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NONSTEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDs) A. Description
Interfere with prostaglandin synthesis
Alleviate inflammation and subsequent discomfort of rheumatoid conditions (GA)
Available in oral and parenteral (IM) preparations CYCLOOXYGENASE INHIBITORS : are preferred because it does not decrease the cytoprotective lining of the stomach.
Celebrex (Celecoxib)
Vioxx (Rofecoxib)(No longer on market as of September 2004)
Bextra (Valdecoxib)(No longer on market as of April 2005) There are also other COX-2 Inhibitors being developed, including:
Prexige Lumiracoxib)
Arcoxia (Etoricoxib) B. Examples
Diclofenac (Voltaren)
Etodolac (Lodine)
Ibuprofen (Motrin)
Naproxen (Naprosyn)
Salicylates (ASA) COX-2 SELECTIVE INHIBITORS are the newest of the NSAIDs
KETOROLAC is the only NSAID that can be administered by injection (intramuscularly or intravenously) and is indicated for the short-term use of severe to moderate pain.
C. Major Side Effects
GI irritation (local effect)
Skin rash (hypersensitivity)
Blood dyscrasias (decreased RBCs, WBCs, platelet synthesis)
CNS and GU disturbances D. Nursing Care
Administer with meals to reduce GI irritation
Monitor blood work
Assess vital signs
Instruct client to report the occurrence of any side effects to the physician
Encourage diet rich in nutrient-dense foods such as fruits, vegetables, whole grains, and legumes to improve and maintain nutritional status and prevent possible drug-induced nutrient deficiencies
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ANTIGOUT AGENTS (Uricosuric agent) A. Description
Act by decreasing uric acid formation and increasing its excretion
Prevent and arrest gout attacks that are caused by high levels of uric acid in the blood
Available in oral and parenteral (IV) preparations B. Examples 1. ALLOPURINOL (ZYLOPRIM): blocks formation of uric acid within the body
Action : Reduces uric acid production by inhibiting xanthine oxidase
Indications: Gout or hyperuricemia, Recurrent calcium oxalate calculi o allopurinol (Allorin, Apo-Allopurinol, Capurate, Zyloprim) o allopurinol sodium (Aloprim)
Allopurinol should not be taken during an acute attack because the initial response to allopurinol is an exacerbation of the symptoms. It is used prophylactically to prevent gout and treat hyperuricemia.
Adverse reactions:
CNS: fever, drowsiness, headache, paresthesia, peripheral neuropathy, neuritis.
CV: hypersensitivity vasculitis, necrotizing angiitis.
EENT: epistaxis.
GI: nausea, vomiting, diarrhea, abdominal pain, gastritis, taste loss or perversion, dyspepsia.
GU: renal failure, uremia.
Hematologic: agranulocytosis, anemia, aplastic anemia, thrombocytopenia, leukopenia, leukocytosis, eosinophilia.
Hepatic: hepatitis, hepatic necrosis, hepatomegaly, cholestatic jaundice.
Musculoskeletal: arthralgia, myopathy.
Skin: rash, exfoliative, urticarial, and purpuric lesions, erythema multiforme, severe furunculosis of nose, ichthyosis, alopecia, toxic epidermal necrolysis.
Other: ecchymoses, chills. Hepatitis, Headache and Fever, Epistaxis, Arthralgia, Alopecia, Abdominal pain, Diarrhea and NV, Rash/Urticaria, Renal Failure and Vasculitis, Toxic epidermal necrolysis, Thrombocytopenia, Anemia and Leukopenia/leukocytosis, Paresthesia
Interactions: Drug-drug
Amoxicillin, ampicillin: May increase possibility of rash. Avoid using together.
Anticoagulants: May increase anticoagulant effect. Dosage may need to be adjusted.
Antineoplastics: May increase potential for bone marrow suppression. Monitor patient carefully.
Chlorpropamide: May increase hypoglycemic effect. Avoid using together.
Ethacrynic acid, thiazide diuretics: May increase risk of allopurinol toxicity.
Uricosurics: May have additive effect. May be used to therapeutic advantage.
Urine-acidifying drugs (ammonium chloride, ascorbic acid, potassium or sodium phosphate): May increase possibility of kidney stone formation. Monitor patient carefully.
Xanthines: May increase theophylline level. Adjust dosage of theophylline, as needed.
Alcohol use: May increase uric acid level. Discourage use together. Effects on lab test results:
May increase alkaline phosphatase, ALT, and AST levels.
May decrease hemoglobin level and hematocrit. May increase eosinophil count.
May decrease granulocyte and platelet counts. May increase or decrease WBC count.
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Nursing Considerations:
To minimize GI adverse reactions, tell patient to take drug with or immediately after meals.
Encourage patient to drink plenty of fluids while taking drug unless otherwise contraindicated.
Monitor uric acid level to evaluate drug's effectiveness.
Monitor fluid intake and output; daily urine output of at least 2 L and maintenance of neutral or slightly alkaline urine are desirable.
Periodically monitor CBC and hepatic and renal function, especially at start of therapy.
Optimal benefits may need 2 to 6 weeks of therapy. Because acute gout attacks may occur during this time, concurrent use of colchicine may be prescribed prophylactically.
Don't restart drug in patients who have a severe reaction.
Look alike-sound alike: Don't confuse Zyloprim with ZORprin.
If patient is taking drug for recurrent calcium oxalate stones, advise him also to reduce his dietary intake of animal protein, sodium, refined sugars, oxalate-rich foods, and calcium.
2. COLCHICINE: COLCHICINE (COLGOUT)
Action: Decreases uric acid crystal deposits by inhibiting lactic acid production by leukocytes; used for acute attacks; Acute gout, acute gouty arthritis. As an antigout drug, may decrease WBC motility, phagocytosis, and lactic acid production, decreasing urate crystal deposits and reducing inflammation. As an antiosteolytic drug, may inhibit mitosis of osteoprogenitor cells and decrease osteoclast activity.
Contraindications & cautions o Contraindicated in patients hypersensitive to drug and in those with blood dyscrasia, serious CV disease,
renal disease, or GI disorders. o Use cautiously in elderly or debilitated patients and in those with early signs of CV, renal, or GI disease.
Incompatibilities: D5W, bacteriostatic normal saline injection.
Therapeutic Effect of Colchicine: decreases the motility of WBCs Adverse reactions
CNS: peripheral neuritis.
GI: nausea, vomiting, abdominal pain, diarrhea.
GU: reversible azoospermia.
Hematologic: aplastic anemia, thrombocytopenia, agranulocytosis with long-term use, nonthrombocytopenic purpura.
Musculoskeletal: myopathy.
Skin: alopecia, urticaria, dermatitis.
Other: severe local irritation if extravasation occurs, hypersensitivity reactions. Myopathy, Abdominal pain, diarrhea and NV, Aplastic anemia, Agranulocytosis with long-term use, Alopecia, Peripheral neuritis. Hypersensitivity reactions (can be Hepatotoxic), Urticaria and Dermatitis, Thrombocytopenia
Interactions: Drug-drug
Clarithromycin, erythromycin, telithromycin, verapamil: May increase the risk of colchicine toxicity. Monitor colchicine levels and adjust dose or stop colchicine as needed.
Cyclosporine: May cause GI, hepatic, renal and neuromuscular toxicity. Use together cautiously.
Vitamin B12: May impair absorption of oral vitamin B12. Avoid using together.
Alcohol use: May impair effectiveness of drug prophylaxis. Discourage use together. Effects on lab test results
May increase alkaline phosphatase, AST, and ALT levels. May decrease carotene, cholesterol, and hemoglobin levels and hematocrit.
May decrease platelet and granulocyte counts.
May cause false-positive urine RBC or urine hemoglobin test results.
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Nursing considerations:
I.V. administration o Give by slow I.V. push over 2 to 5 minutes. o If lower concentration of colchicine injection is needed, dilute with normal saline solution or sterile water for injection and
give over 2 to 5 minutes by direct injection. o Preferably, inject into the tubing of a free-flowing I.V. solution. o Don't inject if diluted solution becomes turbid. o Monitor patient for extravasation because colchicine irritates tissues.
Obtain baseline laboratory test results, including CBC, before therapy and periodically throughout therapy.
Alert: Don't give I.M. or subcutaneously; severe local irritation occurs.
As maintenance therapy, give drug with meals to reduce GI effects. Drug may be used with uricosurics.
Monitor fluid intake and output; keep output at 2 L daily.
Alert: After full I.V. course (4 mg), don't give it by any route for at least 7 days. It's a toxic drug, and overdose may be fatal.
First sign of acute overdose may be GI symptoms, followed by vascular damage, muscle weakness, and ascending paralysis. Delirium and seizures may occur without patient losing consciousness.
Stop drug as soon as gout pain is relieved or at first sign of GI symptoms.
Patient teaching:
Teach patient how to take drug, and tell him to drink extra fluids.
Tell patient to report adverse reactions, especially signs of acute overdose (nausea, vomiting, abdominal pain, diarrhea, unusual bleeding, bruising, tiredness, weakness, numbness, or tingling).
Advise patient to avoid using alcohol while taking drug.
Tell patient with gout to limit intake of foods high in purine, such as anchovies, liver, sardines, kidneys, sweetbreads, peas, and lentils.
