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Rheumatic Fever and Sickle Cell Anemia Guide

This document discusses rheumatic fever and rheumatic heart disease, as well as sickle cell anemia and hemophilia. It defines each condition, discusses occurrence, causes, medical treatment, and the nursing process of assessment, planning, implementation and evaluation. Rheumatic fever is caused by a streptococcal infection and can damage the heart valves. Sickle cell anemia is a genetic blood disorder where red blood cells take on a sickle shape, causing pain and organ damage. Hemophilia is an inherited bleeding disorder where blood does not clot properly due to a lack of specific clotting factors.

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0% found this document useful (0 votes)
218 views32 pages

Rheumatic Fever and Sickle Cell Anemia Guide

This document discusses rheumatic fever and rheumatic heart disease, as well as sickle cell anemia and hemophilia. It defines each condition, discusses occurrence, causes, medical treatment, and the nursing process of assessment, planning, implementation and evaluation. Rheumatic fever is caused by a streptococcal infection and can damage the heart valves. Sickle cell anemia is a genetic blood disorder where red blood cells take on a sickle shape, causing pain and organ damage. Hemophilia is an inherited bleeding disorder where blood does not clot properly due to a lack of specific clotting factors.

Uploaded by

Mamot Mot
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT or read online on Scribd

Rheumatic Fever and Rheumatic Heart Disease

General Information
1. Definition: an inflammatory disease caused by an immune response to group A beta-hemolytic streptococcal infection; affects collagen
(connective) tissue such as heart, joints, central nervous system, and subcutaneous tissue
2. Occurrence: primarily affects school-age children; higher incidence in cold or humid climates, crowded living environments, and with strong
family history of rheumatic fever
3. Medical treatment
a. Antibiotics (penicillin or erythromycin)
1. to eradicate any lingering infection
2. for long-term prophylactic treatment
b. Salicylates to control joint inflammation, fever, pain

Nursing Process
ASSESSMENT (REVISED JONES CRITERIA (AMERICAN HEART ASSOCIATION)
1. Major manifestations
a. Carditis: mitral and aortic valves most commonly affected with symptoms of tachycardia, cardiomegaly, pericarditis, murmurs, congestive
heart failure; carditis is the only manifestation that may cause permanent damage
b. Painful migratory polyarthritis in large joints with manifestations of acute pain, warmth, redness, edema; permanent deformities do not follow
c. Chorea (Saint Vitus’ dance or Sydenham’s chorea): purposeless, irregular movements of the extremities, muscular weakness, emotional
liability, facial grimacing
1. following the acute febrile phase
2. may last for months, but is self-limiting
3. relieved by rest and sleep
d. Erythema marginatum rheumaticum: macular rash with wavy, well-defined border on trunk
e. Subcutaneous nodules: small, nontender swellings in groups over bony prominences
2. Minor manifestations
a. Arthralgia
b. Fever
c. Nonspecific test indicating inflammation
1. elevated erythrocyte sedimentation rate (ESR)
2. elevated C-reactive protein
3. leukocytosis
d. Anemia
e. Prolonged PR and QT intervals on ECG
3. Other
a. Positive throat culture
b. Elevated antistreptolysin (ASO) titer (indicates a preceding streptococcal infection)
PLANNING, IMPLEMENTATION, AND EVALUATION ANALYS IS (SEE. P. 510)

Goal 1: Child will be free from pain and will test comfortably.

Implementatio n
1. Administer salicylates as ordered.
2. Use cradles to keep bed linens off painful joint.
3. Position joints on pillo ws; hand le gently.
4. Encourage use o f relaxation, d istraction and imagery as appropriate.

Evaluatio n
Child does not comp lain of pain, rests and sleeps comfortably.

Goal 2: Child with chorea will be protected from injury.

Implementatio n
1. Use side rails and pad sides o f bed.
2. Provide understanding and emotio nal support; reassure child and family that chorea will
reso lve spo ntaneously.
3. Provide with alternative means to do written work (e.g., typewriter, personal computer, o ral
reports0.
4. Assist child in self-care to pro mote independence and positive self-concep t.

Evaluatio n
Child ambulates without falling, does not sustain injury.

Goal 3: Child and family will be prepared for home care and long-term management.

Implementatio n
1. Emp hasize importance of co mp liance with lo ng-term antib iotic therap y for preventio n o f
serio us heart damage.
a. Prepare child fo r injections of penicillin.
b. Stress seriousness of recurrence and need to seek med ical care for sub sequent infections.
2. Plan for continuation o f schoo l work, realistic reer goals.
3. Refer to co mmunity health nurse for fo llow- up as needed.
4. Instruct parents to take vital signs, ad minister med ications, ensure restrictio ns.

