Professional Documents
Culture Documents
1. Provide education
- Many manifestations of radiation therapy do not develop until
approximately 10-14 days. And some do not subside until several weeks
after treatment.
- The nurse explains the procedure, delivery of radiation, describe the
equipment, the duration and the possible need of immobilizing the patient
4. Dental care
- If you wear dentures, they may no longer fit well because of swollen
gums. If your dentures can cause gum sores, you may need to stop
wearing them until your radiation therapy is over because sores can
become infected.
- Clean teeth and gums thoroughly with a very soft toothbrush after meals
and at least once a day each day.
- Use fluoride toothpaste that contains no abrasives.
- Use unwaxed dental tape to gently floss between once a day.
- Rinse your mouth well with cool water or a baking soda solution after
brushing. Use 1 tsp. baking soda in 1 quart of water.
- Apply fluoride regularly as prescribed by your dentist.
5. Many patients feel tired due to the radiation therapy which can affect their
emotions
7. Side effects can include eating and digestion problems. You may completely
lose interest in food during your treatment.
- Even if you are not hungry, it is important to keep your protein and calorie
intake high.
- Doctors have found that patients who eat can better handle their cancers
and side effects.
- Eat when you are hungry, even when it is not meal time.
- Eat several small meals during the day rather than 2 or 3 large meals.
- Vary your diet and try new recipes.
- If you don’t drink alcohol, ask your doctor if you should avoid alcohol
during your treatment.
- Keep healthful snacks close by nibbling when you get the urge.
Drink milkshakes or prepared liquid supplements between meals.
Patient receives a low residue diet to prevent frequent bowel
movements.
Radiation therapy may cause anorexia which may lead to inadequate
nutrition and hydration so small frequent feedings or use of nutritional
supplements may be required to maintain adequate nutrition.
In radiation therapy, fatigue or malaise also contribute to poor
nutritional intake thus planned rest periods may provide relief of
fatigue providing increased energy for meal preparation or
consumption.
Nutrition – to promote retention of nutrients, administer antiemetics as
prescribed.
Encourage high calorie meals when child is least likely to be
nauseated. Praise a child’s effort to eat.
Provide foods identified by child as special favorites.
Serve easy to swallow food at tolerable temperature.
If mucous membrane of mouth, pharynx or esophagus is irradiated,
modification of diet to bland, soft, or liquid foods will be necessary;
mouth is rinsed frequently with a mild alkaline mouthwash; teeth are
gently cleansed with absorbent cotton or gauze rather than the usual
brush.
Avoids foods that are dry and thick.
9. Miscellaneous.
- A urinary catheter will be in place (if ordered) and must be inspected
frequently to ensure that it drains properly.
- Any profuse discharge should be reported immediately to the radiation
oncologist or gynecologic surgeon.
- Observing the patient for temperature elevation, nausea, and vomiting.
The symptoms may indicate such complications as infection.
- Patient teaching includes informing the patient that abdominal fullness,
cramping, backache, and the urge to void are normal feelings during
therapy.
- Severe should not occur.
- Mild opioid agents, muscle relaxants or sedative medications may be
helpful.
- Private room, with private bathroom and facilities
- Room previously occupied with patients previously treated with
radionuclide treatment should not be used until the room has been
cleansed and surveyed for residual contamination.
- Items such as bedpans, urinals and basins if disposable may be disposed
of as radioactive waste. If these items are not disposable, they shall be
thoroughly washed with soap and running water.
- Any vomitus, gastric contents collected during the first 24 hours by
nasogastric aspiration or excessive sputum should be collected in a
waterproof container and held for disposal by radiation safety division
personnel.
- Wearing of lead apron
- The nurse must deal safety with radioactive body discharges by wearing
gloves and in some instances placing excreta in containers for special
disposal.
- For a child receiving radiation therapy
- Provide ample time to answer questions of children undergoing radiation
therapy
- Advise client to wear loose clothing as skin in the area being treated
might become more sensitive to touch.
Skin changes:
- The patient is observed for possible reactions:
Slight redness for a brief period
Transitory epilation
Erythema with temporary sweat gland activity suppression
Dry desquamation
- For large doses or sensitive skin; observe the following:
Marked erythema followed by purple discoloration
Blister formation and moist desquamation
Slow healing, leaving skin atrophied, thin and very sensitive to
heat, cold and trauma.
Permanent epilation and sweat gland destruction
- After treatment, the area is gently cleansed with tepid water and patted
dry; soap is not used and brisk rubbing is avoided.
- Alcohol, powders, oils, lotions, creams, ointments, deodorants are not
used unless prescribed by the doctor.
- The site is kept dry and may be covered lightly with smooth cloth/cotton
but adhesive tape is contraindicated, used an alternative instead.
- If larynx is treated with radiation, the patient is closely observed 3-4 days
for any difficulty in breathing; edema may develop and occlude airway
necessitating prompt intubation or a tracheostomy.
- Frequent blood cell counts are done because the hemapoetic tissue is
extremely sensitive to radiation.
- Contact with persons with an infection should be avoided especially with
respiratory infection because of the patients lowered resistance.
- Patient should have an extra rest, increased fluid intake and a high
calorie, high protein, high vitamin diet.
- If the patient is allowed to go home, the importance of keeping the
appointments for his treatments is stressed.
Brachytherapy
- The radiation source is used for surface, interstitial, or intracavity applications
1. The nurse should inform the patient that some skin reaction can be
expected but that varies from patient to patient.
2. Do not apply lotions, ointments, cosmetics, etc. to the site of radiation
unless prescribed by the physician. Cornstarch may be used when the skin
is dry and or itchy. Discourage vigorous rubbing or scratching. It may
destroy skin cells.
During treatment:
- Require them to be still for a period of time possibly on an uncomfortable
table.
- Assure patients and the child that during the treatment, just as there is no
sensation from x-ray exposure, the child may will experience no sensation
from radiation exposure.
- Infants are usually prescribed a sedative or conscious sedation before
therapy to ensure that they be still during the procedure.
- To make this approach affective, keep the child fairly active early in the day
and introduce activities after the sedative is administered.
After treatment:
- If head is involved in therapy, alopecia (hair loss) may result.
- Radiation to the head may reduce salivary gland function, leading to a
constantly dry mouth.
- Tooth growth may be halted due to root therapy.
- Radiation to bone marrow may depress blood cell and platelet production.
- Children undergoing radiation therapy need their leukocytes and platelet
counts monitored periodically for changes.
- Use only luke warm water and mild soap. Just let water run over the treated area.
Do not rub.
- Do not wear tight clothing over the treatment area.
