I.

INTRODUCTION
CONGENITAL HEART DISEASE
Congenital heart disease is a type of defect or malformation in one or more
structures of the heart or blood vessels that occurs before birth. These defects occur while
the fetus is developing in the uterus and affect 8-10 out of every 1,000 children. Congenital
heart defects may produce symptoms at birth, during childhood, and sometimes not until
adulthood.
Abnormally formed hearts alter the normal blood flow to the lungs and body. Either
the flow of blood gets re-routed (shunted) or a defective heart valve or a blood vessel
blocks the flow of blood.

Causes of Congenital Heart Defect

In the majority of people, the cause of congenital heart disease is unknown.
However, there are some factors that are associated with an increased chance of getting
congenital heart disease.

These risk factors include:

. Genetic or chromosomal abnormalities in the child such as Down syndrome.
. Taking certain medications or alcohol or drug abuse during pregnancy.
. Maternal viral infection, such as rubella (German measles) in the first trimester of
pregnancy.
. The risk of having a child with congenital heart disease is higher if a parent or a sibling
has a congenital heart defect -- the risk increases from eight in 1,000 to 16 in 1,000.

One third of infants born with CHD develop life-threatening symptoms within the first
few days of life. The infant mortality rate in these cases is as high as 90 percent. In as many
as 80 percent of infants with critical disease, congestive heart failure is the presenting
symptom.
Difficulty in feeding is common and is often associated with tachypnea, sweating
and subcostal retraction. Suspicion of CHD should be raised if feeding takes more than 30
minutes. A history of feeding difficulty often precedes overt congestive heart failure, even if
only by six to 12 hours. On examination, signs of congestive heart failure include an S3
gallop and pulmonary rales. Failure to recognize congestive heart failure as the cause of

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symptoms in infants with CHD often leads to misdiagnosis and treatment for septicemia.
The presence or absence of a heart murmur is unreliable as a basis for the
diagnosis of CHD. Transient murmurs are often heard in infants without cardiac
abnormalities. Furthermore, a murmur is not present in many severe forms of CHD, such as
tricuspid atresia, coarctation of the aorta and transposition of the great vessels. When a
murmur is associated with a cardiac defect, the intensity of the murmur is unrelated to the
severity of the abnormality. However, the nature of the murmur (harsh, blowing or musical),
along with other heart sounds, is useful in differentiating mild defects from severe
abnormalities.
Femoral and brachial pulses should be palpated. In infants with some obstructive
lesions of the left side of the heart, femoral pulses may be palpable, but one or both
brachial pulses may not be palpable.
Suspicion of cyanosis should be confirmed by pulse oximetry. When pulmonary
disorders are the cause of cyanosis, administration of 100 percent oxygen usually
increases the arterial oxygen saturation to at least 95 percent. In patients with cyanotic
CHD, oxygen saturation will only increase to 80 to 85 percent.

Types of Congenital Heart Problems

The most common congenital heart problems include:
• Heart valve defects. Narrowing or stenosis of the valves or complete closure that
impedes or prevents forward blood flow. Other valve defects include leaky valves that
don't close properly and allow blood to leak backwards.
• Defects in the walls between the atria and ventricles of the heart (atrial
andventricular septal defect). These defects allow abnormal mixing of oxygenated
and unoxygenated blood between the right and left sides of the heart. Heart muscle
abnormalities that can lead to heart failure.

ATRIAL SEPTAL DEFECT

Atrial Septal Defect is a form of congenital heart defect that enables blood flow between the
left and right atria via the interatrial septum. The interatrial septum is the tissue that divides
the right and left atria. Without this septum, or if there is a defect in this septum, it is
possible for blood to travel from the left side of the heart to the right side of the heart, or
vice versa. This results in the mixing of arterial and venous blood, which may or may not be

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clinically significant. This mixture of blood may or may not result in what is known as a
"shunt". The amount of shunting present, if any, dictates hemodynamic significance.

Cross-Section of a Normal Heart and a Heart With an Atrial Septal Defect

Figure A shows the normal structure and blood flow in the interior of the heart.
Figure B shows a heart with an atrial septal defect. The hole allows oxygen-rich blood from the left atrium to mix with oxygen-
poor blood from the right atrium.

