General Objectives:
The student will be able to describe the most common cardiovascular diseases among children and their management by the end of this unit.
Specific Objectives:
The student will be able to: 1. Define the most common heart diseases, either the acyanotic or cyanotic heart diseases.
2.
3. Plan the nursing management of each disease. 4. List the methods used in diagnosis of heart disease. 5. Plan the nursing management of congestive heart failure. 6. Identify the etiology of rheumatic fever. 7. Identify the criteria used in diagnosis of rheumatic fever. 8. Plan the nursing management of rheumatic fever. 9. Plan the nursing care for a child undergoing heart surgery.
Fetal Circulation:
The characteristics of fetal circulation ensure that the most vital organs and tissues receive the maximum concentration of oxygenated blood. The fetal brain requires the highest oxygen concentration. The lungs are essentially nonfunctional, and the liver is only partially functional, therefore less blood is needed in these organs in fetal life. During fetal life, blood carrying oxygen and nutritive materials from the placenta enters the fetal system through the umbilicus via the large umbilical vein.
- Oxygenated blood enters the heart by the inferior vena cava because of the higher pressure of the blood entering the right atrium and through the foramen ovale to the left atrium. - In this way, the better-oxygenated blood enters the left atrium and ventricle to be pumped through the aorta to the head and upper extremities.
Blood from the head and upper extremities entering the right atrium from the superior vena cava is directed downward through the tricuspid valve into the right ventricle. From the right ventricle, it is pumped through the pulmonary artery, where the major portion is shunted to the descending aorta via the ducts arteriosus to supply the trunk and lower extremities. Only small amount flows to the non-functioning fetal lungs for the purposes of nutrition.
-1 With cessation of placental blood flow from clamping of the umbilical cord the
expansion of the lungs at birth, the hemodynamis of the fetal vascular system undergo abrupt changes.
-2 With the first breath, the lungs are expanded and oxygen causes pulmonary
vasodilatation, pulmonary pressure start to fall, a systemic pressures given the removal of the placenta start to rise.
-3 Normally, the foramen ovale closes as the pressure in the left atrium exceeds the
pressure in the right atrium and it closes completely at third month of infant life.
(Fig . 1)
Types of Defects:
Congenital heart defects have been divided into 2 categories:
1. Traditionally, a physical characteristics, cyanosis has been used as distinguishing feature, dividing the anomalies into:
-1 Increased pulmonary blood flow. -2 Decreased pulmonary blood flow. -3 Obstruction of blood flow out of the heart. -4 Mixed blood flow in which saturated and desaturated blood mix within the heart
or great arteries.
-Artial septal defect - Coarctation of aorta -Ventricular septal defect - Aortic stenosis -Patent ductus arteriosus - Pulmonic stenosis -Atrioventricular canal
-Tetralogy of fallot -Transposition of great arteries. -Tricuspid atresia -Total anomalous pulmonary venous return. -Tranucus arteriosus - Hypoplastic left heart syndrome
(Table .1) Comparison of acyanotic-cyantoic and hemodynamic classification system of congenital heart disease.
Acyanotic Defects
Most acyanotic defects involve primarily left to right shunting through an abnormal opening. Others result from obstructive lesions that reduce the flow of blood to various areas of the body.
-1 Patent ductus arteriosus (PDA). -2 Atrial septal defect (ASD). -3 Ventricular septal defect (VSD). -4 Pulmonic stenosis (PS). -5 Aortic stenosis (AS). -6 Coarctation of aorta (COA).
Patent Ductus Arteriosus (PDA)
Description and Pathophysiology:
Patent ductus arteriosus is a vascular connection that during fetal life, short circuits that pulmonary vascular bed and directs blood from the pulmonary artery to the aorta. Functional closure normally occurs soon after birth. If the ductus remains patent flow in the ductus is reversed by the higher pressure in the aorta.
(Fig .2)
Incidence:
More common in females (2:1), Higher incidence among premature and commonly associated with maternal rubella.