3. PROBENECID (BENEMID) prevents formation of tophi by inhibiting the reabsorption of uric acid by the kidneys
increases the urinary excretion of uric acid. This uricosuric action is used therapeutically to treat hyperuricemia and gout. It is not effective in acute attacks of gouty arthritis but prevents hyperuricemia and tophi associated with chronic gout. Probenecid may precipitate acute gout until serum uric acid levels are within the normal range; concomitant administration of colchicine prevents this effect. (Probenecid also is used with penicillin, most often in treating sexually transmitted diseases. It increases blood levels and prolongs the action of penicillin by decreasing the rate of urinary excretion.)
Decreases renal excretion of penicillins, thus elevates and prolongs penicillin blood levels
Increases blood levels by decreasing renal excretion of the cephalosporins. This may be a desirable interaction to increase blood levels and therapeutic effectiveness or allow smaller doses. May increase blood levels of acyclovir by slowing its renal excretion. Be alert for nausea, rash, and constipation.
Major Side Effects:
1. Nausea, vomiting (irritation of gastric mucosa) 2. Blood dyscrasias (decreased RBCs, WBCs, and platelet synthesis) 3. Liver damage (hepatotoxicity) 4. Skin rash (hypersensitivity)
Nursing Care:
Administer anti-inflammatory drugs (Prednisone, Indocin) in addition to drugs that will lower serum uric acid during the acute phase
Increase fluids to discourage the formation of renal calculi
Encourage weight reduction if overweight
Monitor serum urate levels to determine effectiveness of treatment
Administer with meals to reduce GI irritation
Instruct client to avoid high purine foods such as organ meats, anchovies, sardines, and shellfish; encourage diet rich in nutrient-dense foods such as fruits, vegetables, whole grains, and legumes to improve and maintain nutritional status and prevent possible drug-induced nutrient deficiencies
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OPHTHALMIC AGENTS A. Description
Produce a variety of actions; e.g., constriction, dilation, anti-inflammatory, anti-infective
Diagnose and treat conditions affecting the eyes
Available in a variety of topical preparations; drugs having a systemic action are available in oral and parenteral (IM, IV) preparations
B. Examples
Miotics: constrict the pupil, pulling the iris away from the filtration angle and improving outflow of aqueous humor) o Physostigmine o Pilocarpine HCl o Timolol maleate (Timoptic)
Mydriatics: dilate pupil (mydriasis) by causing contraction of the dilator muscle of the iris with minimal effect on the ciliary muscle, which lessens the effect on accommodation
o Hyroxyamphetamine (Paredrine) o Phenylephrine HCl (Neo-Synephrine)
Anticholinergics dilate the pupil (mydriasis) by relaxing the ciliary muscle and the sphincter muscle of the iris; paralyze accommodation (cycloplegia); thus facilitating eye examination
o Atropine sulphate o Cyclopentolate (Cyclogyl)
Carbonic anhydrase inhibitors: decrease inflow of aqueous humor in control of intraocular pressure o Acetazolamide (Diamox) o Ethoxzolamide (Cardrase, Ethamide)
Osmotic agents: administered systemically to decrease blood osmolality, which mobilizes fluid from the eye to reduce volume of intraocular fluid
o Glycerin (Glycerol, Osmoglyn) o Mannitol (Osmitrol) o Urea (Urevert)
MAJOR SIDE EFFECTS:
Miotics o Twitching of eyelids and brow ache (increased
cholinergic stimulation) o Headache (vasodilation) o Conjunctival pain (irritation of conjunctiva) o Contact dermatitis (local irritation)
Anticholinergics (decreased parasympathetic stimulation) o Dry mouth (decreased salivation) o Flushing, fever, and ataxia (CNS effect) o Blurred vision (papillary dilation) o Skin rash (hypersensitivity) o Tachycardia (decreased vagal stimulation)
Mydriatics o Brow ache, headache, and hypertension
(vasoconstrictor effect) o Blurred vision (papillary dilation) o Tachycardia (increased sympathetic stimulation)
Carbonic anhydrase inhibitors o Diuresis (increased excretion of sodium and
water in renal tubule) o Paresthesia (fluid-electrolyte imbalance) o Nausea, vomiting (GI irritation) o CNS disturbances (CNS effect)
Osmotic agents o Headache (cerebral dehydration) o Nausea, vomiting (fluid-electrolyte imbalance)
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NURSING CARE:
Instruct client regarding proper method of application and need for medical supervision during therapy
Assess for occurrence of side effects and/or worsening of condition
Encourage diet rich in nutrient-dense foods such as fruits, vegetables, whole grains, and legumes to improve and maintain nutritional status and prevent possible drug-induced nutrient deficiencies
Provide care for the client receiving mydriatics: caution that vision will be blurred temporarily; advise that sunglasses will relieve photophobia; caution about engaging in hazardous activities
INSTILLATION OF EYE MEDICATIONS Purpose: to provide therapeutic effect of medication ordered Nursing care
Position the client with the head slightly backward
Pull lower eyelid down and instill solution in center of conjunctival sac; ointment applied from inner canthus outward; check order:
OD (right eye) OU (both eyes) OS (left eye)
Have client close the eyes gently and instruct that they should not be rubbed
Apply pressure to the nasolacrimal duct if liquid instillation IRRIGATIONS OF THE EAR Definition
Introduction of fluid into the external auditory canal
Usually done for cleansing but can be used to apply antiseptic solutions Nursing care
Verify if tympanic membrane is intact
Assist the client to a sitting position with the head tilted to affected side for an irrigation to facilitate drainage; for instillations the client should lie on the unaffected side
Gently pull up and back on the external ear of an adult, down and forward on a child, to straighten the canal
Direct solution into the canal without exerting excessive force; collect returns in a basin
Dry the outer ear
Record the procedure, type of damage, etc.
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DISEASE MODIFYING ANTI-RHEUMATIC DRUGS (DMARDS) 1. METHOTREXATE (RHEUMATREX, TREXALL)
Methotrexate is now considered the first-line DMARD agent for most patients with RA. It has a relatively rapid onset of action at therapeutic doses (6-8 weeks), good efficacy, favorable toxicity profile, ease of administration, and relatively low cost.
Mechanism: Anti-inflammatory effects of methotrexate in rheumatoid arthritis
Immunosuppressive
Methotrexate can be given orally or by subcutaneous injection.
The onset of action is seen in as early as 4 to 6 weeks.
Side Effects: Most serious complications of methotrexate therapy: o Hepatic cirrhosis Interstitial pneumonitis Severe myelosuppression (quite rare)
Folic Acid Antagonsim SE: o Mild alopecia and hair thinning o Oral ulcers GI upset Stomatitis
Feeling wiped out aka METHOTREXATE FOG = headache and fatigue These side effects can be improved with folic acid supplementation.
2. HYDROXYCHLOROQUINE (PLAQUENIL )
Hydroxychloroquine is an antimalarial drug which is relatively safe and well-tolerated agent for the treatment of rheumatoid arthritis.
sometimes combined with methotrexate for additive benefits for signs and symptoms or as part of a regimen of triple therapy with methotrexate and sulfasalazine.
Mechanism: The mechanism of action of antimalarials in the treatment of patients with rheumatoid arthritis is unknown but is thought to involve changes in antigen presentation or effects on the innate immune system.
Dosage: the drug of choice among antimalarials. Chloroquine is not commonly used because of greater toxicity on the eye.The usual dose of Plaquenil is 400mg/day. It may be prescribed as a single daily dose or in divided doses twice per day
Usual Time to Effect: A period of 2 to 4 months is usual.
Side Effects: Corneal deposits/ Extraocular muscular weakness/Loss of accommodation (and sensitivity to light) /Retinopathy that may progress to irreversible visual loss.
3. SULFASALAZINE (AZULFIDINE)
an effective DMARD for the treatment of RA.
also used in the treatment of inflammatory bowel disease
Its mechanism of action in RA is unknown.
Dosage: The usual dose is 2-3 grams per day in a twice daily dosing regimen. The dose may be initiated at 1 gram per day and increased as tolerated.
Usual Time to Effect: It may take 6 weeks to 3 months to see the effects of sulfasalazine.
Side effects: Hypersensitivity reactions / Mild gastrointestinal complaints are commonly seen and these can be decreased by using enteric coated formulations or administration of the medication with meals.
4. GOLD SALTS/GOLD PREPARATIONS
Gold salts describe ionic chemical compounds of gold
Gold has been used successfully for more than 70 years to treat rheumatoid arthritis (RA).
Gold is one of a class of medications known as disease-modifying antirheumatic drugs (DMARDs), because it not only decreases the pain and swelling of arthritis but also can prevent joint damage and disability.
Gold preparations can be recommended to treat RA as well as other forms of arthritis.
Rheumatologists talking about "gold" usually are referring to one of the injectable forms of gold salts: gold sodium thiomalate (Myochrysine), gold aurothioglucose (Solganal) and gold sodium aurothiosulfate (Aurolate)
There is also an oral tablet that contains gold, auranofin (Ridaura); however, this preparation is distinct from the injectable forms and much less effective.
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Fast Facts
Gold is one of the original medications identified to reduce the symptoms of RA and slow its progression.
Gold usually is given as a weekly injection (and eventually may be given every 4 weeks), although a pill form also exists.
Gold injections can affect kidney function and the bone marrow and require careful monitoring.
Gold largely has been replaced by better tolerated and more effective medications for RA.
Gold injections are given every week for the first 22 weeks. After that, gold may be given less often if it is working.1 Dosing
Adults and teenagers taking aurothioglucose (Solganal) receive intramuscular injections (similar to a vaccine inoculation) once a week.