In acyanotic patients with atrial septal defect (ASD), the direction of the shunt is
from left to right and the magnitude of the left-to-right shunt is determined by the size of the
defect and the relative compliance of the right ventricle (RV) and left ventricle (LV).
Because the compliance of the RV is greater than that of the LV, a left-to-right shunt is
present. The magnitude of the shunt is reflected in the degree of cardiac enlargement. Let it
be assumed that there is a left-to-right shunt of one arrow at the atrial level. As seen (Fig.
C), the right atrium (RA), RV, and main pulmonary artery (PA) and its branches have two
arrows and are therefore dilated.
These findings are translated into the chest x-ray films (Fig. D), which reveal

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enlargement of the RA, RV, and PA as well as an increase in pulmonary vascular markings.
Note that the left atrium (LA) is not enlarged. This is because the increased pulmonary
venous return to the LA does not stay in that chamber; rather, it is shunted immediately to
the RA. The absence of left atrial enlargement is one of the helpful x-ray signs for
differentiating an ASD from a ventricular septal defect (VSD).

Figure C. Block diagram of an atrial septal defect. The number of arrows in each chamber represents the amount of blood to
be handled by that particular chamber. When one redraws the chambers with two arrows larger than normal, one can predict
which will be enlarged.
Figure D. Posteroanterior and lateral view diagrams of chest roentgenograms. Enlargement of the right atrium (RA) and
pulmonary artery (PA) segment and increased pulmonary vascular markings are present in the posteroanterior view. The right
ventricular enlargement is best seen in the lateral view. AO, aorta; IVC, inferior vena cava; LA, left atrium; LAA, left atrial
appendage; LPA, left pulmonary artery; LV, left ventricle; RPA, right pulmonary artery; RV, right ventricle; SVC, superior vena
cava.

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 The dilated RV cavity prolongs the time required for depolarization of the RV
because of its longer pathway, producing a right bundle branch block (RBBB) pattern (with
rsR' in V1) in the ECG. The RBBB pattern in children with ASDs is not the result of actual
block in the right bundle. If the duration of the QRS complex is not abnormally prolonged,
the ECG may be read as mild right ventricular hypertrophy (RVH). Therefore, either RBBB
or mild RVH is seen on the ECG of children with ASD.

The heart murmur in ASD is not caused by the shunt at the atrial level. Because the
pressure gradient between the atria is so small and the shunt occurs throughout the cardiac
cycle, in both systole and diastole, the left-to-right shunt is silent. The heart murmur in ASD
originates from the pulmonary valve because of the increased blood flow (denoted by two
arrows) passing through this normal-sized valve, producing a relative stenosis of the
pulmonary valve (see Fig. C ). Therefore, the murmur is systolic in timing and is maximal at
the pulmonary valve area (i.e., at the upper left sternal border). When the shunt is large,
increased blood flow through the tricuspid valve (denoted by two arrows) results in a
relative stenosis of this valve, producing a diastolic murmur at the tricuspid valve area (i.e.,
lower left sternal border). The widely split S2 that is a characteristic finding in ASD results
partially from RBBB.

The RBBB delays both the electrical depolarization of the RV and the ventricular
contraction, resulting in delayed closure of the pulmonary valve. In addition, the large atrial
shunt tends to abolish respiration-related variations in systemic venous return to the right
side of the heart, resulting in a fixed S2. It should be noted that infants and small children

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rarely manifest with the clinical findings just described even in the presence of a moderately
large ASD (proved by echo studies) until they are 3 to 4 years of age. It is because the
compliance of the RV improves slowly so that any significant shunt does not occur until that
age.
Children with ASD rarely experience congestive heart failure (CHF), even in the
presence of a large left-to-right shunt. The PAs can handle an increased amount of blood
flow for a long time without developing CHF because there is no direct transmission of the
systemic pressure to the PA, and PA pressure remains normal. However, CHF and
pulmonary hypertension eventually develop in the third and fourth decades of life.

An ASD can be small or large. Small ASDs allow only a little blood to flow from one
atrium to the other. Small ASDs don't affect the way the heart works and don't need any
special treatment. Many small ASDs close on their own as the heart grows during
childhood. Medium to large ASDs allow more blood to leak from one atrium to the other,
and they're less likely to close on their own. Most children who have ASDs have no
symptoms, even if they have large ASDs.