Hemodynamics:
Blood from aorta PDA goes to systemic circulation poor systemic circulation. Double pulm. venous return Doubled flow in LA
Assessment:
Clinical manifestation will depend on the size of duct and amount of shunting. Small PDA: asymptomatic and discovered on a routine examination. Large PDA: 1 Classic machinery murmur, which is continuous from systole into diastole. 2 Dyspnea on exertion and easy fatigability. 3 Under weight thin child. 4 Repeated chest infections. 5 Heart rate over 150 b/m, gallop rhythm due to rapid filling of the ventricle. 6 Bounding pluses due to increased systolic pressure. 7 Left heart failure may develop in infancy in severe cases. 8 Enlarged heart size in large PDA.
Therapeutic Management:
Supportive: fluid restriction with diuretics and digitalization for congestive heart failure CHF. 2. Surgical: surgery can be performed at anytime, although it is preferably done at about 6 months of age, surgery maybe done earlier if the child is in difficulty to prevent complications and growth retardation caused by PDA.
1.
Out come:
The child is good with less than 1% mortality.
Complications:
1. Bacterial endocarditis. 2. Congestive heart failure. 3. Pulmonary hypertension.
(Fig.3)
Hemodynamics:
Blood flow from pulmonary veins LA LV ASD poor systemic circulation. double flow in RA Double flow in RV
Assessment:
1 The clinical manifestations depend on the location and size of the defect. The infant with small defects may be asymptomatic. 2 If there is a large left to right shunt and severe mitral incompetence cardiac enlargement and pericardial bulge are seen. These children are easily fatigued and have recurrent pneumonitis. 1 In atrial septal defect, pulse and venous pressure are normal and the heart size is normal or slightly enlarged. 2 Systolic murmur is present. 3 The ausculatory finding of a widely split second heart sound is so unusual in complicated atrial septal defects that the diagnosis is not made without it.
Management:
1. 2.
Supportive: same as that of the VSD. Surgical: surgery is done on affected children before they enter school even if no symptoms are present. If surgery is not done during childhood pulmonary hypertension, atrial arrhythmias and cardiac failure make operation more hazardous in adult life.
(Fig. 4)
Hemodynamics:
to Aorta Blood from LA LV VSD Flow in LA poor systemic circulation RV RV flow Flow in pulmonary circulation (doubled)
Assessment:
The most frequently seen defects are small, so these defects are asymptomatic. Medium sized or larger defects during infancy may produce symptoms such as: dyspnea, slow physical development, feeding difficulties and frequent pulmonary infection. Heart failure, cardiac enlargement and mild cyanosis may also occur in large defects.
Therapeutic Management:
If the defect is small and asymptomatic, treatment is conservative because spontaneous closure may occur before 1 or 2 years of age. If the defect is larger, medical care is given for CHF when it occurs: oral diuretics and digoxin. Surgical repair requires open-heart surgery and cardiopulmonary bypass.
It is an obstructive lesion that interferes with blood flow from the right ventricle. It may occur as a single abnormality or it may be associated with other defects such as those in the atrial or ventricular septa. It may also occur with patent ductus arteriosus. (Fig 5)
(Fig.5)
Pathophysiology:
The pulmonary valve is obstructed by fusion of the cusps of their (ommissures) valve orifice so that their movement is restricted. The passage of blood is obstructed from the right ventricle to the pulmonary artery resulting in increased systolic pressure and hypertrophy of the right ventricle. The degree of change depends on the size of the constricted valvular opening. Another cause of obstruction is a muscular or fibrous that is caused by the failure of involution of an embryonic structure. If the right ventricle cant eject the necessary amount of venous blood into the pulmonary circulation systemic cyanosis occurs. If a patent ductus arteriosus is also present, blood is shunted from the aorta to the pulmonary artery and then to the lungs, partially compensating for the obstruction.
Assessment:
Mild PS: asymptomatic, discovered on routine examination. Severe PS: may present by right heart failure in infancy: cyanosis and cardiac failure may occur, poor exercise tolerance with exertional dyspnea due to insufficient blood flow to the lungs to meet the need for increased cardiac output during exertion. ECG shows gross right ventricular hypertrophy. Radiography shows enlargement of the heart. The murmur and changes in the second heart sound can be analyzed with echocardiography.
Management:
Children having mild and even moderate pulmonic stenosis may need no treatment. Sever defect: -Medical treatment: like in VSD. -Surgical: catheter ballon valvuloplasty if pulmonary valve gradient >60 mmHg. This reduces the narrowing by 75% or more.