Evaluatio n
Child returns to full activity with no resid ual cardiac invo lvement.
SICKLE CELL ANEMIA
General Informatio n
1. Definitio n: autoso mal recessive defect (see F ig. 5-3) found primarily in blacks, resulting in
production of ab normal hemo glob in (hemo glob in S ) and characterized by intermittent ep isodes
of crisis
2. Occurrence: 1:600 b lack Americans
a. Sickle cells trait: heterozygous fo rm (carrier); 1 in 12 black persons is a carrier
b. Sickle-cell d isease: ho mo zygo us form (has the d isease); may have vasoo cclusive crisis:
painful, acute occurrence usually precip itated b y decreased O 2 tensio n, which causes cells
to assume a sickle shape and blood to become viscous, ob struct b lood vessels, and cause
tissue ischemia, infarction, and necrosis
3. Cause: defective form o f hemo globin (hemoglob in S), inherited by autosomal- recessive genetic
transmissio n
4. Med ical treatment: symptomatic treatment of crisis
a. Bed rest to decrease O 2 expenditure
b. Adeq uate hyd ration: oral and IV fluids to increase b lood volume and mobilize sickled cells
c. Electro lyte rep lacement (hypoxia causes metabo lic acidosis)
d. Relief of pain
1. acetaminop hen
2. codeine
3. mo rp hine
4. may use client-contro lled analgesia
e. Blood transfusio ns, for severe drop in hemo glob in (ap lastic crisis)
f. O 2 for severe hypoxia 9o n a short-term basis)
g. Antibiotics to treat concurrent infectio n

Nursing Process
Assessment
1. Parents with sick le cell trait
2. Signs and sympto ms (depend on organ invo lved); not evident until after 6 months o f age
a. Chronic hemo lytic anemia
b. Frequent infectio ns, related to decreased ab ility of sp leen to filter bacteria.
c. Organ deterioration (sp leen, liver, kidney, heart, or CNS)
d. Chronic pain: joints, abdo men, back
e. Bo ne deterio ratio n (osteoporosis, skeletal defo rmities) fro m increase in marro w
3. Manifestations of vasoocclusive crisis
a. Severe abdo minal pain: caused b y organ hypoxia
b. Hand-foo t syndro me: swelling o f hands and feet.
c. Fever: resulting fro m dehydratio n or possible co ncurrent infectio n
d. Artralgia
ANALYSIS (S EE P. 509)
PLANNING, IMPLEMENTATION, AND EVALUATION

Goal 1: Pa rent and child will receive education to prevent bleeding, provide safety measures;
will k now how to treat minor bleeding episodes.

Implementation
1. Prepare parents and child for home care and administration of factor VIII (where available),
a. Teach about the disease.
b. Teach venip uncture proced ure and how to monitor the transfusion.
c. Provide regular fo llow-up (family must be sufficiently motivated and stable to maintain a
homecare program.
2. Teach local treatment measures for minor bleed ing episodes.
a. App ly direct pressure to site (10-15 minutes).
b. App ly ice pack.
c. Immobilize and elevate affected part.
3. Teach safe administration of med ication.
a. Give orally if possible.
b. Avo id injections; if necessary, after injection apply pressure until b leeding s tops.
4. Avoid med ications that increase b leeding (aspirin, phenacetin, phenothiazines, indomethacin
(Indocin).
5. Institute dental precautions: soft toothbrush, water pik, good dental hygiene to avoid
extractions.
6. Encourage appropriate toys, games, and sports.
a. Soft toys for infant
b. Quiet activities (e. g., reading, swimming)
c. Avo id body-contact sport
d. Careful hand ling o f sharp objects
e. Use of electric shavers (nor razors)
7. Use protective devices for young child: padded crib, playpen, side rails, p rotective pad ding.
8. Teach to avoid overweight (causes strain on affected joints).
9. Teach to wear Medic Alert identification.
10. Inform appropriate schoo l personnel.
11. Avoid stressful situations (they increase susceptibility to bleeding)
12. Seek emergency medical treatment in cases of uncontrolled bleeding.

Evaluatio n
Parent and child demonstrate ability to correctly manage home administration of factor
VIII; state medication precautio ns, activities to avoid, and those that are permitted, parent
provides app ropriate pro tect ive devices at home; adeq uately cares for minor b leeding
episodes (e.g., local pressure, ice pack); school personnel and friends are informed abo ut
child’s cond ition and necessary restrictio ns or approp riate action during a bleeding ep isode.
a. Specific identification of trait and disease: Hgb e lectrophoresis (“protein fingerprinting”)
used if screening tests are positive
1. Give informatio n on a va ilab le genetic counseling.

Evaluatio n
Parents receive screening and genetic counse ling as indicated ; demonstrate knowledge of
transmission and implication for subsequent pregnancies.

HEMOPHILIA
General Informatio n

1. Definition, occurrence, and ca use: hereditary coagulation defect, usually transmitted to a ffected
male by female carrier through sex-linked recessive gene (see F ig. 5-3), resulting in prolonged
clotting time; most common type is hemophilia A-factor VIII deficienc y; severity of the
deficiency varies from mild to severe; at risk for a cq uired immunode ficiency syndrome (AIDS0
from contaminated blood products (see Tables 5-9)
2. Medical trea tment
a. Replacement of factor VIII: tra nsfusion o f plasma, fa ctor VIII concentrate, or
cryoprecipitate to prevent bleeding episode s
b. Additional treatment measures for more seve re bleeding episodes
1. immediate administration of factor VIII to control bleeding
2. bed rest with covers off affected area to re lieve pain; temporary immobilization of
affected joints in a slightly flexed position with casts, splints, or tractio n
3. physical therapy to prevent contractures, beginning 48 hours a fter bleeding stops
4. pain relief with seda tives or narcotics

Nursing Process
Assessment
1. Infa nt
a. Umbilical-cord hemorrhage
b. Hemorrhage following circumcision
c. Family history of hemophilia
2. Any a ge
a. Hemarthrosis (bleeding into a joint spa ce) is the most frequent site of bleeding; ma y result
in crippling bony deformities
b. Epistaxis
c. Spontaneous hematuria
d. Hemorrhage following tooth extraction or minor falls and cut
3. Diagnostic laboratory tests: only tests that measure c lotting factors (e.g., P TT) are abnormal;
platelet function tests (e.g., bleeding time) are normal
ANALYSIS (S EE P. 509)
PLANNING, IMPLEMENTATION, AND EVALUATION

Goal 1: Parent and child will receive education to prevent bleeding, provide safety measures;
will know how to treat minor bleeding episodes.