PREVALENCE
ASD (ostium secundum defect) occurs as an isolated anomaly in 5 % to 10% of all
congenital heart defects. It is more common in females than in males (male/female
ratio of 1:2). About 30% to 50% of children with congenital heart defects have an
ASD as part of the cardiac defect.

CAUSES
ASDs occur during a baby's development in the mother's womb and are present at
birth. Before birth, the heart develops from a large tube, dividing into sections that will
eventually become its walls and chambers. If a problem occurs during this process, a hole
in the wall that divides the left atrium from the right may result.
In some cases, the tendency to develop an ASD may be inherited, or genetic. For most
people with an ASD, no one knows exactly why it happens.

PATHOLOGY
1. Three types of ASDs exist–secundum defect, primum defect, and sinus venosus
defect. Another rare form of defect is coronary sinus ASD. Patent foramen ovale (PFO)

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 does not ordinarily produce intracardiac shunts.

2. Ostium secundum defect is

the most common type of ASD,
accounting for 50% to 70% of all
ASDs. This defect is present at
the site of fossa ovalis, allowing
left-to-right shunting of blood
from the left atrium (LA) to the
right atrium (RA) (Fig E).
Anomalous pulmonary venous
return is present in about 10% of cases.

3. Ostium primum defects occur in about 30% of all ASDs, if those that occur as part of
complete ECD are included (see Fig. E). Isolated ostium primum ASD occurs in about
15% of all ASDs. This is discussed in greater detail in the section on partial ECD.

4. Sinus venosus defect occurs in about 10% of all ASDs. The defect is most
commonly located at the entry of the superior vena cava (SVC) into the RA (superior
vena caval type) and rarely at the entry of the inferior vena cava (IVC) into the RA
(inferior vena caval type). The former is very commonly associated with anomalous
drainage of the right upper pulmonary vein (into the RA), and the latter is often
associated with anomalous drainage of the right lung into the IVC.

5. In coronary sinus ASD, there is a defect in the roof of the coronary sinus and the LA
blood shunts through the defect and the coronary sinus ostium into the RA, which
produces clinical pictures similar to those in other types of ASD.

6. Mitral valve prolapse (MVP) occurs in 20% of patients with either ostium secundum
or sinus venosus defects.

SIGN AND SYMPTOMS

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The size of an ASD and its location in the heart determines what kind of symptoms a
person experiences. Most people with ASDs seem healthy and appear to have no
symptoms. Usually, a person with an ASD grows normally and feels well. People with
larger, more severe ASDs might experience some of the following signs or symptoms:
• poor appetite
• poor growth
• fatigue and tiredness during activity
• shortness of breath
• lung problems and infections, such as pneumonia

If an ASD isn't treated in childhood, health problems can develop later, including an
abnormal heart rhythm (know as an atrial arrhythmia) and problems in how well the heart
pumps blood. As kids with ASDs get older, they may also be at an increased risk for stroke,
since a blood clot that develops can pass through the hole in the wall between the atria and
travel to the brain. Pulmonary hypertension (high blood pressure in the lungs) may also
develop over time in older patients with larger untreated ASDs.

DIAGNOSIS
A pediatric cardiologist specializes in the diagnosis and medical management of
congenital heart defects, as well as heart problems that may develop later in childhood. The
cardiologist will perform a physical examination, listening to the heart and lungs, and make
other observations that help in the diagnosis. The location within the chest that the murmur
is heard best, as well as the loudness and quality of the murmur (harsh, blowing, etc.) will
give the cardiologist an initial idea of which heart problem your child may have. However,
other tests are needed to help with the diagnosis, and may include the following:

• Chest x-ray - a diagnostic test which uses invisible electromagnetic energy beams to
produce images of internal tissues, bones, and organs onto film. With an ASD, the heart may
be enlarged because the right atrium and ventricle have to handle larger amounts of blood
flow than normal. Also, there may be changes that take place in the lungs due to extra blood
flow that can be seen on an x-ray.
• Electrocardiogram (ECG or EKG) - a test that records the electrical activity of the heart,
shows abnormal rhythms (arrhythmias or dysrhythmias), and detects heart muscle stress.

