NURSING RESPONSIBILITIES DURING RADIATION THERAPY

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

2. Minimize side effects- In women of child bearing age, RT may cause prolonged or permanent infertility- In prostate radiotherapy, when radioactive seeds have been implanted, there is low, weakly

penetrating radiation for others.- Therefore the client should use a condom for sexual intercourse in the first few weeks after

the procedure.- Also the client should avoid close contact (<6 feet) contact with pregnant women and young

children (younger than 3 years) for more than 5 minutes a day during the first 2 months following implantation.

- If systemic symptoms occur, such as weakness and fatigue occur, the patient may need assistance with ADL and personal hygiene.

- When a patient has a radioactive implant in place, nurses and other health care personnel need to protect themselves as well as the patient from the effects of radiation.

3. Provide a non-stressful environment- Some people who receive radiation to the head and neck experiences redness and irritation

in the mouth, a dry mouth, difficulty in swallowing, changes in taste or nausea.- Other possible side effects include a loss of taste, earaches and swelling- Skin texture might change and jaws may feel stiff

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

6. Patients might feel depressed, afraid, angry, frustrated, alone or helpless- Peer support groups may meet at your hospital- Emotional and spiritual encouragement also is important to the healing process.

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.

8. For lactating mothers undergoing radiation therapy.- Advise pt. not to breastfeed to prevent adverse effects to fetus.- Advise pt. to drink plenty of fluids to prevent dehydration.- Monitor nutritional status.

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.

Internal Radiation Therapy:- Patient should receive a simple explanation of the procedure and necessary precautions

so he will know what to expect and what is expected of him.- Time is taken to answer his questions and dispel misconceptions.

- After implantation, temperature is taken every 4 hours, an increase over 38 degrees is perorted.

- Any radioactive material should be handled with a long forceps, never with hands.- All dressings should be checked before disposal.- Patient’s visitors are required to maintain a 3 feet distance from the patient.- Health workers should know the time at which the radioactive implant is to be removed

and should have necessary equipment in advance and to remind the person responsible for removal.

Nursing responsibilities for the patient receiving radiation therapyTeletherapyThe radiation source is exterior to the tumor such as the use of linear accelerator.

1. Remove all opaque objects such as pins, buttons and hairpins and replace clothing with a gown for body X-rays.

2. Have patient perfectly still; maintain position with the use of foam, plastic, plaster (material) devices and/or variety of other materials that can conform to the patient’s anatomy.

3. Tell the patient there will be no sensation or pain accompanying radiation therapy.4. Advise the patient that he will be alone in the room for the protection of the technician, but will

be in voice contact.5. Determine from the physician what has been told to the patient about radiation therapy6. If series of treatments are to be given, include the patient in the planning phase.

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.

Techniques while working with patients undergoing radiation therapy:1. Put on shoe covers and protective gloves before entering patients room.2. Work quickly but effectively and courteously. Minimize your time in the room.3. Note: No matter how long you are in the room, you will not receive a radiation exposure large

enough to cause adverse effects.4. Leave all trash, linens, and food trays in the room5. After leaving the room, wash your hands.6. Personnel should not smoke, eat or drink in areas where unencapsulated radio active is used in

patient treatment or if the possibilities of contamination of the hands persist.

General procedures for obtaining specimens from therapy patients1. Read the instructions posted in the door.2. Specimen containers must be labeled with radioactive material labels or tape to identify them as

radioactive.3. Put on a face mask if the patient has a tracheostomy or has symptoms of a respiratory infection.4. Never use sink for handwashing/ use telephone/ cellphones while in the room.

Nursing considerations in external radiotherapy:1. It is important that the patient receive an explanation of the procedure and precautions.2. Orient the patient and his family in advance, answer their questions and reassure them that the

treatments are well controlled and adequate protection is used.3. Following the treatment, observe for possible reactions.4. Instruct and suggest care of the skin5. Avoid patient to contact with other persons with infections6. General supportive care applicable to all patients receiving radiotherapy include extra rest, an

increase fluid intake and a high calorie, high protein, high vitamin diet7. When reaction develops, reassure that they are not unexpected and are not an indication of a

recurrence or worsening of his cancerous disease.

Nursing responsibilities in internal radiotherapy:1. An explanation to the patient of the procedure and the precautions2. Place the patient in isolation in a single room and indicate that no visitors are allowed3. Provide a telephone and radio or television and reading materials4. In close contact with patient always wear a lead apron or gown and rubber gloves5. Wear a monitoring badge which records the amount of radiation received by the patient6. Visit patient once in a while7. Nurse should wash hands thoroughly after any contact with patient and other equipment8. Linens, dishes, syringes, needles and other treatment equipment are monitored before being

returned.

For infants and children- No cream, no lotion should be applied to radiation areas until the treatment series is completed.- If creams contain any metal, these could distort or interfere with the entrance of radiation.- If the head will be irradiated, a dental consult may be suggested. This can slow healing of a

tooth extraction.

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.

For clients undergoing radiation:- Clients with radioactive implants are a source of radiation to the immediate environment.

- The nurse who is in close contact with such clients also needs to wear a lead apron.- Nurses must deal safely with radioactive body discharges by wearing gloves and in some

instances placing excreta in containers for special disposal.- The nurse must wash gloved hands well before and after removing the gloves and placed

contaminated materials in a special containers for special disposal.- Nurses must make sure they understand treatment and the precautions they need to take.

Often such clients are restricted to bed or to a confined area to protect others.- These clients need emotional support to deal with the precautions and will likely accept

treatments and precautions better when they know what will happen, when and why.- Exposure of the reproductive organs of mice and rabbits to X rays has caused gene mutations

that resulted in malformed offsprings and geneticist believe that comfortable effects can occur in humans.

- Knowing these, great care is taken to protect both the nurse and patient from unnecessary exposure.

- Chemotherapy and radiation therapy: knowledge of the appropriate routes, doses and reactions is required.

- Infection control: nurses must be aware of standard infection control precautions.- Nausea and vomiting are most likely to occur when the radiation dose is high or if the abdomen

or another part of the digestive tract is irradiated. Sometimes nausea and vomiting occur after radiation to other regions, but in these cases the symptoms usually disappear within a few hours after treatment.

- Nausea and vomiting can be treated with antacids, Compazine, Tigan or Zafran.- Fatigue frequently starts after the 2nd week therapy and may continue until about 2 weeks after

the therapy is finished.- Patients may need help to limit their activities, take naps and get extra sleep at night.