The usual starting dose is 10 milligrams (mg), which is increased to 25 mg once a week for the next two weeks, and then 25 or 50 mg once a week.
Usually after about 6 months, the injections may be given every 2 to 4 weeks.
Adults and teenagers taking sodium thiomalate (Myochrysine) for RA follow a dosing regimen similar to that of aurothioglucose.
For oral gold, the typical starting dose (auranofin or Ridaura) for adult patients with RA is 6 mg once a day or 3 mg twice a day.
After 6 months, your doctor may increase the dose to 3 mg three times a day for maximal effect.
Time to effect: It may take some time to see any improvement of symptoms while taking gold therapy. Most patients experience an improvement after 3 to 6 months of therapy.
SIDE EFFECTS: may develop after a significant amount of gold has accumulated in the body. Oral gold has fewer side effects than gold injected into the muscle.
Common side effects of oral gold include:
Decreased appetite, nausea, and diarrhea. Problems with the skin, blood, kidneys, or lungs (rare).
Common side effects of injected gold include:
An itchy skin rash. Mouth sores.
Rarer side effects include:
Kidney problems (kidney damage that causes loss of protein in the urine). Suppression of blood cell production, which may increase the risk of infection or serious bleeding. (A return to
normal blood cell production may take several weeks after the drug is no longer taken.)
Extremely rare side effects include bowel or lung inflammation.
Drug Interactions
Very little information is available regarding drug interactions with gold therapy, although interactions are uncommon.
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RELATED PROCEDURES 1. COMPUTERIZED TOMOGRAPHY (CT) A. Definition
Cross-sectional visualization of the head or other body cavity determined by computer analysis of relative tissue density as an x-ray beam passes through
Provides information about location and extent of tumors, infracted areas, atrophy, and vascular lesions
Done with or without intravenous injection of dye for contrast enhancement B. Nursing Care
Explain procedure; inform the client that it will be necessary to lie still and that the equipment is complex but will cause no discomfort; infants and cognitively impaired or anxious clients may need to be sedated
Assess for allergy to iodine, a component of the contrast material
Withhold food for approximately 4 hours before contrast testing; dye may cause nausea in sensitive clients
remove wigs, clips, and pins before CT of head
11. MAGNETIC RESONANCE IMAGING (MRI) A. Definition
Uses magnetic fields and radio waves to produce cross sectional images
Produces accurate images of blood vessels, bone marrow, gray and white brain matter, the spinal cord, the globe of the eye, the heart, abdominal structures, and breast tissue, and can monitor blood velocity
B. Nursing Care
Assess ability to withstand confining surroundings because client must remain in the tunnel-like machine for up to 90 minutes; open MRI may be an option for clients who cannot tolerate closed spaces
Instruct client to toilet before test
Have client remove jewelry, clothing with metal fasteners, dentures, hearing aids, and glasses prior to entering scanner
Review history for contraindications: orthopedic hardware; pacemaker; artificial heart valves; or other implants that may be dislodged or malfunction as a result of the magnetic field
111. LUMBAR PUNCTURE A. Definition: involves the introduction of a needle into the subarachnoid space below the spinal cord, usually
between L3 and L4 or L4 and L5
B. Purposes Withdrawal of cerebral spinal fluid for diagnostic purposes or to reduce spinal pressure (normal is 70 to 200 mm H2O)
measurement of spinal pressure (Queckenstedts test involves compression of the jugular veins; normally pressure will rise; but if blockage exists, pressure will not rise)
Injection of dye for diagnostic x-ray examination
Injection of medication such as anesthetics C. NURSING CARE
Explain procedure to the client and obtain a signed consent
Assist the client into a position that will enlarge opening between vertebrae o Lying on side with feet drawn up and head lowered to chest; back near edge of mattress o Sitting on side of bed, leaning on overbed table, feet supported on a stool
After procedure assist the client into a recumbent position; the client should remain recumbent for a few hours, depending on the physicians orders
Label specimens and send to laboratory; note color and amount of fluid
Assess immediate response for signs of shock and complications such as CSF leakage, infection, and brain herniation if space occupying lesion is present
Administer fluids unless contraindicated
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NEUROLOGIC ASSESSMENT A. Definition
systematic evaluation of the cranial nerves, motor and sensory functioning, and mental status to detect neurologic abnormalities
Critical aspects of a complete neurologic assessment are generally extracted and compose a neuro checklist, which is used when the nature of the situation does not warrant complete evaluation
May include the Glasgow Coma Scale B. Nursing Care 1. CRANIAL NERVES
Olfactory (I): ability to identify familiar odors such as mint or alcohol with eyes closed and one nostril occluded at a time
Optic (II): visual acuity measured by use of Snellen chart or by gross estimation with reading material; gross comparison of visual fields with those of examiner; color perception
Oculomotor (III): trochlear (IV), and abducent (VI): ability of the pupils to react equally to light and to accommodate to varying distances; normal range of extraocular movement (EOM) evaluated by asking the client to follow a finger or object with the eyes; also assess for nystagmus (jerking motion of eyes), particularly when eyes are directed laterally
Trigeminal (V): sensations of the face evaluated by lightly stroking cotton across forehead, chin, and cheeks while the clients eyes are closed; ability to clench the teeth (jaw closure)
Facial (VII): symmetry of the facial muscles as the client speaks or is asked to make faces
Acoustic or vestibulocochlear (VIII): hearing acuity determined by a watch tick or whispered numbers; Webers test may be performed by holding the stem of a vibrating tuning form at midline of the skull (should be heard equally in both ears)
Glossopharyngeal (IX) and vagus (X): uvula should hang in midline; swallow and gag reflexes should be intact
Spinal accessory (XI): symmetrical ability to turn the head or shrug the shoulders against counterforce of the examiners hands
Hypoglossal (XII): ability to protrude the tongue without deviation to left or right, and without tremors CALORIC TEST : Test for Oculovestibular Response
If oculocephalic responses are absent, an oculovestibular (caloric test) can be performed to test CN III, VI and VIII. A normal response to ice water instillation occurs when the eyes have conjugate movement and nystagmus toward the irrigated ear. Nystagmus is the involuntary oscillation of the eyeballs and may be horizontal, vertical, oblique, rotary or mixed with various rates of movements. Failure to produce nystagmus with the instillation or warm or cold water into the ear canal indicates a decrease in consciousness with an altered brain stem. However absent cold caloric responses do not always indicate a brain stem disorder. The use of ototoxic drugs, barbiturates, sedatives, phenytoin, or tricyclic anti-depressants or the presence of Menieres disease may produce a false caloric test. In the absence of these conditions, the presence of a negative oculovestibular reflex supports the diagnosis of brain death. A caloric test is contraindicated if a patient has a ruptured tympanic membrane (eardrum) or otorrhea (ear discharge)
Normal Caloric: Eyes indicates to side of ice water application
Abnormal Caloric: Eyes do not deviate to side of ice water application
In medicine, the caloric reflex test (sometimes termed 'vestibular caloric stimulation') is a test of the vestibulo-ocular reflex that involves irrigating cold or warm water or air into the external auditory canal.
Cold or warm water or air is irrigated into the external auditory canal, usually using a syringe. The temperature difference between the body and the injected water creates a convective current in the endolymph of the nearby horizontal semicircular canal. Hot and cold water produce currents in opposite directions and therefore a horizontal nystagmus in opposite directions.[4] In patients with an intact brainstem:
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If the water is warm (44C or above) endolymph in the ipsilateral horizontal canal rises, causing an increased rate of firing in the vestibular afferent nerve. This situation mimics a head turn to the ipsilateral side. Both eyes will turn toward the contralateral ear, with horizontal nystagmus to the ipsilateral ear.
If the water is cold, relative to body temperature (30C or below (ice water)), the endolymph falls within the semicircular canal, decreasing the rate of vestibular afferent firing. The eyes then turn toward the ipsilateral ear, with horizontal nystagmus (quick horizontal eye movements) to the contralateral ear.
Absent reactive eye movement suggests vestibular weakness of the horizontal semicircular canal of the side being stimulated.
In comatose patients with cerebral damage, the fast phase of nystagmus will be absent as this is controlled by the cerebrum. As a result, using cold water irrigation will result in deviation of the eyes toward the ear being irrigated. If both phases are absent, this suggests the patient's brainstem reflexes are also damaged and carries a very poor prognosis[7]
One mnemonic used to remember the FAST direction of nystagmus is COWS o COWS: Cold Opposite, Warm Same. o Cold water = FAST phase of nystagmus to the side Opposite from the cold water filled ear o Warm water = FAST phase of nystagmus to the Same side as the warm water filled ea o In other words: Contralateral when cold is applied and ipsilateral when warm is applied
Testing of Cranial Nerve VIII using a Tuning Fork
WEBER TEST
The tuning fork is set into vibration by striking the tines on the examiners hand or knee. The rounded tip of the handle is placed on the center of the clients forehead or nasal bone. Placement on the teeth (even if the client has false teeth) is a reliable option. The client is asked whether the tone is heard in the center of the head, the right ear, or the left ear. The Weber test is useful in identifying a hearing loss. Normally the sound is heard equally in both ears by bone conduction. If the client is sensorineural hearing loss in one ear, the sound is heard in the other ear. If the client has a conductive hearing loss in one ear, the sound is heard in the other ear.