Description:
Narrowing or stricture of the aortic valve causing resistance to blood flow in the left ventricle and decreased cardiac output. (Fig 6)
(Fig.6)
Pathology:
When there is resistance to blood out flow the left ventricle to the aorta left ventricular hypertrophy occurs, blood backs up in the left atrium, causing increased pressure in that chamber resulting in increased pressure in the pulmonary veins and pulmonary vascular congestion when severe obstruction occurs the pulse pressure in the aorta is narrowed (N.B. pulse pressure is the difference between systole and diastole).
Assessment:
Depend on the severity of the lesion. If there is mild aortic stenosis, the infant may grow normally to be asymptomatic until increased physical growth requires additional cardiac output. In severe obstruction: fatigue due to exercise intolerance, dizziness, fainting and episodes of pulmonary edema occur, decreased cardiac out put also results in faint peripheral pulses and anginal pain. The most prominent physical manifestation of aortic stenosis is the presence of a coarse systolic ejection murmur, usually accompanied by a thrill over the aortic area, radiating to the neck and apex.
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If heart failure occurs in infancy, medical management is carried out: like VSD. Surgical: Ballon valvuloplasty or surgical by open aortic volvotomy or aortic valve replacement should be postponed until child has stopped growing.
(Fig.7)
Assessment:
Blood pressure is higher than normal in the upper part of the body, resulting in headache, dizziness fainting, epistaxis, and later cerebrovascular accidents. In the leg, it is relatively low, resulting in absence or diminishing of the femoral pulse. The legs may be cooler than the arms. If the child exercises muscle cramps in the legs may be due to tissue anoxia.
Surgical: repair consists of resection and anastomosis by aortic graft or subclavian flap angioplasty. If blood pressure is not elevated and heart failure is not a problem, it is wise to postpone the operation until the operation descending aorta is at least 50% of adult size (age of child 3-6 years) to avoid re-stenosis.
Out come:
Surgery should be done if only a minor defect is present to avoid complication, e.g. hypertension, intracranial hemorrhage and stroke.
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Tetralogy of Fallot
The classical tetralogy consists of: 1. Pulmonary stenosis. 2. Ventricular septal defect. 3. Overriding of the aorta: aorta receives blood from both ventricles and this is the cause of cyanosis. 4. Right ventricular hypertrophy. In tetralogy of fallot, the blood normally returns from the systemic circulation to the right atrium and right ventricle. The out flow of the blood from the right ventricle resisted by the pulmonary stenosis so that the blood flows through the ventricular septal defect into the aorta. This is a right to left shunt. Hypertrophy of the right ventricle occurs as a result of the pressure exerted against the pulmonary stenosis, because the blood from the right ventricle is unoxygenated, cyanosis result. Polycythemia develops because the body attempts to compensate for the unoxygenated blood. The resulting increased viscosity of the blood causes slowing of the circulation and possible thrombophlebitis emboi and vascular disease.
(Fig. 8)
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Assessment:
The neonate who has tetralogy of fallot is not cyanotic because of the presence of the patent ductus arteriosus; cyanosis becomes evident after the ductus closes during the first months of life. Clubbing of the fingers and toes (in long standing cases ) (Fig. 9).
(Fig.9) Stunted growth. Intolerance to effort: exercise usually causes severe dyspnea. Infant and toddlers may be able to play for a short time, but then they mustres infants assure a knee chest position rather than extending their extremities when they lie down. Older children, learn that the squatting position relieves dyspnea because: 1. Flexing the legs decrease venous return from the lower extremities which have a very low oxygen content, especially after exercise.
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2. Squatting position increase systemic vascular resistance, which diverts right ventricular blood from the aorta into pulmonary artery increasing pulmonary blood flow. This increases the amount of oxygenated blood in the left side of the heart and eventually into systemic circulation. (Fig.10)
(Fig. 10) Cyanotic spells. (Hypoxic, blue spells). Apansystolic murmur: it is usually associated with thrill. These children dont develop congestive heart failure because the overload of the blood in right ventricle flows freely through the septal defect and the overriding aorta into the systemic circulation.
Management:
Medical: 1. Antibiotic prophylaxis before tooth extraction or GIT and urinary procedures. 2. Treatment of cyanotic spells: -Oxygen therapy.