Nursing Diagnoses and its Nursing Interventions

Nursing Diagnosis: Impairment of skin integrity due to irradiationNurisng interevntions:

- For patients with xerostomia undergoing irradiation- Patient education- Nursing care involves assesing the physical and emotional aspects of the patient before, during

and after a course of head and neck irradiation, and providing interventions, education and support.

- During radiation therapy, the patient should be very gentle with the skin in the treatment area. This nurses can suggest the following:

- Avoid irritatitng treated skin.- When washing, use only lukewarm water and mild soap, pat dry.- Do not wear tight clothing over the area.- Do not rub, scrub or scratch the skin in the treatment area.- Avoid putting anything that is hot or cold, such as heating pad or ice packs on treagted skin.- Ask the doctor or nurse to recommend skin care products that will not cause skin irritation.- Do not use any powders, creams, perfumes, deodorants, body oils, ointments, lotions or home

remedies in the treatment area while you’re being treated and for several weeks afterward unless approved by the doctor.

- Do not apply skin lotion within 2 hours of treatment.- Avoid exposing the radiated area to the sun during treatment, after is over, ask the doctor or

nurses how long you should continue to take extra precautions in the sun.- Avoid extremes of temperature- Avoid rough and tight garments.- Avoid rubbing or scratching the area the nurse needs to explain that during treatment, the

patient must stay in absolute bedrest.- Nurses should know also that over exposure to radiation may include burning and scarring of

the skin or lungs; a tendency to develop cataracts; a tendency to develop cancer; to destroy blood producing tissue.

- 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.

Nursing Diagnosis: Potentials for infection due to bone marrow depressionNursing Intervention:

- Monitor blood counts weekly.- Teach person to avoid infection by frequent handwashing and good nutrition, hygiene and good

habits.- Teach persons signs of infection to report to physician.

Nursing Diagnosis: Potential for bleeding due to BM depression:Nursing Interventions:

- Monitor platelet counts weekly- Teach person to avoid physical trauma and aspirin while platelets are low- Teach person signs of hemorrhage to report to physician- Monitor stool, integument for signs of hemorrhage- Use direct pressure over injection sites until bleeding stops

Nursing Diagnosis: Activity intolerance due to anemiaNursing intervention:

- Discuss fatigue and its causes with person- Encourage good nutrition and plenty of rest

Nursing Diagnosis: Alteration in Nutrition: Less than body requirements due to anemiaNursing intervention:

- Monitor diet for efficient calories- Contact dietitian if indicated- Monitor weight weekly or daily- Assess person’s understanding of nutrition and teach as necessary

Nursing Diagnosis: Alteration in mucous membranes due to irradiationNursing interventions:

- Monitor oral cavity daily- Encourage bland diet, no smoking, no alcohol- Good oral hygiene and saline rinses every 2 hours while awake may help- Ensure professional dental care- Avoid foods that are dry and thick

Care of the teeth, gums, mouth and throat- Avoid spices and coarse foods such as raw vegetables, dry crackers and nuts- Do not eat or drink very hot foods- Do not smoke, chew tobacco or drink alcohol because tobacco and alcohol can further irritate

mouth sores.- Stay away from sugary foods and snacks.- Ask your doctor or nurse to recommend a good mouthwash. The alcohol content in some

mouthwashes has a drying effect on mouth tissues.- Sip cool drinks often throughout the day.- Eat or chew sugar free candy or gum to help keep your mouth moist

- Moisten food with gravies and sauces to make eating easier.- Gentle oral hygiene is essential to remove debris, prevent irritation and promote healing

Mucositis: do not remove membrane

Nursing Diagnosis: Alteration in bowel elimination: diarrhea due to irradiationNursing interventions:

- Monitor stool- Give low residue diet/antidiarrhea medication as prescribed.

Nursing Diagnosis: Alteration in comfort and vomiting due to irradiationNursing interventions:

- Plan rest periods before and after meals- Administer antiemetics as prescribed- Monitor fluids and electrolytes

Nursing Diagnosis: Alteration in comfort: headache due to irradiationNursing Interventions:

- Monitor pain- Administer analgesics as prescribed

Nursing Diagnosis: Disturbance in self concept due to alopeciaNursing interventions:

- Encourage verbalization of feelings- Suggest use of wigs, scarf’s, hats, etc- Instruct person on hair care

Nursing Diagnosis: Alteration in urinary elimination patterns due to irradiationNursing interventions:

- Monitor urine for blood- Monitor for dysuria or urinary frequency- Encourage fluid intake

Nursing Diagnosis: Social isolation due to irradiationNursing Interventions:

- Explain and discuss irradiation precaution- Encourage telephone calls- Suggest television, radio or tape player- Stop by door to say “hello”

HYPERSENSITIVITY REACTIONS Exaggerated or inappropriate response to specific antigen Anaphylaxis, allergies, transfusion reactions, graft rejections

TYPE I – Anaphylactic / Immediate Hypersensitivity ReactionCommon antigens: Insect bites, drugs, food, pollen, x-ray contrast mediumSigns and Symptoms: Urticaria(hives) caused by foods- eggs, fish , nuts, drugs

Atopic allergies – less severe and more common form seen in about 15% of the population. Atopy means inherited hypersensitivity. Common Antigens include:

Inhalants – dust, pollens, mold spore, animal danderContactants – fibers in wool, fur, nylon, plant oils, osaps,

cosmetics, perfumes, hair dyes, nickel in jewelry, clothings, occupational chemicals, changes in temperature and stress

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 – bronchospasm2. Increase in vascular permeability – urticaria(hives or tissue edema3. 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 INursing 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 immunotherapy3. Control the environment – house dust; animal dander; pollens; fungus4. 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

Types of Transfusion Reactions:1. Acute hemolytic Reaction/hemolytic transfusion reaction

- Infusion of ABO incompatible with blood, RBCs or components containing 10 ml or more RBC’s antibodies in the recipients plasma attach to the antigens on transfused RBC’S ---RBC destruction. Chills, fever, low back pain, flushing, tachycardia, tachypnea, hypotension, vascular collapse, hemoglobinuria, bleeding, ARF, shock, cardiac arrest, death

2. Febrile, Non Hemolytic ( most common)- Sensitization to donor’s WBC’s, platelets or plasma proteins- Sudden chills and fever, headache, flushing, anxiety, muscle pain

3. Mild Allergic reaction involves sensitivity to foreign plasma proteins- Flushing, itching, urticaria

4. Anaphylactic reaction- Infusion of IgA protein to IgA deficient recipient who has developed IgA antibody- Anxiety, urticaria, wheezing, tightness and pain chest, difficulty swallowing, progressing to

cyanosis, shock and possible cardiac arrest5. Delayed hemolytic reaction

- An amnestic immune response that occurs 7-14 days after transfusion. Sensitization to RBC antigen not ABO system

- Fever, chills, back pains, jaundice, anemia, hemoglobinuria6. Graft-versus-Host Disease_Pt.

