Congenital heart diseases

Congenital heart diseases
Definition and introduction of congenital heart diseases (CHD):
It includes primarily anatomic abnormalities present at birth that results in abnormal cardiac functions.
The newborn’s heart begins to beat at 28 days of gestation
The heart is completely developed on the 9th week of intrauterine life
Incidence:
4 – 10/100 live births
It is the majority cause of death during the 1st year of life after prematurity
Sexes are affected differently depending on the defect
It is more likely to be with other congenital anomalies e.g. T.E fistula, Renal agenecies and diaphragmatic hernia.
Etiology:
Most of them are unknown
Factors associated with increased incidence:
Prenatal factors:
1. Maternal rubella
2. Radiation
3. Alcoholism
4. age >40 yrs
5. Insulin dependent diabetes
6. Fetal intra uterine cardiac viral disease

Genetic factors: although the influence is multifactorial there is high risk of CHD in children who have:
1. a sibling with a heart defect
2. a parent with CHD
3. chromosomal aberration e.g. Down’s syndrome
4. Born with other congenital anomalies
After birth failure of obliteration of ductus arteriosus or foramen ovali
Altered hemodynamic:
1. Blood flows from high pressure to area of lower pressure and with lower resistance, in response to the pumping action of the heart.
2. The higher the pressure gradient the greater the rate of flow
3. The higher the resistance the less the rate of flow
4. Normally the pressure in the Rt side is lower than the Lt side of the heart
5. The resistance in the pulmonary circulation and vessels entering or leaving these chambers have corresponding pressure.
6. So if there is septal defect, blood will flow from Lt to Rt known as left to right shunt, and no desaturated blood flows directly into the Lt side of the heart so it is acyanotic defect
Cyanotic defects are due to:
Change in the pressure causing blood to flow through Rt - to- Lt Shunt.
Due to increased pulmonary flow through the pulmonary vascular resistance
Or obstruction to the blood flow through the pulmonary valve and aorta
Or due to mixing of the blood between pulmonary and systemic circulation e.g. Truncus arteriosus (the pulmonary artery and the aorta are one single vessel that overrides both ventricles
Classification and clinical consequences:
Depending on the severity of the cardiac defect and the altered hemodynamics two principal clinical consequences can occur:
1st Consequence is Congestive heart failure
2nd Consequence is Hypoxemia
1st Consequence Congestive heart failure:
Occurs mostly in infants.
It is inability of the heart to pump adequate blood to the systemic circulation to meet the metabolic demands of the body
It is a symptom caused by cardiac defect not a disease in itself, it is due to ++ work load on normal myocardium
Pathophysiology of congestive heart failure:
1st category:
Rt sided failure; the Rt ventricle is unable to pump blood to pulmonary artery resulting in increase in the pressure in the Rt atrium and systemic venous circulations leading to liver and spleen enlargement and occasionally edema.
2nd category
Lt sided failure, the left ventricle is unable to pump blood into the systemic circulation leading to increased pressure in the Lt atrium and pulmonary veins.

The lungs become congested leading to increased pulmonary pressure and pulmonary edema.
Congestive heart failure leads to:
Cardiac muscles damage
Decrease the cardiac output
Decrease the flow of blood to the kidneys
Increase the re-absorption of Na and water and increase blood volume
Increase systemic congestion
Distention in neck veins and peripheral veins
Edema and hepatomegaly
Forehead sweating due to sympathetic response
Diagnostic evaluation
Clinical manifestations of congestive heart failure:
? Impaired Myocardial Function:
Tachycardia (occurs early)
Sweating
Decreased urine output
Weakness
Fatigue
Restlessness
Anorexia
Pale cool extremities
Weak peripheral pulses Low blood pressure
Gallop Rhythm heart beats
Cardiomegaly
Pulmonary Congestion:
Tachypnea
Dyspnea
Retraction of ICS in infants Flaring nares
Exercise intolerance
Orthopnea
Cough and hoarseness of voice Cyanosis
Wheezing
Grunting
Systemic Venous Congestion:
• Weight gain (due to edema)
• Hepatomegaly
• Peripheral edema especially periorbital area
• Ascites
• Neck vein distension (children)
Therapeutic management
Goals:
Improve cardiac function
Remove accumulated fluid and Na
Decrease cardiac demands
Improve tissue oxygenation and decrease O2 consumption
Myocardial efficiency improved by giving:
Digitalis glycosides (Lanoxin /Digoxin)
Increase cardiac output
Decrease heart size
Decrease venous pressure
Decrease edema
Regulate heart rate
Nursing alert
Digoxin is not given if:
The apical heart rate in infants is <90 -110
The apical heart rate in young children is <70
Angiotensin-converting enzyme (Captopril/capotin)
Inhibit the normal function of rennin angiotensin in the kidney and vasodilatation occur, decrease pulmonary and systemic vascular resistance and decrease B/P decrease after load
Remove accumulated fluid and Na:
Diuretics. frusamide (Lasix). Thiazide and Spironolactone.
