerve axons and subsequent
slowing of transmission.
• Viral infection, immunization, or other event may trigger the autoimmune response.
• About 30% to 40% of cases are preceded by Campylobacter infection, an acute
infectious diarrheal illness.
• Cell-mediated immune reaction is aimed at peripheral nerves, causing demyelination
and possibly axonal degeneration.
• Paresthesias and, possibly, dysthesias.
• Acute onset of symmetric progressive muscle weakness; most often beginning in the
legs and ascending to involve the trunk, upper extremities, and facial muscles. Paralysis
may develop.
• Difficulty with swallowing, speech, and chewing due to cranial nerve involvement.
• Decreased or absent deep tendon reflexes, position and vibratory perception.
• Autonomic dysfunction (increased heart rate and postural hypotension).
• Decreased vital capacity, depth of respirations, and breath sounds.
• Occasionally spasm and fasciculations of muscles.
• History and neurologic exam. Progressive weakness, decreased sensation, decreased
deep tendon reflexes.
• Lumbar puncture for CSF examinationâ€”low blood cell count, high protein.
• Electrophysiologic studiesâ€”nerve conduction velocity shows decreased conduction
velocity of peripheral nerves.
Management
• Plasmapheresis produces temporary reduction of circulating antibodies to reduce the
severity and duration of the GBS episode.
• High-dose immunoglobulin therapy is used to deduce the severity of the episode.
• ECG monitoring and treatment of cardiac dysrhythmias.
• Analgesics and muscle relaxants as needed.
• Intubation and mechanical ventilation if respiratory paralysis develops.
Complications
• Cardiac dysrhythmias
• Complications of immobility and paralysis
• Anxiety and depression
Nursing Assessment
• Assess pain level due to muscle spasms and dysthesias.
• Assess cardiac function including orthostatic BPs.
• Assess respiratory status closely to determine hypoventilation due to weakness.
• Perform cranial nerve assessment, especially ninth cranial nerve for gag reflex.
• Assess motor strength.
Nursing Diagnoses
• Ineffective Breathing Pattern related to weakness/paralysis of respiratory muscles
• Impaired Physical Mobility related to paralysis
• Imbalanced Nutrition: Less Than Body Requirements, related to cranial nerve
dysfunction
• Impaired Verbal Communication related to intubation, cranial nerve dysfunction
• Chronic Pain related to disease pathology
• Anxiety related to communication difficulties and deteriorating physical condition
• Monitor respiratory status through vital capacity measurements, rate and depth of
respirations, breath sounds.
• Monitor level of weakness as it ascends toward respiratory muscles.
• Watch for breathlessness while talking, a sign of respiratory fatigue.
• Maintain calm environment, and position patient with head of bed elevated to provide for
maximum chest excursion.
• As much as possible, avoid opioids and sedatives that may depress respirations.
• Monitor the patient for signs of impending respiratory failure; heart rate above 120 or
below 70 beats/minute; respiratory rate above 30 breaths/minute; prepare to intubate.
Avoiding Complications of Immobility
• Position patient correctly, and provide ROM exercises (see page 178).
• Encourage physical and occupational therapy exercises to regain strength during the
rehabilitative period.
• Assess for complications, such as contractures, pressure ulcers, edema of lower
extremities, and constipation.
• Provide assistive devices as needed, such as cane or wheelchair, for patient to take
home.
• Recommend referral to rehabilitation services or physical therapy for evaluation and
treatment.
Promoting Adequate Nutrition
• Auscultate for bowel sounds; hold enteral feedings if bowel sounds are absent to prevent
gastric distention.
• Assess chewing and swallowing ability by testing CN V and IX; if function is inadequate,
provide alternate feeding.
• During rehabilitation period, encourage a well-balanced, nutritious diet in small, frequent
feedings with vitamin supplement if indicated.
• Recommend referral to dietitian for evaluation and proper diet therapy.
Maintaining Communication
• Develop a communication system with patient who cannot speak.
• Have frequent contact with patient, and provide explanation and reassurance,
remembering that patient is fully conscious.
• Provide some type of patient call system. Because standard call lights cannot be
activated by the severely weak GBS patient, provide adaptive call light and/or some type
of constant monitoring and surveillance to meet patient's needs.
• Recommend referral to speech therapy for evaluation and treatment.
• Refer to counselor, social workers, or psychologist to develop/enhance coping skills and
regain sense of control.
Relieving Pain
• Administer analgesics as required; monitor for adverse reactions, such as hypotension,
nausea and vomiting, and respiratory depression.
• Provide adjunct pain management therapies, such as therapeutic touch, massage,
diversion, guided imagery.
• Provide explanations to relieve anxiety, which augments pain.
• Turn the patient frequently to relieve painful pressure areas.
Reducing Anxiety
• Get to know the patient, and build a trusting relationship.
• Discuss fears and concerns while verbal communication is possible.
• Reassure patient that recovery is probable.
• Use relaxation techniques such as listening to soft music.
• Provide choices in care, and give patient a sense of control.
• Enlist the support of significant others.
• Be aware that GBS is a significant cause of new long-term disability for at least 1,000
persons per year in the United States, necessitating long-term rehabilitation and
community reintegration. Outcome can range from mild paresthesias to death. The
chance of recovery is significantly affected by age, antecedent gastroenteritis, disability,
electrophysiologic signs of axonal degeneration, latency to nadir, and duration of active
disease.
• Given the young age at which GBS sometimes occurs, the patient and family care must
be treated as an integral unit, assessing family communication, knowledge, adjustment,
and use of support systems.
• Include in caregiver training strategies the need for exercise, positioning, and activity to
prevent secondary complications, such as contractures, deep vein thrombosis (DVT),
hypercalcemia, and pressure ulcers.
• Advise patient and family that acute phase lasts 1 to 4 weeks, then patient stabilizes and
rehabilitation can begin; however, convalescence may be lengthy, from 3 months to 2
years.
• Instruct patient in breathing exercises or use of incentive spirometer to reestablish
normal patterns.
• Teach patient to wear good supportive and protective shoes while out of bed to prevent
injuries due to weakness and paresthesia.
• Instruct patient to check feet routinely for injuries because trauma may go unnoticed due
to sensory changes.
• Reinforce maintenance of normal weight; additional weight will further stress the motor
abilities.
• Encourage the use of scheduled rest periods to avoid over-fatigue.
Guillain-BarrÃ© Syndrome Foundation International, http://www.gbsfi.com.
• Respirationsâ€”24 breaths/minute, deep, unlabored
• Performs assistive ROM exercises every 2 hours; no pressure ulcers or edema present
• Gag reflex present, eating small meals without aspiration
• Uses short phrases and head nodding to communicate effectively
• Verbalizes decreased pain
• Verbalizes reduced anxiety
MYASTHENIA GRAVIS
Myasthenia gravis is a chronic autoimmune disorder affecting the neuromuscular transmission
of impulses in the voluntary muscles of the body. It is due to an antibody-mediated attack
against acetylcholine receptors at the neuromuscular junction. Loss of acetylcholine receptors
leads to a defect in neuromuscular transmission. Cardinal features are muscle weakness and
fatigue. Evidence suggests that the frequency and recognition of myasthenia gravis is
increasing.
• Depletion of acetylcholine receptors at neuromuscular junctions brought about by an
autoimmune attack (see Figure 15-8). In about 90% of patients, no specific cause can be
identified, but genetic make-up is a predisposing factor, suggesting environmental
factors may be involved in development of this disorder.
FIGURE 15-8 Myasthenia gravis. (A), Normal ACh receptor site; (B), ACh receptor site
in myasthenia gravis.
• The reduced number of acetylcholine receptors results in diminished amplitude of end-
plate potentials. Failed transmission of nerve impulses to skeletal muscle at the
myoneuronal junction results in decreased muscle power, clinically manifested as
extreme fatigue and weakness. The pattern of muscle involvement varies among
individuals.
• About 80% to 90% of patients with myasthenia gravis have serum antibodies to
acetylcholine.
• Thyroid gland abnormalities are present in 80% of patients. Thymic tumor is the most
important known cause; 10% of patients with myasthenia gravis have a thymoma.
• Cholinergic crisis can result from overmedication with anticholinergic drugs, which
release too much acetylcholine at the neuromuscular junction.
• Brittle crisis occurs when the receptors at the neuromuscular junction become
insensitive to anticholinesterase medication.
• Women are three times more susceptible to developing myasthenia gravis.
• Extreme muscular weakness and easy fatigability.
• Vision disturbancesâ€”diplopia and ptosis from ocular weakness
• Facial muscle weakness causes a masklike facial expression. Patients may present a
snarling appearance when attempting to smile.
• Dysarthria and dysphagia from weakness of laryngeal and pharyngeal muscles
• Proximal limb weakness, with specific weakness in the small muscles of the hands.
• Respiratory muscle weakness can be life-threatening.
• Impending myasthenic crisis may be triggered by respiratory infection, aspiration,
physical/emotional stress, and changes in medications. Symptoms include:
○ Sudden respiratory distress.
○ Signs of dysphagia, dysarthria, ptosis, and diplopia.
○ Tachycardia, anxiety.
○ Rapidly increasing weakness of extremities and trunk.
• Serum test for acetylcholine receptor (AChR) antibodiesâ€”positive in up to 90% of
patients.
• Edrophonium (Tensilon) testâ€”I.V. injection relieves symptoms temporarily. After
injection, a marked but temporary improvement in muscle strength suggests myasthenia
gravis. It also differentiates myasthenic crisis from cholinergic crisis.
• Electrophysiologic (EMG) testingâ€”reveals decremental response to repetitive nerve
stimulation.
• CT scan to assess enlargement of thymus gland
Management
• With treatment, most patients can lead fairly normal lives.
• Oral anticholinesterase drugs, such as neostigmine (Prostigmin) and pyridostigmine
(Mestinon, Regonol), are first-line treatment for mild myasthenia gravis, enhancing
neuromuscular transmission.
• Immunosuppressive drugs, such as prednisone, are the mainstay of treatment when
weakness is not adequately controlled by anticholinergic medication. Azathioprine
(Imuran) may be added as a steroid-sparing agent. Immunosuppressant treatment is
often permanent.
• Plasmapheresis removes antibodies from the blood and is used for patients in
myasthenic crisis or for short-term treatment of patients undergoing thymectomy.
• Thymectomy for those people with tumor or hyperplasia of the thymus gland
(thymectomy is not usually beneficial in late-onset patients).
• Interventions for myasthenic crisis:
○ Immediate hospitalization and may require intensive care
○ Edrophonium (Tensilon) to differentiate crisis and treat myasthenic crisis;
temporarily worsens cholinergic crisis; unpredictable results with brittle crisis
○ Airway managementâ€”mechanical ventilation, vigorous suctioning, oxygen
therapy, postural drainage with percussion and vibration (Tracheostomy may be
required, depending on duration of intubation. Maintain semi-Fowler's position,
especially in obese patients.)
○ Plasmapheresis
○ Neostigmine (Prostigmin) I.V. for myasthenic crisis
○ Discontinue anticholinergic medications until respiratory function improves; give
atropine to reduce excessive secretions for cholinergic crisis
Complications
• Aspiration
• Complications of decreased physical mobility
Nursing Assessment
• Expect the patient to complain of extreme muscle weakness and fatigue.
• Assess cranial nerve function, motor fatigability with repetitive activity, and speech.
Observe eye muscles (usually affected first) for ptosis, ocular palsy, diplopia.
• Assess respiratory statusâ€”breathlessness, respiratory weakness, tidal volume, and
vital capacity measurements.
Nursing Diagnoses
• Fatigue related to disease process
• Risk for Aspiration related to muscle weakness of face and tongue
• Social Isolation related to diminished speech capabilities and increased secretions
Minimizing Fatigue
• Plan exercise, meals, and other ADLs during energy peaks. Time administration of
medications 30 minutes before meals to facilitate chewing and swallowing.
• Assist the patient in developing realistic activity schedule.
• Provide an eye patch, and alternate eyes for the patient with diplopia to allow safe
participation in activity.
• Allow for rest periods throughout the day.
• Obtain assistive devices to help patient perform ADLs.
DRUG ALERT
Many medications can accentuate the weakness experienced by the patient with myasthenia,
including some antibiotics, antiarrhythmics, local and general anesthetics, muscle relaxants, and
analgesics. Assess function after administering any new drug, and report deterioration in
condition.
Preventing Aspiration
• Assess patient's oral motor strength before each meal.
• Teach patient to position head in a slightly flexed position to protect airway during eating.
• Modify diet as needed to minimize risk of aspiration; for instance, soft, solid foods
instead of liquid. Teach patient that eating warm foods (not hot foods) can ease
swallowing difficulties.
• Have suction available that patient can operate.
• Administer I.V. fluids and nasogastric tube feedings to patient in crisis or with impaired
swallowing; elevate head of bed after feeding.
• Suction the patient frequently if on a mechanical ventilator; assess breath sounds and
check chest X-ray reports because aspiration is a common problem.
Maintaining Social Interactions
• Encourage patient to use an alternate communication method, such as flash cards or a
letter board, if speech is affected.
• Instruct patient to speak in a slow manner to avoid voice strain; refer to speech therapy
as needed.
• Show the patient how to cup chin in hands during speech to support lower jaw and assist
with speech.
• Teach patient to tilt head, and to carry a handkerchief to manage secretions in public.
• Encourage family participation in care.
• Refer patient to the Myasthenia Gravis Foundation to meet other patients with the
disease who lead productive lives.
• Assess home environment for physical and emotional stressors, such as uncomfortable
temperature, draft, loud noises, and encourage avoidance of such.
• Emphasize continued follow-up and compliance with treatment regimen.
• Make referrals to community agencies as indicated, such as home respiratory care,
physical therapy, nutritional services.
• Assess patient frequently for fluctuation in condition, and inform caregivers that this is
common.
• Teach patient and family how to use home suction in case of aspiration. Make sure
everyone in household knows Heimlich maneuver.
• Instruct the patient and family regarding the symptoms of crisis.
• Review the peak times of medications and how to schedule activity for best results. For
patients on anticholinesterase therapy:
○ Stress accurate dosage and times; take anticholinesterase drugs 30 to 45
minutes before meals.
○ Tell patient not to skip medication.
○ Instruct patient to avoid taking medication with fruit, coffee, tomato juice, or other
medications.
○ Inform patient of adverse adverse effects such as GI distress.
• Stress the importance of scheduled rest periods before fatigue develops.
• Teach the patient ways to prevent crisis and aggravation of symptoms.
○ Avoid exposure to colds and other infections.
○ Avoid excessive heat and cold.
○ Inform the dentist of condition because use of procaine (Novocain) is not well
tolerated.
○ Avoid emotional upset; plan ahead to minimize stress.
• Encourage patient to wear a MedicAlert bracelet.
• Stress importance of adequate nutrition; instruct to chew food thoroughly and eat slowly.
• Advise patient to avoid alcohol, tonic water.
• Refer patient/family for more information to: The Myasthenia Gravis Foundation, Inc.,
http://www.myasthenia.org.
• Demonstrates optimal self-care in bathing, eating, toileting, and dressing without fatigue
• Breathes effectively, cough is effective, suctioning own secretions, lungs clear
• Visits with friends, participates in social activities, using alternative method of
communications
TRAUMA
TRAUMATIC BRAIN INJURY
Traumatic brain injury (TBI), also known as head injury, is the disruption of normal brain function
due to trauma-related injury resulting in compromised neurologic function resulting in focal or
diffuse symptoms. Motor vehicle accidents are the most common etiology of injury. TBI is the
leading cause of trauma-related deaths and accounts for 40% of trauma-related injuries, with
70% of patients suffering injury to two body parts and 30% to more than two body parts. The
goal of treatment is to prevent secondary brain injury by providing supportive care (see Chapter
35, page 1142, for emergency management of TBI).
Types of Traumatic Brain Injury
• Concussionâ€”transient interruption in brain activity; no structural injury noted on
radiographics.
• Cerebral contusionâ€”bruising of the brain with associated swelling. Coup injury is the
site of initial trauma; the contra coup injury is the site of rebound injury. Temporal and
frontal lobes are common sites.
• Intracerebral hematomaâ€”bleeding into the brain tissue commonly associated with
edema.
• Epidural hematomaâ€”blood between the inner table of the skull and dura. Frequently
associated with injury or laceration of the middle meningeal artery secondary to a
temporal bone fracture. Arterial bleed is commonly associated with a lucid interval,
followed by unresponsiveness.
• Subdural hematomaâ€”blood between the dura and arachnoid caused by venous
bleeding commonly associated with additional brain injury (contusion, intracerebral
hematoma).
• Diffuse axonal injuryâ€”axonal tears within the white matter of the brain. Frequently
occurs within the corpus callosum or brain stem and at the frontal/temporal poles.
Associated with prolonged coma.
Mechanism of Injury and Effects
• Mechanism of injury to the brain is related to acceleration and deceleration of the brain
(soft gelatin matter) within the skull (hard external surface with sharply edged internal
surface). May be caused by blunt or penetrating injury.
• The initial insult is the primary injury and the injury related to the sequela is the
secondary injury. Cellular changes (release of oxygen-free radicals and
neurotransmitters, calcium loss, and increase in lactate acid) and systemic instability
(hypotension, anemia, hypoxia, hypercarbia, hypovolemia) potentiate secondary injury.
• Neurologic deficits result from primary brain injury (contusion, hematoma, diffuse axonal
injury [DAI] or shearing of white matter) or secondary injury (ischemia and mass effect
from hemorrhage, and cerebral edema of surrounding brain tissue).
• Second impact syndrome (SIS) occurs in repetitive concussion when there is insufficient
time for the brain to recovery from the previous injury. SIS is common in sports-related
injuries and is associated with cerebral edema that can be severe.
• Studies have shown that mild TBI with a positive CT scan is more indicative of moderate
injury, resulting in a more pronounced neurobehavioral presentation and extended
neurologic recovery time frame, beyond the typical 3 months.
• Coagulopathy may result from increased release of intracranial thromboplastin, causing
elevation in PTT, prothrombin time (PT), and fibrinogen levels, which in turn results in
mild clotting dysfunction to disseminating intravascular coagulation (DIC).
• Sympathetic storming may result from uncontrolled release of sympathetic hormones
spontaneously or in response to some stressor. Sympathetic stimulation results in
tachycardia, tachypnea, hyperthermia, diaphoresis, agitation, and dystonia.
• DIâ€”reduced secretion of ADH with excessive fluid and electrolyte loss through the
kidneys due to edema or compression of the pituitary/hypothalamic region; may cause
severe dehydration.
• SIADHâ€”over secretion of ADH with normal to increased intravascular volume and
dilutional hyponatremia.
• Cerebral salt wastingâ€”increase in urinary secretion of sodium accompanied by volume
depletion.
Classification
• Mild (GCS 13 to 15, with loss of consciousness to 15 minutes)
• Moderate (GCS 9 to 12, with loss of consciousness for up to 6 hours)
• Severe (GCS 3 to 8, with loss of consciousness greater than 6 hours)
Associated Injuries: Extracranial Trauma
• Facial trauma and skull fracturesâ€”occur in 20% of major TBI. Temporal skull is
thinnest; frontal or occipital are thickest.
○ Linear fractureâ€”fracture through entire thickness of bone that runs in straight
linear pattern
○ Basilar skull fracture of the anterior fossa results in contusions around the eyes
(raccoon eyes) and rhinorrhea
○ Basilar skull fracture of the posterior fossa results in contusions around the ears
(Battle sign) and otorrhea
○ Depressed fractureâ€”displacement of fracture past the inner table of the skull;
risk of dural tear, CSF leak, and intracranial injury; may be closed or open
○ Facial fracturesâ€”orbital (LeForte I-II), mandible, zygoma, maxillary, nasal
fractures
• Vascular injuriesâ€”vertebral or carotid artery dissection
• Spine fracture with or without SCI
• Soft tissue injuries
• Disturbances in consciousness: confusion to coma
• Headache, vertigo
• Agitation, restlessness
• Respiratory irregularities
• Cognitive deficits (confusion, aphasia, reading difficulties, writing difficulties, acalculi,
memory deficits such as retrograde and antegrade amnesia and difficulty learning new
information)
• Pupillary abnormalities
• Sudden onset of neurologic deficit
• Coma and coma syndromes; persistent vegetative state
• Otorrhea may indicate leakage of CSF from ear due to posterior fossa skull fracture;
rhinorrhea may indicate leakage of CSF from nares due to anterior fossa skull fracture
• Raccoon eyes and Battle sign indicate skull fractures
• Episodes of altered LOC, tachycardia, tachypnea, hyperthermia, agitation due to
sympathetic storming (aggravated stress response)
• Abnormal bleeding due to coagulopathy
• Cardiac arrhythmias due to increased release of catecholamines in stress response
• CT scan to identify and localize lesions, edema, bleeding.
• Skull and cervical spine films to identify fracture, displacement.
• Neuropsychological tests during rehabilitation phase to determine cognitive deficits.
• MRI to identify and diagnosis DAI (MRI is rarely performed as it does not affect medical
treatment).
• CBC, coagulation profile, electrolyte levels, serum osmolarity, ABG values, and other
laboratory tests to monitor for complications and guide treatment.
Management
• Airwayâ€”assess and maintain patent airway
○ Intubate for GCS less than 8 (comatose)
○ Placement of nasogastric tube with intubation to prevent aspiration
• Breathingâ€”all intubated patients should have ventilatory support
○ Oxygen as needed to maintain PaO2 greater than 100 mm Hg
○ Maintain PaCO2 35 to 45 mm Hg
○ Avoid use of hyperventilation
• Circulationâ€”prevent hypotension
○ Maintain SBP above 90 mm Hg through use of vasopressors and albumin
○ Maintain normovolemia
○ Treat symptomatic anemia with packed RBC and iron supplements
○ Treat symptomatic arrhythmias
• Management of increased ICP (see page 480) and cerebral edema
• Management of sympathetic storming with medications such as oxycodone (opiate),
propranolol (beta-adrenergic blocker), clonidine (alpha-adrenergic antagonist),
dantrolene (muscle relaxant), gabapentin (antiepileptic), and bromocriptine (dopamine-
receptor agonist) (Response to medications varies.)
• Supportive careâ€”nutritional support (initiate within 3 to 5 days), rehabilitation services,
skin care
• Antibiotics to prevent infection with open skull fractures or penetrating wounds
• Surgery to evacuate intracranial hematomas, debridement of penetrating wounds,
elevation of skull fractures, or repair of CSF leaks
• Treatment of hypernatremia (due to DI, dehydration, diaphoresis) with fluid replacement,
pitressin (DDAVP) therapy
• Treatment of hyponatremia (due to cerebral salt wasting or SIADH) by monitoring daily
fluid status, fluid restriction, oral salt replacement, and I.V. saline 0.9% or 3% (250 to
500 cc over 3 to 5 hours.
Complications
• Infections: systemic (respiratory, urinary), neurologic (meningitis, ventriculitis)
• Increased ICP, hydrocephalus, brain herniation
• Posttraumatic seizure disorder
• Permanent neurologic deficits: cognitive, motor, sensory, speech
• Neurobehavioral alterations: impulsivity, uninhibited aggression, and emotional lability
• Persistent sympathetic storming
• DIC
• DI, SIADH
• Death
Nursing Assessment
• Monitor for signs of increased ICPâ€”altered LOC, abnormal pupil responses, vomiting,
increased pulse pressure, bradycardia, hyperthermia.
• Monitor for signs of sympathetic stormingâ€”altered LOC, diaphoresis, tachycardia,
tachypnea, hypertension, hyperthermia, agitation, and dystonia. Sympathetic storming is
generally seen in severe TBI (GCS 3 to 8) or minimally responsive patients.
• Monitor cardiac status for hypotension and arrhythmias (bradycardia, elevated T waves,
premature ventricular contractions, premature atrial contractions, and sinus
arrhythmias)â€”common and frequently asymptomatic. Tachycardia with hypotension is
indicative of hypovolemia; patient should be evaluated for additional source of blood
loss.
• Be alert for DIâ€”excessive urine output, dilute urine (specific gravity less than 1.005),
hypernatremia.
• Be alert for SIADHâ€”decreased urine output, concentrated urine, hyponatremia (Na+
less than 134), increased weight, possible decreased hematocrit, decreased serum
osmolarity, slight increase in urinary Na+.
• Monitor laboratory findings and report abnormal values:
○ Abnormal PTT, PT, and fibrinogen levels indicating coagulopathy.
○ Electrolyte imbalanceâ€”alterations in serum potassium (hypokalemia) and
sodium (hypernatremia/hyponatremia) levels are common.
○ Anemiaâ€”related to additional trauma or may be dilutional.
○ Elevated white countâ€”indicating infection related to trauma or invasive
procedures.
○ Hypoxia or hypercarbia.
• Perform cranial nerve, motor, sensory, and reflex assessment.
• Assess for behavior that warrants potential for injury to self or others
NURSING ALERT
Regard every patient who has a brain injury as having a potential spinal cord injury. Cervical
collar and spine precautions should be maintained until spinal fractured has been ruled out. A
significant number of patients are under the influence of alcohol at the time of injury, which may
mask the nature and severity of the injury.
Nursing Diagnoses
• Ineffective Tissue Perfusion (cerebral) related to increased ICP
• Ineffective Breathing Pattern related to increased ICP or brain stem injury
• Imbalanced Nutrition: Less Than Body Requirements related to compromised neurologic
function and stress of injury
• Disturbed Thought Processes related to physiology of brain injury
• Risk for Injury related to altered thought processes
• Compromised Family Coping related to unpredictability of outcome
Maintaining Adequate Cerebral Perfusion
• Maintain a patent airway.
• Monitor ICP, as ordered (see page 481).
• Monitor cerebral oxygenation, temperature, or neurochemicals, as ordered (see page
481). Provide oxygen therapy to maintain PaO2 above 100 and carbon dioxide within
normal range.
• Maintain SBP above 90 to enhance cerebral perfusion and administer treatment for
arrhythmias if patient is symptomatic. Evaluate for additional source of blood loss if
patient is tachycardic and hypotensive.
• Monitor LOC, cranial nerve function, and motor and sensory function as per GCS or
neurologic flow sheet and identify emerging trends in neurologic function, and
communicate findings to medical staff.
• If patient has severe TBI, monitor for signs of sympathetic storming (abnormal stress
response) and identify triggers and effective treatment modalities. Institute nursing
measures that have been found to be helpful, such as maintaining normothermia,
pretreatment before known trigger, cool compress to forehead, and relaxing music.
• Monitor response to pharmacologic therapy, including AED levels, as directed.
• Monitor laboratory data, CSF cultures and Gram stains, if applicable, and institute
prompt antibiotic therapy as directed.
• Monitor for hypernatremia and administer fluid replacement as directed. If due to DI,
administer pitressin replacement therapy.
• Monitor for hyponatremia and administer oral or I.V. salt replacement as directed.
Administer 250 to 500 mL 3% saline solution over 3 to 5 hours.
• Monitor coagulation panel and replace clotting factors at room temperature as directed.
• Assess dressings and drainage tubes after surgery for patency, security, and
characteristics of drainage.
• Institute measures to minimize increased ICP, ischemic changes, cerebral edema,
seizures, or neurovascular compromise such as careful positioning to avoid flexing head,
reducing hip flexion (can reduce venous drainage, causing congestion), and spreading
out care evenly over 24-hour period.
NURSING ALERT
Sympathetic storming places the patient at high risk for secondary brain injury, cardiac
abnormalities, weight loss, skin breakdown, and infection. Be alert to triggers (suctioning,
turning, hyperthermia, infection, auditory stimuli) and treat promptly to control symptoms.
NURSING ALERT
Severe states of hypernatremia and hyponatremia can cause further neurologic compromise
(seizures, nausea, confusion, irritability/agitation, coma). Close monitoring of laboratory values
is indicated to evaluate trends and maintain normal range. Hypernatremia and hyponatremia
should not be reversed quickly, as the rapid change can create rebound cerebral edema and be
detrimental to the patient.
• Monitor respiratory rate, depth, and pattern of respirations; report any abnormal pattern,
such as Cheyne-Stokes respirations or periods of apnea.
• Assist with intubation and ventilatory assistance, if needed.
• Obtain frequent ABG values to maintain PaO2 greater than 100 mm Hg and PaCO2 35 to
45 mm Hg.
• If positive end expiratory pressure (PEEP) is used with mechanical ventilation, monitor
neurologic status carefully. The use of PEEP in the care of critically ill patients after TBI
is controversial. PEEP (5 to 10 cm) is felt to be physiological and not detrimental;
however, excessive PEEP can create increases in intrathoracic pressure, diminish
venous drainage, reduce MAP, and increase ICP.
• Turn patient every 2 hours, and assist with coughing and deep breathing.
• Suction patient as needed; however, hyperventilate the patient before suctioning to
prevent hypoxia.
Meeting Nutritional Needs