Implementation
1. Prepare parents and child for home care and administration of factor VIII (where available),
a. Teach about the disease.
b. Teach venipuncture procedure and how to monitor the transfusion.
c. Provide regular follow-up (family must be sufficiently motivated and stable to maintain a
homecare program.
2. Teach local treatment measures for minor bleeding episodes.
a. Apply direct pressure to site (10-15 minutes).
b. Apply ice pack.
c. Immobilize and elevate affected part.
3. Teach safe administration of medication.
a. Give orally if possible.
b. Avoid injections; if necessary, after injection apply pressure until bleeding stops.
4. Avoid medications that increase bleeding (aspirin, phenacetin, phenothiazines, indomethacin
(Indocin).
5. Institute dental precautions: soft toothbrush, water pik, good dental hygiene to avoid
extractions.
6. Encourage appropriate toys, games, and sports.
a. Soft toys for infant
b. Quiet activities (e.g., reading, swimming)
c. Avoid body-contact sport
d. Careful handling of sharp objects
e. Use of electric shavers (nor razors)
7. Use protective devices for young child: padded crib, playpen, side rails, protective padding.
8. Teach to avoid overweight (causes strain on affected joints).
9. Teach to wear Medic Alert identification.
10. Inform appropriate school personnel.
11. Avoid stressful situations (they increase susceptibility to bleeding)
12. Seek emergency medical treatment in cases of uncontrolled bleeding.

Evaluation
Parent and child demonstrate ability to correctly manage home administration of factor
VIII; state medication precautions, activities to avoid, and those that are permitted, parent
provides appropriate protective devices at home; adequately cares for minor bleeding
episodes (e.g., local pressure, ice pack); school personnel and friends are informed about
child’s condition and necessary restrictions or appropriate action during a bleeding episode.
Goal 2: Child and parents will receive emotional support.

Implementation
1. Encourage realistic career goals.
2. Allow child and family to discuss feeling and concerns about bleeding tendency and treatment,
subsequent absences from school, reactions to peers, and parental protectiveness.
3. Encourage independence while maintaining safety.
4. Urge testing for HIV status.
5. Refer to the local chapter of the National Hemophilia Foundation.

Evaluation
Child seeks independence within reasonable limits; asks question about reactions of school
friends; adolescent seeks out appropriate job opportunities.
CORONARY ARTERY DISEASE (CAD)
CORONARY ATHEROSCLEROTIC HEART DISEASE (CAHD)

Pathophysiology: ATHEROGENESIS

RISK FACTORS

Nonmodifiable Modifiable
Age Stress
Gender Diet
Race Sedentary Living
Heredity Smoking
Alcohol
Hypertension
Diabetes Mellitus
Obesity
Hyperlipidemia / Hypercholesterolema
Behavioral Factors
Contraceptive Pills

A. Nonspecific injury to Arterial Wall (Endothelial Injury)

Desquamation of Endothelial Lining

Increased Permeability / Adhesion Molecules

B. Lipids (LDL, VLDL) and Platelets Assimilate into the Area


C. Oxydized LDL attracts Monocytes And Macrophages to the Site

D. Plaques Begin to Form from cells Which Imbed into the Endothelium

E. Lipids are Engulfed by the Cells (foam cells) and Smooth Muscle Cells
Develop

Coronary Atherosclerotic Heart Disease

Decreased Coronary Tissue Perfusion

Coronary Ischemia

Decreased Myocardial Oxygenation


ANGINA PECTORIS / M YOCARDIAL ISCHEMIA

CAUSES

Atherosclerosis
Hypertension
Diabetes Mellitus
Thromboangitis Obliterans
Polycythemia Vera
Aortic Regurgitation

Reduced Coronary Tissue Perfusion

Diminished Myocardial. Oxygenation

Anaerobic Metabolism

Increased Lactic Acid Production (Lactic Acidosis)

Chest Pain
Causes
 Coronary Atherosclerotic heart Disease
 Coronary Thrombosis / Embolism
 Decreased Blood Flow with Shock and / or Hemorrhage
 Direct Trauma

Myocardial Ischemia Myocardial Oxygen Cellular


Supply Hypoxia

Cardiac Output Myocardial Altered Cell


Contractility Membrane Int.

Arterial Stimulation of Stimulation of


Pressure Baroreceptors Sympathetic Receptors

Peripheral Afterload
Vasoconstriction

Decreased
Myocardial Heart Diastolic Myocardial
Contractility Rate Filling tissue per.