- Try not to rub, scrub or scratch any sensitive spots.
- Avoid exposing the area to the sun during treatment and for at least 1 year after
the treatment is completed.
- If you expect to be in the sun for more than a few minutes, wear protective clothing
and sunscreen. Ask your doctor or nurse about using sunscreen lotions.
- Wash the irritated area gently each day with sitter water alone on a mild soap and
water.
- Use your hand rather than a washcloth to be more gentle.
- Rinse soap thoroughly from your skin.
- Take care not to remove the markings that indicate exactly where the beam of
radiation is to be focused.
- Dry the irradiated area with potting motions rather than rubbing motions, using a
clean, soft towel
- Use no powders, ointments, lotions, or creams on your skin at the radiation site
unless they are prescribed by your radiologist.
- Wear soft clothing over the skin at the radiation site.
- Avoid exposure of the irradiated area to the sun.
- A void heat exposure.
- Mild erythema to moist desquamation similar to appearance to a second-degree
burn.
- The nurse assesses the patient’s skin, nutritional status and general feeling of well
being.
- The skin and oral mucosa are assesses frequently for changes.
- The skin is protected from irritation and the patient is instructed to avoid using
ointments, lotion or powder on the area.
- Pressure is avoided by avoiding tight clothing’s and prolonged lying on the area of
treatment.
- No hot or cold is applied on the site and must be protected from direct sunlight.
- If itching and irritation accompanying erythema, you may suggest application of
plain calamine lotion without phenol; or cornstarch.
• Dryness and pruritus may occur at an accumulated dose of 2000 to
28000 Cgy (1.2) and is caused by obliteration of sebaceous glands
within the field.
• This is an acute phenomenon that correlates with the depletion of
actively proliferating basal cells in the epidermal layer of the skin,
a fixed percentage of which die with each dose fraction of
irradiation.
• Remaining basal cells are stimulated and their cell cycle
shortened.
• Subsequent peeling of the skin is defined as dry desquamation.
• The skin becomes dry and patient may notice itching and burning
sensations.
• Dry skin is susceptible to further injury through scratching and/or
formation of fissures – augmenting the risk of infection and tissue
necrosis.
HYPERSENSITIVITY REACTIONS
• Exaggerated or inappropriate response to specific antigen
• Anaphylaxis, allergies, transfusion reactions, graft rejections
Pathophysiology:
IgE attach to the surface of mast cells and basophils providing a site for allergens to
bond the cells. This causes the cells to releases vasoactive substances including
histamine leading to:
1. Constriction of smooth muscles in the bronchi – bronchospasm
2. Increase in vascular permeability – urticaria(hives or tissue edema
3. Increase in mucus secretions – hay fever and asthma
Symptoms: wheezing, sneezing, rhinitis with conjunctivitis; urticaria, angioedema,
rash: diarrhea; fever,
malaise, joint pains, hematopoietic suppression, anaphylaxis
Sensitizing Dose – initial contact with allergen that triggers the synthesis of specific
antiallergenic IgE
antibodies
Shocking, Challenging Dose – subsequent contact with allergen, indi exhibits the
symptoms of Type I
Nursing Process:
Assessment – history taking
Diagnostic Test – skin test, radioallergosorbent test, one-week food diary test
Nursing Diagnosis: Alerted health maintenance; Knowledge deficit
Implementation:
1. Prevent anaphylactic reaction
- Epinephrine; Benadryl; aminophylline, tracheal intubation; shock therapy
2. Allergen immunotherapy
3. Control the environment – house dust; animal dander; pollens; fungus
4. Facilitate learning – remind physician of allergy if new medications are
prescribed; read all labels of nonprescription drugs before taking the new
drug; examine all labels of new prepared foods for presence of allergens;
avoid eating unknown foods when travelling; use non allergenic soaps and
cosmetics – coat nickel containing jewelry with clean nailpolish; use gloves
to handle allergen; report side effects of prescribed medication
TYPE II – Cytotoxic Hypersensitivity
• Caused by antibodies (IgG and IgM) directed against antigens on a person’s
red blood cells, lymphocytes or platelets or tissue cells. The reaction of
antibodies and antigens usually leads to activation of the complement
system.
• Damage cells by causing lysis as in compatible blood transfusion reactions
Organ Transplantation for end stage or failure and do not respond to conventional
therapy
Recipient: free of irreversible of infection or malignancy
End stage of failure and do not respond to conventional therapy
No anatomical problem that would lead to difficulty of
transplantation
Therapeutic or benefit of the patient
Ability of the family to pay costs; age; functional ability;
rehabilitation potential;
ability to return to work; psychological status; family
support system, ability to
buy post transplantation regimen
Donor: cadaver-brain death; no existing disease; no transmissible
disease; no malignancy; family with no history of death of
unknown causes
Clinical Manifestations:
1. Assess for clinical manifestation of infection
2. Obtain specimens of blood, urine, stool, sputum, throat swabbing, nasal
secretions, pyrogenic exudates for bacteriologic studies
3. Secure/Assist in securing blood smears or other materials for microscopic
studies
4. Assist with spinal aspiration of lumbar tap, BM or any other fluids or tissues
for cytologic, serologic or bacteriologic study
5. Carry out appropriate skin tests for specific diagnostic reactions as directed
Nursing Diagnosis:
1. Fluid and electrolyte imbalance
2. Altered thermoregulatory status
3. Fever
4. Potential for spread of infection
5. Altered respiratory status
6. Altered elimination status
7. Potential for serious systemic complications
8. Ineffective coping and social isolations
9. Knowledge deficit
MEMORY TEST
Testing requires alertness and is not possible in a confused or dysphasic patient.
IMMEDIATE memory – Digit span – Ask patient to repeat a sequence of 5, 6, or 7
random numbers.
RECENT memory – ask patient to describe present illness, duration of hospital stay
or recent events in
the news.
REMOTE memory – ask about events or circumstances of occurring more than 5
years previously.
VERBAL memory – ask patient to remember a sentence or a short story and test
after 15 minutes.
VISUAL memory – ask patient to remember objects on a tray and test after 15
minutes.
COGNITIVE SKILL
Dominant hemisphere disorders
Listen to language pattern – hesitant Expressive dysphasia
- fluent Receptive dysphasia
Does the patient understand Receptive dysphasia
simple/complex spoken commands?
e.g. “Hold up both arms, touch the right
ear with the left fifth finger.”
Ask the patient to name objects Nominal dysphasia
Does the patient read correctly? Dyslexia
Does the patient write correctly? Dysgraphia
Ask the patient to perform numerical Dyscalculia
calculation, e.g. serial 7 test, where 7 is
subtracted serially from 100.