(Fig.11)
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-Give morphine sulfate. -I.V. beta- adrenergic inhibitor. -If acidosis is present give I.V. sodium bicarbonate. Surgical: palliative and total corrective surgery is being done on infants and children of all ages.
The clinical manifestation of cyanosis varies in degree depending on the type and size of the associated defects. Children with minimal communication are severely cyanotic at birth. Those with large septal defects or a patent ductus arteriosus may be less severely cyanotic but have symptoms of congestive heart failure usually before 4 months of age. In these infants the only signs at birth may be cyanosis after crying or feeding and progressive hyperpnea in an attempt to compensate for decreased arterial oxygen saturation. A murmur usually indicates the presence of septal defect or a patent ductus arteriosus cardiomegaly.
Assessment:
(Fig. 12)
Management:
Palliative and corrective treatment used for the treatment of transposition of the great vessels.
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Tricuspid Atresia
Description and Pathology:
Tricuspid valvular atresia is characterized by a small right ventricle, large left ventricle, and usually diminished pulmonary circulation. Blood from the right atrium passes through an atrial septal into the left atrium, mixes with oxygenated blood returning from the lung, flows into the left ventricle, and is propelled into the systemic circulation. The lungs may receive blood through one of three routes: A small ventricular septal defect, Patent ductus arteriosus, and Bronchial vessels. N. B.: it means the absence of the tricuspid valve resulting in no opening between the right atrium and right ventricle. It is usually associated with other defects that allow some shunting of blood into the left side of the heart, then back to the right ventricle or pulmonary artery.
(Fig. 13)
Assessment:
The degree of cyanosis depends on the amount of pulmonary blood flow. Severe cyanosis, dyspnea, anoxic spells and signs of right-sided heart failure are evident early during infancy if the child survives, systemic consequences of cyanosis and polycythemia may develop. Palliative and corrective treatment can be done.
Management:
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Infants:
Cyanosis generalized, especially mucous membranes, lips and tongue. Conjunctiva, cyanosis during exertion such as crying, feeding, straining, or when immersed in water. Dyspnea, especially following physical effort such as feeding, crying or straining. Fatigue, paroxysmal hyperpnea, poor growth and development (failure to thrive). Frequent respiratory tract infection. Feeding difficulties. Hypotonia. Excessive sweating.
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Older Children:
Impaired growth. Fatigue. Orthopnea. Headache. Leg fatigue. Delicate body build. Effort dyspnea. Digital clubbing. Epistaxis.
Intervention:
Administer digoxin as ordered. The childs apical pulse is always checked before administrating digoxin (as general rule the drug is not given if the pulse is below 90-100 b/m in infants and young children or below 70 b/m in older children). Heart rate and volume indicate satisfactory cardiac output.
Expected Outcome:
Intervention:
Allow for frequent of rest. Encourage quite games and activities. Help child to select activities appropriate to age, condition and capabilities. Avoid extremes of environmental temperature. Child determines and engages in activities commensurate with capabilities.
Expected Outcome:
3. Altered growth and development related to inadequate oxygen, nutrients to tissue and social isolation.
Goal:
The patient will: Achieve normal growth.
Intervention:
Provide well balanced highly nutritive diet. Child achieves normal growth.
Expected Outcome:
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Goal: (2)
The patient will: Exhibit adequate iron level.
Goal: (3)
The patient will: Have opportunity to participate in activities.
Intervention:
Avoid contact with infected persons. Provide for adequate rest. Provide optimum nutrition. Child remains free from infection.
Expected Outcome:
Goal: (2)
The patient will: Exhibit positive coping behavior.
Intervention:
Encourage family to participate in care of child while hospitalized. Encourage family to include others in childs care to prevent their own exhaustion. Assist family in determining appropriate physical activity and disciplining methods for childs anorexia. Family copes with childs symptoms in a positive way.
Expected Outcome:
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Goal: (3)
The patient will: Demonstrate knowledge of home care.
Intervention:
Teach skills for home care. Administration of medications. Feeding techniques. Signs that indicate complications. Where and whom to contact for help and guidance. Family demonstrates ability and motivation for home care.
Expected Outcome:
6. High risk for injury (complications) related to cardiac condition and therapies.
Goal:
The patients family will: Recognize signs of complications early.