Myocardial
Oxygen Demand
PATHOPHYSIOLOGY OF PREMATURE VEN TRICULAR CONTRACTIONS

Premature Ventricular Contractions

Ventricular Fibrillations

Cardiac Standstill / Arrest

Dysrhythemias

Cardiac Output

Cardiac Irritability

Myocardial Perfusion
HYPERTENSION

Afterload

Ventricular hypertrophy

Myocardial oxygen demand


Reduced compliance of the ventricle

Myocardial tissue perfusion

Increased risk of myocardial ischemia and infarction

 Accelerates atherosclerosis.
 In hypertension, vasoconstriction  vasopspasm  increased PVR  decreased blood flow to
organs (brains, heart, kidneys, eyes – the end target organs).
 Hypertensive effects on target organs
 Heart – Mycocardial infarction, congestive heart failure, myocardial hypertrophy,
dysrhythmias
 Eyes – blurred / impaired vision, retinopathy, cataract
 Brain – cerebrovascular accident, encephalopathy
 Kidneys – renal insufficiency, renal failure
 Peripheral Blood Vessels – dissecting anaeurysm, gangrene

PATHOPHYSIOLOGY OR HYPERTENSION

Risk Factors

 Family History  Obesity


 Age  Excess Alcohol Consumption
 High Salt Intake  Smoking
 Low Potassium Intake  Stress
Changes in Arteriolar Bed
Systemic Vascular
Resistance

Afterload

Blood Flow to Organs

Beta – receptor
Renal Perfusion Blood Pressure Activation

Hyponatremia Juxtaglomerular cells Hypovolemia

Angiotensinogen Rennin Angiotensin I

Angiotensin – Converting Enzyme (ACE)

Arteriolar Vasconstriction Angiotensin II

Peripheral resistance Adrenal Cortex


Stimulation II

Blood Pressure Aldosterone

Na resabsorption

H2 O reabsorption

Plasma Volume (ECF)


SUMMARY OF CLINICAL MANIFESTATIONS OF HPN

 Headache (especially upon waking). This is the most characteristic sign,


 Epistaxis
 Dizziness
 Tinnitus
 Unsteadiness
 Blurred vision
 Depression
 Noctuia
 Retinopathy, papilledema (on fundoscopy)

*(may be asymptomatic)

COLLABORATIVE MANAGEMENT

 Prevention
 Primary prevention – aimed at reducing the risk factors associated with HPN.
 moderation in sodium intake
 decreased saturated fats diet
 maintenance of IBW
 maintenance of regular pattern of exercise
 cessation of cigarette smoking
 moderation in consumption of alcohol
 stress reduction through effective coping strategies
 Secondary Prevention: focused on identification and control of HPN in high risk groups

 Medical Management
 Diuretics:
 Thiazides
 Chlorothiazide (Diuril)
 Hyrochlorothiazide (Hydrodiuril)
 Chlorthalidone (Hygroton)
 Loop Diuretics
 Furosemide (Lasix)
 Bumetamide (Bumex)
 Ethacrynic Acid (Edecrine)
 Potassium – sparing diuretics
 spironolactone (Aidactone)
 Triamterene (Dyrenium)
 Adrenergic Inhibitors
 Beta – Adrenergic Blockers
o Propranolol (Inderal)
o Pindolol (Visken)
o Nadolol (Corgard)
o Ateno lo l (Teno rmin)
o Metopro lo l (Lopressor)
o Acebutolo l (Secretral)
 Centrally – Acting Alpha Blockers
o Timolol (Blocad ren)
o Methyldopa (Aldomet)
o Clonid ine (Catapress)
o Gua nabenz (Wytensin)
 Perip hally – ActingAdre nergic Antago nists
o Gua nethid ine (Ismelin)
o Reserp ine (Serpasil)
 Alpha 1 Adrenergic Blockers
o Prazosin (Minipress)
o Tolazo line (Prisco line)
o Phento lamine (Regitine)
 Vasolidators
o Hydralazine (Apresoline)
o Na Nitroprusside (N ipride)
o Minozidil (Lo niten)
o Diazo xide (Hyperstat)
 ACE Inhib itors (Angiostensi – Co nverting Enzyme Inhibitors)
o Captopril (Capoten)
o Enalap ril (Vasotec)
o Cila zapril (Vascase)
o Lisinopril (Zestril)
o Ramipril (Altace)
 Calcium Anta gonists
o Amlod ipine Besylate (Norvasc)
o Diltiaze n (Cardizem)
o Felodipine (P lendil)
o Nifedipine (Procard ia, Adalat, Calcibloc)
o Verapamil (Isoptin, Cala n)

 Nursing Inte rventio ns


 Patient Tea ching / Counselling
 Teaching about HPN
 Teaching about the risk factors
 Stress therap y
 Low sod ium, low saturated fat d iet
 Avo id stimulants, e. g., caffeine, alcohol, cigarette smoking
 Regular pattern of e xercise
 Weight reduction if obe sed

 Teaching about med icatio n


 The most common side effects of diuretics are potassium depletion and orthostatic
hypotension.
 The most common side effect of the different antihypertensive drugs in orthostatic
hypotension.
 Take anti-hypertensive medications at regular basis
 Assume sitting or lying position for few minutes
 Change position gradually
 Avoid very warm bath
 Avoid prolonged sitting or standing.
 Avoid alcoholic beverages.
 Avoid tyramine – rich foods (proteins) as follows:
o Aged cheese
o Liver
o Beer
o Wine
o Chocolate
o Yughort
o Herring pickle
o Sausage
o Soy sauce
* these may cause hypertensive crisis

 Preventing Non-compliance
 Inform the client that absence of symptoms does not indicate control BP.
 Advise the client against abrupt withdrawal of medication; rebound hypertension may
occur
 Device ways to facilitate remembering of taking medications e.g. labeled containers

ARTERIAL DISORDERS

 Arterial Occlusive Disorders


 The most common cause is Arteriosclerosis Obliterans (ASO).
 The lower extremities are more commonly affected. The aorta may also be affected.
 Atheromatous plaque develops at the points of branchings, bifurcations, or vessel
narrowing.
 More prevalent among men, 50 to 70 years of age.