• Begin nutritional support as soon as possible after a head injury; provide 140% of energy
requirements (100% in paralyzed patient), with 15% in the form of protein. Administer
H2-blocking agents to prevent gastric ulceration and hemorrhage from gastric acid
hypersecretion.
○ Enteric feedings can be initiated once bowel sounds have returned; continuous
or intermittent
 Elevate the head of the bed after feedings
 Check residuals to prevent aspiration
 Monitor for diarrhea
○ I.V. hyperalimentationâ€”for patients unable to tolerate nasogastric feedings
○ Oral feedingâ€”started when adequate swallowing mechanism is demonstrated
• Consult with dietitian to provide the increased calories and nitrogen requirement
resulting from the metabolic changes of brain injury.
• Monitor glucose levels frequently, utilizing fingerstick samples and glucometer. Insulin
(I.V. drip/sliding scale) may be required to regulate serum glucose levels within a normal
range to avoid hyperglycemia, which elevates lactate levels and worsens the effects of
secondary brain injury.
• Consult speech therapist for bedside or radiographic swallow study before initiation of
oral foods. Recognize that any patient with coma is at risk for swallowing difficulties.
Assessment of swallowing function decreases risk of aspiration. Speech therapy is
essential for retraining and developing adaptive techniques.
NURSING ALERT
Caloric needs of the head-injured patient increase by 100% to 200%. Consult your dietitian to
institute nutritional support within the first 2 to 3 days after injury to support the recovery
process. Weight loss is generally in the form of muscle loss and can be as much as 25 to 30 lb
(11.3 to 13.6 kg).
Promoting Cognitive Function
• Periodically, assess patient's LOC, and compare to baseline.
• Be aware of patient's cognitive alteration, and adjust interaction and environment
accordingly.
• Provide meaningful stimulation using all sensesâ€”visual, olfactory, gustatory, acoustic,
and tactile.
• Observe patient for fatigue or restlessness from overstimulation.
• Involve family in sensory stimulation program to maximize its effectiveness.
• Decrease environmental stimuli when patient is in agitated state.
• Reorient to surroundings using repetition, verbal and visual cues, and memory aids;
routinely orient patient after awakening.
• Use pictures of family members, clock, calendar as outlined by occupational and speech
therapist.
• Encourage family to provide items from home to increase sense of identity and security.
• Anticipate need for additional help with toileting, eating, performing ADLs due to
cognitive impairment.
• Break down ADLs into simple steps that patient can progressively take part in.
• Structure the environment and care activities to minimize distraction and provide
consistency.
• Identify and maintain usual patterns of behaviorâ€”sleep, medication use, elimination,
food intake, and self-care routine.
• Refer patient for cognitive retraining, if appropriate.
Preventing Injury
• Instruct the family regarding the behavioral phases of recovery from brain injury, such as
restlessness and combativeness.
• Investigate for physical sources of restlessness, such as uncomfortable position, signs of
UTI, or pressure ulcer development.
• Reassure patient and family during periods of agitation and irrational behavior.
• Pad side rails, and wrap hands in mitts if patient is agitated. Maintain constant vigilance,
and avoid restraints if possible.
• Keep environmental stimuli to a minimum to avoid confusion and agitation.
• Provide adequate light if patient is hallucinating.
• Avoid sedatives to avoid medication-induced confusion and altered states of cognition.
• Refer family to community support services, such as respite care, faith-based groups,
city and state social services, and resources on the Internet. Suggest the Brain Injury
Association of America, http://www.biausa.org, for further information.
• Assist the family members to establish stress management techniques that can be
integrated into their lifestyle, such as ventilation of feelings, use of respite care,
relaxation techniques.
• Consult with social worker or psychologist to assist the family in adjusting to patient's
permanent neurologic deficits.
• Help the family assist the patient to recognize current progress and not focus on
limitations.
• Observe for signs of postconcussion syndrome (PCS), which include headache,
decreased concentration, irritability, dizziness, insomnia, restlessness, diminished
memory, anxiety, easy fatigability, and alcohol intolerance.
• Be aware that persistence of these symptoms can interfere with relationships and
employability of the patient.
• Encourage the patient and family to report these symptoms and obtain additional
support and counseling as needed. PCS may persist as long as 2 years.
• Act as liaison to coordinate all the home care services the patient will need, while
keeping in touch with the patient's primary care provider, neurologist, and neurosurgeon.
• Provide the necessary education to caregivers in tube feedings, positioning, ROM
exercises, and so forth.
• Make sure that coaches and parents from community recreation programs and schools
are familiar with and follow guidelines for sports-related concussion (see Table 15-4).
TABLE 15-4 American Academy of Neurology Guidelines for Sports-Related
Concussion
SEVERITY RECOMMENDATIONS
Grade 1
Transient confusion without ○ Removal from game and only returned to
loss of consciousness and
the game if remains asymptomatic after 15
resolution of symptoms within
minutes
15 minutes
○ If second grade 1 concussion occurs,
removal from sports activity until
asymptomatic for 1 week
Grade 2
Transient confusion without ○ Removal from sporting event and further
loss of consciousness and
workup if symptoms do not resolve in 1
symptoms persisting longer
week.
than 15 minutes
○ No sporting activity for 1 week.
○ If grade 2 occurs after a grade 1
concussion: removal from sporting event
and no sporting activities for 2 weeks
Grade 3
Loss of consciousness ○ Removal from sporting event.
○ Return to sporting activities if asymptomatic
for 1 week (brief loss of consciousness)
○ Return to sporting activities if asymptomatic
for 2 weeks (prolonged loss of
consciousness)
○ Unconsciousness with neurologic findings
should be transported to nearest
emergency for full evaluation.
○ Removal from sporting activity for 1 year
and discouraged from future participation in
contact sports if any structural findings on
computed tomography scan or magnetic
resonance imaging
• Review the signs of increased ICP with the family.
• Reinforce the lability of cognitive, language, and physical functioning of the person with
brain injury and the lengthy recovery period.
• Teach the family techniques to calm the agitated patient.
○ Therapeutic use of touch, massage, and music
○ Elimination of distractions (television, radio, alarms, crowds)
○ Provide one-on-one communication
○ Distract patients
• No signs of increased ICP
• Respirationsâ€”24 breaths/minute, regular
• Tube feedings tolerated well without residual
• Oriented to person, place, and time
• Less agitated; side rails maintained
• Family reports using respite care
SPINAL CORD INJURY
Spinal cord injury (SCI) is a traumatic injury to the spinal cord that may vary from a mild cord
concussion with transient numbness to immediate and complete tetraplegia. The most common
sites are the cervical areas C5, C6, and C7, and the junction of the thoracic and lumbar
vertebrae, T12 and L1. Injury to the spinal cord may result in loss of function below the level of
cord injury (see Figure 15-9). Spinal cord injury requires comprehensive and specialized care.
The Model Spinal Cord Injury System (MSCIS) is a network of comprehensive, federally funded,
regional SCI centers in the United States. The Department of Veterans Affairs operates 23 SCI
centers. (Also, see Chapter 35, page 1148, for emergency management of SCI.)
FIGURE 15-9 Levels of spinal cord innervation.
• The estimated annual incidence of SCI is about 11,000 new cases per year and the
prevalence is approximately 183 cases per 230,000 persons in the United States. The
average age is 32 and approximately 80% are males. The primary etiologies are motor
vehicle accidents, violence (mainly gunshot), falls, and sports injuries. Most injuries
result in tetraplegia and more patients with SCI are incomplete than complete. (A
complete SCI is absence of motor and sensory function at the lowest sacral segment
affected; see below for a description of incomplete SCI.) About 90% of these patients
are discharged to noninstitutional settings.
• The life expectancy for an individual with SCI is lower (80% to 85%) than that of a
person without SCI. The leading causes of death are pneumonia, emboli, and
septicemia.
• SCI may result from trauma, vascular disorders, infectious conditions, tumor, and other
insults.
• SCI can affect upper motor neurons (UMN) or lower motor neurons (LMN). UMNs
extend from the motor strip in the cerebral cortex of the brain through the corticospinal
tract in the spinal cord, where they synapse with interneurons in the ventral horn. LMNs
originate in the ventral horn, exit the spinal cord at each segment, and extend to the
neuromuscular junction. Each LMN innervates 10 to 2,000 muscle fibers. UMN lesions at
T12 and above result in spasticity. LMN lesions at L1 and below result in flaccidity and
reflex loss.
GERONTOLOGIC ALERT
Older patients are at greater risk for altered glucose metabolism, loss of bone minerals leading
to fractures, musculoskeletal pain and weakness, and greater loss of function with spinal cord
injury.
• Patients with tetraplegia (formerly called quadriplegia) have damage to the cervical
segments of nerves (C1-C8) in the spinal canal. Function may be impaired in the upper
extremities, trunk, pelvic organs, and lower extremities.
• Patients with paraplegia have damage to the thoracic, lumbar, or sacral segments of
nerves in the spinal cord. The arms are unaffected, but function may be impaired in the
trunk, pelvic organs, and lower extremities.
• The International Standards for Neurological Classification of Spinal Cord Injury,
promoted by the American Spinal Injury Association (ASIA), are used (available at
http://www.asia-spinalinjury.org/publications/index.html). The ASIA Impairment Scale is
based upon completeness of injury and motor/sensory function.
ASIA A = Complete; absent sensory and motor function at S4-5.
ASIA B = Incomplete; intact sensory but absent motor function below the neurologic level of
injury (LOI) and includes level S4-5.
ASIA C = Incomplete; intact motor function distal to neurologic LOI, and more than half of key
muscles distal to LOI have muscle grade less than 3.
ASIA D = Incomplete; intact motor function distal to neurologic LOI, and more than half of key
muscles distal to LOI have muscle grade greater than or equal to 3.
ASIA E = Normal; intact motor and sensory function.
• Sacral sensation is intact if there is deep sensation and sensation at the anal
mucocutaneous junction; sacral motor is intact if the patient has voluntary contraction of
the external anal sphincter with digital stimulation.
• The Zone of Partial Preservation (ZPP) indicates areas of partial sensory/motor
innervation below the LOI; the ZPP is applicable only to complete injuries.
• The neurologic level of injury is the lowest neural level with normal sensory and motor
function on both sides of the body. When describing the LOI, the neurologic level is
noted unless stated specifically that the skeletal LOI, which is the level of greatest
vertebral damage, is being discussed.
• Various syndromes (incomplete injuries) may characterize the clinical presentation (see
Table 15-5).
TABLE 15-5 Incomplete Spinal Cord Clinical Syndromes
SYNDROME AFFECTED SITE DEFICIT PRESERVATION
Central cord Central cervical More motor deficit in Sacral sensory; lower
spinal cord upper extremities than extremities have better motor
lower extremities caused function than upper
by medial damage of extremities due to lateral
corticospinal tract sparing of corticospinal tract
Brown- Hemisection of Ipsilateral motor function Ipsilateral sensory function of
Sequard spinal cord and fine touch, vibration, pain and temperature
and proprioception (spinothalamic tract);
(posterior tract); contralateral motor function,
contralateral sensory fine touch, vibration, and
function pain and proprioception (posterior
temperature tract)
(spinothalamic tract)
Anterior cord Main anterior Variable motor deficit; Posterior one-third of spinal
spinal artery of variable sensory deficit of cord (posterior spinal artery);
anterior spinal cord pain and temperature sensory function of
affecting anterior (spinothalamic tract) proprioception, light touch,
two-thirds of spinal vibration (posterior tract)
cord
Conus Conus and lumbar Variable motor deficit; Lesions of proximal conus
medullaris nerve roots in bowel, bladder, and lower may be reflexic (eg,
spinal cord extremity reflexes (flaccid) butocavernosa, micturition)
Cauda Lumbosacral nerve Variable motor deficit; Lesions proximal to level of
equina roots in spinal cord bowel, bladder, and lower injury may be reflexic (eg,
(distal from conus extremity reflexes (flaccid) bulbocavernosa, micturition)
medullaris)
• Sensation function (eg, sensitivity of pinprick/light touch) is tested on each of the 28
dermatomes on both sides of the body. The following grading is suggested: 0 = Absent;
1 = Impaired; 2 = Normal. The external anal sphincter should also be tested (sensory
incomplete if sensate).
• Motor function is tested on each of the 10 paired myotomes on both sides of the body.
The following grading is suggested: 0 = Total paralysis; 1 = Contraction visible or
palpable; 2 = Active movements and full ROM without gravity; 3 = Active movement and
full ROM against gravity; 4 = Active movement and full ROM with moderate resistance; 5
= Normal motor with active movement and full ROM against full resistance. The external
anal sphincter should also be tested (motor incomplete if contraction).
• Most recovery occurs within 6 months of injury; patients with incomplete injuries have
greater recovery than patients with complete injuries.
• Instability exists when ligamentous structures and vertebra cannot protect the vulnerable
spinal cord and movement can further damage the injured spinal cord; stability exists
when ligamentous structures and vertebra can protect the spinal cord from further
neurologic injury.
• Vertebral fractures may be simple, compressed or wedge, dislocated (vertebra overrides
another vertebra), subluxed (vertebra partially dislocated over another vertebrae),
comminuted (vertebrae shattered), or teardrop (vertebrae chipped). Jefferson's fractures,
which may occur with head injuries, involve the C1 level.
• X-ray of spinal columnâ€”include open mouth studies for adequate visualization of C1
and C2.
• MRI of spineâ€”to detect soft tissue injury, hemorrhage, edema, bony injury;
syringomyelia (cystic degeneration in spinal cord) may present as cord compression,
syrinx (cavity) at the fracture site, and kyphosis at fracture site.
• Electrophysiologic monitoring to determine function of neural pathways.
• Urodynamic studies may include urine flow to detect bladder outlet obstruction and/or
impaired bladder contractility; cystometrogram to determine bladder sensation,
compliance, and capacity; sphincter EMG and other studies. The gold standard in
urodynamics is to measure bladder and urethral pressure under fluoroscopy monitoring.
• If DVT or pulmonary emboli are suspected, an ultrasound of the lower extremity or
ventilation/perfusion scan is performed.
• Heterotopic ossification may be diagnosed in the inflammatory stages using ultrasound.
Alkaline phosphatase and ESR are typically elevated.
• Nutritional status should be assessed using nutritional history, anthropometric
measurements, prealbumin (half-life 12 to 36 hours) and transferrin (half-life 6 to 10
days).
• Total lymphocyte count and creatinine height index are also used to establish nutritional
risk.
Management
Requires a multidisciplinary approach because of multiple systems involvement and the
psychosocial aspects of catastrophic injuries.
Immediately After Trauma (Less Than 1 Hour)
• Immobilization with rigid cervical collar, sandbags, and rigid spine board to transport
from the field to acute care facility.
Acute Phase (1 to 24 Hours)
• Maintenance of pulmonary and cardiovascular stability.
○ Intubation and mechanical ventilation, if needed.
○ Vasopressors to maintain adequate perfusion to sustain mean arterial BP at 85
to 90 mm Hg.
○ Medical stabilization before spinal stabilization and decompression.
• Spinal cord immobilizationâ€”use of skeletal tongs.
○ Crutchfield and Vinke tongs require predrilled holes in the skull under local
anesthesia; Gardner-Wells and Heifitz tongs do not.
○ Weight is added to traction gradually to reduce the vertebral fracture; weight
maintained at a level to ensure vertebral alignment.
• Rigid kinetic turning bed to immobilize patients with thoracic and lumbar injuries.
• Surgical interventions are considered when the patient has vertebral instability that may
result in further neurologic damage; an injury that is incomplete at onset may become
complete if instability exists. The objectives are to remove all of the bony and soft tissues
that are compressing the spinal cord, thereby minimizing the possibility of a deteriorating
neurologic status, and stabilize the vertebra surrounding the spinal cord so that
rehabilitation may begin as soon as possible.
○ Decompression, typically using the anterior approach in cervical instances, may
be accomplished by removing the bony structures and soft tissues (eg, fusion,
decompression laminectomy). Realignment of the soft tissues and vertebral
column is required.
○ Stabilization, typically done using the posterior approach, involves the use of
wires, bone grafts, plates, screws, and other fixation devices to prevent
movement at the damaged bony site (eg, fusion, Harrington rods). Harrington
rods, used for thoracolumbar SCI, extend approximately one to three levels
above and below the fracture.
• Methylprednisolone sodium succinate should be administered within 8 hours of injury.
○ Bolus 30 mg/kg administered over 15 minutes; maintenance infusion of 5.4
mg/kg/hr infused for 23 hours
○ Additional benefit may be achieved by administering the maintenance dose for
48 hours.
• Management of neurogenic bladderâ€”Foley catheter
• Pressure ulcer preventionâ€”pressure reduction mattress or kinetic turning frame.
Subacute Phase (Within 1 Week)
• Halo traction is the primary treatment for cervical injuries (see Figure 15-10).
FIGURE 15-10 Halo device.
○ Graphite rings are MRI compatible, lightweight, and radiolucent.
○ Some halos are now open posteriorly, which reduces the incidence of cervical
fracture displacement.
○ The ring is attached to stainless steel pins (two anterior pins, two posterior pins)
and attached to a vest by four connecting rods (also MRI compatible and
radiolucent).
○ Torque wrenches connect the rods to the ring and vest; pressures are typically 8
inches/lb for pins (2 to 5 inches/lb in children) and locking bolts are 28 inches/lb.
○ Pins and locking bolts must be retightened approximately 24 to 48 hours after
placement and periodically thereafter.
○ Pin sites should be cleaned daily with half-strength hydrogen peroxide or soap
and water.
○ Average length of time in a halo vest is 12 weeks, followed by a Philadelphia
collar for 4 weeks.
• GM-1 ganglioside sodium salt I.V., begun within 72 hours after injury, and continued for
18 to 32 days, is believed to enhance neuronal regeneration.
• H2-receptor blockers to prevent gastric irritation and hemorrhage.
• Early mobilization and passive exercise as soon as patient is surgically and medically
stable.
• Hyperalimentation to retard negative nitrogen balance.
• Interventions to prevent thromboembolism (intermediate risk) are based on motor
completeness of injury:
○ Motor Incomplete (ASIA C and D)â€”compression hose; compression boots in
addition to unfractionated heparin (UH) 5,000 units every 12 hours.
○ Motor Complete (ASIA A and B)â€”compression hose; compression boots in
addition to UH with the dosage adjusted to high normal a PTT or low-molecular-
weight heparin 30 mg bid.
○ If the patient is at high risk (ie, motor complete with other risk factors such as
fractures of lower extremities or previous DVT), an inferior vena cava filter should
be considered.
Chronic Phase (Beyond 1 Week)
• Harrington rods, used in conjunction with a body jackets, are used for patients with
thoracolumbar injuries.
• To prevent thrombophlebitis in the chronic phase, compression boots should be
continued for 2 weeks; anticoagulants should also be continued based on motor
completeness of injury:
○ Motor Incompleteâ€”until discharged from hospital (ASIA D) or 8 weeks (ASIA
C).
○ Motor Complete (ASIA A and B)â€”8 weeks.
○ If the patient is at high risk, anticoagulants should be continued for 12 weeks or
until discharged from hospital.
• Management of complications may include treatment of infections with antibiotics;
treatment of respiratory compromise with phrenic nerve pacing, mechanical ventilation,
and other methods; pressure ulcer treatment; management of heterotopic ossification
with calcium chelators and anti-inflammatory agents; drainage of syringomyelia;
management of spasticity with oral or intrathecal antispasmodics, surgical procedure, or
spinal cord stimulation; and management of central neuropathic pain with
anticonvulsants, minor sedatives, antidepressants, nerve block, or surgical procedure.
• Spasticity should be managed by:
○ Maintaining calm, stress-free environment.
○ Allowing ample time for activities such as positioning and transferring.
○ Performing joint ROM exercises with slow, smooth movements.
○ Avoiding temperature extremes.
○ Administering muscle relaxants, such as baclofen (Lioresal) (via pump or orally),
diazepam (Valium), and dantrolene (Dantrium), as prescribed.
• External sphincterotomy may be used for detrusor-sphincter dyssynergia. Other options
include urethral stents and balloon dilatation.
• Clonidine has been used to manage spasticity and facilitate ambulation in patients with
incomplete injuries.
• Resistive inspiratory muscles training shows promise in promoting respiratory muscle
strength and reducing sleep-induced breathing disturbances in patients with tetraplegia.
Resistive training devices are used to perform respiratory maneuvers at scheduled times
during the day.
• Rehabilitation includes medical and psychosocial support, physical therapy, urologic
evaluation, occupational therapy, and multiple other interventions to facilitate an
increased level of function and community participation.
Complications
• Spinal shock lasting a few hours to a few weeks noted by loss of all reflex, motor,
sensory, and autonomic activity below the level of the lesion.
• Respiratory arrest, pneumonia, atelectasis requiring mechanical ventilation with cervical
injury.
• Cardiac arrest may result from initial trauma, worsening of initial injury from edema,
concomitant injuries, and other illnesses.
• Thromboembolic complicationsâ€”in 15% of patients.
• Infectionsâ€”respiratory, urinary, pressure ulcers, sepsis.
• Autonomic dysreflexiaâ€”exaggerated autonomic response to stimuli below the level of
the lesion in patients with lesions at or above T6 is a medical emergency and can result
in dangerous elevation of BP.
• Autonomic dysfunction resulting in orthostatic hypotension, thermodysregulation, and
vasomotor abnormalities.
• Urologicâ€”bladder storage pressure greater than 35 to 40 cm due to neurogenic
bladder may result in renal deterioration; SCI patients who have indwelling urinary
catheters are at increased risk of bladder cancer.
• Paralytic ileusâ€”common in subacute and acute stage.
• Heterotopic ossificationâ€”bony overgrowth that occurs below the level of injury anytime
after SCI.
• Syringomyeliaâ€”cystic formation in the spinal cord may occur any time after SCI.
• Depressionâ€”occurs in 25% of men and 47% of women with SCI.
• Pressure ulcers may occur in up to 35% of persons with SCI.
• Spasticity may result in contractures.
• Amenorrhea occurs in 60% of women with SCI, usually temporary.
• Neuropathic pain occurs in 34% to 94% of patients with SCI.
• Complications can arise from the halo apparatus in persons with cervical injuries.
○ Pin/ring looseningâ€”can result from bone reabsorption. Signs and symptoms
include increased pain, altered pin position, and drainage.
○ Infectionâ€”can result from bacterial infections. Signs and symptoms include
drainage and erythema.
○ Skull/dural penetrationâ€”can result from inner table penetration, usually due to a
fall. Signs and symptoms include a headache, visual disturbances, and CSF leak
from the pin site.
○ Dysphagia and respiratory problemsâ€”can result from halo or vest positioning.
Signs and symptoms include difficulty swallowing and respiratory distress
Nursing Assessment
• Assess cardiopulmonary status and vital signs to help determine degree of autonomic
dysfunction, especially in patients with tetraplegia.
• Determine LOC and cognitive function indicating TBI or other pathology.
• Perform frequent motor and sensory assessment of trunk and extremitiesâ€”extent of
deficits may increase due to edema and hemorrhage. Later, increasing neurologic
deficits and pain may indicate development of syringomyelia.
• Note signs and symptoms of spinal shock, such as flaccid paralysis, urine retention,
absent reflexes.
• Assess bowel and bladder function.
• Assess quality, location, severity of pain.
• Perform psychosocial assessment to evaluate motivation, support network, financial or
other problems.
• Assess for indicators of powerlessness, including verbal expression of no control over
situation, depression, nonparticipation, dependence on others, passivity.
Nursing Diagnoses
• Ineffective Breathing Pattern related to paralysis of respiratory muscles or diaphragm
• Impaired Physical Mobility related to motor dysfunction
• Risk for Impaired Skin Integrity related to immobility and sensory deficit
• Urinary Retention related to neurogenic bladder
• Constipation or Bowel Incontinence related to neurogenic bowel
• Risk for Injury: autonomic dysreflexia and orthostatic hypotension
• Powerlessness related to loss of function, long rehabilitation, depression
• Sexual Dysfunction related to erectile dysfunction and fertility changes
• Chronic Pain related to neurogenic changes
Attaining an Adequate Breathing Pattern
• For patients with high-level lesions, continuously monitor respirations and maintain a
patent airway. Be prepared to intubate if respiratory fatigue or arrest occurs.
• Frequently assess cough and vital capacity. Teach effective coughing, if patient is able
(see Box 15-4).
• Provide adequate fluids and humidification of inspired air to loosen secretions.
• Suction as needed; observe vagal response (bradycardiaâ€”should be temporary).
• When appropriate, implement chest physiotherapy regimen to assist pulmonary drainage
and prevent infection.
• Monitor results of ABG values, chest X-ray, and sputum cultures.
• Tape halo wrench to body jacket or halo traction in the event the jacket must be
removed for basic or advanced life support or respiratory distress.
BOX 15-4 Assisted Coughing
Many patients with tetraplegia have an impairment of the diaphragmatic and intercostal
muscles. The result is a weak or ineffective cough. To increase the mechanical effectiveness of
the patient's cough, perform or teach the assisted cough technique.
• Place the patient in supine, low semi-Fowler's position.
• Place the heels of your hands on the costophrenic angle of the patient's rib cage.
• With the patient's head turned away, ask the patient to hyperventilate and exhale once
or twice. Allow your hands to move with the patient.
• During the next breath, ask the patient to take a deep breath and cough while exhaling.
• As the patient coughs, thrust your hands down and in (inferiorly and medially) to add
power to the diaphragm during exhalation.
• Allow one or two normal breaths, and repeat the procedure.
NURSING ALERT
Incorrect hand placement may cause injury to the internal organs, ribs, and xiphoid process.
Promoting Mobility
• Place patient on firm kinetic turning bed until spinal cord stabilization. After stabilization,
turn every 2 hours on a pressure reduction surface, ensuring good alignment.
• Logroll patient with unstable SCI.
• Perform ROM exercises to prevent contractures and maintain rehabilitation potential.
• Monitor BP with position change in the patient with lesions above midthoracic area to
prevent orthostatic hypotension.
• Encourage physical therapy and practicing of exercises as tolerated. Functional
electrical stimulation may facilitate independent standing and ambulation.
• Encourage weight-bearing activity to prevent osteoporosis and risk of kidney stones.
NURSING ALERT
Never attempt to reposition the patient by grasping a halo or any other stabilization device. This
may result in severe damage to the brain, head, or vertebra.
Protecting Skin Integrity
• Pay special attention to pressure points when repositioning patient. Seating and mobility
requirements must be determined.
• Obtain pressure relief mattress and appropriate wheelchair and cushion.
• Inspect for pressure ulcer development daily over bony prominences, including the back
of head, ears, trunk, heels, and elbows. Observe under stabilization devices for pressure
areas, particularly on the scapulae. Use a risk assessment tool to determine risk of
developing pressure ulcer.
• Keep skin clean, dry, and well-lubricated.
• Turn a minimum of every 2 hours, and instruct patient to perform wheelchair weight
shifts every 15 minutes. Place the patient in prone position at intervals, unless
contraindicated.
• Institute treatment for pressure ulcers immediately, and relieve pressure to promote
healing.
Promoting Urinary Elimination
• Consider use of intermittent catheterization, typically beginning every 4 hours, as an
alternative to an indwelling catheter.
• If patient has an upper motor neuron lesion (above L1) and no indwelling catheter,
promote reflex voiding by tapping the bladder, gently pulling the patient's pubic hair, or
stroking the patient's inner thigh.
• If the patient has a lower motor neuron lesion (L1 or below) and no indwelling catheter,
promote voiding by using a bladder CredÃ©'s method by gently compressing the
suprapubic area to promote voiding.
• Encourage fluid intake of 3,000 to 4,000 mL of fluid per day (2,000 mL per day if
intermittent catheterization is used) to prevent infection and urinary calculi. Space fluids
out over 24-hour period to avoid bladder overdistention. Juices should be encouraged to
help decrease urinary pH (inhibiting stone production) and bacterial adherence to a
catheter.
• Monitor for urine retention by percussing the suprapubic area for dullness, catheterizing
for residual urine after voiding, or using noninvasive devices such as the BladderScan.
• Prophylactic antibiotics for prevention of recurrent UTIs are not supported due to the
increase in resistant organisms.
• The use of biofilms and other materials that inhibit adhesion of pathogens to catheters is
being explored.
Promoting Bowel Elimination