Intervention:
Teach family to intervene during hypercyanotic spells, place child in knee chest position with head and chest elevated. Teach family to recognize signs of complications such as: Increased respiratory effort (tachypnea, retraction, grunting, cough, cyanosis). Cerebral thrombosis (compensatory polycythemia is particularly hazardous when child is dehydrated).
Expected Outcome:
Family recognizes signs of complications and institutes appropriate action.
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Pathophysiology:
Heart failure is often separated into two categories; right sided and left sided failure. In right sided failure, the right ventricle is unable to pump blood effectively into the pulmonary artery resulting in increased pressure in the right atrium and systemic venous circulation. Systemic venous hypertension causes Hepatosplenomegaly and occasionally edema. In left sided failure, the left ventricle is unable to pump blood into the systemic circulation resulting in increased pressure in the left atrium and pulmonary veins. The lungs become congested with blood, causing elevated pulmonary pressure and pulmonary edema.
Clinical Manifestation:
The child may suddenly become dyspnic, cyanotic. Abdominal pain, fever, anorexia, dyspnea, cough; develop suddenly in a young child. Dyspnea, orthopnea or paroxysmal nocturnal dyspnea. Palpitation, tachycardia and profuse sweating, pallor or peripheral cyanosis and cold extremities.
Causes:
1. 2. 3.
4.
Can be classified according to the following changes: Volume overload: especially with left to right shunts that may cause the RV to hypertrophy in order to compensate for the additional blood volume. Pressure overload: resulting from obstructive lesions such as valvular stenosis or coarctation of the aorta. Decreased contractility: primarily factors that affect the contractility of the myocardium, such as cardiomyopathy or myocardial schema from severe anemia or asphyxia, low level of potassium, glucose, calcium or magnesium. High cardiac output demands: in which the body s need for oxygenated blood exceeds the heart out put (even though the volume may be normal), such as in sepsis, hyperthyroidism and severe anemia.
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Assessment:
1. Criteria for impaired myocardial function:
Tachycardia. Decreased urine output. Weakness. Anorexia. Cool extremities. Decreased blood pressure. Tachycardia. Retraction (infants). Exercise intolerance. Cough. Wheezing. Weight gain. Peripheral edema. Neck vein dysfunction.
Sweating. Fatigue. Restlessness. Pale. Weak peripheral pulses. Cardiomegaly. Dyspnea. Flaring nares. Orthopenea. Cyanosis. Grunting. Hepatomegaly. Ascitis.
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Nursing Intervention:
1 Administer digoxin (lanoxin) as ordered. 2 Nursing established precaution to prevent toxicity. 3 Often an E.C.G. rhythm strip is taken to assess cardiac status before administration. 4 Ensure adequate intake of K. 5 Monitor serum potassium levels (decrease enhances digoxin toxicity). 6 Administer medications to decrease over load as ordered. 7 Check blood pressure. 8 Observe for signs of hypotension. 9 Monitor electrolyte levels. Heartbeat is strong, regular and within normal limits for age. 2 Peripheral perfusion is adequate.
1
Expected outcome:
Nursing Intervention:
1 Place inclined posture of 30 to 45 degree tilt mattress support of incubator, place older infant in sent (fowlers position). 2 Avoid any constricting clothing or restraints around abdomen and chest. 3 Administer humidified O2 as prescribed.
Expected outcome:
Respirations remain with normal limits; color is good and infant rest quietly.
Goal: (2)
The patient will: Experience reduction of anxiety.
Nursing Intervention:
1 2 3 4 5 Employ flexible feeding schedule. Handle child gently. Hold and comfort the infant. Employ comfort measures found effective in individual cases. Encourage family to provide comfort. Infant rests quietly and breath easily.
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Nursing Intervention:
1 Maintain neutral thermal environment. -Place newborn in an incubator or under warmer. -Keep infant warm and treat fever promptly. 2 Feed small volumes or frequent intervals using soft nipple with moderately large opening. -Implement gavage feeding if infant becomes fatigues before taking an adequate amount. 3 Time nursing activities to disturb infant as little as possible. 4 Implement measures to reduce anxiety. 5 Respond promptly to crying or other expressions of distress. Expected out come: Infant rest quietly.
Nursing Intervention:
1 2 3 4 Administer diuretics as prescribed. Maintain fluid restriction if ordered. Provide skin care for children with edema. Change position frequently. 5 Use resilient mattress or mattress cover.