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 • Echocardiogram (echo) - a procedure that evaluates the structure and function of the heart
by using sound waves recorded on an electronic sensor that produce a moving picture of the
heart and heart valves. An echo can show the pattern of blood flow through the septal
opening, and determine how large the opening is, as well as how much blood is passing
through it.
• Cardiac catheterization - a cardiac catheterization is an invasive procedure that gives very
detailed information about the structures inside the heart. Under sedation, a small, thin,
flexible tube (catheter) is inserted into a blood vessel in the groin, and guided to the inside of
the heart. Blood pressure and oxygen measurements are taken in the four chambers of the
heart, as well as the pulmonary artery and aorta. Contrast dye is also injected to more
clearly visualize the structures inside the heart. If the echocardiogram has provided enough
information, this procedure is often not needed to evaluate ASD.

TREATMENT
Specific treatment for ASD will be determined by your child's physician based on:

• Your child's age, overall health, and medical history.

• Extent of the disease.
• Your child's tolerance for specific medications, procedures, or therapies.
• Expectations for the course of the disease.
• Your opinion or preference.

Medical Management
1. Exercise restriction is unnecessary.
2. Prophylaxis for infective endocarditis is not indicated unless the patient has
associated MVP or other associated defects. Prophylaxis is indicated in patients
with primum ASD.
3. In infants with CHF, medical management is recommended because of its high
success rate and the possibility of spontaneous closure of the defect.

Nonsurgical Closure
Nonsurgical closure using a catheter-delivered closure device has become a
preferred method, provided the indications are met. Several closure devices that can be
delivered through cardiac catheters have been shown to be safe and efficacious for ASD
closure. These devices are applicable only to secundum ASD with an adequate septal rim.

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Devices available for clinical use have included the Sideris buttoned device, the Angel
Wings device, the CardioSEAL device, and the Amplatzer ASD Occlusion Device. Among
these, the Amplatzer Septal Occluder appears to enjoy widespread use.

Use of the closure device may be indicated to close a secundum ASD, measuring 5
mm or more in diameter (but less than 32 mm), and a significant left-to-right shunt with
clinical evidence of right ventricular volume overload (i.e., p/ s ratio o 1.5:1 or greater or RV
enlargement). There must be enough rim (4 mm) of septal tissue around the defect for
appropriate placement of the device. The timing of the device closure for secundum ASD is
not entirely clear. Considering the possibility of spontaneous closure, it is wise not to use
the device in infancy unless the patient is symptomatic with heart failure.

Advantages of nonsurgical closure include complete avoidance of cardiopulmonary

bypass with its attendant risk, avoidance of pain and residual thoracotomy scars, a less
than 24-hour hospital stay, and rapid recovery. All these devices are associated with a
higher rate of small residual leak than is operative closure.

Surgical Closure
Indications and Timing
1. Surgery is usually delayed until 2 to 4 years of age because the possibility of
spontaneous closure exists and because children tolerate the defect well.
2. If CHF does not respond to medical management, surgery is performed during
infancy, again if device closure is considered inappropriate.
3. If oxygen and other medical therapy are needed for infants with associated
bronchopulmonary dysplasia and the device closure is not considered appropriate,
surgery is performed during infancy.
4. High pulmonary vascular may be a contraindication for surgery.

Procedure
For secundum ASD, the defect is traditionally repaired through a midsternal incision

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under cardiopulmonary bypass by either a simple suture or a pericardial or Teflon patch.
Recently, so-called minimally invasive cardiac surgical techniques with smaller skin
incisions have become popular, especially for female patients.

For ASDs (including simple primum ASDs and sinus venosus defects), one of the
following techniques can be used: midline short transxiphoid incision with minimal sternal
split (preferred), transverse inframammary incision with vertical or transverse sternotomy, or
small lower midline skin incision with either partial or full median sternotomy. The benefit of
this technique appears to be an improved cosmetic result; it does not reduce pain, hospital
stay, or surgical stress.

For sinus venosus defect without associated anomalous pulmonary venous return,
the defect is closed using an autologous pericardial patch. When it is associated with a
pulmonary venous anomaly, a tunnel is created between the anomalous pulmonary vein
and the ASD by using a Teflon or pericardial patch. A plastic or pericardial gusset is placed
in the SVC to prevent obstruction of the SVC.