• Assess bowel sounds, and note abdominal distention. Paralytic ileus is common
immediately after injury.
• Encourage intake of high-calorie, high-protein, and high-fiber (15 g) diet when bowel
sounds return and food is tolerated.
• Assess for loose stool oozing from rectum, and perform rectal examination to check for
fecal impaction; remove fecal matter if necessary.
• Institute a bowel program as early as possible.
○ Schedule bowel care at the same time of day to develop a predictable outcome.
○ Stimulate the gastrocolic reflex 30 minutes before bowel care with food or liquid
intake.
○ Perform bowel care with patient in bowel chair or in left side-lying position; the
procedure should not take more than 2 hours.
○ Use abdominal massage, deep breathing, warm fluids, and leaning forward in the
chair to enhance success.
• For patients with upper motor neuron lesions, perform reflexic bowel care.
○ Insert a glycerin or bisacodyl suppository or mini-enema (4 mL).
○ Alternatively, use digital stimulation with gloved, lubricated fingerâ€”perform a
semicircular motion against posterior rectal wall. Repeat every 5 to 10 minutes
until evacuation is complete.
• For patients with lower motor neuron lesions, perform areflexic bowel care.
○ Perform manual stool elimination.
• Have patient perform Valsalva maneuver (after urinary elimination to prevent
vesicoureteral reflux of urine).
• For chronic constipation without relief from more conservative approaches, consider a
bulk-forming agent or laxative 8 hours before bowel care.
Preventing Autonomic Dysfunction and Orthostatic Hypotension
• Be alert to signs of autonomic dysreflexia (see Standards of Care Guidelines), try to
avoid triggers, and treat as directed.
• Be alert for, prevent, and manage orthostatic hypotension, especially in patients with
cervical SCI.
• Use tilt table as ordered to gradually increase the patient's ability to tolerate sitting after
acute SCI.
• Other conservative strategies consist of use of embolic hose, abdominal binder, and
high-salt diet.
• Administer a sympathomimetic, such as ephedrine or pseudoephedrine, as ordered,
before patient is transferred to wheelchair.
DRUG ALERT
Caution should be exercised for patients with SCI who are taking tricyclic antidepressants
because of autonomic dysfunction. SCI patients are more vulnerable to anticholinergic adverse
effects and orthostatic hypotension. In addition, numerous potential drug reactions are
associated with monoamine oxidase inhibitors and SCI.
Empowering the Patient
• Explain all procedures to the patient. Answer questions.
• Make sure that the patient plays an integral part in decision making about care plan.
Allow the patient to make modifications to treatment plan when possible.
• Schedule procedures and planning sessions when the patient is rested and experiencing
decreased anxiety.
• Praise the patient for incremental gains in function or participation.
• Discuss stress management techniques, such as relaxation therapy, counseling, and
problem solving.
• Refer to vocational training program if the patient expresses an interest.
• Use peer counseling for patient to gain support from others with SCI.
• Be alert for signs of depression (problems with sleep, loss of interest, guilt, loss of
energy, lack of concentration, change in appetite, feeling sad) or risk for suicide, and
refer to mental health counselor. Administer antidepressant medications as directed.
• Explore the use of hands-free environmental control units to control environment (eg,
turn on television).
STANDARDS OF CARE GUIDELINES
Autonomic Dysreflexia
Risk of autonomic dysreflexia occurs after spinal cord injury at the level of T6 or above and may
result in dangerously elevated blood pressure (BP). Follow these assessment and treatment
measures to protect the patient.
Be aware of and try to prevent common causes of autonomic dysreflexia whenever possible:
• Bladder distention, UTI, bladder or kidney stones
• Cystoscopy, detrusor sphincter dysynergia, urodynamic testing
• Bowel distention, bowel impaction
• Constrictive clothing, shoes, or apparatus
• Noxious stimuli such as pain, strong smells, pressure
Be alert for signs and symptoms of autonomic dysreflexia:
• Sudden and significant increase in systolic and diastolic BP 20 to 40 mm Hg above the
patient's baseline. (Normal systolic BP for a person with tetraplegia is 90 to 110 mm Hg.)
In children and adolescents, a systolic increase of > 15 to 20 mm Hg above baseline is
significant.
• Pounding headache
• Bradycardia and/or cardiac arrhythmias
• Profuse sweating, piloerection, and flushing above the level of injury (LOI).
• Blurred vision and spots in visual field
• Nasal congestion
• Apprehension and anxiety
Take the following actions if autonomic dysreflexia occurs:
• Check BP; if elevated, call health care provider immediately.
• Immediately sit the patient up.
• Loosen clothing and other constrictive apparatus.
• Monitor BP every 2 to 5 minutes.
• Check the urinary systemâ€”catheterize patient (use 2% lidocaine jelly and wait 2
minutes); if catheter in place, check for kinks in tubing obstructing drainage; if catheter
blockage suspected, gently irrigate with 10 to 15 mL normal saline (use 5-10 mL in
children younger than age 2); replace catheter if not draining adequately.
• If the BP is < 150 mm Hg systolic, check for impaction (use 2% lidocaine jelly and wait 2
minutes). Remove stool.
• If BP remains > 150 mm Hg systolic, administer immediate release nifedipine 10 mg
(bite and swallow), nitroglycerin ointment 2% 1 inch (2.5 cm) above the LOI, or another
antihypertensive agent.
• If autonomic dysreflexia is still unresolved, check for additional causes (eg, pressure
ulcer, ingrown toenail).
After the episode of autonomic dysreflexia, document the following:
• Monitor BP for at least 2 hours for recurrent hypertension or symptomatic hypotension.
Notify the health care provider as indicated.
• Provide patient teaching for prevention and treatment of complication.
• Make sure all caregivers understand autonomic dysreflexia and that the patient carries
an identification card indicating LOI and emergency information.
Footnote
This information should serve as a general guideline only. Each patient situation presents a
unique set of clinical factors and requires nursing judgment to guide care, which may include
additional or alternative measures and approaches.
Minimizing Alteration in Sexuality and Fertility
• Encourage patient to discuss alternate expression of feelings with partner.
• Advise bowel care and urinary elimination before intercourse.
• Advise women that 90% regain regular menstrual cycles by 1 year. Pregnancy can
occur, and delivery occurs in 40% before 37 weeks gestation. Autonomic dysreflexia
may occur as a complication of delivery.
• Refer patient to a urologist or other health care provider to explore sexuality options.
○ Women with spinal cord injuries experience little sensation during sexual
intercourse, but fertility and ability to bear children are usually not affected.
○ Men with spinal cord injuries may consider implantation of a penile prosthesis or
an assistive device to obtain an erection. Sildenafil (Viagra) has been used to
manage erectile dysfunction in men with SCI. Ejaculation is more common with
lower motor neuron or incomplete injuries; men with injuries at T10 and above
may ejaculate with vibrostimulation.
Reducing Pain
• Assess pain using consistent pain scale. Report changes from baseline or new location
or type of pain.
• Manage neurogenic pain with pharmacological agents as directed.
• Help patient assess the effects of nonpharmacologic treatment such as acupuncture.
Promoting Optimal Function
• Determine short- and long-term functional goals. Expected outcomes should relate to
motor recovery, level of functional independence, social integration, and quality of life.
• Monitor neurologic status, including functional outcomes, periodically throughout the
patient's life span. Functional outcomes may relate to:
○ Respiratory, bowel, bladder, and skin.
○ Bed/wheelchair mobility, transfers, positioning.
○ Standing and ambulation.
○ Independent ADLs, such as eating, grooming, bathing, and dressing.
○ Communication, including speech, computer skills, handwriting, telephone.
○ Transportation, including driving, adapted vehicle use, public transportation.
○ Homemaking, including meal planning and preparation and chores.
• Periodically evaluate the need for an increased level of assistance and equipment as the
patient with an SCI ages.
• Assist the patient in arranging modifications necessary to his home, and in obtaining
financial assistance for modifications to the environment.
• Coordinate continued rehabilitation effort to ensure social support, ongoing
pharmacologic treatment, and monitoring for long-term complications such as
depression, vocational training, and adaptation to home and work environments. Use
Functional Independence Measure or other instrument to set and achieve goals with the
patient in ADLs, transferring, locomotion, and other functional aspects.
• Teach bowel care and urinary elimination procedures to patient and all caregivers to
ensure continuity.
• Teach care of traction and immobilization devices.
• Enlist help of occupational therapist, physical therapist, vocational therapist, recreational
therapist, and other specialists as needed.
• Alert caregivers that autonomic dysreflexia is a complication that may occur up to
several years after SCI involving T6 and above. Teach patient and caregivers preventive
and emergency treatment measures.
• Teach patient and family about the physiology of nerve transmission and how the SCI
has affected normal function, including mobility, sensation, bowel and bladder function.
• Reinforce that rehabilitation is lengthy and involves compliance with therapy to increase
function.
• Explain that spasticity may develop 2 weeks to 3 months after injury and may interfere
with routine care and ADLs.
• Teach patient to protect skin from pressure ulcer development by frequent repositioning
while in bed, weight-shifting and liftoffs every 15 minutes while in a wheelchair, and
avoiding shear forces and friction.
• Teach inspection of skin daily for development of pressure ulcers, using a mirror if
necessary.
• Encourage sexual counseling, if indicated, to promote satisfaction in personal
relationships.
• Teach importance of seat belts.
• Respirations adequate, ABG values within normal limits
• Repositioning hourly, no orthostatic changes
• No evidence of pressure ulcers
• Reflex (or areflexic) voiding without retention
• Bowel evacuation controlled
• No episodes of autonomic dysreflexia
• Verbalizes feeling of control over condition
• Patient and partner exploring sexuality and sexual options
• Reports pain at or lower than 2 to 3 level on a scale of 1 to 10
VERTEBRAL COMPRESSION FRACTURES
Vertebral fractures commonly occur with trauma, but can also be associated with osteoporosis
or cancer.
• The vertebral body is made up of cancellous (soft) and outer cortical (hard) bone. The
fracture creates an area of weakness within the vertebral column.
• This weakness is further stressed and compressed with normal biomechanical stresses
(weight-bearing activities from standing, sitting, and lifting). Over time, the fracture loses
height, compressing the vertebral body.
• The periosteum layer of the bone contains many pain receptors and with weight-bearing
activities that apply pressure on the fractured bone, stimulates the nerve endings,
thereby producing pain.
• Individuals at risk for fracture include:
○ Those with osteoporosisâ€”women over age 50; men over age 70; prolonged use
of steroids.
○ Those with metastatic cancerâ€”breast, lung, renal, prostrate, melanoma,
multiple myeloma.
• Other risk factors include:
○ Smoking.
○ Inactivity.
○ Poor nutrition.
General Considerations
• A vertebral body may fracture without causing debilitating pain.
• Symptoms depend on location, extent of fracture, progression of fracture, and effect on
surrounding structures.
• Most symptomatic fractures result in pain, although the development of instability can
result in sensory changes, loss of reflex, and muscle weakness from canal compromise.
Cervical
• Pain and stiffness in the neck, top of shoulders, and region of the scapula
• Pain with rotation, flexion, and extension
• Paresthesias and numbness of upper extremities
• Weakness of upper extremities
Thoracic/Lumbar
• Middle to lower back pain at site of fracture.
• Pain aggravated with activity and relieved with rest and flexion.
• Progressive kyphosis or postural deformity of the lumbar spine. Progressive thoracic
kyphosis decreases lung capacity and can compromise pulmonary function.
• Point tenderness to palpation on clinical examination.
• Plain X-rays (anterior posterior, AP, and lateral views)â€”evaluate vertebral structure,
height loss, and alignment.
• CT scanâ€”evaluation of extent of fracture and canal involvement.
• MRIâ€”differential diagnosis includes infectious process or metastatic lesion. MRI has
greater sensitivity for soft-tissue abnormalities
• Bone scanâ€”evaluation of microscopic changes within the bone. Identification of
additional metastatic lesions, infectious process, microscopic fractures.
Management
Conservative Treatment
• Orthosis/brace; heat or ice to affected area
• Physical therapy
• Anti-inflammatory drugs
• Analgesics, opioids may be necessary during acute phase.
• Treatment and prevention of osteoporosis
Surgical/Invasive Intervention
• Surgical interventionâ€”spinal instrumentation not considered an option in patients with
advanced osteoporosis.
• Vertebroplastyâ€”injection of methylmethacrylate (bone cement) with barium
(radiopaque) into vertebral body aimed at providing stabilization of vertebral body.
• Kyphoplastyâ€”partial restoration of vertebral height using percutaneous placement of a
balloon into vertebral body, inflation of the balloon with radiopaque solution (creates a
cavity), and deflation and removal of the balloon followed by insertion of
methylmethacrylate (bone cement) with barium (radiopaque). May be done under
moderate sedation or general aanesthesia.
Complications
• Pulmonary embolus due to leakage of cement into venous system following
vertebroplasty or kyphoplasty.
• Spinal cord or nerve root compromise due to leakage of cement following vertebroplasty
or kyphoplasty.
• Muscular spasms related to preprocedure deconditioning and postprocedure change in
posture.
Nursing Assessment
• Perform repeated assessments of motor function and sensation.
• Assess for localized tenderness.
• Assess pain level on scale of 1 to 10.
Nursing Diagnoses
• Acute Pain related to area of compression
• Impaired Physical Mobility related to pain
• Deficient Knowledge regarding vertebroplasty or kyphoplasty
• Readiness for Enhanced Knowledge of postoperative regimen
Minimizing Pain
• Administer or teach self-administration of analgesics as prescribed; inform patient about
potential adverse effects (sedation, constipation, GI upset).
• Administer or teach self-administration of anti-inflammatory drugs as prescribed; advise
taking with food or antacid to prevent GI upset.
• Teach self-administration of muscle relaxants as prescribed; inform patient about
potential adverse effects of sedation.
• Instruct proper application and use of orthosis, if ordered.
• Apply moist ice or heat to affected area of back, per patient-defined relief of pain.
• Inspect skin several times a day, especially under stabilization devices, for redness and
evidence of pressure sore development. Pressure ulcers can cause severe pain.
Maintaining Mobility
• Proper fit and use of lumbar orthosis. Orthosis is not required after vertebroplasty or
kyphoplasty.
• Encourage compliance with physical therapy treatments, as ordered.
Preparing the Patient for Vertebroplasty or Kyphoplasty
• Educate patient about invasive procedure.
○ One to two small punctures with a large bore needle will be made at site of
vertebral body to be treated. Level will be verified using fluoroscopy before
insertion of bone cement.
○ Routine postprocedure care will include assessment of vital signs and neurologic
function, pain control, and ambulation, as ordered.
• Document baseline neurologic assessment to compare with postprocedure
assessments.
Facilitating Recovery Postoperatively
• Monitor vital signs and assess movement and sensation of extremities. Report any new
deficit. CT of spine may be ordered if encroachment on spinal cord or nerve root is
suspected.
• Assess respiratory status and report any breathing difficulties. Chest X-ray or helical CT
may be ordered if pulmonary embolus is suspected.
• Administer analgesics and NSAIDs to control pain from incision and muscular
inflammation due to procedure.
• Enforce bed rest for 2 to 3 hours; patient may turn side to side, as directed; gradually
increase activity as tolerated.
• Position for comfort. May apply heat or ice to affected muscles is spasm occurs.
• Provide meal tray when requested.
• Report any increasing pain, weakness, or breathing difficulties.
• Administer muscle relaxants as needed for spasms.
• Advise patient of 10- to 25-lb lifting restriction for 1 week as ordered and to avoid
strenuous activities; level of activity may be increased gradually as status indicates.
• Demonstrate proper body mechanics to be used for bending, reaching, lifting in all
activities.
• Alternate ice and heat for 20-minute intervals five to six times per day as needed.
• No soaking baths for one week.
• Encourage patient to do stretching and strengthening exercises for back and aerobic
exercise for endurance on a daily basis.
• Physical therapy may be indicated for reconditioning, heat therapy, and massage.
• Instruct the patient to report any changes in neurologic function or recurrence of pain.
• Maintains mobility with active lifestyle
• Verbalizes understanding of procedure
• Vital signs stable, respirations unlabored, out of bed without difficulty
PERIPHERAL NERVE INJURY
Peripheral nerve injury (PNI) is an injury to nerves in the upper extremity (eg, radial, ulnar,
median) or lower extremity (eg, peroneal, sciatic, femoral, tibial). PNI may include damage to
major nerves, the nerve root, plexus (eg, brachial or lumbar), and other peripheral sites.
• The incidence of PNI is approximately 2% to 3% in populations with multiple injuries.
Males have higher incidence than females.
• PNI damage may occur by congenital, traumatic, chemical, pathological, thermal, or
mechanical means. Focal trauma is the most common of all PNI. Injuries can be direct
(eg, gunshot) or indirect (eg, casting).
• The most frequently injured site is the upper extremity, specifically the upper arm.
Childhood PNIs occur predominantly in the lower extremities.
• Injury to the nerve causes impairment in axonal function and possibly disruption of
myelination. Approximately 50% of motor nerves and 75% of cutaneous nerves are
myelinated. Schwann cells contain multiple axons. Myelinated axons enhance
conduction between nodes, accelerating transmission compared to nonmyelinated
axons. Fibers are classified according to diameter, conduction speed, myelination, and
target.
• The cascade of PNI includes:
○ Cell body expands with increased RNA (peaks day 20).
○ The PN closest to the cell body sustains the greatest neuronal damage.
○ Axons develop â€œsproutsâ€ for regeneration within 24 hours after injury.
○ Axons regenerate between 1 to 4 mm/day along neural tube.
○ Distal to the PNI site, Schwann cells and macrophages digest the damaged
neural tube.
○ Proliferating cells (â€œBands of Bungnerâ€) form a column.
○ Neurotrophins (eg, nerve growth factor), produced by the Schwann cells,
stimulate neurons to attach to sprouting axons.
○ After denervation, collagen biosynthesis increases dramatically.
• Sensory regeneration, as opposed to motor regeneration, may take years following a
PNI.
• Nerve injuries are classified according to the Sunderland system, which establishes
grades of nerve function on which to base recovery and need for surgery.
○ 1st degree PNI (neurapraxia)â€”There is a conduction impairment but the
anatomy is intact. Complete recovery is anticipated in 3 months.
○ 2nd degree PNI (axonotmesis)â€”Wallerian degeneration occurs distal to the PNI
site and axons disintegrate. Complete recovery is anticipated.
○ 3rd degree PNIâ€”Scarring occurs in the endoneural tube. Axons recover 1 inch
(2.5 cm) per month. Incomplete recovery is anticipated.
○ 4th degree PNIâ€”(eg, crush injury). Axonal regeneration is blocked by scar
tissue. Surgical repair is typically required.
○ 5th degree PNIâ€”(eg, penetrating trauma). The PN is severed. Surgical
intervention is required.
• Compression neuropathy depends on the amount and extent of compression force.
Edema, connective tissue thickening, and segmental demyelization of large fibers occur.
• Useful function can be achieved when up to 75% of axons are damaged.
• Flaccid paralysis
• Absent deep tendon reflexes
• Atonic/hypotonic muscles
• Progressive muscle atrophy
• Fasciculations peak 2 to 3 weeks after injury
• Trophic changes: skin is warm and dry 3 weeks after injury, then becomes cold and
cyanotic with loss of hair, brittle fingernails, and ulceration
• Causalgia (chronic pain syndrome): Neuropathic pain may be crawling, electric, tingling,
or burning (It typically follows the cutaneous sensory nerve distribution of the PNI.)
• Specifics to area affected:
○ Radial nerve injuryâ€”weakness in extension, possible wrist drop, inability to
grasp objects/make a fist, impaired sensation over posterior forearm and dorsum
of the hand
○ Brachial plexusâ€”difficulty in abduction of shoulder, weakness with supination
and flexion of the forearm (upper trunk) or extension of the forearm (middle
trunk), or paralysis and atrophy of small muscles of the hand (lower trunk)
○ Median and ulnar nerve injuriesâ€”sensory (median nerve) and motor (ulnar) loss
of function in the hand (pronation, opposition of thumb, paralysis of finer flexor
muscles)
○ Femoralâ€”weakness of knee and hip extension, atrophy of quadriceps, absence
of knee jerk, loss of sensation of anterior aspect of the thigh
○ Common peronealâ€”footdrop, sensory loss on dorsum of foot, difficulty with
eversion
○ Sciaticâ€”footdrop, pain across gluteus and thigh, loss of knee flexion,
weakness/paralysis of muscles below knee
• Chronic nerve compression may begin with intermittent signs and symptoms; these may
only occur in specific maneuvers such as digital pressure or position. For example,
damage to the brachial plexus, entrapped at the supra/infraclavicular junction, may elicit
symptoms following arm elevation for 1 minute. In carpal tunnel syndrome (compression
of the median nerve), wrist flexion or external pressure applied proximally to the carpal
tunnel may evoke symptoms.
• If multiple crush sites of the same nerve occur, the patient may be symptomatic, but
each independent site would not result in symptoms.
• The electrodiagnostic examination consists of nerve conduction studies (sensory, motor,
mixed) and needle electrode examination.
○ The electrodiagnostic examination tests only large myelinated axons; it does not
assess pain, temperature, or paresthesia.
○ It can confirm PNI occurrence and determine the type of axon, pathophysiology,
severity, location, and injury prognosis.
• Muscle ultrasonography evaluates the extent of muscle involvement and assesses acute
nerve injuries.
• MRI and electrophysiologic studies such as ENG and EMG detect the site and degree of
nerve injury.
• Muscle imaging may detect atrophy and mesenchymal alteration of skeletal muscles.
• Tinel's sign (tapping the axons of the regenerating nerve produces a paresthesia in the
normal distribution of the nerve) reveals the rate of axonal regeneration.
Management
• Microsurgery reapproximates the severed PN endings. The sooner the repair is
performed, the better the chance of recovery. Microsurgical repair can be done with
tension-free coaptation using technology such as carbon dioxide laser welding, fibrin
gluing, and ring coupling. Autogenous nerve grafts are the gold standard.
• Primary nerve repair (neurorrhaphy) may be done within 1 week of injury (eg, open
woundsâ€”except gunshots). Secondary nerve repair is performed after 1 week (eg,
crush injury with soft tissue damage). In partially transected nerves, surgery may be
delayed 2 to 3 months to determine whether regeneration will take place.
○ Nerve graftingâ€”Two neurorrhaphy sites are used. Thin, cutaneous nerve grafts
with large fascicles and minimal connective tissue are optimal. Common donor
sites include the sacral nerve (lateral aspect of the foot), lateral antebrachial
cutaneous nerve (lateral forearm), and the median antebrachial cutaneous nerve
(medial arm and elbow). Small segments of nerve grafts may be placed to create
a bridge to facilitate axonal and Schwann cell growth. Nerve â€œconduits,â€
connectors of nerve sites, may be composed of bone, vein, artery, silicone, or
other material.
○ End-to-side neurorrhaphyâ€”In end-to-side neurorrhaphy, the severed nerve's
distal end is attached to the side of a healthy nerve.
○ Nerve transferâ€”Ideally, the donor nerve fascicles are in close proximity to the
target muscle motor end plate or target sensory nerve. If the patient has multiple
nerve injuries, such as a complete brachial plexus injury, nerve transfer priority is
given to promoting elbow flexion, shoulder abduction, and external rotation,
respectively. Sensory nerve priorities are given to the ulnar thumb and radial
index finger.
• Tissue expansion is used to compensate for tissue deficit.
• Insulin-like growth factor and acidic fibroblast growth factor have enhanced regeneration
when administered systemically or topically, and other factors are being investigated.
• Corticosteroids may be used to decrease edema.
• Occupational therapy may be consulted to splint or cast the patient. Splinting (eg, hands)
or casting may be indicated to reduce tension on the PNI site and facilitate healing. Day
splints are typically functional splints; night splints are positioning splints. Splint material
depends on the amount of resistance to be exerted by the orthosis, the splint size, and
the patient's compensatory movements.
○ Radial nerve splintâ€”Volnar or dorsal cock-up splints are indicated if wrist
extension is impaired.
○ Median nerve splintâ€”A thumb opposition splint preserves the function of the
hand grip.
○ Ulnar nerve splintâ€”This functional and positioning splint prevents â€œclaw
handâ€ deformity and contractures of fingers 4 and 5.
• Flexibility is primarily due to connective tissues stretching as opposed to muscle
contraction. Passive and active ROM exercises are essential to provide stretch and
prevent contractions. Ultrasound diathermy may be used on deep muscles, and topical
heat may be used for superficial muscles, to promote stretching. Progressive resistance
and strengthening, including isometric activities, are used to restore function. Functional
electrical stimulation may also be used.
• Fibrosis, caused by edema, may be minimized by elevating the affected limb. Using
static graduated compression devices (eg, sleeves, gloves, hose) or sequential
compression devices, distal to proximal wrapping, may also minimize edema. Likewise,
massage may reduce edema.
• Desensitization techniques (eg, scheduled exposure to irritating textures, and vibration)
may be used to manage hyperesthesia. Sensory reeducation may be protective
(compensatory). Sensory restoration is progressive, with temperature and pain returning
first, followed by transient light touch and vibration.
• Neuropathic pain may be managed by traditional analgesics, antidepressants (eg,
tricyclic), anticonvulsants (eg, gabapentin), topical and transdermal agents (eg,
Capsaicin), NSAIDs, alpha-adrenergic agonists (eg, Clonidine), calcium channel
blockers (eg, nicardipine), or transcutaneous electrical stimulation.
• Carpal tunnel syndrome management may include activity modification, NSAIDs, serial
steroid injections, B6, diuretics, and a wrist splint for 6 months. Endoscopic surgical
release of the ligament may be an option.
Complications
• Infection, if injury is penetrating and site becomes contaminated
• Compartment syndrome due to edema or positioning
• Muscle atrophy/flaccid paralysis; disuse syndrome
• Sensory deficit
• Contractures
• Chronic pain
• Nerve damage resulting from surgical repair.
Nursing Assessment
• Perform frequent neurovascular checks of the affected extremity (pressure, vibration,
and two-point discrimination sensation; motor function, strength; pulses; temperature;
capillary refill; degree of swelling).
• Assess degree of pain on a scale of 0 to 10.
• Test reflexes of affected extremity.
• Observe for signs of infection if there is an open wound.
• Assess for concomitant injuries such as head or skeletal trauma.
Nursing Diagnoses
• Risk for Peripheral Neurovascular Dysfunction
• Chronic Pain related to injury
• Risk for Infection secondary to tissue disruption, surgery
Protecting Neurovascular Function
• Administer corticosteroids and diuretics as ordered to decrease swelling and
development of compartment syndrome.
• Keep extremity elevated to promote venous drainage.
• Perform neurovascular check to evaluate status of injury.
○ Incorporate Tinel's sign into assessment.
○ Report any changes in condition.
• Postoperatively assist rehabilitation team in reeducating nerves and muscles to achieve
function.
• Observe for paresthesias, pain, or altered skin integrity in areas of splinting and casting.
Promoting Comfort
• Administer and teach self-administration of analgesics as ordered.
• Elevate extremity.
• Avoid exposing denervated areas to temperature extremes.
• Apply such devices as splints and slings as ordered.
• Maintain mobility with ROM exercises. Perform gently, following administration of
analgesics.
Preventing Infection
• Assess wound and dressing frequently for erythema, warmth, swelling, odor, and
drainage.
• Monitor temperature with vital signs for hyperthermia and tachycardia indicating
infection.
• Encourage deep-breathing exercises and ambulation to prevent pulmonary
complications.
• Teach management of wound and dressing, and management of casts or splints.
• Review analgesia schedule and need for elevation of injured area.
• Teach exercises for involved area.
• Suggest assistive devices to promote independence.
• Stress the importance of complying with long-term rehabilitation, physical therapy, and
follow-up evaluations.
• Support a community accident prevention program including seat belts, industrial
regulations, and sports and recreational safety measures.
• Stable neurovascular status; functional use of extremity.
• Patient reports adequate relief of pain.
• Wound/surgical site is free of erythema, drainage, odor.
CENTRAL NERVOUS SYSTEM TUMORS
BRAIN TUMORS
Intracranial neoplasms are the result of abnormal proliferation of cells within the CNS. A tumor
is a mass of cancerous cells within the brain. It is believed that there is also a 2 to 3 cm
surrounding area of cancer cells with the potential to develop into a tumor. Tumors require blood
to grow and recruit a vascular supply to support the metabolic needs of the tumor. Intracranial
tumors are primary or metastatic tumors, and malignancy depends on cell type and location.
Primary tumors include tumors of the brain itself, the skull or meninges, the pituitary gland, and
the blood vessels. Metastatic tumors spread the primary site of cancer (breast, lung, prostate,
kidney) through the vascular supply and lymphatic systems. Defining primary cancer cell type
determines the treatment modality and influences the overall prognosis.
Primary CNS tumor etiology remains unknown. Glioma research has identified a genetic
mutation of p53 on chromosome 17 that is believed to be responsible for the state of cellular
overgrowth and mutation of p53 occurs in 50% of all cancers. Environmental agents, genetic
mutation, and growth factors continue to be researched as well as attempting to identify a tumor
marker. Primary CNS tumors rarely metastasize outside the CNS.
• May originate in the CNS or metastasize from tumors elsewhere in the body.
• May be benign or malignant; all tumors produce effects of space-occupying lesion
(edema, increased ICP). Malignancy may be related not only to cell type and
invasiveness, but also to location and operative accessibility (ie, the tumor is located in
an area of the brain that will not tolerate compression of the brain structures, or is not
surgically accessible). The World Health Organization grading scale is currently used to
classify gliomas, although other grading scales are available. The grading system
evaluates the probability of tumor recurrence and malignancy from low (Grades I to II) to
high (Grades III to IV).
• May arise from any tissue of the CNS.
• Common tumor types:
○ Gliomasâ€”tumors of the neuroepithelial/glial cells (supportive tissue of the brain;
account for 40% to 50% of intracranial neoplasms):
 Astrocytomaâ€”overgrowth of the astrocyte cells (connective tissue) of
the brain. Tumors are graded on a scale from I to IV that defines growth
pattern, invasiveness, infiltration, cell differentiation, margination, and
necrosis. Grade I (polycystic astrocytoma)â€”slow-growing tumor with
well-defined cells and minimal infiltration; Grade II (astrocytoma)â€”some
atypical cells with higher rate of recurrence and risk of advancing to
Grade III or IV with recurrence; glioblastomaâ€”a Grade III (anaplastic
astrocytoma) that is highly invasive and infiltrative, with poorly marginated
cells and a rapid growth pattern and risk of advancing to Grade IV with
recurrence; Grade IV (glioblastoma multiforme)â€”a malignant tumor that
is highly invasive, infiltrative, and poorly marginated with necrosis and a
very rapid growth pattern (accounts for 55% of gliomas).
 Oligodendrogliomasâ€”overgrowth of oligodendroglial cells with
calcification. Begins as a less invasive tumor but demonstrates
malignancy as it progresses. The frontal and temporal lobes of the
cerebrum are common locations. Rare in children.
 Ependymoma (5% to 6% of intracranial gliomas)â€”overgrowth of the
ependymal cells of the brain. Slow growing; commonly occurs in the floor
of the 4th ventricle; presents with signs and symptoms of increased ICP
and hydrocephalus; 69% of cases occur in children.
 Mixed gliomasâ€”two or more cell types within a tumor.
 Medulloblastomaâ€”most common pediatric malignant tumor. Commonly
located in the 4th ventricle/cerebellar vermis; rapid growth pattern, highly
invasive; high risk for metastasis within CSF.
 Hemangioblastomaâ€”rare, benign tumor commonly located in the
posterior fossa. von Hippel-Lindau disease is multiple hemangiomas
within CNS.
 Colloid cystâ€”a rare cyst that contains neuroepithelial cells; occurs in the
3rd ventricle.
○ Tumors of the meningesâ€”arise from linings of the brain. Can involve the skull;
accounts for 20% of primary brain tumors (90% are benign; 10% are atypical or
anaplastic). Higher incidence in females ages 40 to 70. Rare in children. Tumor
types include Grade I meningiomas (benign, slow-growing, encapsulated lesions
without brain tissue infiltrationâ€”but may have a dural tail); Grade II (atypical
meningiomas), rapid-growing tumors with increased miotic activity and higher risk
of recurrence after resection (with risk of advancing to anaplastic tumor); and
Grade III (anaplastic meningioma), which has malignant features and invasion of
brain tissue.
○ Peripheral nerve tumorsâ€”generally benign tumors that occur secondary to
nerve sheath overgrowth. These tumors include: acoustic neuroma/schwannoma
(located on the 8th cranial nerve); neurofibromatosis type 1 (von
Reclinghausen's) and neurofibromatosis 2.
○ Pituitary tumorsâ€”include pituitary adenoma, which occurs primarily in the
anterior of the pituitary and can be a secreting (prolactin, which causes
amenorrhea/galactorhhea in women, impotence in men, and infertility in both
genders; adrenocorticotrophic hormone, which causes Cushing's syndrome; or
growth hormone, which causes acromegaly) or nonsecreting tumor; or
craniopharyngioma (considered a developmental tumorâ€”a benign cystic lesion
with calcification, occurring in the anterior pituitary margin. (Fifty percent occur in
children.)
○ Germ cell tumors and tumorlike cystsâ€”include dermoid cysts, which occur in
the ectodermal layer and contain hair and sebaceous glands; epidermoid cysts
containing cell debris and keratin; pineal tumor, overgrowth of germ cells, pineal
cells, or mixed germ types (includes teratomas) within the pineal region (more
common in children and males); and cordoma, a rare neoplasm that contains
embryonic remnant occurring along the neuro-axis.
○ Hematopoietic tumorsâ€”include primay malignant lymphoma (rare, diffusely