- Immunodeficient person receives lymphocytes begin to reject cells 4-30 days after the transfusion.

- Anorexia, nausea, diarrhea, high fever, rash, stomatitis, liver dysfunctionPrevention of transfusion Reaction: Accurate laboratory testing; careful blood administration

TYPE III – Hypersensitivitis/Immune Complex- Involves antigens, antibodies (IgG and IgM) and the complement system. When certain

ratios of antigen to antibody occur, the immune complexes are small enough to escape phagocytosis, but they become trapped in the basement membrane under the endothelium of blood vessels, where they activate complement and cause inflammation

- Glomerulonephritis and rheumatoid arthritis- Antihistamines and salicylates; steroids – prednisone; epinephrine

TYPE IV – Cell mediated or Delayed Hypersensitivity Reaction- Usually appears 12-72 hours after exposure to an allergen. Occurs when allergens are taken

up by antigen-presenting cells that migrate to lymph nodes and present the allergen to Tcells, which then proliferate. Some of the new Tcells return to the site of allergen entry into the body, where they produce gamma interferon, which activates macrophages, and tumor necrosis factor, which stimulates an inflammatory response.

- Mycobacterium tuberculosis, poison ivy

Graft and Organ Donation- Types: Isograft/syngraft: Autograft; Synthetic Graft; Xenograft: Allograft- Purposes: Art/Aesthetic; prevention of infection; prevent fluid loss- Forms of Graft: skin graft; flap graft; flee graft- Pre-op and Post-op Care

- Recipient Site: free of infection; good vascularization in the area; cleaned aseptically before surgery/ prevent fluid collection on the graft; prevent infection; prevent graft movement; promote adequate circulation in the area

- Donor Site: celan site; free of infection/ cover dressing during the 1 st 24 hours within mesh gauze until the site is dried up; promote circulation; analgesics; nutrition

Tissue Rejection – healthy defense mechanism of the bodyFirst set rejection: recipient receives unmatched skin

2-3 days the body accepts the skin, there is vascularization6 - 10TH day + lympadenopathy10 – 14th day + appearance of rejection taking place with the appearance of

macrophages and T lymphocytes on the site of transplant12 – 40th day + necrosis, tissue implanted will now shed off

Second set rejection: no vascularization, direct sloughing off tissue

Organ Transplantation for end stage or failure and do not respond to conventional therapyRecipient: free of irreversible of infection or malignancy

End stage of failure and do not respond to conventional therapyNo anatomical problem that would lead to difficulty of transplantation Therapeutic or benefit of the patientAbility 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

Types of Rejection: hyper acute; acute; chronic

Therapies to prevent Rejection: Immunosuppressive drugs; cyclosporine; azaththjioprine; glucocorticoids; ALG

Summary of Hypersensitivity Reactions

Property Type IAnaphylactic

Type 2 Cytotoxic and Cytolytic

Type 3 Immune Complex

Type 4 Cell Mediated or

Delayed ResponseMediators IgE, IgG,

Baasophils mast cells

IgG, IgM, complement

sytem

IgG, IgM T cells, macrophages

Allergens Drugs, stings BT Soluble agents like drugs

PTB, Ca

Response to Skin Test

(+) wheal and flare within 30 minutes

Not done Erythema, edema Tissue induration

Pathophysiology and effect

Secondary to prostaglandin,

bradykinin, serotonin, histamine

Destruction of cells, RBC

Acute inflammatory

reagent

Tissue destruction

Examples Systemic anaphylaxis,

asthma

ABO incompatibility

Serum sickness TB, organ donation

DISRUPTIVE INFLAMMATORY RESPONSES

COMMUNICABLE DISEASE IN CHILDRENNursing Process OverviewAssessment: History Taking: Local or systemic infection; history of travel; any contact with animal or animal products; any animal or insect bites; any illnesses that compromises body defenses; what medications taken; vaccination history

Clinical Manifestations:1. Assess for clinical manifestation of infection2. Obtain specimens of blood, urine, stool, sputum, throat swabbing, nasal secretions, pyrogenic

exudates for bacteriologic studies3. 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 study5. Carry out appropriate skin tests for specific diagnostic reactions as directed

Nursing Diagnosis:1. Fluid and electrolyte imbalance2. Altered thermoregulatory status3. Fever4. Potential for spread of infection5. Altered respiratory status6. Altered elimination status

7. Potential for serious systemic complications8. Ineffective coping and social isolations9. Knowledge deficit

Planning and Implementation:1. Implement therapeutic plan to treat infection2. Ensure hemostasis3. Measure to prevent cross contamination of infection4. Prevent overwhelming infection in the immunocompromised patient5. Relief of symptoms of infection6. Enhance coping mechanism to promote adaptation

Immunization – receiving immunity against a number of dangerous infections.Immunity – ability to combat a particular antigen, passive or active Active Immunity – when the child produces antibodies after the natural invasion of a pathogen

Naturally Acquired Active Immunity – ability to produce antibodies rapidly should be specific antigen invade again; lasting.

Artificially Acquired Active Immunity – when pathogens are artificially injected into the child by immunization. Should be specific antigen enter again, antibodies are produced against the pathogen that are just as lasting as those produced are in naturally acquired active immunity.

Passive Immunity – IgG antibodies that a woman possesses, either through immunization or through having a disease are transferred across the placenta to a fetus in utero.Naturally Acquired Passive Immunity – fetus does not make antibodies but received them.Artificially Acquired Passive Immunity – injection of antibodies made synthetically or obtained

from animal serum to the child to give rapid immunity lasting approximately for six weeks.

Immunization Schedule

Vaccine Indication Age Dose Frequency Route Side effectsBCG

(1 dose at birth)

Tuberculosis At birthSchool entrant

1 dose (0.5 ml)

2x Intradermal deltoid

Pain, fever, local

abscessDPT

(3 doses)0.5 ml 3x IM vastus

lateralisSwelling,

feverOPV 2 drops 3x oral None

HEP B(3 doses)

0.5 cc 3x IM vastus lateralis

Local reaction – swelling,

feverMEASLES 9 months 0.5 cc once Subcutaneous,

deltoid, gluteal

Fever, local reaction

EXAMINATION – HIGHER CEREBRAL FUNCTION

MEMORY TESTTesting 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.