Expected outcome:
Infant exhibits evidence of fluid loss, frequent urination, and weight loss.
5. High risk for infection related to reduce body defenses pulmonary congestion. As nursing diagnosis (4) 6. Altered family processes related to child with life threatening illness. As nursing diagnosis (5)
N.B.: feed cyanotic infant in the knee-chest position, head is elevated, he will suck more strongly, ingest more, tire less, and gain weight. Use soft nipple, frequent burping and pauses of rest.
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Tachycardia, especially during rest and slight exertion. Profuse scalp sweating, especially in infants. Irritability. Respiratory distress. Fatigue. Sudden weight gain. Common signs of Digoxin toxicity: Gastrointestinal: nausea, vomiting, and anorexia. Cardiac: bradycardia, dysrhythmias. Parent guidelines in administrating Digoxin: Give digoxin at regular intervals. Dont mix it with other foods or fluids (inaccurate intake of the drug). If a dose is missed and more than 4 hours has passed withhold the dose and give the next dose at the regular time, if less than 4 hours has elapsed give the next doses.
If the child vomits dont give a second doses. If more than 2 consecutive doses have been missed notify the physician. Dont increase or double the does for missed doses. Keep digoxin in a safe place preferably a locked cabinet.
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Definition:
R.F. is an inflammatory disease of connective tissue involving mainly the joints and heart and less frequently the CNS, skin and subcutaneous tissues. It has a marked tendency to recur.
Incidence:
The incidence of A.R.F peaks between 5-10 years of age. The school age children are he most susceptible to contracting this disease. It may rarely start at earlier age (23years). Boys and girls are equally affected.
Etiology:
R .F. is a poorly understood autoimmune reaction to group A Beta hemolytic streptococcal upper respiratory tract infection (GABHS).
Pathophysiology:
Rheumatic fever is essentially a group of bodily responses to a streptococcal infection following upper respiratory tract infection. R. F. develops in 3 steps: Phase I: GABHS infection of the upper respiratory tract. The attack of GABHS pharyngitis may be extremely mild or moderately severe. Phase II: the symptoms of URTI subside quickly and are followed by a latent or silent period usually lasting for 1-3 weeks, during which the patient is symptom-free. Phase III: the silent period is followed by the onset of acute rheumatic fever. The most acceptable current hypotheses for the development of RF are:
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2. Hypothesis of autoimmunity:
Some streptococcal antigens cross-react with human tissue antigens, and crossreactive anti-heart antibodies have been found in rheumatic fever patients. According to this hypothesis, streptococcal antigens may elicit antibodies capable of reacting not only with the microbial products, but also with the hosts antigens. Thus autoimmunization maybe the underlying basis for the cardiac lesion.
Assessment:
Accurate history should be taking from parents and child, problematic environmental factors or recent exposure are the most efficient ways to diagnose A.R.F. is to strictly and here to the specific onset criteria. The ones major and minor criteria are based on clinical findings are essentially objective. The history and laboratory findings determine the minor criteria.
Fever (38-39C). Arthralgia (pain in joints) without arthritic changes. Abdominal pain. Unexplained epistaxis. Weakness, fatigue, pallor, loss of appetite, weight loss. Elevated acute phase reactants (ESR, CRP). See table (2)
Guidelines for the diagnosis of initial attack of Rheumatic fever (Jones criteria, 1992 update) Major Minor Manifestations Manifestations Carditis Clinical findings Polyarthritis Arthralgia Chorea Fever Erythema marginatum Laboratory findings Subcutaneous nodules Elevated acute-phase Reactants Erythrocyte Sedimenation rate C- reactive protein Supporting Evidence of Antecedent Group A Streptococcal Infection Positive throat culture or rapid streptococcal antigen test Elevated or rising streptococcal antibody titer. Table (2)
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Major Manifestations:
1- Carditis:
Mitral and aortic valves are most affective valves and they become scarred, fibrous areas when healed, stenosis as the leafiers (cusps) of the valves occurs because of their fusing together. This process causes obstruction to the blood flow into the left ventricle or aorta or both. The valve edges may become so scarred that they cant completely close, causing a block flower regurgitation (valvular insufficiency) when the valves close so, the following manifestations will be seen. 1 Tachycardia out of proportion to degree of fever. 2 Cardiomegaly. 3 New murmur or change in preexisting murmurs. 4 Muffled heart sound (ventricle gallop exist that is S3). 5 Friction rub (main manifestation of pericarditis). 6 Pericardial pain. 7 Changes in E.C.G.