Can the patient recognize objects? E.g. Agnosia
ask the patient to select an object from a
group.
Non- Dominant hemisphere
disorders
Note patients ability to find his way Geographical agnosia
around the ward or his home.
Can the patient dress himself? Dressing apraxia
Note the patient’s ability to copy a Constructional apraxia
geometric pattern, e.g. ask the patient
to forma star with matches or copy a
drawing of a cube.
Mild mental function tests and Functional activity questionnaire are used in the
assessment of DEMENTIA
MENTAL BEHAVIOR
Level of Consciousness:
NOMENCLATURE
Abberration - deviation from normal structure of behavior
Decerebrate - deprived of cerebral function
Denervate - to interrupt motor/sensory nerve supply to a party by
drug
injection or operation
Contrecoupinjury - injury to the brain produced on the side opposite that of
the
primary injury
Cerebral Concussion - brain injury resulting from violent jarring of the
brain due to blow
to the head, fall
SURGICAL PROCEDURE
Craniotomy - surgical opening through the cranium
Craniectomy - the surgical removal of a part of the skull
Chordotomy - division of the long tract of the spinal cord, referring usually to
the
antero-lateral pathways that transmit pain
CSF
Hypoglycoorrhakia - low sugar in CSF
Pleocytosis - increased WBC in CSF
Xaantochromia - yellowish discoloration of the CSF
HEAD
Macrocephalous - having an unusually large head
Microcephalous - having an unusually small head
Cephalococle - protrusion of the brain from the cranial cavity
Cephalhematoma - subcutaneous swelling containing blood found in the head
GAIT
“Foot drop” gait - due to weakness in dorsiflexing the ankle, the patient
elevates the
affected foot higher than normal and the foot tends to
point
downward.
Spastic gait - associated with spastic weakness, movement is slowed
and
flexion of the knee and hip joint is slowly and imperfectly
performed; affected leg tends to remain adducted. The
patient has to swing the affected leg around (circunduct)
since he cannot flex and elevate it.
Parkinson Gait - the patient shows loss of arm swing, short-stepped,
with the
trunk developing a forward list, eventually forcing the
patient, with his difficulty in stepping, to have to run
forward to “catch up” with the center of gravity, affected
arm is characteristically held in semiflexion at the elbow
and wrist.
Ataxic - patient show either or both of these abnormalities:
1. He cannot accurately place one foot in front of the
other and leg movement is jerky and uncoordinated:
tends to fall on one side.
2. He may be unable to stabilize his trunk in the vertical
posture so that he tends to jerk back and forth
(titubation) + Rombryg test (sensory)
Titubation - staggering gait
Festination - morbid acceleration of gait
1. Propulsion - tendency to push or fall forward in walking
2. Retropulsion - walking backward, involuntary
Scissors - short, slow steps, with legs alternately crossing over each
other
POSITION
Emprosthothonus - lying with the body in curved and resting upon the
forehead and
feet with face downward.
Opisthotonus - an arched position of the body with the feet and
head on the floor
or bed.
Pleurothotonus - titanic spasm in which the body position is arched
to one side
Orthotonus - titanic spasm marked by rigidity of the body in a straight
line
SENSATION
Paresthesia - peculiar sensation of numbness, prickling, tingling.
Hyperesthesia - unusual sensitivity to pain or sensory stimuli
Neuralgia - severe Lancination pain along the course of a nerve
Myalgia - muscular pain
Agnosia - loss of comprehension of audio-v, visual or other
sensation
1. Auditory – inability to interpret sounds
2. Optic – inability to interpret images seen
3. Tactile – inability to distinguish objects by using sense
of touch
Asteriognosis - is the inability to recognize familiar objects by
touch or
manipulation
Diplopia - double vision
Anopsia - loss of vision in one eye
Homonymous Hemianopsia- loss of one-half of the field of vision in one
eye
Anosmia - absence of the sense of smell
INTRACRANIAL HEMORRHAGE
Extradural/Epidural - bleeding beneath the cranium and outside the dura,
frequently
Subdural Hemorrhage - hemorrhage between the dura and arachnoid;
increasing ICP
develop slowly; personality changes maybe the first
noticeable sign
Subarachnoid Hemorrhage - hemorrhage between the arachnoid and pia
mater into
CSF
NEUROLOGIC SIGNS
A. Cardinal symptoms: increasing or widening pulse pressure
Decreasing PR
Increasing headache
Pappil edema
Decreased mental awareness
Decreased in RR
B. Other signs and symptoms which may or may not develop:
1. Vomiting – may or not be projectile
2. Motor deficits – weakness or paralysis of any part of the body
3. Sensory Disturbances of any part of the body
4. Awkwardness – may mean weakness; difficulty or coordination
5. Speech disturbances
6. Convulsion
7. incontinence/retention
C. Localizing Symptoms
1. Frontal Lobe – aphasia
Confusion
Changes in personality
Jacksonian convulsion- convulsion begins in one part of the
body and
spread in orderly manner to all of the body parts.
2. Parietal Lobe – convulsion, sensory disturbance, asteriognosis
3. Temporal Lobe – defects in visual field, taste or hearing, smell of burning
rubber
4. Occipital Lobe – visual disturbance
5. Cerebellum
Ataxia – muscle coordination especially manifested when voluntary
muscular
movements are attempted.
Tremors, nystagmus, hypotonia
6. Basal Ganglia
Athetosis, chorea, hemiballismus, tremor
Pathopysiology
Prioritization of Problems:
1. Nutrition Imbalanced: less than body requirements r/t oral intolerance and
liver cirrhosis - overt
2. Ineffective Breathing Pattern r/t intra- abdominal fluid collection (ascites) -
overt
3. Fluid Volume Excess r/t compromised regulatory mechanism - overt
4. Impaired Skin Integrity r/t compromised immunologic status - overt
5. Activity Intolerance r/t fatigue - overt
6. Body Image Disturbed r/t personal vulnerability - overt
7. Risk for Injury and bleeding r/t altered clotting mechanism -covert
8. Risk for acute confusion r/t inability of the liver to detoxify certain enzymes or
drugs – covert
Assessment Pathophysiolog Objectives Intervention Rationale Evaluation
y
S: “Nahihirapan Cause: excessive STO: After 8 DX: Monitor Rapid shallow STO: fully met
akong huminga” alcohol hours of health respiratory rate, respirations/dyspne pt is no longer
consumption, care depth and effort smay be present dyspheric and
O: v/s reduced protein interventions pt bec. Of hypoxia and O2 is no longer
Temp: 36.7°C intake, exposure will be free of or fluid needed
BP: 110/60 to certain dyspnea, accumulation in
mmHg chemicals and cyanosis, w/ Auscultate abdomen Factors:
PR: 94/min infectious ABG’s and vital breath sounds, Indicates Pt is very
RR: 18/min schistosomiais capacity w/in noting crackles, developing cooperative and
acceptable wheezes, complications, willing to
Conscious:
Necrosis of liver range rhonchi increasing risk of participate in
dyspheric
cells LTO: After 2 Investigate infection any therapy
Prefers to be
weeks of health changes in level
in bed
Destroyed liver care intervention of consciousness Changes in LTO: fully met if
Prefers to cells are pt will establish pt will establish
sleep mentation may
replaced by scar a normal reflect hypoxemia a normal or
Assisted w/ tissue effective effective
and respiratory
ADL by SO respiratory respiratory
Monitor temp. failure w/c often
Easily pattern pattern
note presence of accompany hepatic
fatigued: Scar tissue chills, increased coma.