Note: Retrograde amnesia – loss of memory of events leading up to a brain injury or insult.Post traumatic amnesia – permanent loss of memory of events for a period following a head injury.

REASONING AND PROBLEM SOLVINGTest patient with two-step calculation, e.g. “I wish to buy 12 articles at 7 pence each. How much change will I receive from L1?

Ask patient to reverse 3 or 4 random numbers.Ask patient to explain proverbs.Ask patient to sort cards into suits.The examiner must compare patient’s present reasoning ability with expected abilities based on

job history and/or schoolwork.

EMOTIONAL STATENote: Anxiety or excitement Depression or apathy Emotional behavior Uninhibited behavior Slowness of movement or responses Personally type or change

COGNITIVE SKILLDominant hemisphere disorders

Listen to language pattern – hesitant - fluent

Expressive dysphasiaReceptive dysphasia

Does the patient understand simple/complex spoken commands?e.g. “Hold up both arms, touch the right ear with the left fifth finger.”

Receptive dysphasia

Ask the patient to name objects Nominal dysphasiaDoes the patient read correctly? DyslexiaDoes the patient write correctly? DysgraphiaAsk the patient to perform numerical calculation, e.g. serial 7 test, where 7 is subtracted serially from 100.

Dyscalculia

Can the patient recognize objects? E.g. ask the patient to select an object from a group.

Agnosia

Non- Dominant hemisphere disordersNote patients ability to find his way around the ward or his home.

Geographical agnosia

Can the patient dress himself? Dressing apraxiaNote the patient’s ability to copy a geometric pattern, e.g. ask the patient to forma star with matches or copy a drawing of a cube.

Constructional apraxia

Mild mental function tests and Functional activity questionnaire are used in the assessment of DEMENTIA

MENTAL BEHAVIOR

Level of Consciousness:

Alert - awake, quick, clear mentation, normal response to tactile, verbal, painful stimuli

Drowsy - responds to stimulus, may be aroused quickly but easily falls asleep; may yawn frequently, fall asleep during meal or lengthy conversation.

Obtunded - can be aroused and responsive, but he’s usually confused and falls backto sleep as soon as he is not directly stimulated

Stuporous - does not respond spontaneously to environment, vigorous, often painfulstimuli are necessary to arouse the patient. When stimulated, he movebut movements are not purposely.

Semi-comatose - Responsive only to deep painful stimulationComatose - no response to any stimulation, movement are absent except for some

muscle reflex contractionConfusion - state of mental confusion and excitementApathy - lack of emotional responseAura - a sensory phenomenon that may precede a convulsion, such as flash of

light, or ringing bells.

HANDOUT IN NEUROLOGIC NURSING

NOMENCLATUREAbberration - deviation from normal structure of behaviorDecerebrate - deprived of cerebral functionDenervate - to interrupt motor/sensory nerve supply to a party by drug

injection or operationContrecoupinjury - injury to the brain produced on the side opposite that of the

primary injuryCerebral Concussion - brain injury resulting from violent jarring of the brain due to blow

to the head, fall

SURGICAL PROCEDURECraniotomy - surgical opening through the cranium

Craniectomy - the surgical removal of a part of the skullChordotomy - division of the long tract of the spinal cord, referring usually to the

antero-lateral pathways that transmit pain

CSFHypoglycoorrhakia - low sugar in CSFPleocytosis - increased WBC in CSFXaantochromia - yellowish discoloration of the CSF

HEADMacrocephalous - having an unusually large headMicrocephalous- having an unusually small headCephalococle - protrusion of the brain from the cranial cavityCephalhematoma - 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 gaitFestination - morbid acceleration of gait

1. Propulsion - tendency to push or fall forward in walking2. Retropulsion - walking backward, involuntary

Scissors - short, slow steps, with legs alternately crossing over each other

POSITIONEmprosthothonus - 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 sideOrthotonus - titanic spasm marked by rigidity of the body in a straight line

MOVEMENTS, COORDINATION, TONECoordination - harmonious action of muscle groups in performing complex

movementApraxia - inability to perform certain acts or purposeful movements

without motor loss.Dyskinesia - defect in voluntary movementsAkinesia - absence of muscle synergia - lack of coordination between muscle groups; movements are in

serial order instead of being made togetherDysmetria - inability to fix the range of a movement; undershoots or

overshootsPass-pointings - tendency to veer to one side of tip of nose or finger when trying

to touch itBradykinesia - extreme slowness of movementSpasm - involuntary, sudden movement or muscular contractionFasciculation - produce localized, incoordinated, involuntary twitching of a single

muscle group while muscles are at rest.Tic - coordinated, stereotyped spasmodic muscular contraction of the

face, neck or shoulder muscles that may be involuntary or the result of a habit

Tremor - rhythmic quivering: involuntary movement of a part of the body resulting from the alternate contraction of opposing muscles1. Coarse Tremors – oscillations are relatively slow (6-7 per sec.)2. Fine Tremors – rapid, characterized by oscillation of 8-10 times per

secondTwitching convulsions - quick spasmodic contraction of muscles paroxysm of involuntary

muscular contractions and relaxations1. Clonic movement - one having intermittent contractions, muscles

alternately contract and relax2. Tonic – one which the contractions are maintained for a time which

usually draw joints into position of flesion/extensionChorea/Choreiform - hallmark of chorea; are purposeless, rapid, jerky usually involving

the movements extremities and trunk with facial grimacing, ex. Flexing and extending fingers

Ballismus - quick jerky shaking movementHemiballismus - quick jerky movement involving half of the bodyAthetosis - repeated involuntary movement of slow, squirming, writhing,

twisting type.Nystagmus - involuntary movement of the eyeballsRigidity - resistance all through the ROMSpasticity - resistance of movement at the beginning then, giving inCogwheel Rigidity - Muscular resistance is characteristically intermittent when the

muscles are palpated.Rest Tremors - involuntary muscle movement at restIntention Tremors - involuntary movement seen when doing somethingHypotonia - decreased muscle toneFlaccidity - muscular weakness, softness and flabbiness, no motor responseNuchal rigidity - stiffness of the neck