CLINICAL MANIF ESTATIONS

 Pain. Intermittent claudication is an aching, persistent, cramplike, squeezing pain that occur
after a certain amount of exercise of the affected extremity. It is relieved by rest.
 Coldness or cold sensitivity. Coldness in the feet with exposure to a cold environment,
associated with blanching or cyanosis due to tissue ischemia.
 Impaired arterial pulsations. Impaired or absent pulse indicates decreased blood flow due to
arterial spasm.
 Color changes. C yanosis or rubor may be observed when the extremities are placed in
dependent position.
 Ulceration and gangrene. May be due to ischemia or trauma. Impaired tissue Edema. Results
from severe obstruction.
 Edema. Results from severe obstruction.
 Sexual dysfunction. Occlusive disease of the terminal aorta decreases the blood supply to the
vascular tree supplying penile circulation. Unsustained erection may be experienced by the
client.

PREVENTION

 Primary Prevention
 Provide information on the effects of the following factors:
 Cigarette smoking. N icotine causes vaso-constriction, spasms of the arteries, reduced
circulation to the extremities. The carbon dioxide inhaled in cigarette smoking reduces
oxygen transport to the tissues.
 Hypertension. Causes elastic tissue in the arteries to be replaced by fibrous collagen
tissue. This reduces arterial elasticity and increases resistance to blood flow.
 Hyperlipidemia. C holesterol and triglycerides contribute to the development of
atherosclerotic plaque in the vessels.
 Obesity. Palces an added burden on the heart and blood vessels. It enhances propensity
to DM, HPN, and hyperlipidemia.
 Physical inactivity. Compromises circulation.
 Emotional stress. Stimulates the sympathetic response which result to vasoconstriction.
Stress may also cause increased cholesterol and platelet levels and HPN.
 Diabetes mellitus. Changes in glucose and fat metabolism enhance atherosclerotic
process.
 Secondary Prevention
 Encourage clients with early symptoms to seek medical care. This is to prevent
complications like infection, injury, thrombosis and amputation.
 Tertiary Prevention
 Rehabilitation is important aspect of management of client with arterial occlusive disorder.
Exercise to develop collateral circulation will be beneficial.

COLLABORATIVE MANAGEMENT

 Medication
 Vasolidators
 Antihyperlipidemics
 Cholestyramine (Questran)
 Colestipol (Colestid)
 Clofibrate (Atromid- S)
 Nicotinic Acid (N iacin)
 Gemfibrocil (Lopid)
 Fluvasten (Lescol)
 Lovastatin (Mevacor)
 Pravastatin (Pravachol)
 Simvastatin (Zocor)
 Probucol (Lorelco)

 Treatment
 Quit smoking
 Control of serum lipid levels
 Skin and foot care
 Diet: low,- fat, low-cholesterol
 Activity: daily walking program
 Surgical Management
 Bypass Graft. This uses a native vein or arterial segment or a synthetic material.
 Endarterectomy. Stripping and removal of atheromatous plaque by surgery (also
atherectomy).
 Endovascular surgery.
 Balloon angioplasty involves insertion of a special catheter through fluoroscopy into the site
of occlusion. The balloon tip of the catheter inflated to compress and rupture the
atheromatous plaque.
 Laser angioplasty invo lves balloon angioplasty and laser.
 Stent involves use of rigid but flexible structure that maintain the integrity of the vascular
wall and patency of the artery.
 Amputation. It is performed in clients with severely advanced arterial occlusive disease and
gangrene. The toes are more frequently involved.

NURSING IN TERVENTIONS

 Promoting Tissue Perfusion


 Maintain warm environmental temperature
 Place legs in slight dependency to promote arterial flow
 Avoid pressure on affected extremity; use padding for support.
 Avoid vigorous massage of extremities.
 Patient teaching includes the following
 Avoid chilling and exposure to cold; use several layers of clothing during cold weather.
 Avoid constricting clothings.
 Avoid crossing the legs.
 Quit smoking

 Maintaining Skin Integrity and Preventing Infection


 Examine the skin on a daily basis for intactness, dryness, redness and lesions.
 Take daily bath and dry the skin gently.
 Apply moisturizing cream / lotion on the skin. Avoid using alcohol.
 Fastidious foot care.
 Wear comfortable, well- fitted pair o f shoe; preferably leather or canvass mate rial.
 Avoid direct heat applica tion over the extremities.
 Consult the physic ian for any signs of skin breakdown, e.g. abrasio ns, lesions a nd
ulcerations.

 Pro moting Activity


 General Exerc ises
 Regular aerobic exerc ise suc h as walking, swimming, jogging, bicycling,
 Do exercises 30 to 45 minutes 3 to 4 times a week.
 Special Exercises
 Buerger – Alle n’s exercise on a daily basis
Lie supine with legs e levated for 2 to 3 minutes.
Sit up in bed and do foot exercises for 3 minutes:
 Dorsiflexion
 Plantar flexion
 Inversion
 Eversion
o Hold the feet in each position for 30 seconds
o Lie quietly supine for 3 minutes.