RINNE TEST
The vibrating tuning fork is shifted between two positions: against the mastoid tube bone (bone conduction) and two inches from the opening of the ear canal (air conduction). As the position is changed, the client is asked to indicate which tone is louder (in front of the ear or behind the ear) or when one of the tones is longer heard. The Rinne test compares air versus sensorineural conduction. With conductive hearing loss, the pathways of normal sound conduction are blocked. However, vibrations against the mastoid bones can bypass the obstruction; therefore, bone conduction last longer or sounds louder than air conduction. With sensorineural hearing loss, the acoustic nerve has decreased ability to perceive vibrations from either route; therefore, normal hearing also reports normal patterns. Normally sound is heard twice as long or as loud by air conduction as it is by bone conduction. With a conductive hearing loss, a client hears bone conduction, sounds louder and longer than air conduction, which constitutes a negative Rinne test finding. With a sensorineural hearing loss, the client hears better by air conduction, which constitutes a positive Rinne test finding.
11. MOTOR FUNCTION (INCLUDING CEREBELLAR FUNCTION)
Balance o Observation of gait o ROMBERG TEST: positive if the client fails to maintain an upright position with feet together when the eyes
are closed
Coordination: ability to touch the finger to the nose when arms are extended or to perform similar tasks smoothly
Muscle strength: evaluated by having the client move symmetrical muscle groups against opposition supplied by the examiner
Sensory function: bilateral testing of the response to light touch with cotton, sharp versus dull stimuli, vibration of a tuning fork
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Mental status (cerebral functioning) o Level of consciousness: determined by the response to stimuli (verbal, tactile, or painful) o Orientation to person, place, and time: determined by general conversation and direct questioning o Judgment, memory, and ability perform simple calculations o Appropriateness of behavior and mood
Reflexes o Deep tendon (biceps, triceps, patellar, Achilles reflexes) with a reflex hammer;
classification from 0 (absent) to 4+ (hyperactive); 2+ is normal o Plantar: planter flexion of the foot when the sole is stroked firmly with a hard object such as a tongue blade;
abnormal adult response (dorsiflexion of the foot and fanning of the toes) is described as a positive Babinski and is indicative of corticospinal tract disease
o OCULOCEPHALIC (dolls-eye movements): when head of comatose client is turned to side, eyes move in opposite direction; absence of reflex suggests brainstem injury; contraindicated with a neck injury
o OCULOVESTIBULAR (caloric test): when warm or ice water is instilled into the ear of a comatose client, nystagmus occurs; eyes deviate towards the stimulated ear if ice water is used and away with warm water; absence of reflex suggest brainstem damage; contraindicated if eardrum is perforated
Accurately record findings; report any deviations
Explain to and reassure the client when the examination must be repeated frequently (q2h)
Coordinate other care with q2h neurologic assessments to promote rest between assessments 111. GLASGOW COMA SCALE A. Definition: technique of objectifying a clients level of responses; clients best response in each area is given a numerical value, and the three values are totaled for a score ranging from 3 to 15 B. Nursing Care
Perform the assessment at appropriate intervals to determine current level of changes in clients level of consciousness; usually every 2 to 4 hours
A score of 7 or less indicates coma
Assess other indicators such as vital signs papillary reaction, movement or extremities, strength, etc. Elements of the scale
Glasgow Coma Scale
1 2 3 4 5 6
Eyes Does not open eyes
Opens eyes in response to painful stimuli
Opens eyes in response to voice
Opens eyes spontaneously
N/A N/A
Verbal Makes no
sounds Incomprehensible
sounds Utters
inappropriate words Confused,
disorientated
Oriented, converses normally
N/A
Motor Makes no
movements Extension to painful
stimuli Abnormal flexion to painful stimuli
Flexion / Withdrawal to painful stimuli
Localizes painful stimuli
Obeys commands
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The scale comprises three tests: eye, verbal and motor responses. The three values separately as well as their sum are considered. The lowest possible GCS (the sum) is 3 (deep coma or death), while the highest is 15 (fully awake person).
BEST EYE RESPONSE (E)
1. No eye opening 2. Eye opening in response to pain. (Patient responds to pressure on the patients fingernail bed; if this does not elicit
a response, supraorbital and sternal pressure or rub may be used.) 3. Eye opening to speech. (Not to be confused with an awaking of a sleeping person; such patients receive a score of
4, not 3.) 4. Eyes opening spontaneously
BEST VERBAL RESPONSE (V)
1. No verbal response 2. Incomprehensible sounds. (Moaning but no words.) 3. Inappropriate words. (Random or exclamatory articulated speech, but no conversational exchange) 4. Confused. (The patient responds to questions coherently but there is some disorientation and confusion.) 5. Oriented. (Patient responds coherently and appropriately to questions such as the patients name and age, where
they are and why, the year, month, etc.)
BEST MOTOR RESPONSE (M)
1. No motor response 2. Extension to pain (abduction of arm, internal rotation of shoulder, pronation of forearm, extension of wrist,
decerebrate response) 3. Abnormal flexion to pain (adduction of arm, internal rotation of shoulder, pronation of forearm, flexion of wrist,
decorticate response) 4. Flexion/Withdrawal to pain (flexion of elbow, supination of forearm, flexion of wrist when supra-orbital pressure
applied ; pulls part of body away when nailbed pinched) 5. Localizes to pain. (Purposeful movements towards painful stimuli; e.g., hand crosses mid-line and gets above
clavicle when supra-orbital pressure applied.) 6. Obeys commands. (The patient does simple things as asked.)
INTERPRETATION Individual elements as well as the sum of the score are important. Hence, the score is expressed in the form "GCS 9 = E2 V4 M3 at 07:35". Generally, brain injury is classified as:
Severe, with GCS 8 - that is also a generally accepted definition of a coma Moderate, GCS 9 - 12 Minor, GCS 13.
Intubation and severe facial/eye swelling or damage make it impossible to test the verbal and eye responses. In these circumstances, the score is given as 1 with a modifier attached e.g. 'E1c' where 'c' = closed, or 'V1t' where t = tube. A composite might be 'GCS 5tc'. This would mean, for example, eyes closed because of swelling = 1, intubated = 1, leaving a motor score of 3 for 'abnormal flexion'
The GCS has limited applicability to children, especially below the age of 36 months (where the verbal performance of even a healthy child would be expected to be poor). Consequently the Paediatric Glasgow Coma Scale, a separate yet closely related scale, was developed for assessing younger children.
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CONTINUOUS PASSIVE MOTION DEVICES (CPM) Definition: a machine that provides for passive range of motion, most commonly for the knee Purposes
Move joint without weight bearing or straining muscles following orthopedic surgery
Stimulate regeneration of articular tissues Nursing Care
Align extremity in padded CPM device
Set Foot Cradle at the angle ordered by the physician
Adjust device according to length of clients extremity (the thigh and lower leg are measured for the CPM of the hip and knee)
Set flexion, extension, and speed dials as ordered by the physician; these are generally increased gradually as tolerated to maximize mobility
Demonstrate use of control cord to client 1. BRACES OR SPLINTS Purposes
Support and protect weakened muscles
Prevent and correct anatomic deformities
Aid in controlling involuntary muscle movements
immobilize and protect a diseased or injured joint Nursing Care
Keep equipment in good repair (e.g., oil joints, replace straps when worn)
Provide adequate shoes (e.g., in good repair, heels low and wide, high top to hold the heel in the shoe)
Examine the skin daily for evidence of breakdown at pressure points
Check alignment of the braces (e.g., leg brace joints should coincide with body joints; back brace should grip the pelvis and trochanter firmly, lacing should begin from the bottom)
11. Mobility: Assistive Devices Purposes
Improve or maintain stability of client with a lower limb disability to prevent injury
Provide security while developing confidence in ambulating
Relieve pressure on weight-bearing joints
Assist in increasing speed of ambulation with less fatigue
Provide for greater mobility and independence A. Nursing Care: USE OF A CANE
Ascertain that the client is able to bear weight on the affected extremity
Ensure that the client is able to use the upper extremity opposite the affected lower extremity
Measure to determine the length of cane required; highest point should be approximately level with the greater trochanter; handpiece should allow 30 degrees of flexion at the elbow with the wrist held in extension
Explain the proper techniques in using a cane o Hold in the hand opposite the affected extremity simultaneously, and then the unaffected leg
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o When climbing, step up with the unaffected extremity and them place the cane and the affected lower extremity on the step; when descending, reverse the procedure
Walk on clients affected side
Observe for INCORRECT USE of the cane o Leaning the body over the cane o Shortening the stride on the unaffected side o Inability to develop a normal walking pattern o Persistence of the abnormal gait pattern after cane is no longer needed
B. Nursing care: CRUTCH WALKING
Ensure proper fit of crutches a. Measure the distance from the anterior fold of the axilla to a point 15cm (6 inches) out from the heel b. Axillary bars must be 5cm (2inches) below axillae and should be padded c. Hand bars should allow almost complete extension of arm with the elbow flexed about 30 degrees when
the client places weight on the hands.