Paralysis - temporary suspension or permanent loss of voluntary motion and sensation in a body part

Spastic Paralysis - involved part of the body is in a state of muscular rigidity or tenseness

Flaccid Paralysis- involved part is completely relaxed or limpParaplegia - paralysis of the lower half of the bodyHemiplegia - paralysis of the longitudinal half of the bodyDiplegia - paralysis of like parts on either side of the bodyQuadriplegia - paralysis of the four extremitiesParesis - muscle weakness of partial or incomplete paralysisBlepharopthosis - dropping of the upper eyelid

SENSATIONParesthesia - peculiar sensation of numbness, prickling, tingling.Hyperesthesia - unusual sensitivity to pain or sensory stimuliNeuralgia - severe Lancination pain along the course of a nerveMyalgia - muscular painAgnosia - loss of comprehension of audio-v, visual or other sensation

1. Auditory – inability to interpret sounds2. Optic – inability to interpret images seen3. Tactile – inability to distinguish objects by using sense of touch

Asteriognosis - is the inability to recognize familiar objects by touch or manipulation

Diplopia - double visionAnopsia - loss of vision in one eyeHomonymous Hemianopsia - loss of one-half of the field of vision in one eyeAnosmia - absence of the sense of smell

SPEECH AND LANGUAGEDysarthria - difficulty in articulationDysphasia - impairment in speechAphasia - loss or the inability to use or understand spoken or written

language; it may exist without intellectual impairment1. Sensory (receptive aphasia) – inability to comprehend or

understand oral or written communication2. Motor (broca’s) aphasia - can’t speak, write although can

comprehend3. Global aphasia – an almost total language loss manifested in

minimal response in every phase of language4. Auditory aphasia – difficulty of understanding spoken word5. Nominal aphasia – inability to attach meaning to words read

Alexia - inability to read, word blindnessAgraphua - inability to express oneself in writing

1. Absolute – complete inability to write2. Acoustic – inability to write words head3. Cerebral – inability to express thoughts in writing4. Motor- inability to write due to muscle coordination5. Optic – inability to copy words

INTRACRANIAL HEMORRHAGEExtradural/Epidural - bleeding beneath the cranium and outside the dura, frequentlySubdural Hemorrhage - hemorrhage between the dura and arachnoid; increasing ICP

develop slowly; personality changes maybe the first noticeable signSubarachnoid Hemorrhage - hemorrhage between the arachnoid and pia mater into

CSF

NEUROLOGIC SIGNSA. Cardinal symptoms: increasing or widening pulse pressure

Decreasing PRIncreasing headachePappil edemaDecreased mental awarenessDecreased in RR

B. Other signs and symptoms which may or may not develop:1. Vomiting – may or not be projectile2. Motor deficits – weakness or paralysis of any part of the body3. Sensory Disturbances of any part of the body4. Awkwardness – may mean weakness; difficulty or coordination5. Speech disturbances6. Convulsion7. incontinence/retention

C. Localizing Symptoms1. 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, asteriognosis3. Temporal Lobe – defects in visual field, taste or hearing, smell of burning rubber4. Occipital Lobe – visual disturbance5. Cerebellum

Ataxia – muscle coordination especially manifested when voluntary muscular movements are attempted.

Tremors, nystagmus, hypotonia6. Basal Ganglia

Athetosis, chorea, hemiballismus, tremor

Pathopysiology

Cause: excessive alcohol consumption, reduced protein intake, exposure to certain chemicals or infectious schistosomiasis

↓Episodes of necrosis involving the liver cells

↓Destroyed liver cells are replaced by scar tissue, the amount of which in time may exceed that of the

functioning liver tissue↓

Early in the disease, the liver is apt to be large and its cells loaded with fat↓

Later as replacing scar tissue contracts, it becomes small↓

Also, its surface often becomes rough, bec the scar within it is disposed in coarse bundles, which contract and pull in the capsule at certain points and cause the island of residual normal tissue and of

new regenerating liver tissue to project in the little lumps↓

Liver Enlargement → Activity Intolerance r/t fatigue↓

Portal Obstruction and Ascites → Ineffective Breathing Pattern r/t↓ intra- abdominal fluid collection (ascites)

Body Image Disturbed r/t personal vulnerabilityInfection and peritonitis → Impaired Skin Integrity r/t compromised

↓ immunologic statusGastrointestinal varices → Risk for Injury and bleeding r/t altered clotting

↓ MechanismEdema → Fluid Volume Excess r/t compromised

↓ regulatory mechanismVit deficiency and anemia → Nutrition Imbalanced: less than body

↓ requirements r/t oral intolerance and liver Cirrhosis

Mental deterioration → Risk for acute confusion r/t inability of the liver to detoxify certain enzymes or drugs

Prioritization of Problems:1. Nutrition Imbalanced: less than body requirements r/t oral intolerance and liver cirrhosis - overt2. Ineffective Breathing Pattern r/t intra- abdominal fluid collection (ascites) - overt3. Fluid Volume Excess r/t compromised regulatory mechanism - overt4. Impaired Skin Integrity r/t compromised immunologic status - overt5. Activity Intolerance r/t fatigue - overt6. Body Image Disturbed r/t personal vulnerability - overt7. Risk for Injury and bleeding r/t altered clotting mechanism -covert8. Risk for acute confusion r/t inability of the liver to detoxify certain enzymes or drugs – covert

Assessment Pathophysiology Objectives Intervention Rationale Evaluation

S: “Nahihirapan akong huminga”

O: v/sTemp: 36.7°CBP: 110/60 mmHgPR: 94/minRR: 18/minConscious:

dysphericPrefers to be in

bedPrefers to sleepAssisted w/ ADL

by SOEasily fatigued:

pallorAppears weak

and restlessOn O2 at 1-2\

LPM/NCIrritable thus

changes position once in a while

(+) coughing, non-productive

Enlarged abdomen (ascites)

A: Ineffective Breathing Pattern r/t

Cause: excessive alcohol consumption, reduced protein intake, exposure to certain chemicals and infectious schistosomiais

Necrosis of liver cells

Destroyed liver cells are replaced by scar tissue

Scar tissue exceeds that of functioning liver tissue

Portal obstruction and ascites

Ineffective Breathing Pattern

STO: After 8 hours of health care interventions pt will be free of dyspnea, cyanosis, w/ ABG’s and vital capacity w/in acceptable rangeLTO: After 2 weeks of health care intervention pt will establish a normal effective respiratory pattern

DX: Monitor respiratory rate, depth and effort

Auscultate breath sounds, noting crackles, wheezes, rhonchi Investigate changes in level of consciousness

Monitor temp. note presence of chills, increased coughing, changes in color/character of sputum Monitor serial ABG’s pulse oximetry, vital capacity measurements, chest x-rays Tx: keep head of bed elevated. Position on sides

Rapid shallow respirations/dyspnesmay be present bec. Of hypoxia and or fluid accumulation in abdomenIndicates developing complications, increasing risk of infection

Changes in mentation may reflect hypoxemia and respiratory failure w/c often accompany hepatic coma.