infiltrating tumor of the brain, occurs in adults, high rate of recurrence), and
secondary lymphoma associated with AIDS.
○ Secondary CNS tumors/metastatic lesionsâ€”commonly from lung cancer (40%
to 50%), breast cancer (14% to 20%), melanoma (10%), renal (5%), and
undetermined primary sites (10% to 15%). Single lesions common with lung and
breast cancer, can have multiple lesions that are unresectable. Indicate systemic
spread of primary cancer. Metastatic lesions account for 30% of all brain tumors.
Manifestations depend on the location and biologic nature of the tumor. If the tumor is in a
noneloquent area of the brain or is slow-growing, specific symptoms may not develop until the
late stages of the process. Instead, the tumor may produce generalized symptoms related to the
increasing size of the tumor and the expanding area of cerebral edema surrounding the margins
of the tumor. This is referred to as the â€œmassâ€ effect of the tumor.
• Generalized symptoms (due to increased ICP)â€”headache (especially in the morning),
vomiting, papilledema, malaise, altered cognition and consciousness.
• Focal neurologic deficits (related to region of tumor):
○ Parietal areaâ€”sensory alterations, speech and memory disturbances, neglect,
visuospatial deficits, right-left confusion, depression
○ Frontal lobeâ€”personality, behavior, and memory changes; contralateral motor
weakness; Broca's aphasia
○ Temporal areaâ€”memory disturbances, auditory hallucinations, Wernicke's
aphasia, complex partial seizures, visual field deficits
○ Occipital areaâ€”visual agnosia and visual field deficits
○ Cerebellar areaâ€”coordination, gait, and balance disturbances, dysarthria
○ Brain stemâ€”dysphagia, incontinence, cardiovascular instability, respiratory
depression, coma, cranial nerve dysfunction
○ Hypothalamusâ€”loss of temperature control, diabetes insipidus, SIADH
○ Pituitary/sella turcicaâ€”visual field deficits, amenorrhea, galactorrhea,
impotence, cushingoid symptoms, elevated growth hormone, panhypopituitarism
• Referred symptoms (related to the vasogenic [extracellular] edema of the tumor
presence)â€”usually present symptoms of ischemia of region distal to the actual lesion.
• Seizures.
• Skull radiographsâ€”to determine bone involvement, identify pineal shift, helpful in
children
• CT scanâ€”with and without contrast to visualize tumor, hemorrhage, shift of midline,
cerebral edema
• EEGâ€”to detect locus of irritability
• Lumbar puncture for elevated CSF protein, cytology; risk of herniation if increased ICP
• Angiogramâ€”to detect and evaluate the vascular supply of the tumor
• MRIâ€”to visualize tumor; more useful than CT in posterior fossa evaluation
• MR spectroscopyâ€”evaluates the neurochemicals located within a core segment of the
lesion; useful in differentiating tumors from infectious lesions
• Functional MRIâ€”evaluates the functional eloquence of the brain tissue affected by the
tumor, and the tissue at risk, for mass effect
• Stereotactic biopsy/surgeryâ€”needed for definitive diagnosis, cell type
Management
Effectiveness of treatment depends on tumor type and location, capsulation, or infiltrative status.
Tumors in vital areas, such as the brain stem, or nonencapsulated and infiltrating tumors, may
not be surgically accessible, and treatment may produce severe neurologic deficits (blindness,
paralysis, mental impairment). Treatment is usually multimodal.
• Surgeryâ€”removal/debulking by way of craniotomy, laser resection, or ultrasonic
aspiration.
○ Craniotomy is the treatment of choice for most tumors; total resection performed
on only 10% to 15% of gliomas; 10% are inoperable.
○ Awake craniotomyâ€”allows intraoperative brain mapping.
○ Image guiding surgeryâ€”computer-generated intraoperative localization of
lesion.
○ Laser resection or ultrasonic aspirationâ€”may augment surgical resection.
○ Endovascular treatmentâ€”embolization of the arterial feeders to the tumor.
Useful preoperatively to reduce surgical risk related to blood loss.
• Radiation therapyâ€”external radiation to tumor bed with 2 to 3 cm border.
○ Conventional therapy daily for 6 weeks; shorter to brain stem.
○ Prophylactic radiation to brain stem for other brain tumors with high risk of
metastasis.
○ Brachytherapyâ€”can use radioisotopes implanted through interstitial catheters to
permit high doses for high-grade malignant tumors.
• Radiosurgeryâ€”stereotactic radiosurgery by way of linear accelerator scalpel or gamma
knife delivers a single, high dose of radiation to a precisely targeted tumor area.
Destroys only targeted abnormal tissue, limiting damage to surrounding brain tissue.
• Chemotherapy (limited agents cross blood-brain barrier)
○ Metastatic tumorsâ€”single or combination drug therapy; may require autologous
bone marrow transplantation (aspirated before chemotherapy and reinfused
afterward to treat bone marrow depression).
○ Primary gliomaâ€”may be used as adjunct to surgery and radiation; this and
other current treatments are palliative rather than curative.
• Shunting procedureâ€”to manage hydrocephalus, which may be obstructive or
nonobstructive depending on location, tumor type, degree of necrosis, and associated
edema and inflammation.
• Supportive therapy and medications.
○ AED therapy.
○ Dexamethasone (Decadron) to reduce swelling and reduce radiation edema; also
given during end stage to enhance quality of life.
• Investigational therapiesâ€”many investigational studies in progress, including:
○ Photodynamic therapyâ€”red light-emitting diodes (LEDs) combined with light-
activated drug porfimer sodium (Photofrin). LED is placed in tumor bed during
surgical resection and the porfimer sodium is given I.V. The two combine to
promote destruction of the tumor.
○ BCNU Wafersâ€”implantable chemotherapy wafers surgically placed into the
tumor bed.
Complications
• Increased ICP and brain herniation; death
• Neurologic deficits from expanding tumor or treatment
Nursing Assessment
• Assess vital signs and signs of increased ICP (see page 479).
• Assess cranial nerve function, LOC, mental status, affect, and behavior.
• Monitor for seizures.
• Assess level of pain using visual analogue scale (0 to 10) or face scale as indicated.
• Assess level of anxiety.
• Assess patient and family patterns of coping, support systems, and resources.
Nursing Diagnoses
• Acute Pain related to brain mass, surgical intervention
• Risk for Injury related to altered LOC, possible seizures, IICP, and sensory and motor
deficits
• Anxiety related to diagnosis, surgery, radiation, and/or chemotherapy
• Imbalanced Nutrition: Less Than Body Requirements related to compromised neurologic
function and stress of injury
• Disabled Family Coping related to changes in roles and structure
Relieving Pain
• Provide analgesics around the clock at regular intervals that will not mask neurologic
changes.
• Maintain the head of the bed at 15 to 30 degrees to reduce cerebral venous congestion.
• Provide a darkened room or sunglasses if the patient is photophobic.
• Maintain a quiet environment to increase patient's pain tolerance.
• Provide scheduled rest periods to help patient recuperate from stress of pain.
• Instruct the patient to lie with the operative side up.
• Alter diet as tolerated if patient has pain on chewing.
• Collaborate with patient on alternative ways to reduce pain such as use of music
therapy.
Preventing Injury
• Report any signs of increased ICP or worsening neurologic condition to health care
provider immediately.
• Adjust care to reduce risk of increased ICP; body positioning without flexion of head,
reduce hip flexion, distribute care throughout the 24-hour period to allow ICP to return to
baseline.
• Monitor laboratory data, CSF cultures and Gram stains, and communicate results to
medical staff.
• Monitor intake and output, osmolality studies, and electrolytes; prevent overhydration,
which can worsen cerebral edema.
• Monitor response to pharmacologic therapy including drug levels.
• Initiate seizure precautions; pad the side rails of the bed to prevent injury if seizures
occur; have suction equipment available.
• Maintain availability of medications for management of status epilepticus (see page
545).
• Initiate fall precautions; side rails up at all times, call light within reach at bedside, assist
with toileting on a regular basis.
• Gradually progress patient to ambulation with assistance as tolerated, enlist help from
physical therapist, occupational therapist early as indicated to prevent falls.
• If the patient is dysphagic or unconscious, initiate aspiration precautions: elevate head of
the bed 30 degrees and position patient's head to the side to prevent aspiration.
• If dysphagic, position the patient upright and instruct in sequenced swallowing to
maintain feeding function (see page 494).
• Maintain oxygen and suction at the bedside in case of aspiration.
• For the patient with visual field deficits, place materials in visual field.
• Provide appropriate care and teaching for patient receiving chemotherapy (see page
140).
• Provide appropriate care and teaching for the patient receiving radiation (see page 152).
• Provide routine postoperative care for the patient undergoing craniotomy (see page
484).
Minimizing Anxiety
• Provide a safe environment in which the patient may verbalize anxieties.
• Help patient to express feelings related to fear and anxiety.
• Answer questions and provide written information.
• Include the patient/family in all treatment options and scheduling.
• Introduce stress management techniques.
• Provide consistency in care, and continually provide emotional support.
• Assess the patient's usual coping behaviors, and provide support in these areas.
• Consult with social worker for community resources.
Optimizing Nutrition
• Medicate for nausea before position changes, radiation, or chemotherapy, and as
needed.
• Maintain adequate hydration within guidelines for cerebral edema.
• Offer small, frequent meals as tolerated.
• Consult with dietitian to evaluate food choices and provide adequate caloric needs
through enteral or parenteral nourishment if unable to take oral nutrition.
• Alter consistency of diet as necessary to enhance intake.
• Recognize stages of grief.
• Foster a trusting relationship.
• Provide clear, consistent explanations of procedures and treatments.
• Encourage family involvement in care from the beginning.
• Establish a means of communication for family with patient when verbal responses are
not possible.
• Consult with social worker and mental health provider when family needs assistance in
adjusting to neurologic deficits.
• Assist family to use stress management techniques and community resources such as
respite care.
• Encourage discussion with health care provider about prognosis and functional outcome.
• Explain the adverse effects of treatment.
• Encourage close follow-up after diagnosis and treatment.
• Explain the importance of continuing corticosteroids and how to manage adverse effects,
such as weight gain and hyperglycemia.
• Encourage the use of community resources for physical and psychological support, such
as transportation to medical appointments, financial assistance, and respite care.
• Refer the patient/family for more information and support to such agencies as the
National Institute of Neurologic Disorders and Stroke, http://www.ninds.nih.gov, and the
National Brain Tumor Foundation, http://www.braintumor.org.
• Reports satisfactory comfort level
• No new neurologic deficits, seizures, falls, or other injuries
• Expresses decreased anxiety
• Nutritional intake meeting metabolic demands
• Patient and family verbalize understanding of treatment and available resources
TUMORS OF THE SPINAL CORD AND CANAL
Tumors of the spinal cord and canal may be extradural (existing outside the dural membranes),
including chordoma and osteoblastoma; intradural-extramedullary (within the SAS), including
meningiomas, neurofibromas, and schwannomas; or intramedullary (within the spinal cord),
including astrocytomas, ependymomas, and neurofibromatosis â€œdumbbell tumors.â€
Vascular tumors can affect any part of the spinal cord or canal.
• Astrocytomas, characterized by asymmetrical expansion in the spinal cord, are more
common in children than adults. Ependymomas, usually with a cyst, are the most
common intramedullary tumor in the adult, but are rare in children. These tumors are
central in the spinal cord.
• Vascular tumors can affect the spinal cord in various ways. Hemangioblastomas often
cause edema and syrinx formation. Cavernomas are located on the dorsal surface of the
spinal cord.
• Approximately 85% of all patients with cancer develop bony metastasis, with the spinal
column as the primary site. Spinal cord compression due to cancer typically presents
with incomplete paraplegia involving the thoracic spine.
• Cause for abnormal cell growth is unknown.
• Extradural tumors spread to the vertebral bodies.
• Spinal cord and/or nerve compression results.
Depends on location and type of tumor and extent of spinal cord compression.
• Back pain that is localized or radiates; may be absent in more than 50% of patients
• Weakness of extremity with abnormal reflexes
• Sensory changes
• Bladder, bowel, or sexual dysfunction
• A plain X-ray or CT scan can detect a pathologic fracture, collapse, or destruction
resulting from a mass.
• MRI is sensitive to tumor detection.
• CT myelography with lumbar puncture is sensitive to tumor detection but may be
uncomfortable and result in complications from lumbar puncture.
Management
• Two surgical approaches may be used to manage spinal cord tumors:
○ Anterior decompression is typically indicated because most spinal cord tumors
are anterior.
○ The posterolateral approach may be used for excision of thoracic tumors.
Endoscopy, or other surgical techniques using instrumentation, can be used to
visualize the anterior part of the cord. In thoracic tumors above T5, posterolateral
decompression negates the need for an anterior thoracotomy or sternotomy.
• Intraoperative somatosensory-evoked potentials and motor-evoked potentials can be
used to â€œmapâ€ the optimal spinal cord site for incision and identify sensory and
motor tracts within the spinal cord. This mapping reduces the neurologic deficits that are
frequently associated with tumor incisions.
• Various techniques are used to remove spinal cord tumors, including the following:
○ Intramedullary tumors are totally resected. Corticosteroids are administered
before and after surgery. MRI verifies tumor characteristics preoperatively (eg,
exact level). Microsurgical laser techniques, ultrasound, and X-rays may be used
intraoperatively. In surgery, every effort must be made to keep the anterior spinal
artery intact.
○ Vascular tumors may be managed in different ways. Hemangioblastomas are
usually removed from the outside inward by exterior coagulation and progressive
tumor shrinkage before removal. Cavernomas are usually removed by exterior
coagulation and progressive tumor shrinkage before removal, but from the inside
outward.
○ Neoplastic tumors may be treated with radiation or surgically excised using an
anterior approach because these tumors typically cause anterior cord
compression.
• Radiation therapy may be used over 2 to 4 weeks; dosing protocols vary. Spinal
radiation before surgical decompression may adversely affect wound healing. In patients
who have a good functional status, radiotherapy to a malignant spinal cord tumor can
significantly improve survival time.
• Corticosteroids, such as dexamethasone and prednisone in moderate to high doses, are
indicated for use before radiation therapy to improve the ambulation rate in the paretic
patient.
○ Corticosteroids are not typically used in nonparetic ambulatory patients.
○ They are tapered over 2 weeks before discontinuing.
• When compared to patients with traumatic SCI, the rehabilitation of patients with spinal
cord tumors is shorter; however, cancer patients have more limited functional
improvement than SCI patients.
Complications
• Spinal cord infarction secondary to compression
• Nerve or spinal compression from tumor expansion
• Tetraplegia or paraplegia due to spinal cord compression
Nursing Assessment
• Perform motor and sensory components of the neurologic examination.
• Assess pain using scale of 0 to 10 as indicated.
• Assess autonomic nervous system relative to level of lesionâ€”pupillary responses, vital
signs, bowel, and bladder function.
• Assess for spinal or nerve compressionâ€”progressive increase in pain, paralysis or
paresis, sensory loss, loss of rectal sphincter tone, and sexual dysfunction.
Nursing Diagnoses
• Anxiety related to surgery and outcome
• Pain related to nerve compression
• Disturbed Sensory Perception (tactile, kinesthetic) related to nerve compression
• Impaired Urinary Elimination related to spinal cord compression
• Risk for Injury related to surgery
Relieving Anxiety
• Provide a safe environment for patient to verbalize anxieties.
• Provide explanations regarding all procedures. Answer questions or refer patient to
someone who can answer questions.
• Refer to cancer and SCI support groups as needed.
• Provide the patient/family with written information regarding disease process and
medical interventions.
• Reduce environmental stimulation.
• Promote periods of rest to enhance coping skills.
• Involve the family in distraction techniques.
• Provide options in care when possible.
Relieving Pain
• Administer analgesics as indicated and evaluate for pain control.
• Instruct the patient in the use of patient control analgesia, if available.
• Instruct the patient in relaxation techniques, such as deep breathing, distraction,
imagery.
• Position patient off surgical site postoperatively.
Compensating for Sensory Alterations
• Reassure patient that degree of sensory/motor impairment may decrease during the
postoperative recovery period as the amount of surgical edema decreases.
• Instruct the patient with sensory loss to visually scan the extremity during use to avoid
injury related to lack of tactile input.
• Instruct the patient with painful paresthesias in appropriate use of ice, exercise, and rest.
• Assess the patient with sensory and motor alterations, and refer to physical therapy for
assistance with ADLs, ambulation.
Achieving Urinary Continence
• Assess the urinary elimination pattern of the patient.
• Instruct the patient in the therapeutic intake of fluid volume and relationship to
elimination.
• Instruct the patient in an appropriate means of urinary elimination and bowel
management (see page 532).
Providing Additional Postoperative Care
• Provide routine postoperative care to prevent complications.
• Monitor surgical site for bleeding, CSF drainage, signs of infection.
• Keep surgical dressing clean and dry.
• Clean surgical site as ordered.
• Pad the bed rails and chair if the patient experiences numbness or paresthesias, to
prevent injury.
• Support the weak/paralytic extremity in a functional position.
• Encourage the patient with motor impairment to use adaptive devices.
• Demonstrate proper positioning and transfer techniques.
• Instruct the patient with sensory losses about dangers of extreme temperatures and the
need for adequate foot protection at all times.
• If the patient has suspected or confirmed neurofibromatosis, suggest referral to genetic
counselor. Also, encourage follow-up for MRI every 12 months to monitor disease
progression.
• Refer to cancer and SCI support groups as needed.
• Asks questions and discusses care options
• Reports that pain is relieved
• Reports decreased paresthesias; ambulatory postoperatively
• Voids at intervals without residual urine
• Incision healing, skin intact
OTHER DISORDERS
SEIZURE DISORDERS
Seizures (also known as epileptic seizures and, if recurrent, epilepsy) are defined as a sudden
alteration in normal brain activity that causes distinct changes in behavior and body function.
Seizures are thought to result from disturbances in the cells of the brain that cause cells to give
off abnormal, recurrent, uncontrolled electrical discharges.
Altered Physiology
• The pathophysiology of seizures is unknown. It is known, however, that the brain has
certain metabolic needs for oxygen and glucose. Neurons also have certain permeability
gradients and voltage gradients that are affected by changes in the chemical and
humoral environment.
• Factors that change the permeability of the cell population (ischemia, hemorrhage) and
ion concentration (Na+, K+) can produce neurons that are hyperexcitable and
demonstrate hypersynchrony, producing an abnormal discharge.
• A seizure may manifest itself as an alterred behavior, motor, or sensory function relating
to any anatomical location in the brain.
Classification
Seizures are classified by the origin of the seizure activity and associated clinical
manifestations.
• Simple partial seizures can have motor, somatosensory, psychic, or autonomic
symptoms without impairment of consciousness.
• Complex partial seizures have an impairment (but not a loss) of consciousness with
simple partial features, automatisms, or impairment of consciousness only.
• Generalized seizures have a loss of consciousness with convulsive or nonconvulsive
behaviors.
• Simple partial seizures can progress to complex partial seizures, and complex partial
seizures can secondarily become generalized.
Etiology
The etiology may be unknown or due to one of the following:
• Trauma to head or brain resulting in scar tissue or cerebral atrophy
• Tumors
• Cranial surgery
• Metabolic disorders (hypocalcemia, hypoglycemia/hyperglycemia, hyponatremia, anoxia)
• Drug toxicity, such as theophylline (Theo-Dur), lidocaine (Xylocaine), penicillin
• CNS infection
• Circulatory disorders
• Drug withdrawal states (alcohol, barbiturates)
• Congenital neurodegenerative disorders
• Nonepileptogenic behaviors can emulate seizures but have a psychogenic rather than
an organic origin.
Manifestations are related to the area of the brain involved in the seizure activity and may range
from single abnormal sensations, aberrant motor activity, altered consciousness or personality
to loss of consciousness and convulsive movements.
• Impaired consciousness
• Disturbed muscle tone or movement
• Disturbances of behavior, mood, sensation, or perception
• Disturbances of autonomic functions
• EEG with or without video monitoringâ€”locates epileptic focus, spread, intensity, and
duration; helps classify seizure type
• MRI, CT scanâ€”to identify lesion that may be cause of seizure
• SPECT or PET scan or MSIâ€”additional tests to identify seizure foci
• Neuropsychological studiesâ€”to evaluate for behavioral disturbances
Management
• Pharmacotherapyâ€”AED selected according to seizure type (see Table 15-6, pages
546 to 549).
TABLE 15-6 Antiepileptic Drugs
GENERIC/T DOSAGE USUAL HALF USUAL MECHAN INDICATIONS DOSE
RADE NAMEFORMS DOSES LIFE TARGET ISM OF RELATED
RANGE ACTION ADVERSE
EFFECTS
Carbamazep ○ Initial 4-12 Modulate
○ S ○ S Double or
ine 20-50, mcg/mL s sodium blurred
u i
Tegretol then 5- channels vision,
s m
Tegretol-XR 14 lethargy
p p
Carbatrol hours; (reduced by
e l
Epitol induces slow dose
n e
own titration)
s p
metabol
i a
ism
o rt
over
n i
first 2
1 a
weeks
0 l
0 ○ C
m
o
g
m
/
p
5
l
m
e
L
x
○ T p
a a
b rt
l i
e a
t l
2 ○ G
0
e
0
n
m
e
g
r
○ C a
h li
e z
w e
t d
a t
b o
1 n
0 i
0 c
m /
g c
l
○ E
o
x
n
t
i
e
c
n
s
d
e
e
i
d
z
R
u
e
r
l
e
e
s
a
s
e
T
a
b
l
e
t
s
1
0
0
m
g
,
2
0
0
m
g
,
4
0
0
m
g
○ E
x
t
e
n
d
e
d
R
e
l
e
a
s
e
S
p
ri
n
k
l
e
C
a
p
s
u
l
e
s
2
0
0
m
g
,
3
0
0
m
g
Clonazepam ○ T ○ 20-40 20-70 Enhances ○ MDrowsiness
Klonopin hours mcg/mL GABA (50%),
a y
C-IV ataxia
b o
Ceberclon ○ (30%),
l c
behavioral
e l
disturbances
t o
(25%),
s n
movement
0 i
disorders,
. c
slurred
5
○ L speech,
m
g e hypersecreti
, n on
1 n
m o
g x
, -
2 G
m a
g s
t
a
u
t
s
y
n
d
r
o
m
e
○ A
t
o
n
i
c
○ A
b
s
e
n
c
e
Diazepam ○ 30-60 Not Enhances
○ P ○ A Sedation
(rectal) hours applicabl GABA
e c
Diastat C-IV e
d u
○
i t
a e
t ○ r
ri e
c p
r e
e ti
c ti
t v
a e
l s
g e
e i
l z
2 u
. r
5 e
m s
g
,
5
m
g
,
1
0
m
g
○ A
d
u
lt
r
e
c
t
a
l
g
e
l
1
0
m
g
,
1
5
m
g
,
2
0
m
g
Ethosuximid ○ 30-60 40-100 Reduces
○ C ○ A GI distress,
e hours mcg/mL current in drowsiness,
a b
Zarontin the T-type hiccups,
p s
calcium sedation
s e
channels
u n
l c
e e
2
5
0
m
g
○ S
o
l
u
ti
o
n
2
5
0
m
g
/
5
m
L
Felbamate ○ 14-23 30-100 Blocks
○ T ○ L Anorexia,
Felbatol hours mcg/mL glycine weight loss,
a e
binding to vomiting,
b n
the insomnia,
l n
NMDA headache,
e o
receptors, somnolence;
t x
modulate rare cases of
s -
s sodium aplastic
4 G
channel, anemia (25
0 a
enhances cases per
0 s
GABA 100,000)
m t
and liver
g a
failure (8
, u
cases per
6 t
100,000)
0 s
have also
0 y
been seen
m n
g d
r
○ S
o
u
m
s
e
p
e ○ C
n o
s m
i p
o l
n e
6 x
0 p
0 a
m rt
g i
/ a
5 l
m s
L e
i
z
u
r
e
s
Gabapentin ○ C ○ 5-9 4-20 Not
○ P
Somnolence,
Neurontin hours mcg/mL known dizziness,
a a
p rt ataxia,
s i nystagmus,
u a weight gain,
l l nausea,
e s vomiting,
1 e blurred
0 i vision,
0 z tremor,
m u slurred
g r speech,
, e peripheral
3 s edema,
0 wdyspepsia,
0 it hiccups
m h
g o
, r
4 w
0 it
0 h
m o
g u
t
○ T
s
a
e
b
c
l
o
e
n
t
d
s
a
6
r
0
y
0
g
m
e
g
n
,
e
8
r
0
a
0
li
m
z
g
e
○ S d
o t
l o
u n
ti i
o c
n /
2 c
5 l
0 o
m n
g i
/ c
5 s
m e
L i
z
u
r
e
s
Lamotrigine ○ 12-50 3-20 Blocks
○ T ○ S Fatigue,
Lamictal hours mcg/mL sodium drowsiness,
a i
up to 70 channels ataxia,
b m
○ hours and dizziness,
l p
with blocks headache,
e l
VPA release of nausea,
t e
glutamate vomiting,
s p
double or
2 a
blurred
5 rt
vision,
m i
nystagmus
g a
, l
1 s
0 e
0 i
m z
g u
, r
1 e
5 s
0 ○ C
m
o
g
m
,
p
2
l
0
e
0
x
m
p
g
a
○ C rt
h i
e a
w l
t s
a e
b i
l z
e u
t r
s e
2 s
m ○ G
g
e
,
n
5
e
m
r
g
a
,
li
2
z
5
e
m
g d
t
o
n
i
c
/
c
l
o
n
i
c
s
e
i
z
u
r
e
s
○ L
e
n
n
o
x
-
G
a
s
t
a
u
t
s
y
n
d
r
o
m
e
○ A
b
s
e
n
c
e
Levetiraceta ○ Adults 7 5-50 Inhibits
○ T ○ P Somnolence
m hours mcg/mL propagati (14.8%),
a a
Keppra on of asthenia
b rt
seizure (14.7%),
l i
by coordination
e a
unknown difficulties
mechanis
t l (3.4%),
m
s o dizziness,
2 n nervousness
5 s , behavioral
0 e problems,
m t decreased
g s blood counts
, e
5 i
0 z
0 u
m r
g e
, s
7
5
0
m
g
Lorazepam ○ T ○ 10-20 50-240 Enhances ○ S Sedation
Ativan C-IV hrs mcg/mL GABA with risk of
a t
respiratory
b a
depression,
l t
amnesia,
e u
abnormal
t s
behavior,
s e
withdrawal
0 p
reactions
. il
5 e
m p
g ti
, c
1 u
m s
g
,
2
m
g
○ S
o
l
u
ti
o
n
2
m
g
/
m
L
○ I
n
j
e
c
ti
o
n
2
m
g
/
m
L
,
4
m
g
/
m
L
Oxcarbazepi ○ Parent 10-35 Modulate
○ T ○ P Headache,
ne 1-2Â½ mcg/mL s sodium drowsiness,
a a
Trileptal hrs for the channels fatigue,
b rt
○ Metabol monohyd nausea,
l i
ite 8-15 roxy dizziness,
e a
hours derivative hyponatremi
t l
a
s o
(hematologic
1 n
toxicity not
5 s
observed to
0 e
date)
m t
g s
, e
3 i
0 z
0 u
m r
g e
, s
6
0
0
m
g
Phenobarbit ○ 40-140 15-40 Enhances
○ C ○ GSedation,
al Generic hrs mcg/mL GABA mental
a e
C-IV dullness,
p n
Solfoton cognitive
s e
Luminal impairment,
u r
hyperactivity,
l a
ataxia
e li
1 z
6 e
m d
g t
o
○ E
n
li
x i
ir c
1 /
5 c
m l
g o
/ n
5 i
m c
L s
, e
2 i
0 z
m u
g r
/ e
5 s
m ○ S
L
i
○ T m
a p
b l
l e
e p
t a
8 rt
m i
g a
, l
1 s
5 e
m i
g z
, u
1 r
6 e
m s
g ○ C
,
o
3
m
0
p
m
l
g
e
,
x
3
p
2
a
m
rt
g
i
,
a
6
l
0
s
m
e
g
i
,
z
6
u
5
r
m
g e
, s
1
0
0
m
g
○ I
n
j
e
c
ti
o
n
3
0
m
g
/
m
L
,
6
0
m
g
/
m
L
,
6
5
m
g
/
m
L
,
1
3
0
m
g
/
m
L
Phenytoin ○ 5-34 hrs10-20 Modulate
○ I ○ GNystagmus,
Dilantin mcg/mL s sodium ataxia,
n e
Cerebyx total 1-2 channels lethargy,
j n
(fosphenytoin mcg/mL propylene
e e
) free (for glycol in I.V.
c r
patients preparation
ti a
with â†“ can cause
o li
protein myocardial
n z
binding) depression,
5 e
0 d bradycardias
m t , other
g o electrocardio
/ n gram
m i changes,
L c hypotension
( /
F c
o l
s o
p n
h i
e c
n s
y e
t i
o z
i u
n r
i e
s s
5 ○ C
0
o
m
m
g
p
/
l
m
e
L
x
p
p
h
a
e
rt
n
i
y
a
t
l
o
s
i
e
n
i
e
z
q
u
u
r
i
e
v
s
a
l ○ S
e i
n m
t p
) l
○ S e
p
u
a
s
rt
p
i
e
a
n
l
s
s
i
e
o
n i
1 z
2 u
5 r
m e
g s
/
5
m
L
,
3
0
m
g
/
5
m
L
○ C
h
e
w
t
a
b
l
e
t
s
5
0
m
g
○ C
a
p
s
u
l
e
s
3
0
m
g
,
1
0
0
m
g
Primidone ○ 4-20 hrs 5-20 Enhances
○ S ○ GSame as
Mysoline (PEMA mcg/mL GABA phenobarbita
u e
Â½ 30- l
s n
36 hrs)
p e
e r
n a
s li
i z
o e
n d
2 t
5 o
0 n
m i
g c
/ /
5 c
m l
L o
n
○ T
i
a
c
b
s
l
e
e
i
t
z
s
u
5
r
0
e
m
s
g
, ○ S
2 i
5 m
0 p
m l
g e
p
a
rt
i
a
l
s
e
i
z
u
r
e
s
○ C
o
m
p
l
e
x
p
a
rt
i
a
l
s
e
i
z
u
r
e
s
Tiagabine ○ 2-9 5-70 Inhibits
○ T ○ P Sedation,
Gabitril hours mcg/mL neuronal dizziness,
a a
and glial memory
b rt
○ uptake of impairment,
l i
GABA inattention,
e a
emotional
t l
lability,
s o
headache,
2 n
abdominal
m s
pain,
g e
anorexia,
, t
tremor
4 s
m e
g i
, z
1 u
2 r
m e
g s
,
1
6
m
g
,
2
0
m
g
Topiramate ○ 12-30 2-25 Modulate
○ T ○ P Speech and
Topamax hours mcg/mL s sodium language
a a
channels, problems,
b rt
○ enhances difficulty with
l i
GABA concentratio
e a
activity, n and
t l
and attention,
s o
modulate confusion,
2 n
s NMDA fatigue,
5 s
receptor paresthesias
m e
, weight loss
g t
, s
1 e
0 i
0 z
m u
g r
, e
2 s
0 ○ L
0
e
m
n
g
n
○ S o
p x
ri -
n G
k a
l s
e t
c a
a u
p t
s s
u y
l n
e d
s r
1 o
5 m
m e
g ○ G
,
e
2
n
5
e
m
r
g
a
li
z
e
d
t
o
n
i
c
/
c
l
o
n
i
c
○ J
u
v
e
n
il
e
m
y
o
c
l
o
n
i
c
e
p
il
e
p
s
y
Valproic ○ 7-20 50-150 Unknown
○ S ○ GGI upset,
Acid/Divalpr hours mcg/mL (may lethargy,
o e
oex Sodium modulate changes in
l n
Depakene sodium menstrual
u e
Depakote channel, cycle,
ti r
Depakote ER enhance thrombocyto
o a
GABA) penia
n li
2 z
5 e
0 d
m t
g o
/ n
5 i
m c
L /
c
○ C
l
a
o
p
n
s
i
u
c
l
s
e
e
2
i
5
z
0
u
m
r
g
e
○ S s
p ○ A
ri
b
n
s
k
e
l
n
e
c
1
e
2
5 ○ M
m y
g o
c
○ E
l
x
o
t
n
e
i
n
c
d
e ○ P
d a
r rt
e i
l a
e l
a o
s n
e s
5 e
0 t
0 s
m e
g i
z
○ T
u
a r
b e
l s
e
t ○ L
1 e
2 n
5 n
m o
g x
, -
2 G
0 a
0 s
m t
g a
, u
5 t
0 s
0 y
m n
g d
r
o
m
e
Vigabatrin ○ 5-7 Not Inhibits
○ T ○ I Drowsiness,
Sabril hours known GABA- fatigue,
a n
transamin ataxia,
b f
○ ase behavioral
l a
(preventin changes,
e n
g GABA weight gain,
t ti
metabolis psychosis (in
5 l
m) predisposed
0 e patients and
0 s upon abrupt
m p withdrawal),
g a hematologic,
s s visual field
c mproblems
o s
r d
e u
d e
t
o
t
u
b
e
r
o
u
s
s
c
l
e
r
o
s
i
s
Zonisamide ○ 27-60 15-40 Modulate
○ C ○ P Drowsiness,
Zonegran hours mcg/mL s sodium psychosis
a a
and T- (2%)
p rt
○ type
s i
calcium
u a
channels
l l
e o
1 n
0 s
0 e
m t
g s
e
i
z
u
r
e
s
○ G
e
n
e
r
a
li
z
e
d
s
e
i
z
u
r
e
s
○ A
b
s
e
n
c
e
○ M
y
o
c
l
o
n
i
c
○ L
e
n
n
o
x
-
G
a
s
t
a
u
t
○ I
n
f
a
n
ti
l
e
s
p
a
s
m
s
• Biofeedbackâ€”useful in the patient with reliable auras
• Surgeryâ€”resective and palliative operations (temporal lobectomy, extratemporal
resection, corpus callosotomy, hemispherectomy)
• Vagal nerve stimulation
Complications
• Status epilepticus (see Box 15-5).
• Injuries due to falls, especially head injuries
Nursing Assessment
• Obtain seizure history, including prodromal signs and symptoms, seizure behavior,
postictal state, history of status epilepticus.
• Document the following about seizure activity:
○ Circumstances before attack, such as visual, auditory, olfactory, or tactile stimuli;
emotional or psychological disturbances; sleep; hyperventilation
○ Description of movement, including where movement or stiffness started; type of
movement and parts involved; progression of movement; whether beginning of
seizure was witnessed
○ Position of the eyes and head; size of pupils
○ Presence of automatisms, such as lip smacking or repeated swallowing
○ Incontinence of urine or feces
○ Duration of each phase of the attack
○ Presence of unconsciousness and its duration
○ Behavior after attack, including inability to speak, any weakness or paralysis
(Todd's paralysis), sleep
• Investigate the psychosocial effect of seizures.
• Obtain history of drug or alcohol abuse.
• Assess compliance and medication-taking strategies.
DRUG ALERT
Nonadherence to medication regimen as well as toxicity of antiepileptic medications can
increase seizure frequency. Obtain drug levels before implementing medication changes.
Nursing Diagnoses
• Ineffective Tissue Perfusion (cerebral) related to seizure activity
• Risk for Injury related to seizure activity
• Ineffective Coping related to psychosocial and economic consequences of epilepsy
Maintaining Cerebral Tissue Perfusion
• Maintain a patent airway until patient is fully awake after a seizure.
• Provide oxygen during the seizure if color change occurs.
• Stress the importance of taking medications regularly.
• Monitor serum levels for therapeutic range of medications.
• Monitor patient for toxic adverse effects of medications.
• Monitor platelet and liver functions for toxicity due to medications.
BOX 15-5 Emergency Management of Status Epilepticus

