Pathophysiology:

>Pleural Effusion
Pleural effusion, which in pediatric patients most commonly results from an infe
ction,
is an abnormal collection of fluid in the pleural space. Pleural effusion develo
ps
because of excessive filtration or defective absorption of accumulated fluid.
Pleural effusion may be a primary manifestation or a secondary complication of m
any disorders.
The etiologic mechanisms involved in the formation of most pleural effusions
include pleural space infection (empyema), abnormal capillary permeability
(exudates), increased hydrostatic or decreased oncotic pressure in the setting o
f
normal capillaries (transudates), abnormal lymphatic clearance (exudates), and
blood in the pleural space (hemothorax).
In children, infection is the most common cause of pleural effusion. Congestive
heart failure constitutes the second most common etiology, followed by malignanc
y.
In a Canadian study of 127 children with pleural effusion, about 50% of
effusions were parapneumonic, 17% were caused by congestive heart failure, 10%
were caused by malignancy, 9% were caused by renal disease, 7% were caused by
trauma, and 6% were associated with other causes.
In another North American report of 210 children admitted with pleural effusion,
Hardie et al showed that 68% of the effusions were parapneumonic (50 of 143
associated with empyema), 11% were caused by congenital heart disease, 5% were
caused by malignancy, and 3% were associated with other causes.
>Congenital Diaphragmatic Hernia (CDH)
The pathophysiology of CDH involves pulmonary hypoplasia, pulmonary hypertension
, pulmonary immaturity, and potential deficiencies in the surfactant and antioxi
dant enzyme system.
Because of bowel herniation into the chest during crucial stages of lung develop
ment, airway divisions are limited to the 12th to 14th generation on the ipsilat
eral side and to the 16th to 18th generation on the contralateral side. Normal a
irway development results in 23-35 divisions. Because airspace development follo
ws airway development, alveolarization is similarly reduced.
Development of the pulmonary arterial system parallels development of the bronch
ial tree, and therefore, fewer arterial branches are observed in CDH. Abnormal m
edial muscular hypertrophy is observed as far distally as the acinar arterioles,
and the pulmonary vessels are more sensitive to stimuli of vasoconstriction. Pu
lmonary hypertension resulting from these arterial anomalies leads to right-to-l
eft shunting at atrial and ductal levels. This persistent fetal circulation lead
s to right-side heart strain or failure and to the vicious circle of progressive
hypoxemia, hypercarbia, acidosis, and pulmonary hypertension observed in the ne
onatal period.
The surfactant system is demonstrably deficient in the lamb model of CDH.Postnat
al administration of surfactant in these lambs is associated with dramatic incre
ases in gas exchange, lung compliance, and pulmonary blood flow. However, in hum
an neonates, reports on the status of the surfactant system are inconsistent.

Infants with CDH also have impairment of the pulmonary antioxidant enzyme system
and are more susceptible to hyperoxia-induced injury.
In addition, a left ventricular smallness and hypoplasia are observed with CDH.
This is believed to arise from decreased in-utero blood flow to the left ventric
le, the mechanical compression of the herniated viscus similar to that observed
in the lungs, and/or a primary yet unidentified developmental defect that simult
aneously causes the diaphragmatic hernia and the lung problems.
>Community Acquired Pneumonia
Pneumonia develops subsequent to the invasion and overgrowth of a pathogenic mic
ro-organism in the lung parenchyma, which overwhelms host defences and produces
intra-alveolar exudates.
The development and severity of pneumonia is a balance between pathogen factors
(virulence, inoculum size) and host factors. The likely microbial causes of CAP
differ according to a number of factors, including differences in local epidemio
logy, the setting (outpatients, hospitalised, or ICU), severity of disease, and
patient characteristics (e.g., sex, age, and comorbidities).
Microbes that are present in the upper airways can enter the lower airways by mi
croaspiration. Nevertheless, the defence mechanisms of the lungs (innate and acq
uired) keep the lower airways sterile. The development of pneumonia indicates a
defect in host defences, exposure to a particularly virulent micro-organism, or
a large inoculum size.
Impaired immune response (e.g., caused by HIV infection or advanced age) or dysf
unction of defence mechanism (e.g., through current or passive smoking, COPD, or
aspiration) leads to greater susceptibility to respiratory infections in patien
ts.
Pathogens can reach the lower respiratory tract by 4 mechanisms:
Inhalation, a common route of entry for viral and atypical pneumonia in younger
healthy patients. Infectious aerosols are inhaled into the respiratory tract of
a susceptible person to initiate infection
Aspiration of oropharyngeal secretions into the trachea, the primary route throu
gh which pathogens enter the lower airways
Haematogenous spread from a localised infected site (e.g., right-sided endocardi
tis)
Direct extension from adjacent infected foci (e.g., tuberculosis can spread cont
iguously from the lymph nodes to the pericardium or the lung, albeit rarely).
Anatomy:
>Pleural Effusion
The inner surface of the chest wall and the surface of the lungs are covered by
the parietal and visceral pleura, respectively. The small amount of fluid (< 1 m
L) between the parietal and visceral pleura in humans forms a thin layer about 1
0 L thick.The protein concentration in the pleura is similar to that of the inter
stitial fluid. Compared with the interstitial fluid in humans, the pleural fluid
has a higher level of bicarbonate, a lower level of sodium and large molecularweight proteins (eg, lactate dehydrogenase [LDH]), and a similar level of glucos
e.