NOTE:
To be effective, perform 4 to 6 c ycles (steps 1 to 3 is one cycle) 4 time a day. C hange position
gradually during the exercise to preve nt orthostatic hypo te nsion.
 Ankle rotations
 Ankle pumps
 Knee extension

Preventing Injury
 Wear comfortable, protective shoes at all times.
 Do not go bare footed.
 Trim toenails stra ight across.
 Avoid scratching or rubbing fee t.
 Check tempera ture of wa ter for bathing and do foot care properly.
 Seek medical treatment for defo rmed nails, corns, calluses, and ulceration. Avo id se lf-
treatment (may cause infection).

ANEURYSM

 It is the lo ca lized, irreversible dilatation of an artery secondary to an a lte ration in the integrity
of its wall.
 Classifica tions of Aneurysm
 Fusiform aneurysm. Involves outpo uching of both sides of the artery.
 Saccular aneurysm. Involves outpouching of only one s ide of the artery.
 Dissecting a neurysm. Involves sepa ration or tear in the tunica intima and tunica med ia.
 The most common type of aneurysm is abdominal aortic aneurysm (AAA).
 The characteristic manifestation of AAA is pulsatile mass over the abdomen. T he other
manifestations are as follows:
 Low back pain
 Lower abdominal pain
 Flank pain
 Collapse
 Shock
 The most common cause of aneurysm is hypertension.
 The most dangerous complication of aneurysm is rupture, causing massive internal
hemorrhage, shock and death.

RAYNUD’S DISEASE

 It is intermittent vasospasm of arteries in the digits that occurs as a result of exposure to cold an
emotional stress.
 It is aggravated by cigarette smoking.
 Women, ages 15 to 40 years are more commonly affected.
 Ulcerations may develop on the fingertips an toes.

PATHOPHYSIOLOGY OF RAYNUD’S DISEASE

Cold exposure
Stress

Digital Artery
Contraction / Spasm

Occlusion of Arteries

Tissue Ischemia
(Blanching to cyanosis of digits; burning, throbbing pain;
Swelling of the area)

Tissue Hypoxia

Tissue Necrosis

Tissue Ulceration

Gangrene
COLLABORATIVE MANAGEMENT

 Medical Management
 Avoid exposure to cold
 Quit smoking.
 Calcium-channel blockers
 Vasodilators
 Anti- inflammatory analgesics
 Sympathectomy to relieve vasospastic symptoms
 Amputation (ulcerations/gangrene)
 Teach effects of smoking on arterial flow. N icotine causes vasoconstriction
 Teach ways to avoid exposure to cold.
 Wear adequate clothing
 Wear gloves when handling frozen foods.
 Caution when cleaning refrigerator
 Wear socks during cold climate
 Discuss importance of reducing emotional stress.
 Avoid drugs that cause vasoconstriction, such as contraceptive pills, beta blockers, and
ergotamines.

VENOUS DISORDERS

 Superficial Thrombophlebitis
 It results from venous thrombosis and inflammation in a superficial vein
 The greater or lesser saphenous veins of the lower extremity are most commonly affected.
 Clinical manifestations are as follows:
 pain
 tenderness
 palpable induration along the course of the vein
(There is no edema)
Medical Manage ment
 Bed rest with leg elevation.
 Local moist heat application.
 Compression support stockings.
 Non-narcotic analgesics.
 Nonsteroidal anti- inflammatory agents. (NSAID)

NURSING IN TERVENTIONS

 Client teaching involves the following:


 Prevention of venous stasis:
 Avoid prolonged sitting or standing
 Elevate legs when sitting
 Avoid crossing the legs at the knee
 Wear compression support stockings.
 Avoid constriction on legs by tight bands such as garters
 Daily exercise and activity
 Prevent recurrence
 Maintain IBW
 Alternate standing with sitting at work or at home
 Regular patterns of exercise.

DEEP VEIN THROMBOSIS

 It is caused by Virchor’s Triad:


 venous stasis
 vessel wall injury
 hypercoagulability of the blood
 it more commonly involves the veins in the lower extremities.
 It is potentially life-threatening because it may lead to pulmonary embolism.
 Clinical manifestations are as follows:
 calf pain (+ Homan’s sign)
 to assess Homans’ sign, flex the knee and dorsiflex this foot
 edema
 tenderness
 palpable induration along the course of the vein

COLLABORATIVE MANAGEMENT ]

 Medical management
 Anticoagulation therapy
 Heparin / IV
 Coumadin / p.o.
 Thrombolytics
 Minimize intake of green leafy vegetables because they contain high Vitamin K, if on
coumadin therapy.
 Prepare protamine SO4 as antidote for heparin.
 Prepare Vit. K as antidote for coumadin.
 Minimize parenteral injections if on thrombolytic therapy. Bleeding is a common side
effect.
 Surgery
 thromboembolectomy.
 Greenfield vena ava filter to prevent pulmonary embolism.

NURSING IN TERVENTIONS

 Maintaining Tissue Perfusion


 Ed rest for 5 to 7 days.
 Elevate legs to promote venous return and prevent edema.
 Compression support stockings.
 Ambulate as able.
 Avoid standing still and sitting for prolonged periods.
 Check pulse distal to the site of thrombosis.
 Assess presence of edema.
 Monitor calf.
 Promoting Comfort
 Administer analgesic to alleviate pain and discomfort.
 Medicate with NSAID to reduce edema.