Status epilepticus (acute, prolonged, repetitive seizure activity) is a series of generalized
seizures without return to consciousness between attacks. The term has been broadened to
include continuous clinical and/or electrical seizures lasting at least 5 minutes, even without
impairment of consciousness. Status epilepticus is considered a serious neurologic emergency.
It has high mortality and morbidity (permanent brain damage, severe neurologic deficits).
Factors that precipitate status epilepticus in patients with preexisting seizure disorder include
medication withdrawal, fever, metabolic or environmental stresses, alcohol or drug withdrawal,
and sleep deprivation.
NURSING INTERVENTIONS
• Establish airway, and maintain blood pressure (BP).
• Obtain blood studies for glucose, blood urea nitrogen, electrolytes, and anticonvulsant
drug levels to determine metabolic abnormalities and serve as a guide for maintenance
of biochemical homeostasis.
• Administer oxygenâ€”there is some respiratory depression associated with each seizure,
which may produce venous congestion and hypoxia of brain.
• Establish I.V. lines, and keep open for blood sampling, drug administration, and infusion
of fluids.
• Administer I.V. anticonvulsant (lorazepam [Ativan], phenytoin [Dilantin]), diazepam
[Valium]) slowly to ensure effective brain tissue and serum concentrations.
○ Give additional anticonvulsants as directedâ€”effects of lorazepam are of short
duration.
○ Anticonvulsant drug levels monitored regularly.
• Monitor the patient continuously; depression of respiration and BP induced by drug
therapy may be delayed.
• Use mechanical ventilation as needed.
• If initial treatment is unsuccessful, general anesthesia may be required.
• Assist with search for precipitating factors.
○ Monitor vital and neurologic signs on a continuous basis.
○ Use electroencephalographic monitoring to determine nature and abolition (after
diazepam administration) of epileptic activity.
○ Determine (from family member) if there is a history of epilepsy, alcohol/drug
use, trauma, recent infection.
Preventing Injury
• Provide a safe environment by padding side rails and removing clutter.
• Place the bed in a low position.
• Do not restrain the patient during a seizure.
• Do not put anything in the patient's mouth during a seizure.
• Place the patient on side during a seizure to prevent aspiration.
• Protect the patient's head during a seizure. If seizure occurs while ambulating or from
chair, cradle head or provide cushion/support for protection against head injury.
• Stay with the patient who is ambulating or who is in a confused state during seizure.
• Provide a helmet to the patient who falls during seizure.
• Manage the patient in status epilepticus.
Strengthening Coping
• Consult with social worker for community resources for vocational rehabilitation,
counselors, support groups.
• Teach stress reduction techniques that will fit into patient's lifestyle.
• Initiate appropriate consultation for management of behaviors related to personality
disorders, brain damage secondary to chronic epilepsy.
• Answer questions related to use of computerized video EEG monitoring and surgery for
epilepsy management.
• Counsel patients with uncontrolled seizures about driving or operating dangerous
equipment.
• Be familiar with state laws.
• Assess home environment for safety hazards in case the patient falls, such as crowded
furniture arrangement, sharp edges on tables, glass. Soft flooring and furniture and
padded surfaces may be necessary.
• Support patient in discussion about seizures with employer, school, and so forth.
• Encourage the patient to determine existence of trigger factors for seizures (eg, skipped
meals, lack of sleep, emotional stress, menstrual cycle).
• Remind the patient of the importance of following medication regimen.
• Tell the patient to avoid alcohol because it interferes with metabolism of antiepileptic
medications.
• Encourage the patient and family to discuss feelings and attitudes about epilepsy.
• Encourage patient to carry or wear a MedicAlert card or bracelet.
• Encourage a moderate lifestyle that includes exercise, mental activity, and nutritional
diet.
• For the surgical candidate, reinforce instructions related to surgical outcome of the
specific surgical approach (temporal lobectomy, corpus callosotomy, hemispherectomy,
and extratemporal resection).
Epilepsy Foundation of America, http://www.efa.org.
• Takes medication as ordered, drug level within normal range
• No injuries observed
• Reports using support services and stress management techniques
NARCOLEPSY
Narcolepsy is a neurologic disorder characterized by abnormalities of REM sleep, some
abnormalities of non-REM sleep, and excessive daytime sleepiness.
• Recent advances suggest that this common sleep disorder may be a neurodegenerative
or autoimmune disorder resulting in the loss of hypothalamic neurons that contain a
peptide, hypocretin (orexin). Hypocretin plays a central role in the timing of sleep and
wakefulness and inhibits REM sleep. The deficiency in hypocretin contributes to the
abnormalities of sleep and wakefulness in narcolepsy.
• Genetic susceptibilityâ€”associated with class II human leukocyte antigens.
• Although considered a hypersomnia disorder, the person does not experience excessive
amounts of sleep in a 24 hour period. Typically, patients with narcolepsy have a normal
amount of sleep over 24 hours. They have abnormal REM sleep that intrudes into
wakefulness.
• Onset is usually between ages 15 and 25.
• Four classic symptoms (all symptoms not present in all patients):
○ Excessive daytime sleepiness is usually the first symptom
○ Cataplexy (abrupt loss of muscle tone after emotional stimulation such as
laughter, anger)
○ Sleep paralysis (powerless to move limbs, speak, open eyes, or breathe deeply
while fully aware of condition)
○ Hypnagogic hallucinations (drowsiness before sleep, usually visual or auditory)
• Symptoms enhanced by high temperature, indoor activity, and idleness.
• Clinical manifestations may abate, but never phase out completely.
• Patient may complain of inability to focus vision or thought process rather than have a
feeling of sleepiness.
• Nocturnal sleep disturbanceâ€”occurs 2Â½ to 3 hours after falling asleep.
○ After being awake for 45 to 60 minutes, the patient will fall back to sleep for
another 2Â½ to 3 hours and then awaken again.
○ This is believed to be the source of the daytime somnolence.
• An overnight polysomnogram in a sleep disorders lab is included in the evaluation to
assess nighttime sleepâ€”indicates the underlying cause for the complaint of sleepiness.
The polysomnogram helps evaluate sleep quality and excludes other disorders, such as
sleep apnea.
• The polysomnogram is followed the next day by an MSLT to assess daytime
sleepinessâ€”indicates severity of the problem. Patients are given four or five
opportunities to nap every 2 hours. Patients with narcolepsy typically fall asleep more
rapidly than the norm of 10 to 15 minutes.
Management
• Long-term treatment is required. Mutual goal-setting is imperative because not everyone
derives benefit from treatment. Even with medication, patients may never attain normal
levels of alertness.
• Nonpharmacologic therapy includes support groups, short naps (10 to 20 minutes, three
times daily), caffeinated beverages, exercise, and avoidance of heavy meals.
• Stimulants prescribed may include pemoline (Cylert), methylphenidate (Ritalin),
dextroamphetamine (Dexedrine), methamphetamine (Desoxyn)
• Antidepressants for cataplexy; protriptyline (Vivactil), desipramine (Norpramin),
fluoxetine (Prozac).
Complications
• Injury related to falling asleep
• Psychosocial problems such as disturbed relationships, loss of employment, depression
Nursing Assessment
• Obtain history of sleep and activity pattern.
• Assess emotional status and social interactions.
• Assess response to medication and lifestyle treatment.
Nursing Diagnoses
• Disturbed Sleep Pattern related to disease process
• Fatigue related to disrupted nighttime sleep
• Ineffective Coping related to interference with activity
Promoting Normal Sleep-Wake Cycle
• Review daily schedule to determine periods of sleep and cataplexy. Advise to wake at
the same time daily.
• Help patient establish nondrug therapies (exercise, diet) that will fit into lifestyle.
• Make sure that the bedroom is dark, cool, and quiet to facilitate sleep.
• Administer or teach self-administration of prescribed medications.
○ Advise of adverse effects of amphetamines, such as nervousness, irritability,
tremors, and GI upset.
○ Warn patient to take only as prescribed and to not increase dosage because of
tolerance and drug dependence
Reducing Fatigue
• Schedule 10- to 20-minute rest periods two to three times per day. Help patient
incorporate naps into lifestyle.
• Encourage patient to incorporate small amounts of caffeinated beverages at intervals,
and smaller, more frequent meals rather than large, heavy meals during the day to
maintain energy.
• Plan diversional activities and relaxation during fatigued periods.
Strengthening Coping
• Encourage active participation in selection of treatment modalities.
• Assist patient in identifying trigger factors of worsening symptoms.
• Teach problem-solving strategy to promote sense of control over activities and
symptoms during the day.
• Review patient coping mechanisms, and reinforce positive ones.
• Encourage use of support groups and community resources.