Alternatively, one may use the Warden procedure. In this procedure, the SVC is
divided above the level of the pulmonary venous entry. The cardiac end of the SVC is
oversewn, and a pericardial baffle is placed in such a way as to drain the pulmonary venous
blood through the sinus venosus ASD into the LA. The proximal SVC is sewn to the right
atrial appendage to drain the SVC blood to the RA.
For coronary sinus ASD, the ostium of the coronary sinus is closed with an
autologous pericardium with care to avoid conduction tissues, provided it is not associated
with persistent left SVC. This results in drainage of coronary sinus blood into the left atrium.

Mortality
Fewer than 0.5% of patients die; however, there is a greater risk for small infants
and those with increased pulmonary vascular resistance.

COMPLICATIONS

Over time, if an ASD isn't repaired, the extra blood flow to the right side of the heart and
lungs may cause heart problems. Usually, most of these problems don't show up until
adulthood, often around age 30 or later. Complications are rare in infants and children.

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Possible complications include:

• Right heart failure. An ASD causes the right side of the heart to work harder
because it has to pump extra blood to the lungs. Over time, the heart may become
tired from this extra work and not pump well.
• Arrhythmias. Extra blood flowing into the right atrium through an ASD can cause
the atrium to stretch and enlarge. Over time, this can lead to arrhythmias (irregular
heartbeats). Arrhythmia symptoms may include palpitations or a rapid heartbeat.
• Stroke. Usually, the lungs filter out small blood clots that can form on the right side
of the heart. Sometimes a blood clot can pass from the right atrium to the left atrium
through an ASD and be pumped out to the body. This type of clot can travel to an
artery in the brain, block blood flow, and cause a stroke.
• Pulmonary hypertension (PH). Pulmonary Hypertension is increased pressure in
the pulmonary arteries. These arteries carry blood from your heart to your lungs to
pick up oxygen. Over time, PH can damage the arteries and small blood vessels in
the lungs. They become thick and stiff, making it harder for blood to flow through
them.

COMMUNITY-ACQUIRED PNEUMONIA (CAP)

Community-acquired pneumonia (CAP) is a disease in which individuals who have not
recently been hospitalized develop an infection of the lungs (pneumonia). CAP is a
common illness and can affect people of all ages. CAP often causes problems like difficulty
in breathing, fever, chest pains, and a cough. CAP occurs because the areas of the lung
which absorb oxygen (alveoli) from the atmosphere become filled with fluid and cannot
work effectively.

Pneumonia is a form of infection that affects the lungs and this infection may be
caused by a variety of different organisms. Even newly born babies as young as 2 to 3
months old may develop pneumonia and this is called infant pneumonia. Such pneumonia
may occur due to group B streptococcus or respiratory syncytial virus. Older babies may
get pneumonia due to viral or bacterial infections.

Doctors normally classify pneumonia in two categories and these include bacterial

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and viral pneumonia. If the baby is afflicted with bacterial pneumonia then the symptoms
may develop rather suddenly. The symptoms associated with this form of infant pneumonia
include high fever, coughing along with rapid breathing. The infant will not want to eat and
may seem extremely unwell or ill. The infant may have problems in breathing and flaring
nostrils or sinking in of chest while breathing can be one of the signs associated with this
condition.

In infant pneumonia the child may be extremely weak and may suffer from diarrhea
or vomiting. The pulse may be fast and the nails and lips of the child may become blue. In
most cases streptococcus pneumoniae bacteria are responsible for this condition but in
some cases Chlamydia pneumoniae and staphylococcus aureus may also be responsible.

Viral pneumonia is also a form of infant pneumonia and this normally starts out in
the form of a cold. Over some time the symptoms get worse and the baby might have
around 101.5 degrees Fahrenheit fever. The baby may also have cough that may worsen
along with rapid breathing and wheezing. The pneumonia may also be accompanied with
other problems such as vomiting, diarrhea and weakness. Viral form of pneumonia is
normally less severe as compared to bacterial pneumonia.

While viral pneumonia cannot progress into bacterial pneumonia it can increase the
susceptibility of the infant towards the bacterial form of disease. The viruses responsible for
this form of pneumonia include parainfluenza virus, flu virus, adenovirus and respiratory
synctial virus (RSV). The breathing of the infant is checked by the doctor and a stethoscope
is used to listen to the breathing sounds so as to detect any abnormal noise.