Indicative of onset infection ex. Pneumonia

Reveals changes in respiratory status developing pulmonary complications

Facilitates breathing by reducing pressure on the diaphragm and minimizes risk of aspiration of secretions

STO: fully metpt is no longer dyspheric and O2 is no longer needed

Factors:Pt is very cooperative and willing to participate in any therapy

LTO: fully met if pt will establish a normal or effective respiratory pattern

Ascites Provide supplemental o2 as indicated

Conserve pt’s strength by providing rest periods and assisting with activitiesChange position in every 2 hours

Assist with paracentesis or thoracentesis as indicated

Ed Encourage frequent repositioning and deep breathing exercises/coughing as appropriateDemonstrate with respiratory adjuncts

Maybe necessary to treat/prevent hypoxia. If respiration/oxygenation inadequate/ mechanical ventilation maybe requiredReduces metabolic and oxygen requirements

Promotes expansion and oxygenation of all areas of the lungsParacentesis and thoracentesis are performed to remove fluid from the abdominal and thoracic cavities respectively.

Aids in lung expansion and mobilizing secretion

Reduces incidence of atelectasis, enhance mobilization of secretions

Assessment Pathophysiology Objectives Intervention Rationale Evaluation

S: “wala akong ganang kumain”

O: v/sTemp: 36.7°CBP: 110/60 mmHgPR: 94/minRR: 18/minConsciousAlways in bed and

asleepAppears weak and

restlessGlobular or

enlarged abdomenProminent

abdominal veinsTenderness on all

quadrantsDull abdomen

upon percussionAnorexia: food

intoleranceSlender body builtIncreased bowel

soundsOral intolerance(-) nausea and

vomiting(-) fever(-) diarrhea

Cause: excessive alcohol consumption, reduced protein intake, exposure to certain chemicals and infectious schistosomiais

Necrosis of liver cells

Destroyed liver cells are replaced by scar tissue

Scar tissue exceeds that of functioning liver tissue

Vit deficiency and anemia

Nutrient imbalanced: less than body requirement

STO: After 8 hours of health care intervention pt will be able to demonstrate progressive weight gain toward goal with pt appropriate normalization of laboratory valuesLTO: After 1 month of health care interventions pt will attain desirable weight with optimal maintenance of health

DX: Measure dietary intake by calorie count

Weigh as indicated, compare changes in fluid status, recent weight history, skin fold measurement.

Tx: Provide diet high in carbohydrates with protein intake consistent with liver function Elevate head of bed during meals.

Offer smaller, more frequent meals Provide salt substitutes, if

Provide information about intake needs or deficienciesIt maybe difficult to use weight as indicator of nutritional status in view of edema and ascites. Skin fold measurement are useful in assessing changes in muscle mass and subcutaneous fat reserves.Provide calories for energy, sparing protein for healing

Reduces discomfort from abdominal distention and decreases sense of fullness produced by pressure of abdominal contents and ascites in the stomach.Decreases feeling of fullness, bloatingSalt substitutes

STO: not metPt was not able to demonstrate progressive weight gain

Factors:Pt doesn’t like to eat because he claims that he is already full

Recommendation:Pt needs encouragementNGT insertion

LTO: fully metif pt will attain desirable body weight with optimal maintenance of health

Not met:If pt will not attain desirable body weight with optimal maintenance of health

allowed, avoid those containing ammonia

Restrict intake of caffeine, gas producing or spicy and excessively hot or cold foods.

Promote undisturbed rest periods especially before meals

Provide oral hygiene before meals aesthetically pleasing setting at mealtime Ed: Suggest soft foods, avoiding roughage if indicated. Recommend cessation of smoking.

Encourage pt to eat meals and supplementary

enhance the flavor of foods and aid in increasing appetite ammonia potentiates risk for encephalopathy.Aids in reducing gastric irtrtation/diarrhea and abdominal discomfort that may impair oral intake and digestion.Conserving energy reduces metabolic demands on the liver and promotes cellular regeneration.Promotes appetite and sense of well-being.

Hemorrhage form esophageal varices may occur in advanced cirrhosis.Reduces excessive gastric stimulation and risk of irritation or bleeding.Encouragement is essential fo the pt w/ anorexia and

feedings gastrointestinal discomfort.

NEUROLOGIC INFECTIONSBACTERIAL 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 meningitiso 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

infectious organisms gain access to meninges and subarachnoid spaces (viral, bacterial, yeast)

Exudate forms↓

Meningeal irritation/inflammation↓

Cortical inflammation↓

Cerebral edema↓

Increased ICP↓

Vasculitis Increased infection Petechial Hemorrhages Neuritis Hydrocephalos ↓ ↓ ↓ ↓ ↓Cortical Brain abscess Septic Emboli Cranial nerve Increased Necrosis Septicemias involvement ICP ↓ ↓ ↓Adrenal DIC Seizures Compression ofHemorrhage brain structures

Hemorrhage HypoxiaInadequate perfusion

Shock ↓DEATH

HEADACHESIs 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.

COMMON TYPES OF HEADACHESI. Migraine

- Are paroxysmal disorders characterized by recurrent throbbing headaches- Episodes begin during puberty or ages 20-40 years- They decrease in frequency and severity with advancing years- Affects 5-10% of the population- Women are more susceptible than men are- Occurs at irregular intervals, frequency varies from several times a week to several times a

yearPATHOPHYSIOLOGY

(vascular theory is currently accepted)- Constriction of intracranial vessels > neurologic symptoms- Intense throbbing headache is due to dilation of extracranial and intranial branches of the

external carotid artery Psychological factors influence migraine headache

o Perfectionisto Fatigueo Excess sleepo Hungero Refractive errorso Bright lighto Surpriseso Mental and emotional excitemento Excessive smokingo High altitudeso Drinking alcoholic beverages

Certain foods that seem to precipitate migraine episodes, food containing beta-phenylethylamineo Chocolateo Cheeseo Citrus fruitso Coffeeo Pork productso Dairy products

Familial tendency

Oral contraceptive may exacerbate migraines or induce their onset in women previously free from significant headaches. It can occur during menstruation.