2-Rheumatic Polyarthritis:
1 It is the most common criterion: typical arthritis occurs in 70% of cases. It occurs during the first 1-2 weeks the febrile period and lasts for a few days in certain affected joints before moving to other joints. 2 Affected joint is red, warm, swollen, very tender, with limited movements + effusion. 3 Migratory: several joints are commonly involved, either together or one after another. 4 Typically the large joints are affected as knees, wrists, ankles and elbows. It rarely affects fingers, toes or spine. 5 It disappears within 12-24 hours from start of salicylate therapy. 6 If untreated it doesnt persist in the same joint for more than 1 week. 7 Rheumatic arthritis leaves the joint intact and doesnt result in chronic disease. N.B.: Rheumatic fever licks the joints but bites the heart.
3- Erythema Marginatum:
1 The lesions are non-pruritic and appear initially as undifferentiated macules on the trunk and inner aspect of the extremities (never on face). 2 Evanescent, and if watched from hour to hour, it will be noted to change gradually.
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5- Subcutaneous Nodules:
1 These occur rarely in the general population but are frequently found in individuals who have severe Carditis or who have had repeated attack of A.R.F. 2 Nodules are generally identified as small (0.5-1Cm) and firm without any tenderness or attachment to the skin. 3 They can be palpated over the extensor surfaces of joints such as elbows, knees, ankles, or over the scalp and spinous processes of the vertebrae. 4 They gradually resolve over a period of time with no residual.
Diagnostic Evaluation:
To diagnose R.F. it is necessary to have: 1 Two major criteria +evidence of preceding GABHS or infection or. 2 One major + 2 minor criteria + evidence of preceding GABHS or infection. 3 Children suspected of having A.R.F. are tested for streptococcal antibodies. The most reliable and most standardized test is an elevated or rising antistreptolysin-o titer (A.S.O.T.). 4 Erythrocyte sedimentation rate (E.S.R.). 5 C- reactive protein. 6 Electrocardiograph. 7 Radiographs.
Therapeutic Management:
The aims of medical management are: 1. Eradication of group AB hemolytic streptococcal infection. 2. Anti-inflammatory agents for Carditis and arthritis. 3. Palliation of the other symptoms. 4. Prevention of recurrents of RF. 1 Penicillin: is the drug of choice to treat GABS infection:
-1 Procaine penicillin 400.000 /day for 10 days, or -2 Oral penicillin V: 200.000 400.000 (125-250mg)/dose 3 times/ day for 10
days, or
Prophylactic Treatment:
Against recurrent R.F is started after the acute therapy and involves monthly intramuscular injections of benzathin penicillin (1-2 million I) IM., two daily oral doses of penicillin (400.000) or one daily oral dose of sulfadiazine orally or erythromycine orally, twice daily. 2 Children who have had acute R.F. are susceptible to recurrent R.F. for the rest of their lives and should be followed medically for at least 5 years.
1
N.B.: Streptococci can be eradicated and R.F. prevented if penicillin is given Early (within 9 days of GABS infection) for a sufficient period of time (10 days
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4 Infective endocarditis.
Nursing Consideration:
The objectives of nursing care for child with A.R.F. are to: 1. Encourage compliance with drug regimens. 2. Facilitate recovery from the illness. 3. Provide emotional support. 4. Prevent the disease.
-1 Alternating warm and cold snacks to the affected joints may reduce swelling
and inflammation and provide direct and immediate reduction of pain. 2 During chorea the only treatment is prevention of injury during the period when involuntary jerking and possibly violent movements occur.
-1 Assist once during walking. -2 Feeding the child to prevent injury. -3 Bed rails to prevent the child from falling out of bed. -4 Restraints to prevent the child from falling from a chair, padding on the
sides of the beds or chair to prevent injury.
