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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

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 .

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.

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

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)

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.

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.

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.

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
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

B. Nursing Care

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 H 2O) 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

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 vestibuloocular 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:

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

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 Eyes Does not open eyes Makes no sounds Makes no movements 2 Opens eyes in response to painful stimuli Incomprehensible sounds Extension to painful stimuli 3 Opens eyes in response to voice Utters inappropriate words Abnormal flexion to painful stimuli 4 Opens eyes spontaneously Confused, disorientated Flexion / Withdrawal to painful stimuli 5 N/A Oriented, converses normally 6 N/A

Verbal

N/A

Motor

Localizes Obeys painful stimuli commands

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. 2. 3. 4. 5. No verbal response Incomprehensible sounds. (Moaning but no words.) Inappropriate words. (Random or exclamatory articulated speech, but no conversational exchange) Confused. (The patient responds to questions coherently but there is some disorientation and confusion.) 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.

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

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

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

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. Movement of a part, e. g. an extremity, in a circular direction. A permanent muscular contraction due to tonic spasm or fibrosis, or to loss muscular balance, with antagonists being paralyzes. 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.

CIRCUMDUCTION

CONTRACTURE

VOLKMANNS CONTRACTURE

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.

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 selfcorrecting. 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.

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. 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.
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 xray examination, the dislocation or subluxation is reduced.

VARUS OR BOWLEGS

DISLOCATIONS AND SUBLUXATIONS

MOTOR ASSESSMENT AFTER SPINAL CORD INJURY Spinal Nerve


C4-5 C5-6 C7 C7 C8 L2-L4 L5-S1 L2-L4 L5 S1

Assessment Technique
Shoulders are shrugged against downward pressure of examiners hands Arm is pulled up from resting position against resistance From the flexed position, arm is straightened out against resistance Index finger is held firmly to thumb against resistance to pull apart Hand grasp strength is evaluated Leg is lifted from bed against resistance Knee is flexed against resistance From flexed position, knee is extended against resistance Foot is pulled up toward hose against resistance Foot is pushed down (stepping on with gas) against resistance

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 Headache o Rapid rise in body temperature; o Weakness or paralysis o decreased pulse rate; o Visual and other sensory disturbances; o changes in respiratory pattern o papilledema o Increased systolic pressure; o Vomiting o widening pulse pressure o Seizures o Restlessness 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

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

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

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

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 nutrientdense 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

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

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

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

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)

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

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 lowheeled 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)

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 ventilation as necessary in myasthenic crisis

PLANNING/IMPLEMENTATION Medications on strict time schedule to prevent onset of symptoms Observe for signs of dyspnea, dysphagia, and dysarthria; may be caused by worsening of myasthenia (myasthenic crisis) or overdose of anticholinergic drugs (cholinergic crisis) Plan activity to avoid fatigue based on the individuals tolerance Avoid people with upper respiratory tract infections Avoid administering morphine to clients receiving cholinesterase inhibitors; these drugs potentiate effects of

morphine and may cause respiratory depression

Administer tube feedings to avoid aspiration if client has difficulty swallowing Administer artificial tears to keep cornea moist if client has difficulty closing eyes Encourage client and family to participate in planning care Ensure that client understands the signs and symptoms of myasthenic and cholinergic crises Myasthenia Gravis Foundation and local self-help groups Patent airway; suction as necessary; provide tracheostomy care; maintain mechanical ventilation as ordered

X. GUILLAIN-BARRSYNDROME (POLYRADICULONEURITIS)
Etiology and pathophysiology It is an acute infectious neuronitis of the cranial and peripheral nerves (demyelination); the immune system overreacts to the infection and destroys the myelin sheath; the syndrome usually is preceded by a mild upper respiratory infection or gastroenteritis 1 to 4 weeks prior to the

onset of neurologic deficits

Symmetrical, bilateral, peripheral polyneuritis characterized by ascending paralysis Can occur at any age; affects men and women equally Cause is unknown; maybe an autoimmune process Recovery is usually from 3 to 6 months or a year; may have residual deficits (10%)

Clinical Findings Subjective: generalized weakness; paresthesia; muscle pain (in the back and calves of legs); diplopia Objective o Paralysis begins in lower extremities (muscle weakness of legs progressing to the upper extremities, trunk and face); ascends within the body; maximal deficit usually by 4 weeks o Paralysis of the ocular, facial and oropharyngeal muscles, causing marked difficulty in talking, chewing, and swallowing

o Respiratory paralysis (paradoxic inward movement of the upper abdominal wall while in supine position, indicating weakness and impending paralysis of the diaphragm) o Increase PR and disturbances in rhythm, transient hypertension and orthostatic hypotension o Autonomic neuropathy (hypertension, tachycardia, diaphoresis) o Abnormal CSF and electrophysiologic studies Treatment is plasmapharesis and infusion of Ig

PLANNING/IMPLEMENTATION Monitor vital signs, breath sounds, and arterial blood gases Maintain airway and keep tracheostomy set at the bedside Monitor functioning of the respirator and suction as necessary

Provide emotional support for the client and family because of the severity of adaptations and lengthy convalescent period

Prevent complications of immobility: skin care; range-of-motion exercises; position changes; coughing and deep breathing; antiembolism stocking

XI. AMYOTROPHIC LATERAL SCLEROSIS (ALS; LOU GEHRIGS DISEASE)


Etiology and pathophysiology Progressive, degenerative corticospinal and anterior horn motor neurons (upper and lower) Men than women in the fourth and fifth/sixth decades Autoimmune diseases and genetic causes are implicated Death from respiratory complications frequently occurs within 3 to 5 years No cure or treatment Clinical Findings Subjective: muscular weakness (progressive weakness and atrophy of the muscles of the arms, legs or trunk); malaise, fatigue Objective o Fasciculations (irregular spasmodic twitching of small muscle groups); spasticity: atrophy o Difficulty in breathing, chewing, swallowing, speaking o Outbursts of laughter or crying o Abnormal electromyography Therapeutic Interventions Physiotherapy to relieve spasticity Supporting respiratory functions Riluzole (Rilutek) to inhibit glutamate accumulation, possibly preventing injury or death of neurons PLANNING/IMPLEMENTATION Encourage client to remain active as long as possible, employing supportive devices as needed Encourage range-of-motion exercises Monitor swallowing ability; positioning and consistency of diet to prevent aspiration Provide alternate means of communication as speech declines Allow client to discuss feeling about life support while still able to speak Monitor respiratory function; increased fluids, positioning, chest physiotherapy, coughing and deep breathing exercises, and suctioning help prevent complication

Support natural defense mechanisms; encourage a diet consisting of nutrient-dense foods, especially those rich in the immune-stimulating nutrients selenium and vitamins A, C, and E. Teach the avoidance of situations that may contribute to infection Provide emotional support for the client and family

XII. ARTHRITIS
Etiology and pathophysiology RHEUMATOID ARTHRITIS (RA) Altered antibodies (rheumatoid factors) combine with IgG to form complexes that are deposited in synovial membranes; inflammation and destructive changes follow, leading to joint deformity and fusion It is an immune complex disorder Systemic effects vasculitis, pulmonary fibrosis, and pericardial disease Etiology unclear; apparent genetic predisposition; incidence higher in women OSTEOARTHRITIS (OA) Enzymatic destruction of articular cartilage Non-inflammatory joint disease with no systemic effects Cause is unknown; secondary osteoarthritis is linked to damage from overuse, injury, infection, or chemicals Risk Factors of OA: o Increased age o Obesity o Previous joint damage o Repetitive use (occupational or recreational) o Anatomic deformity o Genetic susceptibility GOUTY ARTHRITIS (GA) Disorder in purine metabolism that leads to high levels of uric acid in the blood and the deposition of uric acid crystals (tophi) in tissues, especially joints; followed by an inflammatory response Incidence highest in males; a familial tendency has been demonstrated Renal urate lithiasis (kidney stones) may result from precipitation of uric acid in the presence of low urinary pH Clinical Findings Subjective Joint pain o Insidious onset of asymmetric pain in hips, knees, fingers or spine that increases with weight-bearing activity and is relieved by rest (OA) o Symmetrical (bilateral) pain in small joints of hands and feet; knees, shoulders, hips, elbows, and ankles affected as disease progresses; not relieved by rest (RA) o Metatarsophalangeal joint of the great toe (GA) o The metatarsophalangeal joint of the big toe is the most commonly affected (75% of patients). o The tarsal area, ankle, or knee may also be affected. o Less commonly, the wrists, fingers, and elbows may be affected. o The acute attack may be triggered by trauma, alcohol ingestion, dieting, medications, surgical stress, or illness.

o The abrupt onset often occurs at night, awakening the patient with severe pain, redness, swelling, and warmth of the affected joint. Early attacks tend to subside spontaneously over 3 to 10 days even without treatment. Morning stiffness: less than 1 hour with OA; more than 1 hour with RA Anorexia, fatigue, and malaise (RA, GA)