pallor exceeds that of coughing,
Appears weak functioning liver changes in Indicative of onset
and restless tissue color/character infection ex.
On O2 at 1- of sputum Pneumonia
2\LPM/NC
Monitor serial
Irritable thus ABG’s pulse
changes Portal
oximetry, vital
position once obstruction and
capacity
in a while ascites Reveals changes
measurements,
(+) coughing, chest x-rays in respiratory status
non- Ineffective developing
Tx: keep head
productive Breathing pulmonary
of bed elevated.
Enlarged Pattern complications
abdomen Position on sides
(ascites)
Facilitates
A: Ineffective Provide breathing by
Breathing supplemental o2 reducing pressure
Pattern r/t as indicated on the diaphragm
Ascites and minimizes risk
of aspiration of
secretions
Conserve pt’s Maybe necessary
strength by to treat/prevent
providing rest hypoxia. If
periods and respiration/oxygena
assisting with tion inadequate/
activities mechanical
Change ventilation maybe
position in required
every 2 hours Reduces
metabolic and
Assist with oxygen
paracentesis or requirements
thoracentesis
as indicated
Promotes
Ed Encourage expansion and
frequent oxygenation of all
repositioning areas of the lungs
and deep Paracentesis and
breathing thoracentesis are
exercises/cough performed to
ing as remove fluid from
appropriate the abdominal and
Demonstrate thoracic cavities
respectively.
with respiratory
adjuncts Aids in lung
expansion and
mobilizing secretion
Reduces
incidence of
atelectasis,
enhance
mobilization of
secretions
S: “wala akong Cause: excessive STO: After 8 DX: Measure Provide STO: not met
ganang kumain” alcohol hours of health dietary intake by information Pt was not able to
consumption, care intervention calorie count about intake demonstrate
O: v/s reduced protein pt will be able to needs or progressive
Temp: 36.7°C intake, exposure demonstrate Weigh as deficiencies weight gain
BP: 110/60 to certain progressive indicated, It maybe
mmHg chemicals and weight gain compare difficult to use Factors:
PR: 94/min infectious toward goal with changes in fluid weight as Pt doesn’t like to
RR: 18/min schistosomiais pt appropriate status, recent indicator of eat because he
normalization of weight history, nutritional status claims that he is
Conscious
Necrosis of liver laboratory values skin fold in view of edema already full
Always in bed
cells LTO: After 1 measurement. and ascites. Skin
and asleep
month of health fold Recommendation
Appears weak Destroyed liver care :
measurement
and restless cells are replaced interventions pt Pt needs
are useful in
Globular or by scar tissue will attain encouragement
assessing
enlarged desirable weight NGT insertion
changes in
abdomen Scar tissue with optimal muscle mass and
Prominent exceeds that of maintenance of Tx: Provide subcutaneous fat LTO:
abdominal functioning liver health diet high in reserves. fully met
veins tissue carbohydrates Provide calories if pt will attain
Tenderness on with protein for energy, desirable body
all quadrants Vit deficiency and intake consistent sparing protein weight with
Dull abdomen anemia with liver for healing optimal
upon function maintenance of
percussion Elevate head health
Anorexia: food Nutrient of bed during Reduces
intolerance imbalanced: less meals. discomfort from Not met:
than body abdominal If pt will not
Slender body
requirement distention and attain desirable
built
decreases sense body weight with
Increased
of fullness optimal
bowel sounds
produced by maintenance of
Oral health
pressure of
intolerance
Offer smaller, abdominal
(-) nausea and
more frequent contents and
vomiting
meals ascites in the
(-) fever stomach.
Provide salt
(-) diarrhea
substitutes, if Decreases
allowed, avoid feeling of
those containing fullness, bloating
ammonia Salt substitutes
enhance the
flavor of foods
and aid in
increasing
Restrict intake appetite
of caffeine, gas ammonia
producing or potentiates risk
spicy and for
excessively hot encephalopathy.
or cold foods. Aids in
reducing gastric
irtrtation/diarrhe
Promote a and abdominal
undisturbed rest discomfort that
periods may impair oral
especially before intake and
meals digestion.
Conserving
Provide oral energy reduces
hygiene before metabolic
meals demands on the
aesthetically liver and
pleasing setting promotes cellular
at mealtime regeneration.
Ed: Suggest Promotes
soft foods, appetite and
avoiding sense of well-
roughage if being.
indicated.
Recommend
cessation of Hemorrhage
smoking. form esophageal
varices may
Encourage pt occur in
to eat meals and advanced
supplementary cirrhosis.
feedings Reduces
excessive gastric
stimulation and
risk of irritation
or bleeding.
Encouragement
is essential fo the
pt w/ anorexia
and
gastrointestinal
discomfort.
NEUROLOGIC INFECTIONS
BACTERIAL MENINGITIS
- Is an inflammation of the arachnoid, pia, and intervening CSF. The infection spreads throughout the
subarachnoid space about the brain and spinal cord and usually involves the ventricles.
FACTORS PREDISPOSING TO BACTERIAL MENINGITIS
head trauma
systemic infection
post surgical infection
meningeal infection
other systemic illness
When pathogenic organisms enter the subarachnoid space >inflammatory reaction (CFS clouding, exudates
formation, changes in subarachnoid arteries (e.g., engorgement with blood, rapture, thrombosis), and congestion of
adjacent tissues.
The pia arachnoid becomes thickened and adhesions form, especially in the basal cisterns. Little change occurs
in brain structures in the early stages.