• Review the normal sleep cycle and the pathophysiology of narcolepsy.
• Stress the importance of nonpharmacologic measures as an adjunct to treatment.
• Inform the patient of rights of employment conditions under the Americans with
Disabilities Act (see page 198).
• Advise caution with using alcohol, working with machinery, or using dangerous
equipment to prevent injury to self or others during sleepiness or cataplexy.
• If patient drives, advise using caution and avoiding lengthy trips.
• Encourage patient to wear a MedicAlert bracelet.
• Encourage follow-up with health care provider, specialist, and mental health counselor
as needed.
• Refer patient and family to organizations for information, referrals, and group counseling
services such as Narcolepsy Sleep Disorder Association Online Newsletter,
http://www.narcolepsy.com.
• Complies with medication regimen
• Reports working without undue fatigue
• Identifies trigger factors
HEADACHE SYNDROMES
Headaches are one of the most common complaints of people seeking health care. Pain in the
head is a symptom of underlying pathology. The International Headache Society instituted a
classification system that is the standard for defining various types of headaches. It divides
headaches into two categories: Primary headache disorders, which include migraine, tension-
type headache, and cluster headache; and secondary headache disorders. Identifying the
etiology of headaches requires an understanding of the characteristics of each type of
headache.
Primary Headaches
Diagnosis is generally based on the characteristic clinical history and elimination of other
pathology such as stroke, intracranial bleed, AVM, or brain tumor.
• Migraine headacheâ€”consists of initial vasospasm followed by dilation of intracranial
and extracranial arteries; occurs in about 10% of population
○ Caused by hyperactivity to the neurotransmitter serotonin; familial predisposition.
○ Attack may consist of any of five phases: prodrome, aura, headache, resolution,
and postdrome.
○ Classified with or without aura (usually visual); aura is due to reduced cortical
neuronal activity.
• Tension headacheâ€”due to irritation of sensitive nerve endings in the head, jaw, and
neck from prolonged muscle contraction in the face, head, and neck; mild or moderate
intensity that does not prohibit activity.
○ Precipitating factors include fatigue, stress, poor posture.
○ Characterized by hatband distribution
• Cluster headacheâ€”release of increased histamine results in vasodilation
○ Usually unilateral, recurring.
○ Occurs mostly in men.
Secondary Headaches
Headache due to a neurologic or systemic disease
• Mass lesion (tumor, abscess, arteriovenous malformation, subdural or epidural
hematoma)
• Intracranial infection (bacterial/viral/fungal meningitis or encephalitis)
• Inflammation (giant cell arteritis, vasculitis)
• Cerebrovascular disease (subarachnoid hemorrhage, intracranial hemorrhage, occlusive
vascular disease)
• Increased intracranial pressure
• Low-pressure headache (postlumbar puncture, trauma induced)
• Sinus infection, viral infection such as influenza, systemic illness
• Migraine: sensory, motor, or mood alterations precede headache; gradual onset of
severe unilateral, throbbing headache, may become bilateral.
○ With migraine with aura (classic migraine), characteristic aura may include
scintillating scotoma (area of decreased vision surrounded by area of less
abnormal or normal vision with zigzag appearance), hemianopsia (loss of half of
field of vision) and paresthesias; headache follows aura in less than 1 hour;
usually lasts less than a day.
○ With migraine without aura (common migraine), nausea, vomiting, and
photophobia may accompany moderate to severe headache; worsened by
activity; may last 4 to 72 hours and greatly impair activities.
○ Either type of migraine may be triggered in women by hormonal fluctuations
(menses, pregnancy), excess or lack of sleep, change in eating habits, and
certain food additives.
• Tension/muscle contraction: dull, bandlike, constricting, persistent pain and pressure in
the back of the head and neck, across forehead, bitemporal areas; may be tender points
of head or neck.
○ Not aggravated by activity, but may be worsened by noise and light.
○ No nausea and vomiting, but may be associated with anorexia.
• Cluster headache: sudden, sharp, burning, excruciating, unilateral pain; always involving
facial area from neck to temple, and often occurs during the evening or night; more
frequent in men.
○ Occurs in clusters of 2 to 8 weeks followed by headache-free periods.
○ Associated with unilateral excessive tearing, redness of the eye, stuffiness of
nostril on affected side, facial swelling, flushing, and sweating.
○ Attacks last several minutes to several hours. Multiple attacks may occur in 1
day.
• Skull/sinus films to rule out lesions, sinusitis
• CT scan/MRI to rule out lesions, hemorrhage, chronic sinusitis
• Erythrocyte sedimentation rate and other blood studies to help determine inflammatory
process with temporal arteritis
Management
Pharmacologic Treatment
Medications are intended to reduce the frequency, severity, and duration of the headache.
Effectiveness of medication is individualized. Some persons may need a combination of
medications.
• Aspirin, acetaminophen, and NSAIDs for mild to moderate pain of tension, sinus, or mild
vascular headaches.
• Some drugs may abort vascular headaches if taken at the onset, including methysergide
(Sansert), a serotonin antagonist; ergotamine (Ergostat), a vasoconstrictor; or 5HT-
agonists such as sumatriptan (Imitrex).
• Sumatriptan is available in subcutaneous injection as well as oral form.
• Other oral 5HT-agonists include zolmitriptan (Zomig), naratriptan (Amerge), and
rizatriptan (Maxalt).
• Inhalation of 100% oxygen may abort a cluster headache.
• Some drugs may be used continuously as prophylactic treatment for recurrent
migraines, including beta-adrenergic blockers, calcium channel blockers, and
antidepressants.
• Antihistamines and decongestants may be effective for sinus headaches.
• Corticosteroids may be used for temporal arteritis.
• Occasionally, opioid analgesics, muscle relaxants, and antianxiety agents may be
needed for severe pain.
DRUG ALERT
Vasoconstrictors and 5HT-agonists used to abort vascular headaches are contraindicated in
patients with uncontrolled hypertension, coronary artery disease, and peripheral vascular
disease.
Nonpharmacologic Management
• Relaxation techniques, guided imagery, paced breathing.
• Biofeedback, cognitive therapy.
• Trigger identification and control of such factors as intake of alcohol (red wine), skipped
meals, oversleeping, or undersleeping.
• To prevent migraine: avoidance of monosodium glutamate, mixed spices such as
â€œseasoned salt,â€ nitrates and nitrites commonly contained in bacon, hot dogs, or
deli meats.
• Rest in a quiet, dark room at onset of headache.
• If caffeine user, spread caffeine intake evenly over the day.
• Routine exercise program.
Complications
• Usually none from primary headaches.
Nursing Assessment
• Obtain a history of related symptoms, triggering factors, degree of pain, and medications
used.
• Perform a complete neurologic examination to detect any focal deficits or signs of
increased ICP that indicate tumor or hemorrhage.
• Assess coping mechanisms and emotional status.
Nursing Diagnoses
• Acute Pain related to headache
• Ineffective Coping related to chronic and/or disabling pain
Controlling Pain
• Reduce environmental stimuli: light, noise, and movement to decrease severity of pain.
• Suggest light massage to tight muscles in neck, scalp, back for tension headaches.
• Apply warm, moist heat to areas of muscle tension.
• Encourage patient to lie down and attempt to sleep.
• Teach progressive muscle relaxation to treat and prevent tension headaches.
○ Alternately tense and relax each group of muscles for a count of five, starting
with the forehead and working downward to the feet.
○ Try to maintain a state of relaxation of each muscle group until the whole body
feels relaxed.
○ Relaxation of just head and neck may also be helpful if time is limited.
• Teach patient the cause of headache and proper use of medication.
• Encourage adequate rest once headache is relieved to recover from fatigue of the pain.
Promoting Positive Coping