Objective Decreased range of motion Inflammation (swelling, heat, redness) of involved joints (RA, GA) Deformities o Ulna drift, Boutonniere deformity, swan-neck deformity, rheumatoid nodules of hand (RA) o Herberdens and Bouchards nodes (bony hypertrophy) symmetrically occurring on fingers (OA) o Tophi in outer ear, hands, feet, elbows, or knees (GA) Crepitus when joints is moved (OA) Fever (RA, GA) Laboratory findings o RA: presence of rheumatoid factors (RF), elevated erythrocyte sedimentation rate (ESR), decreased RBC, and positive C-reactive protein and anti-nuclear antibody (ANA) tests o GA: elevated serum uric acid Therapeutic Interventions Pharmacologic Management o Acetaminophen (OA) o Nonsteroidal anti-inflammatory drugs (RA, OA, GA) o Disease modifying agents such as methotrexate, hydroxychloroquine, sulfasalazine, gold, azathioprine, and penicillamine (RA) o Antigout agents o Corticosteroids (RA and resistant GA) Weight Loss Physical therapy to preserve joint function; application of heat/cold Use of splints and assistive devices Surgical intervention (RA, GA) o SYNOVECTOMY: removal of the enlarged synovial membrane before bone and cartilage destruction occurs o ARTHRODESIS : fusion of a joint performed when the joint surfaces are severely damaged; this leaves client with no range of motion of affected joint o Reconstructive surgery: replacement of a badly damage joint with a prosthetic device

PLANNING/IMPLEMENTATION Assist with activities that require using affected joints; allow for rest periods Provide for range-of-motion exercises up to the point of pain, recognizing that some discomfort is always present Relieve discomfort and edema by medications or application of heat/cold Allow ample time to verbalize feelings regarding limited motion and changes in life-style; help set realistic goals, focusing on strengths Support client through weight loss program if indicated Encourage client to follow physical therapists instruction regarding regular exercise program and use of supportive devices to maintain independence Administer and teach about prescribed pharmacologic therapy Provide dietary instructions

o o

Encourage 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 and other treatment medications (RA, GA); avoid high-purine foods such as organ meats, anchovies, sardines, and shellfish Increase fluid intake to 2000 to 3000 ml daily to prevent formation of calculi; alkaline-ash diet to increase, discourage precipitation of uric acid and enhance the action of drugs such as Probenecid (GA)

Provide care for the client with RA or OS requiring joint replacement

XIII. OSTEOMYELITIS
Etiology and pathophysiology direct or indirect invasion by Staphylococcus aureus o Indirect entry o Direct entry Clinical Findings Subjective: pain and tenderness of bone; malaise; headache Objective: sepsis such as fever; edema and erythema over bone; positive culture from bone biopsy and positive radionucleide bone scan Therapeutic Interventions Incision and drainage of a bone abscess SEQUESTRECTOMY: surgical removal of the dead, infected bone and cartilage PLANNING/IMPLEMENTATION Monitor neurovascular Functional body alignment and promote comfort Use room deodorizer if a foul odor is apparent Nutrient-dense diet for long-term antibiotic

XIV. INTERVERTEBRAL DISC DISEASE


Etiology and pathophysiology: Protrusion of the nucleus pulposus into the spinal canal compression of the cord or nerve roots as a result of trauma Common site is lumbosacral area (between L4 and L5) herniation occur in the cervical region (between C5 and C6 or C6 and C7) Clinical Findings Subjective o Lumbosacral disc: Acute pain in lower back, radiating across buttock and down leg (sciatic pain)/ pain increases with activities that raise intraspinal pressure/ Pain on affected side o Cervical disc: Neck pain that may radiate to hand/ Weakness of the affected upper extremity Objective o Straightening of normal lumbar curve with scoliosis away from affected side (lumbosacral disc) o Atrophy of biceps and triceps o Elevated CSF protein o Spinal defect on x-ray, myelogram, CT scan, or MRI

Therapeutic Interventions Bed rest with traction to the lower extremities (lumbosacral disc) or cervical traction (cervical disc) Back brace or support; cervical collar Local application of heat Muscle relaxants, analgesics, anti-inflammatory agent Surgical intervention o Laminectomy: excision of the ruptured portion of the nucleus pulposus through an opening created by removal of part of the vertebra o Discectomy: entire disc and cartilaginous plate are removed PLANNING/IMPLEMENTATION Analgesics medications Firm mattress and bed board Make certain that traction and/or braces are correctly applied and maintained and that weights hang freely Fracture bedpan to avoid lifting of hips Frequent and extensive back care to relax muscles and promote circulation Support body alignment at all times Use log-rolling method to turn (instruct client to fold arms across chest, bend knee on side opposite the direction of turn, and then roll over. Weight loss, wearing low-heeled shoes, and appropriate body mechanics Increase fluid intake and encourage diet rich in nutrient-dense foods such as fruits, vegetables, whole grains, and legumes to improve and maintain nutritional status and prevent constipation; use stool softeners to prevent straining Undergoing a repair or a removal of a disc o Explain that pain may persist postoperatively for some time because of edema o Place bedside table, phone, and call bell within reach to prevent twisting o Observe the dressing for hemorrhage and leakage of spinal fluid o Observe for adequate ventilation in clients who have undergone a cervical laminectory o Assess for changes in neurologic function

XV. FRACTURES OF THE EXTREMITES


Etiology and pathophysiology: Break in bone continuity localized tissue response and muscle spasm Trauma or pathologic fractures as a result of osteoporosis, multiple myeloma, or bone tumors Types of Fractures o Complete fracture o Incomplete fracture o Comminuted fracture o Greenstick fracture o Simple (closed) fracture o Compound (open) fracture CLASSIFICATION BY COMMUNICATION WITH THE ENVIRONMENT Open to the environment (bone protrudes through the skin) Closed ( the skin is not broken)

Closed Fractures Uncomplicated fracture with intact skin over the fracture site Called as simple fractures in the past Open fractures Characterized by a break in the skin over the fracture site Wound encompasses the skin (externally) and the fractured bone (internally) Because of the wounds communication with the external environment and extensive tissue damage, open fracture always carries the potential for infection Also called compound fractures Grades of Severity Grade I: Wound smaller than 1 cm. with minimal contamination Grade II: Wound larger than 1 cm. with moderate contamination and moderate soft tissue damage Grade III: Wound larger than 6 to 8 cm. with extensive soft tissue, nerve, and tendon damage and a high degree of contamination. CLASSIFICATION BY FRACTURE PATTERN Linear Fracture o Fracture line is intact o Line may be transverse or oblique o Result of minor or moderate force applied directly to the bone Oblique Fracture o Fracture line occurs at an oblique angle (about a 45 degree angle) to the shaft (axis) of the bone o Usually produced by twisting force. Longitudinal Fracture o Fracture line extends longitudinally Transverse Fracture o Fracture line is straight across the base that is right angle to the bones axis o Transverse fracture is usually caused by an angulations force o Occur in clients with bone disorders, such as Pagets disease, osteomalacia, and osteogenesis imperfecta Spiral Fracture o Fracture line forms a spiral encircling the bone o Caused by twisting force with an upward thrust o Result of indirect forces o When seen in the upper extremities, spiral fractures may indicate abuse

CLASSIFICATION BY TYPE OF FRACTURE Avulsion Fracture Bone fragments are torn away from the body of the bone Avulsion injuries occur when a direct force (pulling) is exerted on a bone with ligamentous resistance in the joint Compression Fracture Produced by a compressive loading force applied to the long axis of the bone Vertebral compression fractures are common in the elderly as a result of osteoporosis Gravity and body weight are the loading forces

Comminuted Fracture A comminuted fracture is produced by high-energy forces (motor vehicle accident) Produce more than one fracture line, and bone fragments are crushed or broken into several pieces Severe soft tissue injury is frequently present Elderly clients suffer comminuted hip fractures during falls Greenstick Fracture Fracture in which one side of the bone is broken and the other side is bent (like a stick of greenwood) Cortex of the bone is buckled or cracked, but bone continuity is not completely disrupted. Also called incomplete fracture Occur in children, whose bones are still soft pliable Impacted fracture Fracture in which one end on the bone is impacted (driven) into the other end Pathologic Fracture
Occurs when bone is weakened as a result of an underlying bone disorder, osteoporosis or tissue Occur with minimal trauma, or even with simple body movements, which would not change normal bone Occur with cancer of the bone Result of repeated stress on a bone, and there is usually no evidence of bone disorder or trauma to explain the fracture Muscles normally allow stress forces to be shunted away from the bone but muscles become fatigued, this protection is lost Commonly seen in marathon runners

Stress (Fatigue) Fracture

CLASSIFICATION OF EPONYM

Named by physicians who first described them

Colles Fracture Common fracture in which the distal radius is fractured within 1 inch or the articular surface Potts fracture Occurs at the radial malleolus of the tibia and fibula and often is associated with ligament, dripping off piece of the medial malleolus or both Tibiofibular articular is seriously disrupted CLASSIFICATION BY APPEARANCE Describes the appearance of the fracture and any bony fragments Burst Fracture Results in multiple pieces of bone; although it is usually found at the ends of bone, it can occur in vertebrae Chip Fracture Small fracture in which a bony process near a joint is fragmented Complete Fracture The fracture line extends through the entire bone substance, that is, the periosteum and cortex are disrupted or both sides of the bone Displaced Fracture Bone fragments are separated at the fracture line or the joint May be described according to the degree of displacement, such as minimal and complete rupture of the internal