Almost any bacteria can enter the body causing meningitis
o The most common are:
Meningoccocus (Neisseria meningitides)
Pneumococcus (Streptoccous pneumonia)
Haemophilus influence
These organisms are often present in nasopharynx.
It is not known how they enter the blood stream and the subarachnoid space.
Clinical manifestations
Headache
Prostration
Chills
Fever
N/V
Backpain
Stiff neck
Generalized seizures
Later stage, confused, stuporous, or semicomatose, petechial, or
hemorrhagic rash may develop
The patient may be irritable at first, but as the infection progresses the
sensorium becomes clouded and coma may develop
o Signs of meningeal irritation:
Nuchal rigidity (rigidity of the neck)
Positive finding of Brudzinski’s sign
Positive finding of Kernig’s sign
MENINGITIS
Exudate forms
↓
Meningeal irritation/inflammation
↓
Cortical inflammation
↓
Cerebral edema
↓
Increased ICP
↓
Hemorrhage Hypoxia
Inadequate perfusion
Shock
↓
DEATH
HEADACHES
Is a symptom of an underlying disorder rather than a disease itself. The cause
must be identified so that appropriate treatment can be given.
Clients often-self treat headaches with OTC medication without prescription.
Most headaches do not indicate serious disease however; the nurse should
encourage clients with persistent or recurrent headaches to seek neurologic
assessment.
Serious disorders that typically produce headache include intracranial tumors
and infection, bacterial or viral meningitis, head injuries, cerebral hypoxia, severe
HPN, acute or chronic diseases of the eye, nose, ear, throat.
MANAGEMENT:
1. Treat the two phases of migraine, vasoconstriction and vasodilation,
analgesics such as acetaminophen may relieve mild H/A.
2. Severe headaches respond to ergot preparations but only if they are taking
30-60 minutes after headache onset. Ergot must be taken before the vessels
become rigid from edema in their walls.
- Prescribed orally IV or rectally
- Once the migraine becomes intense ergot is of little value, stronger
analgesic such as codeine sulfate, diphenhydramine hydrochloride
(Benadryl).
3. Apply pressure on the common carotid artery and the affected superficial
artery.
4. Lying in a dark, quiet room with ice on the back of the neck during acute
episodes.
5. Relaxation techniques, biofeedback, or counseling directed at preventing
episodes by helping the client understand tensions and resolve major life
conflicts.
6. Follow a restrictive diet, avoid food and beverages that contain tyramine and
have vasoactive qualities.
MANAGEMENT:
1. Lying in a dark, quiet room with ice on the back of the neck during acute
episodes.
2. Indomethacin (Indocin) medication of choice
3. Tricyclic antidepressant
4. Supportive care – clients tend to become depressed over their condition and
fearful recurrent episodes. Some feel they cannot survive another episode.
Many things can trigger a migraine headache. It is important for the client to
find out what triggers the headache and avoid the trigger, if possible; if avoidance
of the trigger is not possible, the dose of medication can be adjusted.
Adjusting Medications During Menstrual Cycles. Menstruation and ovulation
may trigger migraines. If medications are taken for migraines, a larger dose may be
required during these times.
Identifying the Role of Stress. Stress may trigger migraines. If stressors cannot
be reduced, then medications may need to be increased. Heat intolerance (such as
vacationing in warm climates) may increase headaches. Other factors related to
stress that might trigger headaches include fatigue, excess sleep, and bright
sunlight causing a glare from water, roads, or car hoods.
HEMOPHILIA
TRANSMISSION OF HEMOPHILIA
STAGES
1. Mild: clotting factor level 6 to 30%
• Bruise easily, tendency to nose/gum bleeding
2. Moderate:2 to 5 %
• More frequent bleeding episodes; excessive bleeding after surgery or
trauma
3. Severe: 1% or less
• Spontaneous bleeding; severe bleeding
• Hemarthrosis
MANIFESTATIONS:
• Diagnosed usually in infancy or early childhood
• History of excessive bleeding into any part of the body sponataneoulsy
following trauma
• History of excessive bleeding following circumcision and dental extraction
• PTT of Hemophilia A and hemophilia B is prolonged
• Platelet count and prothrombin time is normal
TREATMENT
• Replace deficient coagulation factor when bleeding episodes do not respond
to local treatment (ice bags, manual pressure or dressing, immobilization,
elevation and topical coagulants such as fibrin foam and thrombin)
• Since the deficient factors are contained in the plasma, fresh plasma and
blood or fresh frozen plasma Is given.
• In major hemorrhage, adequate blood levels were difficult to maintain
without overloading person’s circulation with large volumes of blood and
plasma.
• In classic hemophilia, treatment of choice in acute bleeding is infusion of
concentrate of antihemophilic factor (Factor VII)
• Concentrates prevent circulatory overload and produce fewer adverse effects
• Usually people who are being transfused with Factor VIII concentrates are
easy to acquire AIDS because donors are not screened that well
MANAGEMENT:
I. Blood Factor replacement Therapy
FFP: all clotting factors present
Cryoprecipitate: factor VIII, fibrinogen
Lyophilized factor VIII concentrates
Vit. K dependent complex: Factor VIII, IX, XI, prothrombin
II. Desmopessin for Mild Hemophilia A
It triggers the release of Factor VIII
CLOTTING FACTORS
1. Factor I – Fibrinogen
2. Factor II – Prothrombin
3. Factor III – Thromboplastin
4. Factor IV – Calcium
5. Factor V – Proaccelerin, labile factor, accelerator globulin
6. Factor VI – omitted
7. Factor VII – Proconvertin, stabile factor, serum prothrombin conversion
accelerator (SPCA)
8. Factor IX – Plasma thromboplastin component (PTC)
9. Factor X - Stuart power factor
10.Factor XI – Plasma Thromboplastin antecedent (PTA)
11.Factor XII – Hageman Factor (HF)
12.Factor XIII – Fibrin Stabilizing Factor
Factor IX
Factor VIII
Factor X
Factor V
Calcium
Prothrombin Thrombin
Plasminogen Activator Urokinase
Plasminogen Plasmin
CARDIAC OUTPUT:
• Influenced by blood volume, which Is greater dependent on body sodium
• Thus, sodium homoestasis is central to blood pressure regulation
GENETIC FACTORS:
• It is now thought that essential hypertension results from an interaction of genetic
and environmental that affect cardiac output or both.
ENVIRONMENTAL FACTORS:
• Environmental factors are thought to contribute to expression of the genetic
determinants of
increased pressure.
• Stress, obesity, physical inactivity, and heavy consumption of salt have all been
implicated as exogenous factors in hypertension.
• In both the major pathways for hypertension – primary renal and primary vascular
defects – heavy sodium intake augments hypertension.