1 The nurse should be alert to any child who has abrupt onset of signs and symptoms of a streptococcal sore throat. 2 After streptococcal pharyngitis has been diagnosed, antimicrobial treatment is given to eradicate the infection. A single injection of benzathine penicillin is the most reliable from the therapy, oral penicillin or erythromycin may be given daily for 10 days, the nurse help the parents to be cooperative. 3 The main nurses role in prevention is to help educate the public as well as the individual patient and family. 4 Massive screening program with throat cultures and support of patient cooperation in therapy can eradicate the disease. N.B.: from the previous discussion about A.R.F. try to develop the appropriate nursing care plan.
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-1 Admission history and physical examination. -2 Baseline vital signs (apical pulse and blood pressure) in all examinations should be
obtained for evaluation at rest and with activity-report any change.
-3 Height and weight measurement for fluid replacement. -4 Pre-operative studies, i.e. E.C.G. Lab Tests should be prepared. -5 Sleep/ awake patterns. -6 Fluid intake: to estimate the childs fluid consumption and which fluids are
preferred.
-7 Additional observation (normal activities, rest be noted & reported)- physical and
emotional stress should be reported.
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Postoperative Care:
Immediate Admission to ICU:
1 2 3 4 Oxygen immediately. Check each catheter in his chest and attached to the suction machine. Check vital signs. If cardioscopy will be in use, attach it to the patient, then EKG, heart rate and rhythm will observed constantly. 5 I.V. fluids must be checked and regulated carefully.
Then:
1. Tell patient that operation is over when he re-awakes. 2. Narcotic may be given as Dr. order. 3. Vital signs are taken each hour or more often if necessary (temperature rectally as cool atmosphere in oxygen tent may affect temperature). 1 Temperature: if there is fever, reduce it by tepid water sponges, ice bags or ice water mattress. 2 Respiration: - Check depth and rate of respiration and chest expansion on both sides is equal. - Do suction if respiration becomes noisy and rapid. 1 Pulse: it should be observed for: regular rhythm and power. 2 Blood pressure: Should be taken and notifying doctor for any change. 4. Observe: skin color, moisture (dry moist). (Warm cold). 5. Monitor fluids: if cut down is used for I.V.; not be too rapid, it must be in proper position (no filtration). Oral fluids are restricted in immediate post-operative period to decrease load on heart, therefore mouth care will also decrease childs thirsty. Input and output of all fluids must be accurately calculated and recorded. Urine must be analyzed for specific gravity to assess kidney function. Fluids requirement is based on childs weight and body surface area. 6. If no voiding within 8-12 hours after operation, catheter may be used. 7. Care for chest tubes (under-water seal). Observe the drainage, bleeding, be sure that they are patent (free from blood clots) and well tighten to patient. Important: be sure that the bottles. Below bed level and observe the amount, color and consistence. If cyanosis, sudden sharp chest pain around the catheter and dyspnea and tachycardia occur. Clamp the chest tube and call Dr. immediately. 8. Encourage child for deep breathing and coughing exercise and support his chest especially over the incision area and praise him. 9. Change position every hour. 10. Support the body with pillows if he cant maintain his position. Encourage him to move himself. 11. Observe: color of legs and its coldness, bleeding or infection at side of operation. 12. To provide rest, good plan of N.C. to decrease disturbance. 13. Encourage patient to be out of bed (according to his condition and severity of operation) on wheel chair after chest tubes have been removed. 14. Child may regress in his behavior (cry- more physical contact- more demanding) understand his behavior as a nurse once his condition improves help him to gain control of his situation. 15. Before discharge: plan of care must be done with the health team and parents.
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References:
1.
Chow MP. Handbook of Pediatric Primary Care. 6th ed. New York: John Whiley and sons co., 1984. 729-744. Wong DL. Whaley and Wongs Nursing Care of Infant and Children. 6th ed. London: Mosby co., 1999. 1583 1649.
2.
3. Oldham KT. Surgery of Infants and Children: Scientific principles and Practice. Philadelphia: lippincott-Raven co., 1997. 999-1004. 4. Madkour A. Essential of Pediatrics. Faculty of Medicine: Egypt, 2001. Pp 133-159.
5.
Finkelmeier B. Cardio thoracic Surgical Nursing.3rd ed. Philadelphia: JB Lippincott co., 2000. 169-180. Woods S. Cardiac Nursing.3rd ed. Philadelphia B Lippincott co., 1995. 820 830.
6.
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