CLASSIFICATION BY POINT REFERENCE Rule of Thirds used to classify fractures by a point of reference on the bone shaft Termed as proximal third, midshaft and distal third Fractures of the midshaft heal more slowly due to the decreased blood supply in that area

CLASSIFICATION BY ANATOMIC LOCATION Described by their anatomic location e.g. the anatomic neck of the humerus or femur, surgical neck of the humerus or femur Fracture including a joint surface is called an articular fracture Fracture near joint but not entering the joint capsule, extracapsular fracture intracapsular fractures are fractures within joint capsule Stages of healing include formation of a hematoma followed by cellular proliferation and callus formation by the osteoblasts; finally ossification and remodeling of the callus

Clinical Findings Subjective: pain aggravated by motion; tenderness Objective o Loss of motion; crepitus (grating sound heard when affected limb is moved o Edema; ecchymosis o E-ray examination reveals break in continuity of bone o Shortening of extremity caused by change in bone alignment Therapeutic Interventions Traction may be used to reduce the fracture or to maintain alignment of bone fragments until healing occurs Skin traction: weights attached to adhesive, which is applied to the skin Bucks extension: immobilized the leg when a client fractures a hip Bryants fraction: fractured femurs in young children Russell traction: balanced traction in which lower leg is supported in a hammock, which is attached to rope and pulleys on a Balkan frame; used to treat fractures of femur (the foot of the bed is usually elevated for countertraction) Skeletal traction applied to the bone: Steinmann pin or Kirschemers wire inserted through bone and skin with weights attached to both ends of pin or wire (may be used in conjunction with a cast) Surgical intervention to alight the bone (open reduction), often with plates and screws to hold fracture in alignment Application of cast to maintain alignment and immobilized limb: may be plaster or fiberglass Use of external fixation device when fractures accompany soft tissue injury

OPEN REDUCTION In open reduction, an incision is made and the fracture is aligned during surgery under direct vision. At the time of surgery, various internal fixation devices may be applied to the fractured bone to maintain alignment, or rods maybe placed through bone fragments, fixed to the sides of the bone, or inserted directly into the bones medullary cavity. For some fractures, open reduction is the treatment of choice, such as for compound fractures that are comminuted or accompanied by serious neurovascular injuries or for fractures with widely separated fragments or with soft tissue interposed between bone fragments. Open reduction is usually needed for fractures of the femur and fractured joints. Although internal fixation devices initially help immobilize a fracture and prevent deformity, they

are not a substitute for bone healing. If proper bone healing does not occur, the metallic internal fixation devices succumb to stress and loosen or break. Examples of open reduction can be seen in the section on fractured hips. CLOSED REDUCTION Closed reduction is a method of fracture realignment. A physician performs closed reduction by manually applying traction to move the ends of a bone together and restore alignment. It should be performed as soon as possible after the injury to reduce the risk of loss of limb function, prevent or delay degeneration of the joint, and minimize the deforming effects of the injury. Closed reduction is performed under general anesthesia or local anesthesia, with or without sedation. Four maneuvers are used for manual reduction. The first step is a longitudinal pull on the distal end of the fracture or extremity. This pull reverses the mechanism that produced the fracture and overcomes the initial muscle spasm, limb shortening, and overriding of bone fragments. The second step is disengagement of the bony ends of the fracture, which is sometimes done by rotating the distal portion. The third step is realignment of the ends of the bone. This is a complex step because several forces from various muscle groups are holding the bony fragments in various positions. Finally, the distraction force is released; forces such as gravity, weight bearing, and muscle contraction begin again and can work to move the fragments once more. Following a closed reduction, x-ray films are taken and either a cast or traction is usually applied. PLANNING/IMPLEMENTATION Provide emergency care Evaluate the clients general physical condition; treat for shock Splint extremity in position found before moving client; consider all suspected fractures as fractures until x-rayed Cover open wound with sterile dressing if available Observe for signs of emboli (fat or blood): severe chest pain, dyspnea, pallor, and diaphoresis Observe for signs of gas gangrene, which develops 2 to 5 days after deep wound injury o Culture shows Clostridium perfringems, C. welchii, and C. Novyi o Bronzed or blackened wound tissue; necrosis o Crepitus; pallor Provide care for a client with a cast Observe for signs of circulatory impairment: change in skin temperature or color, numbness or tingling, unrelieved pain, decrease in pedal pulse, inability to move toes or fingers, prolonged blanching of toes/fingers after compression; compartment syndrome is a serious problem caused by compromised circulated to the muscle; ischemia leads to edema, which further comprises circulation Protect the cast from damage until dry: elevate on pillow; handle with palms of heads only Promote drying of the cast by leaving it uncovered Maintain bed rest until the cast is dry and ambulation is permitted Observe for signs of hemorrhage and measure extent of drainage on cast Observe for irritation caused by rough cast edges, and pad as necessary for comfort and to prevent soiling Observe for swelling and notify the physician if necessary Administer analgesics judiciously and report unrelieved pain Observe for signs of infection(e.g. elevated temperature, odor from cast, swelling) Provide care for a client in traction Check that weights are hanging freely and that the affected limb is not resting against anything that will impeded the pull of the traction Maintain in proper alignment Observe for foot-drop in clients with Russell traction or Bucks extension, because this may indicate nerve damage Observe for signs of thrombophlebitis, a more common complication of Russell traction because there is pressure on the popliteal space in addition to stress of immobility Observe skin for irritation and observe site of insertion of skeletal traction for signs of infection: use surgical asepsis when cleaning site of insertion skeletal traction (an antiseptic ointment be ordered)

Encourage high-protein, high-vitamin diet to promote healing; high-calcium diet is not recommended for the client confined to prolonged bed rest, because decalcification of the bone will continue until activity is restored, and a high calcium intake could lead to formation f renal calculi Encourage fluids to help prevent complications of constipation, renal calculi, and urinary tract infection Teach isometric exercises to promote muscle strength and tone for crutch-walking Teach appropriate crutch-waling technique; non weight bearing (three-point swing-through); weight bearing (four point) progressing to use of cane (see Related Procedures)

XVI. SPINAL CORD INJURY


Etiology and pathophysiology: Sudden impingements on the spinal cord as a result of trauma Cut, compress, or completely sever the spinal cord; the symptoms depend on the location (lumbar, thoracic, cervical) and extent of the damage (complete transaction, partial transaction, compression) and may be temporary or permanent; the sensation and mobility of areas that are supplied by nerves Disruption in NS function, which may result in complete or incomplete loss of motor and sensory function The most common sites are the C5, C6, C7, T12 and L1 Permanent impairment cannot be determined until spinal cord edema has subsided, usually by 1 week Clinical Findings Subjective: paresthesias or loss of sensation below the level of injury Objective Inability to move below the level of the injury Early symptoms of spinal shock Bradycardia Bladder and bowel distension Flaccid paralysis Hypotonia Hypotension Absence of reflexes Inability to perspire in affected parts Lack of sensation below lesion Later symptoms of spinal cord injury Reflex hyperexcitability (spastic paralysis): muscles below site of injury become spastic and hyperreflexic State of diminished reflex excitability (flaccid paralysis) below site of injury follows the state of reflex hyperexcitability in all instances of total cord damage and may occur in some instances of partial cord damage. Total cord damage, location permanent o Sacral region: paralysis (usually flaccid type) of lower extremities (paraplegia) accompanied by atonic o Lumbar region: paralysis of lower extremities that may extend to pelvic region (usually flaccid type) accompanied by a spastic (automatic) bladder and loss of bladder and anal sphincter control o Thoracic region: same symptoms as lumber region except paralysis extends to the trunk below level of the diaphragm o Cervical region: same symptoms as thoracic region except paralysis extends from neck down and includes paralysis of all extremities (quadriplegia); if injury is above C4, respirations are depressed. Partial cord damage either the upper or the lower motoneurons, or both, may be destroyed; lower motoneurons will result in atrophy and flaccid paralysis of involved muscles, whereas destruction of upper motoneurons causes spasticity

(autonomous) bladder and bowel with impairment of sphincter control

AUTONOMIC DYSREFLEXIA: bowel or bladder; leads to: Bradycardia Bowel and bladder distention Severe hypertension Pounding headache Flushed skin Diaphoresis Nasal congestion Goose bumps Therapeutic Interventions Maintenance of vertebral alignment Bed rest with supportive devices or with total immobilization Skeletal traction (crutch field, tongs, halo device) Corsets, braces, and other devices Surgery to reduce pain or pressure and/or stabilize spine (e.g., laminectory, spinal fusion Mechanical ventilation as needed Temperature control via hypothermia PLANNING/IMPLEMENTATION Observation of respiratory and neurologic functioning Maintain spinal alignment; log-rolling method to turn Surgical asepsis with skeletal traction or spinal surgery Skin care to back and bony prominences Maintain body parts in a functional position; prevent dysfunctional contractures Active and passive range-of-motion exercises; exercises by be performed in water Encourage verbalization and accept feelings Include client in decision-making process; encourage independence when possible Involve client, family, and entire health team in developing a plan of care Help with adjustment to altered body image, life-style, and self-concept Set realistic short-term goals so success can be achieved Avoid bumps and bruises; utilize techniques to prevent pressure and examine skin for signs of pressure from positioning, braces, or splints Provide an opportunity to touch, grasp, and manipulate objects of different sizes, weights, and texture to stimulate

tactile sensation

Protect affected limbs by proper positioning during transfer Unaffected extremities to manipulate, move, and stabilized affected parts.