I.1. Classic or Typical Migraineo Preceded by an aura or prodromal phase in which the client may feel depressed, irritable, restlss,

and perhaps anorexico May experience transient neurologic disturbances (visual phenomena, e.g., flashes of lights,

bright spots, distorted vision, diplopia), vertigo, nausea, diarrhea, abdominal pain, paresthesis (numbness of tingling of lips, face, or extremities); may lasts a few minutes or several hours.

o Has a “cresendo” quality. It gradually increases in severity until the pain becomes intense and all-encompassing.>mild discomfort, >prostrating, throbbing pain >seclusion and lie in bed in a darkened room.

o Pain described as dull and boring, pressing, throbbing, or hammering.o Unilateral and may be localized to the front, back, or side of the head, often the temple and eye

areas.o Acute migraine episodes lasts 4-6 hours (accompanied by photophobia, N/V, vertigo, tremor,

diarrhea, excessive sweating or chilliness).o General sensitivity of all sensory organs and client withdraws from light and sound.o Arteries of the head may become prominent and the amplitude of their pulsation increase, scalp

may be very tender, swelling, redness, and excessive tearing of the eyes, and swelling of the nasal mucosa (sometimes accompanied by epistaxis) may occur.

I.2. Atypical or Common Migraineo Begins suddenly with or without prodromal symptoms, may be generalized or unilateral, and may

or may not be accompanied by N/V.

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.

II. Cluster headaches (Histamine headaches)- Sometimes classified as a form of migraine. Most clients experiencing cluster headaches do

not have a history of migraine headaches.- Excruciating painful, unilateral , and tend to occur in clusters. There is usually no aura.- Episodes may occur within a few days, weeks, or occasionally months, followed by a

remission with no symptoms for months or years. Then the headaches again recur in

clusters. Cluster headache may recur at irregular intervals for many years, often related to times of stress anxiety, or emotional upset.

- Men are affected five times more often than are women. Episodes usually begin in middle life and are often worsened by alcoholic consumption.

- The mechanism underlying cluster headache is not well understood but is believed to be in vascular origin. These headaches were formerly believed to be caused by sensitivity to histamine.

- During episode, the client experiences: Excruciating, throbbing, or steady pain arising high in the nostril and spreading to

one side of the forehead, around and behind the eye on the affected side. The nose and affected eye water, and the skin reddens on the affected side Nasal congestion and conjunctival infection are common. Intervention is ineffective because of shortness of episodes.

MANAGEMENT:1. Lying in a dark, quiet room with ice on the back of the neck during acute episodes.2. Indomethacin (Indocin) medication of choice3. Tricyclic antidepressant4. Supportive care – clients tend to become depressed over their condition and fearful recurrent

episodes. Some feel they cannot survive another episode.

III. Tension headaches (muscle Contraction Headaches)- Results from the long-sustained contraction of skeletal muscles around the scalp, face, and

neck and upper back.- Muscles become tender → client tenses more (primary source of many headaches

associated with excessive emotional tension, anxiety and depression.)- Vasodilation of associated cranial arteries may also contribute to muscle irritability and

head pain- Begin in adolescence but occur most often in middle age. They may increase significantly in

menopause. Pre-menstrual headaches are of this type.- Pain is steady, non-pulsatile ache (unilateral or bilateral) in any region of the head, but

more so in the occipital and upper cervical regions and extends diffusely over the top of the head

- Onset is gradual, with N/V (late reaction), could also be accompanied by dizziness, tinnitus or lacrimation

- Pain could be precipitated by combing the hair, wearing a hat or exposure to cold- Maybe unrelieved for weeks, months or years.

MANAGEMENT:1. Eliminate source of stimulation (diseased teeth)2. Psychotherapy for those with prolonged and recurrent muscle tension headaches of

psychological in origin3. Symptomatic relief: massage affected muscles, apply local heat, rest and various relaxation

techniques4. Responds well to a combination of non-narcotic analgesic with an anxiety relieving drug,

occasionally a stronger analgesic is needed (e.g., Codeine sulfate).

CLIENT EDUCATION GUIDE

PREVENTING MIGRAINE HEADACHES

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.

Adjusting Dietary Triggers. Alcohol increases the size of blood vessels (vasodilation) and may increase headache. Some foods contain beta-phenlethylamine and should be considered possible triggers. These items include chocolate, cheese, citrus fruits, coffee, pork products and dairy products. The lack of eating may lower blood sugar and may lead to headache. In this case, small frequent meals may avert headaches.

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

A disorder characterized by impaired coagulation of blood and a tendency to bleed. Hereditary coagulation disorder. both hemophilia A (Factor VIII deficiency) and Hemophilia B

(Factor IX deficiency) are inherited as sex linked recessive disorder and are therefore almost exclusive for males.

Hereditary and limited to males. X-linked recessive disease – it means that, it is common to males but is being transmitted by

females. All daughters of hemophiliacs become carrier. Transmitted by a female trait carrier Absence deficiency or malfunction of any one of clotting factors

TRANSMISSION OF HEMOPHILIA

Genotype of parents Female MaleN Carrier Hemophiliac N Hemophiliac

Carrier+N male 50% 50% 0% 50% 50%N female+Hemophiliac 0% 100% 0% 100% 0%

Carrier+hemophiliac 0% 50% 50% 50% 50%

COMMON TYPES OF HEMOPHILIA

1. Hemophilia A (Classic Hemophilia) 80% hemophiliacs Factor VIII deficiency (anti hemophilic factor)

2. Hemophilia B (Christmas Factor) Factor IX deficiency (Plasma Thromboplastin component)

3. Hemophila C Factor XI deficiency (Plasma Thromboplastin antecedent)

STAGES1. Mild: clotting factor level 6 to 30%

Bruise easily, tendency to nose/gum bleeding2. Moderate:2 to 5 %

More frequent bleeding episodes; excessive bleeding after surgery or trauma3. 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 FACTORS1. Factor I – Fibrinogen2. Factor II – Prothrombin3. Factor III – Thromboplastin4. Factor IV – Calcium5. Factor V – Proaccelerin, labile factor, accelerator globulin6. Factor VI – omitted7. Factor VII – Proconvertin, stabile factor, serum prothrombin conversion accelerator (SPCA)8. Factor IX – Plasma thromboplastin component (PTC)9. Factor X - Stuart power factor10. Factor XI – Plasma Thromboplastin antecedent (PTA)11. Factor XII – Hageman Factor (HF)