Ensure that rubber crutch tips are in good condition
assist in use of proper technique, depending on ability to bear weight and to take steps with either one or both of the lower extremities
FOUR-POINT ALTERNATE CRUTCH GAIT Right crutch, left foot, left crutch, right foot; always three points of support on floor Equal but partial weight bearing on each limb; slow, stable gait Client must be able to manipulate both extremities and get one foot ahead of the other
TWO-POINT ALTERNATE CRUTCH GAIT
Right crutch and left foot simultaneously; always two points of support on the floor More rapid version of the four-point gait and requires more balance and strength
THREE-POINT GAIT
Advance both crutches and the weaker lower extremity simultaneously, then the stronger lower extremity Fairly rapid gait, but requires more balance and strength in the arms and the unaffected lower extremity used when one leg can support the whole body and the other cannot take full weight bearing
SWING CRUTCH GAITS
Swing to gait: place both crutches forward, lift and swing body up to crutches, then place crutches in front of body and continue; always two points of support on floor; requires adequate power in upper arms
Swing through gait: place both crutches forward, lift and swing body through crutches, then place crutches in front of body and continue; a difficult gait that necessitates rolling the pelvis forward and arching the back to get center of gravity in front of hips; requires power in trunk and upper extremities, excellent balance, self confidence, and a bit of daring.
Observe for INCORRECT USE of crutches: o Using the body in poor mechanical fashion o Hiking hips with abduction gait (common in amputees) o Lifting crutches while still bearing down on them o Walking on ball of foot with turned outward and flexion at hip or knee level o Hunching shoulders (crutches usually too long) or stooping with shoulders (crutches usually too short) o Looking downward while ambulating o Bearing weight under arms; should be avoided to prevent injury to the nerves in the brachial plexus; damage to
these nerves can cause paralysis and is known as crutch palsy
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C. Nursing Care: USE OF A WALKER
Assist in selecting a walker o Device should be used when the client is not able to ambulance with a cane; partial weight bearing required o Measurements for a walker are the same as for a cane o Requires strong elbow extensors and shoulder depressors and partial strength in the hands and the wrist
muscles to lift the standard walker; 2- and 4-wheeled walkers are available o Device cannot be used on steps
Assist in ambulating with the walker o Lift the device off the floor and place forward a short distance, then advance between the walker
Two wheeled walkers: raise back legs of the device off the floor, roll walker forward, then advance to it
Four wheeled walkers: push device forward on floor and then walk to it
Observe for incorrect use of the walker o Keeping arms rigid and swinging through to counterbalance the position of the lower extremity o Tending to lean forward with abnormal flexion at the hips o Tending to step forward with the unaffected leg and shuffle leg up to the walker
111. Mobility: WHEELCHAIR Purpose
Support and move a client on a special chair that has wheels; the client is propelled or propels self
Provide mobility for those who cannot ambulate or those who can ambulate but whose ambulation is unsteady, unsafe, or too strenuous
Decrease cardiac workload
Promote independence and stimulate activities Nursing care
Instruct the client that prolonged sitting in one position can cause flexion contractures of the hips and knees and ischial pressure ulcers (encourage the client to change body positions and to use padded cushions and exercises such as push ups every hour to relieve pressure)
Ensure that device is in operating condition (e.g.;., wheel brakes, arm locks, seat belts, swing foot rests); removable arms, laps boards, extra long leg panels, battery or motor propulsion)
Assist client with transfer; keep wheelchair in close proximity to bed or chair when transferring
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CAUSALGIA
The pain syndrome of Causalgia typically has a history of peripheral nerve injury.
The brachial plexus and the median and sciatic nerves are involved most frequently. Although peripheral nerve damage is the usual cause, other conditions may rarely precipitate the problem. Examples of these are sprains, bruises, fractures, amputations, and arterial and venous occlusions.
Assessment findings in Causalgia include burning pain that often severe, persistent, diffuse, spontaneous, and aggravated by motion, touch, or emotional stimuli.
A client with Causalgia may appear apathetic and haggard. The pain may cause emotional disturbance if it is prolonged. If the suffering increases in intensity and the area of involvement spreads, intractable pain may lead to severe depression and even suicide. As with many types of differentiation pain, virtually any stimulus may set off paroxysms of excruciating pain.
Consequently, a person may try to prevent pain by keeping joint rigid or by wrapping the part in moist cloth. Because of a realistic fear of severe pain, a person experiencing Causalgia may adopt elaborate precautions to prevent the paroxysms of pain from being triggered. Those who do not understand the reason and cause additional suffering.
Generally, Causalgia is associated with dystrophic and vasomotor changes. Reflex sympathetic nervous system that may follow not only injuries to nerves but also those to blood vessels, or it may follow fractures or sprains.
Assessment findings of reflex sympathetic dystrophy include rubor or pallor, sweating or dryness, edema, pain, or skin atrophy.
CIRCUMDUCTION
Movement of a part, e. g. an extremity, in a circular direction. CONTRACTURE
A permanent muscular contraction due to tonic spasm or fibrosis, or to loss muscular balance, with antagonists being paralyzes.
VOLKMANNS CONTRACTURE
This serious and potentially crippling condition of the hand or forearm arises from a complication of a fracture around the elbow joint or forearm bones.
It begins as a compartment syndrome that comprises arterial and venous circulation. If it is not relieved, pressure causes prolonged ischemia and muscle is gradually replaced by fibrous tissue that traps tendons and nerves. The typical end result is a permanent, stiff, claw-like deformity of the arm and hand. Numbness and paralysis are also often present.
Volkmanns ischemic contracture most commonly arises after a supracondylar fracture of the humerus. It may also occur following other fracture of the humerus. It may also occur following other fractures of the elbow joint and forearm, crushing injuries of the forearm, and from tight bandages or casts.
To avoid permanent deformity, compartment syndrome must be recognized and treated early. KYPHOSIS
Kyphosis or humpback is excessive posterior curvature of the thoracic spine. Kyphosis can occur at all ages. It may be due to congenital anomaly, tuberculosis, or tumors or it may be compensatory mechanism for lumbar lordosis.
Kyphosis is a classic sign of ankylosing spondylitis. When it occurs in women with osteoporosis, it is called a dowagers hump. The curvature ca become so severe that function of the lungs, heart, and gastrointestinal tract are altered.
General management is with orthotic braces or corsets and exercise to strengthen muscles and ligaments. Osteoporotic women benefit from calcium and estrogen therapy. Spinal fusion with or without fixation rods may be required.
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LORDOSIS
Lordosis is normal curvature of the lumbar spine. It can become exaggerated during pregnancy, with obesity, or in persons with large abdominal tumors. Structural changes in the spine do not occur in these instances, and once the problem is resolved, the condition resolves.
Hyperlordosis, or swayback, is fairly common in young children and in girls before puberty. It is thought to be due to rapid skeletal growth without appropriate growth of soft tissue such as fascia and muscles. This problem is self-correcting.
Permanent Hyperlordosis, which is rare, can occur due to degeneration of the intervertebral discs.
Treatment includes bracing, spinal fusion, or osteotomy. STRAIN
Strain is trauma to the body of a muscle or attachment of a tendon caused by overstretching, misuse, or overextension. Strains usually arise from twisting or wrenching movements. They may be acute or chronic. Strains may occur in any age group and in any body part of the body that contains muscles and tendons.
1st Degree strain is identified by the gradual onset of muscle spasms, discomfort, and loss of ROM. No edema or ecchymosis is present. It involves pulling of the musculotendinous unit.
2nd Degree strain is identified by extreme muscle spasms, pain, and edema, which develop immediately after injury. The area remains tender after acute symptoms subside. Ecchymosis develops within few hours. This type of strain involves tearing or straining of the musculotendinous unit.
3rd Degree strain is identified by severe muscle spasm, point tenderness, and edema at the rim of injury. A sensation of sudden tearing, or snapping or burning sensation is felt. Very limited ROM results from spasms. This degree of injury usually represents a complete rupture of the musculotendinous unit.
o X-ray examination is required to rule out the possibility of fracture. Acute strains require rest and, possibly, splinting.
o Elevate the injured part. o Apply ice packs for the first 24 to 48 hours after injury to reduce swelling. Heat may be prescribed for
comfort, to encourage reabsorption of blood and fluid, and to promote healing. o Surgical repair may be necessary if rupture is present at the tendon-bone interface. During healing *4to 6
weeks) movement of the injured part should be minimal. Activity should never be such that it produces symptoms, such as swelling or pain. After mature scar tissue has formed, the art can be gradually and progressively exercised.
o Avoid overactivity during rehabilitation. SPRAINS
Ankle sprains are the most common injury resulting from recreational sports. A sprain is a ligament injury resulting from overstress causing damage to ligament fibers or their attachment.
They commonly result from sudden injury or forced hyperextension.
Sprains may be mild (grade 1), moderate (grade 2), or severe (grade 3).
A mild sprain tears a few ligament fibers, but there is no loss off function and the ligament is not weakened. Therefore, protection of the ligament is not vital.
A moderate sprain tears a portion of ligament, producing some loss of function. Protection is vital to prevent further tearing.
A severe sprain completely tears a ligament either from its attachment or within the ligament body itself. It is estimated that about 75% of sprains have complete ligament rupture. Complete rupture often requires surgical repair. Approximation of the ligament ends is important to ensure strength of the ligament.
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RECURVATUM
This describes a hyperextension of the knee. Hyperextension of the knee is resisted by both collateral ligaments; both cruciate ligaments; the posterior aspect of the joint capsule, the hamstring and gastroc and the configuration of the condyles. The greater the moment of force tending to produce hyperextension, the greater will be the tensile stress in the ligaments. The paralysis of either the hamstring or quadriceps tends to produce recurvatum.
VALGUS OR KNOCK-KNEES
Term valgus refers to the direction in which the apex of a deformity lies in relationship to the midline. A frontal plane deformity at the knee in which distal end of the tibia is directed away from the midline or median sagittal plane. It is usually associated with coxa vara.
The knees are together and the ankles are apart. Unless the degree of valgus is slight, the subject has rather untoward gait. The knees rubbing together increase the side to side movement of the pelvis and trunk.