Apply anti-embolic stockings


Attempt to establish a schedule pattern of bowel function o Compare clients bowel habits before illness to current pattern; establish a specific and definite time for bowel movement o Provide a diet with bowel-stimulating properties; with emphasis of fruits, vegetables, cereal grains, and legumes because these are rich sources of dietary fiber o Encourage sufficient fluid intake: 2000 to 3000 ml per day o Encourage active and passive activities to develop tone and strength of muscles that can be used o Schedule evacuation after a meal to utilize the gastrocolic reflex (peristaltic wave in the colon induced by entrance of food into a fasting stomach) o Determine if there is an awareness of the need to defecate (e.g. feeling of fullness or pressure in the rectum,

flatus, borborygmus)

o Encourage assumption of a position most near the physiologic position for defecation o Utilize assistive measures to induce defecation by: Teach bearing down and contracting abdominal muscles (Valsalvas maneuver should be avoided by people with cardiac problems) Teach leaning forward to increase intra abdominal pressure by compressing the abdomen against the thighs Provide for adaptation of equipment as necessary (e.g., elevated toilet seat, grab bars, padded backrest Teach the family the bowel training program Attempt to establish bladder function o Determine the type of bladder problem Neurogenic bladder: lesion of the nervous system Spastic bladder (reflex or automatic): lesion of spinal cord above bladder reflex center, in the conus medullaris; loss of conscious sensation and cerebral motor control; bladder empties automatically when the detrusor muscle is sufficiently stretched (about 500 ml) Flaccid bladder (atonic, nonreflex, or autonomous); disorder caused by a lesion of the spinal cord at the level of the sacral conus or below; the bladder continues to fill, becomes distended, and periodically overflows; the bladder muscle does not contract forcefully and therefore does not empty except with conscious effort o Review the clients bladder habits before illness as well as the current pattern of elimination; record output, voiding times, and times of incontinence o Encourage activity o Encourage sufficient fluid intake: 3000 to 4000 ml per 24-hour period, a glass of water with each attempt to void o Restrict fluid after 6 pm to limit amount of urine in bladder during night o Encourage assumption of as normal position as possible for voiding o Establish a voiding schedule Begin trial voiding at the time the client is most often incontinent Attempt voiding every 2 hours all day and 2 to 3 times during the night Time intervals between voiding should be shorter in the morning than later in the day As ability to maintain control improves, lengthen the time between attempts at voiding Time of intervals is not as important as regularity o Determine whether there is an awareness of need or act of urination (e.g., fullness or pressure, flushing, chilling, goose pimples, cold sweats) o Utilize assistive measures to induce urination by teaching the client to: Use Crede maneuver: manual expression of the urine from the bladder with moderate, external pressure downward and backward, from the umbilicus to over the suprapubic area

Bend forward to increase intra abdominal pressure


Stimulate trigger points: areas that, for the individual, will instigate urination (e.g., stroke the thigh, pull pubic hair, touch meatus) Provide for adaptive equipment as necessary (e.g., elevated toilet seats, commode, urinals, drainage systems) Sexual expression and options available; include discussion of penile implants Care for the client experiencing AUTONOMIC DYSREFLEXIA Place in a high-Fowlers position Ensure patency of urinary drainage system Assess for fecal impaction Eliminate other potential stimuli such as drafts Notify physician; administer prescribed antihypertensive When permitted, encourage and support use of tilt table to imitate weight bearing and reduce loss of

calcium from bones

XVII. DOWN SYNDROME


Also called Trisomy 21, is a condition in which extra genetic material causes delays in the way a child develops, both mentally and physically. It affects about 1 in every 800 babies. It is associated with maternal age over 35 as well as with paternal age. Named after John Langdon Down, a British doctor who 1st described the condition in 1887. Normally, at the time of conception a baby inherits genetic information from its parents in the form of 46 chromosomes: 23 from the mother and 23 from the father. In most cases of Down syndrome, a child gets an extra chromosome 21 for a total of 47 chromosomes instead of 46. It's this extra genetic material that causes the physical features and developmental delays associated with DS. Although no one knows for sure why DS occurs and there's no way to prevent the chromosomal error that causes it, scientists do know that women age 35 and older have a significantly higher risk of having a child with the condition. At age 30, for example, a woman has about a 1 in 900 chance of conceiving a child with DS. Those odds increase to about 1 in 350 by age 35. By 40 the risk rises to about 1 in 100.

Signs and Symptoms: Physical characteristics Small rounded skull with a flat occiput/Flat Facial Profile Small nose with depressed bridge (saddle nose)/ Flat Broad nasal bridge Small Ears Short, thick neck High-arched palate Hypoplastic mandible Hypotonic musculature (floppy infant) Hyperflexible/Hyperextensible, lax joints with broad, short, stubby hands and feet Inner epicanthal folds and oblique palpebral fissures (eyes slant upward and outward) Protruding tongue Simian line (transverse palmar crease) Associated characteristics Cardiac anomalies most common congenital defects Atlantoaxial (first and second cervical vertebrae) instability Highly susceptible to upper respiratory infections Increased incidence of leukemia Other Manifestations: Most children with DS typically reach developmental milestones like sitting up, crawling, and walking later than other kids. At birth, kids with DS are usually of average size, but they tend to grow at a slower rate and remain smaller than their peers. For infants, low muscle tone may contribute to sucking and feeding problems, as well as constipation and other digestive issues. Toddlers and older kids may have delays in speech and self-care skills like feeding, dressing, and toilet teaching. Down syndrome affects kids' ability to learn in different ways, but most have mild to moderate intellectual impairment. Kids with DS can and do learn, and are capable of developing skills throughout their lives.

Prenatal Screening and Diagnosis


Two types of prenatal tests are used to detect Down syndrome in a fetus: screening tests diagnostic tests Screening tests estimate the risk that a fetus has DS; diagnostic tests can tell whether the fetus actually has the condition. Screening tests are cost-effective and easy to perform. But because they can't give a definitive answer as to whether a baby has DS, these tests are used to help parents decide whether to have more diagnostic tests. Diagnostic tests are about 99% accurate in detecting Down syndrome and other chromosomal abnormalities. However, because they're performed inside the uterus, they are associated with a risk of miscarriage and other complications. For this reason, invasive diagnostic testing previously was generally recommended only for women age 35 or older, those with a family history of genetic defects, or those who've had an abnormal result on a screening test. However, the American College of Obstetrics and Gynecology (ACOG) now recommends that all pregnant women be offered screening with the option for invasive diagnostic testing for Down syndrome, regardless of age. If you're unsure about which test, if any, is right for you, your doctor or a genetic counselor can help you sort through the pros and cons of each.

Screening tests include:

nuchal translucency testing. This test, performed between 11 and 14 weeks of pregnancy, uses ultrasound to
measure the clear space in the folds of tissue behind a developing baby's neck. (Babies with DS and other chromosomal abnormalities tend to accumulate fluid there, making the space appear larger.) This measurement, taken together with the mother's age and the baby's gestational age, can be used to calculate the odds that the baby has DS. Nuchal translucency testing is usually performed along with a maternal blood test.

Diagnostic tests include:

Chorionic villus sampling (CVS). CVS involves taking a tiny sample of the placenta, either through the cervix or

through a needle inserted in the abdomen. o The advantage of this test is that it can be performed during the first trimester, between 8 and 12 weeks. o The disadvantage is that it carries a slightly greater risk of miscarriage as compared with amniocentesis and has other complications. Amniocentesis. This test, performed between 15 and 20 weeks of pregnancy, involves the removal of a small amount of amniotic fluid through a needle inserted in the abdomen. o The cells can then be analyzed for the presence of chromosomal abnormalities. Amniocentesis carries a small risk of complications, such as preterm labor and miscarriage. Percutaneous umbilical blood sampling (PUBS). Usually performed after 20 weeks, this test uses a needle to retrieve a small sample of blood from the umbilical cord. It carries risks similar to those associated with amniocentesis.