 Varicose Veins
 They are prominent, abnormally dilated veins, usually affecting the lower extremities
because of the effect of gravity on venous pressure.
 More common among women, 30 to 50 years of age.
 Cause of varicose veins are as follows:
 Congenital absence of valves of the veins.
 Hereditary weakness of the valves of the veins (mot common cause).
 Prolonged sitting or standing.
 Wearing of constricting clothings.
 Obesity.
 Thrombophlebitis.
 Pregnancy.
 Disease conditions, e.g., right sided CHF, liver cirrhosis.
 Clinical manifestations are as follows:
 Dilated, purplish, tortuous veins.
 Leg pain
 Leg edema
 Heaviness in the legs

COLLABORATIVE MANAGEMENT

 Medical Management
 Elevation of affected limb for 15 to 30 minutes at a time, average of 20 minute.
 Compression with support stockings.
 Sclerotherapy. It involves injection of a sclerosing agent into the varicose veins. This will
cause thrombosis in the area and prevent inflow of large volume of bloo d. The most
commonly used drug is Na murrhuate.
 Surgery is vein ligation and stripping to relieve pain, reduce swelling, or thrombophlebitis.
 The most effective nursing intervention to prevent thrombophlebitis after vein surgery is
early ambulation.

 Nursing Interventions
 Client Teaching includes the following:
 Wear elastic stockings during activities requiring long periods of standing or during
pregnancy if with family history of varicose veins.
 Moderate exercise and elevation of the legs during sitting to prevent venous congestion.
 After vein ligation and stripping, watch for the following
o Bleeding: elevate the leg, apply pressure over the site, and report to the surgeon.
o Elevate the leg when lying or sitting.
o Take analgesic as ordered, especially 15 to 30 minutes before ambulation.
o Keep elastic bandage snug, and smoothly applied to maintain even pressure.
o Return for follow-up care.

ARTERIAL / VENOUS DISO RDERS


 Buerger’s Disease (Thromboangitis Obliterans)
 It is characterized by diffuse inflammation of the small and medium arteries, followed by
the veins.
 It is more common among males, 30 to 50 years of age.
 It is associated with cigarette smoking, genetic factors, immunologic factors and
coagulation abnormalities.
 The most characteristic manifestation is intermittent claudication.
 Collaborative Management:
 Medical Management
 eliminate cigarette smoking
 calcium – channel blockers
 antiplatelet agents
 sympathectomy (if done on the early stage may eliminate vasospasm
 amputation of ulcerated fingers and toes.
 Nursing Interventions
 (Same as other types of arterial disorders)

DISORDERS AFFEC TING THE RBC’S

 Polycythemia
 ↑ rbc and hgb production.
 Compensatory response to chronic hypoxia.

Hypoxia

↑ erythropoietin production by the kidneys

Stimulation of the bone marrow to ↑ rbc production

 Polycythemia Vera
 Hyperplasia of the bone marrow.
 ↑ rbc (erythrocytosis); ↑ wbc (leukocytosis); ↑ platelets (thrombocytosis)
 Cause is unknown; associated with genetics.
 Pathophysiology
↑ rbc, wbc, platelets

↑ blood viscosity Organ infiltration Capillary


overdistention

Thromboembolism Hepatomogaly Rupture


Splenomegaly
Arthralgia
Cerebral hypoxia Hemorrhage

Hypovolemia

 Signs and Symptoms


 ruddy complexion
 headache
 dizziness
 fatigue
 blurred vision
 hepatosplenomegaly
 increased risk of CVA and MI due to thromboembolism

COLLABORATIVE MANAGEMENT

 Increase fluid intake to reduce blood viscosity.


 Monitor for signs and symptoms of bleeding.
 Monitor for signs and symptoms of thromboembolism.
 Angina
 Claudication
 Thrombophlebitis
 Pruritus
 Administer analgesic as ordered.
 Administer antihistamine to decrease pruritus.
 Therapeutic phlebotomy to reduce circulating volume.
 Chemotherapy to inhibit hyperactivity of the bone marrow.
 Radiation therapy (Na Phosphate / IV)
 Patient teaching: Avoid high altitude; low oxygen levels tend to stimulate the kidneys to
increase secretion of erythropoietin.
ANEMIAS
 Decreased availability of oxygen to the tissues
 Type of Anemia (Adult)
 Iron Deficiency Anemia
 Folate Deficiency Anemia
 Aplastic Anemia
 Pernicious Anemia

 Causes
 Acute/chronic blood loss.
 Inadequate dietary intake of vitamins / minerals needed for the production.
 Decreased rbc production by the bone marrow.
 Increased destruction of rbc.
 Increased demands of vitamins/minerals needed for rbc production.

COMMON CLINICAL MANAGEMENT

 Pallor  Tachycardia / palpitations


 Easy fatigability  Syncope
 Weakness  Brittle hair and nails
 Anorexia  Paresthesia
 Weight loss  Cold sensitivity
 SOB  Amenorrhea
 Headache / Dizziness

IRON DEFICIENCY ANEMIA


 (Microcytic, hypochromic anemia)
 Assessment
 Vinson – P lummer’s Syndrome
 Stomatitis
 Dysphagia
 Atrophic glossitis (smooth, sore tongue)
 Cheilosis (cracks at the side of the lips)
 Koilonychias (spoon – shaped / concave fingernails)
 Pica (craving of non – edible substances like clay, laundry soap, starch, ice, uncooked rice,
etc.)
 Tinnitus
 Cardiovascular symptoms (hgb = 7.5 g / dl.)
 ↑ P R, chest pain, SOB, CHF
 Blood transfusion is necessary

COLLABORATIVE MANAGEMENT

 Medical Management
 Iron S upplement
 Oral
o Ferrous S ulfate
o Ferrous Gluconate
o Ferrous F umarate
 Parenteral: Iron Dextran (Imferon)
o Oral iron should be given p.c. to prevent G.I. irritation.
o Oral liquid iron to be administered with straw to prevent permanent staining of the
teeth.
o Vitamin C increases iron absorption, e.g., orange juice.
o Do not administer with milk, antacid; these will inhibit absorption.
o Imferon: Z – track (deep IM)
o To prevent staining of the skill.
o Do not massage site of injection. To prevent leakage of medication into
subcutaneous layer.
o Iron salts changes color of stool to dark green or black. This is harmless.
 Oxygen therapy for SOB.
 Blood transfusion as needed.