Infant pneumonia causes the child to breathe rapidly so as to take in greater

amounts of oxygen as the air sacs within the lungs might be filled with fluid. Certain tests
may be conducted for diagnosis of this condition and these include blood work, chest X-ray.
Likewise the nose fluid of the infant may also be examined.

The treatment of infant pneumonia is dependent on the extent of sickness of the

child. In case of bacterial pneumonia the doctors may prescribe certain antibiotics. Viral
pneumonia does not respond to the antibiotic treatment and this form of pneumonia may be
treated by taking enough fluids along with rest. In fact replenishing fluids is extremely
crucial so that the child does not get dehydrated due to the fever and rapid breathing that is
observed in pneumonia.

Some other things that can be done in infant pneumonia include using a humidifier
(cool mist) in the child’s room. Based on the doctor’s advice acetaminophen can be

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administered in some cases. A cough medication based on the doctor’s prescription may
also be given to the child. In some cases treatment for bacterial pneumonia may require
hospitalization of the infant.

In many cases the uncomplicated forms of pneumonia can get better in a week’s
time even though the cough may last for some time. If the infant is admitted in the hospital
then the blood oxygen level may be checked through a device called pulse oximetry sensor.
A nasal oxygen mask may also be used so as to facilitate the breathing process. Antibiotics
may be administered through IV and the infant may be given large amount of fluids.

COMPLICATIONS
Despite appropriate antibiotic therapy, severe complications can result from CAP, including:
• Sepsis - Sepsis can occur when microorganisms enter the blood stream and
the immune system responds. Sepsis most often occurs with bacterial
pneumonia; Streptococcus pneumoniae is the most common cause. Individuals with
sepsis require hospitalization in an intensive care unit. They often require
medications and intravenous fluids to keep their blood pressure from going too low.
Sepsis can cause liver, kidney, and heart damage among other things.
• Respiratory failure - Because CAP affects the lungs, often individuals with CAP
have difficulty breathing. If enough of the lung is involved, it may not be possible for
a person to breathe enough to live without support. Non-invasive machines such as
a bilevel positive airway pressure machine may be used. Otherwise, placement of
a breathing tube into the mouth may be necessary and a ventilator may be used to
help the person breathe.
• Pleural effusion and empyema - Occasionally, microorganisms from the lung will
cause fluid to form in the space surrounding the lung, called the pleural cavity. If the
microorganisms themselves are present, the fluid collection is often called
anempyema. If pleural fluid is present in a person with CAP, the fluid should be
collected with a needle (thoracentesis) and examined. Depending on the result of
the examination, complete drainage of the fluid may be necessary, often with
a chest tube. If the fluid is not drained, bacteria can continue to cause illness
because antibiotics do not penetrate well into the pleural cavity.
• Abscess - Rarely, microorganisms in the lung will form a pocket of fluid and
bacteria called an abscess. Abscesses can be seen on an x-ray as a cavity within

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 the lung. Abscesses typically occur in aspiration pneumonia and most often contain
a mixture of anaerobic bacteria. Usually antibiotics are able to fully treat abscesses,
but sometimes it must be drained by a surgeon or radiologist.

MALNUTRITION
Malnutrition is the insufficient, excessive or imbalanced consumption of nutrients. A
number of different nutrition disorders may arise, depending on which nutrients are under or
overabundant in the diet.
Malnutrition may result from:
• Consuming too little food.
• Storage of key nutrients.
• Impaired absorption or metabolism due to disease.
Signs of Severe Malnutrition
• Severe wasting – A child with severe wasting has lost fats and muscle and appears
like skin and bones
• Edema
• Dermatosis
• Eye signs (in the form of Pus and Inflammation, bitot’s spot, corneal clouding and
corneal ulceration)
• Stunting – unusually low height or length for age

Health Maintenance Issues

Growth impairment of infants with acyanotic CHD is directly proportional to the
severity of the hemodynamic disturbance. The most severely affected infants are those with
congestive heart failure. Acyanotic lesions tend to jeopardize weight gain rather than height,
whereas cyanotic lesions tend to affect both height and weight.
Infants with CHD and growth impairment typically show caloric deprivation and a
reduction in adipose stores. Boys are usually more malnourished than girls. Anorexia and
early satiety may be exacerbated by the drugs, such as diuretics, that are administered for
the treatment of congestive heart failure. However, in the absence of congestive heart
failure, a large left-to-right shunt or cyanosis, other causes of failure to thrive should be
explored.