After a baby is born, if the doctor suspects DS based on the infant's physical characteristics, a KARYOTYPE a blood

or tissue sample stained to show chromosomes grouped by size, number, and shape can be performed to verify the diagnosis.
NURSING IMPLEMENTATION

Avoid exposure to persons with upper respiratory infections. Encourage genetic counseling. Prenatal: Encourage prenatal screening for pregnant women older than 35 years of age. Feed to back and side of the mouth Teach use of bulb syringe for suctioning nares Refer to other specialist Nursing Goal : to help the child reach his optimum function

XVIII. CEREBRAL

PALSY

Cerebral palsy (CP) is impaired muscular control resulting from a nonprogressive abnormality in the pyramidal motor. The cause of CP has been unclear; however, it is believed the most common cause of CP is existing prenatal brain abnormalities, especially seen in premature deliveries. The pathological picture is noncharacteristic, meaning that some children exhibit gross abnormalities of the brain, and others exhibit vascular occlusion resulting in atrophy and alterations in the structure of the brain. Anoxia has the greatest effect on the pathological state and the area of insult to the brain . Several classifications of CP exist depending on the area of insult to the brain.

Low birth weight is the major risk factor SPASTIC: hypertonicity of voluntary muscles ATHETOID: abnormal involuntary movement ATAXIC: no muscular control or coordination
Mixed type: combination of spasticity and athetosis

CLASSIFICATION

Signs and Symptoms Choreoid movements: involuntary, irregular, jerking. Persistence of primitive reflexes Persistent tongue thrust. Persistent infantile resting and sleeping posture/Scissoring and extension of legs. Poor sucking/ Feeding difficulties Poor control of posture, balance, and coordinated motion. Abnormal and asymmetrical crawl/Active attempts at motion increase abnormal postures and movements to
other body parts/ Child maintains hips higher than trunk in prone position, with legs and arms flexed or drawn under body. Athetosis: slow, wormlike, writhing movements. Increased or decreased resistance to passive movements Impaired fine motor skills/Abnormal motor performance Rigid and unbending at hip and knee joints when pulled to sitting position Delay in all motor development Drooling and impaired speech articulation. Dystonic movements: disordered muscle tone. Others: Seizures (affects 25%). Sensory deficits may occur: hearing difficulties, visual disturbances,and speech problems. Cognitive impairment (mental retardation) may be present.

Therapeutic Management
Establish locomotion, communication, and self-help with braces and splints, casting, physical therapy, surgery, mobilizing therapy. Gain optimum appearance and integration of motor functions: o Skeletal muscle relaxants (some older children) diazepam (valium) o Antianxiety agents for relief of excessive motion o Anticonvulsants for seizures o Dextroamphetamine or Ritalin for hyperactivity Correct any associated defects with surgery: selective posterior rhizotomy, musculoskeletal procedures. Provide educational opportunities adapted to the individual childs needs and capabilities.

Nursing Care
ASSESSMENT Perform routine physical assessment. Obtain history of childs behavior and attainment of developmental milestones. Assist with diagnostic procedures: electroencephalogram, tomography, screening for metabolic defects, serum electrolytes.

PLANNING
Safe, effective care environment. Help modify environment to conform to needs of child. Physiological integrity o Promote relaxation. o Establish locomotion and communication. o Prevent complications. Psychosocial integrity o Facilitate acquisition of educational opportunities for child. o Promote a positive self-image in child. Health promotion and maintenance o Promote optimum health. o Support family in its efforts to meet the needs of the child. o Promote growth and development.

IMPLEMENTATION Explain or reinforce explanation of condition and treatment. Provide safe environment with padded furniture, side rails on bed, sturdy furniture that does not slip, no scatter rugs or polished floors. Restrain child when in chair or vehicle. Provide helmet for child who is prone to falls. Apply and correctly use braces and splints. Carry out and teach family to perform physical therapy regimen. Encourage sitting, crawling, and walking at appropriate ages. Incorporate play that encourages desired behavior. Promote use of activities to prevent or minimize effects of disease. Maintain a well-regulated schedule that allows for adequate rest and sleep. Help family devise and modify equipment and activities to meet needs of child. Provide extra calories to meet extra energy demands of increased muscle activity. Encourage child to assist in care. Enlist efforts of speech therapist. Promote verbal and nonverbal communication based on childs competencies. Teach family skills needed for care, including expected results of medications and their possible side effects.

XIX. SPINA BIFIDA


Myelodysplasia is abnormal development of any part of the spinal cord in embryonic life (between 24 and 28 days gestation). Spina bifida is a defect in closure of vertebral arches, with varying degrees of tissue protrusion through body cleft. Spina bifida occulta is incomplete fusion of posterior vertebral arches, without accompanying herniation of spinal cord or meninges. Defect of the vertebrae only Meningocele is a hernial protrusion of a saclike cyst of meninges containing spinal fluid. contains only the

meninges and spinal fluid

Myelomeningocele is a hernial protrusion of a saclike cyst containing meninges, spinal fluid, and a portion of the spinal cord with its nerves. the sac contains spinal fluid, meninges and nerves Every child with spina bifida should be screened with latex allergy PREVENTION: Folic acid 0.4 mg is taken daily at least 3 months prior to pregnancy. The dosage is increased to 0.6 mg/day when pregnant Degree of neurological dysfunction is directly related to the anatomical level of the defect. Sensory disturbances usually parallel motor dysfunction (see Signs and Symptoms, below). Neurological impairment o Below second lumbar vertebra Flaccid, areflexic paralysis of lower extremities Sensory deficit Incontinence with constant dribbling of urine Lack of bowel control Joint deformities (e.g., talipes valgus or varus, contractures, kyphosis, lumbosacral scoliosis, hip dislocations) o Below third sacral vertebra No motor impairment Saddle anesthesia with bladder and anal sphincter paralysis (often) Surgical skin coverage and closure of lesion Treatment complications: meningitis, UTI, hydrocephalus decubiti Correction of any associated orthopedic deformities

Pathophysiology

Signs and Symptoms

Therapeutic Management

Nursing Care
ASSESSMENT Perform routine assessment. Assess functional abilities including motor performance and sensory deficits. Assist with diagnostic procedures: transillumination, hip and spinal roentgenographs, renal ultrasound. Observe pressure areas for signs of skin breakdown. Assess for evidence of complications (e.g., enlarging head, dislocated hip, urinary tract infection meningitis). IMPLEMENTATION Apply sterile, moist, nonadherent dressing over sac and moisten with saline or antimicrobial solution as prescribed;

avoid sac contamination by stool and urine.


Use care in cleaning soiled sac.

Position infant on stomach or side.

Place infant on fleece pad to reduce pressure on knees and ankles.


Maintain legs in abduction with pad between knees and roll beneath ankles. Avoid diapering; place infant on diaper or pad and change as needed. Employ meticulous skin care, especially in genital area because of leaking urine and stool. Monitor for signs and symptoms of meningitis: irritability, fever, seizures, and feeding intolerance. Provide gentle range-of-motion exercises to paralyzed extremities as prescribed. Explain or reinforce explanation of condition and treatment. Teach family skills needed for home care, including signs of increased intracranial pressurehydrocephalus is a frequent complication of myelomeningocele.

XX. CONGENITAL HIP DYSPLASIA


Congenital hip dysplasia is an imperfect development of the hip that can affect the femoral head, acetabulum, or both.

Pathophysiology Subluxation: incomplete dislocation or dislocatable hip

Femoral head remains in contact with the acetabulum. Stretched capsule and ligamentum teres cause the head of the femur to be partially displaced. Femoral head loses contact with the acetabulum. It is displaced posteriorly and superiorly over the rim. Ligamentum teres is elongated and taut.

Dislocation

Signs and Symptoms


Infant o Shortening of limb on affected side o Restricted abduction of hip on affected side o Unequal gluteal folds o Positive Ortolani test (performed by skilled person) o Positive Barlow test (performed by skilled person) Older infant and child o Affected leg shorter than the other o Telescoping or piston mobility of joint o Trendelenburg sign o Prominent greater trochanter o Marked lordosis (bilateral dislocations) o Waddling gait (bilateral dislocations) Varies with age of child and extent of dysplasia Newborn to 6 months : Application of external device that maintains proximal femur centered in the acetabulum in attitude of flexion: Pavlik harness most common 618 months : Traction followed by reduction and plaster cast immobilization A brace maintaining abduction may be used after cast removed Older child: Surgical reduction

Therapeutic Management

Nursing Care
ASSESSMENT Perform routine physical assessment: apply Barlows and Ortolanis maneuvers to assess stability of hip. Assess corrective device for proper application and/or maintenance. Assist with diagnostic procedures: ultrasound, CT, MRI. IMPLEMENTATION Explain or reinforce explanation of condition and treatment. Teach family the purpose, function, application, and maintenance of the corrective device (Pavlik harness) or cast. Help family adapt routine nurturing activities and equipment to accommodate corrective device: feeding, sleeping, playing, safety measures (e.g., car seat).