MECHANISMS:
• What then are the primary defect in essential hypertension?
• Two overlapping pathways are proposed:
a. Renal retention of excess sodium
The existence of genetic factors that result in reduced renal sodium
excretion – in the presence of normal arterial pressure – as the
initiating event.
Decreased in sodium excretion leads to an increased in fluid
volume and a high cardiac output.
In the face of an increasing cardiac output, peripheral
vasoconstriction occurs as a result of auto regulation to prevent the
over perfusion of tissues that would ensue from an increase cardiac
output.
Auto regulation leads to an increase in peripheral resistance,
however, and along with it an elevation of blood pressure.
At the higher setting of blood pressure, enough additional sodium
can be excreted by the kidneys to equal intake and prevent fluid
retention.
Thus, an altered but steady state of sodium excretion is achieved
(resetting of pressure natriuresis) but at the expense of stable
increases in blood pressure
b. Vasoconstriction and vascular hypertrophy
Such increased resistance is caused either by factors that induce
functional vasoconstriction or by stimuli that induce structural
changes in the vessel wall like
a. Remodeling
b. Hypertrophy
c. Hyperplasia of smooth muscle cells
Leading to thickened wall and narrowed lumen or by both effects.
Vasoconstrictive influences may consist of:
1. Behavioral or neurogenic factors – as exemplified by the
reduction of blood pressure achieved by meditation
(therelaxation response
2. Increase released of vasoconstrictor agents (eg. Rennin,
catecholamines, endothelin)
3. Increased sensitivity of vascular smooth muscle to constricting
agents.
Such vasoconstrictive influences, if exerted chronically, or repeatedly
may themselves cause structural thickening of the resistance vessels,
thus perpetuating increased blood pressure.
Certain vasoconstrictors (eg. Angiotensin II) also function as growth
factors causing smooth muscle hypertrophy, hyperplasia and matrix
deposition.
Conversely, there is evidence that structural changes in the vessel wall
may occur early in the hypertension, preceding rather than strictly
secondary to the vasoconstriction.
Such evidence has led to a hypothesis that genetic or environmentally
induced defects in intracellular signaling in smooth muscle cells affect
cell cycle genes and ion fluxes that modulate both smooth cell growth
and increased vascular tone resulting in wall thickening and
vasoconstriction respectively.
SUMMARY:
• Essential hypertension is a complex disorder that almost certainly has more
than one cause.
• It may be initiated by environmental factors – stress, salt intake, estrogens…
Which affect the variables that control blood pressure in the genetically
predisposed individual.
• In established hypertension, both increased cardiac output and increased
peripheral resistance contribute to the increased pressure.
VASCULAR PATHOLOGY:
• Hypertension accelerates atherogenesis and causes structural changes in the
walls of blood vessels that potentiate both aortic dissection and cerebral
hemorrhage.
• Hypertension is associated with two forms of small blood vessel disease.
a. Hyaline arteriosclerosis
b. Hyperplastic arteriosclerosis
Both lesions are related to elevations of blood pressure, but other
causes may also be involved.
HYALINE ARTERIOSCLEROSIS:
• The vascular lesion consist of homogenous, pink hyaline thickening of the
walls of arterioles with loss of underlying structural detail and with narrowing
of the lumen.
• It is believed that the lesions reflect leakage of plasma components across
vascular endothelium and increasing extracellular matrix production by
smooth muscle cells.
• Presumably, the chronic hemodynamic stress of hypertension or a metabolic
stress in diabetes accentuates endothelial injury, thus resulting in leakage
and hyaline deposition.
• The narrowing of the arterial lumens causes impairment of the blood supply
to affected organs particularly well exemplified in the kidneys.
• Thus, hyaline arteriosclerosis is a major morphologic characteristic of benign
nephroscerosis in which the arteriolar narrowing causes diffuse renal
ischemia of the kidneys.
HYPERPLASTIC ARTERIOSCLEROSIS:
• Related to more acute or severe elevation of blood pressure and is therefore
characteristic of but not limited to malignant hypertension (diastolic pressure
more than 110 mmHg).
• This form of arteriolar disease can be identified with the light microscopy by
virtue of its onion skin, concentrated laminated thickening of the walls of
arterioles with progressive narrowing of the lumens.
Note:
• The kidneys play a very important role in blood pressure regulation.
• Renal dysfunction is essential for the development and maintenance of both
essential and secondary hypertension.
• The kidney influences both peripheral resistance and sodium homeostasis,
and the rennin-angiotensin system appears central to these influences.
• Rennin elaborated by the juxtaglomerular cells of the kidney transforms
plasma angiotensin to angiotension I.
• angiotension I is converted to angiotension II by angiotension converting
enzyme (ACE)
• angiotension II alters blood pressure by increasing both peripheral resistance
and blood volume.
• Increasing peripheral resistance is achieved largely by its ability to cause
vasoconstriction through direct action on vascular smooth muscle.
• Blood volume is increased by stimulation of aldosterone secretion --- which
increases distal tubular reabsorption of sodium and thus, of water.
• The kidney produces a variety of vasodepressor or antihypertensive
substances that presumably counterbalance the vasopressor effects of
angiotensin. These include:
a. Prostaglandins
b. Platelet activating factor
c. Urinary kalikrein – kinin system
d. Nitric oxide
• When blood volume is reduced; the GPR falls, this, in turn leads to increased
reabsorption of sodium by the proximal tubules in an attempt to conserve
sodium and expand blood volume.
• GFR – independent natriueretic factors, including atrial natriuretic factor
(ANF), a peptide secreted by heart atria in response to volume expansion,
inhibit sodium reabsorption in distal tubules and cause vasodilation.
• Abnormalities in these renal mechanisms are implicated in the pathogenesis
of secondary hypertension in a variety of renal diseases, but they also play
important roles in essential hypertension.