Possible restriction of fluids and decrease Na
Observe fluid intake and out put and Signs of dehydration
Potassium supplement, because Diuretics increase potassium loss
Decrease cardiac demand:
Decrease physical activities, by bed rest, observe body temp.
Treat any infections
Improve breathing ; semi sitting position and sedate irritable children
Increase tissue oxygenation and decrease O2 consumption by applying the mentioned measures and giving humidified cool O2
2nd Consequence Hypoxemia
Hypoxia:
Reduction in tissue oxygenation that results from ?oxygen saturation and PaO2 and results in impaired cellular process
Cyanosis:
Blue discoloration of mucus membrane, skin nail beds of the child with reduced O2 saturation, results from the presence of deoxygenated hemoglobin in a concentration of 5g/dl of blood or more.
Clinical manifestations of Hypoxemia :
Polycythemia
Clubbing of the finger
Hypercyanotic spells
Hypercyanotic spells
Hypercyanotic spells:
Cyanosis and hyperapneia
?Rt -to-Lt Shunt.
Rare < 2 months of age
More common in >1year of age increase in the morning and during feeding, crying and defecation
Possible consequences :
1. CVA
2. Brain abscess
3. ?Development
Congenital Heart Diseases
TYPES OF DEFECTS and Classification
1st Acyanotic 2nd Cyanotic

++Pulmonary Obstruction to --Pulmonary Mixed
blood flow blood flow flow flow
? ? ? ?
- ASD - Tetralogy TPOGA
TPOGV
VSD - Coarctation of of Fallots Truncus
the aorta
arteriosis.
PDA - Tricuspid
Hypoplastic
Artesia
Pulmonic stenosis Lt Heart
Aortic stenosis syndrome
Acyanotic Defects:
Lt – to – Rt shunting through an abnormal opening or obstructive lesions lead to decrease blood flow to various parts of the body.
The most common clinical manifestation is heart failure. Some of them may be asymptomatic. E.g. Patent ductus arteriosus
Patent ductus arteriosus:
Is when the fetal ductus artery connecting the aorta and the pulmonary artery fails to close within few weeks after birth, so the blood flows from the high pressure of the aorta to the lower pressure of the pulmonary artery (Lt – to –Rt shunt
Incidence:
It is most common cardiac anomaly
The ratio is: 2 ?: 1?
Clinical Manifestations:
With or without congestive heart failure
Machinery - like murmur at 2nd Lt ICS
Widened pulse pressure and bounding like pulses resulting from runoff of blood from aorta to pulmonary artery
Risk of bacterial endocarditis and pulmonary vascular obstructive disease in later life from chronic excessive pulmonary blood flow may occur
Medical Management:
Endomethacin (Prostaglandin inhibitor) is successful in helping in the closing of the PDA in newborns
Closure with placement of an occluding device during cardiac cath is done in some institutions
Prognosis is good with < 1% mortality
Surgical Management:
Ligation with, or with out, division of the patent vessel.