 Nursing Interventions
 Pro mote rest to reduce o xygen demands.
 Provide good oral care. To prevent / relieve stomatitis.
 Provide good skin care. To prevent pressure sore.
 Diet: Iron – rich foods
 Organ meats
 Beans
 Green, leafy vegetables
 Raisins; other dried fruits

FOLATE DEFICIENCY ANEMIA (MEGALOBLAS TIC ANEMIA)

 Causes
 Poor dietary intake
 Rarely eat uncooked (raw) fruits and vegetables
 Alcoholism
 Chronic malnutrition
 Pregnancy
 Anorexia nervosa
 Malabsorption
 Malignancy
 Pro longed TPN
 Chronic hemodialysis
 Assessment
 Cracked lips, sore tongue
 Same as Pernicious Anemia
 Collaborative Management
 Well – balance diet
 Folic acid 1 mg. /day
PERNICIOUS ANEMIA

 Macrocytic, hyperchromic anemia


 Causes
 Gastric surgery
 Crohn’s disease

Pathophysiology

↓ IN TRINSIC FACTOR production


By the parietal cells of the stomach

↓VITAMIN B12 absorption

√ ↓RBC production
√ ↓DNA synthesis in maturing RBC (megablastic cells)
√ Impairment of integrity of cells
(mouth, stomach, anus, vagina, axon of neurons)

DIAGNOSTIC TESTS

 Tubeless Gastric Analysis

Diagnex blue / Azuressin tablet



Collect urine specimen

Blue x Blue

HCI is present (-) HCL (Achlorhydria)

(-) Pernicious Anemia (+) Pernicious Anemia

Note: HC L and intrinsic factor are both produced by the parietal cells of the stomach.

 Schilling’s Test
 Most definitive diagnostic test for pernicious anemia.
 Oral radioactive Vitamin B12. to push the radioactive Vit. B12 into the urine.
 Collect 24 – hour urine specimen.
 Decreased excretion of Vitamin B12 in the urine indicate (+)
 Pernicious Anemia.
ASSESSMENT
 “beefy”, red, inflamed tongue (most characteristic manifestation
 Archlorhydria
 Tingling, numbness
 Lack of balance, uncoo rd inated movements
 Confusion
 Paralysis
 Depressio n, psychosis
 Jaundice (faulty erythropoiesis)

 COLLABORATIVE MANAGEMENT
 Vitamin B12 IM
 Daily 7 days
 Weekly 10 weeks
 Monthly LIFETIME (100mg/Mo)
 Hydrochlo ric acid p.o. for 1 week
 Iron therapy
 Blood transfusion as needed
 Physical examination e very six months
* at risk for Gastric Cancer

APLASTIC ANEMIA
 Hypoplasia of the bo ne marrow
 Fat replaces bone marro w

 PANCYTOPENIA
 Anemia
 Leukopenia
 Thrombocytopenia
 Causes
 Congenital
 Acquired
 Idiopathic
 Infections
 Medications
 Heavy metals
 Hepatitis
 Diagnostics tests
 Bone marro w aspiration / biopsy
 Adult
o Posterior Iliac Crest is the most common site.
o Prone position during the proced ure.
o Brief, sharp pain is normally experienced as bone marrow is aspirated.
 Child
o Tibia is the most common site.
o Side – lying position during the procedure.
 Apply pressure at the puncture site to prevent bleeding.

COLLABORATIVE MANAGEMENT
 Medical Management
 Bone marrow transplantation
 Immunosuppressive therapy (Antithymocyte Globulin – ATG)
o Central line 7 – 10 days
 Blood transfusion as necessary
 Stool softeners; high – fiber diet to avoid constipation thereby prevent rectal bleeding.
 Nursing Interventions
 Assess for sign and symptoms of infection, tissue hypoxia and bleeding.
 Frequent rest periods to reduce oxygen demands of tissues.
 Good oral care.
 Use soft-bristled toothbrush / soft swabs to prevent gum bleeding.
 Male clients
o use electric razor
 Avoid ASA administration
 Reverse / Protective Isolation
 Practice asepsis
 Sources of bacteria
o Avoid fresh fruits / fresh flowers in the client’s unit
o Avoid raw foods
 Limits visitors
 Do not allow persons with signs and symptoms of infection to visit.

NEOPLASTIC BLOOD DISORDERS

 Leukemia
 Chronic or acute neoplasm of blood – forming cells in the bone marrow and lymph nodes

 Causes:
 Idiopathic
 Viral
 Genetic
 Radiation
 Chemicals
 Types of Leukemia
 AML (Acute Myelogenous Leukemia)
o Malignant disorder that affects monocytes, granulocytes, erythrocytes and platelets.
o Survival:
 1 – 3 yrs. (with chemotherapy)
 2 – 5 mos. (if untreated)

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