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 Many factors contribute to growth impairment in infants with CHD, including a lower
than normal birth weight, increased caloric requirements and the presence of concomitant
musculoskeletal, central nervous system, renal or gastrointestinal malformations. Mild
gastrointestinal abnormalities, mild steatorrhea and excess protein loss are common in
infants with CHD. Up to 30 percent of infants with CHD have features of various genetic
syndromes. Some of these syndromes, such as fetal alcohol syndrome, are probably under-
diagnosed.
Poor nutrition related to anorexia, fatigability, vomiting, fluid restriction and frequent
respiratory infections also contributes to growth impairment. Systemic and respiratory
illnesses increase the body temperature and the metabolic rate. The metabolic rate can
increase up to 13 percent for each degree centigrade over normal temperature.
Hypertrophic cardiac muscle can use up to 30 percent of the total oxygen consumption of
the body rather the usual 10 percent. After accounting for other energy needs, infants with
CHD may have only one half as much energy available for growth as healthy infants.
In infants who are unable to gain sufficient weight with breast feeding,
supplementation options include a formula with a high caloric density, nocturnal enteral
feeding or continuous 24-hour feeding with a nasogastric or duodenal tube. The latter is the
most effective form of supplementation. A caloric intake of 140 to 200 calories per kg per
day is needed to induce catch-up growth.
Routine childhood health maintenance visits should be scheduled. More frequent
evaluations are needed if congestive heart failure or other problems are present.

A. OBJECTIVES OF THE STUDY

A1. GENERAL OBJECTIVES

The main goal of this case presentation is to enhance our nursing knowledge, skills
and attitudes while conducting a study of the proponents of congenital heart disease
particularly atrial septal defect and right ventricular failure and its relation to
community acquired pneumonia and severe malnutrition.

A2. SPECIFIC OBJECTIVES

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 1. To gather pertinent data from the patient’s chart and the patient’s mother
through interview and assessment.
2. To conduct a thorough physical assessment as a part of the basic baseline
data gathering.
3. To review the anatomy and physiology of the affected areas of the body.
4. To trace the pathophysiology of congenital heart disease, community
acquired pneumonia and severe malnutrition.
5. To obtain, analyze and interpret the patient’s laboratory exams and its
significance to the case.
6. To identify and study prescribed drugs to the patient.
7. To formulate a nursing care plan and health teaching that is appropriate for
the patient’s current condition.

B. DEMOGRAPHIC DATA
B.1. PATIENT’S PROFILE:
Patient Name: Baby K
Address: P.92 Mag Asawang Ilat, Tagaytay City
Date of Birth: October 29, 2009
Age: 9 Months
Sex: Male
Mother: Mommy X
Occupation: Unemployed
Educational Background: HS Graduate

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Father: Daddy Y
Occupation: Tricycle Driver
Educational Background: HS Undergraduate

B.2. CLINICAL DATA

Hospital Name: Dr. Jose Fabella Memorial Hospital
Date/Time Admission: June 25, 2010/10:00 pm
Admitting Diagnosis:
Congenital Heart Disease: Arterial Septal Defect; Primum Large
Right Ventricular Failure
Pneumonia, Severe
Malnutrition, Severe
Admitting Physician: Dr. Rubio
Chief Complain: Cyanosis
Admitted: 7 months age
Weight: 5kg
Vital Signs on Admission: Temperature: 37.3 Pulse:148 bpm
Respiration: 50cpm
Anthropometric: ABW 5 kg <p3 HC 39 cm <p3
CC 35 cm H 61 cm <p3
AC 19
Attending Physician: Dr. Marasigan/ Dr. Magno
Date Discharged: August 13, 2010

B3. MEDICAL HISTORY

HISTORY OF PRESENT ILLNESS:
 Patient was born at home through a “hilot” to a 36 years old G3P3 (3003) with 3-4
times pre natal check-up, she had no cough and colds at unrecalled AOG, TT, no
intake of multivitamins and FeSO4 no exposure to any teratogen. Patient was born
at home assisted by midwife no PROM with circumoral cyanosis, no any consults
done with regard to cyanosis.
 At 1 month old patient breastfeed circum oral, cyanosis was still noted and yellow
color of sclerae, skin pale, noted dyspnea when breastfeeding; no consult was done