Prognosis is good with 1% mortality
Atrial Septal defect (ASD)
An abnormal opening between atria
With a Lt - to – Rt Shunt
Clinical Manifestations:
Characteristic murmur
Pt is at risk for atrial dysrythmia ( may be due to atrial enlargement and stretching of conduction fibers) and pulmonary vascular obstructive disease, later in life due to ? pulmonary blood flow
Management:
Surgical correction:
Closure of moderate – large defects
Open repair with cardiopulmonary bypass
Prognosis:
Very low mortality, <1%
Ventriculo Septal Defect (VSD):
It is an abnormal opening between right and left ventricles, may vary in size ; small pinhole to the absence of the septum, resulting in common ventricle. Frequently associated with other defects
Lt –to – Rt Shunt
Clinical Manifestations:
Congestive heart failure is common
Characteristic murmur
High risk of bacterial endocarditis and pulmonary vascular obstruction disease
Ventricular Septal Defect (VSD)
{Eisenmenger Syndrome }: If pulmonary resistance increase and Lt – to – Rt Shunt is even further reduced and a Rt – to – Lt Shunt results, the unoxygenated blood crosses the VSD to the Lt ventricle and enters the systemic circulation. Combination of pulmonary hyper tension and bidirectional or reversed shunting through {VSD, ASD, or PDA}
Management:
Surgical correction
Palliative: Pulmonary banding on symptomatic infants
Complete repair:
a. Small defect by purse-string
b. Large defect require knitted Dacron patch sewn over the opening
Both (a and b) need cardiopulmonary bypass
Prognosis:
Risk depend on location of the defect
< 5% - 20% mortality also depends on other anomalies in the heart
Pulmonary stenosis (PS)
It is narrowing at the entrance of the pulmonary artery, resistance to blood flow cause RT ventricular hyper atrophy and decrease pulmonary flow
Clinical Manifestations:
Mild cyanosis or cardiac failure
Newborns with severe narrowing will be cyanotic
Characteristic murmur
Cardiomegally is evident in chest X-ray
? Risk of Bacterial Endo Carditis with progressive narrowing lead to increase symptoms
Pulmonary stenosis
Management:
1. Surgical correction
Infants: Transventricular valvotomy Brock procedure
Children: Valvotomy with cardiopulmonary bypass
2. Nonsurgical treatment:
Balloon angioplasty in the cardiac cath to dilate the valve
Prognosis: < 2% mortality
Aortic stenosis AS
There is narrowing or stricture of aortic valve leading to resistance of blood flow in the Lt Ventricle, decrease cardiac output. Lt ventricular hypertrophy and pulmonary vascular congestion.
Clinical Manifestations:
Infants with severe defects:
Decreased cardiac output and faint pulses
Low blood pressure and tachycardia
Poor feeding
Children:
Signs of exercise intolerance
Chest pain
Dizziness when standing for long periods
Characteristic murmur
Risk for bacterial endocarditis
Coronary insufficiency
Ventricular dysfunction
Aortic stenosis
Management:
Surgical correction:
- Commissurotomy
- Patch for extensive narrowing
Nonsurgical correction:
- Dilatation of narrowed valve with balloon angioplasty in the cath lab
Prognosis:
Newborn critical conditions mortality >20%
Older children elective valvotomy has lower risk
Recurrence is possible which will need valve replacement
Coarctation of the aorta (COA)
There is localized narrowing near the insertion of ductus arteriosus resulting in:
Increased pressure in proximal structures to the defect (Head and upper extremities)
Decreased pressure distal to obstruction
(body and lower extremities)
Clinical manifestations:
High B/P and bounding pulses in arms
Weak or absent femoral pulses
Cool lower extremities with low B/P
Signs of congestive heart failure in infants
Older children may experience dizziness, headaches, fainting and epistaxis due to high B/P
Risk of B/P rupture of the aorta, aortic aneurism or stroke
Management
Surgical correction:
- Resection of narrowed portion and end - to - end anastomosis or graft replacement
Prognosis: < 5% in isolated coarctation and high risk in infants and other complex cardiac defects.
Recurrence is possible
Major Cyanotic Defects
Cyanotic defects result from:
1. Obstruction of blood flow to the lungs
2. And Mixing of desaturated blue venus blood with fully saturated red arterial blood within the chambers of the heart
Tetralogy of Fallots (TOF)
It is the most common cyanotic congenital heart disease, the defects include:
1. Ventricular Septal defect
2. Pulmonary stenosis
3. Overriding of the Aorta
4. Rt ventricular hyper atrophy

Clinical Manifestations:
In Infants:
1. Some are acutely cyanosed at birth, others have mild cyanosis that progresses over the 1st year as the pulmonary stenosis worsen
2. Acute episodes of cyanosis and hypoxia (blue spells) usually during crying or after feeding
In Children:
1. With ++ cyanosis ±clubbing of fingers
2. Squatting
3. Poor growth
4. Patients are at risk of emboli, C.V disease,Brain abscess, Seizures and loss of consciousness, or sudden death following an anoxic spell.