• Encourage patient to become aware of triggering factors and early symptoms of
headache, so headache can be prevented or promptly treated. Hunger, lack of exercise,
and erratic sleep schedules may trigger headaches.
• Encourage adequate nutrition, rest and relaxation, and avoidance of stress and
overexertion to better cope with headaches.
• Implement problem solving to help patient manage problems that arise in social or work
situations related to headaches.
• Review coping mechanisms, and strengthen positive ones.
• Teach proper administration of medication.
○ Self-injection of sumatriptan (Imitrex) given subcutaneously with autoinjector.
○ Inhalation of ergotamine (Ergostat) through metered-dose inhaler.
• Teach adverse effects of medications.
○ GI upset, gastritis, and possible ulcer formation with NSAIDsâ€”take with food.
○ Numbness, coldness, paresthesias, and pain of extremities with ergot
derivativesâ€”report to health care provider.
○ Chest pain, wheezing, flushing with sumatriptan (Imitrex)â€”report to health care
provider.
○ Hypotension with beta-adrenergic blockers and calcium channel blockersâ€”arise
slowly, do not exceed prescribed dosage, do not discontinue beta-adrenergic
blockers abruptly.
• Advise avoidance of alcohol, which can worsen headaches.
• Teach about foods that are high in tyramine, which may trigger migrainesâ€”aged
cheese, red wine, liver.
• Teach patient how to perform relaxation techniques to reduce stress and promote inner
well-being.
• Refer for more information to the International Headache Society, http://www.i-h-s.org.
• Reports fewer, less-severe headaches
• Describes use of positive coping mechanisms
HERNIATED INTERVERTEBRAL DISK (RUPTURED DISK)
Herniation of the intervertebral disk is a protrusion of the nucleus of the disk into the annulus
(fibrous ring around the disk) with subsequent nerve compression. The herniation may occur in
any portion of the vertebral column (see Figure 15-11). The pressure on spinal nerve roots or
the spinal cord causes severe, chronic, or recurrent back and leg pain.
FIGURE 15-11 Ruptured vertebral disk.
• The intervertebral disk is a cartilaginous plate made up of gelatinous material in the
enter, known as the nucleus pulposus, and is encapsulated in the fibrous annulus.
• About 90% of herniated disks involve the lumbar and lumbosacral spine. The most
common site is the L4-L5 disk space. The cause of a herniated lumbar disk is usually a
flexion injury, but many patients do not recall experiencing a traumatic event. Cervical
herniation is less common; but when it occurs, is usually in individuals age 45 or older.
• Risk factors for herniation include:
○ Degeneration (aging), trauma, and congenital predisposition
○ Biomechanical factors, such as twisting and repetitive motions in occupational
settings
○ Sedentary occupations
○ Obesity
○ Smoking
• The herniation compresses the spinal nerve root on one side and, with further
degeneration of the disk, may eventually produce pressure on the spinal cord.
• This sequence may take months to years, producing acute and chronic symptoms.
General Considerations
• An intervertebral disk may herniate without causing symptoms.
• Symptoms depend on location, size, rate of development, and effect on surrounding
structures.
• Most symptomatic disk herniations result in pain, sensory changes, loss of reflex, and
muscle weakness that resolve without surgery.
Cervical
• Pain and stiffness in the neck, top of shoulders, and region of the scapula
• Pain in upper extremities and head
• Paresthesias and numbness of upper extremities
• Weakness of upper extremities
Lumbar
• Lower back pain with varying degrees of sensory and motor dysfunction.
• Pain radiating from the lower back into the buttocks and down the leg, referred to as
sciatica.
• A stiff or unnatural posture
• Some combination of paresthesias, weakness, and reflex impairment
• Positive straight-leg raise test: pain occurs in leg below the knee when leg raised from a
supine position.
NURSING ALERT
Cauda equina syndrome is an emergency caused by an acute compression of the cauda equina
area of the spinal cord by massive disk extrusion. Symptoms include bilateral sensorimotor loss,
severe unilateral motor loss, bowel, bladder, or sexual dysfunction. It must be recognized early,
and compression must be relieved to prevent permanent loss of these functions. If pain and
neurologic findings do not subside in response to conservative management, surgical
intervention must be considered.
• Myelogramâ€”demonstrates herniation and pressure on spinal cord or nerve roots
• CT scan or MRIâ€”demonstrates herniation; MRI has greater sensitivity
• Electromyographyâ€”localizes specific spinal nerve involvement
Management
Nonpharmacologic Measures
• Complete bed rest on a firm mattress (2 days usually sufficient) usually results in
improvement in 80% of patients.
• Heat or ice massage to affected area.
• Cervical collar or possibly cervical traction are widely used, although efficacy is not
proven.
• Physical therapy.
• Nonpharmacologic and pharmacologic measures may be used together for 4 to 6 weeks
as conservative management if there is no progressive neurologic deficit.
Pharmacotherapy
• Anti-inflammatory drugs, such as ibuprofen (Motrin) or prednisone.
• Muscle relaxants, such as diazepam (Valium) or cyclobenzaprine (Flexeril).
• Analgesics; opioids may be necessary for several days during acute phase.
Surgical Intervention
• May be done if there is progression of neurologic deficit or failure to improve with
conservative management.
• Surgical procedures include diskectomy (decompression of nerve root), laminectomy,
spinal fusion, microdiskectomy, and percutaneous diskectomy.
• Hemilaminectomy with excision of the involved disk is the surgical procedure most often
indicated for lumbar disk disease.
Chemonucleolysis
• Less-common invasive treatment for lumbar disk herniation
• Injection of chymopapain (Chymodiactin) into herniated disk that produces loss of water
and proteoglycans from the disk, reducing the size of the disk and subsequent pressure
on the nerve root
• May cause severe complications, such as transverse myelitis, allergic reactions,
persistent muscle spasm
Alternative and Complementary Measures
• Acupuncture
• Manipulative therapy
• Massage therapy for adjunct pain relief
• Homeopathic remedies
• Various nutritional supplements
Complications
• Permanent neurologic dysfunction (weakness, numbness)
• Chronic pain with associated psychosocial issues
• Cauda equina syndrome
Nursing Assessment
• Perform repeated assessments of motor function, sensation, and reflexes to determine
progression of condition.
• Assess level at which straight-leg raise test is positive; generally, radiation of pain below
knee at 45 degrees of elevation is considered positive for nerve root involvement;
positive at lesser elevation may indicate worsening condition.
• Assess pain level on scale of 1 to 10.
Nursing Diagnoses
• Acute Pain related to area of compression
• Impaired Physical Mobility related to pain and disease physiology
• Deficient Knowledge related to impending surgery
• Risk for Injury related to surgical procedure
Minimizing Pain
• Administer or teach self-administration of anti-inflammatory drugs as prescribed and with
food or antacid to prevent GI upset.
• Administer or teach self-administration of prescribed muscle relaxant; observe safety
because drowsiness may result.
• Administer or teach self-administration of analgesics as prescribed; be prepared for
sedation.
• Use bed boards under mattress and maintain bed rest except for short trips to bathroom;
maintain supine or low-Fowler's position or side-lying position with slight knee flexion
and pillow between knees.
• Apply dry or moist heat to affected area of back as desired.
• Encourage relaxation techniques, such as imagery and progressive muscle relaxation.
Maintaining Mobility
• Encourage ROM exercises while in bed.
• Properly fit and use a cervical collar (if appropriate to level of injury).
• Apply a back brace or cervical skin traction, if ordered.
• Inspect skin several times a day, especially under stabilization devices, for redness and
evidence of pressure ulcer development.
• Provide massage and good skin care to pressure-prone areas.
• Assist patient with activities at bedside, and discourage lifting or straining of any kind.
• Encourage compliance with physical therapy treatments and activity restrictions as
ordered.
Preparing the Patient for Surgery
• Educate patient about surgical procedure.
○ Procedure is generally short.
○ Small incision will be made on back of neck; second incision will be on hip if a
bone graft is taken from iliac crest for spinal fusion.
○ Routine postoperative care will include frequent assessment of vital signs and
neurologic function, frequent turning and deep breathing, pain control, and
ambulation on the first postoperative day.
• Document baseline neurologic assessment to compare with after surgery.
• Explain your actions to patient as you prepare operative area, administer preoperative
medications, and perform any other preoperative order.
Preventing Complications Postoperatively
• Monitor vital signs and surgical dressing frequently because hemorrhage is a possible
complication.
• If patient has a blood drainage system (Hemovac), check tubing frequently for patency
and secure vacuum seal.
• Assess movement and sensation of extremities, report new deficit.
• Administer analgesics and steroid medications to control pain from incision and swelling
around nerve roots and spinal cord due to surgery.
• Maintain cervical collar if ordered.
• Logroll patient to reposition frequently and encourage coughing and deep breathing.
• Position for comfort with small pillow under head (but avoid extreme neck flexion) and
pillow under knees to take pressure off lower back.
• Provide fluids as soon as gag reflex and bowel sounds are noted.
• Assess for hoarseness, which suggests that cervical surgery resulted in a recurrent
laryngeal nerve injury; this injury may cause an ineffective cough.
• Watch for dysphagia due to edema of the esophagus, and provide a blenderized diet.
• Make sure that the patient voids after surgery; report urine retention.
• Encourage ambulation as soon as possible by having the patient lie on the side close to
the edge of the bed and push up with arms while swinging legs toward floor in one
motion; alternate walking with bed rest, discourage sitting.
• Report any sudden reappearance of radicular pain (may indicate nerve root compression
from slipping of bone graft or collapsing of disk space) or burning back pain radiating to
buttocks (may indicate arachnoiditis).
• Demonstrate and encourage back strengthening, aerobic exercise, and endurance
exercises.
• Make sure that the patient avoids heavy lifting and uses proper body mechanics in all
activities.
• Discourage prolonged bed rest and inactivity.
• Refer for vocational counseling, if indicated.
• If cervical skin traction is ordered for home use, teach the patient how to apply the chin
strap and head halter. The weight should hang freely over the back of a chair or
doorknob near the head of the bed. Make sure the patient maintains proper alignment of
the neck and removes traction before moving the head.
• Educate patient regarding lifestyle changesâ€”smoking cessation, increased activity,
loss of weight.
• Provide instructions regarding back anatomy and back care to reduce symptoms.
• Teach patient the importance of complying with bed rest, use of cervical collar, and other
conservative measures to try to reduce inflammation and heal disk herniation.
• Tell patient who has had a cervical disk herniation to avoid extreme flexion, extension, or
rotation of the neck and to keep the head in neutral position during sleep.
• Encourage the patient with a lumbar disk herniation to remain on bed rest at home with
ambulation to the bathroom only until inflammation and pain are sufficiently reduced;
then ambulation can be increased, but lifting and sitting are discouraged.
• Encourage the patient to do stretching and strengthening exercises of extremities and
abdomen after acute symptoms have subsided. The back can be gently stretched by
lying on the back and bringing the knees up toward the chest.
• Teach the patient about proper body mechanics and the use of leg and abdominal
muscles rather than the back. Knees should be bent on lifting, and load should be
carried close to midtrunk.
• Encourage follow-up with physical therapy as indicated for reconditioning and work
hardening.
• Tell patient to avoid the prone position, long car rides, and sitting in a soft chair.
• Instruct the patient to report any changes in neurologic function or recurrence of
radicular pain.
• Encourage good nutrition, avoidance of obesity, and proper rest to reduce risk of
recurrence.
• Maintains mobility with active lifestyle
• Expresses understanding of preoperative preparation and postoperative care
• Incision healing without signs of infection; patient ambulating with minimal pain