VARUS OR BOWLEGS
A frontal plane deformity of the knee in which the distal end of the tibia is directed toward the midline or median sagittal plane. It is usually associated with coxa valga. The ankles are together and the knees are apart.
DISLOCATIONS AND SUBLUXATIONS
Dislocation and subluxation are both displacements of a joint from its normal position. Dislocation is the separation of both articulating surfaces loses partial contact. These injuries usually occur from direct or indirect pressure to the joint. For example, trying to break a fall down the stairs by holding onto a railing could dislocate the shoulder. A displaced bone may impede blood supply, tear ligaments, rupture blood vessels, damage nerves, and rupture muscle attachments.
Dislocations and subluxations disrupt a joint by tearing the capsule and ligament. They are often accompanied by a fracture of the joint surface. Dislocations and subluxations may or may not produce visible deformity.
Dislocation may alter the length of an affected extremity. Localized joint pain and loss of function may occur. A dislocation differs from a fracture in that it partially immobilizes a joint. X-ray films show the abnormality. Some dislocations reduce themselves, leaving a sprain. Others require therapeutic reduction.
Before treatment, assess and document the neurovascular status of parts distal to the injury. Once diagnosis is confirmed by x-ray examination, the dislocation or subluxation is reduced.
MOTOR ASSESSMENT AFTER SPINAL CORD INJURY
Spinal Nerve
Assessment Technique
C4-5
Shoulders are shrugged against downward pressure of examiners hands
C5-6
Arm is pulled up from resting position against resistance
C7
From the flexed position, arm is straightened out against resistance
C7
Index finger is held firmly to thumb against resistance to pull apart
C8
Hand grasp strength is evaluated
L2-L4
Leg is lifted from bed against resistance
L5-S1
Knee is flexed against resistance
L2-L4
From flexed position, knee is extended against resistance
L5
Foot is pulled up toward hose against resistance
S1
Foot is pushed down (stepping on with gas) against resistance
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MAJOR DISORDERS OF THE NEUROMUSCULOSKELETAL SYSTEM
1. TRAUMATIC BRAIN INJURIES Etiology and Pathophysiology
Result from penetration by bone fragments from structured skull or movement of the brain within the cranial cavity as a result of impact
Fractures Linear: simple break in the bone Depressed: break that results in fragments of bone penetrating brain tissue
Hemorrhages (secondary brain injury) EPIDURAL : hematoma forms between the dura and the skull; may result from a laceration of the middle
meningeal artery SUBDURAL : hematoma forms between the dura and arachnoid layers; generally following venous damage. Intracerebral hematoma
CONCUSSION : temporary disruption of synaptic activity; brief loss of consciousness
CONTUSIONS : bruising of brain tissue, with slight bleeding of small cerebral vessels into surrounding tissues at site of impact (coup) or opposite to site (countercoup) as a result of rebound reaction
Complications include cerebral edema, brain abscess, meningitis, diabetes insipidus Clinical findings:
Subjective: lethargy; indifference to surroundings; altered sensory function (e.g., visual or auditory
Objective Signs of INCREASED INTRACRANIAL PRESSURE (ICP):
o Decreased level of consciousness o Rapid rise in body temperature; o decreased pulse rate; o changes in respiratory pattern o Increased systolic pressure; o widening pulse pressure o Restlessness
o Headache o Weakness or paralysis o Visual and other sensory disturbances; o papilledema o Vomiting o Seizures
Lack of orientation of time and place
Positive Babinski reflex
Seepage of cerebral spinal fluid from nose or ears; usually indicative of basilar skull fracture.
Therapeutic interventions:
Control seizures with anticonvulsants
Mechanical ventilation; hyperventilation constricts cerebral vessels lowering ICP
Reduce cerebral edema with glucocorticoids and loop diuretics
Maintain adequate fluid and electrolyte balance
Surgical intervention in cases of depressed skull fractures or hematomas
Nursing Care of Clients with HEAD INJURIES A. ASSESSMENT
Airway and breathing pattern
Neurologic status (Neurologic Assessment and Glasgow Coma Scale)
Signs of increased intracranial pressure
Circumstances of injury
Presence of glucose in clear drainage from nose or ears, which indicates cerebrospinal fluid
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B. ANALYSIS/NURSING DIAGNOSES
Risk for aspiration related to loss of gag reflex or inability to expectorate
Decreased adaptive capacity: intracranial, related to increased ICP
C. PLANNING IMPLEMENTATION
Institutes neurologic assessments every 15 minutes for several hours, progressing to every hour and then every 4 hours.
Maintain airway by suctioning as necessary (coughing increases intracranial pressure); use an airway or endotracheal tube
Keep the clients head elevated 30 degrees to reduce venous pressure within the cranial cavity
Administer glucocorticoids and/or diuretics if ordered
Institute seizure precautions; administer anticonvulsants if ordered
Monitor for fluid or electrolyte imbalances; diabetes insipidus or syndrome of inappropriate anti diuretic hormone may occur.
If the clients eyes remain open, protect the corneas with moistened pads, mineral oil, or ointment as ordered
Support clients nutritional needs; administer tube feedings or assist with small frequent meals
Position the client to prevent pressure ulcers
Provide range-of-motion exercises and splints to prevent contractures
Provide auditory and tactile stimulation
Assist client to avoid activities that increase ICP such as Valsalvas maneuver, lifting, sneezing, and flexion of head
Recognize that confusion upon return of consciousness may be a defense against additional stress
Utilize hypothermia as ordered to reduce temperature and metabolic demands
Encourage client and family to participate in planning and care
Provide opportunity for expression of grief
D. EVALUATION/OUTCOMES
Maintains a patent airway
Improves level of consciousness
Remains free from complications of immobility
Participates in decisions about administration of care
11. BRAIN TUMORS Etiology and Pathophysiology
Either benign or malignant; they require intervention, because the skull cannot accommodate the increasing size of the tumor and intracranial pressure rises.
Classified according to tissue of origin MENINGIOMA: occurs outside brain from covering meninges; usually benign Acoustic neuroma and optic nerve spongioblastoma: occur from the cranial nerves GLIOMAS: originate in neural tissue; usually malignant and include astrocytoma, glioblastoma,
oligodendroglioma Hemangioblastomas and angiomas: occur from within blood vessels Metastatic Tumors: originate elsewhere in the body, most commonly the lung and breast
Clinical Findings
Subjective: headache that increases when supine or stooping; lethargy
Objectives: signs of increased intracranial pressure abnormal CT scan, MRI, EEG
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Symptoms may vary depending on location of tumor: o Frontal lobe: personality changes, focal seizures, blurred vision, hemiparesis, altered thought processes o Temporal lobe: seizures, headaches, papilledema, receptive aphasia, tinnitus o Parietal lobe: visual loss, motor and sensory focal seizures o Occipital region: focal seizures, visual hallucination, homonymous hemianopsia o Cerebellar region: loss of coordination, tremors, nystagmus
Therapeutic interventions
Radiation therapy and/or chemotherapy
Surgery for partial or complete removal of the lesion Craniotomy with removal of lesion and invaded tissue Stereotactic radio surgery; employs computer-directed radiation to eradicate tissue
Steroids, anticonvulsive, and osmotic diuretics to control symptoms Nursing Care of Clients with Brain Tumors A. Assessment
History
Neurologic status (Neurologic Assessment and Glasgow Coma Scale)
unilateral non reactive and/or dilated pupil progressing to bilateral as intracranial pressure increases
Signs of increased intracranial pressure B. ANALYSIS/NURSING DIAGNOSES
Ineffective breathing pattern related to compromised neurologic function
Decreased adaptive capacity: intracranial, related to increased ICP
Anxiety related to uncertain diagnosis C. PLANNING/IMPLEMENTATION
Perform routine neurologic assessments
Provide emotional support for the client and family; refer to additional resources such as clergy and support groups
Administer analgesics and anti emetics as ordered
Provide small, frequent feedings, supplements, and oral hygiene
provide care for the client requiring brain surgery Obtain consent for surgery and removal of hair After surgery keep the clients head elevated 30 degrees Support respiratory function by encouraging deep breathing, appropriate positioning, and suctioning to
maintain the airway Use strict aseptic technique with ICP monitoring Observe dressings for cerebrospinal fluid leakage or hemorrhage Maintain intake and output Use hypothermia as ordered if the client is febrile; fever increases metabolic needs to the brain
Assist client to focus on abilities rather that disabilities
Emphasize need for continued health care supervision
D. EVALUATION/OUTCOMES
Maintains adequate respiratory function
Oriented to person, place and time
Establishes effective communication
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111. CEREBRAL VASCULAR ACCIDENT (CVA) Etiology and Pathophysiology
Destruction (infarction) of brain cells caused by a reduction in oxygen supply
Caused by a sudden or gradual interruption in the blood supply following an intra cerebral hemorrhage, blockage of vessels by thrombi or emboli, or vascular insufficiency
Symptoms depend on the area of the brain involved and extent of damage; may be masked or delayed because of compensatory collateral circulation through the circle of Willis
Risk factors include hypertension, hyperlipidemia, obesity, smoking, cerebral arterosclerosis, cerebral aneurysm, atrial fibrillation, advanced age
Transient ischemic attacks (TIA) may also occur without causing permanent damage these usually last only a few minutes
Clinical Findings
Subjective: syncope; headache; changes in level of consciousness; transient paresthesias (with TIAs); mood swings
Objective o Convulsions o Hemiplegia on side opposite the lesion (initially flaccid then spastic) o APHASIA ; brain unable to fulfill its communicative functions because of damage to input, integrative, or