Management:
1. Surgical correction:
1. Palliative: To bring back flow to lungs, to create an artificial connection between the pulmonary and systemic circulation
2. Corrective: Closure of VSD - Pulmonic Valvotomy - Patch enlargement of Rt Ventricular out flow tract below the pulmonary valve
Prognosis:
Operative mortality about 5 – 10%
Transposition of Great Arteries or Vessels (TGA or TGV)
Males are affected more than females
Pulmonary artery leaves the Lt ventricle
Aorta exits from the Rt ventricle
With no communication between systemic and pulmonary circulation
Associated defects such as Septal defects or patent ductus arteriosus permits blood to enter the systemic circulation and or pulmonary circulation for mixing of saturated and nonsaturated blood
Clinical manifestations: Depend on other defects
If minimum communication cyanosis is ? and the infant will be depressed at birth
If communication is good congestive heart failure is more common and less severe cyanosis
Heart sounds vary according to defects
Cardiomegally occur after few weeks of life

Management:
Surgical Palliative treatment (To provide intracardiac mixing):
1. Administration of IV prostaglandin E1 to keep the ductus arteriosus open to temporary increase in blood mixing and provide O2 saturation of 75% or to maintain cardiac output.
2. Rashkin procedure: Enlarge septal defect
Complete repair:
Switching the great vessels to their correct anatomic position.
Prognosis: Operative mortality about 5 – 10%
ACUTE RHEUMATIC FEVER
Acute rheumatic fever (ARF) is a systemic disease characterized by inflammatory lesions of connective tissue and endothelial tissue.
It is a primary type of acquired heart disease.
Etiology/Incidence
The pathogenesis is thought to be an autoimmune response to group A beta-hemolytic Streptococcus.
Most first attacks of ARF are preceded by an untreated streptococcal infection of the throat or upper respiratory tract at an interval of 2 to 6 weeks.
ARF is not caused by direct infection by the organism.
ARF is commonly seen in children 5 to 15 years of age, during winter months, and in poorer living conditions.
Incidence is greater in underdeveloped countries, although it is on the rise in the United States.
Altered Physiology
There is cross-reactivity between cardiac tissue antigens and streptococcal cell wall components.
The Streptococcus may no longer be present, but auto antibodies attack one s heart (myocardium, pericardium, or valves)
The unique pathologic lesion of rheumatic fever is the Aschoff body, a collection of reticuloendothelial cells surrounding a necrotic center on some structure of the heart.
The inflammatory process involves the heart, joints, skin, and central nervous system.
The inflammation may involve the leaflets or chordae tendinae of the heart valves, most frequently the mitral or aortic valves, resulting in sclerosis and fusion of valve margins
Valvular incompetence results
There is a high recurrence rate of those with ARF, 75% progress to rheumatic heart disease in adulthood.
ARF is a preventable condition with penicillin treatment of the primary infection. Erythromycin is treatment for those with penicillin sensitivities.
Complications:
Significant chronic heart failure
Pericarditis, pericardial effusions
Aortic/Mitral valve regurgitation
Permanent cardiac damage
Clinical Manifestations and Diagnostic Evaluation:
No single clinical or laboratory finding is characteristic of ARF.
The diagnosis is based on a combination of manifestations
characteristic of this disease and in the absence of other diseases that may mimic it.
For this reason, the Jones criterion is used, and it suggests:
1. The presence of two major criteria
2. Or one major and two minor criteria.
3. Plus evidence of a preceding streptococcal infection are required to establish a diagnosis.
Major Manifestations:
1. CARDITIS: manifested by significant murmurs, signs of Pericarditis, cardiac enlargement, or CHF
2. POLYARTHRITIS: almost always migratory and is manifested by:
3. swelling,
4. heat,
5. redness and tenderness
6. or by pain and limitation of motion of two or more joints.
(The synovial fluid is sterile (
3. Chorea, a CNS disorder that lasts 1 to 3 months purposeless, involuntary, rapid movements often are associated with muscle weakness, involuntary facial grimaces, speech disturbances, and emotional liability
4. Erythema marginatum: are temporary nonpruritic,pink rash.
The erythematus areas have pale centers
and round or wavy margins, vary greatly in size,
And occur mainly on the trunk and extremities.
Erythema is transient, migrates from place to place, and may be brought out by the application of heat.
(Erythema marginatum)
5. Subcutaneous nodules are firm, painless nodules seen or felt over the extensor surface of certain joints, particularly elbows, knees, and wrists, in the occipital region, or over the spinous processes of the thoracic and lumbar vertebrae; the skin overlying them moves freely and is not inflamed.