Neurologic Disorders 2

Diunggah oleh

Informasi Dokumen

Deskripsi Asli:

Hak Cipta

Format Tersedia

Bagikan dokumen Ini

Bagikan atau Tanam Dokumen

Opsi Berbagi

Apakah menurut Anda dokumen ini bermanfaat?

Apakah konten ini tidak pantas?

Hak Cipta:

Format Tersedia

Neurologic Disorders 2

Diunggah oleh

Hak Cipta:

Format Tersedia

Neurologic Disorders

Definitions of Neurologic Findings

Computed Tomography Scan

Performance phase (By the physician or credentialed health care provider)

Nursing and Patient Care Considerations

Nursing and Patient Care Considerations

Promoting Urinary Elimination

Evaluation: Expected Outcomes

NURSING MANAGEMENT OF THE PATIENT UNDERGOING INTRACRANIAL SURGERY

Risk Factors for Stroke

Managing Aberrations in Thought Processes

Patient Education and Health Maintenance

FIGURE 15-6 Appearance of female with Parkinson's disease.

Optimizing Sensory Function

Promoting Bowel Elimination

○ Hematopoietic tumorsâ€”include primay malignant lymphoma (rare, diffusely

BOX 15-5 Emergency Management of Status Epilepticus

Patient Education and Health Maintenance

Promoting Positive Coping

Anda mungkin juga menyukai