12. Factor XIII – Fibrin Stabilizing Factor

Extrinsic System Intrinsic System

Factor III Factor XII

Factor VII Factor XI

Factor IX

Factor VIII

Scheme of clotting Platelet lysisMechanism

Factor XFactor V

CalciumProthrombin Thrombin

Plasminogen Activator Urokinase Plasminogen Plasmin

COMMON BLEEDING AND COAGULATION BLOOD TESTS

TEST DESCRIPTION NORMAL VALUESBleeding time -Evaluation of vascular platelet

factors – the time it takes for a small stab wound to stop

bleeding

2 to 9 minutes

Clotting time (CT) -time required for solid clot to form (less sensitive test than

PTT)

5 to 10 minutes

Prothrombin Time (PT) -indicates rapidity of blood clotting (indicates adequacy of extrinsic coagulation pathways

for factors I, II, V, VII and X)

11 to 16 seconds

Partial Thromboplastin Time (PTT)

-more sensitive test than PT to evaluate adequacy of intrinsic coagulation pathway (Fibrin

formation)

60 to 90 seconds

Activated Partial Thromboplastin (APTT)

-modified PTT; more sensitive; quicker to perform, frequently

used to monitor heparin therapy and hemoglobin

26 to 42 seconds

HYPERTENSION: Elevated blood pressure A sustained blood pressure greater than 90 mmHg or a sustained systolic pressure in excess of

140 mmHg is considered to constitute hypertension. About 90-95 of hypertension is idiopathic and apparently primary (Essential hypertension) Of the remaining 5-10%, most is secondary to renal disease or less often, to narrowing of the

renal artery, usually by an atheromatous plaque (Renovascular hypertension) Infrequently, secondary hypertension is the result of disease related to the adrenal glands.

REGULATION OF NORMAL BLOOD PRESSURE:The magnitude of the arterial blood pressure depends on two hemodynamic variables:

a. Cardiac outputb. Total peripheral resistance

CARDIAC OUTPUT: Influenced by blood volume, which Is greater dependent on body sodium Thus, sodium homoestasis is central to blood pressure regulation

TOTAL PERIPHERAL RESISTANCE: Predominantly determined at the level of the arterioles and depends on lumen size, itself

dependent on the thickness of the arteriolar wall and the effects of neural and hormonal influences that either constrict or dilate these vessels.

Normal vascular tone depends on the competition between:a) Vasoconstricting influences

Angiotensin II Catecholamines Thromboxane Leukotrienes Endothelin

b) Vasodilators: Kinins Prostaglandins Nitric oxide

Certain metabolic products….a. Lactic acidb. Hydrogen ionsc. Adenosine

And hypoxia…can also function as local vasodilators!

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 likea. Remodelingb. Hypertrophyc. 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 arteriosclerosisb. 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. Prostaglandinsb. Platelet activating factorc. Urinary kalikrein – kinin systemd. 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.

PATHOGENESIS OF ESSENTIAL HYPERTENSION: Arterial Hypertension occurs when changes develop that after the relationship between blood

volume and total peripheral resistance. In renovascular hypertension, renal artery stenosis causes decreased glomerular flow and

pressure in the afferent arteriole of the glomerulos and induces rennin secretion by the juxtaglomerular cells.

This initiates angiotension II induced vasoconstriction --- increased peripheral resistance; through the aldosterone mechanism, --- increased sodium reabsorption and increased blood volume.

In Pheochromocytoma, a tumor of the adrenal medulla, catecholamines produced by tumor cells cause episodic vasoconstriction and thus induce 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

The patient will: Perform ADLs and develop alternative means of communicating Avoid injury and maintain adequate calorie intake Express positive feelings about himself Develop adequate coping behaviors and seek support resources

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

Multiple Sclerosis (MS)described as: Elapsing remitting – clear elapses with full recovery lasting disability. Between attacks,

the disease doesn’t worsen Primary progressive – steady progression or worsening of the disease from the onset

with minor recovery or plateaus

Secondary progressive begins as a pattern of clear-cut relapses and recovery but becomes steadily progressive and worsens between acute attacks

Progressive relapsing – steadily progressive from the onset but also has clear, acute attacks. Differential diagnosis must rule out spinal cord, multiple small strokes, syphilis or another infection, thyroid disease and chronic fatigue syndrome

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

The patient will: Perform activities of daily living Remain free from infection Maintain joint mobility And range of motion Express feelings of increased energy and decreased fatigue Develop regular bowel and bladder habit Use support systems and coping mechanism

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 medicationso Adverse drug reactionso Sensory drug reactionso Muscle dysfunctiono Energy levelo Signs and symptoms of infectiono Speecho Elimination patterns vision changeso 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

Precipitating factor that cause acute deterioration: Severe stress, such as myocardial infraction Traumatic injury Viral infections Physical exhaustion

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

The patient will: Maintain a patent airway and adequate ventilation Maintain joint mobility and range of motion (ROM) Maintain daily calorie requirements Seek support systems and exhibit adequate coping behaviors Remain free from infections

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 weaknesso Respiratory statuso Speecho Swallowing abilityo Skin integrityo Nutritional statuso Response to treatmento Complicationso Signs and symptoms of infection

Modifying the home for a Patient with ALSGuidelines:

Explain basic safety precautions, such as keeping stairs and pathways free from clutter, using nonskid mats in the bathroom and in place of loose throw rugs; keeping stairs well lit; installing handrails in stairwells and the shower, tub and toilet areas and removing electrical and telephone cords from traffic areas.

Discuss the need for rearranging the furniture moving items in or out of patient’s care area, and obtaining such equipment as a hospital bed, a commode, or oxygen equipment.

Recommend devices to ease the patient’s and caregiver’s work such as extra pillows or wedge pillows to help the patient sit up, a draw sheet to help him move up in bed, a lap tray for eating, or a bell for calling the caregiver.

Help the patient adjust to changes in the environment. Encourage independence. Advise the patient to keep suction due to handy to reduce the fear of choking due to

secretion accumulation and dysphagia. Teach him to suction himself.

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 patternThe 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 signso Breath soundso Arterial blood gas measurementso Level of consciousnesso Continual respiratory functiono Pulse oximetryo Signs of thrombophlebitiso Signs of urine retentiono Response to medications