(Subcutaneous nodule)
Minor Manifestations :
1. History of previous rheumatic fever or evidence of preexisting rheumatic heart disease
2. Arthralgia—pain in one or more joints without evidence of inflammation, tenderness to touch, or limitation of motion
3. Fever—temperature in excess of 38°C
4. Elevated erythrocyte sedimentation rate (ESR)
5. Positive C-reactive protein (CRP)
6. ECG changes—mainly PR interval prolongation

Supporting Evidence of Streptococcal Infection:
Increased titer of streptococcal antibodies (Antistreptolysin O or ASO titer)
Positive throat culture for group A beta-hemolytic streptococci or recent scarlet fever
Treatment:
Treatment of streptococcal infection—generally intramuscular (IM) penicillin G (Penicillin L-A); erythromycin for patients with penicillin allergy
Prevention of permanent cardiac damage corticosteroids for patients with Carditis
Palliative management of other symptoms—Salicylates prescribed for patients with arthritis (but not while on high-dose corticosteroids due to risk of gastrointestinal bleeding); antipyretics after diagnosis has been established
Prevention of recurrences of ARF
Nursing Interventions:
A. Controlling Infection
Administer medication as prescribed by the healthcare provider.
NURSING ALERT:
Before administering penicillin, elicit a history for possible drug allergy
Administer Salicylates with milk or antacids.
Observe for gastrointestinal upset, ringing in the ears, headaches, bleeding, and disturbances in the mental state.
Report side effects promptly.
Monitor Salicylates blood levels as ordered.
Withhold antipyretics during the diagnostic period as requested.
Prepare the child and family for the expected side effects of steroid therapy, such as rounding facial contour, acne, excessive hair, weight gain.
Watch for mental and emotional disturbances, which may necessitate discontinuing the medication.
Hypertension and the tendency to retain water and sodium may result from steroid therapy. Restrict sodium and fluids, and obtain daily weights as indicated.
Be aware that steroids diminish the child s resistance to infection and may mask symptoms of infection
Do not place a child with an infectious disease in a room with a child with rheumatic fever. Restrict visitors and personnel with infectious diseases from contact with the child on steroid therapy.
Make the family aware that a combination of steroid therapy and stress may lead to the development of gastric ulcers.
Administer antipyretics; alternating schedule of different antipyretics may be required to provide relief of child s fever.
Administer medications punctually and at regular intervals to achieve constant therapeutic blood levels.
Report signs of increased rheumatic activity as salicylates or steroids are being tapered
Observe for the development or disappearance of any major or minor manifestations of the disease.
Monitor carditis by careful documentation of the child s pulse (sleeping pulse counted for 1 full minute), respirations, and blood pressure.
NURSING ALERT:
Do not place a child with an infectious disease in a room with a child with rheumatic fever.
Restrict visitors and personnel with infectious diseases from contact with the child on steroid therapy.
Make the family aware that a combination of steroid therapy and stress may lead to the development of gastric ulcers.
Administer antipyretics; alternating schedule of different antipyretics may be required to provide relief of child s fever.
Administer medications punctually and at regular intervals to achieve constant therapeutic blood levels.
Report signs of increased rheumatic activity as salicylates or steroids are being tapered
Observe for the development or disappearance of any major or minor manifestations of the disease.

Monitor carditis by careful documentation of the child s pulse (sleeping pulse counted for 1 full minute), respirations, and blood pressure.
Maintaining Comfort
Use bed cradle.
Reassure that arthritis is not destructive.
Change positions in bed often to decrease stiffness and decrease skin breakdown.
Support inflamed joints; handle gently.
Provide meticulous skin care.
Position the legs in good body alignment; use a foot board.
Elevate the back of the bed, and support the arms with pillows when child is dyspneic
Providing Safe, Supportive Care for the Child With Chorea :
Place the child in a bed with padded side rails, especially if uncontrolled body movements are severe.
Feed the child slowly and carefully because of uncoordinated movements of the head, mouth, and swallowing muscles.
Avoid the use of sharp eating utensils, and do not use straws.
Provide frequent feedings that are high in calories, protein, vitamins, and iron, because constant movements cause the child to burn calories at a rapid rate.
Spend time talking with the child even though speech may be defective. If severe, use other methods of communication.
Administer sedative, if prescribed.