XXI. COXA PLANA (LEGG-CALV-PERTHES DISEASE)


Coxa plana (Legg-Calv-Perthes disease) is progressive destruction of the femoral head, producing varying degrees of deformity. Self-limited disease Avascular stage o Aseptic necrosis of femoral capital epiphysis with degenerative changes. o Condition produces flattening of upper surface of femoral head. Revascularization stage: bone absorption and revascularization Reparative stage: new bone formation Regenerative stage: gradual reformation of femoral head; may result in residual deformity Intermittent appearance of limp on affected side Pain: soreness or aching o Usually in the groin, in lateral hip, or in vicinity of knee o Worse on rising or at end of a long day o Point tenderness felt over hip capsule Joint dysfunction and limited range of motion Stiffness Disuse atrophy of affected thigh Limb length inequality External hip rotation (late sign) Rest, initially, to reduce inflammation and restore motion Traction to stretch tight adductor muscles (sometimes) Containment of femoral head in acetabulum by nonweight- bearing device (abduction brace, leg cast, leather harness) Surgical correction (sometimes)

Pathophysiology

Signs and Symptoms

Therapeutic Management

Nursing Care
ASSESSMENT Perform routine physical assessment. Assess corrective device for proper application, signs of irritation. Assist with diagnostic procedures: radiography. IMPLEMENTATION Explain or reinforce explanation of condition and treatment. Encourage child to maintain usual activities within limitations imposed by the disorder and its therapy. Teach family purpose, function, application, and maintenance of corrective device. Teach parents skin care measures.

XXII. CLUBFOOT
A congenital anomaly in which the foot is twisted out of its normal shape or position TALIPES: deformity involving the ankle PES: indicating involvement of the foot The cause is unknown. The cause has been attributed to abnormal position and restriction during uterine growth. Others attribute the defect to arrested uterine growth. Some positional deformities are: o TALIPES VARUS: inversion or bending inward o TALIPES VALGUS: eversion or bending outward Correct anomaly by application of successive casts. Maintain correction until normal muscle balance is attained. Surgery done when serial casting has reached plateau. Follow-up observation to avert possible recurrence.

Pathophysiology

Signs and Symptoms

Therapeutic Management

ASSESSMENT Perform routine physical assessment. IMPLEMENTATION Implement cast care as in fractures. Explain or reinforce explanation of condition and treatment. Teach family skills needed for home care. EVALUATION Ensure that cast remains clean and intact and that neurovascular status of toes is intact. Ensure that family demonstrates an understanding of the condition and the ability to provide home care.

XXIII. JUVENILE RHEUMATOID ARTHRITIS


Juvenile rheumatoid arthritis is a chronic inflammatory disease with an unknown inciting agent, a tendency to occur in the prepubertal child, and a slight tendency to occur in families. Similar to adult disease. Chronic inflammation of the synovium. Joint effusion. Limited motion caused by muscle spasm and inflammation. Eventual erosion, destruction, and fibrosis of articular cartilage. Adhesions between joint surfaces; ankylosis of joint (longstanding disease). Growth may be retarded during active disease. Disease pursues one of three courses: systemic onset, pauciarticular, polyarticular. Mode of onset Systemic: only 20% with joint involvement at diagnosis (1) Extra-articular: fever, malaise, myalgia, rash, pleuritis or pericarditis, adenomegaly, splenomegaly, hepatomegaly Pauciarticular: usually joints of lower extremities (knee, ankle, and eventually sacroiliac; sometimes elbow) Extra-articular: acute or chronic iridocyclitis, mucocutaneous lesions, sacroiliitis; eventual ankylosing spondylitis in many (type 2) Polyarticular: any joints; usually symmetrical involvement of small joints Extra-articular: systemic signs minimal (low-grade fever, malaise, weight loss, rheumatoid nodules, and/or vasculitis) Joint characteristics Stiffness and swelling Tenderness May be painful to touch or relatively painless Warm to touch (seldom red) Loss of motion Characteristic morning stiffness or gelling on arising in the morning or after inactivity Suppress inflammatory process with: o Nonsteroidal anti-inflammatory drugs o Cytotoxic drugs o Corticosteroids o Slower-acting antirheumatic drugs (e.g., gold, D-penicillamine) Preserve function and/or prevent deformity with physical therapy, occupational therapy, splinting, and positioning. Reduce pain with analgesia, heat application.

Pathophysiology

Signs and Symptoms

Therapeutic Management

ASSESSMENT Perform routine physical assessment. Observe for joint discomfort and movement. Assist with diagnostic tests: radiography, white blood cell count, rheumatoid factors, erythrocyte sedimentation rate, antinuclear antibodies; latex fixation test used to detect disease in adults is negative in most children.

IMPLEMENTATION o Explain or reinforce explanation of condition and treatment. o Administer and monitor childs response to anti-inflammatory preparations as prescribed. o Carry out or assist with physical therapy plan. o Provide heat to affected joints via bath, hot compresses, paraffin baths. o Carry out range-of-motion activities in appropriate locations (e.g., bath, pool, playroom, etc.). o Encourage activity appropriate to capabilities. o Apply splints and support equipment (e.g., bolsters, sandbags, pillows) as prescribed. o Help modify environment to promote safety and utensils to facilitate self-help. o Employ childs natural affinity for play to encourage motion and activity. o Teach family skills needed for home care. Administration of medications and explanation of possible side effects Purpose and correct application of splints or appliances Modification of environment, clothing, and utensils to facilitate self-help EVALUATION Ensure that child: Demonstrates an understanding of the condition and treatment, as does the family. Is able to move with minimal or no discomfort. Engages in suitable play and self-help activities.

RESPIRATORY SYSTEM ANATOMY AND PHYSIOLOGY


Function of Respiratory System The upper portion of the respiratory system filters, moistens, and warms air during inspiration The lower portion of the respiratory system enables the exchange of gases between blood and air to regulate serum PO2, PCO2, and pH. NOSE A. Structure Anterior nares: exterior openings Nasal cavities: lining is ciliated mucosa; divided by septum; turbinates (conchae) projected from lateral walls Paranasal sinuses draining into the nose: frontal, maxillary, sphenoidal, ethmoidal B. Functions Passageway for incoming and outgoing air, filtering, warming, and moistening Organ of smell: olfactory receptors located in the nasal mucosa PHARYNX A. Structure: composed of muscle with mucous lining, muscular passageway commonly called the throat. Nasopharynx: behind the nose; opens into eustatchian tubes; contains nasopharyngeal tonsils (adenoids) Oropharynx: forms archway behind the mouth; contains palatine tonsils Laryngopharynx: opens into esophagus and larynx B. Functions: passageway to the respiratory and digestive tracts; aids in phonation; tonsils help destroy incoming bacteria LARYNX A. Location: at upper end of the trachea, just below the pharynx B. Structure Formed by cartilage including the thyroid cartilage (Adams apple); epiglottis (the lid cartilage); and choroid (the signet ring cartilage) Vocal cords False cords: folds of mucous lining True cords: fibroelastic bands stretched across the hallow interior of the larynx; the paired vocal cords (folds) and the posterior arytenoids cartilages make up the glottis C. Functions: VOICE production: during expiration, air passing through the larynx causes the vocal cords to vibrate; short, tense cords produce a high pitch; long, relaxed cords, a low pitch; serves as the passageway for air and as the entrance to the lower respiratory tract TRACHEA A. Structure Walls: smooth muscle; contain C-shaped rings of cartilage that keep the tube open at all times Lining: ciliated mucosa Extend from larynx to bronchi; 10 to 12 cm long B. Function: furnishes open passageway for air going to and from lungs

LUNGS A. Structure Divisions Root: consists of the primary bronchus and pulmonary artery and veins bound together by connective tissue Hilum: vertical slit on medial surface of the lung, trough which root structures enter the lung Lobes: three in the right lung, two in the left Apex: pointed upper part of the lung Base: broads, inferior surface of the lung Bronchi tree: consist of the following: Bronchi: right and left, formed by branching at the trachea; right bronchus slightly larger and more vertical than left; each primary bronchus branches into segmental bronchi in each lung; primary and segmental bronchi all contain C-shaped cartilage Bronchioles: small branches off the secondary bronchi, distinguished by lack of C-shaped cartilage and a duct diameter of about 1 mm, which further branch into terminal bronchioles, respiratory bronchioles, and then alveolar ducts Alveoli: microscopic sacs composed of a single layer of extremely thin squamous epithelial cells enveloped by a network of lung capillaries Covering of lung: visceral layer of pleura B. Function Bronchi, bronchioles, alveolar ducts: passage to move air into and out of alveoli Alveoli: provide surface area large enough and thin enough to allow rapid gas exchange type I cells form walls type II cells produce surfactant to prevent alveolar collapse Accessory structures: contribute to the mechanics of breathing Rib cage: 12 pairs of ribs and the sternum provide skeletal support and protection for the heart and lungs Intercostals muscles: located between the ribs, contraction facilitates chest expansion during inspiration by increasing the anterior-posterior and lateral diameter of the chest Diaphragm: separate the thoracic cavity from the abdominal cavity; brains respiratory center controls contraction of the diaphragm via the phrenic nerve; flattens during inspiration to allow greater chest expansion during inspiration; an intact nervous system is essential to proper functioning of the diaphragm