output centers o Dysphagia o Sensory changes; hemianopia (loss of half of visual field) o Alteration in reflexes o Altered bladder and bowel function o CSF is bloody if cerebral or subarachnoid hemorrhage is present o Abnormal EEG, CT Scan, MRI o Cerebral angiography may reveal vascular abnormalities such as aneurysms, narrowing, or occlusions o Signs of increased intracranial pressure
TYPES OF APHASIA
Expressive (motor or Brocas) aphasia: difficulty making thoughts known to others; speaking and writing is most affected
Receptive (sensory or Wernickes) aphasia: difficulty understanding what others are trying to communicate; interpretation of speech and reading is most affected
Global aphasia: affects both expression and reception Therapeutic Interventions
Complete bed rest with sedation as needed
Maintenance of oxygenation by oxygen therapy or mechanical ventilation
maintenance of nutrition by the parenteral route or nasogastric feedings if the client is unable to swallow
Anticoagulant therapy if thrombus or embolus is present; anti platelet therapy
Anti hypertensive and anticonvulsants if indicated
Glucocorticoids may be used to reduce cerebral edema and intracranial pressure
Surgical intervention o To relieve pressure and control bleeding if hemorrhage is present o Carotid endarterectomy to improve cerebral blood flow when carotid arteries are narrowed by
arteriosclerotic patches
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Nursing Care of Clients with CEREBRAL VASCULAR ACCIDENTS A. Assessment
Adequacy of airway and respiratory function
neurologic status (see Neurologic Assessment and Glasgow Coma Scale)
Presence of signs of increased ICP
B. Analysis/Nursing Diagnoses
Risk of aspiration related to dysphagia
altered cerebral tissue perfusion related to interruption of arterial blood flow
Impaired verbal communication related to aphasia
Impaired physical mobility related to hemiparesis
Powerlessness related to loss of abilities
C. Planning/Implementation
Perform neurologic assessments; notes signs of intracranial pressure
Assist with lumbar puncture if performed; may be performed if subarachnoid hemorrhage is suspected (see Lumbar Puncture)
monitor vital signs; avoid using affected extremity for BP because it may produce falsely lowered reading
Maintain patency of the airway by positioning, suctioning, and inserting an artificial airway
Provide for drainage and expansion of lungs by placing client in a low semi-Fowlers position with head turned to side; provide oxygen as necessary
Encourage deep breathing; utilize mechanical ventilation if ordered
Involve all members of the health team when planning care
Assist client and family to set realistic goals; provide encouragement and praise
Accept and explore feelings of fear, anger, and depression; accept mood swings and emotional outbursts
Provide frequent oral hygiene; use artificial tears if blink reflex is absent
Institute seizure precautions
Provide elastic or pneumatic stockings for both legs
Prevent pressure ulcers
Prevent muscle atrophy and contractures o Provide passive range-of-motion exercises; active range of motion and other exercises may be instituted later o Use devices to prevent foot drop, flexion of fingers, external rotation of hips, adduction of shoulders and arms
Provide tube feedings is swallowing and gag reflexes are depressed or absent
Provide food in a form that is easily swallowed (mechanical soft, puree, thickening products); encourage intake of nutrient-dense foods; when client is capable of chewing, introduce dietary fiber to promote normal bowel function
Assist with feeding (e.g., use a padded spoon handle; feed on the unaffected side of mouth; feed in as close to a sitting position as possible)
Encourage the client with speech difficulties to communicate o Be aware of own reactions to the speech difficulties o Evaluate extent of the clients ability to understand and express self o Reinforce what has been learned in Speech therapy o Convey that there is a problem with communication, not with intelligence; try to eliminate anxiety related to
communication attempts o Avoid pushing to point of frustration o Keep distractions at a minimum, since they interfere with the reception and integration of messages o Speak slowly, clearly, and in short sentences, and do not raise voice o Use alternate means of communication o Involve the client in social interactions o Be alert for clues and gestures when speech is garbled
Make a definite transition between tasks to prevent or reduce confusion
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Attempt to prevent fecal impaction and/or urinary tract problems o Provide adequate fluid intake o Provide a diet with enough roughage for sufficient quantity of bowel content and proper consistency for evacuation;
avoid straining at stool because it can raise ICP; administer stool softeners as ordered o Avoid preoccupation with elimination; avoid encouragement of incontinence o Stimulate normal elimination by exercise and activity o Help develop regular bowel and bladder patterns o Respect the individual; provide for privacy and individuality of routine
Create environment that keeps sensory monotony to a minimum; orient to time and place, increase social contacts, provide visual stimuli, extend environment
Provide for self-esteem; encourage wearing own clothes, doing self-care activities, making decisions
help with adjustment to altered body image and self-esteem
D. Evaluation/Outcomes
Maintaining respiratory function
Remains alert and oriented
Communicates effectively
Remains free of client participate in decisions and care
1V. EPILEPSY (SEIZURE DISORDERS) Etiology and pathophysiology storms of transmission
Abnormal discharge of electric impulses by the nerve cells in the brain from idiopathic or secondary causes resulting in: loss of consciousness; convulsions; motor, sensory, behavioral changes
Onset of idiopathic epilepsy generally before age 30; seizures can be associated with brain tumor, CVA, Alzheimers disease, hypoglycemia, head trauma
Types of Seizures
Partial seizures (seizures beginning locally) o Begin with electrical discharge in one limited area/side of the brain o SIMPLE: focal motor or sensory effect; no loss of consciousness o Awareness, Memory and Consciousness are preserved o COMPLEX: cognitive, psycho sensory, psychomotor, or affective effect, brief loss of consciousness o If any of the awareness is impaired, it is called complex
Generalized seizures (bilaterally symmetric and without local onset)
o Begin with a widespread electrical discharge that involves BOTH sides of the brain o ABSENCE (PETIT MAL): (few seconds) brief transient loss of consciousness with or without minor motor
movements of eyes, head, or extremities o MYOCLONIC: brief, transient rigidity or jerking of extremities, singly or in groups o TONIC-CLONIC (GRAND-MAL old name): aura, loss of consciousness, rigidity followed by tonic and
clonic movements, interruption of respirations, loss of bladder and bowel control
STATUS EPILEPTICUS : prolonged repetitive seizures without recovery between attacks, may result in complete exhaustion and lead to death
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Clinical findings (tonic-clonic seizures)
Subjective: seizure often preceded by an aura or warning sensation such as seeing spots or feeling dizzy: loss of consciousness during seizure; lethargy following return to consciousness (postictal phase)
Objective o Shrill cry as seizure begins and air is forcefully exhaled o Tonic and clonic movement of the muscles and incontinence o Abnormal EEG
Therapeutic Interventions
Anticonvulsant therapy continued throughout life; diazepam (Valium) given IV to treat status epilepticus
Sedatives used to reduce emotional stress
Neurosurgery is sometimes indicated if seizures are caused by tumors, abscesses, or vascular problems Nursing Care of Clients with EPILEPSY Planning/Implementation
Provide protection from injury during and after the seizure; nothing should be forced into the mouth because this may cause tongue to occlude airway
Help the client with an aura to plan for self-protection before seizure develops
Encourage use of a medical alert tag
Help plan a schedule that provides adequate rest and reduction of stress
Teach the client and family to observe the aura, initial point of seizure, type of seizure, level of consciousness, loss of bladder and bowel control, progression of seizure, and postictal condition
Encourage expression of feelings about illness and necessary changes in life-style and self-esteem
Assist client and family to accept the diagnosis and develop some understanding of the disease process
Teach that medication must be taken continuously for the remainder of life under continued medical supervision
Refer for job counseling as necessary
Encourage client and family to attend local epilepsy association meetings
Refer Client to state laws regarding driving
Teach about anticonvulsants
V. BELLS PALSY (FACIAL PARALYSIS) Etiology and Pathophysiology
Paralysis that occurs on one side of the face as a result of an inflamed seventh cranial (facial nerve); generally lasts only 2 to 8 weeks but may last longer in older clients
Cause unknown; possible viral link
Most common between ages 20 to 50 years Clinical Findings
Subjective: facial pain; altered taste; impaired ability to chew and swallow
Objective: distortion of face; drooping of mouth on affected side; difficulty with articulation; diminished blink reflex; upward movement of eyeball when closing eye; increased lacrimation
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Therapeutic interventions
Prednisone therapy
heat, massage, and electric stimulation to maintain circulation and muscle tone
Prevention of corneal irritation with eye drops and use of protective eye shield Nursing Care of Clients with BELLS PALSY PLANNING/IMPLEMENTATION
Teach prevention of corneal irritation by using artificial tears, manually closing the eye, and applying an eye shield
Teach importance of keeping face; simple exercises such as blowing; institute only when acute phase is over
Encourage ventilation of feelings
Support nutritional status by providing privacy, small, frequent feedings, and encourage favoring the unaffected side while eating
V1. TRIGEMINAL NEURALGIA (TIC DOULOUREUX) Etiology and Pathophysiology
Incidence higher in women of middle and older age
Disorder of the fifth cranial (trigeminal) nerve characterized by intense knifelike pain along the branches of the nerve