PARKINSON’S DISEASE
Brain disorder causing progressive deterioration, with muscle rigidity,
akinesia, and voluntary tremors
Usual cause of death: aspiration pneumonia
One of the most common crippling diseases in the United States
Affects more men than women
Occurs in middle age or later
Pathophysiology:
• Dopaminergic neurons degenerate, causing loss of available dopamine
• Dopamine deficiency prevents affected brain cells from performing their
normal inhibitory function
• Excess excitatory acetylcholine occurs at synapses
• Nondopaminergic receptors are also involved
• Motor neurons are depressed
Causes:
• Usually unknown
• Exposure to such toxins as manganese dust and carbon monoxide
Common Characteristics:
Muscle rigidity and tremor
Resistance to passive muscle stretching
Akinesia and dysarthria and drooling
High-pitched, monotonous voice, and loss of posture control
Excessive sweating and decreased GI motility
Orthostatic hypotension and oily skin and eyes fixed upward
Complications: injury from falls; food aspiration; urinary tract
infections; skin breakdown
Assessment:
Insidrous (unilateral pill-roll) tremor, which increases during stress or anxiety
and decreases with purposeful movement and sleep
Dysphagia
Fatigue with activities of daily living (ADLs)
Muscle cramps of legs, neck, and trunk
Increased perspiration and insomnia, mood changes
Treatment:
• Small, frequent meals and high-bulk food
• Physical therapy and assistive devices to aid ambulation
• Medication: Dopamine replacement drugs, anticholinergics, antiviral agents,
enzyme-inhibiting agents and tricyclic antidepressants
• Surgery used when drug therapy fails
• Destruction of ventrolateral nucleus of thalamus
New research on the pathogensis of Parkinson’s disease focuses on
damage to the substantia nigra from oxidative stress. Oxidative stress is
believed to:
Alter the brain’s iron content
Impair mitochondrial function
Alter antioxidant and protective systems
Reduce glutathione
Damage lipids, proteins, and deoxyribonucleic acid
Nursing Diagnoses:
• Interrupted family processes
• Imbalanced nutrition: less than body requirements
• Bathing or hygiene self-care deficit
• Disturbed body image
• Chronic low self-esteem
• Constipation
• Dressing or grooming self-care deficit
• Feeding self-care deficit
• Impaired physical mobility, social interaction, verbal communication
• Ineffective coping and risk for injury
Nursing Interventions:
• Take measures to prevent aspiration
• Protect the patient from injury
• Stress the importance of rest periods between activities
• Ensure adequate nutrition
• Provide frequent warm baths and massage
• Encourage the patient to enroll in a physical therapy program
• Provide emotional and psychological support
• Encourage the patient to be independent
Monitor:
Vital signs, intake and output
Drug therapy and adverse reactions to medications
Postoperatively: signs of hemorrhage and increased intracranial pressure
MYASTHENIA GRAVIS
Abnormal fatigability of striated (skeletal) muscles
Sporadic but progressive weakness
Muscle weakness exacerbations by exercise and repetitive movement
Muscle weakness improved by anticholinesterase drugs
Initial symptoms related to cranial nerves
With respiratory system involvement, may be life-threatening
Spontaneous remissions in about 25% of patients
Occurs at any age
Three times more common in women than men
Highest in women ages 18 to 25, in men ages, 50 to 60
Transient myasthenia in about 20%of infants born to myasthenic mothers
Pathophysiology:
• Blood cells and thymus gland produce antibosies that block, destroy, or
weaken neuroreceptors (which transmit nerve impulses)
• The result is failure in transmission of nerve impulses at the neuromuscular
junction
Causes:
• Autoimmune disorder associated with the thymus gland
• Accompanies other immune and thyroid disorders
Common Characteristics:
Weak eye closure, ptosis and
Diplopia
Skeletal muscle weakness; paralysis
Complications in respiratory distress, pneumonia, aspiration
Assessment:
Varying assessment findings
Progressive muscle weakness
Extreme weakness and fatigue (cardiac symptoms)
Ptosis and diplopia (the most common sign and symptom)
Difficulty chewing and swallowing
Jaw hanging open (especially when tired) and
Head bobbing
Symptoms milder on awakening worsen as the day progresses
Short rest periods that becomes more intense during menses, after emotional
stress, after prolonged exposure to sunlight or cold, and with infections
Physical Findings:
Sleepy, masklike expression
Drooping jaw
Ptosis
Decreased breath sounds and tidal volume
Respiratory distress and myathenic crisis
Treatment:
Plasmapheresis
Emergency airway and ventilation management
Diet as tolerated
Activity as tolerated; exercise may exacerbate symptoms
Medication: Anticholinesterase drugs, cortiscosteroids, I.V, immune globulin
Surgery: Thymectomy
MULTIPLE SCLEROSIS
• Progressive demyellination of white matter of brain and spinal cord
• Characterized by exacerbations and remissions
• May progress rapidly, causing death within months
• Prognosis varies (70% lead active lives with prolonged remissions
• Highest in women, among people in northern urban areas, in higher
socioeconomic groups
• Family history increases with living in a cold, damp climate
• Major cause of chronic disability in young adults ages 20 to 40
Pathophysiology:
• Sporadic patches of demyelination occur in the central nervous system (CNS),
resulting in widespread and varied neurologic dysfunction
Causes:
• Exact cause unknown
• Slowly acting viral infection
• An autoimmune response of the nervous system
• Allergic response
• Events that precede the onset:
Emotional distress
Overwork
Fatigue
Pregnancy
Acute respiratory tract infections
• Generic factors possibly also involved
Risk Factors:
• Trauma, Anoxia, and toxins
• Nutritional deficiencies
• Vascular lesions
• Anorexia nervosa
Common Characteristics:
• Dependent on the extent and site of myelin destruction
• Sensory impairment
• Muscle dysfunction
• Bladder and bowel disturbances
• Speech problems and fatigue
• Complications in injuries from falls, urinary tract infections, constipation,
contractures, pressure ulcers and pneumonia
Assessment:
• Symptoms related to extent and site of myelin destruction, extent of
remyelination and adequacy of subsequent restored synaptic transmission
• Visual problems and sensory impairment (the 1st signs)
• Blurred vision or diplopia
• Urinary problems
• Emotional lability
• Dysphagia
• Bowel disturbances (involuntary evacuation or constipation)
• Fatigue (typically the most disabling symptom)
• Poor articulation
• Muscle weakness of the involved area
• Spasticity; hyperreflexia
• Intention tremor and gait ataxia
• Paralysis, ranging from monoplegia to quadriplegia
• Nystagmus scotoma
• Optic neuritis and Ophthalmoplegia
Treatment:
General for acute exacerbations, for the disease process and for related signs
and symptoms
High fluid and fiber intake in case of constipation
Frequent rest periods
Medications: I.V. steroids followed by oral steroids, immunosuppresants,
antimetabolics, alkylating drugs, biological response modifiers