The cells in pleural fluid in healthy humans are small in number and are mostly
macrophages with few lymphocytes and RBCs. In disease state, these parameters ch
ange and large amounts of fluid can accumulate in the pleural space.
The amount of fluid in the pleural space is regulated through a delicate balance
between the oncotic and hydrostatic pressures of the pleural space and the capi
llary intravascular compartments and pleurolymphatic drainage. Chest wall and di
aphragmatic movements enhance absorption of excess pleural fluid, large particle
s, and cells through preformed stomas.
>Congenital Diaphragmatic Hernia (CDH)
The diaphragm is a musculotendinous structure that separates the thoracic cavity
from the abdominal cavity. It is composed of a central nonmuscular portion (cen
tral tendon) surrounded by a muscular rim in addition to the right and left diap
hragmatic crura. The right and left diaphragmatic crura are two muscular bands t
hat originate from vertebral bodies L1-L3 and L1-L2, respectively. These muscula
r bands insert into the dorsomedial diaphragm.
Most diaphragmatic defects are posterolateral, with 85-90% of these occurring on
the left. The label posterolateral may be a misnomer because it is frequently t
he case that much larger areas of the diaphragm are missing and only a posterior
rim of muscle can be found. A hernial sac is present in 10-20% of cases.
The Morgagni defect occurs posterior to the sternum and results from failure of
sternal and costal fibers to fuse at the site where the superior epigastric arte
ry crosses the diaphragm. The Morgagni defect is rare and is rarely a cause for
surgery in the newborn.
>Community Acquired Pneumonia
Pneumonia is an infection of the lung parenchyma. Community-acquired pneumonia r
efers to pneumonia acquired outside of hospitals or extended-care facilities. Nu
rsing homeacquired pneumonia refers to infection acquired in an extended-care fac
ility. Nosocomial pneumonia and hospital-acquired pneumonia describe infections
acquired in the hospital setting. The signs and symptoms of acute pneumonia deve
lop over hours to days, whereas the clinical presentation of chronic pneumonia o
ften evolves over weeks to months.
Nursing Management:
>for Congenital Diaphragmatic Hernia
- instructed the mother to add calories because increased work of breathing requ
ires effort and uses energy. Additional calories can be given by offering more f
eedings, more concentrated feedings, or adding calorie supplements to feedings.
- advised the mother to give vitamins as ordered
- oxygen theraphy @2LPM was given as ordered
- positioned the patient at high-fowlers position to ease difficulty of breathin
g
>for Pleural Effusion
- Elevate head of the patient to promote lung expansion
- Encourage patient to perform deep breathing exercises to promote lung expansio
n
- Provide relaxing environment to promote adequate rest periods to limit fatigue
- Administer supplemental oxygen as ordered to maximize oxygen available for cel
lular uptake

- Maximize respiratory effort with good posture and effective use if accessory m
uscles to promote wellness
- Encourage adequate rest periods between activities to limit fatigue
>for CAP
- Assess the rate and depth of respirations and chest movement. Tachypnea, shall
ow respirations, and asymmetric chest movement are frequently present because of
discomfort of moving chest wall and/or fluid in lung.
- Auscultate lung fields, noting areas of decreased or absent airflow and advent
itious breath sounds: crackles, wheezes. Decreased airflow occurs in areas with
consolidated fluid. Bronchial breath sounds can also occur in these consolidated
areas. Crackles, rhonchi, and wheezes are heard on inspiration and/or expiratio
n in response to fluid accumulation, thick secretions, and airway spams and obst
ruction.
- Elevate head of bed, change position frequently. Doing so would lower the diap
hragm and promote chest expansion, aeration of lung segments, mobilization and e
xpectoration of secretions.
-Teach and assist patient with proper deep-breathing exercises. Demonstrate prop
er splinting of chest and effective coughing while in upright position. Encourag
e him to do so often. Deep breathing exercises facilitates maximum expansion of
the lungs and smaller airways. Coughing is a reflex and a natural self-cleaning
mechanism that assists the cilia to maintain patent airways. Splinting reduces c
hest discomfort and an upright position favors deeper and more forceful cough ef
fort.
- Force fluids to at least 3000 mL/day (unless contraindicated, as in heart fail
ure). Offer warm, rather than cold, fluids. Fluids, especially warm liquids, aid
in mobilization and expectoration of secretions.