MS; tumors in the nerve; compression of the nerve by a small artery or vein
MOST COMMON CAUSE is vascular compression of the nerve by a small artery as the nerve leaves the brainstem
Clinical findings
Subjective: (sharp lancinating pain on one side of the face in one or two of the three divisions) burning or knifelike pain lasting 1 to 15 minutes, usually in lip, chin, or teeth: pain precipitated by brushing hair, eating, cold drafts
Objective: sudden closure of an eye; twitching of mouth and cheek Therapeutic interventions
Anticonvulsants to relieve and prevent acute attacks
Injection of alcohol/glycerol into the ganglion to relieve pain for several months or years until nerve regenerates
Surgical intervention o Severing of the sensory root of the nerve, which will cause loss of all sensation in the area supplied by the nerve
o Microscopic relocation of arterial loop that may cause vascular compression of trigeminal nerve o Janetta Procedure microvascular decompression; the only procedure designed to relieve the source of the
pain
Percutaneous radio frequency trigeminal gangliolysis: thermal lesion destroys nerve, providing permanent relief for most clients
Nursing Care of Clients with TRIGEMINAL NEURALGIA PLANNING/IMPLEMENTATION
Teach factors to limit triggering an attack, which can result in exhaustion o Avoid foods that are too cold or too hot o Chew food on unaffected side o Use cotton pads to gently wash face and for oral hygiene o Keep the room free of drafts; avoiding jarring
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Provide teaching to clients who have sensory loss as a result of treatment o Inspection of the eye several times a day for foreign bodies, which the client will not be able to feel o Warm normal saline irrigation of the affected eye two or three times a day is helpful in preventing a
corneal infection o Dental checkups every 6 months
Teach about anticonvulsants (see Anticonvulsants in Pharmacology) and the need for continued medical supervision
V11. PARKINSONS DISEASE (PARALYSIS AGITANS) Etiology and pathophysiology
Progressive disorder in which there is a destruction of nerve cells in the basal ganglia and substancia nigra of the brain, which results in dopamine deficiency and subsequent generalized degeneration of muscular function
Incidence highest in elderly; suspected causes include neurotransmitter imbalance (dopamine and acetylcholine), unknown virus, cerebral vascular disease, and chemical or physical trauma
Clinical findings
Subjective: mild, diffuse, muscular pain; stiffness and rigidity, particularly of large joints (RIGIDITY OF EXTREMITIES); depression; emotional lability may be present but intelligence is usually not impaired
Objective o Increased difficulty in performing usual activities such as writing, dressing, and eating o Generalized tremor commonly accompanied by pill-rolling movements of the thumb against the fingers;
non-intentional tremors usually reduced by purposeful movements and SLEEP COARSE TREMORS o Various disorders of locomotion (e.g. bent posture, difficulty in rising from sitting position, shuffling
propulsive gait, loss of rhythmic arm swing when walking -bradykinesia) o Mask-like facial expression with unblinking eyes o Low-pitched, slow, poorly modulated, poorly articulated speech o Drooling; difficulty in swallowing saliva o Various autonomic symptoms (e.g., lacrimation, constipation, incontinence, decreased sexual capacity,
excessive perspiration) o Dementia and confusion in 15% to 20% of individuals, especially the elderly
Therapeutic interventions
Medical regimen is palliative rather than curative
Pharmacologic intervention (see Antiparkinson Agents in Pharmacology)
Physiotherapy to reduce rigidity of muscles and prevent contractures Nursing Care of Clients with PARKINSONS DISEASE PLANNING/IMPLEMENTATION
Provide a safe environment
Teach client or family to cut food into small bite-sized pieces or alter the consistency to prevent choking; encourage diet rich in nutrient-dense food such as fruits, vegetables, whole grin to improve and maintain nutritional status and prevent possible drug-induced nutrient deficiencies
Suction to maintain an adequate airway (usually advanced stages)
encourage an adequate intake of roughage and fluids to avoid constipation
Teach activities to limit postural deformities (e.g., use firm mattress without a pillow, periodically lie prone, keep head and neck as erect as possible, think about posture when walking)
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Teach activities to maintain gait as normal as possible; utilize cane or walker as necessary
teach and encourage daily physical therapy to limit rigidity and prevent contractures (e.g., warm baths, passive and active exercises)
Avoid rushing as stress intensifies symptoms
Encourage continuation of medications even though results may be minimal
Teach client and family about Anti Parkinson agents (see Anti Parkinson Agents in Pharmacology)
Assist in setting achievable goals to improve self-esteem
V111. MULTIPLE SCLEROSIS (DISSEMINATED SCLEROSIS) Etiology and pathophysiology
Randomly scattered patches of demyelination in brainstem, cerebrum, cerebellum, and spinal cord.
Chronic debilitating, progressive disease with periods of remission and exacerbation
Cause unknown; viral and immunologic causes have been implicated; current AUTOIMMUNE in origin
ONSET IS INSIDUOUS; Onset in early adult life (20 to 40 years); higher occurrences in females
Greater incidence in Caucasians and those living in cold climates
Fatigue, stress, and heat tend to increase symptoms Clinical Findings
Subjective o Paresthesia; altered position sense; ataxia o Dysphagia o Weakness; fatigue; - begin in upper extremities (from weakness to spastic paralysis) o Blurred vision; diplopia; optic neuritis leading to loss of vision or BLIND SPOTS or WHITE SPOTS in
VISUAL FIELD o Altered emotional affect (depression, apathy, or euphoria)
Objective o CHARCOTS TRIAD : intention tremor, nystagmus, scanning (clipped) speech o Shuffling gait; increased deep tendon reflexes; spastic paralysis o Impaired bowel and bladder function (90% of cases) o Impotence o Cognitive loss (advanced stage) o Pallor of optic discs; blindness; optic neuritis leading to loss of vision or BLIND SPOTS o Increased immunoglobulin G (IgG) levels in the CSF o MRI indicates demyelination PRESENCE OF PLAQUES o CT Scan increased white matter density
PLANNING/IMPLEMENTATION
Incorporate frequent rest periods
Avoid hot baths, which can increase symptoms
Teach use of assistive devices when carrying out activities of daily living
Assist family to understand why client should be encouraged to be active
Assist client and family to plan and implement a bowel and bladder regimen
Explain the disease process to both client and family in understandable terms
Do not encourage false hopes during periods of remission
Spend time listening to both client and family; encourage ventilation of feelings
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Refer client and family to the National Multiple Sclerosis Society
. Encourage counseling and rehabilitation
Explain to client and family that mood swings and emotional alterations are part of the disease process
Help client maintain self-esteem
Teach how to compensate for problems with gait; walk with feet farther apart to broaden base of support; use low-heeled shoes; use assistive devices when necessary (tripod cane, walker, wheelchair)
Teach how to compensate for loss of sensation; use a thermometer to test water temperature; avoid constricting stockings; use protective clothing in cold weather; change position frequently
Teach how to compensate for difficulty in swallowing; take small bites; chew well; use a straw with liquids; eat foods of more solid consistency
Provide a diet rich in nutrient-dense foods such as fruits, vegetables, whole grains, and legumes to improve and maintain nutritional status and compensate for nutrient interactions of corticosteroid medications
Provide skin care to prevent formation of pressure ulcers; turn frequently
Prevent dysfunctional contractures; provide range-of-motion exercises; splints Drug Therapy for MS Clients:
ACTH or Cortisone
Cytoxan and other immunosuppressive drugs
Nursing implications for administration of these drugs should focus on prevention of infection
IX. MYASTHENIA GRAVIS Etiology and pathophysiology
grave muscle weakness
Chronic, progressive, neuromuscular disorder with remissions and exacerbations; there is a disturbance in the transmission of impulses at the myoneural junction resulting in profound weakness ***thymus gland is abnormal
Dysfunction thought to be caused by a reduced number of acetylcholine receptors (AChR) and an alteration of the postsynaptic membrane of the muscle end-plate
Autoimmune theory: it is believed that complement and antibodies to AChR cause accelerated destruction and blockage of the AChR
Highest incidence in young adult females; females between ages 10 and 40 and males between ages 50/60 and 70
Myasthenic crisis refers to sudden inability to swallow or maintain respirations because of the weakness of the muscles of respiration
Clinical Findings
Subjective: Extreme muscle weakness; becomes progressively worse with use, but disappears with rest; dyspnea; dysphagia (difficult chewing and swallowing); dysarthria (difficulty speaking); diplopia
Objective o Physical: COGANS LID TWITCH; Ptosis of the eyelid and diplopia o strabismus; weak voice (dysphonia); myasthenic smile (snarling, nasal smile) mask like effect
Diagnostic Measures: Spontaneous relief of symptoms with administration of subcutaneous neostigmine (prostigmin) or IV administration of endrophonium (Tensilon);
endrophonium used to distinguish myasthenic crisis from cholinergic crisis (toxic effects of excessive neostigmine)
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Therapeutic Interventions
Medications that block the action of cholinesterase at the myoneural junction (see Cholinesterase Inhibitors in Pharmacology)
endrophonium chloride (Tensilon) (used for diagnostic purposes) and neostigmine bromide (Prostigmin) or neostigmine methylsulfate (PMS-Neostigmine, Prostigmin)
Diagnostic Measures: Spontaneous relief of symptoms with administration of subcutaneous/IM/IV neostigmine (prostigmin) or IV administration of endrophonium (Tensilon); endrophonium used to distinguish myasthenic crisis from cholinergic crisis (toxic effects of excessive neostigmine)
X-ray therapy or surgical removal of the thymus may cause partial remission
Corticosteroids or ACTH
Tracheostomy with mechanical vent