Reassure the child about the cause of instability and that symptoms will subside.
Encourage positive parent–child relationships that may have been strained if the onset of symptoms was insidious (e.g., lack of concentration at school, mood swings, deteriorating handwriting, irritability ).
Help the child regain former skills once symptoms begin to subside.
Support the child during periods of ambulation.
Provide activities that require the use of large muscles, and progress to materials that require fine coordination.
Keep the environment calm, and provide increased periods of rest because movements increase with fatigue and increased excitement.
Cont. Nursing Interventions
Maintaining Bed Rest :
Complete or partial bed rest is encouraged.
Help the child understand the restrictions and that progress may be slow.
Initiate appropriate measures to help the child maintain level of development during the lengthy hospitalization.
Arrange for continuation of school and tutors
Facilitate interaction with family, including siblings.
Provide diversional activities that will help the child feel a sense of achievement or satisfaction. Offer quiet play, such as board games, television, radio, reading, and drawing.
Involve child life groups and physical and occupational therapy.
Facilitate contact with peers through writing, tape recording, telephone, or selected visitation.
Cont. Nursing Interventions
Reducing Anxiety for Child and Parent:
Explain ARF and its progression and management, such as the need for intravenous (IV) line and follow-up laboratory work.
Use honest, simple, age-appropriate explanations.
Give the child information about rheumatic fever in understandable terms; for example, "Rheumatic fever is a hard thing to understand because you can t see it. When you scratch yourself, you can see the mark, and you can see the scratch heal.
Rheumatic fever is something that you can t see the healing because it happens to the tissue underneath the skin (and sometimes it happens to the valves in the heart).
Assure the child that healthcare providers know how to treat rheumatic fever.
Communicate information about the child s reactions to all staff members to provide consistent information.
Children may be concerned that they have had a heart attack; reassure that their heart is functioning by letting them listen to it.
Allow the child and parent time to ask questions and express their concerns.
Allow the child to participate in decision making when possible.
Cont. Nursing Interventions
Family Education/Health Maintenance:
Initiate specific preventive teaching to prevent a recurrence or an additional case of rheumatic fever within the family.
Have all family members screened for Streptococcus by referring them for throat cultures.
All people with positive cultures should be treated.
Teach the specific symptoms of streptococcal infections and the need for antibiotics.
Prevent a recurrent attack of rheumatic fever by reinforcing the need for prophylactic antimicrobial therapy.
Penicillin is the drug of choice—either IM Benzathine penicillin G every 28 days, oral penicillin twice daily, or one daily dose of sulfadiazine (Microsulfon)
Continuous prophylaxis is recommended throughout the childhood years and well into adult life, often indefinitely.
Use creativity in recommending methods to remind families about administering the medication.
The child should be taught to assume responsibility for own medication at an early age so that it becomes habitual.
Some children profit from the use of a calendar or special chart. Others find it useful to associate their medication schedule with other routine tasks, such as brushing their teeth.
Encourage administration of prophylactic medication on schedule.
Advise on additional prophylaxis for prevention of infective endocarditic. The American Heart Association s recommendations for the prevention of endocarditic should be observed for children undergoing certain dental procedures and for surgery instrumentation of the upper respiratory tract, genitourinary tract, or lower gastrointestinal tract.
Begin to prepare for discharge early enough with the parents that sufficient adjustments and preparations may be made.
The child should have own bed and preferably own room.
A responsible adult must be in the home to care for child.
The child should have own bed and preferably own room.
A responsible adult must be in the home to care for child.
Provide information about activity restrictions, medications (dosage, schedule, and side effects), dietary instructions, symptoms to report (pain, malaise, anorexia, tachycardia, tachypnea, weight gain), telephone number of healthcare provider, follow-up appointment.
Initiate a community nursing referral; this may be done prior to discharge if a home evaluation is desired or if home care nursing is needed.
Offer financial consultation as available.
Instruct in additional measures to maintain health.
Complete immunization schedules
Regular medical and dental care
The need to seek immediate medical care for signs of streptococcal infections
Cont. Nursing Interventions
Evaluation:
1. Reduction in symptoms; no serious symptoms of medications
2. Stable vital signs; no signs of CHF
3. Patient comfortable as evidenced by unlabored respirations
and no complaints
4. Neurologic status improving and no injuries reported
5. Child coping effectively with activity restrictions
6. Anxiety reduced as evidenced by family cooperation and appropriate discussion of disease management