Respiratory system functions:


primary functions of the respiratory system is the exchange of gases between the external environment and the blood; process of respiration involves ventilation, perfusion, diffusion, and nervous system control; respiration refers to the mechanical and metabolic processes involved with oxygen (O2) transport from the atmospheric air into the blood and car bon dioxide (CO2) transport from the blood back to the atmospheric air VENTILATION: passage of gases between the atmosphere and the lungs; ventilation phases include inspiration and expiration; adequacy of ventilation is influenced by the respiratory system pressures, respiratory tissues properties, airway resistance, lung volumes and capacities, body position, and disease process o Pulmonary ventilation: total volume of gas exchange between the atmosphere and the lungs o Alveolar ventilation: volume of air that undergo gas exchange o Ventilation phases INSPIRATION: nerve impulses travel from brain via phrenic nerve to contract the diaphragm, increasing the diameter of the thoracic cavity; intrapleural pressure increases, becoming more negative compared to atmospheric air; air moves from area of higher pressure (atmosphere) to lower pressure (respiratory system); air moves through structures of the respiratory system to alveoli and pulmonary capillaries where gas exchange occurs EXPIRATION: diaphragm relaxes and pushes upward, decreasing thoracic cavity diameter; intrapleural pressure remains negative compared to atmospheric air, but become less negative than during inspiration; intrapulmonic

pressure becomes higher than atmospheric pressure allowing passive air flow from lung trough respiratory structures into the atmosphere; smaller airways more collapse during expiration, particularly in the supine position

Respiratory system pressures: atmospheric pressure of 760mmhg serves as reference point for comparison to
respiratory pressures Intrapulmonary pressure: also called intra-alveolar pressure; equals atmospheric pressure when glottis is open and there is no air movement Intrapleural pressure: negative pressure produce by opposite forces of elastic recoil between the lungs and the chest wall; with glottis open and alveolar air with the communication with the atmosphere, it measures negative compared to intrapulmonary pressure; with glottis closed, during coughing or with forced expiration, it measured positive compared to atmospheric air, normally negative intrapleural pressure prevent lung collapse Intrathoracic pressure: compared to atmospheric air, negative pressure inside thoracic cavity equal intrapleural pressure, with forced expiration against a closed glottis, intrathoracic pressure becomes positive

Respiratory tissue properties: respiratory vessels and airways are implanted in elastic tissues
Compliance: elastic property of lungs related to elastic and collagen fibers; compliance changes with change in respiratory system pressures and/or change in lung fluid content; higher compliance occurs in lung that is more easily distended; lower compliance occurs in lung that is not easily distended Elastic recoil: ability of lungs to return to original shape after air is expelled; recoil is present is present because of opposing force created by movement of lungs and chest wall Distensibility: ease of lung inflation made more difficult by increased volume lung fluid content or consolidation of lung tissue Stiffness: resistance of lungs to stretch to accommodate air volume; increasing lung stiffness lowers compliance Airway resistance: obstruction to airflow caused by conditions of respiratory system tissues (elastic recoil, compliance), changes in airway diameter (bronchoconstriction, mucus obstruction), and/or pressure differences between atmospheric air and intrapulmonary air Lung volumes and capacities: lung volumes describes normal individual quantities of air exchanged during specific times of the breathing cycle: lung capacities describe combined quantities of lung volumes during specific periods of the breathing cycle Body position: gravity accounts for greater ventilation in dependent areas of lung; with inspiration and body upright, sitting, or standing, airway opening allows for airflow to follow the path of least resistance into the more compliant lung bases PERFUSION: blood flow through the pulmonary capillary bed and to the respiratory system structures: respiratory system circulation includes the pulmonary circulation and bronchial circulation o Pulmonary circulation: pulmonary artery carries deoxygenated (venous) blood from the right ventricle, branches into pulmonary capillaries, and connects to alveoli: CO2 is exchanged for O2 at the pulmonary capillary membranes: capillary membranes merge into pulmonary venules and pulmonary veins that carry oxygenated blood back to the left atrium of the heart o Bronchial circulation: bronchial arteries branching from the thoracic aorta circulate blood to the conducting airways and other respiratory tract tissues; bronchial blood does not circulate to the alveoli and is not included in gas exchange; deoxygenated bronchial blood drains through bronchial capillaries and veins into the vena cava and the right side of the heart; deoxygenated blood from small bronchial veins drains into azygos and pulmonary veins into the left side of the heart then combines with oxygenated blood from the pulmonary circulation o Characteristics of respiratory system circulation: blood pressure resistance to blood flow are lower in pulmonary blood vessels compared to systemic blood vessels; adequacy of pulmonary capillary blood flow depends upon a mean pulmonary arterial pressure (MPAP) that is greater than mean pulmonary venous pressure (MPVP); blood volume in pulmonary capillary bed increases when MPVP exceeds MPAP, causing pulmonary edema; pulmonary blood vessels constrict in response to hypoxia

DIFFUSION: movement of gas from an area of higher pressure to lower pressure; O 2 diffuses from the atmosphere into the alveoli, across the pulmonary capillary membrane and into the pulmonary capillaries for circulation throughout the body; CO2 diffuses out of the pulmonary capillaries across the capillary membrane and into the alveoli to be exhaled; diffusion continues until pressure differences become equal between the two areas FICKS LAW: describes the process of gas diffusion Gas volume = Partial pressure of gas 1 Partial pressure of gas 2 x Surface Area of membrane x Diffusion coefficient/ Membrane thickness Variables that influence gas exchange Partial pressure of gases varies in different lung areas Under normal conditions and in the upright position, ventilation is greater than perfusion in the lung apices; ventilation greater than perfusion yields a V/Q ratio greater than 4:5; perfusion greater than ventilation yields a V/Q ratio less than 4:5 Under normal conditions and in the upright position, perfusion and ventilation are greater in the lung bases Ventilation-perfusion relationship: adequate gas exchange requires alveolar ventilation of about 4 L/min balanced with alveolar capillary perfusion of about 5 L/min Normal ventilation-perfusion (V/Q) ratio: 4:5 V/Q ratio is influenced by partial pressure of O2 and partial pressure of CO2 Average normal PaO2 = 100 mmHg; average normal PaCO2 = 40 mmHg Nervous system control of breathing: initiates within the medulla oblongata and pons of the brainstem Medulla oblongata: controls inspiration, expiration, and breathing pattern Pons: controls rate and depth of respiration Sensory input to brainstem: impulses that influence breathing and respiration are transmitted to the brainstem from chemoreceptors, stretch receptors, proprioceptors, baroreceptors, and the external environment Central chemoreceptors in medulla: increase PCO2 and/or decreased blood ph causes increased alveolar ventilation as a compensatory mechanism to maintain PCO2 and pH at normal levels Peripheral chemoreceptors in the aortic arch and carotid bodies: increased PCO2 causes increased alveolar ventilation Ventilation-perfusion relationships: Normal alveolar-capillary unit with an ideal match of ventilation and blood flow. Maximum gas exchange occurs between alveolar wall and blood. Physiology shunting: A unit with adequate perfusion but inadequate ventilation. Dead space: A unit with adequate ventilation but inadequate perfusion. In the latter two cases, gas exchange is impaired. Stretch receptors in the alveolar septa, bronchi, and bronchioles: prevent overdistention of the lungs when they are inflated PROPRIOCEPTORS in muscles and tendons of moveable joints: stimulate ventilation with exercise to increase oxygen supply during increased oxygen demand BARORECEPTORS in the aortic arch and carotid sinus: alter respiration relative to changes in arterial blood pressure; elevated arterial blood pressure lowers respiration; blood pressure below 80 mmHg increase respiration External environment: factors such as cold, physical stress, air pollution, smoking, and pain alter respiration; infection and fever increase respiration caused by increase oxygen demand Nerve impulses travel from brain stem via phrenic nerve to diaphragm and stimulate muscle construction for breathing

RELATED PHARMACOLOGY
BRONCHODILATORS Reverse bronchoconstriction, thus opening air passages in the lungs Act by stimulating beta-adrenergic sympathetic nervous system receptors, relaxing bronchial smooth muscle Available in oral, parenteral (IM, SC, IV) rectal and inhalation preparations

A METERED-DOSE INHALER (MDI) is a pressurized device containing an aerosolized powder of medication. A SPACER (holding chamber) may also be used to enhance deposition of the medication in the lung and help the patient coordinate activation of the MDI with inspiration. Spacers come in several designs, but all are attached to the MDI and have a mouthpiece on the opposite end Once the canister is activated, the spacer holds the aerosol in the chamber until the patient inhales The patient should take a slow, 3- to 5-second inhalation immediately following activation of the MDI. Examples Adrenergics/Beta 2 Adrenergic Agonists: Stimulates beta receptors in lung Increases vital capacity and decreases airway resistance Indications: asthma, bronchitis, emphysema, relief of bronchospasm occurring during anesthesia, exercised-induced bronchospasm act at beta-adrenergic receptors in bronchus to relax smooth muscle and increase respiratory volume: albuterol (Proventil); epinephrine HCI (Adrenalin; Sus-phrine); metaproterenol sulfate (Alupent); Salmeterol (Serevent) Beta-Adrenergic Agonist Agents Albuterol (Proventil, Ventolin, Volmax) Bitolerol (Tornate) Levalbuterol (Xopenax) Metaproterenol (Alupent) Pirbuterol (Maxair) Salbutamol (Asmavent) Salmeterol (Serevent) Terbutaline (Brethaire, Brethine, Bricanyl) isoetharine (Bronkosol) Non-selective Beta-Adrenergic Isoproterenol (Isuprel)

SE: Nervousness, tremors, restlessness, insomnia, headache, NV, tachycardia, irregular heartbeat, hypertension, cardiac
dysrhythmia, increase effects with other sympathomimetics, decrease with beta blockers

With adrenergic bronchodilators, observe for tachycardia, arrhythmias, palpitations, restlessness, agitation, insomnia. - These signs and symptoms result from cardiac and central nervous system (CNS) stimulation.