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  At 2nd month old condition was still the same no consult done
 at 3rd month cyanosis of the lips still present consulted at a private hospital with
apparently no significant heart finding
 At 4th month still with cyanosis, no consult done, still being breastfeed, mvi started
at 10.3 ml
 At 5th month of age patient has episode of fever, 1st episode of convulsion and still
with cyanosis consulted at the same private hospital, but was sent home with
dicycloverin, Amoxicillin, paracetamol, and was advised New Born Screening but
due to financial problem it was not availed, patient then was sent home; seizure and
fever didn’t occur.
 At 6th month old cyanosis of lips still persisted. Skin was noted to be pale,
jaundice, still no consult done
 At 7th months age (1 week PTA) cyanosis more persisted consulted at hospital in
Tagaytay due to recurrent cough, then was also noted fever of low grade
undocumented no other. CXR was done revealed heart megaly.
 1 day PTA feet were noted with edema, marked fatigue when breastfeeding, very
poor suck and decreased demand for breastfeeding, there was referral to a
Cardiologist.

Immunization: BCG, DPT-3 doses, Hepa B-3 doses

(-)Measles
Nutrition History: Breastfeed still present; can not tolerate soft fluids

Growth & Development: Snuled (birth)

Hold Head (4-5)
Sat with support
Rolled over (side ways only 7 months)
Stood with support
System Review: CNS (-) seizure
PSPI (+) cough; (+) Pleghm; (+) rales
GIT (-) LBM (-) vomitus
GUT (+) no low amount

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HISTORY OF PAST ILLNESS
Previous Admission: Admitted at 7 months age
Chief Complain: Difficulty in breathing
Surgical History: No previous surgeries
Family History: Allergy Asthma (paternal)
Renal Disease (maternal)
Hypertension (both)
Asthma (eldest sister)
CHD (none)
Psychosocial History:
Baby Kyle lives in a two storey house with two bedrooms at Purok 92, Tagaytay City with
his parents and two siblings, a sister and a brother now eight (8) and nine (9) years old
respectively. His father works as a tricycle driver and his mother is a plain housewife.
Work and money was considered as primary stressor and their ways of coping are
laughing and spending time with neighbors, minimal play with his siblings because he was
sick and tired most of the time and watching television.

D. PHYSICAL ASSESSMENT
General Assessment
Vital Signs taken on July 12, 2010 @ 8:00a.m.
Temperature: 37.3 C
Pulse Rate: 136 bpm
Respiratory Rate: 45 cpm
O2 Saturation: 97% (with Nasal Cannula)
D. HEAD –TO – TOE PHYSICAL ASSESSMENT
Head, Eyes, Ears, Nose & Throat
Head circumference larger than ideal for age; Clean scalp, symmetrical head; Anterior
Fontanel palpable1cm wide, 2cm long and flat; posterior fontanel closed; slightly surplus
eyeball, pale conjunctiva; no nasal flaring, moist lips with circumoral cyanosis; sapple neck.

Chest & Lungs

Symmetrical chest; barrel chest; intercostals intact; (+) fine rales, (-) Light brown nipples, no
enlargement and discharges; (-) wheezes; abdominal breather; (+) murmur

Abdomen:

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Globular, non active, no visible signs of veins, Levin edge 1-2 cm subcostal area; No
bruises, hematomas, abrasions, lacerations, fractures, unusual markings, etc. on abdomen;
slightly jaundiced skin warm but not feverish to touch; spleen tip palpable (smooth); left
kidney border palpable (smooth).

Genitalia: Male, no hydrocele, no rashes

Rectal: no rashes

Extremities:
Legs same length and symmetrical; positive pedal edema grade 1, full pulses, positive
circumoral cyanosis, jaundiced skin, cyanosis on fingertips.

Neuro: No head lag noted.

D. DIAGNOSIS
Date Discharged: August 13, 2010
Medical Diagnosis:
Congenital Heart Disease: Atrial Septal Defect (Primum Large)
Right Ventricular Failure
Pneumonia, Severe
Malnutrition, Severe

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