Nursing Diagnoses:
• Activity intolerance
• Interrupted family processes
• Imbalanced nutrition: less than body requirements
• Ineffective role performances
• Disturbed thought processes
• Impaired urinary elimination
• Chronic low self-esteem
• Constipation
• Fatigue
• Impaired physical mobility
• Compromised family coping
• Ineffective coping
• Deficient knowledge chronic pain
• Risk for infection and injury
Nursing Intervention:
• Provide emotional and psychological support
• Assist with physical therapy program
• Provide adequate rest periods
• Promote emotional stability
• Keep the bedpan or urinal readily available because the need to void is
immediate
• Provide bowel and bladder training if indicated
• Administer medications
• Monitor:
o Response to medications
o Adverse drug reactions
o Sensory drug reactions
o Muscle dysfunction
o Energy level
o Signs and symptoms of infection
o Speech
o Elimination patterns vision changes
o Laboratory results
AMYOTROPHIC LATERAL SCLEROSI
Most common motor neuron disease of muscular atrophy
Chronic, progressive and deliberating disease that’s invariably fatal
No cure
Also known as Lou Gehrig’s disease
3 times more common in men than in women
Affects people ages 40 to 70
Pathophysiology:
• An excitatory neurotransmitter that accumulates to toxic levels
• Motor units that no longer innervate
• Progressive degeneration of axons that cause loss of myelin
• Progressive degeneration of upper and lower motor neurons
• Progressive degeneration of motor nuclei in the cerebral cortex and
corticospinal tracts
Causes:
• Exact cause unknown
• 10% of patients with amyotrophic lateral sclerosis (ALS) inherit the disease as
an autosomal dominant trait
• Virus that creates metabolic disturbances in motor neurons
• Immune complexes such as those formed in autoimmune disorders
Common Characteristics:
• Muscle weakness
• Atrophy
• Fasciculations
• Respiratory tract infections
• Complications of physical immobility
Assessment:
Mental function intact
Family history of ALS
Asymmetrical weakness 1st noticed in one limb
Easy fatigue and easy cramping in the affected muscles
Physical Findings:
Location of affected motor neurons
Severity of the disease
Fasciculations in the affected muscles
Progressive weakness in muscles of the arms, legs and trunk
Brisk and overactive stretch reflexes
Difficulty talking, chewing, swallowing and breathing
Shortness of breath and occasional drooling
Treatment:
Rehabilitation
May need tube feedings
No restrictions : as tolerated
Medication: muscle relaxants, dantrolene, Baclofen
I.V. or intrathecal administration of thyrotropin-releasing hormone
Nursing Diagnoses:
Imbaanced nutrition: less than body requirements
Anticipatory grieving
Anxiety
Bathing or hygiene self-care deficit
Dressing or grooming self-care deficit
Feeding self-care deficit
Hopelessness
Impaired physical mobility
Impaired airway clearance
Ineffective breathing pattern
Ineffective coping
Compromised family coping
Deficient knowledge (ALS)
Risk for impaired skin integrity
Risk for infection
Nursing Interventions:
Provide emotional and psychological support
Teach about active exercises and ROM exercises
Promote independence
Teach about meticulous skin care
Turn and reposition the patient frequently
Administer ordered medication
Teach how to perform deep-breathing and coughing exercises
Provide airway and respiratory management
Promote nutrition
Teach about swallowing regimens and aspirations precautions
Monitor:
o Muscle weakness
o Respiratory status
o Speech
o Swallowing ability
o Skin integrity
o Nutritional status
o Response to treatment
o Complications
o Signs and symptoms of infection
GUILLAIN-BARRE SYNDROME
A form of polyneuritis
Acute, rapidly progressive, and potentiaaly fatal
Three Phases:
• Acute – lasting from 1st symptoms, ending in 1 to 3 weeks
• Plateau – lasting several days to 2 weeks
• Recovery – coincides with remyelination and axonal process regrowth;
extends over 4 to 3 years; recovery possibly not complete
Pathophysiology:
Segmented demyclination of peripheral nerves occurs, preventing normal
transmission of electrical impulses
Sensorimotor nerve roots are affected; autonomic nerve transmission may
also be affected
Causes:
Unknown
Virus can cause cell-mediated immunologic attack on peripheral nerves
Risk Factors:
Surgery
Rabies or swine influenza vaccination
Viral illness
Hodgkin’s or some other malignant disease
Lupus erythematosus
Common Characteristics:
Symmetrical muscle weakness initially in lower extremities and progressing
to upper extremities
Parethesia
Diplegia
Dyshagia
Hypotonia
Areflexia
Complications:
Thrombophlebitis
Pressure ulcers, contractures and muscle wasting
Aspiration and respiratory and cardiac compromise
Assessment:
Minor febrile illness 1 to 4 weeks before symptoms
Tingling and numbness (paresthesia) in the legs
Progression of symptoms to arms, trunk and finally, the face
Stiffness and pain in the calves
Physical Findings:
Muscle weakness (major neurologic sign)
Sensory loss, usually in the legs (spreads to arms)
Difficulty in taking, chewing and swallowing
Paralysis of the ocular, facial and oropharyngeal muscles
Loss of position sense
Diminishes or absent deep tendon reflexes
Diagnostic Procedures:
• Cerebrospinal fluid (CSF) analysis may slow a normal white blood cell count,
an elevated protein count and in severe disease, increased CSF pressure.
Others:
• Electromyography may demonstrate repeated firing of the same motor unit
instead of widespread sectional stimulation
• Nerve conduction studies show marked slowing of nerve conduction velocities
Treatment:
Primarily supportive
Possible endocrinal intubation or tracheotomy
Volume replacement
Plasmapheresis
Possible tube feeding with endotracheal intubation
Adequate calorie intake
Exercise program to prevent contractures
I.V. beta-adrenergic blockers and parasympatholytics
I.V. immune globulin and possible tracheostomy
Possible gastrotomy or jejunotomy feeding tube insertion
Nursing Diagnoses:
• Imbalanced nutrition: less than body requirements
• Impaired urinary elimination
• Anxiety and fear
• Impaired gas exchange and impaired physical mobility
• Impaired verbal communication and ineffective breathing pattern
The patient will:
Maintain a patent airway and adequate ventilation
Develop alternate means of expressing self
Maintain required calorie intake daily
Establish routine urinary elimination patterns
Maintain joint mobility and range of motion (ROM)
Nursing Interventions:
Establish a means of communication before intubation is required
Turn and reposition the patient
Encourage coughing and deep breathing
Begin respiratory support at the first sign of dyspnea
Provide meticulous skin care
Administer passive ROM exercises
In case of facial paralysis, provide eye and mouth care
Prevent constipation
Provide emotional support
Administer medications, as ordered
Monitor:
o Vital signs
o Breath sounds
o Arterial blood gas measurements
o Level of consciousness
o Continual respiratory function
o Pulse oximetry
o Signs of thrombophlebitis
o Signs of urine retention
o Response to medications