XANTHINES; act directly on bronchial smooth muscle, decreasing spasm and relaxing. Smooth muscle of the vasculature: aminophylline; theophylline (Elixophyllin; Theo-Dur) Indications: Asthma, emphysema, COPD, CAL METHYLXANTHINES Aminophylline (Phyllocontin) Theophylline immediate release (Aerolate, Slo-phyllin, Theolair) Theophylline extended release (Slo-bid, Theo-Dur, Theo-24, Uni-Dur Uniphyl) SE: Normal level is at 10-20 mcg/ml o Levels >20 mcg/ml nausea (1st sign of toxicity), vomiting, headache, dizziness, insomnia, irritability o Levels >35 mcg/ml tremors (later sign of toxicity), nervousness, tachycardia, palpitations, hypotension, cardiac dysrhythmias, seizures and death With xanthine bronchodilators, observe for tachycardia,arrhythmias, palpitations, restlessness, agitation, insomnia, nausea, vomiting, convulsions. Theophylline causes cardiac and CNS stimulation. Convulsions occur at toxic serum concentrations (>20 mcg/mL). They may occur without preceding symptoms of toxicity and may result in death. IV diazepam (Valium) may be used to control seizures. Theophylline also stimulates the chemoreceptor trigger zone in the medulla oblongata to cause nausea and vomiting.

ANTICHOLINERGICS: inhibit interaction of acetylcholine at receptor sites on the bronchial smooth muscle: ipratropium (Atrovent) Ipratropium bromide (Atrovent) Oxitropium bromide (Oxivent) With ipratropium, observe for cough or exacerbation of symptoms. - Ipratropium produces few adverse effects because it is not absorbed systemically. STEROIDS: exert anti-inflammatory effect on nasal passages: (fluticasone (Flovent) Inhaled and systemic corticosteroids (oral or intravenous) may also be used in COPD but are used more

frequently in asthma. Examples of corticosteroids in the inhaled form are beclomethasone (Beclovent,Vanceril), budesonide
(Pulmicort), flunisolide (AeroBid), fluticasone (Flovent), and triamcinolone (Azmacort). Corticosteroids are the most potent and effective anti-inflammatory medications currently available. They are broadly effective in alleviating symptoms, improving airway function, and decreasing peak flow variability. With inhaled corticosteroids, observe for hoarseness, cough, throat irritation, and fungal infection of mouth and throat. usually does not induce systemic toxicity; risk of oral candida albicans infection (thrush) sore throat, an unpleasant taste in mouth or dysphonia may occur Inhaled corticosteroids are unlikely to produce the serious adverse effects of long-term systemic therapy

MAST CELL STABILIZERS Initially, the inhaled form is used. Cromolyn sodium (Intal) and nedocromil (Tilade) are mild to moderate anti-inflammatory agents that are used

more commonly in children. They also are effective on a prophylactic basis to prevent exercise-induced asthma or in unavoidable exposure to known triggers. These medications are contraindicated in acute asthma exacerbations.
SE: With cromolyn, observe for dysrhythmias, hypotension, chest pain, restlessness, dizziness, convulsions, CNS depression, anorexia, nausea and vomiting. Sedation and coma may occur with overdosage. - Some of the cardiovascular effects are thought to be caused by the propellants used in the aerosol preparation.

LEUKOTRIENE MODIFIER DRUGS were developed to counteract the effects of leukotrienes and are indicated for long-term treatment of asthma in adults and children. The drugs help to prevent acute asthma attacks induced by allergens, exercise, cold air, hyperventilation,

irritants, and aspirin or NSAIDs. They are not effective in relieving acute attacks. However, they may be continued concurrently with other drugs
during acute episodes. SE: With leukotriene inhibitors, observe for headache, infection, nausea, pain, elevated liver enzymes (eg, alanine aminotransferase [ALT]), and liver dysfunction. - These drugs are usually well tolerated. The leukotriene modifiers include three agents with two different mechanisms of action. Zileuton (Zyflo) inhibits lipoxygenase and thereby reduces formation of leukotrienes montelukast (Singulair) and zafirlukast (Accolate) are leukotriene receptor antagonists. Zileuton (Zyflo) is used infrequently because it requires multiple daily dosing, may cause hepatotoxicity, and may inhibit the metabolism of drugs metabolized by the cytochrome P450 3A4 enzymes. It is contraindicated in clients with active liver disease or substantially elevated liver enzymes (three times the upper limit of normal values). A highly elevated ALT and liver dysfunction are more likely to occur with zileuton. When used, hepatic aminotransferase enzymes should be monitored during therapy and thedrug should be discontinued if enzyme levels reach five times the normal values or if symptoms of liver dysfunction develop. zafirlukast (Accolate) and montelukast (Singulair) improve symptoms and pulmonary function tests (PFTs), decrease nighttime symptoms, and decrease the use of beta2 agonist drugs. They are effective with oral administration, can be taken once or twice a day , It can be used with bronchodilators and corticosteroids, and elicit a high degree of patient adherence and satisfaction. However, they are less effective than low doses of inhaled corticosteroids. Montelukast and zafirlukast are well absorbed with oral administration. They are metabolized in the liver by the cytochrome P450 enzyme system and may interact with other drugs metabolized by this system. Most metabolites are excreted in the feces. Zafirlukast is excreted in breast milk and should not be taken during lactation.

Zafirlukast most serious undesirable effects Churg-Strauss Syndrome, which presents with eosinophilia, vasculitic rash, cardiac and pulmonary complications The most common adverse effects reported in clinical trials were headache, nausea, diarrhea, and infection. Zileuton is well absorbed, highly bound to serum albumin (93%), and metabolized by the cytochrome P450 liver enzymes; metabolites are excreted mainly in urine. It is contraindicated in clients with active liver disease or substantially elevated liver enzymes (three times the upperlimit of normal values). When used, hepatic aminotransferase enzymes should be monitored during therapy and the drug should be discontinued if enzyme levels reach five times the normal values or if symptoms of liver dysfunction develop. Elevation of liver enzymes was the most serious adverse effect during clinical trials; other adverse effectsinclude headache, pain, and nausea. In addition, zileuton increases serum concentrations of propranolol, theophylline, and warfarin. Major side effects: dizziness (decrease in blood pressure) CNS stimulation (sympathetic stimulation); palpitations (beta adrenergic stimulation); gastric irritation (local effect) Drugs that increase effects of bronchodilators: Monoamine oxidase inhibitors - These drugs inhibit the metabolism of catecholamines. The subsequent administration of bronchodilators may increase blood pressure. Erythromycin, clindamycin, cimetidine - These drugs may decrease theophylline clearance and thereby increase plasma levels. Drugs that decrease effects of bronchodilators: Lithium - Lithium may increase excretion of theophylline and therefore decrease therapeutic effectiveness Phenobarbital - This drug may increase the metabolism of theophylline by way of enzyme induction. Propranolol, other nonselective beta blockers - These drugs may cause bronchoconstriction and oppose effects of bronchodilators.

Nursing Care
Avoid administration to clients with hypertension, hyperthyroidism and cardiovascular dysfunction Avoid concurrent administration of CNS stimulants (adrenergics and bronchoconstricting agents (beta blockers) Administer during waking hours Asses vital signs, especially respirations Assess intake and output Administer with food. If xanthines, take oral preparation 1 hours before or 2 hours after meals. Peak serum concentration should be taken 1 hours after IV, 1-2 hours following immediate-release dose, 3-8 hours following extended release Demonstrate correct use of inhalers or nebulizers. Teach about MDI. When two puffs are needed, 1-2 minutes should lapse between two puffs. A spacer is used to increase the delivery of the medication.

If a glucocorticoid inhalant is to be used with a bronchodilator, wait 5-15 minutes before using the inhaler containing the steroid for the bronchodilator effect
For steroids, instruct not to use for acute attacks If taking bronchodilators, instruct client to use bronchodilator before corticosteroid aerosol. After inhaling, the client should hold the inhaled drug for few seconds before exhaling. Allow 1-2 minutes to elapse between each inhalation. Rinse mouth with water after inhalations. Keep inhaler clean and unobstructed. Wash in warm water and dry thoroughly. Do not stop abruptly, must taper off gradually. Encourage the use of a diary to record administration of meds and clinical response Bronchodilators are always administered before glucocorticoids when both are given on the same time schedule.